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Phenylephrine plus propranolol improves the balance between myocardial oxygen supply and demand during experimental cardiopulmonary resuscitation
Literature
of resuscitation/Resuscitation
(0.2 mg&g) iv when standard advanced cardiac life support (including multiple I-mg dosages of epinephrine) failed to result in return of spontaneous circulation. Measurements and Main Results: Cardiac arrest patients were separated into those patients with and without detectable serum atria1 natriuretic peptide concentrations, and were termed the ‘low atria1 natriuretic peptide’ and ‘high atrial natriuretic peptide’ groups, respectively. Their aortic pressure response to high-dose (0.02 mgkg) epinephrine was compared. The proportion with positive assayswas compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atria1 natriuretic peptide group was 151 f 82 pg/ml. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) @ = 0.002). The maximal increasein the aortic relaxation-phase pressuresafter high-dose epinephrine was 9 f 7 torr (1.2 f 0.9 kPa) in the low atria1 natriuretic peptide group and 0 * 5 torr (0 f 0.7 kPa) in the high atrial natriuretic peptide group @ = 0.03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 f 13 torr (2.3 f 1.7 kPa) in the low atria1 natriuretic peptide group and 2 * 10 torr (0.3 f 1.3 kPa) in the high atria1 natriuretic peptide group (p = 0.03). Thus, pressor responsesafter high-dose epinephrine administration were observed in patients in the low atria1 natriuretic peptide group, but this responsewas absent in patients in the high atria1 natriuretic peptide group. Conclusions: Cardiac arrest patients receiving CPR have higher circulating atria1 natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonixc the vasopressor response to epinephrine. Blocking this effect of atria1natriuretic peptide may improve outcomes in patients suffering cardiac arrest. Developiog strategies to prevent inhospital cardiac arrest: Aoalyziag respomes of physicians and q orses io tbe boors before the event
Franklin C, Mathew J Critical Care Medicine, Cook County Hospital, Harrison Street, Chicago, IL 60612, USA
1835 West
Crit Care Med 1994;22/2 (244-247) Objective: To determine: (a) the frequency of premonitory signs and symptoms before cardiac arrest in patients on the general medical wards of a hospital; (b) any characteristic patterns in nurse and physician responsesto these signs and symptoms; and (c) whether cardiac arrests on the ward occur more frequently in patients discharged from the medical intensive care unit (ICU) than in other patients. Design: Case series of consecutive patients who had an inhospital cardiac arrest over a 20-month period. Setting: General medical wards of a l,OOObed urban public hospital. Patients: There were 21505total admissions to the medical service in this period. Patients whose cardiac arrests occurred in the Emergency Room and ICU and patients with do-not-resuscitate orders were excluded from the study. Interventions: None. Measurements and Main Results:
83
30 (1995) 79-85
There were a total of 150cardiac arrests on the medical wards (cardiac arrest rate: 7.0/1,000patients) with a hospital mortality rate of 91%. In 99 of 150 cases, a nurse or physician documented deterioration in the patient’s condition within 6 h of crdiac arrest. Common findings included: (a) failure of the nurse to notify a physician of a deterioration in the patient’s mental status; (b) failure of the physician to obtain or interpret an arterial blood gas measurementin the setting of respiratory distress; and (c) failure of the ICU triage physician to stabilize the patient’s condition before transferring the patient to the ICU. Former ICU patients (cardiac arrest rate: 14.7/1,000 patients) were more likely to suffer cardiac arrest than other patients (cardiac arrest rate: 6.8/1,000 patients) (p = 0.004). Conclusions: Cardiac arrests on the general wards of the hospital are commonly preceded by premonitory signs and symp toms. Strategies to prevent cardiac arrest should include training for nursesand physicians that concentrates on cardiopulmonary stabilization and how to respond to neurologic and respiratory deterioration. Special attention should also be devoted to patients who have been discharged from the ICU who are at greater risk for cardiac arrest after ICU discharge than are other medical patients. Pbenylepbrine plus propranolol improves tbe bahce between myocardiai oxygen supply and demaod doriog experimeotal cardlopabnoaary reswwitation
Ditchey RV, Slinker BK Cardiology Unit, Medical Burlington, VT 05401, USA
Center
Hospital
of
Vermont,
Am Heart J 1994; 127/2(324-330) Epinephrine increasescoronary blood flow but may not improve the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation (CPR). The objective of this study was to determine whether this balance can be improved by administering a relatively pure o-adrenergic vasoconstrictor, alone or in combination with a fladrenergic blocker. We measuredcoronary perfusion pressures during CPR and myocardial adenosine 5’-triphosphate (ATP) and lactate concentrations in biopsies obtained immediately after 10mitt of CPR in six control dogs and in three groups of six dogs each given large doses of epinephrine, phenylephrine, or phenylephrine plus propranolol during CPR. Coronary perfusion pressure during CPR was higher in the three treated groups than in the control group, although differences were limited to the early portion of CPR in dogs given epinephrine or phenylephrine alone. Postresuscitation myocardial ATP concentration was significantly higher (29.5 f 3.0 vs. 22.6 l 1.8 nmohmg of protein, p c 0.05) and myocardial lactate concentation tended to be lower (52.8 f 13.6 vs. 78.5 f 15.2 nmopmg of protein) than in the control group in dogs given both phenylephrine and propranolol. In contrast, myocardial ATP concentration tended to be lower than in the control group in epinephrine-treated dogs, and myocardial lactate concentrations were higher than in the control group in dogs treated with either epinephrine @ < 0.05) or phenylephrine alone (p = 0.052). We conclude that the balance between myocardial oxygen supply and demand during CPR
84
Literature
of resuscitation /Resuscitation
can be improved by administering a combination of phenylephrine and propranolol, but not by administering large doses of epinephrine or phenylephrine alone. Interposed abdominal compressho as an adjmwt to cardiopulIllmary resuscitation
Babbs CF, Sack JB, Kern KB Biomedical Engineering Center, Lafayette, IN 47907, USA
Purdue
University,
West
Am Heart J 1994; 12712(412-421) The addition of IAC to otherwise standard CPR provides for the application of external pressureiover the abdomen in counterpoint to the rhythm of chest compression. Interposed abdominal compression is a simple manual technique that can supplement the use of adrenergic drugs to increase both coronary perfusion pressure and total blood flow during CPR. Mechanistically, manual abdominal compressionsinduce both central aortic and central venous pressure pulses. However, owing to differences in venous versus arterial capacitance, the former are usually greater than the latter, so that systemic perfusion pressure is enhanced. Moreover, practical experience and theoretical analysis have suggested subtle refinements in the hand position and technique for abdominal compression that may further improve the ratio of arterial to venous pressure augmentation. Clinical studies confirm that IAC-CPR can improve perfusion pressuresand carbon dioxide excretion during CPR in humans. The incidence of abdominal trauma, regurgitation, or other complications is not increased by IAC. Recently, randomized trials have shown that short-term and long-term survival of patients resuscitated in the hospital by IAC-CPR are about twice that of control patients resuscitated by standard CPR. The technique of IAC has thus evolved to become a highly promising adjunct to normal CPR, which is likely to be implemented in an increasing number of clinical protocols in the 1990s. Traosvnlvular left ventvicuhr assistance in cardiogenic shock secoadary to acute myocardhl infarction. Evidence for recovery from near fatal myogudiel stmming
Smalling RW, SweeneyM, Lachterman B, Hess MJ, Morris R, Anderson HV, Heibig J, Li G, Willerson JT, Frazier OH, Wampler RK Univ. Texas Medical School, Division Fannin, Houston, TX 77030, USA
of Cardiology.
6341
J Am Co11Cardiol 1994;23/3 (637-644) Objectives. The purpose of this study was to test the hypothesis that transvalvular left ventricular assistancewould support the circulation in pat ients with cardiogenic shock secondary to acute myocardial infarction and allow recovery of function in patients with a reversibly damaged (stunned) left ventricle. Background. Cardiogenic shock occurs in 7.5% of patients presenting with acute myocardial infarction, resulting in survival of only 20%. Despite the use of aggressive interventional therapy in patients with shock secondary to anterior myocardial infarction, survival remains as low as 33%. Methods. We studied 11 patients with acute myocardial infarction and cardiogenic shock, as defined by a cardiac index < 2 liters/mm per m*, pulmonary capillary wedge pressure > 18 mmHg and
30 (1995) 79-85
systolic blood pressure ~90 mmHg during positive inotropic therapy. Patients were 57 * I3 years old (mean f SD) and had a mean left ventricular ejection fraction of 25 * 1l%, mean arterial pressure of 69 f 13 mmHg and mean cardiac index of 1.6 f 0.4 liters/mm per m* on admission to the study. Results. During the 1st 24 h of left ventricular assistance,pulmonary capillary wedge pressure decreased from 26 f 4 to 16 f 4 mmHg @ = O.Ol), cardiac index increased from 1.6 f 0.4 to 2.4 c* 0.4 liters/mm per m*, and the dopamine hydrochloride doe decreasedfrom 51 f 92 to 18 f 12 &kg body weight per min. In survivors, cardiac index improved to 3.2 f 0.5 liters/mitt per m* (p = O.Ol), and left ventricular ejection fraction improved to 34 f 5% (p c 0.05). The overall survival in the study group was 4 (36%) of I1 patients (95% confidence interval [CI] 8 to 65%), and 4 (66%) of 6 patients (95% CI 29% to lOO%)with a Q wave anterior myocardial infarction survived. Conclusions. Transvalvular left ventricular support during cardiogenic shock complicating acute myocardial infarction Is feasible and results in significant hemodynamic and functional improvement.
Gut aad muscle timue PO, in endotoxemic dogs during shock and l%L%lSCitptiOll
Vallet B, Lund N, Curtis SE, Kelly D, Cain SM Dept. of Pediatrics, University of Alabama, University Station, Birmingham, AL 35294, USA
J Appl Physiol 1994;76/2 (793-800) There is indirect evidence that tissue hypoxia occurs in human sepsis and surface measures of muscle tissue Po2 (Pti(02)) in hypodynamic endotoxic animals are decreased. This study assessedsystemicand regional tissue oxygenation in a more relevant model of hyperdynamic endotoxicosis. We isolated venous outBow from the left hindlimb and a segment of ileum in six anesthetized dogs to measure muscle and gut 0, delivery and uptake (Vdot on characterO2) and lactate flux, gut intramucosal pH (pH(i)) by tonometry, and Pti(02) by multipoint surfaceelectrodesplaced on mucosal and serosal surfaces of gut and on muscle. We then infused Escherichia cofi lipopolysaccharide (LPS; 2 mgkg) over I h followed by a 2-h infusion of dextran (0.5 ml 0. kg-l. mm-l). LPS infusion significantly decreasedsystemic and gut Vdot on characterQ2, cardiac output (Qdot on character), and blood pressureand increased arterial lactate and gut lactate flux. Resuscitation increased Qdot on character to above baseline and restored systemicVdot on characterQ2. In responseto LPS and then resuscitation, muscle Pti(02) distribution did not change, suggesting little microcirculatory disturbance, although mean Pti(02) first decreasedand the increased.In contrast, gut Vdot on character02 and pH(i) remained low and lactate output remained high, despite restoration of gut blood flow. Gut Vdot on characterO2, lactate flux, pH(i), and Pti(02) histograms were consistent with a marked redistribution of blood flow within the gut wall, away from the mucosa and toward the muscularis. These data show that, in hyperdynamic acute endotoxemia, skeletal muscle Pti(02) and Vdot on character02 are well maintained, but blood flow within the gut is significantly disturbed with mucosal hypoxia.
of resuscitation/Resuscitation
(0.2 mg&g) iv when standard advanced cardiac life support (including multiple I-mg dosages of epinephrine) failed to result in return of spontaneous circulation. Measurements and Main Results: Cardiac arrest patients were separated into those patients with and without detectable serum atria1 natriuretic peptide concentrations, and were termed the ‘low atria1 natriuretic peptide’ and ‘high atrial natriuretic peptide’ groups, respectively. Their aortic pressure response to high-dose (0.02 mgkg) epinephrine was compared. The proportion with positive assayswas compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atria1 natriuretic peptide group was 151 f 82 pg/ml. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) @ = 0.002). The maximal increasein the aortic relaxation-phase pressuresafter high-dose epinephrine was 9 f 7 torr (1.2 f 0.9 kPa) in the low atria1 natriuretic peptide group and 0 * 5 torr (0 f 0.7 kPa) in the high atrial natriuretic peptide group @ = 0.03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 f 13 torr (2.3 f 1.7 kPa) in the low atria1 natriuretic peptide group and 2 * 10 torr (0.3 f 1.3 kPa) in the high atria1 natriuretic peptide group (p = 0.03). Thus, pressor responsesafter high-dose epinephrine administration were observed in patients in the low atria1 natriuretic peptide group, but this responsewas absent in patients in the high atria1 natriuretic peptide group. Conclusions: Cardiac arrest patients receiving CPR have higher circulating atria1 natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonixc the vasopressor response to epinephrine. Blocking this effect of atria1natriuretic peptide may improve outcomes in patients suffering cardiac arrest. Developiog strategies to prevent inhospital cardiac arrest: Aoalyziag respomes of physicians and q orses io tbe boors before the event
Franklin C, Mathew J Critical Care Medicine, Cook County Hospital, Harrison Street, Chicago, IL 60612, USA
1835 West
Crit Care Med 1994;22/2 (244-247) Objective: To determine: (a) the frequency of premonitory signs and symptoms before cardiac arrest in patients on the general medical wards of a hospital; (b) any characteristic patterns in nurse and physician responsesto these signs and symptoms; and (c) whether cardiac arrests on the ward occur more frequently in patients discharged from the medical intensive care unit (ICU) than in other patients. Design: Case series of consecutive patients who had an inhospital cardiac arrest over a 20-month period. Setting: General medical wards of a l,OOObed urban public hospital. Patients: There were 21505total admissions to the medical service in this period. Patients whose cardiac arrests occurred in the Emergency Room and ICU and patients with do-not-resuscitate orders were excluded from the study. Interventions: None. Measurements and Main Results:
83
30 (1995) 79-85
There were a total of 150cardiac arrests on the medical wards (cardiac arrest rate: 7.0/1,000patients) with a hospital mortality rate of 91%. In 99 of 150 cases, a nurse or physician documented deterioration in the patient’s condition within 6 h of crdiac arrest. Common findings included: (a) failure of the nurse to notify a physician of a deterioration in the patient’s mental status; (b) failure of the physician to obtain or interpret an arterial blood gas measurementin the setting of respiratory distress; and (c) failure of the ICU triage physician to stabilize the patient’s condition before transferring the patient to the ICU. Former ICU patients (cardiac arrest rate: 14.7/1,000 patients) were more likely to suffer cardiac arrest than other patients (cardiac arrest rate: 6.8/1,000 patients) (p = 0.004). Conclusions: Cardiac arrests on the general wards of the hospital are commonly preceded by premonitory signs and symp toms. Strategies to prevent cardiac arrest should include training for nursesand physicians that concentrates on cardiopulmonary stabilization and how to respond to neurologic and respiratory deterioration. Special attention should also be devoted to patients who have been discharged from the ICU who are at greater risk for cardiac arrest after ICU discharge than are other medical patients. Pbenylepbrine plus propranolol improves tbe bahce between myocardiai oxygen supply and demaod doriog experimeotal cardlopabnoaary reswwitation
Ditchey RV, Slinker BK Cardiology Unit, Medical Burlington, VT 05401, USA
Center
Hospital
of
Vermont,
Am Heart J 1994; 127/2(324-330) Epinephrine increasescoronary blood flow but may not improve the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation (CPR). The objective of this study was to determine whether this balance can be improved by administering a relatively pure o-adrenergic vasoconstrictor, alone or in combination with a fladrenergic blocker. We measuredcoronary perfusion pressures during CPR and myocardial adenosine 5’-triphosphate (ATP) and lactate concentrations in biopsies obtained immediately after 10mitt of CPR in six control dogs and in three groups of six dogs each given large doses of epinephrine, phenylephrine, or phenylephrine plus propranolol during CPR. Coronary perfusion pressure during CPR was higher in the three treated groups than in the control group, although differences were limited to the early portion of CPR in dogs given epinephrine or phenylephrine alone. Postresuscitation myocardial ATP concentration was significantly higher (29.5 f 3.0 vs. 22.6 l 1.8 nmohmg of protein, p c 0.05) and myocardial lactate concentation tended to be lower (52.8 f 13.6 vs. 78.5 f 15.2 nmopmg of protein) than in the control group in dogs given both phenylephrine and propranolol. In contrast, myocardial ATP concentration tended to be lower than in the control group in epinephrine-treated dogs, and myocardial lactate concentrations were higher than in the control group in dogs treated with either epinephrine @ < 0.05) or phenylephrine alone (p = 0.052). We conclude that the balance between myocardial oxygen supply and demand during CPR
84
Literature
of resuscitation /Resuscitation
can be improved by administering a combination of phenylephrine and propranolol, but not by administering large doses of epinephrine or phenylephrine alone. Interposed abdominal compressho as an adjmwt to cardiopulIllmary resuscitation
Babbs CF, Sack JB, Kern KB Biomedical Engineering Center, Lafayette, IN 47907, USA
Purdue
University,
West
Am Heart J 1994; 12712(412-421) The addition of IAC to otherwise standard CPR provides for the application of external pressureiover the abdomen in counterpoint to the rhythm of chest compression. Interposed abdominal compression is a simple manual technique that can supplement the use of adrenergic drugs to increase both coronary perfusion pressure and total blood flow during CPR. Mechanistically, manual abdominal compressionsinduce both central aortic and central venous pressure pulses. However, owing to differences in venous versus arterial capacitance, the former are usually greater than the latter, so that systemic perfusion pressure is enhanced. Moreover, practical experience and theoretical analysis have suggested subtle refinements in the hand position and technique for abdominal compression that may further improve the ratio of arterial to venous pressure augmentation. Clinical studies confirm that IAC-CPR can improve perfusion pressuresand carbon dioxide excretion during CPR in humans. The incidence of abdominal trauma, regurgitation, or other complications is not increased by IAC. Recently, randomized trials have shown that short-term and long-term survival of patients resuscitated in the hospital by IAC-CPR are about twice that of control patients resuscitated by standard CPR. The technique of IAC has thus evolved to become a highly promising adjunct to normal CPR, which is likely to be implemented in an increasing number of clinical protocols in the 1990s. Traosvnlvular left ventvicuhr assistance in cardiogenic shock secoadary to acute myocardhl infarction. Evidence for recovery from near fatal myogudiel stmming
Smalling RW, SweeneyM, Lachterman B, Hess MJ, Morris R, Anderson HV, Heibig J, Li G, Willerson JT, Frazier OH, Wampler RK Univ. Texas Medical School, Division Fannin, Houston, TX 77030, USA
of Cardiology.
6341
J Am Co11Cardiol 1994;23/3 (637-644) Objectives. The purpose of this study was to test the hypothesis that transvalvular left ventricular assistancewould support the circulation in pat ients with cardiogenic shock secondary to acute myocardial infarction and allow recovery of function in patients with a reversibly damaged (stunned) left ventricle. Background. Cardiogenic shock occurs in 7.5% of patients presenting with acute myocardial infarction, resulting in survival of only 20%. Despite the use of aggressive interventional therapy in patients with shock secondary to anterior myocardial infarction, survival remains as low as 33%. Methods. We studied 11 patients with acute myocardial infarction and cardiogenic shock, as defined by a cardiac index < 2 liters/mm per m*, pulmonary capillary wedge pressure > 18 mmHg and
30 (1995) 79-85
systolic blood pressure ~90 mmHg during positive inotropic therapy. Patients were 57 * I3 years old (mean f SD) and had a mean left ventricular ejection fraction of 25 * 1l%, mean arterial pressure of 69 f 13 mmHg and mean cardiac index of 1.6 f 0.4 liters/mm per m* on admission to the study. Results. During the 1st 24 h of left ventricular assistance,pulmonary capillary wedge pressure decreased from 26 f 4 to 16 f 4 mmHg @ = O.Ol), cardiac index increased from 1.6 f 0.4 to 2.4 c* 0.4 liters/mm per m*, and the dopamine hydrochloride doe decreasedfrom 51 f 92 to 18 f 12 &kg body weight per min. In survivors, cardiac index improved to 3.2 f 0.5 liters/mitt per m* (p = O.Ol), and left ventricular ejection fraction improved to 34 f 5% (p c 0.05). The overall survival in the study group was 4 (36%) of I1 patients (95% confidence interval [CI] 8 to 65%), and 4 (66%) of 6 patients (95% CI 29% to lOO%)with a Q wave anterior myocardial infarction survived. Conclusions. Transvalvular left ventricular support during cardiogenic shock complicating acute myocardial infarction Is feasible and results in significant hemodynamic and functional improvement.
Gut aad muscle timue PO, in endotoxemic dogs during shock and l%L%lSCitptiOll
Vallet B, Lund N, Curtis SE, Kelly D, Cain SM Dept. of Pediatrics, University of Alabama, University Station, Birmingham, AL 35294, USA
J Appl Physiol 1994;76/2 (793-800) There is indirect evidence that tissue hypoxia occurs in human sepsis and surface measures of muscle tissue Po2 (Pti(02)) in hypodynamic endotoxic animals are decreased. This study assessedsystemicand regional tissue oxygenation in a more relevant model of hyperdynamic endotoxicosis. We isolated venous outBow from the left hindlimb and a segment of ileum in six anesthetized dogs to measure muscle and gut 0, delivery and uptake (Vdot on characterO2) and lactate flux, gut intramucosal pH (pH(i)) by tonometry, and Pti(02) by multipoint surfaceelectrodesplaced on mucosal and serosal surfaces of gut and on muscle. We then infused Escherichia cofi lipopolysaccharide (LPS; 2 mgkg) over I h followed by a 2-h infusion of dextran (0.5 ml 0. kg-l. mm-l). LPS infusion significantly decreasedsystemic and gut Vdot on characterQ2, cardiac output (Qdot on character), and blood pressureand increased arterial lactate and gut lactate flux. Resuscitation increased Qdot on character to above baseline and restored systemicVdot on characterQ2. In responseto LPS and then resuscitation, muscle Pti(02) distribution did not change, suggesting little microcirculatory disturbance, although mean Pti(02) first decreasedand the increased.In contrast, gut Vdot on character02 and pH(i) remained low and lactate output remained high, despite restoration of gut blood flow. Gut Vdot on characterO2, lactate flux, pH(i), and Pti(02) histograms were consistent with a marked redistribution of blood flow within the gut wall, away from the mucosa and toward the muscularis. These data show that, in hyperdynamic acute endotoxemia, skeletal muscle Pti(02) and Vdot on character02 are well maintained, but blood flow within the gut is significantly disturbed with mucosal hypoxia.