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Biomedical subjects

W Hess

Publications and source records attributed to W Hess.

At least 73 records · Page 4Linked to original sources
PubMed1979

Haemodynamic effects of dopamine and dopamine combined with nitroglycerin in patients subjected to coronary bypass surgery.

The haemodynamic effects of dopamine and dopamine with nitroglycerin were evaluated in eight patients with coronary heart disease who underwent aortocoronary bypass surgery. The study was performed under anaesthesia and before surgery. Dopamine 8 micrograms kg-1 min-1 alone produced a marked increase of the cardiac index from 2.47 to 3.47 litre min-1 m-2 but only small changes in heart rate (from 65 to 68 beat min-1). This improvement in cardiac performance was accompanied by an increase of the mean pulmonary artery pressure from 10.9 to 21.3 mm Hg and in the left ventricular filling pressure from 6.1 to 13.8 mm Hg with unchanged systemic and pulmonary vascular resistance. Mean arterial pressure increased from 72 to 103 mm Hg. Simultaneous infusion of dopamine (8 micrograms kg-1 min-1) and nitroglycerin (mean dose 0.5 microgram 21.3 to 14.4 mm Hg) and of left ventricular filling pressure (from 13.8 to 7.9 mm Hg). Cardiac index (from 3.47 to 3.34 litre min-1 m-2) and mean arterial pressure (from 103 to 95 mm Hg) were not reduced to the same extent by the addition of nitroglycerin. The combined treatment of dopamine with nitroglycerine seems to be of value in patients with pre-existing high left ventricular filling pressure or with pulmonary hypertension.

Adult↗
PubMed1979

[The haemodynamic effects of dobutamine and dopamine in patients with coronary artery disease. A study performed under general anaesthesia (author's transl)].

The haemodynamic effects of dobutamine (2 microgram/kg . min and 4 microgram/kg . min) and dopamine (4 microgram/kg . min and 8 microgram/kg . min) were studied in 17 patients with coronary artery disease prior to coronary bypass surgery. The study was performed under general anaesthesia (modified neurolept analgesia) and controlled ventilation. Dopamine improved cardiac index significantly, increased mean aortic pressure slightly while heart rate and total peripheral resistance remained unchanged. Dobutamine failed to increase cardiac and stroke index significantly, but increased mean aortic pressure distinctly due to an elevated total peripheral resistance. Both catecholamines increased left ventricular filling and mean pulmonary artery pressure. The HR x ASP-product which is closely related to left ventricular oxygen consumption was found to be augmented to a greater extent during dobutamine. For the above reasons dopamine should be favoured for increasing cardiac output in patients undergoing aortocoronary bypass surgery. Our study does not confirm earlier results which have shown dobutamine to be the preferable catecholamine. The possible reasons for this discrepancy are discussed.

Adult↗
PubMed1979

[Flunitrazepam-pretreatment for prevention of adverse cardiovascular effects following ketamine].

In 18 patients with documented ischaemic heart disease the cardiovascular effects of ketamine (1.5 mg/kg iv) were studied under three different conditions: 1. in awake premedicated patients (n = 6); 2. after the previous administration of flunitrazepam (0.015 mg/kg iv, n = 6) and 3. under conditions of neuroleptanalgesia and muscle relaxation (n = 6). Flunitrazepam prevented or at least attenuated the increases in heart rate (30%), mean arterial pressure (37%), mean pulmonary artery pressure (165%), left ventricular filling pressure (230%), total peripheral resistance (50%), pulmonary vascular resistance (100%) and in the rate-pressure product (66%) which were associated with the use of ketamine as the sole anaesthetic agent. In addition, the flunitrazepam-pretreatment abolished the fall in cardiac index and stroke index which occured in patients given ketamine alone. Flunitrazepam therefore appears to be a promising drug to prevent adverse cardiovascular reactions, when ketamine should be chosen for induction of anaesthesia. Neuroleptanalgesia and muscle relaxation also proved effective in controlling the sympathomimetic actions of ketamine. The response of the mean pulmonary artery pressure and of the ventricular filling pressures to ketamine in this group was even more damped than in the patients pretreated with flunitrazepam alone.

Adult↗
PubMed1978

[Pulmonary hypertension and pulmonary edema caused by intravenous ketamine (author's transl)].

Induction of anaesthesia with ketamine 1.5 mg/kg i.v. in a patient with coronary artery disease caused an increase in mean pulmonary artery pressure from 27 to 65 mmHg, a threefold rise in pulmonary vascular resistance and an increase of the left ventricular filling pressure from 18 to 48 mmHg which was associated with arterial hypoxaemia due to pulmonary edema. Fentanyl (0.01 mg/kg i.v.) promptly reversed the systemic and pulmonary vascular effects of ketamine.

Anesthesia, General↗
PubMed1978

[The influence of sodiumnitroprusside on the oxyhaemoglobin dissociation curve in vitro (author's transl)].

Blood from 16 donors was incubated with 3 microgram sodiumnitroprusside (SNP)/ml blood and the PO2 for halfsaturation of haemoglobin at standard pH and temperature was measured. There was no significant shift of the oxygen dissociation curve. Erythrocyte 2, 3 DPG and met-Hb concentrations did not show significant differences between SNP-treated and control blood. Although the red cells and the haemoglobin are involved in the metabolism of SNP, in clinical doses SNP does not alter the oxygen affinity.

Diphosphoglyceric Acids↗
PubMed1977

Effects of althesin, etomidate and fentanyl on haemodynamics and myocardial oxygen consumption in man.

The acute effects of althesin, etomidate and fentanyl upon haemodynamics, myocardial contractility and oxygen comsumption of the heart were studied in healthy premedicated patients (n = 15) lightly anaesthetized with N2O-O2 (ratio 2:1), 0.3 volumes per cent of halothane and isoflurane respectively. All individuals were ventilated at a normal level. The patients (n = 9) in the halothane group received etomidate 0.3 mg/kg and 20 minutes later althesin 0.075 ml/kg intravenously. In a second group of 6 patients on isoflurane fentanyl 0.01 mg/kg was given. Etomidate did not affect the cardiovascular system significantly. While the decrease in blood pressure after althesin (24 per cent) was the result of a reduction in total peripheral resistance (32 per cent), hypotension associated with fentanyl (23 per cent) was caused by diminished output due to bradycardia (18 per cent). Load data,heart rate, and maximum dp/dt indicated moderate negative inotropic properties only of althesin. Using the complex haemodynamic parameter developed by Bretschneider the myocardial oxygen consumption was calculated. The energy demand of the heart decreased with etomidate, althesin and fentanyl by 14 per cent, 16 per cent and 32 per cent respectively. It is concluded that the risk of cardiovascular depression at induction in patients with impaired myocardial performance and coronary insufficiency can be minimized with etomidate and/or fentanyl.

Adult↗
PubMed1977

Antagonism of morphine with naloxone in dogs: cardiovascular effects with special reference to the coronary circulation.

The cardiovascular effects of naloxone 15 microgram/kg following morphine 2.0 mg/kg were studied in closed-chest dogs during light nitrous oxide-halothane anaesthesia. The bolus injection of naloxone caused an increase in heart rate (73%), cardiac output (20%) and mean arterial pressure (20%). Total peripheral resistance was unaffected. LV dP/dt max and LV dP/dt max/IP increased by 25% and 14% respectively, but positive inotropic effects could not be shown when load data, heart rate and the decrease in left ventricular ejection fraction (22%) were taken into consideration. The cardiovascular stimulation resulted in an increase in myocardial oxygen demand (66%) which was met by an increase in coronary blood flow (59%). The data suggest that the antagonism of narcotics with high doses of naloxone may impair the myocardial oxygen supply in patients suffering from coronary insufficiency. It is concluded that naloxone should be titrated for each patient to ensure adequate reversal of respiratory depression and to avoid circulatory stress.

Animals↗
PubMed1977

Dopamine effects on circulation and myocardial oxygen supply.

We measured the action of dopamine given intravenously at dosage ranging from 2.5 to 320 micrograms/kg per min in closed chest anaesthetized dogs. Dopamine produced a dose-dependent increase in heart rate, cardiac index, mean arterial pressure, total peripheral resistance, pulmonary artery pressure, left ventricular end diastolic pressure, coronary flow and myocardial oxygen consumption. At dopamine dosage of 80-320 micrograms/kg per min, the coronary vascular resistance, the stroke volume index, the efficiency of heart work and the central venous pressure are all decreased. The maximum effect of dopamine on the circulation was seen at a dose between 40 and 80 micrograms/kg per min.

Animals↗
PubMed1977

[Doxapram-induced changes in circulation and myocardial efficiency (author's transl)].

The effects of Doxapram 2.0 mg/kg intravenously on circulation and myocardial oxygen supply were studied in 9 anaesthetized closed chest dogs. Immediately after Doxapram increases in heart rate (maximum+40.5%, 1st min), mean aortic pressure (+49%, 3rd min), cardiac index (+18%, 3rd min), total peripheral resistance (+32%, 3rd min), pulmonary arterial pressure (+48%, 1st min), left ventricular end-diastolic pressure (+79%, 1st min), myocardial blood flow (+38%, 3rd min), myocardial oxygen consumption (+74%, 1st min) and left ventricular work (+76%, 1st min) were observed. The changes in heart rate, mean aortic pressure, myocardial blood flow, myocardial oxygen consumption and heart work were persistent up to 20 min after Doxapram 2.0 mg/kg intravenously. Max dp/dt, coronary vascular resistance and the myocardial efficiency were not influenced after Doxapram.

Animals↗
PubMed1977

[Effect of high dosages of morphine and meperidine on haemodynamics, coronary blood flow and myocardial oxygen consumption in comparison to fentanyl and piritramide (author's transl)].

Although morphine is one of the oldest drugs known to man, it has only recently been used in large doses as an anesthetic agent. The main advantage is the cardiovascular stability. The purpose of this investigation was to study the circulatory response to high equianalgesic doses of morphine and meperidine. In 10 closed chest dogs during normoventilation and light background-anaesthesia (0.5 Vol. % halthane; N2O:O2 = 2:1) 2.0 mg/kg morphine and 15.0 mg/kg meperidine were given at random. Morphine produced a decrease in mean arterial blood pressure by 28%, which was paralleled by an identical fall in total peripheral resistance. No negative inotropic effects were found. In contrast to this, the severe hypotension developing with meperidine (decrease in blood pressure by 54%) was the result of peripheral vasodilatation (46%) and of myocardial depression indicated by a sharp drop in dp/dtmax (59%), dp/dtmax/IP (14%) and in left ventricular ejection fraction (33%). Utilizing the thermodilution technique, the cardiac output remained largely unaffected with both narcotic analgesics, as the increase in heart rate (morphine 27%; meperidine 101%) compensated for the fall in stroke volume (morphine 19%; meperidine 55%). In spite of the altered haemodynamics there was no change in the myocardial energy demand, which was adequately met by the coronary blood flow measured with the pressure-difference technique. Both, morphine and meperidine, produced initially an increase in coronary blood flow and coronary venous oxygen saturation indicating coronary vasodilation. While the mechanism for the change in cardiovascular status with high doses of morphine is vasodilatation probably due to histamine release, the results of this study suggest a peripheral as well as a central (myocardial depression) site of action with meperidine. The results obtained from this study were compared with the data from a previous investigation on equianalgesic doses of fentanyl and piritramide and their clinical implications were discussed.

Animals↗
PubMed1977

[The cardiovascular effects of the inspiratory N2O-concentration during piritramide anaesthesia in the dog (author's transl)].

Administration of nitrous oxide following large doses of narcotics has been reported to impair myocardial performance. In this investigation the effect of the inspiratory N2O-concentration (F1N2O = 0.0; 0.2; 0.4; 0.6; 0.8) upon haemodynamics, inotropism of the heart, coronary blood flow and myocardial oxygen consumption was studied in 8 dogs, which were normoventilated and narcotized with piritramide infused continuously (2.5 mg/kg-h). While 40% N2O(F1N2O = 0.4) decreased cardiac index (18%) and mean arterial pressure (5%) and increased total peripheral resistance (11%) significantly, the remaining inspiratory N2O-concentrations did not affect these parameters considerably. Load data, heart rate and the continuous decrease of LVdp/dtmax from 3170 mm Hg/s (F1N2O - 0.0) to 2175 mm Hg/s (F1N2O = 0.8) indicated negative inotropic properties of high concentrations of nitrous oxide. The myocardial oxygen demand, which was adequately met by the coronary blood flow, decreased with increasing N2O-concentrations initially by 18% (F1N2O = 0.4) due to bradycardia, slight hypotension and reduction in inotropism. Inhalation of 80% N2O, however, returned the energy demand of the heart to control levels (F1N2O = 0.0) resulting from increased myocardial wall-tension (increase in left ventricular end-diastolic pressure by 30%). The efficiency of left ventricular external work decreased from 18.6% (F1N2O = 0.0) to 14.7% (F1N2O - 0.8) indicating that myocardial performance was uneconomically influenced by high inspiratory N2O-concentrations and large doses of narcotics. The clinical implications of the results were discussed.

Anesthesia, General↗
PubMed1977

[The effects of the vasodilator nitroprusside on haemodynamics and myocardial oxygen consumption during drug induced myocardial depression (author's transl)].

The effect of the vasodilator nitroprusside (NP) on haemodynamics and myocardial oxygen consumption during drug induced myocardial oepression was examined in dogs (n = 7). The investigations were performed on closed chest dogs lightly anaesthetized with piritramide and N2O/O2 (ratio 2:1) under controlled ventilation and after beta-adrenergic blockade (1.5 mg/kg propranolol). After a loading dose and a continuous infusion of 0.3 mg/kg X min of pentobarbitone left ventricular maximum dp/dt was reduced to 50% of the control level, which was taken for granted as a standardized myocardial depression. Using an infusion of NP at a mean rate of 7 microgram/kg X min mean arterial pressure was then lowered to 80 mmHg for 20 min. The vasodilator therapy led to an increase in cardiac output and in stroke volume by 16%. Since the calculated endsystolic volume of the left ventricle decreased simultaneously (19%), the ejection fraction increased from 38% to 46%. There was also a significant reduction in left ventricular enddiastolic pressure (46%), which is supposed to result from the combined effects of an improved myocardial performance, a pooling of blood in peripheral vessels (indicated by decreases in enddiastolic volume by 6%, in mean pulmonary arterial pressure by 25% and in central venous pressure by 45%) and an increased ventricular compliance. Since the myocardial wall tension, a major determinant of myocardial energy demand, was lowered by increased ventricular compliance and reduced pre- and afterload, the oxygen consumption of the heart decreased by 22%. The smaller demand was supplied by an unchanged coronary blood flow. The narrowing of the a-v oxygen difference of the heart indicated a coronary dilatation (10%). The results obtained from this study support the clinical observations that NNP may improve an imbalanced ratio between myocardial oxygen supply and demand, in patients with impaired cardiac performance.

Animals↗
PubMed1977

[A comparison of cardiovascular effects of dobutamine and dopamine (author's transl)].

The influences of dobutamine and dopamine 5-40 microgram/kg-min intravenously on hemodynamics and myocardial oxygen consumption were investigated in closed chest dogs (n=9). Heart rate (HR), cardiac index (CI), stroke volume (SVI), mean aortic pressure (MAP), pulmonary artery pressure (PAP), central venous pressure (CVP), left ventricular enddiastolic pressure (LVEDP), myocardial blood flow (MBF) and maximum dp/dt (dp/dtmax) were measured. Total peripheral resistance (TPR), coronary vascular resistance (CVR), myocardial oxygen consumption (MVO2), efficiency of heart work (EME), the ventricular volumes (EDV, ESV) and the ejection fraction (EF) were calculated. When dopamine was infused, the cardiac output rose mainly by an increase of heart rate. During dobutamine an increase of stroke volume and ejection fraction was involved in the improvement of cardiac output. Heart rate and mean aortic pressure increased to a greater extent by dopamine. Dobutamine and dopamine increase myocardial blood flow and oxygen consumption. The comparatively slight effects of dobutamine on afterload and heart rate resulted in smaller increases in myocardial oxygen consumption. The efficiency of external heart work was increased by dobutamine at the doses of 5 microgram and 10 microgram/kg-min. In the higher dose range external myocardial efficiency decreased under dopamine and dobutamine. Load data and heart rate indicate that a greater inotropic effect of dobutamine compared with equal doses of dopamine is involved in the increase of dp/dtmax. The results are discussed in relation to a clinical use of dobutamine and dopamine.

Animals↗