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Hyperbaric Oxygen Therapy And Congestive Heart Failure

Hyperbaric Oxygen Therapy And Congestive Heart Failure

Hyperbaric Oxygen Therapy And Congestive Heart Failure

Introduction

Is congestive heart failure a contraindication to hyperbaric oxygen therapy?

Congestive heart failure (CHF) may be a relative contraindication to hyperbaric oxygen therapy (HBOT) depending on severity and current management. There are a number of known risks and side effects of HBOT most of which are either rare or of minimal consequence. One such complication is an exacerbation of congestive heart failure. When pulmonary edema occurs, it is typically noted in the latter half of a 90-minute treatment and, though rare, this complication can be significant. Patients may do well with simple decompression. Some may require a diuresis while others may require hospitalization and cardio-respiratory support in the Intensive Care Unit. Some deaths are reported in the literature from exacerbations of pulmonary edema during HBOT. [1] 

The Issue

What is the underlying mechanism of pulmonary edema under HBOT?

The underlying mechanism of pulmonary edema under hyperbaric hyperoxia is not entirely clear. One possible mechanism is that of ventricular imbalance, explained below [1][2]:

  • Under hyperbaric hyperoxic conditions, peripheral vasoconstriction results in an increase in left ventricular afterload. This is the equivalent of pushing 500 - 700 cc of excess fluid into the right heart over 10 - 15 minutes (the time to compress the hyperbaric chamber.)
  • On the other hand, this same hyperoxia results in pulmonary vasodilation to allow for matching of ventilation and perfusion. This pulmonary vasodilation results in a lower right ventricular afterload.
  • In the setting of left heart failure, the left ventricle is afterload-dependent. Therefore, any increase in afterload may result in worsening left sided cardiac output.
  • Should these conditions exist during hyperbaric oxygen exposure, there may be an imbalance between the output of the right and left ventricles respectively. A decrease in left heart output relative to the right of only 2% can result in an additional liter of fluid in the pulmonary vascular bed over a 10-minute period of time. This additional pulmonary volume would become symptomatic over time as the disparity between the ventricular outputs continues.
  • Assuming that the mechanism above is correct, the degree of compromise would, in fact, be dependent on the oxygen dose.

Over the past 20 years of practice, we have seen only a few cases of apparent hyperbaric oxygen-induced pulmonary edema. In these cases, there was no correlation with the degree of left ventricular dysfunction as patients with ejection fractions as low as 10-15% have done well while others with only mild impairment have developed symptomatic edema. Patients who experienced pulmonary edema during one treatment did not develop volume overload on subsequent treatments.

Conclusion

What measures need to be taken for patients with CHF undergoing HBOT?

In our opinion, all patients with a history of CHF should be maximally medically managed and well compensated prior to a trial of pressure if the clinical condition allows. One could also consider treating at a lower pressure to potentially lessen the increase in left ventricular afterload. Theoretically, air breaks may be of benefit in reducing the oxygen-induced vasoconstriction and resulting increased afterload.

With regard to a recent myocardial infarction, it would be prudent to address any degree of cardiac dysfunction prior to HBOT especially in the non-emergent setting. This would include allowing time for adequate titration of the various medications prescribed for heart failure. Prior to any trial of pressure patients should be well compensated with respect to their systolic dysfunction. Lastly, patients who suffered a subendocardial infarction are likely to be at greater risk for a subsequent cardiac event. These individuals are also more likely to develop subendocardial ischemia with a subsequent loss in left ventricular diastolic performance, which may lead to an exacerbation of their failure. With this in mind, blood pressure should be adequately controlled and any anxiety with regard to HBOT should be adequately addressed.

References

  1. Weaver LK, Churchill S et al. Pulmonary edema associated with hyperbaric oxygen therapy. Chest. 2001;volume 120(4):1407-9.
  2. Abel FL, McNamee JE, Cone DL, Clarke D, Tao J et al. Effects of hyperbaric oxygen on ventricular performance, pulmonary blood volume, and systemic and pulmonary vascular resistance. Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, In.... 2000;volume 27(2):67-73.

Resources

 

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REFERENCES

  1. Weaver LK, Churchill S et al. Pulmonary edema associated with hyperbaric oxygen therapy. Chest. 2001;volume 120(4):1407-9.
  2. Abel FL, McNamee JE, Cone DL, Clarke D, Tao J et al. Effects of hyperbaric oxygen on ventricular performance, pulmonary blood volume, and systemic and pulmonary vascular resistance. Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, In.... 2000;volume 27(2):67-73.
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