Venous delay, a major source of error in isotopic cardiac output determination.
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
F M Fouad
Publications and source records attributed to F M Fouad.
Automated computer program for radionuclide cardiac output determination.
Radionuclides have provided a safe, reliable, and minimally invasive method for repeated determinations of cardiac output. A completely automated computer program for data analysis is described. Cardiac output values obtained by this technique correlated closely with values obtained by manual determination of the region of interest (r = 0.90 for right-ventricular and 0.98 for left-ventricular outputs, p less than 0.001 for both). Further, cardiac output determined by computer selection of either left-ventricular area of interest or of the "whole heart region" correlated significantly with that simultaneously determined by dye-dilution technique (indocyanine green; r = 0.86, p less than 0.001 for both). The automated approach allows greater objectivity in the selection of the regions of interest, faster turnaround of calculated results, and use of a smaller dose of radionuclide.
Adult↗
Hemodynamics of essential hypertension in young subjects.
Cardiac output was determined in 42 young essential hypertensives (15 to 25 yrs); values ranged from 3.86 to 10.30 L./minute. These differences were not related to magnitude of volemia. Correlation of output to weekly blood pressure average (BPav) was not significant; its relationship to intraarterial pressure (BPia) was not significant in 21 patients aged 20 to 25 and of borderline significance in 13 aged 15 to 19. Blood pressure changes associated with the study (BPia--BPav) were also not consistently related to cardiac output. Six patients had systolic hypertension; only one had elevated stroke volume. These results outline as complex a picture in young essential hypertensives as in older subjects.
Adolescent↗
Hemodynamics of postmyocardial revascularization hypertension.
The evolution of hemodynamic variables during the development of postcoronary bypass hypertension was investigated with use of serial cardiac output determination (indocyanine green dye) in 17 patients. Seven of the 17 patients remained normotensive (Group I) during the follow-up period of 4 to 6 hours after operation, whereas 10 (Group II) had a steady increase in blood pressure (173/101 mm Hg +/- 5.9/2.4 [mean +/- standard error] from 132/78 +/- 4.0/2.5 mm Hg immediately postoperatively, P less than 0.001) during the same time interval. Patients in Group I had no significant change in cardiac output, total peripheral resistance or heart rate. In contrast, patients who became hypertensive had a significant increase in total peripheral resistance (47 +/- 2.9 units/m2 from an initial level of 38 +/- 2.5 units/m2, P less than 0.001) with no significant change in cardiac index (2.73 +/- 0.17 versus 2.66 +/- 0.25 liters/min per m2, P greater than 0.10). Their heart rate, which was rapid initially (102 +/- 3.7 beats/min), remained unchanged during the hypertensive episode (103 +/- 3.0 beats/min). The mean rate of left ventricular ejection was not reduced by the increase in pressure and even tended to increase further in all but one patient. Central venous pressure (measured in all patients) and left atrial pressure (measured in eight patients) remained constant throughout the study in both Groups I and II. The results suggest that the mechanism underlying this type of hypertension is a generalized hemodynamic disturbance possibly related to overall sympathetic overdrive rather than the result of improved cardiac performance induced by myocardial revascularization.
Adult↗
Unilateral stellate block in the treatment of hypertension after coronary bypass surgery. Implications of a new therapeutic approach.
Unilateral stellate ganglion block (right or left) was achieved by local injection of 15 ml of lidocaine in 27 patients with hypertension after coronary bypass surgery. The stellate block led to rapid and sustained control of blood pressure in 18 patients (9 of 15 with right stellate block and 9 of 12 with left stellate block). The reduction in arterial pressure was associated with significant (P less than 0.01) reductions in total peripheral resistance and heart rate but no significant changes in cardiac output or central venous or left atrial pressures. This hemodynamic pattern as well as effectiveness of a unilateral approach suggests that the stellate block reduced arterial pressure by interrupting the afferent limb of a pressor reflex from the heart or great vessels, or both. The procedure was free from side effects and helped avoid prolonged parenteral administration of potent antihypertensive drugs.
Adult↗
Three cases of hypotension and syncope with ventricular pacing: possible role of atrial reflexes.
Hypotension with lightheadedness and near syncope occurred in three patients during effective ventricular pacing. Hemodynamic studies demonstrated a decrease in cardiac output ranging from almost no decrease to 15 percent, presumably related to the loss of effective atrial contraction. The decrease in output was too small to explain by itself the reduced blood pressure, which resulted from paradoxic reduction of total peripheral resistance in one patient and from failure of resistance to increase in two. Baroceptor reflexes (Valsalva response) were normal in all three patients; hence it is suggested that the failure of compensatory increases in total peripheral resistance may be due to a reflex from the sudden atrial distension that occurs during atrioventricular (A-V) dissociation. The fluctuations in arterial pressure during ventricular pacing were synchronous with the appearance of cannon waves in the right atrial pressure tracing. Arterial pressure during A-V dissociation thus appears to be balanced by two opposite reflexes: the baroceptor reflex, which attempts to compensate for reduction in output, and atrial distension, which reduces peripheral resistance.
Blood Pressure↗
Haemodynamics of orally-active converting enzyme inhibitor (SQ 14225) in hypertensive patients.
1. The haemodynamic effects of oral converting enzyme inhibitor (SQ 14225) were assessed in eight patients with severe essential or renovascular hypertension. 2. Mean arterial pressure fell (149 +/- 5 to 127 +/- 8 mmHg, P less than 0.02), because of a fall in total peripheral resistance (6.9 +/- 0.53 to 5.7 +/- 0.40 kPa 1(-1)s m2) without a significant change in cardiac index. Two of the eight patients were non-responders without pressure reduction or a haemodynamic change. Sodium restriction (10 mmol/day) while the same dose of SQ 14225 was continued further lowered arterial pressure (137 +/- 8 to 111 +/- 12 mmHg, P less than 0.05) through further resistance reduction (6.5 +/- 0.53 to 5.2 +/- 0.40 kPa 1(-1)s m2, P less than 0.05). 3. Haemodynamic responses to head-up tilt (increased heart rate and resistance, decreased cardiac index) were unaffected by SQ 14225 regardless of sodium intake. 4. The pattern of reduction in peripheral resistance, with unchanged cardiac index, was similar to that produced by vasodilators acting at both arteriolar and venular levels.
Adult↗
Hemodynamic characteristics in hypertension.
Recent studies have outlined both the importance and limitations of hemodynamic studies in hypertension. Characterization of any type of hypertension cannot be established in terms of cardiac output or total peripheral resistance alone. It depends more on the way in which various factors (hemodynamics, volume, humoral and neural) interrelate than on disturbances of one factor alone. More studies are needed, not so much of each variable alone as of correlations among those variables, e.g. correlations between humoral factors and hemodynamic characteristics. Further, hemodynamic analyses must be extended beyond calculations of TPR to evaluation of other variables such as magnitude and distribution of intravascular volume, indices of aortic distensibility, of velocity of ventricular ejection and of cardiac performance. Interpretation of the results must also take into account factors such as hemodynamic setting, age of patient, neurogenic stimulation and structural changes amongst others. Careful attention to these variables will allow more accurate conclusions regarding characteristics of different types of hypertension, and patterns of response to therapy. Accurate hemodynamic characterization may help orient diagnosis and a rational choice of treatment in initial stages but specially for evaluation of resistant cases.
Aorta↗
Abiotic transformations and decomposition kinetics of 4-carbamoyl-2'-[(hydroxyimino)methyl]-1,1'-(oxydimethylene)-bis(pyridin ium chloride) in aqueous phosphate buffers.
The rate of disappearance of 4-carbamoyl-2'-[(hydroxyimino)methyl]-1,1'-(oxydimethylene) bis (pyridinium chloride) (HI-6) from aqueous phosphate buffers (pH 3.0-9.1) was both pH and temperature sensitive. In midrange buffers (pH 6.0-9.1, mu = 0.2 M) at 37, 25, or 4 degrees C the decomposition followed first-order kinetics consistent with hydroxide-promoted decomposition of the un-ionized drug or with hydrolysis of the ionized oxime anion to result in 4-carbamoyl-2'-hydroxy-1,1'-(oxydimethylene)bis(pyridinium) cation (intermediate 1). The subsequent conversion of intermediate 1 to 4-carboxy-2'-hydroxy-1,1'-(oxydimethylene)bis(pyridinium) cation (intermediate 2) followed higher order kinetics which were consistent with either acid- or base-promoted hydrolysis of the B-ring amide functionality. After approximately 138 days in the dark, the sum of the residual HI-6, intermediate 1, and intermediate 2 in the crude decomposition mixture accounted for 89.9 +/- 10.0% of the initial substrate. Minor byproducts included 4-carbamoyl-2'-carboxy-1,1'-(oxydimethylene)bis(pyridinium) cation, 2-pyridinealdoxime, 2-pyridinecarboxaldehyde, 2-hydroxypyridine, isonicotinamide, isonicotinic acid, and traces of cyanide. In addition, 2-cyanopyridine appeared to be a transient intermediate in more alkaline media. In total, this drug resembles other mono- and bis(pyridinium) aldoximes in terms of the decomposition routes in aqueous solutions at intermediate pHs.
Antidotes↗
Chemical and epidemiological aspects of modified butter oil fractions.
Butter lipids are an important traditional source of dietary energy intake in the form of fat. Butter lost a sizable portion of its market share due to controversies associated with its cholesterol content and high percentage of long-chain saturated fatty acids. Accordingly, the use of vegetable oils and their chemically manipulated counterparts such as those produced by partial hydrogenation or interestrification increased proportionally. However, beginning in 1940, researchers developed several procedures such as temperature-controlled crystallization, refractionation of crystallized butter oil solids, and supercritical carbon dioxide extraction to improve the acceptance of butter oil. Others proposed preparation of synthetic substitutes such as sucrose polyesters to reduce intestinal absorption of fatty acids, thus reducing caloric intake with concomitant reduction in serum cholesterol. The present review provides a summary of the efforts of several attempts to improve the acceptability of butter together with the anticipated epidemiological consequences of long-term consumption of altered butter oil to mammalian health.
Butter↗
Inotropic responsiveness in hypertensive left ventricular hypertrophy: impaired inotropic response to glucagon and vasoactive intestinal peptide in renal hypertensive rats.
Previous studies have shown that left ventricular (LV) hypertrophy in renal hypertensive rats (RHR) is associated with reduced responsiveness to beta-adrenergic stimulation (isoproterenol) but not to calcium or cardiac glycosides. To determine whether this impairment is restricted to beta-receptor agonists or extended to include other stimulants of the adenylate cyclase system, inotropic responses to glucagon and to vasoactive intestinal peptide (VIP) were determined in isolated paced hearts (Langendorff preparation) from RHR and strictly matched sham-operated controls. The response (delta peak LV +dP/dt) to both agonists was significantly reduced in RHR, whether expressed in absolute value or in percent of baseline. It averaged 59.3 +/- 19.3 (SE) mm Hg X s-1 in RHR at the highest dose of VIP (15 micrograms) and a perfusion pressure (PP) of 50 mm Hg as compared with 255 +/- 68.4 in controls (p less than 0.01). The responses to glucagon were determined at two levels of perfusion pressure--50 and 80 mm Hg--to determine the influence, if any, of possible alterations in myocardial perfusion on differences between the normal and hypertrophied hearts. At both PP levels the LV +dP/dt response was significantly lower in RHR--+ 374 +/- 103 vs. + 1,026 +/- 166 mm Hg X s-1 (p less than 0.005) or + 120 +/- 5 vs. + 143 +/- 7% of baseline value (p less than 0.02) for PP of 50 mm Hg; and 392 +/- 154 vs. + 1,732 +/- 251 mm Hg X s-1 (p less than 0.01) or + 112 +/- 4 vs. + 160 +/- 2% (p less than 0.001) for PP of 80 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Hemodynamic and volume changes associated with captopril.
Explore the source record for details and available documents.
Aldosterone↗
Long-term converting enzyme inhibition and sympathetic nerve function in hypertensive humans.
Orthostatic hypotension is uncommon during oral converting enzyme inhibition, even when combined with salt depletion. To assess the mechanisms responsible for the cardiovascular homeostasis in this condition, we studied the blood pressure (BP), heart rate (HR), total plasma catecholamines (CA), and plasma renin activity (PRA) responses after 20 minutes of 60 degrees head-up tilt in four groups of hypertensive patients. Group 1 included seven untreated patients; Group 2, eight patients on converting enzyme inhibitor (captopril) therapy; Group 3, six patients on diuretic therapy and Group 4, 15 patients on combined captopril and diuretic therapy. Long-term converting enzyme inhibition alone or in combination with diuretics resulted in reduction of mean arterial pressure (MAP) associated with a marked increase in PRA and fall in plasma aldosterone concentration (PAC). Pronounced increases in HR and plasma CA on tilt were observed in all groups. In Groups 1, 2, and 3, BP was maintained during tilt; in Group 4, three patients fainted between 5 and 15 minutes while the other 12 had a normal response to tilt. Plasma catecholamines increased more significantly after 15 and 20 minutes of tilt, more in Groups 3 and 4 than in Group 1, while no differences in HR response were observed among groups. Results suggest that sympathetic compensatory mechanisms are adequate in the majority of patients to maintain BP during converting enzyme inhibition even when combined with salt depletion. In a few who exhibited orthostatic hypotension, a vasovagal attack seemed to be responsible for bradycardia and fall in BP.
Adult↗
Hypertension in obese patients: hemodynamic and volume studies.
Distinct hemodynamic and volume characteristics have been suggested for established hypertension in severe obesity, namely, a high cardiac output, and expanded blood volume, and a normal peripheral resistance. To evaluate whether hypertension in moderately obese patients represents a separate entity that can be defined by hemodynamic and volume profiles, we studied these in 50 such patients and compared results with those obtained in 59 nonobese essential hypertensives and 25 normal subjects. Both obese and nonobese hypertensives had a normal cardiac index (men, 2.8 +/- 0.1 vs 2.8 +/- 0.09 liter/min/m2; women, 2.9 +/- 0.1 vs 2.8 +/- 0.1 liter/min/m2, respectively) and similarly elevated total peripheral resistance (men, 47.1 +/- 2.3 vs 46.5 +/- 1.9 U . m2; women, 45.0 +/- 2.4 vs 44.0 +/- 1.3 U . m2, respectively) as compared to normals (cardiac index: men, 2.9 +/- 0.09 liter/min/m2, women, 3.4 +/- 0.2 liter/min/m2; total peripheral resistance: men, 29.4 +/- 1.0 U . m2, women, 28.3 +/- 2.8 U. m2). Volume measurements corrected to body surface area showed that both obese and nonobese hypertensive patients had lower blood volume (men, 2.6 +/- 0.05 vs 2.5 +/- 0.05 liter/m2; women, 2.2 +/- 0.05 vs 2.3 +/- 0.05 liter/m2, respectively) than normals (men, 2.9 +/- 0.08 liter/m2; women, 2.5 +/- 0.08 liter/m2). The results of this study suggest that hypertension in moderately obese subjects is similar in its hemodynamic and volume profiles to hypertension in the nonobese and that the presence of obesity does not alter the hemodynamic characteristics of established essential hypertension.
Adult↗
Sympathetic contribution to the cardiac response to stress in hypertension.
Studies of cardiac performance in hypertension have often been restricted to cardiac output determinations, although the latter alone are inadequate for that purpose. To define the range of cardiac performance in hypertension, the response of left ventricular filling pressure to increased workload (static exercise) was determined in 39 subjects--eight normotensive (NT) volunteers, seven patients with borderline hypertension (BLH), and 24 essential hypertensives (EH), of age-matched groups. A rise of mean pulmonary wedge pressure (PWP) by 5 mm Hg or more during maximum handgrip (HG) was considered "abnormal" for a workload (SBP x HR x 10(-3)) increase of greater than or equal to 25%. All NT subjects and all patients with BLH as well as 16 of the 24 EH (EH-I) showed normal cardiac performance by this definition. In contrast, PWP increased greater than or equal to 5 mm Hg during HG in eight patients with EH (EH-II). The calculated increase in cardiac workload was not significantly different among the four groups (+5, 5.8, 5.4 and 5.5 respectively). Beta blockade (propranolol, 10 mg i.v.) slowed heart rate in all subjects and reduced SBP x HR product in all groups both at rest and during HG. Responses of PWP to HG were widely divergent in the different patients. However, as a group those patients with "impaired cardiac performance" before propranolol (EH-II) had a greater reduction in performance following propranolol than EH-I or NT. This study suggests that adrenergic support of cardiac performance might be important in some hypertensive patients with no evidence of heart failure.
Adult↗
Responses of the stenosed and contralateral kidneys to [Sar1, Thr8] AII in human renovascular hypertension.
To better define the intrarenal hemodynamic effects of angiotensin in human renovascular hypertension, 10 patients underwent renal hemodynamic and functional measurements before and during infusion of a competitive angiotensin analog, [Sar1, Thr8] AII. Eight had technically satisfactory split function studies. Despite a fall in mean arterial pressure (132 +/- 6 to 121 +/- 6 mm Hg, p less than 0.05) and humoral changes consistent with angiotensin-mediated hypertension, the intrarenal effects of this analog were commonly those of an angiotensin agonist, producing vasoconstriction and sodium retention. This was quantitatively greatest in the contralateral kidney, whose preinfusion sodium excretion (86 +/- 30 microEq/min vs 25 +/- 9 microEq/min, p less than 0.02) and glomerular filtration rate (76 +/- 7 ml/min vs 41 +/- 7 ml/min, p less than 0.01) were higher than the stenotic kidney. In some cases, an increase in renal blood flow and rise in sodium excretion were evident during angiotensin blockade, suggesting a tonic intrarenal action of angiotensin. Although renin vein renin values differed markedly between the stenotic and contralateral kidney (ratio = 2.05 +/- 0.30), relative changes in effective renal plasma flow were correlated (r = 0.84: p less than 0.01) during infusion of this analog. These results underscore the differences in sensitivities between vascular beds to the effects of angiotensin II and the major role of the contralateral kidney in renal function and sodium homeostasis in human renovascular hypertension.
Adult↗
Cardiac factors in response to antihypertensive treatment.
The cardiac status of hypertensive patients will influence not only the indications for and choice of antihypertensive agents but can also alter the effectiveness of antihypertensive therapy. The heart may interfere with adequate blood pressure control either because of marked increases in cardiac output or as result of decompensation activating various pressor mechanisms or through the generation of pressor reflexes. Reflex increases in cardiac output may blunt or even nullify the effect of reduction in peripheral resistance by vasodilators. Cardiac decompensation from incidental disease or secondary to some antihypertensive drugs can lead to hypertension rather than reduction in blood pressure. It is particularly liable to develop from excessive fluid retention, particularly when associated with reduction of cardioadrenergic support. Coronary insufficiency from either coexisting coronary disease or triggered by injudicious antihypertensive treatment can stimulate pressor reflexes leading to marked fluctuations in arterial pressure. Alterations in left ventricular relaxation and rapid filling have been reported with some antihypertensive drugs; these changes could conceivably influence blood pressure responses through their effect on reflexes from low pressure baroceptors.
Antihypertensive Agents↗
Evaluation of plasma catecholamines in humans. Correlation of resting levels with cardiac responses to beta-blocking and sympatholytic drugs.
The changes in systolic time intervals (STI) following reduction of adrenergic activity was used to validate supine resting plasma catecholamines (CATs) as an index of sympathetic activity. Blockade of sympathetic activity was achieved by two means in two groups: propranolol (10 mg i.v.) and clonidine (0.3 mg p.o.). The diminished sympathetic effect was evidenced by slowing (p less than 0.01) of heart rate with both drugs and the reduction (p less than 0.01) of blood pressure with clonidine. There was no correlation in our study between resting plasma CATs (norepinephrine alone or total), and changes in heart rate and preejection period (PEP). Moreover, to avoid changes in PEP that could be related to differences in blood pressure levels (clonidine-reduced blood pressure while propranolol did not), the changes in PEP were corrected for the change of mean arterial pressure (MAP) in the same patients (delta PEP/(delta MAP and % delta PEP/% delta MAP). No correlation could be found, still, between resting supine plasma CATs and these ratios. The difficulty in demonstrating a correlation between resting plasma CATs and the immediate cardiac response to adrenolytic agents can be explained by the number of factors influencing plasma levels. Circulating plasma CATs represent the spillover from adrenergic nerve endings, and, therefore, their level would depend on several factors including sympathetic nervous system activity, rate of reuptake, and rate of degradation.
Adrenergic beta-Antagonists↗