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Chandigarh, India
Correspondence to: Ritesh Agarwal, MD, DM, Assistant Professor, Department of Pulmonary Medicine, PGIMER, Sector-12, Chandigarh-160012, India; e-mail: riteshpgi{at}gmail.com
To the Editor:
We read with interest the article by Bendjelid et al (March 2005),1 who present an interesting analysis that the benefit of continuous positive airway pressure (CPAP) in diastolic heart failure (DHF) is due to decrease in left ventricular end-diastolic volume (LVEDV) and mean arterial pressure. However, we do not agree with the authors on the proposed mechanism of CPAP in DHF.
Inadequate LVEDV is the very basis of DHF, and its additional primary lowering by positive pressure could only further limit stroke volume, and hence cardiac output, because of the steep curve for left ventricular diastolic pressure in relation to volume.2 Hence, caution must be used because patients with DHF are sensitive to the preload reduction and may become hypotensive or have severe prerenal azotemia.3 In this context, there may be a theoretical superiority of bilevel positive airway pressure over CPAP because of varying inspiratory and expiratory pressures. But the authors did show improvement in the clinical condition of the patients?
We believe that improvement because of CPAP is probably due to the reduction in heart rate (101 ± 19 beats/min at baseline vs 83 ± 11 beats/min after CPAP). Tachycardia causes an increase in demand for myocardial oxygen and a decrease in coronary perfusion time, which may lead to myocardial ischemia, even in the absence of obstructive coronary artery disease. In addition, there may be insufficient time for complete relaxation, with a resultant increase in diastolic pressure that compromises ventricular filling. CPAP causes a significant decrease in the heart rate, resulting from increased parasympathetic tone in response to CPAP-induced lung inflation.4
However, because of small numbers it is difficult to draw any firm conclusions, unlike systolic dysfunction, in which a recent metaanalysis5 of almost 500 patients conducted showed significant decrease in rates of intubation and mortality, and the numbers needed to treat to prevent one intubation and one death are six and eight, respectively. Thus, pending larger data, CPAP in DHF should be used only under strict experimental conditions with the potential of clinical deterioration due to CPAP per se kept in mind.
References
Geneva University Hospitals, Geneva, Switzerland
Correspondence to: Karim Bendjelid, MD, MS, Chef de Clinique Scientifique, Surgical Intensive Care Division, University hospital of Geneva, CH-1211 Geneva 14, Switzerland; e-mail: karim.bendjelid{at}hcuge.ch
To the Editor:
We read with great interest the comments by Drs. Agarwal and Gupta regarding our article (March 2005)1 entitled "Does Continuous Positive Airway Pressure (CPAP) by Face Mask Improve Patients With Acute Cardiogenic Pulmonary Edema (ACPE) Due to Left Ventricular Diastolic Dysfunction?" The authors do not agree with the proposed mechanism of CPAP in patients presenting with ACPE that was illustrated by our study.
I would like to make the following remarks about their comments. First, the authors should read the introduction to our article in order to appreciate that, as was also the case for them, our expectation prior to performing the study was the contrary of what we actually found.12 Second, they stated that inadequate left ventricular end-diastolic volume (LVEDV) is the basis of diastolic heart failure, and they expected that positive pressure could limit left ventricular filling and cardiac output. However, chronic diastolic heart failure is different from ACPE due to diastolic dysfunction. Indeed, keeping in mind that transthoracic echocardiography underestimates LVEDV,3 in our study,1 as in the study by Ghandi et al,4 patients presenting with ACPE had a normal mean (± SD) LVEDV (107 ± 4 and 109 ± 43 mL, respectively). These results render the authors’ argument irrelevant as inadequate LVEDV was not observed in patients with ACPE due to diastolic dysfunction.
Second, the authors believe that bilevel positive airway pressure should theoretically be more efficient than CPAP for treating patients with ACPE due to diastolic dysfunction. How could additional intrathoracic pressure be better for left ventricular filling, excluding the role of assistance to the respiratory muscles? Moreover, in a recent study,5 therapy with bilevel positive airway pressure did not offer any advantage over CPAP therapy in the treatment of ACPE.
Third, the authors believe that the improvement related to CPAP seen in patients with ACPE due to diastolic dysfunction in our study is due to the reduction in heart rate that causes less myocardial work and better coronary perfusion and left ventricular filling. However, even if this theoretical assumption may be agreed upon, our study does not confirm it, as no increase in ejection fraction and LVEDV was observed during CPAP (Starling curve).1
Finally, Agarwal and Gupta misunderstood our conclusions to mean that the decrease in LVEDV is a helpful mechanism of action of CPAP therapy in patients with ACPE due to diastolic dysfunction. As explained in the "Discussion" section, we think that CPAP, by decreasing respiratory work in patients with cardiopulmonary edema, unloads the heart from the large amount of cardiac output that supplies the respiratory muscles and improves oxygen delivery for other tissues. Physicians should keep in mind that it is not because ACPE is a heart disease affecting the lung that the beneficial effect of CPAP is mandatory related to its hemodynamic effects on the pump. Indeed, as we have already stated in others articles,67 supporting the lung by positive pressure acts as a pulmonary circulatory drive.8
References
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