Left Ventricular End-Diastolic Pressure in Evaluating Left Ventricular Function

Transcription

1 Clin. Cardiol. 4,28-33 (1981) 0 G. Witzstrock Publishing House, nc. Practitioner s Corner Left Ventricular End-Diastolic Pressure in Evaluating Left Ventricular Function A. s. SKANDRAN, M.D., B. L. SEGAL, M.D., A. HAMD HAKK, M.D. The Likoff Cardiovascular nstitute, Hahnemann Medical College and Hospital, Philadelphia, Pennsylvania, USA Summary: There are several factors that could affect the left ventricular end-diastolic pressure. These include heart rate, preload, afterload, pericardial or pleural pressure, diastolic properties of the left ventricle, and the left ventricular inotropic state. Recognition of these factors appears important when considering the left ventricular end-diastolic pressure as an index of left ventricular function. ntroduction Direct measurement of left ventricular end-diastolic pressure (LVEDP) is routinely performed during cardiac catheterization (Fig. 1). ndirect assessment of the LVEDP by measuring the pulmonary artery wedge or pulmonary artery diastolic pressure by means of the balloon-tipped floating catheter is being increasingly used in critical care units. t should be emphasized that the mean pulmonary artery wedge pressure or the pulmonary artery diastolic pressure measured with the balloon-tipped catheter correlates more closely with left ventricular mean diastolic pressure or to left ventricular pressure before atrial contraction rather than LVEDP. This correlation results from a further rise in left ventricular end-diastolic pressure concomitant with atrial contraction, especially in the presence of a noncompliant left Address for reprints: Abdulmassih S. skandrian, M.D. Hahnemann Medical College and Hospital 230 N. Broad Street Philadelphia, PA 19102, USA Rcceived: July 2, 1980 Accepted: September 15, 1980 ventricle (Braunwald and Ross, 1963; Rahimtoola, 1973). Both techniques of measurement (direct and indirect) in experienced hands are simple and safe; there is no question that measurement of the LVEDP or the pulmonary artery wedge pressure has proven to be extremely useful not only in diagnosis but also in therapy and even prognosis. The purpose of this review is to summarize the variables that may affect the LVEDP and the feasibility of using this measurement as an index of left ventricular function. Causes of Abnormal Left Ventricular and Diastolic Pressure Attention to the recording technique, specifically the level of the transducers in relation to the reference point, as well as calibration of the manometric system and the zeroing level before each recording, is important for accurate recording of the LVEDP. An improper transducer level or improper calibration (or both) is probably an important factor in socalled mild elevation of the LVEDP encountered during diagnostic cardiac catheterization in reasonably healthy individuals. The presence and timing of the atrial kick may affect the LVEDP. The atrial kick is absent in patients with atrial fibrillation or junctional rhythm, or in patients with permanent ventricular pacemakers (Fig. 2). Prolongation of the PR interval, as seen in first-degree atrioventricular block, may allow the LVEDP to decline before ventricular systole. Similar observations may be seen in patients with isorhythmic dissociation in whom noticeable changes are evident during consecutive cycles. The cardiac cycles preceded by appropriately timed P waves have higher LVEDP than those with prolonged PR or those where the P wave follows the QRS complex (Fig. 3). Left ventricular end-diastolic pressure also decreases during tachycardia, whether induced by atrial or ventricular pacing or resulting from sinus or junctional

2 ~~ A. S. lskandrian er al.: Left ventricular end-diastolic pressure 29 &=Jh mmhg 40 mmhg... t *.. + _ 1 -t- - - FG. 1 Left ventricular (LV) pressure tracings on a scale of 0-40 mmhg showing a normal left ventricular end-diastolic pressure (LVEDP). FG. 3 Left ventricular (LV) pressure tracing on a scale of mmhg in a patient with complete AV block and an occasional captured beat. Left ventricular end-diastolic pressure (long arrow) varies according to the timing of the preceding A wave (short arrow). FG. 2 Left ventricular (LV) and pulmonary capillary wedge (PCW) pressure on a scale of 0-40 mmhg in a patient with mitral stenosis and atrial fibrillation. Note the absence of A waves in the LV pressure tracing. A mitral valve gradient is present during diastole. Abbreviation: EDP, end-diastolic pressure.

3 30 Clin. Cardiol. Vol. 4, January mechanisms (Linhart et al., 1969). The reduction in enddiastolic volume in these cases is presumably responsible for a decrease in the end-diastolic pressure (Fig. 4). The interaction between the right ventricle, the left ventricle, and the pericardium surrounding these structures is an important factor that may affect the LVEDP (Bemis et Pre Op FG. 4 Left ventricular (LV) pressure on a scale of 0-4Q mmhg showing a normal response to atrial pacing with decrease in LVEDP. End-diastole1 FG. 5 Left ventricular (LV) and right ventricular (RV) pressures recorded on a scale of mmhg in a patient with constrictive pericarditis. Correspondence of ventricular diastolic pressures is shown.

4 A. S. lskandrian et al.: Left ventricular end-diastolic pressure 31 A v3l - ventricle and the completeness of relaxation (Gaasch et al., 1976; Grossman and McLaurin, 1976; Mann et al., 1977). The pressure-volume characteristics of the left ventricle can be altered in several disorders, for example, coronary artery disease (Fig. 7), aortic valve disease, and cardiomyopathy. Whether the alteration in compliance in these cases is related to alterations in chamber or muscle compliance, the resultant effect is similar and raises LVEDP in these patients FG. 6 Left ventricular (LV) and right ventricular (RV) pressures recorded on a scale of 0-40 rnmhg in a patient with pericardial tarnponade. Note equalization of diastolic pressures and elevation of end-diastolic pressures (EDP). - n. 1 al., 1974; Ross, 1979; Shabetai et al., 1979). Under normal circumstances, the intrapericardial pressure is subatmospheric throughout most of the cardiac cycle. The pericardial volume is dependent on the volume of structures it contains, and the pressure-volume characteristics of the pericardium are dependent on its size as well as on the duration of the disorders that result in its stretching. t has been observed that right ventricular overload produces less elevation in LVEDP when the pericardium is open than when the pericardium is intact. Marked right ventricular overloading elevates LVEDP even with an incised pericardium. These observations may suggest that the right ventricle influences LVEDP through two mechanisms: first, by displacing the interventricular septum to the left; and second, by competing with the left ventricle in the available space within the pericardial sac. Constrictive pericarditis and cardiac tamponade are excellent examples of alteration in LVEDP irrespective of the left ventricular systolic function (Shabetai et al., 1979) (Figs. 5 and 6). The size and the ejection fraction of the left ventricle are generally normal in patients with these diseases; however, occasionally they might be abnormal. Such abnormalities can be explained by (1) underlying cardiac disease, (2) extension of the scarring and fibrosis into the myocardium, (3) compression of the coronary vessels on the surface of the heart, (4) reduction of coronary blood flow, especially to the subendocardial layer by the high left ventricular end-diastolic pressure, and (5) low cardiac output and arterial blood pressure. The LVEDP may also be affected by respiration, especially during deep inspiration or during Valsalva or Mueller maneuvers, through changes in the left ventricular afterload, intrapericardial pressure, or right ventricular volume. Many diastolic properties of the left ventricle significantly influence the LVEDP, especially compliance of the left FG. 7 Left ventricular (LV) pressure on a scale of rnrnhg in a patient with coronary artery disease. Note the prominent atrial contribution to left ventricular end-diastolic pressure (LVEDP). t is not unusual to find marked elevation of LVEDP in patients with aortic stenosis and hypertrophic cardiomyopathy, despite a normal-sized left ventricle and a normal ejection fraction (Fig. 8). The atrial kick in these patients is very prominent. The pulmonary artery wedge pressure in some of these patients may be in the low to mid-20s or, occasionally, higher. These observations may explain the etiology of dyspnea on exertion as an early manifestation of the disease. Alterations in the afterload and preload undoubtedly affect LVEDP. Patients with dilated left ventricle, as in chronic mitral or aortic regurgitation, may maintain a normal LVEDP despite a large left ventricular cavity, because of a shift in the pressure-volume curve to the right and below. However, when the steep portion of the curve is approached, there will be a marked increase in the LVEDP, with minimal additional increase in the volume. Patients with acute mitral or aortic regurgitation, on the other hand, experience a dramatic, sudden- rise in LVEDP pulmonary edema develops because of sudden volume overloading. The rigid pericardium

5 32 Clin. Cardiol. Vol. 4, January 'Y- FG. 8 Left ventricular (LV) and aortic (Ao) pressures on a scale of mmhg in a patient with valvular aortic stenosis. An elevated left ventricular end-diastolic pressure (LVEDP) is evident. An LV-Ao gradient is present. FG. 9 Left ventricular (LV) and aortic (Ao) pressure tracings on a scale of mmhg in a patient with severe aortic insufficiency secondary to rheumatic heart disease. Note that the LV-Ao pressures equalize at end-diastole (arrows). FG. 10 Left ventricular (LV) pressure tracings on a scale of mmhg in a patient with coronary artery disease. The left ventricular end-diastolic pressure (LVEDP) is initially normal (control); however, with the onset of angina, an increase in LVEDP is noted. Also shown is ischemic ST depression in the electrocardiogram.

6 A. S. lskandrian et al.: Left ventricular end-diastolic pressure 33 in these patients may be partially responsible for preventing left ventricular dilatation (Fig. 9). A sudden rise in aortic pressure may also increase LVEDP. ncreases in the afterload in patients with aortic stenosis or obstructive hypertrophic cardiomyopathy may be contributory factors in the rise of LVEDP in these patients. Contractility of the left ventricle is certainly an important determinant of LVEDP. Patients with poor left ventricular function generally have elevated LVEDP. However, we have encountered a few patients with left ventricular ejection fractions as low as 10% with normal LVEDP. There are several possible mechanisms to explain the presence of a normal LVEDP in these patients; these include overdiuresis, change in the pressure-volume characteristics of the left ventricle, tachycardia, and, occasionally, the presence of atrial fibrillation. Patients with coronary artery disease during acute myocardial ischemia due to either angina pectoris or acute myocardial infarction have generally elevated LVEDP because of two main mechanisms: an increase in the stiffness of the left ventricle and depression of left ventricular function (Mann et al., 1977). Occasionally, the elevation would be of such magnitude that pulmonary edema may develop. Concomitant mitral regurgitation, due to papillary muscle dysfunction, may further exaggerate the changes in LVEDP. The additional effects on the pericardium and the right ventricle in such cases are still controversial, but may be important (Fig. 10). The angiographic materials currently used during left ventriculography and coronary arteriography produce a rise in LVEDP, even in normal individuals. Therefore, the level of LVEDP post angiography should be used with caution. We have found that some patients with severe coronary artery disease (usually those with left main or three-vessel disease) show a marked rise in LVEDP after left ventriculography. We have suggested that such a marked rise may produce or exaggerate myocardial ischemia through reduction in coronary blood flow (as a consequence of a decrease in the pressure gradient across the coronary vascular bed) (skandrian et al., 1980). The use of LVEDP in describing the Frank-Starling curve should be used with caution in disease states that alter the pressure-volume characteristics of the left ventricle. Even if such a use is justified, the LVEDP depicts one point on the curve; knowledge of the stroke volume or stroke work is required to describe the particular point on the left ventricular function curve. Conclusion Although LVEDP is a useful measurement in patients with various cardiac disorders, it should be emphasized that a normal LVEDP does not exclude left ventricular dysfunction (even a severe degree) nor can the presence of abnormal LVEDP be used to predict left ventricular dysfunction. t has been our impression that there is a need to educate the medical community, especially adult cardiologists, pediatric cardiologists, and cardiac surgeons, to the multiplicity of factors that affect the LVEDP and to emphasize that the clinical implication of LVEDP should be accepted only after a clear understanding of all the determinants that affect this measurement. References Bemis CE, Serur JR, Borkenhagen D, Sonnenblick EH, Urschel CW: nfluence of right ventricular filling pressure on left ventricular pressure and dimension. Circ Res 34,498 (1974) Braunwald E. Ross J Jr: Ventricular end-diastolic pressure: Appraisal of its volume in the recognition of ventricular failure in man (editorial). Am J Med 34, 147 (1963) Gaasch WH, Levine HJ. Quinones MA, Alexender JK: Left ventricular compliance: Mechanisms and implications. Am J Cardiol (1976) Grossman W, McLaurin LP: Diastolic properties of the left ventricle. Ann ntern Med 84, 316 (1976) lskandrian AS, Lichtenberg R. Segal BL, Kimbris D, Bemis CE, Mintz GS: Myocardial ischemia after left ventriculography: Pathophysiology and clinical significance. Carhet Cardiouasc Diagn 6, 17 (1980) Linhart JW, Hildner FJ, Barold SS, Samet P Myocardial function in patients with coronary artery disease. Am J Cardiol23,379 (1969) Mann T, Brodie BR, Grossman W, McLaurin LP: Effect of angina on the left ventricular diastolic pressure volume relationship. Circulation 55,761 (1977) Rahimtoola SH: Left ventricular end-diastolic and filling pressures in assessment of ventricular function (editorial). Chesr 63,858 (1973) Ross J Jr: Acute displacement of the diastolic pressure-volume curve of the left ventricle: Role of the pericardium and the right ventricle. Circulation 59,32 (1979) Shabetai R, Mangiardi L, Bhargava V, Ross J Jr, Higgins CB: The pericardium and cardiac function. Prog Cardiouasc Dis 12, 107 ( 1979)