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Query: UMLS:C0038454 (
stroke
)
147,016
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The efficacy of the phosphodiesterase inhibitor enoximone for reversal of severe postcardiotomy low cardiac output syndrome was investigated in 13 cases of cardiogenic shock refractory to conventional treatment consisting of beta-adrenergic agonists (n = 13) combined with vasodilators (n = 7), and intra-aortic balloon counterpulsation (n = 5). Following a bolus of 1 mg/kg enoximone, cardiac and
stroke
volume indices increased from 1.56 +/- 0.27 l/min/m2 and 16.3 +/- 3.3 ml/m2, respectively, to 2.72 +/- 0.67 and 27.8 +/- 7.1 (both p < 0.001). Mean arterial pressure fell, from 77 +/- 11 to 68 +/- 9 mmHg (p < 0.05), as did atrial filling pressures (LAP and
RAP
), LAP from 21.3 +/- 5.5 to 15.9 +/- 2.9 and
RAP
from 16.6 +/- 2.3 to 13.7 +/- 2.1 mmHg (both p < 0.01). The heart rate rose by only 5%. Enoximone therapy was maintained by a continuous infusion (5-7.5 micrograms/kg/min) for 40.6 +/- 8.6 hours (range 14-92). All hemodynamic parameters remained stable throughout treatment. Six patients died of sepsis and/or multiorgan failure but seven were discharged from hospital. Enoximone thus improved hemodynamic performance significantly in cardiogenic shock after open-heart surgery. It also has proved valuable in cardiac failure when conventional therapy was unsuccessful.
...
PMID:Efficacy of phosphodiesterase inhibitor enoximone in management of postcardiotomy cardiogenic shock. 143 45
Hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting. This hypertension increases myocardial oxygen consumption and can be prevented by application of vasodilators. A possible cause is activation of the renin angiotensin system. Magnesium is a potent vasodilator and has a beneficial effect after myocardial ischaemia. The study was performed to analyse the influence of magnesium infusion on the haemodynamic status and plasma renin activity in patients undergoing aortocoronary bypass grafting. METHODS. Eighteen patients (NYHA classification II-III) undergoing bypass surgery were divided into two groups, a magnesium and a control group. The magnesium group (n = 9) received 0.8 mEq/kg per h magnesium aspartate as an infusion for 15 min while still awake. After induction of anaesthesia, the magnesium infusion was reduced to 0.2 mEq/kg per h and stopped after aortic cannulation was completed. Plasma magnesium levels and concentrations within erythrocytes were measured. Anaesthesia was induced by flunitrazepam (0.01 mg/kg), fentanyl (0.005 mg/kg) and pancuronium (0.1 mg/kg). After intubation, patients were normoventilated with N2O/O2 = 1:1 and isoflurane (0.5-1.0 vol%). Additional doses of fentanyl (0.0025 mg/kg) were injected before the incision and before sternotomy. Mean arterial pressure, heart rate, cardiac index, total peripheral resistance, pulmonary vascular resistance, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, left ventricular
stroke
work index, right ventricular
stroke
work index, intrapulmonary shunt and plasma renin activity were evaluated at five predefined points: (1) prior to magnesium infusion; (2) after magnesium infusion; (3) 10 min following induction of anaesthesia under steady-state conditions; (4) after sternotomy; (5) after aortic cannulation. RESULTS. Concerning the haemodynamic parameters (MAP,
RAP
, PAP, PCWP) no significant difference between the two groups could be demonstrated. In the control group peripheral resistance (TPR) was higher following sternotomy and aortic cannulation than in the magnesium group. Magnesium prevented decrease of the cardiac index (CI) under steady-state conditions, during sternotomy and following aortic cannulation. Left and right ventricular
stroke
work indexes (LVSWI and RVSWI) were higher in the magnesium group. Plasma renin levels were not significantly different between the two groups. CONCLUSION. Patients undergoing cardiac surgery benefit from magnesium administration in the pre-bypass phase. Due to its vasodilating effect, magnesium lowers the output impedance of the left ventricle and improves cardiac pumping function. It opposes detrimental cardiovascular responses to sternotomy and following aortic cannulation. Also of importance is the advantageous effect of magnesium on cardiac arrest elicited by cardioplegia and for reactivation of the ischaemic myocardium.
...
PMID:[Hemodynamics of coronary surgery patients following magnesium aspartate infusion]. 148 73
The aim of this study was to assess the minimum time interval necessary to avoid the development of tolerance during nitroglycerin patch application. We studied 24 patients, aged 23 to 73 years, with ischemic or idiopathic dilated cardiomyopathy (LV EF less than 0.40) and stable clinical conditions during 30 days before the study. All patients had significant reduction of systemic and pulmonary arterial pressure after sublingual nitroglycerin. After the hemodynamic assessment of the response to the first dose of the nitroglycerin patch, the patients were randomized to 1 of 3 chronic treatment groups: continuous patch application (Group A), intermittent application with 4 hours intervals (Group B), intermittent application with 6 hours intervals (Group C). All patients were studied by right heart Swan-Ganz catheterization; the hemodynamic response to a 10 mg multilayer matrix nitroglycerin patch was assessed before and every hour, in the next 4 hours, after both the first application of the patch and after 1 month of therapy; after chronic intermittent therapy, hemodynamic parameters were also measured 24 hours after drug withdrawal. Hemodynamic parameters were significantly changed after the first nitroglycerin patch application: particularly, mean systemic arterial (MAP), right atrial (
RAP
) and pulmonary wedge pressures (PWP) declined from 96 +/- 10, 8.9 +/- 1.8 and 20.1 +/- 5 to 81 +/- 6, 4.7 +/- 1.5 and 12.2 +/- 3 mmHg (-15.6, -47.2 and -59.3%, respectively); systemic vascular resistance (SVR) and heart rate (HR) were reduced from 1645 +/- 121 to 1288 +/- 89 dyne.s.cm-5 and from 85 +/- 7 to 81 +/- 7 b/min; lastly, cardiac index (CI),
stroke
volume (SVI) and
stroke
work index (SWI) increased from 2.3 +/- 0.3, 28.2 +/- 5 and 28.7 +/- 9 to 2.7 +/- 0.3 l/min/m2, 33.3 +/- 5 ml/min/m2 and 31.5 +/- 8 g.m/m2 (+17.4, 18.1 and 9.7%). After 1 month of either continuous or intermittent patch application with 4 hours intervals, hemodynamic parameters returned to control values with no significant change after patch application. In contrast, after intermittent patch application with 6 hours intervals, a persistent hemodynamic response to nitroglycerin patches was still present.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:[The acute, chronic continuous after treatment and chronic intermittent with a variable therapeutic window (4 and 6 hours) hemodynamic effects induced with transdermal nitroglycerin in patients with congestive heart failure]. 176 29
We studied nine patients (56 +/- 7 years) with complete AV-block and permanent dual-chamber pacemaker (DDD) under different pacing modes: ventricle pacing (VVI) 70 bpm, DDD 106 +/- 4 bpm, rate adaptive pacing (VVI-FA) 108 +/- 3 bpm. Exercise was performed supine on the bicycle ergometer at 50 watts for 5 min at each setting. DDD-paced patients showed significantly higher mixed venous oxygen saturation, being 45 +/- 2% after the fourth minute, (VVI 38 +/- 2%, p less than 0.01 and VVI-FA paced patients 40 +/- 1%, p less than 0.01). Pressures were normal under DDD pacing during exercise (
RAP
7 +/- 2 mm Hg; PCP 14 +/- 3 mm Hg) and showed further increase to abnormal levels during VVI (
RAP
13 +/- 2 mm Hg, p less than 0.01; PCP 21 +/- 3 mm Hg, p less than 0.02) and VVI-FA pacing (
RAP
10 +/- 2 mm Hg, p less than 0.05; PCP 20 +/- 3 mm Hg, p less than 0.01).
Stroke
volume increased from 71 +/- 5 ml to 105 +/- 7 ml during VVI and from 64 +/- 7 ml to 81 +/- 7 ml during DDD pacing.
Stroke
volume remained unchanged (69 +/- 5 ml) during VVI-FA pacing. The peak levels of ANP during and after exercise were significantly higher under VVI (951 +/- 248 pg/ml) than under DDD pacing (650 +/- 140 pg/ml, p less than 0.01) and were not different between DDD and VVI-FA pacing (677 +/- 97 pg/ml). These results show that VVI pacing effects a more pronounced increase of ANP level than other pacing modes. Under moderate exercise, rate-responsive pacing compared to VVI pacing showed no differences in mixed venous oxygen saturation and in atrial pressures. Only DDD pacing showed higher oxygen saturation and a normalization of atrial pressures when compared to other types of single chamber pacing.
...
PMID:[Effect of AV synchronization and rate increase on hemodynamics and on atrial natriuretic peptide in patients with total AV block]. 214 4
Endothelin type 1 (ET-1) is an endothelial cell-derived 21-amino acid peptide with potent contractile effects on isolated vascular smooth muscle. The systemic hemodynamic effects of bolus intravenous injections of ET-1 and angiotensin II (ANG II, 300 pmol) were examined in anesthetized male Munich-Wistar rats by measurements of mean arterial (AP) and right atrial (
RAP
) blood pressures and cardiac index (CI, electromagnetic flowmetry) over a 60-min period. ET-1 induced a biphasic pressure response: transient hypotension occurred in the early phase with all doses, followed by a more prolonged dose-dependent elevation of blood pressure in the late phase. Because CI was unchanged during the early phase, the hypotension resulted from systemic vasodilation. On the other hand, the marked rise in AP produced by 300 pmol of ET-1 in the late phase was associated with a significant fall in CI, and thus total peripheral resistance index (TPRI) increased profoundly. A fall in right atrial pressure and significant hemoconcentration were associated with this pronounced vasoconstrictor effect, suggesting that a contraction of plasma volume contributed to the reduction of CI. Additionally,
stroke
and minute work indexes and peak flow velocity became significantly reduced in the late phase for the 300-pmol dose of ET-1. When compared with an equimolar dose of ET-1, 300 pmol of ANG II produced a prompt, more marked, but shorter-lived rise in AP with minimal changes in CI, TPRI,
RAP
, and hematocrit. These results raise the intriguing possibility that endothelin may play a role in both the control of normal vascular smooth muscle tone and in the pathogenesis of vasospastic disorders.
...
PMID:Systemic hemodynamic effects of endothelin in rats. 218 Mar 22
Head-out water immersion is known to increase cardiac filling pressure and volume in humans at rest. The purpose of the present study was to assess whether these alterations persist during dynamic exercise. Ten men performed upright cycling exercise on land and in water to the suprasternal notch at work loads corresponding to 40, 60, 80, and 100% maximal O2 consumption (VO2max). A Swan-Ganz catheter was used to measure right atrial pressure (PAP), pulmonary arterial pressure (PAP), and cardiac index (CI). Left ventricular end-diastolic (LVED) and end-systolic (LVES) volume indexes were assessed with echocardiography. VO2max did not differ between land and water.
RAP
, PAP, CI,
stroke
index, and LVED and LVES volume indexes were significantly greater (P less than 0.05) during exercise in water than on land.
Stroke
index did not change significantly from rest to exercise in water but increased (P less than 0.05) on land. Arterial systolic blood pressure did not differ between land and water at rest or during exercise. Heart rates were significantly lower (P less than 0.05) in water only during the two highest work intensities. The results indicate that indexes of cardiac preload are greater during exercise in water than on land.
...
PMID:Cardiovascular regulation during head-out water immersion exercise. 222 79
A parabolic relationship exists between ventricular external work and arterial load at given preload and contractility. Previous data indicate that the working point falls close to the parabola optimum. By combining the left ventricular (LV) end-systolic pressure-volume relationship (ESPVR) and an equation describing external
stroke
work, optimum values of
stroke
volume (SV), the slope (Emax) of the ESPVR, and arterial resistance (Rp) corresponding with the optimum (i.e., mSV, mEmax, mRp) were obtained. Experiments in anesthetized dogs were performed to test whether mSV, mEmax, and mRp also correspond to observed SV, Emax, and Rp at three different levels of volume load (right atrial pressure,
RAP
) before and after acute depression of LV contractility. Comparisons of observed and optimal values of SV, Emax, and Rp were made before and after LV depression. Before embolization, the ratios were SV/mSV 1.10-1.20 (
RAP
5-15 mmHg); Emax/mEmax 1.21-1.41; and Rp/mRp 0.84-0.69. After LV depression, SV/mSV was 0.80-0.83, Emax/mEmax was 0.78-0.71, and Rp/mRp was 1.56-1.46. The ratios were all significantly changed (P less than 0.01) by the induced LV depression. The present analysis may offer a new tool to detect nonoptimal relations between cardiac and arterial functions.
...
PMID:Optimal matching between canine left ventricle and afterload. 338 92
The effects of 5- and 10-wk treadmill exercise training on cardiorespiratory function were evaluated in the horse. Cardiac output (Q), heart rate (HR), and
stroke
volume (SV), as well as left ventricular (LVP), aortic (AoP), and mean right atrial (
RAP
) pressures and the peak first time derivative of LVP (LV dP/dtmax), were measured at rest and at five different levels of exercise up to 90% of initial predicted maximal HR (HRmax). Oxygen uptake (VO2) and respiratory exchange ratio (R) were also obtained under the same conditions. At rest, although HR was no different after training, LV dP/dtmax was lower at 10 wk (2,369 +/- 502 vs. 1,615 +/- 302 mmHg/s). At the different measured work loads during exercise, Q and VO2 remained unchanged with training, whereas there were consistent trends toward lower LVP, AoP, and LV dP/dtmax and significant reductions in HR and R (both P less than 0.05). In contrast, SV and mean
RAP
were elevated (P less than 0.05) during exercise after the 10-wk training program. Although the observed changes in cardiorespiratory function in response to a training program in the horse are generally similar to those reported for other species, our data also suggest a training-induced increase in venous pressures during exercise as measured by elevated mean
RAP
values.
...
PMID:Effects of training on cardiorespiratory function in the horse. 688 74
Haemodynamic and echocardiographic studies of isosorbide dinitrate were conducted in 12 patients (8 men and 4 women) with left ventricular failure consecutive to recent myocardial infarction. The groups: group I received 5 mg/h and group II 10 mg/h Risordan intravenously. After one hour treatment, group I patients showed a significant fall in both PAP (from 32.3 +/- 5.3 to 26.7 +/- 6.9 mmHg; p less than 0.01) and PCP (from 21.8 +/- 4.7 to 17.3 +/- 7.7 mmHg; p less than 0.05). These haemodynamic changes were amplified after a second hour of treatment: PAP fell to 24 +/- 7.9 mmHg (p less than 0.01) and PCP to 14.2 +/- 4.4 mmHg (p less than 0.001).
RAP
decreased from 7.2 +/- 5.1 to 3.5 +/- 5 (p less than 0.05). There were no changes in heart rate, systemic arterial pressure, peripheral resistance, cardiac index, forward
stroke
work nor, on echocardiography, in ventricular diameters, shortening fraction and VCF. After one hour treatment, group II patients showed a fall in PAP (from 30.5 +/- 4.7 to 21.7 +/- 3.5 mmHg; p less than 0.01), PCP (from 21.7 +/- 4.8 to 14.8 +/- 4.9 mmHg: p less than 0.001) and
RAP
(from 10.3 +/- 2.9 to 7.2 +/- 2; p less than 0.01). The systolic diameter of the left ventricle was reduced from 66.3 +/- 10.6 to 64.3 +/- 11.3 (p less than 0.01). After 4 hours, improvement in PAP and PCP was maintained; the other values remained stable. The effectiveness of Risordan i.v. in left ventricular failure consecutive to acute myocardial infarction is due to reduction of filling pressures in the left ventricule. With the 10 mg/h dose, as opposed to the 5 mg/h dose, the systemic arterial pressure and the double and triple products tend to be reduced, which suggests greater effectiveness.
...
PMID:[Use of isosorbide dinitrate (Risordan) injection in left ventricular failure following acute myocardial infarction (author's transl)]. 711 Sep 69
The acute effects of phenylephrine (PHE) administration or intravascular volume loading on right ventricular (RV) function were examined in 34 patients undergoing elective coronary artery surgery. After anesthetic induction with sufentanil and midazolam, 20 patients received PHE to treat hypotension and increase systemic arterial pressure 20% above baseline values. PHE effectively restored arterial pressure without changing
stroke
index (SI), although RV ejection fraction (RVEF) declined (41.3% to 37.6%) with concomitant increases in RV end-diastolic volume index (RVEDVI) (86.3 to 97.5 mL/m2) and RV end-systolic volume index (51.8 to 63.4 mL/m2). In the first 6 to 8 hours after surgery, 18 patients received intravascular volume expansion with 5% albumin when the clinical perfusion state was inadequate and accompanied by pulmonary artery occlusion pressure (PAOP) less than 15 mmHg and a hemoglobin level greater than 8 g/dL. Volume loading with 500 mL of albumin increased SI(27.0 to 31.8mL/m2), PAOP (12.2 to 15.4 mmHg) and RVEDVI (69.0 to 86.5 mL/m2), although RVEF declined (39.3% to 37.6%). Baseline values of RVEF and SI (but not PAOP or right atrial pressure [
RAP
]) were lower in 9 of 18 patients who exhibited declines in RVEF after volume loading, and
RAP
was a poor indicator of RVEDVI (r = 0.17). RVEDVI (but not
RAP
or PAOP) had significant correlation with SI during volume loading. There was no relationship between the presence of hemodynamically significant right coronary artery stenoses requiring revascularization or other perioperative factors with the response to PHE before revascularization or to volume loading after revascularization.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effects of phenylephrine or volume loading on right ventricular function in patients undergoing myocardial revascularization. 771 51
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