Extrapulmonary Effects of Mechanical Ventilation

Extrapulmonary effects of mechanical ventilation refer to the effects which take place outside the lungs in other body systems during mechanical ventilation. Some of these effects should properly be considered “complications” of ventilation, while others are simply things which we need to be aware of as we care for our patients and make recommendations for therapy. 

The effect of positive pressure invasive mechanical ventilation on the cardiovascular system is well known. Nature did not intend for human beings to breathe with positive pressure, we are supposed to breathe with gentle negative pressure. So the positive pressures that we utilize to invasively ventilate our patients can interfere with the venous return to the heart and thereby impacts the patient’s blood pressure and blood flow to other organs. We must always be cautious of this effect.

However, mechanical ventilation can sometimes be beneficial to other body systems in specific situations. For example, when the patient has a closed head injury, our ventilator can be utilized to intentionally hyperventilate the patient, dropping arterial carbon dioxide levels, and thereby reducing blood flow to the brain. This helps to manage intracranial pressure (ICP) and minimizes brain injury. Many other body systems are impacted by mechanical ventilation. Some Key Examples of complications are listed below:

Cardiovascular Effects

The heart and great blood vessels are subject to the increased intrathoracic pressures which take place during mechanical ventilation. The result of increased intrathoracic pressures decreases cardiac output, resulting in decreased venous return to the heart. This effect is more noticeable in patients who are hypovolemic, or those with cardiac dysfunction, such as congestive heart failure. Therefore, careful continuous monitoring of patient blood pressure is very important during mechanical ventilation. This is especially true when the patient is receiving high levels of Positive-End Expiratory Pressure (PEEP).

It is important to monitor respiratory variation in the arterial pressure waveforms obtained with the insertion of an arterial line. Most patients in the ICU/CCU will have an arterial line in place, and you can actually observe changes in the arterial waveform as the ventilator cycles. Marked dampening of the waveform during the ventilator cycle is an important indication that the ventilator is interfering with cardiac function. If the patient does not have an arterial line in place, observing the pulse oximeter waveform also has value.


The Thoracic Pump Mechanism

It has been known for several decades that positive pressure ventilation (PPV) can reduce cardiac output. This phenomenon can be understood in part by comparing intrapleural pressure changes that occur during normal spontaneous or negative pressure breathing with those occurring during mechanical ventilation.

During spontaneous breathing, the fall in intrapleural pressure that draws air into the lungs during inspiration also draws blood into the major thoracic vessels and heart. This helps the heart to function more efficiently. With this increased return of blood to the right side of the heart and the stretching and enlargement of the right-sided heart volume, the right ventricular preload increases, resulting in an increased right ventricular stroke volume. You may have heard this described as the Frank-Starling mechanism.

During a spontaneous expiration, intrapleural pressure rises causing a reduction in venous return and right ventricular preload, which in turn leads to a decrease in right ventricular stroke volume. Note that these pressure changes affect left-sided heart volumes in a similar fashion.

The negative intrapleural pressures that occur during spontaneous inspiration are transmitted to the intrathoracic vessels. A drop in pressure in the vena cava increases the pressure gradient back to the heart and venous return increases.

The effects on intrathoracic pressures and venous return are quite different when positive pressure is applied to the airway by our mechanical ventilators. During inspiration, increases in airway pressure are transmitted to the intrapleural space and to the great vessels and other structures in the thorax. As the airway pressure rises, the intrapleural pressure rises, and intrathoracic blood vessels become compressed, causing the central venous pressure (CVP) to increase. This increase in CVP reduces the pressure gradient between systemic veins and the right side of the heart, which reduces venous return to the right side of the heart and thus right ventricular filling (preload). As a result, the right ventricular stroke volume decreases.

Vascular pressures within the thorax generally increase in proportion to increases in mean airway pressure and intrapleural pressure (i.e., the higher the pressure, the greater the effects). This phenomenon is particularly evident when one considers the effect of adding positive end-expiratory pressure (PEEP) during PPV. Because PEEP further increases during PPV, it is reasonable to assume that reductions in venous return and cardiac output are greater during PPV with PEEP than with PPV alone. Furthermore, PEEP with assist-control ventilation decreases cardiac output more than when PEEP is used with synchronized intermittent mandatory ventilation (SIMV) or continuous positive airway pressure (CPAP) alone.

Vascular Resistance

During inspiration with high tidal volumes (VT) or when high levels of PEEP are used, the pulmonary capillaries that interlace the alveoli are stretched and narrowed. As a result, resistance to blood flow through the pulmonary circulation increases. This increases right ventricular (RV) afterload. In normal healthy individuals, RV stroke volume is maintained in the face of increased PVR because the RV contractile function is not severely impaired. However, in patients with compromised RV function, the RV cannot overcome these increases in PVR, and overdistension of the RV occurs, resulting in a decrease in RV output.

The LV output may also be decreased when high VTs are used during PPV because the heart is compressed between the expanding lungs (i.e., cardiac tamponade effect). The distensibility of the left side of the heart appears to be directly related to the transmission of positive pressures to the heart from the lung. This effect increases when long inspiratory times and high peak pressures are used.

Coronary Blood Flow

In addition to reduced venous return and alteration in ventricular function, lower cardiac output may be caused by myocardial dysfunction associated with reduced perfusion of the myocardium and the resultant myocardial ischemia. The flow of blood into the coronary vessels depends on the coronary perfusion pressure. The coronary artery perfusion pressure gradient for LV is the difference between mean aortic diastolic pressure and left ventricular end-diastolic pressure (LVEDP); the perfusion pressure gradient for the RV is the difference between mean aortic pressure and pulmonary artery systolic pressure.

Reductions in coronary vessel perfusion can result from any factor that decreases this perfusion pressure gradient. Thus, reductions in cardiac output or blood pressure, coronary vasospasms, or a direct effect of compression of the coronary vessels caused by increases in intrathoracic pressure during PPV can decrease coronary perfusion and ultimately lead to myocardial ischemia. The level of reduction in cardiac output that occurs with PPV depends on several factors, including lung and chest wall compliance, airway resistance (Raw), and the duration and magnitude of the positive pressure.

Intracranial Effects

Mechanical ventilating neurologically injured patients is significantly challenging. Positive pressure ventilation often elevates intracranial pressure. Normal ICP pressures are < 10 mmHg. We must balance the need to maintain brain oxygenation with the need to keep intracranial pressures low. Keeping PEEP levels and tidal volumes low in such patients can be helpful.

Hepatic Effects

Decreased cardiac output, and increase hepatic vascular resistance caused by positive pressure ventilation, adversely affects liver function. It has been shown that bile duct pressure is sometimes elevated during mechanical ventilation, making it harder for the liver and gallbladder function properly.

Renal Effects

The key impact of positive pressure ventilation on the kidneys is an overall decline in renal function with decreased urine volume and sodium excretion. That can result in edema and other resultant adverse effects for the patient.

Gastrointestinal Effects

The mucus membrane layer of the stomach is often damaged during positive pressure mechanical ventilation. Ischemia and secondary bleeding are common in ventilator patients, resultant from the combination of decreased cardiac output and increased gastric venous pressure.

Lung Protective Strategy

This week you will also learn about strategies to prevent harm to the lungs during mechanical ventilation. Taking an example, when the patient has acute lung injury, we implement a “lung-protective strategy” which includes smaller tidal volumes, higher respiratory rates if necessary, and the use of PEEP to keep the alveoli inflated longer in each cycle with resulting improvement in oxygenation. Today we often use smaller tidal volumes, higher respiratory rates, more PEEP, and lower inspired oxygen percentages. All of these steps are taken to protect the patient’s lungs and/or help them recover from the trauma of mechanical ventilation.


For this assignment, you will be addressing key aspects of mechanical ventilation that every Respiratory Therapists needs to understand. 

In your own words, select any three non-pulmonary body systems which are impacted by positive pressure mechanical ventilation, and for each body, system discuss (1) what effect does mechanical ventilation have on that body system, 2) why this effect is occurring, and (3) what steps can be taken to minimize these effects of mechanical ventilation on that body system.


Requirements (Read these carefully)Submit your responses, in your own words, as an essay form, complete sentences, in at least 500 words on a Word document (excluding the prompt, title, cover page, citations/references, quotations). Grammar and spelling count. You must include at least two references (the course text being one of your references) to defend and support your position. Quotes are not included in the word count.