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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension following aorta-coronary bypass operations can contribute to myocardial ischemia. Nitroprusside therapy will reduce afterload, preload, and coronary perfusion pressure. Since both hypertension and its treatment can result in ischemic injury, nitroprusside must be carefully titrated to optimize cardiac function and metabolism. Thirty-one patients undergoing elective coronary bypass grafting were studied during a hypertensive episode (mean arterial pressure [MAP] = 119 +/- 18 mm Hg) and during nitroprusside therapy at an MAP of 97 +/- 11 mm Hg and at an MAP of 80 +/- 11 mm Hg (normotension). Nitroprusside also produced a significant (p less than 0.05) decrease in left atrial pressure (LAP), left ventricular end-diastolic volume index (EDVI) (stroke index divided by ejection fraction by nuclear angiography), stroke index, and stroke work index (SWI). Cardiac lactate extraction (LEx) and the ratio LEx/SWI increased (p less than 0.05) with the initial nitroprusside therapy, but lactate production resulted when the MAP was lowered to 80 mm Hg. Volume loading studies were performed during hypertension in four patients and during nitroprusside therapy in 15 patients. Neither performance nor compliance was significantly altered at an MAP of 97 mm Hg, but compliance decreased at normotension. Both hypertension and its treatment can result in inadequate myocardial metabolism. Nitroprusside should be titrated to maintain MAP between 90 and 100 mm Hg.
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PMID:Effects of postoperative hypertension and its treatment. 660 14

From a hemodynamic point of view, an adequate response to antihypertensive therapy would be restoration of a normal circulatory system. In most patients with mild to moderate essential hypertension considered to need drug therapy, the cardinal hemodynamic disturbance is an increased total peripheral resistance (TPR) and a normal or reduced cardiac output (CO). During a 10- to 17-year follow-up of untreated hypertensives, a gradual increase in TPR, increase in MAP, and a decrease in CO and stroke volume (SV) were seen. Hemodynamic responses to chronic drug therapy were studied at rest and during exercise in 250 men with mild to moderate essential hypertension in WHO Stage I. A significant reduction in TPR was seen on thiazide diuretics, nifedipine and verapamil, but there was no increase of subnormal CO or SV. A greater normalization of central hemodynamics was achieved by prazosin, which induced a reduction in TPR and an increase in CO and SV, particularly during exercise. In contrast, beta-blocker therapy was associated with a chronic reduction in CO and heart rate (HR) and usually no reduction in TPRI below pretreatment values. The chronic CO reduction was associated with an increase in arteriovenous oxygen difference. In 14 patients with therapy-resistant hypertension, a marked increase in TPR was found. Captopril induced a reduction in TPR with rest and exercise, and also a reduction in cardiac output. Prolonged therapy for 5 years with beta-blockers did maintain blood pressure control, but with no further decrease in TPR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic response: decrease in cardiac output vs reduction in vascular resistance. 662 61

the autonomic sympathetic reflexes to sustained handgrip, upright tilt and the Valsalva maneuver, were tested in 26 patients with labile and 26 with fixed essential hypertension. Sustained handgrip increased systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressure, heart rate (HR), cardiac index (CI), tension time index (TTI) (p less than .01), and had no effect on total peripheral resistance index (TPRI) and left ventricular ejection rate index (LVERI) in both groups of patients. However, the response to upright tilt and the Valsalva maneuver was different in the two groups. Upright tilt in labile hypertensives increased DAP, MAP, HR, and TPRI (p less than .001); decreased CI, stroke index (SI) and LVERI (p less than .01) and had no effect on SAP. In fixed hypertensives, it decreased SAP, MAP, CI, SI and LVERI (p less than .001); increased HR (p less than .01) and had no effect on DAP, and TPRI. The diastolic pressure overshoot of the Valsalva maneuver was attenuated in fixed hypertensives compared to labile (p less then .001). Additionally, when the percent changes from control in DAP, MAP, HR and TPRI to sustained handgrip and upright tilt between the two groups were compared, only differences to upright tilt between the two groups were observed. The results of this investigation suggest that upright tilt and the Valsalva maneuver might serve as better predictors of autonomic reflexes in hypertensive patients than the grip test.
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PMID:Hemodynamic correlates of autonomic reflexes in patients with labile and fixed hypertension. 733 96

Dopamine seems theoretically to be a rationale choice when adrenergic support is needed to counter undesired cardiovascular depressant effects of isoflurane. Although the cardiovascular effects of isoflurane (ISO) and exogenous dopamine (DA) are well documented, there are no reports on their pharmacological interaction. The effects of ISO 1.4% (MAC 1.0) on the cardiovascular response to exogenous DA were studied in dogs during chloralose anesthesia. Instrumentation included catheterizations of the femoral artery (for aortic pressures and heart rate, HR), the pulmonary artery (for thermodilution cardiac output, CO, and pulmonary arterial pressures) and the left ventricle (for tip-manometer measured left ventricular end-diastolic pressure, LVEDP). ISO per se decreased HR (-16%), mean arterial pressure (MAP; -33%), CO (-29%), left ventricular dP/dt (LV dP/dt; -51%), and increased pulmonary artery occlusion (PAOP; +64%) and LVEDP (+28%). Prior to ISO, DA increased MAP, CO stroke volume (SV), LV dP/dt and LV dP/dt/SAP (systolic arterial pressure) at the dose 10 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1 DA, besides these effects, increased PAOP and mean pulmonary artery pressure (MPAP). During ISO, DA at the dose 10 micrograms.kg-1.min-1 restored MAP, CO, and SV to pre-ISO control levels, while LV dP/dt was increased to +96% above the pre-ISO control level. At the dose 20 micrograms.kg-1.min-1, DA increased MAP (+33%), LV dP/dt (+172%), PAOP (+132%) and MPAP (+50%) above pre-ISO control levels. The cardiac effects of DA were similar to when it was given alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Are the cardiovascular actions of dopamine altered by isoflurane? 757 20

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg.kg-1) on cardiovascular responses to 50 degrees head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8-40) to 5 (3-10) min (median and range; P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) omega; P < 0.01] of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats.min-1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg.min.1-1, P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1.min-1, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats.min-1 (P < 0.02 compared to control) and MAP remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Naloxone-provoked vaso-vagal response to head-up tilt in men. 760

The effects of calcium gluconate on hemodynamics and saphenous vein graft flow in a group of patients undergoing elective coronary artery bypass grafting who developed ionized hypocalcemia at the end of the surgical procedure were examined. The patients received a central venous bolus of 15 mg/kg of calcium gluconate. Heart rate (HR), arterial pressure (AP), central venous pressure (CVP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), and cardiac output were measured immediately before and 30, 60, 120, 180, and 240 seconds after injection of calcium gluconate. Systemic and pulmonary vascular resistance (SVR and PVR, respectively), cardiac index (CI), stroke volume index (SVI), and right and left ventricular stroke work index (RVSWI and LVSWI, respectively), were calculated. Venous bypass flow velocity (Vbypass-flow) was assessed using a Doppler probe that was attached to the left anterior descending artery (LAD) bypass intraoperatively. Calcium gluconate significantly increased MAP, SVR, and LVSWI from 67 +/- 3 mmHg (mean +/- SEM), 1,128 +/- 128 dyne.s.cm-5 and 25 +/- 3 g.m.beat/m to a maximum of 81 +/- 5 mmHg (P < 0.01), 1,401 +/- 196 dyne.s.cm-5 (P < 0.05), and 32 +/- 4 g.m/beat/m (P < 0.01), respectively. HR, CVP, PAP, PCWP, PVR, CI, SVI, and Vbypass-flow remained unaltered. It is concluded that calcium gluconate administered to moderately hypocalcemic patients increases arterial pressure mainly by peripheral vasoconstriction. Because the increase of arterial pressure, and, thereby, coronary perfusion pressure is not associated with an increase of LAD bypass flow, vasoconstriction in the coronary vascular bed distal to the venous graft cannot be ruled out, and deterioration of the myocardial oxygen supply/demand ratio is strongly suggested.
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PMID:Influence of intravenous calcium gluconate on saphenous vein graft flow in closed-chest patients. 780 43

To study how sepsis affects hemodynamic responses to catecholamines and fluids, either Escherichia coli-infected (septic, n = 8) or sterile (controls, n = 6) fibrin clots were implanted intraperitoneally into 2-yr-old beagles. Hemodynamics were measured at each of four doses of dopamine (0, 5, 10, and 20 micrograms.kg-1.min-1) and norepinephrine (0, 10, 20, and 40 micrograms.min-1), before and after infusion of fluid (Ringer 40 ml.kg-1). Septic animals had lower mean arterial pressure (MAP, P = 0.04), stroke volume index (SVI, P = 0.0001), and left ventricular (LV) ejection fraction (LVEF) (P = 0.0001) than controls. During this time, increasing doses of dopamine and norepinephrine produced corresponding increases (P < 0.001) in LVEF, SVI, and MAP. However, during sepsis, the ability of dopamine to increase MAP diminished, while its ability to increase LVEF and SVI was maintained. Conversely, the ability of norepinephrine to increase LVEF and SVI diminished, but its ability to increase MAP was maintained. During sepsis, fluids alone increased (P < 0.05) MAP, LVEF, SVI, and cardiac index (CI). Fluids with catecholamines also significantly increased (P < 0.05) MAP with only minimal increases in LVEF, SVI, and CI. These data demonstrate that during sepsis without catecholamines, fluids improve cardiac performance and systemic pressures, but with catecholamines, fluids have minimal effects on cardiac performance and augment MAP. Furthermore, during sepsis dopamine is more effective than norepinephrine in increasing LV performance, but norepinephrine is more effective than dopamine in increasing systemic pressures.
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PMID:Hemodynamic effects of dopamine, norepinephrine, and fluids in a dog model of sepsis. 786 96

Neuropeptide Y (NPY), a sympathetic and platelet-derived vasoconstrictor, acts both directly and by potentiating adrenergic responsiveness and therefore may be beneficial in endotoxic shock, where suppressed vascular responsiveness to adrenergic agents is a key factor. This was studied in anesthetized rats. First, infusion of a nonhypotensive dose of endotoxin (lipopolysaccharide, LPS) markedly suppressed the pressor response to increasing doses of norepinephrine (NE), angiotensin II, and vasopressin but did not suppress the response to NPY. Second, in rats rendered hypotensive by intravenous LPS, continuous NE infusion (0.1-1.0 microgram.kg-1 x min-1 started 5 min after LPS for 1 h) did not alter hemodynamics. In contrast, 5 nmol.kg-1 x min-1 of NPY (equipotent to 0.1 microgram.kg-1 x min-1 of NE in normal rats) increased mean arterial pressure (MAP, from 64 to 114% of baseline), total peripheral resistance index (TPRI, from 64 to 154% of baseline), and left ventricular stroke work index (from 36 to 73% of baseline), without changing cardiac index (CI). Third, in a similar experimental protocol, pretreatment of the hypotensive rats with phentolamine blocked the pressor effect of NE infusion, but only partially attenuated the response to NPY. Finally, addition of low-dose NPY to NE infusion improved survival following a lethal dose of LPS compared with treatment with NE alone (P < 0.01). Thus, unlike other vasoconstrictors tested, NPY-mediated vasoconstriction is preserved during endotoxemia. The beneficial effect of NPY is mediated by increased TPRI without reduction in CI; both NPY receptor-mediated vasoconstriction and potentiation of adrenergic responsiveness may be involved.
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PMID:Neuropeptide Y infusion improves hemodynamics and survival in rat endotoxic shock. 790 7

The stroke volume of the left ventricle (SV) was calculated from noninvasive recordings of the arterial pressure using a finger photoplethysmograph and compared to the values obtained by pulsed Doppler echocardiography (PDE). A group of 19 healthy men and 12 women [mean ages: 20.8 (SD 1.6) and 22.2 (SD 1.6) years respectively] were studied at rest in the supine position. The ratio of the area below the ejection phase of the arterial pressure wave (A(s)) to SV, as obtained by PDE, yielded a "calibration factor" dimensionally equal to the hydraulic impedance of the system (Zao = A(s).SV-1). The Zao amounted on average to 0.062 (SD 0.018) mmHg.s.cm-3 for the men and to 0.104 (SD 0.024) mmHg.s.cm-3 for the women. The Zao was also estimated from the equation: Zao = a.(d + b.HR + c.PP + e.MAP)-1, where HR was the heart rate, PP the pulse pressure, MAP the mean arterial pressure and the coefficients of the equation were obtained by an iterating statistical package. The value of Zao thus obtained allowed the calculation of SV from measurements derived from the photoplethysmograph only. The mean percentage error between the SV thus obtained and those experimentally determined by PDE amounted to 14.8 and 15.6 for the men and the women, respectively. The error of the estimate was reduced to 12.3 and to 11.1, respectively, if the factor Zao, experimentally obtained from a given heart beat, was subsequently applied to other beats to obtain SV from the A(s) measurement in the same subject.
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PMID:Assessment of cardiac output from noninvasive determination of arterial pressure profile in subjects at rest. 800 27

The hemodynamic effects of propofol-fentanyl and isoflurane-fentanyl anesthesia during the prebypass period were compared in 42 patients undergoing coronary artery bypass grafting (CABG) and 22 patients undergoing valve replacement (VR) for stenotic lesions. Anesthesia was induced with fentanyl, 25 micrograms/kg, and pancuronium, 0.1 mg/kg, and was maintained with a propofol infusion commenced at 4 mg/kg/h (range 1 to 10 mg/kg/h) or with isoflurane commenced at 1% (range 0 to 2%). Additional fentanyl, 7.5 micrograms/kg, was given before sternotomy. Hemodynamic measurements were made before induction of anesthesia and at various times in the prebypass period. In the VR group, there were no significant differences between the two anesthetics in any hemodynamic variables during the study. Significant decreases (P < 0.05) in mean arterial pressure (MAP 14%), left ventricular stroke work index (LVSWI 29%), and stroke volume index (SVI 24%) occurred after 15 minutes of propofol anesthesia in the CABG group. With isoflurane MAP was well maintained with reductions in LVSWI and SVI of 22% and 20%, respectively. Isoflurane was, however, associated with a significant increase in heart rate (HR) in the CABG group (P < 0.05), whereas no significant change in HR occurred in CABG or VR patients receiving propofol. With both techniques there were no significant changes in right-sided or left-sided filling pressures or in systemic vascular resistance index in the CABG or VR groups, except for a decrease in pulmonary artery occlusion pressure in the propofol VR group and isoflurane CABG group at the time of aortic cannulation. Propofol produced similar hemodynamic changes in the CABG and VR groups. Both anesthetic techniques caused myocardial depression and effectively controlled the autonomic responses to sternotomy in both groups. The study suggests that propofol-fentanyl anesthesia is an acceptable technique for CABG surgery and for VR in patients with stenotic valvular heart disease.
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PMID:Propofol-fentanyl anesthesia: a comparison with isoflurane-fentanyl anesthesia in coronary artery bypass grafting and valve replacement surgery. 806 Dec 62


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