Oakes Academy Tip

As you review airway clearance, it is important to remember that this is the Critical Care exam.
There are unlikely to be that many questions in this area, so just do a basic review of the
information.
Choosing an option is not a difficult task. Be sure to know whether each can be used on
intubated or non-intubated patients. When possible, use less invasive methods first (IPV is
preferred over nasotracheal suctioning, for example). Also, pay attention to anything that suggests
a contraindication to the individual therapy (Ex: low platelets = don't nasotracheal suction, choose
IPV over it).

What This Section Might Cover:

 Recognition of a patient who needs airway clearance, usually due to some level of
respiratory distress.
 Recommendation of a therapy (with close attention to indications, hazards,
contraindications)
 Troubleshooting therapy in progress (such as a desaturation during intrapulmonary
percussive ventilation)
 Evaluating the effectiveness of a therapy, and whether modifications are needed

Equipment/Procedures You Should Recognize:

 Postural drainage (don't worry about memorizing all the position names)
 Intrapulmonary percussive ventilation (IPV)
Provide oscillations aimed towards the insides of the airways (CPT on the inside!), which
can be used in non-intubated patients or intubated patients. Contraindications include
bronchospasm, lung contusion, pneumothorax, pulmonary hemorrhage, subcutaneous
emphysema.
 Mechanical cough assist
This is preferred when a patient doesn't have the mechanical ability to cough, due to
neuromuscular weakness, quadriplegia, etc. This can not be used on intubated patients
without removing them from the ventilator. Be cautious with people who are at risk for
pneumothorax (bullous emphysema, for example).
 Therapeutic bronchoscopy
This is an often preferred choice for intubated patients where the source and scope of
secretions is helpful, or where there are signs/symptoms of mucous plugging (refractory
hypoxemia, worsening lung compliance). The procedure is referred to as a bronchial
alveolar lavage (BAL).
 Abdominal Thrusts
For patients showing signs/symptoms of choking
 Nasotracheal suctioning
Obviously invasive, should not be used as a first resort for most patients
 Intubation
Remember that intubation can be used to facilitate airway clearance when it is
clinically apparent that a patient cannot adequately manage their own secretions, or if the
patient has a high risk of aspiration. Do not consider noninvasive ventilation
when airway clearance is a concern (it is contraindicated).

Signs That Indicate Need

 Sputum
o Increase or decrease in production
 o Consistency (thick is a problem, for example)
 Auscultation (coarse crackles, rhonchi, decreased, maybe wheezing [unilateral])
 Vitals (Tachycardia, Tachypnea usually. Note: If bradypnea, bradycardia, the situation is
emergent!)
 Shortness of breath and/or increased work of breathing (dyspnea)
 ↑ Respiratory tract infections and fever
 ↓ SpO2 and/or worsening ABG (respiratory acidosis with hypoxemia)
 Secretions - ↓ or ↑, thick or discolored
 Chest X-ray changes (decreased volumes, hazy, infiltrates)

Choosing the BEST Option:

 Be progressive: start with the least invasive acceptable therapy and then move up from
there. Be very aware of hazards (if the patient is on heparin, for example, avoid
nasotracheal suctioning which might lead to excessive bleeding).
 Be aware of changing patient status (hemoptysis, hypotension, etc.) that may be a result of
the therapy. Usually you should stop use of that therapy in the presence of significant
adverse reactions

Oakes Academy Tip

Assess the airway! You should put your radar goggles on before taking the exam,
paying very close attention to words that might suggest a difficult airway. In
scenarios, be looking for key terms. Mallampati scores are often mentioned on the
exam, so be aware of scoring system.

Identify risk factors

 History of difficult intubations
 Limited range of motion (trauma, surgery)
 Airway edema
 Anatomic (disability of the jaw or oral cavity)

Management
 Be hyper-aware of alternative intubation techniques, like fiberoptic intubation,
retrograde intubation, awake intubation. Be hesitant to choose options that are
"everyday" choices - you need to address the difficult airway.
 During ACLS: there is a de-emphasis on the need to intubate during a code as long as you
are able to adequately bag-mask ventilate.
 Be very aware of cervical injuries when making a choice to intubate. Do not do anything
that would extend the neck (like direct visualization of the vocal cords by laryngoscope).
Whatever choice you make, protect the injury!

What This Section Might Cover:

 You may be asked to calculate a Mallampati score (no more than a question or two)
 You will be asked to determine if the patient has a difficult airway or not using the score
(and what to do about it)

Equipment/Procedures You Should Recognize:

  Patient must be awake and cooperative
 Performed with patient sitting, head in a neutral position, mouth wide open and tongue
protruding to its maximum. The patient cannot be actively phonating.(voicing sounds - this
moves around the landmarks and an accurate classification cannot be obtained).

Visualizations Interpretation

Class Visibility of hard palate, soft palate, uvula, and

1 tonsils
Indicative of potential for NORMAL intubation
Class Visibility of hard palate, soft palate,
2 upper portion of uvula and tonsils

Class Visibility of hard palate, soft palate, and base of

3 uvula
Indicative of potential for DIFFICULT intubatio
Class carefully
Only hard palate is visible
4

Choosing the BEST Option:

 Remember: if Mallampati is 3 or 4, intubate using specialty equipment (1 or 2 = normal

tube; 3 or 4 = gotta do more!)
Thyromental Distance

Measurement from thyroid notch to the tip of the jaw with the head extended.

 < 6 cm = difficult intubation

 7+ = uncomplicated (easier) intubation

In general the Mallampati score is seen as BETTER than thyromental distancing.

ACCS: Cricoid pressure

What This Section Might Cover:

 This is pretty straightforward - you would be offered the option to apply cricoid pressure,
usually while bagging or intubating.

Equipment/Procedures You Should Recognize:

 This involves placing pressure on the cricoid cartilage with the goal of occluding the
esophagus in order to decrease the risk of aspiration.

Choosing the BEST Option:

 Use of cricoid is recommended in patients who are unable to protect their own airway to
prevent aspiration. So, if the patient is unconscious and you are asked to bag or intubate,
use cricoid if offered it.
Oakes Academy Tip
Use tube exchangers anytime there is an indication to change out an endotracheal tube. Using an
exchanger is preferable to extubating and reintubating. Examples of good times to recommend use
include cuff integrity issues (pilot balloon, pilot balloon line, cuff), tube integrity issues (occlusions
like mucus plugging), improper size ET Tube (usually too small), wrong type of tube (e.g. tube with
metal for a patient going to MRI).

What This Section Might Cover:

 Some type of scenario where an issue with the artificial airway is present. You will be
asked to recognize that a tube exchange needs to occur, and what equipment is MOST
appropriate.

Equipment/Procedures You Should Recognize:

 Airway exchange catheter (Cook Catheter for those who know that term better - the exam
uses the more generic airway exchange catheter). Has a ventilation/oxygenation port.
 Gum elastic bougie: Aids in intubation, good for difficult airways, does not have the ability
to ventilate/oxygenate until ET Tube has been replaced.
 Flexible bronchoscopy: This visualizes the airway, but does provide a "route" to exchange
the tube. It is not the preferred for tube exchange but may be considered when other
options are not available. It is seen as a better option than simply using a direct
laryngoscopic intubation technique.

Choosing the BEST Option:

 Airway exchange catheters allow for ventilation/oxygenation once in so are usually

preferable to a bougie. A bougie is a good option if airway exchange catheter isn't
available.
 Use something! The least safe way to perform a tube exchange is to extubate and
reintubate. Look for the option that uses a device to make the procedure safer.
How The Exam Will Attempt to Deceive You:

 You may not always be offered the "ideal" (airway exchange catheter), so knowing other
methods (hello, bougie) is important.

Oakes Academy Tip

Do not spend time Googling and memorizing the various types of trachs. Instead,
focus on the key types that alter how you would normally do something (for example,
recognizing that a proximal trach might be required for a morbidly obese patient).

What This Section Might Cover:

 Scenarios or questions that expect you to identify when a specialty airway is needed (such
as distal vs. proximal)
 Scenarios or questions that expect you to know how you would alter normal procedures
(such as placing a cuffed trach to ventilate)

Choosing Equipment/Procedures:

 Metal trach: Don't take to MRI (obvious, right?)

 Fenestrations: Used in weaning for moving air through the vocal cords/upper airway
 Cuff Types: Avoid using foam cuffs with a PMV if given option
 Trach Lengths: Distal (for abnormal airways, tumors, tracheomalacia, etc.) vs. Proximal
(usually for obese necks)
 Tight-to-shaft (TTS): Used for patients ready for weaning as well as speaking as the cuff
lays tight against the trach tube allowing for air to move past the tube
 Foam cuff: Good for tracheomalacia, cuff expands to the diameter of the trachea without
putting a lot of pressure on trachea wall
 Uncuffed Trach: Replace with cuffed trach if needing to ventilate

Specialty Endotracheal Tubes

Subglottic suction endotracheal tube

 Port above cuff allows for suctioning of secretions through a specialized channel built into
the endotracheal tube
 Several different names, with the following being the most common:
o Suction above cuff ETT
o Hi-Lo Evac ETT
o Evac ETT
o Subglottic secretions drainage ETT
o Microcuff® Subglottic Suctioning ETT (can use saline to clear clogs in the line)
 Uses
o Suctioning secretions reduces the number of potentially bad things (microbes!)
getting into the lungs. This reduces the risk of aspiration - thus reducing the
potential VAP - a good thing.
o Once a patient is intubated and placed on a ventilator, attach suction tubing to a
specialized suction port on the endotracheal tube using the following criteria:
 Continuous suction no longer recommended
  Intermittent suction pressure placed at around 120 mm Hg - pressures set too
high cause mucosal damage (bleeding may be noted)
 If the line becomes obstructed, use a syringe to inject a "bolus" of air to clear
it.

Wire-reinforced endotracheal tube (also known as Armored ETT)

 An endotracheal tube with metal coils running throughout the length of the tube. The tube
is stronger, so is less likely to kink or bite. Note that a radiopaque line is unnecessary in
this type of tube as the inner coils are visible on the chest radiograph.
 Uses
o Surgical Head/Neck: when airway access is limited (especially during surgery) as
well as in cases where the neck has to be in the flexed or extended positions for long
periods
o Intensive Care: when the patient needs to be in a "neutral" position for a long period
of time
 Cautions
o Caution with use in MRI - most tubes are safe to use in the MRI but this should be
confirmed before taking patient
o Do NOT use as a bite block (once the patient bites it, the tubing won't return fully to
its original shape)

Double-lumen endotracheal tube

 How it works
o Used to achieve independent lung ventilation in cases where one lung needs to be
ventilated while the other is rested
o Specialized tube with one lumen that goes into the right or left bronchus, with the
second lumen remaining in the trachea. There are 2 pilot balloons which can be
inflated depending on whether one lung or both lungs need to be ventilated
o Tubes are specially designed to be used for either the left or right lung
 Uses
o Pneumonectomy
o Lobectomy
o Bronchopulmonary fistula
o Video-assisted thoracoscopic surgery (VATS)
o Lung decortication
o Lung protection where one lung is infected to prevent cross-contamination
o Single lung transplant

ACCS: Specialty Visualization Devices

What This Section Might Cover:

 You will very, very, very likely see questions that ask you to identify a difficult airway and
then choose a method of establishing the airway. Pay close attention to the details given in
the scenario - avoid harm!

Equipment/Procedures You Should Recognize:

 Awake fiberoptic bronchoscopy

 Video-assisted laryngoscopes (such as a Glidescope or McGrath)
 Bougie
 Rigid stylet
  Laryngeal mask airway (LMA), including Fast-Track
 Retrograde wire kit

Choosing the BEST Option:

 General Difficult Airway

(Mallampati 3-4, or when glottal opening cannot be directly visualized):
Use of a Bougie (sometimes called a gum elastic bougie on the exam) is a good option, use
of fiberoptic equipment of any type
Be very suspicious of "normal" options with a difficult airway - such as nasal or oral
intubation. Respond to the difficult airway.

 Obese Patient
Consider altered positioning when presented (such as "extreme sniffing position" with
blankets placed under shoulders)
Use of awake fiberoptic bronchoscopy is a key to maintaining airway patency - consider it in
higher risk patients.

 Inability to Intubate
An LMA is a GOOD option on the exam - especially if multiple attempts to intubate have
failed. Use it as an alternative until a better airway can be established. Do not use if a
patient is awake.

 Trauma: Consider either a retrograde intubation or cricothyroidotomy:

o If URGENT: use cricothyroidotomy as a retrograde can take 4+ minutes to establish
an airway

How The Exam Will Attempt to Deceive You:

 You will be given the option to use "normal" direct laryngoscopic intubation. If there is any
indication that this is a difficult airway, don't do it.

Oakes Academy Tip

Inhaled nitric oxide may show up on the exam. It is a rescue option for a patient who is not
oxygenating well. One of the strengths of this treatment is that it causes pulmonary vasodilation, but
because it has such a short half-life (it stops working quickly), it doesn't cause an issue with
systemic vascular resistance. There are more questions than you might expect on nitric for many
test-takers. This is especially true if you don't use nitric much with adults where you work. Be
prepared to recommend it, manage it, troubleshoot it, and wean/discontinue it.

What This Section Might Cover:

 Scenarios where you are asked to recommend nitric oxide for its ability to treat severe
oxygenation issues - especially ARDS (improves V/Q matching by improving blood flow -
through vasodilation - around the lungs) or for certain cardiac disorders (ones that cause
an intracardiac shunt).
 Asked to respond to equipment troubleshooting (especially Nitric Dioxide [NO 2] build-up)
 Scenarios or questions where you are expected to know dosaging and how/when to
increase therapy and how/when to wean/discontinue iNO.
 Scenarios that require you to recognize signs and symptoms of the effectiveness of iNO (or
ineffectiveness as the case may be), including during weaning of iNO.
Equipment/Procedures You Should Recognize:

 iNO is usually given via a ventilator circuit through a delivery device. It depends on the
flow of the ventilator to deliver to the patient (inadequate flow may result in a build-up of
NO2 which is harmful to the patient). Be sure to "flush" the system with flow before starting
iNO. Note that with some therapies (HFOV, APRV), a one-way valve may be needed to
ensure proper delivery of iNO to the patient.
 A resuscitator bag should also be connected to the blender on the iNO delivery device.
Especially if a self-inflating bag, be sure to squeeze it several times to ensure that NO 2 has
been purged out.
 There is a sampling line that easily is affected by humidity and may cause false alarms.
Always investigate false alarms, but this is one way to troubleshoot.

Choosing the BEST Option:

 Initiate:
o Timing: Initiate after other methods have failed (so optimize ventilator/mode,
consider APRV, etc.)
o Lab: request a methemoglobin level if given the option
o Dose: start at a dosage between 20-40 PPM, then assess the patient-ABG in 30
minutes-for a positive response.
 A positive response includes an increase in PaO 2 (> 20 mm Hg) or SpO2 (>
10%), or an improvement (> 20%) in PAP.
 A response to iNO inadequate (for example, PaO2 is still under 60 torr, but has
increased from 35 torr), consider increasing iNO. Max is 80 PPM.
 No response to iNO (see above bullet point), discontinue it. Remember, iNO
has a very quick half-life, so if no response within 30 minutes when an ABG is
usually drawn, there is unlikely to be one.
 Monitor:
o Be aware of NO2 (see procedures above for minimizing this risk)
o Be aware of methemoglobin (methemoglobinemia requires methylene blue as a
treatment)
 Wean/Discontinue:
o Wean incrementally, usually in half until at 5, then by 1's (so if starting at 40, wean
to 20, then 10, then 5, then 4 . . . )
o Rebound hypertension is a risk. Expect it on the exam. If an increase in PAP and
decrease in CO, PAWP, increase dosage of iNO. Note that systemic BP will unlikely
be affected (iNO has a very short half-life, so it is unlikely to affect systemic
vasculature).
o Rebound hypoxemia may also occur. If this does happen, go back to previous dose
on the iNO.
o If several failed wean attempts, consider waiting 48-hours before reattempting.

Additional Information You May Wish to Consider:

Mechanism of Action

 Selective pulmonary vasodilator, decreasing pulmonary vascular resistance (PVR)

without affecting systemic vascular resistance (SVR)
 May improve blood flow to ventilated alveoli, improving oxygenation (improved V/Q)
 Very short half-life (between 15-30 seconds at dose of 5-80 parts per million [PPM]),
meaning iNO has minimal systemic effect
Potential Uses

Not all are FDA-approved, they are considered "off-label"

 Refractory pulmonary arterial hypertension (PAH) in pediatric/adult populations (usually

made worse by an illness)
 Refractory hypoxemia in ARDS as an emergent life-saving measure when all other options
(ventilator strategies, pharmaceutical intervention, positioning) have been exhausted
 Pulmonary hypertension during initial phase of post-lung transplant and VAD placement
 Acute right heart syndrome (RV Function has decreased [PE] LVEDP)

Other Treatment Options

 May consider the addition of Sildenafil (0.5 mg/kg by I.V. q6hrs). Titrate up to 6
mg/kg/day
 Aerosolized Prostacyclin may have an additive effect
 Aerosolized Iloprost is a potent pulmonary vasodilator approved by the FDA for treatment
of pulmonary hypertension - some studies suggest aerosolized Iloprost combined with
Sildenafil may cause strong pulmonary vasodilation.

Heliox Therapy (Helium-Oxygen)

What This Section Might Cover:

 You may be asked to recommend heliox as a therapeutic intervention

 Equipment set-up and management - pretty basic content

Equipment/Procedures You Should Recognize:

 Heliox is usually administered by a nonrebreather mask (running at 10-15 L/min)

 Two main mixes available: 80/20 and 70/30. Remember the larger number is the helium,
oxygen is the smaller number.

Choosing the BEST Option:

 Indications
o Upper airway tumors (including carcinoma)
o Upper airway obstructions (including a foreign body)
o Asthma exacerbation (usually severe WOB, wheezing, or absent breath sounds)
o Post-extubation stridor
 Use:
o Uncommon to have to pick between mixtures, but if you must, choose 70/30 for
patients with higher O2 needs.
o If a description includes inspiratory "noise" (stridor, musical notes, something like
that), suggest heliox unless the patient is in severe distress (then reintubate)
o Heliox can be run through the ventilator as long as it is calibrated for use. There is
an increased risk of pneumothorax/barotrauma if using heliox with a ventilator not
designed to run with heliox.
o Definitely recommend as an alternative to intubation for an asthma exacerbation as
heliox may enhance aerosol deposition to the lower airways

Additional Information You May Wish to Consider:

  Improved homogeneity of gas distribution resulting in:
o ↑ alveolar ventilation, oxygenation and VT,
o ↓ WOB, PaCO2, gas trapping, auto-PEEP, PIP, Pplat, barotrauma, I:E ratios and
shunting
 Movement of the equal-pressure point of the airways upstream

Delivery using an O2 flowmeter requires flow conversion:

70/30: set flow x 1.6 = total flow delivered
80/20: set flow x 1.8 = total flow delivered

What to Monitor

 ABG sampling
 Arrhythmia
 Dyspnea levels (WOB & SOB)
 Heart rate
 Pulse oximetry
 Pulsus paradoxus

Hazards

 Anoxia - analyze delivered gas

 Barotrauma- via ventilators not designed for helioxf
 Too ↑ or too ↓ bronchodilator - (too ↓ or ↑ of a flow through the nebulizer)

Nitrous Oxide (N2O)

 Nitrous may appear on the exam in the Emergency Department setting. It is used for
procedural sedation.
 Administered as a 30/70 N2O-O2 mix by mouthpiece or mask
 Nitrous may cause respiratory depression, which is an increased risk when other sedatives
(opiates usually) are administered simultaneously
 Important contraindication: DO NOT administer nitrous to patients who have any trapped
air (COPD, pneumothorax, etc.) as nitrous may diffuse into the air-filled area and then
rapidly expand.

Oakes Academy Tip

It should not be surprising to find out that managing mechanical ventilation takes up as much as 25% of the ACCS exam.
For the majority of questions, this means making decisions about what to do next for a patient. That can range from
initiating noninvasive techniques such as NPPV, to conventional ventilation, or in managing patients who aren't doing so
well, such as with APRV, HFOV, NAVA, ASV, etc. This section of review is some of the most complex, particularly if there
are areas you don't have direct experience with. We have worked extra hard to make it all easily understandable, but if
you need additional resources or have questions, simply ask!

Here's the real tip: whenever possible, start out with the least severe option available (such as NPPV), then progress to
conventional options (PRVC, A/C, etc.), and if the patient fails at conventional, then consider more serious options
(HFOV, APRV, etc.). Be on the lookout for contraindications and hazards! For example, increasing PEEP in a patient who
is hypotensive.

Initial Settings
Oakes Academy Tip
There's only one BEST answer on the exam. If you are given 4 sets of initial settings,
there's something "less optimal" about 3 of them so look for it. It might be the tidal
volume or set rate is out of normal range; it might be that one is a more advanced
mode of ventilation (such as PRVC), or there might be something about the
disease/disorder presented that breaks the rules (see diseases/disorders for more on
individual differences).

Assuming relatively normal lung physiology - see individual diseases for alterations

1. Choose Pressure or Volume: the exam doesn't distinguish one as preferred

2. Choose Assist-Control (A/C) or SIMV (with adequate support) when offered
3. If no acceptable A/C or SIMV, choose PRVC or APV. Again, see #2!
Mode
4. APRV and HFOV is strictly saved for when conventional ventilation has failed
(so never for initiation)

Tidal
Volume 6 mL/kg (range is 6-10, but use 6 when possible)

For ARDS: set a tidal volume in the range of 4-8 mL/kg (IDEAL body
weight). Most correct answers will be around 6 mL/kg.

How to Calculate Range

Step 1: Calculate IBW in kg (for exam purposes only, not a bedside calculation)

Female = 46 + 2.5(Height in inches - 60)

Male = 50 + 2.5(Height in inches - 60)

Step 2: Multiply the IBW in kg by 6 (this is the low end of your acceptable
range). Cross out answers below this (unless ARDS)

Step 3: Multiply the IBW in kg by 10 (this is the high end of your acceptable
range). Cross out answers above this

You now have an "acceptable range" (Step 2 -to- Step 3). Any answers outside
range can be ruled out

Example:

Calculate IBW for a 5-ft 6-in male

Formula: 50 + 2.5(height in inches - 60)

= 50 + 2.5(66 - 60)
= 50 + 2.5(6)
 = 50 + 15
= 65 kg
Lower range (65 x 6 = 390 mL)
Upper range (65 x 10 = 650 mL)
Tidal volume should be set between 390-650 mL

18-22 cm H2O
Pressure
Ultimately, pick an answer that will target tidal volume to around 6 mL/kg
(keep Pplat < 35 cm H2O) if pressure mode of ventilation

10-24 breaths/min is considered normal on the exam. Pay close attention to the
I:E Ratio.
Respiratory
 Most rates will be in the 10-18/min range (can be as low as 8)
Rate
 Pick a higher range for ARDS
 Be on the lookout for air trapping when a higher rate is used. Fix by
decreasing TI (= increasing inspiratory flow) or decreasing RR

0.8-1.2 seconds

 Anywhere in this range is considered normal. The exam won't throw

unreasonable answers at you, so don't worry too much about memorizing
this range
 DO be aware of I:E ratio. Normal is 1:2 to 1:3
 Use extended I:E ratio of 1:4 to 1:5 for diseases like COPD, Asthma, CF
 If I:E ratio is too short (1:1, 1:2, or even inverse . . . 2:1), air trapping will
occur (dynamic hyperinflation). To fix, decrease TI by increasing inspiratory
flow or decreasing RR
Inspiratory
 APRV uses much shorter inspiratory times, see that mode for details
Time

Calculations

Total Cycle Time (TCT) = 60 / RR

Expiratory Time TE = TCT - TI

I:E Ratio = TI:TE. Divide both sides by TI to get your appropriate ratio

PEEP
0-6 cm H2O

 Anything over 5 cm H2O is considered therapeutic - so look for a reason

before applying it.
 Use PEEP when refractory hypoxemia (V/Q mismatch). If you are given a
 P/F ratio < 200, that's a clue you may need to increase PEEP.
 It is not uncommon to find higher PEEP (up to 20 cm H 2O) in scenarios
 Do not increase PEEP when a patient is hypotensive or hemodynamically
unstable. Use FIO2 for oxygenation in that case.

Match current FIO2 (if on supplemental O2), assuming PaO2/SpO2 is within normal
range
FIO2
1.0 if no information is given, distress, or in an emergency setting. If all
FIO2 presented as options are similar, don't worry about it.

Oakes Academy Tip

For those who don't work at a hospital with the majority of the "advanced" modes of ventilation at
use, this section can make you wanna go running for the woods. Don't fret it - there are some
things you need to know, but the exam will not be requiring you to connect a real patient to a real
ventilator to run the real mode. We promise. Just focus on the basics (terminology, how you
initiate the mode, how you manage oxygenation and ventilation on the mode, and how you wean
it).

You'll find that the modes/techniques are split into three categories. You'll find information on each
in their respective category pages.

1. Optimizing ventilation. There are no real "modes" here, but more strategies. There are two:
patient positioning and pulmonary vasodilation.

2. Optimizing oxygenation. This one has two important modes in it: APRV and HFOV. You're
likely to encounter both on the exam, but you won't have a gazillion questions on either. There are
a few techniques to review, as well.

3. Optimizing synchrony. The big one here is NAVA, but the exam takes a very light approach
to the mode for now. You do need to understand the EDI catheter (more on that in the NAVA
section) and have some basic knowledge of how the mode works. For techniques, switching modes
is always an option, and increasing or changing sedation is another.

Why does the ACCS use the term "Advanced" modes/techniques? Well, it creates a logical
progression for the critically ill patient. Here's what we recommend as you evaluate patients in ICU:

# Patient has impending respiratory failure

1

Use noninvasive first, unless not indicated

 Requires airway patency

  Requires patient to be conscious
 Requires hemodynamic stability (relative)

# Patient failing #1 or doesn't qualify for #1:

2

Place patient on conventional ventilation

 Pressure or Volume - doesn't matter as long all parameters meet the appropriate
requirements
 Modes - A/C, SIMV, PRVC, APV - doesn't matter
 Ensure appropriate VT, RR, PEEP, FIO2, TI if offered multiple of the above modes. One
off parameter usually rules it out as an option!

# Patient failing #2
3

Transition to advanced mode/technique

 Ventilatory failure: Positional therapy (prone), iNO/prostaglandins (usually a

mention of PAP/PPa)
 O2 Failure: APRV, HFOV, recruitment, iNO/prostaglandins (usually a mention of
PAP/PPa)
 Synchrony: NAVA, sedation

Always wean back to conventional ventilation before extubating

Techniques to Enhance Ventilation

How do you know there's a ventilation issue?

The quick answer is pH and PaCO2, in that order. Let's define a few things for the exam:

 Our goal is to stabilize the pH, not the PaCO2. For most patients this is the same thing (a
sufficient pH is a sufficient PaCO2), but you will also be presented with patients with an
abnormal baseline.
 Treat a low pH (<7.30) until you reach an acceptable level, do not necessarily try to bring
the pH all the way up to normal (7.35). For ACCS purposes, treating a pH up to as low
as 7.30 is reasonable. This is particularly true of ARDS where "fixing" a pH/PaCO 2 to
normal may result in a risk of lung injury.
 Watch work of breathing! WOB is an issue. It might mean the patient is asynchronous
with the ventilator, or if not the vent already, needs to be on one, etc.

Improving ventilation (respiratory acidosis) the conventional way

 Improving ventilation means increasing minute ventilation:

o Increase respiratory rate while ensuring adequate I:E ratio
 o Very cautiously consider increasing tidal volume. Never ever should you ever
increase tidal volume beyond 8 ml/kg IBW. Well almost never, anyhow (they will
most likely not give this option).
o Ensure the patient is not air-trapping. This is where watching your I:E ratio is
very important. Air-trapping results in unventilated areas of the lung where blood is
still flowing by (known as ventilation without perfusion or a pulmonary shunt)

Improving ventilation - some more "advanced" techniques

 Increase perfusion to healthy lung while decreasing perfusion to the sick lung by
positioning the patient.
When ventilation issues are noted to be in a certain location (like right lung), position the
patient to optimize. In short, put the gravity-dependent blood flow next to the healthy lung
regions. Remember this as: BLU GLD (blue gold): Bad Lung Up, Good Lung Down.
Ex: A patient has right-sided pneumonia. Their pH is 7.24, PaCO2 58. What can you do to
address this? Place the patient in a left-lung down position (the good lung is the left
lung).

 Improve perfusion in patients on high O2 by administering iNO or prostaglandins.

Oxygen is a vasoconstrictor and in high amounts may limit perfusion around healthy
alveoli. Think about this - the majority of this super-O2-charged air is being delivered to
the alveoli that are the most healthy (they are more compliant, not atelectatic, and less
filled with "stuff")! This, in turn, causes vasoconstriction in the vessels around those
alveoli. It is a particular issue with ARDS where high FIO2 is necessary to maintain a
sufficient O2. You will usually be given a pulmonary arterial pressure (PAP or PPa) to
confirm the presence of pulmonary hypertension (the source being pulmonary
vasoconstriction).
Ex: A patient has a P/F ratio of 80 on mechanical ventilation. They are noted to have
bilateral infiltrates consistent with ARDS and PAP is elevated. What can you do to address
this? Consider adding inhaled prostaglandins like Flolan, or initiate iNO.

Techniques to enhance oxygenation

How do you know there's an oxygenation issue?

The quick answer is the P/F ratio, which is a reflection of the relationship between oxygenation (PaO 2)
and the FIO2 (delivered oxygen) required to maintain an appropriate oxygenation level. With the P/F
ratio we are essentially asking, "out of X amount of oxygen being delivered to the lungs (F IO2), how
much is getting into the blood where it is needed (PaO 2)?"

 Treat to an adequate PaO2, not a normal one. For ACCS purposes, treating a PaO2 to about
60 torr is reasonable. Treating above that with high FIO2 increases the risk of oxygen
toxicity.
 Throwing oxygen at the problem doesn't often help on the exam - don't be surprised to find
many patients with refractory oxygenation (as the F IO2 goes up, the PaO2 doesn't).
Refractory oxygenation occurs when there is a V/Q mismatch - when the alveoli aren't fully
functioning in gas exchange (atelectasis, consolidation), or when perfusion isn't adequate
(especially with high FIO2 - such as with ARDS).
 It can be more effective to optimize ventilation/perfusion, by either matching them (putting
areas of good ventilation with good perfusion), or by improving it (recruiting lung, for
example)

Improving Oxygenation the conventional way

  Increase FIO2 - this is the obvious way and is indicated in non-ARDS patients who are on
low levels of FIO2. It certainly is most appropriate to increase the F IO2 pre-procedure
(intubation, bronchoscopy, etc.).
 Increase PEEP - a very common method found on the exam is to attempt to increase PEEP
on a patient who has a V/Q mismatch (poor P/F ratio, poor chest radiograph, etc.). Use
this option much more cautiously in patients who are hemodynamically unstable.

Improving Oxygenation - more "advanced" techniques

 Perform a recruitment maneuver.

Recruitment will open atelectatic lung areas, at least temporarily, and improve
oxygenation. The most typical manner of doing this is to place the patient on CPAP of 30-
40 cm H2O for 30-40 seconds, and then place the patient back on their previous settings, or
preferably on a slightly higher PEEP than was previously set.
Ex: A patient on mechanical ventilation, FIO2 1.0, PEEP 10 cm H2O has a steadily declining
SpO2, currently at 91%. What should the ACCS do? Place the patient on CPAP +30 for 30
seconds, then place the patient on PEEP 12 cm H2O.

 Place the patient in prone position.

Proning a patient has been shown to change the dependent areas of the lungs (using
gravity to manipulate blood flow). It is a common option on the ACCS exam in patients
who are oxygenating poorly.

 Place the patient on APRV (BiLevel, BiVent, Dual PAP) ventilation. This mode is
considered a "recruitment mode" and may improve oxygenation (by recruiting alveoli).
Think of it roughly as "inverse I:E ratio ventilation that allows the patient to breathe
spontaneously." If a patient is failing conventional ventilation (normal mode, higher PEEP,
oxygenation is worsening), APRV should be strongly considered. You should also know how
to manage, troubleshoot, and wean APRV.
Review APRV

 Place the patient on HFOV. Yes, the oscillator. Yes, on adult patients. This mode, like
APRV, is a recruitment mode. Like with APRV, you should also know how to manage,
troubleshoot, and wean HFOV.
Review HFOV

Note: There is no better option between APRV and HFOV. If you are given both options,
one is wrong for some particular reason (or both are wrong). You have to be a detective
and figure out what contraindication occurs. For example, if a patient should be able to
breathe spontaneously, APRV is preferred.

Techniques to Enhance Synchrony

How do you know there's a synchrony issue?

Asynchrony occurs when a patient is fighting the ventilator. There's something incorrect with
settings, or something that needs to be addressed in the patient (sedation/paralytic). Clues to
asynchrony (also called dyssynchrony):

 Ventilator graphics display missed triggers, double-triggers, flow starvation, etc. Review
the vent graphics section for details if you need to.
 Patient assessment - increased work of breathing, accessory muscle use, diaphoresis,
tachycardia, tachypnea, hypertension
 Pay particular attention to cardiac patients - asynchrony increases oxygen consumption
during a time when you're trying to allow the patient to rest
Improving synchrony the conventional way

 Look for issues that you can fix

o If missed triggers, make trigger more sensitive
o If auto triggers, make trigger less sensitive
o If flow starved, increase the flow
o Treat a metabolic acidosis if offered (compensation for metabolic acidosis is
tachypnea)
o Consider a different mode - pressure support, if appropriate, more PS if on SIMV
with a lower rate, etc.

 Increase sedation and/or consider paralytics - use this option when oxygen
consumption is a concern (cardiac patients!)
o If issues during weaning with synchrony/anxiety, consider dexmedetomidine
(Precedex) - a very common scenario
o If issues with combativeness, overall restlessness, consider haloperidol (Haldol) or
lorazepam (Ativan)

Improving Synchrony- more "advanced" techniques

 Consider Neurally Adjusted Ventilatory Assist (NAVA)

NAVA is considered a "synchrony" mode of ventilation. It utilizes the electrical activity of
the diaphragm as a trigger (versus flow or pressure). You need to have a general sense of
how the "mode" works, how to troubleshoot it, and have a good understanding of the Edi
catheter.
NAVA mode
Edi catheter

 Consider proportional assist ventilation (PAV)

PAV is also a synchrony mode. It is particularly helpful for patients with work of breathing
issues, including COPDers. As the name implies, the mode provides whatever "amount" of
support the patient needs (as determined by the patient's effort to breathe - flow and
volume).
Review PAV mode

Oakes Academy Tip

It may not surprise you to learn that noninvasive ventilation is a common theme on the ACCS
exam. You should be quite familiar with indications, contraindications, hazards, and settings.
While CPAP will be covered, NPPV (BiPAP - but referred to as NPPV on exam).

A couple keys: NPPV is a critical intervention with patients with COPD. Unless contraindicated, it
can be used to support work of breathing in an acute exacerbation, and as a great option for rapid
weaning after extubation in these patients. CHF (or fluid overload)? Great option, again, unless
contraindicated. Look for any sign of a contraindication before opting for NPPV.

Let's boil down some of the keys:

 Whatever you call it in real life (BiPAP, anyone?), the exam refers to it as noninvasive
positive pressure ventilation (NPPV)
 Use CPAP for fluid balance issues (especially CHF)
  Use NPPV to support work of breathing and impending respiratory failure (COPD, Asthma in
particular)

Ensure the following before recommending:

 The patient must be protecting their airway (NIF, drooling, LOC)

 The patient must have a drive to breathe (RR needs to be within normal range. VT is less
important as it will be boosted by NPPV).
 The patient must neither be in severe distress nor in absolute respiratory failure (pH <
7.30)

High Flow Nasal Cannula (HFNC or HHFNC)

The ACCS in 2018 officially added high flow nasal cannulas (HFNC) and heated high flow nasal
cannulas (HHFNCs) to the exam outline. The devices allow us to deliver fairly precise F IO2s with
higher flow rates (up to about 60 L/min). They are theoretically effective for a few reasons:

1. When flow is set high enough, a HFNC will meet or exceed a patient's minute ventilation. This
means little or no room air is being entrained. This makes it ideal for patients who need high flows!

2. High Flow Nasal Cannulas provide some level of expiratory resistance. Think PEEP. Not exactly,
but kind of like PEEP. The thought is that the expiratory resistance (pseudo-PEEP?) helps to prevent
alveolar and airway collapse on exhalation, preventing or reversing atelectasis. Important note: this
"PEEP-like" effect can't be measured. Heck, it really can't even be estimated.

3. High Flow Nasal Cannulas allow patients to communicate, to eat, to live life a little more normally
than strapping a mask on them and applying CPAP or NPPV.

Recommend therapy when:

 Patients in distress, impending respiratory failure, with high FIO2/high flow needs:
o Asthma
o Carbon monoxide poisoning (FIO2 1.0)
o Pneumonia
o Pulmonary embolus
 Post-extubation respiratory distress. This assumes airway patency (if not, intubate!)
 To facilitate comfort/communication in patients on NPPV (can alternate between NIV and
HFNC)
 Patients with do-not-intubate orders who may be in respiratory distress
 Pre-intubation for patients at high risk (obesity, for example)
 In the case of fluid overload (including CHF), recommend NPPV
 In the case of severe distress, intubate

Equipment

 Nasal Cannula: larger bore (opening) than a normal NC

 Oxygen Supply: often large bore corrugated tubing
 Blender/Heater: because this is a high flow device it overwhelms the body's ability to
effectively heat and humidify inhaled gas. Heated humidity should be added.
o There are different cannula which allows for greater flows of oxygen depending of
the size of the holes in the prongs
 Settings
o FIO2 - a blender that allows for precise setting of O 2 usually from room air up to 1.0
o Flow - set flow that can reach flowrates up to 60 L/min
Initiation and Management

 There are two "settings"

o FIO2: match FIO2 to device patient is on currently. If in doubt use FIO2 1.0, except
COPD when you should choose around 0.50 (for exam purposes. We're not gonna
argue for or against hypoxic drive theory right now).
o Flow: choose a flow in the 15-40 L/min range, if available. 60 L/min is the upper
limit in any scenario.
 If the patient does not improve over a few hours, consider intubation (unless end-of-life)
 Flow set too low will not meet patient's inspiratory demand. Flow set too high may prevent
exhalation (increasing CO2). Look for indications of either in questions.

Weaning and Discontinuing

 Wean FIO2 until below 0.5 (use SpO2 or PaO2)

 Wean flowrates to 20 L/min or below (use work of breathing as an indicator)
 Once weaned below above values, discontinue to other O2 device (venti mask, NC, etc.)

Benefit

 Increased comfort - No mask required!

 Ability to deliver precise flows and FIO2
 Decrease work of breathing
 Improvement of oxygenation
 Secretion mobilization due to heated and humidified air
 Potential CPAP effects with higher flow rates
 Decreases anatomical dead space

Contraindications

 Apnea
 Nosebleeds (severe)
 Obstructed nares
o Postnasal surgery
o Tumors
 Respiratory failure where intubation is necessary

Mask CPAP

 Falls under the umbrella category of noninvasice ventilation (NIV) along with NPPV (you
most likey know this as BiPAP)
 The primary goal of CPAP is to support oxygenation. Remember NPPV helps support
ventilation and/or oxygenation.
 Uses noninvasive interface (mask) as opposed to CPAP on the ventilator which is considered
invasive ventilation

Uses

 Acute cardiogenic pulmonary edema

o Helps decrease venous return lowering the amount of fluid in the lungs or maybe
pushes fluid out of the lungs (depends who you ask). Regardless, it's effective!
o Helps to stent airway open and decrease work of breathing
o Use in conjuction with a diuretic if given the option
 Increasad fluid from procedure such as plasma infusion
  Sleep apnea
o Obstructive - Helps to stent airways open
o Central - Usually only with patients with a combination of CHF as it assists to reduce
airway collapse from increased fluid

Initiation

 There is no hard and fast rule when it comes to initial setttings for CPAP
o General rule of thumb... Keep the pressure below 10 cm H 2O to start. You can
increase pressure if necessary, BUT... increasing CPAP too high can result in
overdistension, leading to hemodynamic compromise, and may result in an increased
risk of gastric insufflation.
 CPAP - Should be titrated to meet oxygen goals.
 FIO2 - Don't forget this other important step when initiating CPAP. Set and titrate together
with CPAP levels to achieve appropriate oxygenation levels
o SpO2 > 92%
o PaO2 - 80 - 100 mm Hg

Considerations

These are similar to NPPV, so they might look familiar

 The patient must be protecting their airway - They need to be awake

 The patient must have a drive to breathe - Otherwise intubate!
 The patient must neither be in severe distress nor in absolute respiratory failure (pH <
7.30, PaO2 < 50 mm Hg)
 As with anytime you strap a mask onto a patient, be weary of anxiety due to the mask
smushed on their face especially if they have a history of anxiety.
o As fluid moves out of the lungs, patient might start to feel less anxiety
from improved WOB

Complications

Minor

 Dry upper airway (use humidification)

 Eye irritation secondary to air leaks
 Gastric distention
 Sinus congestion
 Skin reddening and breakdown (especially around the nose)

Major

 Aspiration (especially with full face masks)

 Hypotension (from too much CPAP/PEEP)

Oakes Academy Tip

You are very likely to see a few graphics questions on the exam. One of those likely to appear is
air trapping (or as it is more fancily known, "dynamic hyperinflation"). You will need to recognize
the graphic, and possibly come up with a solution. There are a few easy options to watch for:
Decreasing the respiratory rate (allowing more time for exhalation), increasing the flow or
 decreasing the TI (inspiratory time).
KEY to watch for: Expiratory flow doesn't return to baseline

How to recognize it

You will probably be given some kind of indication that something is wrong. For example, a patient
with a higher-than-normal respiratory rate, or a specific disease state like COPD, asthma or other
obstructive process. The exam is most likely to provide a scalar clearly showing expiratory flow that
doesn't return all the way to baseline.

Common Causes

 Expiratory resistance results in prolonged exhalation time

 Insufficient expiratory time (usually due to increased respiratory rate either provided from
the ventilator or from patient not being properly sedated/paralyzed with too high of an T I)
 Early collapse of unstable alveoli/airways during exhalation (exhaled air is "blocked" from
flowing out allowing for air to become "trapped" in the lungs)

Complications to Watch For

 Air-trapping prevents CO2 elimination = ABG will become increasingly acidotic despite
increases in minute ventilation (which may only worsen acidosis)
 Severe air-trapping may result in hemodynamic compromise, including cardiac arrest

How to Address It

1. There is such thing as therapeutic air-trapping. DO NOT fix air-trapping related to

APRV (well, ensure it is appropriate - more on that in the APRV section)
2. Increase expiratory time - Remember, there is no way to do this directly, so don't fall
into that trick!
3. Decrease inspiratory time - Make sure I:E ratio is appropriate
4. Decrease respiratory rate - Allows for more time for exhalation
5. Increase inspiratory flow - If TI isn't given, inspiratory flow determines TI. Faster flow
= lower inspiratory time
6. Administer a drug
o Bronchodilator if airway resistance/bronchospasm is suggested. Might have wheezing
present in the scenario.
o Paralytic if severe asthma and no other options are likely + hemo compromise or
overall deterioration
7. Special note: Applying PEEP to counteract intrinsic PEEP is not preferred on the exam,
unless you are given a very specific scenario with a measured auto-PEEP
 o For example: Trigger dyssynchrony (patient is having hard time triggering
ventilator), and an option to apply PEEP at approximately 80% of set PEEP. Yeah,
that's a lot of "ifs"

 Pneumothorax (Rare- DO NOT OVER-PEEP)

Double-triggering

How to recognize it

In the flow or pressure scalar this will show as an easily identifiable "double trigger," so two
waveforms directly next to each other.

Common Causes

 Inadequate inspiratory time, the breath ends before the patient has taken a full breath in

How to Address It

1. Increase inspiratory time - Depending on mode and disease state, this may not be
possible (why? because it increases tidal volume, which may increase risk of injury with
ARDS). In these cases administer a drug (see below).
2. Administer a drug
o Heavier sedation to diminish underlying respiratory drive
o For ARDS a paralytic may be necessary

Auto-Triggering

How to recognize it

Look for a high respiratory rate with no evidence of the patient triggering breaths (negative
deflection on pressure scalar)
Common Causes

 Trigger set incorrectly (it is too sensitive)

 A bounding heartbeat can sometimes cause this - cardiogenic oscillations

How to Address It

1. Change trigger. Adjust sensitivity to prevent auto-triggering. DO NOT lock patient out
(by decreasing sensitivity too much)

Flow Dyssynchrony

How to recognize it

For patients in VOLUME VENTILATION, flow asynchrony shows up as a variable (changing) element
to the inspiratory pressure or to the flow scalar. This bears repeating: Inadequate flow may show up
in the pressure waveform as a "wavy" or "squiggly" element. Note that the flow waveform in this
case MAY appear normal.

This may be referred to as: Flow Asynchrony, Flow Starvation, and Flow Mismatch

From Branson, et al., Respiratory Care Jun 2013, 58 (6) 973-989;

Common Causes

 Inadequate flow

How to Address It
 1. Increase peak flow if given the direct option
2. Decreasing inspiratory time will increase flow

Rate Dyssynchrony (Including Breath Stacking)

How to recognize it

This is "classic" dyssynchrony where the patient is attempting to breathe against the ventilator,
whether during inspiration or exhalation. The ventilator is not responding to the patient's attempt to
trigger a breath.

Common Causes

 Patient is air hungry - minute ventilation (especially tidal volume!) is insufficient for what
patient needs
 Trigger is set inappropriately - usually it is too sensitive (results in auto-triggering)
 Neurological injury

Complications to Watch For

 Results in increased oxygen consumption as patient fights ventilator

How to Address It

1. Change trigger - Adjust sensitivity to prevent auto-triggering. DO NOT lock patient out by
decreasing sensitivity too much
2. Change mode if appropriate - Spontaneous modes allow for more control over the
variables of the breath
3. Administer pharmacologic agent
o Heavier sedation to diminish underlying respiratory drive

Paralytic if oxygen consumption is a concern (for example, cardiac Missed Trigger

How to recognize it

Patient effort that is not followed by the delivery of a breath. It displays as a notch in the expiratory
flow with no breath following.
Common Causes

 Trigger is set inappropriately - usually it is too sensitive (results in auto-triggering in

subsequent breaths due to increase in gas in the lungs)
 Respiratory muscle weakness or decreased respiratory drive
 Dynamic hyperinflation (air-trapping)

How to Address It

1. Change trigger. Try making trigger more sensitive to "catch" patient efforts
2. Consider use of an esophageal probe, such as a NAVA probe or pleural pressure
probe. NAVA can be particularly useful in detecting diaphragmatic electrical activity and
decreasing this type of trigger asynchrony

o patients)

Lung Recruitment Maneuvers

You likely work in one of two types of places: you either do recruitment maneuvers, or you don't. For
exam purposes, recruitment maneuvers are therapeutic responses to refractory hypoxemia.

When to Perform a Recruitment Maneuver

 ARDS or any disorder that results in refractory hypoxemia. There will be a strong clue or
two:
o Worsening or not improving P/F ratio < 300 (usually much lower than that)
o SpO2 that fails to respond to increases in FIO2
o Chest radiograph or CT scan that suggests atelectasis

When Not to Perform a Recruitment Maneuver

 Air trapping diseases (COPD, Asthma)

 Hypotension
 Head Trauma with Increased ICP

How to Perform a Recruitment Maneuver

There's a couple of ways to do a recruitment:

1. Place patient on CPAP of 20-40 cm H2O for 20-40 seconds (anything within that range is
reasonable)
2. Set PEEP by measuring pressures with an esophageal probe
 3. Increase PEEP 1-2 cm H2O at a time (this is called an "incremental PEEP study")
4. Perform a Pressure-Volume maneuver (patient needs to be heavily sedated), and place
PEEP between lower-inflection point and upper-inflection point. This is also called "Open
Lung Ventilation."

Regardless of technique, it is highly recommended that the patient be placed on a higher PEEP
post-maneuver

What to Watch For (Cautions)

 Hypotension: any significant decrease (> 20 mm Hg) in (continuously monitored) blood

pressure is a sign of a decreased venous return to the heart. Stop the recruitment
maneuver immediately.
 Hypoxemia: a decrease in SpO2 < 85% - stop the recruitment maneuver immediately.
 Any arrhythmias or a change in heart rate (> 140 or < 60)

Effectiveness

 A decrease in plateau pressure < 30 cm H2O

 Improvement in P/F (SpO2 or PaO2 improves with FIO2 needs decreasing)
 Improved chest radiograph

Oakes Academy Tip

This section is NOT about the drugs you're used to aerosolizing. That doesn't mean those won't be
on the exam. They will be, but they play a minor role. Check out the Drug Review Table for a list
of the common respiratory drugs you're most likely to find. Even more often, drugs are listed
simply by category (recommend a bronchodilator for bronchospasm, for example)

Narcotics

Used as a significant analgesic. Aerosolized narcotics typically treat severe dyspnea/air hunger (such
as with end-stage COPD, cancers affecting airways). It could be considered in other end-stage
patients without adequate vascular access (IV, etc.).

 Nebulized morphine: 2.5-10 mg up to every 4 hours

Use: recommend primarily in palliative care patients, especially with dyspnea
Adverse: decreased respiratory drive
Notes: may have less systemic adverse effects than administration by IV

 Nebulized Naloxone (Narcan)

1-2 mg in 3 mL NS
Use: reversal of opioid overdose
Notes: provides a low, continuous dose that doesn't abruptly wake patient up but helps
restore respiratory status (not most common route)

Antimicrobials

Used to treat bacterial infections. The exam may list individual drugs or may list "inhaled" antibiotics
as a generic answer choice. Prophylactic use of antibiotics is usually not preferred so avoid choosing
them for anything "preventive" (such as VAP).
  Tobramycin (Tobi)
300 mg 2x/day for 28 days on, 28 days off
Use: management of Pseudomonas and other gram - organisms (especially for CF
patients)
Adverse: bronchospasm is primary (consider pre-treatment with SABA)

 Aztreonam (Cayston)
75 mg every 8 hours for 28 days on, 28 days off
Use: management of Pseudomonas (especially for CF patients)
Alternate cycles with Tobi (28 days on Tobi, then 28 days on Cayston)

 Colistin
75-150 mg 2x/day
Use: P. aeruginosa is primary, but other gram negative organisms as well
Notes: This drug has to be prepared (reconstituted). Do NOT premix as it can become toxic
to the lungs after 24 hours.
Less common option

Pulmonary Vasodilators

As the name implies, vasodilators cause dilation of the blood vessels. It is used to treat pulmonary
hypertension, or to reduce pulmonary arterial pressures. Aerosolized drugs tend to have a more
localized effect on the pulmonary system, so it would not be appropriate for systemic hypertension.

 Epoprostenol (Flolan)
Use: pulmonary hypertension, improve V/Q in severe ARDS, acute right-heart dysfunction
Adverse: Caution if platelets < 50,000, hypotension

 Iloprost (Ventavis)
Use: inhaled prostacyclin/prostaglandin, used to treat pulmonary hypertension, improve
V/Q in severe ARDS (improves P/F ratio), and acute right heart dysfunction
Adverse: Caution if platelets < 50,000, hypotension

 Treprostinil (Tyvaso)
Use: inhaled prostacyclin/prostaglandin, used to treat pulmonary hypertension, improve
V/Q in severe ARDS (improves P/F ratio), and acute right heart dysfunction
Adverse: hypotension

Oakes Academy Tip

Few topics scare people more than the oscillator unless they have experience with it. Remember,
this is a test. There will be no oscillator in the room with you. You really just need to remember a
few keys to do well.

 MAP and Insp % are main determinants of oxygenation (ok, ok, and FIO2, but less so).
Oxygen problem? Increase MAP unless hemodynamic instability.
 Amplitude and Frequency are main determinants of ventilation. Respiratory Acidosis. Either
INCREASE amplitude or DECREASE frequency. If you are given the option to do both, pick
amplitude.

Indications/Contraindications

 Lung protective strategy (so consider with ARDS in particular)

  For ACCS purposes, HFOV is considered a good option when attempts at conventional
ventilation are failing. Usually this means continued hypoxemia (which does not respond to
increasing oxygen).
 Avoid with any indication of hypotension or obstructive disorders (COPD, Asthma, etc.)

Initial Settings

Mean Airway MAP Given: Match conventional MAP (or up to a few higher)
Pressure No MAP Given: Start around 20 cmH2O

~ 40 L/min (or more)

Bias Flow
 Bias flow too low may cause fluctuations in MAP, or may not reach MAP
at all (so increase flow if this is presented)

33%

% Insp Time  Don't typically change

 Possibly consider 50% if severe oxygenation issues. Will exam ever ask
you to do this? We haven't seen it happen

4-8 Hz

 For exam there is really no RIGHT Hz, as long as it is in this range

Hertz
 1 hertz = 60 cycles (a cycle is a set of inspiration + expiration) - YES,
(Frequency)
this is asked.
 Respiratory Acidosis: DECREASE frequency (this is not normal thinking,
so memorize it!)

~ 90 cmH2O
Amplitude (delta
 Clinically this is set to establish adequate chest wiggle (nipple to mid-
P)
thigh is seen as good wiggle)
 Respiratory Acidosis: INCREASE amplitude (opposite of frequency)

Most Common Troubleshooting Scenarios

 Mean Airway Pressure "fluctuating": Normally MAP will stay pretty close to where it is set.
If fluctuating, consider either increasing bias flow or increasing sedation.
 Low Pressure Alarm: Often a leak. Consider patient circuit. "Mushroom" valves are
common causes!
 High Pressure Alarm: Secretions - don't be afraid to suction. Airway resistance (less
common on exam)
 Hemodynamic Deterioration: Especially at higher MAP - decrease MAP directly or indirectly,
ensure bias flow is adequate but not excessive, maybe decrease delta-P
 Oakes Academy Tip
Proning involves flipping a patient from supine to stomach-down with the purpose of improving
ventilation-perfusion matching. Be aware that proning isn't the only option when addressing V/Q
mismatch - pay close attention to details given of the chest radiograph and/or breath sounds.
Unless contraindicated the overall goal is Bad Lung Up, Good Lung Down - so have a real general
idea of some of the chest physiotherapy positions (left and right lateral decubitus, for example).

Consider proning when you suspect a V/Q mismatch in the supine position (refractory
hypoxemia is one clue to that). Evidence supports the benefits of proning in certain
disorders, including:

 ARDS
 Elevated intraabdominal pressure
 Pulmonary edema
 Unilateral lung disease (atelectasis, lung contusion, pneumonia)

Positioning may be contraindicated with COPD, paralyzed patients, pulmonary hemorrhage, and lung
abscesses

Checklist for placing a patient in prone position

 Communication with team members

 Check for contraindications (see above)
 Ensure adequate sedation
 Check length and security of all lines and tubes
 Pre-oxygenate (FIO2 1.0)
 Verify vital signs and hemodynamic status
 Suction endotracheal tube

Patients should be carefully monitored

 All ventilator parameters, including signs of deterioration or improvement (PIP,

Oxygenation, etc.)
 Dislodgement of lines/tubes
 Any improvement is likely to be seen within the first 30 minutes

ECMO

Two major types of ECMO. The exam may ask you to identify which would be most appropriate in a
presented scenario

1. Venovenous (VV ECMO) provides lung support

 Very basically: Blood is removed before the heart/lungs (jugular or inferior vena cava),
where O2 is diffused in and CO2 filtered out, but then returned to the heart (right atrium or
jugular vein)
o This oxygenated blood then circulates through the pulmonary system,
but gas exchange has already occurred via ECMO

2. Venoarterial (VA ECMO): Provides both heart and lung support.

  Very basically: Blood is removed before the heart/lungs (rght atrium or jugular vein),
where O2 is diffused in and CO2 filtered out, then returned after the heart/lungs (descending
aorta or carotid artery)
 The goal is to decrease workload on the heart thus decreasing cardiac oxygen consumption
 A set portion of blood flow can continue through the lungs if desired

When to Use

 Recommend VV ECMO with respiratory patients (the ones with sick lungs) who are
receiving high levels of mechanical ventilation support (think severe ARDS), particularly
when that support is failing.
o Mechanical ventilation goal is to allow lungs to rest while preventing atelectasis
o VT: 4-6 mL/kg IBW
o Set Rate: 4-10 breaths/min
o SpO2: Typically lower than normal (goal is > 85%)
 Recommend VA ECMO for cardiac patients (the ones with sick hearts) where the
workload on the heart needs to be alleviated
o Mechanical ventilation goal is to maintain lung function near normal, utilize
traditional ventilator settings

Management

 For vent rest (VV ECMO patients), once the ventilator support is set, the ABG is managed
on the ECMO side (don't try to fix with the ventilator)
 Wean ventilator FIO2 once stabilized on ECMO
 Sweep controls ventilation while FiO2 is controlled with a blender
 "Whited out" chest radiograph is expected for first 24-hours of support

Cautions

 Use very cautiously in patients with coagulation disorders. Be wary of questions with
indications of a coagulation issue (coagulopathy) - this would be a red flag!
 Evidence of ischemic neurological damage is a relative contraindication (consider the entire
scenario before deciding)

Weaning ECMO

 Reduce the number of sweeps and amount flow of ECMO running, usually over a period of
hours or days. Note that you must increase ventilatory support simultaneously.
 When flow rates reach 10-30 mL/kg/min the patient may be isolated from the ECMO circuit
 Alternatively, a trial separation from ECMO support may be performed on the ventilator

Oakes Academy Tip

You are likely to run across some weaning questions on the exam. Most of these are pretty
straightforward as long as you read them carefully. You will be asked to identify patients ready to
wean (anyone stable and improving). You'll be asked to choose a method of weaning (there's no
one right way, but there are some wrong ways. Ensure safety and allow for as true an SBT as
possible = minimal supports). You'll be asked to evaluate weaning (be sure to review the
parameters - big ones are RSBI, VC, NIF, ABG, and Vitals).
Special Note: Do not "anticipate" failure in weaning. For example, you need to intubate a patient
with significant lung disease. You just "know" that they're going to end up needing a trach, so you
think about skipping an ET tube and go right for traching the patient. The ACCS expects you to give
every patient every chance to succeed. Intubate, aggressively wean, then trach if necessary.

Questions on the Exam

You'll see questions in the following areas:

1. A patient scenario with a bunch of information given to you (vital signs, course of illness,
etc.). You'll be asked whether to determine if the patient should be weaned. The answer is
more likely yes than no. Do not consider daily SBT if:
o Reason for intubating has not reasonably reversed
o Significant hemodynamic instability (including significant use of vasopressors)
o Sedation that impairs drive to breathe (Precedex may be an exception)
2. You'll be asked to choose the appropriate method of weaning. There's no right "one", but
there are wrong options. You need to ensure a patient is on a true SBT (in other words, it
needs to predict their ability to succeed once extubated), but also ensure safety. Do not
"over support" a patient. There are three ways to perform an SBT in addition to a T-Piece
trial:
o Using PS

o Using SIMV

o Using NPPV
3. You'll be asked to evaluate a patient who is weaning, and then make a decision on
whether to extubate. Be sure to review weaning parameters. We break weaning down into
3 categories:

 The patient is passing wean - Parameters are all acceptable, the patient looks good, the
wean has been appropriate (no excessive support). Extubate. If underlying chronic lung
disease, it is reasonable to extubate to NPPV (check settings!) as a "bridge" to extubation.

 The patient is borderline - Some parameters are good, others are poor. Consider
extubating this patient with something in place to support the "poor" parameters.
Remember, the goal is to be aggressive in weaning. For example, a patient has acceptable
VC & RSBI on PS +5 for 30 minutes. The patient coughs on request but the NIF is poor.
What adjuncts could you recommend to encourage a cough?

 The patient is failing wean - Do not continue to wean. Do not extubate. Do not collect
$200, and do not attempt another SBT for 24-hours. Current evidence (and thus the
ACCS) supports "resting" the patient adequately before trialing again. This means choosing
full support on the ventilator.

Prevention of Lung Injury from Mechanical Ventilation

Strategies Used to Prevent Lung Injury

 Use lower tidal volume strategies

6-8 mL/kg, down to as low as 4-6 mL/kg, whatever it takes to keep P plat < 30 cm H2O

 Use of lower inspiratory pressure ventilation on pressure-control modes of

ventilation
Goal is still to target the lower tidal volumes, but they aren't always provided in
exam questions
  Consider lung protective adjuncts: HFOV, APRV, ECMO
Despite what evidence says about HFOV, it is considered equal with APRV and ECMO for
exam purposes in providing longer periods of recruitment with small tidal volumes.
ECMO can bypass lungs altogether, and then lungs receive minimal mechanical ventilation
support to maintain inflation but prevent injury

 Perform recruitment maneuvers and use higher PEEP levels to improve V/Q
matching
There is no specific recruitment maneuver procedure (20 sec at 20 cm H 2O up through 40 sec
at 40 cm H2O have been observed)

Keys to Disease
 ARDS is largely a disease of V/Q mismatch, with refractory oxygenation (meaning PaO 2 does
not meaningfully increase when increasing oxygen)
 Hallmarks of diagnosis include a P/F ratio < 200, bilateral diffuse infiltrates on chest
imaging
 Treatment is mostly supportive (support oxygenation, support ventilation) - see below
 Hypoxemia is unlikely to respond to more oxygen.

In Plain Language: ARDS is an inflammatory lung injury. It causes pulmonary edema (due to the
shift of fluid from capillaries), which results in decreased gas exchange (think V/Q mismatching). It
also results in washed out surfactant. Ultimately this means decreased compliance, atelectasis,
intrapulmonary shunting, and may lead to multiple organ failure.

Clinical Manifestations
General

 Agitated, anxious, confused, restless

 Rapid onset (hours to days after insult)

Respiratory

 Inspection - cough, cyanosis, dyspnea, retractions, tachypnea, ↑ WOB

 Auscultation - ↓ BS, bronchial BS over consolidation, crackles
 Pulmonary Dynamics
↓ CL (total C< 30 mL/cm H2O)
↑ PIP
 ABGs
Oxygenation - refractory hypoxemia (PaO2/FIO2 ≤ 300, really under 200 becomes more
critical)
↑ shunt (>20%)
Ventilation - respiratory acidosis. on ventilator this is okay (permissive hypercapnia),
unless severe

Cardiovascular

 Tachycardia
 Non-cardiogenic: PCWP < 18 mm Hg (higher than that suggests cardiac, not ARDS)
Diagnosis
 Plain Chest Radiograph: Diffuse infiltrates, haziness, white-out (also could show up on a
CT Scan report)
 P/F Ratio < 200 (suspect when < 300, but more definitive < 200)
 Some type of "event" in last 7 days (may or may not present in a scenario)
 Evidence against it being cardiac (may or may not present in a scenario), such as an
echocardiogram

Possible Strategies:
 Initial Ventilation
o If scenario supports ARDS, lean more heavily towards intubation than noninvasive
(HFNC, CPAP, NPPV) options
o The mode isn't all that important: Pressure or Volume, A/C, PRVC, APV. Don't use
advanced ventilation modes initially (HFOV, APRV, ECMO)
o Always use lung protective strategies (low VT in the 4-6 cc/kg range; don't go
above). Allow for permissive hypercapnia. Keep Pplat < 30-35 when possible
o Utilize higher PEEP strategies (> 5 cm H2O)

 Advanced Ventilation Strategies (none of these is more preferred than another on the
exam):
o High-Frequency Oscillatory Ventilation (HFOV) is a recruitment mode of ventilation
that improves V/Q with a high MAP and smaller breaths than dead space ventilation
o Airway Pressure Release Ventilation (APRV) is a recruitment mode of ventilation that
improves V/Q with a high MAP and small, spontaneous tidal volumes
o Extracorporeal Membrane Oxygenation (ECMO) allows oxygenation away from lungs
(outside body) so that lungs can receive just enough ventilation to stay inflated, but
otherwise, rest until ARDS begins to clear
o Prone positioning to treat V/Q mismatch (usually signs of hypoxemia will be
evident)

 Support Oxygen consumption (treat fever!)

 Watch for hemodynamic instability - maintain adequate perfusion (mean arterial

pressure > 60 mm Hg), use of A-Line is smart to monitor status

 Antibiotics to treat evidence of infection (WBC, Fever)

 Nitric oxide for refractory hypoxemia

Trauma (Chest)

Oakes Academy Tip

You should be familiar with chest trauma in general. As with other areas on the ACCS, by able to
recognize signs and symptoms of underlying chest trauma, how to manage emergencies, and how
these might impact upon critical care management (ventilator, shock, ARDS, etc.)

Pulmonary Contusion
"Bruise" of the lung. Results in damage to capillaries, allowing blood and fluids to accumulate in lung
tissue. May interfere with gas exchange, altering V/Q, and is a risk factor for the development of
ARDS.

Flail Chest

Three or more ribs fractured in two or more places

A flail segment develops a paradoxical movement (sucks in on inspiration). Positive pressure

ventilation may mask it.

 Many patients with flail chest are now managed without intubation and MV
o IS, deep breathing, and coughing are important to reduce secretions, prevent
atelectasis, and avoid intubation.
o Aggressive airway clearance and CPT may be limited by chest wall pain
o Monitor closely for respiratory failure

 Patients with flail chest are at significant risk for acute respiratory failure
o Fatigue due to increased WOB
o Pneumothorax, hemothorax, and pulmonary contusions are common
o Associated head injury, abdominal injury, and extremity injury are common

Penetrating Trauma

Effects are very dependent upon what anatomical damage is done with the trauma. Key
considerations:

 Blood loss (may lead to shock)

 Hemothorax (may need to be evacuated)
 Pneumothorax (may need to be evacuated)
 Cardiac injury
 Lung injury

Consider Intubation when:

 Deteriorating respiratory status (fatigue from WOB, depression from analgesia)

 Need for surgery is imminent
 Shock
 Closed Head Injury
 Mechanical Ventilation with normal settings overall
o Ventilate at the lowest possible mean airway pressures due to risks of pulmonary air
leaks (pneumothorax).
o Use PEEP with caution due to barotrauma (esp. unilateral contusion) and
hemodynamic instability due to blood loss and/or head injury.
o Many patients require initial sedation or paralysis.
o Permissive hypercapnia may be employed provided no accompanying head trauma
with ↑ ICP.

Other Strategies to Consider

 Pulmonary Contusions are commonly presented on the ACCS exam

Because contusions are typically "localized" to a certain area of the lung, strongly consider
 patient positioning to address any refractory oxygenation issues
BLU GLD (blue gold) = "Bad Lung Up, Good Lung Down"

 Pain control is an issue

expect scenarios where too much pain medication (opioids especially) have been given
be sure to address pain or indications of pain (tachycardia, hypertension) aggressively,
especially if head trauma

 If an air leak is present (pneumothorax, for example), ventilation may be a challenge.

ECMO is an option in this case - unless coagulation issue as well.

 Be cautious with any type of cardiac injury (especially cardiac tamponade).

any change in positive pressure ventilation may further decrease venous return to the heart
if not intubated, consider carefully before intubating

Exercise and rehab while receiving ventilatory support

Having patients exercise while still receiving mechanical ventilation is a progressively emerging topic
in our profession. And why should it not? The benefits of exercising far outweigh the challenges,
including savings of over $4,000 per patient through the reduction of ventilator days and reduced
length of stay. While you shouldn't find "lots" of questions on the topic, it is not unreasonable to
expect one or two.

The Premise

Exercise is an effective way to combat some of the problems associated with bedrest and critical
care, including:

 A decrease in the incidence of ICU delirium

 A decrease in "ventilator days" (patients wean better)
 A decrease in "hospital length of stay" (muscles stay better conditioned)
 Improved 6-minute walk distance after ICU stay

Patients who aren't ready yet

There are some exclusion criteria related to early mobilization (but not ROM exercises - see below for
differences). As you read through you should find that you don't need to memorize this list, but just
get the picture of a patient who wouldn't qualify - basically they are unstable still. As soon as the
patient is stabilized, consideration for mobility can be given.

Excessive ventilatory support

 FIO2 > 0.6

 PEEP > 10 cm H2O
 RR > 35/min
 pH < 7.25

Hemodynamics

 Vasodilators
 Unstable arrhythmias in last day
 MAP > 140 or < 55
 Pulmonary embolus or DVT in last 24 hours
 Transvenous pacemaker
 Intra-aortic Balloon Pump (IABP)
Labs

 Hemoglobin < 7 g/dL

 Platelets < 20,000

Neurological

 Acute stroke in last 24 hours

What to Recommend on the Exam

Sedation Level Recommendations

Heavily Sedated
Passive Range of Motion Exercises*
RASS -4 to -5

Passive Range of Motion Exercises*

Moderately Sedated
RASS -3 to -2
Sitting Up

Active Range of Motion Exercises*

Active Exercise (pedaling, etc.)

Lightly Sedated
Early Mobilization:
RASS > -2
1. Try Sitting
2. Progress to Standing
3. Progress to Walking
4. Increase duration/distance

*Range of Motion Exercises involves moving the patient's limbs, usually by a physical therapist or
nurse. "Passive" implies the professional is moving the limbs on behalf of the patient. "Active"
implies the patient is being asked to perform the motion on their own.

PEEP Management

Keep this in mind: High PEEP hurts hearts, Low PEEP loses lungs. We just made that up sitting on
our front porch. If it doesn't work for you, keep reading.

What is the goal?

 Optimal opening is the optimal goal. Okay, enough alliterations.

 Physiologically speaking, our goal is to keep the lungs open enough to prevent collapse and
atelectrauma (there is damage done when alveoli slam closed on exhalation, then have to
be popped open each inspiration). However, and this is a big however, if you
overdistend the alveoli with too much PEEP, you cause a decrease in venous return to the
heart. It looks a lot like hemodynamic compromise. Not good.
 If ever given the option, the goal graphically is to place the PEEP somewhere between the
lower inflection point (that's the point of collapse) and the upper inflection point (that's the
point of overdistension). Anywhere in the middle will do just fine.
PEEP Strategies

 Normal (low) PEEP strategy: Patients should be maintained at about 5 cmH2O (4-6 cm
H2O)
 Therapeutic PEEP is > 6 cm H2O: Increase PEEP in presence of refractory hypoxemia (SpO 2
or PaO2 doesn't increase with a rise in FIO2) High PEEP for exam purposes is up to 20 cm
H2O. Use with refractory hypoxemia associated with ARDS, obesity (with esophageal probe)
Note: Do not "automatically" increase PEEP for ARDS. Look for signs of refractory
hypoxemia

Independent Lung Ventilation

Differential/Independent Lung Ventilation

Know the basics: A method of ventilating (with two different ventilators) each lung
separately. There are three ways to accomplish this: double lumen ET Tube, single
lumen ET Tube with a bronchial blocker, and single lumen ET Tube placed in the right or
left mainstem bronchus.

When Should You Use It: When there is a significant pulmonary process affecting one
lung greater than the other (especially when compliance or resistance is significantly
affected). Typically you can better ventilate the healthy lung while allowing for less
ventilation of the affected lung.

Used to ventilate asymmetric lung disease that requires different ventilatory strategies
after conventional therapies have failed (i.e., lateral positioning).

Anatomic:
1. Intrabronchial aspiration
2. Massive unilateral hemoptysis
3. Pulmonary alveolar proteinosis (lung lavage)

Physiologic:
1. Bronchopulmonary fistula
2. Single lung transplant
3. Unilateral lung disease:
a) Hypoxia refractory to high FIO2 and generalized PEEP
b) Overinflation of noninvolved lung
c) PaO2/FIO2 < 150
d) PEEP induced deterioration in oxygenation
e) Significant deterioration in hemodynamics in response to PEEP

Complications:

 Bronchial trauma
 Laryngeal trauma
 Obstruction/malpositioning of DLT

Intrahospital Transport
 Oakes Academy Tip
Generally speaking, it may be preferred to transport a patient on a transport ventilator, when the
option is provided, over bagging that patient through the hospital. Be aware of the differences in
equipment for transport (use of an MRI compatible ventilator, use of a transport ventilator which is
more compact than a bedside ventilator, etc.). You may need to alter settings based upon the
limitation of the ventilator you are using (for example, a patient may be on Pressure Control, but
the transport ventilator only allows for Volume Control. Knowing that you should match the
delivered Tidal Volume and then watch measured PIP carefully).

Indications: Risks and benefits need to be considered, especially in very unstable

patients. Typically you would transport a patient for diagnostic, therapeutic (including
surgical) purposes when the decision is made to not perform at bedside (or can't be
performed at bedside).

Monitoring: Same as during stationary care.

Continuous:

 EKG
 HR
 BP (if invasive line)
 SpO2

Intermittent:

 Auscultation
 Respiratory Rate
 Blood Pressure (no invasive line)
 Peak Pressures
 Tidal Volume

Hazards During Transport

 Accidental extubation or removal of IV access due to movement

 Cardiovascular instability
 Equipment failure
 Hyperventilation (manual ventilation)
 Loss of O2 supply
 Loss of PEEP/CPAP
 Position changes causing ↓ BP, ↓ PaO2, and/or ↑ PaCO2
 May increase risk of aspiration (and thus VAP)

Improving Patient-Ventilator Interaction

The goal is to achieve synchrony between the ventilator and the patient. This is not a
complete discussion but addresses what you are most likely to see on the exam.

STEP 1

Optimize mode and ventilator settings (fix the ventilator first)

  Increasing support (pressure support in particular) is common
 Fix auto-PEEP (decrease inspiratory time and/or respiratory rate)
 Fix trigger (this is rare, but switch to flow trigger from pressure if an option)

STEP 2

Address Patient Issues

 Treat fever (which causes increased metabolic rate = high respiratory drive)
 Treat pain (again, causes increased metabolic rates)
 Know which drugs address pain and sedation (fentanyl is a common one, but morphine may
also appear)
 Treat anxiety (anti-anxiety drug)
 There may be scenarios where it is appropriate to increase sedation or even add a paralytic
o Before increasing sedation, see if there are reasonable options to "fix" the ventilator
settings
o Consider paralytic if severe dyssynchrony such as with asthma. DO NOT GIVE if
patient not on sedation
 If none of this applies, consider other unusual situations
o ET tube too small (change it for a larger tube, preferably with a tube exchanger)
o Water in the circuit (unusual on ACCS)

Cardiac oscillations (heartbeat triggers the ventilator when flow trigger - m Airway instillations
other than for ACLS

Using the mnemonic "NAVEL" helps you remember what common drugs can be instilled:

 Naloxone (Narcan)
Opioid reversal agent. Usually given via IV, IM but can be instilled
 Atropine
If vascular access is unavailable, may consider ET tube instillation
 Valium
Very uncommon administration - especially for ACCS exam - but know it is possible
 Epinephrine
Upper airway bleeding [topical epinephrine (1:20,000) or vasopressin, thrombin,
fibrinogen-thrombin combination, and/or lavage with iced saline]
 Lidocaine
can be instilled to help suppress cough - particularly helpful during procedures like
bronchoscopy
cautiously consider in patients with severe head trauma before suctioning to prevent an
increase in ICP (and decrease in CPP)

Other Drugs Commonly Found on the ACCS Exam that can be instilled:

 Cold Saline
Treatment of hemoptysis: cold saline at 4 degrees Celsius to slow or stop bleeding - usually
when site of bleeding is visualized (less likely to be helpful for significant bleeding!).
Stabilize patient and airway before doing this (such is by placement of a double lumen
endotracheal tube).
 Topical Thrombin
Treatment of hemoptysis: not always successful or available, but works to "clot" the site of
bleeding. Like with cold saline, the site of bleeding should be visualized usually. Stabilize
patient and airway before doing this.
Aerosol Delivery Optimization

Oakes Academy Tip

The ACCS exam doesn't care much for how you deliver medication to a standard room air
breathing patient. The focus instead is on how to most effectively deliver aerosolized drugs
in patients who are on high flow nasal cannulas, noninvasive ventilation, and on the
ventilator. While evidence is still building in these areas, the ACCS has some leanings.

Mechanical Ventilation (using a dual-limb circuit)

A dual-limb circuit has an inspiratory side where gas flows through a humidity device and towards
the patient, as well as an expiratory side which allows for CO2 clearance.

Preferred Method: Vibrating mesh nebulizer (due to the ability to provide relatively equal
particle sizes in the "respirable" range)

Preferred Placement:

 Proper placement should be after the filter but before the patient "wye"
 So where exactly is optimal?
o The optimal location would be placing the nebulizer on the inspiratory limb before
the patient "wye" of the dual circuit with an additional 6 inches of large bore
tubing to allow for the medication to gather during the breath cycle
o Important note: If a patient is receiving passive humidification (aka HME) you must
remove the HME to allow for proper medication delivery otherwise the aerosol will be
deposited into the HME

The following is the flow of gas beginning at the ventilator:

1. Inspiratory filter
2. Humidifier (if active humidification is present)
3. Inspiratory limb
4. Patient "wye" (HME may be present if passive humidification)
5. Endotracheal tube (or tracheostomy tube)
6. Expiratory limb

Noninvasive Ventilation (NPPV) (using a single-limb circuit)

A single limb circuit doesn't have an official inspiratory vs expiratory side. Because of this, a leak
port is added to the circuit to allow for CO2 clearance. Proper placement of the nebulizer is very
important to ensure proper medication delivery.

Preferred Method: Vibrating mesh nebulizer

Placement: In order for the patient to receive the medication it is proper to place the nebulizer in
the breathing circuit but after the leak port. As you picture this, remember that the goal is to
ensure drug doesn't unnecessarily escape out of the leak port.

The following is the flow of gas beginning at the noninvasive ventilator:

 1. Inspiratory filter
2. Humidifier
3. Breathing circuit
4. Leak port
5. Mask (or tracheostomy tube)

High Flow Nasal Cannula (HFNC)

Preferred method: Small volume jet nebulizer with a mouthpiece. If the patient is unable,
consider an aerosol mask.

While in reality aerosolized drugs can be delivered via the HFNC circuit, the ACCS exam does not
treat this as a preferred route of administration. Removing the nasal cannula to provide a treatment
may cause the patient to quickly decompensate and is not preferred.

Chest Radiography - Tubes and Lines

See Approximate Tube\Line Placement on Chest Radiograph

Descriptive Terms for Chest Radiographs

Key Diagnosis Chest Radiograph Descriptive Terms to Watch For

 Blunted costophrenic angles (with one of the below)

 Hyper-expansion (> 7th rib mid-clavicular line)
Air-trapping
 Enlarged airspaces

 Bilateral infiltrates
 Fluffy infiltrates
ARDS
 Reticulogranular pattern (reticular means "net-like")

 Haziness (usually with a location, such as bilateral basilar, or bilateral

apical)
 Low or reduced lung volumes
Atelectasis
 If labeled, may include descriptors like "linear atelectasis" or
"platelike atelectasis"

 Costrophrenic blunting
 Opaque black
Pleural Effusion
 Haziness

 Air bronchograms
Pneumonia  Airspace opacities
 Ground-glass opacities (so not fully consolidated)
Consolidation  Opaque white
 Increased densities
 White-out, infiltrates that are given by location (right-lower lobe, for
 example)

 Absence of vascular markings

 Deep sulcus sign
Pneumothorax
 Tension: Will be described as compressing heart, mediastinal shift

 Bilateral alveolar infiltrates

o With cardiomegaly, vascular engorgement suggests
cardiogenic/CHF
Pulmonary  Butterfly pattern
edema  Interlobular septal thickening
 Interstitial edema
 Presence of Kerley A lines (upper lobes) and Kerley B lines (bases)

 Reticular opacities
Pulmonary
 Honeycombing (destroyed, fibrotic tissue)
fibrosis

 Pulmonary contusion: unilateral, localized haziness

 Hemothorax: Much like pleural effusion (absence of vascular
Trauma
markings)

 Miliary pattern
Tuberculosis  Nodules/nodular pattern

 Centrilobular - Respiratory bronchioles or alveoli

Other Terms  Mass - Can be pulmonary, pleural, mediastinal

Oxygenation Indices

This aspect of the exam is the process of assigning a number to oxygen status. Review some of the
most common indices for determining oxygenation that may appear on the ACCS:

 SpO2: noninvasive, quick measure. Used extensively on ACCS. Be able to make clinical
judgments based on SpO2 in the context of a delivered FIO2.
 PaO2: partial pressure of oxygen in arterial blood (from ABG)
 PAO2: partial pressure of oxygen in alveoli
 P/F ratio: PaO2/FIO2. This is one of the most common bedside indices used.
Normal (100/.21) = about 500
< 200 is consistent with ARDS
Lower P/F ratio is associated with V/Q mismatching (worsening V/Q)

Oakes Academy Tip

Remember, clinically the goal is not necessarily to correct oxygenation to normal, but instead to a
minimum threshold that allows for adequate oxygenation. This is somewhere around a PaO2 of 60,
SpO2 93%. This is particularly important in the overall goal of minimizing oxygen toxicity. The goal
is to wean FIO2 to below 0.50.

Treat to adequate, not to normal.

A quick guide using SpO2 and FIO2 (since that is what is most often given on exam):

SpO2/FIO2

Normal = 100/.21 = 500

Clinically significant = 92/.21 = 440 or below = TREAT at this point

Be just as aware of over-oxygenation. The ACCS takes oxygen toxicity as a serious risk to the
patient. Unless clinically indicated, do not administer higher F IO2.

Assessment of Ventilation

Oakes Academy Tip

What do you think about when you hear "Assessment of Ventilation"? Carbon dioxide? Exactly! It
should be of no surprise that ventilation will be tested on the exam. Most of it will be pretty basic,
like assessing a patient and noting that a minute ventilation of 12 L/min is abnormally high.
Knowing PaCO2 ranges, how it affects pH, and what to do when it is abnormal is important (free
advice: treat the pH, not the PaCO2 primarily. Think COPD retainer!).

How about capnography? Yes, definitely on the exam. You might be asked to interpret numbers
(same as PaCO2 range), or you might be asked to interpret a capnogram.

Be aware of CO2 production as it is likely to be on the exam. This alters due to metabolic processes
(such as fever), diseases, pharmacology (sodium bicarbonate), or with nutrition. For example, a
patient over their nutrition goal (being overfed) will produce excess CO 2 which may complicate
weaning attempts.

Normal Values

 End tidal CO2 (ETCO2, or PETCO2): noninvasive measure. Normal is nearly same as PaCO2
(35-45)
 Partial pressure CO2 (PaCO2): invasive measure, around 35-45 is normal.
 Transcutaneous CO2 (PTCCO2): gaining in popularity (it correlates fairly well with PaCO 2).
Normal is 35-45.
 Minute ventilation (VE): 5-7 L/min

Assessment of Capacity (Ventilatory Mechanics)

Work of Breathing

 At times measured, particularly for weaning

 Normal is 0.5 - 0.7 J/L
 Anything above this would be considered an increased work of breathing
Adequacy

Respiratory Drive: P0.1 (cm H2O)

Normal < 2
Abnormal > 4-6

Respiratory Muscle Strength

Vital Capacity (mL/kg)

Normal 60-80
Abnormal < 60

PIMax (MIP, NIF) (cm H2O)

Normal MORE NEGATIVE THAN (<) - 60
Abnormal (MORE POSITIVE THAN (>) - 30

Respiratory Muscle Endurance

MVV (L/min)
Normal 120-180 L/min
Abnormal < 20

Capnography

A simple and easy to use noninvasive device that can be utilized to continuously monitor exhaled
carbon dioxide in a variety of scenarios.

Also called end-tidal CO2 (ETCO2) monitoring as it measures the carbon dioxide value at the end of a
full exhalation.

Values

 35-45 mm Hg - Normal range (same as PaCO 2 from an ABG)

 < 35 mm Hg - Hyperventilation (not enough carbon dioxide)
 > 45 mm Hg - Hypoventilation (too much carbon dioxide)

Uses

 Monitoring patients during procedures requiring sedation

o When patients are given medications that can suppress the respiratory drive, a
specialized nasal cannula is used to monitor adequate ventilation
 Cardiac arrest
o Monitoring tracheal tube placement
o Monitoring CPR quality
 < 10 mm Hg, consider improving CPR quality
o Can detect the return of spontaneous circulation (ROSC)
 A quick increase and sustaining in CO2 value is a strong indicator of ROSC
 A sharp decrease in CO2 may indicate a loss of ROSC
 Mechanically ventilated patients
o Real-time monitoring of patient's ventilatory status
o Helpful for noninvasive trending of CO2 throughout the day
 Verify endotracheal tube placement using disposable colorimetric capnomentry
o A specialized adaptor is attached to the endotracheal tube after intubation which can
detect the presence of CO2
o When CO2 is detected it causes the device to change colors from purple to yellow.
 o Use the following to help you remember: Yellow = Yes (tracheal
intubation); Purple = Problem (ETT is in the esophagus)

Types

 Sidestream - Used for patients who are not mechanically ventilated via a specialized nasal
cannula (delivers sample to a monitor where value is read)
 Mainstream - Used with mechanically ventilated patients (monitoring occurs directly at the
patient's airway by adapting to the endotracheal tube)

Pathophysiology

Decreased ETCO2

 Pulmonary Embolism - Carbon dioxide increases in the blood but is not exhaled leading to
a decreased ETCO2
 Hyperventilation - Can be due to increased minute ventilation. Consider decreasing RR (or
VT - less likely)

Increased ETCO2

 Fever, agitation, and pain lead to an increased production of carbon dioxide causing an
increased ETCO2
 COPD - These patients may have high PaCO2 values which would translate to increase
ETCO2
 Hypoventilation - Can be due to decrease minute ventilation. Consider increasing RR or VT

Capnogram

The waveform associated with capnography is called a capnogram. There are 4 phases of the
capnogram:
Phase 1 - Referred to as dead space ventilation. This is when exhalation begins and the gas in the
deadspace is removed. CO2 levels should be at or around 0 mm Hg.

Phase 2 - This phase is called the ascending phase. There is a very quick rise in carbon dioxide
which is represented by a straight vertical line in the capnogram and is associated with the carbon
dioxide being released from the lower airways.

Phase 3 - Also known as the plateau phase. This is represented by a horizontal line that has a
minimal rise and occurs when the exhaled CO2 levels out. The end of the line is called end-tidal CO2

Phase 4 - Occurs when inhalation begins and the CO2 levels quickly drop. This quick decrease is
represented by a second vertical line.

Troubleshooting

 A sudden reading of zero can be indicative of a circuit disconnect, make sure to check all
connections
 A slow increase in CO2 is usually an indicator of obstruction due to COPD or asthma,
bronchodilators may be needed

Neurologic Assessment/EEG

Electroencephalogram (EEG)

Main diagnostic application of EEG is epilepsy

Secondary clinical uses:

 Diagnosis of coma, encephalopathies, and brain death

 Monitoring of brain function in ICU:
o Non-convulsive seizures/non-convulsive status epilepticus
o Effect of sedative/anesthesia in patients in medically induced coma
(treatment of refractory seizures or increased intracranial pressure)
o Brain damage in conditions such as subarachnoid hemorrhage

Neurological Assessment

Consciousness

 Modified Glasgow Coma Score (see more)

 Levels of Consciousness (see more)

Neurological Assessment

Vital Signs

 Respiratory Rate (RR)

 Heart Rate (HR)
 Blood Pressure (BP)
 Motor Activity
o Ability to cough/clear secretions
o Grip strength
o Motions: coordination, paralysis, tremors
o Posture:
  Decorticate - flexed arms, extended legs, plantar flexion
 Decerebrate- extended arms, extended legs, plantar flexion
o Pupil size and reaction
 Mental Status
o Emotional state, behavior, comfort, orientation
o Level of Consciousness (LOC)

Glasgow Coma Score

The Glasgow Coma Score (GCS) is used in its modified form (sometimes called the "Modified"
GCS). This is a very common rapid assessment used in critical care.

Lowest possible score = 3 (Comatose)

Highest possible score = 15 (Fully Alert)

General clinical rule of thumb: "Under 8, Intubate"

How it's stated: "Patient has a GCS of 8"

Critical Care Alterations:

 add the letter T (for Tube) after the score in patients who are intubated.
 add the letter C (for Closed) after the score in patients who have closed eyes due to
swelling/trauma
 more detailed approach includes giving each category with its number. Ex: GCS 7T = E3, V1,
M3

MODIFIED Glasgow Coma Score

1 2 3 4 5 6

Eyes Does not Opens to Opens

Opens to Pain --- ---
(E) open Speech Spontaneously

Verbal No Incomprehensibl Confused, Normal

Inappropriate ---
(V) Sounds e Disoriented Conversation

Motor Flexion to Withdraw from Localizes to Obeys

None Extension to Pain
(M) Pain Pain Pain Commands

Motor Responses explained:

Extension to Pain: Note decerebrate posturing (rigid, extended, straightened at elbows)

Flexion to Pain: Note decorticate posturing (arms flexed/bent inward, feet inward)

Withdraw to Pain: Pulls hand away when nailbed is pinched, but doesn't go beyond chin

Descriptive Terms for Levels of Consciousness (LOC)

Alert Awake, oriented and responds appropriately

Confused Inability to think clearly, impaired judgment

Disoriented Beginning loss of consciousness, disoriented to time/place

Lethargic Sleepy, arouses easily, responds appropriately

Obtunded Awakens only with difficulty; then responds appropriately

Does not completely awaken, responds only to deep pain, withdraws or pushes
Stuporous
you away

Semicomatos
Responds only to deep pain, exhibits reflex
e

Comatose No response, flaccid muscle tone

Neurologic Assessment/Stroke

Definition

 When the blood supply to a portion of the brain is suddenly interrupted or when a blood
vessel in the brain bursts
 Brain cells die (ischemia) when they no longer receive oxygen

Symptoms (tend to be sudden)

 Confusion, trouble speaking, or understanding speech

 Numbness or weakness, especially on one side of the body
 Severe headache with no known cause
 Trouble seeing with one or both eyes
 Trouble with walking, dizziness, or loss of balance or coordination

Forms

 Ischemic: blockage of a blood vessel supplying the brain

 Hemorrhagic: bleeding into or around the brain

Diagnosis/Evaluation

You are not likely to be asked to diagnose a stroke straight out, but you should be aware of the basic
findings that suggest one:

 History of stroke in family (or other cardiac issues)

  Presence of clotting disorder or at high risk of clotting (such as long bone fractures -
ischemic)
 Altered level of consciousness (LOC) is common
 Airway patency issues (often with drooling)
 Radiographic evaluation options:
o Arteriography - Definitive diagnosis of an aneurysm
o Computed tomography (CT) - The Brain Attack Coalition recommends that
the CT be performed within 25 minutes of arrival to the ED
o CT angiography and CT perfusion
o Magnetic resonance imaging (MRI) - not recommended for emergency diagnosis of a
stroke

Immediate Management/Treatment

 Determine type of stroke (ischemic or hemorrhagic) by CT scan with contrast:

 If scenario suggests ischemic, consider fibrinolytic
 If scenario suggests hemorrhagic, consider surgical intervention or supportive care
 If any doubt about airway patency or respiratory sufficiency, do not hesitate: intubate

Other Management Considerations

 Blood Pressure
o Increased BP is common. Intervention may not be needed unless BP is really high
(like systolic around 200 or higher)
o BP >160 is present in 60% of patients with an acute stroke. The brain raises the
CPP to enhance blood flow to the damaged tissue. Aggressive use of
antihypertensives can decrease the blood flow to the viable tissue surrounding the
infarction and worsen the neurological deficits.
o Monitor for decreased BP and other complications of therapy (intracranial
hemorrhage, angioedema, bleeding)

 Therapies
o Antithrombolytic therapy (recombinant tissue plasminogen activator [ t-PA],
Activase)
o Fluid Management (be careful)
o Hypertension management
o Oral antiplatelet therapy (aspirin) - if not hemorrhagic
o Thrombolysis (intra-arterial, mechanical)
o Position head midline and head of bed elevated 30 degrees to decrease risk of
aspiration and increase cerebral perfusion

Brain Death

Uniform Determination of Death Act (UDDA):

An individual who has sustained either:

1. Irreversible cessation of circulatory and respiratory functions, or irreversible cessation of all

functions of the entire brain, including the brain stem, is dead.
2. A determination of death must be made in accordance with accepted medical standards.

The AAN identifies four prerequisites that should be met to establish a brain death
diagnosis.
 1. Coma of known cause as established by history, clinical exam, lab testing, and
neuroimaging.
o The standard of care is a computed tomography scan or magnetic resonance imaging
(MRI), the two most commonly used neuroimaging tests.
o Complicating conditions, including hypotension, hypothermia, and hypoxemia, must
be ruled out or reversed before the brain death exam begins
2. Normal or near-normal core body temperature (higher than 36° C)
3. Normal systolic BP (higher than or equal to 100 mm Hg)
4. At least one neurologic exam (some states and hospital protocols require two)
Apnea test, plus one confirmatory test:
o Cerebral angiography
o EEG
o Transcranial Doppler ultrasonography (TCD)
o Cerebral computed tomographic angiography (CTA)

Other
Absence of reflexes

 Brainstem
o No pupillary response
o Negative doll's eye test and caloric test (ice water in ear)
 Corneal - cotton swab test on eyeball
 Cough and gag
 Chloric reflex test (cold water in ear)

Apnea Test
Purpose

To confirm the loss of spontaneous respirations

 Absence of a breathing drive. Tested with a CO2 challenge. (PaCO2 > baseline)

Prerequisites
Note that pre-requisite can include interventions (vasopressors, mechanical ventilation, etc.)

 Eucapnia (PaCO2 35–45 mm Hg). No prior evidence of CO2 retention (i.e., COPD, severe
obesity)
 Absence of hypoxia
 Euvolemia
 Normotension
 Normothermia
 Clinical absence of neurological function and deep coma
 Allow for adequate clearance of drugs in case of a drug overdose or a patient who has been
sedated (especially if obese or has renal or hepatic impairment). This usually takes several
days.

Procedure

 Ensure systolic blood pressure >100 mm Hg.

 Determine patient's baseline PaCO2 level with ABG. If it's not within the normal range (35 -
45 mm Hg), adjust MV until eucapnia is achieved.
 Preoxygenate 10 minutes with 100% oxygen to a PaO2 >200 mm Hg.
  Disconnect patient from the ventilator.
 Maintain oxygenation (insert catheter down ET tube, close to the level of the carina and
deliver 100% O2 at 6 L/min).
o An alternative to delivering O2 at 6 liters at the distal tip of the endotracheal tube is
to use CPAP at 10 cm H2O and 100% O2 at 12 L/M.
 Observe chest and abdomen for movement for 8-10 minutes.
 If no movement seen during this period, obtain another ABG.
 Place patient back on the ventilator.

A positive test and support of the clinical diagnosis of brain death

 A rise in PaCO2 by 20 mm Hg over baseline or a PaCO2 of 60 mm Hg or more.

 Absent respiratory movements for the entire period of the test.
 Abort if systolic BP decreases to 90 mm Hg
 Abort if O2 Sat <85% for >30 seconds.
 If test is inconclusive, but the patient is hemodynamically stable during the procedure, it
may be repeated for a longer period of time (10–15 minutes) after the patient is again
adequately pre-oxygenated.
 If the target increase in PaCO2 isn't obtained, a confirmatory test and written
documentation of why the apnea test was inconclusive is required.

Note

A major goal of the test is to try to maintain near normal body temp and BP, to ensure adequate
perfusion to all organs potentially destined for donation.

Neurologic Assessment: Seizures

Uncontrolled electrical activity in the brain that may lead to symptoms ranging from mild loss of
attention to violent muscular contractions that can lead to death.

Causes

Various individual causes, but key ones you should be aware of (as a seizure might suggest the
diagnosis)

 Brain tumor
 Drugs/medications - including adverse effects to drugs started in hospital
o Theophylline toxicity (keep < 10 mg/L)
 Hypoglycemia
 Infection/high-grade fever
 Injury/trauma
 Severe acidosis (respiratory or metabolic)

Treatment

 Important: Consider intubation for airway patency anytime a seizure is mentioned in a

question
 Drugs: lorazepam (Ativan) is a first choice, phenytoin and other benzodiazepines are
options as well
 If given the option, consider EEG to monitor seizure activity before extubating

Cardiovascular Assessment
 One way to remember treating significant cardiovascular numbers:

 If the number is higher, administer a blocker

 If the number is low, may need more flow (unless asymptomatic, don't you
know)

Heart Rate (beats/min)

 Tachycardia (technical definition = > 100, definitely act if > 120)

Usually symptom of something going on, treating underlying cause is a priority
o hypoxemia, drugs, fever/metabolic processes, pain/anxiety
o If cardiac related, consider "blockers"
 Bradycardia: (< 60, pay attention to symptomatic vs asymptomatic)
Treat symptomatic bradycardia (SOB, chest pain, etc.) aggressively - think atropine
o Cardiac event (junctional rhythms, for example)
o Severe distress (tachycardia will be followed by bradycardia . . . before cardiac
arrest/asystole)

Blood Pressure (mm Hg)

 Hypertensive (~ 140/90 or above)

o Treat if severe (blockers)
 Hypotensive (~ 90/60 or below)
o Key number: mean arterial pressure < 60 = inadequate perfusion so DO
SOMETHING (fluids, inotropics, pressors)

Other Information You May Wish to Review (less likely to be on test)

Inspection/Palpation

 PMI (Point of Maximal Impulse) - 5th left IC space, mid-clavicular line

o often ↓ in COPD and shifted down to left sternal border
o shifts towards a lobar collapse
o shifts away from a tension pneumothorax
o shifts left in cardiomegaly

 Pulmonic Area
2nd left IC space near sternal border
↑ vibrations with pulmonary hypertension

Auscultation - Heart sounds

S1 Closure of A-V Valves (ventricular contraction), beginning systole

S2 Closure of Semilunar Valves (ventricular contraction), during diastole

S3 Rapid ventricular filling during diastole. Abnormal, associated with CHF.

S4 Active filling of ventricles during late diastole. May be normal.

Intensity

Normal = clear sounds

At base of heart: S1 < S2
At apex of heart: S1 > S2

 Abnormal ↑: pulmonary hypertension (S2), cor pulmonale

 Abnormal ↓ (distant or muffled): heart failure, obesity, pneumothorax, pulmonary
hyperinflation, valve abnormalities

Cardiovascular Assessment-Diagnostic Testing

What We Need to Assess

 Right side of heart

o Indicates the "health" of the lungs (and then, less directly, the systemic flow)
o Right atrium is an indicator of fluid status (RAP)
o Right ventricle is an indicator of pulmonary status. Right Ventricular Hypertrophy
can indicate pulmonary hypertension
 Left side of heart
o Indicates the "health" of systemic flow, especially the aorta
o Left Ventricular Hypertrophy can indicate a problem with aorta (stenosis,
insufficiency), or hypertension

Blood tests

 Cardiac Markers include BNP, CPK, Troponin, and Serum Lactate

See section on Cardiac Markers for details

 Electrolytes - check for imbalances which can have a major impact on cardiac function
See section on Electrolytes

 Clotting - clots affect 3 major organs: lungs (PE), brain (CVA), and cardiac vessels (MI)
See section on Coagulation Studies

Electrocardiogram (ECG or EKG)

12-lead EKG is the standard

 Nothing hugely alarming with sinus tachy or brady with regular rhythm (worry more with
SVT and symptomatic bradycardia)
 Ischemia: Inverted T- wave, S-T segment depression
 Injury: ST elevation
 Infarction: Significant Q-wave

Cardiac Tests You May Find on Exam

 Echocardiogram
ultrasound of the heart, used to evaluate pumping functions of heart, and the condition of
the heart valves
recommend if suspect reduced heart function, or for disease involving heart valves
should be the first action in quickly evaluating for cardiac tamponade
  Transesophageal echocardiogram (TEE)
probe in the esophagus to get a better look at heart using echocardiography. Can be done
bedside.

 Cardiac Catheterization
often used to looking at vasculature for emboli, narrowing, etc.
requires patient transport

 Coronary CT Angiography
intravenous contrast administered, then images taken as it travels through coronary
arteries. Note that HR needs to be slowed to < 70/min to be effective (beta blockers are
used for this usually)
better results when patient can perform breath hold (~5 seconds)

 Cardiovascular/Coronary MRI
While it is more expensive and time-consuming, there is no need for contrast and no need
to slow HR using beta blockers

 Urgent Mediastinal Exploration

When hemodynamic compromise that is like cardiac tamponade (from ECHO)

Cardiac Markers

Oakes Academy Tip

Consider cardiac markers when patient's symptoms are consistent with an acute MI. Note that
many of these tests are non-specific for an MI (there are other causes for abnormal results). Use a
combination of symptoms and test results.

Note about values: For ease of memorization, we have left off units .

Test Values Interpretation

BNP (b-type natriuetic failure: Secreted from heart ventricles - indicates heart
peptide) 100-300 failure

Enzyme found in heart and skeletal muscle - may

Creatine kinase 26-174 U/L indicate MI
Other factors may ↑ Creatine kinase (Muscle disease)

< 0.04 Serum marker for cardiac disease

ng/mL
normal Elevates within 3 hours of acute MI, Remains
Troponin elevated for 5-9 days
> 0.40 Other factors may ↑ troponins (PE, Sepsis, etc.)
ng/mL
likely an MI Usually drawn in a series of 3 levels
 Clinically significant levels are generally > 2
0.5-1
Serum Lactate
mmol/L
Indicator of anaerobic metabolism

Cardiac Markers

Oakes Academy Tip

Consider cardiac markers when patient's symptoms are consistent with an acute MI. Note that
many of these tests are non-specific for an MI (there are other causes for abnormal results). Use a
combination of symptoms and test results.

Note about values: For ease of memorization, we have left off units .

Test Values Interpretation

BNP (b-type natriuetic failure: Secreted from heart ventricles - indicates heart
peptide) 100-300 failure

Enzyme found in heart and skeletal muscle - may

Creatine kinase 26-174 U/L indicate MI
Other factors may ↑ Creatine kinase (Muscle disease)

< 0.04 Serum marker for cardiac disease

ng/mL
normal Elevates within 3 hours of acute MI, Remains
Troponin elevated for 5-9 days
> 0.40 Other factors may ↑ troponins (PE, Sepsis, etc.)
ng/mL
likely an MI Usually drawn in a series of 3 levels

Clinically significant levels are generally > 2

0.5-1
Serum Lactate
mmol/L
Indicator of anaerobic metabolism

Hematology (Clotting and Bleeding)

Oakes Academy Tip

We know how important the topic of bleeding is, particularly with procedures we are involved in.
These directly include intubation, bronchoscopy, arterial blood draws, etc. Indirectly we need to be
aware of bleeding and clotting as it relates to pulmonary emboli, and interference with oxygen-
carrying capacity.

Test Values Interpretation

Blood constituent for clotting

Increased Platelets* (thrombocystosis) indicates high risk of

clotting. Consider anticoagulation therapy.

Decreased platelets (thrombocytopenia) indicates increased

risk of bleeding.
150,000-
Platelet
400,000/µL
*Reactive thrombocytosis occurs with certain drugs
(including epinephrine and heparin). This usually does not
need to be treated and does not generally increase the risk
of blood clots.

Transfusion Trigger: If < 50,000/µL consider

transfusing platelets

A measure of the amount of time (in seconds) required for

fibrin clot formation - measures EXTRINSIC PATHWAY,
helpful with determining coumadin dosages

Prolonged PT indicates an increased risk of bleeding (it

takes longer for a clot to form):

 With medication: coumadin, aspirin

 With massive blood transfusion (dilution effect)
Prothrombin Time  Hypothermia
11-13 sec  Liver disease - even mild (diminished clotting factors)
(PT)
 Disseminated intravascular coagulation (DIC)

Decreased PT indicates an increased risk of clotting:

 After fresh frozen plasma (FFP) transfusion

 Vitamin K supplements

Transfusion Trigger: If > 18 seconds, consider

transfusion of fresh frozen plasma/cryoprecipitate

International < 1.3  Ratio of patient's PT to a control PT (INR = Patient PT

Normalized Ratio / Control PT) - DO NOT worry about formula!
(INR)  INR is particularly helpful when monitoring drug
levels, like warfarin (Coumadin)
 Indirect measure of liver function (liver is responsible
for the production of clotting factors)
 Transfusion Trigger: If > 2.0, consider transfusion of
fresh frozen plasma (FFP)/cryoprecipitate

Time it takes, in seconds, for plasma to clot when exposed

to substances that activate contact factors: Measures
INTRINSIC PATHWAY, helpful for heparin dose/level. This is
called PARTIAL due to the absence of tissue factor.

Prolonged aPTT:
Activated partial
thromboplastin time 25-35 sec  Severe liver disease (may be normal with milder
(aPTT) disease)
 Disseminated intravascular coagulation (DIC)
 Massive blood transfusion (dilution effect)

Transfusion Trigger: If > 60 seconds, consider

transfusion of fresh frozen plasma
(FFP)/cryopreciptate

Arrhythmias

OAKES ACADEMY tip

This is not an ACLS exam. Keep that in mind as you review this information. There are intermittent reports
support for the rest of a patient scenario. In other words, you are unlikely to get a question asking you to sim
recommend reviewing the basic arrhythmias and focusing on what to do for each. Check out our Quicktoria
There are a couple of keys.

#1 Does the patient have a pulse. If no, the rhythm strip doesn't matter! Treat it as asystole.
#2 Is the patient stable? If the patient is stable, don't overreact.

See the EKG Quicktorial

Overview of Care

Bradycardia

HR < 60/min with signs of diminished perfusion usually

Exam MAY ask you to treat bradycardia solely based upon EKG presentation

Administering oxygen is always a good idea

Treat pharmacologically (see Rate Control for details)

Bradycardias (Including 1st, 2nd, 3rd degree heart block)

(Treating for symptomatic or accompanied by significant hypotension)
Care:
  Support: O2 as needed
 Stable: Observe unless 2nd degree (type II), 3rd degree - then internal pacing
 Unstable: External pacing, consider parasympatholytic

Tachycardias
(Treating for rate generally > 120, usually not more than 150)
Care:

 Support: O2 as needed
 Stable: Chemical cardioversion, anticoagulation
 Unstable: Synchronized cardioversion

Pulseless (Vfib, Vtach, PEA, Asystole)

Care:

 Provide CPR
 Defibrillate as soon as available
 Do not necessarily jump to intubate - it is not highest priority (over getting return of
circulation)

Congestive Heart Failure (Heart Failure, LVF)

The inability of the left ventricle to maintain adequate cardiac output, thereby failing to provide
sufficient blood flow to meet the metabolic demands of the body.

Usually left heart failure with or without right heart failure.

Causes can include arrhythmias, hypertension-induced, infection, shock, etc.

Clinical Manifestations

 Key: likely to present as shortness of breath, probably moderate-to-severe

respiratory distress. May or may not have classic frothy secretions (flash
pulmonary edema). Hypoxemia and tachycardia are likely to accompany this.
 Cardiac: tachycardia, S3 murmur, hypotension, JVD, hepatomegaly
 Respiratory: tachypnea, dyspnea, orthopnea, coarse crackles/decreased/wheezing,
hypoxemia, pink frothy secretions, pulsus alternans
 CXR: cardiomegaly, Kerley B lines, diffuse infiltrates (pulmonary edema)
 Other: fatigue, irritability, diaphoresis

Treatment

 Key: Use CPAP if offered (8-15 cm H2O to start) on high O2. Give diuretics
aggressively (assuming good kidney function; if not, dialysis may be indicated)
and be cautious with not allowing patient to be fluid overloaded.
 Oxygen - higher is better! Don't hesitate to use 1.0.
 Consider CPAP or NPPV (BiPAP), perhaps Vent, all with adequate CPAP/EPAP/PEEP
 Diurese as appropriate (choices will depend on hemodynamic stability)
 Correct electrolytes or anemia
 Pharmacology: Diuretics, Inotropes, Beta Blockers, Vaso- or Venodilators

Coronary Artery Disease (CAD)

Occlusion of the arteries of the heart resulting in infarction, often due to plaque build-up. May lead
to decreased blood flow. It increases the risk of myocardial infarction. For exam purposes, be aware
of common trigger words that suggest cardiac disease (besides the obvious, "patient has history of
cardiac disease"). Indication of cardiac disease will suggest an answer that is focused on
hemodynamic stability.

Signs and symptoms include:

 SOB, unstable angina, decreased LOC, diaphoresis, lightheadedness, nausea, vomiting,

syncope
 ST or T wave changes (12-lead)
 Elevated cardiac enzymes

Possible actions:

 Oxygen
 Analgesia
 BP management
 Antiplatelet therapy
 Consider: PCI/reperfusion (especially if ST elevation MI - STEMI with or without indication
of acute coronary syndrome)
 If non-STEMI, focus is on finding non-cardiac causes, stress testing

Pulmonary Hypertension

Diseases Pulmonary Hypertension

Minimum # Questions 2

Maximum # Questions 6

Average # Questions 4

Keys to Disease
 Pulmonary artery pressure > 25 (from PA catheter) suggests pulmonary hypertension
 Consider treatment: inhaled nitric oxide or prostaglandins are typical options

A pathological condition of the small pulmonary arteries causing a mean pulmonary arterial pressure
(mPPA) > 25 mm Hg at rest or > 30 mm Hg during exercise.

Causes include cardiac disorders, pulmonary disorders, drugs, and others

Clinical Manifestations

 Progressive exertional dyspnea and fatigue

 Atypical chest discomfort
 Exertional light-headedness or presyncope may accompany dyspnea
 Symptoms are due primarily to insufficient cardiac output

Diagnosis
  Recommend doppler echocardiography (PASP, RV dysfunction, left heart disease,
intracardiac shunt)
 PFT (diffusing capacity reduced, may have mild restrictive process on spirometry and
volumes)
 EKG (peaked P waves)
 Right heart cath to determine severity

Management

 Treat predisposing factors

 Treat respiratory failure (intubate if necessary)
 Careful fluid balance (do not fluid overload which may exacerbate)
 Use vasopressors if needed, but avoid fluid resuscitation if possible
 Use inotropes if needed

Drugs appropriate to consider

 Calcium channel blockers

 Phosphodiesterase Inhibitors (Sildenafil, Tadalafil)
 Prostacyclins (Epoprostenol, Treprostinil, Iloprost)
 Digoxin
 Anticoagulants (warfarin)
 Nitric oxide (iNO)

Arterial Blood Pressures

Oakes Academy Tip

Blood pressure is a good "gauge" for how things are going overall in the body. Remember that
there is a minimum blood pressure required to ensure adequate tissue perfusion (have a goal in
mind of maintaining mean blood pressure > 60). It is also a sensitive indicator for shocks. For
exam purposes, pay close to attention to any blood pressure given as it may help dictate what
treatment is most appropriate (for example, giving dobutamine is appropriate in ventricular
dysfunction, but if the patient is hypotensive it can further reduce blood pressure - NOT what you
want!).

Normal BP

Systolic: < 120

Diastolic: < 80

Mean Arterial Pressure = Systolic + 2(Diastolic) = ~90

* < 60 is a critical level and requires physical or pharmacological intervention (vasopressors, fluid
resuscitation, etc.)

Concerning Values

Borderline sample: 95/65 (map = 75). May NOT have to treat, but be very aware that there is a
reason the ACCS has this BP listed (so avoid further harm at the least)

Tissues not perfusing adequately: anything < 80/50

How do you treat? Fluid resuscitation if not related to bleeding/hemorrhage. Option will read to give
IV fluids, LR, normal saline, something like that. If hemorrhage related, give blood product if an
option (fastest is Type O, if time or available, give Typed + Matched).

Preload

Preload is the amount of blood available for the right atrium/ventricle. Technically speaking, there is
a preload of the right side of the heart and a preload of the left side of the heart.

Imagine you're filling a balloon with water. You are going to use it to squeeze the water out on an
unsuspecting friend. The more water you put into the balloon, the more it stretches, and the more
you'll be able to squeeze when the big moment arrives. This is preload - the amount available for
squeeze. Note that too little preload and there's nothing to squeeze out - a very ineffective
sabotage. Too much preload and you've overworked the vessel, the balloon. That's not effective
either.

More Technical Terminology

Filling pressure (or volume) at end-diastole.

Normal Values

Right Ventricular End-Diastolic Pressure (RVEDP)

 0-6 mm Hg
 0-8 cm H2O

Collected from a pulmonary artery catheter

Affecting Preload

 Vasodilators Reduce Preload

By widening the vessels (which gives more room for the blood that is present).
Nitroprusside is an example.

 Dialysis and Diuretics Reduce Preload

By removing some of the amount/volume of blood that is present

 Positive Pressure Ventilation

By reducing venous return to the heart - worse with higher pressures/PEEP

 A Fluid Bolus will Increase Preload

By increasing the amount/volume of blood/fluid that is present

 Tachycardia Decreases Preload, While Bradycardia Increases Preload

It all has to do will filling time - the more time between each heartbeat, the more time
there is to fill

Factors Determining Preload

 Blood volume (total volume, distribution of volume)

 Filling pressure (atrial pressure, blood volume, venous return)
 Heart rate (duration of diastole: ↑ HR = ↓ fill time)

Afterload
Afterload is the force the heart has to pump against. It is mostly an indication of the pressure of the
aorta (where blood leaves the heart). Technically speaking, there is an afterload of the right side of
the heart (that would be the lungs!) and an afterload of the left side of the heart (the
aorta/systemic circulation), though it is usually the left side that is being referred to when the
generic term "afterload" is used. .

Imagine you are attempting to squeeze a balloon full of water onto an unsuspecting friend. The
friend reaches out and places their hand against the end of the balloon, creating a pressure you
are trying to squeeze against. This is afterload. The more the person messes with the end, the
more difficult it becomes to squeeze out the water - narrowing the end, completely blocking it,
etc.

More Technical Terminology

Total force opposing ventricular ejection

Normal Values

Pulmonary Vascular Resistance (PVR) is an approximation of pulmonary afterload

Normal = 20-200 dynes•sec•cm-5

 Force the right ventricle must overcome to maintain pulmonary blood flow
 Pulmonary blood vessel resistance to blood flow

Systemic Vascular Resistance (SVR) is an approximation of systemic afterload (+ aortic

pressure/compliance)

Normal = 800-1600 dynes•sec•cm-5

 Force the left ventricle must overcome to maintain systemic blood flow
 Peripheral blood vessel resistance to blood flow

Factors Determining Afterload

 Aortic stenosis increases systemic afterload (SVR)

By decreasing the amount of "give" the aorta has to accept the squeezed fluid from the
heart

 Vasoconstriction (including by that caused by high F IO2) increases systemic

afterload
By decreasing the space available - the vessels are smaller - after the heart

 Pulmonary hypertension increases pulmonary afterload (PVR)

By increasing the pressure against which the right side of the heart must pump

 Systemic hypertension increases afterload (SVR)

By increasing the pressure against which the left side of the heart must pump

 Vasodilators, beta blockers decrease systemic afterload

Pulmonary vasodilators (iNO, prostaglandins) decrease pulmonary afterload (by
decreasing CO)
By increasing the space available - the vessels are larger/dilated - after the heart
Ex: Nitroprusside, milrinone
  Vasopressors usually increase systemic afterload
By decreasing the space available - the vessels are larger/dilated - after the heart
Ex: Norepinephrine, epinephrine, dopamine

Clinical Notes

A decrease in afterload results in an increase in preload (Frank-Sterling curve)

Contractility

Contractility is the strength of the squeeze, the force of the contraction. This term contractility
refers to that strength of squeeze without considering the impact of preload or afterload.

You have a balloon filled with water which you are planning to use it to squeeze the water out on
an unsuspecting friend. The strength with which you squeeze the balloon - that's contractility.
Your goal is for a nice big squeeze so you'll scrunch every muscle you can into a nice big squeeze.

More Technical Terminology

The inotropic (force) state of the myocardium. This is the inherent ability to increase the force of
contraction independent of heart rate, preload, or afterload

Normal Values

There really is no direct measure of contractility.

 Cardiac Output (CO) and Cardiac Index (CI) are approximations. See Cardiac Output for more
details
 Stroke Volume (SV), the amount of blood ejected by either ventricle per contraction, is
another approximation. Normal is 60-130 mL/beat

Affecting Contractility

 Positive inotropics increase the strength of contractility

Use when there is low CO (cardiogenic shock)
Ex: Digoxin, epinephrine, norepinephrine, dobutamine

 Negative inotropics decrease the strength of contractility

Use with cardiac failure - allows the heart to "rest", alleviating symptoms and improving
survival
Beta Blockers block the effects of epinephrine on beta receptors
Calcium channel blockers relaxes the vessels
Antiarrhythmics slow the electrical conduction of the heart

Notes

Under normal circumstances, ventricular contractility (inotropy) will increase when afterload
increases (activation of catecholamines does this)

Rate Control

Rate control usually refers to the manipulation of heart rate, often using drugs. A heart rate "target"
is important. Tachycardia does not give sufficient filling time (preload suffers) which decreases the
heart's effectiveness. Bradycardia, on the other hand, may not provide a sufficient enough blood
flow to allow for adequate oxygen delivery (and CO2 removal).
Decreasing Heart Rate

Treating tachycardia varies. It is determined by how stable the patient is, what type of tachycardia
it is (SVT, for example), and what the rate is.

 Vagal Stimulation
Slows, or temporarily stops, heart conduction, reducing the heart rate.
o Suctioning
o Bronchoscopy
o Endotracheal tube too low
o "Bearing down" for a bowel movement

 Negative Chronotropic (heart rate) Drugs

o Beta Blockers
o Acetylcholine
o Digoxin
o Verapamil
o Diltiazem

Increasing Heart Rate

Treating bradycardia is usually only indicated if the patient is symptomatic or HR < 60/min.
Atropine, epinephrine, and dopamine are the drugs of choice.

 Positive Chronotropic (heart rate) Drugs*

o Atropine
o Dopamine
o Dobutamine
o Epinephrine
o Milranone

*While not often tested, remember that beta-agonists like albuterol, terbutaline, salmeterol, etc. have +
chronotropic effects for some patients. These drugs are NOT used to increase heart rate.

Intrinsic Rate Control

Node Rate

SA 60-100

AV 40-60

Purkinj
20-40
e

Cardiac Output

Definition

the amount of blood pumped by the heart each minute

Cardiac Output = Heart Rate x Stroke Volume

CO = HR x SV
Measurement

Pulmonary Artery Catheter directly measures cardiac output (using Fick method or thermodilution)

 Normal CO = 4-8 L/min

This is often then calculated as the cardiac index (CO/Body Surface Area)

 Normal CI = 2.9 - 4.2 L/min/m2

Low Cardiac Output Causes

 Positive Pressure Ventilation (decreases venous return to heart) - some pressure

is too high (IP, Phigh, PEEP)
 ACLS: Do not hyperventilate to ensure adequate venous return (unmeasured
impact on CO)
 Heart failure
 Hypovolemia
 Pulmonary hypertension
 Right ventricular failure

High Cardiac Output Causes

 Sepsis
 Renal disease
 Liver disease

Affecting Cardiac Output

 Volume (fluid resuscitation) increases cardiac output

By increasing the amount of fluid available (preload)

 Inotropic drugs increase cardiac output

By increasing the squeeze of contractility
Ex: Dobutamine, Dopamine, Milrinone, Epinephrine, Norepinephrine

 Diuretics and dialysis decrease cardiac output

By removing volume (decreasing preload)

 Beta blockers decrease cardiac output

By increasing the size (dilation) of the vessels after the heart (reducing afterload)

 Calcium channel blockers decrease cardiac output

By causing smooth muscle relaxation (reduces afterload)

Oxygen Delivery

Oakes Academy Tip

Oxygen delivery is an important concept to wrap your mind around ... as a concept ... as in we
need to understand what is at stake when we say something like "impaired oxygen delivery." What
is happening at a physiological level? For exam purposes, it is extremely unlikely that you will have
to do the math related to these. We present the basic formulas as they help clue you into what
 elements makeup delivery, consumption, and extraction.

 Oxygen delivery
Is the rate at which oxygen gets from the lungs to the circulation.
Oxygen Delivery = Cardiac Output x Oxygen Content

 Oxygen consumption
Is the rate at which oxygen gets from the circulation to the tissues
VO2 = Q x C(a-v)O2

 Oxygen extraction
Is the proportion of oxygen in circulation that is removed before it returns to the lungs
O2 Extraction Ratio = C(a-v)O2/CaO2

Causes of Decreased Oxygen Delivery

 A decrease in cardiac output will decrease oxygen delivery

o Cardiac disease
o Hypovolemia
 Treat by supporting cardiac output, usually with pharmacology (inotropics, for example)

Causes of Increased Metabolic Demand

 Elevated in ARDS, sepsis - More oxygen is required to maintain aerobic metabolism

 Treat by supporting metabolic demand, usually with oxygen at lower end, ECMO at high
end

Anaphylactic Shock

Recognize it on the exam.

 Anaphylactic shock is an easy one to identify as it involves a life-threatening allergic

reaction
 Hypotension + respiratory distress are particular clues
 Some type of "hint" is usually provided by way of a trigger:
o Drugs - especially a new drug the patient hasn't been on before
o Antibiotics
o Blood products
o Contrasts (like as in CT scan contrast)

Respond appropriately to it.

 Remember that anaphylaxis is more likely to affect the airway than other shocks (requiring
emergent intubation)
 Remove the antigen (stop the new drug, etc.) if this is obvious.
 Giving epinephrine is a key step with this type of shock. Then support by giving inotropes,
pressors, volume.

Cardiogenic Shock

Recognize it on the exam.

  There will be some mention of (including lab values, radiology, etc.) cardiac cause.
 As with other shocks, we are most concerned with hypotension, especially once it results in
hypoperfusion (roughly systolic BP < 90 mm Hg).

Respond appropriately to it.

 Initially: give oxygen oxygen and treat hypotension (inotropes in particular, pressors,
mechanical)
 Then: some surgical/procedural intervention is often indicated.
 A few common causes to consider:
o Acute MI (significant)
o Myocarditis (pharmacology)
o Cardiac tamponade (pericardiocentesis)
o Severe valve dysfunction (surgical intervention)

Sepsis and Septic Shock

Sepsis is a very common scenario presented on the ACCS exam. These patients are nearly always
presented as hypotensive (or on hemodynamic supports). Treat aggressively with antibiotics,
pressors. Other systems failing is also common (especially kidneys).

 Fever: almost always present on exam

 BP: almost always hypotensive. Severe hypotension = severe sepsis

Definitions
Yes, you may be asked to classify sepsis (just basic stuff, don't worry). Here's a couple keys you
should know:

 Sepsis: Milder fever, mild hypotension (MAP > 60)

 Severe Sepsis / Septic Shock: Severe: higher fever (> 100 F), MAP < 60 which results
in other systems affected:
o Kidneys: Decreased or no urine output
o Respiratory: Distress apparent if not intubated
o Other: platelets (thrombocytopenia) is common

Treatments
 Give antibiotics (broad-spectrum initially) immediately
 Fluids and vasopressors to support adequate blood pressure
 Support what's failing: Ventilator, dialysis, etc.

Hypovolemic Shock

Recognize it on the exam.

 A decrease in the effective circulating blood volume. Obviously this will have an impact on
hemodynamic function, and the severity will be partially based upon the amount of fluid
loss.
 The question will need to give strong hint that patient is bleeding (post-surgical, trauma,
post-procedure) or has a non-bleeding loss of fluid (dehydration, burn, sepsis). Remember,
not all bleeding is visible ("blood on the floor plus four more - intrathoracic, abdominal,
thigh, head")
  Note that by the time a patient is hypotensive (this is referred to as decompensated shock),
they have likely lost 1/3 or more of their blood volume. The body will first vasoconstrict to
maintain BP. Once the system is unable to further compensate, the patient becomes
hypotensive.
 Certainly treat hypotension, but administering fluid with strong suspicion of hypovolemia is
indicated as well (pallor is a first indication, present history is the best indication).

Respond to it appropriately.
 Goal is to replace volume lost. Particularly if hemorrhagic (bleeding), we suggest the
following order:
 Support with pressors, inotropes
 Support with supplemental oxygen
o Give Type O blood (available in ED quickly)
o Give normal saline if #1 is not an option
o Give typed, cross-matched blood as soon as it is available (it takes time for this to
happen, so if patient is just admitted, it will delay care waiting)
 Red blood cells, plasma, and platelets are all priorities.
 Inotropes may help circulate available volume more effectively

Specific cases to look for:

 Hemorrhage (blood on the floor + 4 more:)

o Chest (hard to judge how massive is bleeding, questions may include chest tube
drainage amount, > 1L is concerning)
o Abdomen (again, hard to judge how massive, may have distension, may affect
respiratory status)
o Head (including scalp)
o Thighs (thighs can hold over 1L of blood!)
 Other Causes:
o Dehydration
 Vomiting and diarrhea, both severe
 Over-diuresis
 Diabetes
 Heat exhaustion
o Third Spacing
 Burns
 Trauma
 Sepsis
 Ascites

Neurogenic Shock

Recognize it on the exam.

 Neurogenic shock is just like it sounds like - originating from the nervous system. it is an
altered signal that results in massive peripheral vasodilation and systemic hypoperfusion.
 Some common causes include:
o Brain or spinal cord trauma
o Drugs
o Insulin shock

Respond appropriately to it.

  Treat the cause, if possible
 Support oxygen and ventilation
 Use vasopressors to address hypovolemia

Acute Respiratory Distress Syndrome (ARDS)

Diseases ARDS

Minimum # Questions 11

Maximum # Questions 19

Average #
Questions 15

Keys to Disease
 ARDS is largely a disease of V/Q mismatch, with refractory oxygenation (meaning PaO 2 does
not meaningfully increase when increasing oxygen)
 Hallmarks of diagnosis include a P/F ratio < 200, bilateral diffuse infiltrates on chest
imaging
 Treatment is mostly supportive (support oxygenation, support ventilation) - see below
 Hypoxemia is unlikely to respond to more oxygen.

In Plain Language: ARDS is an inflammatory lung injury. It causes pulmonary edema (due to the
shift of fluid from capillaries), which results in decreased gas exchange (think V/Q mismatching). It
also results in washed out surfactant. Ultimately this means decreased compliance, atelectasis,
intrapulmonary shunting, and may lead to multiple organ failure.

Clinical Manifestations
General

 Agitated, anxious, confused, restless

 Rapid onset (hours to days after insult)

Respiratory

 Inspection - cough, cyanosis, dyspnea, retractions, tachypnea, ↑ WOB

 Auscultation - ↓ BS, bronchial BS over consolidation, crackles
 Pulmonary Dynamics
↓ CL (total C< 30 mL/cm H2O)
↑ PIP
 ABGs
Oxygenation - refractory hypoxemia (PaO2/FIO2 ≤ 300, really under 200 becomes more
critical)
↑ shunt (>20%)
Ventilation - respiratory acidosis. on ventilator this is okay (permissive hypercapnia),
unless severe

Cardiovascular
  Tachycardia
 Non-cardiogenic: PCWP < 18 mm Hg (higher than that suggests cardiac, not ARDS)

Diagnosis
 Plain Chest Radiograph: Diffuse infiltrates, haziness, white-out (also could show up on a
CT Scan report)
 P/F Ratio < 200 (suspect when < 300, but more definitive < 200)
 Some type of "event" in last 7 days (may or may not present in a scenario)
 Evidence against it being cardiac (may or may not present in a scenario), such as an
echocardiogram

Possible Strategies:
 Initial Ventilation
o If scenario supports ARDS, lean more heavily towards intubation than noninvasive
(HFNC, CPAP, NPPV) options
o The mode isn't all that important: Pressure or Volume, A/C, PRVC, APV. Don't use
advanced ventilation modes initially (HFOV, APRV, ECMO)
o Always use lung protective strategies (low VT in the 4-6 cc/kg range; don't go
above). Allow for permissive hypercapnia. Keep Pplat < 30-35 when possible
o Utilize higher PEEP strategies (> 5 cm H2O)

 Advanced Ventilation Strategies (none of these is more preferred than another on the
exam):
o High-Frequency Oscillatory Ventilation (HFOV) is a recruitment mode of ventilation
that improves V/Q with a high MAP and smaller breaths than dead space ventilation
o Airway Pressure Release Ventilation (APRV) is a recruitment mode of ventilation that
improves V/Q with a high MAP and small, spontaneous tidal volumes
o Extracorporeal Membrane Oxygenation (ECMO) allows oxygenation away from lungs
(outside body) so that lungs can receive just enough ventilation to stay inflated, but
otherwise, rest until ARDS begins to clear
o Prone positioning to treat V/Q mismatch (usually signs of hypoxemia will be
evident)

 Support Oxygen consumption (treat fever!)

 Watch for hemodynamic instability - maintain adequate perfusion (mean arterial

pressure > 60 mm Hg), use of A-Line is smart to monitor status

 Antibiotics to treat evidence of infection (WBC, Fever)

 Nitric oxide for refractory hypoxemia

Aspiration (Pneumonia)

Aspiration pneumonia: lung infection caused by chronic aspiration of colonized oropharyngeal

secretions.
Aspiration pneumonitis: acute lung inflammation following aspiration of gastric contents.

Clinical Manifestations

 Pneumonia: signs of infection with purulent sputum

  Pneumonitis: Sudden tachypnea and dyspnea, cough, crackles, wheezing, cyanosis,
hypoxemia, may progress to respiratory failure. PFTs variable

CXR

 Patch, mottled, segmental consolidation (depending on position when aspirated),

atelectasis, abscess

Preventive Measures

• Airway Clearance (suction)

• Oxygen Therapy

• Bronchodilators

• Therapeutic Bronchoscopy

• Invasive ventilatory support, if severe

• Antibiotics if indicated

• Steroids

Atelectasis

Incomplete expansion, non-aeration, and/or collapse of alveoli.

Clinical Manifestations

 Asymptomatic to ↑ dyspnea / ↑ WOB

 ↑ RR / ↑ HR
 ↓ chest expansion
 Tracheal shift (same side)
 Chest pain, fever, restless
 Refractory hypoxemia (capillary shunting)
 Auscultation: end-inspiratory crackles, decreased

PFTs - restrictive

CXR: often areas of opacification (gray/white lung regions instead of black). More severe: elevation
of diaphragm on affected side, displacement of heart/trachea towards affected side.

Treatments

 Oxygen to treat hypoxemia, though may be refractory (unresponsive to O2)

 Correct underlying cause.
 Lung inflation therapy: Increase PEEP on vent, consider CPAP, IPV if retained secretions

Drug Overdose

Symptoms
  Obtunded/Stuporous
 Respiratory depression
 Ineffective spontaneous breathing (either hypo or hyperventilation)
 Cardiovascular compromise (hypotension and/or arrythmias)

Treatments

Mechanical ventilation if apnea, acute respiratory failure, impending respiratory failure

Monitor closely for:

 Aspiration
 Hemodynamic stability
 Level of Consciousness (LOC)
 Patient-ventilator synchrony

Alveolar Hypoventilation Syndrome

Acute or chronic breathing disorder featuring inadequate alveolar ventilation, causing an increased
PaCO2.

Causes include chest wall deformities, COPD, Neuromuscular disorders, and Obesity Hypoventilation
Syndrome

Clinical Manifestations

Vary based upon cause, but are all consistent with what you would expect with hypoventilation:

 Atelectasis
 Hypoxemia
 Respiratory acidosis
 Polycythemia
 Cor pulmonale

Treatment

 Use PEEP/CPAP to offset chest wall

 Treat any possible underlying causes

Neuromuscular Disorders

Rapid Onset

 Botulism
 Cervical spinal cord injury
 Guillian Barre
 Myasthenia gravis
 Tetanus

Gradual onset

 ALS
 Post polio sydrome
  Progressive thoracic deformities (scoliosis, kyphosis)

Resulting Patient Challenges

 Aspiration from airway muscle weakness

 Atelectasis from inadequate lung inflation
 Pneumonia from impaired cough/mucociliary clearance

Treatments

 Mechanical ventilation when acute respiratory failure; best initiated when respiratory
acidosis noted
 Allow for adequate support
 Wean when primary neuromuscular deficit has reversed. Consider gradual weaning/trach.

Myasthenia Gravis

An auto-immune disorder of neuromuscular transmission of the voluntary (skeletal) muscles

characterized by muscle weakness and easy fatigability, which often affects the respiratory muscles.

Clinical Manifestations

 Extreme weakness and fatiguability

 Aspiration potential (choking, coughing, inability to manage secretions)
 Respiratory insufficiency
 Weakness tends to be descending (Myasthenia Gravis = MG = MIND to GROUND)
 Myasthenic crisis: acute event characterized by respiratory compromise
 Tensilon Test: Give edrophonium. If this is myasthenia gravis, the patient improves
temporarily. If it is a cholinergic crisis the patient will worsen.

Treatment

 Monitor pulmonary mechanics (vital capacity, NIF/MIP)

 Anti-cholinesterase drugs (pyridostigmine)
 Manage airway patency early on by supporting cough (cough assist), secretions (NT
suction)
 When patient is failing, do not delay: intubate

Guillian-Barre' Syndrome (GBS)

Ascending muscular paralysis & profound autonomic dysfunction, often idiopathic (no known cause)

Clinical Manifestations

 Ascending muscular weakness, pain, and paralysis: MAY LEAD TO CHEST

MUSCLE/DIAPHRAGM PARALYSIS
 Difficulty swallowing, risk of aspiration (choking, coughing)
 Hypotension
 Bradycardia
 Bronchorrhea
 Diagnose by Electromyogram (EMG - measures muscle activity), CSF (protein level > 500
mg/dL)

Treatment
  Monitor pulmonary mechanics (vital capacity, NIF/MIP)
 Plasmaphoresis
 Manage airway patency early on by supporting cough (cough assist), secretions (NT
suction)
 When patient is failing, do not delay: intubate

Chronic Obstructive Pulmonary Disease (COPD)

Diseases COPD

Minimum # Questions 10

Maximum # Questions 16

Average #
Questions 13

Keys to Disease
 COPD is a progressive disease characterized by airflow limitation that is not fully reversible.
The ACCS is likely to focus on patients who are in an acute exacerbation, or with COPD as a
complicating factor with something else.
 Diagnosis is primarily by spirometry
 Be on the lookout of issues related to sputum production and/or work of breathing
 Be quick to recommend NPPV (BiPAP) for patients in distress, avoiding intubation unless
NPPV is contraindicated. Also recommend for patients who are weaning—extubate to
NPPV.

In Plain Language:

A preventable and treatable disease with some significant extrapulmonary effects that may
contribute to the severity in individual patients. Its pulmonary component is characterized by airflow
limitation that is not fully reversible. The airflow limitation is usually progressive and associated with
an abnormal inflammatory response of the lung to noxious particles or gases.

Diagnosis

The exam should not cover diagnosis in detail (it is a critical care exam, after all). However, it may
be helpful to remember the basics (spirometry: FEV1/FVC < 70% predicted). Also, the exam is likely
to present patients with comorbidities. The presence of comborbidities increases the severity of
dyspnea in patients with COPD.

Clinical Manifestations

You are likely very familiar with the clinical manifestations of COPD, including dyspnea, sputum
production, work of breathing, abnormal breath sounds, etc. Lab values at baseline include
polycythemia, Chronic Respiratory Acidosis (compensated with high PaCO 2, low PaO2). These
symptoms vary based upon type and severity of disease. Any significant worsening of symptoms
may indicate an exacerbation. Be on the lookout, too, for signs of active infection (change in color or
consistency of secretions, fever, respiratory distress, etc.).
Treatment/Strategies

This exam will focus on critical care management of the COPD patient. You are not likely to manage
questions about chronic management, although it may be mentioned as a patient who is not
compliant with management may end up hospitalized. You are not likely to be asked questions about
patient education, although lack of education may contribute to a patient ending up in the hospital.

 Administer oxygen if the patient is hypoxemic (the exam will not test on hypoxic drive
theory. treat hypoxemia.)
 Consider short-acting beta agonists like albuterol when indicated (wheezing, for example)
 Be quick to consider NPPV (BiPAP) unless contraindicated. Use it as a an alternative to
intubating, and use it as method for rapidly extubating a COPD patient (this decreases VAP
risk)
 Air hunger is a common asynchrony scenario. Increase flow when given the option.
Increase IPAP if an option on NPPV.
 Treat the ABG, but don't overtreat it. The goal is to normalize pH and PaO2. Don't worry
about the PaCO2 on its own.
 If on a ventilator, ensure adequate exhalation time (auto-PEEP is a significant concern.
Check the flow waveform to ensure it returns to baseline at end exhalation). It is advisable
to increase PEEP on the ventilator to offset patient's auto-PEEP, but do so carefully (look for
signs of hemodynamic compromise or increased work of breathing).

Pneumonia

Introduction
Inflammatory process of the lung's air spaces.

Diagnosed by CXR infiltrate, plus 2 or more of:

 Fever (< 38ºC)

 ↑ WBC
 Purulent sputum.

Clinical Note: Often abbreviated clinically as PNA

 Hospital Acquired Pneumonia (HAP), or Nosocomial: A Pneumonia that occurs 48-

hours or more after admission, with no apparent signs or symptoms at time of admission.
 Ventilator Associated Pneumonia (VAP): Forms > 48-72 hrs after intubation.
 Healthcare-Associated Pneumonia (HCAP): Occurs in non-hospitalized patient with
healthcare contact, with 1 or more of the following:
o IV therapy, wound care, IV chemo is last 30 days
o Resident of Long-term care facitlity or Nursing Home
o Clinic (including Hemodialysis) in last 30 days
o Admission in Acute Care Hospital is last 90 days

Microbiology
Most Common Pathogens (not exhaustive):

 Gram Negative Bacilli

o P. aeruginosa (Pseudomonas aeruginosa)
o E. coli (Escherichia coli)
o K. pneumoniae (Klebsiella pneumoniae)
 o Acinetobacter spp
 Gram Positive Cocci
o S. aureus (Staphylococcus aureus)
 MRSA (Methycillin-Resistant S. Aureus)
o Streptococcus spp

Clinical Note
The quality of the sputum sample obtained is essential in correct diagnosis (and, therefore,
appropriate treatment). Numerous tools are available, including:

 Above carina: (Nasal Tracheal Suction, Endotracheal Suction (with clean catheter, even if
inline) and
 Below carina: (Bronchial Alveolar Lavage (BAL) via Bronchoscopy, or Mini-BAL)

Post-Operative Pulmonary Complications

Diseases Post-Surgical

Minimum # Questions 8

Maximum # Questions 14

Average #
Questions 11

Keys to Disease
 One of the biggest respiratory risks post-surgery is atelectasis. Strategies to prevent and
treat atelectasis are important themes.
 Hallmarks of diagnosis include deteriorating oxygenation, haziness on chest radiograph,
decreased breath sounds
 Treatment includes emphasis of PEEP/EPAP/CPAP as being more important than Oxygen
(due to V/Q mismatch). If on a ventilator, consider a recruitment maneuver (it may even
be a preferred first step before PEEP as it is a quick response)
 Hypoxemia is unlikely to respond to more oxygen.

In Plain Language: When we don't breathe deeply, our alveoli collapse. This is the whole concept
behind an incentive spirometer (an option you are less likely to find on the critical care exam, but
who knows!). The best way to treat atelectasis is to prevent it, so if that is an option, go for it.
Otherwise we should treat it by doing more than throwing oxygen at it (the highest amounts of
oxygen still can't get into collapsed lung regions).

Oakes Academy Tip

Atelectasis is very, very likely to appear in multiple questions on your exam. Expect to find
evidence of atelectasis (usually plain radiograph, though breath sounds are a possibility). The
patient will likely be hypoxemic and you will be given the option to battle the problem with oxygen.
Resist the urge. Look first for an option to increase PEEP or start NPPV.
Post-Operative Pulmonary Complications (PPC) (the most
common surgical complication)
Definition of PPC: Atelectasis on a chest radiograph or respiratory failure necessitating intubation
and MV

Atelectasis and reduced lung volume develop from:

 Anesthesia
 Pain
 Pharmacologic agents
 Positioning
 Respiratory muscle dysfunction
 Surgical trauma

Diagnosis

 Symptoms (new onset cough, fever, abnormal breath sounds, ↑ RR, ↑ HR, dyspnea, altered
mental status)
 Laboratory values (hypoxemia, leukocytosis, microbiology of sputum)
 Radiographic criteria (atelectasis or new infiltrates)
 Pneumonia
 Need for mechanical ventilation > 48 hrs

Common Post-Operative Therapy Techniques

 Aggressive SBT/extubation when appropriate clinically

 Consider adjuncts: IPV for example
 If on vent, PEEP to prevent atelectasis, or to recruit atelectatic lung regions
 If not on vent, consider CPAP or NPPV (BiPAP)
 Patient positioning (remember: blue gold [BLU GLD] Bad Lung Up, Good Lung Down)
 If a patient has signs of atelectasis and is on higher PEEP already, consider a therapeutic
bronch.
 Consider early mobility if patient is stable enough (even on ventilator)

Trauma (Chest)

Oakes Academy Tip

You should be familiar with chest trauma in general. As with other areas on the ACCS, by able to
recognize signs and symptoms of underlying chest trauma, how to manage emergencies, and how
these might impact upon critical care management (ventilator, shock, ARDS, etc.)

Pulmonary Contusion

"Bruise" of the lung. Results in damage to capillaries, allowing blood and fluids to accumulate in lung
tissue. May interfere with gas exchange, altering V/Q, and is a risk factor for the development of
ARDS.

Flail Chest

Three or more ribs fractured in two or more places

A flail segment develops a paradoxical movement (sucks in on inspiration). Positive pressure
ventilation may mask it.

 Many patients with flail chest are now managed without intubation and MV
o IS, deep breathing, and coughing are important to reduce secretions, prevent
atelectasis, and avoid intubation.
o Aggressive airway clearance and CPT may be limited by chest wall pain
o Monitor closely for respiratory failure

 Patients with flail chest are at significant risk for acute respiratory failure
o Fatigue due to increased WOB
o Pneumothorax, hemothorax, and pulmonary contusions are common
o Associated head injury, abdominal injury, and extremity injury are common

Penetrating Trauma

Effects are very dependent upon what anatomical damage is done with the trauma. Key
considerations:

 Blood loss (may lead to shock)

 Hemothorax (may need to be evacuated)
 Pneumothorax (may need to be evacuated)
 Cardiac injury
 Lung injury

Consider Intubation when:

 Deteriorating respiratory status (fatigue from WOB, depression from analgesia)

 Need for surgery is imminent
 Shock
 Closed Head Injury
 Mechanical Ventilation with normal settings overall
o Ventilate at the lowest possible mean airway pressures due to risks of pulmonary air
leaks (pneumothorax).
o Use PEEP with caution due to barotrauma (esp. unilateral contusion) and
hemodynamic instability due to blood loss and/or head injury.
o Many patients require initial sedation or paralysis.
o Permissive hypercapnia may be employed provided no accompanying head trauma
with ↑ ICP.

Other Strategies to Consider

 Pulmonary Contusions are commonly presented on the ACCS exam

Because contusions are typically "localized" to a certain area of the lung, strongly consider
patient positioning to address any refractory oxygenation issues
BLU GLD (blue gold) = "Bad Lung Up, Good Lung Down"

 Pain control is an issue

expect scenarios where too much pain medication (opioids especially) have been given
be sure to address pain or indications of pain (tachycardia, hypertension) aggressively,
especially if head trauma
  If an air leak is present (pneumothorax, for example), ventilation may be a challenge.
ECMO is an option in this case - unless coagulation issue as well.

 Be cautious with any type of cardiac injury (especially cardiac tamponade).

any change in positive pressure ventilation may further decrease venous return to the heart
if not intubated, consider carefully before intubating

Pulmonary Edema

Accumulation of vascular fluid in alveoli or pulmonary interstitium

High-pressure pulmonary edema - (cardiogenic, hydrostatic)

 Transudation: due to a volume/ pressure overload of the pulmonary circulation

 Causes: acute MI, arrhythmias, CHF, infection, hypervolemia, LVF, renal failure, shock,
valve disease

Permeability pulmonary edema - (non-cardiogenic, neurogenic)

 Exudation: due to an ↑permeability of the pulmonary capillary membrane

 Causes: ARDS, CNS (hemorrhage, trauma, stroke, tumors, ↑ ICP),drowning, smoke
inhalation, O2 toxicity
 Varies with severity of underlying disorder (↑severity as ↑fluid).

Clinical Manifestations

 General: Sudden anxiety, restlessness, orthopnea, cyanosis, hypoxemia, diaphoresis

 Respiratory: ↑ RR, dyspnea, cough (dry to pink, frothy fluid), basal crackles/wheezing,
SOB, ↓ CL
 Cardiovascular: ↑ HR, ↓ BP, cold clammy skin, JVD, peripheral edema

Chest Radiograph

 Interstitial: Haziness of vasculature and hilar

 Alveolar: Irregular, poorly defined ascinar shadows forming a "butterfly" or "bat wing"
pattern.
 Both: Disparity between upper and lower lobe venous calibers. LVH when due to CHF. Air-
bronchograms

Treatment

 Treat underlying cause.

 Oxygen as needed,
 Diuretics, inotropes and afterload reducing agents, morphine
 CPAP, NPPV (BiPAP), mechanical ventilation with PEEP
 Cardioversion/resuscitation if needed.

Cardiogenic Pulmonary Edema

Pulmonary edema due to volume or pressure overload of the pulmonary circulation. This is the most
common type of pulmonary edema.

2 Major Causes
  Intravascular volume overload: from increased intake or decreased output, renal failure
 Left ventricular dysfunction: from acute MI, aortic stenosis, pericarditis

Pathophysiology
 PCWP > 18-20 mm Hg — gradual movement of fluid into lungs (onset of pulmonary
congestion)
 PCWP > 30-35 mm Hg — rapid movement of fluid into lungs (acute pulmonary congestion)

Diagnostics
 In assessment, watch for:
o pink, frothy secretions (this is a giveaway!)
o basic signs of respiratory distress (tachypnea, tachycardia, you know the drill . . . )
o breath sounds may include crackles, diminished breath sounds
 EKG: variable, depending on cause
 Chest Radiograph:
o Batwing
o ↑ heart size if left ventricular function
o Kerley B lines

Management
 Support adequate oxygenation and ventilation:
o CPAP or NPPV (especially with distress/work of breathing)
o Diurese (furesemide, bumetanide)-monitor hemodynamics, intake/output
o If initial trial of CPAP/diuretic is unsuccessful, consider intubation
 Patient position: Fowler's or sitting with feet down.
 Hemodynamics: maintain optimal cardiac output with inotropics, NOT fluids

Myocardial Infarction (MI)

Severe heart failure leads to hypoxemia, ↑ WOB, ↑ work of myocardium

Causes include acute MI, fluid overload, ↑ BP, tacycardia

Careful monitoring and assessment of the effects of PPV on hemodynamics, as well as fluid and
electrolyte balance is essential.

Treatments

Support oxygenation, ventilation, circulation

 Oxygenation - favor high end of spectrum (start with FIO2 1.0)

 Ventilation - consider BiPAP, or if unstable, ventilation
 Circulation - fluid balance, inotropic support, vasodilators, diuretics

Be aware of the interaction of mechanical ventilation and hemodynamics. Decreases venous return
to the heart, which actually may be beneficial with fluid overload (severe CHF). Be aware that
ventilator in this case may assist with hemodynamic support, which can then end up reversing with
weaning.
Myocardial Infarction (MI)

Severe heart failure leads to hypoxemia, ↑ WOB, ↑ work of myocardium

Causes include acute MI, fluid overload, ↑ BP, tacycardia

Careful monitoring and assessment of the effects of PPV on hemodynamics, as well as fluid and
electrolyte balance is essential.

Treatments

Support oxygenation, ventilation, circulation

 Oxygenation - favor high end of spectrum (start with FIO2 1.0)

 Ventilation - consider BiPAP, or if unstable, ventilation
 Circulation - fluid balance, inotropic support, vasodilators, diuretics

Be aware of the interaction of mechanical ventilation and hemodynamics. Decreases venous return
to the heart, which actually may be beneficial with fluid overload (severe CHF). Be aware that
ventilator in this case may assist with hemodynamic support, which can then end up reversing with
weaning.

Pulmonary Embolism (Pulmonary Infarction)

Blockage of part of pulmonary vascular bed by blood-borne material, sometimes causing pulmonary
infarction (necrosis).

Causes:

 Blood stasis: Bed rest, CHF, obesity, pregnancy, post-operative

 Air: Complication of CVP line placement
 Fat (bone marrow): Fractures, particularly long bones (legs)
 Foreign material: Drug abuse, indwelling catheters, tumors

Clinical Manifestations:

 Dyspnea and sharp chest pain (sudden)

 Tachypnea
 Cough (may or may not be productive)
 Breath sounds: non-specific
 Tachycardia

Treatment

 Maintain proper oxygenation and ventilation

 Hemodynamic support (volume resuscitation, vasopressors)
 Dissolve clot (fibrinolytics)
 Types: Blood (thrombolytic), Fat (steroids)
 Prevent future emboli (anticoagulant therapy such as heparin, warfarin, IVC filter)
o NOTE: IVC filter is only choice if patient is actively bleeding (subdural hematoma,
internal bleeding, etc.)

Restrictive Lung Disease (Disorder)

Disease/disorder characterized by a ↓ lung volumes/capacities

Causes include fibrosis, pleural effusion, pneumothorax, ARDS, atelectasis, obesity, etc.

Clinical Manifestations: dyspnea, hypoxemia, polycythemia, cyanosis, respiratory alkalsosis

(early)/acidosis (late), ↓ lung volumes

Sleep Apnea

Frequent cessation of breathing during sleep (> 10 sec)

Types

Obstructive: anatomic obstruction of the upper airway (largely the tongue). Ventilatory efforts
continue

Exact cause is unknown, but CHF, Stroke, Brain Lesions, and Cerebrovascular Diseases are all
possible contributors
Clinical Manifestations: Snoring and apnea with increasingly desperate efforts to inhale. May awaken
gasping for air.
Treatment: In Critical Care: CPAP or NPPV (BiPAP), may extubate a pt directly to CPAP

Central: No ventilatory effort (no signal is sent to phrenic nerve to initiate breath)

Can be caused by obesity, anatomic deformities

Clinical Manifestations: Apnea with no signs of obstruction
Treatment: May need trach for night ventilator support; negative pressure ventilation, phrenic nerve
pacemaker

Mixed: Combination of obstructive and central

Transfusion-Related Lung Injury

Oakes Academy Tip

It is important to recognize transfusion-related lung injury. This one's easy. The scenario will
mention the patient has received blood product (usually Fresh Frozen Plasma). Confirm it is a
reaction by looking specifically for sudden dyspnea and symptoms of non-cardiogenic pulmonary
edema (coarse crackles, wheezes, hypoxemia). Hypotension and fever are also common and may
or may not be mentioned in the question.

What do you recommend? Stop the transfusion. FIRST. Then consider supportive treatment
(CPAP, BiPAP, Lasix, etc.)

Description

A serious blood transfusion complication characterized by:

 Acute onset of non-cardiogenic pulmonary edema

 Acute lung injury (ALI), which may progress to
 Acute respiratory distress syndrome (ARDS)

With no acute lung injury (ALI) prior to transfusion, the diagnosis of TRALI is:
 1. Acute onset, hypoxemia, bilateral lung infiltrations on the chest radiograph, and no
evidence of circulatory overload
2. Occurrence during transfusion or within 6 hr of completion
3. No other risk factor for lung injury

Clinical Presentation

 Dyspnea/Shortness of Breath
 Hypoxemia
 Hypotension
 Fever
 Bilateral pulmonary infiltrates
 Normal cardiac function

Management

 STOP transfusion
 THEN support symptoms by:
o Consider CPAP (or BiPAP) within normal parameters
o Diuresis is an acceptable option on ACCS
o Treat any wheezes with an aerosolized bronchodilator (this is a confirmed acceptable
response on exam)
o Severe distress may require mechanical ventilation
 Consider ECMO for short durations in severe cases, usually when mechanical ventilation is
failing

Upper Airway Obstructions

Oakes Academy Tip

Recognizing upper airway obstruction is important on every exam, and the ACCS is no exception.
This is often presented as a scenario where the patient develops post-extubation stridor.

Things to look for:

 Extubating a patient intubated for airway patency, or that could impact airway patency
 Thyroid or neck surgeries
 Anaphylaxis
 Major oral surgery/abscess

The treatment algorithm depends on severity of symptoms. When all else fails, reintubate. In
lesser severity (stridor but no substantial respiratory distress), consider systemic steroids, racemic
epinephrine, and a cool aerosol.

Fluid Assessment

Urine Output Averages

 600-1,800 mL/day (female is slightly lower in the range; male is slightly higher in the range)
  40 mL/hr
 > 0.5 mL/kg/hr

Fluid Excess (Hypervolemia)

Signs & Symptoms

 ↑ body weight, ↑ CO, ↑ BP

 ↑ PAP, ↑ CVP, ↑ JVD
 ↓ Hgb, ↓ Hct
 Bounding pulse
 Coarse crackles on auscultation
 Pitting edema
 Pulmonary edema
 ↑ UO from overload

Causes

 Iatrogenic: Fluid overloading patient (such as with fluid resuscitation)

 Heart Failure
 PPV (↓CO, ↑ADH)
 Renal system malfuntion
 Blocked Foley

Strategies

 Diurese patient: Pay close attention to diuretic choice in the presence of hemodynamic
instability
 Fix underlying cause (ventilator, Foley, etc.)
 Administer CPAP/EPAP/PEEP (or titrate up) if fluid pulmonary edema from overload

Fluid Deficit (Hypovolemia)

Signs & Symptoms

 ↓ body weight
 ↑ HR, ↓ BP (postural)
 ↓ PAP, ↓ CVP, ↓ JVD
 ↑ Hgb, Hct
 Poor peripheral pulse
 Dry mucous membranes
 Extremities: cool/pale
 Trunk: warm/dry
 ↓ Skin elasticity
 ↑ UO (diuresis)
 ↓ capillary refill

Causes

 Dehydration
 Starvation
 Shock (usually due to a fluid shift)
 Burns
  Diarrhea/Vomiting

Strategies

 IV Fluids - fluid resuscitation

 Pharmacologic: administer vasopressors if significant impact on cardiovascular system
 Support underlying cause (feeding, shock )

Acute Kidney Injury

A usually reversible decline in kidney function - common in patients critical care, especially when
poorly perfusing (MAP < 60 torr).

What to Look For

 Decreased urine output (though not always)

 Serum Creatinine will be high
 Blood Urea Nitrogen (BUN) will be high
 Net fluid balance is like to be high (+)
o Fluid retention may be apparent (legs, ankles, feet)

Causes of Impaired Blood Flow to Kidneys

 Hypotension (fluid loss)

 Cardiac arrest
 Infection
 Liver failure

Causes of Damage to the Kidneys

 Chemotherapy drugs
 Toxins (alcohol, heavy metals, cocaine)

Treatment

 If the kidney is not functioning, don't administer most diuretics. Mannitol is the exception
to this.
 If patient is hemodynamically stable, hemodialysis is an acceptable option.
 If patient is not hemodynamically stable, continuous renal replacement therapy (CRRT) is
preferred.

ABG Analysis

Oakes Academy Tip

It will probably not be a shock to find out that there will be a health sprinkling of arterial blood
gases on the ACCS. We're going to make a bold prediction that if you are sitting for this exam, you
feel comfortable with doing basic ABG interpretation. You can make vent changes after looking at
an ABG, knowing that a respiratory acidosis probably means you need to increase the minute
ventilation in one way or another. The ACCS knows this as well, and you really won't be tested on
these items. Instead you will be tested on some slightly more advanced thinking . . . how to
manage the ABG of an acute-on-chronic COPDer, DNI/DNR orders, significant metabolic acidosis
scenarios, common ABG errors (air in sample, analyzer error, etc.). Not all ABGs presented are
important, but train yourself to look at them, especially if the values are outside of normal, with a
weary eye.

Be sure you know the NBRC normal values:

pH 7.35-7.45

PaCO2 35-45

PaO2 80-100

HCO3 22-26

The ACCS exam is pretty straightforward with values. It is either in normal range (no action
absolutely required to fix it) or out of range (you must do something to address the abnormal
value). This may be different than clinical practice.

Relevant ABG goals for ACCS exam can be found in the disease section, but here are a few to get
you started.

Respiratory Acidosis

Most respiratory acidosis gases are due to some level of respiratory insufficiency so consider what
respiratory intervention you need (this needs to be in context to the remainder of the scenario). For
some disease this might mean treating less aggressively (using lung protective strategy), allowing a
reasonable respiratory acidosis and a minimum goal for oxygenation (PaO 2 > 60). Read the entire
scenario. Read it twice. There's likely some keyword in there to point you towards where you should
be going.

For example: COPD: Compensated respiratory acidosis (for example, pH 7.35, PaCO 2 55, PaO2 66,
HCO3- 30. Some clinicians are tempted to treat the high CO2, despite the normalized pH).

Metabolic Acidosis

The key to treating a metabolic acidosis is to treat the underlying cause whenever possible.
Remember that any respiratory symptoms (such as tachypnea) are likely to be compensation from
the metabolic acidosis. You may not need to intubate immediately, even with a poor pH, but the
patient needs to be stable (consider respiratory intervention if the patient is tiring, isn't protecting
their airway, has major LOC changes, hemodynamic compromise, etc.)

For example: Diabetic Ketoacidosis: DKA is distinguished by the usual severely low HCO3- (for
example, pH 7.15, PaCO2 20, PaO2 92, HCO3- 6, BE -18. This is not considered respiratory failure - no
intubation is required - unless the patient is tiring, needs to protect their airway, etc.).

Metabolic Alkalosis

Less commonly found on the exam, but certainly could be. The body's compensation will be to
hypoventilate (RR will drop). Again, treat the underlying cause. Watch for signs that respiratory
drive is too low to adequately deliver oxygen.
Respiratory Alkalosis

Less commonly found on the exam, but certainly could be. This patient is hyperventilating (or we are
hyperventilating the patient), by definition. Some neurological disorders cause this. It can also be
an early sign of distress in patients with Asthma (and other disorders). Placing a patient into a
respiratory alkalosis used to be the "gold standard" for head injury (it causes cerebral
vasoconstriction), but most guidelines today recommend very mild hyperventilation if used at all
(how mild? like PaCO2 at the low end of normal: 35-39 torr).

Urine Output

Urine Output Averages

 Males fall into the higher output range than females

 600-1,800 mL/day
 40 mL/hr
 > 0.5 mL/kg/hr

Fluid Balance

 Positive fluid balance - Urine output is less then the input

o For example: Patient has had 5 L/day input and an output of 1 L/day
 The patient has a positive fluid balance of 4 L/day

 Negative fluid balance - Urine output is less then the input

o For example: Patient has had 4 L/day input and an output of 5 L/day
 The patient has a negative fluid balance of 1 L/day

Terminology

 Oliguria - <500 mL/day

o Low fluid intake
o Kidney injury (acute)
o Obstruction (partial)
o Dehydration
 Anuria - < 100 mL/day (almost no urine output)
o Kidney failure (acute or chronic)
o Diabetic ketoacidosis
o Obstruction (total)
o Hypertension (blood vessels in kidneys become injured leading to kidney failure)
 Polyuria - > 3 L/day
o Diabetes
o Increased fluid intake
o Diuretics
 Hematuria - Blood in the urine
o Can be due to a contusion to the kidney

GI Assessment/Abdominal Distention

You should be well aware of the impact of abdominal pressures on pulmonary function.

The Basics:

 Normal abdominal pressure is about 5 mm Hg

  Intra-abdomonal Hypertension is a sustained pressure of at least 12 mm Hg
 Abdominal compartment syndrome is a sustained pressure of > 20 mm Hg (with new organ
failure)
 Critical illnesses often contain some element of abdominal distension

Common Causes:

 Blunt abdominal trauma- intra-abdominal bleeding - most common

 Shock - vasoconstriction shunts blood away from the skin, muscles, kidneys, and
gastrointestinal tract in favor of the heart and brain
 Acute pancreatits
 Abdominal aortic aneurysm
 Ileus - mechanical obstruction of the bowel
 Massive volume resuscitation following major illness, surgery, or trauma.

Measurement

 Indwelling bladder catheter (invasive)

 Doppler (nonvasive) - good for estimate

Clinical Significance

 Abdominal
o Decreased perfusion → hypoxia and progressive organ failure (from release of
cytokines and histamine)
o Hypoxia → impaired gut–mucosal barrier function →bacterial translocation, sepsis
and MODS.
o Compression of abdominal vena cava → impaired venous return →decreased CO
 Thoracic
o Elevation of the diaphragm → impeding diaphragm descent and direct cardiac
compression
o Increased intrathoracic pressure → elevated intravascular (PA) and intracardiac
pressures → decreased CO
o Compression of the lung → decreased FRC, atelectasis, decreased compliance, and
V/Q mismatch - → pulmonary dysfunction
 Kidney: Decreased urine output (> 15-20 mm Hg)
 Neuro: Increased ICP → obstruction in cerebral venous out?ow

Respiratory Quotient

Respiratory quotient is the ratio of CO2 produced to O2 consumed.

Equation:

Volume of CO2 Produced/min

Volume of O2 consumed/min
Normal

200/250 = 0.8

If the quotient is off, it changes the needs of the patient, can impact weaning, etc. For the ACCS it is
particularly important to consider the nutrition impact of this.
ACCS- Anticipate Care Based on Nutrition Status

Go
To Outline

Section IIE Nutritional Status

Estimated
Question
Count

Basic Recall 1

Applied
3
Knowledge

Total Questions 4

Oakes Academy Tip

This is a surprising area of the exam for most people, but remember it only comprises 4 questions
(4 questions out of 150 scored). FOUR! We recommend doing some reading and maybe lightly
study the information, but don't get overly concerned about this content area.

Content Review
1. Complications of Malnutrition
(Protein Wasting, Hypoglycemia, Respiratory Muscle Catabolism)

2. Complications of Feedings
(Aspiration, central line infection, refeeding syndrome, malplacement of feeding tube)

3. Routes of Feeding
o Enteral Nutrition (EN)
o Parenteral Nutrition (PN) or Total Parenteral Nutrition (TPN)

4. Morbid Obesity

5. Metabolic Studies
caloric requirements, exhaled gas analysis

Patient Assessment/Metabolic/Nutrition/General
 Oakes Academy Tip
Nutrition is one of those areas that many RTs feel inadequate in. After all, most of us don't receive a lot of e
outside our role (isn't that what the nutritionist is for?) at the bedside. Let's boil it down to a few important thi
1: Nutrition can impact upon respiratory status, with a particular emphasis on weaning failure.

2: Most questions won't contain nutrition information. If it is there (REE, for example), be suspicious. Evalua

3: Most common scenario is overfeeding >> leads to excess CO2 and higher minute ventilation needs >> lea

 Nutrition is the interaction between diet and metabolism.

 Malnutrition = Imbalance between diet and metabolism (both over and under nutrition)
 Malnutrition associated with advanced lung disease has been termed the "pulmonary
cachexia syndrome."

Nutrition Goals
 Prevent loss of lean body mass (maintain homeostasis)
 Reduce stress-induced derangements
 Reduce oxidative stress
 Maintain immune response

Nutritional support is generally provided for patients with an ICU stay of > 2-3 days or MV 3-5 days

It is tailored to each individual patient.

Malnutrition Causes
 Many patients are malnourished prior to admission (poor diet, GI dysfunction).
 Severe illness often increases metabolioc demand (stress, infections, hyperthyroidism,
endocrine disorders, burns, trauma, surgery, and other critical illnesses)
 Commonly diarrhea/vomiting, NG tube output, hemodialysis.
 Muscle wasting (immobilization, medications (steroids)

Signs of Malnutrition
 Loss of appetite
 Unintentional weight loss
 Muscle wasting
 Mental confusion
 Sensory loss
 Motor weakness.
 Dull and dry hair
 Conjunctival dryness
 Receding gums

Malnutrition or Underfeeding can lead to:

 Muscle breakdown/wasting
 Muscle weakness (Increased fatigue, decreased strength/endurance)
  Decreased cough/atelectasis/subsequent pneumonia
 Decreased diaphragm mass and function
 Increased respiratory muscle work
 Increased WOB
 Prolonged weaning
 Prolonged MV, ICU stay

Infectious complications (increased tracheal bacteria colonization, impaired immune function)

Increased morbidity/mortality (MSOD)

Ventilatory drive decrease

Electrolyte imbalances

Malnutrition/Overfeeding can lead to:

 Excessive CO2 production (prolonged weaning)

 Infectious complications
 Increased morbidity/mortality
 Liver dysfunction
 Many other complications

Complications of Feedings

Aspiration

 Enteral nutrition (feeding tube) increases risk of aspiration, likely due to impaired ability to
protect airways
 In all patients where it is possible, keep the head of the bed up at least 30 degrees. If not
possible, elevate as much as possible.
 If high-risk of aspiration, or not tolerating gastric feeds, consider "post-pyloric" feeding, a
feeding tube inserted surgically beyond the stomach (jejunum or duodenum, for example).

Malplacement of feeding tube:

If feeding tube is placed into lungs, there are two possible findings with mechanical ventilation:

 If feeding tube is set to suction: Expiratory tidal volume will be less than delivered volume
(same as a leak!)
 If feeding tube is set to feed: Aspiration is possible, expect coarse crackles, deterioration of
respiratory status
 If suspected to be in the lungs, STOP feed or suction, then assess placement. If any doubt,
pull the feeding tube

Refeeding Syndrome:

 Potentially fatal
 From enteral, parenteral, or oral feeding
 Results from the change in fluid and electrolyte status in sudden feeding of malnourished
patients. Scenarios to be on the lookout for:
o History of alcoholism
o Eating disorders such as anorexia
o Severe diarrhea, vomiting (over days)
o Oncology patients undergoing chemotherapy
 o Elderly patients
 Results in:
o Respiratory failure (issues with diaphragmatic strength), cardiovascular compromise
(CHF), rhabdomyolysis, seizures, delirium. Electrolytes are likely to be low
(potassium, magnesium, phosphorus)
o Note that phosphorus < 2 mg/dL should be corrected
 Preventing and Treating
o For patients at high-risk, gradually introduce nutrition over hours - SLOW
o If evidence of refeeding syndrome, immediately stop feed, treat electrolytes, then
introduce slowly

Central Line Infection

 Repeat after us: Any invasive line has the potential for infection.
 Then this: The ACCS exam is likely to combine symptoms of infection with the
presence of lines
 Types: Bacterial or fungal (bacterial is more common)
 Prevention: Hand hygiene, sterile insertion
 What to do: Remove the line, treat with antibiotics

Hyperglycemia

 Most common with parenteral nutrition - glucose control is a critical aspect of critical care

Patient Assessment/Metabolic/Enteral Nutrition

Patients with functioning GI tract, but cannot ingest enough nutrients orally (unable or
unwilling)

Specific indications
 Prolonged anorexia
 Severe protein-energy undernutrition
 Coma or depressed sensorium
 Liver failure
 Inability to take oral feedings due to head or neck trauma or neurologic disorders
 Critical illnesses (eg, burns) causing metabolic stress
 Bowel preparation for surgery in seriously ill or undernourished patients
 Disorders that may cause malabsorption (eg, Crohn's disease)

Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill
patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition:
Executive Summary

Summary
1. EN is the preferred route of feeding over parenteral nutrition (PN) for the critically ill patient
who requires nutrition support therapy. (It should be given to all patients who are not
expected to be on a full oral diet within 3 days).
2. In the ICU patient population, neither the presence nor the absence of bowel sounds and
evidence of passage of flatus and stool is required for the initiation of enteral feeding.
 3. Enteral feeding should be started early within the first 24 – 48 hours following admission.
The feedings should be advanced toward goal over the next 48 –72 hours
4. Gastric access will be adequate for most patients and will be confirmed by radiography NOT
auscultation alone.
5. Either gastric or small bowel feeding is acceptable in the ICU setting. Critically ill patients
should be fed via an enteral access tube placed in the small bowel if at high risk for
aspiration, show intolerance to gastric feeding, or potential for delayed gastric emptying
(sepsis, diabetic gastroparesis, head trauma, or narcotic use).
6. In the setting of hemodynamic compromise (patients requiring significant hemodynamic
support, including high-dose catecholamine agents, alone or in combination with large
volume fluid or blood product resuscitation to maintain cellular perfusion), EN should be
withheld until the patient is fully resuscitated and/or stable.
7. Specialty high-lipid, low-carbohydrate formulations designed to manipulate the respiratory
quotient and reduce CO2 production are not recommended for routine use in ICU patients
with acute respiratory failure.
8. Patients with ARDS and severe acute lung injury (ALI) should be placed on an enteral
formulation characterized by an anti-inflammatory lipid profile (i.e. omega-3 fish oils,
borage oil) and antioxidants.
9. In the critically ill obese patient, permissive underfeeding or hypocaloric feeding with EN is
recommended.

Procedure
If tube feeding is needed for:

≤ 4 to 6 wk - Use small-caliber, soft nasogastric or nasoenteric (eg, nasoduodenal)

If nasal injury or deformity - may use orogastric or oroenteric tube

> 4 to 6 wk - usually requires gastrostomy or jejunostomy tube, placed endoscopically, surgically, or

radiologically.
Choice depends on physician capabilities and patient preference

Complications
Mechanical
 Aspiration of enteral feeding (reflux) (increased respiratory distress, pneumonia /sepsis)
 Clogging or obstruction of tube
 Inadvertent tracheal intubation (pneumonia and sepsis)

Gastrointestinal
 Abdominal distension
 Diarrhoea
 Vomiting

Metabolic
 Hyperglycaemia
 Hypophosphataemia
 Hypercapnia – due to excess carbohydrate or glucose calories
Assess for Risk of Aspiration

The following measures have been shown to reduce risk of aspiration:

1. Maintain head (shoulders) elevated to 30°–40° (pts with femoral lines can be at 30°, if no
contraindication)
2. Routinely verify appropriate placement of feeding tube
3. Clinically assess GI tolerance:
o Abdominal distension/fullness/discomfort
o Constipation/cramps
o Excessive residual volumes
o Nausea/vomiting/diarrhea
o Respiratory distress/aspiration
4. Remove naso/oro enteric feeding tubes ASAP.
5. High-risk (aspiration) or intolerant to gastric feeding, delivery of EN should be fed via an
enteral access tube placed in the small bowel.
6. Agents to promote motility, such as prokinetic drugs (metoclopramide and erythromycin) or
narcotic antagonists (naloxone and alvimopan), should be initiated where clinically feasible.
7. Diverting the level of feeding by postpyloric tube placement should be considered.
8. Use mouthwash (chlorhexidine) 2 x day to reduce VAP.
9. Blue food coloring and glucose oxidase strips, as surrogate markers for aspiration, should
not be used in the critical care setting.

Patient Assess/Metabolic/Parenteral Nutrition

Definition
IV nutrition support using a formulation of amino acids, carbohydrates, lipids, electrolytes, MVI,
minerals, and supplemental medications (Insulin or H2 blockers)

Indications
 Patients who do not have a functioning GI tract
 Disorders requiring complete bowel rest, such as:
o Acute abdomen
o GI bleed
o Ileus/obstruction
o Long term GI work-up (requiring day after day of NPO at midnight)
o Short bowel syndrome
o Some stages of Crohn's disease or ulcerative colitis

Cautions
 Should not be used routinely in patients with an intact GI tract.
 Causes more complications than enteral, does not preserve GI tract structure and function
 PN is associated with more infectious, metabolic, and fluid complications than EN
 Prolonged PN may lead to atrophy of the gastrointesinal tract.
 PN is also approximately four times the cost of enteral feeding.
 The potential for enteral feedings should be reevaluated daily in patients on PN.

Complications
 5 to 10% have CVP complications
  ≥ 50% have catheter-related sepsis
 > 90% have glucose abnormalities (hyperglycemia or hypoglycemia) or liver dysfunction

Types
Partial parenteral nutrition
Supplies only part of daily nutritional requirements, supplementing oral intake.

Total parenteral nutrition (TPN)

Supplies all daily nutritional requirements.
A central venous catheter is usually required.

IV Access
 Central Access (TLC, PICC, Hickman, Port-A-Cath)
 Peripheral solutions (10% glucose) may be infused via central or peripheral venous
catheters

NOTE: X-ray confirmation of newly inserted CVC or PICC placement is mandatory before
beginning infusion

When to Use
Quick Summary
If the patient is presented as sick (often multi-system dysfunction), and not tolerating enteral feeds
(oro- or nasogastric), consider use of parenteral feeds. A line should be placed (PICC line is the one
we hear about commonly). Remember, there are somewhere around 4 questions on the exam
covering these areas so don't go wild memorizing everything below; just read through and have a
working sense.

General
 First 7 days after admission to ICU - If early EN not feasible or available, no nutrition
support therapy should be provided.
 If patient is previously healthy, no evidence of protein calorie malnutrition, and EN is not
available - PN should be reserved and initiated only after the first 7 days of hospitalization.
 If evidence of protein-calorie malnutrition and EN is not feasible - it is appropriate to initiate
PN ASAP following admission and adequate resuscitation.
 PN should be initiated only if the duration of therapy is anticipated to be 7 days or more.
 Usecentral venous access device to administer high osmolarity PN mixture for full
nutritional needs.
 Use peripheral venous access devices for low osmolarity (< 850 mOsmol/L) mixtures for a
proportion of the nutritional needs and to mitigate negative energy balance.

Dosing
 All ICU patients - Mild permissive underfeeding should be considered at least initially. Once
energy requirements are determined, 80% of these requirements = energy goal or dose of
parenteral feeding.
 As the patient stabilizes, increase PN to meet energy requirements. For obese patients (BMI
≥ 30), the dose of PN with regard to protein and energy provision should follow the same
recommendations given for EN.
  During acute illness, provide energy as close as possible to the measured energy
expenditure in order to decrease negative energy balance.
 In the absence of indirect calorimetry, ICU patients should receive 25 kcal/kg/day
increasing to the energy target over the next 2–3 days.

Surgery
 If undergoing major upper gastrointestinal surgery and EN is not feasible, PN should be
provided under very specific conditions.
 If the patient is malnourished, PN should be initiated 5–7 days preoperatively and
continued into the postoperative period.
 PN should not be initiated in the immediate postoperative period - delay for 5–7 days (if EN
not feasible).

Initiating
 In patients stabilized on PN, periodically repeat efforts to initiate EN.
 As tolerance improves, increase volume of EN energy and decrease volume of PN energy.
 Do not terminate PN until ≥ 60% of target energy requirements are being delivered by EN.

Obesity - Nutrition

Malnutrition often exists during critical illness

Overfeeding may result in excess CO2 production and prolonged ventilator days

2009, the Society for Critical Care Medicine and American Society for Parenteral and
Enteral Nutrition joint consensus statement:

 Use hypocaloric enteral feeding for obese ICU patients - 60% to 70% of target caloric
requirements, or 11 to 14 kcal/kg actual body weight per day.
 Estimation of target caloric requirements:
Obesity-adjusted weight with a 25% correction of excess weight above the
IBW as follows:
Adjusted body weight = (actual weight - IBW) 0.25 + IBW

Nutritional Assessment

Resting Energy Expenditure (REE)

 Calculates Resting Energy Expenditure (REE). This is the amount of energy required to
maintain the current metabolic state. Think of it as a patient's current "baseline."
 Energy expenditure from the measurement of oxygen consumption (VO 2) and carbon
dioxide production (VCO2) reflects the energy needs at the cellular level.
Uses Modified Weir Equation to determine requirements (O 2 consumption (VO2) vs CO2
production (VCO2)

Respiratory Quotient (RQ)

VCO2/VO2

 Normal is around 0.8 (this varies some but treat anything > 1.1 as abnormal)
 Review the Respiratory Quotient and what it means
  Measured by Indirect Calorimetry
Indirect calorimetry is potentially inaccurate when:
o High FIO2 or PEEP on a ventilator
o Leak
 Active leak (chest tube)
 ET Tube cuff leak
o Pain
o Fever or shivering
o Hypo or hyperventilation
o Hypoventilation
o Vasoactive drugs
o Acidosis or alkalosis

Total Energy Expenditure (TEE)

Total energy expenditure is how much energy is utilized daily to maintain current state. It is equal to
the sum of:

 Resting metabolic rate (RMR, or resting energy expenditure rate), which is normally about
70% of TEE
 Energy dissipated by metabolism of food (10% of TEE)
 Energy expended during physical activity (20% of TEE)

TEE ranges from:

 25 kcal/kg/day for sedentary and not under stress to about

 40 kcal/kg/day for people who are critically ill.

Conditions that increase metabolic demand can increase resting metabolic rate (and thus
impact TEE):

 Burns
 Critical illnesses
 Endocrine disorders, including hyperthyroidism
 Infections
 Surgery
 Trauma

18 – 25 kcal/kg/day is considered most appropriate for critically ill patients

Obese – may use adjusted or IBW and provide underfeeding (60-70% of target)

Initial caloric GOALS = 25 - 35 kcal/kg of IBW

 In critical care we often aim for 50-65% of initial caloric goals initially, then increase as the
patient tolerates
 Consider parenteral nutrition if 100% of goal isn't met by 7-10 days of enteral nutrition

Indicators of lean body mass

 Body mass index (BMI)

 Body composition analysis
 Body fat distribution
 Nitrogen balance
  Response to skin antigens
 Muscle strength measurement
 Indirect calorimetry

Metabolic Assessment-Endocrine Disorders

Oakes Academy Tip

It is probably not all that important to know each endocrine disorder, but the ACCS content outline
does suggest that you should be comfortable assessing for endocrine disorders (but pretty
generically). It may be more likely that diabetes is included in a scenario, and perhaps treating a
patient with a severe metabolic acidosis (such as diabetic ketoacidosis).

Typical laboratory tests that should trigger you to think "endocrine". Knowing values is likely
unimportant:

 ACTH: Reflection of cortisol production by the adrenal glands

 TSH: Reflection of thyroid hormone production
 PTH: Reflection of parathyroid hormone / regulates blood calcium
 Aldosterone: Reflection of salt/water balance
 Insulin, Glucagon: Involved in glucose regulation

Selected Disorders

 Pituitary dysfunction: Diabetes inspidus, Inappropriate ADH secretions (retention of

fluids)
 Hypoparathyroidsm: Tetany (bronchospasm, laryngeal spasm, seizures, cardiac
dysrhythmias)
 Hyperparathyroidism: Fatigue, muscle weakness
 Cushing's Syndrome: Commonly due to corticosteroid use

Feeding Tube Placement

Verification is essential

 X-ray is the only reliable method to verify initial placement of blindly inserted feeding tubes.
 Secondary confirmation (via pH or carbon dioxide testing, visualization of tube at exit site)
must be performed regularly to ensure tube location.

As the lack of CO2 is used to determine improper ETT placement, the presence of CO2 is
increasingly being used to identify improper nasogastric or oral feeding-tube placement.

Note:

 ET or trach tube cuffs do not prevent pulmonary malposition.

 Aspiration risk is high when tubes are placed in the esophagus or gastroesophageal
junction.
 Pulmonary malplacement may occur silently, without coughing, dyspnea, or oxygen
desaturation and cause pneumonia, pneumothorax, perforations, empyema, and BP fistula.

Increased risk of malplacement occurs with:

  Artificial airways
 Confused/uncooperative
 Cranio-facial trauma
 Decreased cough-gag reflex
 Sedation/decreased consciousness

GI Assessment/Ileus

Partial or complete blockage of the small and/or large intestine by functional (adynamic or paralytic
ileus) or mechanical bowel obstruction.

Clinical Effects

 May lead to increased intra-abdominal pressures, possible to compartment syndrome.

Anytime there is increased abdominal pressures, these may transmit to the pleural space,
making it more difficult to ventilate a patient.
 Increased risk of Ventilator Associated Pneumonia

Treatments

 Adequate hydration status

 Avoidance of drugs known to impair intestinal perfusion
 Stimulation of gastric and intestinal motility
 Proper nutrition
 Treat any accompanying ACS

GI Assessment/GI Bleed

GI Bleed
Major risk factors

 MV for > 48 h (#1 cause)

 Coagulopathy
 Hepatic or renal disease
 Hypotension
 Major surgery
 Major trauma
 Sepsis
 Severe burns

Probable causes

 Stress-related mucosal damage (SRMD)

 Esophageal mucosal injury from nasogastric tubes, gastroesophageal reflux (GER), and
duodenogastroesophageal (bile) reflux

Prevention

 Aggressive hemodynamic support to ensure adequate tissue perfusion

 Enteral feeding
 Ranitidine (H2-receptor blocker)
 Stress ulcer prophylaxis
Coagulation

Coagulopathy refers to abnormal bleeding and particularly to problems with clotting. This can be a
result of the blood vessels themselves, platelets, or something in the coagulation cascade. For exam
purposes, mentions of coagulopathies will often tag-team on some other factor, such as whether you
should give heparin (it's not as simple as a no - may consider for DIC), fresh frozen platelets (yes),
etc. Some procedures should be avoided (biopsies, trachs, some line placements, etc.)

Major Causes to Watch for and Treat

 Vitamin K deficiency
 Liver disease (look for INR and PTT to be elevated)
 Disseminated intravascular coagulation (DIC)
o The abnormal and excessive generation of thrombin and fibrin in the blood (both
factors in clotting)
o Platelets "aggregate" (gather)
o Symptoms: skin puncture sites bleed persistently, ecchymoses (discoloration under
skin) form at site of injections.
o Diagnosis: evolves rapidly
 Thrombocytopenia (low platelet count)
 Elevated PTT and PT
 Increased plasma d-dimer (this is used for DVT, PE, and DIC - but only rules
out as other things can increase it as well)
o Three common possibilities:

1. A thrombosis made up of aggregated platelets can enter bloodstream

(increases risk of PE, stroke, MI)
2. Increased bleedability at sites of procedures (think: bronch, intubation, ABG
draw, A-line placement)
3. Severe GI bleed (as evidenced by distended abdomen)
o Treatment

 Note that heparin may be used if DVT present

 Replacing platelets
o Bottom Line: Be very aware of coagulation when DIC is mentioned.

Respiratory Concerns of Coagulation Disorders

 Venous thromboembolism
 Pulmonary coagulopathy can occur in pneumonia and ALI/ARDS
 Percutaneous lung biopsy - avoid if platelets < 100,000 or INR > 1.4

Exam Strategies

 When there is any indication of coagulopathy, be very cautious about proceeding with any
invasive procedures
o ECMO - remember this involves cannulation
o Blood draws (ABG)
o Line placement (a-line, PA line, central line)
o Procedures (bronch, any biopsies, trach, PEG, etc.)
 When there is any indication of coagulopathy, be aware of what drugs are indicated
(heparin, Coumadin, tPA - more on those in the drug section)
o Do NOT give anticoagulants (like Heparin) if active bleeding - often GI is used but
anything can be mentioned - hemoptysis, hematuria, etc. Do give heparin to
prevent or treat thrombosis, emboli. Do NOT give with fat emboli (won't work)
 o Give warfarin only if indication that heparin has been given before
o Enoxaparin is very common choice with thrombosis, emboli
o ONLY give tPA if hemodynamically unstable with evidence of PE
o Don't give anticoagulants if head bleed, GI bleed and risk of thrombosis, emboli -
inferior vena cava filter instead
 If platelets are low with bleeding, strongly consider platelets transfusion
o This will not help immediately!

Hematology (Leukocytes)

Oakes Academy Tip

White blood cells are one of the best indicators of immune system health we have. Abnormally
high values often suggest an infectious process. Abnormally low values can indicate an
overwhelmed or suppressed immune system. The ACCS exam will not ask a bunch of question
asking you to regurgitate terms and values, but you will be expected to thoughtfully consider
values in the context of a situation. For example, if a patient has a WBC of 11,500 you should
immediately look to see if the patient is febrile - both indicators of an infection. Couple this with a
central line placed a few days ago, and you can make the connection that a catheter-related
infection is likely.

Test Values Interpretation

More generally referred to as White Blood Cells (WBCs)

 Increased leukocytes (leukocytosis)

Leukocytes o Infection
5,000-
o Steroids (systemic) may elevate the count (mostly
(White Blood 10,000/µL
neutrophils) - Note that there will not be banding
Cells)
(see below)
 Decreased leukocytes (leukopenia) indicate the potential
for immunosuppression

Differential (%) of WBC:

Neutrophils 40-75%
Increased (> around 8,000/µL) neutrophil count (neutrophilia):

 Infection, probably bacterial but could be viral

 Corticosteroids (systemic) "falsely" increase the count

Decreased (< 1,500/µL) neutrophil count (neutropenia):

 Chemotherapy and Radiation therapy

 Leukemia
 Certain infections (sepsis, HIV/AIDS, Hepatitis)

Neutropenia suggests the patient is immunosuppressed, unable to

fight off infection. Neutropenic precautions (reverse isolation) are
 necessary to protect the patient from infection.

Bands are immature neutrophils

Bands Near 0%  the presence of them may indicate an active infection.

This is referred to as "bandemia," "banding," or simply an
increased band count.

Increased (> 4,000/µL) lymphocyte count (lymphocytosis)

Lymphocytes 20-45%
 Infection, but more likely viral (mononucleosis,
cytomegalovirus)

Increased (> 950/µL) monocyte count (monocytosis)

 Infection, usually bacterial (tuberculosis, bacterial

Monocytes 2-10% endocarditis)
 Leukemias, some types
 Autoimmune disease (lupus, rheumatoid arthritis)
 Sarcoidosis

Increased (> 500/µL) eosinophil count (eosinophilia)

Eosinophils 1-6%  Allergic reactions

 Asthma
 Allergy to drugs

Basophils 0-1% Increased (> 150/µL) basophil count (basophilia) is RARE

Trauma/Spinal Cord

Respiratory dysfunction is a major cause of morbidity and mortality in spinal cord injury (SCI)

Manifestations by location of injury

 High lesions (ie, C1 or C2) - VC 5-10% of normal, cough is absent

 Lesions at C3 through C6 - VC 20% of normal, cough is weak and ineffective
 High thoracic cord injuries (ie, T2 through T4) - VC 30-50% of normal, cough is weak
 Lower cord injuries - respiratory function improves
 Injuries at T11 - respiratory dysfunction is minimal; VC essentially normal, cough is strong

Pathophysiology
  Aspiration
 Decreased lung and chest wall compliance
 Decreased VC
 Excessive oxygen cost of breathing due to distortion of the respiratory system
 Hypoventilation/respiratory failure
 Impairment/paralysis of respiratory muscles
 Ineffective cough/atelectasis

History

Underlying cardiopulmonary comorbidity such as COPD or heart failure.

Degree of respiratory dysfunction is dependent on:

 Level of the spinal cord injury (loss of ventilatory muscle function from denervation)
 Preexisting pulmonary comorbidity (COPD or heart failure)
 Associated chest wall or lung injury (pneumo/hemothorax, pulmonary contusion)
 Loss of ventilatory muscle function from denervation and/or associated chest wall injury
 Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion
 Decreased central ventilatory drive - head injury or drugs

Monitor

Obtain baseline VC, FEV1(if possible) and ABGs and periodically until stable

Observe/monitor:

 RR, chest wall expansion, abdominal wall movement, cough

 Chest wall and/or pulmonary injuries
 Pulse oximetry

Watch for signs of Respiratory Failure:

 Increased WOB, dyspnea

 Accessory muscle use
 Rapid, shallow breathing
 Hypercarbia
 Cyanosis - late sign

Other findings of respiratory dysfunction

 Agitation, anxiety, restlessness

 Decreased air entry
 Decreased chest wall expansion
 Increased accessory muscle use
 Increased heart rate
 Moist cough
 Pallor, cyanosis
 Paradoxic movement of the chest wall
 Crackles, rhonchi

Complications
  Aspiration - nasogastric decompression of the stomach is mandatory
 Atelectasis – due to decreased VC & FRC
 Decreased coughing – resulting in the of retained secretions, atelectasis, and pneumonia
 Increased WOB - due to decreased compliance
 Muscle fatigue/respiratory failure
 V/Q mismatch - due to sympathectomy and/or adrenergic blockade
 Sepsis or pneumonia - follows treatment with high-dose methylprednisolone

Treatments

 Oxygen therapy as needed

 Close monitor for respiratory failure (VC and NIF)
 Maintain airway:
o Intubation -
 Direct laryngoscopy – method of choice with in-line mobilization
 Blind nasal intubation – is an option
 Fiberoptic intubation with cervical spine control is an option
 Indications for intubation:
 Acute respiratory failure
 Decreased level of consciousness (Glasgow score < 9)
 Increased respiratory rate with hypoxia
 PCO2 > 50 mm Hg
 VC < 10 mL/kg
o Aggressive airway clearance
o Atelectasis/pneumonia prevention using manually assisted coughing and/or
mechanical insufflations-exsufflation
o Prevent/treat VTE
 Mechanical compression devices
 Heparin therapy
o Mechanical Ventilation
 Promote spontaneous ventilation as much as possible
 PEEP to prevent atelectasis
 Larger VT and sigh breaths to avoid atelectasis
o Weaning and long term – respiratory muscle training
o Phrenic nerve pacing

Intubation may cause severe bradyarrhythmias from vagal

stimulation.
Topical lidocaine spray can minimize or prevent this reaction.
Notes
Oral suctioning may cause significant bradycardia.

Preoxygenation with 100% oxygen may be preventive.

American Spinal Injury Association Impairment Scale (ASIA)

A = Complete

No motor or sensory function is preserved below the neruological level*.

B = Incomplete

Sensory but not motor function is preserved below the neurological level* and includes the sacral
segments S4-S5.

C = Incomplete

Motor function is preserved below the neurological level*.

Also, more than half of the key muscles below the neurological level have a muscle grade less
than 3.

D = Incomplete

Motor function is preserved below the neurological level*, and

At least half of the key muscles below the neurological level have a muscle grade of 3 or more –
full ROM.

E = Incomplete

Motor and sensory function is normal.

-------------------------------------------------------------------------------

*Neurological level refers to the nerve level of injury.

Example: C4 ASIA A -complete injury. Motor and sensory function is lost below C4 nerve.

-------------------------------------------------------------------------------

Common Terms

Paraplegia - motor and/or sensory loss in trunk, legs, and pelvic organs. Arm function is spared.

Tetraplegia (old term = quadriplegia) - motor and/or sensory loss in arms, trunk, legs, and
pelvic organs.

ICU Myopathy

Found particularly in patients with an extended or complicated ICU stay. It is characterized by

general muscle weakness (which does not affect vital muscles of breathing). Certain drugs may
increase the risk (steroids, sedation, paralytics)

Clinical Manifestations

 Absent deep tendon reflexes

 Failure to wean
 Flaccid muscles

Treatment (prophylactic)

 Avoidance of high risk drugs when possible (NMBAs, for example)

 Early mobilization
 Optimized nutrition plan
Rhabdomyolysis

The breakdown of muscle fibers resulting in muscle necrosis and the release of intracellular muscle
constituents into the circulation

Common Findings

 Acute renal failure

 Disseminated intravascular coagulation (DIC) - tiny thrombi form from fibrin, often a sign of
advanced organ failure (sepsis, for example)
 Hypovolemia
 Hyperkalemia
 Metabolic acidosis

Signs and Symptoms

 Increased creatinine kinase (CK)

 Triad of complaints:
o Muscle pain
o Weakness
o Dark urine
 Other:
Malaise, fever, tachycardia, nausea/vomiting, abdominal pain

Treatment

 Key treatment: fluid resuscitation - often large amounts

 Manage acute renal failure - by diuretics if some function, or dialysis
 Treat electrolytes that are out of balance (K+, Na+, Ca++)
 Platelets (or factor replacement) if bleeding

Other potential causes (you don't need to memorize these):

 Drugs of abuse
 Exercise induced (severe exercise, status asthamaticus)
 Immunologic
 Infectious (viral or bacterial)
 Inherited
 Metabolic – electrolyte disorders
 Medications
 Diuretics
 Muscle relaxants
 Neuromuscular blocking agents
 Prolonged immobilization
 Sedatives – etomidate and propofol
 Traumatic - crush syndrome (such as lying on side for long period), burns, electrical injury

Therapeutic Hypothermia (Targeted Temperature Management)

"Therapeutic Hypothermia" and "Targeted Temperature Management" both involve lowering the body
temperature below normal. The main difference is the range of temperatures used:

 Therapeutic Hypothermia (TH): body temperature 32-34 C Do not use with significant
bleeding
 Targeted Temperature Management (TTM): body temperature < 36 C
Purpose

 Improves survival chances in post-cardiac arrest patients

 Improves neurological outcome in post-cardiac arrest patients

Indications

 Patients who have achieved "ROSC" (return of spontaneous circulation) post-cardiac arrest
 Patients who are not following commands or showing purposeful movement post-cardiac
arrest
 Mean blood pressure (MAP) > 65 mm Hg

Contraindications

 Do-not-resuscitate status
 With severe bleeding, if given the choice, choose TTM over TH

Management

 Cooling Phase
o Treatment should be started within 6 hours once ROSC is achieved
o Targeted temperature is approximately 36 C to be reached within 24 hours post-
ROSC. There is a range, which generally doesn't go below 32 C.
 Maintenance Phase
o 24-48 hours of cooling
o Mechanical Ventilation
 Still humidify circuit; consider HME
 Minimize oxygen consumption (so full support modes). Maintain SpO2 > 94%
o Maintain stable BP, use vasopressor support like norepinephrine if needed
 Rewarming Phase
o Warm at around 0.5 C/hour - so takes 6-8 hours
o Do not allow fever
o Monitor BP as hypotension (from vasodilation) is possible

Methods

Use of one or multiple is reasonable. There is little evidence to support any one method over
another.

 Internal cooling
o Cold Saline: intravenous infusion of cooled isotonic saline (4 C) with a pressure bag.
Temp drops by 2 C/hour on average. 1L x 15 min = Drop 1 C. Do not use if fluid
overload is a concern (CHF history, renal failure, for example)
 External (Surface) cooling. Temp drops by 0.5 - 1 C per hour.
o Cooling blankets
o Thermoregulation device, such as Arctic Sun®
 Cold water runs through special pads which are attached to the patient's skin
 Temperature is regulated by a special machine at the foot of the bed
o Cool water and fans

Complications

 Shivering
 o Shivering increases O2 consumption + increases body temperature (!)
o Administer sedation to control shivering, regardless of sedation scale
o Use paralytics if needed, but may mask seizures (so consider EEG)
 Cardiac
o Slows conduction, results in bradycardia with HR as low as the 40s at lower temps
o Do not intervene for HR, but monitor BP instead
o If Vfib or pulseless Vtach, defibrillation
 Hyperglycemia
o Insulin resistance results in high glucose levels
o Administer insulin to maintain glycemic control
 Electrolyte imbalance
o Decreases primarily in: Na, Mg, Phosphate
o Treat each as needed
 Coagulopathy
o Clotting is less effective
o STOP and REWARM if significant bleeding
 Decreased drug metabolism
o Cold temperatures decrease the elimination of a drug from the system (so delayed
effect)
o Rewarm and allow time for the drug to wear off before making any end-of-life
(apnea test) decisions
 Infection
o Leukocytes are not as effective, particularly if TH/TTM is > 24 hours
o Treat underlying infection when present

Albumin

Normal Albumin: 3.5 - 5.5 g/dL

Albumin is a strong reflection of chronic liver (hepatic) function

Interpreting

 Serum albumin is normal with acute hepatitis

 Serum albumin decreases (hypoalbuminemia):
o Chronic liver disease (hepatitis, cirrhosis)
o Hypovolemia
o Burns
o Ascites
o Malnutrition
 Serum albumin increases with (hyperalbuminemia):
o Dehydration
o Severe diarrhea

Treatment

 As with most disorders like these, treating the underlying cause is the most effective
strategy
 Administer albumin (human serum) for hypovolemia, severe burns
 For hyperalbuminemia, treat dehydration by giving fluid

Hematology (Red Blood Cells)

 Oakes Academy Tip
Red blood cells are important in determining oxygen-carrying capacity. Abnormally high values
suggest some type of chronic lung disease (or could simply mean the person lives at a high
altitude). Abnormally low values can indicate anemia—consider recommending packed red blood
cells (PRBCs).

Know the normal values listed below, and pay particular attention to hemoglobin. Know when
to transfuse PRBCs (don't transfuse to "normal range," but instead use a transfusion trigger - see
below). As with most things in critical care, treat patients who are symptomatic more
aggressively than those who are not.

Test Normal Values Interpretation

Red Blood Cells (RBCs)

Erythrocytes
(Red Blood 4-6 million per mcL ↑ polycythemia (possible sign of chronic lung disease)
Cells)
↓ anemia (impact on O2 carrying capacity)

Grams of hemoglobin in 100 mL of blood

Hemoglobin 13-18 g/dL ↑ polycythemia (possible sign of chronic lung disease)

↓ anemia (impact on O2 carrying capacity)

% blood volume occupied by RBCs

Hematocrit 36-55 % ↑ polycythemia (possible sign of chronic lung disease)

↓ anemia (impact on O2 carrying capacity)

Transfusion Trigger:

 Remember, transfusing blood product has its own risks and complications, most commonly
nonhemolytic fever
 When hemoglobin is under 8 g/dL consider a transfusion of RBCs (usually PRBCs)
o If patient is symptomatic or reason is cardiac (tachycardia, hypotension, significant
dyspnea), transfusing at a trigger of about 10 g/dL would be appropriate.
o For patients actively bleeding, transfusing based on a number is difficult but don't delay
treatment waiting for typed and crossed blood to arrive
 After transfusion, recheck hemoglobin levels, as early as 15 mins after transfusion

Hematology (Clotting and Bleeding)

Oakes Academy Tip

We know how important the topic of bleeding is, particularly with procedures we are involved in.
These directly include intubation, bronchoscopy, arterial blood draws, etc. Indirectly we need to be
aware of bleeding and clotting as it relates to pulmonary emboli, and interference with oxygen-
carrying capacity.

Test Values Interpretation

Blood constituent for clotting

Increased Platelets* (thrombocystosis) indicates high risk of

clotting. Consider anticoagulation therapy.

Decreased platelets (thrombocytopenia) indicates increased

risk of bleeding.
150,000-
Platelet
400,000/µL
*Reactive thrombocytosis occurs with certain drugs
(including epinephrine and heparin). This usually does not
need to be treated and does not generally increase the risk
of blood clots.

Transfusion Trigger: If < 50,000/µL consider

transfusing platelets

A measure of the amount of time (in seconds) required for

fibrin clot formation - measures EXTRINSIC PATHWAY,
helpful with determining coumadin dosages

Prolonged PT indicates an increased risk of bleeding (it

takes longer for a clot to form):

 With medication: coumadin, aspirin

 With massive blood transfusion (dilution effect)
Prothrombin Time  Hypothermia
11-13 sec  Liver disease - even mild (diminished clotting factors)
(PT)
 Disseminated intravascular coagulation (DIC)

Decreased PT indicates an increased risk of clotting:

 After fresh frozen plasma (FFP) transfusion

 Vitamin K supplements

Transfusion Trigger: If > 18 seconds, consider

transfusion of fresh frozen plasma/cryoprecipitate

International < 1.3  Ratio of patient's PT to a control PT (INR = Patient PT

Normalized Ratio / Control PT) - DO NOT worry about formula!
(INR)  INR is particularly helpful when monitoring drug
 levels, like warfarin (Coumadin)
 Indirect measure of liver function (liver is responsible
for the production of clotting factors)

Transfusion Trigger: If > 2.0, consider transfusion of

fresh frozen plasma (FFP)/cryoprecipitate

Time it takes, in seconds, for plasma to clot when exposed

to substances that activate contact factors: Measures
INTRINSIC PATHWAY, helpful for heparin dose/level. This is
called PARTIAL due to the absence of tissue factor.

Prolonged aPTT:
Activated partial
thromboplastin time 25-35 sec  Severe liver disease (may be normal with milder
(aPTT) disease)
 Disseminated intravascular coagulation (DIC)
 Massive blood transfusion (dilution effect)

Transfusion Trigger: If > 60 seconds, consider

transfusion of fresh frozen plasma
(FFP)/cryopreciptate

Transfusion Refusal

Oakes Academy Tip

This section follows common sense. If a patient has an objection to blood product based on cultural
or religious reasoning, your answer choice needs to respect the belief system. What if the patient's
life is in the balance? It doesn't matter: Choose an option that respects the belief.

 Unless otherwise stated, this includes packed red blood cells (PRBCs), fresh frozen plasma
(FFP), platelets, etc. Look for other potential non-human options such as Vitamin K and
Factor 7.
 In an emergency, if the patient is unable to provide consent, something in writing should be
in place or a hospital may administer blood product. What does this mean? A neighbor, for
example, can't just say, "Hey I know this person doesn't want blood products." There
needs to be some documentation of the fact.
 Note that for some religions (Jehovah's Witnesses, for example), transfusing your own
blood is not an acceptable solution either.
 Note: You will not be expected to know what religious beliefs correlate with the refusal of
blood product. The scenario will be clear.

Cardiac Markers

Oakes Academy Tip

 Consider cardiac markers when patient's symptoms are consistent with an acute MI. Note that
many of these tests are non-specific for an MI (there are other causes for abnormal results). Use a
combination of symptoms and test results.

Note about values: For ease of memorization, we have left off units .

Test Values Interpretation

BNP (b-type natriuetic failure: Secreted from heart ventricles - indicates heart
peptide) 100-300 failure

Enzyme found in heart and skeletal muscle - may

Creatine kinase 26-174 U/L indicate MI
Other factors may ↑ Creatine kinase (Muscle disease)

< 0.04 Serum marker for cardiac disease

ng/mL
normal Elevates within 3 hours of acute MI, Remains
Troponin elevated for 5-9 days
> 0.40 Other factors may ↑ troponins (PE, Sepsis, etc.)
ng/mL
likely an MI Usually drawn in a series of 3 levels

Clinically significant levels are generally > 2

0.5-1
Serum Lactate
mmol/L
Indicator of anaerobic metabolism

D-Dimer Lab Test

D-dimer is a waste product of the clotting process.

Normal: < 0.5 µg/mL

> 0.5 is reported as "positive"

< 0.5 is reported as "negative"

Causes of a Positive D-Dimer:

 Evaluation of thrombus formation, including pulmonary embolus

 Monitoring anticoagulation therapy
 Disseminated intravascular coagulation (DIC)
  Others: Pregnancy, inflammation, trauma, post-surgery, liver disease, heart disease,
hosptialization

Important Note: Note that lots of things cause a + D-Dimer. Its use in diagnosing a PE is
limited. Its use in ruling out a PE is helpful.

 A patient has a PE: the d-dimer will be positive

 A patient doesn't have a PE: the d-dimer may still be positive (for any of the reasons
above)
 Therefore, if the d-dimer is negative, the patient is unlikely to have a PE. If the d-
dimer is positive, the patient may or may not have a PE.

Lactate

Lactic acid (lactate with an extra proton) is a byproduct of anaerobic metabolism.

Normal in hospitalized patients: < 2.0 mmol/L

Increase in lactic levels

 Hyperlactatemia is mild elevation (2-4 mmol/L) - no change in blood gas

 Lactic acidosis is moderate-to-severe elevation (> 4 mmol/L) - causes metabolic acidosis

Causes of lactic acidosis

 Tissue hypoperfusion (hypovolemia, cardiac failure, sepsis, cardiopulmonary arrest)

o Hypoperfusion leads rapidly to hypoxia, which leads to lactic acidosis
 Diabetic ketoacidosis (anion gap acidosis)
 I.V. epinephrine
 Inhaled beta agonists (continuous nebulization at high doses)

Treatment

 Support or treat the underlying cause when known

 Sodium Bicarbonate
o Administration of sodium bicarb: severe acidosis (pH < 7.2). Bicarbonate is a
temporary fix until the cause can be addressed
o Rapid infusion of bicarbonate may increase PaCO2 and worsen lactate production
o Goal: give 1-2 mEq/kg IV bolus, then repeat after 30-60 mins if pH hasn't improved
satisfactorily

Procalcitonin (PCT)

A biomarker that strongly indicates sepsis that is bacterial in nature, meanin it is an indication of
when to initiate antibiotics

Normal: < 0.15 ng/mL

(basically should be 0!)
Increase in serum procalcitonin

 Mild elevation (0.15 - 2 ng/mL)

o bacterial infection (mild-to-moderate)
o untreated end-stage renal failure
 Moderate - Severe elevation (> 2 ng/mL)
o bacterial sepsis
o severe bacterial infections (pneumonia, for example)
o major burns
o severe trauma
o major surgery (abdominal, cardiothoracic)

Acid-Base Balance

Oakes Academy Tip

Blood gases are common on the exam. No surprise, right? Let's be clear ... there are no questions testing
are from the RRT level exam. There are no questions asking you to outright analyze and classify an ABG. Y
make a decision about what to do next. For example:

pH 7.17
PaCO2 23 torr
PaO2 90 torr
HCO3- 8 mEq/L
BE -21 mEq/L

What should you do next? Start NPPV (that's a theme on the exam, too!)? Intubate? Treat the metabolic a
recognize this as a metabolic acidosis, likely diabetic ketoacidosis.

Arterial Blood Gas Values

Normal Range for

Notes
Exam*

 pH as low as 7.25 for lung protection (ARDS)

 Consider bicarbonate if pH < 7.20
pH 7.35-7.45
Venous: 7.32-7.43

 Treat pH as more important than PaCO2

 Abnormal baselines due to COPD are likely to be presented
PaCO2 35-45 torr
PvCO2: 41-50 torr

PaO2 80-100 torr  PaO2 as low as 60 torr in ICU

 When V/Q mismatch (estimate with P/F ratio), prioritize
PEEP over FIO2 in "fixing" PaO2
 PvO2: 25-40 torr

SaO2 > 95% SvO2: ~70%

 Only consider bicarbonate if pH is exceptionally low (<

HCO3 -
21-28 mEq/L 7.20)

 Amount of acid that must be added to 1L blood to restore

pH to 7.40
BE -2 to +2 mEq/L
 Indicator of cause of metabolic acidosis

*Ranges vary some regionally and by laboratory. Of particular importance is bicarbonate which is
reported as wide as 21-28, but also as 22-26, 22-28, etc. For ACCS purposes the "exact" normal
range isn't worth worrying about - just remember this list and you'll be okay.

Sampling Errors

Sampling errors may be included within a scenario where you have an option to question a result.
The three most common:

 Air bubbles: Some indication of air in sample. ERROR: False high PaO2, false low PaCO2
 Not icing sample: If not analyzing ABG within 15 minutes, put on ice. Scenario should
mention extended time at room temperature. ERROR: False low PaO2
 Heparin: The scenario would have to state something about "liquid heparin" in syringe.
ERROR: False low PaCO2, pH

Anion Gap

The purpose of the anion gap is to help determine the cause of a metabolic acidosis.

Normal:
< 11 mEq/L

Calculating the Anion Gap:

You may be given an anion gap on the exam, or you may be given the elements to calculate it
yourself.

AG = Na - (Cl + HCO3)
Normal AG

Sodium = 135
Chloride = 100
HCO3 = 25

AG = 135 - (100 + 25)

AG = 10

Note: Some people include potassium in the anion gap, which increases the normal range to around
12-16

Interpreting the Anion Gap

An elevated anion gap strongly suggests a metabolic acidosis

Anion Gap Metabolic Acidosis

Accumulation of acids or impaired H+ excretion

Causes

 Alcoholic or Starvation (Ketoacidosis)

 Lactate (Lactic Acidosis)
 Ketones (Diabetic Ketoacidosis)
 Salicylates
 Carbon monoxide poisoning
 Dehydration
 Renal failure
 Hyperalbuminemia

Non-Anion Gap Metabolic Acidosis

Decrease in base

Causes

 Diarrhea
 Renal tubular acidosis
 Sudden decrease in PaCO2 to normal after hyperventilating (for example: severe asthmatic
being placed on mechanical ventilation)

Ketones

Produced in the liver in the absence of sufficient amounts of insulin. Insulin is needed to convert
glucose into energy. When there is insufficient insulin, the body turns to adipose (fat) instead, and
the byproduct of this is ketones (an acid).

 Ketones can be detected in urine (ketonuria) or in blood/serum (ketonemia)

 Nitroprusside testing is a manner of measuring ketones. It may result in False-Negative
results, or may underestimate the amount of ketones in blood.
 Increased anion gap is common with ketoacidosis

Diabetic Ketoacidosis (DKA)

Look for: nausea, vomiting, change in mental status, extreme tachypnea, Kussmaul breathing
Alcoholic Ketoacidosis

Look for: Nausea, vomiting, abdominal pain, hepatomegaly, tachycardia

AFB Smear and Culture

Culture and sensitivity

Culture

Identification and bacterial count of an organism.

Bacterial counts assist in deciding whether a wound or fluid is colonised or infected.

Colonized - bacteria multiply but do not elicit a host response

Infected - bacteria multiply, plus a pathological response

Numbers of bacteria are expressed as colony-forming units (cfu) (e.g. 104cfu/ml)

A cfu is a colony arising from a single viable bacterium.

Sensitivity

Identifies organisms based upon their sensitivity to antibiotics.

Gram Stain

Gram stains are performed on body fluid or biopsy when infection is suspected.

It differentiates bacterial species into two large groups:

Gram-positive - stain dark blue or violet

Two types – cocci and bacilli

Gram-negative - stain red or pink

Patients at risk of or showing early signs of sepsis should be cultured for infection. Lab results from
blood, urine, stool, and sputum should all be considered. If presence of micro-organisms (gram +,
gram -, AFB) then strongly consider administration of antimicrobials (antibiotics). For certain
sputum-based infections consider inhaled antimicrobials (such as tobramycin for pseudomonas).

For example, if sputum culture shows gram negative rods, be prepared to recommend treatment with
tobramycin.
It would not be advisable to recommend inhaled antimicrobials for infections present in blood, urine,
and/or stool (use systemic instead).

Test Normal Value Clinical Significance Clinical Increases

AFB + Smear = poss active + Culture indicates MTb present

Smear No organisms seen case of MTb (or one of 50 in culture site (i.e., lungs,
and False negative? (5,000- other species, including stomach, kidneys, GI, blood,
Culture 50,000 organisms/mL = non-myobacteria spp.) marrow, sterile body fluids,
 tissue, wound aspirate)
+)

No growth on
myobacterial agar x 6-8
wks incubation is
generally negative for
MTb

Co-Oximetry

< 3% is normal
CoHb
< 10-15% for smokers

MetHb < 1% is normal

Carboxyhemoglobin (COHb)

Carboxyhemoglobin is formed when carbon monoxide (CO) attaches to hemoglobin. Hemoglobin,

unfortunately, actually prefers CO to O2. The CO steals seats on the hemoglobin that are usually
taken up by oxygen. It gets worse though - to some degree carboxyhemoglobin reads just like
oxyhemoglobin. This means patient appearance is pink and SpO2 reads normal.

KEY: A patient with CO poisoning appears normal (including some labs) but is actually
hypoxic. It is critical to treat the hypoxia aggressively and minimize the amount of time spent
hypoxic. The half-life of CO is about 3-4 hours on room air; this is cut in half with 100% O2,
and drops to about 20 minutes with hyperbaric treatment.

Absolute Rule #1: If there is any suspicion that the patient has been exposed to carbon monoxide
(house fire, car exhaust, etc.), treat with 100% oxygen (high-flow with high-FIO2, or nonrebreather).
Ignore SpO2; ignore ABG; Ignore patient color. Even if considering further treatment (hyperbarics),
start max O2 with the highest flow available right away.

Absolute Rule #2: When treating numbers, prioritize COHb level. SaO2 will often decrease with
CO, but SpO2 and PaO2 are likely to be normal. The patient may have a metabolic acidosis, though
not always. Note that smokers may have a baseline COHb level of up to 15%. A scenario on the
ACCS would need to state that the patient has a known elevated baseline (this is a very unlikely test
question).

Absolute Rule #3: If changes in mental status, including unconsciousness, protect the airway by
intubating immediately. Always start FIO2 at 1.0. Because there is unlikely to be a typical V/Q
mismatch, using high levels of PEEP is unnecessary.

COHb Treatment
 Treat with 100% oxygen:
> - High Flow option WITH high FIO2 if available
10% - Nonrebreather at 12-15 L/min if above not available
- Note: NRB is preferred over high flow options presented only with lower FIO2.

patient may have severe metabolic acidosis + be unconscious. If unconscious, intubate

and hyperoxygenate (FIO2 1.0, PEEP doesn't benefit oxygenation)
>
25% Treat with hyperbarics, if available

2-2.5 ATA for 1-2 hours

Other Considerations:

 Avoid hyperventilation & sodium bicarb (shifts oxy-heme curve further to left)
 Consider Steroids
 Watch for latent deterioration (usually 4-9 days later), pulmonary edema, MI, CHF.

Methomoglobin

Treatment

 Methemoglobin levels should be drawn before starting any drug from list above (when
possible), then monitored for the duration of administration intermittently (typically daily)
 Indicated for > 30% (lower % in patients with anemia or cardiovascular disease)
 Administer Methylene Blue (IV) (1–2 mg/kg of a 1% solution over 5 min)- reduces
methemoglobin to hemoglobin.
 May be repeated - if no clinical response observed within 1 hr
 Note: A dose greater than 7 mg/kg of methylene blue can cause methemoglobinemia.

Drugs that cause Methemoglobinemia

Methemoglobin level:

Level Symptoms

> 15% Asymptomatic or cyanosis with a gray-brown hue - unresponsive to oxygen

> 20-
Fatigue, headache, tachycardia, dizziness, weakness develop
30%

Dyspnea, bradycardia, hypoxia, cardiac arrhythmias, metabolic acidosis, seizures,

> 45%
coma, and cardiac arrhythmias

> 70% Rapidly fatal

Drugs that induce methemoglobinemia

 Benzocaine
  Dapsone
 Lidocaine
 Nitric oxide (iNO)
 Nitroprusside
 Sodium nitrate

Treatment

 Methemoglobin levels should be drawn before starting any drug from list above (when
possible), then monitored for the duration of administration intermittently (typically daily)
 Indicated for > 30% (lower % in patients with anemia or cardiovascular disease)
 Administer Methylene Blue (IV) (1–2 mg/kg of a 1% solution over 5 min)- reduces
methemoglobin to hemoglobin.
 May be repeated - if no clinical response observed within 1 hr
 Note: A dose greater than 7 mg/kg of methylene blue can cause methemoglobinemia.

Endocrine Assessment

Oakes Academy Tip

The endocrine system isn't one of those obvious areas of the exam that you expect to see. Just reme
questions, but this page will get you up to speed on what is most likely to appear. Want a quick and

1 Cortisol increases with stress, including ICU patients. If severe septic shock, treat with low-dose
2 Treat glucose > 180 mg/dL with insulin. Treat glucose < 80 mg/dL with glucose (usually in saline)
3 Don't discontinue thyroid drugs for hypothyroidism in ICU. If hyperthyroidism (low TSH), treat ca

Cortisol

Normal: 5-24 mcg/dL (varies throughout the

day)

Stress increases levels to 40-50 mcg/dL

 Increases in critically ill patients, and particularly so with sepsis

 If NO sepsis, or less severe sepsis (hemodynamically stable with or without drugs), do not
give steroids
 If severe septic shock (not hemodynamically stable despite fluid + drugs) give low dose
steroids (decreases cortisol levels)
 ACTH stimulation (ACTH produces cortisol) is not a reliable indicator of the need for steroids

Serum Glucose

ICU Normal: 140-180 mg/dL (varies throughout the day)

 We know this isn't "normal" normal ... but it is the ICU
normal

 The most common problem in critical care is with hyperglycemia. This is so much the case
that you can use glucose as one marker of severity of illness.
 The term used in critical care is "glycemic control" as the goal is to maintain in a safe
range. There are adverse effects of both hypo- and hyperglycemia. Usually hypoglycemia
occurs when hyperglycemia is too aggressively treated with insulin.
 Note that actual normal glucose is around 80-110 mg/dL (so similar to diastolic-to-systolic
blood pressure - unrelated but easy to remember). The goals are a bit different in critical
care to avoid hypoglycemia.
 Uncontrolled hyperglycemia is associated with worse outcomes in:
o Post-surgical patients
o Trauma patients
o Traumatic brain injury
 Treating
o > 180 mg/dL hyperglycemia: Treat with insulin (yes, you may be asked to do this
on exam)
o 110-140 mg/dL mild hyperglycemia: There's probably another priority in the answer
options (so don't generally treat, may result in hypoglycemia)
o < 110 mg/dL: Consider treating with glucose, includes option for saline with
glucose.
o < 80 mg/dL: Absolutely treat with glucose

Thyroid

Normals vary by the type of test (assay) that is used. Treat this section as "high," "normal," or
"low."

Of most importance for exam is TSH, though you should have a basic understanding of T3 and T4.

Thyroid-stimulating hormone (TSH)

 Thyroid-stimulating hormone (TSH) is a lab indicator of thyroid function

 High TSH = Hypothyroidism
o Signs/Symptoms
 Weight gain
 Puffy skin
 Lethargic
o Drugs that increase TSH: Haloperidol, amiodarone
o ICU Treatment
 Synthetic thyroid hormones (Levothroid, Synthroid, etc.)
 Low TSH = Hyperthyroidism or Nonthyroid Illness (ICU)
o Signs/Symptoms
 Weight loss
 Tremors
 Tachycardia
 Hypertension
o Drugs that decrease TSH: Steroids, dopamine, amiodarone
o ICU Treatment
 Treat cardiac symptoms with beta blockers
 Anti-thyroid drugs are slow
Hypo versus Hyper - this is opposite of what you're used to with terminology!

Serum T3

 NOT a direct measure of thyroid function. Always low with hyperthyroidism, but many
causes for high/normal
 Used mostly to determine whether a low TSH is due to thyroid or non-thyroid
 Measure when low or undetectable TSH:
o Low T3 with Low TSH = Probable hyperthyroidism
o Normal/High T3 with Low TSH = Probably nonthyroid cause (hypoxia(!), ischemia)

Serum T4

 Similar to T3 as a low serum T4 is common in critically ill patients, but doesn't mean a
patient definitely has thyroid malfunction
 T4 is unreliable in ICU patients

BUN and Creatinine Labs

BUN and creatinine are indicators of kidney function. Remember that kidneys can fail acutely
(especially during shock when perfusion is inadequate) or chronically. Diuresing a patient with
furosemide aka Lasix (or other diuretics) requires adequate kidney function. If inadequate,
mechanical dialysis may be necessary. If the patient is hemodynamically stable, hemodialysis is
acceptable. If the patient is unstable, consider bedside renal replacement therapy which is more
gentle (and doesn't require fluid loss during the process).

Blood Urea Nitrogen (BUN)

The liver forms urea, which is then excreted by the kidney. Presence of high urea suggests the liver
is working but the kidneys are not.

 Normal Value: 6-20 mg/dL

 High BUN suggests impaired kidney function
 Look for causes of false highs: high-dose steroids, high-protein diet, GI bleed

Creatinine

Creatinine is produced during muscle energy metabolism. Usually, it is filtered by the kidneys
(based on GFR).

 Normal Value: around 0.6-1.3 (lower part of range for women; higher part of range for
men)
 High creatine suggests impaired kidney function/damage
 Do not interpret creatinine if a patient is on dialysis

Liver Assessment

Bilirubin

Normal Total Bilirubin: 0-

1 mg/dL
  Indicates health of the liver: bilirubin is a byproduct of hemoglobin breakdown
 Jaundice is an external sign of liver failure
 Causes of hyperbilirubinemia
o Sepsis
o Shock
o Acute and chronic pancreatitis
o Hepatitis
o Sarcoidosis
o Tuberculosis

Ammonia

 Increased ammonia
o GI bleed
o Parenteral nutrition
o Steroid administration
o Treatment
 Treat the cause
 Drugs: Sodium benzoate, sodium phenylacetate
 Decreased ammonia
o Drugs: Salicylates, valproate, etc.
o Acute + chronic liver failure
o Renal tubular acidosis
o Treatment
 Treat the cause (acetylcysteine for acetaminophen toxicity, for example)
 Liver transplantation, if indicated

AST and ALT

ALT: Alanine aminotransferase

 Female: 19-25 international unit/L

 Male: 29-33 international unit/L
 High levels indicate the potential for liver disease
 ALT is more liver-specific than the AST
 The greater the number, the greater the injury

AST: Aspartate aminotransferase

 Female: 9-32 international unit/L

 Male: 10-40 international unit/L
 High levels indicate the potential for liver disease
 The greater the number, the greater the injury

Pleural fluid analysis

Pleural effusion is the excessive accumulation of pleural fluid

Transudation: Plasma passing from vessels into pleural space due to hydraulic or osmotic
abnormalities (↓ proteins, ↓ LDH).
Causes: atelectasis, CHF, hypoproteinemia, lymphatic obstruction, liver cirrhosis, nephrotic
syndrome, pericarditis.

Exudation: Inflammatory effusion resulting from capillary damage or lymphatic blockage (↑

proteins, ↑ LDH).
Causes: acute pancreatitis, cancer, drugs, infections (TB), post-MI syndrome, pulmonary embolism,
rheumatoid arthritis, sarcoidosis, SLE

Symptoms
depend on size of effusion and symptomology:

• If small and/or minimal symptoms, may just be observed

• Oxygen Therapy, as needed

• Treat underlying cause (see causes above in Etiology)

• Thoracentesis or Thoracostomy Tube

• Pleurodesis* (malignancy)

• Shunt

Clinical manifestations
are dependent on amount of fluid: dyspnea, cough, pain, ↑RR, orthopnea, ↓ BS, egophony, ↓
fremitus, dull to percussion (on affected side), progressing to tracheal deviation and CV compromise
with massive effusion > 300 mL.

Urine Analysis

Oakes Academy Tip

Spend enough time looking through a urine analysis textbook and you'll have increased respect for
nephrologists. For exam purposes you need to be on the lookout for infection, especially if a
catheter is placed. Other scenarios throughout the exam may contain supporting information using
pH, color, etc.

Interpreting

 Color:
o Cloudy suggests a possible infection
o Blood (hematuria) suggests trauma, anticoagulant therapy, hypertension
 pH Range: 4.5 to 8.0
o 4.5-6.9 Acidotic:
 Metabolic acidosis (ketoacidosis, for example)
 Respiratory acidosis (respiratory failure)
 Urinary system disorders (UTI - E coli, uremia, chronic renal failure)
 Certain drugs (ammonium chloride)
o 7.0-7.9 Alkalotic
 Metabolic alkalosis (vomiting, gastric lavage)
 Respiratory alkalosis (hyperventilation)
 Urinary system disorders (UTI - pseudomonas)
 Certain drugs (sodium bicarb, potassium citrate, acetazolamide)
  Leukocytes present
o Possible infection in kidneys or urinary tract (bacterial or non-bacterial)
o Inflammation in kidneys or urinary tract (trauma)
 Nitrite Reaction (positive or negative)
o Presence of potential UTI
 Glucose - Presence of ketones (ketonuria):
o Diabetes
o Vomiting
o Starvation
o Alcoholism

Cerebral Spinal Fluid (CSF)

Fluid from around the spinal cord and in the cerebral space. It is usually collected through a lumbar
puncture (LP).

Normal Cerebral Spinal Fluid (CSF)

 Red Blood Cells: should not be present in normal CSF. Presence includes bleeding
 White Blood Cells: Normally < 5. Significantly increased with infection or inflammation of
the CNS
 Cytology: investigation for abnormal cells, such as tumor cells, indicative of cancer

Peritoneal Fluid

Accumulated fluid in the abdominal region (which is called ascites)

Transudative: includes liver disease/cirrhosis, CHF, nephrotic

Exudative: includes trauma, infection, pancreatitis, cancer

Treatment is based upon the underlying cause (see individual diseases/disorders for treatment
suggestions). Be aware of the impact of ascites on ventilator strategies (pressure from the abdomen
will transfer to the pleural space. Increasing PEEP may help offset this pressure).

CT Scans

A CT scan is a series of x-rays that produce cross-sectional images of the body part being scanned.

CT scan of the chest

(images may appear on the exam that require you to identify basic issues. See our Quicktorial here
for a review)

 Provides more information than a chest x-ray

 Overall excellent information for assessing pneumonia, pulmonary edema, pleural effusion
 If "with contrast" this is better for blood vessels/mediastinum
 Requires transporting patient (sometimes inappropriate option because of this - consider
thoracic ultrasound if available and indicated)

CT scan of the brain

 Often used to monitor patients with neurological deficit (head bleed, swelling/trauma,
etc.).
 Should be a priority when changes in mental status are noted
 The exam question will give a reported finding. No images will need to be assessed.
CT Scan of the abdomen

 Often used to assess abdominal distension. Be aware of the impact of distension on the
pulmonary system (it is harder to ventilate a patient, particularly if supine).
 The exam question will give a reported finding. No images will need to be assessed.

MRI Scan

Uses magnets and radio waves to create detailed images, does not use radiation. Certainly be very
wary of this option if the patient has specialized equipment that may react to the MRI (such as an ET
Tube with metal coiling used in neuro surgery).

 Indications include investigating tumors or other disorders (abscess, lesions) of the chest wall,
heart, mediastinum, and pleura
 May be useful in looking at perfusion - pulmonary or cardiac (pulmonary hypertension, for
example)
 Requires transporting a patient

Ultrasound

Uses high-frequency sound waves to create images

Thoracic Ultrasound
Excellent at detecting pleural fluid accumulation, especially if a small amount. May be able to
determine type of fluid, transudate vs. exudate. may be looking at pleural space, or vascular status
(fluid load, emboli)

 Indications:
o Suspicion of pleural fluid (when chest radiograph shows haziness)
o Suspicion of pneumothorax
o To place chest tube, or perform thoracentesis
o To assess/determine movement of the diaphragm
 Portable - can be done at bedside (good choice for suspicion of pleural effusions)

Echocardiography

 Diagnostic ultrasound specifically for the heart and valves. Indicated when heart failure,
diagnosis of heart disease

Nuclear Scans

CT Angiography, Spiral Computer Tomography

 Recommend for detecting of a pulmonary embolus

 Requires transporting patient (is usually necessary transport)

V/Q Scan

 Can be used for detecting a pulmonary embolus or quantifying a V/Q mismatch

 Requires transporting patient (so use more with PE suspicion than non-PE V/Q)
 Requires more time to perform (set-up, procedure, etc.) so perhaps consider CT first if
offered for critical care

Cerebral Blood Flow

  Nuclear scans may be used to determine "brain death." Consider utilizing this in patients
not meeting the criteria for bedside apnea testing.

Angiography

Angiography is a scan WITH CONTRAST that looks at the inside of the blood vessels/organs and
helps diagnose related diseases and blockages. Most of these involve going to the Cath Lab, which
involves transporting the patient (so be cautious in recommending in unstable patients). There are
various types you should know for the ACCS:

Pulmonary Artery Angiography

 Looks at the blood vessels around the lungs (through a catheter)

 Consider when suspicion of pulmonary embolus

Coronary Angiography

 Looks at the blood vessels in and around the heart, as well as the chambers of the heart
 Consider for stenosis, and for determining presence and amount of blockage in vessels.

Gastrointestinal Angiography

 Looks at the blood vessels in the GI region (may be upper or lower)

 Consider when signs/symptoms of active hemorrhage. Helps locate source and location of
bleed.

Bronchial artery embolization

 This is a procedure used to treat severe, ongoing, or recurrent hemoptysis (caused by

pneumonia, lung cancer, tuberculosis, bronchiectasis, etc.)
 Contrast is given, then X-rays are taken. A catheter is finally inserted and granules are
injected to clot the vessel and stop bleeding.

ACCS- Prevent Ventilator-Associated Events

Go
To Outline

Section IIF Preventing VAE

Estimated
Question
Count

Basic Recall 1

Applied
5
Knowledge

Total Questions 6
Content Review
Causes

 At highest risk are patients with decreased immune systems

 Majority of VAE is aspiration-related, meaning cuff pressures are important (and not too
much pressure)
 Breaking the closed circuit (disconnecting ventilator for many reasons) creates a portal for
VAE

Signs & Symptoms

For screening and diagnosis:

 For exam purposes, a normal sputum sample (from closed suction catheter) is often
described as unusable (not deep enough in lungs)
 Mini-BAL - A mini bronchoalveolar lavage is performed by the RT specifically to obtain a
better sample to rule out VAP
 BAL - A bronchoalveolar lavage is performed by a physician and assisted by an RT
 If given the option between the two, mini-BAL is less expensive, gains same information,
unless indication that something else needs to be investigated (presence of hemoptysis, for
example)

Signs and Symptoms to suggest the presence of infection, possibly VAP:

 Sputum production (often yellow, thick)

 ↑ WBC (> 12,000)
 Fever (> 38ºC)
 Tachypnea

Preventing ventilator-associated events

1. Daily Oral Care: use chlorhexidine or similar

Decreases bacteria common in saliva, which may end up "micro-aspirated" into lungs (leak
around ET tube cuff)
When Not to: something obvious (jaw wired shut if inaccessible)

2. Elevation of the head of the bed to between 30º and 45º

Decreases risk of aspiration, reflux
When Not to: significant unstable hypotension, procedures

3. Minimize intubation time

o Aggressively wean patient using daily "sedation vacation" (SAT - spontaneous
awakening trial) and daily assessment of readiness to extubate (SBT -
spontaneous breathing trial)
When not to: Patient is significantly unstable hemodynamically or is worsening
overall (for example, P/F ratio is worsening)
o Consider use of NPPV: consider use as an adjunct in patients who are stable but the
reason for intubating still hasn't fully reversed (they present as "on the mend")
When not to: Intubated for airway patency, failed wean completely. If borderline,
consider extubating to NPPV

4. Ventilator circuit care

Minimize any disconnections from circuit - any option in a question that encourages
disconnecting circuit is unlikely to be the correct response. Always drain
 condensation/secretions away from the patient. Do not routinely change or rinse patient
circuit on a ventilator - change only when visibly soiled or non-functioning.

5. Use Specialty Airways that discourage microbial growth on the ET tube itself, such as
silver-coated ET tubes (Removed in the 2018 update). Preventing "micro-aspiration" (as
secretions leak down around the cuff) is also important, such as with the use of
polyurethane cuffs and subglottic suctioning. This includes the use of the subglottic tube
which allows for removal of secretions on top of the ET tube cuff.

6. Assessment of cuff integrity and pressure. Maintain cuff pressure of at least 20 cm

H2O. Under this increases the risk of VAP (via microaspiration). Note that cuff pressures
should not be too high due to the risk of tissue necrosis. Cuff pressures should be checked
regularly and documented.

7. Peptic ulcer disease (PUD) prophylaxis. Patients should receive a proton pump
inhibitor (look for drugs that end in azole like pantoprazole or omeprazole, or drugs that
end in tidine, including famotidine and ranitidine). These drugs help prevent reflux, one of
the known causes of VAP.

8. Deep venous thrombosis (DVT) prophylaxis. There are various methods for doing
this:
o Ambulation: if a patient is stable enough, assisting them to walk is great. Yes, this
may be presented on the exam!
o Compression/Sequentials: placed on lower legs, mechanically squeeze which mimics
the effect of walking to a degree. DO NOT USE if trauma to the legs, burns, etc.
o IVC Filter (e.g. Greenfield filter): placed in inferior vena cava, this filter is meant to
prevent any clots from traveling to vital organs. This is invasive, but if the first two
options aren't provided or are contraindicated, this is an acceptable response.
o Heparin or another anticoagulant: often used prophylactically in higher-risk patients

9. Do NOT administer antibiotics prophylactically to prevent VAE: This may build

resistance in the patient. Only administer antibiotics for signs/symptoms of
pneumonia/infection.

Infection Prevention Measures

Preventing infections (including sepsis) is a critical aspect of the care we provide. You may have
heard the old cliche, "the best intervention is prevention." For exam purposes, you should know that
while not every situation can be controlled (things happen in emergencies), we should take
reasonable steps to prevent the introduction of an infection.

Examples of how you might see this on the exam

Understanding the importance of standard precautions

 hand-washing or using an approved gel/foam for hand hygiene

 use of personal protective equipment, such as a mask, gown, goggles, gloves whenever the
risk of exposure is present

Understanding the importance of transmission-based precautions (or "isolation")

 This is a fancy term for contact, droplet, airborne, etc

 You may be asked about placing patients together (cohabiting) in disaster-type scenarios.
The goal should be to cohabit like-infections. For example, patients with Cdiff should be
cohabited with other patients with Cdiff. It's not always possible, but it is the priority.
Closely monitoring skin integrity

 Skin integrity related to an endotracheal tube or tracheostomy tube is most common, but
other skin integrity issues may be mentioned
 Skin should not be in contact with anything for more than a few hours without being
repositioned
 Rotate endotracheal tube and monitor skin integrity every shift (the exam doesn't focus on
an exact amount of time, but refers to things that must be done "each shift")
 Remember the "Key 3 of Integrity" =
o Red: skin is likely to be red and inflamed looking, possibly with pus (yellow),
ecchymosis
o Hot: the site itself will be warm or hot to the touch. This may or may not be
presented in a scenario
o Swelling: this can be described as swollen, edematous (or just edema), or puffy

Catheter/Tube Care

 The area around insertion must be kept sterile if possible

 Remove catheters at first sign of infection
 Avoid catheters if other options are available
o Foley should be removed as soon as clinically possible
o Be careful about recommending pulmonary artery catheters (and central, a-lines to a
lesser degree)
o Get ET tube out as soon as clinically possible (so daily SBT!)
o Remove NG/OG as soon as clinically possible (and don't jump to things like PEG
tubes too quickly)

The Big No-No (take this one to the bank)

Do NOT give antibiotics to prevent infection. Antibiotics are only given with some indication that
there's an infection (usually fever, WBC, and the Key-3-of-Integrity)

End of Life Care

Introduction
End of life is defined as a phase of life when a person is living with an illness that will worsen and
eventually cause death. It is not limited to the short period of time when the person is moribund.

Palliative Care
 Palliative care at the end of life involves meeting the physical, psychological, social, and
practical needs of patients and caregivers.
 It combines active and compassionate therapies to comfort and support individuals and
families nearing the end of life.
 Palliative care is both a philosophy of care and an organized, highly structured system
for delivering care.

Goal of palliative care

 Prevent and relieve suffering

 Support the best possible quality of life for patients and their families, regardless of the
stage of the disease or the need for other therapies.
Hospice
 Hospice care is end-of-life care provided by health professionals and volunteers giving
medical, psychological and spiritual support to both the patient and their family.
 Usually, a hospice patient is expected to live 6 months or less due to a life-limiting illness
that no longer responds to cure-oriented treatments.
 It neither prolongs or hastens death.

Goal of Hospice Care

 Help those who are dying have peace, comfort and dignity.
 Control pain and other symptoms, so a person can remain as alert and comfortable as
possible.
 Provide services to support a patient's family.

Withdrawal of Life Support

Symptom Management

Problem Symptom Therapy

Dyspnea, stridor, Steroids

Airway edema
increased WOB (methylprednisolone)

Diruetics (furosemide)
Dyspnea, stridor,
Excessive secretions Anticholinergics
increased WOB
(glycopyrrolate,
scopolamine)

Propofol
Inadequate sedation Anxiety
Benzodiazapines
(midazolam, lorazepam)

Opiates (morphine,
Inadequate analgesia Pain fentanyl,
hydromorphone)

Care of Organ Donors

Oxygenation and ventilation
  Optimize gas exchange (SpO2 > 95%; SvO2 > 70%) and acid-base balance.
 Proper ventilatory strategy to maintain lung integrity and meet the gas-exchange criteria
has not been determined.
 Low VT appears to be beneficial in ALI and ARDS
 Check ABGs regularly
 Use low levels of PEEP as needed
 Recruitment strategies to improve gas exchange and to prevent atelectasis have
increased the number of lungs judged suitable for transplant.
 The maximal safe interval for the lung to remain ischemic, even when cooled, has not been
defined - 6 hours is the selected limit.

Major Indications for Lung Transplantation by Procedure

Single-Lung Transplantation

 Chronic obstructive lung disease

 Pulmonary fibrosis
 Alpha-1 antitrypsin deficiency
 Sarcoidosis

Bilateral Lung Transplantation

 Cystic fibrosis
 Chronic obstructive lung disease
 Pulmonary fibrosis
 Pulmonary hypertension
 Bronchiectasis

Brain Death

Uniform Determination of Death Act (UDDA):

An individual who has sustained either:

1. Irreversible cessation of circulatory and respiratory functions, or irreversible cessation of all

functions of the entire brain, including the brain stem, is dead.
2. A determination of death must be made in accordance with accepted medical standards.

The AAN identifies four prerequisites that should be met to establish a brain death
diagnosis.

1. Coma of known cause as established by history, clinical exam, lab testing, and
neuroimaging.
o The standard of care is a computed tomography scan or magnetic resonance imaging
(MRI), the two most commonly used neuroimaging tests.
o Complicating conditions, including hypotension, hypothermia, and hypoxemia, must
be ruled out or reversed before the brain death exam begins
2. Normal or near-normal core body temperature (higher than 36° C)
3. Normal systolic BP (higher than or equal to 100 mm Hg)
4. At least one neurologic exam (some states and hospital protocols require two)
Apnea test, plus one confirmatory test:
o Cerebral angiography
o EEG
o Transcranial Doppler ultrasonography (TCD)
 o Cerebral computed tomographic angiography (CTA)

Other
Absence of reflexes

 Brainstem
o No pupillary response
o Negative doll's eye test and caloric test (ice water in ear)
 Corneal - cotton swab test on eyeball
 Cough and gag
 Chloric reflex test (cold water in ear)

Apnea Test
Purpose

To confirm the loss of spontaneous respirations

 Absence of a breathing drive. Tested with a CO2 challenge. (PaCO2 > baseline)

Prerequisites
Note that pre-requisite can include interventions (vasopressors, mechanical ventilation, etc.)

 Eucapnia (PaCO2 35–45 mm Hg). No prior evidence of CO2 retention (i.e., COPD, severe
obesity)
 Absence of hypoxia
 Euvolemia
 Normotension
 Normothermia
 Clinical absence of neurological function and deep coma
 Allow for adequate clearance of drugs in case of a drug overdose or a patient who has been
sedated (especially if obese or has renal or hepatic impairment). This usually takes several
days.

Procedure

 Ensure systolic blood pressure >100 mm Hg.

 Determine patient's baseline PaCO2 level with ABG. If it's not within the normal range (35 -
45 mm Hg), adjust MV until eucapnia is achieved.
 Preoxygenate 10 minutes with 100% oxygen to a PaO2 >200 mm Hg.
 Disconnect patient from the ventilator.
 Maintain oxygenation (insert catheter down ET tube, close to the level of the carina and
deliver 100% O2 at 6 L/min).
o An alternative to delivering O2 at 6 liters at the distal tip of the endotracheal tube is
to use CPAP at 10 cm H2O and 100% O2 at 12 L/M.
 Observe chest and abdomen for movement for 8-10 minutes.
 If no movement seen during this period, obtain another ABG.
 Place patient back on the ventilator.

A positive test and support of the clinical diagnosis of brain death

 A rise in PaCO2 by 20 mm Hg over baseline or a PaCO2 of 60 mm Hg or more.

 Absent respiratory movements for the entire period of the test.
  Abort if systolic BP decreases to 90 mm Hg
 Abort if O2 Sat <85% for >30 seconds.
 If test is inconclusive, but the patient is hemodynamically stable during the procedure, it
may be repeated for a longer period of time (10–15 minutes) after the patient is again
adequately pre-oxygenated.
 If the target increase in PaCO2 isn't obtained, a confirmatory test and written
documentation of why the apnea test was inconclusive is required.

Note

A major goal of the test is to try to maintain near normal body temp and BP, to ensure adequate
perfusion to all organs potentially destined for donation.

Moving Patients

Introduction
This section of the exam is likely to be general in nature. Some general thoughts to consider:

Unknown Biological Disaster

 When possible, keep disaster victims separate from current hospital patients. It
may be necessary to cohort current patients (put patients with similar conditions, like
MRSA, together).
 Consider putting masks on patients to decrease chances of exposure.
 Have a designated decontamination area.
 When possible, designate hospital staff to work with disaster victims, with separate staff to
work with current hospital patients.

Other considerations
 Be prepared to move patients on ventilators
 Outside staging areas may be necessary with larger disasters
 Facilities should have disaster policies and routine disaster drills to be as best prepared as
possible

Disaster Management

Disasters causing Mass Casualty Respiratory Failure

(MCRF)
 Biological (bacteria, toxins, viruses)
 Chemical (lung-damaging, nerve, blood, and blister agents, chemical spills)
 Epidemics and febrile illness (natural-SARS, pandemic flu; man-made- anthrax, botulism)
 Trauma (natural disaster, accidents, fire, explosion, terror attack, war)
 Weapons of Mass Destruction (chemical, biological, radiological, nuclear, explosives -
CBRNE)

Triage
 A system should be used to briefly assess each disaster victim, and mark them for easy
identification of triage level. Respiratory rate over 30/min usually requires
 immediate care, as do positional airways (patient is breathing but has periods of
apnea, often dependent on airway position).
 Triage levels vary:
o Deceased (beyond help)
o Injured who can be helped by immediate transportation
o Injured with less severe injuries whose transport can be delayed
o Minor injuries not requiring urgent care
 Resources are then provided based upon the triage designations - resources include use of
space and equipment, as well as staff attention

Note: Most mass casualty injuries result in ARDS

Goals
 Provide support
 Relieve suffering
 Mitigate further harm
 Maximize survival
 Save lives

Equipment and Supply Management

For equipment, you will be asked to prioritize care based on disaster scenarios. This will involve
making decisions about which equipment to stockpile, what features are ideal, and how then to
decide who should get the equipment

The Disaster Ventilator

Use the common sense rule. What makes sense if you were overwhelmed with critical care
patients? You're not going to spend lots of time analyzing graphics, and you're not going to have
time to manage advanced modes or equipment (like oscillators).

 Important Elements
o Basic modes are essential (or a basic mode)
o Battery-operated/back-up - battery life is a priority
o Air compressor (so no air hose needed) - anything to minimize use of valuable
hospital resources which may not work
o Basic alarms and monitoring
o Training on how to use the equipment available - the goal is to use the basic
equipment to manage patients as well as possible, so perhaps things like recruitment
maneuvers, PEEP titration, etc.
 Elements that are NOT important
o Variability of modes/advanced modes
o Display of waveform graphics
o Ultimately avoid recommending any advanced equipment! (NO ECMO, NO oscillators,
etc.)

Equipment Modifications

Oxygen: if malfunctioning, fire etc. and central supply becomes unavailable:

 Always ensure zone valve disconnects unit from the main supply (esp with fire)
 Remember, the 50 PSI outlets are all connected and run through the zone valve
  Consider "back feeding" the unit with H cylinders if given option (so 1 H cylinder supplies
whole unit)

A-Line Insertion

Introduction
Arterial lines are used in the monitoring of hemodynamic parameters via an intra-arterial catheter

Indications
 Conditions of instability where careful monitoring is needed
 Assessment of therapeutic interventions

Insertion
Two methods: Percutaneous (most common), Surgical cutdown
Radial artery is most common

Notes
 Ensure aseptic technique
 Ensure collateral circulation (just like with an ABG, using modified Allen's test)
 Insert needle and catheter into artery (this is called cannulizing the artery)
 Verify position using waveform, pressure
 Attach heparinized flush line, gently flush

Calibrating
 Patient should be supine or as close as possible to supine.
 First, place transducer at appropriate level in relation to patient
 Place at level of catheter tip in the cannulated artery. (To get an accurate reading of aortic
root pressure and CPP, place both the transducer and catheter tip [i.e., extremity] at level
of right atrium, phlebostatic axis)

Zeroing is the process of balancing the transducer to atmospheric pressure (important in verifying
accurate information)

 Complete each shift

 Ensure no air bubbles
 Turn stopcock on transducer off to patient and open to air
 Adjust zero to read zero on display
 Adjust cal to appropriate readout
 Check for return to zero
 Close stopcock to air, open to patient

It used to be standard practice to calibrate against a known pressure using a mercury manometer.
This is no longer recommended (due to risk of an embolism)
-Line Interpretation (Pressures)

Arterial Pressures
Parameter Normal (Range) Reflective of:
BP systolic 120 mm Hg (100-140 mm Hg) LV systolic pressure
BP diastolic 80 mm Hg (60-80 mm Hg) Runoff and aortic elasticity
BP (MAP) 93 mm Hg (70-95 mm Hg) CO x SVR
Pulse Pressure 40 mm Hg (20-80 mm Hg) SV and arterial compliance

Increased Arterial Pressures

 Aortic insufficiency
 Systemic hypertension
 Inotropes or Vasopressors

Decreased Arterial Pressures

 Arrythmias (a-fib, PVC)
 Stroke volume decreased (left ventricular failure, shock, cardiac tamponade)
 Vasodilators

***Always ensure proper transducer level and proper zeroing***

A-Line Management/Troubleshooting

Artifact, Noise
 Catheter whip (avoid excessive length, change tip position)
 Patient movement

Dampened Waveform
 Air in system or catheter (aspirate catheter, flush system)
 Clot in system or catheter (aspirate clot with syringe)
 Catheter tip against vessel wall (check for free backflow of blood, reposition tip)
 Improper zero (re-zero)
 Incorrect stopcock position (fix)
 Loose connection (fix)
 Tubing kink (fix)
 Falsely low reading (suspected)
 Incorrect zero (re-zero)
 Loose connection (fix)
 Transducer level too high (LOWER transducer level)
 Altered tip location (fix)

Falsely high reading

  Incorrect zero (re-zero)
 Transducer level too low (INCREASE transducer level)
 Altered tip location (fix)

No waveform showing
 Occlusion of catheter (attempt to aspirate clot, if unable - remove catheter)
 Incorrect zero (re-zero)
 Incorrect monitor or pressure range settings (check monitor)
 Kink in catheter (reposition)
 Loose connection (fix)
 Stopcock off to patient (adjust)

Unable to flush
 Blood clot at tip (aspirate clot, if unable - remove catheter)
 Kink in tubing (fix)
 Pressure bag improperly inflated (ensure proper pressure to drive flush)
 Catheter tip against vessel wall (reposition wrist/catheter)
 Stopcock not open (fix)

Mini-BAL

Introduction
Blind sampling of the smaller airways using a protected double catheter that
enables a bronchoalveolar lavage and collection of fluid specimen. This procedure is often
performed directly by the Respiratory Therapist (versus assisting, as occurs with a BAL).

Indication
 Need for a sputum sample to test for presence of infection (pneumonia). Can be
particularly helpful for thick secretion as the lavage will loosen the secretions. Also helpful
when unable to get a "clean" sample through sputum production.
 A bronchoscopy will obtain the same results, but a mini-BAL tends to be less time-
consuming and expensive.

Complications
 Bronchial irritation and/or hemorrhage
 Pneumothorax
 Vagal reflex (bradycardia, hypotension)

Esophageal Probes

There are two types of esophageal probes likely to be covered on the ACCS exam:

 Transpulmonary Pressure Monitor: Placement of an esophageal balloon catheter that

allows for direct measurement of esophageal pressure. Esophageal pressure is a rough
estimate of pleural pressure, which can then be used to calculate transpulmonary pressure.
 Transpulmonary Pressure = Peak Inspiratory Pressure - Pleural (aka esophageal)
Pressure

How is this used?

o Transpulmonary pressure can be used to set PEEP levels.
o Transpulmonary pressure is thought to be a more accurate reflection of actual harmful
pressures in the lungs (as compared to peak inspiratory pressure).
o There are times when PIP may not reflect just distending pressures (those harmful
ones), but other pressures falsely register into the PIP. These false readings include
obesity, chest wall deformities, pleural effusions (especially large ones), distended

Set PEEP to transpulmonary pressure of:

end - EXpiratory 0-10 cm H2O

end
≤ 25 cm H2O
- INspiratory

 Neurally Adjusted Ventilatory Assist (NAVA) probe: For exam purposes, NAVA (a mode
of ventilation) is used primarily to improve synchrony between the ventilator and the patient.
A NAVA esophageal probe is required to work with NAVA. The probe is a specialized gastric
(usually nasogastric but may be orogastric) tube with an array of electrodes (called the Edi
catheter) which is positioned in the esophagus to optimally detect the electrical activity of the
diaphragm.

Insertion:
o A measurement is taken - from bridge of nose to the earlobe to the xiphoid process.
This is called the "NEX" measurement
o The insertion distance (cm) is then calculated using a formula
o The Edi should be dipped in water - NOT LUBRICANT - and then inserted to the distance
calculated
o Positioning needs to be verified:
On EKG: P, QRS should be present in top leads
P waves will decrease and disappear; QRS will decrease - this signifies
catheter is likely in place

Oakes Academy Tip

Questions in this content area are likely to be more general than specific. As you know, an RT is
expected to not just do what a physician says, but to think critically about orders and care plans,
making appropriate recommendations. If you offered an option to just agree with a physician, think
carefully before selecting it.

Repeat after us: "I should not simply agree with the physician or other health team member. I
should perform my own assessment and suggest modifications when appropriate."

Common sense, right?

Keep this "common sense" in mind as you read through questions. This is particularly difficult if you
work or have worked in an environment where what the physician says goes. Look for answers that
respectfully redirect what a team member has originally suggested. How might you see this?

A physician orders 500-mcg/kg/min continuous propofol. The patient becomes hypotensive. You
are asked what you want to recommend, ranging from discontinuing propofol to changing drugs to
simply continuing the current course. You are being asked to analyze the physician's decision in the
context of a changing patient status.

Troubleshoot Systems: Chest Tube Drainage

Note that chest tubes may be referred to as thoracostomy tubes. A thoracostomy is a

procedure in which a chest tube is placed.

What This Section Might Cover:

 While chest tube drainage is not a major concept on the exam, it may cover some of the
basics of troubleshooting
 You will likely be given a scenario with a chest tube that is not working properly and have
to choose between a few options on how to resolve the problem.

Equipment/Procedures You Should Recognize:

 Bubbling in Water Seal Chamber

o Causes: Pneumothorax (reduce PEEP), Disconnection (tighten connection, replace
drainage system if needed)
 Absence of Bubbling or Drainage
o Causes: Tube kinked or occluded (gently milk tube to clear occlusion, fix kink),
Malposition of tube (reposition via CXR)

Choosing the BEST Option:

 Remember, that increased PEEP can cause an increased air leak, so consider decreasing
PEEP if given the option
 Always make sure that all connections are secure before making any decisions to adjust
any other parameters.

How The Exam Will Attempt to Deceive You:

 You most likely be given a choice to clamp a chest tube at some point on the exam. DO
NOT clamp a chest tube unless you are sure that the pneumothorax has resolved!

Troubleshoot Systems: Bronchoscopy

What This Section Might Cover:

 You are most likely to see a scenario in which a bronchoscope is being used during a
procedure such as a therapeutic bronchoscopy and a situation will arise asking you to
identify and/or troubleshoot the problem.

Equipment/Procedures You Should Recognize:

 There are a few different types of bronchoscopes, though the test will not focus on this
much:
 o Flexible bronchoscopy: used for most diagnostic and therapeutic bronchoscopies
o Rigid bronchoscopy: primarily used to retrieve foreign bodies
 The bronchoscopy procedure is used to perform airway clearance (washout, this is also
called bronchial alveolar lavage), or to view/assist in exploring (exploratory bronchoscopy,
goal is to visualize the airways) and/or to perform lung biopsies (requires the use of
needles/clips/clamps, and are more likely to result in bleeding, a common presentation on
the exam).
 Mini-BAL is a slightly different procedure, performed directly by the RT, and is used to get a
sample of sputum from the lungs to rule out/diagnose VAP. It can be often used to
differentiate from other sources of pneumonia (such as community-acquired).

Choosing the BEST Option:

 Biopsy
o Air leak/pneumothorax
 Stop procedure, recommend chest tube placement if moderate-to-severe
o Moderate-or-severe bleeding
 Administer cold saline, epinephrine, or lidocaine. Stop procedure only if
massive bleeding/accompanying hypotension.
 A double lumen tube for single lung ventilation may be necessary, but this is a
less common option.
 Drug complications
o If a patient is not intubated but being given opioid, be ready to recommend reversal.
If intubated, ensure adequate vent support
 Hypoxemia
o Pre-oxygenate, give additional oxygen during procedure if needed, stop procedure if
severe
 Laryngospasm/Bronchospasm
o Pre-treat at-risk patients, stop procedure if severe
 Scratch or tear to the airways resulting in bleeding
o See above for bleeding
 Swelling of the mucous membranes of the airways
o Racemic epinephrine particularly if patient becomes stridorous

Hemodynamic Troubleshooting

Artifact, Noise
 Catheter whip (avoid excessive length, change tip position)
 Patient movement

Dampened Waveform
 Air in system or catheter (aspirate catheter, flush system)
 Clot in system or catheter (aspirate clot with syryinge)
 Catheter tip against vessel wall (check for free backflow of blood, reposition tip)
 Improper zero (re-zero)
 Incorrect stopcock position (fix)
 Loose connection (fix)
 Tubing kink (fix)
 Falsely low reading (suspected)
 Incorrect zero (re-zero)
 Loose connection (fix)
 Transducer level too high (fix - should be at level of the heart)
  Altered tip location (fix)

Falsely high reading

 Incorrect zero (re-zero)
 Transducer level too low (fix - should be at level of the heart)
 Altered tip location (fix)

No waveform showing
 Occlusion of catheter (attempt to aspirate clot, if unable - remove catheter)
 Incorrect zero (re-zero)
 Incorrect monitor or pressure range settings (check monitor)
 Kink in catheter (reposition)
 Loose connection (fix)
 Stopcock off to patient (adjust)

Unable to flush
 Blood clot at tip (aspirate clot, if unable - remove catheter)
 Kink in tubing (fix)
 Pressure bag improperly inflated (ensure proper pressure to drive flush)
 Catheter tip against vessel wall (reposition wrist/catheter)
 Stopcock not open (fix)

Pulmonary Artery Catheters

Other Names Used

 PA line
 PA catheter
 Swan Ganz catheter
 flow-directed, balloon-tipped pulmonary arterial catheter

Placement

We recommend knowing the values in GREEN below, or if you want to be more prepared learn the
values in Yellow, then remember to ADD 10 to RV, 10 to PA, 10 to wedge

Total
Distance from Total
to RA to RV to PA Distanc + wedge
(all veins) in WEDGE
e

subclavian 10-15 cm 30-35 cm 40-45 cm

jugular 15-20 cm + 10 cm + 10 cm 35-40 cm + 10 cm 45-50 cm

femoral 30-40 cm 50-60 cm 60-70 cm

RA = Right Atrium, RV = Right Ventricle, PA = Pulmonary Artery

Higher end of ranges = taller heights; lower end of ranges = shorter heights
The ACCS exam may present a scenario where a patient has a pulmonary artery line and you are
asked what to do. You may be given a catheter tip location, a distal port, a proximal port, or the
total distance. Here are some things to remember:

 Key: Even though it is an ARTERIAL catheter, it is placed via the VEIN (remember, the
pulmonary artery is on the deoxygenated side of circulation!)
 Key: We use waveforms to determine placement, as well as distance and chest
radiograph:
o RA waveform = the PA catheter tip is in the right atrium. Fix: fill balloon with 1.5
mL saline, reposition pt left-side down
o RV waveform = the PA catheter tip is probably coiled in the right ventricle. Fix:
withdraw slightly, then advance with balloon inflated again
o PA waveform = the PA catheter tip is correctly positioned in the right or left
pulmonary artery
o Wedge waveform = either in wedge purposely, OR the PA catheter tip is in a distal
pulmonary artery (too far). Fix: withdraw a few centimeters
Note that wedging with balloon should show wedge waveform. If not, placement
should be questioned.
 Key: To withdraw the catheter, always use a deflated balloon (you are coming back
against flow)
 Key: To advance the catheter, inflate the balloon, then allow it to float the proper cm
distance (see chart above)
 Key: The distal port is the normal port used for determining the correct distance
 Chest radiograph: the tip should curve but should not have any loops, coils, or knots. It
should be below the level of the left atrium on radiograph.

If the distance is listed as beyond the chart above, you need to deflate the balloon and
withdraw. The distal port often ends up in the right ventricle, coiled.
Ex: A patient has a pulmonary artery catheter being placed via the jugular vein. The distal port is
noted to be in the right ventricle. The introducer is noted to be at 50 cm. What should the specialist
do? Answer: deflate and withdraw.

If the distance is below the range in the chart above, or if the distal port is noted to be in
the right atrium, or ascending/descending vena cava (ascending if subclavian, jugular or
descending if femoral), the correct answer is to inflate the balloon with 1.5 mL of air OR
LESS
Ex: A patient has a pulmonary artery catheter being placed by femoral vein. The introducer is noted
to be at 20 cm with a right atrial pressure waveform. What should the specialist do? Answer: inflate
with 1.5 mL of air and allow it to float 10 cm more.

Measurements

 Measurements should be taken at end-expiration to minimize effects of pleural

pressures on intracardiac pressures

 The transducer must be positioned level with the left atrium (at the
phlebostatic axis which is a fancy way of saying 4th intercostal space, mid-
axillary)
o If the transducer is above the left atrium it will underestimate the actual pressure
(by 0.7 per 1 cm above)
o If the transducer is below the left atrium it will overestimate the actual pressure (by
0.7 per 1 cm below)

 The system should be zeroed every shift or when inaccurate results are
suspected. Zeroing eliminated the interference of external factors.
 o Stopcock closest to the transducer is turned off (closed to patient)
o Remove the cap (open to air)
o "zero" the line on the monitor - this calibrates known zero with measured zero
o Replace cap (closed to air)
o Open stopcock closest to the transducer (open to patient)

 Getting a wedge pressure is controversial (it can cause a pulmonary infarction)

o Also called: pulmonary artery occlusion pressure (PAOP), pulmonary artery wedge
pressure (PAWP), pulmonary capillary wedge pressure (PCWP)
o This estimates left ventricular pressure (LVEDP to be exact)
o To place the catheter into "wedge position" the ballon is inflated (about 1.5 mL of air
or less). A wedge waveform should be visible. Once pressure is measured, the
balloon should immediately be deflated and confirmation of PA pressure waveform
noted.
Leaving the catheter in WEDGE position is dangers = pulmonary infarction

ACCS Drug Review

Important Notes as you study:

This presentation is copyrighted. Please help us by not copying or sharing this page.

This is meant to be a quick reference. Some drugs contain additional information (click on
them to go that info)

Generic drug names are always presented on the exam. We have included brand names only
when we think they might help clarify what you already know (for example most of us call
naloxone "Narcan." Narcan is the brand name, but is also the common name, so we
included it!

For best viewing on a mobile device, turn the device to landscape.

New! Pharmacology Digital Flashcards

you'll go to Quizlet where you'll need our password: alveoli1

Yes, there's an app (search for Quizlet on your app store)

Key:
drugs that have a common nebulized form (sometimes this is not the most common form, like
with morphine)
drugs that can be instilled by endotracheal (or tracheostomy) tube
drugs that should be avoided with kidney (renal) failure - or a major consideration
drugs that should be avoided with liver (hepatic) failure - or a major consideration

generic name
Category Things to Know
(Brand*)

Pain Management (Analgesia). Treat for indications of pain. Note that opioids may cause
respiratory depression - look for this! How pain is measured varies:
 Awake and alert: pain scale

Sedated: asynchrony on ventilator, ↑ HR, ↑ BP, ↑ RR, restlessness/combativeness

Paralyzed: ↑ HR, ↑ BP

Use: any indication of pain (vitals, pain

scale)

fentanyl citrate Adverse: respiratory depression

(Sublimaze) Pain
(opioid) Reverse: naloxone (Narcan)
(Duragesic) = patch
Notes: You may also come across sufentanil
and remifentanil (both opioid-based as
well)

Use: any indication of pain (vitals, pain

scale)

Adverse: respiratory depression, cardiac

morphine Reverse: naloxone (Narcan)

Pain
(opioid)
Notes: nebulize for SOB (related to cancer
that causes dyspnea)
May be instilled via ET tube
large doses would be required for
continuous sedation, so not an optimal
choice for that

Use: any indication of pain (vitals, pain

scale)
hydromorphone
(Dilaudid) Pain
Adverse: respiratory depression, cardiac,
(opioid)
reduce dosage for renal failure

Reverse: naloxone (Narcan)

Use: for management of moderately severe

pain
ketorolac
Adverse: Do not use if renal failure +
(Toradol) Pain
hypotensive due to volume
(NSAID)
Notes: often used in combination with an
opioid as it decreases the required opioid
dose to adequately manage pain

Ibuprofen Use: for mangement of pain

Pain
(NSAID) Notes: like, ketorolac, ibuprofen is often
 used in combination with an opioid

Reverses: Opioids (fentanyl, morphine,

hydromorphone)
naloxone
Opioids may cause respiratory depression or
(Narcan)
(opioid reversal) cardiac effects. If it is clinically
significant, reverse.

Quick duration, may require several doses

(adverse effect will reappear)

Anxiety (Benzodiazepines): Often used more for sedation than anxiety. Note that
benzodiazepines have a tendency to accumulate in the system, resulting in excessive sedation.
Metabolism occurs in the liver, so be very cautious about use in patients with any indication of
hepatic impairment. Benzodiazepines play a role in the development (NOT TREATMENT) of ICU
delirium.

Use: anxiety (weaning, NPPV), drug/alcohol

withdrawal
lorazepam
(Ativan) Anti-anxiety
Adverse: may interact with narcotics and
(benzodiazepines)
suppress respiratory drive

Reverse: flumazenil

Use: procedural sedation, anxiety (weaning,

NPPV), drug/alcohol withdrawal

Adverse: may interact with narcotics and

midazolam
suppress respiratory drive
(Versed) Anti-anxiety
(benzodiazepines)
Reverse: flumazenil

Note: Use in either kidney or liver failure

will prolong the effect of the drug (it
takes longer to leave the system)

Use: anxiety (weaning, NPPV), drug/alcohol

withdrawal, seizures

diazepam Adverse: may interact with narcotics and

(Valium) Anti-anxiety suppress respiratory drive
(benzodiazepines)
Reverse: flumazenil

Note: Not often used in critical care due to

"drug accumulation" issues

flumazenil Reverses: Benzodiazepines (lorazepam,

(reversal agent for
 midazolam, diazepam, etc.)

Administer when excessively drowsy while

(Romazicon) benzodiazepines)
on benzodiazepines

Look for drugs that end in PAM or LAM

Continuous Sedation (common). Consider propofol as a stronger choice over dexmedetomidine

as it is less expensive, readily available. If patient is struggling with "wake up" for wean, or if
refractory hemo instability related to propofol, then consider dexmedetomidine. Note that these
drugs are preferred over bezodiazepines as they are less likely to cause delirium.

Use: pain, sedation (procedural, ventilator)

Intermittent: a bolus of propofol given for a

procedure (such as for combative
patients, or a very short procedure).
Note that propofol has such as quick
half-life that intermittent use is difficult.

Continuous: an IV infusion that is

maintained at the lowest rate to achieve
adequate sedation (usually based on
RASS score)

propofol Adverse: respiratory depression, hypotension

Sedation
(Diprivan)
Reverse: wears off quickly, no need to reverse
(just stop)

Notes: stop before weaning/extubating.

Propofol can store in fat tissue and thus may
take longer than expected to "clear" in obese
patients.

Propofol Infusion Syndrome: with high,

extended doses, abrupt onset of bradycardia,
rhabdomyolysis, renal failure, and overall lactic
acidosis. Keeping doses as low as possible is
recommended.

dexmedetomidine Sedation Respiratory drive doesn't diminish regardless of

(Precedex) dose/level of sedation

Use: ICU sedation, procedural sedation, has

some analgesia

Adverse: decreases in HR, BP. Life-

threatening bradycardia (on higher
 doses)

Reverse: atipamezole (very rarely needed)

Notes: Consider for patients who are having

trouble weaning (doesn't affect
respiratory drive - patient can remain
sedated for wean)

Sedation (Barbiturates) - these are relatively uncommon for sedation, but may appear on
exam. There will be a specific reason (like refractory intracranial hypertension)

Use: ICU sedation, seizures, and as a rescue

therapy for very high ICP that is
unresponsive to other drugs (as it has
adverse effects) = refractory intracranial
pentobarbital
hypertension
(Nembutal) Sedation
(barbiturate)
Adverse: may decrease HR, RR, BP, Reduce
dose for kidney/liver failure (risk of
propylene glycol toxicity exists)

Reverse: physostigmine

Use: ICU sedation, seizures, alcohol

withdrawal, sedative withdrawal
(difficulty weaning drugs/sedation), and
as a rescue therapy for very high ICP
that is unresponsive to other drugs (as it
phenobarbital
Sedation has adverse effects) = refractory
(barbiturate) intracranial hypertension

Adverse: may decrease HR, RR, BP, Reduce

dose for dialysis (but not CRRT)

Reverse: physostigmine

Doesn't technically reverse, but is an

arousal agent
physostigmine
(Arousal Agent)
(Antilirium)
If clinically significant decrease in RR, HR, or
BP, administer

Sedation (Induction for RSI)

etomidate Onset: 15-45 seconds, Duration: 3-12

(Amidate) Sedation minutes

Use: Very common induction agent for RSI;

 useful for hemodynamically unstable
patients

Adverse: may cause seizure activity, may

increase ICP

Exam Notes: do not use if a better option

with seizures OR with traumatic brain
injury (high ICP)

Onset: 45-60 seconds, Duration: 10-20

minutes

Use: Common induction agent for RSI -

causes analgesic and amnesiac qualities
as well

Adverse: May cause hypertension, may

increase ICP
ketamine
Sedation Exam Notes:
(Ketalar)
good option for awake intubation
(preserves respiratory drive)

may be a preferred option for

intubating a patient with severe
asthma

do NOT use in patients who are

hypertensive

Anti-Delirium in ICU - Delirium is known to complicate weaning from the ventilator, as well as
cause patients to be more asynchronous with the ventilator. The goal is to PREVENT delirium
when possible, including avoiding the use of benzodiazepines whenever possible.

Use: gold standard for ICU delirium - does

have a sedative effect and suppress
respiratory drive

haloperidol Adverse: bronchospasm/laryngospasm

Anti-delirium
(Haldol) (rare, no need to pre-treat), cardiac
(rare)

Reverse: no, give epinephrine if reaction

enough to be anaphylactic

risperidone Anti-delirium Less common option than haloperidol,

(Risperdal) recommend only if haloperidol is not an option
 for some reason

Use: ICU delirium

For severe kidney/liver failure, use lower

dosaging (or haloperidol if an option)

Neuromuscular Blockade Agents (NMBAs) = Paralytics. Use during intubation is common,

be very aware of underlying issues. If anticipated difficult airway, do not administer. For use of
NMBA continuously, patient obviously must be intubated, recommend very cautiously. Important:
pay attention to succinylcholine which is the only non-reversible paralytic.

Use: RSI (onset is quick), may use during

ventilation (not often used),

Adverse: do not use with patients who are

hyperkalemic or at risk of becoming so
succinylcholine Paralytic (burns, Guillain Barre)
(Anectine) (depolarizing NMBA)
Reverse: NO, "succs" because it is the only
paralytic on exam that can't be reversed

Notes: MUST give sedative first; MUST

manage airway

Use: RSI, may use during mechanical

ventilation (less common drug)

Adverse: anaphylaxis, bradycardia

Notes:

Not a first line option for most

patients (interacts with many
atracurium Paralytic (non-
other drugs). Off-label use for
(Tracrium) depolarizing NMBA)
ARDS, off-label use for shivering
related to therapeutic
hypothermia

May be preferred in patients with

renal or hepatic insufficiency

MUST give sedative first; MUST

manage airway

Use: facilitate mechanical ventilation (not

cisatracurium Paralytic routine), RSI (less common)
(Nimbex) (non-depolarizing
NMBA) Adverse: bradycardia (more than the other
NMBAs), may take longer time to
 ONSET

Reverse: edrophonium, neostigmine,

pyridostigmine

Notes: MUST give sedative first; MUST

manage airway

Use: facilitate mechanical ventilation (not

routine), not RSI

Adverse: tachycardia, hypertension

Paralytic
mivacurium
(non-depolarizing
(Mivacron) Reverse: edrophonium, neostigmine,
NMBA)
pyridostigmine

Notes: MUST give sedative first; MUST

manage airway

Use: facilitate mechanical ventilation (not

routine), not RSI

Adverse: tachycardia, hypertension, takes

pancuronium longer to wear off in kidney/liver failure
Paralytic
(Pavulon) patients (double the time)
(non-depolarizing
NMBA)
Reverse: edrophonium, neostigmine,
pyridostigmine

Notes: MUST give sedative first; MUST

manage airway

Use: RSI (great option due to quick onset)

Adverse: tachycardia, hypertension, takes

longer to wear off in liver failure patients
rocuronium
Paralytic
(Zemuron) Reverse: edrophonium, neostigmine,
(non-depolarizing
pyridostigmine
NMBA)

Notes: MUST give sedative first; MUST

manage airway
Requires higher dose than normal with
liver failure

Use: RSI, facilitate mechanical ventilation

vecuronium Paralytic (not routine)
(Norcuron) (non-depolarizing
NMBA) Adverse: bradycardia (rare), reduce dosage
with liver failure patients

Reverse: edrophonium, neostigmine,

 pyridostigmine

Notes: MUST give sedative first; MUST

manage airway

Reverses all paralytics EXCEPT

succinylcholine
Give if significant adverse reaction to
edrophonium reversal of paralytic NMBA (cardiac!)

(also used in diagnosis of myasthenia

gravis)

Reverses all paralytics EXCEPT

neostigmine succinylcholine
reversal of paralytic
(Prostigmin) Give if significant adverse reaction to
NMBA (cardiac!)

Reverses all paralytics EXCEPT

succinylcholine
pyridostigmine reversal of paralytic
Give if significant adverse reaction to
NMBA (cardiac!)

Airway drugs (not bronchodilators). Each is usually given for a very specific reason. You will find
some of these scenarios on your ACCS exam.

Use: nebulized drug indicated when stridor

(reduces inflammation/edema)

racemic epinephrine Adverse: cardiac (uncommon)

Airway
Notes: pay close attention to overall patient
assessment. If severe distress/stridor,
intubate. If mild-to-moderate (semi-
stable), consider racemic epi

lidocaine Use: nebulized as a local anesthetic for

Airway procedures (tracheostomy,
bronchoscopy, etc.)

cold saline
Use: Instilled usually for airway bleeding
Airway
during a procedure (esp. bronchoscopy)

Use: anticholinergic primarily for drying up

glycopyrrolate
Airway excessive secretions, especially with
(Robinol)
end-of-life care ("death rattle")
Respiratory Drugs: this is a selection of common respiratory drugs that you may find on the
exam. There won't be anything all that challenging - questions will involve the drugs but unlikely
focus on them. The exception to this is doxapram which is reported to show up in several
questions for most people on the exam.

Use: cleaves the disulfide bonds in infected

acetylcysteine
pulmonary secretions
(Mucomyst)
Mucolytic
May cause bronchospasm so consider pre-
treating with albuterol

Use: bronchodilation, acceptable for ANY

wheezing (yes, we said ANY wheezing)
albuterol
Beta agonist
Note that albuterol may be listed OR the
generic category "bronchodilator" may
be used

Use: bronchodilation when evidence of

albuterol/ipratropium
bronchospasm
(Duoneb in neb)
Beta agonist +
(Combivent in MDI)
anticholinergic Consider in patients with COPD - Duoneb is
usual option in ICU as pt flows are not as
important

dornase alfa
Use: primarily for cystic fibrosis patients -
(Pulmozyme)
Mucolytic helps "cleave" mucus to make it more
manageable

Use: respiratory stimulant (uncommon

doxapram
Stimulant drug) - IM or IV, consider with COPD
(Dopram)
with acute hypercapnia

ipratropium bromide
Use: prevents bronchoconstriction (if the
Anticholinergic
patient has reactive airways)

levalbuterol
Use: bronchodilation, specifically
(Xopenex)
Beta agonist recommend when cardiac adverse
effects noted with albuterol

Use: long-acting bronchodilation (prevents

tiotropium bromide Anticholinergic bronchoconstriction) for chronic lung
 disease (COPD)
(Spiriva)
Generally not recommended in critical care -
especially as a new drug

Pulmonary Vasodilators. These drugs are used to treat high pressures in the lungs (pulmonary
hypertension - not necessarily a chronic version, but related to refractory hypoxemia/ARDS).

Use: inhaled prostacyclin/prostaglandin,

used to treat pulmonary hypertension,
epoprostenol improve V/Q in severe ARDS (improves
(Flolan) Inhaled P/F ratio), and acute right heart
prostaglandins dysfunction

Adverse: Caution if platelets < 50,000,

hypotension

Use: inhaled prostacyclin/prostaglandin,

used to treat pulmonary hypertension,
treprostinil
improve V/Q in severe ARDS (improves
(Tyvaso) Inhaled
P/F ratio), and acute right heart
prostaglandins
dysfunction

Adverse: hypotension

Use: inhaled prostacyclin/prostaglandin,

used to treat pulmonary hypertension,
iloprost improve V/Q in severe ARDS (improves
(Ventavis) Inhaled P/F ratio), and acute right heart
prostaglandins dysfunction

Adverse: Caution if platelets < 50,000,

hypotension

Use: inhaled prostacyclin/prostaglandin,

used to treat pulmonary hypertension,
improve V/Q in severe ARDS (improves
Inhaled P/F ratio), and acute right heart
inhaled nitric oxide
prostaglandins dysfunction

Adverse: rapid discontinuation may cause

rebound pulmonary hypertension

Cardiac - Tachycardia

adenosine (slows HR)

Cardiac
(Adenocard)
Used for supraventricular tachycardia
lidocaine
(Xylocaine)
Cardiac Used to treat Vtach and Vfib

Used to treat torsades de pointes (a specific

magnesium Cardiac
form of Vtach)

Use: Nonselective Beta Blocker reduces HR

and BP
propanolol
(Inderal) Adverse: Use with caution in kidney/liver
Cardiac
failure

Hemo: - Chronotrope, ↓ HR, ↓ BP, ↓

Contractility

(decreases HR)
verapamil
(Calan, Verelan) Use for SVT (second line - calcium channel
Cardiac
blocker)

Adverse: reduce dosage for kidney/liver

failure

Cardiac - Bradycardia

(increases HR)
atropine
Cardiac
Use for bradycardia (symptomatic)

No longer used with asystole/PEA

(increases HR)

dopamine Cardiac Use for bradycardia (use atropine first, but

then consider dopamine)

Hemo: ↑ Rate, ↑ Contractility

epinephrine Cardiac (increases HR)

Asystole, pulseless rhythms (VT, VF)

Symptomatic bradycardia (unresponsive to

 atropine/pacing) - low doses

Anaphylaxis

Severe asthma (especially when

unresponsive to SABA)

Cardiac - Arrhythmias

amiodarone (corrects rhythm)

(Cordarone, Nexterone,
Pacerone) Cardiac Use: anti-arrythmic, including a-fib

Adverse: reduce dose or don't use with

severe liver failure

diltiazem Use: angina, hypertension, arrhythmias

(Cardizem)
Cardiac
Adverse: reduce dose or don't use with
severe liver failure

Cardiac - Hypertension

Use: treats hypertension, heart failure

hydralazine
Cardiac Adverse: may cause hypotension (obviously,
right?), CNS depression, consider
reducing dose with kidney/liver failure

Use: Beta Blocker drug: treats

labetalol hypertension
(Normodyne)
Cardiac
Adverse: may cause hypotension (obviously,
right?), consider reducing dose with liver
failure

Use: Selective Beta Blocker drug: treats

metoprolol hypertension, angina
(Lopressor)
Cardiac
Adverse: may cause hypotension (obviously,
right?), CNS depression, reduce initial
dose with liver failure

Use: Phosphodiesterase inhibitor that

milrinone Cardiac directly vasodilates = low CO, acute CHF
(Primacor)
 Adverse: thrombocytopenia, Reduce dose
with kidney failure

Hemo: + inotrope with minimal chronotropic

action that ↓ Preload, ↓ Afterload

Use: Calcium Channel Blocker drug: treats

nicardipine
hypertension, angina
(Cardene)
Cardiac
Adverse: use low end of dosing for renal
failure (20 mg)

(decreases BP through vasodilation)

Use: severe heart failure, Low CO

sodium nitroprusside Use: to treat hypertensive crisis

(Nipride)
Cardiac
Adverse: choose another drug if availablein
pts with renal failure

Hemo: ↓ Preload, ↓ Afterload

Renal: poor renal function increases risk of

thiocyanate toxicity

Cardiac - Hypotension

(increases BP)

dobutamine Used to treat hypotension (esp. refractory) -

Cardiac
(Dobutrex) inotropic properties

Hemo: ↑ HR, ↑ Contractility, ↓ Preload, ↓

Afterload

Use: vasopressor for hypotension, a first

choice drug for septic shock
norepinephrine
Cardiac Adverse: bradycardia, cardiac, dyspnea
(Levophed)
Note: not first choice for hypovolemic shock
(you need to fluid resuscitate!)

phenylephrine
Cardiac (increases BP)

Use: hypotension when other options are

 ineffective or significant adverse effects

Note that phenylephrine is also the active

ingredient in Sudafed for nasal
decongestant

hemodynamically: increases PAP

Adverse: bradycardia (rare)

Hemo: ↑ Contractility, ↑ Afterload, Does not

increase HR

Cardiac - Other Drugs

a derivative of digitalis (a plant)

Use: + Inotropic drug used to treat CHF

(right-heart)

Adverse: Digitalis toxicity occurs when drug

accumulates (kidney failure especially)

Symptoms include nausea, vomiting,

abdominal pain, change in LOC,
digoxin delirium
(Digox, Lanoxin)
Cardiac
If suspected, serum digoxin level
should be requested (> 2.6 ng/mL
is toxic, though it can manifest at
lower amounts)

Treatment: fluid resuscitation and

discontinue drug, then support
whatever isn't working
(respiratory!)

Adverse: be very cautious in use with renal

failure, reduce dosage

Use: chest pain (angina) by venodilation

(systemic + pulmonary)
nitroglycerin Cardiac
Adverse: hypotension

Hemo: ↓ Preload, ↓ Afterload

vasopressin Use (1x) for pulseless arrest

Cardiac
vasopressin is no longer recommended as
 an ACLS drug but may still appear on
exam

Coagulation

prophylactic and treatment for patients at risk

for or with heparin-induced thrombocytopenia
argatroban (HIT) - prevents fibrin formation
Anticoagulation
(Acova)
Use: at-risk patients undergoing
percutaneous coronary intervention
(PCI)

(diminishes platelet cascade - so prevents

clotting)
clopidogrel
Antiplatelet
(Plavix) Use: unstable Angina (STEMI or non-
STEMI)

Use: Stroke (CVA)

heparin Anticoagulation There are two types of heparin: unfractionated

and low molecular weight. You are unlikely to
ex: be asked to pick between the two, but we
recommend choosing low molecular weight if
enoxaparin you are as it has more predictable
(Lovenox) anticoagulation effects. It is more common
today.

Use: prophylactic for deep vein thrombosis

(DVT) - so think hip surgery, long-bone
fractures (trauma), coagulopathy

Use: treatment of DVT and PE, acute

coronary syndromes (unstable angina,
myocardial infarctions)

Adverse: Bleeding is a primary concern. In a

scenario with this drug noted, be wary of
details related to suctioning,
bronchoscopy, etc. It doesn't mean you
can't recommend those options but do
so with caution.

Notes: the question or answer option is

likely to include the word heparin, but
remember that there are multiple
formulations of heparin and they all end
 in "parin" (heparin, enoxaparin,
dalteparin, etc.). The goal of this drug is
to PREVENT the "parin" of stuff to form a
clot. Okay, it's a really bad mnemonic
but it worked for our brains.

Key: Technically heparin doesn't break up a

current clot. Recommend with
uncomplicated PE (no hemodynamic
effects) or to prevent further clots.
Heparin or warfarin are usually given
even when tPA is indicated.

This drug is a fibrinolytic (clot buster). Keep it

separate in your mind from heparin and
warfarin, which prevent further clotting but
don't actually affect any present clots. tPA
drugs break up the clot but have serious
bleeding adverse effects.

Use: confirmed pulmonary embolus (PE) in

certain situations. Consider this drug as
an extreme reaction to a PE - if any
reason not to give it, then certainly do
not. Almost always this will involve
some kind of hemodynamic
tPA deterioration. The presence of a PE
(Alteplase) Fibrinolytic doesn't insinuate the automatic need for
(Reteplase) tPA. Let's simplify this: give tPA if
confirmed PE with hemodynamic issues.
Do not give tPA if confirmed PE without
hemodynamic effects.

Contraindications: Do not give if active

bleeding (especially anything head-
related), post-surgical. Bleeding is a
serious risk.

If the question writers are feeling fancy they

may refer to tPA as "Recombinant tissue
type plasminogen activator." They like
to throw out fancy terminology from
time to time.

warfarin Use: prophylactic for deep vein thrombosis

(Coumadin) Anticoagulation (DVT), just like heparin

Use: treatment of a thromboembolism,

myocardial infarction. Prevents further
damage.

Key: Technically warfarin doesn't break up

 a current clot. Recommend with
uncomplicated PE (no hemodynamic
effects) or to prevent further clots.
Heparin or warfarin are usually given
even when tPA is indicated.

Diuretics

Use: watch in particular for cardiac effects

(CVP!) of fluid status - recommend when
fluid overloaded
acetazolamide
Use: old use as a respiratory stimulant
(Diamox)
Diuretics (especially with metabolic alkalosis which
causes respiratory depression as a
compensatory mechanism)

Adverse: Ineffective if kidney/liver

impairment is moderate-to-severe

Use: watch in particular for cardiac effects

(CVP!) of fluid status. Bumex is usually
bumetanide
a second-line option.
(Bumex)
Diuretics
Adverse: Ineffective if kidney (anuria) or
liver impairment (hepatic coma) is
moderate-to-severe

Use: watch in particular for cardiac effects

(CVP!) of fluid status - recommend when
furosemide
fluid overloaded
(Lasix)
Diuretics
Adverse: May be effective with mild acute
kidney failure, otherwise don't use with
kidney impairment

Use: this drug may be effective even if

kidney function is impaired (give a test
dose) - do not use if severe kidney
mannitol
impairment
(Osmitrol)
Diuretics
Use: reduction of cerebral edema and ICP

Adverse: Don't give simultaneously with

blood product

Gastric Drugs
pantoprazole
Gastric There are two main proton pump inhibitors
(Protonix)
(PPIs) that you should be familiar
with. Recommend either for prevention of VAP
or erosive gastritis:

Use: short-term prophylactic for ventilator-

associated pneumonia (proton pump
omeprazole inhibitors (PPIs) are on the VAP bundle
Gastric
(Prilosec) as they help prevent reflux which causes
aspiration, which causes pneumonia).

Use: treatment for erosive gastritis (yes,

this has been tested)

famotidine
Gastric There are two main histamine h2 agonists that
(Pepcid)
you should be familiar with. Recommend either
for prevention of VAP or erosive gastritis:

Use: short-term prophylactic for ventilator-

associated pneumonia (histamine h2
agonists are on the VAP bundle as they
ranitidine
Gastric help prevent reflux which causes
(Zantac)
aspiration, which causes pneumonia).

Use: treatment for erosive gastritis (yes,

this has been tested)

Anti-Infective Drugs. There are three categories of organisms we seek out: bacteria, viruses,
and fungi. Most common are bacterial infections in ICU. Anitbiotics are given with evidence of
infection (fever + increased WBC, bands often present), not as a preventative measure.

Antibiotics:

Gram + (less likely - these are "nicer" organisms, + attitude!) = penicillins, cephalosporins

Gram - (more likely in ICU - these are not nice, - attitude!) = mycins

Fungals:

Treat with an antifungal (flucanazole is common)

Viral:

Varies by virus. Remember that anti-virals slow down replication of the virus, but there's no
virus-killer!

Antibiotic Use: management of Pseudomonas

aztreonam (especially for CF patients)
(Cayston)
Alternate cycles with Tobi (28 days on Tobi,
then 28 days on Cayston)
 Use: Administer if an indication of a fungal
flucanazole disorder. Use is unusual. "Azole" is a
Antifungal
(Diflucan) quick clue that it is likely an antifungal
drug.

Use to treat gram negative organisms,

gentamycin Antibiotic much more common in ICU than
penicillin

Use: Antibiotic used for bacterial-based

pneumoinias (which is most of them). If
signs/symptoms of pneumonia, this is a
levofloxacin good drug to recommend.
Antibiotic
(Levaquin)
Note: Do not use prophylactically. Question
must contain some evidence of infection
(WBC, fever, culture)

penicillin Treats Gram + organisms, so not all that

(amoxicillin) Antibiotic common in ICU. Read carefully before choosing
(ampicillin) this.

Use: combo antibiotic. Recommend for

piperacillin/
pneumonia, including aspiration.
tazobactam Antibiotic
Although this drug is used commonly in
(Zosyn)
ICU, it does not appear often on test.

polymixin
(Colistin) Used to treat gram-negative bacilli
Antibiotic
(pseudomonas aeriginosa, acinetobacter)

Treatment of tuberculosis (usually in

rifampin Anti-TB
addition to other drugs)

tobramycin
(Tobi) Used to treat pseudomonas aerigunosa,
Antibiotic
especially in cystic fibrosis patients

trimethoprim/
Use: Consider with moderate-to-severe
sulfamethoxazole Antibiotic
infections, including COPD exacerbations
(Bactrim)
 Use: As a broad-spectrum antibiotic,
particularly used for MRSA. Consider
when a question gives information that a
line and/or catheter has been placed
(most common: central line, urinary
vancomycin Antibiotic cathter). Look for fever, WBC to also be
mentioned.

Use: As narrow-spectrum treats C-diff, and

some of the "coccal" (enterococcal,
staphylococcal, streptococcal)

Other Drugs

Use: This should be the primary drug used

to treat fever (febrile, hyperthermia)

Adverse: extreme caution with liver

acetaminophen
impairment. Do not give if severe.
anti-pyretic
Notes: administration is a key to "issues"
like O2 consumption, ventilator weaning,
with a patient identified as having a
fever. Be prepared to recommend!

Use: for severe, life-threatening metabolic

acidosis (pH < 7.20)

Adverse: Do NOT use for respiratory

acidosis as it will increase CO2
production (you will worsen the
problem!)
bicarbonate
miscellaneous
(sodium bicarb) Notes: It is usually better to treat the cause
of the metabolic acidosis, if known, versus
giving sodium bicarb. For example, if a
patient is hyperglycemic (DKA),
administering insulin is much more
effective than sodium bicarb. This drug
will appear frequently on the exam but is
often the incorrect choice!

Use: Keep it pretty generic. If indication of

hyperglycemia, administer insulin. DO
NOT administer for hypoglycemia (keep
glucose the two separate!)
insulin
management
Notes: Treat glucose > 180 mg/dL in ICU
with insulin, don't use normal ranges
- review this section if you need to
 Use: For treatment of hypothyroidism
(levels too low)
levothyroxine thyroid replacement
(Synthroid) therapy
Notes: if thyroid function is high, stop
treatment

Use: Drug given to treat methemoglobin.

methemoglobinemia
methylene blue Note: Know the drugs that may result in
treatment
methemoglobinemia. Inhaled nitric oxide is
common, but there are others.

Use: Treat seizures in critical care

phenytoin, Notes: lorazepam is first choice for trying

fosphenytoin anticonvulsant to get seizures under control. Note that
(dilantin) seizures are usually caused by
"something" unless idiopathic, so look
for cause and treat it

Use: Common steroid given for any sign of

an inflammatory process. This includes
drugs used to manage
diseases/disorders like Asthma.
solumedrol miscellaneous Recommend for treatment of upper
airway stridor.

Adverse: solumedrol aggravates gastritis, so

do not recommend