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Mechanical Ventilation

Mechanical ventilation improves oxygenation by providing an increased fraction of inspired oxygen (FiO2) and positive end-expiratory pressure (PEEP) to prevent alveolar collapse.  The goal is to maintain arterial partial pressure of oxygen (PaO2) at 55-80 mm Hg, which roughly corresponds to oxygen saturations >88%-95%. 

Invasive mechanical ventilation may be required in hypercapnic patients with poor mental status (eg, somnolence, lack of cooperation, inability to clear secretions), hemodynamic instability, or profound acidemia (pH <7.1).


💻 Modes

Volume-cycled (controlled) ventilation (VCV): Ventilator will deliver a set tidal volume irrespective of the pressure that it generates.

Assisted VCV - Mode of ventilation where the ventilator is triggered by an initiated breath from the patient  ❗ The ventilator will not generate a breath without the patient’s effort.    

Controlled VCV - Requires the operator to assign a set minute ventilation by determining an appropriate tidal volume and respiratory rate ✅ This mode will generate breaths whether the patient is spontaneously breathing or not.    

Assist-controlled (ACV) volume-cycled ventilation - Combination of the aforementioned two.  (ii) The ventilator will generate breaths whenever triggered by the patient’s spontaneous breathing. (iii) Will also deliver set tidal volumes to make sure the predetermined minute ventilation is achieved    

Intermittent Mandatory Ventilation (IMV) - Essentially ACV + spontaneous ventilation (SV) (ii) The ventilator will allow SV, assist with spontaneous breaths, and generate its own breaths.  Advantage of IMV:  When SV occurs, muscle atrophy is reduced. 2. Risk of lung hyperinflation and the generation of intrinsic PEEP is minimized.  Disadvantage of IMV:  Spontaneously breathing through a breathing circuit and mechanical ventilator is difficult.  A patient typically requires a pressure support of 10 cm H2O to overcome that resistance.  Because of this, IMV becomes much more similar to ACV, as there is no longer any truly SV occurring.

Pressure-cycled ventilation (PCV): Indicates that the ventilator generates a constant pressure that is applied to inflate the lungs (i) This principle is important to remember anytime someone is on PCV, as one can see variability in the inflation volumes depending on the patient’s lung compliance.    Advantages of PCV: Generates a decelerating inspiratory flow pattern. This effectively decreases the peak inspiratory pressure (PiP) and can thereby improve gas exchange.  Disadvantages of PCV: Changes in lung mechanics will change the resultant inflation volumes. Therefore, it is imperative that the delivered tidal volumes are monitored to prevent the occurrence of volutrauma💥.

Pressure support ventilation (PSV)  The spontaneously ventilating patient has each tidal volume “supported” with a set pressure.  When the patient initiates a spontaneous breath, the ventilator is triggered to apply a positive pressure and augment each tidal volume.    

Pressure support settings  (i) Typically range from 5 to 20 cm H2O depending on the patient’s needs.    

Common indications for PSV: Weaning a patient from ventilatory support  This can be particularly beneficial when a patient has a minimal oxygen requirement but may be deconditioned and require additional pressure support for adequate ventilation. (ii) The amount of pressure support can be reduced on a regular basis until the patient is then able to ventilate without the need for pressure support and possibly ready for discontinuation of mechanical ventilation. Contraindication to PSV:  A patient receiving neuromuscular blocking agents. Since PSV has no backup set respiratory rate, ventilating a paralyzed patient with this mode would be catastrophic.

"T Piece" for weaning



🔢 Settings

Fraction of inspired oxygen (FiO2): The concentration of oxygen in the gas mixture with which the patient is ventilated.  Immediately following an endotracheal intubation and the initiation of mechanical ventilation, most patients should be placed on 100% inspired oxygen.  An FiO2 of 1.0 should be used until adequate arterial oxygenation is documented. A short period of ventilation with a FiO2 of 1.0 is not dangerous to the patient and offers some clinical advantages. 

(1) Protects the patient against hypoxemia if unrecognized problems occur as a result of the endotracheal intubation

(2) Using the FiO2 measured with a FiO2 of 1.0, a clinician can more easily estimate the shunt fraction and calculate the next desired FiO2.    

(a) The degree of shunt while receiving a FiO2 of 1.0 can be estimated by applying the rule 700—FiO2.   

(b) For each difference of 100 mm Hg, the shunt fraction is 5%.      

(i) For example, if the FiO2 is 500 mmHg while receiving a FiO2 of 1.0, then the shunt fraction is estimated at 10%.      

(ii) A shunt fraction of 25% should remind the clinician to consider the use of PEEP.      

(iii) A low FiO2, despite a FiO2 of 1.0, should prompt a search for complications related to endotracheal intubation and positive-pressure ventilation.    

Tidal volume:  The volume of gas the ventilator will deliver to the patient with each breath.  For a patient without preexisting lung disease, 10 to 12 mL/kg is a commonly used tidal volume for the assist-control mode.  For patients with a history of obstructive pulmonary disease, such as COPD, a smaller tidal volume of 8 to 10 mL/kg is commonly used.  In the setting of ARDS, it is suggested that the lungs may function best, and volutrauma may be minimized, with a lower tidal volume of 6 to 8 mL/kg in the assist-control mode

(1) These lower volumes may lead to slight hypercarbia.

(2) However, this elevated PCO2 is typically recognized and accepted without correction, leading to the term permissive hypercapnia.

Peak airway pressure:  The pressure measured by the ventilator in the major airways.  Strongly reflects airway resistance.  As the tidal volume increases, so too does the pressure required to drive that volume into the lung.  Persistent peak pressures higher than 45 cm H2O are a risk factor for barotraumas and should be avoided.

(1) Therefore, tidal volumes suggested by the above rules are only estimates.

(2) May need to be decreased in some patients in order to keep peak airways pressures < 45 cm H2O

Plateau pressures Pressures measured at the end of the inspiratory phase of a volume-cycled tidal volume.  Most modern ventilators are programmed not to allow expiratory airflow for a set time, typically a half of a second.  The pressure measured to maintain this lack of expiratory airflow is the plateau pressure.  It has been suggested that the plateau pressure should be monitored as a means to prevent barotraumas in patients with ARDS.

(1) Barotrauma can be minimized when the plateau pressure is maintained < 30 cm H2O.  

Respiratory rate  The frequency of breaths delivered per minute during mechanical ventilation. 

Minute ventilation (MV)MV = RR × TV  Typical respiratory rates range from 8 to 16 breaths/min but really depend on the desired PCO2

(a) Higher respiratory rate decreases PCO2.    (b) Lower respiratory rate increases PCO2 (2) A situation where a higher-than-normal PCO2 may be desired is in the case of weaning a patient from mechanical ventilation.    (a) The higher PCO2 is required for the patient’s drive to breathe. (3) A situation when one may desire a lower-than-normal PCO2 is in the case of elevated intracranial pressure.    (a) The low PCO2 causes cerebral vasoconstriction and a decrease in cerebral blood flow and a theoretical decrease in intracranial pressure.    (b) If a respiratory rate is too high, the risks include the following: (i) Inadequate expiratory time      (ii) “breath stacking”      (iii) The development of intrinsic PEEP can occur.      (iv) In order to minimize this risk, the I:E ratio can be adjusted to allow more expiratory time and completion of the expiratory phase.    

I:E ratio  Defined as inspiratory time + inspiratory pause time:expiration.   This ratio is usually set to 1:2 or 1:2.5 in an attempt to mimic the usual pattern of spontaneous breathing.  A higher I:E ratio is the equivalent to a longer inspiratory time.

(1) This adjustment may improve oxygenation by increasing the mean airway pressure and allowing redistribution of gas from more compliant alveoli to less compliant alveoli.

(2) However, this also increases the risk of “breath stacking” (leading to intrinsic PEEP), and barotrauma by reducing the expiratory time.

(3) It is important to keep in mind, however, that a higher I:E ratio is generally less well tolerated by the patient and typically necessitates a deeper level of sedation.   

A lower I:E ratio is the equivalent to a longer expiratory time.

(1) This can be particularly useful when obstructive pulmonary disease is present such as asthma or COPD.

(2) It is also useful in settings where high minute ventilation is required, necessitating a higher-than-normal respiratory rate

(a) The risk of breath stacking must be minimized.    

Positive end-expiratory pressure (PEEP) A positive pressure applied at the end of the expiratory cycle.  PEEP is generally effective when used in patients with diffuse lung disease that results in a decrease in FRC.  PEEP works by increasing end-expired lung volume and preventing airspace closure at the end of expiration.  Essentially “splinting” the alveoli open.  Most patients who require mechanical ventilation may benefit from the application of 5 cm H2O of PEEP.  It can limit the amount of atelectasis that frequently accompanies endotracheal intubation and mechanical ventilation in the supine position.  More importantly, PEEP can be utilized to permit lower levels of FiO2, while preserving adequate oxygenation.  This is important in limiting lung injury that may result from prolonged exposure to high inspired oxygen concentrations (FiO2 > 0.6).

The addition of PEEP is typically justified when a FiO2 of 60 mm Hg cannot be achieved with a FiO2 of 0.6.  The addition of PEEP is also justified when the estimated initial shunt fraction is >25%. Therefore, the use of PEEP should have a well-defined indication.

Higher levels of PEEP, in the range of 5 to 15 cm H2O, have been shown to improve oxygenation in more severe alveolar filling disorders such as cardiogenic pulmonary edema in ARDS.  The mechanism behind this is likely redistribution of fluid from the alveoli to the interstitium and opening up collapsed alveoli.  ❗ Cx:  In the hypovolemic patient, PEEP increases intrathoracic pressure and can impede venous return.  This commonly results in hypotension and hemodynamic instability.  PEEP also increases intra-alveolar pressures and thus places patients at increased risk for barotrauma.


The PaO2, an important measure of oxygenation, is influenced mainly by FiO2 and PEEP.  The arterial partial pressure of carbon dioxide (PaCO2), a measure of pulmonary minute ventilation, is affected mainly by the respiratory rate (RR) and tidal volume (TV). 

Immediately following intubation, a high FiO2 (eg, >60%, or 0.6) is usually provided, and ventilator settings can subsequently be adjusted based on the results of the first arterial blood gas analysis.  Cx: Prolonged, high FiO2 can cause oxygen toxicity as it can lead to the formation of proinflammatory oxygen free radicals and predispose to atelectasis as alveolar nitrogen is displaced, resulting in worsened oxygenation.  Although there is no strict cutoff FiO2 value for oxygen toxicity, FiO2 levels <60% are considered generally safe.  

Airway Pressures

Measurement of airway pressures can be useful in mechanically ventilated patients.  The peak airway pressure (the maximum pressure measured as the tidal volume is being delivered) equals the sum of the resistive pressure (flow x resistance) and the plateau pressure.

Peak airway pressure = resistive pressure + plateau pressure

The plateau pressure is the pressure measured during an inspiratory hold maneuver, when pulmonary airflow and thus resistive pressure are both 0.  It represents the sum of the elastic pressure and positive end-expiratory pressure (PEEP).

Plateau pressure = elastic pressure + PEEP

Elastic pressure is the product of the lung's elastance and the volume of gas delivered.  Because elastic recoil is inversely related to lung compliance, the elastic pressure can be calculated as tidal volume/compliance.  Decreased compliance (eg, pulmonary fibrosis) causes stiffer lungs and higher elastic pressure.


Airway Pressure



Centrally from the brain, such as oversedation


Injury to the spinal cord near levels C3, C4, or C5 is associated with the potential loss of diaphragmatic function.

Injury to peripheral nerves can also be associated with ventilatory failure as is the case when phrenic nerve loss occurs following certain surgical procedures.

Additionally, any lower motor neuron disease such as Guillain-Barre, poliomyelitis, or amylotrophic lateral sclerosis can contribute to muscle weakness and impending ventilatory failure.

Autoimmune diseases such as myasthenia gravis can create a state of increasing muscle weakness that can lead to the inability to expire CO2.

Damage to structures of the chest wall such as rib fractures or flail chest may impair adequate ventilation

Morbid obesity, abdominal hypertension, or the presence of restrictive dressing (abdominal binders) can all bring about this effect.

Pleural effusions, pneumothoraces, and hemothoraces

Any patient with evidence of laryngeal edema, bronchospasm, laryngospasm, or the presence of a foreign body is at an increased risk for ventilatory failure.

Any process that thickens the alveolar membrane where gas exchange occurs

Thickened alveolar membranes can be the result of pulmonary fibrosis, where an abnormal and excessive amount of fibrotic tissue is deposited in the pulmonary interstitium.

Thickened alveolar membranes can also be the result of the accumulation of fluid in the area of gas exchange, as in the case of pulmonary edema.

Anatomic deadspace (i) An example would be something as simple as rapid, shallow breathing. (ii) Since the conducting airways typically occupy 150 mL or 1 to 2 mL/kg, when one takes breaths of 150 to 200 mL, these small tidal volumes do not reach the alveoli.

Shunt: Acute respiratory distress syndrome (ARDS)/ALI, airway collapse, pneumonia, or pulmonary contusion.


Delayed Emergence

Return to consciousness after anesthesia (emergence) typically occurs within 15 minutes of extubation; at a minimum, patients should be responsive with intact protective (eg, gag) reflexes within 30-60 minutes of the last administration of an anesthetic or adjuvant agent (eg, opiate, muscle relaxant).  Delayed emergence occurs when a patient fails to regain consciousness within the expected window.  The etiology is typically multifactorial but generally occurs due to 1 of 3 major causes:

  • Drug effect:  Preoperative drug ingestion (eg, opiates, benzodiazepines, illicit drugs, anticholinergic drugs, antihistamines) may potentiate anesthetic effects.  Prolonged anesthesia duration or higher medication doses may also delay emergence.
  • Metabolic disorder:  Common etiologies include hyper- or hypoglycemia, hyper- or hypothermia, hyponatremia, and liver disease.
  • Neurologic disorder:  Intraoperative stroke, seizure (or postictal state), or elevation of intracranial pressure can cause prolonged alterations in mental status.

Management of acute respiratory failure includes ventilatory support (eg, bag and mask, reintubation); reversal agents (eg, naloxone) may also be indicated.


Malignant hyperthermia


  • Genetic mutation alters control of intracellular calcium
  • Triggered by volatile anesthetics, succinylcholine, excessive heat


  • Masseter muscle/generalized rigidity
  • Sinus tachycardia
  • Hypercarbia resistant to increased minute ventilation
  • Rhabdomyolysis
  • Hyperkalemia
  • Hyperthermia (⌛late manifestation)


  • Respiratory/ventilatory support
  • Immediate cessation of causative anesthetic
  • Dantrolene

MH is an autosomal dominant or sporadic skeletal muscle receptor disorder marked by excessive calcium release following exposure to succinylcholine or a volatile anesthetic (eg, halothane).

In MH, sustained muscle contraction leads to:

  • Hypercarbia (due to increased levels of cellular metabolism) that does not improve with increased minute ventilation (tachypnea)
  • sinus tachycardia
  • masseter/generalized muscle rigidity
  • Myoglobinuria, with dark urine (due to muscle breakdown) 🍖
  • hyperthermia (late manifestation due to the sustained contractions generating more energy than the body can dissipate; not usually present initially).

Most cases arise shortly after induction or during maintenance of anesthesia, but symptoms can occur soon after anesthetic cessation.  Urgent treatment with dantrolene (a skeletal muscle relaxant) and supportive care are required to prevent death.


Airway deterioration

Severe hypoxemia (eg, PaO2 <60 mm Hg on room air) 

In patients unable to maintain adequate oxygen saturations, bag-valve-mask ventilation (BVM) with 100% oxygen (to keep oxygen saturation ≥ 88%) should be initiated.  If BVM does not result in adequate oxygenation (ie, oxygen saturation remains low, as in this patient), endotracheal intubation using a video laryngoscope (to facilitate direct visualization of the epiglottis) should be attempted.

However, given the risk of rapid respiratory deterioration, failure of a single attempt at endotracheal intubation with a video laryngoscope (as in this patient) should immediately prompt the establishment of a surgical cricothyrotomy by the most experienced provider available (preferably an otolaryngologist or general surgeon).  Cricothyrotomy establishes an airway below the epiglottal swelling and potential obstruction.


Pheochromocytomas and paraganglionomas

Pheochromocytomas and paraganglionomas are catecholamine-producing tumors arising from chromaffin cells of the adrenal medulla or extra-adrenal paraganglia, respectively.

Hypertension in pheochromocytoma can be intermittent or sustained.  Paroxysms of severe hypertensioncan be precipitated by increases in intra-abdominal pressure (eg, tumor palpation, positional changes), surgical procedures, and a number of medications, particularly anesthetic agents.  In addition, nonselective beta blockers can cause a state of unopposed alpha adrenergic stimulation leading to vasoconstriction and paradoxical hypertension.  For this reason, alpha adrenergic blockers (eg, phenoxybenzamine) should be administered prior to beta blockers in patients with pheochromocytoma.


Noninvasive positive-pressure ventilation

Noninvasive positive-pressure ventilation is the application of positive airway pressure using a mechanical ventilator, without the presence of an endotracheal tube.

(1) Bilevel positive airway pressure (BiPAP) (a) A noninvasive form of positive-pressure ventilation that is used to increase oxygenation by providing high-flow positive airway pressure (b) Cycles between high positive pressure and a lower positive airway pressure depending on its timing in the respiratory cycle (2)

Continuous positive airway pressure (CPAP)    (a) Another form of NPPV that is used for increasing ventilation by providing CPAP