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K H Lindner

Publications and source records attributed to K H Lindner.

At least 109 records · Page 6Linked to original sources
PubMed1996

Cardiovascular function during the postresuscitation phase after cardiac arrest in pigs: a comparison of epinephrine versus vasopressin.

OBJECTIVE: The administration of vasopressin during cardiopulmonary resuscitation (CPR) provides significantly more vital organ blood flow when compared with epinephrine during cardiac arrest in pigs. The effects of this potent vasoconstrictor on postresuscitation cardiovascular function remain unknown. The purpose of this study was to compare the effects of vasopressin and epinephrine on cardiovascular function in the postresuscitation phase after CPR. DESIGN: Prospective, randomized, experimental study. SETTING: University research laboratory. SUBJECTS: Domestic pigs, 12 to 14 wks of age. INTERVENTIONS: Sixteen pigs were randomly allocated to receive either 0.045 mg/kg of epinephrine or 0.4 U/kg of vasopressin after 4 mins of cardiac arrest. MEASUREMENTS AND MAIN RESULTS: Hemodynamics, left ventricular contractility, and myocardial blood flow were measured for an interval of 240 mins after successful CPR. Differences between animals treated with epinephrine vs. vasopressin were most pronounced 15 mins after restoration of spontaneous circulation. At this time, mean aortic pressure was 64 +/- 6 (SEM) mm Hg in the epinephrine group and 84 +/- 6 mm Hg (p < .05) in the vasopressin group. Systemic vascular resistance was 1285 +/- 72 dyne.sec/cm5 in the epinephrine group and 2314 +/- 130 dyne.sec/cm5 (p < .001) in the vasopressin group. Cardiac index was 140 +/- 9 mL/min/kg in animals treated with epinephrine and 99 +/- 9 mL/min/kg (p < .01) in animals treated with vasopressin. Myocardial contractility (dp/ dtmax/P) was 52.8 +/- 3.4/sec with epinephrine as compared with 36.3 +/- 2.9 sec-1 (p < .01) with vasopressin. Left ventricular epicardial blood flow was 241 +/- 35 mL/min/100 g with epinephrine and 142 +/- 22 mL/min/100 g (p < .05) with vasopressin. Four hours after CPR, no significant differences were observed between groups. CONCLUSIONS: In the early postresuscitation phase, vasopressin provided higher systemic blood pressures and there was a reversible depressant effect on myocardial function when compared with epinephrine. Overall cardiovascular function was not irreversibly or critically impaired after the administration of vasopressin in this pig model of cardiac arrest.

Animals↗
PubMed1996

Release of endogenous vasopressors during and after cardiopulmonary resuscitation.

OBJECTIVE: To assess whether plasma endothelin, adrenaline, noradrenaline, arginine vasopressin, adrenocorticotropin, and cortisol concentrations were higher during cardiopulmonary resuscitation in patients in whom resuscitation was successful than in those in whom it failed, and to measure the concentrations of these hormones in the immediate post-resuscitation phase. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a university hospital. PATIENTS: 60 patients with cardiac arrest out of hospital. INTERVENTIONS: Blood samples were drawn and blood pressure and heart rate were measured during cardiopulmonary resuscitation, before and after the first dose of adrenaline was given and at 5, 15, 30, and 60 minutes after the restoration of spontaneous circulation. Plasma hormone concentrations were measured by radio-immunoassays. RESULTS: 24 of the 60 patients were successfully resuscitated and admitted to hospital: 36 were not. During cardiopulmonary resuscitation before adrenaline was given, the plasma concentration of endothelin (mean (SEM)) in resuscitated and in not resuscitated patients was 4.3 (0.9) pg/ml and 5.5 (0.4) pg/ml respectively (NS), adrenaline was 14.1 (2.0) ng/ml and 25.3 (3.6) ng/ml (P < 0.01), noradrenaline was 5.0 (0.9 ng/ml) and 8.4 (1.1 ng/ml) (P < 0.05), arginine vasopressin was 193 (28) pg/ml and 70 (9) pg/ml (P < 0.001), adrenocorticotropin was 128 (34) pg/ml and 57 (6) pg/ml (P < 0.05), and cortisol was 18 (3) microgram/dl and 15 (2) microgram/dl (NS). During cardiopulmonary resuscitation after adrenaline was given endothelin in resuscitated and in not resuscitated patients was 4.0 (1.0) pg/ml and 5.3 (0.5) pg/ml (NS), adrenaline was 145 (16) ng/ml and 201 (21) ng/ml (P < 0.05), noradrenaline was 3.9 (0.9) ng/ml and 8.3 (1.1) ng/ml (P < 0.01), arginine vasopressin was 177 (27) pg/ml and 58 (9) pg/ml (P < 0.001), adrenocorticotropin was 234 (92) pg/ml and 85 (9) pg/ml (P < 0.001), and cortisol was 17 (2) microgram/dl and 13 (2) microgram/dl (NS). CONCLUSIONS: Despite a tremendous adrenosympathetic response, the lower arginine vasopressin and adrenocorticotropin concentrations during cardiopulmonary resuscitation in patients in whom resuscitation failed may influence vital organ perfusion and hence the success of resuscitation. Plasma concentrations of arginine vasopressin and adrenocorticotropin may have a more important effect on outcome than previously thought.

Adrenocorticotropic Hormone↗
PubMed1996

Cerebral oxygenation during cardiopulmonary resuscitation with epinephrine and vasopressin in pigs.

BACKGROUND AND PURPOSE: Administration of vasopressin during cardiopulmonary resuscitation (CPR) improves vital organ blood flow compared with epinephrine, but the effect of vasopressin on cerebral oxygenation and cerebral venous hypercarbia during CPR has not previously been studied. METHODS: Fourteen pigs were allocated to receive either epinephrine (0.2 mg/kg) or vasopressin (0.4 U/kg) after 4 minutes of ventricular fibrillation and 3 minutes of CPR. Cerebral blood flow was determined by radiolabeled microspheres, and arterial and cerebral venous blood gases were measured. RESULTS: Cerebral blood flow, measured before and 90 seconds and 5 minutes after drug administration, was 9 (3; 12), 25 (19; 27), and 18 (10; 23) mL/min per 100 g (median and 25th and 75th percentiles, respectively) in the epinephrine group and 12 (5; 16), 51 (48; 70), and 53 (45; 63) mL/min per 100 g in the vasopressin group (P<.05 at 90 seconds, P<.01 at 5 minutes between groups). Five minutes after drug administration, cerebral venous Pco2 was 63 (59; 68) mm Hg in the epinephrine group and 47 (43; 55) mm Hg in the vasopressin group (P<.01); at the same time cerebral venous pH was 7.18 (7.17; 7.20) and 7.26 (7.22; 7.36) (P<.01) in the epinephrine and vasopressin groups, respectively. Cerebral oxygen extraction ratio, calculated before and 90 seconds and 5 minutes after drug administration, was 0.42 (0.32; 0.57), 0.47 (0.41; 0.57), and 0.56 (0.56; 0.64) in the epinephrine group and 0.43 (0.38; 0.45), 0.38 (0.25; 0.44), and 0.35 (0.33; 0.49) in the vasopressin group (P<.05 at 90 seconds and 5 minutes). CONCLUSIONS: Compared with epinephrine, vasopressin not only increases cerebral blood flow but also improves cerebral oxygenation and decreases cerebral venous hypercarbia when administered during CPR in pigs.

Acid-Base Equilibrium↗
PubMed1995

Angiotensin II augments reflex activity of the sympathetic nervous system during cardiopulmonary resuscitation in pigs.

BACKGROUND: During hypotensive states, angiotensin II augments reflex activity of the sympathetic nervous system. The purpose of the present study was to assess the effects of this vasoconstrictor on myocardial blood flow and plasma catecholamine concentrations during and after CPR. METHODS AND RESULTS: After 4 minutes of ventricular fibrillation and 3 minutes of open-chest CPR, 14 pigs (24 to 26 kg) were randomized into two groups receiving either saline (n = 7) or 0.05 mg/kg angiotensin II (n = 7). Arterial plasma catecholamine concentration was measured with high-pressure liquid chromatography. Organ blood flow was measured with radiolabeled microspheres. During CPR, after drug administration, left ventricular myocardial blood flow was significantly higher in the angiotensin II-treated group than in the control group. During CPR, median epinephrine concentrations before and 90 seconds and 5 minutes after drug administration were 63.0, 35.2, and 22.5 ng/mL, respectively, in the control group and 63.2, 139.8, and 154.2 ng/mL, respectively, in the angiotensin II group (P < .001 at 90 seconds and P < .01 at 5 minutes). At the same times, median norepinephrine concentrations were 52.6, 59.8, and 33.9 ng/mL, respectively, in the control group and 42.5, 98.7, and 111.3 ng/mL, respectively, in the angiotensin II group (P < .01 at 5 minutes). Restoration of spontaneous circulation was possible in all of the angiotensin II-treated pigs, whereas only 3 of the 7 saline-treated pigs could be resuscitated. At 5 minutes after successful resuscitation, epinephrine was 6.8 ng/mL in the control group and 16.1 ng/mL in the angiotensin II group (P < .05). CONCLUSIONS: During CPR, angiotensin II appears to increase coronary perfusion pressure and myocardial blood flow, not only by direct peripheral arteriolar vasoconstriction via angiotensin II receptors but also by inducing a massive catecholamine release with adrenergic peripheral vasoconstriction.

Angiotensin II↗
PubMed1995

Vasopressin improves vital organ blood flow during closed-chest cardiopulmonary resuscitation in pigs.

BACKGROUND: This study was designed to compare the effects of epinephrine with those of vasopressin on vital organ blood flow during closed-chest cardiopulmonary resuscitation (CPR) in a pig model of ventricular fibrillation. METHODS AND RESULTS: Vasopressin was compared with epinephrine by randomly allocating 28 pigs to receive either 0.2 mg/kg epinephrine (n = 7), 0.2 U/kg vasopressin (low dose) (n = 7), 0.4 U/kg vasopressin (medium dose) (n = 7), or 0.8 U/kg vasopressin (high dose) (n = 7) after 4 minutes of ventricular fibrillation and 3 minutes of closed-chest CPR. Left ventricular myocardial blood flow, determined by use of radiolabeled microspheres during CPR, before and then 90 seconds and 5 minutes after drug administration was 17 +/- 2, 43 +/- 5, and 22 +/- 3 mL.min-1.100 g-1 (mean +/- SEM) in the epinephrine group; 18 +/- 2, 50 +/- 6, and 29 +/- 3 mL.min-1.100 g-1 in the low-dose vasopressin group; 17 +/- 3, 52 +/- 8, and 52 +/- 6 mL.min-1.100 g-1 in the medium-dose vasopressin group; and 18 +/- 2, 95 +/- 9, and 57 +/- 6 mL.min-1.100 g-1 in the high-dose vasopressin group (P < .001 at 90 seconds and 5 minutes between epinephrine and high-dose vasopressin, and P < .01 at 5 minutes between epinephrine and medium-dose vasopressin). At the same times, calculated coronary systolic perfusion pressures were 12 +/- 2, 36 +/- 5, and 18 +/- 2 mm Hg in the epinephrine group; 10 +/- 1, 39 +/- 6, and 26 +/- 5 mm Hg in the low-dose vasopressin group; 11 +/- 2, 49 +/- 6, and 38 +/- 5 mm Hg in the medium-dose vasopressin group; and 10 +/- 2, 70 +/- 5, and 47 +/- 6 mm Hg in the high-dose vasopressin group (P < .01 at 90 seconds and 5 minutes between epinephrine and high-dose vasopressin); and calculated coronary diastolic perfusion pressures were 15 +/- 2, 24 +/- 2, and 19 +/- 2 mm Hg in the epinephrine group; 13 +/- 1, 25 +/- 2, and 20 +/- 1 mm Hg in the low-dose vasopressin group; 13 +/- 2, 25 +/- 2, and 21 +/- 2 mm Hg in the medium-dose vasopressin group; and 13 +/- 2, 35 +/- 3, and 24 +/- 2 mm Hg in the high-dose vasopressin group (P < .05 at 90 seconds between epinephrine and high-dose vasopressin). Total cerebral blood flow was significantly higher after high-dose vasopressin than after epinephrine (P < .05 at 90 seconds and P < .01 at 5 minutes between groups). Five animals in the epinephrine, 5 in the low-dose vasopressin, 7 in the medium-dose vasopressin, and 6 in the high-dose vasopressin groups were successfully resuscitated and survived the 1-hour observation period. CONCLUSIONS: We conclude that administration of vasopressin leads to a significantly higher coronary perfusion pressure and myocardial blood flow than epinephrine during closed-chest CPR in a pig model of ventricular fibrillation.

Animals↗
PubMed1995

Are the effects of noradrenaline, adrenaline and dopamine infusions on VO2 and metabolism transient?

OBJECTIVE: To determine whether noradrenaline, adrenaline and dopamine have persistent actions on VO2 and metabolism. DESIGN: Descriptive laboratory investigation. SETTING: Laboratory of the Department of Anaesthesiology at a University Hospital. SUBJECTS: 9 volunteers. INTERVENTION: VO2 and the plasma concentration of glucose and free fatty acids were measured prior to and during a 4 h infusion of saline (control), noradrenaline (0.14 microgram/kg min) adrenaline (0.08 microgram/kg min) or dopamine (7 micrograms/kg min), n = 9 each. VO2 was measured using an open circuit gas exchange system. MEASUREMENTS AND MAIN RESULTS: VO2 increased from 250 +/- 22 ml/min to 280 +/- 38 ml/min during noradrenaline, to 298 +/- 30 ml/min during adrenaline and to 292 +/- 39 ml/min during dopamine infusion. The plasma glucose concentration increased from 6.2 +/- 0.6 mmol/l to 8.8 +/- 0.8 mmol/l, 13.2 +/- 1.4 and 7.3 +/- 0.4 mmol/l during infusion of noradrenaline, adrenaline or dopamine, respectively. The plasma free fatty acid concentration increased from 0.28 +/- 0.10 mmol/l to 0.79 +/- 0.21 mmol/l during noradrenaline and to 0.52 +/- 0.09 mmol/l during dopamine. In contrast, free fatty acid values averaged baseline values at the end of the adrenaline infusion after an initial increase to 0.72 +/- 0.31 mmol/l. CONCLUSIONS: Administration of noradrenaline, adrenaline or dopamine resulted in persistent increases in VO2 in volunteers. With the exception of the transient adrenaline effect on fatty acids the metabolic actions were steady during 4 h of adrenergic stimulation. Since the adrenergic effect on VO2 is persistent over time a similar action in patients (e.g. septic shock) during treatment with adrenoceptor agonists may be important. Thus, an increase in VO2 during therapy may not only reflect an oxygen debt but also a pharmacodynamic action of adrenoceptor mediated calorigenic and metabolic induction.

Adult↗
PubMed1995

Right ventricular function after coronary artery bypass grafting in patients with and without revascularization of the right coronary artery.

OBJECTIVES: To evaluate the influence of revascularization of a stenosis of the right coronary artery on right ventricular function. DESIGN: Prospective study. SETTING: Single institutional study in a university hospital. PARTICIPANTS: 20 patients with different degrees of stenosis of the right coronary artery undergoing elective coronary artery bypass grafting. INTERVENTIONS: In 10 patients, bypass surgery included revascularization of a significant stenosis of the right coronary artery (group 1). In 10 other patients, the pathology of the right coronary artery was judged to be not significant, without indication for revascularization (group 2). MEASUREMENTS AND MAIN RESULTS: Using the fast-response thermodilution pulmonary artery catheter, right ventricular function was estimated perioperatively. After termination of extracorporeal circulation, there was an increase in right ventricular volumes in group 2 (p < 0.05) and an initial decrease in group 1 (p < 0.05), with higher volumes in group 2 compared with group 1 (p < 0.05). The ejection fraction increased in group 1 (p < 0.05) and decreased in group 2 after operation (p < 0.05), with higher values in group 1 compared with group 2 (p < 0.05). In addition to these findings, the pressure-volume relationship showed a leftward and upward shift in group 1 and a rightward shift in group 2 postoperatively. CONCLUSIONS: These results indicate that right ventricular depression can occur after bypass grafting in patients with a moderate stenosis of the right coronary artery that is not revascularized. Revascularization of more severe stenosis of the right coronary artery appears to preserve postoperative right ventricular function.

Cardiac Volume↗
PubMed1995

Unchanged 5'-deiodinating activity during the induction of a nonthyroidal illness.

We investigated the formation of a "nonthyroidal illness" (NTI) in pigs undergoing ventricular fibrillation (VF) and resuscitation. Seven minutes after VF twenty-one pigs received either Epinephrine (E: 45 micrograms/kg B.W.; n = 7), Norepinephrine (NE: 45 micrograms/kg B.W.; n = 7), or Vasopressin (VP: 0.8 U/kg B.W.; n = 7). We determined the serum concentrations (sc) of total T4 (TT4), FT4, total T3 (TT3) and rT3 120 min before, during (t0), and 5, 15, 60 and 120 min after VF. At the end of the observation period we figured out the in-vitro T3-generation (kM, Vmax), the in-vitro rT3-generation, the in-vitro rT3-decomposition (kM, Vmax) and the content of cytosolic sulfhydryls (total sulfhydryls, non-protein bound sulfhydryls) in liver and kidney specimen. Animals not undergoing VF served as controls (C) for parameters measured in the intracellular compartment. TT4- and TT3-sc decreased to 3.3 +/- 0.6 micrograms/dl (p < 0.05, vs. t0) and 15.2 +/- 4.1 ng/dl (p < 0.05, vs t0), resp. FT4-sc remained stable for five minutes (2.63 +/- 0.41 ng/dl) before declining to 1.8 +/- 0.39 ng/dl (p < 0.05, vs. t0). The rT3-sc raised finally to 46.9 +/- 7.3 ng/dl (p < 0.05, vs t0). Iodothyronine sc did not exhibit differences between E-, NE- and VP-treatment. Neither in-vitro T3-generation, nor in-vitro rT3-generation, nor in-vitro rT3-decomposition nor intracellular sulfhydryl content were affected by the events of VF and resuscitation as compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effect of 7.2% hypertonic saline/6% hetastarch on left ventricular contractility in anesthetized humans.

BACKGROUND: Although a positive inotropic effect of hypertonic saline has been demonstrated in isolated cardiac tissue as well as in animal preparations, no information exists about a possible positive inotropic action of hypertonic saline in humans. The aim of this investigation was to determine whether a clinically relevant positive inotropic effect can be demonstrated in humans. METHODS: Twenty-six patients without cardiovascular disease were randomized to receive 4 ml/kg of either 7.2% hypertonic saline/6% hetastarch or 6% hetastarch (control) at a rate of 1 ml.kg-1.min-1 while under general endotracheal anesthesia. Transesophageal echocardiography was used to evaluate left ventricular function. Arterial pressure, heart rate, and left ventricular end-systolic and end-diastolic diameter, area, and wall thickness were measured immediately before and after administration of either solution. Fractional area change, end-systolic wall stress, and the area under the end-systolic pressure-length relationship curve (ESPLRarea) were calculated. ESPLRarea was used to assess left ventricular contractility. RESULTS: Administration of hypertonic saline/hetastarch resulted in a significant decrease of mean arterial pressure and end-systolic wall stress from 77 +/- 14 (mean +/- SD) to 64 +/- 17 mmHg (P < 0.01) and from 52 +/- 14 to 32 +/- 11 10(3) dyne/cm2 (P > 0.01), respectively. End-diastolic area and fractional area change increased from 16.5 +/- 2.9 to 21.7 +/- 3.3 cm2 (P < 0.01) and from 0.53 +/- 0.07 to 0.70 +/- 0.06 (P < 0.01), respectively, whereas there was only a minor change of ESPLRarea from 38 +/- 13 to 44 +/- 13 mmHg.cm (P < 0.05). CONCLUSIONS: The apparent improvement of left ventricular systolic function in response to hypertonic saline/hetastarch is caused mainly by the combined effect of increased left ventricular preload and reduced left ventricular afterload. A possible positive inotropic action of hypertonic saline/hetastarch is not likely to be clinically relevant.

Adult↗
PubMed1995

Concentrations of prolactin and prostaglandins during and after cardiopulmonary resuscitation.

OBJECTIVES: To assess differences in plasma prolactin and prostaglandin concentrations in resuscitated and nonresuscitated patients during cardiopulmonary resuscitation (CPR), and to compare changes of prostaglandin and prolactin concentrations with hemodynamic variables in the immediate postresuscitation phase. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a university hospital. PATIENTS: Twenty-nine patients ranging in age from 39 to 87 yrs with out-of-hospital cardiac arrest. INTERVENTIONS: Venous blood samples were taken during CPR and at 5, 15, 30, and 60 mins after restoration of spontaneous circulation in order to measure plasma concentrations of prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 by immunoassay. Heart rate and blood pressure were measured at 5, 15, 30, and 60 mins after restoration of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: In 15 patients, restoration of spontaneous circulation was achieved; in the remaining 14 patients, successful resuscitation was not possible. During CPR, the mean plasma prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 concentrations were 95.9 +/- 13.6 micrograms/L, 357 +/- 61 ng/L, 228 +/- 28 ng/L, 277 +/- 66 ng/L, and 375 +/- 78 ng/L, respectively, in resuscitated patients, and 23.9 +/- 5.6 micrograms/L (p = .0001), 192 +/- 22 ng/L (p = .005), 202 +/- 31 ng/L (p = .528), 221 +/- 40 ng/L (p = .713), and 344 +/- 77 ng/L (p = .780), respectively, in nonresuscitated patients. At 60 mins after restoration of spontaneous circulation, the mean plasma prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 concentrations were 50.1 +/- 9.5 micrograms/L, 306 +/- 42 ng/L, 503 +/- 87 ng/L, 278 +/- 55 ng/L, and 355 +/- 30 ng/L, respectively. Mean values of systolic arterial blood pressure were 114 +/- 12 mm Hg at 30 mins and 123 +/- 18 mm Hg at 60 mins. No significant correlations were found between hemodynamic values and plasma concentrations of prolactin or prostaglandins. CONCLUSIONS: Prolactin and prostaglandin concentrations were increased during cardiac arrest and CPR. Successful initial resuscitation was associated with increased prolactin and prostaglandin F2 alpha concentrations during CPR. Decreased concentrations in non-resuscitated patients may have been a result of exhaustion of the neuroendocrine and eicosanoid systems, or may be due to differences in bioavailability at the site of blood sampling based upon differences in hemodynamics.

Adult↗
PubMed1994

[What's new in cardiopulmonary resuscitation? American Heart Association].

A strong consensus was reached for several changes in the guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC) in the 1992 conference on CPR and ECC held by the Emergency Cardiac Care Committee of the American Heart Association. These new recommendations, together with differing recommendations of the European Resuscitation Council, are described. An unresponsive person with spontaneous respirations should be placed in the recovery position if no cervical trauma is suspected. Compared with endotracheal intubation, other airway-protecting devices such as combination esophageal-tracheal tubes are of minor acceptance. During ventilation, the time for filling the lungs is increased to 1.5-2 s to decrease the likelihood of gastric insufflation. Delivery of i.v. drugs can be enhanced by an i.v. flush of sodium chloride. In endotracheal drug administration, higher doses and drug dilution are recommended. In infants and children up to 6 years of age, the value of intraosseous drug administration is emphasized. For pulseless adult victims, the initial dosage of epinephrine of 1 mg i.v. remains unchanged. For repeat doses, high-dose epinephrine up to 0.1 mg/kg is classified as of uncertain but possible efficacy. For lidocaine, the recommended i.v. dosage is 1.5 mg/kg. Sodium bicarbonate and calcium are not routinely recommended for resuscitation. For atropine, the maximum dose is 0.04 mg/kg. If hypomagnesaemia is present in recurrent and refractory ventricular fibrillation, it should be corrected by administration of 1 to 2 g magnesium sulfate i.v. Thrombolytic agents are classified as useful and effective in acute myocardial infarction and should be administered as early as possible. Glucose-containing fluids are discouraged for resuscitative efforts.

Cardiopulmonary Resuscitation↗
PubMed1994

[Perioperative endothelin, ACTH and cortisol plasma concentrations in coronary bypass patients].

STUDY OBJECTIVE: To follow up endothelin (ET), adrenocorticotropic hormone (ACTH), and cortisol levels in patients undergoing aortocoronary bypass grafting (CABG) and to determine whether these are extracted from plasma by the pulmonary circulation. DESIGN: Convenience sample trial. SETTING: University hospital. PATIENTS: Eight male routine CABG patients without appreciable concomitant disease. INTERVENTIONS: Patients were given anaesthesia in a strictly standardised manner using etomidate, flunitrazepam, fentanyl, and pancuronium. Nitroglycerin was administered prior to cardiopulmonary bypass (CPB) at 2 mg/h and dopamine as the only catecholamine starting from CPB weaning until the end of sampling at 3.5-5 micrograms/kg.min. Samples were drawn in rapid sequence from cannulated radial and a distal pulmonary arteries (Swan-Ganz catheter) at eight sampling times starting after induction of anaesthesia and catheter placement and finishing 22 h after the end of operation. MEASUREMENTS AND RESULTS: ET levels were determined by an ET-1, 2, 3-sensitive radioimmunoassay (RIA), ACTH and cortisol by commercially available RIA kits. There was significant (P = 0.032, linear regression analysis) correlation between ET and cortisol from pulmonary arterial samples. ET was significantly (P = 0.042, two-tailed Wilcoxon test) extracted by the pulmonary circulation after induction of anaesthesia. This pulmonary-systemic arterial difference nearly disappeared intraoperatively, but tended to be restored 22 h after the end of operation at an approximately twofold increased level. CONCLUSIONS: No interrelation between ET and the hypothalamic-pituitary-adrenal axis could be established by the ET, ACTH, and cortisol plasma levels. However, the significant correlation between perioperative ET and cortisol lends further support to the hypothesis of ET release by cortisol from vascular smooth-muscle cells. There is a net pulmonary clearance of ET in patients prior to CABG that is lost intra- and early postoperatively, but tends to be restored on the 1st day thereafter at an increased level.

Adrenocorticotropic Hormone↗
PubMed1994

Influence of phenylephrine bolus administration on left ventricular filling dynamics in patients with coronary artery disease and patients with valvular aortic stenosis.

BACKGROUND: Left ventricular diastolic function is known to be impaired in patients with coronary artery disease and patients with valvular aortic stenosis. Phenylephrine is frequently administered as an intravenous bolus in these patients perioperatively to increase coronary perfusion pressure. Although this is common practice, there is no information about the effect of phenylephrine bolus administration on left ventricular filling dynamics. METHODS: Twenty patients with coronary artery disease (group 1), 15 patients with valvular aortic stenosis (group 2), and 10 subjects without cardiovascular disease (group 3, control) entered the study. Left ventricular filling was evaluated using transesophageal pulsed Doppler echocardiography before and after phenylephrine injection given to patients whose mean blood pressure has decreased by more than 20% (and was not higher than 90 mmHg). We recorded the transmitral blood flow velocity curve and measured peak early and peak atrial flow velocity, acceleration and deceleration time of the early flow velocity peak, and mitral valve diameter. We calculated the ratio of peak early to peak atrial flow velocity (PE/PA), acceleration and deceleration rate of the early flow peak, and peak filling rate. RESULTS: Phenylephrine effectively restored arterial pressure in all three groups. However, in group 1, phenylephrine administration resulted in a reduction of PE/PA, acceleration rate of the early flow peak, and peak filling rate from 1.25 (mean) to 0.75 (P < 0.001), 411 to 276 cm/s2 (P < 0.001), and 439 to 305 ml/s (P < 0.001), respectively. In contrast, in group 2, intravenous phenylephrine increased PE/PA, acceleration rate of the early flow peak, and peak filling rate from 0.76 to 0.97 (P < 0.001), 365 to 503 cm/s2 (P < 0.05), and 321 to 388 ml/s (P < 0.01), respectively. In the control subjects, phenylephrine caused a transient reduction of PE/PA and peak filling rate from 1.71 to 1.39 (P < 0.001) and 618 to 524 ml.s-1 (P < 0.001), respectively. CONCLUSIONS: Phenylephrine bolus administration causes an alteration of left ventricular filling in coronary artery disease patients that seems to be more marked than that seen in normal subjects. In patients with aortic stenosis no deleterious effects were observed in response to phenylephrine.

Adult↗
PubMed1994

Pressure-time product and work of breathing during biphasic continuous positive airway pressure and assisted spontaneous breathing.

The pressure-time product (PTP) and work of breathing (W) were measured in 19 intubated patients during weaning from mechanical ventilation after aortocoronary bypass surgery. The patients were supported by two different ventilatory modes: biphasic continuous positive airway pressure (Biphasic CPAP; a ventilatory mode that permits spontaneous breathing at two different levels of airway pressure during inspiration and during expiration) and pressure-support ventilation (denominated as assisted spontaneous breathing, ASB). Our aim was to compare the energy cost of breathing imposed by both modes. The PTP was obtained by integrating the area enclosed by the esophageal and chest-wall static recoil pressure curves. The W performed by the patient (Wp) was calculated using Campbell's diagram method, based on the esophageal pressure curve and normalized per liter of ventilation. Two comparable support levels, corresponding to a high and a low degree of mechanical support, were studied for each ventilator mode. The levels of support were generally higher than that necessary to overcome inspiratory resistance. We found significantly higher PTP values during biphasic CPAP than during ASB (p < 0.01), whereas the Wp was the same with biphasic CPAP and ASB at both support levels. We conclude that because of the higher PTP values measured during biphasic CPAP, this mode of ventilation appears to have been more exhausting for our patients. The discrepancy between PTP and Wp is probably due to the different mechanisms of support given by the two ventilatory modes and the greater patient effort is related to those respiratory cycles that are not helped by the ventilator and which represent nearly half of the breaths during biphasic.

Aged↗
PubMed1994

The effect of ephedrine bolus administration on left ventricular loading and systolic performance during high thoracic epidural anesthesia combined with general anesthesia.

We investigated the effect of ephedrine on left ventricular function in patients without cardiovascular disease under high thoracic epidural anesthesia combined with general anesthesia. Because the epidural block was extended to all cardiac segments, ephedrine was assumed to be deprived of its centrally mediated actions. Left ventricular (LV) function was assessed using transesophageal echocardiography. We measured arterial pressure (AP), heart rate (HR), LV end-systolic and end-diastolic diameter and area (ESA, EDA), wall thickness, and LV ejection time before and after intravenous ephedrine bolus administration. We calculated area ejection fraction (EFA), end-systolic wall stress (ESWS), and mean velocity of circumferential fiber shortening (mVcfc). Ephedrine had a biphasic effect on left ventricular function. It transiently decreased EDA from 18.9 to 16.5 cm2 (mean), whereas EFA and mVcfc were increased from 33% to 49%, and from 1.88 to 2.67 circumferences/s, respectively. During the second phase, ephedrine increased mean arterial pressure (MAP) from a baseline value of 62 to 87 mm Hg, EDA was restored to 19.3 cm2, and EFA and mVcfc remained above baseline (52% and 2.64 circumferences/s, respectively). ESWS was not significantly increased from baseline. We conclude that ephedrine improves left ventricular contractility, even in the presence of high thoracic epidural anesthesia, without causing relevant changes of left ventricular afterload.

Adult↗
PubMed1994

Frequency of ventricular fibrillation as a predictor of defibrillation success during cardiac surgery.

The purpose of this study was to record median frequency of ventricular fibrillation (VF) in patients undergoing cardiopulmonary bypass for cardiac surgery, and to assess whether defibrillation success depends upon median VF frequency. Data were collected from 20 patients undergoing aortocoronary bypass grafting. Using computerized fast Fourier transformation of the signal from the electrogram, median VF frequency was assessed from onset of VF until aortic cross-clamping and during the 4-s period immediately before each defibrillation during the reperfusion phase. During VF, when an adequate coronary perfusion was maintained by cardiopulmonary bypass prior to aortic cross-clamping, median VF frequency (5.8 +/- 0.1 Hz to 6.2 +/- 0.1 Hz) remained constant for the entire observation interval (96 +/- 25 s; mean +/- SEM). A total of 42 defibrillations were performed: 22 resulted in supraventricular rhythm, 10 in VF, 6 in asystole, and 4 in electromechanical dissociation (EMD). Median VF frequency before defibrillation resulting in supraventricular rhythm was 4.7 +/- 0.17 Hz. In contrast, median VF frequencies before unsuccessful defibrillation resulting in persistent VF (3.5 +/- 0.28 Hz; P < 0.05), EMD (2.9 +/- 0.15 Hz; P < 0.01), or asystole (2.8 +/- 0.28 Hz; P < 0.01) were significantly lower. Above a threshold of 3.0 Hz, the probability of successful defibrillation increased as median VF frequency increased. The probability of success was 100% at a frequency of > or = 5.5 Hz. We conclude that median VF frequency is a reliable noninvasive variable which can be used to predict defibrillation success during the reperfusion phase after cardiac surgery.

Cardiopulmonary Bypass↗