Cardiopulmonary resuscitation: state of the art.
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Blood Pressure↗
Biomedical subjects
M H Weil
Publications and source records attributed to M H Weil.
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↗
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↗
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↗
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↗
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↗
Resolution of lactic acidosis after sedation of a patient with acute myocardial infarction and left ventricular failure.
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Acidosis, Lactic↗
Reversible impairment of myocardial contractility due to hypercarbic acidosis in the isolated perfused rat heart.
BACKGROUND AND METHODS: Striking increases in PCO2 of the myocardium have recently been documented during cardiac arrest. The purpose of the present study was to investigate selective effects of hypercarbia as distinct from acidosis on left ventricular contractile function and oxygen utilization. An isolated, spontaneously beating rat heart preparation was utilized. The perfusate was equilibrated with gases containing 5%, 10%, 20%, and 30% CO2. In a subset of experiments, the [H+] was adjusted independently of PCO2 by decreasing the concentration of HCO3-. RESULTS: When the PCO2 of the perfusate was progressively increased from 36 to 146 torr (4.8 to 29.5 kPa), the left ventricular systolic pressure (LVSP) generated by the isolated heart and the maximum rate of pressure change in the left ventricle (dP/dt) were decreased to 20% of their control values. However, comparable acidosis in the absence of hypercarbia produced only minimal decreases in the LVSP or dP/dt such that contractility remained at greater than or equal to 88%. Increases in the perfusate PCO2 but not in the perfusate H+ were highly correlated with decreases in both myocardial contractility and oxygen consumption (r2 = .88). CONCLUSION: Hypercarbia rather than acidosis accounts for decreased contractility and oxygen utilization in the isolated perfused rat heart.
Acidosis↗
Hypothermia after cardiac arrest.
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Animals↗
Unaccounted for anion in metabolic acidosis during severe sepsis in humans.
OBJECTIVE: To quantitate the contribution of lactate, phosphate, urate, total serum proteins, and unidentified anions to the anion gap in patients with severe sepsis. DESIGN: Thirty critically ill patients with evidence of severe sepsis and systemic hypoperfusion were prospectively studied. MEASUREMENTS: The anion gap was calculated as [Na+] + [K+] - [Cl-] - [HCO3]. A corrected anion gap was calculated as the anion gap minus the anionic contribution of lactate, phosphate, urate, and total serum proteins. The corrected anion gap is a marker of unmeasured anion less unmeasured cation concentration. RESULTS: The mean anion gap was 21.8 +/- 1.4 mmol/L and the corrected anion gap was 3.7 +/- 0.8 mmol/L. The mean arterial blood lactate concentration was 5.9 +/- 0.8 mmol/L. The magnitude of the lactate concentration correlated linearly with the anion gap (r2 = .61, lactate = 0.4 anion gap - 3.9, n = 30, p less than .01). The corrected anion gap was greater than 0 in 24 (80%) of 30 patients. The magnitude of the corrected anion gap correlated linearly with the anion gap (r2 = .66, corrected anion gap = 0.5 anion gap - 6.3, n = 30, p less than .01). Since the slope of the regression line for estimating corrected anion gap from anion gap was 0.5, the contribution of unmeasured anions was as important as lactate in determining the anion gap. CONCLUSION: These data indicate that lactic acidosis does not entirely account for the metabolic acidosis during severe sepsis. Furthermore, the increased corrected anion gap suggests the presence of an unidentified anion (or anions) that is (or are) responsible, in large part, for the development of metabolic acidosis in patients with sepsis.
Acid-Base Equilibrium↗
Hypercarbic acidosis reduces cardiac resuscitability.
BACKGROUND AND METHODS: Marked increases in myocardial hypercarbia and acidosis accompany cardiac arrest and resuscitation. To investigate whether hypercarbic acidosis independent of oxygenation is of itself detrimental to cardiac resuscitation, three groups of six Sprague-Dawley rats were ventilated with gas mixtures containing concentrations of inspired CO2 (FICO2) of 0.0, 0.3, or 0.5, with oxygen fractions held constant at 0.5. After 4 mins of ventricular fibrillation, mechanical chest compressions were initiated with a pneumatic thumper; 2 mins later, transthoracic defibrillation was attempted. RESULTS: Each animal ventilated with FICO2 of 0.0 or 0.3 was successfully resuscitated. However, none of the animals ventilated with FICO2 of 0.5, in which aortic pH was less than 6.67 and aortic PCO2 was greater than 200 torr (greater than 26.7 kPa), was resuscitated (p less than .001). This finding contrasted with a second control group of seven identically treated animals which, in the absence of cardiac arrest, demonstrated no adverse effects after ventilation with an FICO2 of 0.5. CONCLUSIONS: Increases in FICO2 to levels of 0.5 under conditions of constant arterial oxygenation and controlled coronary perfusion pressure preclude successful resuscitation in this rodent model of CPR.
Acidosis, Respiratory↗
Redefining ischemia due to circulatory failure as dual defects of oxygen deficits and of carbon dioxide excesses.
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Carbon Dioxide↗
Pulmonary ventilation/perfusion defects induced by epinephrine during cardiopulmonary resuscitation.
BACKGROUND: Epinephrine has been shown to impair pulmonary excretion of CO2 during resuscitation. This phenomenon was investigated in a rodent model of cardiac arrest and conventional resuscitation. METHODS AND RESULTS: The effects of racemic epinephrine were compared with the selective alpha 1-agonist methoxamine and with saline placebo during cardiac resuscitation in 15 Sprague-Dawley rats mechanically ventilated with gas containing 70% oxygen. Epinephrine and methoxamine but not saline placebo significantly increased coronary perfusion pressure from approximately 32 to 55 mm Hg. Following epinephrine, end-tidal PCO2 decreased from approximately 10 to 5 mm Hg. This was associated with a time-coincident decrease in PaO2 from approximately 130 to 74 mm Hg and an increase in PaCO2 from approximately 26 to 40 mm Hg. These changes indicated increases in alveolar dead space ventilation concomitant with increases in pulmonary arteriovenous admixture. No such effects were observed after administration of either methoxamine or saline placebo. Each of the 15 rats was successfully resuscitated. However, a significantly larger number of transthoracic countershocks were required after epinephrine compared with methoxamine or placebo before return of spontaneous circulation. CONCLUSIONS: Epinephrine induced ventilation/perfusion during cardiopulmonary resuscitation as a result of redistribution of pulmonary blood flow.
Animals↗
Peripheral vascular tone in sepsis.
Septic shock is characterized as a distributive form of circulatory failure. We examined the relationship of changes in forearm arterial, venous, and microvascular tone to the severity of sepsis. The study population consisted of ten control patients, 15 patients with sepsis, and eight patients with sepsis and shock. Patients treated with inotropic, vasopressor, or vasodilator drugs were excluded from the study. Forearm venous capacity (MVC), forearm venous tone (F-VT), arterial blood flow (FBF), forearm arterial resistance (FAR), and hyperemic response (FBF-RH) were measured using air plethysmography. MVC was decreased and VT increased in septic and septic shock patients. FBF was decreased with modest increases in FAR in septic and septic shock patients. FBF-RH was significantly reduced in both septic and septic shock patients. Decreases in FVT and attenuation of the reactive response to hyperemia occurred early in sepsis in patients without clinical evidence of hypoperfusion. In our patients, progressive vasodilatation in skeletal muscle was not associated with severe sepsis. These changes appear to be proportional to the severity of sepsis and are most pronounced in patients with circulatory failure.
Aged↗
End-tidal carbon dioxide tension as a monitor of native blood flow during resuscitation by extracorporeal circulation.
In a porcine model of cardiac arrest, we investigated end-tidal carbon dioxide tension as a monitor of native blood flow during resuscitation by extracorporeal circulation. After 15 minutes of cardiac arrest and after precordial compression and transthoracic countershocks had failed, extracorporeal circulation consistently restored spontaneous circulation. Native end-tidal carbon dioxide tension, which averaged 29.8 +/- 1.0 mm Hg before arrest, was only 5.2 +/- 0.8 mm Hg during precordial compression. After the start of extracorporeal circulation, native end-tidal carbon dioxide tension was measured during 15-second interruptions of pump flow. End-tidal carbon dioxide tension progressively increased with a corresponding increase in native cardiac index. The correlation coefficients between end-tidal carbon dioxide tension and native cardiac index averaged 0.92 +/- 0.03 (mean +/- standard error of the mean). When end-tidal carbon dioxide tension exceeded 15 mm Hg, mean aortic pressure in each instance was 60 mm Hg or greater, and the animal was successfully weaned from extracorporeal support. We conclude that end-tidal carbon dioxide tension serves as a reliable monitor of blood flow through the lung and therefore of native cardiac output during weaning from extracorporeal circulation. It therefore indicates when native cardiac output is likely to be adequate to sustain spontaneous circulation.
Animals↗
Monophosphoryl lipid A induces tolerance to the lethal hemodynamic effects of endotoxemia.
Monophosphoryl lipid A (MPL) is a nontoxic derivative of lipid A. In this study, the induction of tolerance by MPL to the hemodynamic effects of lethal endotoxemia was tested. Ten Sprague-Dawley rats were received either Salmonella minnesota MPL 0.5 mg/100 g intravenously (i.v.) or equivalent volume of diluent (control) i.v. on day zero. On day 3 S. minnesota endotoxin (LPS) 5.0 mg/100 g was administered i.v. Cardiac output (CO), arterial lactate (L), and central venous oxygen saturation (SvO2) were measured before and 3 and 6 hr after LPS administration. Survival was determined at 72 hr. At 6 hr, CO was 217 +/- 11 ml/kg/min in controls, and 435 +/- 28 ml/kg/min in the MPL animals (P less than 0.01). Arterial lactate was 2.6 +/- 0.3 mmol/liter in controls and 1.3 +/- 0.2 mmol/liter in MPL animals at 6 hr (P less than 0.05). The controls died 7.5 +/- 1.3 hr after LPS administration, whereas all the MPL-pretreated animals survived. These data indicate that MPL induces tolerance to the acute hemodynamic effects of LPS and enhances survival from lethal endotoxemia.
Animals↗
Cardiac resuscitation by extracorporeal circulation after failure of conventional CPR.
After cardiac arrest, return of cardiac function and effective circulation are contingent on prompt restoration of myocardial blood flow. Because conventional closed-chest CPR has limited hemodynamic efficiency, we investigated venoarterial ECC utilizing peripheral vascular access as an alternative for cardiac resuscitation. Ventricular fibrillation was induced in domestic pigs by alternating current delivered to the endocardium of the right ventricle. Conventional closed-chest CPR was begun after 10 minutes. In each instance, precordial compression and external defibrillation failed to restore a viable rhythm. ECC was begun at 15 minutes at an average flow rate of 183 ml/kg/min. In each of eight animals, sinus rhythm was restored. In six of these eight animals, spontaneous circulation was reestablished after an average interval of 152 minutes. When epinephrine was administered concomitantly with ECC in an additional eight animals so as to maintain mean aortic pressure between 60 and 100 mm Hg, sinus rhythm and spontaneous circulation were reestablished in each pig after an average of only 23 minutes. The effects of ECC in conjunction with epinephrine were then compared with those of conventional precordial compression in conjunction with epinephrine (sham ECC). In contrast to ECC, which successfully resuscitated each of five animals, none of five sham ECC-treated animals was resuscitated by continued precordial compression and maximal doses of epinephrine (p less than 0.01). We conclude that ECC in conjunction with epinephrine emerges as a highly effective experimental intervention for resuscitation when conventional techniques of precordial compression and external defibrillation fail to reverse cardiac arrest.
Animals↗
[Determinants of survival in cardiopulmonary resuscitation].
Prognostic indices for survival after cardiopulmonary resuscitation (CPR) were investigated in 14 male Sprague-Dawley rats (500 +/- 50 g) and in 16 domestic pigs (25 +/- 4 kg). Arterial and venous blood gas and lactate measurements in association with the coronary perfusion pressure (CPP) and the end-expiratory CO2 concentration (ETCO2) were evaluated. Additional parameters in the porcine studies were coronary venous blood gas measurements and intramyocardial pH. Volume controlled ventilation was established and catheters were placed in the thoracic aorta and in the right atrium in both animal species. Additionally in the pigs, the pulmonary artery and the great cardiac vein were catheterized and intramyocardial pH was measured with a glass pH electrode placed in the diaphragmatic left ventricular myocardium. Ventricular fibrillation was induced with a direct current and external chest compression was initiated after four minutes in the rats and after three minutes in the pigs. Transthoracic DC defibrillation was attempted with 10J after two minutes of compression in the rats and with 300J after eight minutes of compression in the pigs. Eight of 14 rats and eight of 16 pigs were successfully resuscitated. Significant veno-arterial gradients for pH and pCO2 but not for lactate were observed during CPR in both animal species. With the exception of arterial pH in the pigs (p less than 0.05), neither arterial nor venous blood gas measurements nor intramyocardial pH separated resuscitated from non-resuscitated animals. However, CPP and ETCO2 significantly separated resuscitated from non-resuscitated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Acid-Base Equilibrium↗