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Biomedical subjects

M H Weil

Publications and source records attributed to M H Weil.

At least 91 records · Page 5Linked to original sources
PubMed1994

Cardiac resuscitation by retroaortic infusion of blood.

Current methods of closed-chest cardiac resuscitation generate coronary perfusion pressures that rarely exceed one fourth of normal, and this decreases with prolongation of cardiac arrest. The resuscitation effort is therefore almost uniformly unsuccessful when precordial compression is initiated after 8 minutes of untreated cardiac arrest. This report introduces a new option for cardiac resuscitation by infusion of oxygenated blood into the ascending aorta such as to transiently increase the pressure gradient for coronary perfusion. Thirty-six anesthetized, mechanically ventilated normovolemic rats were investigated. Cardiac arrest was induced with an alternating current delivered through an electrode catheter advanced into the right ventricle. Ventricular fibrillation was untreated for 4, 6, or 8 minutes, after which resuscitation was attempted without blood infusion, with infusion of oxygenated blood, or with infusion of oxygenated blood containing 30 mg/kg epinephrine. The boluses of blood were delivered through a catheter advanced from the right carotid artery into the ascending aorta. Except for mechanical ventilation and direct current precordial countershock for electrical defibrillation, no other mechanical resuscitation intervention, and specifically no precordial compression, was administered. None of six control animals that received either no retroaortic infusion or right atrial infusion was resuscitated after 4 minutes of untreated ventricular fibrillation. Each of five animals was successfully resuscitated by retroaortic infusion after 4 minutes of untreated cardiac arrest; one was resuscitated after 6 minutes, and none was resuscitated after 8 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Myocardial hypercarbic acidosis reduces cardiac resuscitability.

BACKGROUND: The severity of spontaneous myocardial hypercarbic acidosis during cardiac arrest previously has been predictive of the likelihood of restoring spontaneous circulation. The present study investigated whether hypercarbia itself impairs cardiac resuscitation. Since coronary perfusion pressure is the overriding determinant of cardiac resuscitability, we used a porcine model of cardiac arrest in which coronary perfusion pressure was controlled. METHODS: In 31 domestic pigs anesthetized with pentobarbital, the lungs were mechanically ventilate. Myocardial carbon dioxide tension and hydrogen ion concentration were measured by sensors advanced into the myocardium. After 15 min of untreated ventricular fibrillation, venoarterial extracorporeal circulation was initiated. Animals were randomized to receive a carbon dioxide gas fraction in the extracorporeal perfusate of 0.00, 0.10, 0.30, or 0.50 with oxygen concentration maintained constant at 0.50. Extracorporeal flow was adjusted to maintain a coronary perfusion pressure in the range of 60-80 mmHg, a level of predictive resuscitability. RESULTS: The proportion of animals successfully resuscitated and the proportion of animals maintaining spontaneous circulation for 60 min or longer decreased with increasing perfusate PCO2 and concurrent increases in myocardial CO2 tension in the absence of altered oxygen utilization (P < .01). CONCLUSIONS: Hypercarbia, in this experimental setting, was therefore a quantitative determinant of both myocardial resuscitability and the restoration of spontaneous circulation.

Acidosis↗
PubMed1993

Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation.

OBJECTIVE: To define changes in intramyocardial pH and PCO2 during cardiac arrest and resuscitation. DESIGN: Prospective and observational trial. SETTING: Mammalian research laboratory utilizing a porcine model of cardiac arrest. SUBJECTS: Sixteen domestic pigs. INTERVENTIONS: Ventricular fibrillation was induced by an alternating current delivered to the epicardium. Precordial compression was begun after 3 mins of untreated cardiac arrest and was initially adjusted to produce a coronary perfusion pressure of 10 mm Hg. Electrical defibrillation was attempted after an additional 8 mins of precordial compression. MEASUREMENTS AND MAIN RESULTS: A rapid-response, ion-selective field effect transistor sensor was adapted for measurement of intramyocardial PCO2. Intramyocardial PCO2 progressively increased from 54 to 346 torr (7.2 to 46.1 kPa) during the 11-min interval of cardiac arrest. Intramyocardial hydrogen ion concentrations were simultaneously measured with a glass electrode. The intramyocardial hydrogen ion value increased from 65 nmol/L (pH 7.20) to 441 nmol/L (pH 6.38) over the same interval. The increases in myocardial PCO2 were inversely correlated with coronary perfusion pressure and with the likelihood of successful resuscitation. Within 30 mins after successful cardiac resuscitation, myocardial PCO2 had almost completely returned to prearrest levels. CONCLUSIONS: Striking increases in myocardial PCO2 and hydrogen ion values accompany the global myocardial ischemia of cardiac arrest. The increases in myocardial PCO2, rather than decreases in pH, reflected more precisely the hemodynamic efficacy of the resuscitation effort, correlated inversely with coronary perfusion pressure, and predicted the likelihood of successful resuscitation.

Acidosis, Respiratory↗
PubMed1993

Progressive myocardial dysfunction after cardiac resuscitation.

OBJECTIVE: To investigate left ventricular function by the Langendorff method after successful cardiac resuscitation in rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: University research laboratory. SUBJECTS: Adult, male Sprague-Dawley rats. INTERVENTIONS: Myocardial function was investigated in three subsets of isolated, perfused rat hearts that were harvested either before inducing ventricular fibrillation (controls) or at defined intervals after successful resuscitation from ventricular fibrillation. Ventricular fibrillation was induced with an electrode catheter advanced into the right ventricle of 15 mature, mechanically ventilated Sprague-Dawley rats. After an interval of 4 mins of untreated ventricular fibrillation and an additional 5 mins of precordial compression, spontaneous circulation was restored by a direct current, transthoracic countershock. The heart of each animal was then harvested at either 2 or 20 mins after successful cardiac resuscitation. The same model was utilized for harvesting the controls. Animals were randomized to each of the three subsets immediately before induction of cardiac arrest. MEASUREMENTS AND MAIN RESULTS: There was a progressive decrease in myocardial contractility of the isolated, perfused hearts. Mean left ventricular systolic pressure was 128 +/- 8 mm Hg in control animals. In hearts harvested at 2 mins after successful resuscitation, the maximal generated pressure was reduced to 106 +/- 9 mm Hg. When harvested at 20 mins after successful resuscitation, it was reduced to 81 +/- 11 mm Hg. There were corresponding decreases in the mean maximal rate of left ventricular pressure increase (dP/dtmax) from 2880 +/- 110 to 2470 +/- 120 mm Hg/sec at 2 mins and to 1810 +/- 135 mm Hg/sec at 20 mins. These decreases in contractility were associated with striking decreases in myocardial relaxation and compliance. CONCLUSION: These studies, therefore, document progressive systolic and diastolic myocardial dysfunction immediately after successful cardiac resuscitation with restoration of spontaneous circulation.

Animals↗
PubMed1993

Regional blood flow during closed-chest cardiac resuscitation in rats.

Quantitative measurement of regional blood flow during cardiac arrest and resuscitation has been confined to large animals. We report on a rodent model utilizing radioactive microspheres during cardiac arrest and resuscitation for investigation of regional blood flow. Ventricular fibrillation was electrically induced in 10 pentobarbital-anesthetized Sprague-Dawley rats. Resuscitation was attempted by precordial compression followed by external direct current countershock. During precordial compression, cardiac output corresponded to 12% of prearrest flow. Similarly low flows were observed in the myocardium and brain. However, much lower flows were observed in the adrenal glands, kidneys, intra-abdominal viscera, skin, and skeletal muscle. Five of ten animals were successfully resuscitated. During precordial compression, resuscitated animals had significantly higher cardiac output (13.1 +/- 4.1 vs. 8.6 +/- 1.46 ml/min), myocardial blood flow (0.70 +/- 0.24 vs. 0.22 +/- 0.15 ml.min-1.g-1), cerebral blood flow (0.17 +/- 0.04 vs. 0.06 +/- 0.02 ml.min-1.g-1), and adrenal blood flow (1.09 +/- 0.60 vs. 0.27 +/- 0.16 ml.min-1.g-1). Thirty minutes after successful resuscitation, cardiac output and myocardial, cerebral, renal, and adrenal blood flows and blood flow to splanchnic viscera (with the exception of the spleen) had returned to > or = 70% of prearrest flows. These studies confirm the conclusion of earlier investigations in larger animals that visceral blood flow during cardiac arrest and precordial compression is preferentially distributed to the brain and myocardium. Successful cardiac resuscitation is contingent on threshold levels of myocardial blood flow that exceed 0.4 ml.min-1.g-1.

Adrenal Glands↗
PubMed1993

Augmented efficacy of external CPR by intermittent occlusion of the ascending aorta.

BACKGROUND: After prolonged cardiac arrest, conventional methods of closed-chest cardiac compression are ineffective. This is primarily because of failure to generate minimal threshold levels of coronary perfusion pressure for cardiac resuscitation. This report introduces a new option for cardiac resuscitation by use of a combination of intermittent ascending aortic balloon occlusion, aortic infusion, and precordial compression to increase the pressure gradient for coronary perfusion. METHODS AND RESULTS: Twenty anesthetized, mechanically ventilated, normovolemic domestic pigs were investigated. A 10F balloon catheter was advanced from the left femoral artery into the ascending aorta. Ventricular fibrillation was induced with an AC current delivered through an electrode catheter advanced into the right ventricle. Precordial compression was initiated after 7 minutes of untreated ventricular fibrillation. The animals were randomized to one of four groups: (1) balloon occlusion with proximal infusion of oxygenated saline, (2) balloon occlusion alone, (3) proximal aortic infusion together with epinephrine without balloon occlusion, and (4) injection of epinephrine without balloon occlusion or proximal infusion. For balloon occlusion, the balloon was inflated for 30 seconds during each minute of cardiopulmonary resuscitation. In the subsets of animals that received infusions, oxygenated saline (30 mL) was injected into the proximal aorta immediately after balloon occlusion. Epinephrine was used in two subsets: It was injected as a bolus in amounts of 30 micrograms/kg into the right atrium at 30 seconds after start of precordial compression and repeated as required to maintain coronary perfusion pressure within the range of 25 to 30 mm Hg. Defibrillation was attempted at 1 minute after start of precordial compression and at 1-minute intervals thereafter. Resuscitation attempts were continued until there was return of spontaneous circulation or for a total of 30 minutes after start of precordial compression. Coronary perfusion pressure generated by precordial compression was significantly increased after balloon occlusion. Each of 10 animals was successfully resuscitated and survived for 48 hours after balloon occlusion whether or not it was combined with infusion. Three of five animals were resuscitated by a combination of infusion and epinephrine in the absence of aortic occlusion, but none survived for 48 hours (P = .02). Only one epinephrine-treated animal was successfully resuscitated and survived for 48 hours in the absence of balloon occlusion or infusion (P < .05). CONCLUSIONS: Ascending aortic balloon occlusion with or without proximal aortic infusion strikingly increased resuscitability and 48-hour survival after cardiac arrest under conditions when conventional methods failed.

Animals↗
PubMed1993

Gastric intramural PCO2 during peritonitis and shock.

OBJECTIVE: To define whether increases in gastric intramural tissue CO2 and H+ increase during experimentally induced peritonitis with circulatory shock as they do under conditions of hemorrhagic shock and cardiac arrest. DESIGN AND SETTING: Peritonitis was induced in Sprague-Dawley rats by cecal ligation and fecal spillage. MEASUREMENTS AND RESULTS: Over an interval of 260 +/- 20 min in 5 animals, there was a progressive reduction in mean aortic pressure from 153 +/- 12 to 40 +/- 20 mm Hg and a decline in cardiac index from 429 +/- 135 to 178 +/- 7 ml/min. This was associated with increases in gastric intramural [H+] from 34 +/- 5 to 217 +/- 93 mmol/L (p = 0.001). Arterial blood lactate content concurrently increased from 0.9 +/- 0.1 to 4.6 +/- 0.7 mmol/L (p = 0.001). Only a late increase in gastric intramural PCO2 from 45 +/- 5 to 128 +/- 38 mm Hg (p = 0.01) was observed. CONCLUSION: In contrast to the gastric acid base changes that accompany hemorrhagic shock, in which there is an early and prominent increase in both PCO2 and [H+] in close relationship to decreases in cardiac output and arterial pressure, there was a prominent increase in gastric [H+] but only a delayed rise in gastric intramural PCO2. Arterial blood lactate and central venous oxygen saturation were earlier indicators of perfusion failure. Since the bicarbonate concentration in the stomach wall was substantially greater than that of simultaneously measured arterial blood, this has bearing on the current clinical method of gastric tonometry which assumes that arterial blood bicarbonate is equivalent to gastric wall bicarbonate.

Animals↗
PubMed1993

Comparison of gastric luminal and gastric wall PCO2 during hemorrhagic shock.

Measurement of gastric wall PCO2 has emerged as a promising monitor of perfusion deficits during low-flow states of circulatory shock. In the present study, gastric luminal PCO2 measured with the gastric tonometer was compared with the PCO2, measured directly in the wall of the stomach during hemorrhagic shock in two groups of five Sprague-Dawley rats. One group was pretreated with the H2 blocker, ranitidine. During a 120-min interval of hemorrhage, tonometer PCO2 increased from 60 +/- 7 mmHg to 90 +/- 10 mmHg, and time-coincident gastric wall PCO2 from 52 +/- 5 mmHg to 131 +/- 14 mmHg. Following reinfusion of shed blood, tonometer PCO2 remained elevated for an interval exceeding 60 min, but gastric wall PCO2 returned to control levels within approximately 10 min. Ranitidine pretreatment did not alter the relationships between gastric wall PCO2 and tonometer PCO2. These observations indicate that gastric luminal PCO2 underestimates relatively rapid increases in gastric wall PCO2 during profound hemorrhagic shock in rats.

Animals↗
PubMed1993

Pathophysiology and treatment of circulatory shock.

Circulatory shock is a syndrome characterized by imbalance between oxygen supply and demand. Myriad different mediators are responsible for the systemic manifestations of shock. The therapeutic approach requires initial interventions directed at increasing oxygen delivery followed by definitive therapy for the causative process. Areas of ongoing research involve mediated-directed therapy, reperfusion injury, and immunologic interventions directed at reducing infectious complications in the survivors of circulatory shock.

Animals↗
PubMed1992

Extracorporeal circulation as an alternative to open-chest cardiac compression for cardiac resuscitation.

Open-chest direct cardiac compression represents a more potent but highly invasive option for cardiac resuscitation when conventional techniques of closed-chest cardiac resuscitation fail after prolonged cardiac arrest. We postulated that venoarterial extracorporeal circulation might be a more effective intervention with less trauma. In the setting of human cardiac resuscitation, however, controlled studies would be limited by strategic constraints. Accordingly, the effectiveness of open-chest cardiac compression was compared with that of extracorporeal circulation after a 15-min interval of untreated ventricular fibrillation in a porcine model of cardiac arrest. Sixteen domestic pigs were randomized to resuscitation by either peripheral venoarterial extracorporeal circulation or open-chest direct cardiac compression. During resuscitation, epinephrine was continuously infused into the right atrium, and defibrillation was attempted by transthoracic countershock at 2-min intervals. Systemic blood flows averaged 198 ml.kg-1.min-1 with extracorporeal circulation. This contrasted with direct cardiac compression, in which flows averaged only 40 ml.kg-1.min-1. Coronary perfusion pressure, the major determinant of resuscitability on the basis of earlier studies, was correspondingly lower (94 vs 29 mm Hg). Extracorporeal circulation, in conjunction with transthoracic DC countershock and epinephrine, successfully reestablished spontaneous circulation in each of eight animals after 15 min of untreated ventricular fibrillation. This contrasted with the outcome after open-chest cardiac compression, in which spontaneous circulation was reestablished in only four of eight animals (p = .038). We conclude that extracorporeal circulation is a more effective alternative to direct cardiac compression for cardiac resuscitation after protracted cardiac arrest.

Acidosis↗
PubMed1992

Cardiac anaphylaxis in the Sprague-Dawley rat.

Anaphylactic shock was induced in pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats that had been sensitized 21 days earlier to crystallized ovalbumin. The sensitization was confirmed by passive cutaneous anaphylaxis test. Antigen challenge produced an immediate reduction in mean aortic pressure from 168 to 67 mm Hg within 1 minute after intravenous injection of ovalbumin. Plasma histamine increased from 4.5 to 128 ng/ml within 5 minutes after injection of antigen. There were no changes in airway or esophageal pressures after antigen challenge. Left ventricular diastolic pressure was increased, and contractility, as measured by the rate of change of left ventricular pressure (dP/dt), was decreased over an interval exceeding 90 minutes. When isolated, constant flow--perfused hearts from sensitized Sprague-Dawley rats were challenged with antigen, decreases in left ventricular function were observed associated with decreased positive and negative maximum rate of change of left ventricular pressure (dP/dtmax). This experimental model in the rat therefore demonstrated selective myocardial impairment with reduced inotropism and lusitropism after anaphylaxis.

Anaphylaxis↗
PubMed1992

Monophosphoryl lipid A attenuates the effects of endotoxic shock in pigs.

Monophosphoryl lipid A (MPL) is a nontoxic lipid A derivative that maintains many of the beneficial immunomodulatory activities of the parent lipopolysaccharide molecule, including the induction of tolerance to endotoxin. The hemodynamic effects of Salmonella minnesota MPL (300 mg/kg) and S. minnesota lipopolysaccharide (300 micrograms/kg) were compared in 20 minipigs. Decreases in cardiac output and arterial pressure and increases in pulmonary artery pressure and lactic acidosis were significantly greater in animals treated with lipopolysaccharide. These changes were associated with peak tumor necrosis factor (TNF) levels of 1373 +/- 79 U/ml in animals treated with LPS and 157 +/- 31 U/ml in animals treated with MPL. Ten minipigs were subsequently randomized to receive S. minnesota MPL (30 micrograms/kg) or diluent intravenously 48 hours before receiving S. minnesota lipopolysaccharide (300 micrograms/kg IV). MPL significantly attenuated lipopolysaccharide-induced decreases in mean arterial pressure, cardiac index, stroke volume index, and mixed venous oxygen saturation. At baseline, no significant difference could be seen in TNF levels between diluent and MPL pigs. TNF levels peaked 2 hours after LPS infusion at 1190 +/- 156 U/ml in diluent pigs and at 539 +/- 126 U/ml in MPL pigs (p less than 0.05). Each of the pigs pretreated with MPL survived endotoxic shock, whereas only one of the five diluent pigs survived. These observations are consistent with the induction of endotoxin tolerance by pretreatment with MPL.

Animals↗
PubMed1991

Buffer solutions may compromise cardiac resuscitation by reducing coronary perfusion presssure.

OBJECTIVE: --To investigate the effects of hypertonic buffer solutions on coronary perfusion pressure (CPP) and resuscitability during experimental closed-chest cardiac resuscitation. DESIGN: --Randomized, placebo-controlled trial. SETTING: --Mammalian research laboratory. PARTICIPANTS: --Forty-four domestic pigs. INTERVENTIONS: --Cardiac arrest was induced by ventricular fibrillation in mechanically ventilated pigs anesthetized with pentobarbital sodium. Precordial compression was started at the third minute of untreated ventricular fibrillation and maintained for an interval of 8 minutes. A hypertonic solution of sodium bicarbonate, Carbicarb (an equimolar mixture of sodium bicarbonate and sodium carbonate [International Medication Systems, Ltd]), or sodium chloride or an isotonic solution of sodium chloride was infused into the right atrium over a 1-minute interval starting at the sixth minute of ventricular fibrillation. Restoration of spontaneous circulation was attempted by DC transthoracic countershock after 11 minutes of ventricular fibrillation. MAIN OUTCOME MEASURES: --Plasma osmolality, CPP, and cardiac resuscitability. RESULTS: --Infusion of hypertonic buffer and sodium chloride solutions increased plasma osmolality from an average of 280 to 330 mOsm/kg. This was accompanied by a significant decrease in the aortic pressures and CPPs generated during precordial compression. No such changes occurred after infusion of isotonic sodium chloride. Restoration of spontaneous circulation, as in earlier studies, was contingent on the levels of CPP prior to attempted defibrillation. Accordingly, none of 13 animals in which the CPP declined to less than 10 mm Hg after infusion of the hypertonic solutions were successfully resuscitated. This contrasted with nine animals that received isotonic sodium chloride and served as controls. Coronary perfusion pressure consistently exceeded 10 mm Hg in these control animals, and spontaneous circulation was restored in each instance. CONCLUSIONS: --Hypertonic solutions and specifically buffer solutions administered in the absence of vasopressor agents may adversely affect cardiac resuscitation efforts by reducing CPP below critical thresholds.

Animals↗
PubMed1991

Long-term survival of patients with AIDS, Pneumocystis carinii pneumonia, and respiratory failure.

OBJECTIVE: --To evaluate the long-term survival of patients admitted to the medical intensive care unit, Cook County Hospital, Chicago, Ill, with Pneumocystis carinii pneumonia and acute respiratory failure. DESIGN: --Cohort study over a 4-year period. SETTING: --Municipal teaching hospital. PATIENTS: --Seventy-three consecutive patients who had 75 episodes of P carinii pneumonia and acute respiratory failure were followed up from the time of hospital admission until their deaths or the termination of the study. OUTCOME MEASURES: --Duration of survival from the time of initial hospital admission with diagnoses of P carinii pneumonia and acute respiratory failure. RESULTS: --Consistent with recent reports of improved short-term outcome, the immediate hospital survival was 47% (35/75). The 1-year survival was 37% (95% confidence interval, 26% to 49%). Two patients have survived for 40 months. Almost three quarters of the patients who survived hospitalization lived for at least 1 year. CONCLUSIONS: --The long-term prognosis for patients with the acquired immunodeficiency syndrome, P carinii pneumonia, and acute respiratory failure is now substantially better than anticipated. Respiratory failure due to P carinii pneumonia does not necessarily signify the terminal phase of human immunodeficiency virus infection. Accordingly, patients with the acquired immunodeficiency syndrome, P carinii pneumonia, and acute respiratory failure can be appropriate candidates for life support in medical intensive care units.

Acquired Immunodeficiency Syndrome↗