blood pressure. In essence, in a spontaneously breathing patient with baseline P
thoracic=^ - 10, the LV has to generate pressure of 110 to obtain systemic pressure of
100 (must overcome intrathoracic pressure of - 10 + MAP 100). If there is MAP of
10 or intrathoracic P =+10, the heart has to generate P of 90 only to systemic
pressure of 100.
The dominant effect of PPV on lung and cardiac mechanics is through the
Paiarway. Effects due to phasic changes such as ∆P are minor.
To some extent, pulmonary vascular resistance is modulated by lung
volume. When there is atelectasis, large pulmonary vessels are not straight,
increasing pulmonary vascular resistance. Smaller lung vessels are not taut so
resistance in these vessels is low. When lungs are over distended, resistance
through the straightened pulmonary vessels are low, but the large perialveolar
pulmonary vessels are impressed by the overly distended alveoli, increasing PVR.
Therefore when the lung is atelectatic or over distended, PVR can increase.
Hypoxia, respiratory alkalosis, metabolic alkalosis also decreases PVR. Note that it
is the change in pH and not the CO2 that modulates PVR.
(^)
III. Consensus Statement on Oxygen Delivery in a Critically Ill Patient
Hemodynamic stability must be maintained.
Normovolemia must be achieved.
Colloid and crystalloid resuscitation are equivalent.
Aggressive attempts for supranormal O2 delivery show no outcome advantage.