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Dr. Alpert is Robert S. and Irene P. Flinn Professor of Medicine, Head, Department of Medicine, University of Arizona Health Science Center, Tucson, AZ.
Correspondence to: Joseph S. Alpert, MD, FCCP, Robert S. and Irene P. Flinn Professor of Medicine, Head, Department of Medicine, University of Arizona Health Science Center, 1501 North Campbell Ave, Tucson, AZ 85724-5024
It is a platitude known to all second-year medical students that the most common cause of right ventricular failure is left ventricular failure. It is decidedly less well known that right ventricular dysfunction has an effect on left ventricular form and function. In 1910, the French physiologist P. I. Bernheim postulated an interaction between the left and right ventricles such that an alteration in the function of one ventricle led to an alteration in the function of the other ventricle.1 He specifically proposed that left ventricular dilatation or hypertrophy would cause the right ventricle to be compressed with a resultant decrease in right ventricular function. Today, we know what Bernheim did not know, that decreased right ventricular function secondary to left ventricular dilatation/hypertrophy is the result of increased right ventricular afterload secondary to passive pulmonary hypertension (elevated left ventricular filling pressure leads to increased pulmonary arterial diastolic and systolic pressures).
In recent years, it has been clearly documented in experimental animal models and in patients that right ventricular dilatation and hypertrophy shift the interventricular septum leftward, thereby causing decreased left ventricular cavity size, contractility, compliance, and ejection fraction as well as increased left ventricular diastolic pressure. This phenomenon has been coyly described as "the reverse Bernheim phenomenon," even though Bernheim never actually suggested such a term. The physiologic terms most commonly employed to describe this phenomenon are "ventricular interaction or ventricular interdependence." The observed changes in left ventricular function can occur in normal hearts or in those of patients with cardiac disease. The reverse Bernheim phenomenon has been noted in patients with both volume and pressure overload of the right ventricle.
The restraining pericardium plays an important role in furthering ventricular interaction secondary to acute changes in right ventricular volume/function, since pericardial stretch cannot occur acutely. The restraining influence of the pericardium ensures that a sudden increase in right ventricular volume occurs at the expense of left ventricular volume as a result of the leftward shift of the septum. Even in chronically dilated right ventricles, pericardial restraint ensures that the interventricular septum will shift to the left, thereby decreasing left ventricular volumes and altering systolic and diastolic function. In patients with right ventricular pressure overload, such as the patients described by Marcus et al in this issue of CHEST (see page 1761), there is a second potential mechanism for altering left ventricular function: the myocardial hypertrophic process that is affecting the right ventricle produces concomitant hypertrophy of the interventricular septum. Left ventricular compliance is altered by the septal hypertrophy. Both mechanisms probably play a role in changing left ventricular diastolic function.
Marcus et al used nuclear MRI to study left and right ventricular volumes and filling rates as well as septal curvature, and pulmonary arterial flow curves in 12 patients with rather severe primary pulmonary hypertension. Their work confirms and extends previous studies in this area. Marcus et al noted that the interventricular septum bowed into the left ventricle during diastole, although it continued to curve into the right ventricle during systole when left ventricular pressure was higher than right ventricular pressure. The leftward shift in the septum during diastole led to slower filling rates in the left ventricle as compared with the right. As expected, right ventricular volumes were increased compared with a normal population while left ventricular end-diastolic volume was decreased. Right ventricular ejection fraction was markedly depressed while left ventricular ejection fraction declined modestly. Stroke volume from both ventricles was depressed. The normal rightward bowing of the septum during systole was halved in the pulmonary hypertensive patients as compared with normal individuals.
The authors concluded that right ventricular pressure overload caused an alteration in septal bowing that encroached on the left ventricle thereby reducing its diastolic filling. This led to a decrease in stroke volume by the Frank-Starling mechanism.
Similar effects have been observed in patients with severe pulmonary disease with resultant pulmonary hypertension. Vizza et al2 observed a direct correlation between right and left ventricular ejection fraction in a large cohort of patients with severe pulmonary disease. A subset of their patient population underwent lung transplantation with a consequent reduction in pulmonary hypertension. In these latter patients, right and left ventricular ejection fraction improved. Schena et al3 studied 30 patients with advanced COPD. The results in this study were similar to those reported by Marcus et al: increased right ventricular volume, a leftward shift in the interventricular septum, and reduced left ventricular volume and diastolic function.
In conclusion, experimental and clinical observations support the concept of the reverse Bernheim phenomenon, ie, a leftward shift of the interventricular septum secondary to right ventricular pressure and volume overload. This septal shift alters left ventricular volume as well as diastolic and, to a lesser extent, systolic function. Patients with a wide array of severe pulmonary diseases are prone to develop the reverse Bernheim phenomenon.
References
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