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Clinical and physiologic complications of mechanical ventilation: Overview

Clinical and physiologic complications of mechanical ventilation: Overview
Author:
Robert C Hyzy, MD
Section Editor:
Polly E Parsons, MD
Deputy Editor:
Geraldine Finlay, MD
Literature review current through: Jan 2024.
This topic last updated: Oct 30, 2023.

INTRODUCTION — Positive pressure mechanical ventilation is a lifesaving therapy. The ventilator forces air into the central airways, and the resulting pressure gradient causes air to flow into the small airways and alveoli. Mechanical ventilation is directly associated with several complications that need to be recognized by clinicians who manage critically ill patients.

The complications of positive pressure ventilation are discussed in this topic review. Key steps in initiating mechanical ventilation are provided separately. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit".)

PULMONARY EFFECTS — Common pulmonary complications of mechanical ventilation include barotrauma, lung injury, and pneumonia. Others include endotracheal tube complications, respiratory muscle weakness, and secretion retention.

Barotrauma — Pulmonary barotrauma is a well-known complication of positive pressure ventilation. Consequences include pneumothorax, subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum. Pulmonary barotrauma during mechanical ventilation is discussed in detail separately. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Ventilator-associated lung injury — Ventilator-associated lung injury (VALI) refers to lung injury that occurs due to mechanical ventilation. It is clinically indistinguishable from lung injury or acute respiratory distress syndrome due to other causes. VALI is discussed separately. (See "Ventilator-induced lung injury".)

Aspiration and ventilator-associated pneumonia and microbial colonization — Patients who are mechanically ventilated are at high risk for the development of aspiration and ventilator-associated pneumonia (VAP). Further details regarding prevention, diagnosis, and management of aspiration and VAP are provided separately. (See "Aspiration pneumonia in adults" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults" and "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

Mechanically ventilated patients act as reservoirs for hospital-acquired pathogens, including Staphlococcus, Pseudomonas, and Aspergillus species. Acinetobacter and Candida appear to be emerging pathogens in this population [1]. An observational cross-sectional surveillance study of 51 acute and long-term care facilities in the state of Maryland reported a 31 percent prevalence for Acinetobacter baumannii (among which almost one-half were carbapenem-resistant) and a 7 percent prevalence for Candida auris (among which one-third were newly identified). Prevalence rates were higher among patients in long-term care facilities than those in acute care hospitals. This study supports prevention programs targeted at mechanically ventilated patients, particularly those in long-term care facilities.

Endotracheal tube complications — In addition to complications of endotracheal tube (ETT) insertion, the ETT is also associated with acute and chronic complications during the course of mechanical ventilation, the diagnosis and management of which are provided separately. (See "Direct laryngoscopy and endotracheal intubation in adults" and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients".)

Respiratory muscle weakness — Respiratory muscle weakness is common in patients who are mechanically ventilated, even if only ventilated for a short time [2]

Respiratory muscle weakness may be due to the following:

Diaphragm weakness – Mechanical ventilation can cause diffuse diaphragmatic muscle atrophy (typically both leaflets), a phenomenon called ventilator-induced diaphragmatic dysfunction (VIDD). VIDD does not appear to correlate with peripheral neuromuscular weakness [3].

Diaphragmatic weakness may develop as early as the first day of mechanical ventilation. The longer the duration of mechanical ventilation, the higher the likelihood of significant VIDD [4,5]. Patients receiving a greater percentage of controlled ventilation (>25 percent) during the first 48 hours of assist-control mechanical ventilation also exhibit a greater degree of diaphragmatic atrophy [6].

Weakness of other respiratory muscles – Atrophy of respiratory muscles other than the diaphragm (table 1) can also develop in patients undergoing positive pressure ventilation. It can occur independent of and does not correlate with diaphragmatic weakness [3].

Respiratory muscle weakness is more likely to be encountered in those who have undergone prolonged mechanical ventilation and usually presents as difficulty weaning from mechanical ventilation. It may be associated with prolonged intensive care unit stay and a higher risk of complications (eg, pneumonia, need for tracheostomy) [7].

The optimal approach to potentially prevent respiratory muscle weakness (including VIDD) is unknown [2].

The mechanism of respiratory muscle weakness is probably similar to that of general peripheral neuromuscular weakness in critically ill patients and includes disuse atrophy, oxidative stress, high metabolic demand, lipid accumulation, and proteolysis [2].

Content describing the evaluation and management of neuromuscular weakness in the spontaneously breathing patient as well as evaluation and management of bilateral and unilateral diaphragm weakness and critical illness-associated peripheral neuromuscular weakness are provided separately. (See "Diagnostic evaluation of adults with bilateral diaphragm paralysis", section on 'Patients who are intubated' and "Diagnosis and management of nontraumatic unilateral diaphragmatic paralysis (complete or partial) in adults", section on 'Sniff test' and "Management of the difficult-to-wean adult patient in the intensive care unit", section on 'Investigational strategies (inspiratory respiratory muscle training)' and "Neuromuscular weakness related to critical illness".)

Reduced mucociliary motility — Positive pressure ventilation appears to impair mucociliary motility in the airways. In a series of 32 patients, bronchial mucus transport velocity was frequently impaired and associated with retention of secretions and pneumonia [8].

The administration of mucolytics is poorly studied and in general, is not routine. One randomized trial of 922 patients receiving mechanical ventilation reported that routine, compared with as needed, nebulization of the mucolytic acetylcysteine together with salbutamol did not reduce the number of ventilator days, length of stay, or mortality but did result in more tachyarrhythmias and agitation [9]. Whether the tachyarrhythmias were beta-2 agonist-related is unclear.

NONPULMONARY CLINICAL EFFECTS — Mechanical ventilation has an impact on several organ systems throughout the body. This includes the cardiovascular, gastrointestinal, and renal system as well as the peripheral and central nervous system. Some of these effects are directly related to changes in intrathoracic pressure from mechanical ventilation itself while in others it is hard to distinguish effects due to mechanical ventilation from effects due to the underlying disease.

Cardiovascular — The hemodynamic effects of mechanical ventilation are the result of positive airway pressure being transmitted to the surrounding structures of the thorax. The extent to which this occurs varies according to chest wall and lung compliance. Transmission of airway pressure is greatest when there is low chest wall compliance (eg, fibrothorax) or high lung compliance (eg, emphysema); it is least when there is high chest wall compliance (eg, sternotomy) or low lung compliance (eg, acute respiratory distress syndrome, heart failure).

Hypotension — Hypotension is common in mechanically ventilated patients. In a series of over 2900 patients, within one hour of intubation, 43 percent developed cardiovascular instability defined as systolic pressure <65 mmHg at least once, <90 mmHg for >30 minutes, new or increased need of vasopressors or fluid bolus >15 mL/kg [10].

Positive pressure ventilation frequently decreases cardiac output, which may cause hypotension. There are several mechanisms that contribute to the fall in cardiac output:

Decreased venous return – Intrathoracic and right atrial pressure increase during positive pressure ventilation, thereby reducing the gradient for venous return. This effect is accentuated by positive end-expiratory pressure (PEEP) or intravascular hypovolemia [11].

Reduced right ventricular output – Alveolar inflation during positive pressure ventilation compresses the pulmonary vascular bed. This increases pulmonary vascular resistance, thereby reducing right ventricular output [12]. This effect is mitigated by increasing the central venous blood volume.

Reduced left ventricular output – Increased pulmonary vascular resistance can shift the interventricular septum to the left, impair diastolic filling of the left ventricle, and reduce left ventricular output. An exception can occur in patients with left ventricular failure, however, where increased intrathoracic pressure from positive pressure ventilation may improve left ventricular performance by decreasing both venous return and left ventricular afterload [13].

Falsely elevated hemodynamic measurements — Positive pressure mechanical ventilation may falsely elevate hemodynamic measurements, particularly when PEEP is applied or auto-PEEP in present.

The effect of positive pressure ventilation on falsely elevating the pulmonary arterial occlusion pressure (PAOP) (figure 1) and central venous pressure (CVP) are well established [14]. The "true" PAOP can be estimated by subtracting one-half of the PEEP level from the PAOP or CVP if the lung compliance is normal or one-quarter of the PEEP level if lung compliance is reduced [15]. As an example, for a patient with normal lung compliance who is receiving a PEEP of 12 cm H2O and whose PAOP is measured as 18 mmHg, the true PAOP is estimated to be 12 mmHg. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)

Venous thromboembolism — Mechanically ventilated patients are at high risk of venous thromboembolism (VTE). The degree of risk and prevention of VTE in this population are discussed separately. (See "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults", section on 'Intensive care unit patients' and "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults", section on 'High-risk patients'.)

Gastrointestinal

Stress ulceration — Positive pressure ventilation for greater than 48 hours is a risk factor for clinically important gastrointestinal bleeding due to stress ulceration. Details regarding prevention, diagnosis, and management of stress ulcers are provided separately. (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention".)

Hypomotility — Positive pressure ventilation may also be associated with gut hypomotility, although the mechanism is unclear and may relate to the underlying illness or medications. Hypomotility usually manifests as intolerance to enteral feeding and places the patient at risk of aspiration. Enteral feeding is discussed separately. (See "Nutrition support in intubated critically ill adult patients: Enteral nutrition".)

Correction of electrolytic abnormalities and avoidance of drugs that adversely affect gastric motility (eg, opiates) can reduce the risk of gastrointestinal hypomotility. While methylnaltrexone has been used intermittently for opioid-induced hypomotility, its routine addition to regular laxatives appears to be of no value [16].

In mechanically ventilated patients with enteral feeding intolerance, erythromycin, with or without metoclopramide, may be useful in deceasing gastric residual volume, but the rate of successful feeding may be no different to placebo [17]. Management of enteral feeding is discussed in detail separately. (See "Nutrition support in intubated critically ill adult patients: Enteral nutrition", section on 'Monitoring and management of complications'.)

Other gastrointestinal effects — Other gastrointestinal complications seen in patients receiving positive pressure ventilation include the following, although it is uncertain whether these complications are due to mechanical ventilation or the critical illness [18,19]:

Erosive esophagitis (See "Pathophysiology of reflux esophagitis".)

Diarrhea (See "Nutrition support in intubated critically ill adult patients: Enteral nutrition", section on 'Diarrhea'.)

Acalculous cholecystitis (See "Acalculous cholecystitis: Clinical manifestations, diagnosis, and management".)

Positive airway pressure (especially PEEP) is also associated with decreased splanchnic perfusion, the clinical impact of which is uncertain [20]. The mechanism underlying this association is unknown but may be related to decreased cardiac output [21]. Decreased splanchnic perfusion may manifest as elevated plasma aminotransferase and lactate dehydrogenase levels [22].

Acute kidney injury — Mechanical ventilation is associated with the development of acute kidney injury (AKI). In one study, approximately 5 to 6 percent of ventilated individuals developed AKI requiring renal replacement therapy [23]. In a prospective cohort study of 29,269 critically ill patients, positive pressure ventilation was an independent risk factor for acute renal failure (odds ratio 2.11, 95% CI 1.58-2.82) [23].

AKI during invasive mechanical ventilation is associated with increased intensive care unit (ICU) mortality, increased ventilator days, increased length of ICU stay, prolonged mechanical ventilation, and impaired weaning [23-25].

The mechanism for renal injury during positive pressure ventilation is unknown, but it is likely multifactorial. Hypotheses include renal injury through the release of inflammatory mediators (eg, interleukin-6) and impaired renal blood flow due to decreased cardiac output, increased sympathetic tone, or activation of humoral pathways [26].

The evaluation and management of AKI are discussed separately (See "Evaluation of acute kidney injury among hospitalized adult patients" and "Overview of the management of acute kidney injury (AKI) in adults".)

Neurologic

Peripheral neuromuscular weakness — Peripheral neuromuscular weakness of critical illness is common among patients who undergo mechanical ventilation. The pathogenesis is multifactorial (eg, immobilization, prolonged use of sedatives, use of neuromuscular blocking agents, and critical illness). The causes, diagnosis, prevention, and management of neuromyopathy of critical illness are discussed in detail elsewhere. (See "Neuromuscular weakness related to critical illness".)

Increased intracranial pressure — Positive pressure ventilation increases intracranial pressure (ICP). This is probably the result of elevated intrathoracic pressure impairing cerebral venous outflow. Factors associated with increased ICP include lower respiratory system compliance, lower mean arterial pressure and lung recruitment, and increased arterial carbon dioxide tension [27]. Management of ICP in patients with traumatic brain injury is discussed separately. (See "Management of acute moderate and severe traumatic brain injury", section on 'Intracranial pressure management'.)

Disordered sleep — Disordered and disrupted sleep is common among patients in the ICU [28-30]. For example, in a prospective cohort of 20 patients who were mechanically ventilated for lung injury, none experienced normal sleep according to 24-hour polysomnography [28]. However, studying sleep quality in the ventilated patient is challenging. Conventional sleep staging is not possible in up to one-third of awake, nonsedated mechanically ventilated patients without delirium. Such patients lack typical sleep stage-2 markers and are felt to have previously uncharacterized states of "atypical sleep" or "pathologic wakefulness" with sleep fragmentation and the absence of rapid eye movement [30,31].

Sleep disorder in critically ill patients is thought to be multifactorial and due to acute illness itself, noisy environment, the disruptive daily routine care, loss of circadian rhythm, and medications including sedatives. Environmental factors may be the least important, with one study reporting that patient care activities and noise accounted for less than 30 percent of arousals and awakenings [32]. The mode of mechanical ventilation may also influence sleep quality, particularly pressure support ventilation [33,34]. The impact of newer modes, such as proportional assist ventilation and neurally adjusted ventilation, on sleep is unknown.

The clinical impact of sleep disturbance is unclear but may contribute to delirium while in the ICU [35]. Sleep disturbance persists even after discharge in up to 67 percent of patients but generally resolves slowly with time [36]. Another study reported that patients over the age of 65 years in the ICU who slept more during the day than at night had greater cognitive impairment during recovery [37]. (See "Post-intensive care syndrome (PICS) in adults: Clinical features and diagnostic evaluation", section on 'Cognitive impairment'.)

How best to improve sleep quality in the ICU is unknown since measuring sleep and classifying sleep disordered breathing in ICU patients is difficult. In addition, it is unknown whether reducing sedatives, maintaining normal circadian rhythms, and limiting external stimulants, which are commonly performed, have any impact of sleep quality. Experts also endorse the use of assist-controlled ventilation rather than pressure support ventilation during the night in critically ill patients, although the impact of this strategy is unclear [38,39].

Miscellaneous neurologic effects — Delirium and memory or cognitive impairment that occur during mechanical ventilation are likely multifactorial and partly related to the underlying lung disease or possibly hippocampal apoptosis [40]. (See "Diagnosis of delirium and confusional states" and "Delirium and acute confusional states: Prevention, treatment, and prognosis" and "Delayed emergence and emergence delirium in adults" and "Post-intensive care syndrome (PICS) in adults: Clinical features and diagnostic evaluation", section on 'Clinical features'.)

Other — Positive pressure ventilation appears to induce inflammation. In a randomized trial of 44 patients, those who received positive pressure ventilation using large tidal volumes and low PEEP had higher concentrations of inflammatory mediators in their blood and bronchoalveolar lavage fluid than patients who received smaller tidal volumes and high PEEP [41].

Positive pressure ventilation may also promote translocation of tracheal bacteria into the bloodstream, according to one animal study [42]. Translocation was most pronounced during ventilation with large tidal volumes and low PEEP.

Prolonged bedrest has also been associated with insulin resistance [43] and joint contractures [44]. During mechanical ventilation, the head of the bed is frequently raised to prevent aspiration, which may increase the risk of sacral pressure ulcers by increasing the pressure on the skin in the sacral region [45].

PHYSIOLOGIC EFFECTS

Auto-PEEP — Auto-positive end-expiratory pressure (auto-PEEP, also called intrinsic PEEP) exists when there is positive airway pressure at the end of expiration due to incomplete exhalation [46]. In other words, inspiration is initiated before expiratory airflow from the preceding breath is complete. This process is also commonly referred to as dynamic hyperinflation (DHI) and can reduce venous return to the heart and consequently cause hypotension. The causes, impact, and management of auto-PEEP are discussed separately. (See "Positive end-expiratory pressure (PEEP)".)

Heterogenous ventilation — The distribution of positive pressure ventilation is never uniform because the amount of ventilation is a function of three factors that vary from region to region within the lungs:

Alveolar compliance

Airway resistance

Dependency (upper versus lower lung zones)

Compliant, nondependent regions with minimal airway resistance are best ventilated. In contrast, stiff, dependent regions with increased airway resistance and diminished respiratory compliance (lung, chest wall, and abdomen) are poorly ventilated. The heterogeneity of ventilation is accentuated in patients who have both airways disease and parenchymal lung disease.

Heterogenous ventilation may have limited to negligible clinical effect but, when severe, may result in hypoxemia as well as DHI in more compliant, overventilated areas and atelectasis in less compliant, underventilated areas, thereby contributing to barotrauma and atelectasis, respectively.

Heterogenous ventilation in patients with acute respiratory distress syndrome is managed using low tidal volume ventilation and moderate to high levels of PEEP. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Low tidal volume ventilation: Initial settings'.)

Heterogenous ventilation from airways disease requires interventions related to causes including suctioning of secretions, bronchodilator therapy, and adjustment of ventilator settings, such as decreased respiratory rate and tidal volume or increased inspiratory flow rate. (See "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Dynamic hyperinflation'.)

Ventilation/perfusion mismatch — Mechanical ventilation can alter two opposing forms of ventilation/perfusion (V/Q) mismatch. By increasing ventilation (V) more uniformly, the institution of positive pressure ventilation can worsen dead space (in areas that are poorly perfused) but improve shunt (in areas where perfusion is well preserved), resulting in extreme forms of V/Q mismatch (figure 2). (See "Measures of oxygenation and mechanisms of hypoxemia", section on 'Ventilation-perfusion mismatch'.)

Increased dead space – Dead space reflects areas that are overventilated relative to perfusion (V>Q; high V/Q). Positive pressure ventilation increases alveolar dead space by increasing ventilation in alveoli that do not have a corresponding increase in perfusion, thereby worsening V/Q mismatch. Dead space should be suspected in those with concomitant worsening hypercapnia and evidence of auto-PEEP or DHI when minute ventilation is unchanged. (See "Measures of oxygenation and mechanisms of hypoxemia", section on 'Ventilation-perfusion mismatch'.)

Reduced shunt (ie, improved shunt) – Shunt reflects areas that are underventilated relative to perfusion (V<Q; low V/Q). Patients with respiratory failure frequently have increased intraparenchymal shunting due to areas of focal atelectasis that continue to be perfused (ie, regions that are underventilated relative to perfusion). Treating atelectasis with positive pressure ventilation, especially PEEP, can reduce intraparenchymal shunting by improving alveolar ventilation, thereby improving V/Q matching and oxygenation. (See "Measures of oxygenation and mechanisms of hypoxemia", section on 'Ventilation-perfusion mismatch' and "Positive end-expiratory pressure (PEEP)".)

EQUIPMENT MALFUNCTION — Occasionally, respiratory distress and disruption of gas exchange can occur in mechanically ventilated patients when the ventilator or circuit malfunctions. Evaluation and management of the ventilated patient in respiratory distress and contribution of equipment malfunction are discussed separately. (See "Assessment of respiratory distress in the mechanically ventilated patient" and "The ventilator circuit", section on 'Troubleshooting problems with the circuit'.)

SUMMARY

Pulmonary complications – While positive pressure mechanical ventilation can be lifesaving, it can potentially be associated with several complications. Common pulmonary complications include the following:

Barotrauma – (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Lung injury – (See "Ventilator-induced lung injury".)

Pneumonia – (See "Aspiration pneumonia in adults" and "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults" and "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

Endotracheal tube complications – (See "Direct laryngoscopy and endotracheal intubation in adults" and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients".)

Respiratory muscle weakness (diaphragmatic and other respiratory muscles) (table 1) – (See 'Respiratory muscle weakness' above.)

Secretion retention – (See 'Reduced mucociliary motility' above.)

Nonpulmonary complications – Positive pressure ventilation may reduce cardiac output, causing hypotension, and may falsely elevate instrumentally measured hemodynamic parameters (eg, pulmonary arterial occlusion and central venous pressures (figure 1)). (See 'Cardiovascular' above.)

In addition, it is associated with the following:

Gastrointestinal stress ulceration, gut hypomotility, and decreased splanchnic perfusion – (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention".)

Acute kidney injury – (See 'Nonpulmonary clinical effects' above and "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention" and "Evaluation of acute kidney injury among hospitalized adult patients".)

Peripheral neuromuscular weakness – (See "Neuromuscular weakness related to critical illness".)

Increased intracranial pressure, disordered sleep, memory and cognitive impairment, inflammation, and impaired immunity – (See 'Increased intracranial pressure' above and 'Miscellaneous neurologic effects' above and 'Disordered sleep' above.)

Physiologic effects – Physiologic effects of positive pressure mechanical ventilation include intrinsic positive end-expiratory pressure, heterogenous ventilation, and altered ventilator/perfusion mismatch (increased dead space, decreased shunt (figure 2)). (See 'Physiologic effects' above.)

Equipment malfunction – Occasionally, respiratory distress and disruption of gas exchange can occur in mechanically ventilated patients when the ventilator or circuit malfunctions. (See "Assessment of respiratory distress in the mechanically ventilated patient" and "The ventilator circuit", section on 'Troubleshooting problems with the circuit'.)

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References

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