No abstract

We hypothesized that both acute and chronic accumulation of myocardial interstitial edema (extravascular fluid [EVF]) would compromise cardiac function. We also postulated that excess fluid within the myocardial interstitial space would potentiate interstitial fibrosis, thus further compromising function. Dogs were divided into three groups: 1) control, 2) chronic pulmonary hypertensive with right heart failure, and 3) chronic arterial hypertensive. The quantity of EVF, expressed as the unitless blood-free (wet weight-dry weight)/dry weight ratio, and interstitial fibrosis (collagen content) were determined and correlated with cardiac function at baseline and after acute elevation of coronary venous pressure and reduction of cardiac lymph flow. Control EVF was 2.90±0.20 (mean±SD), which increased to 3.45±0.16 after acute (3-hour) elevation of coronary sinus pressure. This EVF significantly compromised cardiac function. The EVF in chronically hypertensive dogs and in dogs with chronic right heart pressure elevations was 3.50+0.30 and 3.50±0.08, respectively. End-diastolic left ventricular interstitial fluid pressure increased from a control value of 14.9+3.1 (at EVF=2.9) to 24.8+3.7 (at EVF=3.5).An EVF of 3.5 produced -30% reduction of the heart's ability to maintain cardiac output at a left atrial pressure of 15 mm Hg. The compromised function in these chronic models is exacerbated after acute elevation of coronary venous pressure and reduction of cardiac lymph flow. Collagen levels were elevated by at least 20% in the chronic hypertensive dogs and in the nonhypertrophied left ventricles of dogs with chronic right heart pressure elevation. We conclude that acute myocardial edema compromises cardiac function and that chronic right heart pressure elevation and chronic arterial hypertension produce left ventricular myocardial edema, which also compromises function in these common pathological conditions. The presence of myocardial edema in these chronic models also potentiates interstitial fibrosis, leading to a further decrease in the heart's ability to function normally. (Circulation Research 1991;68:1713- has also been shown to stimulate fibrosis within the myocardial interstitial matrix.9-1' The increased deposition of collagen within the myocardial interstitial space during chronic arterial hypertension and ventricular hypertrophy compromises cardiac function.12 We believe this deposition of collagen may result from the combined effects of cardiac interstitial remodeling during hypertrophy and the presence of small volumes of myocardial edema.6'13 We hypothesized that acute and chronic accumulation of myocardial edema could directly compromise cardiac function in a predictable manner. We also postulated that myocardial fibrosis secondary to small volumes of chronic edema could diminish the heart's ability to function normally. Both the presence of myocardial edema and the edema-induced deposition of interstitial matrix material could increase myocardial stiffness, increase oxygen diffusion distances, and alte...

The heart, perhaps more than any other organ, is exquisitely sensitive to increases in microvascular permeability and the accumulation of myocardial interstitial oedema fluid. Whereas some organs can cope with profound increases in the interstitial fluid volume or oedema formation without a compromise in function, heart function is significantly compromised with only a few percent increase in the interstitial fluid volume. This would be of little consequence if myocardial oedema were an uncommon pathology. On the contrary, myocardial oedema forms in response to many disease states as well as clinical interventions such as cardiopulmonary bypass and cardioplegic arrest common to many cardiothoracic surgical procedures. The heart's inability to function effectively in the presence of myocardial oedema is further confounded by the perplexing fact that the resolution of myocardial oedema does not restore normal cardiac function. We will attempt to provide some insight as to how microvascular permeability and myocardial oedema formation compromise cardiac function and discuss the acute changes that might take place in the myocardium to perpetuate compromised cardiac function following oedema resolution. We will also discuss compensatory changes in the interstitial matrix of the heart in response to chronic myocardial oedema and the role they play to optimize myocardial function during chronic oedemagenic disease.

Intra-abdominal fluid volume and hydrostatic pressure were elevated by positive pressure infusion of Tyrode solution into the peritoneal cavity of anesthetized dogs. The compliance of the peritoneal cavity fell from 10.8 to 0.56 ml X mmHg-1 X kg-1 of body wt as intra-abdominal pressure increased from 0 to 40 mmHg. Intrathoracic pressure also increased as elevated peritoneal pressure caused diaphragmatic bulging. Cardiac output and stroke volume were reduced by 36% after an intra-abdominal pressure rise of 40 mmHg; in contrast, heart rate did not change. Flow in the celiac, superior mesenteric, and renal arteries was reduced by 42, 61, and 70%, respectively. Pressure in the femoral vein increased to 46 mmHg, while flow in the femoral artery decreased by 65%. Whole-body O2 consumption, pH, and arterial PO2 decreased as intra-abdominal pressure rose. The peritoneal cavity, with its high initial compliance, affords the body an ideal location for the temporary accumulation of small to moderate volumes of fluid during episodes of increased vascular pressure or permeability. The marked alterations in the hemodynamic properties of the cardiovascular system are indicative of the physiological changes that occur when intra-abdominal fluid accumulation becomes excessive and peritoneal pressure rises to high levels.

Fluid accumulation in the cardiac interstitium or myocardial edema is a common manifestation of many clinical states. Specifically, cardiac surgery includes various interventions and pathophysiological conditions that cause or worsen myocardial edema including cardiopulmonary bypass and cardioplegic arrest. Myocardial edema should be a concern for clinicians as it has been demonstrated to produce cardiac dysfunction. This article will briefly discuss the factors governing myocardial fluid balance and review the evidence of myocardial edema in various pathological conditions. In particular, myocardial microvascular, interstitial, and lymphatic interactions relevant to the field of cardiac surgery will be emphasized.