Mechanical ventilation is a procedure often performed in patients in respiratory

failure, which is defined broadly as the inability to meet the body’s needs for
oxygen delivery or carbon dioxide removal. A ventilator delivers air, usually with an
elevated oxygen content, to a patient’s lungs via an endotracheal tube to facilitate
the exchange of oxygen and carbon dioxide.The indications for mechanical
ventilation include airway protection, treatment of hypoxemic respiratory failure
(low blood oxygen), treatment of hypercapnic respiratory failure (elevated carbon
dioxide in the blood), or treatment of a combined hypoxic and hypercapnic
respiratory failure. On some occasions, patients are also intubated and placed on
mechanical ventilation for procedures. However, intubation and initiation of
mechanical ventilation require a great degree of vigilance, as committing to this
therapy can affect the patient’s overall course of treatment.

Mechanical ventilation is managed by Respiratory Therapists (RTs), highly-trained

medical professionals who specialize in the care of respiratory illnesses. In addition
to managing ventilators, RTs have expertise in other forms of oxygen
administration and respiratory support, provide medications for respiratory
disorders, and assess patients for extubation readiness. RTs are essential for the
appropriate care of mechanically ventilated patients. Conversely, mechanical
ventilation traditionally has not been taught as a core component of many medical
and nursing practices outside of Critical Care and Anesthesiology. As such, to
collaborate effectively with RTs in the care of ventilated patients, additional
education is warranted. Ventilator management can seem intimidating due to
varied and confusing terminology (with many clinicians using synonyms for the
same modes or settings), slight variation among brands of ventilators, unfamiliarity,
or ceding management to others.

For COVID-19 patients, ventilators are often crucial, given the nature of the illness.
But note that intubation and initiation of mechanical ventilation require a great
degree of vigilance. The data supporting the importance of good ventilator
management continues to increase, and appreciating the fundamental principles of
ventilation is essential for all clinicians involved in the care of these patients.

The objectives of this course are to:

1. Familiarize clinicians with common terms in mechanical ventilation

2. Review key principles of pulmonary physiology relevant to mechanical ventilation

3. Discuss the basic principles of selecting ventilator settings

4. Develop strategies for caring for ventilated patients with ARDS and obstructive
lung disease, as well as COVID-19 specific management

5. Review the daily assessment of ventilated patients

6. Provide strategies for evaluating patients for extubation readiness

A learner who understands these concepts will be well-positioned to collaborate

with colleagues in Intensive Care and Respiratory Therapy in caring for critically ill,
mechanically ventilated patients.

The list below includes terms that will be repeated throughout the course. You can
also find them defined in the "Glossary" page (accessible from the tabs at the top
of each page in the course).

Annotate
Reading
A discussion of the principles of mechanical ventilation must begin with a review of
important physiologic concepts. We will begin with a review of gas exchange, and
the concepts of shunt and dead space ventilation.

Gas Exchange:
This diagram represents a normal cluster of alveoli with a normal capillary,
delivering carbon dioxide (CO2) and picking up oxygen (O2).

The above diagram is highly simplified for conceptual emphasis.

Carbon dioxide travels dissolved in the blood. Approaching the alveolus, the
CO2 easily crosses through the blood, across the capillary wall, and into the
alveolus.
Because CO2 crosses so readily into the alveolus from the serum, ventilation
occurs readily. This means that the major determinants of CO 2 in the blood are the
rate of production (increased with elevated metabolic demand, such as in sepsis or
exercise) and the rate of elimination, largely determined by the minute ventilation.
The minute ventilation is the amount of air moving through the lungs in one minute,
quantified as the tidal volume (green shaded arrows) and the respiratory rate
(represented by the back and forth arrows.) The higher the minute ventilation, the
lower the CO2. Normal minute ventilation is about 6-8 L/min. In times of stress, with
increased CO2 production, the minute ventilation may be 10-15 L/min.

Conversely, the path for oxygen is less simple. Oxygen is transported largely
bound to hemoglobin inside the red blood cells. The hemoglobin in this schematic
demonstrates the four binding sites per hemoglobin molecule inside the red blood
cells. Oxygen is represented by small blue dots. The concentration of oxygen is
high in the alveoli, and it diffuses down the concentration gradient, into the
capillary, into the RBC, and binds with Hgb.

While this binding allows for great efficiency in carrying oxygen, the multiple steps
for oxygen transport, as compared to the simplicity of CO 2, explains some of the
differential clinical effects seen with ventilation and oxygenation.

A small amount of oxygen is carried dissolved in the plasma, but compared to the
amount bound to hemoglobin, this amount is trivial. The oxygen-carrying capacity
of the blood is described by the equation:

Delivery of Oxygen = Cardiac Output x (Hgb x 1.39 x Oxygen Saturation) +

(PaO2 x 0.003)

This equation intuitively makes sense, as the more Hgb available to carry oxygen,
the more oxygen that can be delivered.

Annotate

Additional Resources
Trucorp has created an app (TruVent) that teaches the primary principles of
mechanical ventilation. The app also allows users to create custom simulations
that mirror real life situations. As of April 5, 2020, they are offering a 7 day trial.

Issues with Oxygenation

Hypoxemia
There are five broad physiologic causes of hypoxemia: shunting, VQ mismatch,
alveolar hypoventilation, diffusion defect, and decreased partial pressure of
oxygen. Understanding these mechanisms allows the clinician at the bedside to
quickly develop a differential diagnosis for hypoxemia and target diagnostics to
assess for the precise etiology. We will review each mechanism in detail.

Shunts, or blood bypassing normal gas exchange, is one of the most common
causes of hypoxemia. A classic example of a shunt is an intracardiac shunt. In this
example, much of the blood passes by the alveoli, participating in normal gas
exchange. However, a small amount is diverted through the heart, bypassing the
lungs. This deoxygenated blood mixes with the oxygenated blood, leading to
hypoxemia.

When an area of the lung is perfused, but not ventilated, that results in an intra-
pulmonary shunt. In other words, the inspired oxygen cannot reach the alveoli for
gas exchange. There are several different causes of intra-pulmonary shunts,
including atelectasis, pneumonia, pulmonary edema, acute respiratory distress
syndrome (ARDS), hemothorax or pneumothorax, hyperinflation or auto-PEEPing.
All of these pathological processes prevent effective gas exchange at the alveoli.
When an area has ventilation, but no perfusion, this is dead space. In other words,
the airways are functioning normally, but there is a disease process in the
vasculature. The best example would be a patient in cardiac arrest who is
intubated and ventilated, but there is an interruption of chest compressions. Dead
space can be anatomic and physiologic, such as oxygenation but lack of gas
exchange that occurs in the upper airways, like the trachea. There can also be
pathological causes of dead space, such as this diagram of microthrombi blocking
a capillary.
Other examples of dead space include low cardiac output and hyperinflation, as
occurs in obstructive lung disease. In diseases such as chronic obstructive lung
disease (COPD), there can be a significant level of hyperinflation or auto-PEEP,
which can lead to vasoconstriction of the capillaries involved in gas exchanged,
thereby leading to impaired gas exchanged. Dead space ventilation can lead to
both hypoxia and hypercapnia, due to CO2 retention.
Hypoxic Vasoconstriction

When an area of the lung is hypoxic, or there is impairment in the oxygen delivery,
the lung tries to optimize ventilation and perfusion ration (V/Q matching) by means
of hypoxic vasoconstriction. In this schematic below, the cluster of alveoli is not
receiving oxygen. Therefore, the arterioles leading to the alveoli constrict, diverting
blood away from this under-ventilated area, in an effort to improve oxygenation.

Atelectasis and Derecruitment

Maximizing V/Q matching, by preventing atelectasis, is a key principle in the

management of respiratory failure. Alveolar derecruitment, or atelectasis, leads to
the creation of shunts. Atelectasis has multiple detrimental effects in ventilated
patients. First, atelectasis decreases the surface area for gas exchange.
Atelectasis on a large scale is derecruitment. Derecruitment is compounded by
excessive lung weight (such as with pulmonary edema), chest wall weight (as with
morbid obesity), abdominal contents and distention (as with small bowel
obstructions), and even cardiac compresses (as with pericardial effusion). The
addition of sedation and paralysis to positive pressure ventilation can further
augment this derecruitment. This diagram reflects the pressures leading to
compression of the lungs when lying a patient supine – the weight of the heart, the
weight of the chest wall, the weight of the abdominal contents, and the weight of
the lungs themselves.
Compliance and Resistance
Two other important physiologic concepts to review are compliance and resistance.

Resistance is the impedance of flow in the tubing and airways and therefore can
only occur when there is airflow. According to Ohm’s Law:

Resistance (R) = Δ pressure /Δ volume

R = (Peak inspiratory pressure – Plateau pressure) / Tidal volume
R = (PIP- Pplat) / (TV)
Assuming a constant tidal volume, the resistance equation can be simplified to:

R ≈ (PIP- Pplat)
Normal airway resistance should be ≤ 5 cmH20. Resistance is a factor in
ventilating all patients but can become particularly important when ventilating
patients with COPD or asthma. The resistance in a system increases with
decreasing diameter. While common examples include a very small endotracheal
tube (ETT) or bronchospasm leading to narrowing of the airways, recall that a
“decrease in the diameter” can also occur at just one point, such as with kinking or
biting of the ETT, or a mucous plug in a large airway.

Compliance refers to the distensibility of the system and is the inverse of

elastance. In other words, it a measure of the lung’s ability to stretch and expand.
The more elastic a system, or higher the “recoil,” the lower the compliance. A
common analogy to understand the concepts of elastance is to analyze the recoil
of springs. Imagine a very tightly wound and stiff spring. This spring is difficult to
stretch and wants to stay in the coiled position. This spring would have high
elastance and low compliance. Envision a second, loosely coiled spring. Very little
force is required to stretch out this spring, and therefore, it has low elastance but
high compliance.

Although compliance commonly is used to describe the lung parenchyma,

remember that compliance actually involves all components of the system. In other
words, a patient with pulmonary edema may have low compliance due to an issue
with the lung parenchyma, but another patient may have similarly low compliance
due to severe chest wall stiffness after a third-degree burn. Clinically, knowing the
exact cause of decreased compliance in a given patient can be challenging.
Physicians should not, therefore, always assume that it is always related to “stiff
lungs.”

In the schematic below, the top “lungs” are healthy. The lungs on the left have a
resistance problem or impairment in airflow. The lungs on the right have a
compliance problem or impairment in stretch and recoil. In this diagram, both
figures could have elevated peak inspiratory pressures (PIP), due to the excess
pressure generated in the system. However, only the right-hand figure would have
an elevate plateau pressure (Pplat), since this process occurs when there is an
absence of airflow.

Compliance (C) = ∆ volume / ∆ pressure

C = Tidal volume / Plateau pressure – Positive end expiratory pressure

C = (TV) / (Pplat – PEEP)

Therefore, when troubleshooting high-pressures on the ventilators, two values are

needed. The peak inspiratory pressure (PIP) is the maximum pressure in the
system and includes both resistance and compliance. An inspiratory pause stops
all airflow, thereby removing resistance, and only leaving compliance, as illustrated
in this diagram below. The plateau pressure, or Pplat, is, therefore, a measure of
compliance.
These values can be displayed on the ventilator screen. On most ventilators, the
PIP is always seen, while the Pplat is seen by pushing the “inspiratory hold” or
“inspiratory pause” button on the ventilator. An elevated PIP and normal Pplat is
indicative of increased airway resistance. An elevated PIP and elevated Pplat is
indicative of abnormal compliance.  
Determining whether the patient has a resistance problem or a compliance
problem can assist in the differential diagnosis of respiratory failure, as outlined in
the table below.

High Resistance Low Compliance

High PIP, Low/Normal Pplat High PIP, High Pplat

Kinked/obstructed ETT Mainstem intubation

Mucus plugging Atelectasis

Bronchospasm Pulmonary edema

ETT too narrow (small) ARDS

Coughing Hemo/pneumothorax

Bronchospasm (obstructive lung disease) Pneumonia

  Pulmonary fibrosis (restrict

  Air-trapping with accumulat

  Obesity

  Abdominal compartment sy

  Circumferential burns of the

  Scoliosis

  Supine position
Air trapping, also referred to as breath-stacking, can lead to the development of
auto-PEEP, or intrinsic PEEP (iPEEP). These pressures should be differentiated
from the set PEEP, or extrinsic PEEP (ePEEP). ePEEP refers to the additional
end-expiratory positive pressure set during mechanical ventilation to prevent
alveolar collapse and recruitment. In contrast, auto-PEEP, or iPEEP, is a
pathophysiological process that can occur when the ventilator initiates the next
breath prior to complete exhalation. While this is most common in patients with
prolonged expiratory phases, such as asthma or COPD, it can also occur in
patients who have a fast respiratory rate or those who are being ventilated with
large tidal volumes. The amount of auto-PEEP can be measured by pressing the
“expiratory hold” or “expiratory pause” button on the ventilator. When this button is
pressed, the ventilator will display the total PEEP. The auto-PEEP is the difference
between the total PEEP and the set PEEP.

Auto-PEEP (iPEEP) = Total PEEP – ePEEP

The schematic represents the effects of air trapping. Please note that this diagram
is for illustration purposes only and does not represent the expected tracings on
actual ventilator screens.

Air trapping, or autoPEEP, can lead to significant adverse cardiopulmonary effects.

The increased intrathoracic pressure from autoPEEP can decrease venous return
and lead to hemodynamic instability, even cardiac arrest in severe cases. The
increased pressures may also result in a pneumothorax or pneumomediastium.
Additionally, air trapping can lead to ineffective ventilation due to collapse of the
capillaries responsible for gas exchange, with worsening hypercarbia and
hypoxemia. While this may seem like a paradox, as one may assume that
increasing the minute ventilation, or moving more air, will improve ventilation, there
is a limit to the beneficial effects. Once the lungs are overdistended, gas exchange
is ineffective. In these circumstances, allowing the patient sufficient time to exhale
can decrease CO2 retention.

Auto-PEEP is the positive end-expiratory pressure caused by the progressive

accumulation of air (air trapping), due to incomplete expiration prior to the initiation of the
next breath.

Anticipating Physiologic Changes

Critically ill patients are at high risk of deterioration with intubation and initiation of
mechanical ventilation. Much of this text is devoted to reviewing the effects of
positive pressure ventilation (PPV) can have on pulmonary physiology. However,
mechanical ventilation can also have extra-pulmonary effects that warrant review.
Specifically, PPV leads to an increase in the intrathoracic pressure, which has
different effects on the right and left ventricles. For the right ventricle, the PPV will
lead to decreased preload via decreased venous return. This is shown by the blue
and white arrowheads indicating increased pressure. The distention of the alveoli
can also lead to increased afterload on the right ventricle. The inset illustrates the
compression of small capillaries by distended alveoli, leading to an increase in
pulmonary vascular resistance.
Note, however, that there is a U-shaped curve for changes in the pulmonary
vascular resistance. Both atelectasis and overdistention can increase the afterload
on the right ventricle.
The effects on the left ventricle are slightly different. PPV also decreases the left
ventricular preload, given the impact on the right ventricle. However, the increased
intrathoracic pressure also decreases the transmural pressure, or the afterload, on
the left ventricle. While we use this principle to care for those with congestive heart
failure (CHF), it can lead to an increase in stroke volume and cardiac output.
However, in excess, these impacts on the cardiovascular system can lead to a
decrease in the cardiac output and hypotension, especially in the intravascularly
depleted patient, those with shock physiology, or with air trapping. Additionally,
PPV leads to a decrease in the left ventricular afterload.

When intubating and placing the patient on the ventilator, the clinician should
anticipate these effects. A volume-depleted patient, such as a patient with a GI
bleed, may have hemodynamic collapse with initiation of positive pressure
ventilation.

When initiating mechanical ventilation, the practitioner must be conscientious to

ensure adequate gas exchange to meet the metabolic demands of the patient. For
example, a patient in severe metabolic acidosis with respiratory compensation
might be very tachypneic. One must be cognizant to increase the respiratory rate
on the ventilator to help meet the patient’s metabolic demands. Failure to do so
can be detrimental for the patient, and lead to rapid decompensation.

Along the same lines, the practitioner must be careful to set and then adjust the
ventilator settings to prevent further decompensation or injury. For example,
excessive volumes on the ventilator can lead to volutrauma and impaired gas
exchange. Excess pressure can lead to hemodynamic instability or barotrauma.
These concepts will be explored further in the content on Ventilator Management in
ARDS.
At least once a day, likely in the setting of morning ICU rounds, all patients on
mechanical ventilation must be assessed by a multidisciplinary team. The ideal
structure will vary with institutional norms, however, we recommend rounds with all
members of the care team, including the attending physician, residents, nurse
practitioners, physician assistants, bedside nurse, and respiratory therapist as
available.

While the exact structure of rounds will vary between institutions and between
units, we recommend a systematic approach. Some intensive care units will take a
problem-based approach, reviewing each medical problem in detail, then
developing a plan to address that problem. (eg, Respiratory failure, renal failure,
etc). Others take a systems-based approach, using each body system as a prompt
for considering the relevant problems and developing an assessment and plan.
Which approach is preferable is a matter of personal preference and local norms,
but what is most important is maintaining a thorough, detailed approach to the
recent clinical data. A sample ICU rounding script is included at the end of these
readings. Please note that this is provided in a data/assessment/plan format. Some
ICUs will provide all data together, including vital signs, ventilator settings,
infusions and other medications, physical exam findings, lab data, and imaging,
then move to assessment, then plan; others organize things differently. 

The daily assessment usually starts with review of the vital signs, including any
vasoactive medications required to maintain those vital signs.  For COVID patients,
most authors are recommending one member of the care team perform a physical
exam and report back to the rest of the team.

Neurologic System:
Many patients with COVID-19 are requiring very high doses of sedation and even
occasionally neuromuscular blockade to maintain ventilator synchrony. Each day,
the medical team should assess the patient's current level of sedation, appropriate
analgesia, current trajectory on the ventilator including synchrony or the ability to
liberalize, and make a determination about the appropriate sedation and analgesia
plan. In general, while a patient continues to have moderate-to-severe ARDS
requiring controlled ventilation, most patients will require fairly deep sedation.
However, as soon as the patient is demonstrating pulmonary improvement,
lightning sedation and especially allowing for daily awakening trials, is one of the
most important things one can do to reduce ventilator days. 

Delirium is a very common problem in the  Intensive Care Unit, and this can
contribute to prolonged mechanical ventilation.  While specific medical treatments
for delirium have not proven to reduce its incidence, close attention to the ambient
environment can be beneficial.
 An excellent recent article 1 recommends the following points:

 Agitation and delirium

o Minimize sources of environmental agitation, such as ventilator dyssynchrony and ambient

noise

o Attend to patients’ audiovisual disortentation by helping re-orient

o Do not use physical restraints to address agitation, whenever possible, rather determine
and address the source of the agitation

 Sedation and pain management

o Use of sedation should be minimal and include daily sedation interruptions

o Frequently assess and treat pain

o Be aware of painful stimuli, including suctioning, turning, and the mobilizing patient

 Sleep

o Use of hypnotic drugs should occur only when strictly necessary and only after addressing
sleep disruptions caused by pain and noise

 Early mobilization

o As a patient begins to  demonstrate clinical Improvement, early mobilization is critical to

reducing deconditioning and improving the odds of extubation

o Patient should engage in bed rest as little as possible and participate in multidisciplinary
rehabilitation

Cardiovascular System:
Hypotension is common with COVID-19, due in large part to use of high doses of
sedatives and analgesics to maintain ventilator synchrony, relative volume
depletion in an effort to optimize the lungs, and vasoplegia from sepsis. Trends in
heart rate and blood pressure over the last 24 hours should be assessed every
day, including evaluation of the doses of vasopressin required to maintain blood
pressure goals. The blood pressure goal for most patients should be a mean
arterial pressure of 65 mmHg. In patients with chronic hypertension,  a study found
that maintaining a mean arterial pressure greater than 75 mmHg was associated
with a reduced risk of need for renal replacement therapy. Therefore, given the
patient's underlying conditions and kidney function, the clinician may adjust the
MAP goals accordingly.
 The patient should be assessed for improving, worsening, or unchanged
hemodynamic status. Attempts should be made to verify the etiology of any
hemodynamic perturbations, including worsening or recurrent sepsis, hypovolemia,
cardiogenic shock, or far less likely, unobstructive cause of shock. As indicated
given the underlying concern, the cardiac function can be evaluated with an EKG 
or echocardiogram. 

In addition to assessing the patient's hemodynamic status and determining goals,

the patient's hemodynamics must be monitored closely after any change in the
ventilator.   Changes in the intrathoracic pressure can lead to variations and heart
rate and blood pressure.

The hemodynamic goals for the day should be clearly delineated, and the plan for
achieving them outlined. 

Pulmonary System:
The initial assessment of the patient on the ventilator begins with reviewing their
current ventilator settings as well as the trends over the last 24 hours. The basic
vital signs that should be reviewed every day include the motors in elation, title
volume, pressure, plateau pressure, driving pressure, PEEP, respiratory rate, and
FiO2. Additionally, the milliliters per kilogram of predicted body weight, and
PaO2/FiO2 ratio should be assessed every day. 

Specifically, for different modes of ventilation, it is important to check different

parameters:

 In volume assist control, check peak pressure and plateau pressure.

 In pressure assist control and pressure support, check peak tidal volume and minute
ventilation.

 When patients are breathing spontaneously, it is important to monitor changes in minute

ventilation.

The appropriate limits for these parameters are patient-specific. Alarms are
generally set slightly above or below the current monitored values, to alert the
patient’s care team if their condition changes.

In addition, make sure that plateau pressure is < 27 cm H 2O (or 30 in patients with
ARDS) and consider if higher PEEP is appropriate. Aggressive action should be
taken to decrease PEEP and wean the patient off.
Any changes in trends over the last 24 hours that should be evaluated for etiology.
In reviewing these settings, the clinician can begin to make assessments as to
whether the patient is doing better, worse, or staying the same.

If the patient is doing worse, indicated by increasing FiO 2, the need to increase the
PEEP, or decreased compliance, the clinician should assess for the underlying
issue. Issues can include derecruitment, pulmonary edema, or the development of
pneumonia, and others. Additionally, specifically in COVID-19, patients require
prolonged weaning from the ventilator. Attempting to make rapid ventilator changes
may result in some deterioration. The clinicians should decide what the next best
step is, often including deepening sedation, ensuring ventilator synchrony,
increasing the PEEP, performing a recruitment maneuver, or proning.

If the patient is doing better, defined as requiring less FiO 2, lower PEEP, or
improved compliance, the clinician may consider liberalizing the ventilator settings.
Many will use a PaO2/FiO2 ratio greater than 200 as a cut-off for changing the
patient to pressure support ventilation.

Note that not every patient who appears ready for a pressure support will be. The
ventilator screen below shows a patient in severe respiratory distress on pressure
support, with a high respiratory rate (36) and very high tidal volume (1013),
indicating lung-injurious ventilation. This patient was changed back to volume
control ventilation.
 Patients should be evaluated every day for readiness for a spontaneous breathing
trial (SBT). To determine, consider if:

 The patient is stable and/or improving medically.

 The FiO2 requirements are 0.5 or less.

 The PEEP requirements are 10 cm H2O or less.

 The patient can make spontaneous efforts

After changes to ventilator settings, be sure to monitor:

o Blood pressure

o Arterial blood gas for sufficient oxygenation and acid-base balance

o When using venous blood gases consider pH and use SpO2 for oxygenation

Arterial blood gases 

When it comes to checking arterial blood gases (ABGs), the American Thoracic
Society outlines six steps, which we summarize here:

1. Assess that consistency of pH and hydrogen

2. Check if acidemia or alkalemia is present by checking if the pH < 7.35 or pH > 7.45,
respectively

3. Check if the disturbance is respiratory or metabolic by checking in which direction the pH

and PaCO2 change (if opposite directions they indicate a respiratory disturbance and if
same direction that means metabolic)

4. Does the disturbance have a high enough correction factor (will generally NOT return the
pH to normal)?

5. Calculate the anion gap (>AG= [Na+]-( [Cl-] + [HCO3>-] )-12 ± 2) and see if it is normal (12
meq/L)

6. If there is an anion gap, evaluate its relationship to the decrease in bicarbonate.

Renal:
Approximately 35% of patients with ARDS well developed acute kidney injury at
some point during their critical illness. Acute kidney injury has a high attributable
mortality. However, simply providing more fluids does not necessarily improve
renal outcomes. A large study published in 2006 found that keeping a negative
fluid balance in patients who were not in shock was associated not only with better
pulmonary outcomes, but also renal outcomes. The hourly urine output, total body
balance for the last 24 hours, BUN, creatinine, as well as other electrolytes should
be assessed daily. 

The patient should be determined to have improving or worsening acute kidney

injury, and a decision should be made regarding the patient volume status.

For patients with worsening renal failure, determined by lower urine output despite
adequate circulating volume, rising creatinine, or failure to clear medications or
electrolytes, the next step is to evaluate when the patient might need dialysis. The
indications for emergency dialysis are severe acidemia, hyperkalemia, toxic
ingestions (unlikely), volume overload leading to pulmonary compromise, or
uremia. 

GI/Nutrition: Nutrition is essential for healing in any critically ill patient. The patient
should be assessed for an appropriate nutrition plan including tolerance of tube
 feeds. Liver injury is common and critically ill patients, often due to shock liver.
Bowel regimens are essential in patients who are receiving Opioids as this can
cause substantial constipation.

Heme:
The hemoglobin, platelets, coagulation factors should be assessed as indicated. In
patients with COVID-19, Ddimers are frequently elevated, and higher levels
correspond to worse outcomes. Patients with unexplained drops in hemoglobin
should be evaluated for bleeding or hemolysis. Please note that the average
critically ill patient loses 40 to 70 mL of blood a day simply from phlebotomy. Most
patients should be transfused if there are signs of hemodynamically significant,
active bleeding or a hemoglobin of less than 7. Additionally, the anticoagulation
plan should be determined, if indicated.

ID:
The white blood cell count, maximum temperature for the last 24 hours, current
temperature, and culture data should all be reviewed. If the patient is on antibiotics,
they should be reviewed as well as the day of antibiotics noted. For patients with
isolated COVID-19, procalcitonin levels are often low, but they can be used to
evaluate the patient for a superimposed bacterial pneumonia. Imaging should be
reviewed for evidence of ongoing infection. If the patient has a known infection, it
should be assessed as to whether it is improving for worsening. The patient should
also be assessed for any evidence of new infections. If the patient is showing
clinical improvement on antibiotics, but does not have any clear evidence of
infection and negative cultures, stopping antibiotics should be considered. All
antibiotics in the ICU should have a planned duration.

Endo:
The patient’s glucose control should be reviewed. Steroids are not routinely
recommended for patients with COVID-19, but can be administered if the patient
has another condition that is steroid-responsive. Patients who have underlying
thyroid issues should have their medications continued while they are in the
intensive care unit. If the patient does not have adequate glucose control, the
regimen should be adjusted, using an insulin drip if necessary.

Ppx: Reduce risk for  ventilator-associated pneumonia (VAP):

o Hand wash diligently

o Raise head of bed to 30-45 degrees (if permissible given patient’s specific situation)

o Use aseptic technique while suctioning

 Suction as minimally as possible using the lowest pressure possible

 Hyperoxygenate the patient pre and post suctioning

 Do not add normal saline to the ET tube

o Give sedation interruptions

o Evaluate viability of extubation

o Provide prophylaxis for deep vein thrombosis

Ventilator Alarms
There are some alarms that must be considered:

 Minute ventilation: when using pressure targeted modes it can mean that respiratory
system mechanics have changed or the patient’s respiratory drive has changed.

 The peak pressure alarm is important in volume assist control. It indicates that respiratory
system mechanics have changed, but whether that is due to a change in resistance or
elastance (compliance) needs to be assessed by looking at the peak and plateau
pressure.

o Changes in plateau pressure are a result of changes in compliance

o Changes in PEEP and/or tidal volume will also alter plateau pressure.

When troubleshooting high-pressure ventilator alarms, PIP is key. 

The peak airway pressure (PIP) should be displayed on the ventilator screen, while
the plateau pressure (Pplat) is obtained by holding the “inspiratory hold” or
“inspiratory pause” button on the ventilator. An elevated PIP and normal Pplat is
indicative of increased airway resistance. An elevated PIP and elevated Pplat is
indicative of abnormal compliance. Determining whether the patient has a
resistance problem or a compliance problem can assist in the differential diagnosis
of respiratory failure.

SAMPLE ICU ROUNDING SCRIPT

In general, approach each patient presentation with a snapshot in your mind.  Before
starting the presentation, ask yourself:

 Is this patient getting worse, getting better, or staying the same?

 What are the patient’s top 1,2,3,4 issues? (As indicated.) 

Thinking about this global assessment will focus your presentation.  An example would be, “Mr.
P is now ICU day #7, and he is not really getting better. His major issues are the COVID-
related ARDS, now with a superimposed pneumonia, as well as acute kidney injury.” – then
you know what issues below you really need to focus on.

Different ICUs will organize these data differently, but these are the key concepts to focus on,
using a data/assessment/plan structure in an organ system-based approach.

Neuro: (Data) Neuro exam, delirium – CAM; Current RASS and RASS goals, sedative
requirements, pain medication, results of any recent neuro imaging

(Assessment) Is pain well controlled? The sedation plan appropriate? Mental status
improving/declining?

(Plan) Do we need to lighten or deepen sedation? Do we need to change pain/sedation

medications? Do we need imaging? Do we need EEG? Neuro consult?

Cardiovascular:(Data) HR, BP, - and trends for both over last 24 hours, cardiac rhythm, the
type of shock – distributive, cardiogenic, hypovolemic, obstructive; current volume status,
current pressor or inotrope requirements – include medication, current dose, and any trends or
changes, EKG, troponin, BNP, use of any antihypertensives or anti-arrhythmics

(Assessment) Is the hemodynamic status improving/worsening?  Is the patient

hypo/eu/hypervolemic? Is the rate/rhythm controlled?

(Plan) What are our hemodynamic goals (HR, MAP)? Will we give fluid/diurese? Will we
change our pressors/inotropes? Do we need an echo? Should we consult Cardiology?

Pulmonary: (Data) Type of respiratory failure – hypoxemic, hypercarbic; h/o underlying lung

disease, current ventilator settings – the mode, the TV, RR, PEEP, FiO 2, the PIP, Plat, the
minute ventilation; PaO2/FiO2 ratio, recent  proning, use of inhaled pulmonary vasodilators,
most recent ABG, use of bronchodilators, any home medications for pulmonary conditions,
incentive spirometry, results of any recent SBT, results of any recent chest imaging

(Assessment) Is the respiratory failure improving/worsening?  List barriers to extubation –

recent SBT results, mental status, airway patency, unresolved shock, deconditioning;

(Plan) Can we change the ventilator? Can the patient be put on pressure support? SHould we
perform an SBT, if not already done? Can we extubate? Does the patient continue to require
proning or pulmonary vasodilators? Do we need to add medications?

Renal: (Data) BUN, Cr, UOP, total body balance for last 24 hrs, Na, K, other lytes, AKI -
causes of AKI

(Assessment) Improving/worsening AKI, Volume status – can include here or CV, or can

repeat as appropriate,
(Plan) Volume goals for the day. Do we plan to diurese/give fluids? Does the patient meet any
criteria for dialysis?

GI/Nutrition: (Data) underlying liver condition, acute liver injury, abdominal exam, LFTs, INR
as indicated, nutrition plan and tolerance

(Assessment) Is the liver function improving/worsening?  Are the bowels working? 

(Plan) Nutrition plan for the day. Bowel regimen? Do we need to check imaging? 

Heme: (Data) Underlying condition, Hgb, Plts, coags, Ddimer, fibrinogen

(Assessment) Are counts improving? Any evidence of bleeding or clotting? 

(Plan) Anticoagulation plan, transfusion goals

ID: (Data) WBC, Tmax, Tcurrent, culture data, current abx with day, procalcitonin

(Assessment) Is the infection improving/worsening? Any concern for new infections?

(Plan) Planned course, any other evaluations for sources (like CT or US)

Endo: (Data) Glucose, steroids, thyroid issues

(Assessment) Adequate glucose control?

(Plan) Changes to regimen?

Ppx: GI prophylaxis, DVT prophylaxis, PT, up OOB

Just as important as knowing when and how to put a patient on a ventilator, it is
important to know when and how to remove them from this support (also known as
“weaning”). An adage from Critical Care is that preparation for extubation starts as
soon as the patient is intubated. With COVID-19, the patients are generally
requiring prolonged periods of intubation, with many reports quoting 10 to 14 days.
Regardless, the onus falls on the clinicians caring for any mechanically ventilated
patient to assess the patient's daily for signs of stability or improvement. With any
signs of improvement, assessment for extubation readiness should begin.

Patients’ conditions should be assessed continually and, once gas exchange and
compliance improve, the level of support can be reduced. For most patients, the
first step in moving towards extubation readiness is to move from assist control
ventilation to pressure support ventilation. As discussed in previous readings,
pressure support ventilation allows for spontaneous ventilation. The patient
engages their diaphragm and sets their own respiratory rate, flow, and tidal
volume. The following ventilator screen illustrates a patient who is ready to be
changed to pressure support. The patient was arousable with lightening sedation,
has good pulmonary mechanics as indicated by the low PIP of only 22 with a TV of
400, has a low PEEP requirement, and is only on 50% FiO 2. On these settings, the
patient’s ABG was also reassuring, at 7.37/38/110. (Note: in addition to changing
to pressure support, the FiO2 could also be decreased to 40% given the more than
adequate PaO2.)
 Once the patient has been placed on pressure support, physiological
measurements including MIP (maximal inspiratory pressure),fRVT (respiratory
frequency to tidal volume ratio, or rapid shallow breathing index) and others can be
used to assess a patient’s readiness to wean. 

If the following criteria are met, the patient should undergo a spontaneous
breathing trial (SBT) to determine if they are ready to attempt extubation. 

Criteria for Performing Spontaneous Breathing Trial*

 Improvement of underlying condition that led to intubation

 Relative hemodynamic stability

o HR < 130
o Mean arterial pressure (MAP) adequately supported on a stable dose of vasopressors

 Presence of a cough reflex (often elicited by suctioning)

 Burden of secretions that can be handled by cough strength. (Patients with a robust cough will be able to clear more secretio

 Adequate oxygenation

o Usually SpO2 > 90% on 40% FiO2 and PEEP ≤ 8

o Ability to maintain the current oxygenation status once extubated.

 Adequate ventilation

o pH > 7.3 with a PCO2 near baseline

o Minute ventilation that a patient can maintain after extubated, usually < 12 L/min

 Minimal ventilator settings

o On pressure support ≤ 10 cmH2O

o On PEEP ≤ 8 cmH2O

o Maintaining tidal volumes ≥ 5 mL/kg PBW

o Respiratory rate < 35

o FiO2 ≤ 50%

*These values are provided for general education purposes. Most institutions have
their own specific criteria. Please refer to your institution’s protocols for details. 

The following screen shows a patient on pressure support, 10/5 (10 cm H 20 driving
pressure over 5 cm H2O of PEEP). This patient is marginal, as the tidal volume with
10 cm H2O of driving pressure is 400, which is acceptable, but the respiratory rate
is 30. The patient should be assessed for non-pulmonary causes of tachypnea,
such as pain, anxiety/agitation, fever, etc. It is reasonable to decrease the pressure
support of 10 cm H2O and reassess both the tidal volumes and respiratory rate. It is
difficult to predict how patients will do; often the best course is to give them a trial
and assess. 
 Spontaneous breathing trials are used to assess a patient’s readiness to wean by
removing ventilation support for 30 minutes and evaluating the patient’s ability to
breathe on their own during this time. There are many ways to perform SBTs,
including pressure support of 5/5, 0/5, and 0/0, as well as “T-piece trials” in which
the patient is taken off the ventilator and supported with blow-by humidified
oxygen. Each approach has its proponents, and institutional guidelines vary. The
most important concept to consider is the available respiratory support options
once the patient is intubated, and ensure they are able to pass with that level of
support. 

Criteria for Passing Spontaneous Breathing Trials*

 Clinical Appearance

o No evidence of respiratory distress

 Cyanosis, diaphoresis, accessory muscle use, grimacing

 Pulmonary mechanics

o Ratio of respiratory rate : tidal volume < 105

o Respiratory rate < 30 breaths per minute

o Tidal volume < 5 mL/kg PBW

 Oxygenation and ventilation

o SpO2 > 90% on 40% FiO2

o PaCO2  ≤ 50mmHg or a

o pH ≥ 7.3 or decrease in pH of ≤ 0.07

 Hemodynamics

o Change in SBP to  > 90 or < 180 mmHg

o HR < 130 beats per minute

o No new dysrhythmias 

*These values are provided for general education purposes. Most institutions have
their own specific criteria. Please refer to your institution’s protocols for details.

The screen below demonstrates a patient who is doing well on an SBT. They are
on pressure support, 5/5, and have large tidal volumes of 735 mL, indicating good
compliance. They are breathing at a slow rate of 14, and they are on a low FiO 2 of
25%. This patient would be an excellent candidate for extubation, assuming there
are no other barriers. 
If a patient’s spontaneous breathing trial is successful, the next step is to assess
for other barriers to extubation. A helpful approach is to go head to toe:

Assessment for Barriers to Extubation:

Head: Is the patient awake, following commands? If not, does the clinician believe s/he will be able to cough and
agitated, does it seem related to the ETT? Is there a plan for agitation management? Is pain adequately controlle

Face/Neck: Any facial trauma? Tongue or lip swelling? (Note: this may be seen in a patient who was previously
not preclude extubation, but all clinicians should be aware) Does the patient have a cuff leak? 

Chest: Does the patient have any chest trauma/other pathology (eg, rib fractures, etc) that may preclude adequa
 Abdomen: Any planned procedures or diagnostics that should happen before extubation? What is the nutrition p
tube feeds before extubation? (Note: most patients with prolonged intubations have oropharyngeal muscle weak

If there are no barriers to extubation, the patient may be extubated. In preparation,

gather supplies that would be needed for oxygenation post-extubation (nasal
cannula, oxygen mask, CPAP or BPAP, etc.), as well as supplies that would be
needed to intubate the patient again if extubation fails:

 Endotrachial tubes (ETTs) of appropriate sizes

 Bag mask with positive end expiratory-pressure (PEEP) valve

 Airway bougies

 Tube exchangers

 Traditional direct laryngoscope

 Video laryngoscope

 Flexible bronchoscope

 Drugs needed for induction

 Suction catheter

For extubation:

1. Put the patient in an upright, seated position.

2. Suction the ETT and oral cavity. Remove all secretions above the ETT cuff using
subglottic suction, if available, or insert a small bore catheter on the side of the
ETT for removal of secretions above the ETT cuff.

3. Remove the ETT from the holder.

4. Ask the patient to take a deep breath and exhale.

5. During exhalation, deflate the cuff and smoothly remove the ETT. 

Note: If an orogastric tube is present, it will be removed alongside the ETT and
may need to be replaced by a nasogastric tube, if the patient is not ready for oral
intake of medications and nutrition.
6. Suction the oral cavity.

7. Ask the patient to take a deep breath and cough out all secretions.

8. Provide supplemental oxygen through a nasal cannula, oxygen mask, etc., as

appropriate.

After extubation, it is important to monitor the patient carefully. Make sure they
have adequate oxygenation and provide supplemental oxygen as appropriate. If
necessary, consider CPAP/BPAP if a patient requires additional support. Use
bronchodilators as needed, provide secretion management, maintain airway
hydration and patent central airway, and encourage patient behaviors that reduce
the potential for re-intubation:

 Coughing

 Deep breathing

 Sitting up

 Moving around if appropriate

Risk factors that suggest a patient will need to be re-intubated

include:

 Pneumonia

 Weak cough

 Frequent suctioning

 Rapid shallow breathing index >58 breaths per minute per liter

 Positive fluid balance in the 24 hours prior to extubation

(Extubation process and post-extubation recommendations modified from Saeed F,

Lasrado S. Extubation. [Updated 2019 Jul 21]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2020 Jan-. Available
from: https://www.ncbi.nlm.nih.gov/books/NBK539804/)

Annotate
 This 2007 report from the European Respiratory Journal about weaning from
mechanical ventilation is the product of the Sixth International Consensus
Conference on Intensive Care Medicine. It discusses recommendations for
assessing patients’ readiness for weaning, the usual process for weaning, and risk
factors for weaning failure.

 This 2019 paper presents a comprehensive protocol for ventilator weaning and
extubation that includes risk assessment checklists for the different stages of
weaning and extubation.
 Mode settings
There are three settings common to every conventional mode of ventilation:

1. FiO2 - the amount of oxygen delivered to the patient

2. PEEP - pressure maintained in the respiratory system at the end of exhalation

 Maintaining PEEP keeps an open lung and prevents atelectasis

3. Trigger sensitivity - criteria used to see if the patient is making an effort (flow-
triggered and pressure-triggered)

The three most common modes of ventilation include volume assist control,
pressure assist control, and pressure support.  Assist control modes (pressure or
volume) are typically used in the acute phase of mechanical ventilation, or when
the patient has no or very minimal drive to breath.  Pressure support is used when
patients have an intact respiratory drive. Their nuances are included in the table
below.

Volume Flow Pressure Cycle

Controlled Controlled Determined by Volume

Volume Assist
respiratory or Time
Control (VAC)
system

Pressure Determined by Variable Controlled Time

Assist Control Respiratory System
(PAC)

Determined by Variable Controlled % of

Pressure
respiratory system and Peak
Support (PS)
patient demand
Volume Assist Control (AC-VC) requires a frequency of respirations per minute.
Patients can trigger additional breaths greater than the devised respirations per
minute. If the trigger criteria is not being met, the machine will trigger all of the
breaths. When patients are starting to interact with the ventilator, a spontaneous
mode such as pressure support should be considered.

The tidal volume should be 6-8 mL/kg of ideal body weight. The weight should be
predicted weight, NOT actual weight, as actual weight will overestimate the tidal
volume. 

To calculate predicted weight we relied on the work of emDocs, and the group

recommends using the equation 50 + 2.3 x (height [in] - 60) for men and 45 + 2.3 x
(height [in] - 60) for women. 

Current practice based on several trials suggests that the patient should be
ventilated with “lower” tidal volumes of 6–8 mL/kg. Flow is the speed at which the
tidal volume is delivered (50-60L/min will minimize discomfort when patients start
making an effort). PEEP should always be set at a minimum of 5 cmH 2O, to reduce
atelectasis.

The inspiratory flow is commonly set between 50 and 60 L/min and a minimum I:E
ratio of 1:1.5 to 1:2 (affected by respiratory rate as well). Common inspiratory times
are 0.75–1 s. In certain circumstances, such as in airway obstruction with asthma,
allowing more time for exhalation is beneficial. In these cases, one can increase
the inspiratory flow or decrease the I:E ratio, to 1:3 or 1:4.

The inspiratory pause helps distinguish between resistive pressure and elastic
pressure (compliance of the respiratory system). The inspiratory pause allows the
ventilator to display the plateau pressure, which is helpful for monitoring the
patient’s respiratory system mechanics (resistance and compliance).  It also
prolongs the inspiratory time to the common time of 0.75-1 s.

Pressure Assist Control (AC-PC) similarly requires a frequency of respirations

per minute. The inspiratory time is the length of time the pressure is maintained
while the rise time is the time the ventilator will take to reach the set pressure. The
default setting for rise time is generally acceptable at 0.1 sec. As resistance or
elastance of the respiratory system changes, a result will be changes in tidal
volume and minute ventilation. Consequently, it is very important to monitor
the tidal volume and keep it in the proper range in AC-PC.  The I:E ratio is the
simplest parameter to monitor if there is enough time to exhale. It must be
maintained at 1:2 or higher to ensure there is enough time to exhale. If the patient
starts spontaneously breathing, this will affect I:E and it is worth considering
transition to spontaneous breathing. Similar to volume assist control, the inspiratory
flow is commonly set at 60L/min and tidal volume should be 6-8 mL/kg.
 Pressure Support (PS) is distinguished from AC-PC because breaths are cycled
off by a % of peak flow, as opposed to time. It is important to adjust the default
settings for the % of peak flow to initiate the cycling off of each breath, as it
depends highly on the resistance and elastance of the lungs.

Levels to monitor:

o Volume Assist Control

 Elevated peak pressure and/or plateau pressure will result from abnormal
resistance and elastance due to ARDS, COPD, asthma, intra-abdominal
hypertension, etc.

o Pressure Assist Control

 Significant changes to tidal volume and minute ventilation will result from abnormal
resistance and elastance due to ARDS, COPD, asthma, intra-abdominal
hypertension, etc.

PEEP can be increased to improve oxygenation. However, it should not be so

much to overdistend the lungs.  The risk of potential injury increases when plateau
pressure is greater than 27 cm H2O.

pH should be kept between 7.35 and 7.45. To increase pH, increase minute
ventilation. To decrease pH, decrease minute ventilation. However, Minute
Ventilation should not be increased to the point that PaCO 2 < 30 mmHg. Cerebral
perfusion may be impacted with levels that low.  In management of ARDS,
permissive hypercapnia is often considered to minimize injury to the lung and a pH
7.25 is considered the lower acceptable limit.
 Acute Respiratory Distress Syndrome, (ARDS) is a condition of diffuse alveolar
damage and inflammation, secondary to any number of possible processes. While
ARDS always causes hypoxemia, not all hypoxemia is ARDS. ARDS is the most
common severe complication of COVID-19, contributing to the severe morbidity
and mortality of the infection. ARDS is defined by 4 criteria:

1. The condition must be acute (< 7 days)

2. The findings are not solely explained by cardiogenic pulmonary edema

3. The chest X-ray must have bilateral opacities

4. While on at least 5 cmH2O of positive pressure ventilation, the ratio of PaO2 to

FiO2 (expressed as a decimal, such as 0.7) must be < 300

1. Mild ARDS is a PaO2/FiO2 ratio of 200-300

2. Moderate ARDS is 100-199

3. Severe ARDS is < 100

Positive pressure ventilation, especially with large tidal volumes or high pressures,
has been shown to cause injury in both patients with ARDS as well as patients who
do not yet have ARDS. Of all the interventions in critical care, few have been as
reproducibly beneficial to patients as low tidal volume ventilation.

Many of the maneuvers used in severe hypoxemia to improve oxygenation and

ventilation can be deleterious in the long term. Increasing the mean airway
pressure (MAP) is one of the major goals of positive pressure ventilation, and
higher MAPs are often associated with improved oxygenation. The factors that
increase MAP are those that either increase the pressure in the airways, such as
tidal volume, PEEP, or AutoPEEP, or the amount of time the positive pressure is
delivered, such as the inspiratory time.

However, despite short-term improvement in oxygenation, high pressures in the

alveoli are also associated with worse long-term outcomes. Therefore, the clinician
has to balance the risk of increasing the MAP with using good, evidence-based
ventilator management.

Tidal volumes are best represented in both mLs and mLs/kg of predicted body
weight. The predicted body weight is a surrogate for the patient’s anticipated lung
volume. Lung volumes depend upon a patient’s height and biological sex. Actual
body weight should never be used as a replacement for the predicted body weight.

The ventilator screen below shows an example of a low tidal volume strategy. The
patient was set on 330 ml/kg, or 6.35 ml/kg of PBW, as indicated in the bottom left-
hand corner.
Once the initial tidal volume is selected, the pressures should be assessed. In
ARDS, as well as other patients, maintaining a Pplat < 30cm H 2O is key to
preventing ventilator-induced lung injury. Note that the Pplat will be determined by
the tidal volume given and the compliance of the respiratory system. ARDS usually
results in decreased compliance, resulting in stiff lungs. Interestingly, in patients
with COVID19, their compliance seems to be higher than other patients with
comparable ARDS.

Using an inspiratory hold, the Pplat should be confirmed to be less than 30 cm H 20.
If Pplat is > 30 cm H20, a lower tidal volume should be initiated, even down to
4ml/kg.

In this image, an inspiratory hold has been performed, providing a Pplat of 32. This
tells us two things:
4. There is a minimal difference between the PIP (35 cmH2O) and the Pplat (32 cmH2O)
indicating that the patient has only a compliance problem without a resistance problem.

5. The Pplat is too high. The tidal volume should be lowered to 5 ml/kg PBW and
reassessed.

PEEP is the next setting to address. Clearly, oxygenation is a critical factor for
these patients. PEEP increases the mean airway pressure (MAP) and thereby
improves oxygenation. PEEP additionally can help prevent further derecruitment. A
physiologic goal in setting PEEP is to prevent atelectasis without extending into
overdistention. A theoretical optimal PEEP would be at the red “X”, and each
breath would move up and down the pressure/volume slope as indicated by the
light blue arrow.
Many of these patients will need moderate to high PEEPs of 8-16 cmH 2O, and at
times, even greater. The PEEP may contribute to the Pplat, and therefore, the
Pplat should be checked with any PEEP change, just as with any TV change. The
time when an increase in PEEP will not, or will only minimally, increase the Pplat is
when the patient is derecruited and increasing the PEEP helps recruit collapsed
lung. In this instance, the increase in PEEP can actually improve compliance, and
therefore not increase the
Pplat. 

This is the principle behind performing a recruitment maneuver and a “BestPEEP”

trial to find a PEEP that optimizes compliance – preventing both atelectasis and
overdistention. This is discussed in more detail below.

Driving pressure (∆P) is the term that describes the pressure changes that occur
during inspiration, and is equal to the difference between the plateau pressure and
PEEP (Pplat – PEEP). For example, a patient with a Pplat of 30 cmH 2O and a
PEEP of 10cmH20 would have a driving pressure of 20cmH2O. In other words,
20cmH2O would be the pressure that extered to expand the lungs. Studies have
shown that a driving pressure of < 15 cmH2O is associated with better outcomes in
patients with ARDS.
While most patients will be started on a FiO 2 of 100%, especially if hypoxemic, the
FiO2 should be decreased as tolerated after checking an ABG (arterial blood gas).
Oxygen toxicity is increasingly appreciated in numerous conditions, as decreasing
the FiO2 as much as is safely tolerated is appropriate.(7-9) A reasonable target is
an SpO2 of 92-96%.

The following ventilator screen illustrates settings for a patient with ARDS. The tidal
volume is 400, which is appropriate for the patient’s height and sex. The respiratory
rate is 30, to maintain minute ventilation of approximately 12. A PEEP of 18 is
required, and the patient is still on 100% FiO2. Note that the PIP is 47, and the
Pplat is 43. The clinicians can try to decrease the tidal volume, however, these
values are so far from 30 cmH2O, it is unlikely that they will be able to achieve this
goal.
An ABG (arterial blood gas) provides important information, allowing the clinician to
calculate the PaO2 to FiO2 (P/F) ratio, and thereby categorize the severity of the
patient’s ARDS.

Patients being ventilated with low tidal volumes will require a higher rate to
maintain minute ventilation. Most patients with ARDS will require RR of 20 breaths
per minute or greater. This is especially important to consider as many patients
with ARDS will be hypermetabolic, with increased CO2 production.
  
Initial Ventilator Settings in ARDS

Tidal Volume 4-8 ml/kg PBW, starting with 6 ml/kg

Respiratory Rate Higher, often > 20 breaths per minute

PEEP ≥ 8 cmH2O, avoiding overdistention

FiO2 Decrease as tolerated, SpO2 ≥ 92%

Severe Hypoxemia
At times, patients may have refractory, severe hypoxemic respiratory failure. After
checking all ventilator settings as described above, the clinician should employ
additional evidence-based maneuvers.
At times, a patient may be well sedated yet dyssynchronous with the ventilator.
Ventilator dyssynchrony is associated with worse outcomes and should be
avoided. A recent trial, published in 2019, did not find improved mortality with
neuromuscular blockade use in ARDS. However, neuromuscular blockade was
also not associated with increased harm. As such, it can be considered in patients
who remain dyssynchronous with the ventilator despite appropriate sedation. This
image of the ventilator shows how a patient looks when dyssynchronous. The
waveforms should be smooth and fairly regular. When they are jagged and
irregular, the patient is fighting the ventilator. Additionally, note that while the
patient is set on low tidal volume ventilation at 380 ml, the patient is actually taking
in about 800 ml through significant respiratory efforts.
In well-sedated and possibly chemically relaxed patients, the first maneuver is to
provide a recruitment maneuver. Recalling that derecruitment is a common cause
of hypoxemia, gently recruiting alveoli can improve oxygenation. The damage to
the lungs is heterogeneous. Some areas are atelectatic, some are fluid-filled, some
are already over distended, and some are even normal. The concept behind a
recruitment maneuver is simple: the application of sustained pressure to open up
collapsed alveoli. However, there are two potential downsides.

However, note that the normal and overdistended areas may also become even
more overdistended. This overdistention from the previously “good” parts of the
lung can lead to decreased gas exchange during the recruitment, causing
desaturation. This effect should be temporary and improve after the maneuver.
The second effect is that the patient can become hemodynamically unstable, due
to a significant increase in the intrathoracic pressure and resultant decrease in
preload and increase in right ventricular afterload. Again, this should be temporary
and resolved with a reduction in the pressure, but in unstable or preload dependent
patients, this can precipitate hemodynamic collapse. Recruitment maneuvers
should never be performed without a respiratory therapist, nurse, and physician
present. All clinicians should be aware of the risks of transient hypoxemia and
hypotension.
There are many methods of performing recruitment maneuvers. One of the
methods least likely to cause hemodynamic perturbations is to serially increase
PEEP in small increments. A trial of large increases in PEEP (25 cmH 2O, 35
cmH2O, then 45cmH2O with a final PIP of up to 60 cmH2O) was stopped early for
futility. As such, we recommend a more gradual approach.

Once the patient is stabilized after intubation, the recruitment maneuver and the
best PEEP can be determined, using a decremental compliance PEEP trial. This
can be repeated every 24 hours for patients who continue to require high levels of
ventilatory support.

The FiO2 should be set at 1.0 and the patient appropriately sedated, and relaxed if
needed. The ventilator should be set to pressure control ventilation, with a PC of
15 cmH2O, inspiratory time of 3 sec, rate of 10 breaths per minute. Then, increase
PEEP 3 cmH2O every 5 breaths until the applied PEEP is between 25 to 35 cmH 2O
and the maximum PIP is between 40 to 50 cmH 2O. Ventilate at this level for 1 min.
If the patient desaturates or becomes hypotensive at any point, stop, and return to
the prior PEEP. This illustration indicates the step-wise PEEP approach.
From here, the best compliance decremental PEEP trial should be performed. The
next step is to change to volume control ventilation (VCV) at 4-6 ml/kg PBW and
set PEEP at 20 to 25 dependent on patient severity of lung injury. The respiratory
rate should be set to a rate that does not result in autoPEEP, usually 20 to 30
breaths/minute. Measure dynamic compliance, then decrease the PEEP by 2
cmH2O, holding for 30 seconds at a time, and reassessing dynamic compliance
each time. Initially the compliance will increase as PEEP is decreased, but with
derecruitment, compliance will decrease. Once it is obvious that compliance is
decreasing, the trial can be stopped. A clear pattern will indicate the PEEP with the
best compliance. To set the ventilator, recruit the lung a second time, then set at
the best PEEP + 2cmH2O to optimize oxygenation as well. The illustration below
demonstrates the concept.
Below is an example from clinical practice. The patient was placed on PEEP of 20,
a tidal volume of 400, and an incremental best PEEP trial performed as described.
The values were written on the patient’s white board at the time of the testing, and
a worksheet with the driving pressure and compliance were then filled in to
determine the optimum PEEP. As both 10 and 12 had good compliance, 12 cmH 2O
was selected in this example.

PEEP (cm H2O) Pplat (cm H2O) Driving Pressure (cm H2O)

20 37 17

18 37 19

16 33 17
 14 29 15

12 26 14

10 24 14

For patients with a PaO2/FiO2 ratio of less than 150, the next maneuver is proning
the patient, or placing them in the proned position, to improve oxygenation to the
posterior lungs. Proning the patient improves V/Q matching and allows the patient
to have gas exchange along the posterior aspects of the lungs. Proning has been
shown to improve mortality in severe ARDS in a large multi-center study.
Additionally, patients with COVID-19 seem responsive to proning. However, this
maneuver requires specialized expertise and a coordinated effort amongst
providers to avoid dislodging the endotracheal tube and patient harm. If a patient
has such severe hypoxemia that non-Intensivists are considering proning, expert
consultation should be sought.

Another consideration is the administration of inhaled pulmonary vasodilators, such

as inhaled nitric oxide (not to be confused with nitrous oxide, the anesthetic agent)
or prostacyclins, such as epoprostenol. Hypoxemic patients generally have
heterogeneous lung pathology, with some damaged areas not participating in
oxygenation and ventilation, as well as some relatively unharmed areas that are
doing the bulk of gas exchange. Inhaled pulmonary vasodilators will vasodilate the
areas that are participating in gas exchange, effectively increasing blood flow to the
good areas of the lung and allowing the ineffective areas to continue to have
hypoxemic vasoconstriction. This principle is illustrated in the diagram below.

Finally, patients with severe, refractory hypoxemia may be referred to an

extracorporeal membrane oxygenation (ECMO) center for consideration of ECMO
support. The data for venovenous (VV) ECMO in severe ARDS not related to
COVID-19 are mixed. The largest trial, the EOLIA trial,14 ECMO for severe ARDS
was stopped early at 249/331 patients enrolled for predefined futility. There was no
significant mortality benefit at day 60, but 28% of the conventional treatment group
had crossover to ECMO rescue. This has led to a lot of controversy as to how the
results of the trial should be interpreted. Although it is a negative trial, proponents
of ECMO note that when patients from the control group received ECMO, it was
started later when they were sicker, and 7 crossover control patients even
underwent VA ECMO for arrest. They also note that conventional treatment had a
high rate of failure necessitating ECMO.

The role of ECMO in COVID-19 remains to be determined. Some centers are

reporting successes, with new decannulation reported each day. However, others
note that the natural history of COVID-19 appears to be a very prolonged
respiratory failure. As such, some have expressed concerns that the respiratory
failure could result in protracted ECMO runs with concomitant high rates of
complications. As such, many are making referrals and initiating VV ECMO while
data are being collected to determine best practices.

The image of a ventilator screen above shows an inspiratory pause to calculate a

plateau pressure (Pplat). The gold star shows where flow has ceased to allow
pressures to equilibrate. The Pplat is 18cmH 2O in this example. The ventilator
automatically calculates a compliance of 40 mL/cmH 2O. A normal compliance is
about 80–100 mL/cmH2O, and expected for a ventilated patient is approximately 60
mL/cmH2O, as all ventilated patients are less compliant than those breathing with
normal respirations.
Additional Resources
Continulus, an accredited, continuing education platform for healthcare providers,
is offering free lectures related to COVID-19. One of them is Foundational Aspects
of Mechanical Ventilation by a critical care nurse of 22 years. The lecture is
designed to help medical professionals understand the importance of mechanical
ventilation in the adult ICU, describe critical ventilator settings and apply
knowledge of mechanical ventilation to patients with acute respiratory distress
syndrome. The document got good reviews on social media.

Treatment for severe acute respiratory distress syndrome from COVID-19, by

Michael Matthay, J. Matthew Aldrich, and Jeffrey E. Gotts, was published in the
Lancet on March 20, 2020, and recommends an escalating approach to treating
patients with ARDS from COVID-19.

We have also put together prone positioning guidelines that provide general

instructions for how to prone a patient and how to return them to the supine
position. Be sure to work with experienced critical care clinicians when deciding
whether or not to use proning for a patient and to perform this procedure safely.
Asthma
In asthma, the patient has a constriction of the bronchial smooth muscles in the
airways, leading to reversible air trapping. This is indicated in the schematic. Note
that the bronchial muscles do not extend into the small airways.

Intubation of an asthmatic is a dreaded complication of this illness, as asthmatics

can deteriorate rapidly on the ventilator without close monitoring and active
management. The goal with a ventilated asthmatic is to prevent breath-stacking or
autoPEEP, and the hemodynamic instability that can result.
Before discussing the ventilator management of asthma, clinicians should note that
intubation of an asthmatic should trigger even more active management with
medications, rather than less. Intubated asthmatic patients should continue to
receive aggressive treatment with bronchodilators, steroids, magnesium, as well as
deep sedation and possibly even neuromuscular blockade in the initial hours after
intubation, in an effort to relax the chest wall musculature and gain control of the
situation.

Please note that neuromuscular blockade only works on skeletal muscle and
therefore, will not bronchodilate smooth muscle in the airways. In addition, it is very
critical to be aware of the patient’s intravascular volume status, as the excess
positive pressure can lead to hemodynamic collapse. Moreover, the excess
pressure, including the auto-PEEP, can result in barotrauma, such as the
development of a pneumothorax very quickly in this patient population. The
ventilator screen below demonstrates the effects of reactive airways disease on
pulmonary mechanics. This patient had unexpected bronchospasm after being
intubated. Note the elevated peak inspiratory pressure (PIP) of 45 despite the
relatively low tidal volume of 365. The patient’s resistance was too high for her to
even receive the full tidal volume, as the ventilator was only able to deliver 320ml
before stopping.
Checking the plateau pressure (Pplat) confirmed that this was a resistance
problem, rather than a pure compliance problem. Her PIP was 39 at the time the
inspiratory hold was performed, but her Pplat was only 28. The delta between 39
and 28 indicates a significant resistance component.
This patient was treated with continuous bronchodilators with rapid improvement in
the bronchospasm. Her PIP returned to normal within minutes.

Four ventilator maneuvers increase expiratory time, namely, decreasing the

respiratory rate, decreasing the I:E ratio, decreasing the inspiratory time, or
increasing the inspiratory flow. Of these, decreasing the respiratory rate is the most
effective means to allow more time to exhale.

The figure shows a schematic of 30 seconds with two patients, set with the same
I:E ratio of 1:2. The first patient has a rate of 10 breaths per minute, allowing 6
seconds per breath cycle. The second patient has only 3 seconds per breath cycle,
given the respiratory rate of 20. The blue represents inspiration, the red the time for
exhalation. Note that even with the same I:E, the lower rate offers a substantially
longer time to exhale.
In looking further at this diagram, one can imagine the effects of changing the I:E
ratio, the inspiratory flow, or the I time. Fig 9.3 shows a hypothetical example of the
effects of these changes in a patient on volume control. In a given patient, the
exact values will vary, but the purpose of the illustration is to show the relationship
among the parameters of I:E, inspiratory time, and inspiratory flow.

In addition to a slow respiratory rate, a low I:E ratio, a short inspiratory time and/or
a fast inspiratory flow rate, asthmatics should also be ventilated with low tidal
volumes. Considering that the larger the tidal volume, the more the patient has to
exhale, this is fairly intuitive.

In monitoring an intubated asthmatic, looking for air trapping is key. In the vent
tracing below, note that the flow tracing, in the middle, does not return to the
baseline before the next breath. (Red arrows) This represents that the patient is
still exhaling when the next breath is given, leading to air trapping. Seeing this
pattern on the ventilator can be an early clue that the patient is air trapping. If you
were caring for this patient, how would you address this air trapping?

In this patient, you could first decrease the respiratory rate, or increase sedation if
the patient is over-breathing. The I:E ratio is only 1:2, so changing the I time to
make a ratio of 1:3 or 1:4 is also appropriate. Also continued treatment with
bronchodilators to decrease the bronchospasm associated with this disease will
also mitigate the excess auto-PEEP.
Recall that to quantify the pressure exerted by air trapping, one should check for
autoPEEP by checking an expiratory hold button on the mechanical ventilator. In
this tracing, what is the autoPEEP, or the intrinsic PEEP? What is the total PEEP?

The intrinsic PEEP is 11, and the total PEEP is 12. This indicates that the patient
was only set on 1 of PEEP (an unusual - and not recommended - setting, used in
this circumstance for demonstration purposes only.)

Thus, to set the ventilator for an asthmatic, select a low tidal volume of 6-8 mL/kg
of predicted body weight. The respiratory rate should be low, less than 20 breaths
per minute, and often around 10. The I:E ratio should be changed to 1:3 or less.
PEEP should be set at 5 cmH2O. The FiO2 should be down-titrated as tolerated.
These patients continue to receive heavy sedation, possibly NMB if required,
continuous bronchodilators, and close monitoring for breath stacking and
autoPEEP. AutoPEEP should be monitored periodically or after any ventilator
change with an expiratory hold. Arterial blood gases (ABGs) should be checked to
ensure that the patient is being adequately ventilated.

Permissive hypercapnia is the concept of tolerating a PaCO 2 > 40mmHg and a pH

> 7.20 to 7.25 for the sake of achieving another goal. In the case of asthma, the
goal is to allow time to exhale and prevent air-trapping. Permissive hypercapnia is
a reasonable strategy, especially early in ventilating the asthmatic.

Initial Ventilator Settings in Asthma

 Tidal Volume 6-8 ml/kg PBW

Respiratory Rate 6 - 14 breaths/minute, allowing for permissive hypercapnia

PEEP ~ 5 cmH2O

FiO2 Decrease as tolerated, SpO2 ≥ 92%

The following ventilator screen demonstrates these settings. The patient is set at
6ml/kg at 350 mls, with a respiratory rate of 14, a PEEP of 5, and a FiO 2 40%.
Note, however, that the patient is not synchronous with the ventilator and is taking
large tidal volumes. This can be a very dangerous situation, leading to worsening
air-trapping and possibly hemodynamic compromise. This patient needs to be
deeply sedated and neuromuscular blockade administered if needed. Additionally,
the patient should continue to receive bronchodilators and all other appropriate
medical treatments.
COPD
There are two types of obstructive lung disease falling under the umbrella of
COPD, namely, chronic bronchitis and emphysema. While some patients may
have one or the other, many will exist on the continuum.
Chronic bronchitis can resemble the asthmatic schematic above, with the notable
exception that muscles hypertrophy and are not entirely reversible. Additionally,
chronic bronchitis is associated with increased mucous production.

Emphysema is a disease of parenchymal destruction. Not only is there loss of

alveoli, resulting in decreased surface area, or decreased diffusion area (leading to
an increased DLCO), but the small airways can become floppy due to the loss of
other tissues holding them open.
Understanding the pathophysiology of COPD is important for considering how to
best ventilate these patients. It should be noted, however, that most patients with
COPD have some mixing of elements of chronic bronchitis and emphysema.
These conditions exist on a spectrum rather than a dichotomy.

Most patients with COPD are now managed with BPAP, with improved outcomes
over intubation. However, on occasion, a patient with COPD is not a candidate for
BPAP or fails to improve with a trial of BPAP, mandating intubation and invasive
mechanical ventilation. Many of the principles that apply in mechanical ventilation
for asthma also apply in COPD. Both are obstructive diseases, and in both
processes, the patients require adequate time to exhale. Therefore, low tidal
volumes, low rates, and low I:E ratios are appropriate. However, a key difference
involves the role of PEEP.

Patients with COPD are at high risk of developing autoPEEP. Due to their
obstructive disease, they require additional time to exhale. However, the
mechanism of obstruction can differ between asthma and COPD, especially COPD
with emphysematous changes as illustrated above. With the destruction of
parenchyma, the small airways can collapse with exhalation, trapping air behind. In
this circumstance, this trapped air leads to autoPEEP. Increasing the set PEEP, to
match the autoPEEP, is not necessarily an intuitive solution. However, as
illustrated by the diagram below, increasing the PEEP to prevent collapse of these
small airways can allow the patient to exhale more fully.
Reexamine the tracing of Fig 9.5 from the Asthma section, imaging that this patient
has COPD. If this patient has 11 of autoPEEP, or intrinsic PEEP, what PEEP
would you select?

To match the autoPEEP, 11cmH2O would be an appropriate PEEP selection.

Lastly, patients with COPD are often chronically hypoxemic. Indications of chronic
hypoxemia physical exam findings of chronic hypoxemia can be demonstrated with
nail clubbing. Additionally, can include an elevated hemoglobin level on the CBC,
indicating the patient’s compensation for their chronic lung disease. Because these
patients are baseline hypoxemic, and ventilation is often a relatively greater issue
for them than hypoxemia, the oxygen saturation for a patient with COPD should be
targeted at 88-92% in most circumstances. This is increasingly important as more
data demonstrating the risks of hyperoxia continue to accumulate.

Initial Ventilator Settings in COPD

Tidal Volume 6-8 ml/kg PBW

Respiratory Rate 6 - 20 breaths/minute, allowing for permissive hypercapnia

PEEP 5-15 cmH2O - may need to match autoPEEP for patients with significant emphysema

FiO2 Decrease as tolerated, SpO2 target 88-92%

This ventilator screen demonstrates a patient with COPD with severe

dyssynchrony. The PIP is 54, indicating severe pathology. The irregular waveforms
indicate the dyssynchrony. The patient is set at a respiratory rate of 16 but is
breathing at 24.
An expiratory hold was performed and demonstrated a total PEEP of 29, with a set
PEEP of 10. This indicates a high autoPEEP of 19. Therefore, this is a very high-
risk situation. This patient was deeply sedated, NMB administered, and the ETT
was disconnected from the ventilator to allow the patient to exhale.
Once sedated and relaxed, the patient was placed back on the ventilator at a rate
of 12, with frequent expiratory holds to check the autoPEEP.

The slideshow Management of Severe Obstructive Lung Disease by Dr. Craig Rackley,

pulmonologist and assistant professor of Medicine at Duke University Medical Center,
gives the basics of treating obstructive lung disease and includes a thorough case study.

https://slideplayer.com/slide/11985536/
 In waveform analysis, the scalars of interest are volume vs time, pressure vs time,
and flow vs time.

In volume assist control, it is common to have a constant flow pattern, which will
show up as straight in the flow scalar. Adding an inspiratory pause (when flow =
0) will indicate a plateau pressure in the pressure scalar. In volume assist control,
effort will cause changes to the pressure waveform.

In pressure assist control, pressure is held constant over time. The rise time is
the time it takes to reach the pressure provided during inspiration. To find
the plateau pressure, use an inspiratory pause. In pressure assist control, effort
by the patient will change the flow waveform.

To understand patient behavior, it is important to understand asynchrony, which

includes:

o Neurological timing and ventilator timing is out of sync

o Flow starvation (the ventilator does not meet the demand of the patient)

o Patient is unable to meet the trigger criteria.

In volume assist control, you will see patient effort in the form of negative
scooping in the pressure waveform, if flow demand is not entirely met for the
patient. Patients with COVID-19 often have excessive efforts when they interact
with the ventilator. As a result, it is important to monitor the occlusion pressure,
or p0.1, to ensure it is not too high and to watch for significant scooping in the
pressure waveform.
The figure above shows patient effort in volume assist control with a normal
amount of scooping (and p0.1 of 2.35 cmH 2O). The figure below indicates
excessive effort, which many COVID-19 patients display when they begin to
interact with the ventilator, with p0.1 of 4.7.
In pressure assist control, patient effort should change the flow waveform. In this, it
is important to check if the flow reaches 0 as pressure reaches 0 during inspiration
or if there is dampening of the peak expiratory flow during exhalation to ensure the
patient is not experiencing asynchrony with breath timing. This can be adjusted by
shortening or lengthening the inspiratory time. Similarly, p0.1 can be monitored to
evaluate whether a patient is experiencing excessive effort in which increasing
support should be done in an attempt to reduce respiratory drive provided tidal
volume is not excessive. PEEP can also be adjusted to attempt to improve the
patient’s drive.

In pressure support, it may be necessary to alter the % of peak inspiratory flow that
causes cycling off to eliminate asynchrony. If the patient is demonstrating
excessive effort, increasing the pressure support will help decrease the patient’s
drive. However, if increasing pressure support does not decrease the p0.1,
reducing the drive must be prioritized. PEEP can also be adjusted to attempt to
improve the patient’s drive.

Delayed cycling is another phenomena where the patient wants to exhale but the
machine has not cycled off yet. In pressure assist control, if there is an increase in
pressure at the end of inspiration with a subsequent rapid deceleration in the
expiratory flow, then the patient is most likely experiencing delayed cycling. As a
result, the inspiratory time should be shortened. However, the time should be not
shortened so much that it causes premature cycling, in which the patient’s effort
lasts longer than the ventilator’s cycle off criteria. This will manifest as a
dampening in the peak expiratory flow. Premature cycling can also occur in
pressure support, when the cycling-off percentage is too high. This flow scalar will
look similar to that for premature cycling in pressure assist control.
 
 In the figures above, delayed cycling (top) and premature cycling (bottom) in
pressure assist control are noticeable by analyzing the flow scalar. The inspiratory
time should be shortened for delayed cycling and lengthened in premature cycling.

Ineffective efforts are another form of asynchrony that generally occurs when
patients are overassisted (too much pressure support) or have too high of airway
resistance. Delayed cycling is a common cause of ineffective efforts. 

Reverse triggering is another form of asynchrony where the ventilator triggers a

breath that then triggers an effort from the patient. This can also lead to breath
stacking. The first thing to check when noting reverse triggering is to see if it is bad
timing or reflex. To check this, first reduce the respiratory rate. After reducing the
respiratory rate, if the patient is triggering the breaths, it was simply bad timing. 

However, if the reverse triggering still continues, a few steps should be taken:

o Turn off sedation if possible.

o Increase tidal volume to a maximum of 8 mL/kg of IBW.

 Keep plateau pressure less than or equal to 27 cmH 2O, and less than 30cmH2O for
COVID-19 patients (typical ARDS guidelines).

o If there is a known injurious pattern (breath stacking) and sedation cannot be

stopped, consider NMB agents to protect the lung and minimize the possibility of
barotrauma.

https://www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/
mechanical-ventilation/ventilator-waveform-analysis.php
 According to Brigham and Women’s Hospital COVID-19 Critical Care Clinical
Guidelines, people with COVID-19 generally present respiratory symptoms. More
specifically,

 46-82% have a cough

 20-64% experience shortness of breath

 5-25% exhibit upper respiratory symptoms, including nasal/sinus congestion

The Brigham and Women’s Hospital guidelines further state that approximately

20% of those with COVID-19 develop ARDS and 2-25% have a respiratory viral co-
infection. While the most common cause of ICU admission for COVID-19 patients
is hypoxemic respiratory failure. Among those admitted, intubation is often required
within 12 to 24 hours. Of COVID-19 patients who die, about half die from
respiratory failure and a third die from concomitant respiratory and heart failure.

Many patients with COVID-19 are presenting with hypoxemia disproportionate to

their imaging findings. Hypoxemia arises in ARDS through a mismatch of
ventilation and perfusion, predominantly due to shunt,1–3 with shunt fractions
much greater than would be anticipated for their relatively compliant lungs. Patients
with COVID-19 have scattered, peripheral ground glass opacities on chest
computed tomography scans, indicating ineffective lung units, and as such, shunt
appears to be a major cause of the hypoxemia. Dr. Gattioni and colleagues report
disproportionate blood flow to these areas, possibly accounting for the profound
hypoxemia.3 They suggest at least two distinct phenotypes, with the low
recruitability phenotype presenting with low elastance, high compliance, low
recruitability, but yet substantial hypoxemia. They posit that a mechanism for this
profound hypoxemia could be loss of V/Q matching from pulmonary arterial
vasoplegia. Later, patients progressed to the H phenotype, with high elastance, low
compliance, high recruitability, and need for higher PEEP.

The CT scan below demonstrates the mild-moderate ground glass findings in

COVID-19.
On presentation, patients are presenting with substantial hypoxemia, with many
having oxygen saturations in the 70s, 80s, 90s, and they deteriorate with any
exertion. Chest x-ray imaging will vary substantially depending upon where the
patient is in the course of their illness.

The initial mode of treatment involves providing supplemental oxygen immediately

to improve the oxygen saturation. Although patients may or may not be
complaining of dyspnea, nearly all hypoxemic patients are noted to be tachypneic.
Patients who are tachypneic, generating large tidal volumes, can still induce lung
injury from generating large negative intrathoracic pressure and therefore a large
transpulmonary pressure. As such, the hypoxemia should be treated to decrease
hypoxemic drive.

The role of high-flow nasal cannula and non-invasive positive pressure ventilation
are controversial in COVID-19. The concerns are for healthcare workers, as the
risk of aerosolization has been noted with these modalities, especially non-invasive
positive pressure ventilation. Although there are limited data regarding the use of
HNFC in COVID-19, a small study of patients with Influenza A showed that 45%
avoided intubation, although all more severe patients were eventually intubated.4

Similarly, non-invasive positive pressure ventilation (NIPPV) is a common means

of respiratory support in many patients, but its use in COVID-19 should be limited.
NIPPV failed in 57-85% of patients with Influenza A H1N1 associated ARDS, and
with failing patients having a higher ICU mortality than those treated with invasive
mechanical ventilation.4,5 Some component of this may be due to patients
continuing to generate those large tidal volumes and continuing to induce self-
inflicted lung injury.6 Subjects with SOFA score ≥ 5 had a higher risk of NIV failure
(odds ratio = 3.3, 95% CI 2.4-4.5).5 A small study of COVID-19 patients in Wuhan
found that 76% failed NIPPV, and the mortality rates were similarly high for both
groups.6 NIPPV also aerosolizes the virus7 and many recommend that it should be
avoided in most circumstances.7,8 However, there may well be a role for judicious
use of non-invasive ventilation in COVID-19. Each institution is developing their
own policies and procedures, with some adopting the process widely and others
not using it at all.

When the decision is made to intubate a patient, the patient can have significant
clinical deterioration with COVID-19. The patient arrives with a high work of
breathing, generating substantial negative intrathoracic pressure to maintain
minute ventilation and V/Q matching. When the patient is intubated, the induction
agents and paralytics are administered, the patient is laid in a recumbent position,
and the patient will be derecruited.
Recruiting the patient can be a substantial endeavor. Typically, we use a bag
method with a PEEP valve to recruit patients and prepare them to be placed on the
ventilator immediately after intubation. If this method is to be used, a HEPA filter
must be placed between the endotracheal tube and the bag. However, many
institutions are now foregoing any bagging and instead placing the patient directly
on the ventilator to reduce the risk of aerosolization. An advantage is that the
patient does not receive any high tidal volume, high-pressure breaths from the
bagging. The downside, however, is that recruitment may take longer, and these
patients may be profoundly hypoxemic during that time period.
Once the patient is placed on the ventilator, general principles of good ventilator
management still apply. The patient should be placed on low tidal volume
ventilation, starting with a tidal volume of 6 ml/kg of predicted body weight. The
plateau pressure should be checked and monitored, ensuring a value less than 30
cm of water. The driving pressure should be less than 15 centimeters of water.
These patients likely require a moderate PEEP at least. We recommend starting
with a PEEP of 8 and adjusting from there. Please refer to the section on
“Ventilation in ARDS” for an in-depth review of performing a recruitment maneuver
and a best PEEP trial to assess a patient's compliance to find the optimal peep.
While PEEP can improve oxygenation, too much PEEP can be deleterious,
causing increased intrathoracic pressure, lung injury, and hemodynamic
compromise if severe.

For patients with COVID-19 who have a PaO 2 / FiO2 ratio of less than a 150, the
next step should be placing the patient in a prone position. Many institutions have
protocols or guidelines for prone positioning. Prone positioning has been shown to
improve mortality in patients with ards, and authors are reporting good outcomes
with proning in patients with COVID-19. Although a simple procedure, it requires a
systems-based approach, with investment from nurses, respiratory therapists, and
physicians alike. All attention must be on the patient's endotracheal tube, invasive
lines, and position during the turns. Additionally, close attention must be paid to
patients in a prone position to ensure that their orbits and eyes are protected, that
pressure points are well-supported, that medical equipment is not trapped under
the body, possibly causing opportunity for injury or bedsores. Most protocols
involve leaving the patient in the prone position for 12 to 16 hours. The patient will
be reproned as long as their PaO2 / Fi20 ratio remains less than 150 while they are
supine. When the patient’s PaO2 / FiO2 ratio starts to improve, the patient no longer
requires routine proning.
For patients with persistent severe hypoxemia, inhaled pulmonary vasodilators can
be considered. Inhaled epoprostenol is an excellent pulmonary vasodilator,
however, it is not recommended in COVID-19 as it mandates frequent ventilator
circuit changes. Therefore, if an inhaled pulmonary vasodilator is needed, inhaled
nitric oxide is preferred. We start at 20 parts per million and assess the patient for
an improvement in SpO2. If the patient does not have at least a 20% improvement
in the SpO2, the inhaled pulmonary vasodilator is unlikely to be effective and should
not be continued. If the patient is responsive, the pulmonary vasodilator can be
continued with gradual weaning as a patient improves clinically over the next
several days.

Bacterial superinfection has been noted in about 20 to 30% of patients with

COVID-19, and as such, many patients will require antibiotics. Procalcitonin can be
useful for assessing COVID-19 alone.

Steroids are not routinely recommended for COVID-19 treatment. However,

patients who have another indication for steroids, such as asthma or adrenal
insufficiency, should receive them. The surviving sepsis campaign recommends
use of steroids in severe Arts, however, this is not a universal recommendation.

The role of other medications including hydroxychloroquine, azithromycin, and

statins, are unclear. We encourage everyone to refer to local protocols for
guidance on the use of these medications. Some medications, such as Remdesivir,
are being evaluated in clinical trials.

Although CT scans have been shown to be fairly sensitive for the diagnosis of
COVID-19, once the diagnosis is made, we do not encourage the routine use of CT
scans. Not only does a CT scan pose risk to a critically ill patient, mandating travel
with the associated risks of line pulls, hemodynamic instability, and hypoxemia, but
this can lead to infection control issues mandating the cleaning of the scanners as
well.

Patients with COVID-19 have been noted to be fairly hypercoagulable with many
authors reporting thromboembolic disease, clotting of dialysis lines, and other
clinical manifestations of hypercoagulability. D-dimer levels can be quite elevated
coming into the thousands. The best practices for initiation of therapeutic
anticoagulation, in the absence of a documented thromboembolism, are unclear at
this time. some clinicians are using markedly elevated D-dimer levels, such as
greater than 2000, as an indication for anticoagulation, whereas others are basing
it upon clotting of lines and other clinical markers.

Bronchoscopy is an aerosolizing procedure and as such, should be minimized or

avoided in patients with COVID-19. Additionally, suctioning can be aerosolizing
and all healthcare workers in the room should be aware and in appropriate PPE
before these procedures are performed.

https://covidprotocols.org/