Download Perioperative heart-lung interactions

Cardiovascular insufficiency with initiation and withdrawal of mechanical ventilation
Michael R. Pinsky, MD, Dr hc, Professor of Critical Care Medicine, Bioengineering,
Cardiovascular Disease and Anesthesiology
Department of Critical Care Medicine, University of Pittsburgh
E-mail: [email protected]
The hemodynamic effects of ventilation are multiple and complex, but can be grouped into
four clinically relevant concepts. First, spontaneous ventilation is exercise. In patients increased
work of breathing, initiation of mechanical ventilatory support will improve O2 delivery to the
remainder of the body by decreasing O2 consumption. To the extent that mixed venous O2 also
increases, arterial PO2 will also increase without any improvement in gas exchange. Similarly,
weaning from mechanical ventilatory support is a cardiovascular stress test. Patients who fail to
wean also manifest cardiovascular insufficiency during the failed weaning attempts (1).
Improving cardiovascular reserve or supplementing support with inotropic therapy may allow
patients to wean form mechanical.
Second, changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at
high lung volumes compress the heart in the cardiac fossa similarly to cardiac tamponade. As
lung volume increases so does the pressure difference between airway and pleural pressure.
When this pressure difference exceeds pulmonary artery pressure, pulmonary vessels collapse as
they pass form the pulmonary arteries into the alveolar space increasing pulmonary vascular
resistance. Thus, hyperinflation increases pulmonary vascular resistance, pulmonary artery
pressure, impeding right ventricular ejection. Spontaneous ventilation that induces dynamic
hyperinflation and rapid mechanical breaths that cause auto-PEEP can both induce acute cor
pulmonale. Decreases in lung volume below functional residual capacity, as occurs in acute lung
injury, alveolar collapse and increased pulmonary vasomotor tone by the process of hypoxic
pulmonary vasoconstriction (2). Recruitment maneuvers, positive-end expiratory pressure and
continuous positive airway pressure may reverse hypoxic pulmonary vasoconstriction and reduce
pulmonary artery pressure.
Third, spontaneous inspiration and spontaneous inspiratory efforts decrease intrathoracic
pressure. Spontaneous inspiratory efforts often occur during positive-pressure ventilation and can
be quite forceful. Since diaphragmatic descent increases intra-abdominal pressure, these
combined effects cause right atrial pressure inside the thorax to decrease, but venous pressure in
the abdomen to increase, markedly increasing the pressure gradient for systemic venous return.
Furthermore, the greater the decrease in intrathoracic pressure the greater the increase in left
ventricular afterload for a constant arterial pressure (3). Thus, spontaneous inspiratory efforts
increase LV afterload and can induce acute cardiogenic pulmonary edema. Mechanical
ventilation, by abolishing the negative swings in intrathoracic pressure will selectively decrease
left ventricular afterload, as long as the increases in lung volume and intrathoracic pressure are
small (4).
Finally, positive-pressure ventilation increases intrathoracic pressure. Since diaphragmatic
descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous
return is less than would otherwise occur if the only change were an increase in right atrial
pressure (5). However, in hypovolemic states, positive-pressure ventilation can induce profound
decreases in venous return. Increases in intrathoracic pressure decreases left ventricular afterload
and will augment left ventricular ejection. In patients with hypervolemic heart failure, this
afterload reducing effect can result in improved left ventricular ejection, increased cardiac output
and reduced myocardial O2 demand (6).
Using the obligatory changes in venous return induced by positive-pressure breathing, one
can readily identify which patients are volume responsive and by how much (7). Use of the
associated arterial pulse pressure variation or its derived stroke volume variation, resuscitation
algorithms can be created to sustain adequate blood flow in high risk patients decreasing
morbidity and mortality (8).
References:
1. Lemaire F, JL Teboul, L Cinoti, G Giotto, F Abrouk, G Steg, I Macquin-Mavier, WM Zapol.
(1988) Acute left ventricular dysfunction during unsuccessful weaning from mechanical
ventilation. Anesthesiology 69:171-9.
2. Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T, Ando S, Bradley TD. (2003)
Cardiovascular effects of continuous positive airway pressure in patients with heart failure
and obstructive sleep apnea. N Engl J Med 348: 1233-41.
3. Buda AJ, Pinsky MR, Ingels NB, et al. (1979) Effect of intrathoracic pressure on left
ventricular performance. N Engl J Med 301:453-9.
4. Jardin F, Farcot JC, Boisante L. (1981) Influence of positive end-expiratory pressure on left
ventricular performance. N Engl J Med 304:387-92.
5. Van den Berg P, Jansen JRC, Pinsky MR. (2002) The effect of positive-pressure inspiration on
venous return in volume loaded post-operative cardiac surgical patients. J Appl Physiol
92:1223-31.
6. Denault AY, Gorcsan J 3rd, Pinsky MR. (2001) Dynamic effects of positive-pressure
ventilation on canine left ventricular pressure-volume relations. J Appl Physiol 91: 298-308.
7. Michard F, Boussat S, Chemla D, Anguel N, Mercat A, Lecarpentier Y, Richard C, Pinsky
MR, Teboul J-L. (2000) Relation between respiratory changes in arterial pulse pressure and
fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care
Med 162: 134-8.
8. Pinsky MR, Payen D. (2005) Functional hemodynamic monitoring. Crit Care 9:566-72.