Urapidil versus clonidine. Acute haemodynamic effects during control of intraoperative hypertensive episodes.
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Biomedical subjects
Publications and source records attributed to W Hess.
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In 8 patients with coronary artery disease (CAD) classed as NYHA II or III, anesthesia was induced with high-dose fentanyl (0.05 mg/kg) and pancuronium (0.1 mg/kg). The patients were ventilated normally with the aid of a mask (O2: air 1:1, tidal volume 10 ml/kg with a rate of 10/min) for 5 min and then intubated. In 8 further patients with CAD NYHA class II or III, anesthesia was induced with 0.02 mg/kg flunitrazepam, N2O/O2 1:1 and isoflurane 0.5 vol%; they were relaxed with pancuronium (0.1 mg/kg) in combination with a bolus of 0.005 mg/kg fentanyl. These patients were also ventilated normally for 5 min and then intubated. Measurements of cardiovascular dynamics included cardiac output (CO), heart rate (HR), arterial pressure (AP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), myocardial blood flow (MBF), and arterial and coronary sinus oxygen and lactate contents. Cardiac index (CI), stroke volume index (SVI), total peripheral resistance (TPR), myocardial oxygen consumption (MVO2), coronary vascular resistance (CVR), coronary perfusion pressure (CPP), myocardial oxygen content difference (AVDO2cor) and myocardial lactate extraction rate (LE) were calculated from standard formulas. Measurements and an electrocardiogram were taken before anesthesia, after induction of anesthesia and after intubation. The hemodynamic parameters HR, AP, CI, CPP were relatively stable in patients anesthetized with high-dose fentanyl and pancuronium, whereas we found greater decreases in these parameters with the balanced anesthesia technique. Determinants of myocardial oxygen demand were higher in the high-dose fentanyl group; therefore, myocardial blood flow and oxygen consumption did not decrease to the same extent as in the balanced anesthesia group.(ABSTRACT TRUNCATED AT 250 WORDS)
Unlike the left ventricle, the right ventricle is a thin-walled, low-pressure, volume-displacement pump that ensures adequacy of left ventricular filling and maintains a low pressure in the venous system. In healthy human subjects, there is no burden for right ventricular systolic emptying, because normal pulmonary vessels have a low impedance and show a passive recruitment when cardiac output increases. However, under a pathological condition like right-sided heart failure, the right ventricle may exert profound influences on the circulatory state. Right-sided heart failure most often results from primary or secondary pulmonary arterial hypertension. Pharmacologic vasodilation of the hypertensive pulmonary vascular bed is an ideal therapy for right-sided heart failure. The bipyridine derivative amrinone has positive inotropic and direct vasodilator properties, and therefore seems suitable for the therapy of right ventricular dysfunction accompanied by pulmonary arterial hypertension. In one study, 12 patients with right ventricular failure due to mitral valve stenosis were evaluated, and it was found that amrinone increased cardiac output by 25% and decreased pulmonary artery pressure by 30% to 50%. In a second study, the hemodynamic properties of amrinone versus sodium nitroprusside were compared in patients with aortic or mitral valve failure (n = 17), when both agents lowered systemic vascular resistance equally. Pulmonary vascular resistance decreased significantly (25%) only in the amrinone group.
The effects of the non-depolarizing muscle relaxants pancuronium (Pancuronium) and vecuronium (Norcuron) (0.1 mg/kg) on myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, cardiovascular dynamics and electrocardiogram were studied in two groups of eight patients undergoing coronary artery bypass surgery. After an introduction of anaesthesia with 0.015-0.02 mg/kg rohypnol, isoflurane (0.5 Vol%) and N2O/O2 neuromuscular blockade was induced with pancuronium or vecuronium combined with a single dose of 0.005 mg/kg fentanyl. Measurements and electrocardiogram were performed before anaesthesia, in steady state of anaesthesia and after relaxation with pancuronium or vecuronium, combined with fentanyl. The measurements consisted of heart rate (HR), cardiac index (CI), stroke volume index (SVI), mean arterial pressure (AP), total peripheral resistance (TPR), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), right atrium pressure (RAP), myocardial blood flow (MBF), coronary vascular resistance (CVR), myocardial oxygen consumption (MVO2), coronary ateriomixed venous oxygen content difference (AVDO2cor), myocardial lactate extraction (LE) and rate pressure product (RPP). In the vecuronium group heart rate (HR) decreased significantly greater (21%) than in the pancuronium group (9%). Therefore myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) diminished more in the vecuronium (48% resp. 35%) than in the pancuronium group (31% resp. 18%). The higher metabolic demand in the pancuronium group induced a significantly lower coronary vascular resistance (CVR). All the other hemodynamic parameters did not differ significantly in both patients groups. In all the patients we could not observe ST-segment depressions or elevations in the ECG, increases of PCWP or myocardial lactate productions.(ABSTRACT TRUNCATED AT 250 WORDS)
The bipyridine derivative amrinone is a specific phosphodiesterase III blocking agent. In vitro and in vivo studies show a dose-dependent increase in myocardial contractility induced by amrinone. In patients with congestive heart failure, the inotropic and vasodilator effects of amrinone contribute to cardiac improvement. When amrinone is used, the increase in myocardial oxygen consumption due to increased contractility is offset by the reductions in preload and afterload. In hearts with very high wall tension, myocardial oxygen consumption may even decrease with amrinone. Amrinone therapy is not accompanied by significant increases in heart rate. Tachyphylaxis has not been observed. The elimination half-life ranges between 2.5 and 3.5 h. A large quantity of amrinone is excreted unchanged, and therefore in cases of renal impairment the possibility of cumulation exists. The main adverse reaction of amrinone is a reversible thrombocytopenia induced by a dose-dependent decrease in platelet survival time. Therefore, frequent platelet counts are necessary when amrinone is administered. Numerous studies in patients with chronic congestive heart failure confirmed the beneficial hemodynamic effects of amrinone. Experience in the treatment of acute perioperative heart failure with amrinone are still limited, but the present results are encouraging; an additive effect of amrinone to catecholamines seems especially promising in the therapy of severe postoperative low-cardia-output syndrome.
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A patient with mitral valve stenosis (NYHA IV) suffered a pulmonary artery rupture after valve replacement and weaning from bypass. This event coincided with the measurement of pulmonary capillary wedge pressure. Anticoagulation aggravated the endobronchial bleeding to a near fatal outcome. By intubating with a double-lumen endobronchial tube and clamping the right pulmonary artery, the pulmonary hemorrhage and its complications could be controlled. After antagonizing the heparin dose and supporting the right heart with epinephrine bleeding was reduced substantially, following which the right pulmonary artery was declamped. In older patients or patients with pulmonary hypertension the following procedures for preventing pulmonary artery rupture should be taken: before inflating the balloon the catheter should be withdrawn into a large vessel; after inflation the balloon the catheter can be advanced to the wedge position.
The hemodynamic parameters of 24 cardiosurgical patients with low cardiac output syndrome (LCOS) after weaning from bypass were evaluated retrospectively. These patients were additionally treated with amrinone if the conventional therapy with catecholamines and vasodilators did not reach satisfying hemodynamic results. 14 patients underwent aorto-coronary bypass surgery, 10 patients underwent valve repair. Their disability by NYHA class was III and IV. One third of these patients died between the first and the fifth day postoperatively. Hemodynamic assessment was performed after weaning from bypass and after the start of amrinone therapy and was continued the first 24 hours in the intensive care unit, as long as the patients were dependent on amrinone. The platelet count was determined every eight hours after surgery. Under the supplementary therapy with amrinone we found an increase of the arterial pressure and cardiac index and decrease of heart rate and total peripheral resistance. These salutary hemodynamic changes could be sustained in the postoperative period. The platelet count dropped from nearly 100,000/mm3 in mean (first measurement post-op.) to 58,000 in mean (the lowest value during 48 hours on intensive care). 2 patients showed a decrease to 11,000 and 15,000/mm3 with petechial bleedings. These findings indicate that on the one hand amrinone seems to be a promising drug in cases of severe LCOS when conventional therapy fails, but on the other hand a marked decrease of the platelets can occur. Therefore a frequent control of platelet count has to be performed when using amrinone.
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Hemoglobin as a vehicle for oxygen carries roughly 65 times the volume of oxygen that would otherwise be transported by simple solution in plasma. Conformational shifts of the molecule induce a cooperative oxygen-hemoglobin affinity. This property is reflected in the sigmoidal shape of the oxygen-hemoglobin dissociation curve. The affinity of hemoglobin is affected by temperature, hydrogen ions, carbon dioxide, and intraerythrocytic 2,3-DPG, with all these factors mutually influencing each other. Physiologic conditions associated with shifts in hemoglobin-oxygen affinity are oxygen uptake in the lung, oxygen delivery in the capillaries, and particularly oxygen delivery in working muscle, diaplacental oxygen transfer, and the regulation of erythropoesis. Hemoglobin-oxygen affinity attains pathological significance for oxygen supply during respiratory or metabolic alkalosis when the hemodynamic and tissue responses of the individual are limited: the increased affinity can critically lower capillary oxygen tension. Methemoglobin and carbon monoxide shift the oxygen dissociation curve to the left, so that intoxication with both substances reduces both total oxygen capacity and oxygen delivery of the remaining hemoglobin able to bind oxygen. This effect of methemoglobin and carbon monoxide must be considered in intensive care of intoxicated victims. Transfusions of large volumes of stored red cells, whose hemoglobin shows high affinity, can force the capillary oxygen tension down, especially in patients with impaired cardiac performance. The lowered oxygen affinity of patients with chronic renal disease and anemia must be preserved by avoiding an increase in the acidotic plasma pH. In the neonate, hemoglobin possesses a high affinity for oxygen physiologically; the hemodynamic reserve of the neonate is limited. Therefore, the hemoglobin content plays a crucial role in oxygen transport capacity during the initial months of extrauterine life. Consequently, red cell transfusion must be started much earlier in neonatal surgery than in adults. The red cells must be fresh, or at best "rejuvenated". Normally, oxygen affinity is not relevant for oxygen supply, but the position of the oxygen-hemoglobin dissociation curve may be a critical factor in the situations described above, particularly when blood flow is additionally restricted.
Intraoperative neuromonitoring, especially evoked potential monitoring, has gained interest in recent years for both the anesthesiologist evaluating cerebral function and the neurosurgeon wishing to avoid neuronal lesions during intracranial operations. Before evoked potential monitoring can be introduced as a routine method of intraoperative management, experience with this method particularly in intensive care units, is imperative. We recorded evoked potentials with the Compact Four (Nicolet) and Basis 8000 (Schwarzer Picker International) computer systems. Preoperative derivations should be done with the same apparatus used intraoperatively and parameters of peri- and intraoperative derivations should not be changed. The patient's head must be fixed in a Mayfield clamp in order to avoid artefacts during trepanation. The possible artefacts due to apparatus, patient, or anesthesia are summarized in the tables. The derivations of evoked potentials should be supervised by a person who is not involved in the anesthesia or the surgical procedure; this condition may change in the future with full automatization of the recording technique and alarms. Good communication between surgeon, anesthesiologist, and neurophysiological assistant is a prerequisite. The modality is chosen in accordance with the affected neuronal system: visual-evoked potential (VEP) monitoring in the management of processes affecting the visual pathway, brain stem auditory-(BAER) and somatosensory-evoked potential (SSEP) monitoring in lesions affecting these pathways, in particular space-occupying lesions of the posterior fossa. VEP monitoring may be useful, but we observed alterations of the responses without changes in the level of anesthesia or manipulation of the visual pathways. In space-occupying processes of the cerebellopontine angle, BAER could not be developed in nearly all cases because the large underlying tumor had caused the disappearance of waves II-V. In these cases SSEP monitoring could be carried out. Despite these difficulties, evoked potential monitoring seems useful. We believe, however, that it is not routinely used in operating rooms at present because alterations of the responses can be due to different causes; for the neurosurgeon, the problem as to which interdependent degrees of alteration in evoked potentials are related to neuronal disturbances remains unsolved.
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In 16 patients with necrotizing pancreatitis and in 6 patients with edematous-interstitial pancreatitis, hemodynamic studies were conducted between the first and the 12th day after the onset of illness. Patients with necrotizing pancreatitis had a high cardiac index of 4.47 +/- 0.75 L/min X m2 and a low total peripheral vascular resistance of 884 +/- 180 dyn X s/cm5, a low mean pulmonary vascular resistance of 84.3 +/- 25.7 dyn X s/cm5, and a high pulmonary shunt fraction of 24.2% +/- 6.6% of the cardiac output. This hyperdynamic vascular pattern was not found in patients with edematous-interstitial pancreatitis associated with gallstone disease. The group of patients with edematous-interstitial pancreatitis had a cardiac index of 3.21 +/- 0.8 L/min X m2, a total peripheral vascular resistance of 1337.8 +/- 248.2 dyn X s/cm5, a mean pulmonary vascular resistance of 130.7 +/- 48.2 dyn X s/cm5, and a pulmonary shunt fraction of 13.6% +/- 3.5% of the cardiac output. There was a significant difference between the patients with necrotizing pancreatitis and those with edematous-interstitial pancreatitis in the following hemodynamic parameters: heart rate (p less than 0.02), cardiac index (p less than 0.01), total peripheral vascular resistance (p less than 0.001), arteriovenous oxygen difference (p less than 0.02), and pulmonary shunt fraction (p less than 0.01). These findings in patients with necrotizing pancreatitis demonstrate an opening of intrapulmonary shunts and peripheral vasodilatation probably due to the release of pancreatitis-associated toxic agents in the early phase of the disease.
The aim of this study was to investigate the haemodynamic effects of amrinone in patients with pulmonary hypertension and impaired right ventricular function. Twelve patients with mitral stenosis (NYHA classification III and IV) took part in the study. The haemodynamic measurements were performed in the steady state under anaesthesia prior to surgery. The patients received a bolus injection of 1.5 mg kg-1 amrinone; haemodynamic measurements were taken at 3, 5, 10, 15, 20 and 30 min. Amrinone increased cardiac index by approximately 30%, heart rate rose from on average 76 to 82 beats per minute. Whereas pulmonary capillary pressure did not change significantly, mean pulmonary artery pressure fell clearly from 33 to 28 mmHg. A decrease in the elevated pulmonary vascular resistance of about 40% was calculated. The higher the initial value for resistance in the pulmonary circulatory system, the more marked was the reduction (r = 0.96). The study shows that amrinone induces a vasodilation in the pulmonary circulatory system. A reduction in ventricular afterload is of great significance particularly for the therapy of right heart insufficiency. Amrinone therefore appears to be a suitable substance with its observed vasodilating and its well known positive inotropic effects for the treatment of right heart failure in cases of pulmonary hypertension.
Forty patients scheduled for elective aortocoronary bypass surgery were entered in a double-blind study set up to compare the haemodynamic effects of 20 mg nifedipine (n = 20) and placebo (n = 20), both administered with the premedication. Global left ventricular function was normal in all patients. Anaesthesia was induced and maintained with standardized doses of fentanyl, flunitrazepam, and pancuronium together with 50% N2O. Cardiovascular responses to anaesthesia, intubation, skin incision, sternal retraction, and aortic manipulation were investigated. Throughout the study nifedipine produced a marked decrease in systemic vascular resistance. The reduction of left ventricular afterload was associated with an increase in cardiac index. In contrast to other reports, we observed no severe hypotension after nifedipine administration. Mean arterial pressure in patients from the nifedipine group was lower than in the placebo group only prior to anaesthesia. Since no negative drug interactions between nifedipine and the anaesthetic agents were observed, we conclude that the established cardiovascular benefit of nifedipine should be continued during anaesthesia.
The haemodynamic effects of isoflurane- and modified neurolept-anaesthesia were evaluated in 24 patients undergoing coronary artery bypass grafting. 12 patients (isoflurane group) were anaesthetized after an induction with 1.5 mg/kg methohexital and a unique dose of 0.005 mg/kg fentanyl with isoflurane (0.5-1.5 Vol%), N2O/O2 and pancuronium. 12 patients (neurolept group) received fentanyl (0.04 mg/kg), flunitrazepam, pancuronium and N2O/O2. Haemodynamic measurements were made before anaesthesia, in steady state anaesthesia, after sternotomy, after extracorporal circulation, after thoracic closure and one, two and four hours after the end of the operation. Between both groups we could not find significant differences in the haemodynamic parameters RAP, PAP, PCWP, PVR, CI, SVI, AP and CPP. However in the isoflurane group the peripheral vascular resistance (TPR) was significantly lower in steady state anaesthesia and after sternotomy. In the neurolept group the heart rate (HR) was significantly higher after bypass than in the isoflurane group. We believe, that at this time fentanyl analgesia was reduced. Before extracorporal bypass, patients with isoflurane anaesthesia had a lower arterio-mixed venous oxygen content difference (AVDO2) than patients with neurolept anaesthesia. Therefore it can be supposed that isoflurane lowers the oxygen demand more than neurolept anaesthesia. After surgery neurolept anaesthetized patients showed postanaesthetic shivering more frequently than those in the isoflurane group. We suggest that the vasodilating effect of isoflurane induces a homogeneous heat gain during warming the patients up, and that, therefore, in patients of the isoflurane-group AVDO2 and TPR were lower than in the patients of the neurolept-group during the first postoperative hours.(ABSTRACT TRUNCATED AT 250 WORDS)