Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEMODYNAMICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1987

Arterial vasodilator, systemic and coronary hemodynamic effects of nisoldipine in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

The systemic and coronary hemodynamic and neurohumoral effects of nisoldipine, a calcium antagonist drug with high vascular specificity, were investigated in 17 patients with chronic congestive heart failure (CHF). Brachial artery infusions (n = 9) decreased forearm vascular resistance in a dose-dependent manner, attesting to its powerful arterial vasodilator properties. A dose of 3 micrograms/kg intravenously decreased mean blood pressure 16% and systemic vascular resistance 33%, while increasing stroke index 19% and ejection fraction 21% at rest and similarly during exercise. Pulmonary capillary wedge pressure decreased significantly during exercise. Intravenous infusion of nisoldipine increased rest coronary sinus flow 10% (p less than 0.05, n = 7), decreased rest and exercise coronary vascular resistance 28% and 19% (p less than 0.01) and rest myocardial oxygen consumption 14% (p less than 0.05). In 13 patients similar systemic hemodynamic results were found after treatment with oral nisoldipine, 2 X 20 mg for 4 weeks. Stroke index and stroke work index increased long-term more than acutely (31% and 12.4% vs 19% and 4.5% at rest, both p less than 0.05), which may indicate a compensated mild cardiodepressant effect of intravenous nisoldipine. Changes in forearm vascular resistance after intra-arterial administration did not correlate with changes of systemic vascular resistance after intravenous administration, suggesting that factors other than vascular calcium entry blockade importantly influence hemodynamic responses. Elevated control plasmas norepinephrine and renin levels, on average, did not change during chronic therapy but individual changes were compatible with a reduction of sympathetic activity in patients with hemodynamic improvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Central and renal hemodynamic effects and hormonal response to diltiazem in severe congestive heart failure.

The central and renal hemodynamic effects and the hormonal response to single doses of 60 mg and 90 mg of diltiazem were evaluated in 10 patients with severe chronic left ventricular (LV) systolic dysfunction (ejection fraction 0.22 +/- 0.08). Diltiazem administration resulted in only mild and mostly statistically insignificant changes. After 60 mg, only heart rate (from 86 +/- 10 beats/min at baseline to 79 +/- 14 beats/min at 4 hours) and pulmonary vascular resistance (from 231 +/- 108 to 165 +/- 74 dynes s cm-5 at 4 hours) changed significantly. Administration of 90 mg of diltiazem resulted in no significant change in any of the measured or calculated central hemodynamic variables. Individual data, however, revealed an increase stroke volume index in 3 patients but a decrease in 1 patient and a persistent increase in mean pulmonary artery wedge pressure in another patient. These hemodynamic changes were not associated with symptomatic deterioration in any of the patients. Both renal blood flow and glomerular filtration rate were impaired at baseline on both days and did not show a significant change 1, 2 and 4 hours after diltiazem administration. Similarly, no significant change was noted after either diltiazem dose in plasma catecholamine levels and renin concentration. In conclusion, administration of 60 to 90 mg of diltiazem in patients with severe chronic LV systolic dysfunction results in only mild and mostly insignificant acute effects on central and renal hemodynamics, plasma hormonal levels and patient clinical status.

Diltiazem↗
PubMed1989

Hemodynamic effects of lisinopril after long-term administration in congestive heart failure.

To determine whether acute effects of the angiotensin converting enzyme inhibitor lisinopril are maintained during long-term therapy, 19 patients were studied using right-sided heart catheterization before an initial randomized dose of lisinopril and again after 12 weeks of maintenance lisinopril therapy. During initial evaluation, lisinopril produced significant decreases in mean systemic arterial pressure, pulmonary artery wedge pressure, systemic vascular resistance, mean pulmonary arterial pressure, mean right atrial pressure and pulmonary vascular resistance, and concomitant increases in cardiac index and stroke volume index. After 12 weeks of therapy with lisinopril, the dosage of which was titrated to produce optimal relief of symptoms of congestive heart failure (CHF), repeat hemodynamic studies revealed persistent significant reductions in baseline systemic arterial pressure, pulmonary artery wedge pressure, mean pulmonary arterial pressure and systemic vascular resistance. However, the increases in cardiac index and stroke volume index were not statistically significant. To determine if further acute hemodynamic changes occur during long-term therapy, the patients were readministered a dose of lisinopril. This caused further decreases in systemic arterial pressure, mean pulmonary arterial pressure, pulmonary artery wedge pressure, systemic vascular resistance and mean right atrial pressure, and an increase in cardiac index. Lisinopril did not change stroke work index at either initial or rechallenge study. This study indicates that in patients with CHF treated with lisinopril, acute hemodynamic effects persist after 12 weeks of therapy, and acute hemodynamic response continues to occur upon drug readministration.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Comparison of right ventricular impedance, pulse pressure and maximal dP/dt for determination of hemodynamic stability of ventricular arrhythmias associated with coronary artery disease.

By monitoring hemodynamic parameters, a future generation of automatic implantable defibrillators will provide tiered therapy of ventricular arrhythmias according to the associated hemodynamic compromise. Changes in intracardiac impedance permit beat-to-beat assessment of ventricular volumes and make this parameter attractive as a rapid discriminator of hemodynamic compromise during arrhythmias. Beat-to-beat changes in right ventricular (RV) impedance were measured before, during and after 27 episodes of ventricular tachyarrhythmias induced in 17 men (64 +/- 7 years, mean +/- standard deviation; left ventricular ejection fraction 41 +/- 11%). Impedance was measured using a tripolar lead system and was compared to ventricular tachycardia cycle length, RV pulse pressure and maximum systolic RV dP/dt as indicators of systemic hemodynamic compromise. The average decreases in systolic blood pressure and mean arterial pressure during ventricular tachycardia were 48 +/- 23% and 46 +/- 26%, respectively (mean +/- standard deviation; p less than 0.001 for each). Right ventricular impedance decreased an average 39 +/- 22% from its baseline value (p less than 0.001) during ventricular tachycardia. The percent change in impedance from baseline during ventricular tachycardia correlated significantly with the percent decrease in systolic and mean arterial pressure (r = 0.45 and 0.42, respectively; both p less than 0.05). Right ventricular dP/dt correlated the most poorly of all parameters with changes in blood pressure while impedance X RV pulse pressure correlated best with changes in mean and systolic pressure (r greater than or equal to 0.82, p less than 0.001).

Aged↗
PubMed1991

Effects of prolonged infusion of human alpha calcitonin gene-related peptide on hemodynamics, renal blood flow and hormone levels in congestive heart failure.

We have previously demonstrated that short-term infusion of calcitonin gene-related peptide (CGRP) has beneficial effects in congestive heart failure. The effects of prolonged infusion of CGRP on hemodynamic functions, plasma hormones and renal blood flow were studied in 9 patients with congestive heart failure (New York Heart Association class III or IV, ejection fraction less than 35%). Hemodynamic variables were measured at 30-minute intervals for 8 hours during CGRP infusion (8 ng/kg/min) and for 2 hours after discontinuation. CGRP caused a decrease in right atrial (28%, p less than 0.05), pulmonary artery (22%, p less than 0.02), pulmonary artery wedge (37%, p less than 0.001) and systemic arterial (18%, p less than 0.05) pressures. Systemic vascular resistance decreased more than pulmonary vascular resistance. Cardiac output (72%, p less than 0.001) and stroke volume (60%, p less than 0.02) increased. Heart rate did not change. There was no evidence of tolerance throughout the infusion. The hemodynamic effects were lost within 30 minutes of stopping CGRP. Renal blood flow (34%, p less than 0.01) and glomerular filtration rate (43%, p less than 0.01) increased. Atrial natriuretic peptide decreased (p less than 0.05), while plasma cortisol (p less than 0.02) increased. Plasma epinephrine, norepinephrine, renin activity, aldosterone and growth hormone were unchanged. It is concluded that in patients with severe congestive heart failure, CGRP has sustained beneficial effects on hemodynamic functions and has no adverse effects on hormones. Unlike many other vasodilators, CGRP also increases renal blood flow and glomerular filtration.

Calcitonin Gene-Related Peptide↗
PubMed1994

Measurement of long-term hemodynamic changes and the use of 24-hour blood pressure monitoring to evaluate treatment.

Hemodynamic studies at rest as well as during exercise are useful for profiling the hemodynamic derangements in essential hypertension and for evaluating the changes produced by antihypertensive therapy. Modern, lightweight, 24-hour ambulatory blood pressure monitoring devices can provide useful information in understanding circadian variation of blood pressure, and also in evaluating blood pressure control over 24 hours. We have studied in > 400 patients the hemodynamic profiles of most of the commonly used antihypertensive agents. Results from our study of amlodipine, a novel calcium antagonist, are presented as an example. Nineteen patients with mild-to-moderate essential hypertension underwent invasive hemodynamic studies while at rest, supine, and sitting, and during 50, 100, and 150 W bicycle exercise in the sitting position. Systolic, diastolic, and mean arterial blood pressure decreased 16% (p < 0.01) at rest and during exercise, and total peripheral resistance was reduced 18%. Blood pressure during the daytime and during sleep was reduced approximately 16%. The reductions in systolic and diastolic pressures were similar. There were no significant changes in heart rate or cardiac output. Amlodipine was well tolerated. Two patients developed ankle edema, which disappeared when the dose was reduced, and in 1 patient the drug was withdrawn because of nondrug-related side effects.

Adult↗
PubMed1976

Comparative effects of lidocaine and procainamide on acutely impaired hemodynamics.

Controversy exists regarding the relative safety of intravenously administered lidocaine and procainamide to patients with acutely impaired hemodynamics. Accordingly, their effects were studied in 15 such patients, 14 with acute myocardial infarction and one with cardiomyopathy and severe congestive heart failure. All had elevated levels of pulmonary capillary wedge pressure (greater than 15 mm Hg) and/or low cardiac index (less than 2.5 liters/min/m2). Patients were given lidocaine, a 100 mg bolus followed by a 3 mg/min infusion and, after at least a 30 minute recovery period, procainamide, a 100 mg bolus over 2 minutes followed by a 20 mg/min infusion for 20 to 25 minutes. Hemodynamic measurements were compared early and late in the infusion of each drug. Small, clinically insignificant differences were observed in the hemodynamic responses to the drugs, and no clinically significant deterioration occurred with either. Conventional therapeutic doses of intravenous procainamide can be administered by this regimen, to patients with acute myocardial infarction complicated by cardiac failure or low cardiac output, without producing deleterious hemodynamic effects.

Acute Disease↗
PubMed1978

Hemodynamic responsiveness to short- and long-acting vasodilators in left ventricular failure.

Vasodilators acutely reduce afterload and improve hemodynamics in congestive heart failure. Intravenous nitroprusside reduces left ventricular filling pressure and increases cardiac output while modestly reducing blood pressure and not changing heart rate in patients with heart failure in whom this response is characteristic. Comparably reduced blood pressure during nitroprusside infusion in normal subjects or hypertensive patients without failure results in a decrease in cardiac output and tachycardia. Long-acting vasodilators are also effective in patients with congestive heart failure. Nitrates, predominant venodilators, decrease left ventricular filling pressure as much as nitroprusside does, but increase cardiac output less. Hydralazine, an arterial dilator, increases cardiac output similarly to nitroprusside but decreases filling pressure less. Combining hydralazine with nitrates results in hemodynamic effects almost identical to those of nitroprusside. The quinazoline derivatives, trimazosin and prazosin, are also effective vasodilators, which act on both arteries and veins in patients with congestive heart failure. The hemodynamic response to vasodilators is influenced by the underlying hemodynamic status, as the change in cardiac output is directly related to base line ventricular filling pressure as well as systemic vascular resistance, and inversely related to the base line cardiac output. Response to vasodilators does not appear to be altered by age, diabetes, acute myocardial infarction or the cause of congestive myocardiopathy.

Blood Pressure↗
PubMed1984

Angiotensin II levels, hemodynamics, and sympathoadrenal function after low-dose captopril in heart failure.

The angiotensin converting enzyme inhibitor captopril improves the altered hemodynamics in many patients with chronic heart failure, but the first dose may precipitate hypotension. Ten patients with chronic heart failure were studied, nine with high plasma concentrations of renin and one with a low concentration. Frequent measurements of plasma concentrations of angiotensin II, renin, and catecholamines were made over 60 minutes after a small dose (6.25 mg) of captopril and related to concurrently measured hemodynamic variables. Captopril caused a decrease in systemic and pulmonary artery pressure and an increase in cardiac index, and these changes coincided with reductions in the plasma concentrations of angiotensin II and increases in plasma concentrations of renin. The hemodynamic changes were accompanied by reductions in the plasma concentrations of norepinephrine but transient increases in plasma concentrations of epinephrine in patients in whom vasomotor syncope developed. The patient with a low plasma renin concentration showed little hemodynamic response to the drug. It is concluded that vasomotor syncope occurs quite frequently in patients with severe chronic heart failure after captopril in a small dose and is associated with a selective increase in epinephrine secretion from the adrenal medulla.

Aged↗
PubMed1984

Hydralazine therapy in chronic congestive heart failure. Sustained central and regional hemodynamic responses.

Central and regional hemodynamic parameters were evaluated at baseline and following three months of placebo or hydralazine therapy (100 mg orally every eight hours) in 20 patients with idiopathic dilated cardiomyopathy. Both control (placebo) and hydralazine groups were comparable with respect to functional classification (New York Heart Association classes III and IV) and baseline hemodynamic variables. In the hydralazine group, cardiac index increased 25 percent (2.4 +/- 0.4 to 3.0 +/- 0.5 liters/minute/m2), renal blood flow increased 26 percent (648 +/- 199 to 815 +/- 229 ml/minute), and limb blood flow was augmented by 35 percent (6.8 +/- 3.0 to 9.2 +/- 4.6 ml/dl/minute) with long-term therapy. These changes were significant (all p less than 0.05) when compared with both baseline values and values in the control group. Both central and regional hemodynamic parameters remained unaltered in the control group. Long-term hydralazine therapy (three months) elicited a favorable circulatory response in this group of patients with chronic congestive heart failure. Central or regional hemodynamic tolerance to oral hydralazine failed to develop in the majority of patients.

Administration, Oral↗
PubMed1995

Favorable hemodynamic effects of magnesium sulfate in preeclampsia.

OBJECTIVE: Our purpose was to evaluate the hemodynamic effects of magnesium sulfate in preeclamptic and preterm labor patients. STUDY DESIGN: Fifteen preeclamptic patients at 32.4 +/- 3.3 (mean +/- SD) weeks' gestation and 11 preterm labor patients (31.3 +/- 2.8 weeks) were hemodynamically monitored in the lateral recumbent position by thoracic electrical bioimpedance (BoMed, Irvine, Calif.) before and during high-dose magnesium sulfate bolus and infusion. Cardiac index, systemic vascular resistance index, mean arterial pressure, heart rate, and stroke index were all recorded at baseline and during magnesium sulfate infusion. All patients received a standard crystalloid infusion. Data analysis continued until the patient received epidural placement or other antihypertensive therapy or was delivered. RESULTS: At baseline the systemic vascular resistance index was 2465 +/- 718 F.ohm/m2 and the cardiac index was 3.6 +/- 1.0 L/min/m2 for the preeclamptic patients. These were significantly different compared with the preterm labor patients, who had a systemic vascular resistance index of 1377 +/- 563 F.ohm/m2 and 4.6 +/- 1.2 L/min/m2. Magnesium sulfate infusion resulted in a rapid, sustained fall in systemic vascular resistance and a rise in cardiac index in the preeclamptic patient. This effect was evident at least 4 hours after initiation of the bolus and infusion. In the preterm labor patients the hemodynamic effects of magnesium sulfate were minimal and were noted only during the magnesium sulfate bolus. CONCLUSION: Magnesium sulfate infusion appears to have a prolonged hemodynamic effect in the preeclamptic patient. Sustained reduction in systemic vascular resistance and an increase in cardiac index is found in patients with preeclampsia but not in preterm labor.

Cardiac Output↗
PubMed1995

Systemic hemodynamic and regional circulatory effects of centrally administered endothelin-1 are mediated through ETA receptors.

Central endothelin (ET) has been implicated in the regulation of the cardiovascular system. The effect of intracerebroventricular (i.c.v.) administration of ET-1 or IRL 1620 (5, 15 and 45 ng) on the systemic hemodynamics and regional circulation was studied in anesthetized rats using a radioactive microsphere technique. Systemic hemodynamics and regional blood circulation were determined before (baseline) and at 30 min after the injection of each dose of ET-1 or IRL 1620. Administration of saline (5 microliters, i.c.v.) did not produce any significant cardiovascular effects. The lower doses of ET-1 (5 and 15 ng) did not produce any significant effect on blood pressure (BP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR) and regional blood circulation. However, the higher dose (45 ng) produced a transient rise (26%) followed by a sustained fall (48%) in BP. The decrease in BP was accompanied by significant decreases in CO (44%) and SV (39%), while HR and TPR were not affected. ET-1 (45 ng, i.c.v.) also produced a significant reduction in blood flow to the brain (75%), heart (49%), kidneys (66%), GIT (40%), portal system (52%) and musculo-skeletal system (38%), while blood flow to the skin was not affected. To determine pharmacological specificity of the central effects of ET-1, studies were performed in rats pretreated with BQ-123, a specific ETA receptor antagonist. Pretreatment with BQ-123 (10 micrograms, i.c.v.), 15 min prior to the administration of ET-1, completely antagonized the systemic hemodynamic as well as the regional circulatory effects of ET-1 (45 ng, i.c.v.). In order to determine whether stimulation of central ETB receptors produces any cardiovascular effects, studies were performed using IRL 1620, a specific ETB receptor agonist. Administration of IRL 1620 (5, 15 and 45 ng, i.c.v.) did not produce any effect on systemic hemodynamics and regional blood circulation in rats. It is concluded that ETA but not ETB receptors are involved in the central cardiovascular actions of ET.

Animals↗
PubMed1983

Hemodynamic effects of the arteriolar vasodilators hydralazine, dihydralazine and endralazine in the conscious spontaneously hypertensive rat.

The hemodynamic effects of the vasodilators hydralazine, dihydralazine and endralazine were studied in conscious, unrestrained spontaneously hypertensive rats (SHR) equipped for chronic hemodynamic measurements. The arteriolar vasodilators hydralazine (0.3 mg/kg i.a.) and dihydralazine (0.3 mg/kg i.a.) caused a rapid fall in blood pressure and peripheral resistance, lasting up to 24 h in the case of dihydralazine. Immediately after injection, the cardiac output and heart rate were increased significantly. These effects only lasted for 1-2 h. The hemodynamic pattern of the new vasodilator endralazine (0.1-1 mg/kg i.a.) was very similar, with a duration of action similar to that of dihydralazine. The role of baroreceptor reflexes in the early hemodynamic effects of vasodilators was studied by comparing the effects of 0.3 mg/kg hydralazine in baroreflex-denervated and non-denervated SHR. The decrease in blood pressure and peripheral resistance was significantly larger in the denervated SHR, whereas increases in cardiac output and heart rate were almost completely absent in these animals. These data suggest that baroreceptor reflexes oppose the early fall in blood pressure and peripheral resistance induced by vasodilators. However, the activity of the baroreflex seems of very short duration, suggesting a rapid adaptation to the prevailing blood pressure. Moreover, the data show that endralazine is an effective arteriolar vasodilator in conscious SHR.

Animals↗
PubMed1992

Cardiovascular effects of the new nitric oxide donor, pirsidomine. Hemodynamic profile and tolerance studies in anesthetized and conscious dogs.

The hemodynamic profile of pirsidomine, a new donor of NO (nitric oxide), was evaluated in dogs. In anesthetized dogs, the intravenous or intraduodenal administration of pirsidomine (0.3-10 mg/kg) decreased dose relatedly the preload and afterload of the heart, total peripheral resistance, cardiac output, left ventricular work and myocardial oxygen consumption. In conscious renal-hypertensive dogs, oral administration of pirsidomine (1.0-10 mg/kg) caused a marked and sustained decrease in systolic blood pressure and left ventricular end-diastolic pressure, which was accompanied by a slight and transient increase in heart rate and contractility. The diastolic blood pressure was affected less than in anesthetized dogs. Similar hemodynamic effects were obtained with M1 (3-(1-(2,6-dimethylpiperidino))-sydnonimine; 0.3-1 mg/kg), the main metabolite of pirsidomine, and with the known NO donor, isosorbide-5-mononitrate (IS-5-MN; 2-10 mg/kg). Tolerance development after repeated administration of pirsidomine and IS-5-MN was also investigated. In anesthetized dogs, repeated intraduodenal administrations of pirsidomine did not attenuate the response whereas tolerance occurred with hemodynamically equieffective doses of IS-5-MN. In conscious dogs, long term oral treatment, three times daily every 8th h for 5 days, revealed tolerance to IS-5-MN, slight or no tolerance to pirsidomine, and no cross-tolerance between the two agents. The results indicate that pirsidomine possesses an antianginal hemodynamic profile similar to that of its main metabolite, M1, and of IS-5-MN. This suggests a common mode of action via the release of NO.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Systemic and hepatic hemodynamics after variceal hemorrhage: effects of propranolol and placebo.

Hepatic and systemic hemodynamics were measured in 19 cirrhotic patients with variceal bleeding enrolled in a controlled trial of propranolol for the prevention of rebleeding. The patients were studied on three separate occasions. The first study was performed before randomization within 24 h of the bleeding episode, once hemodynamic stabilization had been achieved. The second study was performed after 10 days of treatment, and the third after 6 mo without rebleeding. Propranolol dosage was titrated according to blood levels. Wedged and free hepatic venous pressures and the hepatic venous pressure gradient were recorded. Hepatic blood flow and cardiac output were also measured. Before treatment, the groups of patients treated with propranolol (n = 11) or placebo (n = 8) were comparable according to clinical, biochemical, and hemodynamic parameters. After 10 days, hepatic venous pressure gradient decreased similarly in the two groups (-20% in the propranolol group, -25% in the placebo group). Cardiac output fell only in the propranolol group (-40%). Hepatic blood flow remained unchanged in either group. After 6 mo, hepatic venous pressure gradient remained lower than the values from the first (within 24 h of bleeding) study in both the propranolol group (n = 5) and the placebo group (n = 6). Our results suggest that portal pressure increases shortly after hemorrhage with a return to baseline values 10 days later, and that propranolol does not further magnify these changes. Spontaneous changes in hepatic hemodynamics after variceal hemorrhage must be taken into account when evaluating the effect of pharmacologic agents on portal pressure.

Adult↗
PubMed1992

Effect on hemodynamics of a liquid meal alone and in combination with propranolol in cirrhosis.

Thirteen patients with alcoholic cirrhosis had splanchnic and systemic hemodynamics assessed before and after ingestion of a standard liquid meal of 700 kcal (consisting of isocaloric proteins, lipids, and carbohydrates). Half of the patients (n = 6) were randomized to a treatment group receiving intravenous infusion of propranolol in combination with the meal. No significant effects were observed on systemic hemodynamics after the meal alone. Heart rate (-14%; P less than 0.01) and cardiac index (-24%; P less than 0.01) decreased after meal in combination with propranolol. The mean hepatic venous pressure gradient increased significantly after ingestion of the meal alone with a maximal effect after 30 minutes (+13%; P less than 0.05) and returned to baseline values after 2 hours. Meal in combination with propranolol had no significant effect on the hepatic venous pressure gradient. Hepatic blood flow increased substantially after the meal alone with a maximal effect after 30 minutes (+28%; P less than 0.01), whereas no significant effect was observed after meal in combination with propranolol. Azygos blood flow increased significantly after the meal alone (+36%; P less than 0.05), whereas this effect was abolished in combination with propranolol. In conclusion, ingestion of a peroral mixed meal in cirrhotic patients has, contrary to what is observed in normal controls, no effects on systemic hemodynamics. Substantial changes in splanchnic hemodynamics were observed, and these effects were all abolished when the meal was administered in combination with propranolol.

Analysis of Variance↗
PubMed1985

Carbohydrate metabolism and the hemodynamic response to shock.

To investigate the temporal relationship of changes in carbohydrate metabolism to changes in the hemodynamic stability of the dog in protracted hemorrhagic shock, 30 animals were studied. Blood pressure was maintained at 60 mm Hg for 12 hr during which hemodynamic and metabolic parameters were studied. In early shock cardiac output was decreased and peripheral resistance increased. After 2 hr cardiac output began to increase and peripheral resistance began a progressive decline despite the continuing hypotensive state. Hemodynamic decompensation was essentially complete at 5 hr. There was early and marked mobilization of carbohydrate stores. Muscle glycogen was rapidly mobilized over a 5-hr period. Serum glucose and blood lactate levels rose and remained elevated for 8 hr. Amino acid degradation remained at high levels throughout the experimental period. Hemodynamic decompensation began well before significant depletion of carbohydrate stores and was complete well before the relative exhaustion of the available reserves.

Amino Acids↗
PubMed1988

Hemodynamic effects of radical left ventricular scar resection in patients with and without congestive heart failure.

To evaluate the hemodynamic changes that occur following radical left ventricular scar resection we studied 40 patients (mean age, 59.2 years; 36 males) with complete hemodynamic evaluation preoperatively (preop) and 5 to 12 days postoperatively (postop). Severe congestive heart failure (CHF) was present in 15 patients, ventricular arrhythmias in 19, and angina in 19 patients preop. The operation consisted of extensive scar resection with complete myocardial revascularization (average 2.4 grafts per patient). Ten patients required intraaortic balloon pump assist for up to 8 days postop. Postoperative left ventricular ejection fraction (EF) was estimated with multiple gated acquisition scanning. A significant rise in heart rate was observed in the whole group of patients postop (P = 0.000). In the group of patients with CHF preop the EF was increased from 25.1 +/- 8.4% (mean +/- SD) preop to 30.9 +/- 11.2% postop (P = 0.003), the cardiac index was increased from 2.2 +/- 0.5 liters/min/m2 preop to 2.7 +/- 0.5 liters/min/m2 postop (P = 0.02), and the pulmonary artery wedge pressure was decreased from 22.0 +/- 7.7 mm Hg preop to 15.5 +/- 4.3 mm Hg postop (P = 0.005). In the patients without active CHF preop no improvement in the above hemodynamics was noted. In conclusion, radical left ventricular scar resection significantly increased EF and CI and decreased PAW in patients with preop CHF, whereas in the absence of CHF this procedure resulted in minimal hemodynamic changes.

Adult↗