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ABSTRACT: To evaluate the effect of cardiac arrest and cardiopulmonary resuscitation (CPR) on blood chemistry in a canine model.
Evaluative canine animal study.
Animal laboratory accredited by the Association for Assessment and Accreditation of Laboratory Animals.
Twenty-six adult mongrel dogs.
The dogs underwent an episode of induced fibrillatory cardiac arrest for 3 minutes followed by 10 minutes of standard CPR. Blood samples were taken at baseline (before cardiac arrest), after 10 minutes of ventricular fibrillation, and 10 minutes after successful resuscitation for determination of blood chemistries and hematologic parameters.
Glucose, blood urea nitrogen, serum creatinine, sodium, potassium, chloride, calcium, phosphorus, uric acid, alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, protein, albumin, cholesterol, triglycerides, iron, white blood cell count, red blood cell count, and hematocrit were measured. Significant changes (p<0.05) in values obtained during CPR versus baseline values were noted for all laboratory parameters except blood urea nitrogen, chloride, and alkaline phosphatase. Eighteen dogs achieved return of spontaneous circulation (ROSC); their laboratory values were obtained after CPR. Significant changes (p<0.05) after ROSC compared with baseline were noted for all laboratory values except chloride, blood urea nitrogen, uric acid, alkaline phosphatase, glucose, potassium, calcium, triglycerides, iron, red blood cell count, and hematocrit.
Results indicate that significant changes in blood chemistries and hematologic parameters occur during and after CPR. Clinicians should note these normal laboratory parameter changes when interpreting laboratory data in patients who experience cardiac arrest.
Pharmacotherapy 10/2001; 21(10):1187-91. · 2.90 Impact Factor
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ABSTRACT: Over the past decade, the conceptual understanding of heart failure has changed significantly. Several large clinical trials have demonstrated that pharmacologic interventions can dramatically reduce the morbidity and mortality associated with heart failure. These trials have extended the therapeutic paradigm for treating heart failure beyond the goal of limiting congestive symptoms of volume overload. This two-part article presents an evidence-based guideline to assist primary care physicians in evaluating and treating patients with heart failure. Part I describes the new paradigm of heart failure and offers guidance for diagnostic testing. Part II presents a treatment guideline.
American family physician 10/2001; 64(5):769-74. · 1.70 Impact Factor
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ABSTRACT: Several large clinical trials conducted over the past decade have shown that pharmacologic interventions can dramatically reduce the morbidity and mortality associated with heart failure. These trials have modified and enhanced the therapeutic paradigm for heart failure and extended treatment goals beyond limiting congestive symptoms of volume overload. Part II of this two-part article presents treatment recommendations for patients with left ventricular systolic dysfunction. The authors recommend that, if tolerated and not contraindicated, the following agents be used in patients with left ventricular systolic dysfunction: an angiotensin-converting enzyme inhibitor in all patients; a beta blocker in all patients except those who have symptoms at rest; and spironolactone in patients who have symptoms at rest or who have had such symptoms within the past six months. Diuretics and digoxin should be reserved, as needed, for symptomatic management of heart failure. Other treatments or treatment programs may be necessary in individual patients.
American family physician 10/2001; 64(6):1045-54. · 1.70 Impact Factor
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ABSTRACT: Coenzyme Q10 (CoQ10) is an antioxidant and plays an important role in the synthesis of adenosine triphosphate. Studies suggest that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors reduce CoQ10 levels; however, no studies have directly compared HMG-CoA reductase inhibitors in a randomized crossover fashion.
Twelve healthy volunteers received either 20 mg pravastatin (P) or 10 mg atorvastatin (A) for 4 weeks in a randomized crossover fashion. There was a 4- to 8-week washout period between the 2 phases. CoQ10 levels and a lipid profile were obtained.
There was no difference in CoQ10 levels from baseline to post-drug therapy for either P or A (0.61 +/- 0.14 vs 0.62 +/- 0.2 microg/mL and 0.65 +/- 0.22 vs 0.6 +/- 0.12 microg/mL, respectively; P >.05). There was a significant difference in low-density lipoprotein (LDL) levels from baseline to post-drug therapy for both P and A (97 +/- 21 vs 66 +/- 19 mg/dL and 102 +/- 21 vs 52 +/- 14 mg/dL, respectively; P <.01). There was no significant correlation between LDL and CoQ10.
P and A did not decrease CoQ10 despite a significant decrease in LDL levels. These findings suggest that HMG-CoA reductase inhibitors do not significantly decrease the synthesis of circulating CoQ10 in healthy subjects. Routine supplementation of CoQ10 may not be necessary when HMG-CoA reductase inhibitor therapy is administered.
American Heart Journal 09/2001; 142(2):E2. · 4.65 Impact Factor
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B E Bleske
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ABSTRACT: Understanding of the pathophysiology of chronic systolic heart failure evolved from a purely mechanical model to one in which a cascade of neurohormones and biologically active molecules are thought to be critical in the development, maintenance, and progression of the disease. Two important neurohormonal systems are the sympathetic nervous and renin-angiotensin-aldosterone systems. Initially, increases in norepinephrine concentrations from the sympathetic nervous system and in angiotensin II and aldosterone are beneficial in the short term to maintain cardiac output after an insult to the myocardium. However, long-term exposure to these neurohormones causes alterations of myocytes and interstitial make-up of the heart. These alterations in myocardium lead to progression of heart failure and, eventually, death.
Pharmacotherapy 12/2000; 20(11 Pt 2):349S-358S. · 2.90 Impact Factor
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ABSTRACT: The purpose of this double-blind study was to determine the effect of intravenous ethanol administration on defibrillation efficacy in 18 patients with an implantable defibrillator. The equivalent of 60 ml of 100 proof ethanol did not impair defibrillation efficacy.
The American Journal of Cardiology 02/2000; 85(1):117-9, A9. · 3.37 Impact Factor
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ABSTRACT: Diurnal variation in plasma norepinephrine (PNE) levels is well documented in healthy individuals but not in patients with heart failure. Therefore, we attempted to determine variations in PNE levels over 24 hours, measured hourly, in six patients with an ejection fraction below 40% and a history of heart failure of longer than 3 months. Three controls without a history of heart failure also were evaluated. Both patients and controls had diurnal variations in PNE, with highest levels occurring during the day and lowest at night. When data in patients were evaluated by 6-hour time intervals the mean value for 6:00 A.M.-12:00 noon was approximately twice as high as 12:00 midnight-6:00 A.M. (689+/-329 vs 338+/-166 pg/ml, p<0.05, respectively). Patients also had significant peak to trough variation in PNE levels compared with controls (959+/-396 vs 386+/-84 pg/ml, p<0.02, respectively). These results suggest that significant intrapatient variations in PNE occur over 24 hours in patients with heart failure. These variations may have to be accounted for when evaluating and treating patients with heart failure.
Pharmacotherapy 09/1999; 19(8):984-8. · 2.90 Impact Factor
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ABSTRACT: Plasma pharmacokinetics of oral furosemide have been shown to be influenced by degree of decompensation in patients with congestive heart failure (CHF). This open-label, sequential comparison trial was conducted to determine whether CHF decompensation also alters the pharmacokinetics and pharmacodynamics of torsemide. Twelve patients with CHF, defined by either hemodynamic parameters or clinical signs and symptoms, were enrolled. On admission for treatment of their CHF, the patients were given 100 mg oral torsemide (phase A). A second dose of oral torsemide 100 mg was administered after hemodynamic parameters and clinical signs and symptoms of decompensated CHF resolved (phase B). Plasma and urine samples were collected over a 24-hour period for determination of torsemide concentrations and urine sodium. Hemodynamic measurements and physical signs and symptoms also were evaluated. During phase A, patients had significantly greater urine output and fractional sodium excretion compared with phase B. A significant increase in the area under the plasma concentration-time curve (AUC) was observed during phase B compared with phase A. However, no significant differences in maximal excretion rate of torsemide were noted between phase A and phase B. Heart failure status slightly affects the plasma pharmacokinetics of torsemide; however, this does not significantly alter the maximal urinary excretion rate of torsemide.
The Journal of Clinical Pharmacology 09/1998; 38(8):708-14. · 2.91 Impact Factor
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ABSTRACT: Delay in epinephrine administration during cardiopulmonary resuscitation (CPR) due to technical difficulties in obtaining an access site may be detrimental. To avoid this potential delay, we have previously shown that intranasal administration of phentolamine and epinephrine is a rapidly obtainable and feasible route of administration during CPR. A randomized blinded dose ranging study was performed in a controlled laboratory environment. Thirty mongrel dogs were randomized to one of the following dosage regimens: phentolamine, 0.25 or 2.5 mg/kg/nostril; epinephrine, 0.075, 0.75, or 7.5 mg/kg/nostril. Phentolamine was administered intranasally 1 minute before the intranasal administration of epinephrine to improve absorption. Each dog underwent 3 minutes of ventricular fibrillation followed by 7 minutes of closed chest CPR. Epinephrine was administered was administered at 3 minutes of CPR. Data from 26 dogs were included for analysis. Treatment B (0.25 and 7.5 mg/kg/nostril of phentolamine and epinephrine, respectively) produced the greatest elevation in coronary perfusion pressure (17 +/- 11 vs. 4 +/- 3 mm Hg for the next highest group, P < .003) and in epinephrine plasma concentrations (1,403 +/- 1,400 vs 290 +/- 182 ng/mL for the next highest group, P > .05). In addition, treatment B had the highest resuscitation rate, 100% (5/5) versus 0% to 50% for the other groups (P < .05). These data show that there is a dose response effect, with 0.25 and 7.5 mg/kg/nostril of phentolamine and epinephrine being the optimal dose studied. In addition, when administered in appropriate doses, intranasal epinephrine reaches the systemic circulation and increases coronary perfusion pressure and successful resuscitation during CPR in this canine model.
American Journal of Emergency Medicine 03/1996; 14(2):133-8. · 1.98 Impact Factor
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ABSTRACT: Recent studies in dogs have suggested that the disposition of S- and R-propranolol may depend on the input rate of drug delivered to the liver. Therefore, this study was designed to determine whether differences in the disposition of S- and R-propranolol occur in humans when altering the input rate of propranolol by giving different dosage forms of the drug. Twelve healthy subjects were enrolled in a single-dose, 4-way crossover pharmacokinetic study in which racemic propranolol was given according to 1 of 4 treatments: one 80-mg immediate-release (IR) tablet, phase A; two 80-mg IR tablets, phase B; a 160-mg controlled-release capsule, phase C; or a 10-mg IV bolus, phase D. The results showed no significant differences in the ratios of S/R-propranolol for AUC, clearance, or overall mean concentration among the oral dosage groups. Significant differences in these parameters including Cmax S/R ratio were seen between the oral phases and the IV phase. These differences appear to be related more to the route of administration than to the low input rate. However, at high concentrations there may be input-rate alteration in S/R ratios. Specifically, for phase B, which had the highest Cmax concentrations, the Cmax S/R ratio was significantly lower than the other oral dosage groups A and C (Cmax S/R ratios: 1.44 versus 1.54 and 1.54, respectively; P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
The Journal of Clinical Pharmacology 04/1995; 35(4):374-8. · 2.91 Impact Factor
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ABSTRACT: The primary role of epinephrine for the treatment of ventricular fibrillation (VF) and pulseless electrical activity (PEA) is to increase blood flow to the myocardium and central nervous system and ultimately improve survival. However, despite the administration of epinephrine, survival following VF or PEA is low. In an attempt to improve outcome from VF and PEA, alternative adrenergic agonists (methoxamine, phenylephrine, norepinephrine) which have different pharmacological properties than epinephrine have been evaluated. In order to determine the role of alternative adrenergic agonists for the treatment of VF and PEA this paper will compare the pharmacological properties and pharmacodynamic effects of these drugs to epinephrine. Specifically, receptor physiology along with the effects of adrenergic agonists on coronary perfusion pressure, survival, myocardial oxygen demand, and cerebral blood flow will be discussed.
Resuscitation 01/1995; 28(3):239-51. · 3.60 Impact Factor
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ABSTRACT: Limited information exists regarding the influence of dosage-release formulation on inhibition of drug metabolism. Therefore, the purpose of this study was to evaluate the effect of immediate-release (IR) and sustained-release (SR) verapamil on the pharmacokinetic parameters of propranolol in 12 healthy men. IR propranolol, 160 mg, was administered alone (Phase A) and following either IR verapamil, 80 mg t.i.d., (Phase B) or SR verapamil, 240 mg q.d., (Phase C) in a randomized crossover fashion. Of the 12 subjects enrolled, only seven were able to be analyzed secondary to assay interference. Oral clearances for L-propranolol for Phases A, B, and C were 198 +/- 70, 156 +/- 76, and 143 +/- 85 L/h, respectively. Oral clearances for D-propranolol for Phases A, B, and C were 203 +/- 96, 172 +/- 96, and 152 +/- 102 L/h, respectively. No significant differences were observed. However, when the verapamil groups (Phase B and C) were combined and compared to Phase A, a significant decrease in clearance for propranolol isomers was observed. In conclusion, due to the unexpected low numbers of patients evaluated, no significant differences in oral clearance were observed among the three treatment phases. However, there is a trend suggesting that SR verapamil had the greatest effect on propranolol clearance, which may warrant caution when changing from one formulation to another.
Therapeutic Drug Monitoring 05/1994; 16(2):216-20. · 2.49 Impact Factor
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ABSTRACT: The results of a study evaluating the appropriateness of drug and defibrillation therapy given during cardiac arrest at two hospitals are reported. A retrospective study was performed to evaluate and compare the appropriateness of therapy given during adult cardiac arrest at a large teaching hospital (hospital 1) and at a smaller nonteaching hospital (hospital 2) as measured by conformance to advanced cardiac life support (ACLS) guidelines and by less stringent alternative criteria based on published data and clinical judgment. Patients included in the study were older than 18 years and had experienced at least one of five types of cardiac arrest: ventricular fibrillation, asystole, ventricular tachycardia, electromechanical dissociation, or bradycardia. The type of drug administered, the drug dosage, and the timing of dosages were evaluated, as were the timing of defibrillation attempts and the energy used for such attempts. Treatment decisions were considered inappropriate if they did not conform to standard (ACLS) or alternative criteria. In hospital 1, there were 1137 assessable decisions recorded for 75 cardiac arrests; of these, 205 (18%) were inappropriate according to standard criteria, and 96 (8.4%) were inappropriate according to alternative criteria. In hospital 2, there were 827 assessable decisions recorded for 57 cardiac arrests; of these, 173 (21%) were inappropriate according to standard criteria, and 98 (11.2%) were inappropriate according to alternative criteria. Inappropriate therapy during cardiac arrest occurred with a similar frequency in a large teaching hospital and in a smaller, nonteaching hospital. The number of inappropriate treatments was smaller when more liberal standards of therapy were used.
American journal of hospital pharmacy 01/1994; 50(12):2538-45.
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ABSTRACT: Sodium bicarbonate is administered during cardiopulmonary resuscitation (CPR) for the treatment of systemic acidemia. However, the effect of administering standard-dose sodium bicarbonate on the vasopressor effect of epinephrine is unknown. This study compared the effects of sodium bicarbonate or normal saline on the vasopressor effect of epinephrine in 18 pigs. After 10 minutes of unassisted ventricular fibrillation, CPR was started using a pneumatic chest compression device. Two minutes after the start of CPR, sodium bicarbonate (1 mEq/kg) or normal saline (1 mL/kg) was administered into the right ventricule followed 1 minute later by epinephrine (0.2 mg/kg). Defibrillation was attempted at 8 minutes of CPR (18 minutes of ventricular fibrillation). Results demonstrated no significant differences in aortic systolic, aortic diastolic, or coronary perfusion pressure (CPP) between the two groups (1 minute after epinephrine, CPP was 22.6 +/- 13.3 mm Hg versus 21.1 +/- 20.7 mm Hg for the sodium bicarbonate and normal saline groups, respectively). However, when the data were stratified according to pH < 7.4 and pH > 7.4, the peak change in CPP was 12.7 +/- 21 mm Hg when pH < 7.4 and was 5.2 +/- 7.4 when pH > 7.4 (P = .33). Resuscitation was also similar between the two groups (two of nine for sodium bicarbonate and one of nine for normal saline). In conclusion, the standard recommended dose of sodium bicarbonate did not alter the vasopressor effect of epinephrine or resuscitation compared with normal saline in this closed chest model of ventricular fibrillation and CPR.
American Journal of Emergency Medicine 09/1993; 11(5):439-43. · 1.98 Impact Factor
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ABSTRACT: Systemic acidosis occurs during cardiac arrest and cardiopulmonary resuscitation (CPR). The present study investigated the effect of different modes of sodium bicarbonate administration on blood gas parameters during CPR. Arterial and venous blood gases were obtained during 10 minutes of CPR which was preceded by 3 minutes of unassisted ventricular fibrillation in 36 dogs. Following 1 minute of CPR, the animals received one of four treatments in a randomized and blinded manner: normal saline (NS), sodium bicarbonate bolus dose 1 mEq/kg (B), sodium bicarbonate continuous infusion 0.1 mEq/kg/min (I), and sodium bicarbonate bolus dose (0.5 mEq/kg) plus continuous infusion 0.1 mEq/kg/min (L+I). Eleven dogs completed NS, 8 B, 8 I, and 9 L+I protocol. Following NS infusion, both arterial and venous pH declined consistently over time. Significant differences compared with NS treatment in venous pH were observed at 12 minutes of ventricular fibrillation (L+I, 7.27 +/- 0.05; NS, 7.15 +/- 0.05; B, 7.20 +/- 0.05; I, 7.24 +/- 0.04, each bicarbonate treatment versus NS, and L+I versus B, (P < .05). The B group had an elevated venous PCO2 (mm Hg) concentration following 6 minutes of ventricular fibrillation compared with NS, L+I, and I groups (81 +/- 14 versus 69 +/- 10 versus 68 +/- 10 versus 71 +/- 8, respectively, (P = .07). Arterial pH and PCO2 values showed a similar trend as the venous data with the L+I group demonstrating arterial alkalosis (pH > 7.45) at 12 minutes of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
American Journal of Emergency Medicine 12/1992; 10(6):525-32. · 1.98 Impact Factor
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ABSTRACT: Epinephrine improves coronary perfusion pressure during CPR. However, administration of epinephrine during CPR may be delayed or omitted if IV or endotracheal access is not established. Therefore, the objective of this study was to determine if intranasal administration of epinephrine during CPR would provide an alternate route of drug administration that is readily accessible and requires no special technical skills.
Randomized blinded study performed in a controlled laboratory environment.
Twenty mongrel dogs weighing 19.5 +/- 4.6 kg.
All dogs received either IV epinephrine 0.015 mg/kg or intranasal epinephrine 14 mg per nostril. Phentolamine (5 mg per nostril) was administered intranasally one minute before nasal administration of epinephrine to improve absorption. Each dog underwent three minutes of ventricular fibrillation followed by seven minutes of CPR with a pneumatic chest compression device. Epinephrine was administered at two minutes into CPR.
Seven dogs were excluded because of inadequate baseline coronary perfusion pressure or compression device displacement, leaving a total of 13 dogs for analysis (six IV epinephrine, seven intranasal epinephrine). Baseline coronary perfusion pressure (mean +/- SD) was similar for IV epinephrine and intranasal epinephrine (16.9 +/- 7.1 mm Hg versus 18.2 +/- 13.8 mm Hg, respectively, P = .84). For IV and intranasal epinephrine, coronary perfusion pressure increased to 21.4 +/- 9.2 mm Hg and 24.4 +/- 18.7 mm Hg one minute after epinephrine, respectively (P = .73). Five minutes after epinephrine coronary perfusion pressure was 18.2 +/- 8.7 mm Hg and 24.3 +/- 13.9 mm Hg for IV epinephrine and intranasal epinephrine, respectively (P = .38). The rate of successful resuscitation was similar for both groups, five of seven dogs for intranasal epinephrine and four of six dogs for IV epinephrine (P = .66).
Intranasal epinephrine has similar effects on coronary perfusion pressure and resuscitation compared with standard-dose IV epinephrine. Therefore, the nasal route for administration of epinephrine appears to be an acceptable alternate method of drug delivery during CPR and compares favorably with standard IV therapy in the canine model. Because of the obvious benefits to human patients, these observations suggest further investigation.
Annals of Emergency Medicine 10/1992; 21(9):1125-30. · 4.13 Impact Factor
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ABSTRACT: Ciprofloxacin decreases the clearance of antipyrine and other drugs which, in part, undergo oxidative metabolism. Based on these findings, the authors hypothesized that ciprofloxacin may decrease the clearance of quinidine, a drug which also undergoes oxidative metabolism. The purpose of this study was to evaluate the effect of ciprofloxacin on the pharmacokinetic and ECG parameters of quinidine in seven healthy men. Oral quinidine sulfate 400 mg was administered alone (Phase A) and after oral ciprofloxacin pretreatment (Phase B) in a randomized crossover fashion with a 2-week washout period between each phase. During Phase B, ciprofloxacin pretreatment (750 mg every 12 hours) was administered for 5 days before and 24 hours after quinidine administration. Quinidine serum samples were obtained over a 24-hour period. QRS and QTc intervals were measured over a 12-hour period. There were no significant differences in clearance (20.3 +/- 3.3 L/hr vs 20.1 +/- 2.3 L/hr, P = .836), half-life (7.9 +/- 1 hr vs 7.8 +/- 0.8 hr, P = 0.8), maximum concentration (1.4 +/- 0.6 mg/L vs 1.5 +/- 0.6 mg/L, P = 0.613), or time to maximum concentration (1.5 +/- 0.2 hr vs 1.5 +/- 0.1 hr, P = 0.571) for quinidine between Phase A and Phase B, respectively. The largest decrease in clearance observed for Phase B compared to Phase A was 10%. There was also no significant difference in the degree of QRS and QTc prolongation between Phase A and Phase B. From these results, it appears that ciprofloxacin in the dose given does not alter the pharmacokinetic or ECG parameters of quinidine. Therefore, no adjustment in the dose of quinidine is needed when coadministered with ciprofloxacin.
The Journal of Clinical Pharmacology 11/1990; 30(10):911-5. · 2.91 Impact Factor
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ABSTRACT: The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.
Clinical pharmacy 06/1990; 9(5):339-57.
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ABSTRACT: Previous studies have indicated that methoxamine (an alpha adrenergic receptor agonist) may provide an advantage compared to epinephrine (a mixed alpha and beta adrenergic agonist) during cardiac arrest and CPR. To test this theory, we compared the effects of bolus injections of epinephrine vs. methoxamine on survival, hemodynamic variables, blood gases, and blood lactate concentrations during ventricular fibrillation and CPR in 12 dogs. Each dog underwent a 3-min fibrillatory arrest followed by 10 min of fibrillation and CPR, at which time the animals were defibrillated. Epinephrine (0.05 mg/kg, n = 6) or methoxamine (2 mg/kg, n = 6) was administered at the start of CPR. Both epinephrine and methoxamine produced identical survival rates (5/6) with no differences in coronary perfusion pressure gradients or blood gases (aortic, venous, or great cardiac venous pH, PaO2, or PaCO2) during CPR. Also, there were no differences between the two study groups in myocardial lactate or oxygen extraction ratios during CPR. We conclude that in the dosages tested in our experimental model, epinephrine and methoxamine produce similar results in the variables which we measured.
Critical Care Medicine 01/1990; 17(12):1310-3. · 6.33 Impact Factor
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ABSTRACT: There are limited data on the effects of Class IB and IC antiarrhythmic drug combination for the treatment of ventricular tachycardia. The present study evaluated this combination in 12 patients who had sustained ventricular tachycardia (SuVT) during programmed electrical stimulation (PES) and failed IC antiarrhythmic therapy. Following combination of lidocaine and a IC agent (7 with encainide and 5 with flecainide), two had no inducible ventricular tachycardia (VT) and one had nonsustained VT (NSVT). In seven of nine patients who still had SuVT, the mean VT cycle length increased 40 +/- 25 msec post combination compared to IC antiarrhythmic therapy. Seven patients who had a favorable response to the initial combination (less than 10 beats of NSVT, or greater than or equal to 10 beats of VT with a greater than 100 msec increase in cycle length compared to baseline and no hemodynamic compromise) were then placed on IC + oral IB agent (5 with mexiletine, 2 with tocainide). Similar effects on VT inducibility and cycle length were observed following the oral combination. In conclusion, the addition of lidocaine to IC therapy produced favorable effects on induced ventricular tachycardia in 58% of patients compared to IC agent alone. Also, a positive PES response to lidocaine and IC therapy corresponded to a similar positive response when either mexiletine or tocainide was substituted for lidocaine.
The Journal of Clinical Pharmacology 12/1989; 29(11):998-1002. · 2.91 Impact Factor
