IPPV and PEEP

• IPPV is artificial ventilation produced by imposing a positive pressure from a sealed circuit into the airway, followed by passive expiration, usually at atmospheric pressure
• The major physiological difference from spontaneous ventilation is in the range of airway and intrathoracic pressures involved
• Spontaneous ventilation involves small pressure excursions above and below atmospheric pressure in airway pressure
• IPPV involves much higher airway pressures in inspiration, typically 15-25 mmHg in a healthy adult
• Much of this pressure is transmitted to increase intrathoracic pressure
• Positive end-expiratory pressure (PEEP) is a modification of IPPV such that the expiratory airway pressure does not fall as low as atmospheric pressure. A typical level of PEEP is 5-15 mmHg

Consequences of IPPV and PEEP:

The physiological effects of IPPV with ZEEP or PEEP relate to the mean increase in intrathoracic pressure and as such PEEP has a more significant effect.

Respiratory effects:

• IPPV results in minor changes in the spatial distribution of ventilation which is only relevant in patients with acute lung injury.
• PEEP increases lung volume, re-expands collapsed alveoli and therefore improves ventilation in these areas.
• Both delivery of IPPV and PEEP results in aparatus deadspace which may or may not influence the overall deadspace (sometimes it is cancelled by a reduction in anatomical deadspace).
• There is a slight worsening of V/Q ratios with IPPV but this is often not significant.
• PEEP increases FRC whilst IPPV with ZEEP does not.
• IPPV and PEEP do not change oxygenation in healthy patients, but may have significant benefits is diseased patients by increasing the FRC above closing capacity, reducing airways resistance and improving recruitment and maintaining patency in alveolar units

Cardiovascular effects:

• IPPV and PEEP cause a reduction in cardiac output by reducing venous return to the right atrium because of increased introathoracic pressure.
• With normal inspiration there is negative intrathoracic pressure which acts as a pump to draw blood into the chest from the major veins and this is abolished with postive intrathoracic pressure.
• The reduction in RV filling leads to less LV filling, which is exacerbated in hypovolaemic states.
• Increased airway pressures lead to increased pulmonary vascular pressures and this increases RV strain.
• While PEEP may improve PaO2 the decrease in CO may actually lead to decreased O2 delivery to the tissues (remember that DO = CO(sats x Hb + dissolved O2)).
• There is some increase in peripheral vascular resistance to counter the decreased CO but this is often inadequate.

Renal effects - prolonged IPPV causes increases in oedema, this is believed to be from a combination of increased ADH and the reduced pressure gradient at the glomerulus caused by decreased arterial pressures and increased CVP

Immunological effects - occur from increased neutrophil retention in the pulmonary vasculature due to their reduced calibre with IPPV and PEEP.