Complications Associated With Invasive Mechanical Ventilation

Although frequently life saving, invasive mechanical ventilation is also associated with numerous complications, some of which can be life threatening in themselves (Table 11 [24k PDF*]). The expression ‘associated with’ is important conceptually, as many adverse effects that occur while a patient is being mechanically ventilated cannot be shown conclusively to arise directly from the ventilator or its operation. Nosocomial pneumonia in the ventilated patient, for example, is more likely a consequence of critical illness and the breakdown of normal host defenses than of the ventilator per se. Since they are related temporally and clinically to intubation and mechanical ventilation, however, it is logical to consider all such complications together here.

Physiologic effects of positive-pressure ventilation

Initiating positive-pressure mechanical ventilation in any patient alters pulmonary mechanics and respiratory function. Several of these changes are more ‘effects’ than ‘complications’ in that they are direct, predictable results of changes in lung volume and intrathoracic pressure. In several instances, although these effects have been well known for years, the precise mechanisms remain uncertain.

Impaired cardiac function

The effects of positive-pressure ventilation on cardiac function are more common with the application of PEEP, but may also occur when mechanical ventilation is used without PEEP, especially in volume-depleted patients and those who have pre-existing cardiac disease.

Several mechanisms for decreased cardiac function have been postulated, and which is most important remains unclear. However, most investigators agree that two mechanisms predominate:

• reduced right ventricular preload as a result of raised mean intrathoracic pressure (which is an absolute effect of positive pressure ventilation); and
• increased right ventricular afterload because of increased lung volume (which need not occur if gas trapping does not occur and if tidal residual volumes are physiologic).

Compared with spontaneous breathing, positive-pressure ventilation increases both peak and mean intrathoracic pressure, and thus increases the pressure gradient that must be overcome by venous blood as it returns to the right atrium. Mean intrathoracic pressure is further increased by application of PEEP, and in the presence of relative hypovolemia, even small amounts of PEEP can compromise cardiac function. Patients who have pre-existing right ventricular dysfunction are at increased risk for cardiac impairment on addition of PEEP. Some investigators have suggested that the reduction in venous returns may be the result of an increase in inferior vena caval resistance because of the increase in lung volume rather than the decrease in driving pressure grouping venous return.

Marked increases in lung volume cause an increase in pulmonary vascular resistance. This increases right ventricular afterload, which may compromise the forward output of that chamber. The increase in right ventricular volume associated with raised pulmonary vascular resistance may in turn impair left ventricular function, since both ventricles share the interventricular septum, pericardial sac, and certain circumferential muscle fibers.

Positive-pressure ventilation does not always impair cardiac function, and in certain circumstances it may even improve it. Although the work of spontaneous breathing normally accounts for a small proportion of overall oxygen consumption, this may increase drastically during acute respiratory failure. When cardiac function is severely impaired, as in cardiogenic shock, the heart may not be able to meet the demands imposed by this excessive work of breathing. In addition, the increase in juxtacardiac pressure that occurs as a result of the increase in intrathoracic pressure induced by positive pressure causes a functional reduction in left ventricular afterload.

Increased intracranial pressure

Positive pressure ventilation can increase jugular venous pressure, which in turn can impede venous return from the brain and raise increased intracranial pressure (ICP).

Normally, over a wide range of CPP (i.e. mean arterial pressure minus ICP), cerebral blood flow is kept constant through autoregulation, and changes in ICP or cardiac output have little effect. When ICP is elevated, however, as after head injury, autoregulation is lost, the relationship of cerebral blood flow to CPP becomes linear, and either an increase in ICP or a drop in cardiac output can reduce cerebral blood flow. Fortunately, conditions such as ARDS that require high levels of PEEP to support oxygenation also markedly reduce lung compliance, so that less pressure is transmitted to the jugular venous system.

Gastric distention

Gastric and intestinal distention with air may occur when manual ventilation with bag-and-mask raises mouth pressure above lower esophageal sphincter pressure. During mechanical ventilation via a cuffed endotracheal tube, it is also not uncommon for patients who have low respiratory system compliance to develop gastric distention, presumably because tracheal pressure exceeds both cuff pressure and lower esophageal sphincter pressure in the presence of a closed or occluded mouth. Distention can be massive (‘meteorism’), and gastric rupture has been reported. Placement of a small-bore nasogastric tube usually prevents or alleviates this problem.

Respiratory alkalosis

Respiratory alkalosis is among the most common adverse occurrences during mechanical ventilation. Severe alkalemia may precipitate cardiac arrhythmias or seizures. Unintentional respiratory alkalosis (pH >7.55 units) developed in 11% of ventilated patients in one series, and was associated with an increased overall mortality rate. Dyspnea, agitation, and pain are the most common causes in patients who do not suffer severe central nervous system dysfunction or chronic liver disease, and appropriate ventilator adjustment, combined with sedation as required, controls the alkalosis in most instances.

Renal and hepatic effects

Fluid retention and edema are common in patients who receive mechanical ventilation. Reductions in renal blood flow and impairment in renal function, especially with the use of PEEP, have been documented by a number of investigators, who postulate mechanisms that include elevation of serum antidiuretic hormone, excessive aldosterone effect, and (more recently) reduced levels of atrial natriuretic peptides.

Liver dysfunction is also fairly common in ventilated patients, which has led some investigators to conclude that positive-pressure ventilation causes hepatic impairment. A fall in portal blood flow has been documented with PEEP therapy, but the clinical importance of this is unclear. As with a number of the other adverse effects discussed here, it may be difficult to separate the effects of mechanical ventilation on renal and hepatic function from manifestations of the patient’s underlying disease process.

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