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Hypokalemia in out-of-hospital cardiac arrest
ABSTRACTS
HYPOKALEMIA IN OUT-OF-HOSPlTAL CARDIAC ARREST David M. Salerno, MD, PhD; Richard W. Asinger, MD; Frank L. Mikell, MD; Ernest Ruiz, MD; Morrison Hodges, MD, FACC. Hennepin County Medical Center and the University of Minnesota, Mimeapolis, Minnesota. Hypokalemia exacerbates ventricular ectopy and lowers ventricular fibrillation (VF) threshold. To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest (CA), we reviewed the initial serum potassiums (K+l and arterial pH values obtained in the emergency room from 151 consecutive pts resuscitated from CA between 1978 and 1980. For comparison, the same variables were reviewed from 62 comecutive pts who had acute transmural myocardial infarction (AM11 without CA between 1979 and 1980. The observed serum K+ (Kol was normalized (Knl to DH7.40 bv the formula: Kn = Ko +6 (PH - 7.40). The following data-were obtained: P AMI (n) ( ) E&&9, Rs Ko (mm/L) 7.36 (134) < .005 3.53 (128) t.001 62 of 128 (48%) Kn < 3.5mRo/L 7 of 39 (18%) < .005 34 of 128 i27%j Kn < 3.0 mEq/L 2 of 39 ‘(5%) < .Ol Since CA ots are a diverse Erouo. we also COmBred two major subets of&CA to AM1 pts. +he subgroup of CA ‘pts whose initial rhythm was VF but who did not evolve AMl after resuscitation (primary VF) more frequently had Kn < 3.5 mEq/L than did pts with AMI tut no CA (22 of 54 vs 7 of 39; p < .05). Also, VF pts who proceeded to evolve transmural AMI immediately after reslscitaticn were more likely to have Kn < 3.5 mEq/L than were AMI ptswho did not have CA (12 of 23 vs 7 of 39; p < .025). Therefore, we conclude that hypokalemia is prevalent immediately following out-of-hospital CA, whereas it is uncommon in AMI in the absence of CA. Hypokalemia is severe in some CA pts and ttus may be a causative factor in their arrest. z.
NESDA Y, APRIL 27, 1982 AM CALCIUM BLOCKING DBUGS IN ISCHEMIC HEART DISEASE 8:30- lo:oo RANDOMIZED PLACEBO-CONTROLLED STUDY OF NZFEDIPINE IN PATIENTS WITH VASOSPASTIC ANGINA Edgar C. Schick, MD, FACC, Chang-seng Liang, MD, Frederick A. Hewler, MD. FACC. Nicholas Z. Kerin, MD, FACC, Frederick k. Kahl;MD, FACC, Kenneth M. Kent, MD, FACC, R. Joe Noble, MD, FACC, Bernard Tabatznik, MD, Richard W. Terry, MD, FACC, Boston University Medical Center, Boston, MA and Collaborating Institutions A multicenter randomized study compared the efficacy of nifedipine (N) to placebo (P) in vasospastic angina. Patients with reversible ST elevation, angiographic coronary spasm, or positive ergonovine response who improved during open-label nifedipine therapy (2 to 60 months) were studied. After a 2 week single-blind baseline period during which nifedipine was continued at pre study levels, patients entered the double-blind randomized phase, receiving nifedipine or placebo for 4 weeks or until symptoms required premature termination. Other antiangina1 medicines were continued unchanged. The efficacy of randomized treatment was based on the investigators' overall clinical assessment at the end of the randomized phase. The results of treatment during the double-blind phase were: P P value N Patients Angina/week (median) Nitroglycerin/week (median) Premature termination Therapy effective
13 0 0 0 11
15 3.4 0.5 5 2
0.04 0.06 0.03
The efficacy of nifedipine in the treatment of vasospastic angina, previously reported only in open-label studies, has now been validated in a randomized double-blind trial.
VENTRICULAR ELECTRICAL INSTABILITY DURING THE FIRST YEAR FOLLOWING MYOCARDIAL INFARCTION David A. Richards, FRACP: David V. Cody, FRACP: Alan R. Denniss, MB; Paul A. Russell, FRACP; John B. Uther, MD, FRACP; Alan A. Young, FRACP; Westmead Centre, Sydney, Australia.
COMPARISON OF THE ANTIANGINAL EFFICACYOF IQUR CALCIUM ION ANTAGONISTSWITH PROPRANOLOL V. Bala Subramanian, MD, FACC, M.J.Bowles,MRCP, N.S. Khur&,!MBBS,A.B.Davies, MBBS, E.B.Raftery, MD, FACC, NorthvlckPark IIospitsl & ClinicalResearchCentre, H-w, Middlesex,U.K.
The aim of this study was to ascertain whether instananeous death within 1 year of myocardial infarction could be predicted by the ability to induce a sustained ventricular tachyarrhythmia in the laboratory 6-28 days after acute infarction. Ventricular electrical stability was assessed in 165 hemodynamically stable survivors of acute infarction (age 54?10 years),onnoantiarrhythmictherapy, and in 111 control patients without ischaemic heart disease (age 44+14 years). Ventricularelectrical stability was assessed by programmed stimulation (PS) ofthe RV with a drive chain of 8 beats followed by single and paired extrastimuli at the apex and qtflow tract at twice diastolic threshold and 20 mA. Patients were considered unstable if PS induced a sustained ventricular tachyarrhythmia lasting > 10 sec. Other patients were considered stable. Whereas all control patients were stable, 23% of infarct survivors were unstable. Stable and unstable infarctsurvivorsweresimilar in termsofage and clinical status in hospital. However the cumulative mortality for unstable patients at 1 year was significantly higher (p
Ve have evaluatedfour calciumion antagonists, comparing their mode of action vith a standard beta blocker. The drugs evaluated were proprenolol(P 240 mg/day)in 24 patients,diltiaaem(D 360 mg/day)in 20 patients, nicerdipine(Nit 60 mg/day)in X, patients,nifedipine (Nif 60 mg/day)in 28 patients,and verapamil(V 36) mg/ day) in 28 patients. All drugs were administered in three divideddoses deily for four weeks and all trials were identicalend placebocontrolled. The efficacy was assessedby serialmultistagetreadmillexercise tests with a computerassistedexercisesystem, The time requiredtc produceangina (exercisetime),resting heart rate (RHR)maximalheart rate (MHR),heart rate increasedper minuteof exercise(AHR) peak ST depression (MSTI)and MSTi/exercise time @ STI) were calculated. The resultsare shownin the Table. P D Nit Nif V Exercisetime c22 +39 +42 +67 +75 tll t4 -8 Restingheart rate -26 -20 Max. heart rate -23 -3 t 5 t4 -1 AHR MST1 (CM51
Ig
1416 -50
-25
-25
-37
-11
MSTI/Ex.time -28 -50 15: 15; 1 mm time t82 +17 +73 +75 +49 (All values expressedas per cent changescomparedto placebo This study suggeststhat verapamiland diltiazemare the two most suitablecalciumion antagonistsfor treatment of chronicstableangina.
March 1992
The American Journal of CARDIOLOGY
Volume 49
929
HYPOKALEMIA IN OUT-OF-HOSPlTAL CARDIAC ARREST David M. Salerno, MD, PhD; Richard W. Asinger, MD; Frank L. Mikell, MD; Ernest Ruiz, MD; Morrison Hodges, MD, FACC. Hennepin County Medical Center and the University of Minnesota, Mimeapolis, Minnesota. Hypokalemia exacerbates ventricular ectopy and lowers ventricular fibrillation (VF) threshold. To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest (CA), we reviewed the initial serum potassiums (K+l and arterial pH values obtained in the emergency room from 151 consecutive pts resuscitated from CA between 1978 and 1980. For comparison, the same variables were reviewed from 62 comecutive pts who had acute transmural myocardial infarction (AM11 without CA between 1979 and 1980. The observed serum K+ (Kol was normalized (Knl to DH7.40 bv the formula: Kn = Ko +6 (PH - 7.40). The following data-were obtained: P AMI (n) ( ) E&&9, Rs Ko (mm/L) 7.36 (134) < .005 3.53 (128) t.001 62 of 128 (48%) Kn < 3.5mRo/L 7 of 39 (18%) < .005 34 of 128 i27%j Kn < 3.0 mEq/L 2 of 39 ‘(5%) < .Ol Since CA ots are a diverse Erouo. we also COmBred two major subets of&CA to AM1 pts. +he subgroup of CA ‘pts whose initial rhythm was VF but who did not evolve AMl after resuscitation (primary VF) more frequently had Kn < 3.5 mEq/L than did pts with AMI tut no CA (22 of 54 vs 7 of 39; p < .05). Also, VF pts who proceeded to evolve transmural AMI immediately after reslscitaticn were more likely to have Kn < 3.5 mEq/L than were AMI ptswho did not have CA (12 of 23 vs 7 of 39; p < .025). Therefore, we conclude that hypokalemia is prevalent immediately following out-of-hospital CA, whereas it is uncommon in AMI in the absence of CA. Hypokalemia is severe in some CA pts and ttus may be a causative factor in their arrest. z.
NESDA Y, APRIL 27, 1982 AM CALCIUM BLOCKING DBUGS IN ISCHEMIC HEART DISEASE 8:30- lo:oo RANDOMIZED PLACEBO-CONTROLLED STUDY OF NZFEDIPINE IN PATIENTS WITH VASOSPASTIC ANGINA Edgar C. Schick, MD, FACC, Chang-seng Liang, MD, Frederick A. Hewler, MD. FACC. Nicholas Z. Kerin, MD, FACC, Frederick k. Kahl;MD, FACC, Kenneth M. Kent, MD, FACC, R. Joe Noble, MD, FACC, Bernard Tabatznik, MD, Richard W. Terry, MD, FACC, Boston University Medical Center, Boston, MA and Collaborating Institutions A multicenter randomized study compared the efficacy of nifedipine (N) to placebo (P) in vasospastic angina. Patients with reversible ST elevation, angiographic coronary spasm, or positive ergonovine response who improved during open-label nifedipine therapy (2 to 60 months) were studied. After a 2 week single-blind baseline period during which nifedipine was continued at pre study levels, patients entered the double-blind randomized phase, receiving nifedipine or placebo for 4 weeks or until symptoms required premature termination. Other antiangina1 medicines were continued unchanged. The efficacy of randomized treatment was based on the investigators' overall clinical assessment at the end of the randomized phase. The results of treatment during the double-blind phase were: P P value N Patients Angina/week (median) Nitroglycerin/week (median) Premature termination Therapy effective
13 0 0 0 11
15 3.4 0.5 5 2
0.04 0.06 0.03
The efficacy of nifedipine in the treatment of vasospastic angina, previously reported only in open-label studies, has now been validated in a randomized double-blind trial.
VENTRICULAR ELECTRICAL INSTABILITY DURING THE FIRST YEAR FOLLOWING MYOCARDIAL INFARCTION David A. Richards, FRACP: David V. Cody, FRACP: Alan R. Denniss, MB; Paul A. Russell, FRACP; John B. Uther, MD, FRACP; Alan A. Young, FRACP; Westmead Centre, Sydney, Australia.
COMPARISON OF THE ANTIANGINAL EFFICACYOF IQUR CALCIUM ION ANTAGONISTSWITH PROPRANOLOL V. Bala Subramanian, MD, FACC, M.J.Bowles,MRCP, N.S. Khur&,!MBBS,A.B.Davies, MBBS, E.B.Raftery, MD, FACC, NorthvlckPark IIospitsl & ClinicalResearchCentre, H-w, Middlesex,U.K.
The aim of this study was to ascertain whether instananeous death within 1 year of myocardial infarction could be predicted by the ability to induce a sustained ventricular tachyarrhythmia in the laboratory 6-28 days after acute infarction. Ventricular electrical stability was assessed in 165 hemodynamically stable survivors of acute infarction (age 54?10 years),onnoantiarrhythmictherapy, and in 111 control patients without ischaemic heart disease (age 44+14 years). Ventricularelectrical stability was assessed by programmed stimulation (PS) ofthe RV with a drive chain of 8 beats followed by single and paired extrastimuli at the apex and qtflow tract at twice diastolic threshold and 20 mA. Patients were considered unstable if PS induced a sustained ventricular tachyarrhythmia lasting > 10 sec. Other patients were considered stable. Whereas all control patients were stable, 23% of infarct survivors were unstable. Stable and unstable infarctsurvivorsweresimilar in termsofage and clinical status in hospital. However the cumulative mortality for unstable patients at 1 year was significantly higher (p
Ve have evaluatedfour calciumion antagonists, comparing their mode of action vith a standard beta blocker. The drugs evaluated were proprenolol(P 240 mg/day)in 24 patients,diltiaaem(D 360 mg/day)in 20 patients, nicerdipine(Nit 60 mg/day)in X, patients,nifedipine (Nif 60 mg/day)in 28 patients,and verapamil(V 36) mg/ day) in 28 patients. All drugs were administered in three divideddoses deily for four weeks and all trials were identicalend placebocontrolled. The efficacy was assessedby serialmultistagetreadmillexercise tests with a computerassistedexercisesystem, The time requiredtc produceangina (exercisetime),resting heart rate (RHR)maximalheart rate (MHR),heart rate increasedper minuteof exercise(AHR) peak ST depression (MSTI)and MSTi/exercise time @ STI) were calculated. The resultsare shownin the Table. P D Nit Nif V Exercisetime c22 +39 +42 +67 +75 tll t4 -8 Restingheart rate -26 -20 Max. heart rate -23 -3 t 5 t4 -1 AHR MST1 (CM51
Ig
1416 -50
-25
-25
-37
-11
MSTI/Ex.time -28 -50 15: 15; 1 mm time t82 +17 +73 +75 +49 (All values expressedas per cent changescomparedto placebo This study suggeststhat verapamiland diltiazemare the two most suitablecalciumion antagonistsfor treatment of chronicstableangina.
March 1992
The American Journal of CARDIOLOGY
Volume 49
929