The effects of ventilation

Spontaneous ventilation can be assisted or replaced by delivering an intermittent positive pressure to the lungs. This is what happens when an unconscious patient is ventilated by hand with a bag and mask. In the past "iron lungs" were used to apply an intermittent negative pressure to the thorax, but manual intermittent positive pressure ventilation (IPPV) was introduced during a large polio epidemic in Copenhagen in 1952. Mortality rates were much more favourable than those following previously used techniques. This heralded the introduction of intensive care units.

During IPPV there is reversal of the thoracic pump - the normal negative intrathoracic pressure during spontaneous inspiration, which draws blood into the chest from the vena cavae, a significant aspect of venous return. With IPPV, venous return decreases during inspiration and, if a positive pressure is added during expiration as well (positive end-expiratory pressure or PEEP), venous return will be impeded throughout the respiratory cycle. This can cause hypotension. The degree of impairment of venous return is directly proportional to the mean intrathoracic pressure. So changes in ventilatory pattern, not just pressures, can cause cardiovascular changes.

At high lung volumes the heart may be directly compressed by lung expansion. This prevents adequate filling of the cardiac chambers. Ventricular contractility is also affected. Elevated intrathoracic pressures directly reduce the left and right ventricular ejection pressure which is the difference between the pressure inside and outside the ventricular wall during systole. As a result, stroke volume is reduced for a given end-diastolic volume. This is usually detrimental, but in failing hearts IPPV can improve cardiac output by reducing filling pressures and returning the heart to a more favourable portion on the Frank-Starling curve.

IPPV indirectly produces an overall decline in renal function with a reduced urine volume and sodium excretion. Hepatic function can also be adversely affected by the decrease in cardiac output, with increased vascular resistance and elevated bile duct pressure. The gastric mucosa does not have an autoregulatory capability. Therefore mucosal ischaemia and surgical bleeding may result from a decreased cardiac output and an increased gastric venous pressure.

These physiological changes during IPPV can be precipitously revealed when intubating critically ill patients. Marked hypotension and cardiovascular collapse can occur as a result of uncorrected volume depletion prior to intubation. This is compounded by the administration of anaesthetic drugs, which vasodilate and reduce circulating catecholamine levels as patients lose consciousness.

The effects on cardiac output are seen in both invasive and non-invasive IPPV, but the effects are not as dramatic in non-invasive ventilation as the patient is awake and breathing spontaneously, with the ventilator acting only as an assistant.

Table 4.2 Advantages and disadvantages of volume versus pressure control


Volume control

Pressure control


Delivers a set tidal volume

If airway pressures are

no matter what pressure

high, only small tidal

this requires. This can

volumes will be delivered.

cause barotrauma

Not good if lung compliance keeps changing


Poor compensation

Compensates for leaks well (e.g. poor fitting mask or circuit fault)


Many volume control ventilators cannot apply PEEP

PEEP easily added

PEEP, positive end-expiratory pressure.

PEEP, positive end-expiratory pressure.

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