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PubMedDate not supplied

Pacemaker hemodynamics: clinical implications.

Our review of the current literature and experience in caring for pacemaker patients suggests that a consideration of hemodynamics is a logical way to approach pacemaker selection and programming. Multiple clinical factors enter into the selection of a pacemaker or pacemaker programming settings in each case. It appears that in patients with sinus node disease, atrial-inhibited or dual-chamber pacing provides the best chance for preventing the development of chronic atrial fibrillation with its attendant risks of embolism and stroke. It is clear that AV synchrony has beneficial hemodynamic effects at rest in most patients. The results of Labovitz would suggest that in patients with marked left atrial enlargement, this may be less so. The results of Stewart et al would further suggest that in patients with retrograde VA conduction, dual-chamber pacing is preferable. Retrograde VA conduction can be intermittent and this makes it difficult to use its absence on a single test to decide on the type of pacemaker to use. It appears that baseline left ventricular function does not determine the relative improvement in cardiac output observed with AV synchrony or rate-adaptive pacing. However, in patients with severe congestive heart failure even a small improvement in cardiac output may result in significant clinical improvement. Studies have shown that in any given patient, there may be an optimal AV interval at rest. In general, this ranges from 100 to 150 milliseconds. In normal individuals the optimal AV interval shortens with increased heart rate during exercise in a predictable and linear fashion. The hemodynamic benefits of a shortened AV interval with faster heart rates in pacemaker patients have not yet been shown. Intuitively, however, this would appear to be a desirable approach and will probably be added to the design of future generations of dual-chamber pacemakers. Studies of the effect of different pacing modes on secretion of atrial natriuretic factor are intriguing and may contribute more to our understanding of pacing hemodynamics in the future. During exercise, heart rate increase is more important than AV synchrony and this has been shown by several studies. Thus, in active patients with chronotropic incompetence due to sick sinus syndrome, the addition of rate-adaptive pacing is important. Because single-chamber rate-adaptive atrial pacing leaves the patient exposed to the risk of future development of AV block and DDD pacing does not provide chronotropic support, it is likely that the new rate-adaptive dual-chamber (DDDR) devices will be used in a significant number of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1991

Variability of hemodynamic values and plasma catecholamine concentrations over a one-hour period in conscious, restrained rats.

Restrained conscious rats have been widely used for physiological and pharmacological hemodynamic studies. In this condition, the variability of the circulation is unclear. Repeated measurements in restrained normal rats showed stable systemic hemodynamics (cardiac output ranging from 130 +/- 14 to 174 +/- 10 mL/min, mean arterial pressure ranging from 109 +/- 9 to 117 +/- 5 mmHg) and splanchnic hemodynamics (splanchnic blood flow ranging from 8.51 +/- 1.89 to 13.01 +/- 1.45 mL min-1 100 g-1 body wt) over a period of 1 hr. Slight but not significant hemodynamic variations, however, occurred in pulmonary blood flow. Similarly, plasma noradrenaline concentrations did not vary over this period (plasma noradrenaline level ranging from 186 +/- 36 to 358 +/- 64 pg/mL). These plasma noradrenaline concentrations were similar to those measured in a group of conscious unrestrained rats 3 hr after recovery from surgery (292 +/- 60 pg/mL). A significant correlation was observed between plasma noradrenaline concentration and heart rate.

Animals↗
PubMed1985

Leukotrienes on porcine hemodynamics and prostanoid release.

We studied the effect of intracoronary leukotriene B4, C4, D4 and E4 (0.1-3 micrograms) on coronary artery blood flow and resistance in anesthetized pigs. Conventional hemodynamics were measured, and the peripheral electrocardiogram was obtained in lead II. Thromboxane B2 and 6-keto-prostaglandin F1 alpha (as breakdown products of thromboxane and prostacyclin, respectively) were measured during the influence of leukotrienes on the heart. All leukotrienes except B4 reduced coronary flow. Peak reduction was produced by 3 micrograms of each eicosanoid: C4 = 96 +/- 4%+; D4 = 98 +/- 2%+; E4 = 82 +/- 8%+. Coronary resistance increased after the same dose B4 = 65 +/- 18%; C4 = 225 +/- 94% (P less than 0.01); D4 = 442 +/- 118%+; E4 = 110 +/- 43% (+ = P less than 0.001). Increase in filling pressure and heart rate but blood pressure reduction and diminution in left ventricular d P/dtmax were observed with leukotriene C4, D4 and E4. The S-T segments of the electrocardiogram were elevated, thus indicating myocardial ischemia during the blood flow reduction. Indomethacin (5 mg/kg i.v.) had no effects on the leukotriene-induced hemodynamic sequelae. Thromboxane B2 concentration in coronary sinus blood plasma increased by 132-176% (P less than 0.05) at peak leukotriene effects on blood flow. Thus, leukotriene C4, D4, and E4 are vasoconstrictors in the situ porcine heart. Leukotriene B4, however, exerts no hemodynamic effects. The electrocardiographic ischemia and changes in hemodynamics indicate actions on coronary resistance and myocardial depression. These eicosanoids may contribute to cardiac dysfunction and vasospasm in coronary artery disease.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Enalapril in congestive heart failure: acute and chronic invasive hemodynamic evaluation.

Following hemodynamic evaluation using invasive and noninvasive methods, 73 patients were treated in an open, uncontrolled, multicenter study with single oral doses of enalapril maleate 1.25 to 40 mg until the optimal dose for each patient (based upon hemodynamic response) was achieved. Diuretics were withheld and reinstituted only if necessary. Hemodynamic measurements were made at 0 (predrug), 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours postdrug. Patients were discharged on their optimal dose, treated 1 to 4 months and then rehospitalized for repeat hemodynamic measurements. The optimal enalapril single dose was associated with the following mean peak responses: increased cardiac index 42% (SE = 6) and decreased pulmonary capillary wedge pressure 40% (SE = 3), systemic vascular resistance 39% (SE = 2), and mean arterial pressure 23% (SE = 1.5). These changes persisted during chronic therapy. Chronic treatment with enalapril also improved exercise capacity 40% (P less than 0.01), ejection fraction 18% (P less than 0.05) and clinical status (N.Y.H.A. functional class, P less than 0.01). Ten and 20 mg/day, taken as once- or twice-daily regimens, were the most commonly effective doses.

Adult↗
PubMed1996

Acute hemodynamic and long-term clinical effects of isradipine in patients with coronary artery disease and chronic heart failure. A double-blind, placebo-controlled study.

To assess the acute hemodynamic and long-term clinical effects of isradipine, a calcium antagonist of the dihydropyridine class, we performed a double-blind, placebo-controlled parallel study in 19 patients with coronary artery disease (CAD) and stable chronic heart failure (CHF). Their mean age was 56 +/- 5 years, and left ventricular ejection fraction (LVEF) was 0.18 +/- 0.05. Patients were treated with diuretics and digoxin only. All were clinically stable and in sinus rhythm. The acute hemodynamic study showed that (intravenous) isradipine increased cardiac index (+36%) and stroke volume index (+30%) (both P < 0.001), while systemic vascular resistance (-33%) and mean arterial pressure (-10%) decreased (both P < 0.005). Filling pressures and heart rate were not affected. Of the 19 patients, 17 completed the 12 week study; 2 patients on placebo (1 death, 1 side-effects) but no patient on isradipine (5 mg 3 times daily) dropped out. After 12 weeks, peak oxygen consumption (VO2), LVEF, echocardiographic indices, and other clinical parameters were unaffected by treatment. Repeat invasive hemodynamic measurements showed that the initial improvement by isradipine was not present anymore. In conclusion, despite a beneficial acute hemodynamic effect, isradipine has no favorable clinical influence during prolonged treatment in patients with mild to moderate CHF.

Calcium Channel Blockers↗
PubMed1995

Blunted natriuresis and abnormal systemic hemodynamic responses to C-type and brain natriuretic peptides in rats with cirrhosis.

BACKGROUND/AIMS: The effects of C-type and brain natriuretic peptides (CNP and BNP, respectively) on renal excretion of sodium and hemodynamics have not yet been studied in cirrhosis. METHODS: This study aimed to examine the effects of saline, CNP (300 ng.kg-1.min-1 i.v. for 30 min) and BNP (600 ng.kg-1.min-1 i.v. for 30 min) on natriuresis and diuresis in normal and rats with cirrhosis. Moreover, regional and systemic hemodynamics were measured prior to and following CNP and BNP administration in normal rats and rats with cirrhosis with ascites. RESULTS: In rats with cirrhosis, the effects of CNP or BNP or natriuresis and diuresis did not significantly differ from the effects of saline. CNP significantly decreased portal pressure and systemic vascular resistance and significantly increased the cardiac index. BNP significantly decreased portal tributary blood flow, portal pressure and cardiac index. In normal rats, natriuresis and diuresis were significantly higher with CNP and BNP than with saline. Systemic hemodynamics were not changed by CNP. A decrease in arterial pressure was the sole BNP-induced hemodynamic change. CONCLUSIONS: In conclusion, this study shows that the natriuretic response to pharmacological doses of CNP and BNP is blunted in rats with cirrhosis. This blunting may be related to an activation of the endogenous antinatriuretic systems secondary to systemic vasodilation (by CNP) or to a decreased cardiac index (by BNP). Finally, this study shows that CNP and BNP have a portal hypotensive action.

Animals↗
PubMed1995

Uterine and fetal hemodynamics and fetal cardiac function after atenolol and pindolol infusion. A randomized study.

OBJECTIVE: To evaluate the short-term effects of intravenously given atenolol and pindolol on utero- and umbilicoplacental vascular impedance, fetal hemodynamics and cardiac function in patients suffering from pregnancy-induced hypertension. STUDY DESIGN: A total of 24 women were randomized to receive atenolol or pindolol infusion. By using pulsed color Doppler techniques, uterine, placental arcuate, umbilical fetal middle cerebral and renal arteries were examined before, at the end and 30 min after the end of infusion. Pulsatility indices (PI) were calculated to assess vascular impedance. Fetal myocardial function was evaluated by using pulsed Doppler and M-mode echocardiography. Peak systolic velocities from the ascending aorta and pulmonary trunk, and also inner diameters and fractional shortenings of both ventricles were measured. RESULTS: Both drugs significantly decreased maternal blood pressure. Immediately after the infusion, maternal heart rate was significantly decreased in both groups; but the decrease was clearer and lasted longer in the atenolol group. Pindolol caused no changes in utero- or umbilicoplacental vascular impedance, while atenolol increased it in the nonplacental uterine artery. After atenolol infusion, PI in the umbilical artery was higher than after pindolol. Pindolol had no effects on fetal hemodynamics, while atenolol decreased PI value in the fetal renal artery. Peak systolic velocity in the pulmonary trunk was decreased after atenolol. Pindolol did not affect the fetal cardiac function. In subgroups with originally increased utero- or umbilicoplacental vascular impedance, the responses in uterine and umbilical vascular impedance and in fetal hemodynamics and cardiac function after atenolol and pindolol were different compared to whole groups. CONCLUSION: Differently acting antihypertensive agents seem to affect differently uteroplacental vascular impedance. Atenolol may have some direct effects on fetal hemodynamics and cardiac function. According to our results, pindolol seems to be more preferable in the treatment of pregnancy-induced hypertension than atenolol.

Adrenergic beta-Antagonists↗
PubMed1989

Hemodynamic effects of innominate artery occlusive disease. Evaluation by Doppler ultrasound.

Between 1976 and 1987 we saw 20 patients presenting with stenosis or occlusion of the innominate artery with a measurable hemodynamic effect. This corresponds to less than 0.1% of our patients subjected to noninvasive vascular testing. The hemodynamic sequelae involved the vertebral as well as the carotid arteries. The majority of the cases (n = 17) showed a vertebral steal and only minor concomitant alterations of carotid artery flow. Only three patients had a carotid steal in addition to the vertebral steal. In general, the vertebral steal is predominant over the carotid steal and precedes the latter. We propose a phenomenological classification of innominate artery disease following the severity of hemodynamic changes. Type I shows systolic deceleration or alternating flow in the right vertebral artery and only minor changes in the carotid arteries. Type II is characterized by reversed flow in the ipsilateral vertebral artery and systolic deceleration in the carotid arteries and type III by alternating flow or even complete steal in the carotid arteries in addition to vertebral artery steal. Continuous wave Doppler ultrasound is a valuable noninvasive method for examinating innominate artery occlusive disease and its hemodynamic sequelae. In special cases the additional use of duplex- and transcranial sonography is useful.

Adult↗
PubMed1991

Implications of echocardiographically assisted diagnosis of pericardial tamponade in contemporary medical patients: detection before hemodynamic embarrassment.

Identification of suspected pericardial tamponade and the decision to perform invasive drainage of the pericardial space have historically been based on classic bedside findings. Two-dimensional echocardiography has improved detection of pericardial effusion, but it may be excessively sensitive in evaluation of patients for hemodynamic embarrassment. Therefore, 50 consecutive medical patients were examined who were identified by echocardiography to have probable tamponade (defined as the presence of right heart chamber collapse in the presence of a pericardial effusion) and who underwent combined right-sided cardiac catheterization and percutaneous pericardiocentesis. All patients had elevated pericardial pressure. However, many had minimal evidence of hemodynamic compromise (94% had systolic blood pressure greater than or equal to 100 mm Hg and 58% had a cardiac index greater than or equal to 2.3 liters/min per m2). Pericardiocentesis resulted in hemodynamic improvement, but frequently did not alleviate dyspnea or correct tachycardia. Patients with malignancy as the cause of tamponade had a high mortality rate (the cumulative probability of survival in such patients was only 17% at 1 year). Echocardiographically assisted diagnosis of pericardial tamponade in medical patients results in the identification of a substantial subset of patients with only subtle evidence of hemodynamic compromise. This subset of patients differs sharply from medical patients described in previous reports with classic tamponade. Although the patients can be managed by invasive catheter pericardiocentesis with few complications, the natural history and the optimal management strategy for this group are not resolved.

Cardiac Catheterization↗
PubMed1991

Experimental pericardial effusion: relation of abnormal respiratory variation in mitral flow velocity to hemodynamics and diastolic right heart collapse.

Pericardial effusion is associated with an abnormal increase in respiratory variation in mitral flow velocity. However, the relation of the changes in flow velocity to pericardial pressure, hemodynamics and two-dimensional echocardiographic findings is not established. Therefore, 11 sedated dogs with extensive hemodynamic instrumentation were studied with two-dimensional and Doppler echocardiography during four stages of progressively larger pericardial effusion. During all stages of effusion, respiratory variation in peak mitral flow velocity in early diastole and left ventricular isovolumetric relaxation time was increased compared with baseline (p less than 0.05). This increase was seen at the earliest stage of effusion (mean pericardial pressure 4.2 +/- 1.4 versus -0.8 +/- 0.9 mm Hg at baseline, p less than 0.05), and preceded the appearance of unequivocal diastolic right heart collapse in every dog. Maximal respiratory variation coincided with the appearance of right atrial collapse (mean pericardial pressure 7.1 +/- 2.4 mm Hg; mean inspiratory decrease in aortic pressure 9.5 +/- 2.6 mm Hg; mean aortic pressure 88.2 +/- 15.2 versus 102.2 +/- 11.2 mm Hg at baseline, p less than 0.05; and cardiac output 3.8 +/- 1.2 versus 5.5 +/- 1.3 liters/min at baseline, p less than 0.05), but did not increase at stages associated with more severe hemodynamic compromise. In addition, the respiratory changes in peak mitral flow velocity in early diastole were associated with simultaneous changes in the diastolic transmitral pressure gradient. It is concluded that in this model of acute pericardial effusion 1) increased respiratory variation in early diastolic mitral flow velocity, peak mitral flow velocity in early diastole and left ventricular isovolumetric relaxation time occurs almost immediately as pericardial pressure increases and persists at all stages of increasing pericardial effusion; 2) the abnormal respiratory variation occurs before equalization of intracardiac pressures and before the onset of unequivocal right heart collapse; 3) the respiratory variation occurs as a result of changes in the diastolic transmitral pressure gradient; and 4) the magnitude of the respiratory change is not necessarily predictive of pericardial pressure or severity of hemodynamic compromise, especially at the more severe stages of pericardial effusion.

Animals↗
PubMed1993

Sustained hemodynamic response to flosequinan in patients with heart failure receiving angiotensin-converting enzyme inhibitors.

OBJECTIVES: We evaluated the short- and long-term effects of flosequinan in 47 patients with severe heart failure despite ongoing captopril treatment. BACKGROUND: There have been no previous evaluations of the long-term hemodynamic effects of any direct-acting vasodilator in patients with heart failure receiving an angiotensin-converting enzyme inhibitor. Flosequinan is an arterial and venous vasodilator with actions similar to those of the hydralazine-isosorbide dinitrate combination. METHODS: After baseline hemodynamic measurements using balloon-tipped pulmonary artery and radial arterial catheters, patients were randomized to receive 50, 100 or 150 mg of flosequinan daily. Hemodynamic variables were measured immediately before and after short-term flosequinan administration and after 8 weeks of therapy. RESULTS: With short-term flosequinan administration, mean arterial, right atrial and left ventricular filling pressures decreased by 6.4 +/- 1.1, 3.8 +/- 0.5 and 7.3 +/- 0.7 mm Hg, respectively (all p < 0.001). Cardiac index increased by 0.5 +/- 0.1 liters/min per m2, systemic vascular resistance decreased by 616 +/- 105 dynes.s.cm-5 and heart rate increased by 4 +/- 1 beats/min (all p < 0.001). After 8 weeks of long-term flosequinan administration, the vasodilator effect of a dose of flosequinan persisted. Compared with pretreatment baseline values, mean arterial, right atrial and left ventricular filling pressures at the peak effect of flosequinan were decreased by 3.5 +/- 1.3, 2.8 +/- 0.7 and 5.1 +/- 1.3 mm Hg, respectively (all p < 0.01). Systemic vascular resistance had decreased by 585 +/- 95 dynes.s.cm-5, cardiac index had increased by 0.5 +/- 0.1 liters/min per m2 and heart rate had increased by 10 +/- 2 beats/min (all p < 0.001). CONCLUSIONS: The arterial and venous vasodilator flosequinan exerts both short- and long-term sustained hemodynamic effects in patients with heart failure receiving angiotensin-converting enzyme inhibitors.

Adult↗
PubMed1994

Improved exercise hemodynamic status in dilated cardiomyopathy after beta-adrenergic blockade treatment.

OBJECTIVES: This study was performed to investigate exercise hemodynamic status in a double-blind, placebo-controlled trial and was a substudy in the Metoprolol in Dilated Cardiomyopathy Trial. BACKGROUND: Previous open studies have shown beneficial effects on exercise hemodynamic status after beta-adrenergic blocking agent therapy in patients with congestive heart failure. METHODS: The study included 41 patients with idiopathic dilated cardiomyopathy with ejection fraction < 0.40 (metoprolol, 20 patients; placebo, 21 patients) whose hemodynamic status was investigated at rest and during supine submaximal exercise, at baseline and after 6 and 12 months of treatment. Myocardial metabolism was evaluated in a subset of 19 patients. RESULTS: Metoprolol-treated patients responded favorably, as expressed by improved exercise cardiac index ([mean +/- SD] placebo 4.8 +/- 1.6 to 4.7 +/- 1.8 liters/min per m2, metoprolol 4.3 +/- 1.1 to 5.4 +/- 1.9 liters/min per m2, p = 0.0001) and stroke work index (placebo 44 +/- 20 to 41 +/- 27 g.m/m2, metoprolol 35 +/- 16 to 58 +/- 28 g.m/m2, p < 0.0001). Exercise systolic arterial pressure increased (placebo 161 +/- 25 to 151 +/- 23 mm Hg, metoprolol 155 +/- 29 to 165 +/- 37 mm Hg, p = 0.0003) as well as exercise oxygen consumption index (placebo 463 +/- 194 to 474 +/- 232 ml/min per m2, metoprolol 406 +/- 272 to 507 +/- 298 ml/min per m2, p = 0.045). There was a significant increase in exercise duration in the metoprolol group (63 +/- 38 s) compared with the placebo group (-24 +/- 42 s) (p = 0.01). Net myocardial lactate extraction increased in the metoprolol group, suggesting less myocardial ischemia (placebo 17 +/- 22 to 9.5 +/- 6.4 mmol/min, metoprolol -32 +/- 100 to 42 +/- 45 mmol/min, p = 0.03). Peripheral levels of norepinephrine tended to decrease at rest and during exercise, whereas myocardial net spillover was unchanged. CONCLUSIONS: Metoprolol improved hemodynamic status in patients with dilated cardiomyopathy at rest and had a more pronounced effect during exercise. These positive effects were achieved along with improved or stable myocardial metabolic data.

Analysis of Variance↗
PubMed1994

Short-term effects of naloxone on hemodynamics and baroreflex function in conscious dogs with pacing-induced congestive heart failure.

OBJECTIVES: The purpose of this study was to determine the effects of naloxone on systemic hemodynamics and reflex function in dogs with congestive heart failure induced by rapid pacing. BACKGROUND: We have shown previously that naloxone, an opiate receptor antagonist, improves cardiac output, aortic blood pressure, systolic performance and the baroreflex function in conscious dogs with chronic right-sided congestive heart failure. However, whether endogenous opioids also play a role n mediating the reduction of myocardial and baroreflex function in animals with left heart failure remains controversial. METHODS: We administered naloxone (1 mg/kg body weight) and normal saline solution to 15 dogs with pacing-induced congestive heart failure (225 beats/min for 8 weeks) and 11 control dogs. In addition to systemic hemodynamic measurements, the slope of pressure-area relation obtained from echocardiography with intravenous bolus injection of phenylephrine was taken as a load-independent index of myocardial contractility. Baroreflex function was estimated by the slope of the regression line relating systolic aortic pressure and RR interval. RESULTS: Plasma beta-endorphin levels were elevated in dogs with congestive heart failure. Naloxone administration increased heart rate, mean aortic pressure, first derivative of left ventricular pressure, cardiac output and myocardial contractility in pacing-induced congestive heart failure. These changes correlated significantly with basal plasma beta-endorphin levels and were accompanied by increases in plasma beta-endorphin and catecholamines after naloxone administration. However, unlike the hemodynamic and cardiac effects of naloxone, baroreflex function did not change after naloxone in dogs with congestive heart failure. CONCLUSIONS: The increase in basal plasma beta-endorphin suggests that the endogenous opiate system is activated in left-sided congestive heart failure. Because naloxone improves the systemic hemodynamics and myocardial contractile function under this condition, the endogenous opioids appear to play an important role in mediating the myocardial depression that occurs in heart failure. However, the endogenous opiate system has no apparent effect on the regulation of baroreflex control in heart failure induced by rapid pacing.

Animals↗
PubMed1995

Intracoronary amiloride prevents contractile dysfunction of postischemic "stunned" myocardium: role of hemodynamic alterations and inhibition of Na+/H+ exchange and L-type Ca2+ channels.

OBJECTIVES: This study sought to establish the effect of amiloride on stunned myocardium and to determine the role of hemodynamic alterations and inhibition of sodium/proton (Na+/H+) exchange and L-type cytosolic calcium (Ca2+) channels. BACKGROUND: Amiloride is a nonspecific agent that may reduce reperfusion injury, but its effect on reversible dysfunction or stunned myocardium is unclear. METHODS: Ninety-seven open chest dogs undergoing 15 min of left anterior descending coronary artery occlusion and 3 h of reperfusion with monitoring of hemodynamic variables, systolic shortening and myocardial blood flow were randomized to seven intracoronary infusions: control dogs (5% dextrose, n = 16); low dose amiloride (1 mg/min, n = 14); high dose amiloride (5 mg/min) with (n = 12) and without (n = 16) atrial pacing; sodium nitroprusside (20 micrograms/min, n = 16); hexamethylene amiloride (a specific inhibitor of Na+/H+ exchange, 60 micrograms/min, n = 14); and nifedipine (a specific inhibitor of L-type Ca2+ channels, 5 micrograms/min, n = 9). Drug infusions were started 40 min before occlusion and stopped at 30 min after reperfusion. RESULTS: Forty-three dogs were excluded because of ventricular fibrillation or high collateral flow. The incidence of ventricular fibrillation was similar in all groups to that in control dogs. Systolic shortening completely recovered (p = NS vs. baseline; p < 0.01 vs. control group) by 2 h after reperfusion in the low dose amiloride group and 30 min in the high dose group (p < 0.01 vs. low dose). High dose amiloride increased myocardial blood flow and had positive inotropic and negative chronotropic effects (p < 0.05 vs. control group). Atrial pacing did not attenuate recovery. The only effect of low dose amiloride was increased myocardial blood flow after reperfusion. Systolic shortening did not deteriorate after washout of drug effects. Sodium nitroprusside and nifedipine similarly increased myocardial blood flow, but systolic shortening never recovered. Hexamethylene amiloride had no hemodynamic effects, and systolic shortening never recovered. CONCLUSIONS: Amiloride prevented the contractile dysfunction of myocardial stunning but did not prevent arrhythmias. Hemodynamic alterations, increased myocardial blood flow and inhibition of Na+/H+ exchange or L-type Ca2+ channels alone did not account for the improved function. Inhibition of Na+/Ca2+ exchange may be the mechanism of improved postischemic function.

Amiloride↗
PubMed1987

Naloxone does not improve hemodynamics following graded hemorrhage in a canine model.

Two recent studies have demonstrated no improvement in hemodynamic parameters or survival following naloxone administration in hemorrhagic shock. This finding is in contrast to those of earlier studies, which consistently demonstrated a beneficial effect. The current study evaluated naloxone's ability to improve hemodynamics when administered following a fixed-volume hemorrhage, during a period of partial hemodynamic compensation. Thirteen conditioned beagles were anesthetized with pentobarbital (25 mg/kg intravenously), endotracheally intubated, and instrumented with a femoral arterial line and a pulmonary artery thermodilution catheter. Animals were then subjected to an estimated 50% graded hemorrhage (45 ml/kg) over one hour. Following hemorrhage, animals were observed for 90 minutes, then reinfused with shed blood over 30 minutes, and finally observed for an additional 60 minutes. Six animals received naloxone (2 mg/kg intravenously) 30 minutes after completion of hemorrhage and then 2 mg/kg/hr for the duration of the study. Seven control animals received an equivalent volume of saline. Heart rate, mean arterial pressure, central venous pressure, cardiac output, arterial and mixed venous blood gases, and serum lactate level were measured at regular intervals throughout the study. Cardiac index and systemic vascular resistance index were calculated at the same intervals. Overall, there were no statistically significant differences in the mean data values for mean arterial pressure, cardiac index, systemic vascular resistance index, or lactate, although lactate values were consistently higher in the naloxone group (two-tailed independent Student's t test). We conclude that naloxone does not significantly improve hemodynamics when administered after a fixed-volume hemorrhage.

Animals↗
PubMed1990

Epidural anesthesia with the Trendelenburg position for cesarean section with or without a cardiac surgical procedure in patients with severe mitral stenosis: a hemodynamic study.

The hemodynamic effects of epidural anesthesia (EA) with the Trendelenburg position were studied in seven patients with severe mitral stenosis undergoing emergency cesarean section (CS) because of hemodynamic deterioration. In six patients, the CS was immediately followed by an open mitral commissurotomy under general anesthesia, whereas in one patient, the CS was performed alone. A significant reduction in heart rate (120 +/- 5 to 83 +/- 7 beats/min; P less than 0.001) was observed after induction of EA. Mean arterial pressure (MAP) decreased (78 +/- 9 to 55 +/- 5 mm Hg; P less than 0.01) simultaneously with reduction of the pulmonary capillary wedge pressure (PCWP) (37 +/- 4 to 15 +/- 4 mm Hg, P less than 0.001) and cardiac index (CI) (2.4 +/- 0.3 to 1.8 +/- 0.32 L/min/m2; P less than 0.001). However, PCWP could be adjusted by selecting the appropriate angle of the Trendelenburg position. When the PCWP was approximately 25 mm Hg, MAP and Cl increased to 72 +/- 7 mm Hg and 3.1 +/- 0.4 L/min/m2, respectively, and a satisfactory hemodynamic state was achieved. Systemic vascular resistance decreased after induction of EA (2,250 +/- 250 to 1,750 +/- 450 dyne.s.cm-5; P less than 0.001), and remained unchanged during the perioperative period. It is concluded that the combination of epidural anesthesia with tilting of the table is a safe method for urgent CS in pregnant women with critical mitral stenosis in whom termination of pregnancy is indicated because of hemodynamic deterioration.

Adult↗
PubMed1995

Relationship of insulin, race, and hypertension with hemodynamic reactivity to a behavioral challenge.

Insulin is a modulator of blood pressure and may play a role in the pathogenesis of hypertension. This study examined the relationship between fasting insulin level and cardiovascular reactivity in hypertensive and normotensive black and white patients. Eighty-one patients were studied after 3 days of hospitalization on an isocaloric diet providing 200 mmol Na+ and 100 mmol K+ per day. Fasting insulin levels were determined on the morning of the second hospital day; a median split was used to determine high- and low-insulin groups. On the next day of hospitalization we examined blood pressure and hemodynamic responses to a speaking challenge. Hemodynamic responses were determined with impedance cardiography. Reactivity was studied as the percentage change from resting baseline. There were significant race by blood pressure level interactions for systolic and diastolic blood pressure reactivity (P < or = .01). Black hypertensives showed more blood pressure reactivity than either the white hypertensives or the white normotensives; black normotensives had less blood pressure reactivity than the other groups. Insulin grouping interacted with blood pressure level and race on the reactivity of the underlying hemodynamic measures (total peripheral resistance, stroke volume, and heart rate; P < or = .02). Fasting insulin level had no relationship to blood pressure reactivity. On the other hand, insulin level interacted with blood pressure level and race on the underlying hemodynamics controlling blood pressure, namely total peripheral resistance and stroke volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Hemodynamics in white coat hypertension compared to ambulatory hypertension and normotension.

Hemodynamic alterations associated with the blood pressure response in subjects with white coat hypertension may provide insight into the pathophysiologic mechanisms of this condition. Systemic arterial hemodynamics were investigated with a recently validated method based on noninvasive estimates of aortic root pressure and flow in 28 subjects with white coat hypertension (diastolic pressure > or = 90 mm Hg measured by the general practitioner [GP arterial pressure] and ambulatory daytime pressures < 140/90 mm Hg), in 23 subjects with previously untreated, ambulatory hypertension (GP diastolic pressure > or = 90 and < 115 mm Hg and ambulatory daytime diastolic pressure > or = 90 mm Hg), and in 32 normotensive subjects. The groups did not differ significantly concerning age, gender, body surface area, heart rate, stroke index and cardiac index, but total peripheral resistance index was increased and total arterial compliance reduced in the white coat group and the hypertensive group compared to the normotensive group. The subjects in the white coat group with a systolic arterial pressure during echocardiography that was > 5 mm Hg higher than the ambulatory daytime systolic pressure (n = 19) had increased cardiac index, increased total peripheral resistance, and decreased total arterial compliance compared to the normotensive group. The subjects in this group with a hemodynamic pattern characterized by a high ratio of cardiac index/peripheral vascular resistance were significantly younger than the subjects with the opposite pattern. Thus, the blood pressure increase in subjects with white coat hypertension is associated with increased cardiac output, increased peripheral vascular resistance, and reduced total arterial compliance, but the hemodynamic pattern may be influenced by age.

Adult↗