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Hypotensive episodes occur frequently during hemodialysis; they are often sudden and difficult to prevent despite careful clinical control. Their etiology was studied by investigating the hemodynamic response of five patients submitted to ultrafiltration during their three first dialyses. A Swan Ganz catheter was inserted and left in position for 5 days. Simultaneous determination of cardiac output, mean pulmonary artery (PAP) and capillary and systemic arterial pressures were recorded. 10 hypotensive episodes were observed. In 3 patients in whom the first hypotensive episode occurred 10 minutes after the start of dialysis, there was a significant drop in PAP, cardiac index and stroke index while heart rate and peripheral resistance remained unchanged. Paradoxical bradycardia was observed. In 4 patients hypotension was observed more than one hour after initiation of dialysis. Before the hypotensive episode there was moderate elevation of heart rate and peripheral resistance and an insignificant reduction in PAP. Cardiac index and stroke index were diminished. The decrease in MAP was only 2 mm Hg. Hypovolemia is the most important factor in hemodialysis-induced hypotension but other factors such as vagal stimulation, autonomic neuropathy and osmotic disequilibrium can interfere with blood pressure control and trigger hypotension. Methods of preventing hypotension during dialysis, including the infusion of low molecular weight dextran, are discussed.
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PMID:Hemodynamic evaluation of hypotension during chronic hemodialysis. 88 13

Antiarrhythmic and hemodynamic effects of i.v. disopyramide phosphate (1.7 mg/kg b.wt. over 2 min) have been studied in nine patients, several in various degrees of cardiac decompensation, with sinus rhythm and persistent ventricular ectopic beats (VEBs). In one case with primary cardiomyopathy, with greater than 30 VEBs/min, disopyramide (DE) abolished the arrhythmia for 30 min, but precipitated brief dysponea. Other side-effects were tolerable and mainly attributable to anticholinergic effects of the drug. DE either abolished or significantly reduced the arrhythmia in all cases. For 30 min, only one patient showed VEBs, and in three patients no VEBs were seen for three hours. Changes in cardiac output and pulmonary artery (PAP) and central aortic pressures were measured in eight patients. Negative inotropic effects were indicated in seven by an increased diastolic PAP/stroke volume ratio and in seven by a decreased central aortic (dp/dt)max. Patients with high control values for diastolic PAP showed marked reductions in cardiac output, stroke volume and stroke work. In predicting myocardial depressant effects of DE, the control values for diastolic PAP seemed to be superior to central venous pressure, cardiac index and systolic time intervals. Mean arterial pressure measured 5 and 10 min after drug administration showed no significant change, indicating that vasoconstrictor reflexes were well preserved, and a pressure level significantly above the control value was reached from the 20th min. It is concluded that DE is potent in suppressing VEBs but exerts negative inotropic effects that may be of clinical importance. The optimal antiarrhythmic dose is probably lower than that used in the present study.
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PMID:Hemodynamic and electrocardiographic effects of disopyramide in patients with ventricular arrhythmia. 125 72

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.
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PMID:[Hemodynamics of coronary surgery patients following magnesium aspartate infusion]. 148 73

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.
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PMID:Prostacyclin for the treatment of pulmonary hypertension in the adult respiratory distress syndrome: effects on pulmonary capillary pressure and ventilation-perfusion distributions. 211 82

An animal model of coronary artery spasm-coronary thrombosis-acute myocardial infarction (CAS-CATH-AMI) was obtained by injecting ergonovine(0.22 mg/kg) directly into the left coronary artery (LCA) of 17 dogs under general anesthesia. Various parameters of the experimental group were compared with those of the control group consisting of 5 dogs. The following changes were observed: increased average arterial blood pressure (MAP), pulmonary capillary wedge pressure (PCWP), stroke volume (SV, P less than 0.05), PAP (P less than 0.01) transient decreased cardiac output (CO); elevated ST-T in EKG; ventricular arrhythmia in 60% of animals; transient spasm of 50%-75% of LCA in the LCA angiographs; enhancement of platelet aggregation and TXB2 (P less than 0.01) and decline of 6 Keto-PGF1 alpha, SAO2 (P less than 0.05), indicating acute hypoxia and high coagulating pathophysiological changes after CAS. Pathological examination one hour after CAS induction revealed CATH(53%) in addition to CAS induced morphological changes of the CA and myocardium, as well as necrosis of the corresponding sites in its early stage. This study provides a reproducible animal model of CAS-CATH-AMI for research of coronary heart disease and pathomorphological criteria for the diagnosis of CAS. It also shows that CAS may lead to CATH-AMI, therefore, prevention of CATH and AMI is possible.
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PMID:Animal model of coronary artery spasm-coronary thrombosis-acute myocardial infarction. A study on hemodynamics, EKG, coronary angiography, biochemistry and pathology. 211 65

The effects of negative extra-thoracic pressure ventilation (NETPV) on respiratory system and hemodynamics were examined in ten normal dogs. Changes of the parameters obtained during intermittent NETPV (INETPV), and NETPV with negative end-expiratory pressure (CNETPV) were compared with those during IPPV and CPPV. Animals' chests and upper abdomens were confined in an acryl box. In INETPV and CNETPV, the dogs were ventilated with the negative extra-thoracic pressure ventilator (Kimura, OKT-100). Positive and negative pressure ventilation was carefully matched for tidal volume and the increase in FRC obtained with PEEP and the end-expiratory negative extra-thoracic pressure (EENETP). EENETP of -11.6 cmH2O produced the same FRC change as PEEP of 10.6 cmH2O did. Gas exchanges did not differ in any modes. INETPV did not change any hemodynamic parameters without PAP. In CNETPV, heart rate increased, and CVP, cardiac index (CI) and stroke volume (SV) decreased significantly (P less than 0.05), but tmCVP and tmPCWP did not change. The decreases of CI and SV (100----89.1, 88.8%) in CNETPV were significantly smaller when compared with CPPV (100----78.8, 74.5%). In CPPV, meanBP, CVP, tmCVP, tmPCWP, CI, SV changed significantly. The mechanisms of the decrease of CI and SV by CNETPV seemed to be different from those by CPPV.
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PMID:[Effects of negative extra-thoracic pressure ventilation on respiratory system and hemodynamics in normal dogs]. 225 33

The hemodynamic effects of ketamine, 1.5 mg/kg, or sufentanil, 3.4 +/- 0.3 micrograms/kg, were studied prospectively for the anesthetic induction of 20 patients with cardiomyopathies undergoing cardiac transplantation. Plasma epinephrine (EPI), norepinephrine (NE), and sufentanil levels were also obtained. Measurements were taken at various times before induction and following intubation. Following ketamine, progressive increases (P less than 0.05) in mean arterial pressure (28%, MAP), mean pulmonary artery pressure (56%, PAP), central venous pressure (109%, CVP), and pulmonary capillary wedge pressure (84%, PCWP) occurred over time, whereas the cardiac index (CI), stroke volume index (SVI), and stroke work index (SWI) remained unchanged or decreased. The use of sufentanil was associated with no significant changes in MAP, PAP, CVP, PCWP, CI, SVI, or SWI. The heart rate (HR) did not significantly change in either group. Plasma NE significantly increased (31%) in the ketamine group, peaking at 10 minutes; whereas EPI levels did not significantly change in either group. Plasma sufentanil did not reflect the microgram/kg or microgram/BSA administered dose, suggesting individualized distribution kinetics. Since perioperative morbidity and mortality did not differ between groups, both ketamine and sufentanil are acceptable drugs for the anesthetic induction for cardiac transplantation. However, the dissimilar hemodynamic effects caused by ketamine and sufentanil suggest that this conclusion may not be applicable to the patient with a cardiomyopathy undergoing noncardiac surgery.
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PMID:Cardiac transplantation: a prospective comparison of ketamine and sufentanil for anesthetic induction. 253 97

The majority of epidemiological studies on the benefits and risks of oral contraceptive (OC) use have been conducted during the late 1960s and early 1970s when OCs had 50 mcg of estrogen. Based on these studies, the risk of death due to OC use for nonsmokers 35-39 years old was lower than using no contraceptive at all (14.1 deaths/100,000 women/year vs. 25.7 deaths/100,000 women/year). In addition to smoking, other contraindications include women with a history of angina, myocardial infarction, blood clots or stroke, estrogen dependent cancer, hypertension, a known lipid disorder, and women with hepatitis or cirrhosis of the liver. Suitable 35 year old candidates for OC use would be nonsmokers with blood group O, at low risk for cardiovascular disease, and who might receive additional benefits, including those with severe dysmenorrhea or hypermenorrhea and possibly those who have a strong family history of osteoporosis, early menopause, or ovarian cancer. Practitioners should take a thorough history of these women and give a physical examination with a blood pressure check. They should also administer screening tests, such as a PAP test, mammograms, a lipoprotein profile, and a glucose test. After the practitioners have deemed these women to be healthy based on the examination and the results of the screening test, they then should prescribe only a low dose OC containing 50 mcg of estrogen. Today most estrogen based OCs contain 35 mcg and research on their effects have not yet begun. Scientists expect to find that the dose response effects for risks for thromboembolism, myocardial infarction, stroke, and gallbladder disease to be lower in users of the low dose preparations.
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PMID:Risks and benefits of oral contraceptive use in women over 35. 323 16

The prospective human studies considered above reveal that in some patients protamine is associated with decreases in SBP and SVR, especially when administered rapidly. Cardiac output increases reflexly, except perhaps in patients with less compliant ventricles, which are more dependent on preload to maintain stroke volume. In the latter, decreases in filling volume associated with protamine can lower CO. Regardless of the rate of administration, protamine does not produce predictable, acute increases in PAP, although increases in PAP may occur during idiosyncratic reactions (see the section on idiosyncratic reactions below). Left atrial or aortic administration of protamine may not confer protection from its hemodynamic or idiosyncratic sequelae (see below). Little evidence exists to conclude that protamine directly depresses contractility of the human heart.
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PMID:Protamine: a review of its toxicity. 388 48

In order to test the clinically supposed development of tolerance during chronic high-dose nitrate therapy, we studied a total of 24 patients with angiographically proven coronary heart disease at rest and during ergometric exercise (supine position, 50 w for 3 min). Pulmonary arterial pressure (PAP, floating catheter), arterial blood pressure (cuff method), cardiac output (Fick principle), heart rate, and exercise capacity (w X min) were measured at rest and exercise before and during chronic (4 weeks) oral therapy with 5-isosorbide mononitrate (5-ISMN), 3 X 20 mg/day (n = 14) and 3 X 50 mg/day (n = 10). After acute administration, both doses of 5-ISMN decreased mean PAP at rest and during exercise (rest: by 25% with 20 mg and by 29% with 50 mg; exercise: by 30% with 20 mg and by 45% with 50 mg), whereas cardiac output and stroke volume were only reduced by 5-ISMN at rest. During chronic treatment with 60 mg and 150 mg 5-ISMN, and additional administration of 20 mg or 50 mg respectively lowered PAP at rest by 15% and 19%; during ergometric exercise PAP was 22% and 14% lower than during ergometry before any drug treatment. The exercise capacity slightly increased during treatment to 60 mg 5-ISMN, whereas it decreased by 25% on chronic treatment with 150 mg 5-ISMN per day. Our results show that acute administration of 5-ISMN in either dose (20 mg and 50 mg) exerts unloading effects on the heart and will increase the exercise tolerance. In contrast to the higher dose of 150 mg 5-ISMN per day, chronic treatment with the lower dose of 60 mg 5-ISMN daily will not result in drug tolerance.
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PMID:Dose dependence of tolerance during treatment with mononitrates. 666 25


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