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Biomedical subjects

K H Lindner

Publications and source records attributed to K H Lindner.

At least 127 records · Page 7Linked to original sources
PubMed1994

Right ventricular function during weaning from respirator after coronary artery bypass grafting. Comparison of two different weaning techniques.

The purpose of this investigation was to determine right ventricular function during weaning from controlled ventilation comparing a biphasic positive airway pressure ventilatory support system (BiPAP [Respironics]) with pressure support ventilation (PSV). In 22 patients following coronary artery bypass grafting, both weaning techniques were used in randomized chronological order for 60 min each. Right ventricular end-systolic (RVESV) and end-diastolic volume (RVEDV) and ejection fraction (RVEF) were evaluated using the fast-response Swan-Ganz catheter. In comparison to PSV, the BiPAP system resulted in a significantly higher mean pulmonary artery pressure (20.6 +/- 5.0 vs 19.3 +/- 4.2 mm Hg, p = 0.0158), pulmonary vascular resistance index (206 +/- 55 vs 181 +/- 61 dyn.s.cm-5.m2, p = 0.0355), RVESV (92.2 +/- 36.3 vs 77.2 +/- 30.4 ml, p = 0.0017), and RVEDV (176.4 +/- 48.5 vs 161.8 +/- 43.3 ml, p = 0.0061), while the RVEF was significantly lower (46.0 +/- 11.9 vs 51.8 +/- 12.4 percent, p = 0.0012). No differences in left ventricular function or arterial blood gas analyses were measured during both study periods. In summary, the RV afterload was higher with the BiPAP system compared with PSV which suggested that this was due to differences in the respiratory support between both weaning modes. Because of the Frank-Starling mechanism, this higher afterload did cause a small but significant increase in RV volumes and a significant decrease in RV ejection fraction with the BiPAP system.

Aged↗
PubMed1993

Metabolic and haemodynamic effects of dopamine plus domperidone in volunteers.

There are no studies of the relationship between infusion rate of dopamine and the arterial and venous dopamine plasma concentration and the resulting haemodynamic and metabolic effects. Dopamine was administered to seven volunteers using five infusion rates (1, 3, 6, 9, 13 micrograms/kg per minute) in an escalating sequence lasting for 30 min for each step. Since dopamine can cause nausea and vomiting, this relationship was investigated after administration of domperidone for infusion rates above 3 micrograms/kg per minute. Haemodynamic effects were assessed using 2-dimensional echocardiography. During the highest infusion rate the arterial plasma dopamine concentration reached 1,379 +/- 181 nmol/l. There was a linear correlation between the dopamine infusion rate and both the arterial and the venous plasma concentration. There was no significant change in heart rate or diastolic blood pressure. Systolic blood pressure, ejection fraction and cardiac index increased in a dose-dependent manner. Systemic vascular resistance decreased during the two low doses of dopamine and was not different from baseline values during the three high infusion rates. The plasma concentrations of glucose and non-esterified fatty acids increased from 5.3 +/- 0.4 to 0.68 +/- 0.9 nmol/l, and from 360 +/- 119 to 971 +/- 307 mumol/l, respectively, during the 13 micrograms/kg per minute infusion rate. As the plasma noradrenaline concentration increased up to 7.84 +/- 2.46 nmol/l in correlation to the dopamine plasma concentration, an indirect sympathomimetic effect may contribute to the actions of dopamine plasma concentration.

Adult↗
PubMed1993

Effect of phenylephrine bolus administration on global left ventricular function in patients with coronary artery disease and patients with valvular aortic stenosis.

BACKGROUND: Although phenylephrine bolus administration is frequently used to increase coronary perfusion pressure in patients with coronary artery disease or valvular aortic stenosis, there are no data describing its effect on left ventricular function (LVF). METHODS: Twenty patients scheduled for elective coronary artery bypass grafting (group 1) and 18 patients scheduled for elective aortic valve replacement (group 2) entered the study. The effect of phenylephrine was compared with that of norepinephrine in those patients who developed a defined degree of arterial hypotension under general anesthesia. These patients were randomized to receive an initial bolus of either phenylephrine (1 micrograms/kg) or norepinephrine (0.05 micrograms/kg) followed by a bolus of the other drug after arterial pressure and heart rate (HR) had returned to baseline. Transesophageal echocardiography was used to evaluate LVF. Arterial pressure, HR, ejection time, and LV diameter, area, and wall thickness were recorded immediately before and for 3 min after bolus administration. Fractional diameter shortening, fractional area change, mean heart rate corrected velocity of circumferential fiber shortening (mVcfc), and LV meridional end-systolic wall stress (ESWS) were calculated. RESULTS: Both substances effectively restored arterial pressure in both groups. However, in group 1, phenylephrine administration resulted in a reduction of fractional area change from 0.51 (median) to 0.39 (P = 0.0007) and a reduction of mVcfc from 1.16 to 0.61 circ/s (P = 0.0001). End-systolic wall stress increased from 98 to 186 10(3) dyne-cm-2 (P = 0.0001). Administration of norepinephrine to group 1 and administration of either substance to the group 2 patients did not cause any significant changes of LVF. CONCLUSIONS: The results indicate that phenylephrine given as an intravenous bolus to patients with CAD anesthetized with fentanyl causes a transient impairment of LV global function and that phenylephrine bolus administration is well tolerated in patients with valvular aortic stenosis.

Aged↗
PubMed1993

Effects of norepinephrine, epinephrine, and dopamine infusions on oxygen consumption in volunteers.

OBJECTIVE: To determine the relationships between plasma concentrations of norepinephrine, epinephrine, and dopamine and oxygen consumption (VO2) during infusion of these catecholamines. DESIGN: Prospective, randomized variable dose, pharmacologic study in which a noncumulative infusion-rate design was used. SETTING: Laboratory of the Department of Anesthesiology at a University Hospital. PATIENTS: Twenty-one normal volunteers. INTERVENTIONS: After a control period of 20 mins, norepinephrine (three infusion rates; 0.06 to 0.2 microgram/kg/min; n = 7), epinephrine (four infusion rates; 0.02 to 0.2 microgram/kg/min; n = 7), or dopamine (three infusion rates; 3 to 12 micrograms/kg/min; n = 7) was administered to normal volunteers (n = 21) for the purpose of constructing plasma concentration/VO2 response curves. MEASUREMENTS AND MAIN RESULTS: Systolic and diastolic blood pressure, heart rate, plasma concentrations of norepinephrine, epinephrine, and dopamine, and VO2 were measured at the end of the control period and at the end of each catecholamine infusion. VO2 was measured using a ventilated canopy system and a differential oxygen sensor. Typical hemodynamic responses to vasopressors were seen during adrenergic receptor agonist infusions. VO2 increased from 132 +/- 7 to 153 +/- 10 mL/min/m2 during the highest infusion rate of norepinephrine, from 133 +/- 7 to 182 +/- 11 mL/min/m2 during the highest infusion rate of epinephrine, and from 132 +/- 13 to 163 +/- 8 mL/min/m2 during the highest infusion rate of dopamine (p < .05; paired t-test). Increases in VO2 were correlated with the logarithms of the corresponding plasma catecholamine concentrations. Effects on VO2 and hemodynamic responses occurred at similar plasma concentrations for each of the three catecholamines. CONCLUSIONS: Administration of norepinephrine, epinephrine, or dopamine results in marked increases in VO2 in volunteers. In patients, the administration of catecholamines or sympathomimetics to attain optimal values of cardiac index, oxygen delivery (DO2), and VO2 may increase the oxygen demand and thus obscure the DO2-VO2 relationship.

Blood Pressure↗
PubMed1993

Influence of high thoracic epidural anesthesia on left ventricular contractility assessed using the end-systolic pressure-length relationship.

The effect of high thoracic epidural anesthesia (TEA on left ventricular contractility was studied in a prospective clinical trial. Forty-eight patients with ASA physical status 1 and 2 and without cardiovascular disease were included in the study. Thirty-six patients scheduled for elective upper abdominal surgery were randomly assigned to Group 1 (TEA, bupivacaine 0.25%, n = 12), Group 2 (TEA, bupivacaine 0.5%, n = 12) or to Group 3 (control without TEA, n = 12). TEA induced a sensory block which extended over all cardiac segments. In order to assess the effect of systemically absorbed bupivacaine, we studied a separate group of patients who received lumbar epidural anesthesia without involvement of the cardiac segments: Group 4 (LEA, bupivacaine 0.5%, n = 10). Left ventricular contractility was assessed using the end-systolic pressure-length relationship. Left ventricular dimensions were measured by transesophageal echocardiography. All hemodynamic measurements were performed under general anesthesia. There was no significant difference in systolic or diastolic arterial pressure, heart rate, left ventricular end-systolic and end-diastolic cross-sectional areas and left ventricular wall stress between the four groups. Left ventricular maximum elastance as a measure of left ventricular contractility was significantly (P < 0.001) reduced in Groups 1 and 2 [8.1 (+/- 3.5) and 9.6 (+/- 4.4) kPa.cm-1, respectively] as compared to Groups 3 and 4 [18.4 (+/- 8.8) and 17.7 (+/- 7.7) kPa.cm-1, respectively]. No significant difference could be demonstrated between Groups 1 and 2 or between Groups 3 and 4. It is concluded that high TEA severely alters left ventricular contractility even in subjects without pre-existing cardiac disease.

Abdomen↗
PubMed1993

Effects of active compression-decompression resuscitation on myocardial and cerebral blood flow in pigs.

BACKGROUND: This study was designed to assess the effects of a modified cardiopulmonary resuscitation (CPR) technique that consists of both active compression and active decompression of the chest (ACD CPR) versus standard CPR (STD CPR) on myocardial and cerebral blood flow during ventricular fibrillation both before and after epinephrine administration. METHODS AND RESULTS: During a 30-second period of ventricular fibrillation cardiac arrest, 14 pigs were randomized to receive either STD CPR (n = 7) or ACD CPR (n = 7). Both STD and ACD CPR were performed using an automated pneumatic piston device applied midsternum, designed to provide either active chest compression (1.5 to 2.0 in.) and decompression or only active compression of the chest at 80 compressions per minute and 50% duty cycle. Using radiolabeled microspheres, median total myocardial blood flow after 5 minutes of ventricular fibrillation was 14 (7 to 30, minimum to maximum) STD CPR versus 30 (9 to 46) mL.min-1 x 100 g-1 with ACD CPR (P < .05). Median cerebral blood flow was 15 (10 to 26) mL.min-1 x 100 g-1 with STD CPR and 30 (21 to 39) with ACD CPR (P < .01). When comparing STD with ACD CPR, aortic systolic (62 mm Hg [48 to 70] vs 80 [59 to 86]) and diastolic (22 [18 to 28] vs 28 [21 to 36]) pressures, calculated coronary systolic (30 [22 to 36] vs 49 [37 to 56]) and diastolic (18 [16 to 23] vs 26 [21 to 31]) perfusion pressures, end-tidal CO2 (1.4% [0.8 to 1.8] vs 2.1 (1.8 to 2.4]), cerebral O2 delivery (3.1 mL.min-1 x 100 g-1 [1.5 to 4.5] vs 5.3 [3.8 to 7.5]), and cerebral perfusion pressure (14 mm Hg [4 to 22] vs 26 [6 to 34]) were all significantly higher with ACD CPR: To compare these parameters before and after vasopressor therapy, a bolus of high-dose epinephrine (0.2 mg/kg) was given to all animals after 5 minutes of ventricular fibrillation. Organ blood flow and calculated perfusion pressures increased significantly in both the STD and ACD groups after epinephrine. The differences observed between STD and ACD CPR before epinephrine were diminished 90 seconds after epinephrine but were again statistically significant when assessed 5 minutes later, once the acute effects of epinephrine had decreased. No difference in short-term resuscitation success was found between the two groups. CONCLUSIONS: We conclude that ACD CPR significantly increases myocardial and cerebral blood flow during cardiac arrest in the absence of vasopressor therapy compared with STD CPR:

Animals↗
PubMed1993

Effect of angiotensin II on myocardial blood flow and acid-base status in a pig model of cardiopulmonary resuscitation.

The effect of angiotensin II on myocardial blood flow and acid-base status during cardiopulmonary resuscitation (CPR) was assessed. Fourteen pigs were allocated randomly to receive either 0.9% saline (n = 7) or 0.05 mg/kg angiotensin II (n = 7) after 4 min of ventricular fibrillation and 3 min of open-chest CPR. Total myocardial blood flow (measured with radiolabeled microspheres) before, 90 s, and 5 min following drug administration was 74 +/- 18, 62 +/- 12, and 54 +/- 11 mL.min-1 x 100g-1 (mean +/- SD) in the control, and 72 +/- 17, 125 +/- 25, and 74 +/- 20 mL.min-1 x 100 g-1 in the angiotensin II group (P < 0.001 at 90 s and P < 0.05 at 5 min). The PCO2 of coronary venous blood at 90 s after drug administration was 82 +/- 8 mm Hg in the control group as compared to 47 +/- 9 mm Hg in the angiotensin II group (P < 0.001). Only three of the seven control group animals could be resuscitated successfully, whereas all of the angiotensin II-treated pigs survived the 1-h observation period (P < 0.05), during which neither arterial hypertension nor bradycardia was observed. Angiotensin II was associated with an improvement of myocardial blood flow during CPR and short-term resuscitation success. The increase in myocardial perfusion is associated with a lower coronary venous PCO2 and a higher coronary venous pH. The authors conclude that angiotensin II administration facilitated cardiopulmonary resuscitation.

Acid-Base Equilibrium↗
PubMed1993

Effect of phenylephrine bolus administration on left ventricular function during high thoracic and lumbar epidural anesthesia combined with general anesthesia.

The effect of phenylephrine (PHE) boluses on left ventricular (LV) function was examined in patients without cardiovascular disease who developed arterial hypotension during high thoracic epidural anesthesia (TEA) combined with general anesthesia (GA) (group 1) or lumbar epidural anesthesia (LEA) combined with GA (group 2). LV function was assessed by transesophageal echocardiography (TEE) before and after central venous injection of 1 microgram/kg PHE. Fractional diameter shortening (FDS), end-systolic wall stress (ESWS), and rate-corrected velocity of circumferential fiber shortening (mVcfc) were determined. PHE effectively restored arterial blood pressure in both groups with a peak effect between 30 and 45 s after injection. FDS was reduced from 38% to 25% (mean, P < 0.01) in group 1 and remained unchanged in group 2. ESWS increased from 70 to 143 x 10(3) dyne.cm-2 (P < 0.01) and from 57 to 86 x 10(3) dyne.cm-2 (P < 0.05), in groups 1 and 2, respectively. mVcfc was significantly reduced from 1.11 to 0.80 circ/s (P < 0.05) in group 1 and was not altered in group 2. The authors conclude that PHE given as an intravenous bolus to patients under high TEA plus general anesthesia causes a transient impairment of LV function.

Abdomen↗
PubMed1993

The effect of phenylephrine bolus administration on left ventricular function during isoflurane-induced hypotension.

By using transesophageal echocardiography, we examined the effect of phenylephrine (PHE) bolus administration on left ventricular function in 16 patients with no known cardiovascular disease during isoflurane-induced hypotension. PHE was compared with norepinephrine (NE). The patients received an intravenous bolus of PHE (2 micrograms/kg) or NE (0.1 microgram/kg) in random order. The second substance was administered after levels of arterial blood pressure and heart rate returned to baseline levels. We determined fractional area change, end-systolic wall stress, and rate-corrected mean velocity of circumferential fiber shortening. Both substances effectively restored arterial blood pressure. However, after PHE, fractional area change decreased from 0.45 to 0.31 (mean) and rate corrected mean velocity of circumferential fiber shortening from 0.88 to 0.57 circumference/s, whereas both variables remained unchanged in response to NE. End-systolic wall stress increased after PHE and NE from 47.4 to 91.2 and from 54.0 to 65.2 10(3) dyne/cm2, respectively. We conclude that phenylephrine, given as intravenous bolus to patients under isoflurane hypotension, causes a transient impairment of left ventricular systolic performance.

Adult↗
PubMed1993

Effect of vasopressin on hemodynamic variables, organ blood flow, and acid-base status in a pig model of cardiopulmonary resuscitation.

Based upon the hypothesis that vasopressin (antidiuretic hormone) may increase vascular resistance during ventricular fibrillation, the effects of this potent vasoconstrictor were studied in a porcine model of ventricular fibrillation. Vasopressin therapy was compared to epinephrine by randomly allocating 14 pigs to receive either 0.045 mg/kg of epinephrine (n = 7) or 0.8 U/kg of vasopressin (n = 7) after 4 min of ventricular fibrillation and 3 min of open-chest cardiopulmonary resuscitation. During cardiopulmonary resuscitation, myocardial blood flow before and 90 s and 5 min after drug administration was 57 +/- 11, 84 +/- 11, and 59 +/- 9 mL.min-1 x 100 g-1 (mean +/- SEM) in the epinephrine group, and 61 +/- 5, 148 +/- 26, and 122 +/- 22 mL.min-1 x 100 g-1 in the vasopressin group (P < 0.05 at 90 s and 5 min). At the same times, mean cardiac index was not significantly different between the groups. After drug administration, coronary venous PCO2 was significantly higher and coronary venous pH was significantly lower in the epinephrine as compared to the vasopressin group. All pigs in both groups were resuscitated and survived the 2-h observation period. We conclude that vasopressin improves vital organ perfusion during ventricular fibrillation and cardiopulmonary resuscitation. Vasopressin seems to be at least as effective as epinephrine in this pig model of ventricular fibrillation.

Acid-Base Equilibrium↗
PubMed1993

Pharmacokinetics and technique of endotracheal and deep endobronchial lidocaine administration.

To determine absorption characteristics of endotracheal lidocaine, we administered lidocaine to hemodynamically stable patients by different techniques. Blood samples were taken for measurement of lidocaine plasma concentrations (fluorescence polarization immunoassay), and pharmacokinetics were calculated by regression analysis. Plasma concentrations at 1.5 and 2 min after drug administration were higher (P < 0.05) after instillation into the endotracheal tube (1.40 +/- 0.19 and 1.26 +/- 0.14 microgram/mL) than after deep endobronchial administration (1.00 +/- 0.08 and 0.83 +/- 0.05 microgram/mL). A biphasic absorption with a division of the area under the curve (AUCtot) into two parts (AUC1 and AUC2) could be assumed. After tube instillation, the AUC1/AUCtot ratio (2.6%) was higher (P < 0.05) than after deep endobronchial instillation (1.1%). To achieve high plasma concentrations within a short time, AUC1, representing a nearly instantaneous absorption, seems to be more important than AUC2, representing a higher but delayed absorption (depot effect). Because deep endobronchial lidocaine administration accentuated the late absorption, presumably by preventing drug distribution to the whole lung, this technique was detrimental to obtaining high plasma concentrations within a short period of time.

Adult↗
PubMed1992

Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers.

Noradrenaline and adrenaline were infused IV at 5 different rates (0.01-0.2 micrograms.kg.min-1) for 30 min to volunteers. The plasma catecholamine concentrations were determined by HPLC and electro-chemical detection. At the highest infusion rate, the arterial and venous plasma concentrations of noradrenaline increased from 1.18 to 44.1 nmol.l-1 and from 1.14 to 31.9 nmol.l-1, respectively, and of adrenaline from 0.29 to 23.9 nmol.l-1 and from 0.28 to 19.3 nmol.l-1, respectively. The peripheral venous plasma concentration of noradrenaline averaged 76% of the arterial concentration, and of adrenaline it was 73%. There was a linear relationship between the peripheral venous and arterial plasma noradrenaline and adrenaline concentrations at therapeutic doses.

Adult↗
PubMed1992

Stress hormone response during and after cardiopulmonary resuscitation.

The purpose of this study was to assess whether plasma adrenocorticotropin, cortisol, vasopressin, and renin concentrations are higher in resuscitated than in nonresuscitated patients during cardiopulmonary resuscitation, and whether there are possible correlations between these hormones and blood pressure or heart rate in the immediate postresuscitation phase. Of 34 consecutive patients (36-85 yr of age) with out-of-hospital cardiac arrest, 20 could be successfully resuscitated and admitted to hospital, whereas in the remaining 14 patients restoration of spontaneous circulation could not be achieved. During cardiopulmonary resuscitation, median adrenocorticotropin, cortisol, vasopressin, and renin concentrations in the external jugular vein were 237 pg/ml, 32.6 micrograms/dl, 122 pg/ml, and 46.5 ng/l, respectively, in resuscitated patients, and 45 pg/ml (P = 0.018), 18.4 micrograms/dl (P = 0.481), 88 pg/ml (P = 0.049), and 11 ng/l (P = 0.017), respectively, in nonresuscitated patients. Median adrenocorticotropin, cortisol, vasopressin, and renin concentrations were 101 pg/ml, 34.6 micrograms/dl, 22 pg/ml, and 25 ng/l, respectively, 60 min after successful resuscitation. No significant correlations were found between hormone levels and blood pressure or heart rate, but there was a significant negative correlation between the interval from collapse to the start of cardiopulmonary resuscitation and plasma cortisol concentrations during cardiopulmonary resuscitation (Spearman rank correlation coefficient = -0.967, P less than 0.001), indicating an impaired cortisol release from the adrenal cortex. The lower hormone concentrations of the nonresuscitated patients measured during cardiopulmonary resuscitation might indicate an impairment in neuroendocrine response.

Adrenocorticotropic Hormone↗
PubMed1992

Plasma catecholamine concentrations after successful resuscitation in patients.

OBJECTIVES: To measure plasma catecholamine concentrations after cardiopulmonary resuscitation (CPR) and to correlate catecholamine concentrations with heart rate (HR), BP, and plasma glucose and lactate concentrations. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a University Hospital. PATIENTS: Ten patients (58 to 85 yrs) with out-of-hospital cardiac arrest. INTERVENTIONS: At 1, 5, 15, 30, and 60 mins after restoration of spontaneous circulation, blood samples were drawn and BP and HR were measured. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography and plasma glucose and lactate concentrations were measured by enzymatic methods. MAIN RESULTS: Median plasma epinephrine and norepinephrine concentrations were 136.3 micrograms/L (136,300 pg/mL), range 27.6 to 397.6 micrograms/L (27,600 to 397,600 pg/mL), and 4.7 micrograms/L (4700 pg/mL), range 1.8 to 14.5 micrograms/L (1800 to 14,500 pg/mL), respectively, at 1 min. Median plasma epinephrine and norepinephrine concentrations decreased to 8.7 micrograms/L (8700 pg/mL), range 1.2 to 55.0 micrograms/L (1200 to 55,000 pg/mL) and 1.9 micrograms/L (1900 pg/mL), range 1.3 to 5.8 micrograms/L (1300 to 5800 pg/mL), respectively, at 60 mins after restoration of spontaneous circulation. Epinephrine concentrations decayed with a semilogarithmic decay pattern. The half-life for the alpha phase was 2.2 mins and was 38.7 mins for the beta phase. Mean values of systolic arterial pressure were between 136 +/- 23 mm Hg at 1 min and 120 +/- 15 mm Hg at 30 mins. Median plasma glucose concentrations were between 8.2 mmol/L (147.7 mg/dL; range 5.8 to 11.2 mmol/L [104.5 to 201.8 mg/dL]) at 1 min and 13.9 mmol/L (250.4 mg/dL; range 9.7 to 16.6 mmol/L [174.8 to 299.1 mg/dL]) at 30 mins. Lactate values were between 11.4 mmol/L (range 4.7 to 16.5) at 1 min and 5.2 mmol/L (range 2.7 to 12.5) at 60 mins. No significant correlations were found between circulating catecholamine concentrations and the other variables. CONCLUSIONS: After CPR, plasma catecholamine concentrations remained at high values but they did not lead to increases in BP, HR, or circulating glucose concentrations.

Aged↗
PubMed1992

Effects of diltiazem on oxygen delivery and consumption after asphyxial cardiac arrest and resuscitation.

BACKGROUND AND METHODS: Calcium-channel blockers may attenuate vasospasm after transient ischemia and improve organ blood flow after resuscitation. Our aim was to assess the effect of diltiazem on systemic oxygen delivery and consumption, hemodynamics, electroencephalogram (EEG), and organ blood flow after restoration of spontaneous circulation. After a 3-min period of asphyxial cardiac arrest, 14 pigs (20 to 27 kg) were randomly allocated to treatment with either diltiazem (0.1 mg/kg bolus followed by an iv infusion of 0.025 mg/min/kg over 120 mins) or placebo, given at 5 mins after successful resuscitation. Organ blood flow was measured using tracer microspheres 120 mins after resumption of spontaneous circulation. RESULTS: Median systemic oxygen delivery index values at 30, 60, and 120 mins after restoration of spontaneous circulation were 18.2 mL/min/kg (range 14.8 to 20.7), 16.8 mL/min/kg (13.2 to 20.8), and 19.6 mL/min/kg (16.9 to 21.0), respectively, in the diltiazem group and 13.1 mL/min/kg (11.2 to 14.6), 11.9 mL/min/kg (10.3 to 13.3), and 14.7 mL/min/kg (11.4 to 17.2), respectively, in the control group (p less than .05 for all three comparisons). At the same points in time, median systemic oxygen consumption indices were 3.2 mL/min/kg (range 2.2 to 3.7), 2.1 mL/min/kg (1.9 to 3.0), and 2.6 mL/min/kg (1.8 to 3.8) in the diltiazem group and 2.8 mL/min/kg (2.1 to 4.0), 2.7 mL/min/kg (1.7 to 4.3), and 2.3 mL/min/kg (1.6 to 3.8) in the placebo group (NS). Diltiazem enhanced the postarrest recovery of EEG total power. Right and left cerebral blood flow 120 mins after restoration of spontaneous circulation was significantly (p less than .01) higher in the diltiazem group in comparison with the control group. CONCLUSIONS: Diltiazem causes an increase in systemic oxygen delivery index by promoting vasodilation, but it does not change systemic oxygen consumption index in comparison to placebo treatment. It may be that an impairment in local autoregulation and/or in oxidative metabolism at the cellular or subcellular level was the reason why diltiazem did not improve these derangements. The observed increase in cerebral blood flow and in EEG recovery may be beneficial to the brain after a period of asphyxia.

Acid-Base Equilibrium↗