Consider PEEP
Andrea Y. Tan MD
Ibtesam A. Hilmi MB, CHB, FRCA
Positive end-expiratory pressure (PEEP) is defined as an elevation of alveolar pressure at the conclusion of passive expiration that exceeds atmospheric pressure. PEEP is categorized as applied/extrinsic PEEP or auto/intrinsic PEEP. Extrinsic PEEP is delivered directly through a mechanical ventilator or through a tight-fitting face mask at the end of exhalation. PEEP maintains the patient’s airway pressure above atmospheric level by exerting pressure to oppose passive emptying of the lung. Intrinsic PEEP occurs when the lungs fail to deflate fully prior to the next breath, which maintains the alveolar pressure above the atmospheric pressure. If otherwise unspecified, PEEP usually refers to extrinsic PEEP. Both extrinsic PEEP and intrinsic PEEP are covered in this chapter.
EXTRINSIC PEEP
Why Use PEEP?
PEEP is used to completely or partially replace the function of the respiratory muscles and therefore correct hypoxemia secondary to alveolar hypoventilation. PEEP is effective in improving arterial oxygenation simply through increasing functional residual capacity (FRC), reducing venous admixture, shifting tidal volume, preventing loss of pulmonary compliance, and decreasing the work of breathing.
Effects of PEEP
Respiratory System.
Extrinsic PEEP improves oxygenation by directly affecting alveolar gas exchange and pulmonary mechanics of the respiratory system. Overall, alveolar gas exchange improves through redistribution of fluid within the alveoli. As a result, there is a decrease in intrapulmonary shunting and an improvement in arterial oxygenation. With the addition of PEEP, arterial oxygenation goals may be achieved with a lower fraction of inspired oxygen (FIO2) and therefore a decreased risk of oxygen toxicity. In terms of lung mechanics, FRC increases and lung compliance improves. PEEP is also responsible for prevention of alveolar collapse, which is of critical importance because the repetitive collapse of lung units at the end of expiration may lead to ventilator-induced lung injury (VILI).
Cardiovascular System.
From the cardiovascular standpoint, the addition of PEEP causes a significant increase in intrathoracic pressure. As a result, there is a decrease in venous return and decrease in right and left ventricular
preload. This leads to a decline in cardiac output. Biondi et al. showed that at low levels of PEEP the predominant effect is right ventricular (RV) preload reduction. Above 15 cm H2O PEEP, RV volumes increase and RV ejection fraction (EF) decreases, consistent with increased RV afterload and declines in RV contractility, presumably as a result of increased RV wall stress.
preload. This leads to a decline in cardiac output. Biondi et al. showed that at low levels of PEEP the predominant effect is right ventricular (RV) preload reduction. Above 15 cm H2O PEEP, RV volumes increase and RV ejection fraction (EF) decreases, consistent with increased RV afterload and declines in RV contractility, presumably as a result of increased RV wall stress.
Several possible factors can lead to decrease in cardiac output during application of PEEP. In addition to changes in loading conditions, the leftward septal displacement, systolic and diastolic ventricular interdependence and altered cardiac geometry can all affect cardiac output during the application of PEEP. In any case, the decline in cardiac output may progress toward hypotension and subsequent hypoperfusion of critical organs.
The adverse effects of PEEP on the cardiovascular systems cannot be overlooked. One study has revealed that PEEP may cause tricuspid regurgitation. The combination of increased pulmonary artery pressures, increased vascular resistance, and altered RV geometry may all affect tricuspid valve function. This is critical because the presence of undiagnosed tricuspid regurgitation during mechanical ventilation may invalidate cardiac output values as well as the derived parameters that are determined through thermodilution.
Liver.
Effects of PEEP on the hepatic system are also noticeable. The drop in cardiac output causes a decrease in splanchnic blood flow and subsequent decrease in hepatic and portal blood flow. However, an increased in hepatic outflow resistance as a result of impaired venous drainage can lead to the observed liver congestion and hinder the hepatic perfusion. The use of PEEP causes a downward shift of the diaphragm, which further compresses the liver and worsens the hepatic perfusion.
Renal.
PEEP causes a decrease in urinary output, sodium excretion, and creatinine clearance. The mechanisms responsible for the decreased urine output are most likely multifactorial, including a decrease in cardiac output, renal blood flow, intravascular volume, and reflex sympathetic nerve activation. There is also an altered release of various hormones including catecholamines, renin-angiotensin-aldosterone, antidiuretic hormone, and atrial natriuretic factor, which contributes to the effects of PEEP on renal function. The patient’s volume status and the amount of applied PEEP both contribute to alterations in renal function.
Central Nervous System.
The effects of PEEP on cerebral mechanics are numerous. As PEEP is added, there is a notable rise in right atrial pressure. This further translates to an increase in superior vena cava pressure and a decrease in cerebral venous return, resulting in an increase in intracranial pressure (ICP). Other influencing variables include intracranial compliance and body positioning. When the head is elevated above the chest, the transmitted intrathoracic pressure to the intracranial venous sinuses is decreased.
As a result, ICP is minimally affected. In patients with normal ICP, the effect of PEEP can be easily overcome by maintaining normal intravascular volume and systemic blood pressure.
As a result, ICP is minimally affected. In patients with normal ICP, the effect of PEEP can be easily overcome by maintaining normal intravascular volume and systemic blood pressure.
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