Biomedical subjects

A W Goertz

Publications and source records attributed to A W Goertz.

11 recordsLinked to original sources

PubMed1997

[Effectiveness, side effects and costs of postoperative pain therapy: intravenous and epidural patient-controlled analgesia (PCA)].

PURPOSE: Improvement of the quality of analgesia, reduction of side effects and costs by application of epidural (PCEA) in comparison to intravenous patient-controlled analgesia (PCA) in postoperative pain treatment. METHODS: 62 patients with upper abdominal surgery took part in this randomised prospective study which was approved by the local ethics committee. Epidural catheters were inserted at T 8/9 (group PCEA). General anaesthesia was performed with propofol, sufentanil 2 micrograms/kg, pancuronium, enflurane and O2:N2O = 1:2. Postoperative analgesia consisted of epidural bupivacaine 0.25% + sufentanil 2 micrograms/ml (BS). (bolus 0.05 ml/kg, lockout 10 min) in group PCEA, or of intravenous morphine (bolus 2 mg. lockout 10 min) in group PCA. The following parameters were recorded until the evening of postoperative day 4: pain intensity at rest (VASR, 1-10) and on coughing (VASH, 1-10), blood pressure, heart rate, blood gas analysis, ability to ambulate, pruritus, nausea/vomiting (PONV), patient satisfaction (0-4), time and expenses for postoperative pain treatment. RESULTS: Median VASR (1 vs 2) and VASH (3 vs 4.5) were lower, cough intensity (2 vs 1) and patient satisfaction score (4 vs 3) were higher in PCEA compared to PCA. Ability to ambulate, pruritus, PONV, haemodynamics, paO2 and paCO2 were comparable. Postoperative pain treatment with PCEA was more time-consuming (407 vs 299 min) and expensive (71 vs 40 S/day) than PCA. CONCLUSION: PCEA in comparison to PCA after major abdominal surgery provides superior analgesia with comparable side effects at approximately 80% higher costs.

Abdomen↗

PubMed1995

Analgesic and hemodynamic effects of epidural clonidine, clonidine/morphine, and morphine after pancreatic surgery--a double-blind study.

This study characterizes analgesia an hemodynamics after epidural clonidine 8 micrograms/kg (Group C) or clonidine 4 micrograms/kg+morphine 2 mg (Group CM) in comparison to epidural morphine 50 micrograms/kg (Group M). Forty-five patients scheduled for pancreatectomy in combined general/epidural anesthesia were studied. The study drugs were administered 75 min postoperatively and for 10 h pain intensity (visual analog scale [VAS]), heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were measured; filling pressures were kept > 5 mm Hg. Adequate analgesia could be achieved within 1 h in all patients of Groups C and CM, but only in six patients of Group M (P < 0.001). Quality of analgesia was comparable in all groups (VAS reduction 82% +/- 20%, mean +/- SD) but duration of analgesic action was longer in Groups CM (586 +/- 217 min) and M (775 +/- 378 min) compared to Group C (336 +/- 119 min) (P < 0.001). In Group M, no hemodynamic alterations occurred. In Groups C and CM, HR, CO, and MAP were reduced significantly compared to baseline within the first 15-90 min, while stroke volume and systemic vascular resistance remained stable. We conclude, that hemodynamic alteration after epidural clonidine under conditions of stable filling pressures is caused mainly by a decrease in HR. It is not an effect of analgesia but of the intrinsic antihypertensive action of clonidine.

Analgesia, Epidural↗

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↗

PubMed1994

Influence of intravenous calcium gluconate on saphenous vein graft flow in closed-chest patients.

The effects of calcium gluconate on hemodynamics and saphenous vein graft flow in a group of patients undergoing elective coronary artery bypass grafting who developed ionized hypocalcemia at the end of the surgical procedure were examined. The patients received a central venous bolus of 15 mg/kg of calcium gluconate. Heart rate (HR), arterial pressure (AP), central venous pressure (CVP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), and cardiac output were measured immediately before and 30, 60, 120, 180, and 240 seconds after injection of calcium gluconate. Systemic and pulmonary vascular resistance (SVR and PVR, respectively), cardiac index (CI), stroke volume index (SVI), and right and left ventricular stroke work index (RVSWI and LVSWI, respectively), were calculated. Venous bypass flow velocity (Vbypass-flow) was assessed using a Doppler probe that was attached to the left anterior descending artery (LAD) bypass intraoperatively. Calcium gluconate significantly increased MAP, SVR, and LVSWI from 67 +/- 3 mmHg (mean +/- SEM), 1,128 +/- 128 dyne.s.cm-5 and 25 +/- 3 g.m.beat/m to a maximum of 81 +/- 5 mmHg (P < 0.01), 1,401 +/- 196 dyne.s.cm-5 (P < 0.05), and 32 +/- 4 g.m/beat/m (P < 0.01), respectively. HR, CVP, PAP, PCWP, PVR, CI, SVI, and Vbypass-flow remained unaltered. It is concluded that calcium gluconate administered to moderately hypocalcemic patients increases arterial pressure mainly by peripheral vasoconstriction. Because the increase of arterial pressure, and, thereby, coronary perfusion pressure is not associated with an increase of LAD bypass flow, vasoconstriction in the coronary vascular bed distal to the venous graft cannot be ruled out, and deterioration of the myocardial oxygen supply/demand ratio is strongly suggested.

Aged↗

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

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↗

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

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

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↗

PubMedDate not supplied

Effect of phenylephrine bolus administration on left ventricular function during postural hypotension in anesthetized patients.

STUDY OBJECTIVE: To investigate the effect of intravenous (IV) phenylephrine (PHE) bolus administration on left ventricular function in patients who developed postural hypotension during isoflurane anesthesia in the head-up tilt (reverse Trendelenburg) position. DESIGN: Prospective "before-after" trial. SETTING: Operation theater of a university medical center. PATIENTS: 15 ASA physical status I and II patients without cardiovascular disorders. INTERVENTIONS: The anesthetized patients were tilted from a supine horizontal to a 30-degree reverse-Trendelenburg position. Once a steady state was achieved, PHE 3 micrograms/kg was administered as an IV bolus dose. MEASUREMENTS AND MAIN RESULTS: Transesophageal echocardiography was used to assess left ventricular function. We measured blood pressure (BP); heart rate; left ventricular end-systolic and end-diastolic area, diameter, and wall thickness; and ejection time at baseline and after tilt, immediately before and for a period of 3 minutes after PHE injection. We calculated fractional area change (FAC), mean velocity of circumferential fiber shortening (mVcf), and end-systolic wall stress. Head-up tilt caused a reduction of mean arterial pressure [from 68 to 54 mmHg (mean)], end-systolic and end-diastolic left ventricular area (from 9.7 to 6.5 cm2 and from 19.2 to 13.1 cm2, respectively) and end-systolic wall stress (from 56 to 33 10(3).dyne/cm2). FAC and mVcf remained unaltered. PHE administration restored baseline values or overcompensated the changes caused by tilt. FAC slightly decreased in response to PHE (from 0.51 to 0.43), end-systolic wall stress increased to 83 10(3).dyne/cm2, and mVcf remained unchanged. CONCLUSION: PHE bolus administration effectively restored BP and cardiac filling, which were reduced after head-up tilt, without causing a relevant impairment of left ventricular function or an increase in end-systolic wall stress above the upper normal limit.

Adult↗