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Contribution of External Forces to Left Ventricular Diastolic Pressure: Implications for the Clinical Use of the Starling Law

Kent Dauterman, MD; Peter H. Pak, MD; W. Lowell Maughan, MD; Amit Nussbacher, MD; Sigemituzo Arie, MD; Chun-Peng Liu, MD; and David A. Kass, MD
[+] Article and Author Information

From the Johns Hopkins Medical Institutions, Baltimore, Maryland. Instituto di Coracao, Sao Paolo, Brazil. Veterans General Hospital, Taipei, Taiwan. Requests for Reprints: David A. Kass, MD, Division of Cardiology, Carnegie 530, Johns Hopkins University Hospital, 600 North Wolfe Street, Baltimore, MD 21287. Grant Support: In part by National Public Health Service Grants HL-47511 and AG-12249; the American Heart Established Investigator Award (Dr. Kass); the Merck Clinician Scientist Award (Dr. Pak); and a grant from Academica Sinica (Dr. Liu).


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1995;122(10):737-742. doi:10.7326/0003-4819-122-10-199505150-00001
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Objective: To test whether a substantial proportion of measured resting left ventricular diastolic pressure stems from forces external to the left ventricle (such as right-heart filling) in normal and chronically diseased hearts.

Design: Nonrandomized study with single intervention.

Setting: University hospital.

Patients: 29 patients referred for cardiac catheterization who had normal left ventricles and ejection fractions (n = 12); chronic heart disease due to idiopathic dilated cardiomyopathy (n = 6); ischemic heart disease (n = 6); or left ventricular hypertrophy (n = 5).

Intervention: Acute reduction of external forces imposed on the left ventricle using balloon obstruction of inferior vena caval inflow to the right heart.

Measurements: Continuous catheter-derived left ventricular pressure-volume data before and after abrupt obstruction of inferior vena caval inflow. Diastolic pressures were measured at the same volume just before atrial systole before and after sudden decrease of external (right-heart and pericardial) forces. The resulting decline in pressure was a measure of the contribution of these external forces to resting left ventricular diastolic pressure.

Results: The decline in pressure when external forces were released averaged −19%±13% with minimal change in left ventricular end-diastolic volume ( −3.66%±6.7%) and cardiac output ( −5%±8%). In all patients combined, the decline in pressure when external forces (Delta Pd) were released correlated with resting left ventricular diastolic pressure (LVPd) given by: Delta Pd = 0.38 x (LVPd − 6) (r = 0.86, P < 0.0001). This indicates that when resting diastolic pressure was more than 6 mm Hg, almost 38% of the pressure was due to external factors. This percentage was similar among all subgroups. Furthermore, the left ventricular diastolic pressure could be reduced by this percentage with only minimal compromise to ventricular filling and cardiac output.

Conclusions: A substantial proportion of measured resting left ventricular diastolic pressure stems from forces extrinsic to the left ventricle rather than from diastolic stiffness in the left ventricle itself. This markedly influences the dependence of cardiac output on filling pressure and has important implications for clinical application of the Starling law.

Figures

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Figure 1.
Measurement of the contribution of external forces to resting left ventricular diastolic pressures.dd

A. Stable resting left ventricular pressure-volume loop. End-diastolic pressure is shown at the lower right corner (●). The diastolic pressure-volume boundary forms the lower side of the loop. B. After obstruction of inferior vena caval inflow. Downward shift of the left ventricular diastolic pressure-volume relation is indicated by dashed loop. C. With continued obstruction of inferior vena caval inflow. D. By subtracting the pressure from the diastolic pressure-volume relation from that at an identical volume on the initial resting pressure-volume loop, this downward shift is quantified (Delta P ); Delta P reflects the component of initial resting pressure that is not due to filling of the left ventricle per se but that stems from forces extrinsic to the left ventricle. DPVR = diastolic pressure-volume relation.

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Figure 2.
Relation between initial resting left ventricular diastolic pressure (LVPd) and the component of this pressure that is due to external forces (Delta Pd).

Four groups of patients are shown: patients with normal hearts (◆), those with hypertrophic cardiomyopathy ▿), those with dilated cardiomyopathy (■), and those with ischemic heart disease (●). The data fell along a single relation that was well fit by linear regression. The slope (0.38) indicates that above an initial pressure of 6 mm Hg, 38% of the resting left ventricular diastolic pressure was due to forces external to the left ventricle.

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Figure 3.
Implication of external contributions to the resting left ventricular diastolic pressure on clinical application of the Starling Law.ddd

Reducing the resting left ventricular diastolic pressure (LVP ) by 19% was principally achieved by removing the extrinsic forces contributing to this resting pressure. This occurred with almost no change in either left ventricular end-diastolic volume (EDV) or cardiac output (CO). However, after these external forces were removed, there was a much tighter correspondence between changes in LVP and EDV and therefore between CO and (according to the Starling law). Lowering LVP by an additional 19% (total decrease, −38%)would require a marked reduction in cardiac filling, corresponding to an almost 60% decrease in CO.

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