Jump to comment:

• Beneficial Hemodynamic Effects Of Positive-pressure Ventilation In Patients With Heart Failure
  Mohamad Abdelsalam Abdelkader
  Published on: 16 March 2004

• Published on: 16 March 2004

  Beneficial Hemodynamic Effects Of Positive-pressure Ventilation In Patients With Heart Failure

  • Mohamad Abdelsalam Abdelkader, King Fahd Hofuf Hospital

  Dear Editor

  Positive-pressure ventilation may be associated with adverse cardiovascular effects, particularly when using large tidal volumes and / or high PEEP. The increased intra-thoracic pressure decreases venous return to the heart with subsequent reduction of cardiac filling, cardiac output and blood pressure. On the other hand, positive-pressure ventilation may have beneficial hemodynamic effects. If the pos...

  Show More

  Dear Editor

  Positive-pressure ventilation may be associated with adverse cardiovascular effects, particularly when using large tidal volumes and / or high PEEP. The increased intra-thoracic pressure decreases venous return to the heart with subsequent reduction of cardiac filling, cardiac output and blood pressure. On the other hand, positive-pressure ventilation may have beneficial hemodynamic effects. If the positive airway pressure is timed to occur during systole and the airway pressure is released during diastole, cardiac output can sometimes be increased and the mechanical ventilator can actually function as a partial ventricular assist device ( as if the ventilator is squeezing the heart when the intra -thoracic pressure is increased during systole) . Based on clinical observation, many patients with decompensated heart failure (who were intubated and ventilated because of acute pulmonary oedema) improved significantly several hours after mechanical ventilation. Compensatory tachycardia, ventricular ectopics and gallop rhythm decreased and many patients showed much better diuretic response. In addition, some patients with underlying Coronary artery disease - CAD - demonstrated ECG evidence of improved myocardial ischemia after initiation of positive- pressure ventilation (nitrates and calcium antagonists were not given to those patients with borderline B.P for fear of exaggerated ventilator - induced hypotension). It should be remembered that ventilator-induced hypotension is a potential complication in volume-depleted patients rather than the fluid-overloaded patients with heart failure. We can assume that mechanical ventilator may be particularly useful to patients with decompensated heart failure as it may augment ventricular contraction, improve arterial oxygenation and hence myocardial O2 supply and reduce preload (as a result of increased intra-thoracic pressure and reduced venous return). Preload reduction not only reduces pulmonary congestive symptoms but also decreases left ventricular end-diastolic diameter ( L.V.EDD ), L.V wall tension and therefore cardiac work and myocardial O2 demand (the same mode of action of nitrates that may explain the ECG evidence of improved ischemia in some patients with CAD shortly after intubation. It is to be remembered that L.V wall tension depends on L.V.EDD - determined by preload - and intra-ventricular pressure - determined by after load. Positive - pressure ventilation may also be beneficial in the clinical setting of acute pulmonary oedema in which up to 40 – 50 % of the cardiac output may be taken up by the overacting respiratory muscles of the severely distressed patients. After intubation, ventilation and sedation (with or without muscle paralysis), mechanical ventilator provides "rest" to the overacting respiratory muscles and allows redistribution of the cardiac output from the respiratory muscles to the heart, brain and kidneys. This may lead to improved coronary blood flow and myocardial O2 supply which may further enhance myocardial contractility and reduce myocardial ischemia. In addition, renal blood flow may also be increased which may explain the enhanced diuretic response in heart failure patients after intubation and mechanical ventilation. In conclusion, positive-pressure ventilation may have several beneficial effects in patients with decompensated heart failure who are intubated because of acute pulmonary oedema and hypoxemic respiratory failure. This may include increased cardiac output, improved myocardial ischemia (due to increased O2 supply and reduced O2 demand) and increased renal perfusion and diuretic response. Finally, this issue needs more evaluation using echocardiography (to assess L.V function and regional wall motion), invasive hemodynamic monitoring (to measure cardiac output, PCWP and pulmonary artery pressure) as well as biochemical markers of heart failure such as the recently available B-type natriuretic peptide that may be of value in assessing the severity of heart failure.

  References

  1. Pinsky HR. Cardiovascular effects of ventilatory support and withdrawal. Anaesth. Analg 1994; 79: 567 – 576

  2. Veisprille A. The pulmonary circulation during mechanical ventilation. Acta Anesthesiol Scand 1990; 34 (Suppl):51-62.

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top