Biomedical subjects

R J Kahn

Publications and source records attributed to R J Kahn.

At least 37 records · Page 2Linked to original sources

PubMed1995

Methylene blue administration in septic shock: a clinical trial.

OBJECTIVE: A release of nitric oxide has been incriminated in the cardiovascular alterations of septic shock. Since guanylate cyclase is the target enzyme in the endothelium-dependent relaxation mediated by nitric oxide, we studied the acute effects of methylene blue, a potent inhibitor of guanylate cyclase in patients with septic shock. DESIGN: Prospective clinical trial. SETTING: Medical-surgical intensive care unit in a university hospital. PATIENTS: Fourteen patients with severe septic shock requiring adrenergic therapy. INTERVENTIONS: Short-term intravenous infusion of methylene blue. MEASUREMENTS AND MAIN RESULTS: Hemodynamic measurements were obtained at baseline, and 30, 60, and 90 mins after the infusion of 2 mg/kg of methylene blue. Methylene blue administration was followed by a progressive increase in mean arterial pressure (from 61.1 +/- 7.6 to 71.7 +/- 12.0 mm Hg at 60 mins, p < .01). Pulmonary arterial pressure, cardiac filling pressures, cardiac output oxygen delivery, and oxygen consumption were not significantly affected. Left ventricular stroke work increased from 42.5 +/- 17.9 to 48.9 +/- 14.5 g.m after 60 mins (p < .05). Arterial lactate concentration decreased from 3.4 +/- 1.4 to 2.7 +/- 1.3 mmol/L (p < .05). Since these effects were transient, a second dose of methylene blue was administered 90 mins later to six patients and was followed by a similar response. No adverse effect was observed. CONCLUSIONS: In septic shock patients, the administration of methylene blue results in a transient and reproducible increase in arterial pressure, associated with an improvement in cardiac function, but does not increase cellular oxygen availability. The significant reduction in blood lactate concentration is probably related to the reductor effect of methylene blue, rather than to an improvement in tissue oxygenation.

Adult↗

PubMed1995

Combined measurements of blood lactate concentrations and gastric intramucosal pH in patients with severe sepsis.

OBJECTIVE: To compare the prognostic value of blood lactate concentrations, gastric intramucosal pH, and their combination in patients with severe sepsis. DESIGN: Prospective, noninterventional study. SETTING: Medical/surgical intensive care unit of a university hospital. PATIENTS: The study included 35 consecutive patients (44 to 82 yrs) with severe sepsis as defined by fever or hypothermia (rectal temperature > 38.3 degrees or < 35.5 degrees C), tachycardia (heart rate > 100 beats/min), tachypnea (respiratory rate > 20 breaths/min) or mechanical ventilation, abnormal white blood cell count (> 10 or < 6 x 10(3) cells/mm3), hypotension (systolic arterial pressure < 90 mm Hg), and evidence of organ dysfunction (oliguria or deterioration of mental status). INTERVENTIONS: Arterial lactate concentration and intramucosal pH were measured at the time of study entry, and at 4 and 24 hrs later. Hemodynamic data and oxygen-derived variables were determined at the time of study entry and 24 hrs later. Arterial blood and balloon saline gases were also determined to obtain the pH gap (arterial pH-intramucosal pH) and the PCO2 gap (intramural PCO2-PaCO2). MEASUREMENTS AND MAIN RESULTS: Of the 35 patients, 19 survived the intensive care unit stay. At the time of study admission, 23 (66%) patients had an increased lactate concentration (> 2 mEq/L) and 26 (74%) had a low intramucosal pH (< 7.32). Initially, there were no significant differences in blood lactate concentrations between nonsurvivors and survivors (3.2 +/- 1.5 vs. 2.8 +/- 2.3 mEq/L). Lactate concentrations remained high in nonsurvivors and progressively decreased in survivors (4 hrs: 3.3 +/- 1.1 mEq/L in nonsurvivors vs. 2.2 +/- 0.9 mEq/L in survivors [p < .01]; 24 hrs: 3.5 +/- 2.0 mEq/L in nonsurvivors vs. 1.9 +/- 1.1 mEq/L in survivors [p < .05]). Intramucosal pH was lower in the nonsurvivors than in the survivors initially (7.19 +/- 0.15 in nonsurvivors vs. 7.30 +/- 0.14 in survivors [p < .05]), at 4 hrs (7.18 +/- 0.17 in nonsurvivors vs. 7.29 +/- 0.13 in survivors [p = .06]), and at 24 hrs (7.19 +/- 0.31 in nonsurvivors vs. 7.30 +/- 0.17 in survivors [p < .05]). Of the 23 patients with initially high lactate concentrations, 12 (60%) of the 20 patients with low intramucosal pH died, as compared with one (33%) of the three patients with normal intramucosal pH (p = .052). Of the 14 patients with persistently high lactate concentrations at 24 hrs, all nine (100%) patients with low intramucosal pH, but only two (40%) of five patients with normal intramucosal pH died (p < .001). No significant relationship was found between lactate or intramucosal pH and oxygen-derived variables. Intramucosal pH correlated better with gastric intramural PCO2 (r2 = .58) than with arterial bicarbonate or base deficit/excess. Intramural PCO2 was a more specific predictor of mortality than intramucosal pH. When compared with patients with normal lactate concentrations, those patients with high lactate concentrations had a higher pH gap (0.22 +/- 0.22 vs. 0.07 +/- 0.13 [p < .01]) and PCO2 gap [21.0 +/- 33.9 vs. 1.8 +/- 9.8 torr [2.79 +/- 4.5 vs. 0.24 +/- 1.34 kPa]; p < .01). CONCLUSIONS: Both lactate concentrations and intramucosal pH represent reliable prognostic indicators in severe sepsis, and their combination improves the prognostic assessment in these patients. Both variables are better prognostic indicators than oxygen-derived variables. Intramural PCO2 appears to be a more specific variable than intramucosal pH, which partially reflects systemic metabolic acidosis. Combined determinations of blood lactate concentrations and intramucosal pH or intramural PCO2 may help to predict outcome from severe sepsis.

APACHE↗

PubMed1995

Early hemodynamic course of septic shock.

OBJECTIVE: To assess the relative contributions of changes in vascular tone and changes in cardiac function to hemodynamic recovery from septic shock. DESIGN: Case series, observational study. SETTING: Multidisciplinary department of intensive care in an academic hospital. PATIENTS: Sixty-seven patients with septic shock (prolonged hypotension, signs of tissue hypoperfusion, signs of sepsis, suspected source of infection, or documented bacteremia). In addition to the antibiotic therapy and the removal of the source of sepsis whenever possible, each patient received intravenous fluids and vasoactive agents (dopamine, norepinephrine, and dobutamine). Each patient was also treated with mechanical ventilation. Twenty-four (36%) patients survived their intensive care unit course. INTERVENTIONS: Hemodynamic measurements were obtained at baseline, after initial resuscitation (as soon as apparent hemodynamic stability was achieved), after 12 hrs, and after 24 hrs. MEASUREMENTS AND MAIN RESULTS: There were no significant differences in hemodynamic or oxygen-derived variables at baseline between the survivors and the nonsurvivors. During the initial resuscitation period, only the survivors demonstrated a significant increase in mean arterial pressure (from 69 +/- 17 to 82 +/- 18 mm Hg; p < .02) and left ventricular stroke work index (from 25.2 +/- 11.0 to 35.5 +/- 19.4 g.m/m2; p < .05). The increases in cardiac index and systemic vascular resistance were greater in the survivors than in the non-survivors, but the differences did not reach statistical significance. Study of the left ventricular function curves indicated an improvement of left ventricular function in the survivors but not in the nonsurvivors. CONCLUSION: An early improvement in left ventricular function is a hallmark of the survivors from septic shock.

Adolescent↗

PubMed1994

Effects of dobutamine and prostacyclin on cerebral blood flow velocity in septic patients.

PURPOSE: Both dobutamine and prostacyclin (PGI2) have been used to increase oxygen delivery in septic patients, but their effects on cerebral blood flow have not been well studied. METHODS: In 10 septic patients with altered mental status, stable hemodynamic status, and normal lactatemia, we investigated the effects of successive infusions of dobutamine at 5 micrograms/kg/min and PGI2 at 5 ng/kg/min on mean blood flow velocity in a middle cerebral artery, using transcranial Doppler flowmetry. RESULTS: Mean flow velocity increased with dobutamine (from 52 +/- 4 to 62 +/- 6 cm/s, P < .005) but not with PGI2 (from 55 +/- 5 to 57 +/- 5 cm/s, P = not significant). Each substance significantly increased cardiac index. Dobutamine increased arterial pressure from 85 +/- 6 to 91 +/- 5 mm Hg (P < .05), but PGI2 decreased it from 87 +/- 6 to 77 +/- 5 mm Hg (P < .005). With each agent, mean flow velocity was correlated with cardiac index (r = .51, P < .001) but not with arterial pressure. PGI2 reduced PaO2 from 103 +/- 10 to 82 +/- 6 mm Hg (P < .005). Cerebral oxygen delivery (estimated by the product of mean flow velocity and arterial oxygen content) increased by 19% with dobutamine but remained unchanged with PGI2. CONCLUSIONS: Dobutamine and PGI2 at the administered doses exert different effects on arterial pressure and middle cerebral artery flow velocity in septic patients. According to these data, dobutamine increases cerebral oxygen delivery more than PGI2.

Adult↗

PubMed1994

Effects of dobutamine on oxygen consumption in septic patients. Direct versus indirect determinations.

Dobutamine has been proposed as a means of disclosing a pathologic oxygen supply (DO2) dependency in critically ill patients. Like other catecholamines, however, dobutamine might increase cellular metabolism, so that oxygen consumption (VO2) would increase regardless of the presence or absence of a supply dependency. This study investigated the effects of graded doses of dobutamine on VO2 in stable, septic patients. Since it has been suggested that the use of reverse Fick equation to determine VO2 can induce a spurious VO2/DO2 dependency owing to a mathematical coupling of data, we determined VO2 both by respiratory gas analysis (VO2DIR) and from the reverse Fick equation (VO2INDIR). In 12 adult patients with signs of sepsis but an otherwise stable hemodynamic status (normal blood lactate levels, and no change in vasoactive drugs or fluid administration for at least 2 h), a dobutamine infusion was administered at a dose of up to 10 micrograms/kg/min in increments of 2 micrograms/kg/min every 10 min. Complete hemodynamic and gas measurements were obtained at baseline, at each dose of dobutamine, and 20 min after discontinuation of the infusion. All of the measured parameters were similar at baseline and after discontinuation of the dobutamine infusion. Dobutamine induced a dose-related increase in the cardiac index (from 3.84 +/- 0.97 to 6.19 +/- 1.56 L/min/m2, p < 0.01) and DO2 (from 501 +/- 123 to 801 +/- 219 ml/min/m2, p < 0.01). Both VO2DIR and VO2INDIR increased, from 161 +/- 37 to 183 +/- 40 ml/min/m2 and from 140 +/- 29 to 168 +/- 42 ml/min/m2, respectively (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Sotalol poisoning associated with asystole.

Sotalol overdose has special features because this beta-blocker has the potential to lengthen the Q-T interval and to initiate severe arrhythmias such as ventricular tachycardia or fibrillation. We describe the case of a 70-year-old woman who ingested 6.72 g sotalol with suicide attempt. Despite administration of activated charcoal, glucagon, atropine and isoprenaline, two episodes of asystole occurred, requiring cardiopulmonary resuscitation. Further treatment included ventricular pacing and dopamine. The patient recovered without neurologic nor cardiac sequelae.

Aged↗

PubMed1993

Relationship between oxygen uptake and oxygen delivery in septic patients: effects of prostacyclin versus dobutamine.

OBJECTIVE: To compare the effects of prostacyclin (PGI2) and dobutamine on the relationship between oxygen delivery (DO2) and oxygen uptake (VO2) in stable septic patients. DESIGN: Prospective study using a crossover design with alternate order of medications. PATIENTS: Seventeen patients with documented sepsis and a stable hemodynamic status with normal blood lactate concentrations. Eleven patients were mechanically ventilated. Eight patients eventually died. INTERVENTIONS: DO2 and VO2 were calculated before and after a 20-min infusion of 5 ng/kg/min of PGI2 followed or preceded by 5 micrograms/kg/min of dobutamine. MEASUREMENTS AND MAIN RESULTS: Both medications increased cardiac output significantly. At the dose used, PGI2 infusion reduced mean arterial pressure from 90.8 +/- 16.8 to 81.5 +/- 17.3 mm Hg (p < .01) and PaO2 from 97 +/- 25 torr to 82 +/- 22 torr (from 12.9 +/- 3.3 to 10.9 +/- 2.9 kPa) (p < .01) and increased venous admixture from 17.5 +/- 0.6% to 23.8 +/- 8.2% (p < .01). Dobutamine had no significant influence on these variables. PGI2 increased DO2 by 19% (from 470 +/- 105 to 557 +/- 117 mL/min/m2, p < .01) while dobutamine increased DO2 by 27% (from 463 +/- 103 to 589 +/- 156 mL/min/m2, p < .01). PGI2 increased VO2 by 5% (from 148 +/- 38 to 155 +/- 36 mL/min/m2) while dobutamine increased VO2 by 10% (from 146 +/- 36 to 161 +/- 41 mL/min/m2, p < .01). Accordingly, there was an identical decrease in oxygen extraction with PGI2 (from 32.4 +/- 8.2% to 28.6 +/- 7.1%, p < .01) and dobutamine (from 32.4 +/- 8.3% to 28.5 +/- 7.8%, p < .01). The responses to these medications were similar in survivors and nonsurvivors. CONCLUSIONS: PGI2 and dobutamine at the doses used have similar effects on oxygen extraction in critically ill, septic patients, but dobutamine increases DO2 more consistently and is better tolerated than prostacyclin.

Aged↗

PubMed1993

Administration of nebivolol after coronary artery bypass in patients with altered left ventricular function.

This prospective, double-blind study used invasive monitoring and echo-Doppler techniques to compare the hemodynamic effects of nebivolol, a new beta 1-selective beta-blocking agent with those of atenolol in patients recovering from coronary artery bypass grafting surgery. Five milligrams nebivolol and 50 mg atenolol equally decreased heart rate (HR) and blood pressure (BP) but, nebivolol, in contrast to atenolol, caused no decrease in stroke index (SI), cardiac index (CI), and right ventricular ejection fraction (RVEF). These differences appeared to be related in part to different peripheral effects of the two agents because nebivolol administration was associated with a reduction in systemic vascular resistance (SVR). After < or = 10 days of treatment, acceleration of aortic flow velocity increased and isovolumic relaxation time decreased with nebivolol but not with atenolol treatment. Both drugs were equally well tolerated. Therefore, nebivolol shares most of its effects with classical beta 1-blockers but is devoid of the potentially harmful effects on cardiac output (CO) and peripheral resistance.

Adrenergic beta-1 Receptor Antagonists↗

PubMed1993

Relation between oxygen consumption and oxygen delivery in patients after cardiac surgery.

The relative contributions of oxygen delivery (DO2) and oxygen extraction (O2ER) to the increase in cellular oxygen uptake (VO2) after cardiopulmonary bypass were studied prospectively in 36 patients after coronary artery bypass grafting (n = 18), valve replacement (n = 17), and removal of a left atrial tumor (n = 1). VO2 was calculated from the Fick equation and DO2 from thermodilution cardiac output and arterial oxygen content. During the first 24 h after cardiac surgery, there was a strong relation between VO2 and DO2 (VO2 = 28 + 0.27 x DO2, r = 0.79, P < 0.0001) but not between VO2 and oxygen extraction. Mixed venous oxygen saturation (SVO2) was usually reduced when cardiac index was below 2.0 L.min-1.m-2. Patients with a prolonged intensive care unit course (> 24 h) had lower cardiac index and lower SVO2 than the other patients. Therefore, the progressive increase in VO2 after cardiac surgery is accomplished primarily by an increase in cardiac output and DO2. It is usually when cardiac function is compromised that O2ER increases and SVO2 decreases.

Aged↗

PubMed1993

Serum cytokine levels in human septic shock. Relation to multiple-system organ failure and mortality.

PURPOSE: Cytokines have been associated with the development of sepsis and diffuse tissue injury following septic or endotoxic challenges in humans. Furthermore, relative organ-system dysfunction, not specific organ dysfunction, appears to predict outcome from critical illness. We hypothesized that persistence of inflammatory cytokines within the circulation, reflecting a generalized systemic inflammatory response, is associated with multiple-system organ failure (MSOF) and death from critical illness. In addition, since hepatic function is central to host-defense homeostasis, we further reasoned that critically ill patients with hepatic cirrhosis would have an increased incidence of MSOF and death following sepsis associated with a persistence of cytokines in the blood. PATIENTS AND METHODS: We measured serum levels of tumor necrosis factor (TNF), interleukin (IL) 1, IL-2, IL-6, and interferon gamma (IFG) serially for the first 48 h following the onset of hypotension (systolic blood pressure < 90 mm Hg) thought likely to be due to sepsis in all patients presenting to one ICU. These data were correlated with initial severity of shock and retrospective determination of septic or nonseptic origin, preexistent hepatic cirrhosis, subsequent development of MSOF, and outcome. RESULTS: Fifty-three specific episodes of shock in 52 patients were recorded (35 septic and 18 nonseptic episodes). Mortality was higher in septic patients (41 vs 17 percent, p < 0.01), as was the development of MSOF (29 vs 6 percent, p < 0.001), incidence of cirrhosis (21 vs 0 percent, p < 0.01), and TNF levels over the study interval (p < 0.01). Nonseptic patients also had an initial elevation in TNF over 48-h levels (p < 0.05) that were higher than serum levels reported for normal subjects (chi 2, p < 0.05). There was no relation between peak TNF level and outcome. Sixty-seven percent of the cirrhotic patients had development of MSOF and died, while only 30 percent of the noncirrhotic patients had development of MSOF or died (p < 0.05). The TNF and IL-6 levels in patients who had MSOF or who died were both elevated and did not decrease over time independent of presence or absence of sepsis (p < 0.01). Similarly, IL-6 levels after 12 h were higher in cirrhotic patients than in noncirrhotic septic patients (p < 0.05). No elevation in IL-1, IL-2, or IFG was seen in any patient subpopulation. CONCLUSIONS: TNF and IL-6 serum levels are higher in septic than in nonseptic shock, but the persistence of TNF and IL-6 in the serum rather than peak levels of cytokines predicts a poor outcome in patients with shock.

Cytokines↗

PubMed1992

Addition of enoximone to adrenergic agents in the management of severe heart failure.

OBJECTIVE: To assess the hemodynamic effects of the addition of small bolus doses of the phosphodiesterase inhibitor enoximone to adrenergic therapy in patients with severe heart failure. DESIGN: Open label, prospective study. SETTING: Multidisciplinary department of intensive care in a university academic hospital. PATIENTS: Twelve surgical patients after cardiac surgery and ten medical patients with ischemic or dilated cardiomyopathy who had signs of altered tissue perfusion associated with a low cardiac index (less than 2.25 L/min/m2), despite adrenergic therapy. INTERVENTIONS: Small iv bolus doses of 0.25 mg/kg of enoximone. MEASUREMENTS AND MAIN RESULTS: This treatment resulted in significant increases in cardiac index and left ventricular stroke work index without significant changes in heart rate or mean arterial pressure. Furthermore, the effects of half this dose (i.e., 0.125 mg/kg), studied in 11 patients, demonstrated a significant drug-induced increase in mean (+/- SD) cardiac index (from 1.58 +/- 0.29 to 1.84 +/- 0.27 L/min/m2, p less than .01) without change in mean arterial pressure (from 74.5 +/- 12.1 to 76.5 +/- 12.6 mm Hg, nonsignificant). CONCLUSIONS: Direct iv injections of enoximone can significantly increase the cardiac index in critically ill patients treated by adrenergic agents for severe heart failure. The administration of small doses of enoximone is effective and has minimal effect on arterial pressure.

Adult↗

PubMed1992

Veno-arterial carbon dioxide gradient in human septic shock.

Recent reports have shown that venous hypercarbia, resulting in a widening of the veno-arterial difference in PCO2 (dPCO2), is related to systemic hypoperfusion in various forms of low-flow state. Although septic shock usually is a hyperdynamic state, other factors can influence the CO2 production and elimination, and thus dPCO2 in septic shock This study examined the dPCO2 and acid-base balance together with cardiac output measurements and oxygen-derived variables in 64 adult patients with documented septic shock. For a total of 191 observations, a significant exponential relation between dPCO2 and CO was found. At time of first measurement, 15 patients had an increased dPCO2 (above 6 mm Hg) and a higher mixed venous PCO2 (PvCO2) (47.2 +/- 10.0 vs 35.9 +/- 7.3 mm Hg, p less than 0.001). These patients had a lower cardiac index (2.9 +/- 1.3 vs 3.8 +/- 2.0 L/min.m2, p less than 0.01), a higher oxygen extraction ratio, but a similar VO2 than patients with normal dPCO2. The higher dPCO2 could also be related to an impaired CO2 elimination as indicated by a higher PaCO2 and a lower PaO2/FIO2 in these patients. Nonsurvivors had a significantly higher dPCO2 than survivors (5.9 +/- 3.4 vs 4.4 +/- 2.3 mm Hg, p less than 0.05) in the presence of similar cardiac output. The higher dPCO2 in these patients was probably related to the higher blood lactate levels (7.7 +/- 5.3 mmol/L vs 4.5 +/- 2.8 mmol/L, p less than 0.01) and the more severe pulmonary impairment (SaO2 90 +/- 8 percent vs 95 +/- 4 percent, p less than 0.001). Arteriovenous oxygen content difference (dAVO2) and VO2 were similar in survivors and nonsurvivors. In conclusion, dPCO2 patients with septic shock is related principally to cardiac output but apparently also to the degree of pulmonary impairment. Although dPCO2 is larger in nonsurvivors, its prognostic value is modest.

Adult↗

PubMed1992

Administration of anti-TNF antibody improves left ventricular function in septic shock patients. Results of a pilot study.

In this pilot study, murine monoclonal anti-TNF antibody (2 mg/kg) was administered to ten patients within 24 h of septic shock which persisted after initial resuscitation with intravenous fluids and adrenergic agents. This treatment resulted in a reduction in heart rate (from 122 +/- 10 to 113 +/- 10 beats per minute at 4 h, p less than 0.01) associated with an increase in LVSWI (from 26.5 +/- 5.6 to 31.5 +/- 10.5 g.m2 at 2 h, p less than 0.05), indicating in the absence of change in cardiac filling pressures, an improvement in ventricular function. Arterial oxygenation improved concurrently in six patients. These changes, however, appeared transient. The improvement in cardiac function following anti-TNF antibody administration in patients is in keeping with recent experimental studies indicating the role of TNF in the myocardial depression characterizing septic shock.

Aged↗

PubMed1992

Myocardial depression characterizes the fatal course of septic shock.

The relationship between cardiac and vascular abnormalities was studied in 68 patients with established septic shock. At time of hemodynamic evaluation, after initial resuscitation, there was no significant difference in arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac index between the 38 survivors of shock and the 30 patients who died of shock, but the left ventricular stroke work index and the right ventricular (RV) stroke work index were higher in survivors than in those who died (mean +/- SD: 25.0 +/- 9.1 vs 20.1 +/- 9.4 gm/m2 [p less than 0.05] and 6.6 +/- 3.6 vs 4.8 +/- 2.8 gm/m2 [p less than 0.05], respectively). Survivors had also higher thermodilution RV ejection fraction and lower RV end-diastolic volumes than had those who died (43.9% +/- 16.3% vs 31.1% +/- 13.7% [p less than 0.01] and 82 +/- 30 vs 99 +/- 31 ml/m2 [p less than 0.05], respectively). Calculated systemic vascular resistance was similar in the two groups, but vasopressors had been required in 22 (58%) of 38 survivors and 25 (83%) of 30 patients who died (p less than 0.01). Moreover, when the patients were separated into two groups according to their cardiac output, higher or lower than 3 L/min/m2, in both subgroups patients who died had lower blood pressure than had survivors. Blood lactate levels were significantly lower in survivors than in nonsurvivors (5.1 +/- 2.1 vs 8.1 +/- 4.7 mEq/L, p less than 0.01). Final data obtained before recovery of shock or death indicated that the survivors had higher arterial pressure, lower pulmonary artery pressure and right atrial pressure, higher stroke volume, and higher RV ejection fraction than had the patients who died. No survivors but all patients who died had been treated with vasopressors. These data therefore indicate that death as a result of septic shock is characterized by both myocardial depression and altered vascular tone and both are probably interrelated.

Female↗

PubMed1992

Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation.

The infusion of prostaglandin E1, a vasodilating substance with predominant effects on the pulmonary vasculature, has been found effective in the management of pulmonary hypertension associated with various diseases. The reported experience with prostaglandin E1 after cardiac transplantation is, however, limited. We used prostaglandin E1 in 18 patients in whom acute right ventricular failure developed after orthotopic cardiac transplantation. The infusion was started within 24 hours after operation in 16 patients and was continued for up to 7 days. Maximal doses of prostaglandin E1, administered via a central venous catheter, ranged from 30 to 120 ng/kg/min. Norepinephrine was simultaneously infused via a left atrial catheter in 10 patients to prevent a reduction in systemic arterial pressure. The prostaglandin E1 infusion resulted in significant reductions in mean arterial pressure and pulmonary vascular resistance and simultaneous increases in cardiac index and stroke index. Mean arterial pressure was stable and left ventricular stroke work increased. The alveolar oxygen tension/forced inspiratory oxygen index tended to decrease during the infusion. Three patients died, two of right heart failure and one of multiple organ failure associated with cardiac allograft rejection. In patients in whom right ventricular failure associated with pulmonary hypertension develops after cardiac transplantation, prostaglandin E1, combined with norepinephrine whenever the arterial pressure declines, can effectively reduce pulmonary artery pressures and improve global cardiac function without compromising systemic perfusion.

Adult↗

PubMed1991

Hemodynamic evaluation of bisoprolol after coronary artery surgery in patients with altered left ventricular function.

Bisoprolol is a new cardioselective beta1 adrenergic blocking agent without intrinsic sympathomimetic activity but with minimal effects on myocardial contractility. Bisoprolol was compared to propranolol in 24 patients after cardiac surgery for coronary artery bypass graft (CABG). Each patient had been treated preoperatively with beta-blocking agents and had a cineangiographic left ventricular ejection fraction between 35% and 55%. Patients were randomized to receive orally either 10 mg of propranolol three times a day or 5 mg of bisoprolol once a day. Both drugs resulted in a significant and similar decrease in heart rate. This was associated with significant decreases in cardiac index, stroke index, and thermodilution right ventricular ejection fraction 6 hours after administration of propranolol, but not after bisoprolol. Systolic function measured by Doppler techniques significantly increased in the 10 postoperative days in patients under bisoprolol but not significantly after propranolol. Each drug was well tolerated during the 10 postoperative days, and the recovery was uneventful in each patient. These results indicate that in patients with altered systolic function after CABG, bisoprolol is susceptible to reduce heart rate with less cardiovascular alteration than propranolol.

Adrenergic beta-Antagonists↗

PubMed1991

Echocardiographic signs of cardiac rejection during the first week after cardiac transplantation.

The early recognition of acute rejection after heart transplantation remains an important clinical problem. In this study we explored the value of echo-Doppler techniques to identify the rejection during the first week after cardiac transplantation. The study included 22 patients with an average age of 48 +/- 9 years. Ultrasonic measurements were obtained by 2-dimensional 84 degrees phased array sector scanner with pulsed Doppler incorporated. The stroke index (SI), the peak outflow blood velocity pulsed (POBVP), the peak outflow blood acceleration pulsed (POBAP), the peak flow velocity in early diastole (PFVE), the peak flow velocity during atrial systole (PFVA), the PFVA/PFVE ratio, the mitral valve pressure half-time (PHT) and the fractional shortening (FS) were calculated. On the seventh day after transplantation, a percutaneous right ventricular endomyocardial biopsy was systematically performed. For the entire group, the SI, PHT and the FS relation were not significantly influenced during the week of evaluation. The POBVP and the POBAP transiently decreased but returned to baseline on the seventh day. An increment in the PFVA/PFVE ratio was observed in 4 patients, and acute allograft rejection was documented in 3 of them. On day 7 after transplantation, PFVA and PFVA/PFVE were significantly higher in patients with rejection. No patient with normal PFVA/PFVE ratio had allograft rejection. No patient with rejection showed signs of altered systolic function as measured by SI, POBVP, POBAP and FS. These data therefore indicate that the assessment of the diastolic function using Doppler techniques (PFVA/PFVE) can be helpful to detect signs of acute allograft rejection occurring early after heart transplant.

Echocardiography, Doppler↗

PubMed1990

Addition of phosphodiesterase inhibitors to adrenergic agents in acutely ill patients.

The addition of enoximone, a phosphodiesterase inhibitor, to adrenergic agents has been found useful in increasing cardiac output in severe heart failure. In one study of 13 patients in cardiogenic shock already receiving adrenergic support, enoximone was administered as a bolus of 0.5 mg/kg over 20 minutes. Pulmonary artery occlusion pressure decreased significantly from 21.7 +/- 5.8 mm Hg to 19.8 +/- 6.0 mm Hg (P less than 0.01) and cardiac index increased markedly. A second study investigated the effects of the addition of small boluses of enoximone to adrenergic agents in low flow states associated with heart failure (n = 8) or postoperative states after cardiac surgery (n = 10). Each of the 18 patients was treated with dobutamine; 12 patients were also treated with dopamine and 4 with noradrenaline. Enoximone was administered as small but increasing intravenous boluses. No significant change in mean arterial pressure was observed, but on 0.5 mg/kg of enoximone pulmonary artery occlusion pressure decreased significantly from 24.6 +/- 8.7 mm Hg to 19.4 +/- 9.9 mm Hg (heart failure) and from 18.2 +/- 3.3 mm Hg to 15.3 +/- 3.8 mm Hg (cardiac surgery) after the initial dose of 0.125 mg/kg. Cardiac index increased markedly after enoximone, 0.25 mg/kg. These changes were significant after the initial dose of 0.125 mg/kg. Thus, the addition of even small doses of enoximone to adrenergic agents can markedly increase cardiac index without significant effect on arterial pressure in medical or surgical cardiac patients.

Adult↗