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Hemodynamic response to graded exercise after chronic beta-adrenergic blockade.

The effect of sustained beta-adrenergic blockade (BB) on the hemodynamic response to graded exercise has been studied in 31 patients with high blood pressure. Hemodynamic investigations were conducted during a control period and were repeated after 1 mo of BB. Similar readjustments were observed at rest and during submaximal and maximal exercise. No significant change occurred in maximal physical working capacity during beta blockade. This resulted from hemodynamic readjustments. Maximal exercise heart rate was reduced by 34%, and this was compensated for by a 31% enhancement in stroke index. Consequently cardiac index decreased by only 14%. In the Fick equation the decrease in cardiac index was further compensated by an increase of the total arteriovenous O2 difference of 8%, thereby maintaining O2 delivery to the tissues. At maximal exercise mean brachial artery pressure dropped 14.5%, while mean pulmonary artery pressure increased by 20%. It is concluded that the compensatory action of the stroke volume, resulting from the interaction of an increased preload and a decreased impedance, played a major role in the hemodynamic readjustments following chronic BB to maintain maximal working capacity.

Adult↗

Factors that determine the hemodynamic response to inhalation anesthetics.

The hemodynamic response to inhalation anesthesia is influenced by three factors: 1) the specific drug, 2) the dose, and 3) individual characteristics of the subject. To investigate the importance of these factors on the cardiovascular response, we administered five doses [0, 0.5, 1.0, 1.5, and 2.0 minimum alveolar concentration (MAC)] of enflurane, halothane, and isoflurane to each of six dogs. Twelve hemodynamic variables were measured. For all variables, a change in the dose of each drug produced a consistent effect in each dog. Increases in dose resulted in significant decreases in seven variables [left ventricular ejection fraction, cardiac index (CI), stroke volume index (SVI), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), left ventricular stroke work index (LVSWI), and heart rate (HR)] and a significant increase in one variable [central venous pressure (CVP)]. In contrast, the response of individual dogs to different drugs was not consistent. For seven variables [MAP, MPAP, LVSWI, CVP, pulmonary capillary wedge pressure (PCWP), end-diastolic volume index (EDVI), and end-systolic volume index (ESVI)], a significant difference in the responses of a dog to two drugs was greater than zero, whereas a significant difference in the response of at least one other dog to the same two drugs was less than zero (discordant dog-drug interactions). Thus, in contrast to the consistency of the cardiovascular response to changes in dose, the hemodynamic response to different drugs was inconsistent among dogs. We also studied the effect of fluid challenge on hemodynamic response at 1.5 or 2.0 MAC of the three drugs given to each dog.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗

Hemodynamic and norepinephrine responses to pacing-induced heart failure in conscious sinoaortic-denervated dogs.

The present study was undertaken to determine the effects of chronic sinoaortic (baroreceptor) denervation (SAD) on the hemodynamic and sympathetic alterations that occur in the pacing-induced model of congestive heart failure. Two groups of dogs were examined: intact (n = 9) and SAD (n = 9). Both groups of dogs were studied in the control (prepace) state and each week after the initiation of ventricular pacing at 250 beats/min. After the pacemaker was turned off, hemodynamic and plasma norepinephrine levels returned toward control levels in the prepaced state and after 1 and 2 wk of pacing. However, by 3 wk all hemodynamic and norepinephrine levels remained relatively constant over the 10-min observation period with the pacemaker off. With the pacemaker off, left ventricular end-diastolic pressure went from 2.7 +/- 1.4 (SE) mmHg during the prepace state to 23.2 +/- 2.9 mmHg in the heart failure state in intact dogs (P < 0.01). Left ventricular end-diastolic pressure increased to 27.1 +/- 2.2 mmHg from a control level of 4.2 +/- 1.9 mmHg i SAD dogs (P < 0.0003). Mean arterial pressure significantly decreased in intact and SAD dogs. Resting heart rate was significantly higher in SAD dogs and increased to 135.8 +/- 8.9 beats/min in intact dogs and 136.1 +/- 6.5 beats/min in SAD dogs. There were no significant differences in the hemodynamic parameters between intact and SAD dogs after pacing. Plasma norepinephrine was significantly lower in intact than in SAD dogs before pacing (197.7 +/- 21.6 vs. 320.6 +/- 26.6 pg/ml; P < 0.005). In the heart failure state, plasma norepinephrine increased significantly in both intact (598.3 +/- 44.2 pg/ml) and SAD (644.0 +/- 64.6 pg/ml) groups. There were no differences in the severity or the magnitude of the developed heart failure state in SAD vs. intact dogs. We conclude from these date that the arterial baroreflex is not the sole mechanism for the increase in sympathetic drive in heart failure.

Animals↗

Postnatal hemodynamic changes in very-low-birthweight infants.

The purpose of this study was to characterize postnatal changes in regional Doppler blood flow velocity (BFV) and cardiac function of very-low-birthweight infants and to examine factors that might influence these hemodynamic changes. Mean and end-diastolic BFV of the middle cerebral and superior mesenteric arteries, cardiac output, stroke volume, and fractional shortening were measured in 20 infants birthweight 1,002 +/- 173 g, gestational age 28 +/- 2 wk) at 6, 30, and 54 h after birth and before and after feedings on days 7 and 14. Postnatal increases in cerebral BFV, mesenteric BFV, and cardiac output were observed that were not associated with changes in blood pressure, hematocrit, pH, arterial PCO(2), or oxygen saturation. The postnatal pattern of relative vascular resistance (RVR) differed between the cerebral and mesenteric vasculatures. RVR decreased in the middle cerebral but not the superior mesenteric artery. Physiological patency of the ductus arteriosus did not alter postnatal hemodynamic changes. In response to feeding, mesenteric BFV and stroke volume increased, and mesenteric RVR and heart rate decreased. Postprandial responses were not affected by postnatal age or the age at which feeding was initiated. However, the initiation of enteral nutrition before 3 days of life was associated with higher preprandial mesenteric BFV and lower mesenteric RVR than was later initiation of feeding. We conclude that in very-low-birthweight infants over the first week of life 1) systemic, cerebral, and mesenteric hemodynamics exhibit region-specific changes; 2) asymptomatic ductus arteriosus patency and early feedings do not significantly influence these postnatal hemodynamic changes; and 3) cardiac function adapts to increase local mesenteric BFV in response to feedings.

Blood Flow Velocity↗

Measurement of hemodynamics in human carotid artery using ultrasound and computational fluid dynamics.

The objective of the study was to investigate the feasibility of using computational fluid dynamic modeling (CFD) with noninvasive ultrasound measurements to determine time-variant three-dimensional (3D) carotid arterial hemodynamics in humans in vivo. The effects of hyperoxia and hypoxic hypercapnia on carotid artery local hemodynamics were examined by use of this approach. Six normotensive volunteers followed a double-blind randomized crossover design. Blood pressure, heart rate, and carotid blood flow were measured while subjects breathed normal air, a mixture of 5% CO(2) and 15% O(2) (hypoxic hypercapnia), and 100% O(2) (hyperoxia). Carotid artery geometry was reconstructed on the basis of B-mode ultrasound images by using purpose-built image processing software. Time-variant 3D carotid hemodynamics were estimated by using finite volume-based CFD. Systemic blood pressure was not significantly affected by hyperoxia or hypoxic hypercapnia, but heart rate decreased significantly with hyperoxia. There was an increase in diastolic flow velocity in the external carotid artery after hypoxic hypercapnia, but otherwise carotid blood flow velocities did not change significantly. Compared with normal air, hyperoxic conditions were associated with a decrease in the width of the region of flow separation in the external carotid artery. During hyperoxia, there was also an increase in the minimum and a decrease in maximum shear stress in the bifurcation and hence a reduction in cyclic variation in shear stress. Hypoxic hypercapnia was associated with a reduced duration of flow separation in the external carotid artery and an increase in the minimum shear stress without affecting the cyclic variation in shear stress. This study demonstrates the feasibility of using noninvasive ultrasound techniques in conjunction with CFD to describe time-variant 3D hemodynamics in the human carotid arterial bifurcation in vivo.

Adult↗

Age-dependent cerebral hemodynamic effects of indomethacin in the newborn piglet.

With recent discussions in the literature regarding prophylactic use of early (within the first 12 h after birth), low-dose indomethacin to reduce the incidence and severity of intraventricular hemorrhage, knowledge pertaining to the cerebral hemodynamic effects of indomethacin in this age group is of significant interest. The cerebral circulation is known to undergo significant changes during the first few days of postnatal life. In the present study, we have investigated the hypothesis that postnatal adaptive changes influence the cerebral hemodynamic response to indomethacin in an age-dependent manner. Near-infrared spectroscopy with indocyanine green was used to measure cerebral hemodynamics, cerebral metabolic rate of oxygen, and cerebral oxygen extraction fraction in 39 newborn piglets. Piglets were grouped by age and received either 0.2 mg/kg indomethacin (14 were <13 h of age and 12 were >13 h of age) or saline (8 were <13 h of age and 5 were >13 h of age) infusions. In a subgroup of indomethacin-treated piglets (9 less than and 7 greater than 13 h of age), Doppler flow ultrasound was used to diagnose and monitor the presence and persistence of patent ductus arteriosus. Age was a significant factor in the cerebral hemodynamic response to indomethacin with piglets <13 h of age exhibiting delayed increases in cerebral blood flow and cerebral blood volume at 150 min post-indomethacin infusion.

Adaptation, Physiological↗

Changes in renal and systemic hemodynamics after NO-synthase inhibition in males with family history of hypertension.

BACKGROUND: Nitric oxide (NO) plays an important role in the regulation of blood pressure and renal hemodynamics. METHODS: To further investigate the role of NO in human hypertension, we studied the effect of systemic injection of N(G)-monomethyl-L-arginine (L-NMMA) on renal hemodynamics, urinary sodium excretion (FE(Na)), systemic hemodynamics and several vasoactive hormones in 5 healthy male subjects with (group H) and without (group N) family history of hypertension. An intravenous infusion of L-NMMA (3 mg/kg over 10 min) or placebo was given in a randomized, double-blinded manner. GFR and ERPF were measured by inulin- and PAH-clearances. Norepinephrine infusion (0.1 microg/kg/min over 60 min) served as vasoconstrictive control infusion. RESULTS: L-NMMA induced a significant decrease in ERPF (-135 +/- 49 vs. 7 +/- 31 ml/min/1.73 m(2) with placebo, p < 0.05), a decrease in FE(Na) (-1.2 +/- 0.6% with L-NMMA vs. 0.0 +/- 0.1% with placebo), and a significant increase in diastolic blood pressure (+7 +/- 1 vs. -2 +/- 1 mm Hg with placebo) in group N, only. A sustained drop in plasma renin activity (-0.1 +/- 0.1 vs. 0.3 +/- 0.1 ng/ml/h with placebo) could also be seen in this group, only. Subjects with family history of hypertension showed minor or even no response (changes in diastolic blood pressure: L-NMMA: 5 +/- 3 mm Hg, placebo: 0 +/- 2 mm Hg; changes in ERPF: L-NMMA: -89 +/- 57 ml/min/1.73 m(2), placebo: -34 +/- 28 ml/min/1.73 m(2); changes in plasma renin activity: L-NMMA: -0.0 +/- 0.3 ng/ml/h, placebo: -0.1 +/- 0.2 ng/ml/h). The vasoconstrictive effect of norepinephrine infusion did not differ between both groups. CONCLUSION: Our data indicate that systemic NO synthetase inhibition by L-NMMA results in a blunted effect on systemic blood pressure and the renal hemodynamic system in subjects with family history of hypertension.

Adult↗

[Effects of active and passive movement stimuli on cerebral hemodynamics and the cerebral metabolism].

INTRODUCTION: In contrast to the well-examined cardiovascular changes during movement stimuli, up to now changes of cerebral hemodynamics and cerebral metabolism have rarely been studied. We investigated the question if active and passive movement stimuli cause changes in the cerebral hemodynamics and the cerebral metabolism. METHOD: Active and passive repetitive movement stimuli on 14 volunteers (8 females, 6 males, age 35 +/- 8 years) were examined. As a parameter of cerebral hemodynamics the mean and the peak blood flow velocity (mCBFV(MCA), pCBFV(MCA)) in the middle cerebral artery (MCA) were recorded by transcranial Doppler sonography. At the same time the noninvasive blood pressure (Penaz method) and the CO(2) expiration concentration were investigated on 8 volunteers of the collective. As cerebral metabolic parameters we examined in 4 volunteers additionally the cerebral respiratory chain enzyme cytochrome aa3 (ccytaa3) and the cerebral oxygen saturation (cHbO(2)) by the transcranial near infrared spectroscopy. With each volunteer 4 measurement series were carried out with a special active and passive exercise program for the right upper as well as the right lower extremity. Each measurement series was formed according to the evoked flow test (R. Aaslid): Exercises were carried out for 20 s, followed by a break of 20 s; this was repeated 10 times for each series. RESULTS: During active exercises of the right lower extremity we found an increase of 13.6% (p < 0.001) of pCBFV(MCA) and an increase of 3.8% (p = 0.003) of mCBFV(MCA). During passive exercises of the lower extremity the increases ran up to 12.3% (p < 0.001) for pCBFV(MCA) and 3.4% (p = 0.004) for mCBFV(MCA). The increases of pCBFV(MCA) came up to 12.5% (p < 0.001) at active exercises of the right upper extremity, those of mCBFV(MCA) to 3.5% (p = 0.15). During passive exercises of the upper extremity the pCBFV(MCA) increased by 12.2% (p < 0.001) and the mCBFV(MCA) by 4.6% (p = 0.007). Significant increases of ccytaa3 were measured during active exercises of the upper extremity (1.6%; p = 0.04) and of the lower extremity (2.7%, p = 0.007). We also found an increase of ccytaa3 during passive exercises of the upper extremity (1.5%, p = 0.04). Significant changes of cHbO(2) were measured with 2.5% (p < 0.05) at active exercises of the lower extremity. CONCLUSION: These studies show that active as well as passive clinical exercises cause an increase of cerebral blood flow velocity. We attribute the increase of cerebral hemodynamics and cerebral metabolism to cerebral activation and autoregulative mechanisms.

Adult↗

Epinephrine affects hemodynamics of noninnervated normal and all-trans retinoic acid-treated embryonic chick hearts.

OBJECTIVE: To study the acute effect of epinephrine on hemodynamics of noninnervated normal and retinoic-acid-treated embryos. DESIGN: Prospective interventional study design. METHODS: A total of 190 stage 15 (50-55 h of incubation) chick embryos were randomly treated with 1 microg all-trans retinoic acid and reincubated. At stage 20 (day 3) and stage 24 (day 4), dorsal aortic flow velocities were measured with a 20-MHz pulsed Doppler velocity meter, in normal and retinoic-acid-treated embryos. Flow velocity waveforms were assessed both before and after the administration of epinephrine (5 or 10 microg). RESULTS: Epinephrine caused a significant increase (p < 0.05) in heart rate, peak and mean velocities, peak acceleration, peak and mean blood flows, stroke volume and dorsal aortic area of both stage 20 and stage 24 normal and retinoic-acid-treated chick embryos. However, before epinephrine administration, stage 24 retinoic-acid-treated embryos displayed a significantly lesser increase in all outcome variables with the exception of dorsal aortic area. This was even observed after epinephrine administration. The effect of retinoic acid on cardiac output could not be compensated by epinephrine application. CONCLUSION: Epinephrine affects hemodynamics in both normal embryos and retinoic-acid-treated embryos prior to sympathetic innervation. A significant difference in hemodynamics exists between stage 24 normal and retinoic-acid-treated embryos. The underlying mechanism for the observed hemodynamic changes will need to be investigated.

Animals↗

Hemodynamic effects of combined treatment with lignocaine, procainamide and practolol in acute myocardial infarction.

In the treatment of refractory ventricular tachyarrhythmias antiarrhythmic drugs must sometimes be combined. An electrophysiologically appropriate combination is lignocaine and procainamide and, when needed, a beta-blocking agent. The hemodynamic effects of this treatment were studied in 6 patients in the acute phase of myocardial infarction. After a control period, an infusion of lignocaine was started and 1 h later procainamide/placebo was added in a double-blind system and finally also practolol/placebo. The drugs were given intravenously in ordinary doses. Hemodynamics were studied by bedside catheterization. During triple treatment heart rate and aortic pressures fell significantly whereas right atrial mean pressure increased compared to the control period. Stroke volume, cardiac output and pulmonary artery pressures were unchanged. Most of the changes appeared when practolol was added. Following the procainamide injection a transient fall in aortic pressures was noted. Lignocaine gave no hemodynamic effects. The number of ventricular premature beats was reduced in all patients and no patient had ventricular tachycardia during treatment. In these patients it was possible to combine lignocaine, procainamide and practolol in the acute phase of myocardial infarction. However, 3 patients developed hypotension, 1 sinus bradycardia and 1 had a short run of nodal tachycardia. It is concluded that this kind of combined treatment, because of its potential risks, should be restricted to critical clinical situations and then it ought to be hemodynamically controlled.

Adult↗

Hemodynamics in borderline hypertension: acute effect of furosemide.

In order to identify the hemodynamics of borderline essential hypertension, radionuclide angiography was performed before and after bolus injection of furosemide (40 mg i.v.) both at 3 min (i.e. before diuretic effect) and at 30 min (i.e. after diuretic effect) in 16 borderline (B) patients and in 14 age-matched WHO classification I-II essential hypertensives (H) patients. 14 age-matched normotensive (N) subjects were used as controls. B patients were further subdivided into two subgroups according to a cardiac index under or above 3 liter/min/m2 in basal conditions. Baseline hemodynamic characteristics showed higher values of mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both H and B patients when compared with N subjects (p less than 0.001). Furthermore, B and H patients exhibited lower values of left ventricular peak filling rate (PFR) than seen in N subjects (p less than 0.01 and p less than 0.05, respectively). H patients demonstrated higher peak systolic blood pressure/endsystolic volume ratio (PSP/ESV) than seen in N subjects (p less than 0.05). PFR positively correlated with peak emptying rate (PER) only in N and B patients (p less than 0.05). After furosemide administration, even though differences were observed in the absolute values, B and H patients showed similar hemodynamic patterns. Only the B subgroup with cardiac index (CI) greater than 3 liter ('volume-dependent' patients) showed a decrease in left ventricular end-diastolic volume index (LVEDVI) at 30 min associated with a lowering of stroke index (SI; p less than 0.005 for both), when compared with pre-drug values. In B patients with CI less than 3 liter ('afterload-dependent' patients) no differences were observed either at 3 min or at 30 min in comparison with values obtained prior to drug administration. Moreover, in this subgroup, like in H patients, there was a negative correlation (p less than 0.01) between 3-min percent change of SVRI and 3-min percent change of SI. Our data suggest that in 'borderline' hypertension: (a) there may be an increase in peripheral resistance, as in established hypertension, especially when age-matched groups are considered; (b) the earliest sign of compromised left ventricular function is the reduction in diastolic PFR but, unlike established hypertension, this index is still correlated with systolic function; (c) cardiac output might be even somewhat reduced and also negatively correlated with vascular resistance ('afterload-dependent' hearts); (d) furosemide (acute administration) might contribute to a better definition of hemodynamic behavior.

Adult↗

Efficacy and safety of flosequinan, given over 3 days, evaluated by continuous hemodynamic monitoring.

The hemodynamic effects of flosequinan, a new balanced vasodilator, were evaluated in 12 patients with chronic congestive heart failure. The drug was added to diuretics and digitalis and given as an oral dose of 100 mg, once daily in the morning, over 3 days, and hemodynamic monitoring was performed before the first dose and for 72 h thereafter. Hemodynamic improvement, peaking between 1 and 2 h after oral administration, was observed on all 3 days. On day 1 pulmonary capillary wedge pressure (PCWP) was reduced from 27.8 +/- 8.6 to 13.0 +/- 3.1 mm Hg and cardiac output (CO) increased from 3.3 +/- 0.6 to 4.5 +/- 0.9 liters/min (p less than 0.05). After 12-16 h the effect was slightly attenuated but remained significant at 24 h. A similar response was observed after the doses given on days 2 and 3. At 72 h PCWP was 15.5 +/- 4.1 mm Hg and CO 3.8 +/- 1.1 liters/min (p less than 0.05 for the difference from baseline). Heart rate was slightly increased only at 2 h after the dose. Pulmonary arterial and right atrial pressure and systemic and pulmonary vascular resistances were significantly reduced (except for systemic resistance at 72 h). In conclusion, flosequinan produces hemodynamic improvement in patients with chronic congestive heart failure. The response to subsequent doses is similar to the response to the first dose.

Aged↗

Hemodynamic mechanisms of the effect of nitroglycerin in patients with acute myocardial infarction.

We studied the hemodynamic response to intravenous nitroglycerin (NTG) in 40 patients with and without acute heart failure (hemodynamic subsets I-IV) during acute myocardial infarction. Hemodynamic measurements were performed by right heart catheterization. The results showed that NTG response influenced mainly the preload and to a lesser extent the afterload, however these changes were dependent on initial hemodynamic status. The changes in mean arterial pressure and cardiac index were predominantly related to pretreatment pulmonary wedge pressure and slightly to systemic vascular resistance. Response to NTG could be predicted with 85% probability as a decrease of pulmonary wedge pressure, with 58% probability as a decrease in mean arterial pressure and cardiac index, and with 32% probability as an increase in cardiac index and a decrease in systemic vascular resistance. These results indicate that NTG therapy could have optimal results in patients with elevated pulmonary wedge pressure and normal cardiac index, while in the subsets with low mean arterial pressure or low cardiac index potentially deleterious decrease in these values could occur. Therefore the optimal condition for use of intravenous nitroglycerin in the patients with acute heart failure is isolated pulmonary congestion.

Adult↗

Sympathetic and hemodynamic response to volume removal during different forms of renal replacement therapy.

Sympathetic and hemodynamic response to a constant volume removal was investigated during pure ultrafiltration, hemofiltration, acetate hemodialysis, and bicarbonate hemodialysis in the same ESRD patients. Small solute removal rates were matched. The sympathetic response resulting in an increase of total peripheral vascular resistance was found to be qualitatively adequate in ultrafiltration and hemofiltration, but not in acetate and bicarbonate hemodialysis. This inadequate response to volume removal explains the clinically observed hemodynamic instability during hemodialysis. The purpose of the study was to substantiate the, compared to hemodialysis, improved tolerance to fluid withdrawal during ultrafiltration and hemofiltration with hemodynamic data and to correlate hemodynamic and sympathetic changes during the different treatment modalities of uremia.

Adult↗

Systemic hemodynamics and renal function in cirrhotic patients during plasma volume expansion.

Systemic hemodynamic impairment (hepatocirculatory failure) has been suggested as one of the possible factors which may explain the renal hemodynamic alterations found in the late stage of liver cirrhosis, typical of the hepatorenal syndrome. 20 patients, divided into two groups of 10 sodium retainers and 10 sodium excretors, affected by liver cirrhosis with portal hypertension and ascites, were studied. Renal functional parameters (diuresis, urinary and plasma electrolytes, urine to plasma osmolality and creatinine ratios and creatinine clearance) were evaluated before and after acute volume expansion with 1,000 ml of 10% dextran in saline, infused through a catheter located in the right atrium. Hemodynamic tests (cardiac index, systemic vascular resistance, right atrial pressure and capillary wedge pressure) were performed before, during and after expansion. Cardiac index decreased in 6 patients (sodium excretors) after a 500-ml infusion and rose again after 1,000 ml in 5 of them. The remaining 14 patients showed a progressive and significant increase of cardiac index. A strong inverse relationship between cardiac index and systemic vascular resistance was observed (r = -0.87; p less than 0.001). The mean left-ventricular function curve showed a slow response in most sodium excretors and a normal response in the sodium-retaining group, without significant difference between the two groups. Sodium excretion significantly improved after expansion in both groups of patients. No relationship was found between hemodynamic response and renal function. These data show that cardiocirculatory function is normal, even in sodium-retaining cirrhotics.

Adult↗

Localizing role of hemodynamics in atherosclerosis in several human vertebrobasilar junction geometries.

Atherosclerosis is a common finding in the vertebrobasilar junction and in the basilar artery. Several theories try to link the process of atherogenesis with the forces exerted by the flowing blood. An attractive relation has been found between the locations in vessels at which atherosclerotic plaques are often present and the locations in models where complicated flow patterns exist. Most of the studies provided data on bifurcations. Finding a similar relation in an arterial confluence would certainly add to the credibility of the (causal) relationship between hemodynamics and atherosclerosis. Further support can be provided if variations of the geometry result in changes of the location of the atherosclerotic lesions, corresponding to the changes of the flow force distribution. In our previous numerical and experimental work, the influence of geometric and hemodynamic parameters, such as asymmetrical inflow, confluence angle, and blunting of the apex, on the flow in vertebrobasilar junction models has been investigated in detail. Recirculation areas and distribution of the wall shear stress have been computed. In this anatomic study, the effect of modulation of these geometric and hemodynamic parameters on the flow pattern is compared with the size and location of plaques in human vertebrobasilar junctions and basilar arteries. In addition, a comparison is made between the preferential areas of atherosclerotic plaques in junctions and bifurcations to demonstrate the localizing role of hemodynamics in atherogenesis. The apex of the vertebrobasilar junction and the lateral walls of the basilar artery appeared to be prone to atherosclerosis. In 43 of 85 vertebrobasilar junctions, a plaque was found at the apex. Furthermore, the summed plaque thickness at both lateral walls differs significantly (paired t test, P=.03) from that at the walls facing the pons and the skull base. In contrast, several authors found that the lateral walls of the mother vessel and the apex in bifurcations are often spared. Modulation of the various parameters in the models changed the size of the regions with low wall shear stress and/or recirculation areas dramatically. A comparable effect was found in the occurrence of plaques in the human vertebrobasilar junction; eg, for an atherosclerotic plaque at the apex, a predicted probability larger than 0.5 was computed for blunted apexes and for sharp-edged apexes with a confluence angle exceeding 90 degrees. Apparently, two geometric risk factors for an atherosclerotic plaque at the apex can be distinguished: a blunted apex and a large confluence angle.

Aged↗

Hemodynamic findings in 123 patients with acute myocardial infarction on admission.

Hemodynamic and clinical evaluations of 123 patients with acute myocardial infarction were performed during the first hour of admission to the hospital. In the 123 patients, the right atrial pressure was less than 10 mm Hg in 49 patients, the right atrial oxygen saturation was less than 70% in 97 patients, the arteriovenous oxygen difference was greater than 5.0 vol% in 78 patients. The arterial Po2 was less than 90 mm Hg in 101 of 107 patients who could be evaluated while breathing room air. The cardiac index was depressed below 3.0 L/min/m2 in 65 of 98 patients. The hemodynamic findings generally correlated with the clinical status of the patient; however, within each clinical class of patients there was a wide spectrum of values for each measurement evaluated. There was also considerable overlap of the values found within each clinical classification. It is concluded that hemodynamic evaluation of patients with acute myocardial infarction presents a profile of the patient which is frequently different from the profile that clinical evaluation presents. An objective hemodynamic classification of patients with acute myocardial infarction may provide a more useful index for the evaluation of the patient's prognosis and for the assessment of preventative therapy.

Adult↗

Acute effects of oral pirbuterol on myocardial oxygen metabolism and systemic hemodynamics in chronic congestive heart failure.

Pirbuterol hydrochloride, an orally effective beta-adrenergic agonist, improves hemodynamic abnormalities in patients with congestive heart failure, but its effects on myocardial oxygen consumption (MVO2) and coronary blood flow have not been characterized. We studied the effects of 20-30 mg of oral pirbuterol on myocardial metabolic and hemodynamic parameters in 12 patients (six with coronary artery disease) with chronic CHF refractory to standard medical therapy. Pirbuterol induced an increase in cardiac index (1.7 +/- 0.1 to 2.3 +/- 0.2 l/min/m2, p less than 0.05) and a fall in systemic vascular resistance (1884 +/- 118 to 1391 +/- 69 dyn-sec-cm-5, p less than 0.01) 2 hours after administration. Pulmonary capillary wedge pressure fell from arterial and right atrial pressures did not change. Heart rate remained constant. Arterial-coronary sinus oxygen content difference narrowed (from 12.9 +/- 0.4 to 11.1 +/- 0.3 vol%, p less than 0.05), while no significant change occurred in MVO2. Myocardial oxygen extraction ratio and myocardial lactate extraction ratio did not change, and no patient developed angina or electrocardiographic evidence of myocardial ischemia. Patients with coronary artery disease had hemodynamic and myocardial metabolic responses similar to those without coronary artery disease. Pirbuterol effects substantial acute hemodynamic improvement in patients with chronic congestive heart failure without increasing requirements for coronary blood flow or myocardial oxygen delivery and without provoking myocardial ischemia.

Adult↗