Respiratory system
- decreased lung compliance
- more uneven distribution of ventilation
- increase in dead space and in ratio of dead space to tidal volume
Patients with normal lungs
- fall in FRC and increased alveolar to arterial oxygen gradient
- due to extensive dependent atelectasis
Patients with abnormal lungs
- in patients who have been hypoventilating near residual volume, mechanical
ventilation will increase FRC and tidal volume
Cardiovascular system
Positive pressure ventilation results in:
- rise in pleural pressure
- rise in intra-abdominal pressure
- increased lung volumes
All these produce cardiovascular changes.
The extent of
these changes relative to any given level of airway pressure will depend on the
lung and chest wall compliance and airway resistance
In any individual patient the overall effects will depend on the patient's
underlying pathophysiology.
Preload
LV preload is usually (but not invariably) reduced by a variety of mechanisms
Venous return

- in a volume resuscitated patient
- venous return does not fall
- intrathoracic pressure is positive rather than negative but
- intra-abdominal pressure also rises
- pressure gradient between abdomen and thorax is maintained
- in a patient with an open abdomen
- venous return should fall
- intra-abdominal pressure does not rise
- pressure gradient not maintained

- in a volume depleted patient
- collapse of
intra-abdominal veins and SVC occurs
- result of positive pressure intrathoracic pressure
- in abdomen collapse appears to occur behind the liver as a result of
positive pleural pressure transmitted through the diaphragm and liver
- in superior vena cava
- results in a fall in venous return, RV stroke volume and hence LV
preload
- changes in LVEDV do not necessarily parallel changes in RVEDV
- RV and LV confined by pericardium
- as a result increase in RVEDV decreases LV compliance and vice versa
- in a patient with pulmonary hypertension a reduction in venous return
as a result of positive pressure ventilation will reduce the size of a
dilated RV and hence increase LV compliance and LV preload

Pulmonary vascular resistance
- decreased RV stroke volume and hence LV preload because of compression of
pulmonary vessels by positive alveolar pressure
LV compliance
- at high lung volumes lungs compress the heart reducing LV compliance and
hence LV end-diastolic volume
Afterload
- afterload = wall tension (T) during contraction

where Ptm= transmural pressure, R=radius and H=wall thickness
- transmural pressure=intraventricular pressure-pleural pressure
- pleural pressure increased by positive pressure
- therefore transmural pressure and afterload must be decreased by positive
pressure ventilation
Myocardial oxygen consumption
- myocardial oxygen consumption was previously thought to be determined by
stroke work. However it is now known that it is determined by the sum of
stroke work and elastance-defined potential work. The latter is the
potential energy in the ventricle at end-systole. Figure below illustrates this
relationship. Myocardial oxygen consumption is proportional to the shaded
area. As mechanical ventilation generally decreases preload and afterload it
shifts the pressure-volume loop to the left and
down decreasing elastance-defined potential work and thus myocardial
oxygen consumption.

- in patients with coronary artery disease reducing myocardial oxygen
consumption may improve the balance between oxygen demand and supply
resulting in an improvement in LV function. Thus in these patients
mechanical ventilation may increase LV contractility.
Cardiac output
- overall effect depends on whether ventricle is normal or abnormal
- in a patient with normal LV contractility increased intrathoracic pressure
decreases LVEDV more than LVESV resulting in a fall in stroke
volume (figure below)
Fig. 1

- in a patient with decreased LV contractility,
intrathoracic pressure decreases LVEDV less than LVESV resulting in a rise in stroke volume (figure
below). Note the decreased slope of the end systolic pressure volume
relationship due to decreased contractility

Renal
- renal blood flow falls if cardiac output falls
- Decreased sodium secretion due to fall in cardiac output and decreased
secretion of atrial natriuretic factor
- Increased water retention due to increased secretion of ADH, particularly in
children.
CNS
- increased
intrathoracic pressure decreases venous drainage from head and may
increase ICP. If, however, mechanical ventilation results in a decrease in PaCO2
ICP may actually fall
- NB adverse effects of mechanical ventilation are far outweighed by benefits
in brain injured patients
Further
reading
Jardin F, Vieillard-Baron A. Right ventricular function and
positive pressure ventilation in clinical practice: from hemodynamic subsets to
respirator settings. Intensive Care Med 2003; 29:1426-1434
Pinsky MR. The hemodynamic consequences of mechanical
ventilation: an evolving story. Intensive Care Med 1997; 23:493-503
Pinsky MR. Recent advances in the clinical application of
heart-lung interactions. Curr Opin Crit Care 2002; 8:26-31
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