Hoffman R, et al. Go!dfronk's Toxicologic Emergencies . 8th ed.

New York: McG raw-Hill, 2006.

cardiotoxicity, coma, and death (Table 60- 1). Antimuscarinic findings are commonly appreciated in poisoned patients, including dry skin and mucous membranes,

diminished or absent bowel sounds, urinary retention, and

sinus tachycardia. Acute cardiovascular toxicity must be

recognized and treated expediently. Sinus tachycardia is a

very common early finding, but typically does not result in

hemodynamic compromise. That said, severe poisonings

frequently progress to induce wide complex tachycardias

and refractory hypotension. CNS toxicity can range from

disorientation and agitation to outright lethargy. Early

subtle alterations in levels of consciousness can quickly

progress to obtundation and coma. Generalized tonicclonic seizures occur in -4o/o of all patients who present

with CA poisoning and in 13o/o of those who subsequently

experience cardiopulmonary arrest.

DIAGNOSTIC STUDIES

� Laboratory

Although quantitative assays for serum CA concentrations

do exist, their limited availability and prolonged turnaround times preclude any clinical utility. Furthermore,

serum levels correlate poorly with clinical significance.

There are no additional laboratory studies useful for the

diagnosis or management of patients with CA poisoning.

� Electrocardiogram

The electrocardiogram (ECG) is the most useful and r eadily available modality for the evaluation of patients with

potential CA poisoning. It not only provides rapid, distinctive, and diagnostic findings suggestive of toxicity, but also

facilitates the provision of targeted therapy. ECG abnor ­

malities develop within the first 6 hours of ingestion and

typically resolve by 36-48 hours.

The classic ECG pattern in moderate to severely poisoned patients is sinus tachycardia with right axis devia ­

tion of the terminal 40 msec of the QRS complex (terminal

R-wave in lead aVR) associated with prolongation of the

PR, QRS, and QT intervals (Figure 60-1). Life-threatening

complications are far more likely when the QRS c omplex is

prolonged beyond 100 msec. Thirty percent of patients will

experience seizures with a QRS > 100 msec, and the risk of

ventricular tachycardia increases drastically when the QRS

complex exceeds 160 msec.

MEDICAL DECISION MAKING

A high index of suspicion combined with a thorough history, physical examination, and ECG analysis is required to

establish the diagnosis of CA toxicity. Keep in mind that

patients with intentional overdoses may neither be reliable

nor forthcoming regarding their ingestions. Every effort

must be made to ascertain the exact time of ingestion,

specific agent and amount consumed, and the presence of

CYCLIC ANTIDEPRESSANTS

Cook County Hospital-ER

Vent. rate

PR interval

QRS duration

QT/QTc

P-R-T axes

1 1 6 BPM

1 58 ms

••• Age and gender specific ECG analysis •••

Sinus tachycardia

1 08 ms Biatrial enlargement

336/467 ms

85 259 71

Right superior axis deviation

No previous ECGs available

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Figure 60-1 . ECG findings in a patient with chronic pain who mistook his Elavil for Tylenol #3 and ingested

approximately 500 mg. Note sinus tachycardia, the prolonged QRS interva ls, and the terminal R-wave in aVR .

any co-ingestants. Once identified, the treatment for CA

toxicity should be initiated without delay (Figure 60-2).

TREATMENT

All patients require large-bore intravenous (IV) access and

continuous cardiac monitoring. Early intubation is recommended for patients with CNS depression and/or hemodynamic instability, as they have the potential for rapid

deterioration. Furthermore, respiratory acidosis secondary

to ventilatory insufficiency can exacerbate the cardiotoxicity of CA poisoning.

...... Gastrointestinal Decontamination

The induction of emesis with syrup of ipecac is no longer

recommended given the potential for sudden decompensation and secondary aspiration.