Congestive heart failure following chronic tachycardia

The mechanics of left ventricular contraction were analyzed in quantitative terms from isovolumic contractions in six dogs in which congestive heart failure developed following 13 to 29 days of chronic pacemaker-induced ventricular tachycardia. Twenty-four hours following cessation of stimulation, heart failure was evidenced in the intact sedated dogs by elevated left ventricular end-diastolic pressures (average, 28 mm. Hg), ascites, and the presence of a protodiastolic gallop sound. Aortic pressure, heart rate, and the ratio of stroke volume to end-diastolic volume were decreased while the ratio of left ventricular mass to body weight was unchanged, and cardiac output was increased, presumably secondary to hypervolemia. Left ventricular function was substantially reduced, contractile element velocity-tension relations were altered, and V_max was significantly reduced (failure 2.37 ± 0.40 circumferences per second vs. control 3.0 ± 0.03). The maximum isovolumic tension development for any given end-diastolic volume also was decreased in five of six animals. Left ventricular myocardial stores of creatine, creatine phosphate, and adenosine triphosphate were significantly depressed. These findings indicate that the syndrome of heart failure following chronic tachycardia, characterized by elevated left ventricular end-diastolic pressure and ascites, is associated with significant depression of the left ventricular contractile state and total energy stores.     

Left ventricular function in patients under peritoneal dialysis treatment

M-Mode echocardiogram and systolic time intervals were obtained in 24 patients with end-stage chronic renal failure before and after peritoneal dialysis in order to evaluate their left ventricular function. Before dialysis 9 patients (group A) showed an echocardiographic pattern of dilated cardiomyopathy, i.e. increased left ventricular end-diastolic dimension (EDD) and volume (EDV), reduction of fractional shortening (FS%), of circumferential fiber shortening (Vcf) and of ejection fraction (EF). Seven patients (group B) had the morphological and functional features of asymmetric septal hypertrophy: ratio of interventricular septum to posterior wall thickness (IVS/PWT) greater than 1.3, reduced EDD and EDV. Eight uraemics (group C) had no specific feature of cardiac disease, but only aspecific echocardiography signs of myocardial derangement. Peritoneal dialysis appeared to be associated with gradual improvement of the contractile state in group A patients, with reduction in echocardiographic asymmetric septal hypertrophy in group B uraemics, and with an aspecific increase in cardiac performance in group C patients. It is concluded that: end-stage chronic renal failure may have echocardiographic pattern of dilated or asymmetric hypertrophic cardiomyopathy; peritoneal dialysis significantly improves the morphological and functional derangements of both clinical conditions.     

Congestive Renal Failure: The Pathophysiology and Treatment of Renal Venous Hypertension

Longstanding experimental evidence supports the role of renal venous hypertension in causing kidney dysfunction and “congestive renal failure.” A focus has been heart failure, in which the cardiorenal syndrome may partly be due to high venous pressure, rather than traditional mechanisms involving low cardiac output. Analogous diseases are intra-abdominal hypertension and renal vein thrombosis. Proposed pathophysiologic mechanisms include reduced transglomerular pressure, elevated renal interstitial pressure, myogenic and neural reflexes, baroreceptor stimulation, activation of sympathetic nervous and renin angiotensin aldosterone systems, and enhanced proinflammatory pathways. Most clinical trials have addressed the underlying condition rather than venous hypertension per se. Interpreting the effects of therapeutic interventions on renal venous congestion are therefore problematic because of such confounders as changes in left ventricular function, cardiac output, and blood pressure. Nevertheless, there is preliminary evidence from small studies of intense medical therapy or extracorporeal ultrafiltration for heart failure that there can be changes to central venous pressure that correlate inversely with renal function, independently from the cardiac index. Larger more rigorous trials are needed to definitively establish under what circumstances conventional pharmacologic or ultrafiltration goals might best be directed toward central venous pressures rather than left ventricular or cardiac output parameters.     

Myocardial depression in shock: A survey of cardiodynamic studies

The question as to whether myocardial depression occurs in hemorrhagic shock and, if so, its importance was reinvestigated. For this purpose the cardiodynamic changes which occur after simple hemorrhage, during prolonged hypotension (50 to 30 mm. Hg), during reinfusion of all the withdrawn blood, and during spontaneous circulatory failure following infusion, were studied in the same animal. In different series of experiments in which the same standard technique was used, we studied changes in calibrated arterial pressure pulses, cardiac output by a modified Stewart method, alterations in effective venous pressure, ventricular volume and pressure curves, inferior vena cava flow, and electrocardiograms by standard and chest leads.Following simple hemorrhage sufficient to reduce mean arterial pressure to 50 mm. Hg, the changes in ventricular action are all secondary to reduction in venous return and decrease in effective central venous pressure. Electrocardiograms reveal no significant changes. Changes in the contour of the central arterial pulse consist in abridgement of the period of systolic ejection and development of a primary spike followed by a peaked summit, and this is followed by a deep incisura. As a result of decreased venous pressure, ventricular filling is slower, initial tensions decrease in both ventricles, and their diastolic size is smaller. Pressure and volume curves indicate that the ventricles expel their diminished volumes with good velocity.If severe posthemorrhagic hypotension is prolonged for 135 minutes, death results from an oligemic type of failure unless blood is reinfused. However, such reinfusion is of only temporary benefit; a slow spontaneous circulatory failure and eventually death follow. Irreversibility develops during the period of prolonged hypotension. This includes depression of the myocardium, for while venous return continues to decrease slightly, effective venous and initial ventricular pressures return to or above control levels and the diastolic size of the ventricles augment. Nevertheless, the stroke volume and cardiac output decrease. Myocardial depression is further indicated by a subminimal stroke volume when venous pressures are elevated to normal levels and by development of S-T depression in electrocardiograms.Reinfusion of blood restores arterial pressures and pulses as well as cardiac output to normal, but in order to do so the ventricles are required to operate under supernormal conditions of high venous pressure and initial tensions. As soon as these re-establish at normal levels, cardiac output decreases, and the ventricles pump less efficiently due to a depressed state of the myocardium. As arterial pressure declines to ca. 70 mm. Hg, reduction in venous return becomes so great that the myocardial depression is obscured but is detectable by special tests. A progressive circulatory failure develops despite the fact that blood volumes are not significantly decreased. This represents a form of normovolemic shock due solely to default of the peripheral circulation and of the myocardium. The preduction of venous return is of paramount importance, but circulatory failure is hastened by coexistent myocardial depression.Since the functional state of the myocardium and the capacity of the coronary responses at the time of shock-producing catastrophies may often be below par, myocardial depression may play as significant a subsidiary role in some cases of human shock as it did in our animals submitted to a particular type of hemorrhage and shock. The problem deserves further careful exploration by cardiologists.     

Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.     

Cardiac tamponade. Report of a case after insertion of transvenous endocardial electrode

The effects of acute myocardial infarction on hemodynamics and cardiopulmonary volumes were studied in two groups of anesthetized closed-chest dogs: a non-shock group (intracoronary thrombus obstruction) and a shock group (intracoronary microspheres). Moderate blood volume expansion was carried out with donor dog blood and the effects were compared with those in a group of normal dogs.The shock dogs had greater decreases in cardiac output and left ventricular work than the non-shock group. In neither were true cardiopulmonary volume or LV end-diastolic volume increased over controls at two hours. With moderate blood volume expansion, improvement in Frank-Starling performance occurred in the infarct dogs with no significant changes in cardiac output or work among the normal dogs.In experimental myocardial infarction, blood volume expansion therefore improved cardiac performance independent of prior reductions in ventricular or central blood volume as a result of infarction. However, such benefits must be weighed against the threat of pulmonary edema with rising LV end-diastolic pressures and possible increased oxygen costs accompanying the increases in cardiac output and left ventricular work.     

Cardiac performance in rats with renal hypertension.

To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.     

Regional vascular adjustments during recovery from myocardial infarction in rats

Left ventricular function and systemic regional blood flow (radioactive microspheres, 15 +/- 5 mu) were studied 1, 3, 10 or 42 days after left coronary occlusion in conscious rats. One day after coronary occlusion, vascular resistance in the skeletal muscle and cutaneous beds increased while stroke work and left ventricular systolic pressure were depressed. Regional blood flow and hemodynamic data were similar for sham and infarction groups at 3 and 10 days after surgery, except for left ventricular end-diastolic pressure, which was significantly increased in rats with infarction (sham versus infarct: 11.5 +/- 1.0 versus 18.4 +/- 3.2 at day 3 and 12.2 +/- 1.4 versus 19.9 +/- 3.2 at day 10) (p less than 0.05). At 42 days after myocardial infarction, manifest heart failure occurred as documented by decreased cardiac output and left ventricular systolic pressure and elevated left ventricular end-diastolic pressure and vascular resistance in the cutaneous, skeletal muscle and renal beds. In a separate group of animals with moderate (33.2 +/- 2% of left ventricle) and large infarctions (45 +/- 1.3% of left ventricle), regional blood flow was compared with the sham group. Rats with a large infarct demonstrated significant (p less than 0.05) reduction in flow to kidney, gut and liver. In rats with a medium sized infarct, only renal blood flow was significantly reduced. It is concluded that in this model of myocardial infarction, early cardiocirculatory depression is followed by a partially compensated state with increased left ventricular end-diastolic pressure and subsequent systemic and regional vasoconstriction which, in turn, may contribute to late deterioration of heart failure.     

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.     

Hemodynamic effects of nitroprusside on cardiovascular system

The effects of nitroprusside (NP) on hemodynamics, especially on venous flow velocity of the inferior vena cava (IVC) were evaluated in 20 remote myocardial infarction patients. NP was given beginning at 10 micrograms/min, with subsequent increments of 10 micrograms/min every 5 minutes until the systolic blood pressure was reduced to about 30 mmHg. Pressure was measured by a catheter-tip micromanometer. Flow velocity of IVC was measured by a catheter-tip flow velocity probe. NP significantly decreased left ventricular systolic pressure, left ventricular end-diastolic pressure, mean aortic pressure, right ventricular systolic pressure, right ventricular end-diastolic pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure, systemic vascular resistance index (SVRI) and left ventricular volume. Cardiac index (CI) was unchanged and stroke volume index was decreased. IVC pressure was unchanged, while right atrial (RA) pressure decreased. Subsequently, the pressure difference between IVC and RA increased significantly. The amplitude of IVC flow velocity decreased significantly. Twenty patients were classified into two groups according to whether or not the CI increased by NP. CI increased in 9 patients (group I) and decreased in 11 patients (group D). Compared to group D, control CI and the slope of end-systolic pressure-volume relation were less and the difference between IVC pressure and RA pressure was greater in group I. The patients with higher control SVRI had greater increase in CI during NP. In our study, the greater the depression of cardiac performance and the higher the SVRI, the greater the improvement of left ventricular pumping function during NP.     

Isosorbide dinitrate and intra-aortic balloon pumping in preinfarctional angina. Effects on central circulatory dynamics.

The dynamics of the central circulation were measured by a radionuclidic technique in 18 men with high-risk preinfarctional angina who received therapy with isosorbide dinitrate (n equals 18), intra-aortic balloon pumping (n equals 8), or both (n equals 8). Administration of 5 mg of isosorbide dinitrate sublinqually was associated with a reduction in stroke volume index (SVI), cardiac index (CI), systemic arterial blood pressure, and left ventricular end-diastolic volume (LVEDV) and with increased left ventricular ejection fraction (LVEF). Intra-aortic balloon pumping did not alter SVI or CI, but decreased systolic blood pressure and LVEDV and increased LVEF and diastolic blood pressure. The combination of therapy with isosorbide dinitrate and intraaortic balloon pumping resulted in decreased SVI, systolic blood pressure, and LVEDV and increased LVEF. Thus, therapy with isosorbide dinitrate reduced left ventricular preload, and intra-aortic balloon pumping reduced blood pressure, which resulted in a decreased LVEDV and an increase in LVEF. Therapy with isosorbide dinitrate and intra-aortic balloon pumping act to alter central circulatory dynamics in favor of reducing myocardial oxygen demand.     

Role of circulatory congestion in the cardiorespiratory failure of obesity.

The role of circulatory congestion in the cardiorespiratory dysfunction of massive obesity was investigated in 18 patients. They were hypervolemic and had increased cardiac outputs proportionate to their weight. The average resting left ventricular filling pressure was within the upper limits of normal, but it increased to abnormally high levels with increased venous return of passive leg raising, and further during exercise. The elevations in pressure were associated with high resting central blood volumes which increased significantly with exertion. These findings are consistent with reduced distensibility of the central circulation in these congested patients. Weight reduction was accompanied by a decrease in central blood volumes and restoration of a normal left ventricular response in three of four patients and a return toward normal in one. The improvement in ventricular function with relief of edema and dyspnea. In 14 patients with normal or only minimal alveolar hypoventilation, there were no significant transpulmonary diastolic pressure gradients despite a marked increase in left ventricular end-diastolic pressures. One patient, after regaining weight, subsequently had an abnormal gas exchange and an increased pulmonary vascular resistance. He and two others with severe alveolar hypoventilation demonstrated cor pulmonale on a background of left ventricular dysfunction and congestion of the circulation. Two other patients, the least obese of the group, had hypoventilation and cor pulmonale with normal left ventricular pressures. Hypervolemia and a hyperdynamic state are common features of the obese patients. High cardiac output is maintained despite marked circulatory congestion which may result in generalized anasarca and increased ventricular filling pressures. This clinical syndrome may be present in obese patients without intrinsic heart disease and may be reversible with weight reduction. The central circulatory congestion may contribute to the development of the alveolar hypoventilation syndrome in certain obese patients.     

Effect of chronic rapid ventricular pacing on total vascular capacitance.

BACKGROUND. Rapid right ventricular pacing (RRVP) at 250 bpm for 3-6 weeks produces chronic heart failure manifested by a reduction in cardiac output and increases in right atrial, pulmonary artery, and capillary wedge pressures. METHODS AND RESULTS. One week after splenectomy and pacemaker placement, vascular capacitance, unstressed volume, and compliance were determined in 19 anesthetized dogs from pressure-volume curves using transient circulatory arrests induced by acetylcholine. Nine dogs were restudied 31 +/- 1 days later without RRVP, and 10 dogs underwent RRVP at 250 bpm and were restudied at 23 +/- 8 and 38 +/- 8 days in cardiac failure and after 1 and 2 weeks of postpacing recovery. Control animals had no changes in vascular capacitance or compliance. Dogs undergoing RRVP exhibited a marked increase in mean circulatory filling pressure (5.4 +/- 0.4 to 10.5 +/- 1.5 mm Hg) during the development of cardiac failure with a reduction in unstressed volume (81.9 +/- 5.7 to 43.9 +/- 8.1 ml.kg-1) without changing total vascular compliance. Total blood volume decreased (95.4 +/- 6.2 to 66.7 +/- 6.5 ml.kg-1) primarily due to a reduction in packed cell volume. The pressure gradient for venous return and overall venous resistance was unaltered. Central blood volume as a proportion of total blood volume increased (9.3 +/- 1.7% to 16.0 +/- 2.7%). Arterial compliance and capacity and pulmonary vascular compliance were reduced. In the 2-week postpacing period, except for a reduced cardiac response to a volume load, all of these parameters returned to baseline values. CONCLUSIONS. Chronic RRVP induced cardiac failure with a marked reduction in total vascular capacitance due to a reduction in unstressed volume without altering compliance. The rise in mean circulatory filling pressure was limited by a reduction in total blood volume.     

Functional state of the left ventricle in patients who have had a myocardial infarct according to ultrasonic scanning data

In most patients who had suffered from myocardial infarction 3 1/2 to 12 months (7.6 months on the average) previously and had no clinical symptoms of circulatory insufficiency, ultrasonic scanning of the heart showed normal stroke volume and stroke index, and normal minute volume and cardiac index against the background of low indices of left ventricular contractility function (ejection fraction, % delta S, VcF) and large end-diastolic and end-systolic left ventricular volumes. Normal stroke ejection was achieved due to an increase of the end-diastolic volume, the decrease in the contractility of the left ventricular was thus compensated for with the participation of the Frank-Starling mechanism.     

Experimental myocardial infarction. IX. Efficacy of hyperbaric oxygenation in ventricular failure after coronary occlusion in intact conscious dogs

In this study of the efficacy of hyperbaric oxygenation in the therapy of left ventricular failure after experimental myocardial infarction, 6 intact dogs underwent a 20 minute control period of exposure to 100 percent oxygen at 3 atmospheres absolute of pressure. The procedure increased arterial PO₂ to more than 1,600 mm Hg and mean aortic pressure by 8 percent (0.05 <P < 0.10); left ventricular end-diastolic pressure increased from 8.0 to 9.7 mm Hg (P < 0.05) without change in heart rate, cardiac output, stroke volume, left ventricular minute work, stroke work or total peripheral resistance. One hour later, coronary occlusion was produced and resulted in left ventricular failure, manifested by an increase in heart rate and left ventricular end-diastolic pressure and by a fall in stroke volume and stroke work. Ten minutes after occlusion, the dogs underwent a second hyperbaric exposure period, and mean aortic pressure increased by 9 percent (0.05 <P < 0.10), left ventricular minute work by 9 percent (P < 0.01) and stroke work by 17 percent (0.05 <P < 0.10). The increased work was performed at the expense of an increase in left ventricular end-diastolic pressure from 13.1 to 17.4 mm Hg (P < 0.01). Other variables remained stable. An additional 8 dogs that underwent coronary occlusion while breathing room air had stable hemodynamic values over the ensuing hour except for a progressive increase in left ventricular end-diastolic pressure. It is concluded that hyperbaric oxygenation did not improve left ventricular function impaired by experimental myocardial infarction in intact, conscious dogs, even though given at a time when the ischemic lesion was potentially reversible.     

Insulin-like growth factor I improves cardiovascular function and suppresses apoptosis of cardiomyocytes in dilated cardiomyopathy.

To investigate how insulin-like growth factor I (IGF-I) modulates cardiovascular function and myocardial apoptosis in heart failure, the therapeutic effects of IGF-I were determined in a canine model of dilated cardiomyopathy. The animals were paced at 220 beats/min, and the left ventricular (LV) chamber became dilated after 2 weeks. A subset of paced dogs was treated with s.c. injections of IGF-I from week 3 to week 4. After 4 weeks of pacing, untreated paced dogs developed significant ventricular dysfunction. IGF-I-treated paced dogs showed better cardiac output, stroke volume, LV end-systolic pressure, and LV end-diastolic pressure. Moreover, pulmonary wedge pressure and systemic vascular resistance were increased in the untreated group and decreased in the IGF-I-treated group. IGF-I treatment was associated with less thinning of the ventricular wall. Compared with the controls, untreated paced dogs showed increased apoptosis of cardiac muscle cells, which was partially suppressed by IGF-I treatment. The myocardial apoptotic index was negatively related to the thickness of the ventricular wall and to cardiac output, suggesting that ventricular remodeling/dysfunction involves the occurrence of myocardial apoptosis. Due to the close resemblance between this experimental model of dilated cardiomyopathy and human heart failure, the results of this study provide evidence that IGF-I may be a potential therapeutic agent for the failing human heart.     

Effects of glucose-insulin-potassium (GIK) on myocardial blood flow and metabolism in canine endotoxin shock

Glucose-insulin-potassium (GIK) has beneficial effects during endotoxin shock, possibly through improvement of myocardial function, but the mechanism is not clear. We have studied the effects of GIK on left ventricular function, coronary flow, and oxygen consumption in controls and dogs treated with endotoxin (1.5 mg/kg-1). The animals were anaesthetized (etomidate 4 mg/kg-1/hr-1) and ventilated (N2O:O2 = 2:1). We have measured left ventricular pressure, left ventricular end-diastolic pressure (LVEDP) and LVdP/dt, systemic blood pressure, cardiac output (CO; thermodilution), coronary blood flow (CBF; radioactive microspheres), and oxygen content and lactate in arterial and coronary sinus blood. Endotoxin caused a rapid fall of CO and blood pressure with a temporary recovery followed by gradual circulatory collapse. GIK infusion (50% glucose, 2 g/kg-1 bw, 8 mmol KCl, and 3 U insulin/kg-1 bw) increased CO (56%), CBF (61%), blood pressure (21%), LVEDP (77%), and LVdP/dt (28%), and systemic vascular resistance decreased (23%). Stroke work (80%) and tension time index (42%) decreased during shock, but GIK temporarily improved these variables. The ratio of stroke work, respectively tension time index to oxygen consumption, suggests that myocardial efficiency decreased during shock and improved after GIK. Endotoxin decreased the ratio of endo- to epicardial flow. GIK did not change this ratio. However, for the same endo to epi ratio, increased CBF implies increased flow to endocardium.     

Quantitative two-dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement

In 14 patients requiring aggressive therapy for circulatory failure resulting from massive pulmonary embolism, hemodynamic and two-dimensional echocardiographic data were obtained at bedside (acute phase) and again after circulatory improvement (intermediate phase) and during recovery. The acute stage was characterized by a low cardiac output state despite inotropic support (cardiac index 1.9 +/- 0.6 liters/min per m2) associated with increased right atrial pressure (12.4 +/- 4.2 mm Hg), increased right ventricular end-systolic and end-diastolic area (12.4 +/- 3.4 and 15.4 +/- 4.1 cm2/m2, respectively) and reduced right ventricular fractional area contraction (20.1 +/- 8.6%). Two-dimensional echocardiography also revealed interventricular septal flattening at both end-systole and end-diastole and markedly decreased left ventricular end-diastolic dimensions. Left ventricular fractional area contraction remained normal. Hemodynamic improvement occurred during the intermediate phase as shown by restoration of cardiac index (3.3 +/- 0.6 liters/min per m2), decrease in right atrial pressure (8.3 +/- 4.8 mm Hg), reduction in right ventricular end-systolic area (9.0 +/- 3.6 cm2/m2 at the intermediate stage and 6.1 +/- 1.8 cm2/m2 at recovery) and end-diastolic area (10.5 +/- 3.6 cm2/m2 at the intermediate stage and 8.9 +/- 2.9 cm2/m2 at recovery) and improvement in right ventricular fractional area contraction (31.5 +/- 16.4%). The interventricular septum progressively returned to a more normal configuration at both end-systole and end-diastole, and left ventricular diastolic dimension steadily increased. It is concluded that circulatory failure secondary to massive pulmonary embolism was mediated through a profound decrease in left ventricular preload, resulting from both pulmonary outflow obstruction and reduced left ventricular diastolic compliance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute myocardial infarction complicated by left ventricular dysfunction and respiratory failure. The effects of continuous positive airway pressure

The cardiopulmonary effects of continuous positive airway pressure (CPAP) were studied in 14 patients with acute myocardial infarction complicated by circulatory and respiratory failure. Cardiac performance, lung mechanics, and gas exchange were assessed during 50 percent mechanical ventilatory support at end-expiratory airway pressure levels of 0, 5, 10, and 15 mm Hg. The increase in airway pressure resulted in significantly improved arterial blood oxygenation (p less than 0.001) and in a substantial reduction in the spontaneous respiratory effort (p less than 0.001). We observed a slight decrease in stroke volume index (p less than 0.05) with increasing airway pressure in patients who had moderate left ventricular dysfunction, and a trend of improvement (NS) in those who had severe pump failure. Relatively high levels of CPAP can be used to improve pulmonary function in patients with acute myocardial infarction and left ventricular failure. In fact, circulatory depression is less likely to occur when cardiac performance is poor.     

Mechanisms of decreased left ventricular preload during continuous positive pressure ventilation in ARDS

Continuous positive pressure ventilation is associated with a reduction in left ventricular preload and cardiac output, but the mechanisms responsible are controversial. The decrease in left ventricular preload may result exclusively from a decreased systemic venous return due to increased pleural pressure, or from an additional effect such as decreased left ventricular compliance. To determine the mechanisms responsible, we studied the changes in cardiac output induced by continuous positive pressure ventilation in eight patients with the adult respiratory distress syndrome. We measured cardiac output by thermodilution, and biventricular ejection fraction by equilibrium gated blood pool scintigraphy. Biventricular end-diastolic volumes were then calculated by dividing stroke volume by ejection fraction. As positive end-expiratory pressure increased from 0 to 20 cm H2O, stroke volume and biventricular end-diastolic volumes fell about 25 percent, and biventricular ejection fraction remained unchanged. At 20 cm H2O positive end-expiratory pressure, volume expansion for normalizing cardiac output restored biventricular end-diastolic volumes without markedly changing biventricular end-diastolic transmural pressures. The primary cause of the reduction in left ventricular preload with continuous positive pressure ventilation appears to be a fall in venous return and hence in right ventricular stroke volume, without evidence of change in left ventricular diastolic compliance.