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...

Forty-six patients with severe nonpenetrating brain injury [Glasgow Coma Scale (GCS) 4-7] were randomized to standard management at 37 degrees C (n = 22) and to standard management with systemic hypothermia to 32 to 33 degrees C (n = 24). The two groups were balanced in terms of age (Wilcoxon's rank sum test, p > 0.95), randomizing GCS (chi-square test, p = 0.54), and primary diagnosis. Cooling was begun within 6 h of injury by use of cooling blankets. Metocurine and morphine were given hourly during induction and maintenance of hypothermia. Rewarming was at a rate of 1 degree C per 4 h beginning 48 h after intravascular temperature had reached 33 degrees C. Muscle relaxants and sedation were continued until core temperature reached 35 degrees C. There were no cardiac or coagulopathy-related complications. Seizure incidence was lower in the hypothermia group (Fisher's exact text, p = 0.019). Sepsis was seen more commonly in the hypothermia group, but difference was not statistically significant (chi-square test). Mean Glasgow Outcome Scale (GOS) score at 3 months after injury showed an absolute increase of 16% (i.e., 36.4-52.2%) in the number of patients in the Good Recovery/Moderate Disability (GR/MD) category as compared with Severe Disability/Vegetative/Dead (SD/V/D) (chi-square test, p > 0.287). Based on evidence of improved neurologic outcome with minimal toxicity, we believe that phase III testing of moderate systemic hypothermia in patients with severe head injury is warranted.

Respiratory muscle fatigue is considered a common cause of weaning failure but its detection is hampered by the lack of a satisfactory diagnostic test. Abdominal paradox has been proposed as a valuable clinical index of fatigue and thus its presence may lead to curtailment of weaning trials. However, sensitivity and specificity of this sign as a predictor of weaning outcome is unknown. We hypothesize that abnormal ribcage-abdominal (RC-Ab) motion is a common finding in the early stages of weaning and its presence does not inevitably imply an unsuccessful weaning outcome. We tested this hypothesis in patients undergoing a weaning trial: one group had a successful weaning outcome and were extubated (n = 10) and the other group failed the trial (n = 7). Normal RC-Ab motion was separately characterized in 17 healthy subjects. Employing a calibrated respiratory inductive plethysmograph, quantitative assessment of asynchrony and paradox was obtained by computing several indices from series of breaths at fixed time periods using the Konno-Mead method of analysis. During the weaning trial, both groups of patients displayed significant increases in asynchrony and Ab paradox compared to normal values. As a group, patients who failed the trial displayed significantly greater asynchrony and paradox of the RC and Ab than patients with a successful outcome. However, there was considerable overlap between the individual patients in the 2 study groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Our data suggest that current clinical CPB management impacts postoperative renal function. We found that patients with normal preoperative renal function who developed postoperative ARF had longer CPB duration, lower CPB perfusion flow, and longer periods on CPB at pressures < 60 mmHg compared to patients with no post CPB ARF. However, our data do not allow us to separate these CPB-related factors from the potential influence of perioperative low cardiac output syndrome as a cause for postoperative ARF. Thus, future clinical studies are required to elucidate CPB-induced ARF and to optimize CPB management for ARF prevention.