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Procaine amide overdosage in myocardial infarction
Clinical
PROCAINE
AMIDE JAMES
Reports
OVERDOSAGE
IN
MYOCARDIAL
E. DOHERTY, AND
M.D., WELDON S.ABBO~‘, JOHN C. DAVIS, JR., M.D. LITTLE
INFARCTION M.D.,
ROCK, ARK.
VERDOSAGE with oral procaine amide* has not, to our knowledge, been reported previously in myocardial infarction. It is the purpose of this case report to present such a patient, treated conservatively, with recovery.
0
CASE REPORT J. B. H., a white man, aged 48 years, was admitted Nov. 2, 1952 to the University Hospital with an eighteen-hour history of nausea and vomiting, dyspnea, profuse sweating, and constricting substernal pain which radiated into the neck and down the medial aspect of both arms. Physical examination revealed blood pressure llO/SO mm. Hg, pulse 100, respirations 22, temperature 99” F. orally. The heart was not enlarged. Heart sounds were distant and occasional premature contractions were noted. No murmurs were heard. The remainder of the physical examination was negative. An electrocardiogram was obtained and revealed typical findings of an acute anterior myocardial infarction. The patient was given initial doses of Dicumarol, and continuous intravenous heparin was administered for the first three days of hospitalization. The prothrombin time was thereafter maintained at about 40 seconds with daily doses of Dicumarol. The premature contractions noted on admission were demonstrated by electrocardiogram to be ventricular in origin. The patient was then given procaine amide 0.5 Gm. orally every six hours with considerable reduction in number of premature beats. Physical signs remained much the same. The blood pressure varied from 94/70 to 110/80 mm. Hg. On Nov. 13, 1952 he was given 5.0 Gm. of procaine amide through error. One hour later he complained of numbness of his extremities, blurring of vision, nausea without vomiting, and dizziness. These symptoms subsided gradually over a period of about three hours after onset or four hours after the medication was administered. Blood pressure determinations during this period varied from 92/75 to lOO/SO mm. Hg, and the pulse from 90 to 100. Fortunately, an electrocardiogram had been obtained about one and one-half hours before medication was given (Fig. 1). Serial tracings were taken throughout the next 24 hours (Fig. 2 and Fig. 3). Toxic effects demonstrable were: prolongation of QRS complex from 0.10 second to 0.14 second, Q-T prolongation from 0.44 second to 0.54 second, P-R prolongation from 0.18 to 0.20 second (Lead II), and alteration of the T wave in Leads II, III, AVr,, AVF, and VI (Fig. 2). All these changes gradually returned to original levels within approximately eight hours. A tracing made the following day (Nov. 14) about 20 hours after medication (Fig. 3) shows no change over the tracing performed before procaine amide was administered. cine,
From the Division of Cardiology, Department Little Rock, Arkansas. Received for publication Feb. 7, 1963. ‘F’roneatyl,
Squibb.
of Medicine.
456
University
of Arkansas
School
of Medi-
Fig.
l.-Electrocardiogram
. ..on J. B. H. performed one and one-half hours Findings characteristic of subacute anterior
prior to admInistration myocardial infarction.
of overdose
of procaine
amide.
DOHERTY
ET
AL.
:
PROCAINE
AMIDE
OVERDOSAGE
457
458
AMERICAN
HEART
JOURNAL
DOHERTY
ET
AL.
:
PROCAINE
AMIDE
OVERDOSAGE
459
The patient was given no treatment during this period but was observed very closely. The following day he was asymptomatic and remained so until discharged from the hospital (Dec. 3, 1952). He was seen in the cardiac clinic Jan. 6, 1953 and continues to convalesce satisfactorily. SUMMARY
A case of myocardial infarction has been presented in which ten times the prescribed dose of procaine amide (5.0 Gm.) was inadvertently administered. Recovery was uneventful and toxic symptoms disappeared eight hours later. No treatment was administered.
PROCAINE
AMIDE JAMES
Reports
OVERDOSAGE
IN
MYOCARDIAL
E. DOHERTY, AND
M.D., WELDON S.ABBO~‘, JOHN C. DAVIS, JR., M.D. LITTLE
INFARCTION M.D.,
ROCK, ARK.
VERDOSAGE with oral procaine amide* has not, to our knowledge, been reported previously in myocardial infarction. It is the purpose of this case report to present such a patient, treated conservatively, with recovery.
0
CASE REPORT J. B. H., a white man, aged 48 years, was admitted Nov. 2, 1952 to the University Hospital with an eighteen-hour history of nausea and vomiting, dyspnea, profuse sweating, and constricting substernal pain which radiated into the neck and down the medial aspect of both arms. Physical examination revealed blood pressure llO/SO mm. Hg, pulse 100, respirations 22, temperature 99” F. orally. The heart was not enlarged. Heart sounds were distant and occasional premature contractions were noted. No murmurs were heard. The remainder of the physical examination was negative. An electrocardiogram was obtained and revealed typical findings of an acute anterior myocardial infarction. The patient was given initial doses of Dicumarol, and continuous intravenous heparin was administered for the first three days of hospitalization. The prothrombin time was thereafter maintained at about 40 seconds with daily doses of Dicumarol. The premature contractions noted on admission were demonstrated by electrocardiogram to be ventricular in origin. The patient was then given procaine amide 0.5 Gm. orally every six hours with considerable reduction in number of premature beats. Physical signs remained much the same. The blood pressure varied from 94/70 to 110/80 mm. Hg. On Nov. 13, 1952 he was given 5.0 Gm. of procaine amide through error. One hour later he complained of numbness of his extremities, blurring of vision, nausea without vomiting, and dizziness. These symptoms subsided gradually over a period of about three hours after onset or four hours after the medication was administered. Blood pressure determinations during this period varied from 92/75 to lOO/SO mm. Hg, and the pulse from 90 to 100. Fortunately, an electrocardiogram had been obtained about one and one-half hours before medication was given (Fig. 1). Serial tracings were taken throughout the next 24 hours (Fig. 2 and Fig. 3). Toxic effects demonstrable were: prolongation of QRS complex from 0.10 second to 0.14 second, Q-T prolongation from 0.44 second to 0.54 second, P-R prolongation from 0.18 to 0.20 second (Lead II), and alteration of the T wave in Leads II, III, AVr,, AVF, and VI (Fig. 2). All these changes gradually returned to original levels within approximately eight hours. A tracing made the following day (Nov. 14) about 20 hours after medication (Fig. 3) shows no change over the tracing performed before procaine amide was administered. cine,
From the Division of Cardiology, Department Little Rock, Arkansas. Received for publication Feb. 7, 1963. ‘F’roneatyl,
Squibb.
of Medicine.
456
University
of Arkansas
School
of Medi-
Fig.
l.-Electrocardiogram
. ..on J. B. H. performed one and one-half hours Findings characteristic of subacute anterior
prior to admInistration myocardial infarction.
of overdose
of procaine
amide.
DOHERTY
ET
AL.
:
PROCAINE
AMIDE
OVERDOSAGE
457
458
AMERICAN
HEART
JOURNAL
DOHERTY
ET
AL.
:
PROCAINE
AMIDE
OVERDOSAGE
459
The patient was given no treatment during this period but was observed very closely. The following day he was asymptomatic and remained so until discharged from the hospital (Dec. 3, 1952). He was seen in the cardiac clinic Jan. 6, 1953 and continues to convalesce satisfactorily. SUMMARY
A case of myocardial infarction has been presented in which ten times the prescribed dose of procaine amide (5.0 Gm.) was inadvertently administered. Recovery was uneventful and toxic symptoms disappeared eight hours later. No treatment was administered.