Positive end-expiratory pressure (PEEP) is ordered for a mechanically ventilated patient. The nurse understands that PEEP serves which purpose?

Choice A rationale

While PEEP can eventually lead to improved lung compliance, its primary and immediate mechanical purpose is not the reduction of the work of breathing. In fact, excessively high levels of PEEP can sometimes increase the work of breathing by causing overdistention of the alveoli, making it harder for the patient to initiate a breath or move air effectively. Its therapeutic focus remains on gas exchange rather than the muscular effort of ventilation.

Choice B rationale

This choice is scientifically incorrect because PEEP is specifically designed to increase the functional residual capacity, which is the volume of air remaining in the lungs at the end of a normal expiration. By maintaining positive pressure, PEEP prevents the total collapse of the lungs during the expiratory phase. Decreasing this capacity would lead to widespread atelectasis and a significant decline in the surface area available for gas exchange at the alveolar-capillary membrane.

Choice C rationale

Tidal volume is the amount of air moved in or out of the lungs during a single respiratory cycle and is typically determined by the ventilator settings or the patient's effort. While PEEP improves the environment for air delivery, it is not used as a primary mechanism to increase the specific volume of a single breath. Instead, it maintains a baseline pressure that keeps the respiratory architecture open for the duration of the cycle.

Choice D rationale

The fundamental purpose of PEEP is to improve oxygenation by keeping alveoli open at the end of expiration, a process known as recruitment. This prevents atelectasis and increases the surface area for gas exchange. By maintaining open alveoli, it reduces intrapulmonary shunting, where blood flows past unventilated lung tissue. This mechanism allows for a lower fraction of inspired oxygen to be used while maintaining adequate arterial oxygen tension and systemic delivery.

Choice A rationale

Systemic vascular resistance (SVR) specifically measures the resistance the left ventricle must overcome to eject blood into the systemic circulation. It does not directly cause an increase in pulmonary vascular resistance (PVR), which is the resistance in the lung's blood vessels. While severe left sided heart failure can eventually lead to pulmonary backup, an increase in SVR itself is a systemic afterload issue. Respiratory rate changes are usually secondary to compensatory mechanisms or distress rather than a direct hemodynamic effect.

Choice B rationale

An increase in systemic vascular resistance usually results in an increase in arterial blood pressure, as pressure is the product of flow and resistance. If resistance increases and the heart maintains its output, the pressure will rise. Mean arterial pressure (MAP) typically increases with higher SVR unless the heart's pumping ability fails significantly. Therefore, decreasing blood pressure is generally the opposite of what is expected when SVR increases, provided the cardiac compensatory mechanisms are still functioning effectively.

Choice C rationale

Increasing systemic vascular resistance represents increased afterload. According to the Frank Starling law and basic hemodynamics, as afterload increases, it becomes harder for the heart to pump blood out, which typically leads to a decrease in stroke volume and subsequently a decrease in cardiac output. It would be highly unusual for cardiac output to increase in response to higher resistance unless there was a massive increase in contractility or heart rate to compensate for the added pressure work.

Choice D rationale

Increased systemic vascular resistance raises the afterload on the left ventricle, forcing the myocardium to work harder to eject blood. This increased workload directly leads to higher myocardial oxygen demands. Simultaneously, the higher resistance often leads to a reduction in stroke volume and cardiac output because the ventricle cannot empty as efficiently against the high pressure. Normal SVR ranges from 800 to 1200 dynes/sec/cm-5. High SVR can lead to heart strain and decreased systemic perfusion.