Adverse Effects and Complications of Endotracheal Intubation and Invasive Mechanical Ventilation-Part 1



Immediate Adverse Effects/Complications (Typically Manifest During or Immediately After Intubation)

Arrhythmia/Cardiac Arrest (see Cardiac Arrest)

Clinical

  • Atrial Fibrillation (AF) (see Atrial Fibrillation)
  • Cardiac Arrest (see Cardiac Arrest)
    • In Emergency Endotracheal Intubations Performed in Critically Ill Patients Suffering Deterioration, the Rate of Cardiac Arrest was 1 in 50 and was Associated with Hypoxemia in 83% of Cases (and 63% of the Cases of Hypoxemia were Associated with Inadvertent Esophageal Intubation) (Anesth Analg, 2004) [MEDLINE]
    • In Emergency Department Intubations, Early Post-Intubation Cardiac Arrest Occurred in Approximately 2% of Cases and was Associated with Preintubation Systolic Hypotension (PLoS One, 2014) [MEDLINE]
    • In Intubations of Critically Ill Intensive Care Unit Patients, Post-Intubation Cardiac Arrest Occurred in 1 of 40 Procedures, Had High Immediate and 28-Day Mortality Rates, and was Associated with Defined Risk Factors (Crit Care Med, 2018) [MEDLINE]
      • Absence of Preoxygenation: odds ratio 3.584 (1.287-9.985)
      • Pre-Intubation Hypotension (SBP <90 mm Hg): odds ratio 3.406 (1.797-6.454)
      • Pre-Intubation Hypoxemia: odds ratio 3.991 (2.101-7.583)
      • Age > 75 y/o: odds ratio 2.251 (1.080-4.678)
      • Obesity (BMI>25): odds ratio 2.005 (1.017-3.951)
    • Reverse Shock Index Predicts Post-Intubation Cardiac Arrest (Int J Emerg Med, 2023) [MEDLINE]: n = 127
      • Reverse Shock Index = systolic blood pressure/heart rate
      • In Multivariate Analysis, Age, Reverse Shock Index, Oxygen Saturation, and Total Bilirubin were Significantly Associated with Post-Intubation Cardiac Arrest
      • Patients with Reverse Shock Index <1 had a Significantly Higher Risk of Developing Post-Intubation Cardiac Arrest (Odds Ratio 5.22; 95% CI: 1.83-14.86, p = 0.002)
      • Reverse Shock Index Sensitivity, Specificity, Positive Predictive Value, Negative Predictive Value, and Diagnostic Accuracy for Predicting Post-Intubation Cardiac Arrest were 51.11%, 83.33%, 90.2%, 36.23%, and 59.17%, Respectively
      • ROC Curve for Reverse Shock Index Showed an Area Under the Curve (AUC) of 0.66
  • Pulseless Electrical Activity (PEA) (see Pulseless Electrical Activity)
    • Typically Occurs Due to Initiation of Positive-Pressure Ventilation in a Patient with Shock
    • Pulseless Electrical Activity was the Most Common Rhythm in Post-Intubation Early Cardiac Arrest (Occurred in 78.1% of Cases) (PLoS One, 2014) [MEDLINE]
  • Ventricular Fibrillation (VF) (see Ventricular Fibrillation)
  • Ventricular Tachycardia (VT) (see Ventricular Tachycardia

Atelectasis/Mucous Plugging (see Atelectasis)

Mechanism

  • Large Airway Mucous Plugging, Resulting in Obstructive Atelectasis

Diagnosis

  • Bronchoscopy (see Bronchoscopy): useful to rapidly assess for large airway mucous plugging

Clinical

  • Increased Peak Airway Pressure (PIP) on Mechanical Ventilator (When Using a Volume-Cycled Ventilation Mode) (see Invasive Mechanical Ventilation-General)
  • Unilaterally Absent Breath Sounds on the Obstructed Side

Auto-Positive End-Expiratory Airway Pressure (Auto-PEEP or Intrinsic PEEP) (Am Rev Respir Dis, 1982) [MEDLINE]

Risk Factors for the Development of Auto-PEEP

  • Airway Obstruction with Expiratory Flow Limitation (Due to Asthma, COPD, etc) (Crit Care Med, 2000) [MEDLINE]
    • Expiratory Flow Limitation Impairs Exhalation and Lung Emptying
    • Expiratory Flow Limitation is More Prominent in the Supine Position than in the Semirecumbent Position (Am J Respir Crit Care Med, 1994) [MEDLINE]
  • Expiratory Flow Resistance (Due to Small Endotracheal Tube, Kinked Endotracheal Tube, Ventilator Tubing, Exhalation or PEEP Valve, or Patient-Ventilator Dyssynchrony)
    • Expiratory Resistance Impairs Exhalation and Lung Emptying
  • High Minute Ventilation (VE)
    • High Minute Ventilation (VE) May Due to Any/All of the Following
      • High Set Respiratory Rate (RR) on the Ventilator
      • High Patient-Driven Respiratory Rate (RR) (Due to Fever, Sepsis, Pain, Agitation, Anxiety, etc)
      • High Set Tidal Volume (VT) on the Ventilator
      • High Patient-Driven Tidal Volume (VT) (Due to Fever, Sepsis, Pain, Agitation, Anxiety, etc)
  • High Inspiratory/Expiratory (I/E) Ratio
    • While the “Normal” I/E Ratio for a Normal Spontaneously-Ventilating Patient is 1:2, a “High” I/E Ratio Cannot Be Numerically Defined for All Patients, Since Patients with Significant Airway Resistance (i.e. Airway Obstruction Due to Status Asthmaticus, etc) May Develop Auto-PEEP Even at a Relatively “Normal” I/E Ratio
  • Time-Constant Inequality of Lung Units
    • Some Lung Units (Especially in the Setting of Airway Obstruction) Empty Heterogeneously, Resulting in the Development of Auto-PEEP Even at a Relatively Low Minute Ventilation (VE)
  • Altered Respiratory System Compliance (Due to Expiratory Muscle Activity): impairs exhalation
    • Altered Respiratory System Compliance May Also Interfere with the Accurate Measurement of Auto-PEEP (Am J Respir Crit Care Med, 1995) [MEDLINE]

Physiology

  • Next Ventilator Breath is Triggered Before the Airway Pressure Returns to Baseline (i.e. Zero)
  • Unlike Applied PEEP Which Distributes Evenly, Auto-PEEP Distributes Predominantly to Lung Units with the Highest Airway Resistance and Lowest Compliance (Chest, 1995) [MEDLINE]

Diagnosis

  • Auscultation (or Palpation) of Continued Expiratory Airflow at the Point When the Next Ventilator Breath is Initiated
    • Physical Exam Has a Positive Predictive Value of 95% and a Negative Predictive Value of 58% in Detecting the Presence of Auto-PEEP, Suggesting that it is Useful to Diagnose Auto-PEEP, But Not to Rule Out Auto-PEEP (Am J Respir Crit Care Med, 1999) [MEDLINE]
  • Observation of Pressure Waveform Not Returning to Baseline Between Breaths
  • Expiratory Hold (0.5-1.0 sec) on Ventilator (i.e. Occlusion of Exhalation Port on Ventilator)

Clinical Effects

  • Dynamic Hyperinflation Amplifies the Respiratory Variation of Arterial Pulse Pressure and Contributes to Pulsus Paradoxus in Mechanically Ventilated Patients [MEDLINE]
  • Dyspnea (see Dyspnea)
  • Hypotension (see Hypotension)
    • Due to Decreased Venous Return to the Right Side of the Heart, Resulting in Decreased Cardiac Output (Especially in the Setting of Hypovolemia)
  • Increased Risk of Barotrauma (Mainly Due to Increased Lung Volume): see below
  • Increased Work of Breathing
    • Due to the Fact that the Patient Must Overcome the Residual Positive Airway Pressure to Generate a Negative Pressure Deflection to Trigger the Next Ventilator Breath
    • Due to Ventilation at High Lung/Chest Wall Volumes (Lung and Chest Wall are Less Compliant at High Lung Volumes)
  • Introduction of Errors in the Measurement of the Mean Alveolar Pressure and Static Lung Compliance (Am J Respir Crit Care Med, 1996) [MEDLINE]
  • Introduction of Errors in the Measurement of Pulmonary Capillary Wedge Pressure (PCWP) (see Hemodynamics)
  • Patient-Ventilator Dyssynchrony: see below

Management

  • Treat Airway Obstruction
  • Increase the Inspiratory Flow Rate and/or Decrease the Respiratory Rate (RR) to Decrease the Inspiratory/Expiratory (I/E) Ratio (to 1:3, 1:4, 1:5, etc)
    • This Lengthens the Expiratory Time, Allowing a Longer Duration to Expire the Gas in the Lung
    • In Rare Cases, Transient Removal of the Patient from the Ventilator May Allow Gas Emptying from the Lungs
  • “Permissive Hypercapnia” (Decrease the Respiratory Rate and/or Tidal Volume to Purposely Underventilate the Patient): allowing the pCO2 to increase to as much as 70-100 mm Hg
    • Physiology
      • Permissive Hypercapnia was First Utilized in Status Asthmaticus
      • Permissive Hypercapnia Decreases the Tidal Volume (VT) (Which Will Decrease the Total Volume of Gas Which Must Be Exhaled During Expiration) and the Respiratory Rate (Which Will Allow a Longer Expiratory Time)
    • Contraindications
    • Technique
      • Maintenance of pH >7.2 Can Be Achieved with Either Sodium Bicarbonate (or Tris-Hydroxymethyl Aminomethane, THAM) Administration: however, sodium bicarbonate administration may be ineffective in increasing the pH in this setting
      • Many Patients Require Deep Sedation (and Paralysis, if Necessary) to Maintain a Low Minute Ventilation (VE)
  • Measures to Decrease the Metabolic Rate (Decreasing Carbon Dioxide Production and Therefore, the Ventilatory Demand)
  • Measures to Decrease the Expiratory Flow Resistance
    • Use Larger Diameter Endotracheal Tube
    • Frequent Suctioning
  • Use Synchronized Intermittent Mandatory Ventilation (SIMV) Mode to Decrease Breath Stacking, Instead of Assist Control (AC)
  • Application of Extrinsic PEEP: this may decrease the amount of auto-PEEP
    • Mechanisms
      • Decreases Dynamic Airway Compression
      • Counteracts the Critical Closing Pressure that Causes Small Airway Collapse in Asthma/COPD
    • Technique
      • Add PEEP to the Point Just Below Where the PIP and Plateau Pressures Start to Increase
      • Use Extrinsic PEEP in an Amount <50-80% of the Amount of Auto-PEEP
    • Clinical Efficacy
      • The Efficacy of Applied PEEP in Decreasing Auto-PEEP Depends on the Level of PEEP Used and Whether Flow Limitation is Present
      • Applying PEEP to Lungs Without Flow Limitation Simply Distends Them Further and Can Cause Barotrauma or Hypotension

Bronchospasm (see Bronchospasm)

Epidemiology

  • In Patients with Underlying Reactive Airways Disease, Postoperative Bronchospasm Occurs Commonly with Endotracheal Intubation (Masui, 1995) [MEDLINE]: bronchospasm occurs in 8.9% of patients with reactive airways disease undergoing endotracheal intubation with general anesthesia
  • In Patients with Underlying Reactive Airways Disease, the Incidence of Postoperative Bronchospasm was Higher with Thoracic/Abdominal Surgery (39.5%), as Compared to Other Surgeries (10.4%) (Masui, 1995) [MEDLINE]

Mechanisms

  • Aspiration of Acidic Gastric Contents During Intubation, Resulting in Airway Irritation
  • Underlying Obstructive Lung Disease

Clinical

  • Increased Peak Airway Pressure (PIP) on Ventilator (see Invasive Mechanical Ventilation-General)
    • Increased Peak-Plateau Pressure Difference (≥5 cm H2O): reflecting an increase in airway resistance
  • “Shark Tooth” Pattern on End-Tidal CO2 (see Capnography)

Dental/Lingual/Orolabial/Pharyngeal/Laryngeal Mucosal Injury

Epidemiology

  • Common (Int Anesthesiol Clin, 1989) [MEDLINE]

Mechanisms

  • Trauma Caused by Bite Block, Laryngoscopy Blade, Endotracheal Tube Metal/Plastic Stylet, or Endotracheal Tube

Clinical

  • Oropharyngeal Bleeding

Emesis with Aspiration (see Aspiration Pneumonia)

Epidemiology

  • May Occur When Endotracheal Intubation is Performed in the Presence of Gastric Contents

Physiology

Endotracheal Tube Cuff/Ventilator Circuit Leak

Mechanisms

  • Defective Endotracheal Tube Cuff System
    • Laceration of Endotracheal Tube Cuff (Typically on the Teeth During Intubation)
    • Puncture of Pilot Balloon
    • Puncture of Pilot Balloon Tubing
  • Intact Endotracheal Tube Cuff System
    • Discrepancy Between Endotracheal Tube Size and Tracheal Diameter (Especially in a Patient with Tracheomalacia, etc)
    • Endotracheal Tube Cuff Underinflation
    • High Peak Airway Pressure (PIP): may result in leak around the endotracheal tube cuff
    • Inadvertent Tracheal Placement of Nasogastric/Orogastric Tube (see Nasogastric-Orogastric Tube)
    • Proximal Migration of the Endotracheal Tube
    • Ventilator Circuit Leak

Diagnosis

  • Check Endotracheal Tube and Ventilator Circuit for Disconnections or Leaks
  • Monitor Endotracheal Tube Cuff Pressure with Manometer
  • Bronchoscopy (see Bronchoscopy): useful to rapidly determine the location of the endotracheal tube tip, in cases where endotracheal tube proximal malpositioning is suspected
    • With a Suspected Cuff Leak, if the Endotracheal Tube Tip is in the Appropriate Position, This Makes the Diagnosis of Endotracheal Tube Cuff Rupture More Likely as the Etiology

Clinical

  • Endotracheal Tube Cuff Leak
    • In One Study of Patients with Lost Volume on the Ventilator and Suspected Endotracheal Tube Cuff Rupture, 61% of the Leaks Were Actually Due to Endotracheal Tube Dislodgment and Only 39% Were Due to a Ruptured Cuff (Crit Care Med, 1993) [MEDLINE]
    • Audible Leak from Air Passing Through Around the Cuff of the Endotracheal Tube
    • Decreased Peak Airway Pressure (PIP) on Ventilator
    • Extent and Leak and Patient Tolerance of the Endotracheal Tube Cuff Leak are Variable (Anesth Analg, 2013) [MEDLINE]
    • Inability to Maintain Endotracheal Tube Cuff Pressure
    • “Lost Volume” on the Ventilator (Inspired Tidal Volume > Expired Tidal Volume)
  • Ventilator Circuit Leak
    • Decreased Peak Airway Pressure (PIP) on Ventilator
    • “Lost Volume” on the Ventilator (Inspired Tidal Volume > Expired Tidal Volume)

Treatment

  • Endotracheal Tube Cuff Leak Due to a Ruptured/Damage Endotracheal Tube Cuff
    • Requires Reintubation
  • Endotracheal Tube Cuff Leak Due to Damaged Pilot Ballon Tubing
    • Pilot Ballon Tubing Can Be Repaired by Cutting the Pilot Ballon Line Prior to Site of Leak (If Feasible) and Repaired Using a Commercially-Available Kit
    • Leak in Pilot Ballon Tubing Can Also Be Repaired by Cutting the Pilot Ballon Line Prior to Site of Leak (If Feasible) and Using a Peripheral Intravenous Catheter (BMC Anesthesiol, 2022) [MEDLINE]
      • Time to Repair Leak: 27.8 ± 1.5 s in the endotracheal tube group (and 20.4 ± 1.1 s in the laryngeal mask airway group)
    • Reintubation is Required in Cases Where the Leak Cannot Be Remedied Using One of the Above Methods
  • Ventilator Circuit Leak
    • Replace Ventilator Circuit Tubing

Endotracheal Tube Tip Malpositioning

Epidemiology

  • In One Study of Patients with Lost Volume on the Ventilator and Suspected Endotracheal Tube Cuff Rupture, 61% of the Leaks Were Actually Due to Endotracheal Tube Dislodgment and Only 39% Were Due to a Ruptured Cuff (Crit Care Med, 1993) [MEDLINE]

Mechanisms

  • Inadvertent Placement of the Endotracheal Tip Either Proximally (i.e. Endotracheal Tube Cuff Above the Vocal Cords) or Distally (i.e. Mainstem Bronchial Intubation)

Diagnosis

Clinical

  • Proximal Endotracheal Tube Migration
    • Decreased Peak Airway Pressure (PIP) on Ventilator
    • Hypoxemia (see Hypoxemia)
    • “Lost Volume” on the Ventilator (Inspired Tidal Volume > Expired Tidal Volume) (see Invasive Mechanical Ventilation-General)
    • Requirement for Increasing Volume to Maintain Endotracheal Tube Cuff Pressure: caution should be exercised in cases such as these, as unrecognized excessive inflation of the cuff may occur in the posterior oropharynx in a patient with a proximally-migrated endotracheal tube
  • Distal Endotracheal Tube Placement
    • Hypoxemia (see Hypoxemia)
    • Increased Peak Airway Pressure (PIP) on Ventilator (see Invasive Mechanical Ventilation-General)
    • Unilaterally Absent Breath Sounds (on the Non-Ventilated Side)
    • Pneumothorax (on the Overventilated Side) (see Pneumothorax): use of large tidal volume delivered unilaterally may particularly predispose to the development of pneumothorax on the ventilated side

Inadvertent Esophageal Intubation

Clinical

Inadvertent Right/Left Mainstem Bronchial Intubation

Diagnosis

  • Bronchoscopy (see Bronchoscopy): useful to rapidly identify and treat large airway mucous plugging and identify endotracheal tube tip location
  • Chest X-Ray (CXR)/Chest CT (see Chest X-Ray and Chest Computed Tomography): useful to exclude pneumothorax and diagnose atelectasis
  • Thoracic Ultrasound (see Thoracic Ultrasound): useful to exclude pneumothorax

Clinical

  • Unilaterally Absent Breath Sounds: on the non-ventilated side
  • Hypoxemia (see Hypoxemia)
  • Pneumothorax (see Pneumothorax): use of large tidal volume delivered unilaterally may particularly predispose to the development of pneumothorax on the ventilated side

Kinked Endotracheal Tube

Mechanism

  • Kinking at Endotracheal Tube Securement Device (Hollister, etc): common
  • Kinking in Posterior Oropharynx: less common
  • Kinking at Teeth (i.e. Patient Biting the Endotracheal Tube): most common site of kinking

Diagnosis

  • Bronchoscopy (see Bronchoscopy): useful to rapidly evaluate endotracheal tube patency

Clinical

  • Increased Peak Airway Pressure (PIP) on Ventilator

Prevention

  • Use of a Bite Block to Prevent Kinking of the Endotracheal Tube at the Teeth is Routinely Recommended

Post-Intubation Hemoptysis (see Hemoptysis)

Diagnosis

  • Bronchoscopy (see Bronchoscopy): useful to rapidly evaluate for a potential endotracheal/endobronchial etiology of hemoptysis

Mechanisms (Any of the Following Mechanisms May Have Increased Risk of Demonstrating Hemoptysis in the Setting of Coagulopathy)

  • Preexisting Etiology of Hemoptysis (Diffuse Alveolar Hemorrhage, etc)
  • Bronchial Wall Mucosal Injury Due to Inadvertent Mainstem Intubation
  • Laryngeal Wall Mucosal Injury
  • Oropharyngeal Trauma
  • Tracheal Wall Mucosal Injury

Post-Intubation Hypotension (see Hypotension)

Epidemiology

  • Post-Intubation Hypotension is the Most Common Complication of Intubation
  • Up to 40% of Patients Intubated in the ICU Setting Experience Significant Procedure-Related Hypoxemia or Hypotension (Crit Care, 2015) [MEDLINE]
  • Risk Factors for Post-Intubation Hypotension (Crit Care, 2015) [MEDLINE]
    • Simplified Acute Physiologic Score II (SAPS II): odds ratio 1.02 (p<0.001)
    • Age 60-75 y/o: odds ratio 1.96 (p<0.002 vs <60 y/o)
    • Age >75 y/o: odds ratio 2.81 (p<0.001 vs <60 y/o)
    • Acute Respiratory Failure as the Indication for Intubation: odds ratio 1.51 (p=0.04)
    • First Intubation in the ICU: odds ratio 1.61 (p=0.02)
    • Noninvasive Ventilation Required for Preoxygenation: odds ratio 1.54 (p=0.03)
    • Inspired FIO2 >70% After Intubation: odds ratio 1.91 (p=0.001)

Mechanisms

  • Positive-Pressure Ventilation Increases Intrathoracic and Right Atrial Pressure -> Decreases Venous Return to the Right Side of the Heart -> Decreases Right Ventricular Cardiac Output
    • This Effect is Accentuated by the Concomitant Presence of Auto-PEEP, Extrinsic PEEP, and/or Hypovolemia (Anesthesiology, 1975) [MEDLINE]
    • The Use of Pharmacologic Agents with Vasodilator Properties (Opiates, Benzodiazepines, Propofol, etc) Can Further Exacerbate this Effect
    • This Effect May Be Most Pronounced Immediately After Intubation and Initiation of Mechanical Ventilation in a Patient Who is Hypovolemic and Has Just Received Vasodilating Sedatives (Such as Midazolam, Propofol, etc) or Analgesics (Fentanyl, etc)
  • Positive-Pressure Ventilation Causes Alveolar Inflation with Compression of the Pulmonary Vascular Bed -> Increases Pulmonary Vascular Resistance (PVR) -> Decreases Right Ventricular Output (Crit Care Med, 2010) [MEDLINE]
    • Passive Leg Raise Maneuver Has Been Demonstrated to Increase Central Blood Volume and Mitigate this Effect (Crit Care Med, 2010) [MEDLINE]
  • Positive-Pressure Ventilation Causes Alveolar Inflation with Compression of the Pulmonary Vascular Bed -> Increases Pulmonary Vascular Resistance (PVR) -> Shifts the Intraventricular Septum Toward the Left (with Impaired Diastolic Left Ventricular Filling) -> Decreases Left Ventricular Cardiac Output
  • Peri-Intubation Pneumothorax (see Pneumothorax): may occur due to large tidal volume during bag-valve-mask ventilation
  • Use of Vasodilating Medications During Intubation

Interaction Between Airway Pressures and Thoracic Structures

  • Hemodynamic Effects of Positive-Pressure Mechanical Ventilation are Due to Transmission of the Airway Pressure to the Adjacent Thoracic Structures
    • Transmission is Greatest When There is Low Chest Wall Compliance (Due to Fibrothorax, etc) or High Chest Wall Compliance (Due to COPD, etc)
    • Transmission is Least When There is High Chest Wall Compliance (Due to Sternotomy, etc) or Low Lung Compliance (Due to ARDS, Pulmonary Edema, etc)

Clinical

  • Hypotension (see Hypotension)
    • Pulseless Electrical Activity (PEA) Arrest May Occur in Severe Cases
  • Sinus Tachycardia (see Sinus Tachycardia)

Prevention

  • Prophylactic Intravenous Fluid/Vasopressors Prior to and/or During Endotracheal Intubation
    • Especially Indicated in Patients with Marginal Pre-Intubation Blood Pressure and/or Known Hypovolemia
    • PREPARE II Randomized Trial of Intravenous Fluid Bolus Prior to Endotracheal Intubation (JAMA, 2022) [MEDLINE]: n = 1,067 (in 11 intensive care units in the United States)
      • In Critically Ill Adults Undergoing Endotracheal Intubation, Administration of an Intravenous Fluid Bolus (as Compared to No Fluid Bolus) Did Not Significantly Decrease the Incidence of Cardiovascular Collapse or 28-Day Mortality Rate
  • Use of Ketamine (see Ketamine)
    • In an Analysis of Data from the Prospective, Multicenter, Observational Japanese Emergency Airway Network (JEAN-2) Study (from Feb, 2012-Nov 2017), Ketamine Manifested Less Post-Intubation Hypotension in Hemodynamically-Unstable Patients in the Emergency Department, as Compared to Midazolam or Propofol (Sci Rep, 2019) [MEDLINE]

Post-Intubation Hypoxemia (see Hypoxemia)

Epidemiology

  • Up to 40% of Patients Intubated in the ICU Setting Experience Significant Procedure-Related Hypoxemia or Hypotension (Crit Care, 2015) [MEDLINE]

Mechanisms

  • Aspiration of Oropharyngeal/Gastric Contents During Intubation
  • Atelectasis/Mucous Plugging (see Atelectasis: unilaterally absent breath sounds
  • Inadvertent Esophageal Intubation: bilaterally absent breath sounds
  • Inadvertent Right (or Left) Mainstem Intubation: unilaterally absent breath sounds
  • Pneumothorax (see Pneumothorax)
  • Transiently Altered V/Q Matching Due to the Introduction of Positive-Pressure Ventilation

Diagnosis

Treatment

  • Once Life-Threatening Etiologies are Promptly Excluded, Oxygenation Can Be Carefully Monitored for Improvement Over Time

Sinus Tachycardia (see Sinus Tachycardia)

  • Mechanisms
    • Paralysis with Inadequate Sedation: this may especially occur when a short-acting sedative (such as etomidate, etc) is utilized in conjunction with a long-acting paralytic (such as rocuronium, etc)
    • Positive-Pressure Ventilation in Hypovolemic Patient, Resulting in Decreased Venous Return to Right Side of the Heart with Decreased Cardiac Output
    • Sympathetic Nervous System Response Due to Glottic Stimulation: see below

Sympathetic Nervous System Response

Mechanisms

  • Glottic Stimulation from Laryngoscopy Blade/Endotracheal Tube (Typically in the Setting of Inadequate Sedation): since the glottis is highly innervated
  • Paralysis with Inadequate Sedation: may occur following rapid sequence intubation with a short-acting sedative (such as etomidate, etc) and a long-acting paralytic (such as rocuronium, etc)

Clinical

  • Arrhythmias
  • Hypertension (see Hypertension)
  • Myocardial Ischemia
  • Sinus Tachycardia (see Sinus Tachycardia)
    • Note that Sinus Tachycardia May Alternatively Represent a Normal Physiologic Response to Hypovolemia Induced by Positive-Pressure Ventilation (and Decreased Venous Return to the Right Side of the Heart): it is critical to rule out hypovolemia as the etiology in this case

Prevention of Sympathetic Nervous Response Due to Glottic Stimulation

  • Sympatholytic Agent

Prevention of Hypertensive/Tachycardic Response Due to Paralysis with Inadequate Sedation

  • Ensure Adequate Sedation at All Times During Administration of Paralytic Agents

Tracheobronchial Mucosal Injury

Mechanisms

  • Tracheal Wall Mucosal Injury
  • Bronchial Wall Mucosal Injury Due to Inadvertent Mainstem Intubation

Diagnosis

  • Bronchoscopy (see Bronchoscopy)
    • Bronchoscopy is Recommended to Rapidly Determine the Site of Post-Intubation Hemoptysis (Larynx vs Tracheal Mucosal vs Endobronchial Mucosal vs Diffuse Alveolar Hemorrhage): this is especially useful in patients with pre-existing diffuse alveolar hemorrhage who only manifest hemoptysis after intubation

Clinical

  • Post-Intubation Hemoptysis (see Hemoptysis)
    • Hemoptysis May Be Significant in Patients with Coagulopathy

Vagal Response

Epidemiology

  • Laryngoscopy-Related Vagal Response is More Common in Young Patients

Mechanisms

  • Due to Laryngoscopic Stimulation

Clinical

Ventilator-Induced Lung Injury (VILI)/Barotrauma

Definitions

  • Ventilator-Induced Lung Injury (VILI): lung injury due to volume-related overstretching (“volutrauma”), high frequency of stretching, and/or high velocity/acceleration of stretching
    • VILI Likely Develops Regionally in the Lung When Low Resistance/High Compliance Lung Units Receive a Disproportionately Large Regional Tidal Volume in the Setting of High Alveolar Distending Pressures
    • Pathologically, VILI Appears as Diffuse Alveolar Damage
    • VILI is Associated with Cytokine Release and Bacterial Translocation
    • Barotrauma: clinically apparent type of alveolar injury which presents as extra-alveolar air in various locations (mediastinum, pleural space, etc)

Epidemiology

  • Mechanical Ventilation Itself Increases the Risk of Barotrauma
    • Development of Auto-PEEP During Mechanical Ventilation Further Increases the Risk of Barotrauma
    • Noninvasive Positive-Pressure Ventilation Probably Has a Similar Mechanism of Barotrauma as Invasive Mechanical Ventilation, But the Rate of Barotrauma is Lower (Due to Use of Lower Pressures) (Rev Bras Ter Intensiva, 2008) [MEDLINE]
  • Incidence of Barotrauma in ARDS is Approximately 10% (NEJM, 2000) [MEDLINE] (Intensive Care Med, 2002) [MEDLINE] (NEJM, 2004) [MEDLINE]

Physiology

  • Ventilator Factors Which May Cause Alveolar Overdistention, Resulting in Alveolar Rupture
    • Positive-Pressure Ventilation Itself
      • All Patients on Mechanical Ventilation are at Risk for Barotrauma, Since Positive-Pressure Ventilation Increases the Transalveolar Pressure (Alveolar Pressure – Adjacent Interstitial Space Pressure)
    • High Tidal Volume
      • Inappropriately High Tidal Volume Set During Bag-Valve-Mask Ventilation
      • Inappropriately High Tidal Volume Set on Ventilator (During Volume-Cycled Ventilation)
      • Inadvertent Right (or Left) Mainstem Intubation with Inappropriately High Tidal Volume Applied to a Single Lung
    • High Plateau Pressure (Pplat)
      • Plateau Pressure is the Pressure Applied to the Small Airways and Alveoli
      • While There is No Safe Plateau Pressure Under Which Barotrauma Does Not Occur, the Greatest Risk of Barotrauma Occurs with Plateau Pressure ≥35 cm H2O or Static Compliance <30 mL/cm H2O (Intensive Care Med, 2002) [MEDLINE]
    • High Peak Inspiratory Pressure (PIP)
      • There is No Absolute Safe Threshold for PIP Under Which Barotrauma Does Not Occur
      • PIP is Probably Less Associated with the Risk of Barotrauma than the Plateau Pressure, Although Some Data are Conflicting (Crit Care Med, 1983) [MEDLINE] (Chest, 1994) [MEDLINE] (Am J Respir Crit Care Med, 2002) [MEDLINE]
    • High Positive End-Expiratory Pressure (PEEP)
      • High PEEP Probably Only Contributes to an Increased Risk of Barotrauma When Open Lung Ventilation (High PEEP or Recruitment Maneuvers, Usually with Lung Protective Measure Such as Low Tidal Volume with Plateau Pressure ≤30 cm H2O) Strategies are Ineffective in Recruiting Atelectatic Lung Units in ARDS or When Lung Protective Ventilation (Low Tidal Volume with Plateau Pressure ≤30 cm H2O) is Not Utilized
    • Mode of Ventilation (Volume-Cycled vs Pressure-Cycled) Does Not Appear to Be Associated with the Risk of Barotrauma (PLoS One, 2011) [MEDLINE] (Cochrane Database Syst Rev, 2015) [MEDLINE]
  • Disease Factors Which May Cause Alveolar Overdistention, Resulting in Alveolar Rupture
    • Acute Respiratory Distress Syndrome (ARDS): due to decreased lung compliance, resulting in increased alveolar pressure (Am J Respir Crit Care Med, 1995) [MEDLINE] (Intensive Care Med, 2004) [MEDLINE]
    • Asthma (see Asthma): due to dynamic hyperinflation, resulting in increased alveolar pressure (Intensive Care Med, 2004) [MEDLINE]
    • Chronic Obstructive Pulmonary Disease (COPD) (see Chronic Obstructive Pulmonary Disease): due to dynamic hyperinflation, resulting in increased alveolar pressure
    • Interstitial Lung Disease (ILD) (see Interstitial Lung Disease): due to decreased lung compliance, resulting in increased alveolar pressure (Intensive Care Med, 2004) [MEDLINE]
    • Langerhans Cell Histiocytosis (see Langerhans Cell Histiocytosis): due to cystic lung disease, resulting in escape of air
    • Necrotizing Pneumonia (see Necrotizing Pneumonia and Pulmonary Gangrene): due to cavitating lung disease, resulting in escape of air
    • Pneumocystis Jirovecii Pneumonia (see Pneumocystis Jirovecii): due to cavitating lung disease, resulting in escape of air
  • Other Factors Which May Cause Alveolar Overdistention, Resulting in Alveolar Rupture
    • Bronchoscopy During Mechanical Ventilation: may result in prolonged increase in plateau pressure
    • High Tidal Volume During Bag-Valve-Mask Ventilation: may result in prolonged increase in plateau pressure
    • High Tidal Volume Ventilation in Pneumonectomy Patient: may result in prolonged increase in plateau pressure
    • Right Mainstem Bronchial Intubation: may result in prolonged increase in plateau pressure
    • Severe Central Airway Obstruction: may result in prolonged increase in plateau pressure

Anatomic Path of Air Dissection

  • Air from Torn Alveolus Enters the Perivascular Interstitium, Dissecting Along the Bronchovascular Sheath into the Pulmonary Hila and Subsequently Into the Mediastinum, Causing Pneumomediastinum (in the Setting of Blunt Trauma to the Lung, This Tracking of Air Has Been Termed the “Macklin Effect”) (see Pneumomediastinum) (Chest, 2001) [MEDLINE]
  • From Pneumomediastinum, Air Can Dissect Upward into the Soft Tissues of the Neck (Causing Subcutaneous Emphysema), into the Pleural Spaces (Causing Pneumothorax on Either Side), Inferiorly into the Peritoneum (Causing Pneumoperitoneum), or Rarely, into the Pericardium (Causing Pneumopericardium)

Diagnosis

  • Bronchoscopy (see Bronchoscopy): useful to rapidly identify and treat large airway mucous plugging and identify endotracheal tube tip location
  • Chest X-Ray (CXR)/Chest CT (see Chest X-Ray and Chest Computed Tomography): useful to exclude pneumothorax and diagnose atelectasis
  • Thoracic Ultrasound (see Thoracic Ultrasound): useful to exclude pneumothorax

Clinical Harbingers of Possible Barotrauma

  • Bleb (intrapleural Air Collection) (see Bullae): this represents a form of interstitial emphysema
  • Deepening of the Sulcus (Deep Sulcus Sign)
  • Hyperlucency Over the Upper Abdominal Quadrants
  • Linear Air Streaking Toward the Hilum
  • Perivascular Air Halos
  • Pneumatoceles (see Cystic-Cavitary Lung Lesions)

Clinical Manifestations

  • Pneumothorax with/without Bronchopleural Fistula (see Pneumothorax and Bronchopleural Fistula)
  • Pneumomediastinum (see Pneumomediastinum)
  • Pneumopericardium (see Pneumopericardium)
    • Epidemiology
      • Rare Manifestation of Barotrauma
  • Pneumoperitoneum (see Pneumoperitoneum)
    • Epidemiology
      • Uncommon Manifestation of Barotrauma
  • Pulmonary Interstitial Emphysema
    • Epidemiology
      • Rare Manifestation of Barotrauma: (occurs particularly with usual interstitial pneumonia from idiopathic pulmonary fibrosis) (Am J Surg Pathol, 2014) [MEDLINE]
    • Physiology
      • Air Dissects Through the Alveolar Walls into Adjacent Lung Interstitium, Causing an Inflammatory Reaction
      • Can Progress to Pneumothorax, Air Cysts within the Lung Parenchyma, and Air Embolism
  • Subcutaneous Emphysema (see Subcutaneous Emphysema)
    • Epidemiology
      • Common Manifestation of Barotrauma
  • Subpleural Air Cyst
    • Epidemiology
      • Uncommon Manifestation of Barotrauma
  • Tension Lung Cyst
    • Epidemiology
      • Uncommon Manifestation of Barotrauma
  • Venous Air Embolism (see Air Embolism) (Am Rev Respir Dis, 1993) [MEDLINE]
    • Epidemiology
      • Uncommon Manifestation of Barotrauma

Prevention

  • General Comments
    • While Both Barotrauma and Volutrauma Likely Contribute to Alveolar Injury, Limiting Alveolar Pressure Appears to Be the Most Effective Measure to Prevent Barotrauma
  • Avoid Dynamic Hyperinflation (in Asthma and COPD): hyperinflation is progressive (dynamic) since air accumulates in the lung with each breath as a result of a failure to achieve complete exhalation before the onset of the next breath
    • Treatment of Bronchospasm (see Obstructive Lung Disease): usually with bronchodilators, corticosteroids, etc
    • Use Low Tidal Volume Ventilation: reduces amount of air in each breath which needs to be exhaled
    • Use Short Inspiratory Time/Longer Expiratory Time: allows adequate time for expiration
    • Use Lower Respiratory Rate (Even Using Permissive Hypercapnia in Some Cases)
  • Maintain Low Plateau Pressure (Pplat ≤30 cm H2O): being cautious to avoid Pplat >35 cm H2O
    • Targeting Even Lower Plateau Pressures May Further Reduce the Risk of Barotrauma (Am J Respir Crit Care Med, 1999) [MEDLINE]
  • Maintain Low Tidal Volume Ventilation (6 mL/kg Predicted Body Weight) (N Engl J Med, 2000) [MEDLINE]
  • Neuromuscular Blockade
    • In in Systematic Review and Meta-Analysis, Use of Neuromuscular Blockade is Associated with a Decreased Risk of Barotrauma (Crit Care, 2013) [MEDLINE]
  • Use Appropriate Amounts of PEEP
    • PEEP is Standardly Titrated Per the FIO2/PEEP Table as was Used in the 2000 Study on Low Tidal Volume Ventilation (N Engl J Med, 2000) [MEDLINE]
  • Use Low Respiratory Rate: even using permissive hypercapnia in some cases

Management-General

  • Since the Occurrence of Any Barotrauma in the Setting of Mechanical Ventilation for ARDS Suggests Either a Patient with More Severe ARDS (at Higher Mortality Risk) or a Suboptimal Ventilation Strategy (or Both), the First Priority Should Be Measures to Optimize the Ventilation Management
    • Use Lung Protective/Low Tidal Volume Ventilation (Ideally to 6 mL/kg PBW) and Adjust the Respiratory Rate to the Minimum Required to Maintain an Adequate pH (i.e. Permissive Hypercapnia)
      • Use Sedation and Pharmacologic Paralysis as Necessary to Maintain Ventilator Parameters
    • Avoid Patient-Ventilator Dyssynchrony and Overbreathing
      • Use Sedation and Pharmacologic Paralysis as Necessary to Maintain Synchrony
    • Decrease Both the Auto-PEEP and Extrinsic PEEP (As Allowed by Oxygenation)
      • Target a Low I/E Ratio (Around 0.33) to Maintain a Low Mean Airway Pressure
      • Shorten Inspiratory Time with Higher Inspiratory Flow Rate (Around 70-100 L/min)
      • Lengthen Expiratory Time
      • Avoid Inverse Ratio Ventilation
      • Use a Low Compressible Volume (Non-Disposable) Ventilator Circuit
    • Treat Bronchospasm
    • Treat Underlying Etiology of Respiratory Failure to Minimize the Total Duration of Mechanical Ventilation

Management-Pneumothorax (see Pneumothorax)

  • Chest Tube (see Chest Tube)
    • Chest Tube is Generally Required for Mechanical Ventilation-Associated Pneumothorax, Since >30% of These Progress to Tension Pneumothorax

Management-Chest Tube with Air Leak (i.e. Bronchopleural/Alveolopleural Fistula) (see Bronchopleural Fistula): ventilator changes should aim to decrease the plateau pressure (to Pplat ≤30 cm H2O)

  • Optimization of Ventilation Management: as above
  • Continue Chest Tube Drainage (see Chest Tube: while this may seem obvious, prematurely removing a chest tube in a patient with an air leak from a bronchopleural fistula can result in the rapid development of tension pneumothorax (which can be potentially fatal)
  • Use the Least Amount of Chest Tube Suction Which Maintains Lung Inflation and Decreases the Amount of Air Leak
  • Optimize Body Position and Patient’s Sedation/Pharmacologic Paralysis to Minimize the Air Leak
  • Other Less Established Techniques

Management-Pneumomediastinum (see Pneumomediastinum)

  • Optimization of Ventilation Management: as above
  • Rare Cases of Tension Pneumomediastinum May Require Mediastinotomy For Decompression

Management-Pneumopericardium (see Pneumopericardium)

  • Optimization of Ventilation Management: as above
  • Rare Cases with Tamponade May Require Pericardiocentesis with Drain Placement for Decompression

Management-Pneumoperitoneum (see Pneumoperitoneum)

  • Optimization of Ventilation Management: as above
  • Barotrauma-Associated Pneumoperitoneum is Usually Self-Limited and Doesn’t Require Specific Intervention (Other than Ventilator Adjustments, Such as a Decrease in Plateau Pressure, etc)
  • Rare Cases of Pneumoperitoneum-Associated Abdominal Compartment Syndrome May Require Lapartotomy/Laparoscopy for Surgical Decompression (to Both Relieve the Compartment Syndrome and to Exclude a Perforated Viscus)

Management-Pulmonary Interstitial Emphysema

  • Optimization of Ventilation Management: as above
  • Treat Underlying Etiology

Management-Subcutaneous Emphysema (see Subcutaneous Emphysema)

  • Optimization of Ventilation Management: as above
  • Manage Underlying Pneumothorax (If Present) (see Pneumothorax): as above
  • Blowhole Incision (see Blowhole Incision)

Management-Venous Air Embolism (see Air Embolism)

  • Optimization of Ventilation Management: as above
  • Standard Management

Prognosis

  • In Mixed Populations, Mechanical Ventilation-Associated Barotrauma is Associated with an Increased Mortality Rate (Chest, 1986) [MEDLINE]
  • ARDS-Associated Barotrauma is Associated with an Increased Mortality Rate: likely related to the fact that the barotrauma is a marker for patients with worse ARDS (Crit Care Med, 1995) [MEDLINE] (JAMA, 1994) [MEDLINE]


References

Acalculous Cholecystitis (see Acalculous Cholecystitis)

Acute Kidney Injury (AKI) (see Acute Kidney Injury)

Arrhythmia/Cardiac Arrest (see Cardiac Arrest)

Arytenoid Cartilage Dislocation

Aspiration Pneumonia (see Aspiration Pneumonia)

Auto-Positive End-Expiratory Pressure (Auto-PEEP or Intrinsic PEEP) (see Invasive Mechanical Ventilation-General)

Bronchospasm (see Bronchospasm)

Constipation (see Constipation)

Decubitus Ulcer (see Decubitus Ulcer)

Deep Venous Thrombosis (DVT) (see Deep Venous Thrombosis)

Dental/Lingual/Orolabial/Pharyngeal/Laryngeal Mucosal Injury

Diarrhea (see Diarrhea)

Endotracheal Tube Cuff/Ventilator Circuit Leak

Endotracheal Tube Tip Malpositioning

Erosive Esophagitis (see Esophagitis)

Esophageal Injury

Gastrointestinal Stress Ulceration (see Peptic Ulcer Disease)

Ileus (and Gastrointestinal Hypomotility) (see Ileus)

Gastrointestinal Ulceration (see Peptic Ulcer Disease)

Impaired Mucociliary Motility

Increased Intracranial Pressure (see Increased Intracranial Pressure)

Induction of Inflammatory Response

Insulin Resistance

Intensive Care Unit (ICU)-Acquired Weakness (see Intensive Care Unit-Acquired Weakness)

Joint Contracture

Laryngeal Injury

Laryngotracheal Stenosis (see Tracheal Stenosis)

Laryngotracheomalacia (see Tracheobronchomalacia)

Neurologic Complications

Oxygen Toxicity (see Oxygen)

Patient-Ventilator Dyssynchrony

Pharyngitis (see Pharyngitis)

Positive Pressure-Induced Artifacts Introduced into the Measurement of Hemodynamic Pressures

Post-Intubation Hypoxemia (see Hypoxemia)

Post-Intubation Hypotension (see Hypotension)

Sleep Disruption

Swallowing/Speech Impairment (see Dysphagia)

Tracheoarterial Fistula (see Tracheoinnominate Artery Fistula)

Tracheoesophageal Fistula (see Tracheoesophageal Fistula)

Translocation of Tracheal Bacteria into the Bloodstream

Ventilator-Induced Diaphragmatic Dysfunction (VIDD)

Ventilator-Induced Lung Injury (VILI)/Barotrauma

Vocal Cord Granuloma

Vocal Cord Paralysis

Vocal Cord Ulceration