eMedicine Specialties > Cardiology > Arrhythmias

Sudden Cardiac Death: Differential Diagnoses & Workup

Author: Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Coauthor(s): Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago; Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, Division of Cardiology, University of California, Los Angeles School of Medicine; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Contributor Information and Disclosures

Updated: Oct 21, 2009

Differential Diagnoses

Aortic Stenosis
Tetralogy of Fallot
Cardiomyopathy, Dilated
Torsade de Pointes
Cardiomyopathy, Hypertrophic
Ventricular Fibrillation
Coronary Artery Atherosclerosis
Ventricular Premature Complexes
Ebstein Anomaly
Ventricular Tachycardia
Lown-Ganong-Levine Syndrome
Wolff-Parkinson-White Syndrome
Myocardial Infarction
Myocardial Ischemia

Other Problems to Be Considered

Arrhythmogenic RV dysplasia
Brugada syndrome

Workup

Laboratory Studies

  • Cardiac enzymes (creatine kinase, myoglobin, troponin): Elevations in these enzyme levels may indicate ischemia and MI. The extent of myocardial damage usually can be correlated to the extent of elevation in the enzyme levels. Patients are at increased risk for arrhythmia in the peri-infarct period.
  • Electrolytes, calcium, and magnesium: Severe metabolic acidosis, hypokalemia, hyperkalemia, hypocalcemia, and hypomagnesemia are some of the conditions that can increase the risk for arrhythmia and sudden death.
  • Quantitative drug levels (quinidine, procainamide, tricyclic antidepressants, digoxin): Drug levels higher than the levels indicated in the therapeutic index may have a proarrhythmic effect. Subtherapeutic levels of these drugs in patients being treated for specific cardiac conditions also can lead to an increased risk for arrhythmia. Most of the antiarrhythmic medications also have a proarrhythmic effect.
  • Toxicology screen: Looking for drugs, such as cocaine, that can lead to vasospasm-induced ischemia is warranted if suspicion exists. Obtaining levels of drugs (antiarrhythmics) also may be warranted.
  • Thyroid-stimulating hormone: Hyperthyroidism can lead to tachycardia and tachyarrhythmias. Over a period of time, it also can lead to heart failure. Hypothyroidism can lead to QT prolongation.
  • Brain natriuretic peptide (BNP): BNP has predictive value especially in post MI patients and in patients with heart failure. Although preliminary and not conclusive, emerging data support the notion that an elevated BNP level may provide prognostic information on the risk of SCD, independent of clinical information and LVEF.

Imaging Studies

  • Chest radiography: This may reveal whether someone is in congestive heart failure. It also can show signs suggesting LV enlargement or RV enlargement. Signs of pulmonary hypertension also may be evident on the chest radiograph.
  • Echocardiography: Two-dimensional echocardiography with Doppler is essential in the evaluation of SCD. A number of studies have demonstrated that the use of 2-dimensional echocardiogram to evaluate left wall motion abnormalities after an acute MI (using the LV wall-motion score index) is useful in predicting the risk for major cardiac events, including sudden death. A decrease in the ejection fraction and worsening wall motion abnormalities upon exercise echocardiography in patients who have had an MI has been suggested to confer increased risk of cardiac death.
  • Nuclear imaging techniques: Resting thallium or technetium-99m scintigraphy is helpful in assessing myocardial damage after MI. A larger defect has been associated with greater risk for future cardiac events. Exercise nuclear scintigraphy is very sensitive for detecting the presence, extent, and location of myocardial ischemia. Gibson et al found that pharmacologic-stress nuclear (dipyridamole or adenosine) scintigraphy was better than submaximal exercise ECG and coronary angiography in predicting cardiac death and other cardiac events. These tests can be very helpful in patients with low functional capacity such as chronic obstructive pulmonary disease, peripheral vascular disease, or orthopedic problems. The Multi-Center Post-Infarction Research Group provided evidence that resting ejection fraction was the most important noninvasive predictor of SCD and other cardiac events in patients with MI.

Other Tests

  • Electrocardiogram: This study is indicated in all patients. Evidence of MI, prolonged QT interval, short QT interval, epsilon wave, Brugada sign, short PR, a WPW pattern, or other conditions should be sought.
  • Signal-averaged ECG (SAECG) has been variably reported to be useful in analysis of patients with SCD. What may be more useful is analysis of T wave alternans in patients with VT, VF, and/or SCD. Small changes in T amplitude are not detected in 12-lead ECG. Microvolt T wave alternans (MTWA) amplifies the alternans and may be used in the workup to predict the risk of SCD. However, to date, the use of T wave alternans to predict which patients with ischemic or nonischemic cardiomyopathy would benefit from ICD placement has not been conclusive.
  • Genetic testing: The value of genetic testing in conditions such as congenital long QT and HCM is still being evaluated. Some studies have recommended the testing of siblings and close relatives of people with SCD due to these conditions.

Procedures

  • Coronary angiography: Perform cardiac catheterization in patients who survive SCD to assess the state of ventricular function and the severity and extent of CAD.
    • The number of vessels with severe obstruction and the degree of LV dysfunction are important variables in predicting cardiac events. Ejection fraction is the best predictor of significant cardiac events and survival.
    • Coronary angiography also can help identify coronary anomalies and other forms of congenital heart disease.
    • Angiography is performed with the aim of identifying patients who may benefit from revascularization. Revascularization is indicated when ischemic myocardium is present as the underlying substrate of VT/VF.
  • Electrophysiology studies: In targeted patients, EPS play diagnostic, prognostic, and therapeutic roles. EPS usually are performed after ischemic and structural heart disease has been diagnosed and addressed. These studies have been used to identify patients who have inducible versus noninducible sustained monomorphic VT. The presence of inducible sustained VT, at baseline or when the patient is on antiarrhythmic medications, confers a higher risk for sudden death. Significantly lower ventricular function also has been observed in patients with inducible sustained VT. Inducible bundle-branch reentrant VT can be seen in patients with DCM and in the postoperative period after valvular replacement. As many as 20% of patients with HCM have inducible sustained monomorphic VT. The identification of accessory pathways also is possible with these studies. EPS are performed with an eye toward the following:
    • Ablation of VT foci, eg, bundle branch VT, RVOT VT, and some cases of idiopathic LV tachycardia
    • ICD implantation, which is generally the case in survivors of SCD

More on Sudden Cardiac Death

Overview: Sudden Cardiac Death
Differential Diagnoses & Workup: Sudden Cardiac Death
Treatment & Medication: Sudden Cardiac Death
Follow-up: Sudden Cardiac Death
Multimedia: Sudden Cardiac Death
References
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Further Reading

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Keywords

cardiac arrest, sudden cardiac death, cardiac arrhythmias, heart attack, myocardial infarction, heart failure, cardiac disease, coronary artery disease, coronary heart disease, congestive heart failure

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Contributor Information and Disclosures

Author

Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians and American Heart Association
Disclosure: Nothing to disclose.

Coauthor(s)

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, Division of Cardiology, University of California, Los Angeles School of Medicine; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Arnold S Baas, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, and American Society of Echocardiography
Disclosure: Pfizer Honoraria Speaking and teaching

Medical Editor

Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx  Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

 
 
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