Electrocardiographic abnormalities in acute heroin overdosage

Sections

Abstract
Patients and methods
Results
Discussion

Details

Author: Frederik L GLAUSER , Robert L. DOWNIE, W. Richard SMITH
Pages: 85 to 89
Creation Date: 1977/01/01

Electrocardiographic abnormalities in acute heroin overdosage

Frederik L GLAUSER *
Robert L. DOWNIE
W. Richard SMITH Department of Medicine, University of California, Irvine, California

Abstract

Twenty-one of 25 acutely overdosed heroin addicts had abnormalities noted on their admission electrocardiograms. The most common findings were non-specific ST-T changes in 17 patients, sinus tachycardia in 11, and left or right atrial enlargement in 8. Five patients had more serious arrhythmias (4 atrial fibrillation and 1 ventricular tachycardia). For the entire group the initial PaO 2was 74.8 ± 48.2 torr. This degree of oxygenation was only achieved with the use of high dose supplemental oxygen. The 5 patients with the more serious arrhythmias had comparable PaO 2s but this was only achieved with higher supplemental oxygen concentrations. We conclude that electrocardiographic alterations (other than arrhythmias) are very common in acute heroin overdosage and may be related to hypoxemia. The abnormal cardiac rhythms may be due to the direct effects of heroin or its metabolites.

Heroin addiction is associated with a multitude of medical complications which can affect various organ systems including the heart [ (1)] . Within the last six years several reports have appeared documenting electrocardiographic abnormalities in heroin users [ (2)] , [ (3)] , [ (4)] , [ (5)] . These studies dealt with either a small series of patients or patients who used methadone or heroin in a chronic fashion. No one, to our knowledge, has extensively studied the electrocardiographic changes which occur in patients with acute heroin overdosage. This retrospective analysis of the electrocardiograms (ECG), arterial blood gases and selected electrolytes in 25 consecutively hospitalized patients acutely overdosed on heroin is an attempt to correct this deficiency.

Patients and methods

All heroin abuse patients, admitted to Orange County Medical Center between July 1974 and June 1975 were eligible for this study if they met the following criteria: [ (1)] acute heroin overdosage as evidenced by lethargy, semi-coma or coma; [ (2)] a history of intravenous injection within the previous 12 hours; [ (3)] ECG, arterial blood gases (PaO 2, PaCO 2, pH), serum potassium and calcium obtained within 2 hours of admission. Recent heroin use was confirmed by both history and response to morphine antagonists or urinary findings of morphine.

In an attempt to dissect out the role of hypoxemia, hypercapnia, and acidosis versus the specific effects of heroin we also analysed the ECG, arterial blood gases and electrolytes in 25 consecutively hospitalized age-matched patients acutely overdosed on barbiturates (hereafter designated barbiturate overdose patients).

* Frederick L. Glauser, M.D., Pulmonary Division B, Veterans Administration Hospital, Long Beach, California 90801.

These patients had to meet the following criteria to be eligible for this study: [ (1)] acute barbiturate overdosage as evidenced by lethargy, semi-coma or coma; [ (2)] a history of oral ingestion within the previous 12 hours; [ (3) ] ECG, arterial blood gases, serum potassium and calcium obtained within 2 hours of admission. Recent drug use was confirmed by history and urinary findings of barbiturate or its metabolites.

Non-cardiogenic pulmonary oedema was diagnosed as follows: bilateral alveolar infiltrates without cardiomegaly on chest radiographs; tachypnea and/or end inspiratory rales; [ (3)] no evidence of pulmonary infection by sputum smears or cultures; [ (4)] rapid resolution of the alveolar infiltrates. Electrocardiographic interpretation was taken from a standard textbook [ (6)] . Special criteria were as follows: non-specific ST changes - ST depression of 0.5 mm in leads I, II, aVL, aVf, V2-6 and ST depression of > 30.75 mm in lead III. Non-specific T changes -T 10 per cent following R wave in all leads except III where T was accepted as upright, flat or inverted.

Arterial blood gases were measured on a Radiometer PM 71 blood gas apparatus. Serum potassium and calcium determinations were performed on the Technicon Autoanalyzer.

Results

The mean age for the 25 heroin abuse patients (21 men, 4 women) was 25.4 + 6.3 years and for the drug overdose patients (14 women, 11 men) 31.2 + 14.4 years. Twelve heroin abuse patients had evidence of pulmonary oedema on their admission chest radiograms; 2 had localized infiltrates compatible with a diagnosis of pneumonia and 1 had evidence of segmental atelectasis. Four barbiturate overdose patients had radiographic evidence of pulmonary oedema; 4 had localized infiltrates compatible with a diagnosis of pneumonia and 1 had segmental atelectasis.

ECG findings are listed in the table. The most common abnormalities in the heroin abuse population were non-specific ST-T changes and sinus tachycardia.

Electrocardiographic alteration in addicts and drug overdose patients *

 

Addicts

Drug overdose

Normal
4 5
Non-specific ST-T changes
17 16
Sinus tachycardia
11 13
Left or right atrial enlargement
8 3
Left ventricular hypertrophy
4 1
Peaked T waves
3
-
Intraventricular conduction delay
2 1
1st degree A-V block
2
-
Right or left axis deviation
4 2
PVCs, PACs
2 2
Atrial fibrillation
4
-
Ventricular tachycardia
1
-

*Each patient may have one or more abnormalities present on the ECG.

Four patients experienced atrial fibrillation, 1 patient experienced ventricular tachycardia. The barbiturate overdose group showed a similar distribution of abnormalities (see table) except that, in no cases, was atrial fibrillation or ventricular tachycardia apparent.

The initial arterial blood gases in the heroin abuse population were PaO 2 - 74.8 ± 48.2 torr, PaCO 2 - 47.2 ± 22.3 torr, pH - 7.31 ± 0.13. In 11 patients the F 1O 2 was accurately known being 0.50 ± 0.29. Of the remaining patients, 9 were receiving supplement oxygen by nasal cannulae with a mean flow of 4 ± 2.2 L/min. In the barbiturate overdose patients the initial PaO 2 was 75.6 ± 51.3 torr, PaCO 2- 44.6 ± 18.6 torr, pH - 7.33 ± 0.11 (as compared to addicts p = NS). In 18 patients the F 1O 2was accurately known being 0.45 ± 0.25 (NS). Of the remaining patients, 4 were receiving supplemental oxygen by nasal cannulae with a mean flow of 3.8 ± 2.0 L/min (NS). The serum potassium was 4.2 ± 0.79 meq/L and calcium 9.3 ± 1.2 mg per cent in the heroin and 4.4 ± 0.3 meq/L and 9.2 ± 1.1 mg per cent in the barbiturate overdose group (NS). The three addicts with low potassium (3.5 meq/L) had non-specific ST or T wave abnormalities; one heroin patient had an intraventricular conduction delay and another had 1st degree AV block and left atrial enlargement. The one individual who had an elevated serum potassium (>5.0 meq/L) had only a sinus tachycardia. None of the barbiturate overdose patients had abnormally elevated or depressed serum potassiums.

When the five heroin cases with the more serious arrhythmias (4 atrial fibrillation, 1 ventricular tachycardia) were considered together and compared to the other 20 heroin and the 25 barbiturate overdose patients there were no significant differences in age, PaO 2, PaCO 2, pH, serum potassium or calcium. The F 1O 2in this group was higher (0.80 ±0.28, 2 patients) as was the amount of supplemental oxygen administered (6.0 ± 1.2 L/min, 3 patients). In addition, 4 of these 5 patients had evidence of pulmonary oedema.

Discussion

Hypoxaemia, hypercapnia, respiratory acidosis, the vagotonic and cholinesterase inhibitory effects of heroin, and the effects of heroin metabolites and adulterants have all been postulated to be the mediators of the cardiac abnormalities found in heroin patients (1-5). Nonetheless, the etiology of the arrhythmias and electrocardiographic abnormalities remains obscure. Most investigators have hypothesized that hypoxaemia may play a central role in the cardiac disturbances found in this group of patients. At first glance our findings would seem to contradict this viewpoint since the heroin patients' mean PaO 2 was 74.8 ± 48.2 torr and the barbiturate overdose patients' was 75.6 ± 51.3 torr. However this degree of oxygenation was only achieved in most cases with the use of supplemental oxygen (Results, table). This implies that severe hypoxaemia was initially present in each group. In contrast the PaCO 2 and pH for both groups deviated only minimally from the normal range (see table).

Of the heroin patients 84 per cent (and 80 per cent of barbiturate overdose patients) had some ECG change, the most common being non-specific ST-T changes and sinus tachycardia (see table). This incidence is higher than that found by Lipski et al., in an investigation of the ECGs of 75 asymptomatic individuals admitted to a methadone programme. Eighteen of 34 (55 per cent) patients taking heroin only, had abnormalities noted in their ECG. Of 15 patients who had taken heroin within 4 hours of their ECG, 68 per cent had abnormalities, the most frequent of which were prolonged QT intervals and bradyarrhythmias. Whether any of their subjects experienced hypoxaemia is not recorded.

Although the 5 patients in this study who experienced arrhythmias (4 atrial fibrillation, 1 ventricular tachycardia) needed higher F 1O 2s to maintain adequate oxygenation there was no statistically significant difference between their PaO 2s, PaCO 2s, pH serum potassiums and calciums and those of the rest of the heroin or barbiturate overdose group. In addition, individual patients in this latter group had the same degree of hypoxaemia without experiencing arrhythmias. Thus, in contrast to the relatively benign ECG alterations, it does not appear that we can attribute these serious rhythm disturbances to severe hypoxaemia. In contrast Duberstein and Kaufman, felt that hypoxaemia was the major cause of atrial fibrillation found in 6 of 149 heroin patients (5). Five of the 6 patients had an average pH of 7.06, PaO 2 - 30 torr, PaCO 2 - 57 torr. Reversion to sinus rhythm occurred in all cases after treatment with nalorphine and oxygen.

The discrepancy between our findings and those of Duberstein and Kaufman is not apparant. It could be argued that their patients suffered much greater degrees of hypoxaemia compared to ours and thus arrhythmias were initiated. On closer analysis this postulate does not seem tenable as 5 of the heroin and 4 of barbiturate overdose patients had PaO 2s 40 torr and none experienced abnormal cardiac rhythms. It is possible that the known effects of heroin (or of its morphine metabolites) on the heart may account for the arrhythmias found in this and Duberstein and Kaufman's series. Morphine (depending on the dosage employed) is known to have both a vagolytic and vagomimetic action which, experimentally, can result in bradycardias, sinus tachycardias, or second degree AV blocks [ (7)] . It is therefore conceivable that the pharmacologic actions of morphine were primarily responsible for the arrhythmias. This hypothesis is strengthened when the following is considered: ( a) only the heroin and not the barbiturate group experienced arrhythmias even though they were comparable regarding arterial blood gases and electrolytes; ( b) the patients described by Duberstein and Kaufman had reversal of their arrhythmias after oxygen and nalorphine treatment. Although these authors felt the relief of hypoxaemia led to conversion of the arrhythmias it is possible that nalorphine antagonized the effects of morphine and thus terminated the abnormal heart rhythm and ( c) in subjects with a normal myocardium exposure to severely hypoxic mixtures (resulting in a mean PaO 2 of 31 torr) during exercise does not result in arrhythmias [ (8)] . These findings would imply that hypoxaemia itself, even during stressful situations, does not cause alterations in heart rhythms in patients with a basically normal myocardium.

References

001

A. D. Steinberg and J. S. Karliner, "The clinical spectrum of heroin pulmonary edema", Arch. Intern. Med. 122 :122. 1968.

002

J. Lipski, B. Stimmel and E. Donosa, "The effect of heroin and multiple drug abuse on the electrocardiogram", Amer. Heart Journ. 86 :663, 1973.

003

M. Labi, "Paroxysmal atrial fibrillation in heroin addiction", Ann. Intern. Med. 71 :951, 1969.

004

D. Gann, N. Mansour and D.J. Crosby, "Atrial fibrillation and pulmonary edema in acute heroin intoxication", Arizona Med. 28 :672, 1971.

005

J.L. Duberstein and D.M. Kaufman, "A clinical study of an epidemic of heroin intoxication and heroin induced pulmonary edema" , Amer. Journ. Med. 51 :704, 1971.

006

R. Ashman and E. Hull, Essentials of electrocardiography . New York, 1937. The Macmillan Co.

007

F. Urthaler, J.H. Isobe and T.N. James, "Direct and vagally mediated chronotropic effects of morphine studied by selective perfusion of the sinus node of awake dogs", Chest 68 :222, 1975.

008

C.A. Guenter, "The effects of acute severe arterial hypoxemia on the electrocardiogram during exercise ", Chest 68 :149, 1975.