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Microvascular, interstitial, and lymphatic interactions in normal heart
Insights
This study quantifies fluid exchange forces in the heart, revealing that increased interstitial hydrostatic pressure is key to preventing myocardial edema during venous pressure elevation. Lymph flow significantly rises with pressure.
Area of Science:
- Cardiovascular Physiology
- Myocardial Fluid Dynamics
- Edema Formation Mechanisms
Background:
- Control of transmicrovascular fluid exchange in the heart is vital for preventing myocardial edema.
- Understanding the forces and flows governing cardiac fluid balance is crucial.
Purpose of the Study:
- To quantify absolute values of forces and flows governing fluid balance in the normal heart.
- To determine the interrelationships between these variables under control and elevated venous pressure conditions.
Main Methods:
- Measured arterial pressure (Pa), coronary sinus pressure (Pcs), interstitial fluid pressure (Pint), plasma protein concentration (Cp), and oncotic pressures (tau cap, tau int).
- Recorded interstitial protein concentration (CL) and left ventricular lymph flow rate (Jv).
- Evaluated parameters under control conditions and during graded elevations in venous pressure.
Main Results:
- Control values: Pa (125 mmHg), Pcs (7.3 mmHg), Pint (14.9 mmHg), CL/Cp (0.82), Jv (7.0 ml/h).
- Elevating Pcs eightfold increased Pint to 50 mmHg and Jv sixfold.
- A filtration-independent CL/Cp value for total plasma protein was unobtainable; a washdown value for beta-lipoprotein was 0.04.
Conclusions:
- The heart's system relies on a substantial increase in interstitial hydrostatic pressure to limit edema.
- A large surface area of myocardial exchange vessels and less sensitive lymphatics contribute to this mechanism.
- This highlights the importance of hydrostatic pressure regulation in preventing cardiac edema.
Abstract:
Control of transmicrovascular fluid exchange in the heart is of critical importance in the prevention of myocardial edema formation. To quantify the absolute values for, and the interrelationships between, the forces and flows governing fluid balance within the normal heart, the following variables were measured: arterial pressure (Pa), coronary sinus pressure (Pcs), myocardial interstitial fluid pressure (Pint), plasma protein concentration (Cp), and oncotic pressure (tau cap) along with interstitial protein concentration (CL), interstitial oncotic pressure (tau int), and left ventricular lymph flow rate (Jv). All parameters were recorded under control conditions and during graded venous pressure elevations. Control values were Pa, 125 +/- 21 mmHg; Pcs, 7.3 +/- 1.3 mmHg; Pint, 14.9 +/- 3.1 mmHg; CL/Cp, 0.82 +/- 0.12; and Jv, 7.0 +/- 2.7 ml/h. As Pcs was elevated to eight times control, Pint increased from 15 to 50 mmHg and lymph flow rose sixfold. A filtration-independent value for CL/Cp could not be obtained for total plasma protein, although a washdown CL/Cp value for beta-lipoprotein of 0.04 was obtained. Our data indicate that a large surface area of myocardial exchange vessels coupled with lymphatics of relatively low sensitivity to extravascular volume expansion produce a system that relies on a large increase in interstitial hydrostatic pressure to limit edema formation.