APPLIED

ICU NOTES
By Dr. Mohamed Erfan
1st EDITION
Volume II
2025

APPLIED ICU NOTES

BY
DR. MOHAMED ERFAN

Dr. Mohamed Erfan

EGYPT 2025
PAGE |1 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Preface& Acknowledgment
All praise is due to Allah, the Most Merciful and Benevolent. I extend my deepest
gratitude to my parents, whose unwavering support and guidance have been
instrumental in my journey. To my wife, daughter, and sons, I offer heartfelt thanks
for their patience, love, and encouragement.

This book, "ICU Notes," aims to provide concise, easily digestible insights into
critical care medicine. Its purpose is to serve as a valuable resource for
candidates preparing for board exams, as well as to enhance the knowledge and
practice of intensivists.

I hope that these notes will prove beneficial to healthcare professionals and
contribute to improved patient care in intensive care units.

Mohamed Ibrahim erfan

Erfanmohamed1984@gmail.com
00201281221443
Mansoura – Egypt
2025
PAGE |2 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

TABLE OF CONTENTS
Chapter number TITLE Page number
Section I: procedures
1 Arterial Catheterization 4
2 Central Venous Catheterization 6
3 Endotracheal Intubation 11
4 Percutaneous Tracheostomy 16
5 Chest Tube Insertion 19
6 Paracentesis 24
7 Lumbar puncture 26
8 Thoracocentesis 30
9 Pericardiocentesis 33
10 Pulmonary Artery Catheterization 37
Alternative Hemodynamic Monitoring
(Esophageal Doppler - Transpulmonary Thermodilution –
11 Pulse Contour Analysis – Partial CO2 Rebreathing – 43
Thoracic Bioimpedance & Bioreactance)
Functional Hemodynamic Monitoring
12 (Static & Dynamic) Markers Of Volume Responsiveness 49
13 Extracorporeal Therapy In ICU 54
14 Basic Critical Care Ultrasound 66
15 Difficult Airway Management 90
Section II : Common ICU Drugs & Equations
16 Common ICU Drugs 101
17 Common Equations in ICU 131
Section III : Traces & Curves
18 ECG in Critical Care 136
19 Mechanical Ventilation 151
20 PAC Waveforms 192
21 PiCCO Analysis 198
22 Esophageal Doppler CO Monitoring 200
23 IABP Waveforms 201
24 CVP Waveforms 203
25 ROTEM Analysis 205
26 ICP Waveforms 221
27 Arterial waveforms 223
28 Capnography 226
29 CRRT curves 228
30 ABG Interpretation 232
Section IV : Important Trials In Critical Care
31 Important Trials in Critical care 248
PAGE |3 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Section I: Procedures
PAGE |4 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

1 Arterial Catheterization
Indications
 Direct arterial hemodynamic monitoring in unstable patient
 Frequent ABG measurements in unstable patients with respiratory insufficiency
 Less commonly, for placement of IABP or direct drug administration (thrombolytics).
Complications
 Thrombosis (the most common)  Limb ischemia
 Local or systemic infection  Peripheral neuropathy
 Hematoma  Insertion site pain
 Pseudoaneurysm  HIT (for heparin-flushed lines)
 Hemorrhage  Significant blood loss from frequent
 Retroperitoneal hematoma (femoral) blood testing
Prevention of Complications
 With careful sterile technique during catheter placement,& radial A preference.
 Routine catheter care, dressings should be changed every 48 hours.
 Careful sterile technique when drawing blood samples from the catheter.
 A lines are less likely to become infected than CVC because of higher pressure bl flow.
 For febrile patients, A lines do not necessarily need to be removed unless no other infectious
source is identified. However, it should be removed as soon as they are no longer needed.
Equipment of catheterization
1. maximal sterile barrier precautions 3. suture or fixation device
2. intravascular catheter 4. noncompliant tubing,
5. flush device which pressurized flush solution
6. transducer & electronic monitoring equipment including connecting cable & monitor with
amplifier and display screen.
7. Real-time ulcrasonography is recommended to increase success rate of vessel cannulation.
How the Equipment work
 The tubing is connected to transducer, which is connected to electronic monitor via cable.
 The noncompliant tubing transmits pressure waveform from artery to transducer, which
converts pressure waveform to electrical waveform.
 The electric waveform is amplified and displayed on oscilloscope screen.
 The flush device allows continuous fluid infusion to prevent thrombus formation and is
pressurized to prevent backup of high-pressure arterial blood into the tubing.
Cannulation Site
 Radial artery is the most common site followed by femoral artery. Although both have similar
complication, the radial site is preferred with lower infection risk.
 Less common sites include dorsalis pedis, brachial, and axillary arteries.
 The radial & ulnar arteries are distal branches of brachial artery & are located on lateral &
medial sides of wrists, respectively. They are connected by deep & superficial palmar arches
in hand. These arterial anastomoses are taken into consideration when radial line is placed,
as potential complication of radial artery catheterization is thrombosis. If thrombosis occurs,
collateral circulation from ulnar artery through palmar arches ensures adequate blood flow
to hand. Peripheral vascular disease that occludes the palmar arches could interrupt blood
flow to the hand if radial artery thrombus occurs.
 The Allen test can identify patients who have compromised collateral palmar circulation. it
is performed by raising patient's arm to 45 degrees, with the examiner compressing radial
& ulnar arteries with both hands. The patient is asked to repeatedly open & close hand to
drain the blood. Once pallor develops, one artery is released and the time to palmar flushing
is timed. Positive if ≤ 7 seconds, equivocal if 8-14 sec, and negative if ≥15 sec with evidence
for a lack of adequate collateral circulation. The test is repeated with the other artery. Results
PAGE |5 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

may be difficult to interpret for patients on vasopressors and those unable to cooperate.
Thus, many have abandoned the routine performance of the Allen rest.
Types of Arterial Catheters
 3 types are used (similar angiocatheter to peripheral IV without guidewire assistance).
 Guidewire kits offer preloaded system or separate guidewire using Seldinger technique.
 No method is superior, and kit selection is based on provider preference and availability.
 Catheter gauge and length vary on the basis of arterial site.
Steps For Radial Artery Cannulation
1. Position the supine patient's hand with 30-60 degrees of extension by propping the dorsal
wrist surface on a rolled towel or other supporting structure with the ventral surface up.
2. Remove all objects from wrist& cleanse skin with antiseptic sol (chlorhexidine or Betadine)
3. Create a sterile field by draping wrist and donning sterile gown & gloves (a reasonable rule
is to gown & mask when placing objects in patient that will remain in place and act as a
potential source of infection).
4. Palpate radial A on patient's ventral wrist with the 1st 2 fingers of nondominant hand 3-4 cm
proximal to crease at the base of thenar eminence. If employing ultrasonography, use a
sterile sleeve and identify pertinent structures including the radial artery.
5. For conscious patients, infiltrate a liberal volume (>2 mL) of local anesthetic.
6. With the dominant hand, hold the catheter like a pencil between the first and second fingers.
7. While palpating gently, or visualizing with US probe, with nondominant hand, enter the skin
at 30-45 angle with catheter tip just caudad to the fingertips of nondominant hand. Pressing
too firmly on the radial artery can occlude flow and make cannulation difficult.
8. Advance the catheter toward the artery until a flash of blood enters the catheter tip.
9. If using simple catheter-over-needle configuration, advance the tip of needle slightly further
into A to ensure that tip of catheter is in A lumen (go to step 12 if using device with wire).
10. While holding the needle steady, advance catheter gently forward into A lumen with slight
twisting motion.
11. Remove the needle; correct placement= pulsatile flow (if using C without wire, go to 15).
12. If using kit with guidewire, when blood flash occurs, hold needle steady & advance guidewire
into A lumen with little resistance. US, if available, should document imraluminal guidewire.
13. If using a preloaded guidewire, advance the catheter over the wire and into A lumen. If using
separate guidewire, remove needle while leaving guidewire in place & replace with catheter.
14. Remove the needle and wire; correct placement should result in pulsarile blood flow.
15. Connect the catheter to the transducer tubing and Rush device.
16. Secure the catheter to the skin with suture or adhesive device.
17. Cleanse the skin and catheter with antiseptic solution and cover with sterile dressing.
Tips
 If 1st attempt is unsuccessful, reposition catheter& try again, less steep angle↓ traversing A
 If further attempts are unsuccessful, try advancing needle through A when the initial blood
flash is seen in catheter tip. Next, slowly withdraw catheter until bl. flash occurs again &
attempt to advance guidewire through catheter & into A lumen. Once guidewire is in place,
the catheter can be advanced.
 A is transfixed initially with no blood flow. Thus, catheter should be withdrawn slowly as
success can be achieved while withdrawing the catheter.
 Deliberate palpation of A, focused technique, & real-time US will aid in a successful result.
 For FA cannulation, a kit similar to CVC kit is used. FA lies in femoral triangle bordered
superiorly by inguinal ligament, laterally by sartorius muscle, & medially by adductor longus.
 From lateral to medial positions in the triangle lie FN, FA & FV.
 FA is palpated with nondominant hand or with US guidance. Cannulation of A is performed
in the same manner as CVC cannulation. A Flow may be nonpulsatile during cardiac arrest.
PAGE |6 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

2 Central Venous Catheterization

Indications
 Administration of noxious medications (vasopressors, chemotherapy, & TPN)
 Hemodynamic monitoring (CVP, measurement of central venous hemoglobin saturation)
 Therapies requiring rapid blood flow rates (hemodialysis, plasmapheresis),
 Insertion of invasive devices (pulmonary artery catheters or transvenous pacemakers)
 Rapid large-volume fluid or blood product administration,
 Emergency venous access, when peripheral access is inavailable or inadequate
Contraindications
 Known thrombosis of the target vessel
 Infection over the site of entry.
 No definitive cut-off for CVC insertion in coagulopachic or thrombocycopenic;
 However, subclavian site is avoided in coagulopathy due to inability to monitor for
bleeding or adequately compress this site if bleeding occur.
 Use of micropuncrure kit or correction of coagulopathy with FFP & platelet transfusion
may be useful prior to the procedure.
Complications
 Mechanical: arterial puncture, pneumothorax, hemothorax, air embolus, retroperitoneal hge.
 Infectious complications : CVC-associated bacteremia, cellulitis.
 CVC-associated thrombosis or stenosis.
Canulation Site Selection
 Although conflicting data exist, general consensus is that risk of infection is least with
subclavian & highest with femoral cannulation. Avoid FV due to infectious complications.
 CDC guidelines for cannulation site selection recommend avoiding femoral cannulation in
adult because of ↑ venous thrombosis and restriction of patient mobility.
 Subclavian cannulacion should be avoided in patients with coagulopathies for the
aforementioned reasons or with advanced kidney disease due to risk of subclavian stenosis.
 Ultrasound Guidance in CVC Insertion
 It is used both to identify the location of target vein and its accompanying artery and to
assess the vein for thrombosis or stenosis.
 ↓ (complication, number of attempts to cannulate the vein, & duration of the procedure).
 IJV is anterolateral to carotid artery, and femoral vein is medial to femoral artery.
 Vein can be identified on US by its compressibility. Veins is completely compressible
(anterior & posterior walls should approximate) with pressure applied with US probe.
 If vein is not compressible, there should be suspicion for venous thrombosis.
 Veins can also be identified using spectral color or pulsed wave Doppler, as flow in
arteries is typically pulsatile and flow in veins is not. However, this can be misleading in
certain clinical conditions, such as with severe tricuspid regurgitation.
 US-guided IJV cannularion is usually performed in the classic short axis approach by
holding the probe transversely to have a cross-sectional view of artery & vein.
 However, long-axis & novel medial- oblique approaches have also been described.
 In the oblique axis, US probe is applied oblique to the axis of vein so that the larger SA
of vein is available, and carotid artery is away from the needle path. This provides better
real-time needle and guidewire visibility.
 However, none of the approaches has been found to be superior to others in terms of
first insertion success rate, overall success rate, & incidence of carotid artery puncture.
 ↑ cross-sectional area (CSA) of IJV has been found to ↑ success rate of cannulation.
 This done by application of PEEP= 10-15 during cannulation in MV patients >> ↑ CSA
& anterioposrerior diameter of IJV and ↓ carotid artery overlap underneath vein.
PAGE |7 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Obtain informed consent before performing cannulation& based on the policies of each
institution. All present must agree on the patient identification, the procedure being
performed, and the site of the procedure. Sterile precautions must be observed, including
hand hygiene, full sterile drape, sterile gloves, sterile gown, mask with face shield, and hair
covers. All present in the room should wear masks and hair covers. It is helpful to have a
nonsterile assistant present during the procedure.
 The following guidelines are for CVC placement via Seldinger's guidewire technique.
Internal Jugular CVC Placement (US guidance is preferred)
1. Place patient in Trendelenbmg position, and patient turn his head 45 degrees to the direction
opposite the site of catheter placement.
2. If ultrasound is available, use it to identify the vascular structures prior to sterilizing the
procedure site. Evaluate the vein for patency and compressibility to ensure that there are
no contraindications to catheterization (venous thrombosis or stenosis).
3. Prepare the US for sterile use by applying nonsterile gel to transducer. (Alternatively, this
may be performed by a nonsterile assistant.
4. Don sterile gown, sterile gloves, mask with face shield, and hair cover.
5. Prepare the skin with antiseptic solution (e.g., chlorhexidine or Beradine).
6. Use a sterile full-body drape with a sire hole or surgical towels to cover the body, head, and
face, exposing only the necessary skin.
7. Flush all ports to ensure appropriate functioning. (If US is not available, proceed step 14)
8. With help from a nonsterile assistant, lower the ultrasound transducer into the sterile plastic
sheath. Make sure to avoid contact between the transducer and the outer surface of the
plastic sheath. The nonsterile assistant should then pull the plastic sheath to cover the
length of the transducer probe that will come into contact with the sterile field.
9. Place sterile gel on the procedure site. Confirm location of the vessels using US again.
10. Once the site is confirmed, anesthetize the skin & subcutaneous tissue.
11. Use ultrasound to maintain a transverse view of the vein and artery. While holding US probe
over vein with the nondominant hand, use the dominant hand to hold the introducer needle.
12. Enter the skin with introducer needle, bevel up, just cephalad to US transducer at 45 angle.
13. With US transducer, locate the tip of the introducer needle. Move the US transducer &
introducer needle together in order to visualize the tip of the introducer needle throughout
its approach to the target vein, aspirating while advancing. Once the vein is cannulated,
dark blood will enter the syringe. (Skip to seep 18 if using direct US guidance.) (Fig 1.1)
14. Identify triangle formed by 2 heads of sternocleidomastoid& sternum& palpate CA(Fig 1.2)
15. Anesthetize the skin and subcutaneous tissue.
16. Palpate the carotid pulse. Lateral to carotid pulse, advance 22-gauge needle (finder needle),
bevel up, at 30-45-degree angle to the patient, directed at the ipsilateral nipple while
aspirating. If no venous blood return is noted, withdraw the needle and change the angle to
a more lateral and then more medial position. Maintain palpation of the carotid pulse. When
venous blood is aspirated, make note of the angle and depth of the finder needle, and
remove the finder needle. If the carotid artery is entered (bright red and/or pulsatile blood),
remove the needle and hold pressure.
17. At the same site and angle as the internal jugular vein was encered with the finder needle,
insert the introducer needle until free fl.ow of dark venous blood is noted (Fig 1.2).
18. Securely hold the needle, remove the syringe (placing a finger over the needle hub to reduce
the risk of air embolism), and insert the guidewire. The guidewire should advance with little
resistance. Always maintain control of guidewire.
19. While holding guidewire, remove the introducer needle. Once introducer needle is outside
the patient's skin, hold the guidewire at the entry site and slide the needle off the guidewire.
20. Use US to confirm correct placement of guidewire within the lumen of target vein. Obtain
transverse view of IJV , and identify the wire within the lumen of vein. Trace the tract of
PAGE |8 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

guidewire from skin insertion site into the insertion into vein. Move US transducer in caudal
direction to follow the course of guidewire toward SVC . Continue moving transducer
caudally confirming the guidewire remains within lumen of vein for its entire course through
the neck. US transducer probe can then be rotated 90 degrees to confirm the guidewire is
within the lumen of vein in the longitudinal axis (Fig 1.3).
21. Using a scalpel, make a small incision in the skin at the entry site. Ensure that the cutting
edge of scalpel is facing away from guidewire & perform stabbing morion to make incision.
22. Pass the dilator over guidewire, dilate tract to the depth of the target vein& remove dilator.
23. Ensure that the distal pore of catheter is open. Pass the catheter over guidewire. When
catheter is near the entry site, feed guidewire out until it emerges from the distal port of
catheter. Grasp guidewire distally & insert catheter to desired depth ( 15-16 cm for right
subclavian vein,18-20 cm for left SCV, 16-17 cm for right IJ vein, 17-18 cm for left IJ vein).
24. Hold catheter in place & withdraw guidewire. Ensure that guidewire is intact once removed.
25. Flush all pores to ensure that they are functioning properly, and place caps on all pores.
26. Secure the catheter with suture or a commercially available sucureless kit.
27. Cleanse the site with antiseptic solution and place a sterile dressing.
28. Obtain chest radiograph for placement (tip should reside in SVC) & to evaluate for PTX.

Fig 1.1 Needle insertion using US

guidance
Figure 1.2. IJV anatomy

Figure 1.3. IJV with verification of guidewire placement. A: Transverse view. B: Longitudinal
view. Arrowhead: carotid artery, Asterisk: IJV , White arrow: guidewire within IJV.
PAGE |9 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Femoral CVC Placement (US guidance if preferred)

1. Place patient in supine position, with ipsilateral thigh slightly abducted & externally rotated.
2. If using US, follow steps 2 to 13, followed by steps 18 to 27 from IJV catheter placement.
Remember when locating femoral vein with US that FV typical lies medial to FA. If US is
unavailable, follow steps 4 to 7 from IJV catheter placement above, followed by steps below.
3. Palpate FA pulse inferior to the inguinal ligament. FV is medial to FA (Fig. 1.4). With the
introducer needle bevel up, enter the skin 1 cm medial to the pulse, inferior to the inguinal
ligament, at 30-45 angle (Fig. 1.5). Continue to aspirate as the needle is advanced until the
return of venous blood. If the needle is advanced 5 cm with no return of venous blood,
withdraw while continuing to aspirate, angle more medially, and try again. If FA is entered
(bright red andlorpufsatile blood), hold pressure.
4. Follow seeps 18 through 27 for IJV CVC placement. For femoral site, the entire length of
catheter is inserted (20 cm) and secured in place.

Figure 1.4. Femoral vein anatomy Figure 1.5 Femoral vein cannulation
P A G E | 10 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Subclavian CVC Placement

1. Place patient in Trendelenburg position, and place a towel roll between scapulae. Keep
head in neutral position or toward side of line placement to help direct guidewire inferiorly.
2. Don sterile gown, sterile gloves, mask wich face shield, and hair cover.
3. Prepare the skin with antiseptic solution (e.g., chlorhexidine or Betadine).
4. Use a sterile full-body drape with a site hole or surgical towels to cover the body, head, and
face, exposing only the necessary skin.
5. Flush all ports of the catheter to ensure appropriate functioning.
6. Place the index finger of nondominant hand at the sternal notch and thumb of the same
hand on clavicle where it bends over 1st rib (approximately where lateral third & medial two-
thirds of clavicle meet). SCV should traverse a line between index finger & thumb (Fig. 1.6).
7. Anesthetize skin & SC tissue just inferior to the clavicle and lateral to the thumb.
8. With the introducer needle, bevel up, enter the skin lateral to the thumb and inferior to
clavicle (2 cm inferior & 2 cm lateral to the bend in clavicle). Aim at the index finger (sternal
notch), aspirating while advancing. It is imperative to keep the needle parallel to the floor
during advancement. If clavicle is contacted, depress the entire needle with thumb until it
passes under clavicle, rather than changing the angle of approach. Dark blood will enter the
syringe when vein is cannulated. If there is no blood return after advancing the needle 5 cm,
withdraw the needle while continuing to aspirate (frequently the vein has been pierced, and
successful blood flow will be obtained during withdrawal). Redirect the needle more
cephalad, and try again. Multiple repeated attempts are not recommended. Once
appropriate venous return is noted, rotate the bevel of the needle 90 degrees inferior (bevel
now poincing toward the patient's feet).
9. Follow steps 18 through 28 for IJV CVC placement.

Figure 1.6. Subclavian vein anatomy & cannulation

P A G E | 11 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

3 Endotracheal Intubation
Uses
 Maintains airway patency.  Facilitates pulmonary toilet.
 Assures delivery of MV defined breaths.  Prevent aspiration.
Indications
 Airway obstruction,  Respiracory failure,
 Encephalopathy,  Cardiopulmonary arrest.
Risks & Complications
 Trauma to oropharynx,  Emesis with aspiration of gastric
 Hypoxemia from prolonged attempts, contents
 Unrecognized misplacement of ETT  Death.
Required Preparations
 Assessment of airway anatomy facilitates recognition of potentially difficult intubations.
 An abbreviated assessment should be performed even in emergent cases. A commonly
utilized assessment tool follows the "LEMON" mnemonic (Table 3.1).
Table 3.1 LEMON Airway Assessment
 Look externally
 General impression of difficulty airway (anatomy, habitus,
dentition, tongue, trauma, facial hair)
 Evaluate (3-3-2 rule) Patient should have at least:
 3 finger breadths between incisors with mouth opening
 3 finger breadths within the thyromental distance
 2 finger breadths between hyoid and thyroid cartilage
 Mallampati Score (Fig. 3.1)
 I & II predict easy laryngoscopy
 Ill predicts a difficult laryngoscopy
 IV predicts a very difficult laryngoscopy
 Obstruction/Obesity
 Supraglottic mass, secretions, blood or redundant tissue
 Neck Mobility
 Spinal disease or C-collar immobilization

Figure 3.1. Mallampati classification.

 Pay attention to
 dentition & dental appliances,
 mobility of tongue & its size relative to oropharynx or Mallampati score (Fig. 3.1),
 range of extension & flexion of the cervical spine,
 mobility of the jaw  presence of stridor.
P A G E | 12 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 A difficult intubation may be anticipated in patients with thick necks, narrow mouth openings,
facial hair, large tongues, and limited motion of cervical spine.
 Successful intubation requires overcoming the normal barriers to objects entering the
trachea, including reflexes arising from laryngeal stimulation, mal-alignment of major axes
of the upper airway, and anatomic barriers of tongue & epiglottis.
 Endotracheal intubation is uncomfortable procedure, and even patients with decreased
mental status may cough and resist attempts at intubation. In addition, laryngeal stimulation
↑ sympathetic tone with consequent ↑ in BP, HR, and ICP.
 Judicious use of appropriate medications can blunt the potential adverse physiologic effects
while providing analgesia, sedation, and amnesia. Decisions regarding use of specific
agents are based on knowledge of their advantages and disadvantages relative to patient's
clinical status and comorbidities (Table 76.2).
 Only practitioners skilled in endotracheal intubation should administer paralytic agents.
Table 3. 2 Medications Used For Intubation
P A G E | 13 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Rapid-sequence intubation (RSI)

 It is employed when airway control is emergent, the airway is predicted to not be difficult,
and gastric insuffiation is contraindicated.
 RSI includes simultaneous administration of paralytic & laryngoscopy attempt prior to
bag-valve mask ventilation.
 Vasopressors should be available in the event of hemodynamic decompensation.
 All necessary equipment should be immediately available prior to intubation attempts.
Table 3.3 Necessary Equipment Prior to Laryngoscopy Attempt
 Suction equipment
 Endotracheal tube
 Usually 7.0-8.5 for adult patients
 Test balloon prior to attempt
 Stylet
 Lubricant
 Syringe for balloon inflation
 Supraglottic device
 Bag-valve-mask connected to 15 L/min oxygen
 PEEP vaIve for bag-vaIve-mask
 Laryngoscope with blade loaded and alternate sizes available
 Oropharyngeal or nasopharyngeal airway
 End-tidal CO2 detector (favor continuous over colorimetric)
 Tracheal tube introducer (e.g., Bougie)
 Monitor with pulse oximetry, BP, HR, cardiac rhythm
 Medications (analgesia, sedative, paralytic,
 Tape or ETT holder
HOW TO INTUBATE
 The "sniffing" position, achieved by flexing neck 30 degrees & extending head at adanto-
occipital joint to 20 degrees, helps align the oral, laryngeal, and pharyngeal axes (Fig. 3.2).

Figure 3.2. Anatomic axes for endotracheal intubation.

A. head in neutral position, axis of mouth (M), axis of trachea (T) & axis of pharynx (P) are
not aligned with one another.
B. If head is extended at atlanto-occipital joints, axis of mouth is correctly placed. If back of
head is raised off the table with pillow, thus flexing cervical vertebral column, axes of
trachea & pharynx are brought in line with axis of mouth.
P A G E | 14 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Placement of towels under the occiput supports maintenance of this position.

 Pre-oxygenation is achieved using highflow O2 system for at least 3 min prior to induction.
 Oropharygneal airway, nasopharyngeal airway, or jaw thrust is frequently required after
induction to maintain upper airway patency.
 Apneic oxygenation via nasal cannula is continued during laryngoscopy to ↓ desaturation.
 Laryngoscope is used to displace tongue & lift epiglottis away from glottic opening.
 Laryngoscope blades vary in size & shape.
 Blade sizes from 0 to 4 with higher the number corresponding to larger blades.
 Curved blade (Maclntosh) has a broad, flat surface, and tall flange.
 Straight blades (include Miller, Wisconsin, and Phillips) vary with regard to their width,
presence and size of flange, and shape of distal end.
 Curved blades apply upward traction to the base of tongue at vallecula, indirectly lifring
epiglotcis while straight blades lift epiglotcis directly (Figs. 3.3 & 3.4).
 Choice of specific equipment should be left to the individual practitioner.
 In general, straight blades allow visualization of larger portion of vocal cords as epiglottis
is removed from the field of view. It may be difficult to control large tongue with Miller
blade, which is relatively narrow.

Fig 3.3. Intubation with Macintosh blade, Fig 3.4. Intubation with Miller blade, used
used anterior to the epiglottis. to hold epiglottis (posterior to epiglottis).
 Video laryngoscopy should be utilized for novice users. Similar to direct laryngoscopy,
several shapes and sizes of video laryngoscope blades are available.
 As with any procedure, a verbal time-out to identify medicacion strategy, health care team
roles, and airway algorithm is recommended.
 With the patient in "sniffing" position, laryngoscope is held in left hand and blade is inserted
into the right side of mouth to the base of tongue. The blade is then moved to midline
sweeping tongue to left. Laryngoscope handle & blade should align with nasal septum.
 Tip of straight blades is advanced to epiglottis, while tip of curved is placed in vallecula.
 Vocal cords are exposed by elevating the epiglottis through lifting motion using arm &
shoulder in a plane 45 degrees from the horizontal. Wrist must be kept stiff to avoid a prying
motion that uses teeth as a fulcrum.
P A G E | 15 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Once the vocal cords are visualized, ETT is advanced from right side of mouth with the tip
directed so that it intersects the tip of the laryngoscope blade at the level of glottis allowing
the operator to view the entry of the tube into the trachea (Fig. 3.5).

Figure 3.5. Endotracheal intubation , showing correct method for intubating victim
 ETT is advanced through vocal cords until the cuff disappears.
 Remove stylet& inflate cuff with sufficient air to prevent leakage during bag valve ventilation.
 ETT must be held firmly in place at all times to prevent displacement.
 Attempts at intubation should take no longer than 1 minute.
 In patients where there is difficulty intubating the trachea, repeated attempts ↑ risk of trauma
& hypoxemia. A supraglottic airway device offers temporary airway while more skilled
provider is contacted for assistance.
Additional Techniques
 Cricoid pressure (Sellick maneuver)
 ↓ aspiration by compressing esophagus between cricoid cartilage & vertebral column
 Applied prior to intubation attempts & maintained till confirmation of correct ETT position
 Bimanual laryngoscopy using right hand to manipulate thyroid cartilage or hyoid bone may
improve visualization of the vocal cords. Assistant must apply identical pressure to facilitate
optimal visualization. Alternatively, the "BURP" maneuver (backward, upward, rightward
pressure) can be employed, though typically with less success than bimanual laryngoscopy.
 Alternate approaches to endocracheal intubation
 Video laryngoscopy, optical stylet, (supraglottic& laryngeal) airways& fiberoptic intubatn
 Video laryngoscopy-guided intubation is safe& ↓ esophageal incubations in ER& ICU.
 Supraglorcic and laryngeal tube airways are placed blindly into upper airway & form a
seal over the laryngeal inlet to ventilate and oxygenate patients while partially occluding
the esophagus allowing for directed ventilation into the trachea.
Confirmation
 Correct tube placement is established via visualization of ETT through vocal cords,
condensation within ETT , visualization of chest expansion, and auscultation over
epigastrium & lung fields during ventilation.
 Continuous end-tidal CO2 confirmation is preferred, although colorimetric end-tidal CO2
detection devices may be used.
 A chest radiograph should be reviewed to document appropriate ETT placement.
 Upon confirmation of placement, ETT is secured in place with tape or commercial device.
 Initial ventilator management is an integral component To any airway and should not be
overlooked, especially if paralytics were administered.
 Regardless of outcome, debriefing session for feedback of team members is recommended
to improve future attempts.
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4 Percutaneous Tracheostomy
Introduction
 Tracheostomy is creation artificial airway between neck surface & cervical trachea.
 There are 2 main tracheostomy techniques.
 Surgical approach uses surgical dissection to form tract between neck surface& trachea.
 Percutaneous approach has been developed, use Seldinger technique to form tract
between neck surface& trachea. Although not suitable for all patients, percutaneous has
potential advantages over surgical approach in appropriately selected ICU patients.
 A meta-analysis showed a lower rate of peristomal bleeding& postoperative infection
with percutaneous tracheostomy.
 Percutaneous tracheostomies are performed in ICU, risk of adverse events associated
with transporting these patients is reduced, and scheduling flexibility is increased.
 Lastly, some research supports percutaneous tracheostomies as the more cost-effective
tracheostomy approach for ICU patients.
 The remainder of this chapter will focus on percutaneous tracheosromies.
Indications
1. Upper airway obstruction. Surgical approach is more appropriate for upper airway
obstruction due to tumor.
2. Need for long-term mechanical ventilation.
3. Access for frequent suctioning and other airway care.
4. Treatment of severe obstructive sleep apnea when CPAP is ineffective or not tolerated.
Contraindications
 Difficult-to-palpate neck anatomy
 History of prior neck surgery or radiation.
 Patients with high ventilatory and oxygenation requirements may be better served by
surgical approach because of the reduced ability to ventilate around the bronchoscope and
likelihood of greater PEEP loss during the procedure.
 Coagulopathies
 It should be corrected prior to proceeding, although no well-validated thresholds.
 One center described low rate of complications for percutaneous tracheostomy in
significant thrornbocytopenia as long as platelets were administered before procedure.
 Hypovolemia & hypotension are relative contraindications. Hypotension can be worsened
because of significant amount of sedatives needed to perform the procedure.
Complications
1. More common early complications
 Transient hypotension and minor bleeding during the procedure.
 Massive hemorrhage from damage to innominate vessels ( but rare).
 Pneumothoraces & cardiac arrests are uncommon early complications.
 Fractured tracheal rings occur frequently, although clinical significance is unknown.
2. Late complications
 Stomal infections, bleeding, accidental decannulation, and tracheal stenosis.
 Bronchoscopic visualization reduces, although does not eliminate, older described
complications such as posterior tracheal perforation.
 Although still under investigation, there is growing evidence that ultrasound-guided
percutenous tracheosomy may improve the safety of the procedure.
 Tracheal stenosis rates vary widely in the literature, with some reports finding them to be
rare and others finding them to be more common in PT compared with surgical T.
 The use of different techniques & study population selection may explain some of the
discrepancies in the literature. When stenosis develops in patients who have undergone PT
, they tend to be subglottic in location & may be more challenging to correct surgically.
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Timing of Tracheostomy Procedure In Critically Ill Patients

 Most patients receive tracheostomies in ICU because of difficulty weaning from MV or
because they cannot protect and clear their own airways.
 Potential advantages of tracheostomy over prolonged ETT include greater comfort, ↓
sedation requirements, ↑ ability to participate in rehabilitation, and facilitated weaning.
 Optimal timing for tracheostomy in ICU patients is controversial. If prolonged intubation is
predicted at admission, a tracheostomy on day 1 or 2 may be appropriate. In most patients,
a tracheostomy is considered after 1-2 weeks of endotracheal intubation.
 The preponderance of evidence supports earlier tracheostomy over prolonged ETT, and a
recent meta-analysis including 12 studies suggested that early tracheostomy is associated
with more ventilator-free days, shorter ICU stays, ↓ sedation requirements, & improved
long-term mortality when compared to late tracheosromy.
Procedure for Percutaneous Tracheostomy
 Approaches differ slightly on the basis of operator preferences and particular brand of PT
kit used. The following description describes the Ciaglia technique modified by the use of a
single dilator with a hydrophilic coating.
1. Explain procedure including risks and benefits. Obtain consent.
2. Preprocedure US is performed in the longitudinal plane with a linear probe to identify the
cricoid cartilage and the tracheal cartilages for the identification of the puncture site. US in
transverse plane identifies aberrant blood vessels & thyroid gland and may prevent bleeding
complications. It is supported by observational data suggesting that preprocedural US is
safe & led to a change in preplanned insertion sites in a significant proportion of cases.
3. A team approach makes the procedure more efficient and optimizes patient safety.
Bronchoscopist is responsible for bronchoscopic guidance and maintenance of the airway.
He should be skilled in airway management in case of accidental excubation during the
procedure. Video bronchoscopy is advantageous because it allows the operator to see the
interior of the trachea continuously during the procedure. The nurse assists with intravenous
anesthesia during the procedure. A respiratory therapist makes appropriate changes to the
ventilator throughout the procedure. The operator performs the procedure and
communicates to other members of the team to ensure coordination.
4. Increase FiO2 to I 00%.
5. Monitor BP/ 3-5 min; monitor other (HR, pulse oximetry, and airway pressure, continuously).
6. A variety of anesthetic regimens can be used, although combinations of benzodiazepine
and short-acting narcotic or propofol work well. Traditionally, after deep sedation is
achieved, a paralytic is administered to prevent coughing. Currently, we perform most of our
procedures without a paralytic and have not had significant problems with this approach.
7. A small pad is placed under the shoulders to slighdy extend the neck. The neck is prepared
with chlorhexidine and a large surgical drape is used to completely cover the patient, with a
small opening at the neck. The operator scrubs and dons a hat, protective eyewear, a mask,
and sterile gloves and gown.
8. The operaror selects the appropriate incision site by palpating the thyroid and cricoid
cartilages and the sternal notch. Typically, the space between the first and second, or
second and third cartilaginous rings can be approached with an incision halfway between
the cricoid cartilage and the sternal notch.
9. After creating a skin wheal with lidocaine, the needle is raised to form a 90-degree angle
with the trachea. The tract is anesthetized and the needle is advanced slowly while
continuously aspirating. Air bubbles will appear when the needle penetrates the trachea.
10. 1.5-2 cm incision through skin & superficial SC tissue is made either horizontally or vertically.
11. A small, curved Kelley clamp is used to dissect a tract down to the trachea.
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12. Bronchoscopist carefully withdraws ETT over bronchoscope until tip lies just below vocal
cords & tracheal lumen is visible. Firm pressure is applied to trachea with Kelly clamp to
confirm placement between the appropriate cartilaginous rings.
13. Under continuous bronchoscopic visualization, catheter-over-needle apparatus is advanced
through skin incision, between selected tracheal rings& into trachea. Catheter is advanced
off the needle into trachea while needle is withdrawn.
14. The guidewire is threaded through the catheter coward the carina.
15. The catheter is removed, leaving the guidewire in place.
16. A punch dilator is advanced through the trachea and then removed.
17. Next, the curved dilaror is inserted over the wire inro the trachea. Remove dilator.
18. Load cracheoscomy tube onto dilator and advance over guidewire. PT tubes have tapered
ends that allow for easier tracheal insertion.
19. Next, the bronchoscopist removes the bronchoscope from the en do tracheal cube and
quickly inspects through the tracheosromy tube to ensure proper placement. The patient is
reconnected ro mechanical ventilation through tracheosromy tube.
20. The bronchoscopist can inspect the trachea above the tracheostomy tube to rule out active
bleeding, suction blood and secretions, confirm the cracheosromy ballon is completely in
the airway, and then remove ETT.
21. Tracheostomy tube is sewed into place, secured with ties, & dressed appropriately.
22. The tracheostomy tube is changed on day 10 -14.

Other Techniques
 Other techniques of percutaneous dilatational tracheostomy include Griggs method, Ciaglia
Blue Rhino technique, Frova's single-step screw-type dilator technique (PercuTwist),
balloon dilatational technique (blue dolphin), and Fanroni translaryngeal technique.
 A systematic review and meta-analysis could not demonstrate the superiority of any
technique, although it was found that the translaryngeal technique was associated with more
complications, and there were more frequent needs to convert to an alternative technique.
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5 Chest Tube Insertion

Definition
 Thoracostomy refers to the insertion of a hollow, flexible tube into the pleural space.
Indications
1. Drainage of air or fluid from the pleural space.
2. Administration of therapeutic pleural agents such as sclerosants.
Contraindications
1. Bleeding diatheses (PT or PTT > 2 times normal, platelets <50,000, or creatine > 6) should
be corrected in nonemergent settings.
2. History of thoracic surgery or pleurodesis on the side of proposed insertion requires
additional caution, as lung tissue can become adherent to chest wall after these procedures,
resulting in lung injury or hemorrhage during insertion. Image guidance or operating room
placement may be required.
Complications
 they are less studied than complications associated with other thoracic procedures.
 The site of placement (ER, ICU, or OR) & circumstances of placement (emergent or elective)
are important.
 One study looked at complications from chest tubes inserted by pulmonary fellows with
attending supervision. Many, although not all, of patients were in ICU. The largest number
of chest tube placements in study were for ventilator-associated or iatrogenic PTX.
 Classified as early (1st 24 hours) or late and by tube size (≤14 F or larger).
 Early: tube not being placed in pleural space, nonfunctional tubes, & lung laceration.
 Late complications: nonfunctional tubes, site infection, and leak around tube.
 All complications were more common with small tubes (36%) versus larger tubes (9%).
 Others : hemothoraces from intercosral vessel injury or intra-abdominal placement.
 Infections associated with it are uncommon. Prophylactic antibiotic use is supported by one
meta-analysis in trauma patients, but is probably not justified in other clinical situations.
Imaging
 Confirmation of the suspected pleural process prior to tube placement is imperative to avoid
inadvertent damage to lung or other organs and attendant morbidity and mortality.
 In cystic or emphysematous lung dse, large bullae can mimic PTXs on upright radiographs.
 Tumors with associated atelectasis can be mistaken for pleural effusions.
 In the postoperative setting, diaphragmatic paralysis or injury with resultant diaphragmatic
elevation on routine chest radiograph may be confused with significant pleural effusion.
 Attempted chest tube placement can cause significant morbidity in these situations.
 Lateral decubirus films may help confirm the existence of free-flowing air or fluid.
 If any doubt exists, or in difficult cases, chest CT or ultrasound should be performed.
Site Selection
1. Physical examination
 Findings consistent with pleural effusion include decreased breath sounds on
auscultation, dullness to percussion, loss of tactile fremims, and asymmetric chest wall
expansion with inspiration.
 Findings consistent with pnewnothoraces include hyperresonance and decreased
breath sounds. In tension PTX, shift of mediasrinal structures may be observed.
2. For free-flowing air or fluid, chest tubes are traditionally placed in the "Triangle of Safety,"
delineated by lateral border of the pectoris major or anterior axillary line (anteriorly), lateral
border of latissimus dorsi or middle axillary line (posteriorly) & 5th intercostal space
(inferiorly). Alternatively, 2nd interspace in midclavicular line can be used for drainage of
PTXs with small, percutaneous catheters.
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3. Loculaced air or fluid collections often require image guidance by US or fluoroscopy for
optimal tube placement. A good understanding of the overlying anatomy is requfred in this
situation to prevent damage to anatomic structures during tube insertion.
4. Avoid any overlying cutaneous abnormalities such as cellulitis, candidiasis, burns or wounds
Choosing The Optimal Tube Size And Approach
 The blunt dissection and guidewire (also known as Seldinger) methods are the 2 most
commonly used techniques for tube thoracostomy (Table 5. 1).
 Different indications dictate appropriate tube size and approach.
 Chest Tube Sizes
 reported in French (F), where 3 F equals 1 mm of outer diameter, so that 24 F = 8 mm.
 Large bore CT (LBCT > 20 F) were used for most pleural diseases requiring drainage.
 Small bore CT (SBCT=8-14 F) are less painful & easier to place with few complications.
 SBCT are equally as efficacious in PTXs (1ry, 2ry, traumatic& iatrogenic) and malignant
pleural effusions. Recent data suggests that SBCT may be as effective as LBCT for
managing infected pleural spaces.
 Indications for LBCT include bronchopleural fistulae, PTX in MV patients, & hemothorax.
 SBCT are not sufficient to adequately drain air from the space in bronchopleural fistulae
because amount of air leak is too large. The same is often true in patienrs on PPV. 20-
28 F tube is preferred in these instances & can be placed either by guidewire technique
or by blunt dissection depending on the degree of air leak & clinical situation.
 Hemothoraces (pleural fluid hematocrit at least 50% of peripheral blood hematocrit)
require at least 32 F tube to prevent tube blockage and allow adequate drainage.
 Loculared air or fluid collections are often more readily approached by realrime, image-
guided, guidewire approach. Anaromically, free flowing air will accumulate anteriorly &
apically in supine position, therefore, chest tubes placed for simple PTXs are placed in
anteroapical direction. In contrast, fluid accumulates in posterior & basal diaphragmatic
gutters, so chest tubes placed for effusions are placed in inferoposrerior direction.
Table 5.1 Chest Tube Size & Insertion Method by Indication

a = Based on clinical situation and expertise with available procedures.

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Procedure Steps
A- Blunt Dissection Approach
1. Explain benefits, risks, alternatives, and obtain consent.
2. Gather necessary equipment (Table 5 .2). Kits prepared ahead of time can simplify it.
3. Patient is placed in semirecumbent position with head & shoulders about 30 degrees off
bed. Ipsilateral arm is placed above head for exposure of axilla& to ↑ distance between ribs
Table 5.2 Materials Necessary for Blunt Dissection Thoracostomy

A=Chlorhexidine or Betadine. B= to anesthetize skin. C= to anesthetize tract and pleura.

4. Clean the area with antiseptic and sterilely drape.
5. After appropriate site & corresponding inferior rib identification, SC infilrrate 1% lidocaine
without epinephrine (Fig. 5. 1).
i. Next, inject lidocaine down to appropriate rib. Move needle superiorly, over the rib in a
stepwise fashion, aspirating as you advance, stopping to inject lidocaine every 1 to 2 mm.
ii. Confirm entry into the pleural space with aspiration of air for pneumothoraces or fluid for
effusions by aspirating the syringe as it is advanced.
iii. Next, withdraw syringe while aspirating until no air or fluid return & inject lidocaine to
generously anesthetize parietal pleura. 25-40 mL achieve adequate local anesthesia.

6. Make skin incision through SC tissue that is wide enough to insert a finger (1 - 2 cm).
7. Using medium-sized Kelly clamps, bluntly dissect to the cop of the selected rib. This is done
by applying forward pressure with clamps while opening, relaxing forward pressure while
closing, and repeating as necessary. Once rib is reached, continue with blunt dissection
over the top of rib. A rush of air or fluid signals entry into pleural space. When entering , do
not push too far, to prevent lung injury.
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8. Place finger through tract into the pleural space, sweep circumferentially around the entry
site to confirm the lack of adherent lung in the direction of chest tube placement.
9. Clamp the end of the chest tube with a Kelly clamp and guide into the pleural space.
Direction is generally anteroapical for drainage of air and inferoposterior for drainage of fluid.
Depending on body wall size, insert to 10 to 12 cm at the skin.
10. Attach external end of tube to drainage system. Drainage of air or fluid as well as evidence
of respiratory variation suggest proper placement into the pleural space.
11. Securely suture tube to prevent dislodgment. Some operators place mattress suture at time
of insertion, leaving the ends loose, which they use to close incision at time of tube removal.
12. Using occlusive gauze to seal the skin around tube is controversial. Some authors argue
that this leads to skin breakdown.
13. Dress area with a generous amount of gauze and tape.
14. Check chest x-ray for proper placement.
15. Check on chest tube output, signs of respiratory variation, and the presence of air leaks at
least daily. Evaluate site for bleeding or signs of infection.

B- Guidewire Approach
 Note: this approach may vary slightly, depending on kit used.
1. Obtain consent, position patient, obtain materials as per Table 78.2 & guidewire insertion
kit & prepare area as for blunt dissection approach. Multiple companies make preassembled
kits containing most of the necessary materials; check kit labeling to ensure all materials
are available.
2. Anesthetize rib & pleural space in selected interspace using technique described above.
3. Insert the introducer needle just superior to the appropriate rib. Stop just past the point
where fluid or air is aspirated.
4. Remove syringe & cover needle opening with finger to prevent excessive air entry. Introduce
wire into pleural space. Remove needle from patient, leaving guidewire in pleural space.
5. Make a small skin nick at the wire entry site to allow introduction of dilators and chest tube.
6. Using sequential dilators, dilate tract into pleural space, tactile feedback is present when
dilator has punctured through parietal pleura (can be described as a giving way, or "pop.")
Dilators should be advanced only a small amount (1 cm) beyond this point to ensure proper
tract formation, while using caution to avoid further advancement potential harm to the lung.
7. Introduce chest tube over the wire into the pleural space. Confirm that all openings are in
pleural space (depending on body wall size, typically at 8-12 cm at the skin). Remove wire.
8. Connect chest cube to drainage system.
9. Suture tube in place and dress with gauze and tape.
10. Check chest x-ray for proper placement.

Drainage Systems
 The most common drainage system for hospitalized patient is 3 bottles drainage system.
 The functions of 3 bottle system are most commonly incorporated into one container today.
 1st column serves as drainage repository, collecting fluid that drains from pleural space.
 2nd column serves as a water seal, which prevents retrograde air entry into pleural space.
 3rd column allows for adjustment of the negative pressure applied to the pleural space.
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Guidelines For Chest Tube Removal

 Timing of removal: after resolution of the initial indication for placement.
 For PTXs, a fully expanded lung with resolution of the air leak
 For pleural fluid, a maximum drainage of 100-150 ml/day.
 There is no consensus regarding timing of pulling during respiratory cycle, nor regarding the
practice of tube clamping, placing on water seal, or continuing suction until removal.
 Our approach is to remove from suction, that is, place on water seal once the indication for
placement has resolved. We then perform a follow-up chest x-ray 12-24 hours later. If there
is no significant air leak or reaccumulation of air or fluid, the tube is removed. In difficult
cases, tube can be clamped for 2-4 h, with moniroring & repeat CXR to confirm stability.
Removal Steps
1) Gather materials- suture removal kit, gauze, 1.0 silk suture, needle driver, scissors, 10-mL
1% lidocaine without epi, 10-mL syringe with 25-g needle, cape.
2) Patients can be given a small amount of narcotic prior to removal where clinically indicated.
3) Remove sutures
4) Have patient make a full inspiration & pull tube out quickly while occluding the track with
gauze in your other hand.
5) Approximate the wound.
i. For LBCT: by tying previously placed mattress suture or by placing new suture.
ii. For SBCT: by simple occlusive dressing should suffice.
6) Follow-up CXR after 12-24 h (or sooner, if indicated) to rule out recurrence of PTX or pleural
fluid.
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6 Paracentesis
Indications
 Diagnostic paracentesis: in patients with suspected SBP or ascires of unknown cause.
 Therapeutic paracentesis: in patients with significant SOB or abdominal discomfort TO
alleviate symptoms.
Contraindications
 DIC.
 Small bowel obstruction (NGT should be placed prior to procedure).
Complications
 Rare and usually without clinical consequence.
 Ascitic fluid leak
 Causes: largebore needle , large skin incision , or Z-track has not performed.
 Controlled by repeated paracentesis to relieve tension in abdomen if ascitic fluid cannot
be decreased with diuretic ttt.
 Perforation if the needle punctures the bowel wall. Even if perforation does occur, it rarely
results in clinically significant secondary peritonitis.
 Bleeding
 Causes: inadvertent puncturing of artery or vein & in renal diseases
 It is uncommon , but can be fatal.
 Prevention by selecting the site that avoids inferior epigastric vessels.
 Treatment is usually supportive, and rarely requires further intervention.
Site detection & Preparations
 Many patients undergoing paracentesis (especially those with underlying liver disease) are
coagulopathic and thrombocycopenic at time of procedure, however no need to correct
coaguloparhy or transfuse platelets prior to procedure.
 With Hx of prior abdominal surgery ( the area of the surgical scar should be avoided)
 Patients with urinary retention should undergo bladder catheter insertion prior to procedure.
 The most common sites of paracentesis are abdominal left lower quadrant, suprapubic, or
right lower quadrant regions. Physical examination, particularly percussion & examination
for shifting dullness, can help determine ideal site.
 When available, US should be used to aid in selecting the ideal procedure site.
 When performing a paracentesis, the catheter should not be inserted through infected skin.
 Once the site has been determined and all present agree on the identification of the site,
and the procedure being performed, one can proceed with paracentesis.
Steps (US guidance, if available, is the preferred method)
1. Site identification by US where ascitic fluid is present& no bowel or solid organ then mark it.
2. At a minimum, sterile gloves & mask with face shield are worn. Additional sterile equipment
should be used according to hospital policy.
3. The patient should be placed supine with the head of bed slightly elevated.
4. Prepare site with antiseptic solution (chlorhexidine or Betadine)& sterile drape is placed.
5. Using 22 or 25 gauge needle, local anesthesia with 1 % lidocaine is injected, starting with
SC wheel followed by deeper anesthesia. While injecting the deeper tissues, maintain
continuous negative pressure on the syringe, and inject lidocaine periodically. Maintain an
angle of entry perpendicular to abdominal wall.
6. When ascitic fluid is obtained, inject lidocaine around the peritoneum.
7. Ideally, a catheter specifically designed for paracemesis (Caldwell needle) should be used,
although large-bore IV catheter may be used. Attach 10-mL syringe to the catheter.
8. Using scalpel, make small incision in skin at insertion site to facilitate insertion of catheter.
9. Using Z-tract technique, pull skin 2 cm caudad prior to inserting catheter. This causes the
tract to close, and thus reduces the rate of leakage when the catheter is withdrawn.
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10. Insert catheter slowly, with continued -ve pressure on syringe. When ascitic fluid is obtained,
stop advancing needle/catheter system, advance catheter over needle, & remove needle.
11. Obtain adequate amount of ascitic fluid for diagnostic studies (at least 25 mL). Culture
bottles should be inoculated at the bedside to increase yield.
12. If therapeutic paracencesis is performed, tubing should be connected from to vacuum bottle.

Diagnostic Considerations
 Diagnostic studies performed on ascitic fluid are determined by clinical situation (Table 6.1).
 Other less common diagnostic studies include triglycerides (chylous ascites), amylase
(pancreatic ascites), mycobacterial culture (tuberculous ascites) and bilirubin (bile leak).
 If there is concern for SBP, fluid should be sent for cell count and culture.
 Cell count >250 polymorphonuclear cells/mm3 without 2ry source of infection
(perforated viscous) or a grossly bloody cap suggests SBP.
 The definitive diagnosis is based on positive culture results. In patients with findings
suggestive or diagnostic of SBP, empiric ttt should be initiated with 3rd cephalosporin
(cefcriaxone or cefotaxime) or fluoroquinolone (ciprofloxacin or levofloxacin) pending
culture results and sensitivities.
 The routine use of albumin infusion (6 - 8 g /L fluid removed) after large-volume paracentesis
(≥ 5 L) is controversial but has been shown to ↓ circulatory dysfunction& precipitation of
hepacorenal syndrome.

Table 6.1 Common Clinical Situations & Pertinent Studies for Ascitic Fluid

SBP= spontaneous bacterial peritonitis;

SAAG (serum ascites albumin gradient) = (serum albumin) − (ascites albumin)
TP= total protein.
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7 Lumbar Puncture
Indications
 It is useful to remember the old adage, "If you consider an LP, you should do it."
 Delay in the diagnosis of meningitis leads to inappropriate ttt & difficulty in later establishing
the diagnosis when the patient fails to improve.
 Prompt diagnosis of SAH results in early ttt of aneurysms & prevention of rebleeding.
Table 7.1 Common Indications for Lumbar Puncture
o Diagnosis of bacterial, viral, fungal, parasitic, or mycobacterial meningitis
o Diagnosis of carcinomatosis meningitis
o Diagnosis of subarachnoid hemorrhage
o Assessing CNS & meningeal inflammation for diagnosis of conditions, including
multiple sclerosis, Devic disease, & neurosarcoidosis
o Measuring CSF protein levels for diagnosis of Guillain- Barre syndrome
o Measuring intracranial pressure for diagnosis of pseudotumorcerebri
o Removing CSF for ttt of pseudotumor cerebri or normal-pressure hydrocephalus

contraindications to LP
 Coagulopathy: LP may cause epidural hematoma leading to compression of cauda equina.
 No studies have established cutoffs, but INR>1.4, PTT>50, and/or platelet
<100,000/mm3 are corrected with FFP and/or platelet transfusions prior to LP.
 Those targets can be lowered in hematologic disorders & thrombocyropenia resistant
to correction, and the risk to benefit should be assessed individually.
 With altered mental status, papilledema, focal neurologic deficit, or if there is suspicion for
SAH, head CT should be obtained prior to LP.
 Signs of herniation and large posterior fossa masses preclude an LP because the pressure
drop following CSF removal can precipitate tonsillar herniation.
 Local skin infections
 Known spinal cord tumors
 Recent neuro-surgical instrumentation.
Complications
 Post LP headaches
 Place your in supine position for 1 h to ↓ this headache immediately after LP.
 Fluids, caffeine, acetaminophen, & NSAIDs are effective in most post-LP headaches.
 headache worsens with sitting up or standing & resolves when lying down. If headaches
persist > 5 days, epidural blood patch may be required
 Dural tear & persistant CSF leakage
 Supine position does not prevent pose-LP headaches due to dural tear& persistent leak.
 Reduced by appropriate spinal needle selection and proper technique.
 Rarely, paresthesias or pain referred to one leg.
 During the procedure, this indicates impingement of nerve root, & spinal needle should
be retracted, repositioned further toward midline, & then reinserted.
 Careful controlled insertion of needle helps avoid such nerve damage.
 When symptoms of cord compression occur following procedure,
 There is concern for intraspinal epidermoid tumor or epidural hematoma.
 MRI or CT & neurosurgical consultation are mandatory if any mass is discovered.
 Other rare complications
 Cerebral herniation syndromes
 Spontaneous rupture of subarachnoid arterial aneurysm. These can be avoided by
careful physical examination and, when indicated, brain imaging prior to LP.
P A G E | 27 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Technique
1. Informed Consent must be obtained prior to performing LP according to policy of institution.
2. Collect the Supplies to gather the following:
 sterile 20-gauge or smaller spinal needle with a styler,
 sterile 25-gauge needle and syringe for local anesthesia, 1-2% lidocaine solution
 topical antiseptic, sterile drape and gauze,
 sterile manometer, sterile surgical gloves, and tubes for collection of the fluid.
 With more experience, smaller gauge spinal needle, preferably a Sprotte needle, helps
reduce post-LP headaches.
 In morbidly obese patients, needle longer than the standard 3.5 in may be necessary.
3. Position the Patient
 Lateral decubitus positioning to accurately measure intracranial CSF pressure. Patient
is positioned such that hips& shoulders are squarely above one another, back is parallel
to wall,& patient is curled up with knees& chin tucked deeply into torso (Fig. 7.1).
 Sitting position aids in determining midline of spine,↑space between spinous processes,
& may ↑ filling of lumbar cistern, thus improving chance of successful LP. Patient is
positioned such that back is straight& arched outward, with chin tucked deeply into chest.
 Choice of positioning is determined by indications, patient comfort& operator experience.
4. Find the L4-5 Space
 In most adults, spinal cord ends at L1 (in few adults it ends at L2).Therefore, L3-4, L4-5,
& L5-S1 spaces represent safe and effective locations ro insert a spinal needle.
 In most adults, line (Tuffier, Fig. 7.1) drawn across tops of both iliac crests crosses L4
spinous process or L4- 5 space. Use spinous space on or immediately below Tuffier line.
 Attention to superficial anatomy helps ensure appropriate placement of spinal needle.

Figure 7.1. Positioning the patient. Tuffier line is indicated by the dashed line.
5. Scrub & Anesthetize the Space
 Scrub the location with antiseptic solution (chlorhexidine or Becadine). There are
adequate data that chlorhexidine is safe alternative to Betadine& does not ↑ risk of
neurologic complications.
 Using (sterile gloves, sterile drape at selected location with lumbar space exposed).
 Lidocaine is injected SC & 2 cm deep along the expected track of spinal needle.
6. Insert the Spinal Needle
 Spinal needle with its styler in place should then be introduced through skin in a tract
that is angled toward navel or about 15 degrees cephalad.
 Needle must be entered at midline & orthogonal to plane of the back.
 Bevel initially perpendicular to long axis of body to ↓ tearing of dura& post-LP headache.
7. Advance the Spinal Needle
 After penetrating skin & SC fat, needle should traverse supraspinatus ligament,
interspinous ligaments, ligamentum Ravum, epidural space, & finally dura (Fig. 80.2).
P A G E | 28 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Severe pain may indicate being away from midline.

Figure 7.2. The ideal tract of the spinal needle.

 Once needle has been inserted about 3-4 cm, or if a "pop" or sudden loss of resistance
is experienced, remove stylet to check for CSF If no CSF is obtained, replace the styler
& advance needle another 2-3 mm and remove styler again to check for CSF.
 Once lumbar cistern has been entered, CSF should flow freely through spinal needle,
and stylet can be replaced to limit CSF leakage until it can be collected or manometer
can be attached to measure CSF pressure.
 Hitting bone while inserting needle indicates either incorrect angling of needle or skin
has been entered away from midline. When this occurs, retract the needle to SC tissue,
reposition its angle so thar it is closer to being 15 degrees or less cephalad & more
directed toward midline, and then enter again. This procedure can be repeated few times
until tract free of bone is achieved. After several attempts at 1st lumbar space, using L3-
4 space (space immediately above the Tuffier line) is permissible, but using any higher
spaces risks inserting the needle into tip of spinal cord.
 On occasion, LP needle is inserted to hub without obtaining CSE This problem can be
avoided by using a needle that is sufficiently long, ensuring correct entry point & angle,
and occasionally by sitting up the patient.
 Fluoroscopic or US guidance may be necessary in obese or uncooperative patients.
8. Measure CSF Pressure & Collect Fluid
 Once needle has entered lumbar cistern, manometer can be used to measure "opening"
CSF pressure.
 This measurement is accurate only when patient is in lateral decubitus position & relaxed
enough to allow visible respiratory excursions of CSF in manometer.
 Normal pressure is 8 - 22 cm H20, although it can be slightly higher in normal obese
patients or in patients on positive pressure ventilation.
 The fluid in manometer should be collected for CSF analysis. Sufficient CSF should be
collected for all of the necessary tests, and additional fluid should be collected & saved
in case further testing is desired.
 If the opening pressure >50, the minimum amount of fluid necessary should be collected.
P A G E | 29 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 If CSF appears bloody initially & later it clears, this suggests a "traumatic" tap, whereby
the needle had punccured a vein en route to lumbar cistern.
 Xanthochromia, or a yellowish tint to fluid, indicates either blood products > 12- 24 hours
old in subarachnoid space or greatly elevated protein levels.
 Careful replacement of stylet before & after collection helps avoid excessive CSF leak.
 After CSF collection, closing pressure can be measured if necessary.
 Replace stylet before removing the needle.
 Samples collected should be sent for cell count with differential, chemistry, & Gram
stain/culture; additional studies may be included based on suspected underlying
diagnosis . CSF analyses are listed in Table 7.2.
 Of note, samples should be analyzed as soon as possible after collection, as cell counts
are prone to decline markedly over the course of hours.

Table 7.2 Common Tests for CSF Analysis

(ordered based on clinical concern)
o Complete cell count and differential
o CSF glucose and protein levels
o Gram stain and bacterial, fungal, and mycobacterial cultures
o Cytology and wet mount inspection
o Spectrophotometer analysis for xanthochromia
o CSF lgG & albumin, serum lgG & albumin levels to determine
IgG index =(CSF lgG/CSF albumin)/(S. lgG/S. albumin)
o Oligoclonal bands
o PCR tests for HSV, VZV, EBV, CMV, enteroviruses, TB,
arboviruses, & toxoplasmosis
o Other: cryptococcal antigen testing, syphilis (VDRL or FTA-ABS),
cysticercosis, histoplasmosis, coccidioidomycosis, & malaria

VDR=Venereal Disease Research Laboratory

FTA-ABS=fluorescent treponemal antibody absorption
P A G E | 30 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

8 Thoracocentesis
Definition
 Inserting a needle and/or catheter into pleural space for aspiration of air or fluid.
Indications
1. To evaluate pleural effusions of unknown etiology.
2. To exclude empyema or complicated parapneumonic effusions in febrile patients with
pleural effusions.
3. Therapeutic removal of air or fluid from the pleural space.
Relative Contraindications
1) Uncooperative patient.
2) Cutaneous abnormality such as an infection at the proposed sampling site.
 Note. There are no data to confirm that uncorrected bleeding diathesis (PT or PTT > 2 times
normal, INR > 1.5, platelets <50,000, or creatine >6) ↑ risk of hemorrhagic complications.
 However, one must consider risks & benefits for each procedure before proceeding without
correcting coagulopathy or thrombocytopenia.
Complications
 Major complications such as pneumothorax, significant bleeding or REPE
 Minor complications, such as pain or failed procedure/dry tap.
 Operator experience& US guidance↓ risk of complications, emphasizing importance of
having proper background knowledge& experience in performance of procedure.
 REPE is a feared, but rare complication of therapeutic thoracemesis. The pathophysiology
is unclear, bur has been hypoth esized co be due to excessive negative pleural pressure
during pleural drainage procedures. Symptoms include anterior chest or neck pain/pressure
and intractable cough. Therapy is supportive.
 Factors affect hemorrhagic complications are number of needle passes & location on chest.
 Although guidelines recommend correcting thrombocyropenia (platelets <50,000) or
coagulopathy (INR > 1.5), there are little data to support this practice, and growing literature
suggests it is unnecessary. We recommend taking into account the risk to benefit ratio for
each case individually when considering correcting bleeding risk.
History
1) Measure coagulation factors in patients with risk factors or Hx suggestive of bleeding.
2) Screen for allergies to local anesthetics.
3) The urgency of procedure (benefits of rapid diagnosis & ttt of empyema/parapneumonic
effusion or relief of tension PTX) can help guide the need for correction of coagulopathy or
thrombocytopenia or holding of anticoagulant medications.
Site Selection
1. Physical examination findings consistent with pleural effusions include ↓ breath sounds,
dullness to percussion, loss of tactile fremitus, & asymmetric diaphragmatic excursion.
2. Lateral decubitus film, ultrasound, or CT of chest can exclude alternative diagnoses that
mimic pleural fluid on standard PA and lateral chest radiographs.
3. Using ultrasound for site selection is recommended by British Thoracic Society & considered
standard of care in America. US-guided thoracentesis can be performed safely on MV.
4. Radiographic and physical examination can be used for site selection if US is not available,
but at least 1 cm of fluid should layer out on lateral decubitus film to safely sample effusion.
5. US guidance is recommended if two unsuccessful, or "dry caps" are performed.
P A G E | 31 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Procedure
1) Explain the procedure, risks, benefits, alternatives; answer questions and obtain consent.
2) There are a number of commercially available procedure kits that simplify gathering of
needed equipment (Table 8.1 lists necessary equipment for thoracentesis).
3) Sit patient up with arms draped forward over a bedside table or procedure stand to maximize
the intercostal space and amount of fluid in the posterior gutter. If patient is intubated (or
unable to sit up), our preference is to roll him so that intended side for thoracentesis is up.
4) With US, identify diaphragm between mid-scapular line& posterior axillary line. Go 1 rib
space up. Mark site where at least 1.5 cm of fluid is between chest wall & underlying lung
(Fig. 81.1).
5) If US is not available, percuss down the chest until area of dullness is reached and go one
interspace below area of dullness. Avoid the paraspinal area to avoid incercostal vessels.
Do not go below 9th rib interspace to avoid splenic or hepatic laceration (Fig. 81.2).
6) Don a mask and sterile gloves.
7) Cleanse the chosen site with an appropriate annsepnc (chlorhexadine or beradine).
8) Cover surrounding area with sterile drape or towels.
9) Use 25-gauge needle attached to 10-mL syringe filled with lidocaine to create skin wheal
over the top of the appropriate rib.
10) Use 22-gauge needle to go through the wheal while aspirating. It is important to keep needle
perpendicular to skin surface at all times. Advance by few millimeters at a rime, injecting
lidocaine with each stop, until fluid is aspirated. At this point, withdraw slowly until flow of
fluid stops & inject the remainder of lidocaine to properly anesthetize pleura. Remember,
skin, top of rib, and parietal pleura require the most anesthetic.
11) If using needle without catheter device, insert needle into previously anesthecized tract until
fluid is aspirated. Collect fluid for studies.
12) If using needle with catheter device, first make skin nick with a scalpel. Insert needle &
catheter device through skin nick and advance while aspirating, making certain to keep
device perpendicular to skin surface and in line with the anesthetized tract. After fluid is
aspirated, advance needle & catheter 2-3 mm further into pleural space and then advance
catheter off needle into pleural space while preventing the needle from advancing further.
Remove the needle, leaving the catheter in place.
13) Using large syringe, remove fluid for studies. Samples for chemical evaluation are typically
sent in mint green top blood tube, and cell counts in lavender top blood tube. Cytology and
microbiology samples for study can be sent in small, sterile containers. Although submission
of large amounts of cytology fluid is commonly advocated, the yield for diagnosis appears
to be independent of fluid amount submitted.
14) If performing therapeutic procedure, connect catheter to syringe and collection bag system.
Vacuum bottles or wall suction devices should not be used for thoracentesis, as this
associated with ↑ risk for PTX & may ↑ risk for re-expansion pulmonary edema (REPE).
15) Cough is expected as underlying atelectatic lung re-expands. Shoulder/scapular pain or
unilateral posterior chest pain may be due to catheter induced irritation of diaphragm or
pleura. Slowing rate of fluid removal or temporarily stop it until pain improves is acceptable.
16) It is recommended to stop procedure when patient develops symptoms of intractable cough
or anterior chest/neck discomfort (thought to be signs of ↑ negative pleural pressures) or
after approximately 1,500 mL of pleural fluid is removed to avoid REPE. Alternacively, one
can monitor pleural manometry, if available, and keep pleural pressures < -20 cm H20.
17) Remove catheter during exhalation, as this is when intrathoracic pressure is positive,
decreasing the likelihood of entrainement of air, that is, PTX. Cover site with sterile dressing.
18) Chest x-rays are commonly performed to exclude PTX, but data suggest thar they may not
be needed unless there are concerning symptoms or problems with the procedure that
suggests that the lung may have been punctured.
P A G E | 32 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Table 8.1 Materials Necessary for Thoracentesis

A=Chlorhexadine or Betadine. B=To anesthetize skin. C=To anesthetize tract and pleura.
D=For chemical analysis. E=For cell count. F= For cultures and cytology.

Figure 8.1. US image depicting diaphragm& 1.5 cm of fluid between chest wall & lung

Figure 8.2. appropriate needle location for sampling of pleural effusion.

P A G E | 33 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

9 Pericardiocentesis
Cardiac Tamponade
 fluid accumulates in pericardia! space& prevents filling of cardiac chambers.
 In acute situation , fluid may be bloody, purulent, inflammatory, or rarely transudative.
 It is a clinical diagnosis classically marked by Beck's triad(hypotension, jugular venous
distension& muffled heart sounds).
 These signs are a result of ↓ SV & VR from pressure effect of fluid in the pericardia! sac.
 Additional signs: pulsus paradoxus (↓SBP > 10 during inspiration), electrical alternans &
low voltage on ECG.
 The most common cause of tamponade is malignancy.
Table 9.1 Causes of Cardiac Tamponade in ICU
 Neoplasm
 Infectious pericarditis (viral, bacterial, tubercular, parasitic)
 Uremia
 Post MI with ventricular rupture
 Complication of catheter-based procedure (pacemaker lead
insertion, central line placement, or coronary catherization)
 Compressive hematoma after cardiothoracic surgery
 Traumatic hemopericardium
 Systemic autoimmune diseases (SLE, RA)
 Aortic dissection
 Drugs (hydralazine, procainamide, isoniazid, minoxidil,
anticoagulant)
 Idiopathic
 It is recommended to perform a transthoracic echocardiogram to confirm the presence of
effusion & ideal window for needle insertion, before proceeding to pericardiocentesis.
 In postcardiac surgery patient, transesophageal echocardiogram may be preferred because
of the possibility of a loculared, posterior effusion (Fig. 9.1).
 The amount of fluid necessary to cause camponade varies & depends on rapidity of
accumulation.
 In cases of malignant effusions, fluid may collect gradually and stretch pericardia! sac to the
point that it contains over 1 L of fluid before creating tamponade.
 In contrast, trauma may quickly lead to tamponade with only 100-200 mL of fluid or blood.
 The decision to perform a bedside pericardiocencesis is based on hemodynamic instability
& development of obstructive shock.
 Intubation should be avoided if possible because it will worsen shock caused by tamponade.
 Vasopressors have limited capacity to improve organ perfusion in this setting.
 The procedure entails insertion of a needle into pericardia! sac, followed by insertion of
guidewire, successive dilations, & placement of pericardia! drainage catheter.
Indications of Pericardiocentesis
 Emergent treatment of cardiac tamponade.
 Diagnostic or therapeutic procedure for pericardia! effusions.
Safety Considerations
 The safety of the procedure is dramatically improved with use of echocardiography to guide
needle placement and by personnel with experience in performing procedure (Fig. 9.2) .
 Ideally, to reduce the risk of complications, the procedure should be performed using real-
time echocardiography or fluoroscopy (risk = 1.3-1.6% of procedures).
 This increases to 20.9% in emergent situations, without echocardiography.(Fig. 9.3)
P A G E | 34 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Figure 9.1. PLAX echo of large posterior pericardial effusion (PEF).

Pericardiocentesis is being undertaken with echo guidance. A: large posterior pericardial fluid
collection B:Agitated saline is injected via pericardiocentesis needle. There is now echo
contrast in previously clear pericardial space confirming that needle is in pericardium

Figure 9.2. Pericardiocentesis

Figure 9.3. Echocardiogram from subcostal position in moderate pericardial effusion.

Note the approximate 1.5-cm distance between pericardium & RV free wall (arrows), implying
significant distance between pericardium& heart, which may confer a decreased risk of
pericardiocentesis if approached from the subcostal position.
P A G E | 35 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Complications of Pericardiocentesis
1. Myocardial injury & laceration, ventricular perforation, coronary artery laceration.
2. Pneumothorax 6. liver& stomach lacerations.
3. ventricular arrhythmias 7. Air embolism.
4. Infection. 8. vascular injury (internal mammary a),
5. Peritoneal puncture, 9. Failed drainage, & death.
 Major complications such as ventricular rupture and death are rare.
Contraindications to Pericardiocentesis
 Relative: (coagulopathy, INR > 1.4), (platelets <50,000) & small effusions in posterior,
loculated space.
 Absolute: Aortic dissection associated with hemopericardium & patients with this condition
should have immediate surgery.
Types of Pericardiocentesis
A. Surgical procedure such as subxiphoid pericardiostomy
 It is preferred in cases where effusions are likely malignant & time is available (Fig. 9.4).
 It allows for a pericardia! window, which reduces the rate of recurrence.
B. Bedside Pericardiocentesis
 Leaving a catheter in place for prolonged drainage after pericardiocentesis has a similar
rate of recurrence as placing a pericardia! window.
 Catheter drainage is typically left in place for 24-48 hours as rate of fluid output
diminishes to < 25 ml/day.
 The following steps outline it (ideally performed with realtime US guidance).
Steps For Bedside Pericardiocentesis
1. Gather the necessary equipment, which available in prepackaged pericardiocemesis kit.
a) Antiseptic (betadine or chlorhexidine) f) Needles(18 ga, 1.5 in); (25 ga, 5/8 in)
b) Local anesthetic (lidocaine 1 %) g) Spinal needle, 18 ga, 7.5 to 12 cm
c) Sterile drapes,gown, cap& face mask h) Guidewire
d) Syringes, 20 mL and 60 mL i) Pericardiocentesis catheter
e) Scalpel, no. 11
2. Patient positioning:
 Ensure patient is on cardiac moniroring with supplemental O2.
 If time permits, decompress stomach with NGT.
 Place the head of bed at 45-degree angle to cause fluid to collect inferiorly & to bring
heart closer to anterior chest wall.
3. Identify insertion site:
 Locate xiphoid process & left costal margin by palpation. The most common sites of
needle insertion are marked by black dots below.
 When using echocardiographic guidance, probe can identify safest site for needle
insertion. This is generally subxiphoid site, however parasternal & apical approaches
are also possible, depending on where the pericardia! collection width is greatest.
4. Prep site: Use sterile technique with antiseptic solution, drapes, & anesthetize skin with
lidocaine if time allows.
5. Needle insertion: 1st make small incision at insertion site with scalpel. Fill 20-mL syringe
with 10 mL of sterile saline, evacuate air, and attach to 18-gauge needle. As needle is
advanced, place constant suction on syringe. Stop too inject saline (0.5-1 mL) intermittently
to prevent tissue from clogging the needle.
6. Needle angle: needle should be advanced toward left shoulder at 30-45 degree angle to
abdominal wall, needle is slowly advanced past the posterior rib border of left costal margin,
then flattened to 15-degree angle.
P A G E | 36 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

7. Needle advancement: Continue advancing needle until pericardia! fluid is returned. ST

elevation or abrupt ECG changes indicate myocardial injury. In this case, needle should be
slowly withdrawn back.
8. Aspiration: remove 20-mL syringe & replace with larger available syringe to continue to
aspirate as much fluid as possible. In shock due to tamponade, removal of as little as 50
mL of fluid can cause rapid improvement in CO. If time is available & echo guidance is being
utilized, injection of agitated saline into pericardia! space can confirm the correct positioning
of the needle tip, prior to guidewire insertion. If bloody aspirate is obtained, it can be injected
into a dish and observed for clotting. Pericardial Fluid with blood will often not clot, blood
aspirated from ventricle will clot
9. Pericardia/ drain placement: It prevents reaccumulation of fluid in the next 1-2 days. 1st
insert guidewire found in the pericardiocentesis kit into needle. Remove needle over wire,
& keep the wire in hand to avoid losing its place. Slide 6-8 French dilator over wire to form
a tract. A larger skin incision may be needed to advance dilator. Remove dilator, and then
advance drainage catheter over guidewire into pericardiaJ space. Guidewire is removed &
discarded leaving catheter available for draining . Suture in place & cover with sterile
dressing. Fluid can be removed through 3-way stopcock until hemodynamic srability.
10. Continued catheter drainage: There are 2 options for continued drainage of pericardial
fluid, catheter may be directly connected to cubing & placed on suction bulb; or tubing can
be left to gravity drainage, to maintain patency, tubing should be flushed with saline every
1-2 hours. Another alternative is to fill tubing & catheter with urokinase. In this case, the
tubing must then be opened every 2 -4 hours to drain for 1 hour.
11. Diagnostic studies: depending on the clinical situation. fluid may be sent for cell count with
differential, glucose, protein, Gram stain, culture (aerobic, anaerobic, AFB), hematocrit,
lactate dehydrogenase, cyrology, tumor markers, , rheumatoid factor (RF), & ANA.
12. Postprocedure CXR should be performed to evaluate positioning of drain & rule out
pneumothorax. A repeat transthoracic echocardiogram should reveal resolution of effusion.

Fig 9.4.Subxiphoid approach to pericardiocentesis with pressure& ST seg monitoring

(hollow, thin-walled, 18-gauge needle is connected via 3 -way stopcock to aspiration syringe filled with 1%
Xylocaine& to short length of fluid-filled tubing connected to pressure transducer. Sterile V lead of ECG
attached to metal needle hub. Needle is advanced until pericardial fluid is aspirated or injury appears on
ECG. Once fluid is aspirated, stopcock is turned so needle-tip pressure is displayed against simultaneously
measured RAP from RT heart catheter. When needle-tip position within pericardial space is confirmed, J-
tipped guidewire is passed through needle, needle is removed,& catheter with end& side holes is advanced
over guidewire& connected via 3-way stopcock to both transducer & syringe. This permits, 1st drainage using
catheter rather than sharp needle&, 2nd documentation that tamponade physiology is relieved when RAP
falls & intrapericardial pressure is restored to level at or below zero.
P A G E | 37 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

10 Pulmonary Artery Catheterization

 Since its inception in 1970s, the clinical use of PAC has been controversial.
 PAC provides direct pressure measurements from RA, RV, PA & PCWP + measuring CO
by thermodilution.
 PAC rapidly gained favor when it was recognized how inaccurate physician assessments of
these parameters were.
 Use of PAC became widespread & bedside management was influenced by hemodynamic
parameters; however, no clinical validation of its benefit had been performed.
 Routine use of PAC should be avoided due to:
 Trials in different patient populations, including surgical patients, patients with acute MI,
CHF& ALI have shown no benefits, & possibly ↑ risk, from use of PAC.
 Study by ARDS clinical trials network found no differences in outcomes of patients with
ARDS who had their fluid balance guided by use of CVP monitoring or use of PAC.
 Newer, noninvasive techniques to assess hemodynamic parameters are being refined
and are reducing dependence on PAC.
 PAC still has a role:
 In PA hypertension & congenital heart D& with complex fluid management issues.
 As new therapies emerge, information on treatment benefits may require invasive
assessment of hemodynamic parameters.
 The clinician using PAC needs to ask how the information obtained from PAC will change
management of specific patient, and be alert to possibly the greatest danger of the device:
misinterpretation of its hemodynamic measurements.
 PAC should be used for the shortest time possible & with understanding that it is unlikely to
alter the clinical course of a patient with multiple complex medical problems (Table 10.1 ).
Table 10.1 Contraindications,Indications& Complications of PAC Placement
P A G E | 38 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Procedure Technique
 The easiest insertion sites are right IJV or left SCV ; however, FV or brachia! V can be used.
 Prior to starting the procedure, evaluation of any contraindications to PAC should be made.
 In cases with suspected RV dysfunction, PAH, TR, or RA enlargement, consideration should
be given to placing PAC with fluoroscopic guidance, as direct visualization enhances ability
to pass PAC in difficult cases.
 IV lines, pressure bags, transducers, and zeroing apparatus should all be assembled and
ready prior to the sterile insertion of PAC.
 It is useful to have an assistant or nurse available for the procedure.
 A sterile procedural field should be used, with strict attention to handwashing, mask and cap
usage, sterile glove and gown use, as well as full-length drapes.
 The introducer catheter is inserted in similar manner to CVC using Seldinger technique.
 The introducer catheter is slightly different in that dilator is advanced through the introducer
rather than as separate piece of equipment, as occurs with a regular CVC insertion.
 Additionally, the guidewire and dilator are removed together at the conclusion of the
introducer insertion, which leaves the introducer alone in the vessel.
 PAC (Fig. 10.1) should have all ports flushed and balloon checked for leaks prior to insertion.
In addition, the operator should check that balloon tip does not protrude beyond inflated
balloon as this can increase the risk of vascular rupture.

 All pores of PAC should be attached to pressure transducers and flushed prior to insertion.
 Waving of catheter tip prior to insertion with verification of waveform on monitor confirms
that the catheter pores are correctly attached.
 Prior to starting the procedure, a final check to verify that the protective catheter sheath has
been inserted over the catheter should be performed.
 The catheter should be oriented prior to insertion to match natural curve in the catheter to
projected course through the vasculature.
 PAC is advanced through introducer,& when tip is in RA, balloon should be inflated gently.
 Distance from insertion site to RA will vary depending on site, 15-20 cm from RIJV or LSCV.
 Once balloon is inflated and lock on inflating syringe has been activated, the catheter is
advanced & waveforms on the monitor are inspected.
 RA waveform ↑ in amplitude as RV is entered, at approximately 30 cm (from RIJ approach).
 Passage of catheter through RV is arrhythmogenic & should not be of prolonged duration.
 Conversion of RV waveform to PA waveform, as catheter tip traverses pulmonary valve, is
identified by ↑ in diastolic pressure & development of dicroric notch(often at 40 cm).
P A G E | 39 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Difficulty in traversing the pulmonary valve is not uncommon in patients with PAH from any
cause and, if excessive catheter length has been advanced without this transition occurring,
the most likely explanation is that catheter is coiled in enlarged RV. If this occurs, balloon
should be deflated & catheter withdrawn until RA tracing is obtained, after which balloon
should be inflated and the procedure attempted again.
 PCWP tracing is identified by loss of arterial tracing to flatter tracing of lower amplitude than
PA diastolic pressure (often at 50 cm). (Fig. 10.2 for pressure tracings as PAC advances).
 At this point, balloon should be deflated & PA waveform observed. Gentle reinflarion of
balloon while feeling for ↑ resistance & monitoring waveform for overwedging is crucial.
 The 1.5 mL balloon should be fully inflated when wedge tracing is obtained. If wedge tracing
is obtained & balloon is partially inflated, this signifies that catheter tip is too distal & ↑ risk
of PA rupture by full inflation of balloon. With this scenario, catheter should be gently
withdrawn 1-2 cm with balloon deflated, & balloon inflation performed again to obtain a
wedge tracing optimally at full balloon inflation. If there is no wedge tracing obtained with
full inflation, catheter should be advanced with balloon inflated till wedge tracing is obtained.
 PAC should never be withdrawn with the balloon inflated and should never be advanced
without the balloon inflated, as this can result in perforation of heart or PA.
 Once insertion is completed,
 Distance of insertion from introducer site should be recorded as a reference point.
 Catheter should be secured with tape & sterile dressing
 Chest x-ray should be obtained to verify catheter course, tip position, and to rule out
any complications from the procedure, such as a pneumorhorax.
 As catheter warms up in patient's body, it tends to soften& migrate distally, which ↑ risk
of overwedging, pulm infarction, & PA rupture with balloon inflation, so re-evaluation
with daily CXR & cautious inflation of balloon & inspection of waveforms (Table 10.2).
Table 10.2 Hemodynamic Parameters Obtained by PAC in Different Clinical Situations
P A G E | 40 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN
P A G E | 41 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Cardiac Output Determination

 Once PAC has been verified to be correctly placed, hemodynamic data can be obtained.
 Catheter system must be opened to air to set zero point as atmospheric pressure & catheter
transducer must be referenced to the level of the heart.
 CO is determined by both thermodilucion and Fick calculation.
 For thermodilurion,
 Known volume (5-10 mL) of cold saline is injected through proximal pore of PAC. The
distal pore has thermistor which records change in temperature of blood over time &
displays this as thermodilucion curve.
 Area under the thermodilucion curve is proportional to CO (PA flow rate) as long as
there is not incracardiac shunt (falsely elevated CO) or TR (falsely low CO).
 Normally, 3 thermodilution curves with minimal variance (<10%) are used to derermine
the mean CO utilizing the Stewart Hamilton equation.

Figure 10.3 CO measurement. Analyzing thermodilution curves

P A G E | 42 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 The Fick equation can also be used to calculate CO.

O2 consumption
CO =
Arteriovenous oxygen content difference X 10
 O2 consumption is normally assumed & calculated by using value for O2 consumption
at rest of 110-125 mL/min/m2 depending on age and sex.
 AV oxygen content calculation requires a simultaneous ABG (SaO2) & sampling of blood
from distal port of PAC (SvO2) and is calculated as follows:
AV O2 content difference = 1.34 X Hb concentration X (SaO2 – SvO2).

Tips
 Pressure measurements are all measured at end-exhalation, when intrathoracic pressure
most approaches atmospheric pressure.
 Use of mainstream end-tidal CO2 detector is useful to determine this point in intubated
patients. In nonintubated, review of hemodynamic tracings can identify fluctuations in
pressure associated with normal respiration and end-exhalation can be identified.
 Utilization of all the hemodynamic data obtained from PAC, together with knowledge of
patients clinical scenario, can greatly aid in interpretation of the data.
 PAC has a unique ability to identify diverse etiologies of shock, including hypovolemia,
cardiogenic, and distributive/septic shock. In addition, patients with predominantly RV
dysfunction and patients with pericarclial tamponade can be identified.
 Use of continuous oximetry during catheter insertion can also identify stepups in O2
saturations which can help diagnose intracardiac left to right shunts.
 Titration of inotropes, fluids, and vasodilators can be performed with serial measurements
from PAC to optimize tissue oxygen delivery & hemodynamics.
P A G E | 43 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

11 Alternative Hemodynamic Monitoring

 No hemodynamic monitoring technique can improve patient outcomes by being utilized.
 The ideal hemodynamic monitor should provide accurate & reproducible measurements of
clinically relevant variables that are able to guide therapy, should be easy to use with rapid
response times, be operator independent and cause no harm.
 The perfect system does not exist and different approaches may be required in single
patient during different phases of their illness.
 There are several noninvasive or minimally invasive techniques that measure CO, include
esophageal Doppler, transpulmonary thermodilution, pulse contour analysis, partial CO2
rebreathing, and thoracic electrical bioimpedance and bioreactance.
 The focus of this chapter is to describe these techniques, both their advantages, and
limitations with a special focus on the esophageal Doppler.
Esophageal Doppler
 It involves placing transducer into esophagus until approximately midthoracic 35-40 cm &
rotating probe to achieve optimal signal.
 Blood flow velocity is measured by changes in the frequency of reflected sound waves.
 It is most useful when obtaining serial measurements to detect trends & response to therapy,
absolute values are not as important as trend analysis.
 Improved outcomes utilizing esophageal Doppler-guided management have been shown in
surgical patients undergoing orthopedic procedures but there is lack of outcome data in
most ICU patients.
 It has been utilized in trauma patients, medical ICU, intraoperative & postoperative care.
 Measurement of CO is based on measuring velocity of blood flow through descending aorta.
 Stroke volume (SV) is estimated from derivation of velocity time integral (VTI) multiplied by
aortic cross-sectional area (Fig. 11.1). then , CO is determined (CO= HR x SV).

Figure 11.1. Method for determining volumetric flow. It is applicable for any laminar flow for
which cross-sectional area (CSA) of flow chamber can be determined. The product of CSA&
time velocity integral (TVI) is SV. Then CO can be calculated.
 Also, provides measure of preload termed corrected flow time . FTc is systolic FTc for HR;
it is represented on monitor display as waveform's base (normal values 330 - 360 ms).
 Achieving the longest possible FTc , correlates with finding optimal LV filling or preload.
 Maximum or peak velocity is waveform's height=measure of contractility (normal ↓ with age)
Preload ======> Flow time Peak velocity by age
Contractility===> Peak velocity 20 yrs = 90 -120 cm/s
Afterload =====>Velocity and flow time 50 yrs = 70 -100 cm/s
70 yrs = 50 - 80 cm/s
P A G E | 44 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Both FTc & peak velocity helps to optimize resuscitation efforts in clinical situations.
 In hypovolemic shock monitor displays narrow waveform base with corresponding
decrease in FTc (<330 ms) & relatively normal peak velocity. The administration of fluid
would widen waveform base, or lengthen FTc.
 In myocardial depression, the initial waveform shows low peak velocity & normal FTc.
Inotropic ttt improves peak velocity or contractility in such a situation (Fig. 11.2).

Figure 11.2 Esophageal Doppler waveforms in (A)normovolemia (B) hypovolemia(C) LV failure

1ry measurements are stroke distance (area under waveform during systole), peak velocity &
ejection time during systole (flow time). During hypovolemia & HF, stroke distance is ↓ . In
addition, ideally, during hypovolemia, flow time is ↓ but peak velocity is maintained, whereas
during HF, flow time is normal but peak velocity is ↓.
Advantages of Esophageal Doppler
 Able to rapidly obtain a set of hemodynamic numbers which are easy to interpret.
 It is possible to leave it in place as long as 72 hours, but it is important to test position of
probe to ensure the optimal signal.
 The device is safe to use in most patients including patients with coagulopathies.
 Probe placement in patients with known varices is a relative contraindication.
Drawback to Esophageal Doppler
 Its limitation to sedated and mechanically ventilated patients.
 There are assumptions in calculating SV& CO that affect its ability of precise measurements.
 SV is estimated from proportion of blood flow that reaches descending aorta. It is
assumed that there is constant 70/30 division of flow between descending aorta (70%)
& brachiocephalic A supplying head & neck as well as the upper extremities (30%).
 CSA of aorta is estimated based on nomogram utilizing characteristics of patient (age,
gender, & weight). Therefore, if significant aortic pathology (aneurysm or dilation) is
present, the absolute derived values may not be accurate.
 The mathematical model assumes that aorta is cylindrical with constant laminar flow
running parallel to esophagus. In reality, flow may be turbulent due to arrhythmia,
anemia, or aortic valve disease.
 The presence of any of these factors makes it difficult to obtain consistent signal.
P A G E | 45 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Severe kyphoscoliosis may alter the angle of interrogation of probe so that it is not
optimally positioned to measure flow in descending area. If this angle >15-30 degrees,
measurements will be inaccurate.
Trans-Pulmonary Thermodilution
 In contrast to PA thermodilution technique, transpulmonary thermodilucion measures CO
by detecting a cold bolus within peripheral arterial system. The cold injectate is administered
through a CVC and detected by a thermistor-tipped arterial catheter placed into radial,
axillary, or femoral artery.
 CO is calculated by the Stewart-Hamilton equation similar to PA thermodilution.
 The benefit with the transpulmonary technique is the ability to obtain CO readings as well
as other markers of preload (global end-diastolic volume [GEDV], inrrathoracic blood
volume [ITBV]), and extravascular lung water (EVLW), without a PA catheter.
 Transpulmonary CO values are generally greater than the PA thermodilution values. It has
been proposed that there is an unaccounted loss of cold indicator in che lung which would
explain the difference as well as overcorrection for recirculation artifact.
 Thermodilution measurements can be used not only to measure flow, but also to measure
the volume through which flow is measured (from the point of injection to point of detection).
 Figure 11.3 depicts typical thermodilucion curve utilizing transpulmonary thermodilution &
explains the concept of mean transit time (MTt) & downslope time (DSt).

Figure 11.3. Diagrammatic representation of temperature-time curve during a

thermodilution measurement, plotted on linear-linear (top) and log-linear scales (bottom), dotted
lines in each case represent what curve would have looked like in the absence of recirculation
of thermal indicator. Note that the decay of the thermal curve becomes linear when graphed on
semi-log scale (bottom). Also shown are typical points used to measure MTt & DSt.
 The derived volumes can be seen graphically in Figure 11.4:
P A G E | 46 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Intrathoracic thermal volume (ITTV) = CO X Mean transit time of thermal indicator

 Pulmonary thermal volume (PTV) = CO X Downslope time of thermal indicator
 Global end-diastolic volume (GEDV)= ITTV – PTV, provides preload marker of
moderate strength.
 Intrachoracic blood volume (ITBV) = 1.25 X GEDV - 28.4 (ml)
 Extravascular lung water (EVLW) = ITTV – ITBV, used to help guide fluid
administration or distinguish between hydrostatic pulmonary edema & ALI.
 The clinical utility of EVLW
 It is not clear. ↑ EVLW may be used as indication of early pulmonary edema.
 It has been found that mortality is greater when EVLW > 15 mL/kg.
 However, currently there is no established protocol using EVLW in sepsis or ALI/ARDS.
 The value for EVLW is subject to error in certain situations.
o Overestimated in severe lung injury.
o Underestimated in acute pulmonary embolism where loss of perfusion affects the
ability of thermal indicator to detect all areas of lung water.

Pulse Contour Analysis

 Use arterial pressure waveform to predict vascular flow & calculate SV.
 Most devices require calibration to provide a correction factor for differences in the arterial
system. Indeed there are several assumptions necessary to derive the aortic pressure
waveform from the shape of the peripheral pulse. Therefore, most models use either
transpulmonary thermodilution or lithium dilution techniques as a reference point to derive
CO. Cw-rent systems available include: PiCCO (Pulsion Medical Systems, Munich,
Germany), PulseCO (LiDCO Ltd, Cambridge, UK), and Flo Trac/Vigileo (Edwards
LifeSciences, Irvine, California, USA).
 Thermodilution is used in the PiCCO device, lithium is the indicator for PulseCO, while the
Flo Trac/ Vigileo device does not require any dilution technique.
 Pulse contour analysis requires arterial line placement, and for the PiCCO or PulseCO
devices a central venous catheter must be placed for calibration. Each device uses a
different mathematical model of pressure and flow that must account for the changes in
aortic impedance, arterial compliance, and systemic resistance.
 Calibration is generally needed to derive the correction factors for these mathematical
algorithms.
 The Flo Trac/Vigileo uses demographic data co extrapolate its correction factor. Pulse
contour analysis provides continuous CO monitoring in contrast to PAC thermodilution
technique which is intermittent.
 CO provided by pulse contour analysis is subject to error as well. These devices are limited
by dynamic changes in vascular resistance which would require recalibration. Ir is generally
recommended to recalibrate the PiCCO and PulseCO devices every 8 hours. The Flo
Trac/Yigileo does not require calibration, but may not be reliable in patients with reduced
peripheral resistance such as in sepsis. Performance is also affected by the presence of
AR, aortic aneurysm, and dampened waveforms. The PulseCO system canner be used in
patients taking lithium therapy or paralytics because this alters the sensor's ability to detect
the indicator.
 Such limitations should be taken into account when deciding which hemodynamic
monitoring device to use. These devices can provide useful information like PPV & SVV in
patients who are totally mechanically ventilated (no spontaneous respirarory effort), in
normal sinus rhythm & on MV with adequate tidal volumes.
P A G E | 47 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Partial Carbon Dioxide Rebreathing

 This technique relies on a modified Fick principle to calculate CO. The Fick equation is
based on the belief that oxygen uptake from lung is completely transferred into bloodstream.
 Therefore, CO is calculated as ratio between O2 consumption & arteriovenous difference in
O2 content.
 In partial CO2 rebreathing technique, Fick principle is applied to CO2 instead of O2.
 Several devices are necessary to obrain the appropriate measurements. These consist of
CO2 infrared sensor, air-flow or pressure pneumotachometer, pulse oximeter & disposable
rebreathing loop. No central lines are required to measure CO2 content.
 Venous CO2 value is eliminated from equation by measuring CO2 under normal &
rebreathing conditions.
Modified Fick equation
𝐂𝐎 = 𝐯𝐂𝐎𝟐 (𝐍) − 𝐯𝐂𝐎𝟐 (𝐑)
𝐒 𝐗 ∆𝐞𝐭𝐂𝐎𝟐
 It requires estimate of venous CO2, arterial CO2 content & adjustment for slope of CO2
dissociation curve.
 Venous content is represented by change in CO2 during normal (N) minute ventilation
versus rebreathing (R) conditions.
 Arterial CO2 is estimated from end-tidal CO2 at the end of both maneuvers multiplied by the
slope (S) of CO2 dissociation curve.
 Intrapulmonary shunt can affect this equation by changing blood flow participating in gas
exchange. Degree of shunting in severe lung injury may not be easily estimated and
adjusted by system.
 Some devices incorporate SpO2 & PaO2 on blood gases to account for shunting.
Nonetheless, underlying lung disease, varying tidal volumes, & hemodynamic instability can
alter the precision of this technique which is not recommended or widely used.

Thoracic Bioimpedance
 SV is estimated from changes in electrical resistance over time as low magnitude, high-
frequency current is applied. Patient does not detect low level of current.
 It is considered the least invasive of the available devices. It requires placement of 6
electrodes: 2 on upper chest wall or neck, & 4 on the lower.
 The electrical current follows the path of least resistance, which is aortic blood flow. As left
heart contracts, there is a change in aortic blood volume & therefore ↓ in impedance.
 For SV calculation , amount of electrically participating tissue is estimated from gender,
height & weight of patient.
 Surrounding tissue fluid volume is important in precision of impedance measurements.
 Change in surrounding tissue fluid volume & effect of respiration on pulmonary blood
volume must be accounted for in calculation of aortic blood flow.
 There is very limited use of it in ICU& devices using bioreactance are more reliable due to:
 It is sensitive to acute changes in tissue water content (pul edema, effusions& anasarca)
 Electrodes cannot be moved during measurement because it is calculation of change
over time.
 The calculation also depends on constant R-R interval, therefore arrhythmias will cause
error in measurement of SV and CO.
 Measurements are also affected by temperature and humidity.
P A G E | 48 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Thoracic Bioreactance
 The most widely used device is NICOM (Cheetah Medical, Portland, Oregon) device which
measures bioreactance or phase shift in voltage across the thorax.
 It measures thoracic impedance& tracks changes in amplitude& direction (measured in
degrees) of impedance.
 Pulsatile blood flow causes these phase shifts in impedance & vast majority of thoracic
pulsatile flow is generated by aortic blood flow.
 NICOM device incorporates a sensitive phase shift detector& therefore noninvasively
measures aortic flow.
 The system is totally noninvasive & consists of high-frequency sine wave generator (75 kHz)
& 4 dual electrode stickers which establish electrical contact with thorax.
 2 stickers are placed on each side of thorax and CO is determined separately from each
side of the body with the final noninvasive CO averaged from these two values.
 Bioreactance-based measurements are more accurate than bioimpedance as they do not
measure static impedance and also do not depend on distance between electrodes.
 Signals are averaged over 1 minute so can be used with cardiac arrhythmias.
 Validation studies of NICOM have shown good correlation between NICOM-derived CO
compared to CO obtained by thermodilution techniques & with esophageal Doppler.
 It is noninvasive, can be used in ventilated, nonventilated & cardiac arrhythmias patients.
 There are conflicting data whether NICOM can track changes in CO to functional challenges
like fluid boluses and passive leg raises in different ICU populations.
 NICOM is not reliable when electrocautery is being simultaneously applied for > 20 s/min.

Conclusion
 The decision to use one form of hemodynamic monitoring over the other depends on
understanding of limitations of each device and assessing each patient's unique situation.
 At Washington University, the esophageal Doppler is often used for its easy placement in
critically ill, ventilated patients, ease of interpretation, and quick results. It provides
intermittent CO monitoring as well as hemodynamic indices of cardiac preload, contractilicy
and afterload.
 Regardless of the method chosen, clinical picture, physical examination findings and all
other available data should be integrated to adequately determine the hemodynamic status.
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12 Functional Hemodynamic Monitoring

 Hemodynamic instability is very common in ICU. Clinical impressions regarding a patient's
hemodynarnic profile can often be erroneous resulting in potentially harmful interventions.
 The need for accurate hemodynarnic information to guide patient care resulted in
widespread use of PAC.
 The lack of benefit observed in RCT& inherent invasiveness of PAC has renewed interest
in alternative modes of hemodynamic monitoring & assessment of volume responsiveness.
 Basic principles of hemodynamic optimization focus on improving O2 delivery to the tissues
by restoring adequate circulating volume, restoring perfusion by optimizing CO & MAP &
ensuring adequate O2 carrying capacity (optimal Hb & Hb saturation with O2).
 Volume responsiveness refers to ↑ in CO or SV that occurs in response to fluid challenge.
Static Markers Of Volume Responsiveness
 Figs. 12.1 & 12.2 explain the concept of volume responsiveness by depicting the Frank-
Starling curve of a normal heart.

Figure 12.1 Volume responsive: ↑ SV in Figure 12.2 Volume unresponsive:

response to fluid challenge in normal Minimal ↑ of SV volume despite volume
biventricular function & on steep portion expansion in normal BV function on flat
(low preload) of Frank–Starling curve. portion (high preload) of Frank–Starling.

 Clinicians have generally utilized static hemodynamic values, most commonly intravascular
pressures, to predict which patients will benefit from fluid challenges.
 Table 12.1 summarizes static markers used in ICU to help predict volume responsiveness.
Central Venous Pressure
 Figure 12.3 shows normal CVP tracing.
 CVP tracings in disease states are often characteristic:
1) In AF, a wave is lost.
2) In AV dissociation, large cannon a waves occur as atrium contracts against closed TV.
3) In TR , large fused cv wave is seen.
4) TS results in giant a-waves & reduced y descent.
5) In constrictive pericarditis, y descent is prominent & becomes steeper during inspiration
6) In cardiac camponade, x descent is preserved & y descent is attenuated.
 CVP is used extensively in ICUs to make clinical decisions regarding volume status due to
high prevalence of CVC lines & ease of acquisition from existing catheter. However, there
is no association between CVP and circulating blood volume.
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 CVP is intravascular pressure in major thoracic veins, measured relative to atmospheric

pressure. It provides estimate of RAP as it is ideally measured at the junction of SVC& RA.
 There are many factors chat affect CVP including blood volume, vascular tone, RV function
and compliance, TV disease, cardiac rhythm, intrathoracic pressure (respiratory efforts and
PEEP) as well as patient position.
 The ability of any CVP value to accurately predict volume responsiveness is in 56% range.
 ↓ CVP is a relatively late sign of intravascular volume depletion particularly in patients with
intact vascular rone. For all these reasons, CVP alone should not be utilized to guide fluid
management decisions, but should be combined with knowledge of the patients underlying
pathophysiology and additional hemodynamic parameters.

Table 12.1 Static Markers of Volume Responsiveness

P A G E | 51 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Figure 12.3. Normal CVP tracing

 a wave: atrial contraction, c wave: TV closure & bulging into RA or transmitted
pulsation from carotid artery, x descent: atrial relaxation, v wave: atrial filling, y wave:
atrial emptying.
 S1= MV& TV closure, S2= AV & PV closure.
 P:atrial depolarization QRS: ventricular depolarization T: ventricular repolarization.
P A G E | 52 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Dynamic Markers Of Volume Responsiveness

 It is possible at bedside & consists of challenging patients Frank-Starling curve.
 The principle is to induce change in preload & monitor the response by documenting
changes in SV, CO, or other surrogates.
Commonly used techniques of inducing a change in preload are:
1) Infusing a fluid bolus,
2) Passive leg raising which autotransfuse 200-300 ml of blood in LL back to central circulation
3) Utilizing the natural cyclic changes that occur in RV SV, LV preload & ultimately LV SV due
to mechanical ventilation-induced changes in RV preload.
 Large MV- induced changes in LV SV will occur in patients with biventricular preload
reserve with no change occurring if one or both of the ventricles is preload independent.
 To utilize this technique, patient needs to be in normal sinus rhythm, totally mechanically
ventilated with no spontaneous breathing attempts and tidal volume needs to be
adequate (8-10 mL/kg).
Common techniques for detecting change in preload induced by challenges above:
1) Dynamic real-time monitoring of SV or CO
 Utilizing esophageal or suprasternal Doppler, bedside echocardiography,or others.
 ↑ SV or CO by > 15% with fluid challenge or in response to PLR = volume responsive.
 ↑ SV or CO by 10-15% range= likely volume responsive & if associated with evidence
of end-organ hypoperfusion, the patient may benefit from fluid loading.
 ↑ SV or CO by< 10%= not volume responsive & is functioning on flatter portion of Frank-
Starling curve.
2) Dynamic changes in descending aortic blood flow velocity utilizing esophageal Doppler. A
similar cutoff of 10-15% is used for volume responsiveness if this technique is used.
3) Measuring arterial pulse contour analysis and pulse pressure or stroke volume variation.
 PPV or SVV > 10-12% predict volume responsiveness with high sensitivity & specificity
PPV = 100 × (PPmax - PPmin)/(PPmax + PPmin)/2
SVV = 100 × (SVmax - SVmin)/(SVmax + SVmin)/2

Figure 12.4. Arterial pressure tracing showing the presence of PPV & SVV.
P A G E | 53 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Functional hemodynamic monitoring& assessment of volume responsiveness used in

1. Hemodynamic instability (MAP <65 mm Hg),
2. Evidence of tissue hypoperfusion (UOP <20 mL/hr, anxiety, confusion, lethargy, HR> 100
b/min, lactate >2.2 mmol/L).
 These criteria should be met before embarking on fluid challenges as many individuals in
ICU may be fluid responsive, but may not be in need of fluid administration.
 Clinical scenario determines need for utilizing any hemodynamic monitoring & intervention
strategy.
 Once hemodynamically unstable, the next step in evaluation is determination of preload
responsiveness using one of dynamic markers noted above with adequate fluid boluses.
 If the patient is preload responsive, serial fluid boluses & serial evaluations of continuing
preload responsiveness should be performed until the patient is no longer hemodynamically
unstable or no longer preload responsive.
 The septic patient who is persistently hypotensive and no longer preload responsive will
require vasopressors titrated.
 In addition, further diagnostic workup with bedside echocardiography should be performed
to identify cardiogenic dysfunction which would benefit from inotropic support or to identify
another cause (pericardia! tamponade, RV dysfunction in acute pulmonary embolism, etc.).

ScvO2 Monitoring
 Used in ICU as surrogate of true SvO2 and reflects balance between O2 delivery & demand.
 A normal SvO2 is between 65 & 75% and studies in critically ill patients which
simultaneously measured the variables, show that ScvO2 is about 5-7% > SvO2 but that
the variables track in the same direction with changes in a patient's condition.
 ScvO2 is therefore useful for trend analysis.
 The determinants of the ScvO2 are shown in Figure 12.5.

Figure 12.5. Variables affecting the ScvO2.

P A G E | 54 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

13 Extracorporeal Therapy in ICU

 Extracorporeal literally means outside of the body.
 ECT is a kind of mechanical supportive therapy used to perform physiologic functions of
various organs outside the body.
 ECTs are used in patients admitted to ICU with single or multiorgan failures as a rescue and
supportive care to assist the failing organs.
 ECT include
 RRT=renal replacement therapy for kidney,
 ECMO = extracorporeal membrane oxygenation for lungs & heart,
 ECCO2R = extracorporeal CO2 removal for the lungs,
 Liver dialysis devices for the liver,
 Extracorporeal ventricular assist device for heart failure, etc.
 The other forms of ECT are
 Plasmapheresis/filtration for the removal of a harmful antibody,
 Hemoperfusion therapy for roxin removal,
 ECT for removal of endotoxins &/or inflammatory mediarors in sepsis (Table 13.1).
Table 13.1 Types of Extracorporeal Therapy
 Renal replacement therapy
 Hemoperfusion
 ECMO
 ECCO2R
 Liver dialysis devices
 Extracorporeal ventricular assist device
 Plasmapheresis/filtration

Extracorporeal Membrane Oxygenation (ECMO)

 ECMO is being used increasingly over the past 2 decades as a lifesaving extracorporeal
modality, to treat critically ill patients with refractory respirarory and/ or cardiac failure.
 The basic principle of ECMO is to draw deoxygenated blood from patient, run it through
oxygenator to allow gas exchange, and return oxygenated blood to patient. A pump is used
to drain the blood from the body and to maintain flow through the circuit and oxygenaror.
Types of ECMO
A. Basic ECMO Mode: VV & VA
 ECMO mode is named as per site of drainage of blood & site of return of blood to patient.
 ECMO is subdivided into 2 categories- venovenous & venoarterial ECMO (Fig. 13.1 ).
 In VV, deoxygenated blood is drained from vein& returned back to venous circulation
after oxygenation.
 In VA, deoxygenated blood is drained from venous circulation& after oxygenation,
oxygenated blood is returned to arterial circulation (through artery).
 If oxygenated blood is returned to peripheral artery (commonly FA), it is termed
peripheral VA. In central VA, blood is drained from RA& returned to ascending aorta.
 Indications & contraindications of ECMO have been enumerated in Table 13.2.
B. Hybrid ECMO Modes
 There is also a complex category called hybrid ECMO (known as high-flow ECMO) in
which 1 or 2 extra cannulas are inserted to overcome shortcomings of VV or VA ECMO.
 Patients on VV ECMO for respiratory failure, who develop cardiogenic shock or RV
failure, can be managed with VVA ECMO mode by putting another return cannula in
artery to support the failing heart.
 Similarly, patients on VA ECMO developing cerebral hypoxia can be managed with VAV
ECMO mode by putting another return cannula in a vein.
P A G E | 55 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Figure 13.1. VV ECMO & VA ECMO.

Table 13.2 Indications & Contraindications of ECMO

AOI=age-adjusted oxygenation index. APSS=age; PaO2/FiO2, Pplateau Score.

P A G E | 56 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

The ECMO Circuit

 The components of ECMO circuit are (Fig. 13.2).:
1. Cannula (drainage& return) 5. oxygenator,
2. tubing, 6. oxygen blender
3. blood pump, 7. heat exchanger
4. console,

Figure 13.2. Simplified ECMO circuit.

1. Cannula:
 Most C are made from polyurethane,with wire reinforcement to prevent occlusion/kinking
 Modern cannulas are heparin coated & have radiopaque marker.
 Available in various sizes (6 - 51 Fr).
 Size of Cannula is determined by size of vessel, flow requirement, & mode of ECMO.
 Drainage or access C have larger diameter & multiple perforations to maximize venous
drainage and to prevent collapse.
 Return C are smaller than venous C (in both length & internal diameter).
 Recently, double-lumen cannula is also available for VV ECMO.
2. Circuit Tubing
 Made from polyvinylchloride with biocompatible coating to ↓ systemic inflammation.
 Length of the circuit should be adequate for easy handling but with minimum possible
tubing length to ↓ resistance & reduce exposure to the extracorporeal surface.
 ECMO circuits have various pressure monitors at different levels (before pump, before
oxygenator& after oxygenator) & integrated flow monitor device to measure blood flow.
 Tubing is coated with biocompatible lining to ↓ inflammatory response & thrombosis.
3. Pump
 Pump (responsible for flow) may be either centrifugal (commonly used) or roll pump.
 Flow depends on rotation speed of pump/min (RPM), which controlled from console.
 Flow generated by the pump is preload dependent and afterload sensitive.
 Preload determinanrs are: volume status, venous tone & drainage cannula
characteristics (position, length, & diameter ).
 Afterload determinants are: systemic vascular resistance, resistance offered by
membrane oxygenacor, and return cannula characteristics (length & diameter).
4. Oxygenator
 Called artificial lung or membrane oxygenator or membrane lung
 Responsible for oxygenation & decarboxylation. It is placed distal to pump in circuit.
P A G E | 57 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 Modern oxygenators have hollow fiber of polymethylpentene (PMP), which are extremely
efficient in gas exchange. Have low resistance to blood flow & minimal plasma leakage.
more durable, easy to prime, & less thrombogenic, & cause less hemolysis.
 The gas flows through hollow fibers, & blood flows outside the fiber channel.
 The fiber walls act as interface between blood & gas, where gas exchange occurs.
 Factors responsible for oxygenation and decarboxylation are mentioned in Table 13.3.
 The new-generation oxygenators may contain an built-in heat exchanger.
Table 13.3 Factors Affecting Oxygenation & Decarboxylation
Factors Affecting Oxygenation Factor Affecting CO2 Removal
 Blood flow  Sweep gas flow
 FiO2 delivered to the oxygenator  Blood CO2 concentration
 O2 carrying capacity of blood  Surface area for gas exchange
 Degree of recirculation
5. Blender & Heat Exchanger
 The gas is delivered to oxygenator from a blender with flow meter to regulate gas flow.
 Blender provides & regulates desired O2 fraction(21-100%) to oxygenator.
 Hear exchanger is essential to maintain temp of blood circulating in circuit & prevent
hypothermia. Also is used for cooling to ↓ overall metabolism (less CO2 production &
less O2 consumption) when required.
ECMO Setting & Initiation
A. Cannulation
 Vascular access is achieved by cannulation of large vessels in neck or groin (Table 13.4)
 Cannulation can be done either by using percutaneous approach (Seldinger technique)
or by cutdown or a combination of curdown and Seldinger technique.
 For central cannulation, the RA & aorta are directly cannulated via thoracotomy.
Table 13.4 Cannulation Site for ECMO

B. Priming of ECMO Circuit

 Done by crystalloid or blood under strict aseptic conditions, to remove air from circuit.
 Nature of priming solution depends on baseline Hb, age & weight, clinical scenario, etc.
C. ECMO Initiation
 Once cannulation is done & primed circuit connected to cannulae, adequate
anticoagulation is achieved, pump is turned on& ↑ pump speed to provide forward flow.
 Adjust sweep gas flow to keep gas flow to blood flow ratio 1:1& Monitor circuit pressures.
 Once ECMO is established, ↓ ventilator settings & titrate vasopressor/inotrope dose.
P A G E | 58 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

 In VV ECMO, the target is to maintain adequate oxygenation,

 In VA ECMO, the target is to maintain adequate BP as well as oxygenation.
D. Anticoagulation
 Systemic AC (mostly bolus & infusion of UFH) is required with ECMO to prevent clotting.
 Consensus on AC targets is lacking. Often aPTT , activated clotting time (ACT), anti-Xa
levels, and thromboelasrography (TEG) parameters are used to titrate anticoagulation.
 Anticoagulation may be stopped while on ECMO, in case of significant bleeding.
E. Ventilator Setting in Patients on ECMO
 There are no standard guidelines regarding this. However, lung ultraprotective strategy
is followed to ↓ the harmful effect of MV on the already injured lungs.
 VALI can be limited by reducing tidal volume & airway pressures.
 As gas exchange is almost fully supported by ECMO, ventilarory strategy is aimed at
healing of injured lungs by ↓ tidal volume ( <6 mL/kg) to achieve a safe Pplateau (Pplat
<25 cm H20), low RR (5-10/min), and moderate PEEP (10-15 cm H20).
 Pressure control modes may be the most logical mode, but volume control mode with
strict limit of Ppeak may be equally effective.
 Patients on VA ECMO, primarily for cardiac support, may be put on spontaneous modes
or extubated even while on ECMO.
Table 13.5 Complications of ECMO

Table 13.6 Difference between VV ECMO & VA ECMO

P A G E | 59 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Weaning from ECMO

 Daily assessment should be done to wean off from ECMO at the earliest.
 Extracorporeal support is decreased as the native organ function improves. Weaning should
be considered when extracorporeal support is < 30% of total native heart or lung function.
 Weaning from excracorporeal support differs between VV and VA ECMO (Table 13.7).
 Weaning from VV ECMO:
 It is integral part of comprehensive patient care. As cardiac function is adequate, gas
exchange efficacy is tested before starting weaning.
 With recovery in native lung function (improvement in oxygenation, lung compliance,
radiologic improvement, etc.), sweep gas flow is gradually reduced while maintaining
low blood flow. If patient is able to maintain oxygenation, sweep gas flow is switched off.
 During weaning process, ventilatory management should be optimized & patient must
be vigilantly monitored for hemodynamic disturbances & respiratory distress.
 If patient remains stable during weaning (1-6 hours), ECMO can be discontinued.
 Weaning from VA ECMO:
 It is a complex process and standardized weaning protocols are lacking. It depends on
indication for which ECMO was initiated and should be individualized accordingly.
 Weaning should be considered once heart is adequately recovered (assessed by
echocardiography), with resolution of primary pathology & hemodynamic stability (no or
minimal ionotropic support) achieved for at least 24 hours.
 ↓ blood flow gradually with simultaneous assessmem of cardiac function by echo.
 When patient remains stable at minimal blood flow (1 L/min) for 30-60 min,
discontinuation of excracorporeal support can be considered.
Table 13.7 Weaning from ECMO

TDSa= lateral mitral valve annular peak systolic velocity.

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Evidences for use of ECMO

 Evidence for VV ECMO is based on 2 large RCTs: CESAR trial & EOLIA trial.
1. In CESAR trial (2009),
o 180 adult patients with severe ARDS (defined as Murray Score >3 or
uncompensated hypercapnic respiratory acidosis with arterial pH <7.2 despite
optimal ventilatory strategy) were recruited and assigned to either ECMO group or
conventional management group.
o ECMO group had significantly better survival without disability at 6 months
compared to conventional management group (63% vs. 47%),
o Although 24% of cases assigned to ECMO group did not receive ECMO as they
either died before ECMO initiation or improved with conventional management at
ECMO center.
o Patients with high Ppeak (>30 cm H20) & FiO2 >0.8 for >7 days were excluded.
o The trial was criticized for heterogeneous ventilation strategies for the conventional
management group & for the fact that about one-fifth of patients transferred to
ECMO center did not require ECMO as they improved with standard lung-protective
ventilation. However, the authors concluded that severe ARDS should be referred
to ECMO center for further evaluation and management.
2. In EOLIA trial (2018),
o 249 patients with severe ARDS (defined as PaO/FiO2 < 50 for >3 hours or P/F <80
mm Hg for >6 hours) were randomly assigned to either ECMO group to receive
early ECMO (as soon as entry criceria were satisfied) or conventional management
group to receive lung-protective ventilation and late ECMO as a rescue therapy.
o Although there was 11 % difference (35% vs. 46%) in 60-day mortality favoring use
of early ECMO, the study was stopped early after recruitment of 75% of the planned
sample size as it met predefined stopping criteria.
o Survival was higher (65% vs. 43%) in early ECMO (2 vs. 6 days after onset)
compared with in those who received late ECMO as rescue therapy.
o It was concluded that severe ARDS who fail to respond to optimal conventional
management should be managed with ECMO as an early rather than late rescue
therapy.
o From the available evidence, ECMO should be considered beneficial for those who
do not respond to conventional management, and ECMO should be used in early
course of disease (within 7 days) rather than in later stage as a rescue therapy.
o In ECMO centers , 25% of patients will improve & recover without ECMO,& 60-70%
of those who require ECMO will survive. But potential risk involved in shifting
unstable patient to ECMO center should be weighed against benefits of ECMO..
 No controlled trial of VA ECMO,
 As assignment of a control group is not justified.
 Studies show that among adult patients with refractory out-of-hospital cardiac arrest,
survival is about 22% with 50% of those who survived by receiving ECMO during
resuscitation having a good neurologic recovery.
 Similarly, among patients who received ECMO for cardiac arrest, severe cardiogenic
shock, or failure to wean from cardiopulmonary bypass following cardiac surgery,
survival rates are about 20-50%, and ECMO-CPR (e-CPR) is associated with better
survival compared co conventional CPR.
Summary
 ECMO is a supportive therapy rather than a disease-modifying ttt in. It should be performed
only by clinicians with experience in its initiation, maintenance, and discontinuation.
 Best results are obtained if we chose the right patient, the right type of ECMO, and the right
type of configuration (site and management) and anticipate complications.
P A G E | 61 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Extracorporeal CO2 Removal (ECCO2R)

 It is a modified kind of VV ECMO with a low blood flow rate (0.4-1 L/min), which provides
partial respiratory support with removal of CO2 without much effect on oxygenation.
 Hypercapnia is a major issue in COPD & in patients receiving lung-protective ventilation
strategy. It may be associated with adverse effects such as cerebral vasodilacation, cardiac
depression, and arrhythmia. So, ECCO2R may be beneficial in these situations by
protecting various organs from the deleterious effects of hypercapnia.
 Usually heparin-coated, wire-reinforced, double-lumen cannula is used, but 2 different
single-lumen cannulae can be used for drainage & return. Centrifugal pump is present in
circuit to draw blood & membrane lung through which blood passes for CO2 removal.
 After CO2 removal, the decarboxylated blood is returned back to the body (Fig. 13.3).
 The mechanism of ECCO2R is similar to that of VV ECMO except for having low blood flow
rate. The sweep gas contains very minimal CO2 to create diffusion gradient across the
membrane lung, through which blood containing high CO2 passes.
 There is another system in which the pump is not required as blood flows in circuit across
membrane due to pressure difference between arterial and venous systems.
 Complications are related to catheter insertion (catheter site bleeding, infection), related to
therapy (hemolysis), or related to device failure (pump failure, clot/air in the circuit).
 As far as the evidence for the use of ECCO2R is concerned, at present, it is used for
research purpose only, and being a new concept, its success in patient recove1y depends
on the clinical situation in which it is used.

Figure 13.3 ECCO2R

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Therapeutic Plasma Exchange (TPE)

Defenition
 The process in which plasma is separated from cellular components & discarded, and the
rest along with equivalent amount of replacement fluid is circulated back to patient
 In plasmapheresis, plasma is separated from cellular components & collected for use; the
rest is returned back to patient without any replacement fluid.
 It is based on the principle that, with removal of plasma, molecules responsible for disease
pathogenesis such as cycokines, antibodies, and/or immune complexes are removed & the
removed plasma is replaced by fresh plasma or other replacement fluid.
 In TPE, large volume of patient's plasma (1-1.5 times) is removed and thereby about 60-
70% of intravascular culprit substances are removed. Plasma is replaced by equivalent
amount of replacement fluid & the commonly used replacements are albumin, albumin with
saline as a minor component, and plasma.
 The anticoagulant used in TPE depends on the device, and most devices use citrate.
 The time interval between sessions is decided by the disease process, response to therapy,
component to be removed (IgG), & adverse effects of TPE such as bleeding complications.
 TPE is relatively safe, but the incidence of adverse effects varies from 4-30%. Most of the
adverse reactions are mild and easily resolved
2 Steps Of TPE Process
1. 1st step, blood is withdrawn from patient and filtered by using filter of desired size
(membrane filtration method) or centrifuged on the basis of density (centrifugation method)
to separate plasma from cellular components,
2. 2nd step, the filtered plasma is discarded & the rest of the components are recirculated along
with infusion of replacement fluids (Fig. 86.4).
Indications
a) Acute inflammatory demyelinating polyneuropathy (AIDP),
b) Chronic IDP (CIDP), d) Wegener's granulomarosis,
c) Goodpasture's syndrome, e) Myasthenia gravis,
f) Trombotic thrombocyropenic purpura (TTP),
g) Hyperviscosiry syndrome in monoclonal gammopathies, etc.
Complications
 Related to intravascular catheter, anticoagulant (bleeding risk),
 Filtration of medications (treatment failure), & transfusion of plasma transfusion related
acute lung injury (TRALI) or infusion of the replacement fluid (allergy to albumin).
P A G E | 63 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Extracorporeal Therapy In Sepsis

Pathophysiology of Sepsis
 Sepsis is life-threatening organ dysfunction caused by dysregulated host response to
infection.
 In any infection, host recognizes the pathogens by presence of certain molecular patterns
or endotoxins called pathogen-associated molecular patterns (PAMPs). Neutrophils
recognize these PAMPs with help of toll-like receptors & other pattern recognition receptors.
 Once neutrophils recognize the infecting agent, innate immunity & leukocytes are activated,
leading to release of cyrokines, both proinflammatory and anti-inflammatory.
 This release of cytokines damages the host cells & the injured host cells express damage-
associated molecular patterns (DAMPs). DAMPs further activate leukocytes, and lead to
massive release of both proinflammatory and anti-inflammatory cytokines (cytokine storm)
in response to infection and dysregulated immune response.
 This excessive as well as unbalanced host immune response to infection during sepsis
leads to organ dysfunction and may lead to death.
 After the initial cyrokine excess phase, there is a phase of immune paralysis, in which
healthcare-associated infections and viral reactivations occur & add to morbidity &mortality.
Management of Sepsis
 It is aimed at organ support, proper antimicrobial& adequate source control in timely manner
 Despite all these standard treatment options, mortality from sepsis remains high. So,
removal of harmful cytokines by ECT may be the next level of treatment in sepsis.
 There are various proposed hypotheses such as the peak concentration theory, threshold
immunomodulacion concept, iceberg theory, and mediator delivery hypothesis to support
the role of ECT in removal of cytokines in the treatment of sepsis.
 ECT is adjuvant therapy for sepsis, hypothesized to control cytokine storm & associated
organ dysfunction.
 The rationale behind such approach is to remove excess cytokines, endoroxins, or both.
This can achieve immune homeostasis & ↓ damage caused by immune dysregulation.
 Different therapies have been developed to address certain steps of immune dysregulation.
Table 13.8 Advantages and disadvantages of ECT in sepsis

 Various ECTs tried in sepsis are discussed under 4 headings (Table 13.9).
P A G E | 64 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Table 13.9 Types of Extracorporeal Therapy in Sepsis

P A G E | 65 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Indications to ECT in Sepsis

 It is not clearly defined and is evolving.
 Before starting ECT in sepsis, it should be ensured that standard treatment protocol has
been aptly followed and sepsis management is optimized as per existing guidelines.
 Consider ECT in septic shock with multiple organ failure (at least 2 organs) with worsening
hemodynamics, despite implementation of standard sepsis management protocol.
 While using ECT in sepsis, consider various factors as severity of sepsis, course of disease,
cytokine trends, mortality risk, cost-effectiveness & probability of organ failure reversal.
 At present, ECT in sepsis is being used on a case-to-case basis as per the treating
physician's judgment rather than on the basis of any evidence-based criterion.
Timing of ECT in Sepsis
 Timing is very important, although it has not been clearly defined.
 Too early initiation may not be justifiable as many patients recover with standard therapy,
whereas delayed therapy may fail due to irreversible organ failure that has set in.
Contraindications to ECT in Sepsis
 No absolute contraindications.
 However, factors such as response to standard care, futility of therapy & irreversible organ
damage should be considered before starting therapy.
Evidences
 High-volume Hemofiltration (HVHF):
 Small studies have shown that use of HVHF improves hemodynamics & ↓ mortality.
 IVOIRE trial is large RCT failed to show any benefit in mortality or hemodynamics.
 CytoSorb®:
 Multiple case series showing improvement in hemodynamics & ↓ in mortality.
 RCT did not show any survival benefit, in spite of significant ↓ in cytokine levels.
 Coupled Plasma Filtration Adsorption (CPFA):
 Small observational studies shown promising results in hemodynamic improvement.
 COMPACT 1 & 2 are 2 large multicenter trials, they did not show any benefit; rather, it
was found to be associated with increased adverse effects.
 Polymyxin B Hemoperfusion (Toraymyxin)
 It is the most extensively investigated therapy for endotoxin removal.
 EUPHAS (old) showed improvement in hemodynamics, organ function & 28-d mortality.
 ABDOMIX trial: results of EUPHAS were not replicated here; rather, this tial ↑ mortality.
 EUPHRATES study (2018) failed to show any mortality benefit
 Aiteco® LPS Adsorber:
 Only few case series reported reduction in cytokine levels & hemodynamic improvement.
ASSET trial is RCT, which was terminated early due to patient recruitment issues.
 oXiris® membrane:
 Multiple small case series showed favorable outcomes , but no large CRT to support it.
 Hemopurifier®:
 It has been used successfully for the treatment of severe Ebola virus disease.
Summary
 As sepsis is interplay between various types of both proinflammatory and anti-inflammatory
cytokines, nonselective removal of cytokines may not be effective.
 Cytokines may have pleiotropic properties& same cytokine may have contradictory function
 ECT works by modulating or decreasing the harmful effects of cytokines, but at the same
time may also reduce the beneficial effects.
 Cytokine trend is a dynamic phenomenon and proper timing of ECT is not yet clear.
 At present, evidences are not in favor of using ECT in routine care of sepsis. so, better
understanding of pathophysiology of sepsis is required for optimal use of ECT in sepsis
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14 basic critical care ultrasound

Introduction
 It refers to clinician-performed and interpreted bedside US to help diagnose & manage
critically ill patients with cardiopulmonary failure.
 Comparable to physical examination,
 It is noninvasive, rapid & repeatable exam performed by the provider directly caring for
patient & is designed to answer specific clinical questions.
 Results are immediately available to guide time-sensitive decision-making.
 Multiple focused examinations are performed serially to document clinical responses to
specific interventions.
 It differs from standard echocardiography & US, which provide delayed, comprehensive,
and mostly single examinations for diagnostic purposes, which are interpreted by physicians
who are disassociated from the clinical care of patient.
 Advantages of critical care US:
 Ideal for bedside use  Avoids patient transportation
 diagnostic& for procedural guidance.  repeatable.
 Involves no ionizing radiation  extension of physical examination.
 Barriers to the use of US in the critically ill include:
 Inadequate training,(operator dependent)
 Cost of equipment,
 Difficulty achieving adequate windows because of (obesity, dressings, incisions)
 Risk of transmitting infections if cleaning protocol of probes & device is not followed.
 Appropriate clinical application of the technology is dependent on the knowledge & skill of
operator/interpreter. Expertise in Critical Care US requires combination of didactic training,
+ many hours of bedside scanning & image interpretation sessions to review common
pathologies. It is best learned at the bedside from a mentor who is an expert in the field.
Table 14.1 Comparison of Bedside US with Diagnostic Modalities in ICU
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Basic US Physics
 US refers to sound waves with frequency of >20 kHz, which is too high for human ear to
hear. These high frequency waves are used to generate images of internal organs & can
detect blood flow velocities.
 Sound waves (vibrations) are transmitted through different media (solid, liquid, or gas) and
are governed by the following relationship: propagation velocity = frequency X wavelength.
 In body tissues, sound waves propagate at approximately 1500 meters/second. Therefore,
if the frequency of waves is 1000 Hz (cycles / sec), the wavelength is 1.5 m which is
obviously inadequate for human US imaging since many of tissues of interest are only mm
thick. Therefore, extremely high frequency waves are utilized in medical US (2 to 15 MHz).
 US waves with higher frequency will deliver higher resolution images but this needs to be
balanced with the ability of the US waves to penetrate into the body.
 Lower frequency US waves tend to be less attenuated by tissue and so penetrate further.
 US waves are generated by a piezoelectric crystal transducer within US probe. Electrical
energy is converted by the crystals into movement and vibrations which set up US waves
which propagate into the surroundings. The unique properties of each crystal will determine
the frequency of the waves generated.
 Transducer probes generate sound waves but also receive returning waves from tissues.
 Pulses of sound waves are generated by transducer & then received back. It is this pulsed
natured of the signal and the time delay between generation and reception which allows for
US machine to derive the distance of the structure of interest from the probe.
 Thousands of pulses per second are possible with modern machines. The returning waves
are converted back to electrical signal which is amplified and processed to generate the
final image which will provide information about depth and tissue characteristics of the
structures encountered by the sound waves.
 Modern transducer probes have these crystals arranged in electronically steered or phased
arrays, to generate complete image from multiple wavelets that are generated in series of
radial lines.
 Echogenicity of particular tissue is determined by the degree of reflection of US waves at
tissue interfaces.
 If most of the waves are reflected back, tissue will appear very bright or echogenic (bone
reflects most US waves & will not allow for visualization of structures deeper to bone).
 If most of the waves penetrate through the interface without reflection, the tissue will
appear darker or black (hypoechoic) and this is seen with fluids.
 Varying degrees of gray are seen in tissue imaging, dependent on properties of tissue.
The Ultrasound Machine
Modes
1. 2D or B-mode (brightness mode):
 Standard, familiar, default mode which generates slice images. The machine processes
the returning sound waves and displays structures as gray scale cross-sectional image.
2. M-mode(motion mode):
 Plots morion over rime. This mode provides excellent temporal resolution and is useful
for visualizing moving structures and measuring cavity dimensions.
3. Doppler:
 Doppler effect, 1st described by Christian Doppler in 1843, refers to frequency change
that occurs in echo signal when object moves toward or away from source of US waves.
 If wave source is moving toward an observer, waves are compressed causing decrease
in wavelength. The opposite applies if wave source is moving away from observer.
 The major limitation of Doppler is the need to align US beam with the direction of the
blood flow. This angle should at maximum be 15 degrees to ensure accuracy.
P A G E | 68 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

A. Continuous Wave Doppler:

 utilizes continuous cycle of US waves with simultaneous acquisition of returning
echoes. US machine analyses the complex mix of returning echoes & Doppler shifts
and generates a spectral Doppler layout from which it is able to discern the direction
of flow as well as the peak velocity and mean velocity.
 Used to measure high velocity flows in heart, across valves & estimate PA pressure.
B. Pulse Wave Doppler:
 allows for discrimination for where a particular Doppler shift signal arises from US
beam axis (the sample volume).
 Utilized in assessing blood velocity at specific location of interest & is best used with
low velocity flows as it is susceptible to phenomenon called aliasing (Nyquist limit).
 We routinely use it to assess velocity of blood in aortic outflow tract to estimate SV.
C. Color Doppler:
 is a form of pulsed wave Doppler utilizing a grid with multiple interrogation points
(pixels) and is generally used superimposed on the 2D image as a way ro determine
direction and velocity of flow in a large sample area.
Adjustable Settings
1. Gain:
 Adjustments in gain allow operator to change brightness & should be set to allow the
maximum contrast resolution for area of interest.
 Many machines have total gain, near gain, and far gain settings and users should try
set uniform gain across the image.
 Excessive gain should be avoided.
2. Depth:
 Depth should be adjusted so that the area of interest is viewed in middle of screen.
 Appropriate depth settings can often improve resolution.
Transducers
 Transducers vary by frequency and footprint (Table 14.2).
 Frequency:
 Number of cycles of compressions& rarefactions that occur in 1 second & inversely
proportional to wavelength.
 Higher frequency transducers generate higher resolution images, but do not
penetrate deeply into tissues. These are used to visualize superficial structures like
vessels & nerves, so are used for procedures like central line insertion. Most linear
vascular probes have a frequency of 5 -10 MHz.
 Lower frequency transducers (1-5 MHz) are commonly used as phased array probes
for cardiac, lung & abdominal imaging as they provide more penetration to visualize
deeper structures.
 Footprint: size and shape of probe area in contact with skin.
Standard Transducer Movements
 Slide/Move: movement of ultrasound footprint across skin surface (example: slidingprobe
vertically down anterior chest to evaluate lung slide between different rib spaces).
 Rotate: turning clockwise or counterclockwise without angling or changing the location on
the body, in order to obtain orthogonal plane (moving from parasternal LAX to PSAX).
 Tilt/Rock: angling the transducer on its long axis on che same tomographic plane (when
IVC is visualized horizontally across the screen with probe placed perpendicular to
abdomen, rocking the probe upward will demonstrate IVC entering the RA).
 Angle: angling the transducer without moving it, in order to view adjacent tomographic
planes (angling the probe side to side to appreciate aorta running laterally to IVC).
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Table 14.2 Characteristics, Uses & Advantages of 3 Commonly Used Transducers

Lung US & Evaluation of Acute Respiratory Failure

Key Points
 Air is enemy of US as its reflective properties inhibit US from reaching underlying structures.
 Lung Us is therefore generally restricted to patterns seen at the pleural surface.
 > 90% of etiologies of acute respiratory failure involve pleural surface & cause US artifacts.
These artifacts create specific patterns that correlate to traditional physical exam findings.
 These artifacts or lung US signatures, define lung US. They include lung slide, A-lines, B-
lines, consolidation, and effusion.
 Lung US is superior compared to chest x-ray & CT in detection of pneumothorax, normal
aeration patterns, interstitial syndrome, consolidation & pleural effusion.
 Bedside Lung US in Emergency protocol (BLUE) is a rapid noninvasive exam which
provides a decision tree framework to help delineate the most likely etiology in patients with
acute respiratory failure (Fig. 14.1).
Performing the Exam
1. Probe Selection (Fig. 14.2)
a) Phased array probe
 Set depth 15 cm to evaluate for consolidation, pleural effusion& to identify diaphragm.
 Able to appreciate lung slide, however provides less resolution of pleural surface
compared to linear probes.
 Decreasing the gain setting will often make the pleural line more apparent.
 Has the advantage of not needing to switch transducers to perform rapid & sequential
lung, cardiac, and abdominal exam in a deteriorating patient.
b) High frequency, linear probe
 Has better resolution of superficial srructures, making it easier to evaluate pleural
interface, including detecting lung slide & lung point.
c) Micro convex probe
 Small footprint allows for easy visualization between ribs. Frequencies 5-8 mHz.
2. Machine Settings
 Basic/abd setting:avoid advanced(cardiac presets)which ↓artifacts that define lung US
P A G E | 70 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Figure 14.1. A decision tree utilizing lung US to guide diagnosis of severe dyspnea.

Figure 14 .2. Normal lung US using linear probe (left) & phased array (right).
Notice the higher resolution with linear probe, however only able to penetrate few cm.
P A G E | 71 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

3. Probe Positioning (Fig 14.3)

 Sagittal/longitudinal, indicator pointing to 12 o' dock, perpendicular to chest wall.
 Bilateral anterior chest-examine artifacts between multiple rib spaces over anterior
chest, starting apically and moving down.
 Convention is to include both adjacent rib shadows on the image to assess
underlying pleura and lung.
 Multiple parallel and vertical scan lines are recommended.
 Bilateral posterior and lateral axillary position:
 Obrain image in mid-axillary& posterior axillary lines,
 Identify diaphragm, evaluate for atelectasis& pleural fluid,& assess subdiaphragmatic
structures (liver/spleen).
 To do this correctly, start very posteriorly & angle probe toward horizon.

Fig 14.3. To evaluate for A, B lines& lung

slide, place transducer on anterior chest
perpendicular to chest wall & slide between rib
spaces with indicator at 12 o’clock.
To evaluate for pleural effusions,
atelectasis/consolidation&subdiaphragmati
c structures, place it in mid-axillary line with
indicator at 12 o’clock. Slide it superiorly&
inferiorly until diaphragm is identified.
To completely evaluate this area, may need
to move the transducer more posteriorly while
angling upward toward the horizon.

Figure 14.4. Lung slide (movement between visceral & parietal pleura) = bright,
shimmering line between rib shadows (left). M mode of movement beneath pleural line.
If lung is in contact & moving below pleural line, grainy or sandy pattern is seen (middle
sandy beach). If there is no movement or lung is not in direct contact with parietal pleura,
then linear pattern is seen (right= stratosphere/barcode signs).
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The Five Lung Signatures

1. Lung Slide
 Characteristics:
 Horizontal hyperechoic line approximately 0.5 cm deep to origin of rib shadows.
 Dynamic finding, as shimmering, sparkling, glimmering, twinkling appearance.
 Represents the movement of visceral on parietal pleura.
 Often more apparent at the lung base than at the apex of the lung.
 Presence of lung slide rules out pneumothorax at the point of interrogation.
 Lung pulse is not the same as lung slide, but refers to pulsation of pleural line
interface with each cardiac pulsation, & also able to rule out PTX when seen.
 By M mode:
 Normal lung slide results in "sandy beach sign" due to movement of underlying
lung, underneath pleural line (sand on a beach) as opposed to the relatively
stationary superficial soft tissue structures (seen as "waves" on M mode).
 If PTX is present, M mode finding is stratosphere or barcode sign (consists of
multiple horizontal lines without haziness generated by lung motion) (Fig. 14.4).
 Lung POINT sign:
 Referring to the point or edge of PTX . Sliding lung is seen coming in & out of US
image as patient breaths, & juxtaposed to area with absent lung slide.
 It is very specific for PTX but not very sensitive, as it is not always seen and
depends on pneumothorax location related to probe position.
Differential Diagnosis for Loss of Lung Slide
 Pneumothorax  Severe pneumonia or ARDS with significant loss of
 Prolonged apnea lung compliance
 Prior Hx of pleurodesis  Examination on left side with right mainstem intubation
 Bullous lung disease  MV modes without significant tidal volume(HFOV)
 Adhesions  Pulmonary contusions
2. A Lines
 Characteristics
 They are a reverberation artifact, with serial repetitions of the pleural line.
 A lines are horizontal lines and are each separated by an equal distance (this is a
reverberation artifact of the original distance from the probe co the pleural line).
 A lines are the normal expected pattern and represent aerated lung.
 Differential Diagnosis
 Normal lung,
 COPD/asthma,
 PTX (A lines + absent lung slide)
 P embolism (without P infarct)
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3. B Lines
 Characteristics
 Vertical, hyperechoic, dominant lines.
 Originate at pleural surface & extend to bottom of screen without fading.
 Efface A lines where the two intersect.
 Move in synchrony with lung slide.
 Their presence excludes pneumothorax.
 Represents thickened subpleural interlobular septae surrounded by air-filled alveoli.
 The more B lines and closer they are together, generally signifies a more severe
involvement of interlobular septae & progressive alveolar involvement.
 Differential Diagnosis
 ARDS, cardiogenic pulmonary edema both interstitial and alveolar, pneumoma, lung
contusion, interstitial lung disease.
 Multiple anterior & symmetric B lines: Generally signifies cardiogenic pulm edema.
 Asymmetric B lines interspersed with normal areas of A lines: noncardiogenic
edema/ARDS, pneumonia (Fig. 14.5).

Figure 14.5. A lines, created by reflections of pleural line, are equidistant horizontal lines (left).
B lines are dominant, bright vertical lines that move with pleura, extend to bottom of screen, and
represent thickened, fluid-filled interlobular septae (right).
4. Consolidation
 Characteristics:
 The lung is no longer air filled & so no A or B lines are seen. Consolidated lung appears
like any other solid organ ("hepatization" of the lung).
 Best seen in lateral views just above the diaphragm. Often associated with effusions.
 Air bronchograms may be seen in the consolidated lung:
 appear as hyperechoic artifact which moves with respiration& represents movement
of air within bronchi of consolidated lung, suggesting preserved patency of proximal
airway.
 Dynamic air bronchograms can differentiate pneumonia (present) from simple
atelectasis ( absent).
 Differential Diagnosis:
 Atelectasis, pneumonia, ARDS, tumor or mass, lung contusion.
5. Pleural Effusion
 Characteristics
 Pleural fluid is anechoic (black) on US.
 Most effusions are free Rowing, so patient should be positioned to optimize view.
 US can detect very small pleural effusions, before they are seen on CXR.
 There should be at least 1 cm of pleural fluid before thoracentesis is performed.
 US of pleural fluid reveals it to be dynamic, meaning movement with respiration.
 It is important to define the boundaries of the pleural fluid:
 The boundaries of the pleural space consist of chest wall, diaphragm, & lung.
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 This is a routine but extremely important component of pleural US, to avoid

misidentifying diaphragm and confusing it with perirenal fascia.
 Misidentification of diaphragm can result in major injury if thoracentesis is attempted
with resultant subdiaphragmatic injury to liver or spleen.
 Fluid characteristics:
 Simple fluid is anechoic.
 Exudates may not be anechoic & may have swirling debris in fluid (plankton sign)
 Complex effusions may have multiple fibrous strands and septations within the
effusion which are often not seen with CT.
 This may signify loculation of fluid & could be due to parapneumonic effusion,
empyema, or resolving hemothorax (Fig. 14.6).

Figure 14.6. 3 Examples Of Lung Consolidation& Effusions. Consolidated lung has a similar
echogenicity to abdominal organs. Effusions are anechoic or black. Notice echogenic material in
pleural fluid in the right image, can be seen in complex effusions & suggests the need for chest-
tube. Diaphragm is hyperechoic line above abdominal structures. Spine seen posteriorly. C,
consolidation; E, effusion; A, abdominal structures; S, spine.
Approach to Acute Respiratory Failure
 An algorithmic approach using combination of lung US,& LL venous exam is recommended
when utilizing US to help determine an etiology for acute respiratory failure.
 In clinical practice, history, exam findings, laboratory data& basic imaging are combined with
the knowledge of bedside US exam to determine what is the most likely etiology for RF.
 This algorithm is known as BLUE protocol (Fig. 14.1) and is reviewed conceptually below by
a simple approach to bedside lung US.
A. Is there a pneumothorax? Is lung slide present?
 If NO, PTX is possible. Is there Lung point present to confirm PTX? Are B lines or lung
pulse present which will rule out PTX at the probe position?
 Consider other causes of loss of lung slide as noted in above.
B. Are the lungs normally aerated (dry) as signified by an A-line predominant pattern?
 Yes, most likely diagnosis is COPD/Asthma, pulmonary embolism (proceed to evaluate
LL for DVT).
C. Is there an interstitial or alveolar process (wet) as signified by B lines?
 Are B lines diffuse, bilateral & symmetric? suggestive of cardiogenic pulm edema.
 Are B lines occasional, asymmetric, & interspersed with normal areas of A lines?
suggestive of noncardiogenic edema or pneumonia.
D. Is there an asymmetric A/B profile (one lung has A pattern, the other has B pattern)?
 Suggestive of pneumonia which may be confirmed by finding of lung consolidation &
dynamic air bronchograms.
E. Is a pleural effusion present and does it appear to be simple or complex? Is it safe to
proceed with thoracentesis?
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Focused Echocardiography
Key Points
 Bedside echocardiography is goal-directed and problem-oriented.
 Why is my patient hypotensive? What is the cause of hemodynamic instability?
 Is there a pericardia! effusion? Is there tamponade physiology?
 Is the LV function normal? Hyperdynamic? Moderately or severely depressed?
 What is the RV size and function? Are there signs of RV strain?
 Are there any gross valvular or wall motion abnormalities?
 Is IVC normal? Distended? Collapsible?
 Can more fluid be tolerated?
 Phased array probe is used with cardiac setting (indicator on right side of screen).
 5 standard views are obtained with the patient in a supine position.
 Complements, does not replace, standard comprehensive echocardiography.
 It is extension of physical exam- findings should support clinical suspicion & narrow
differential diagnosis.
Limitations
 Limited quantitative measurements and poorer image quality with portable bedside machines
compared to comprehensive echocardiography.
 Some significant findings are difficult to appreciate, including subtle wall motion abnormalities,
valvular vegetations, and RV hypertrophy.
 Obtaining greater than two cardiac views may not be possible due to patient body habitus,
COPD/lung disease, bandages, and positioning.
 Misinterpretation ooccur when image is foreshortened or off axis, or less than 2 views are
obtained, or image quality is poor;& interpreter is not conscious of these limitations.
 Referral for standard, comprehensive echocardiography should be considered in situations
where findings are inconclusive or fall beyond the scope of point-of-care exam.
Image Acquisition & Interpretation
 Image window: position on patient’s chest (parasternal, apical, & subcostal) (Fig. 14.7).
 Image plane: 3 standard planes defined by American Society of Echocardiography
a) Long Axis (sagittal plane): vertical bisection through LV apex & center of aortic valve.
b) Short Axis (transverse plane): perpendicular to long axis, cross sections of ventricles.
c) Four Chamber (coronal plane): LV apex to base, bisecting mitral & tricuspid valves.
1. Parasternal Long Axis (PLAX)
 Image Acquisition:
 Indicator toward patient’s right shoulder (11 o’clock).
 Probe just left of sternum (between 2nd & 5th rib space).
 Image Optimization:
 Slide up & down along left aspect of the sternum to locate the best viewing window.
 Stay close to the sternum to avoid lung interference.
 Find the interspace in which the inferior aspect of the septum is horizontal.
 Rotate so that mitral and aortic valves are in the same plane.
 LV should be seen in its longest axis and aortic valve cusps should be symmetric.
 Tilt away from sternum so that mitral and aortic valves are in the center of screen.
 The apex should not be visualized.
 Adjust depth so descending aorta in view (14 to 16 cm) (Fig. 14.8).
 Normal Structure & Function:
 RV outflow tract, aortic outflow tract, & LA approximately the same size.
 LV systolic function: visualize myocardial thickening, symmetrical inward endocardial
movement, anterior leaflet of mitral valve approximates the septum (<1 cm).
 Mitral & aortic valves: leaflets come together with normal opening & closing.
 Is There a Pericardial Effusion?
 Appears as anechoic space between the myocardium and pericardium.
 Nonloculated effusions generally collect posteriorly in dependent areas.
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 Anterior fat pad can be misinterpreted as an anterior effusion since it is located between
myocardium & pericardium.
 Ascites and left-sided pleural effusions can be mistaken for pericardial effusions.
 Use the descending aorta to differentiate between pericardial and pleural effusion.
 Pericardial effusions taper anterior to descending aorta.
 Pleural effusions extend posterior to the descending aorta.
 Is There LV Dysfunction?
 Dilated chamber, decreased myocardial thickening.
 Diminished MV opening, anterior leaflet >1cm from septum.
 Is the LV Hyperdynamic?
 Small chamber size with anterior mitral valve leaflet contacting the septum.
 End diastolic cavity obliteration.
 Is the RV Overloaded?
 RV outflow tract larger than the aorta and left atrium.
 Paradoxic septal motion.
 Pitfalls of PLAX:
 Only visualizing RVOT , so unless severely abnormal, unable to evaluate RV size.
 May overestimate LV function in underresuscitated septic or hypovolemic patients.
 Off-axis views lead to underestimation of LV size & overestimation of function.
 Inaccurate assessment of MV or AV function:
 normal appearing valves may have significant regurgitation.
 vegetations may be subtle and can be missed by bedside ultrasound.
 heavily calcified appearing AV may not be hemodynamically significant.
2. Parasternal Short Axis (PSAX)
 Image Acquisition:
 From a good PLAX , rotate probe clockwise 60 - 90 degrees, until LV is circular.
 Image Optimization:
 Center LV in the screen between the rib shadows.
 Find the midventricular level by tilting probe along right shoulder–left hip axis until
papillary muscles are visualized (come into view just below MV, like a fish-mouth).
 Papillary muscles at 4 & 7 o’clock positions.
 Normal Structure & Function:
 Circular LV with small, crescent-shaped RV.
 LV systolic function: endocardium moves symmetrically toward center, equal ventricular
thickening, papillary muscles approximate during end systole (Fig. 14.9).
 Is There LV Dysfunction?
 Dilated cavity with decreased contraction.
 Obvious wall motion abnormalities or akinesis which may be global or in a specific
coronary artery distribution.
 Is There RV Overload?
 Large, ovoid-shaped RV.
 Septum moves toward LV cavity during early systole, progressing to septal flattening (
D-shaped LV).
 Is the LV Hyperdynamic?
 Small LV cavity with touching papillary muscles.
 Pitfalls of PSAX:
 Off-axis evaluation, in which LV appears elliptical, causes inaccurate assessment of
segmental wall movements & septal motion.
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Figure 14.7. Cardiac exam probe positions. A: Parasternal long axis. B: Parasternal
shoraxis. C: Apical long axis. D: Subcostal long axis. E: Subcostal IVC.
P A G E | 78 APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN

Figure 14.8.
A. Normal PLAX. AoV, aortic valve; D,
descending aorta; LA, LV, MV.
B. Circumferential pericardial effusion.
The posterior aspect lies between
posterior wall of LV& pericardium,
pericardial fluid is superior to descend a.
C. Severe LV dysfunction in diastole (left)
&systole (right), anterior leaflet of MV
barely opens& does not approximate
septum. cavity is dilated& walls hardly
move inward during contraction.
D. RV overload causing septal deviation
toward LV.
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Figure 14.9. A: Normal PSAX during systole. S=septum; P=papillary muscle. B: Severe LV
dysfunction during systole. C: RV overload with flattening of septum. D: Pericardial effusion.
3. Apical Four Chamber (A4C)
 Image Acquisition:
 Probe placed over cardiac apex at the point of maximal apical pulsation.
 Indicator is facing between patient’s axilla & the bed (about 2 to 3 o’clock).
 Probe is positioned in line with long axis of heart & tilted upward toward the base.
 Depth approximately 14 - 18 cm to image the entire heart, including the atria.
 Image Optimization:
 Deep inhalation may help bring the heart closer to probe and improve the view.
 Positioning the patient with left lateral tilt of the thorax often improves the view.
 Locate the apex of heart made up by LV& RV and center at the top of the screen.
 Slide/rock the transducer until interventricular septum is centered horizontally in the
image and ventricles are fully visualized in their longest axis.
 Rotate until both MV & TV are seen in the same plane.
 Angle transducer superiorly to appreciate the entire heart, including atria (Fig. 14.10).
 Normal Structure & Function:
 RV is triangular & 2/3 the size of LV. The majority of apex is created by LV.
 RV function: systolic shortening occurs in long axis. Visual tricuspid annular plane
systolic excursion (TAPSE) refers to the distance that lateral annulus of TV moves during
systole (M-mode, normal 15 - 20 mm).
 Mitral & tricuspid valves: open and close normally.
 Is the RV Dilated?
 Moderate dilation: RV 60 to 100% of LV.
 Severe dilation: RV larger than LV.
 Paradoxic septal movement present.
 Is There RV Dysfunction?
 Decreased free wall motion.
 TAPSE <15 mm.
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 McConnell’s sign: hypokinesis or akinesis of mid RV free wall & hyperkinesis of apex.
 Is There LV Dysfunction?
 Dilated chamber with decreased MV opening.
 Wall motion abnormalities which can be global or in a specific coronary distribution.
 Pitfalls of A4C:
 Challenging view to obtain in a critically ill supine patient.
 Off-axis imaging: inaccurate assessment of LV/RV function and size.
 Endocardium not always visualized, limiting assessment of LV function.
 It can be difficult to differentiate between acute and chronic RV volume/pressure
overload. Chronic RV dilation is normally associated with hypertrophy of RV free wall.

Figure 14.10.
A. Normal apical 4-chamber view (A=apex).
B. RV hypertrophy & dilation.
C. TAPSE with normal RV function (left) &
impaired function (right).
D. LV dilation & dysfunction.
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4. Subcostal Four Chamber (S4C)

 Image Acquisition:
 Gently place the probe under xiphoid process flat against patient’s abdomen with the
indicator pointing toward 3 o’clock.
 Probe is held differently to the other positions, with hand overlying probe (Fig. 14.7).
 Image Optimization:
 Apply pressure to keep the probe under rib cage & tilt upward, bringing handle of probe
toward patient’s abdomen.
 Direct beam anteriorly until heart comes into view, gentle pressure may be required.
 If bowel gas is obscuring view, move the probe slightly to left (patient’s right) & use the
liver as an acoustic window.
 Rotate the probe until the entire LV, including the apex, is visualized (Fig. 14.11).
 Normal Structure & Function:
 Compare size of chambers, LV/RV gross ventricular function, septal motion.
 Is There Tamponade?
 Does pericardial effusion cause RA or RV free wall collapse during systole or diastole
respectively?
 Is There RV Overload?
 RV size, visual TAPSE, septal abnormalities.
 Pitfalls of S4C:
 Off-axis imaging will lead to inaccurate assessment of LV/RV size & function.
 Difficult to obtain in obese, muscular, or postsurgical patients.
 Some patients unable to tolerate the pressure needed to obtain image.
 Bowel gas or abdominal distention can be challenging.

Fig 14.11.
A. Normal subcostal 4-chamber view.
B. Pericardial effusion.
C. RV & LVhypertrophy.
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5. Subcostal Inferior Vena Cava (SIVC)

 Image Acquisition:
 Place the probe in midline, on abdominal preset, with indicator facing patient’s head.
 Angle or slide the transducer until the IVC is seen horizontally across the screen.
 Image Optimization:
 Rock probe slightly inferiorly & tilt toward patient’s left until IVC is seen entering RA.
 Rotate until IVC traverses horizontally& hepatic vein is entering IVC (Fig. 14.12).
 Normal Anatomy & Function:
 Normal IVC size is 1.5 - 2.5 cm with some variation with respiration.
 Increasing age, respiratory effort & positive pressure ventilation affect IVC diameter.
 Use of IVC Diameter to Assess Preload:
 We caution against solely using IVC diameter to assess volume status, & prefer more
functional hemodynamic monitoring with response in SV to fluid challenges or passive
leg raise.
 At extremes, IVC diameter can be useful to assess preload responsiveness:
 If IVC <1 cm, patient is likely preload responsive, particularly if they are on PPV.
 If IVC <1.5 cm & exhibits >50% collapsibility, likely preload responsive.
 If IVC >1.5 cm but still has >50% collapsibility, patient may be preload responsive
but need to use other measures of preload responsiveness.
 If IVC >1.7 cm& exhibits<50% collapsibility, unlikely to be preload responsive.
 Pitfalls of SIVC:
 Limited use in patients on positive pressure ventilation or in respiratory distress.
 Useful at extremes.
 Aorta can be misidentified as IVC, especially in severely hypovolemic patient in which
IVC may be very small or completely collapsed.
 Identify IVC& aorta to ensure you are truly assessing IVC& not mistaking it for aorta

Figure 14.12. A: Subcostal IVC view (H=hepatic vein). B: M-mode through IVC. Dilated IVC
without respiratory variation (left) compared to small, completely collapsing IVC (right).
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Measuring Stroke Volume by Bedside Echocardiography

 Volume of blood traveling through particular chamber is determined by the following:
 Volume = Time period of flow × mean Velocity of flow × Cross Sectional Area of chamber
 With pulsatile blood flow, when velocity is frequently changing, use velocity time integral:
Volume = VTI × CSA
 VTI is also referred to as the stroke distance in some texts.
 The standard location to measure SV is in the left ventricular outflow tract (LVOT)
 This simple maneuver requires 2 standard echocardiographic views.
a) 1st is PSLAX at AV level, measure LVOT diameter during systole with AV wide open.
 Use caliper to measure LVOT diameter at this point (Normal LVOT=1.8 - 2.2 cm).
 Then LVOT is halved to obtain the radius of LVOT.
 The cross-sectional area of LVOT is then obtained by using this equation:
CSA = π r2 (π is 3.14)
b) 2nd is apical 5-chamber = standard A4C view with slight upward tilt of beam to visualize
LVOT,then Pulsed W Doppler to obtain sample from LVOT,below AV level.
 Pulse wave Doppler profile at that point is obtained and VTI is calculated as area
under VTI envelope using standard US calculations(normal LVOT VTI=18-22 cm)
 SV is obtained by multiplying the VTI by CSA.
 Serial VTI assessments are easily obtainable without need to measure LVOT diameter.
 Serial VTI measurements can be used as a surrogate for SV to assess response to fluid
loading or inotropic support (Fig. 14.13).

Figure 14.13. LVOT diameter & LVOT VTI to calculate SV.

SV=CSA x LVOT VTI.

LVOT diameter = 2 cm, so CSA = 3.14 ---- LVOT VTI = 17.92 ----- SV = 56 mL.
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Point of care US (POCUS) in Shock

 Shock requires rapid recognition, evaluation, and treatment.
 Unfortunately, etiology is not always clear by history & physical exam alone. POCUS by an
experienced user can quickly & accurately differentiate between distributive, hypovolemic,
obstructive, and cardiogenic shock.
 Focused cardiac, lung& IVC takes< 5 min. often combined with LL DVT screen (Table 14.3).
1) Using the phased array probe in abdominal mode, scan anterior lung fields looking for lung
slide (yes or no), also A & B lines (A, B, or A/B pattern)
2) Switch to cardiac presets & perform focused cardiac exam evaluating overall LV size &
function, RV size & function, and presence of pericardial effusion (yes or no)
 LV function: hyperdynamic? normal? mod/severely depressed?
 RV size: <2/3 LV? normal septal movement?
3) Finally, evaluate IVC .
 Fixed, dilated Vs small, collapsing can help support or rule-out certain diagnoses.
 Fixed & dilated >2.5 cm, no respiratory variation
 Small & collapsing <1.5 cm, > 50% variation with respiration
Table 14.3 US Findings in Different Etiologies of Shock

Pneumothorax
 The presence of lung slide, lung pulse, or B lines rules-out pneumothorax.
 Evaluate multiple areas on anterior chest of supine patient to rule-out pneumothorax.
 Absence of lung slide suggests pneumothorax, however this is not a specific finding.
 Loss of lung slide is also seen with severe pneumonia/ARDS, prior pleurodesis, bullous lung
disease, examination on left with right mainstem intubation, and prolonged apnea.
 Lung point confirms the diagnosis of PTX, however, if concerned for tension PTX, do not spend
extra time searching for this finding.
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Tamponade
 Presence of pericardial effusions are often easily identified; however, assessing hemodynamic
importance can be difficult.
 Hemodynamically significant pericardial effusion always associated with fixed& dilated IVC.
 The presence of RV collapse during diastole or RA collapse in systole supports hemodynamic
significance.
 Any questionable pericardial effusion warrants cardiology consultation, and if time allows,
evaluation with a more comprehensive echocardiographic exam evaluating for respiratory
variation in mitral valve inflow velocities and pulmonary vein inflow velocities.
Acute LV Failure
 LV dysfunction as a cause of acute hypotension requires more than just depressed LV function
on cardiac US.
 Gross visualization of LV contraction and anterior mitral valve excursion are the recommended
initial techniques to evaluate overall LV function.
 Attention should be focused on whether the decrease in LV function is segmental and in a
coronary distribution, global or classic for stress-induced cardiomyopathy (apical ballooning
and basilar hyperkinesis).
 Findings should be confirmed in at least 2 different cardiac views.
 Acutely decompensated LV failure may have additional US findings associated with increased
CVP including bilateral B lines & fixed, dilated IVC.
 If, after full clinical assessment, LV dysfunction is considered to be the cause of hypotension &
poor perfusion (cardiogenic shock), consider early initiation of Dobutamine or mechanical
support.
 Repeated exams showing improved LV function & ↓ B line severity as well as improving SV
can be used to guide interventions such as inotropy, diuresis, and/or afterload reduction.
Hypovolemic/Septic Shock
 Both distributive & hypovolemic shock will appear similarly on bedside ultrasound.
 Findings are hyperdynamic LV, predominantly A line pattern on lung exam& collapsible IVC.
 LV cavity is always obliterated during systole& endocardial borders appear to be “kissing.”
 Attention to technique is important as off-axis views may make LV cavity appear underfilled.
 Keep in mind other states that will make the LV appear hyperdynamic.
 Include LV hypertrophy, MR, supraventricular arrhythmias& decompensated RV failure.
 Once hyperdynamic state is observed, other US findings may be helpful in differentiating
between hypovolemia and sepsis.
 Abdominal free fluid suggest hypovolemia related to acute bleeding or decompensated
cirrhosis.
 US evidence of infection are abscess, hydronephrosis or lung consolidation, may suggest
sepsis as 1ry cause. Additional imaging & laboratory testing is required for final diagnosis.
RV Pressure/Volume Overload
 Pulmonary circulation in health is normally low pressure, high capacitance system & thin-walled
RV will dilate with substantial & sustained acute ↑ in pressure (acute cor pulmonale).
 The majority with PE as a cause of shock will have features of RV dysfunction on POCUS.
 RV size & function are best evaluated in A4C, S4C, or PSAX by direct comparison with LV.
 Normally in A4C view, RV should be triangular & <60% of LV.
 As RV enlarges, it’s shape becomes more ovoid & it may progress to being the dominant
chamber at apex ( normally, the majority of apex is made-up by LV).
 Septal bowing, bouncing, or paradoxical movement suggests pressure/volume overload of
RV (best appreciated in PSAX view). Septal changes range from septal bouncing to
complete flattening (D-shaped LV).
 Assess RV function by measuring longitudinal movement of RV free wall at TAPSE level
 TAPSE is obtained by M-mode through intersection of RV free wall & tricuspid annulus &
measuring the distance traveled. This can also be assessed visually in S4C view.
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 McConnell’s sign
 often seen with acute RV dysfunction,
 It refers to hypokinesis or akinesis of mid RV free wall and hyperkinesis of apex.
 It is best seen in the A4C & S4C views.
 It is not specific for pulmonary embolism & can be seen in ARDS or other conditions
associated with acute RV strain.
 US findings of RV dysfunction are used with other standard clinical assessments (history,
examination, ECG findings, BNP, troponin, lactate, Chest CT, DVT screen) in patients with
evolving acute cor pulmonale from pulmonary embolism. This added risk stratification which
US provides, allows for reasoned approach to the use of anticoagulation, thrombolytic therapy,
inotropic support, and fluid administration.
 To assess chronicity of any process affecting RV, evaluate RV free wall thickness
 A previously healthy RV free wall should not exceed 5 mm in thickness.
 If RV free wall is thickened, this would be suggestive of a more chronic process which has
allowed the RV to hypertrophy over time.
 Another clue to a chronic process would be elevation of PA pressure, which is easily
obtained utilizing continuous wave Doppler analysis of TR jet velocity.
 Estimated PASP= 𝟒𝐕 𝟐 (where V is maximal TR jet velocity). Normally, estimated RAP
based on IVC characteristics is added to this value to estimate PASP.
Deep Vein Thrombosis
 Traditional duplex & triplex vascular studies include compression, color & spectral doppler.
 Most point-of-care evaluations of DVT used in ER & ICU use the compression portion only.
 Proximal deep V of LL are external iliac, common FV, deep FV, superficial FV& popliteal V.
 The reader is encouraged to learn venous anatomy of LL in order to perform DVT screening.
 Image Acquisition
 A high frequency transducer is used (5 to 12 MHz).
 Compared to veins, arteries appear more round, thick walled, pulsatile, smaller & require
substantial pressure to be compressed.
 Venous structures generally compress with gentle pressure.
 Ideal patient position is supine with leg externally rotated and knee flexed.
 Start with transducer in transverse position near iliac artery.
 The external iliac vessels should be identified here.
 Normal veins should compress fully with complete collapse of the opposing walls.
 Firm downward pressure is required. Pressure needed to completely collapse the vein is
much less than that needed to compress the adjacent artery.
 Failure to fully compress the vein suggests the presence of acute thrombus.
 Acute thrombi are often not visible with US. Subacute or chronic thrombi which are
organized will be visible within the vessel lumen.
 Common femoral vein:
 Start just proximal to great saphenous V, slide down CFV, compressing every 1-2 cm.
 Identify each branching point until just beyond division into superficial & deep FV.
 Popliteal:
 Place the transducer in transverse plane within popliteal fossa. Popliteal vein is superficial
to artery in the center of the fossa.
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Basic Critical Care US of Abdomen

Key Points
 FAST exam can detect as little as 100-260 mL of free peritoneal fluid.
 The type of fluid cannot be differentiated by US exam alone.
 Sonographic appearance of injured liver or splenic tissue is subtle and difficult to appreciate.
 Presence of free peritoneal fluid is a surrogate marker for solid organ injury following trauma.
 Hydronephrosis & bladder outlet obstruction can be rapidly diagnosed with bedside US,
expediting appropriate therapies.
 Identification of renal cysts/masses or bladder masses require further evaluation& are beyond
the scope of POCUS.
Free Peritoneal Fluid
 FAST exam evaluates gravitationally dependent areas in RUQ, LUQ, and pelvis. This exam
was developed to look for hemoperitoneum in trauma patients.
 All types of free fluid, including blood, ascites, bile, lymph, and urine will appear black. Fluid
with higher levels of protein (clotted blood, loculated fluid, pus) are more echogenic.
 Both the curvilinear or phased-array probes may be used.
1. RUQ:
 Evaluate the hepatorenal recess (Morrison’s pouch), under diaphragm, & inferior pole of
kidney (right paracolic gutter).
 Image Acquisition:
 Place probe in coronal plane(indicator at 12 o’clock) in midaxillary line at xiphoid level
 Center the hepatorenal recess in the center of the screen.
 Fluid in the hepatorenal recess will appear as anechoic space between the 2 organs.
 Tilt probe anteriorly & posteriorly, making sure to evaluate inferior pole of the kidney.
 Angle the transducer superiorly to image under the diaphragm.
2. LUQ:
 Evaluate under diaphragm, spleen, splenorenal space & left kidney (paracolic space).
 Image Acquisition:
 Left kidney is located more posterior and superior compared to right kidney.
 Start with the probe in posterior axillary line as close to bed as possible (may help to
have patient role into right decubitus position if possible).
 Once the left kidney is centered on the screen, fan the space above and below to
evaluate the inferior pole and the splenorenal space.
 Angle superiorly to appreciate the area under the diaphragm.
3. Pelvis:
 Fluid accumulates in rectovesicular space in men or pouch of Douglas in women.
 Image Acquisition:
 Start with the transducer just above the pubic symphysis in transverse plane with the
indicator toward the patient’s right.
 Tilt inferiorly until the bladder is visualized.
 Adjust depth so that the posterior part of bladder is located in the top half of image.
 Fan through the entire length of the bladder, from the fundus to the neck.
 Rotate 90 degrees and scan the entire bladder in the sagittal plane (Fig. 14.14).
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Figure 14.14.
 Left= Free fluid in RUQ around liver & within hepatorenal space.
 Right= Free fluid seen around spleen under the diaphragm in LUQ.

Renal Ultrasound
 Normal kidney:
 Gerota’s fascia creates a bright outline of kidney.
 The underlying renal cortex appears grainy & slightly less echogenic than surrounding liver
or splenic tissue.
 The renal sinus, which contains calyces & renal pelvis, appears hyperechoic due to fat
between the renal sinuses.
 The fluid-filled medullary pyramids and renal calyces appear black.
 Kidneys are positioned slightly obliquely with inferior poles more anterior & lateral.
 Imaging the full length of kidney requires slight (15 to 30 degree) rotation of transducer.
 In longitudinal axis, kidney appears in the shape of a football.
 In the transverse, view it is C-shaped.
 Image Acquisition
a) Right Kidney:
 Place transducer in coronal plane in mid to anterior axillary line at the level of xiphoid.
 Aim the probe slightly posteriorly to visualize the kidney.
 Center the kidney in the middle of the screen, then rotate counter clockwise 15 to 30
degrees to appreciate the longest axis.
 Assess the entire kidney by tilting the probe anteriorly and posteriorly.
 Rotate 90 degrees to evaluate the short axis.
 Tilt to evaluate the superior and inferior pole.
b) Left Kidney:
 Start with the transducer in the posterior axillary line.
 Center the kidney, rotate 15-30 degrees clockwise to find longest axis, then fan through
kidney.
 Rotate 90 degrees& tilt superiorly and inferiorly to evaluate the entire length of kidney.
 Hydronephrosis
 Differentiated by mild, moderate, and severe:
a) Mild: increased fluid within the calyces with preservation of renal papillae.
b) Moderate:rounding of calyces with ballooning of papillae. Preservation of outer cortex
c) Severe: large calyces and pyramids filled with fluid surrounded by thinned cortex.
 Compared to renal cysts, in hydronephrosis, all dilated areas of fluid can be traced back to
the collecting system.
 Unilateral hydronephrosis is likely 2ry to obstructive uropathy & may be associated with
pyelonephritis. DD for obstruction (ureteral stone, or retroperitoneal mass/adenopathy).
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 Bilateral hydronephrosis suggests bladder outlet obstruction and a sonographic bladder

exam should be performed at a minimum (Fig. 14.15).

Figure 14.15. Normal kidney (left). Mild/moderate hydronephrosis (right).

Bladder Ultrasound
 Evaluate for bladder distention& differentiate between true ↓urine production (empty
decompressed bladder)& postobstructive renal F caused by urinary retention (Fig. 14.16).
 With ↓ UOP, it is valuable test to make sure that Foley catheter is not blocked and to verify the
position of the Foley balloon within the bladder.
 Pelvic ascites can mimic the bladder.
 Bladder volume is calculated using measured height, width, and length:
Volume = 0.75 × w × h × 1
 Qualitative assessment: bladder dome is half way to umbilicus in a distended bladder.
 Image Acquisition
 Curvilinear probe is recommended since wider footprint allows visualization of entire UB
 Place transducer in transverse plane just superior to pubic symphysis& below umbilicus.
 Aim transducer inferiorly to appreciate the anechoic, fluid-filled bladder.
 Measure width and length in the transverse plane.
 Rotate probe 90 degrees to evaluate the long axis.
 Measure height in the sagittal (long) axis.

Figure 14.16 Transverse bladder

view with distended bladder
despite presence of Foley catheter
(inflated catheter balloon visible).
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15 Difficult Airway Management Strategies

Introduction
 Effective airway management involves addressing the challenges encountered in difficult
airway situations and potential complications, ranging from aspiration and esophageal
intubation to more severe outcomes, such as dental injury, hypoxic brain injury, and even death.
 It requires a comprehensive approach that includes airway evaluation, preparation for difficult
airway management, actual management of difficult airway (both anticipated & unanticipated),
and confirmation of tracheal intubation, extubation, and follow-up care.
 To explore the latest approaches to difficult airway management, this article aims to review
various guidelines, with a focus on 2022 ASA & 2015 DAS guidelines.
Incidence
 Incidence of difficult & impossible face mask ventilation are 1.4–5.0% & 0.07–0.16%,
respectively.
 The incidence rates of difficulty and impossibility of intubation with a classic laryngoscope are
5–8% and 0.05–0.35%, respectively.
 The success rate of intubation using video laryngoscope ranges from 97.4% to 99.6%.
 The incidence of impossibility of placing the supraglottic airway (SGA) ranges from 0.2 to 8%.
 The incidence of situations “cannot intubate, cannot oxygenate” ranges from 0.0019 to 0.04%.
Evaluation Of The Airway
 Healthcare providers involved in airway management must be able to identify and assess risk
factors for difficult airways.
 Predicting a difficult airway allows the implementation of prophylactic measures and provides
valuable time for adequate preparation.
 Various predictive factors indicate the risk of a difficult airway, including demographic
information, history or medical records, and physical examination findings (Table 1).
Table 1. Methods to Evaluate a Difficult Airway
Demographic information Age, sex, BMI, weight, & height
History of difficult intubation (sedation & anesthesia records)
History or medical record Distorted airway anatomy
Snoring and obstructive sleep apnea
Diabetes mellitus
Findings of diagnostic tests (e.g., radiography & CT)
Measurement of facial and jaw features
(mouth opening, ability to prognath, head& neck mobility,
prominent upper incisors, presence of beard & upper lip bite test)
Anatomical measurement
Physical examination (Mallampati & modified Mallampati scores, thyromental distance,
sternomental distance, interincisor distance, neck circumference,
ratio of neck circumference to thyromental distance, ratio of
height to thyromental distance, hyomental distance, and
hyomental distance ratio)
Measurements obtained from ultrasound
(skin-to-hyoid distance, tongue volume & distance from skin to
epiglottis)
 Although these factors can facilitate the prediction of difficult airways, there are no ideal
predictive factors available.
 Among the aforementioned predictive factors, a history of difficult airways is crucial. However,
the upper lip bite test, shorter horizontal distance, retrognathia, and Wilson score have been
recommended as predictors (Table 2).
 Wilson score is composite scoring that combines various evaluation techniques (Table 3).
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 Among these, upper lip bite test (inability to bite upper lip with lower incisors) is recommended
as bedside test that healthcare providers can easily perform to predict difficult airways (Fig. 1).
 Several mnemonic acronyms help recall risk factors for difficult intubation, mask ventilation,
SGA placement, and surgical airway procedures (Table 4).

Table 2. Recommended Predictors of Difficult Airway

Test Methods +VE LR (95% CI) Specificity (95% CI)
Upper lip bite Protrude the chin forward& bite 14 (8.9–22) 0.96 (0.93–0.97)
upper lip with the lower incisors
Short Range of < 3–5.5 cm 0.97 (0.94–0.98)
6.4 (4.1–10)
hyomental
distance
Mandible measuring < 9 cm
Retrognathia 6.0 (3.1–11)
from angle of jaw to tip of chin 0.98 (0.90–1.0)
or subjectively short
Weight, Cervical spine mobility
Wilson score ↓ jaw mobility, Retrognathia 9.1 (5.1–16) 0.95 (0.90–0.98)
Prominent incisors
LR: likelihood ratio, CI: confidence interval.

Table 3. Wilson Score (Range, 0-10)

Parameter 0 1 2

Weight (kg) < 90 90–110 >110

Cervical spine
> 90° 90° <90°
mobility
Interincisor gap ≥ 5 cm Interincisor gap < 5 cm Interincisor gap < 5 cm
Impaired jaw or able to protrude & only able to & unable to protrude
mobility lower teeth past protrude lower teeth lower teeth to meet
upper teeth to meet upper teeth upper teeth
Retrognathia Normal Moderate Severe
Prominent incisors Normal Moderate Severe

Table 4. Mnemonic Acronyms of the Risk Factors for a Difficult Airway

Intubation Face mask ventilation Supraglottic airway Surgical airway
LEMON MOANS RODS SHORT
Look Mask seal Restricted mouth Surgery
Evaluate 3-3-2 Obstruction, obesity Obstruction Hematoma
Mallampati Age > 55 years Disrupted or distorted Obesity
Obstruction, obesity No teeth Stiff lungs or C-spine Radiation
Neck Stiff lungs or C-spine Tumor
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Fig. 1. Upper lip bite test. The upper lip bite test, which involves instructing patients to bite their upper lip
with their lower incisors, offers a classification system based on the following criteria: Class 1, the lower
incisors extend beyond the vermilion border of the upper lip; Class 2, the lower incisors can bite the lip but
cannot extend above the vermilion border; Class 3, the lower incisors cannot bite the upper lip at all.
Preparation For Difficult Airway Management
 Involves the presence of a healthcare provider skilled in airway management along with another
healthcare provider dedicated to monitoring the patient’s condition, including vital signs.
 Before the initiation of airway management, all necessary equipment should be readily
available within the workspace and a portable storage unit should be accessible at all times in
emergency situations (Table 5).
 It is essential to explain the procedure adequately and obtain consent from the patient or the
responsible person before initiating airway management.
 Basic patient monitoring devices should be attached to assess vital signs before the procedure.
Table 5. Airway Management Equipment
 Self-inflating resuscitation bag
 Suction tubing, Yankauers, suction catheters & appropriate connectors
 Face masks
 Oropharyngeal and nasopharyngeal airways
 Classic laryngoscope blades and handles
 Video laryngoscope
 Endotracheal tubes
 Tracheal tube introducer (bougie)
 Stylets
 Equipment for emergency invasive airway management
(cricothyroidotomy)
 Supraglottic airway
 Water-soluble medical lubricant
 Nasal cannula and oxygen face mask
 Standard ASA monitoring (pulse oximetry with variable pitch pulse tone,
ECG, end-tidal CO2 monitoring, BP& HR measurements)
 Anesthetic induction, maintenance, and rescue medications
 Other medications

Preoxygenation
 Adequate preoxygenation is crucial before initiating airway management. When sufficient
preoxygenation is performed, it takes approximately 9 min for oxygen saturation to ↓ to 80%.
 Therefore, sufficient preoxygenation time is essential for patient safety during difficult airway
management.
 Methods are providing O2 for (3 min through normal breathing or 1 min through vital capacity
breathing)
 Even after sufficient preoxygenation, continuous oxygen administration should be maintained
during airway management procedures
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Anticipated Difficult Airway Management

 In situations where a difficult airway is anticipated, the healthcare provider performing airway
management is responsible for selecting appropriate strategies and techniques (Fig. 2).
A. Awake Intubation
 Indications:
a) difficult laryngoscopy
b) difficult face mask V or SGA
c) risk of aspiration,
d) risk of rapid desaturation,
e) difficult emergency invasive airway.
 Methods for awake intubation include video laryngoscopy, fiber optics & invasive access
techniques such as tracheostomy and cricothyroidotomy.
 Awake intubation requires patient cooperation. However, in pediatric or uncooperative
patients, intubation may have to be performed after induction of general anesthesia,
regardless of the possibility of airway management challenges. In these cases, additional
preparation and personnel are required.
 Recommendations for awake intubation are presented in Table 6.
Table 6. Recommendations for Awake Intubation
1. Awake tracheal intubation must be considered in the presence of predictors of difficult
airway management.
2. Cognitive aid such as checklist is recommended before& during awake tracheal intubation
3. Supplemental oxygen should always be administered during awake tracheal intubation.
4. Effective topicalization must be established and tested. The maximum dose of lidocaine
should not exceed 9 mg/kg of lean body weight.
5. The careful use of minimal sedation can be beneficial & should be administered by
independent practitioner. Sedation should not be used as substitute for inadequate airway
topicalization.
6. The number of attempts should be limited to 3, with one additional attempt allowed if a more
experienced operator is present (3 + 1).
7. Anesthesia should only be induced after a two-point check (visual confirmation and
capnography) has confirmed the correct position of the tracheal tube.
8. All departments should support anesthetists in attaining and maintaining competency and
skills in awake tracheal intubation.

 In awake intubation, appropriate positioning of ETT can be confirmed by visual confirmation

to observe passing through the vocal cord and capnography because tip of ETT can be
located in oropharynx or nasopharynx while still allowing capnographic monitoring (Fig. 3).
 The essential factors in awake intubation are conveniently described using the acronym
“STOP” (sedation, topicalization, oxygenation, and performance).
 Furthermore, the characteristics of available drugs and considerations for specific situations
are discussed in detail.

Fig. 3. Malposition of ETT where EtCO2 can be

measured. The appropriate location of ETT is
within trachea. However, in cases where the
tip of ETT is positioned in oropharynx or
nasopharynx, capnography can still be
measured.
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B. Intubation after induction of general anesthesia

1. Intubation
 During intubation, it is important to perform sufficient preoxygenation & maintain O2
supply throughout airway management.
 Up to 3 intubation attempts are allowed; additional attempts may be made if a more
experienced healthcare provider is available.
 With each new attempt, the following variations should be introduced: (1)
repositioning the patient, (2) using a video-laryngoscope, (3) changing the blade size
of the laryngoscope, or (4) externally manipulating the larynx.
 If difficulties are anticipated, even with a new attempt, it may be appropriate to
proceed to the next step without making 3 attempts.
2. Face mask ventilation
 If intubation fails after GA induction, face mask ventilation should be attempted.
 Evaluation of the adequacy of face mask ventilation through EtCO2 monitoring.
 If adequate O2 supply can be achieved through face mask ventilation, alternative
methods can be considered: (1) awakening the patient (2) using SGA or (3) using
invasive access.
3. SGA
 If O2 supply through face mask ventilation fails, SGA can be considered.
 If successful oxygenation is achieved with SGA, 4 options can be considered: (1)
awakening the patient, (2) performing intubation through SGA, (3) proceeding with
ventilation using SGA, or (4) using invasive access methods.
4. Invasive access (emergency pathway)
 Should be considered when attempting oxygenation through face mask ventilation or
SGA.
 The available options include surgical cricothyrotomy, needle cricothyrotomy with a
pressure-regulated device, large-bore cannula cricothyrotomy, surgical
tracheostomy, retrograde wire-guided intubation, percutaneous tracheostomy, and
rigid bronchoscopy.
5. Extracorporeal membrane oxygenation (ECMO)
 In cases where difficult airways are expected, it may be necessary to apply ECMO
before initiating airway management or prepare for ECMO before proceeding.
6. Declaration of failure & call for help
 When O2 supply fails, it is crucial to declare failure, call for help, & maintain
awareness of the limited number of attempts& elapsed time. Patient awakening
should be considered if feasible.

Unanticipated Difficult Airway Management

 When encountering unanticipated difficult airway, it is crucial to call for assistance &
optimize oxygenation.
 Following these initial steps, strategic decisions must be made (Fig. 4).
 A rapid response based on difficult airway management guidelines (including 2022 ASA
guideline & 2015 DAS guideline) is essential.
 Specifically, the following steps must be considered:
1) decide whether to awaken the patient or attempt to restore spontaneous breathing,
2) choose between noninvasive and invasive airway management,
3) consider combination techniques in noninvasive airway management,
4) consider ECMO as an option .
 To effectively manage unanticipated difficult airway situations, consistent education &
practice are essential to improve individual competencies and promote efficient &
systematic team approach through team dynamics.
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Confirmation Of Tracheal Intubation

 Various methods can be used to confirm tracheal intubation, such as direct visualization
of the vocal cords, observation of increased chest movements, and auscultation.
 The recommended methods include capnography and EtCO2 monitoring.
 In cases of uncertainty about tracheal intubation, 2 approaches can be considered: (1)
perform extubation followed by reintubation and (2) perform a reassessment through
visualization techniques such as flexible bronchoscopy, ultrasonography, or radiography.

Extubation Of Difficult Airways

 Difficulties may occur even after extubation. Therefore, formalized strategies and
preparations are necessary to ensure safe extubation.
 Consequently, DAS extubation guidelines can be used
 The selected strategy may vary depending on the nature of procedure or surgery, the
patient’s vital signs and condition, and the expertise and preferences of the healthcare
providers.
 Table 7: essential considerations that must be considered while preparing for extubation
Table 7. Comprehensive Extubation Checklist
 Assess readiness for extubation (spontaneous breathing & vital signs)
 Conduct with clinicians skilled in airway management
 Choose the appropriate time and place for extubation
 Decide the extubation strategy (awake extubation or deep extubation)
 Prepare reintubation
 Consider extubation with airway exchange catheter or supraglottic airway
 Provide supplemental O2 throughout the extubation process
 Assess the need for tracheostomy
 Post-extubation care (consider steroids and/or racemic epinephrine)

Follow-Up Care
 To ensure continued safety among patients undergoing difficult airway management,
information must be shared with patients or persons responsible for difficult airway
management and documented.
 This information includes the presence of a difficult airway, the cause of the difficult
airway, the solution strategies for the difficult airway, and what to tell medical personnel
when performing other procedures or surgery.
 Additionally, patients must be registered in a difficult airway management system.
Guidelines
 Table 8 presents the latest airway management guidelines.
Conclusion
 It is essential to remember that difficult airway situations can occur anytime and
anywhere.
 First, it is crucial to improve the ability of the healthcare professional to predict difficult
airways. Predicting and adequately preparing patients for such situations can improve
patient safety. Consequently, healthcare providers must be trained in the proficient use
of airway management equipment, and it is important to ensure that the necessary
equipment is readily available.
 Therefore, algorithms that are easily accessible in such situations are recommended.
 In difficult airway management situations, considerations are necessary when selecting
equipment and techniques. Accordingly, it is important to develop guidelines specific to
each hospital based on the experience, preferences, and capabilities of the medical
team, as well as the availability of equipment.
 Mastering difficult airway management goes beyond theoretical knowledge& requires
practical experience. Therefore, implementing regular training through simulation-based
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education is the key to improving competence and improving patient safety in difficult
airway scenarios.
 Before initiating airway management, it is crucial to provide sufficient explanations and
share algorithms with patients and their fellow medical staff. Open communication helps
ensure that participants understand the plan and actively participate in the process.
 Patients with difficult airways should receive detailed explanations of the causes and
potential solutions before obtaining informed consent. Sharing this information in a
documented format ensures that both the patient and healthcare team have a clear
understanding of the challenges and proposed strategies, which fosters a sense of
shared responsibility for optimal patient care.
 Patient safety in difficult airway management can be facilitated through the prediction of
a difficult airway, thorough preparation, simulation-based education, development of
algorithms suitable for each medical site, and sufficient communication in pre-procedural
explanation and post-management care.

Fig. 2. American Society of Anesthesiologists difficult airway algorithm (2022)

1) Low- or high-flow nasal cannula, elevated position of the head throughout the procedure,
and noninvasive ventilation during preoxygenation
2) Awake intubation techniques include flexible bronchoscope, video laryngoscopy, direct
laryngoscopy, combined techniques, and retrograde wire-aided intubation
3) Invasive airway techniques include surgical cricothyrotomy, needle cricothyrotomy with
a pressure-regulated device, large-bore cannula cricothyrotomy, or surgical
tracheostomy. Elective invasive airway techniques include above and retrograde wire-
guided intubation and percutaneous tracheostomy. Moreover, consider rigid
bronchoscopy and ECMO
4) Other options include, but are not limited to, alternative awake technique, awake elective
invasive airway, alternative anesthetic techniques, induction of anesthesia (if unstable or
cannot be postponed) with preparation for emergency invasive airway, and postponing
the case without attempting the above options
5) Consideration of size, design, positioning, and first versus second-generation SGA may
improve the ability to ventilate
6) Includes postponing the case or postponing the intubation and returning with appropriate
resources (e.g., personnel, equipment, patient preparation, awake intubation)
7) Alternative difficult intubation approaches include, but are not limited to video-assisted
laryngoscopy, alternative laryngoscope blades, combined techniques, intubating SGA
(with or without flexible bronchoscopic guidance), flexible bronchoscopy, introducer, and
lighted stylet or light wand. Adjuncts that may be used during intubation attempts include
tracheal tube introducers, rigid stylets, intubating stylets, or tube changers & external
laryngeal manipulation
8) Other options include, but are not limited to, proceeding with the procedure using a face
mask or SGA ventilation. The pursuit of these options usually implies that ventilation will
not be problematic.
SGA: supraglottic airway, CICV: cannot intubation, cannot ventilation.
 Fig. 2. American Society of Anesthesiologists difficult airway algorithm (2022)
1) Low- or high-flow nasal cannula, elevated position of head throughout procedure & noninvasive MV during preoxygenation
2) Awake intubation techniques include flexible bronchoscope, video laryngoscopy, direct laryngoscopy, combined techniques, and
retrograde wire-aided intubation
3) Invasive airway techniques include surgical cricothyrotomy, needle cricothyrotomy with a pressure-regulated device, large-bore
cannula cricothyrotomy, or surgical tracheostomy. Elective invasive airway techniques include above and retrograde wire-guided
P A G E | 97

intubation and percutaneous tracheostomy. Moreover, consider rigid bronchoscopy and ECMO
4) Other options include, but are not limited to, alternative awake technique, awake elective invasive airway, alternative anesthetic
techniques, induction of anesthesia (if unstable or cannot be postponed) with preparation for emergency invasive airway, and
postponing the case without attempting the above options
5) Consideration of size, design, positioning, and first versus second-generation SGA may improve the ability to ventilate
6) Includes postponing the case or postponing the intubation and returning with appropriate resources (e.g., personnel, equipment,
patient preparation, awake intubation)
7) Alternative difficult intubation approaches include, but are not limited to video-assisted laryngoscopy, alternative laryngoscope
blades, combined techniques, intubating SGA (with or without flexible bronchoscopic guidance), flexible bronchoscopy, introducer,
and lighted stylet or light wand. Adjuncts that may be used during intubation attempts include tracheal tube introducers, rigid stylets,
intubating stylets, or tube changers & external laryngeal manipulation
8) Other options include, but are not limited to, proceeding with the procedure using a face mask or SGA ventilation. The pursuit of
these options usually implies that ventilation will not be problematic.
APPLIED ICU NOTES - VOLUME II - BY DR. MOHAMED ERFAN
Fig. 4. DAS management of unanticipated difficult tracheal intubation (2015)
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Section II :
Common ICU Drugs& Equations
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16 ICU Drugs
A- Drug-Drug Interactions
Table 16.1 Cytochrome P450 Enzyme Substrates, Inhibitors& Inducers
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(continued) Cytochrome P450 Enzyme Substrates, Inhibitors& Inducers

Table 16.2 Drugs with Serotonergic Propertiesa

A= combination of these agents may increase risk for serotonin toxicity manifested by
triad of symptoms including: (1) cognitive changes, (2) autonomic instability, & (3) NM
excitability.
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Table 16.3 Frequent Drug–Drug Interactions in Critically Ill Patients

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(continued) Frequent Drug–Drug Interactions in Critically Ill Patients

A = ↑ increase serum/tissue concentration; ↓ decrease serum/tissue concentration.

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Table 16.4 Drugs Associated with QT-Interval Prolongation

The combination of these agents may increase the risk for adverse arrhythmic event
including torsades de pointes.
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B- Commom Drud Dosages & Side Effects

 Toxicities were classified as “rare” & “common” in relative fashion for each
agent.
Shock Medications
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Respiratory Disorders Medications

A= mmediate-release form. HPA, hypothalamic–pituitary–adrenal; BID, twice

daily; QID, four times a day; PO, by mouth.
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Cardiac Disorders Medications

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A=Usual starting doses are listed for furosemide and torsemide; dosing is
highly variable and much larger doses are often used.
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Electrolytes Abnormalities Medications

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Endocrine Disorders Medications

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Temperature Disorders Medications

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Toxicology Disorders Medications

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Infectious Diseases Medications

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Hepatic & GIT Disorders Medications

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Neurology Disorders Medications

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Hematopoetic Disorders Medications

Oncologic Emergencies Medications

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Medication of Pregnancy Related Emergencies

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17 Common Equastions & Rules of Thumb in ICU

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Section III
Curves& Traces
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18 ECG in critical care

 Brugada syndrome:
 Genetic disorder with abnormal electrical activity of heart > increases the risk of
abnormal rhythms & sudden cardiac death, at rest and may be triggered by a fever.
 25% of patients have a family history of this condition. May be due to a new genetic
mutation or certain medications. The common involved gene is SCN5A which
encodes the cardiac Na channel.
 Has 3 forms of ECG pattern.( Pseudo-RBBB+STE in V1&2):
1. Coved ST + STE ≥ 2
mm+ down sloping ST
+ negative T
2. Saddle-back ST+ STE
≥2 + positive or biphasic
T, seen in healthy.
3. Either 1 or 2 +STE < 2
mm, seen in healthy.

 Hypothermia: Temp< 35, has the following ECG changes:

 Osborn (J) wave: convex positive
deflection (negative in aVR & V1) at
junction of QRS & ST, not
pathognomonic, seen in: hyperCa, head
injury, SAH & IC hypertension.
 Bradyarrhythmia’s: sinus bradycardia, AV block, slow AF.
 Prolonged PR, QRS & QT interval.
 Ventricular ectopy, cardiac arrest, VF, VT, shivering waves (artifact).
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 Wellens sign: inverted T wave may extend to V6:

 De Winter T wave: anterior STEMI equivalent that presents with no obvious STE+
peaked T or ST depression in pericardial leads.

 Arrhythmogenic right ventricular dysplasia (ARVD): AD, +ve family Hx of cardiac

arrest, Hx of palpitation, syncopal attack, sudden arrest in 10%, 2 nd cause of death in
young after HOCM. Characteristic Epsilon wave+ T inversion from v1 to v3+ absence
RBBB, D by ECHO, MRI, treated by urgent ICD, Radiofrequency ablation for repeated
symptomatic.
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 Right ventricular outflow tachycardia (RVOT): LBBB+ Inferior access= can be normal
or RT axis deviation but not left axis+ Pericordial transition usually at or after V3. Acute
termination in stable by vagal maneuver or adenosine or verapamil if BP is adequate.If
RVOT with ARVD, adenosine will not be effective. If unstable do cardioversion.
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 R on T sign: high risk of Torsade de pointes, R on PVC wave came on T of previous

wave.

 VT versus SVT with BBB: Likelihood of VT include:

 Absence of typical RBBB or LBBB morphology.
 Extreme axis deviation (northwest axis): QRS positive in aVR & negative in I &
aVF.
 Very broad QRS complexes>160 ms.
 AV dissociation: P& QRS at different rates. P superimposed on QRS& difficult
to discern.
 Capture beats: occur when SAN transiently captures V in the midest of AV
dissociation producing QRS of normal duration.
 Fusion beats: occur when a sinus & ventricular beat coincide to produce a hybrid
complex (see Dressler beat).
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 Na channel blocker in ECG (eg: TCA toxicity)

 Sinus tachycardia + 1st degree AV block (P hidden in T, seen in V1-2).
 wide QRS + positive R in aVR >3 mm + prolonged PR & QT.

 Treatment of WPW syndrome: antiarrhythmic cause prolongation of accessory

pathway= class III: sotalol, amiodarone or class IA-C: procainamide & flecainide.
 Myxedema coma : Significant bradycardia-low volt R in limb leads - spread inverted T.
 Short P-R interval: WPW syndrome or Junctional rhythm.
 Prolonged QTc > 0.44 sec (measured from start of QRS to end of T wave), causes:
 Electrolytes: hypO (Ca, K, and Mg).
 Medications: TCA, antiarrhythmic (amiodarone, phenothiazine, haloperidol).
 Systemic diseases: SAH, cardiac ischemia, hypothyroidism.
 Congenital: Romano-Ward S, Jervell & Lange-Nielsen S (associated with defenses).
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 Electrolyte disturbance & ECG changes:

 HypoCa: Prolonged ST and QT intervals.
 HyperCa: shortened ST segment- widened T, short QT interval, Osborn wave.
 HypoK: ST depression- shallow, flat, inverted T - Prominent U wave, prolong QT.
 HyperK: peaked T waves- Flat P waves- widened QRS complex- Prolonged PR.
 HypoMg: Tall peaked T waves- Depressed ST segment, PR prolongation, U waves,
Widened QRS, prolong QT interval, tachycardia.
 HyperMg: prolongation of the PR interval and widening of the QRS complex.
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 Trifascicular block= RBBB + Lt Axis deviation (Lt Ant fascicular B) + HB 1 or 2 or

3.
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 Inferolateral STEMI + Posterior: Horizontal STD in V1-3+ Tall, broad R V2-3

+Dominant R (R/S ratio > 1) in V2 + Upright T in V2-3
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WPW + AF
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19 Mechanical ventilation
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Mechanical ventilator curves

 Types of waveforms (scalars and loops):
 Scalars: plot pressure, volume, or flow against time.
Time is x–axis.
o Pressure–time.
o Volume–time.
o Flow–time.
 Loops: plot pressure or flow against volume, no time component.
o Pressure–volume.
o Flow–volume.

 Basic shapes of waveforms:

1. Square wave:
o Represents constant parameter.
o Example: pressure setting in PC mode or flow rate in
VC mode.

2. Ramp wave:
o Represents variable parameter.
o Can be accelerating or decelerating.
o Vary with changes in lung characteristics.

3. Sine wave:
o With spontaneous or unsupported breathing.

 Types of waveforms (volume – pressure)

1) VC – SIMV:
o Volume modes: shape of
pressure wave will be ramp
for mandatory breaths.

2) PC – SIMV:
 Pressure modes: shape of
pressure wave will be square
shape.
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A. Pressure Waveform:

 Baseline for pressure waveform will be higher when PEEP is added.

 Area under the entire curve represents mean airway pressure.

 Negative deflection just before waveform with patient triggered breaths.

 Uses of pressure waveform: it can be used to assess:
1. Air trapping (auto–PEEP) 5. Breathe Type (Pressure
& airway Obstruction. vs. Volume).
2. Bronchodilator Response. 6. PIP and Pplat
3. Respiratory Mechanics 7. Asynchrony.
(C/Raw). 8. Triggering Effort.
4. Active Exhalation.
 Peak pressure:
 Definition: is a maximum pressure generated in the circuit.
 Peak pressure = airway resistance pressure + plateau pressure.
 Causes of elevated peak pressure:
a. Endotracheal tube being kinked (or chewed on).
b. Ventilator tubing being full of fluid.
c. Heat and moisture exchanger being waterlogged.
d. Secretions building up on the inside of the endotracheal tube.
e. Bronchospasm.
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 Airway Resistance Pressure:

 Definition: is a pressure produced by
the resistance of whole circuit (hoses –
ETT – bronchi).
 Presents only while flow is
occurring& relates directly to dynamic
compliance of chest.
 If flow stops → airway resistance
pressure drops to zero → airway
pressure can be estimated from
difference between P peak& P plat.
 Increased (Raw) due to ↑ PIP with
normal P plat.

 Air–Trapping (Auto–PEEP):
 Measurement by expiratory hold so the
trapped air makes expiratory pressure
waveform rises above baseline.
 Acceptable auto–PEEP < 5 cm H2O.

 Plateau Pressure (Alveolar Compliance Pressure):

 Definition: a pressure in lung after all
flow has stopped (alveolar pressure
generated by the delivered volume).
 Directly related to the compliance of the
lung parenchyma (static compliance).
 P plateau = VT / Compliance.
 ↓ Lung compliance by ↑ entire waveform
because more pressure is needed to
achieve the same tidal volume & the
difference between PIP & P plat remains
normal.
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B. Volume Waveform:
 Volume waveform will have mountain
peak appearance at the top.
 There will also be plateau if inspiratory
pause time is set or inspiratory hold
maneuver is applied to the breath.
 Can be used to assess:
o Air trapping (auto–PEEP).
o Leaks.
o Tidal Volume.
o Active Exhalation.
o Asynchrony.
 If exhalation side doesn’t return to
baseline it could be from air–trapping
or air leak.

C. Flow Waveform:
 Volume control mode= square waveform--Pressure control mode= ramp
waveform.

 Can be used to assess:

o Air trapping (auto–PEEP).
o Airway Obstruction.
o Bronchodilator Response.
o Active Exhalation.
o Breathe Type (Pressure vs.
Volume).
o Inspiratory Flow.
o Asynchrony.
o Triggering Effort.
 Auto–Peep (air trapping):
o Expiratory portion of the
waveform doesn’t return to
baseline before the start of the
next breath starts.
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 Bronchodilator response:
o Known by ↑ Peak expiratory
flow rate& expiratory portion
returns to baseline sooner.

D. Pressure/Volume Loops:
 Inspiratory curve is upward – Expiratory curve is downward.
 Spontaneous breaths go clockwise– positive pressure breaths go counterclockwise.
 The bottom of the loop will be at the set PEEP. It will be at 0 if there’s no PEEP set.
 If imaginary line is drawn down the middle of
loop:
o Area to right = inspiratory resistance.
o Area to left = expiratory resistance.
 Can be used to assess:
o Lung over distention
o Airway obstruction
o Bronchodilator Response.
o Respiratory Mechanics (C/Raw).
o WOB.
o Flow Starvation.
o Leaks.
o Triggering Effort.
 Dynamic compliance (C dyn):
o The top part of P/V loop represents C dyn.
o C dyn = 𝚫 𝐯𝐨𝐥𝐮𝐦𝐞 / 𝚫 𝐩𝐫𝐞𝐬𝐬𝐮𝐫𝐞.

 P–V loop in pressure modes:

o Almost square shaped because of pressure
limiting during inspiration.
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 Beaking:
o Pressure continues to increase with little or
no change in volume (bird beak).
o Correct it by ↓ VT delivered.

 Increased resistance:
o ↑ Expiratory resistance by secretions &
bronchospasms.
o ↑ Inspiratory resistance by kinked ETT&
patient biting tube.

 Leak:
o The expiratory portion of the loop doesn’t
return to baseline.

 Compliance:
o Increased with emphysema& surfactant
therapy.

o Decreased with ARDS, CHF& atelectasis.

 Inflection Points:
o Lower inflection point
represents point of alveolar
opening (recruitment).
o Some lung protection
strategies for treating ARDS,
suggest setting PEEP just
above the lower inflection point.
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E. Flow/Volume Loops:
 The shape of inspiratory portion of curve will
match the flow waveform.
 The shape of expiratory flow curve
represents passive exhalation.
 Used to determine PIF – PEF – VT.
 Looks circular with spontaneous breaths.
 Can be used to assess:
o Air trapping.
o Airway Obstruction.
o Airway Resistance.
o Bronchodilator Response.
o Insp / Exp Flow.
o Flow Starvation.
o Leaks.
o Water or Secretion accumulation.
o Asynchrony.
 Leak:
o Expiratory part does not return to
baseline.
o It can also occur with air–
trapping.

 Airway obstruction:
o Reduced peak flow: expiratory
part of the curve (scoops) with
diseases that cause small
airway obstruction (e.g. asthma
– emphysema).
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 Air Trapping (Auto–Peep):

 Causes:
o Insufficient expiratory time.
o Early collapse of unstable alveoli/airways during exhalation.
 How to identify it on the graphics:
o Pressure/Volume Loop= the loop doesn’t meet at the baseline.

Pressure W= by exp hold W above baseline. Flow W= exp flow not return to baseline.

Exp part of volume W doesn’t return to baseline. F/V Loop doesn’t meet at the baseline.

 Correction:
o Give treatment.
o Adjust I–time.
o Increase flow.
o Add PEEP.
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 Airway Resistance Changes:

 Causes:
o Bronchospasm.
o ETT problems à too small – kinked – obstructed – patient biting.
o High flow rate.
o Secretion build–up.
o Damp or blocked expiratory valve/filter.
o Water in the HME.
 How to identify it on the graphics:

Pressure wave ↑ PIP + normal plateau. Flow W= ↑ expiratory side& ↓ exp FR.

Volume W= ↑ exp W to reach the baseline. F/V loop= ↓ exp flow+ exp scooping.

P/V loop= wide loop bulge to right = ↑ insp Correction:

resistance & to left = ↑ exp resistance. o Give treatment.
o Suction patient.
o Drain water.
o Change HME.
o Change ETT.
o Add bite block.
o Reduce PF rate.
o Change expiratory filter.
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 Decreased Compliance:
 Causes:
o ARDS--Atelectasis.
o Consolidation—Fibrosis—Hyperinflation.
o Pneumothorax--Pleural effusion.
o Abdominal distension--Congestive heart failure.
 How to identify it on the graphics:
Pressure wave ↑ = PIP + ↑ plateau. P/V loop= more horizontal.

 Increased Compliance:
 Causes: emphysema or surfactant therapy.
 How to Identify it on the graphics:
o Pressure wave: ↓ PIP + ↓ plateau.
o Pressure/Volume loop: Stands more vertical (upright).

 Leaks:
 Causes:
o ETT cuff leak-chest tube leak-Broncho pleural fistula-nasogastric tube in trachea.
o Loose connections-ventilator malfunction-faulty flow sensor.
 How to identify it on the graphics:
o Pressure wave= decreased PIP.
o Flow wave= PEF decreased.
F/V loop = exp not return to baseline. P/V loop = exp not return to baseline.

Volume W= exp wave not return to Correction:

baseline. o Check possible causes listed above.
o Do leak test & make sure all
connections are tight.

 Asynchrony:
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 Causes:
o Air hunger (flow starvation).
o Neurological Injury.
o Improperly set sensitivity.
 How to identify it on the graphics:

F or P wave: tries to inhale/exhale in the middle of W →erratic flows/dips or dip in

pressure in the waveform.

P/V loop: patient makes effort to F/V loop: patient makes effort to breathe
breathe causing dips in loop either causing dips in loop either Insp/Exp.
Insp/Exp.

 Correction:
o Try to ↑ (flow rate – inspiratory time – RR).
o Change the mode from partial to full.
o If neurological →paralytic or sedative.
o Adjust sensitivity.
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 Rise Time
 Inspiratory rise time determines the amount of time it takes
to reach the desired airway pressure or peak flow rate.
 In pressure Support mode →used to assess if ventilator is
meeting patient’s demand.
 In SIMV: rise time = percent of the breath cycle.
 Too fast rise time:
o Definition: overshoot in pressure wave causing
pressure spike.
o Correct it by ↑ the rise time to open the valve slowly.

 Too slow rise time:

o Definition: slanted pressure wave causing ↓ VT.
o Correct it by ↓ the rise time to open the valve faster.

 Inspiratory Cycle Off:

 Definition: cycling of MV flow from inspiration to expiration, in Pressure Support
mode.
 Other names:
o Inspiratory flow termination.
o Expiratory flow sensitivity.
o Inspiratory flow cycle.)%(
o E–cycle, etc…
 In this example MV is set to cycle
inspiration off at 30% of patient’s peak
inspiratory flow.

 Too high: cycling off too soon causing

too small breath (not enough VT).

 Too low: too long breath which forces

the patient to actively exhale (exhalation
spike) causing ↑ WOB.
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 Phases Of The Ventilator Breath Delivery: 4 phases

1. Trigger Phase= the onset of patient effort to onset of flow delivery.
2. Flow/Inspiratory Phase= the onset of flow delivery to the termination of
inspiratory flow
3. Cycling Phase= the breath termination when ventilator inspiration ends.
4. Expiratory Phase = relaxation of resp muscles before next breath is initiated.

1 - Trigger phase 2- Flow/inspiratory phase

3 - cycling phase 4 - Expiratory phase

Patient Ventilator Asynchrony

 Ventilator asynchronies may occur at any phase of mechanical breathing.
A. Trigger Asynchronies:
1. Optimal Triggering.
2. Auto-Triggering.
3. Trigger Delay.
4. Ineffective Efforts.
5. Double Triggering.
6. Intrinsic PEEP.
7. Intrinsic Diaphragmatic Rate.
B. Flow Asynchronies:
1. Flow Mismatch.
2. Inadequate Driving Pressure.
3. Inappropriate Pressurization Rate (Rise time).
C. Cycling Asynchronies: premature cycling or delayed cycling.
D. Expiratory Asynchronies.
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Patient ventilator asynchrony

Triggering Asynchrony
1. Ineffective Triggering (Wasted Efforts)
 Refers to a patient’s inspiratory effort but not followed by a ventilator cycle.
 Definition: ↓ in pressure drop (≥ 0.5 cmH2o) + simultaneous ↑ in flow.
 Occurred with COPD, asthma, intrinsic peep and diminished respiratory drives
(such as deep sedation & brain stem injuries). Additionally, improper triggering
thresholds of the ventilator could lead to ineffective triggering.
 Occur during both mechanical inspiratory and expiratory phase, under both
pressure support & mandatory ventilation. Expiratory asynchrony due to short Te.
 Detected by airway pressure and flow waveforms combined with Pes or EAdi
signals which can improve the accuracy and sensitivity.
 Correction by
a) ↓ autopeep by ↓ minute ventilation.
b) ↓ inspiratory time to decrease tidal volume
c) ↓ PS and/or VT.
d) Applying extrinsic peep to ↓ patient’s inspiratory effort to trigger ventilator
e) Adjust the expiratory trigger sensitivity (ETS) to make it more sensitive to
the patient's activity
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Ineffective triggering, during expiratory & inspiratory phase; in PSV.

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Ineffective triggering during pressure assist-control ventilation (PA/C)

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↑ ETS to 30 % after red line which fix ineffective efforts

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2. Double triggering
 Definition: 2 cycles separated by a very short expiratory time (< ½ of the mean
inspiratory time, the 1st cycle being patient-triggered.
 For most patients, there is a pressure drop and flow change in the pre-inspiratory
phase, which indicates an inspiratory effort of the patient.
 Inspiratory asynchrony due to short mechanical Ti or Air hunger.
 Classification: 3 types according to 1st breathe triggering: patient-triggered, auto-
triggered& ventilator-triggered.
 Caused by a greater inspiratory effort and an insufficient level of PS.
 Lead to hyperinflation, even ventilator-induced lung injury.
 Commonly mistaken for the patient actively generating a 2nd breath (breath 2) after
delivery of a mechanically timed breath (breath 1) or air hunger.
 Closer analysis is recommended by utilizing esophageal manometry to compare
and contrast pleural pressure & ventilator’s airway pressure and flow changes.
 Correction:
a) Prolonging the Ti,
b) ↓expiratory flow-cycle %
c) Switching to PSV mode,
d) ↓ Patient’s respiratory effort through sedation.
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Double triggering occurring during pressure support ventilation (PSV)

 Example below-the addition of the esophageal pressure scalar waveform (pes- paux
waveform) reveals a DT is present because of the subsequent delivery of breaths
during a single active inspiratory effort (see ↓ in pleural pressure).
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3. Reverse Triggering
 Definition: inspiratory efforts triggered by ventilator in a repetitive & consistent
manner.
 Pes & EAdi, as an indicator of the patient’s inspiratory effort, combined with the flow
and airway pressure, can be used to identify reverse triggering.
 It has been observed in deeply sedated, brain-dead, and those with ARDS.
 Lead to hyperinflation, VILI, due to high VT & higher Pplat in VCV mode.
diaphragmatic Ms damage, ↑(WOB, O2 consumption, VT& transpulmonary P)
 Correction: by adjustment of mechanical rate or tidal volume & NM blockers.

Reverse triggering during pressure assist control ventilation

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Reverse triggering in PAC with EAdi

 Detection of patient effort that is ‘triggered’ by a ventilator is simpler to detect during

PC ventilation, because the flow will change when the effort occurs early enough in
the inspiratory phase (red arrows above).
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 During VCV the effort can be detected in the pressure-time tracing if flow is constant
since flow will not usually change in response to patient effort.
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4. Auto-Triggering
 Definition: an assisted breath delivered by the ventilator that is not triggered by the
patient (without a prior airway pressure decrease).
 Expiratory asynchrony with short cycles without any efforts
 Caused by: inappropriately high triggering sensitivity, flow change produced by the
cardiac oscillations, water condensation and leaks of the ventilator circuit.
 Lead to: hyperventilation, misjudgment of the patient’s spontaneous breath leading
to hypoventilation, even wrong clinical decisions.
 In pressure support ventilation, auto-triggering could be detected by an absence of
airway pressure decrease before inspiration, and could also be distinguished by
trigger sensitivity adjustment. Therefore, careful evaluation of the patient and
inspection of the airway pressure and flow signals are important to detect auto-
triggering. Besides, Pes & EAdi monitoring help in detection of auto-triggering.

 Correction by: avoid leaks & water condensation - ↓ trigger sensibility.

 Auto-triggering caused by leak in the circuit. Note that there is no drop of the airway
pressure in the pressure/time waveform (upper waveform) at the beginning of the
inspiratory phase which means that the breaths are not patient triggered.
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Flow Asynchrony
1. Insufficient Flow (Flow Starvation)
 When the ventilator’s flow setting is lower than the patient’s demand, a dish-out of
pressure waveform could be observed.
 In flow-targeted breaths, such as VCV (figure below is V A/C )
 The inspiratory flow or peak flow is usually set by the clinician.
 When the patient’s inspiratory demand is higher than peak flow of ventilator, a
downward deflection of pressure-time waveform could be observed.
 The accessory respiratory muscle of the patient may be used.
 Correction by: ↑ peak flow of ventilator, changing to pressure mode, or ↓
patient’s inspiratory demand.

 On pressure-targeted breaths, such as PSV & PCV ( figure below P A/C)

 The speed of flow delivery depends on the rise time set by the clinician.
 When the patient’s respiratory demand is higher, a drop of pressure-time
waveform could be seen.
 Correction By: shortening the rise time, ↑ applied pressure, or ↓ patient’s
respiratory demand.
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2. Excessive Flow
 When the ventilator flow setting is higher than the patient’s demand,
 A peaking of pressure waveform (overshoot) at the beginning of the inspiration could
be observed.
 Correction by:
a) ↓ inspiratory flow in VCV.
b) ↓ applied pressure or prolonging rise time in PCV.

Excessive flow delivery (overshoot) during pressure support V (PSV)

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Cycling Asynchrony
1. Premature (Early) Cycling
 Definition: termination of ventilator cycle despite the patient’s effort continued.
 Mechanism:
 Inspiratory Ms continue to contract after the end of ventilator inspiration, sharp
↓ in expiratory flow followed by ↑ then ↓ gradually to baseline.
 For some patients, the inspiratory muscle contraction may cause the ventilator
to deliver a 2nd breath, which is identified as double triggering, sometimes, it is
difficult to distinguish from ineffective triggering, while Pes & EAdi signals may
help to identify the deflection at the beginning of the expiratory phase is
caused by either the unfinished inspiratory effort or another new inspiratory
effort that fails to trigger the ventilator.
 Along with short Ti, double triggering is an indication of premature cycling
 Caused by: high inspiratory demand, short ventilator Ti & high flow-cycling %.
 Result in a larger tidal volume and even lung injury. It may cause double triggering
causing delivery of higher tidal volumes, breath stacking, and ↑ WOB.
 Correction by:
a) Prolonging ventilator Ti, trying to match the neural Ti with ventilator Ti
b) Increasing pressure support,
c) Lowering flow-cycling percentage (ETS) by 10% to lengthen Ti.
d) Decreasing the patient’s respiratory demand.
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Early cycling during PSV

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2. Delayed cycling
 Definition: patient’s expiratory effort starting before the ventilator switch to expiratory
phase, which is indicated by a spike in the airway pressure waveform and rapid
decrease of inspiratory flow towards the end of mechanical inspiration.
 Inspiratory asynchrony - Longer mechanical Ti
 It may be difficult to detect depending on the pressure and flow waveforms only when
there is no patient’s expiratory muscle contraction, we need Pes & EAdi signals
indicating the patient’s neural expiratory starting.
 Recognized by an end-inspiratory peak in the pressure curve caused by an active
expiratory effort, also a change in slope of inspiratory flow towards baseline.
 Caused by excessive support, long Ti, and large tidal volume,
 Lead to insufficient expiratory time, large tidal volume, air-trapping, and peepi.
 Correction by
a) Adjusting cycling off threshold, including ↓ Ti, ↓ applied pressure& ↑ flow-
cycling % (ETS), as well as switching to PS mode.
b) The optimal Ti &cycling need to be adjusted according to patient’s demand.
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Delayed cycling during (P A/C) mode

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Delayed cycling is typically described in COPD, reduction in inspiratory flow is

smaller, probably due to dynamic hyperinflation and airway resistance.

Delayed cycling + expiratory efforts.

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Answer is Flow Starvation

Weaning trial in patient with tracheostomy, describe the abnormality?

Answer is ineffective trigger
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Reverse triggering

Answer is missed trigger due to Auto-PEEP

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Q: patient with ETT cuff was left deflated by mistake

Answer: Auto-trigger due to leak (Volume is continuously decreasing)
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Double triggering. Must be spontaneous mode

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Early Cycling

Late cycling
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Patient with Broncho-pneumonia & the cause of asynchrony is secretions

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20 Pulmonary artery catheter

 It is useful to consider the hemodynamic data in a schematic representation of heart.

Figure: normal resting pressures at right heart catheterization

 Vascular resistance is expressed as metric units (dynes/sec/cm-5) or resistance units
(mmHg/L/min). The difference between them is that metric units are greater by a factor of
80. Resistance units are also called Wood units after the cardiologist who introduced them.
 What are the normal O2 saturation values encountered during RT heart catheterization?
 SVC: 70%  RV: 75%
 RA: 75%  PA: 75%
 Wedged position, blood aspirated from distal port: 98%
PAC insertion waveforms
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Hemodynamic data from the PAC in different clinical scenarios

Cardiogenic shock
 Clinical signs of hypoperfusion in conjunction with hemodynamic data demonstrating
decreased cardiac index and markedly elevated PAOP.

Right heart failure

 Increases in RV end-diastolic and mean RA pressures.
 If caused by LV failure, these increases will be accompanied by ↑ in PAOP & ↓ CI.
 In isolated RV infarct, RAP will be disproportionately elevated compared to PAOP.

Figure: RV infarct cardiogenic shock

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Septic shock
 In the early stages: low arterial pressure, normal or low PAOP & ↑ SI/CI may be manifest.
 In the later stages of the disease LV failure may occur.

Ventricular septal defect (VSD)

 Acute ventricular septal rupture: right heart catheterization may show a step-up in oxygen
saturations of blood (>7%) in the pulmonary artery compared to RA.
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Acute mitral regurgitation

 In addition to a systolic murmur, a giant V wave occurs in the PAOP waveform.
 With a simultaneously recorded ECG, the PAOP V wave of acute MR occurs (well after the
T wave), while the peak PA systolic wave (occurs within the QRS).

Figure: V wave Pcwp

Acute massive pulmonary embolism

 Moderate pulmonary hypertension is seen in acute PE. However, the RV & PA systolic
pressures rarely exceed 50-55 mmHg.
 At greater pressures in the acute setting the RV dilates and can fail.
 The finding of a PASP >55 mmHg indicates chronicity as the thin walled RV requires time
to hypertrophy to generate the higher pressure.
 The RAP is elevated and greater than the PAOP which is usually normal or low.
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Cardiac Tamponade
 The hemodynamic hallmark is equalization of RA, RV, PA diastolic & PAOP pressures.

Comparison of minimally invasive CO monitoring techniques

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 End expiratory occlusion test: ↑ CI > 5% during holding expiration, means fluid responder.

The first 3 are validated by many studies

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21 PICCO - Thermodilution curve

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 EVLWI= lung water (3-7 ml/kg). If > 10 ml/kg = clinical pulmonary oedema.
 PVPI (normal<3) = permeability= EVLW / pulmonary blood volume (PBV),
 Guide fluid management in risk of fluid overload (septic shock & ARDS).
 If high indicated non cardiogenic pulmonary edema (ALI& ARDS)
 Differentiate cardiogenic (↑ hydrostatic P) & non-cardiogenic PO (↑ permeability)
 ITBV = 1.25 * (GEDV relates to preload, but not to fluid responsiveness).

 How to read PiCCO ?

1) Initially assess the cardiac index (as a marker of contractility)
2) Assess the prelaod state (The most reliable marker is GEDVI)
3) Assess EVLWI ( To assess amount of lung water)
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4) If EVLWI is elevated you should assess pulmonary permeability index to assess

the integrity of the pulmonary capillary vascular membrane
 EVLWI>10 & PVPI>3 =↑ memb permeability=non cardiogenic PO (ARDS)
 EVLWI > 10 & PVPI < 3 = Hydrostatic pulmonary edema(cardiogenic).

22 Esophageal Doppler CO monitoring

 Flow time is corrected (FTc) = LV Ejection time:
 Indicates preload & inversely related with SVR.
 Normal range = 300-360 msec - depends on HR 60bpm.
 High in low SVR, (vasoplegia) ↓ afterload such in sepsis or drug induced.
 Low in vasoconstriction, indicate hypovolemia needs fluid resuscitation.
 Peak Velocity (PV):
 Indicates contractility
 Normal value = 90-120m/sec
 Low in LVF or β–blockade. Treated by inotropic support
 High with inotropes treatment or during exercise.
 Both PV & FTc used to evaluate afterload
 Low FTc >>>> need fluid
 Low PV >>>> need inotrope
 Low PV + Low FTc >>>> need to decrease afterload by vasodilators.
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23 IABP
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 Answer: too early inflation of balloon, leading to the LV continue to pump against an
obstruction which will increase LV work. Correction by delaying the inflation time.

 Answer: late deflation, leading to blunting of the assisted systole (it obstructs cardiac
outflow & may worsen cardiac performance.
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24 CVP
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25 ROTEM
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AF/CLD corrected by 1ST PCC / VIT K

Low fibrinogen = fibrinogen or CRYO

Fibrinogen dose is: 9 - A5 = X/2 = FIB g or CRYO = fib g x 4 or 5 = x unit

Thrombocytopenia = plat transfusion

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Hyper fibrinolysis = TXA 1g within 3h the 1g q8h

Hyper- coagulable state (PE) = thrombolysis

Exogenous Heparin effect = Protamine sulphate (1 mg/100 u heparin) max=50 mg

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Rare cases

Hyper fibrinolysis = TXA (repeat ROTEM) → +/- plat& fibrinogen

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Heparin effect = protamine sulphate

Low fibrinogen = fibrinogen/ cryo = Prolonged CT IN EXTEM= PCC/FFP

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Thrombocytopenia = plat transfusion

Low level of platelets

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Hyper-fibrinolysis

Heparin
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Hyper-fibrinolysis TXA
Low fibrinogen  FIB or CRYO

Normal ROTEM + Bleeding Exclude surgical cause

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26 ICP waveforms
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 Preserved cerebral blood flow auto-regulation: when BP goes up, ICP goes down.
 In case of loss of auto-regulation with massive increase in ICP: MAP & CPP not go up
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28 Capnography

Causes of ↓ EtCO2 over a short time:

1) Cardiac:↓CO (cardiac arrest,
hypotension, cardiogenic shock.
2) Vascular: V/Q mismatch (massive PE).
3) Pulmonary: interference with gas
exchange (pul edema) unlikely in above
trace.
4) Equipment problem: C. failure or sample
line being kinked.
5) blockage of circuit: anywhere from ETT
to ventilator
6) An ETT cuff leak.
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29 CRRT Waveforms
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Patient with intercostal drain for PTX, explain the volume- flow loop pattern
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30 ABG interpretation
 6 Steps Approach is Used for A.B.G Interpretation to reach a proper diagnosis:
1. Validity of ABG
2. Acidemia or Alkalemia?
3. Respiratory or Metabolic (Primary Disorder)?
4. Compensated or Not?
5. Mixed or Pure Primary?
6. Oxygenation.
1) Validity of ABG:
 When PH = 7.4 → H = 40
A. 1st rule: any ↑ or ↓ in PH by 0.3& its folds→ ↓ H by half or ↑ H by doubling.
o Examples:
 If PH = 7.7, H will Decrease by Half ( H = 20 )
 If PH = 7.1, H will Increase by Double (H = 80 )
 If Changes in PH by less than 0.3 → go to the 2nd rule.
B. 2nd rule: ↑ or ↓ in PH by 0.01 & its folds→ ↓ or ↑ H by 1.
o Examples:
 If PH = 7.25, H will Increase by 15.
 If PH = 7.55, H will Decrease by 15.
 The Previous Rules are used to know The Expected H According to PH in A.B.G.
 Then We Apply The Following Equation to Know the H in The A.B.G.
H = 24 x PaCo2/HCO3
If Both Equal Each Other (+/- 10%), this means That A.B.G. is Valid.
 Another So Easy Equation to know the Validity of A.B.G:
24 X PaCO2/HCO3 = (7.8 - PH) x 100
 DD of invalid A.B.G: several Factors affect the Accuracy of ABG,
 The Presence of Air Bubbles in the Sample, especially if they constitute >
1-2% of blood Volume.
 If the Sample was left > 15 Minutes.
o Blood consumes O2 and Produce CO2 as it is a living Medium.
o Also glycolysis can cause significant changes in PH, PaCO2 & PaO2
after 15 Min at RM Temp.
o This can be minimized by placing the sample in ice, so the sample can
be stored for nearly 30 minutes with little effect on accuracy.

 Heparin is acidic and can ↓ PH and also ↓ PaCO2 due to dilutional effect,
heparin use can be dropped out if the sample will be used immediately.
 The type of syringe: glass is better than plastic.
 The device is Well calibrated or not.
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2) Acidemia or Alkalemia?

3) Respiratory or Metabolic (Primary Disorder)?

 1ry disorder: Acidemia or Alkalemia is either Respiratory or Metabolic.
 In ABG we should look to: PH, PaCO2 & HCO3 to know the AB Disorder.
 Rules:
 PaCO2 reflects the Respiratory Part & HCO3 reflects the Metabolic Part.
 To know the 1ry Disorder (Respiratory or Metabolic), remember (RO ME)
o Respiratory (PaCO2) Opposite (PH), Metabolic (HCO3) Equal (PH).
o When PH goes in opposite direction with (PaCO2), this means 1ry
Respiratory Disorder.
o When PH goes in The Same direction with (HCO3), this means 1ry
Metabolic Disorder.
o Examples:
 If PH = 7.31 and PaCO2 =50, so 1ry Respiratory Acidosis.
 If PH = 7.31 and HCO3 =15, so 1ry Metabolic Acidosis.
4) Compensated or Not?
 There is no over-compensation.
 The compensation comes from the opposite system:
 In Respiratory disorders (reflected on PaCO2), compensation occurs via the
kidney (Reflected on HCO3).
 In Metabolic disorders (Reflected on HCO3), compensation occurs via the
Lung (reflected on PaCO2).
 Types of Compensation: either Full or Partial compensation.
a) Full compensation: means that PH Returns to normal range (7.35 - 7.45).
o Examples:
 PH=7.36, PaCO2=28, HCO3=16→Fully-compensated Metabolic
Acidosis.
 PH=7.36, PaCO2=55, HCO3=35 → Fully-compensated Res. Acidosis.
b) Partial compensation:
o The change is too large for compensation to restore normal PH.
o PH is out of normal range together with changes in the opposite
compensatory arm and these changes go with the Primary disorder.
o Examples:
 PH=7.30, PaCO2=30, HCO3=14 → partially compensated Metabolic
Acidosis.
 PH=7.6, PaCO2=48, HCO3=33→partially compensated Met Alkalosis
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c) Decompensated Metabolic or Respiratory disorder:

o Means that PH is out of normal range without any change in the opposite
compensatory arm (other ppposite Part within the normal range) or these
changes not go with the primary disorder.
o Examples:
 PH=7.27, PaCO2=53, HCO3=24→decompensated Resp Acidosis.
 PH=7.53, PaCO2=40, HCO3=30→decompensated Met Alkalosis.
5) Mixed or Pure Primary?
 To know if the acid-base disturbance is mixed or pure 1ry, you should know:
 Acidemia or Alkalemia is either Metabolic or Respiratory.
 Respiratory compensation is Immediate in Metabolic changes.
 Metabolic compensation (Renal) is delayed (full compensation occurs after
48 hours).
 Actual means the number present in the ABG paper (patient number).
 Expected means the number calculated by the next equations.
1. In Metabolic Acidosis respiratory compensation is immediate
Expected PaCO2 = {(1.5 x HCO3) +8} ± 2
 If Expected PaCO2 = Actual PaCO2 → only 1ry Metabolic Acidosis not mixed.
 If Expected PaCO2 > or < Actual PaCO2= added Respiratory element, so
mixed Metabolic and Respiratory.
 Example :
o In a patient with renal failure, Serum HCO3 is 15,
o Expected PaC02 = (1.5x15) +8) ± 2 = 30.5 ± 2.
o If Actual PaCO2 is between 28.5-32.5 → only 1ry Metabolic Acidosis not
mixed.
o If Actual PaCO2 > 32.5 → mixed respiratory acidosis with the 1ry
Metabolic Acidosis.
o If Actual PaCO2 < 28.5 → mixed respiratory alkalosis with the 1ry
Metabolic Acidosis.
 Anion Gap:
 In Metabolic Acidosis, you should calculate Anion GAP, to differentiate between
High Anion Gap (HAGMA) from Normal Anion Gap Metabolic Acidosis (NAGMA).
Anion Gap= Na - (Cl+HCO3)
 Normal Anion Gap = 12±4 (8-16)
 AG is corrected to the level of Albumin, ↓ in Albumin by 1, will ↓ AG by 2.5-3
 Normally, added Acids equals the consumed Bicarbonate if there is only one
Metabolic Acidosis disorder (1ry Metabolic Acidosis).
 In HAGMA, the ↑ in AG means ↑ in Added Acids.
 Added Acids= Measured AG - 12
 Expected HCO3 = 26 - Added Acids
o If Expected HCO3 = Actual HCO3 → no added either Metabolic Alkalosis
or Metabolic Acidosis.
o If Expected HCO3 > Actual HCO3 → added Metabolic Acidosis (Mostly
NAGMA).
o If Expected HCO3 < Actual HCO3 → added Metabolic Alkalosis.
 Another Approach to HAGMA (delta gap = delta AG – delta HCO3)
 Delta AG = Patient’s AG - 12 mEq/L
 Delta HCO3 = 26 mEq/L - Patient’s HCO3
 If there is just one Acid-Base Abnormality, there Should be a 1 : 1
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 Correlation between the rise in AG & a Corresponding drop in HCO3.

 ↑ AG by 10 → ↓ HCO3 by 10. So delta gap = 10 -10 = 0, so there is one Acid-
Base Problem here.
 Variation of the Delta Gap from Zero is either, Added Metabolic Alkalosis or
NAGMA, (Mixed Acid-Base Problem).
 NB: Understanding the AG
 To fully understand the AG, you should know that body fluids are electro-neutral
(total concentration of Cations = total concentration of Anions)
 (Na+ k+ Ca+ Mg) = (Cl+ HCO3+ Albumin+ Organic Anions+ PO4+ SO4)
 Anion Gap equals
1. = Na - (Cl + HCO3)
2. = (Albumin+ Organic Anions+ PO4+ SO4) - (k+ Ca+ Mg)
3. = (Unmeasured Anions - Unmeasured Cations)
 The AG equation Shows that the measured ions (Na, Cl and HCO3), used to
give information about the unmeasured Anions and unmeasured Cations.
 ↑ Unmeasured Anions or ↓ Unmeasured Cations → will ↑ AG.
 In NAGMA you should differentiate between GIT loss of HCO3 & Renal loss via
calculating the Urinary AG.
 Causes of high AG Metabolic Acidosis (HAGMA):
a) ↑ Endogenous Acid production: Lactate or Ketoacidosis.
b) Accumulation of Endogenous Acids with Renal Failure.
c) Toxins: Methanol, Ethylene Glycol and Salicylates.
 Causes of Normal AG Gap Metabolic Acidosis (NAGMA):
a) Loss of HCO3, in diarrhea or renal loss.
b) Renal tubular acidosis (loss of HCO3).
c) Carbonic anhydrase inhibition.
2. In Metabolic Alkalosis compensation is immediate through Hypoventilation.
Expected PaCO2 = {(0.75 x HCO3) + 21} ± 2
 ↑ HCO3 by 1 → ↑ PaCO2 by 0.6-0.7
 If Actual PaCO2 is > or < Expected PaCO2 → added Respiratory disorder to
the 1ry Metabolic Alkalosis.
3. In Respiratory Acidosis: it is either Acute or Chronic.
 Metabolic compensation (Renal compensation) is weak and delayed, which is
completed after 48 hours.
 In Acute Respiratory Acidosis compensation is weak.
o Causes: acute severe Asthma, respiratory depression central or
peripheral , air way obstruction
o ↑ PaCO2 by 10 above 40 → ↑ HCO3 by 1 above 26.
o IF PaCO2 =80, the Expected HCO3= 26 (Mean for
 In Chronic Respiratory Acidosis (COPD):
o Metabolic (Renal) compensation is completed.
o ↑ PaCO2 level by 10 above 40 → ↑ HCO3 level by 4 above 26.
 If Actual HCO3 < Expected HCO3 → added Metabolic Acidosis to the 1ry
Respiratory Acidosis.
 If Actual HCO3 > Expected HCO3 → added Metabolic Alkalosis to the 1ry
Respiratory Acidosis.
4. Respiratory Alkalosis: it is either Acute or Chronic.
 Compensation via the kidney (Metabolic) is delayed (after 2 days).
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 In Acute Respiratory Alkalosis: ↓ PaCO2 by 10 → ↓ HCO3 by 2

 In Chronic Respiratory Alkalosis: ↓ PaCO2 by 10 → ↓ HCO3 by 5
 If Actual HCO3 > or < Expected HCO3 → this means there is added Metabolic
disorder to the 1ry Respiratory Alkalosis.
6) Oxygenation: look for
A. Respiratory Failure has 2 types:
 Type 1: Hypoxemia (↓PaO2) with normal or decreased PaCO2.
 Type 2: Hypoxemia with hypercarbia.
o ABG is the only investigation, can document, specify & quantitate RF.
o High PaCO2, Moderately low PaO2 and Acidic PH, indicate ventilatory
failure
o Low PaCO2, Low PaO2 and Alkaline PH, indicate primary oxygenation
failure.
o The management plan will be ventilatory support in the former case & O2
therapy in later Case.
o Hypoxemia: PaO2 < 80mmHg &/or SO2 < 92%.
o Hypercarbia: PaCO2 > 45mmHg.
B. The P/F ratio (PaO2 / FiO2):
 The Smaller the Value, the Worse the Patient’s Gas Exchange.
 Commonly Used in Patients on Mechanical Ventilation as part of the
assessment of whether they have ARDS or not?
 P/F ratio < 300 is consistent with ARDS (provided Meets the other criteria).
C. A-a gradient = (PAO2 - PaO2)
 The difference between PaO2 in Alveoli (PAO2) and in arterial blood (PaO2).
 The Normal Gradient < 20
 PAO2=(FiO2x713)-(PaCO2x1.25)
 713= diference between barometric Pressure at sea level (PB=760mmHg) and
the humidification of inspired air inside airways (PH2O=47 which is the water
vapor pressure in MmHg and it is subtracted as only the dry alveolar gas
pressures are measured). 1.25=respiratory quotion or the ratio of O2 uptake to
CO2 exhaled.
 If A-a gradient > 20 = highly suspicious of ventilation perfusion mismatch ●
(especially pulmonary embolism).
 Age affects A-a Gradient :
o If aged 40, so A-a gradient=24
o If aged 60, so A-a gradient=31
o If aged 80, so A-a gradient=38.
 Oxygenation is the transfer of adequate O2 from Alveoli to the blood.
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Oxygenation Dissociation Curve

 Interpretation of PO2
 Requires knowledge of the sigmoid oxy-hemoglobin dissociation curve.
 The Sigmoid Shape derives from the fact that hemoglobin consists of 4 subunits,
and binding of O2●to one subunit facilitates the binding of O2 to the other units.
 Binding of O2 to hemoglobin results in conformational changes to the molecular
subunits, making the histidine residues less ready to accept H+.
 So, deoxy-hemoglobin is a better H+ acceptor than is oxy-hemoglobin, allowing
deoxygenated ● blood to transport more CO2 (in the form of H + HCO3) than
oxygenated blood does, this is called the Haldane Effect.
 Deoxygenated hemoglobin is also more ready to bind CO2 in the form of carbamino
compounds at terminal amine groups.
 Conversely, the presence of H+ reduces hemoglobin’s affinity for O2, so, a low PH
shifts the dissociation curve to the right, making hemoglobin more ready to give up
O2 at a given PaO2, this is called the Bohr Effect.
 The Bohr and Haldane Effects, make useful physiological sense, the high O2
environment of the lungs oxygenates hemoglobin and so, causes H+ release and
reformation of CO2 to be expired, while the high CO2 environment of the tissues
acidifies red cells and so, facilitates O2 release.
 Acidosis, hypercarbia and increased temperature are all features of the local
circulation in metabolically active tissues, & they all ↑ O2 unloading from hemoglobin.
 PaO2:
 Reflects gas exchange in lungs, normally, it ↓ with age due to ↓ elastic recoil of lung.
 The Expected PaO2= 100-(Age X 0.25)
 The decrease in PaO2 less than Expected indicates hypoxemia and this can result
from hypoventilation or Mismatch of V/Q.
 PaO2 < 60mmHg warrants immediate therapeutic intervention.
 2.3 DPG (Diphosphoglycerate):
 Present in RBC, It reduces hemoglobin affinity for O2.
 Increases in chronic hypoxia and anemia.
 Progressively decreases in stored blood.
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 Ventilation:
 (Alveolar Ventilation, Ventilation of CO2).
 The PaCO2 directly reflects the adequacy of alveolar ventilation.
 Causes of Metabolic alkalosis:
 Current or Recent diuretic use.
 Excess Alkali administration.
 Refeeding alkalosis.
 Excess Mineralocorticoid activity: Cushing's, Conn's Syndrome.
 Exogenous Steroids.
 Vomiting.
 Nasogastric Suction.
 Causes of Acute Respiratory Acidosis:
 CNS depression, e.g, drugs, CNS event.
 Neuromuscular disorders, e.g, Myopathies, Neuropathies.
 Acute airway obstruction, Upper airway, e.g, laryngospasm, bronchospasm.
 Severe Pneumonia or Pulmonary Edema.
 Impaired lung Motion, e.g, Hemothorax, Pneumothorax
 Thoracic Cage injury, e.g, flail chest
 Causes of Chronic Respiratory Acidosis:
 Chronic lung disease: Obstructive or Restrictive.
 Chronic NM disorders (Poliomyelitis, Multiple Sclerosis and Muscular dystrophy).
 Ventilatory Restriction (Kyphoscoliosis, Spinal arthritis and Obesity).
 Causes of Respiratory Alkalosis (Acute or Chronic):
 Anxiety.
 Hypoxia.
 Lung disease (Pneumonia, Pulmonary Embolism) with or without hypoxia.
 Psychogenic hyperventilation.
 CNS diseases: Pain, Infections and Tumors.
 Pregnacy.
 Excessive Mechanical Ventilatory Rate.
 Drug Use, eg, Salicylates, Catecholamines, Progesterone.
 Acidemia: Refers to a Low blood PH
 Acidosis: Refers to any Process that, IF left Unchecked, will lead to Acidemia.
 Alkalemia: Refers to a high blood PH
 Alkalosis: Refers to any Process that, IF left Unchecked will lead to Alkalemia.
 Hypoxemia: PaO2 is lower than Normal.
 Hypoxia:
 The Clinical Condition of the Patient is very important in interpreting ABG.
 Venous Blood Gas :
 PH: 0.03 lower than Arterial PH (Basically the Same).
 PaO2: 40-50 MmHg.
 PaCO2: 5-7 higher than Arterial PaCO2 (46 Rather than 40).
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 Base excess (BE) :

 A measure of metabolic acid level, & is normally Zero.
 Changes are termed excess or Deficit.
 The base excess may be used to estimate the amount of treatment (Neutralization)
required to overcome the metabolic acidosis (or alkalosis).
 BE of minus 10= the Patient has a metabolic acid excess (acidosis) of 10 mEqL/L”.
 Bicarbonate Dose :
 If NaHCO3 is administered, it should be given as a Slow infusion rather than an ●
IV bolus, in quantities designed to raise blood PH to levels not greater than 7.2 ●
(Serum HCO3 Concentration ~10 Mmol/l) with Close Monitoring.
 HCO3 Requirement= desired [HCO3]–Measured [HCO3]×HCO3 Space
 HCO3 Space from this Equation [0.4 + (2.6/ [HCO3])] × Body Weight.
 50% of total deficit be given Over 3 - 4 h& the remainder replaced over 8-24 hours.
 IV bolus should be reserved for cardiac life Support and not metabolic acidosis.
 HCO3 in DKA is only allowed when the Arterial PH ≤ 7.1
 ABG vs VBG:
 PH VBG~0.04 lower,
 HCO3 (VBG~2mEq lower; calculated value on BG, BMP more accurate),
 CO2 (VBG~8 mmHg higher).
 VBG can screen for hypercapnia w/ pCO2 cutoff ≥45mmHg (100% sensitivity) but
does NOT accurately assess degree of hypercapnia. When in doubt, check ABG
 Severe acidemia (pH<7.2) →vasodilation, ↓ inotropy/MAP, ↓ response
catechols/pressors, arrhythmia, ↑ K, insulin resistance, AMS.
 Severe alkalemia (pH >7.6) →vasoconstriction, ↓ coronary/cerebral perfusion, SVT/VT,
↓ K/Ca/Mg/Phosphorus, AMS, seizure, hypoventilation.
 STEP-WISE APPROACH:
1. Is there acidemia (pH <7.36) or alkalemia (pH >7.44)?
2. Is 1ry disorder metabolic (parallels pH Δ) or resp (opposite pH Δ)?
3. Is pt compensating? (respiratory takes min-hrs, renal 3-5d)
4. Is there an anion gap? Calculate regardless of pH or HCO3
AG = Na – (Cl + HCO3) = unmeasured anions – unmeasured cations
Correct AG for albumin: AGc = AG + 2.5(4 – albumin)
Negative AG: ↑↑Na, lipids (interfere w/ chloride), bromide intox
5. If there is ↑ AG metabolic acidosis (AGMA), calculate “delta-ratio”
Δ/Δ = Δ AG /Δ HCO3 = AG – (albumin x 2.5) / (24 – HCO3)
6. Osm gap = 2(Na + K) + Urea/2.8 + glucose/18 + EtOH/4.6 –serum Osm.
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How to Assess Acid-Base Status?

 In real life, intensivists rarely give the blood gas a long thought and rather use a quick pattern
recognition. For example, on the blood gas shown that lactate 10.2 mM will likely be instantly
spotted. The ABG disorder (SBE −10 mM & low pH) well matches with lactate elevation.
Normal pCO2 means no compensation and minute ventilation should be ↑.
 All looks fine and likely no further analysis will be attempted. So develop your own
systematic way how you will be looking at ABG strip. Having a mental checklist will reduce
the chance you overlook something important.
 Sometimes the situation in less clear and a systematic way of deciphering AB disorder is
needed. This is because various AB disorders can offset each other & may not be visible.
 There are many approaches for assessment of AB status & most based on 2 principles:
1. PH is determined by ratio HCO3 act/pCO2. This explains directions into which PH is
driven, for example, by increase of pCO2 in respiratory acidosis and also
compensations, for example, why bicarbonate retention by the kidney would restore pH
back towards normal in respiratory acidosis.
2. Electroneutrality—this simple rule dictates that in all body compartments the sum of
cations must equal the sum of anions. Electroneutrality is the hallmark of Stewart
approach, but some extensions of classical approach (such as the use of anion gap) are
based on electroneutrality, too.
1. Simplified Electroneutrality-Based Method
This image of ion gamblegram is very useful tool in assessment of
complex AB situation, hatched area=strong ions (always ionized).
 Difference between strong cations& ions (SID, strong ion difference)
is important variable determining AB status.
 A=negative charges on non-HCO3 weak acids, albumin & phosphate
 The marker of metabolic disorders HCO3= SID − A. In turn, any ↑
SID or ↓ A will cause proportional ↑ HCO3 (metabolic alkalosis).
Analogously, metabolic acidoses could be caused by ↓ SID or ↑ A.
 The quantity of change can be assessed (↓SID by 10 mEq will cause
↓ of SBE by 10 mEq. This concept is useful for quantitatively
dissecting combined AB disorder.
 SID = Na – Cl (reference 35 mEq) and [A−] to 0.3 Alb [in g/L], i.e. 40
g/L of albumin would hold 12 mEq of negative charges.
Then, the analysis of acid-base status may occur in the following steps:
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1) Assess SID deviation from 35 mEq and predict influence on BE.

 < 35 = low SID acidosis (hyperchloridemic), SBE would be negative.
 > 35 = high SID alkalosis, SBE would be positive.
 Example, SID= 146–107 = 39, which would lead to SBE = +4 mEq/L.
2) Assess weak acids & their influence on SBE. Note that A should be 12 mEq can be
calculated as 0.3 Alb [g/:]
 < 12 mEq/L = metabolic alkalosis: hypoalbuminaemic
 > 12 mEq/L = metabolic acidosis: hyperalbuminaemic, would be rare)
 Example, if albumin= 30 g/L of albumin, we would estimate A = 9 mM, which would
lead to SBE = +3 mEq/L (less A = more space for HCO3 & hence cause alkalosis).
3) Detect unmeasured anion by comparing predicted SBE (in steps 1 & 2) to the one on
ABG . The difference between 2 determine the quantity of non-Cl strong anions such as:
 Lactate
 unmeasured anions: as ketones (starvation, DKA), sulphates (renal failure), or
organic acids derived from toxic alcohols or other species
 Example, Predicted SBE from changes in SID& A to be +4 & +3 , respectively, so
predicted SBE +7 mEq/L. On ABG, SBE = −10 , i.e. 17 mEq/L lower & therefore 17
mEq/L of strong anions are in search. We see lactate= 10 therefore there must be 7
mEq/L of another strong acid, unknown at present.
4) Assess respiratory disorder by comparing pCO2 with predicted value.
 Predicted CO2 by Winter’s formula.= HCO3nact/5 + 1 kPa (±0.3) kPa
5) Making sense out of it—distinguishing causes from consequences, summarising
the finding and putting them into clinical context.
 Example, 1st ABG in ER from 67-year-old lady with HX of DM2 on metformin& CLD
attributed to alcohol consumption in the past who was brought in with 3-day history of
worsening back pain and vomiting. Now she is febrile 38.9 °C, confused & hypotensive.
O2 at 15 L/min was applied, blood cultures were taken &IV piptazobactam was given
 After performing steps 1–4 of our AB analysis, we have identified following disorders:
a) High SID metabolic alkalosis (SBE +3)
b) Hypoalbuminaemic alkalosis (SBE +4)
c) Lactic acidosis (SBE -10)
d) Unknown anion acidosis (SBE -7)
e) Respiratory acidosis (pCO2 1 kPa higher)
 1st 2 alkalosis are attributable to CLD (poor nutrition explains ↓ albuminaemia & 2ry ↑
aldosteronism& mild high SID alkalosis are often seen with cirrhosis).
 Elevated lactate is worrisome, as it could be a sign of sepsis, which was suspected &
acted upon. Unknown ion requires attention—plausible options are non-diabetic ketosis
(starvation, alcoholism), renal failure, or toxic alcohols.
 Renal failure was confirmed as creatinine was 385 μmol/L & UOP was low.
 Alcohol level was 0. Hypoventilation is probably a result of altered consciousness.
 In light of this, this lady was treated by i.v. fluids, glucose, thiamine,& antibiotics. She later
grew Staph aureus from blood cultures and was found to have spondylodiscitis as the
source of sepsis.
 Indeed, there are other approaches allowing a comprehensive acid-base analysis, which
will give very similar results, such as corrected AG approach, delta/delta, or others.
 It is no surprise that strong ions in infused fluids influence acid-base status of the patients
by changing SID of extracellular fluid & to lesser extent by diluting weak acids (albumin).
 As a rule of thumb, following rules may apply
 Fluids with SID <24 (such as normal saline or Ringers with SID =0) are acidifying.
They may be used in the treatment of high SID alkaloses.
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 Fluids with SID 24–40 (e.g. IsoLyte or Hartmanns) are considered balanced, i.e. not
significantly altering acid base. This is achieved by replacing chloride by
metabolisable organic anion such as lactate, acetate, or gluconate.
 Fluids with SID >40 are alkalising.(as Plasma-Lyte SID = 50) could be used as
maintenance fluids to compensate for normal saline used as a dilutant for most ICU
drugs. Others (8.4% Na-HCO3 SID = 1600 mEq/L) only to treat metabolic acidosis.
 SID= Na – CL=35, so deviation from 35, rather than chloride level itself is a useful
measure of SID-related disorders as hyperCl acidosis or hypoCl alkalosis. This also
explains why solutions with SID = 0, such as normal saline makes patients more acidotic.
 Low albumin = alkalosis (SBE +3 mEq/L for every 10 g/L below normal albumin).
 Winters formula pCO2 = HCO3 act/5 + 1 (±0.3) kPa with metabolic acidosis.
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Management Of Acid-Base Disorders

 Treat The Underlying Cause.
1) Metabolic acidosis:
 Acute:
 In BICAR-ICU, pts with metabolic acidosis (pH <7.2) tx w/ IV HCO3 for goal
pH >7.3 had no Δ in overall mortality but ↓ RRT initiation. A subset of pts w/
AKIN stages 2-3 had improved mortality at 28 days.
 For pH <7.1 or HCO3- <6: if HDS, can start isotonic HCO3 gtt. Monitor
VBG/ABG q1h. Bolus admin is controversial due to c/f CO2 accumulation →
hypercapnia, hypernatremia, hypocalcemia, hypertonicity, hypervolemia,
overshoot alkalosis
 For bicarb to have full effect on serum pH, pt must be able to increase minute
ventilation to ventilate off CO2
 Special considerations:
 Toxic alcohols: tx with NaHCO3, fomepizole, or HD (if vision Δ, AKI,
methanol >50mg/dL, ethylene glycol >300mg/dL)
 Salicylate poisoning: NaHCO3 to urine pH >6.5 or HD (if level >80mg/dL,
coma, AKI, hypervolemia)
 Chronic: in CKD, replete with PO NaHCO3 for goal HCO3 >22.
2) Metabolic alkalosis: replete volume, K, & Cl
 Treat both (1) underlying cause of metabolic alkalosis & (2) cause of renal
retention of HCO3
 If saline responsive: NS w/ KCl until urine pH >7. For pts w/ CHF/cirrhosis &
alkalosis 2/2 diuresis, consider K+-sparing diuretic
 If saline resistant: for mineralocorticoid excess → use K+-sparing diuretic
(amiloride) & consider surgical removal of adenoma
 If pH >7.6 & persistently volume overloaded, give acetazolamide vs KCl + loop
diuretic with close K+ monitoring
3) Respiratory acidosis: treat underlying process; adjust vent settings if intubated.
NaHCO3 unlikely to be helpful, theoretically harmful if unable to ventilate subsequent
CO2 produced. For every 100mEq HCO3 administered, 2.2L CO2 must be exhaled
4) Respiratory alkalosis: address underlying cause (correct hypoxemia, treat
pain/anxiety/fever); adjust vent settings if intubated
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Renal Tubular Acidosis (RTA)

 Consider in any pt w/ hyperchloremic or non-AG metabolic acidosis (NAGMA) or
hyperK (Type IV). R/o GI losses & excessive Cl use first!
 Pathophysiology:inappropriate retention of acid or inadequate excretion of HCO3
 - excretion; urine pH should be <5.3; this
process is defective in RTAs

 Etiologies:
 Proximal RTA (Type II): new ↓ set point for proximal tubule HCO3- reabsorption
so more HCO3 spills into urine
 Primary (rare): Na-HCO3 co-transporter defect
 Acquired: amyloidosis, MM, post-renal transplant, heavy metals (Pb, Cd,
Hg, Cu), ↓ Vit D, Wilson’s disease, PNH
 Meds: acetazolamide, cisplatin, tenofovir, aminoglycosides, topiramate
 Often a/w Fanconi Syndrome: glycosuria (w/ serum gluc <180),
hypouricemia, aminoaciduria
 Distal RTA (Type I): inability to secrete H+ in distal tubule
 Primary: genetic loss of H+ or HCO3 transporters in intercalated cells
 Acquired: autoimmune disease (RA, SLE, SS); hypercalciuria (any cause);
obstructive nephropathy; SCD, MM, amyloid, cryoglobulinemia,
tubulointerstitial injury, renal transplant rejection, cirrhosis, glue sniffing
(toluene)
 Meds: amphotericin B, Lithium , fosfamide
 Type IV: effective hypoaldosteronism:↓ aldo secretion OR tubular resistance →
↑K → ↓ NH3 synthesis → ↓ NH4+ excretion
 Acidosis due to inhibition of ammonia-genesis by hyperK of any cause
 Hyporeninemic hypoaldosteronism (most common): diabetic nephropathy,
CIN, NSAIDs, calcineurin inhibitor, HIV
 ↓ Aldo production: ACEi/ARB > heparin > adrenal insufficiency, severe illness
 Aldosterone resistance: (ENaC inhibition) K-sparing diuretic, trimethoprim,
pentamidine
 Workup: clinical history (PMH – autoimmune or malignancy, med review, stones),
response to HCO3 supplementation
 ABG/VBG, BMP (AG, HCO3, K), UA (pH). urine Ca/Cr to differentiate proximal
vs distal RTA
 Estimate of U NH4+: UAG = Na + K - Cl (less useful if ↑ U anions or UNa < 25)
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Section IV
Important Trials In Critical Care
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31- Important Trials in

Critical Care

River’s trial
EGDT reduced mortality
1. CVP 8-12mmHg (IVF)
2. MAP >65mmHg (NA)
3. ScvO2 >70%, achieved with packed RBC transfusions and dobutamine if necessary
4. UOP >0.5mL/kg/h
Non- blinded1– Single center2 – Hi mortality in the control arm3 – Which one helped best (of 4)4

ProCESS
In early septic shock, no difference in-hospital mortality at 60 days with management driven by
EGDT Vs usual care

ProMISe
EGDT did not improve mortality at 90 days Vs standard therapy including IV fluids and
vasopressors

ARISE
In critically ill patients presenting to ED with early septic shock, EGDT did not reduce all-cause
mortality at 90 days. Another nail in the coffin for EGDT and specifically continuous central
venous co-oximetry, liberal blood transfusion policy and probably dobutamine

Kumar
Q: Does a delay Abx in septic shock increase mortality?
A: Yes

Annanne study
Low dose HC and fludrocortisone reduced the risk of death in patients with septic shock and
relative adrenal insufficiency without increasing adverse events
1) 1ry outcome is not 28-ds mortality
2) 25% received Etomidate, which caused adrenal insufficiency.)

CORTICUS
Q: Did HC in Severe septic shock improve 28-day mortality?
A: No

ADRENAL
Q: Septic shock + Vasopressors + MV, HC 200mg/d  Mortality benefit?
A: NO
BUT  Shock reversal time1 – MV duration2 – LOS3 – Blood transfusion4

PROWESS-SHOCK
Q: Among patients with severe sepsis, does activated protein C (APC) improve survival?
A: NO!
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CITRIS-ALI (Vitamin C Sepsis)

This RCT of vitamin C in sepsis-induced ARDS showed no difference in the primary outcome
of reduction in SOFA or biomarkers (did not significantly improve organ dysfunction scores or
alter markers of inflammation and vascular injury)

CESAR
The study highlights the importance of involving specialist units, LPV and ECMO as an option
in refractory respiratory failure, 24% of the ECMO arm didn’t receive it
It does not show that ECMO is better than conventional ventilation

EOLIA
Q: Severe ARDS refractory to traditional therapies benefit from early initiation of V-V ECMO?
A: NO mortality benefit!

SUPERNOVA
Q: ECCO2R facilitate Ultra-LPV in moderate ARDS?
A: Yes but outcome is unclear (Phase II trial, REST trial is still recruiting)

PReVENT
Q: In MV patients without ARDS, does LTV (6mL/Kg) Vs 10mL/Kg, reduce the number of
ventilator-free and mortality at day 28?
A: NO

ACURASYS
MC RCT Significant mortality benefit in severe ARDS who were treated with EARLY NMBA
(Cisatracurium)

PROSEVA
Q: In severe ARDS (P/F ratio <150 mmHg), did prone positioning reduces 28-day mortality?
A: YES!

OSCAR
Q: HFOV reduce mortality & ALI in ARDS?
A: NO

OSCILLATE
A: In moderate to severe early ARDS, HFOV reduce in-hospital mortality?
Q: NO, increase it!!

3CPO
In Acute cardiogenic pulmonary edema, NIV improved breathlessness but not short- or longer-
term survival

FLORALI
Q: Acute T1RF, HFNC Vs standard oxygen (FM / NIV) prevent intubation?
A: NO! BUT, (1) (--) Mortality @ 90 days! (2) (--) Discomfort @ 1 hour
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ABC
The use of Spontaneous awakening trials (SAT) during this trial appears to accelerate weaning,
(greater risk of self-extubation and increased nursing workload)

BALTI 2
IV β2 agonist in ARDS  No effect + may cause harm

Meduri paper
Prolonged methylprednisolone in un-resolving ARDS  improvement in lung injury and MODS
scores and reduced mortality.

FACCT
Q: ARDS I&V – Conservative Vs Liberal IVF reducing mortality?
A: (--) MV days – LOS NOT mortality

TracMan
Q: High risk of prolonged MV, does early (4) Vs late (10) tracheostomy (--) mortality at 30 days?
A: No

HYPERION
Q: In patients with coma following cardiac arrest with a non-shockable rhythm, does moderate
hypothermia vs. normothermia, improve neurological outcome?
A: YES (NB. Recognized no in the control arm developed fever)

COACT
Q: In adult OOHCA (arrhythmia-associate) without STEMI, is immediate PCI superior to
delayed angiography in improving 90-day survival?
A: NO, a strategy of good supportive management without the need for immediate PCI, would
seem reasonable in most instances except CS, persistent arrhythmias or significant cardiac h/o

CULPRIT-SHOCK
Q: MI + MVD + CS … MVD PCI Vs Culprit improve outcome?
A: NO + More RRT in MVD PCI (III in ESC 2018)

SHOCK
In patients with CS, emergency revascularization did not significantly reduce overall mortality
at 30 days. However, after six months there was a significant survival benefit

IABP-SHOCK II
Q: In patients with acute MI + CS, did IABP reduce (30 days) mortality?
A: No

PAC-Man
Q: PAC (--) mortality?
A: NO

SEPSISPAM
Q: MAP 85 Vs 65 in septic shock (--) mortality?
A: NO, but higher MAP  (--) renal dysfunction in CKD
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SOAP II
Q: Dopamine Vs NA in decreasing shock mortality?
A: NO

SURVIVE
Levosimendan Vs Dobutamine in AHF did not significantly reduce all-cause mortality at 180
days

LIDO
Q: Levosemindan Vs Dobutamine in low COP?
A: Improvement in HD 24 hours and (--) mortality at 180 days

Liu
Q: Terlipressin Vs NA reduced 28-day mortality in septic shock?
A: NO

VASST
Q: Mortality (28-days) benefit for Vasopressin Vs NA in septic shock?
A: NO

PEITHO
Q: Thrombolysis in sub-massive PE?
A: HD improvement but no mortality benefit attributed to it

IRONOUT-HF
Q: In patients with iron deficiency + Symptomatic HFrEF, does oral iron replacement improve
exercise capacity (VO2)?
A: NO

RED-HF
Q: In LV systolic dysfunction of darbepoetin targeting a hemoglobin >13 g/dL (--) Mortality or
hospitalization?
A: NO

Pivetta
Q: In (ED) with acute dyspnea, does lung US compared to standard approach, improve the
diagnostic accuracy for acute decompensated heart failure?
A: Yes, whereas the addition of CXR and NT-pro BNP did not

DRAIN
Q: IVi Vs IV Furosemide improve decongestion @ 72 hrs?
A: Yes (small trial)

EXTEND
Q: AIS 4.5-9 hrs Alteplase improved 90 ds functional outcome?
A: Yes (stopped early, so further evidence needed)
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MR CLEAN
Q: In patients with large proximal anterior AIS, does intra-arterial (IA) intervention in addition
to usual care offer improved neurological outcomes?
A: IA therapy within 6 hours of symptom onset improved functional independence at 90 days
without increasing ICH or mortality

SWIFT PRIME
Q: In patients with AIS due to large vessel occlusion, IV t-PA and Solitaire FR within 6 hours of
symptom onset lead to better function outcome than those subjects treated with IV t-PA alone?
A: YES!

STICH
Q: TBI + ICH, early hematoma evacuation Vs initial conservative ttt (--) Mortality & disability
at 6M?
A: Yes (larger trial needed)

ISAT
Q: IC aneurysms endovascular coiling Vs clipping?
A: Survival free of disability at 1 year is significantly better with endovascular coiling

DECRA
Unchanged mortality + Worse disability outcome in decompressive craniotomy

CRASH I
Q: Did HC in TBI reduce death or disability?
A: No

CRASH II
Q: Did TXA in trauma with significant hge reduce death risk?
A: Yes (it did not reduce amount of blood transfusion BTW)

CRASH III
Q: TXA within 3 hours from injury, compared with placebo, reduce head injury associated in-
hospital 28-days mortality?
A: Yes!

PRODEX/MIDEX
Dexdor = Midazolam/Propofol in sedation + Improved communication

SLEAP
Q: MV + Opioids + BNZ … (--) SH to light sedation reduce time to extubation?
A: NO!!!!

6S
HES increased (1) Death (2) RRT

CHEST
Q: 6% HES Vs 0.9% NS IVF resuscitation
A: ++ RRT rate
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VISEP
Q: In patients with severe sepsis and septic shock, Intensive insulin therapy + HES reduce
morbidity and mortality Vs conventional insulin therapy and Ringer's lactate?
A: No, Harmful

CRYSTMAS
HES Vs. 0.9% NS in the initial phase of fluid resuscitation in severe sepsis patients  Less
volume to achieve HD stability without any difference for adverse events in both groups

CRISTAL
Q: Among ICU patients with hypovolemic shock, does fluid resuscitation with colloids reduce
mortality at 28 days when compared to crystalloids?
A: NO!

ALBIOS
20% HAS in severe sepsis will improve HD, but will not reduce mortality

SAFE
Q: HAS Vs 0.9% NS?
A: NO, TBI worse outcomes with HAS

ABLE
Fresh blood (stored for < 8 days) is no better than blood stored up to 42 days

TRICC
In critically ill patients, restrictive transfusion (Hb >7 g/d) is associated with better survival
compared to liberal strategy (Hb >10 g/dl)

TRISS
In septic shock, transfusion at Hb7 g/dl had similar mortality at 90 days but used 50% fewer
PRBCs compared with those who underwent transfusion at Hb 9 g/dl

IVOIRE
No benefit in septic shock for HVHF at 70 mL/kg/h when compared with contemporary SVHF
at 35 mL/kg/h (underpowered as stopped early)

RENAL
Q: In AKI  Hi intensity CVVH (--) Mortality (Effluent flow rate 40 Vs 25 ml/kg/h)
A: NO
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Van den Berghe study

Q: In post-operative patients requiring mechanical ventilation, does tight glycemic control
(<110 mg/d) Vs conventional insulin therapy (--) mortality?
A: Yes! (But, (1) Single center (2) CTCCU

NICE-SUGAR
Q: Conventional (≤180) Vs Tight glycemic control (81-108 mg/dL) effect on mortality?
A: In medical ICU patients, tight glycemic control led to more deaths

CALORIES
Early TPN is neither more harmful nor more beneficial than PN

EDEN
Q: Initial Trophic Vs Full-Energy EN in MV with Acute Respiratory Failure
A: Same outcome