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4 EKG Abnormalities: What Are the Lifesaving Diagnoses?

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4 EKG Abnormalities: What Are the Lifesaving Diagnoses? CASE c Nathaniel J. Ward, MD; Clinton J. Fox, MD; 4 EKG abnormalities: Kevin S. Kralik, MD; Samir Haydar, DO, MPH, FACEP; John R. Saucier, What are the MD, FACEP Tufts University School of Medicine, Maine Medical lifesaving diagnoses? Center, Department of Emergency Medicine, Portland These conditions may not have [email protected] associated findings on physical The authors reported no potential conflict of interest exam. See if you can make the relevant to this article. diagnosis based on the EKG tracings. hen evaluating a patient with a history of chest PracTIce pain, palpitations, syncope, and/or new-onset recommendaTIons W seizures, an electrocardiogram (EKG) may be the › Consider placement of an key to identifying a potentially life-threatening condition. automatic implantable Here we present 4 cases in which EKG findings were the clue cardioverter-defibrillator to underlying medical conditions that, if left untreated, could for all patients with a type be fatal. Because each of these conditions may not have asso- 1 Brugada pattern on EKG ciated findings on a physical exam, early recognition of these accompanied by syncope, EKG findings can be lifesaving. documented ventricular arrhythmia, or aborted c sudden cardiac death. B CASE 1 A 15-year-old boy suddenly collapses while walking, and bystanders report seizure-like activity. The patient doesn’t › Always look for EKG remember the event. Vital signs and physical exam are normal, findings suggestive of Wolff- and his blood glucose level is 86 mg/dL (normal: 70-100 mg/dL). Parkinson-White syndrome in otherwise healthy patients He doesn’t take any medications and denies illicit drug use or presenting with syncope. C recent illness. What EKG abnormality (FIGURE 1) likely explains the cause › Refer all patients with of the patient’s collapse? suspected hypertrophic cardiomyopathy to Cardi- z ology for a transthoracic The EKG abnormality and diagnosis. The patient’s echocardiogram. B EKG revealed a prolonged QT interval (FIGURE 1, BrackeTS). His QTc (QT interval corrected for heart rate) was .470 sec- Strength of recommendation (SOR) onds, which is at the high end of the normal range for his A Good-quality patient-oriented age and gender.1 The patient had no family history of syn- evidence B Inconsistent or limited-quality cope, sudden cardiac death (SCD), or seizure disorder. patient-oriented evidence Evaluation uncovered a calcium level of 4.4 mEq/L (normal: C Consensus, usual practice, opinion, disease-oriented 4.5-5.5 mEq/L) and a phosphate level of 7.8 mg/dL (normal: evidence, case series 2.4-4.1 mg/dL). This patient had a low parathyroid hormone from pri- mary hypoparathyroidism. His conduction abnormality was treated with both oral calcium and vitamin D supplements. 368 THE JOURNAL OF FAMILY PRACTICE | JULY 2014 | VOL 63, NO 7 FIGURE 1 Case 1: 15-year-old boy, syncopal episode z Etiology and epidemiology. A pro- activity (in LQTS1). They likely are caused by longed QT interval may be the result of a torsades de pointes and ventricular fibrilla- primary long QT syndrome (LQTS) or an ac- tion. A brief aura may precede these arrhyth- A common error quired condition from electrolyte imbalance, mias, and patients may experience urinary or in measuring medication effect, or toxin exposure. fecal incontinence.5 the QT interval In the United States, the incidence of The key to making a diagnosis of LQTS occurs when a genetic mutation that causes LQTS is 1 in is correctly measuring the QT interval. The physicians 2500 people.2 Patients with LQTS usually re- QT interval is measured from the beginning inadvertently main asymptomatic unless the QT interval is of the Q-wave to the end of the T-wave as include a further prolonged by a condition or medica- measured from the intersection of a line tan- U-wave in the tion. There are several hundred congenital gent to the downslope of the T-wave and the measurement. LQTS subtypes based on specific ion channel isoelectric line. This can be difficult to deter- defects; the most common is LQTS1, with an mine in EKGs showing bundle branch block inherited defect in the KCNQ1 gene, which or an irregular rhythm, such as atrial fibril- regulates the slow potassium ion channel. Acquired LQTS is much more common than congenital LQTS.3 Many drugs have TaBle 1 been linked to an increased risk of LQTS, in- Medications that can prolong cluding certain antiarrhythmics, antibiotics, the QTc interval4 and antipsychotics (TABLE 1).4 In addition, electrolyte disturbances such as hypokale- Amiodarone mia, hypocalcemia, and hypomagnesemia Azithromycin can be etiologic factors. Chloroquine Be aware that an acquired LQTS may mask an underlying congenital LQTS. There- Chlorpromazine fore, patients in whom the offending agent Droperidol or condition is corrected should still have a Haloperidol follow-up EKG. Screening family members Methadone for LQTS is worthwhile, even in those with- out symptoms. Moxifloxacin I MA z G Clinical features. Patients with symp- Ondansetron E © JOE tomatic LQTS may have dizziness, palpita- Procainamide G tions, and syncope. SCD also is possible. ORMAN Sotalol These signs and symptoms may be triggered by strong emotions (in LQTS2) or physical Thioridazine JFPONLINE.COM VOL 63, NO 7 | JULY 2014 | THE JOURNAL OF FAMILY PRACTICE 369 FIGURE 2 Case 2: 14-year-old boy, syncopal episode with fever lation (AF).6,7 A common error in measuring dure can be used instead of, or in addition the QT interval occurs when clinicians inad- to, beta-blockers. If the patient’s syncope First rule out or vertently include a U-wave in the measure- persists, AICDs are an option. AICDs can be treat any causes ment.1 Some EKG machines may provide QT lifesaving, but patients run the risk of adverse of acquired interval and QTc measurements. Normal QT effects that include inappropriate shocks and LQTS by taking intervals are ≤.450 seconds for men and ≤.470 infection.10 As the result of these therapies, a medication seconds for women.8 mortality associated with LQTS has dropped history and It is essential to confirm the QT inter- to approximately 1%.11 evaluating val by using the Bazett formula (QTc equals the patient's the QT in seconds divided by the square CASE 2 c A 14-year-old boy has a syncopal electrolytes. root of the RR interval in seconds) for all pa- episode while at rest. A similar event oc- tients with a history that suggests a possible curred 3 years earlier; at that time, an echocar- arrhythmia. diogram and EKG were normal. For 2 days, he’s Our patient had hypocalcemia, which had a cough and low-grade fever. His tempera- on an EKG can cause T-wave widening with ture is 102ºF and he has a productive cough. a normal ST segment, rather than a normal Based on this EKG (FIGURE 2), what is the T-wave with a long ST segment, as is typically likely diagnosis? What is the significance of his seen in LQTS. This distinction may be diffi- fever? cult to discern and should not preclude the search for either an acquired prolonged QTc z The EKG abnormality and diagnosis. or an underlying LQTS.9 This patient’s EKG showed a type 1 Brugada z Treatment. First rule out or treat any pattern (FIGURE 2, ARROWS), which strongly causes of acquired LQTS by taking a careful supported the diagnosis of Brugada syn- medication history and evaluating the pa- drome (BS). BS is an inherited condition tient’s electrolytes. Once these have been ad- caused by a genetic defect in cardiac ion dressed, a beta-blocker is first-line therapy channel function that leads to characteristic for symptomatic patients.5 EKG changes and a predisposition to ventric- Unfortunately, up to 20% of individuals ular fibrillation.12 In this case, the fever likely treated with beta-blockers may continue to unmasked these EKG findings. have syncope.5 For these patients, options in- The patient was transferred to a local hos- clude a left cardiac sympathetic denervation pital for treatment of community-acquired (LCSD) or placement of an automatic im- pneumonia, and ultimately received an AICD. plantable cardioverter-defibrillator (AICD). z Etiology and epidemiology. BS was An LCSD involves removal of the left-sided first described in 199213 and is a major cause stellate and/or thoracic ganglia. This proce- of SCD, responsible for up to 4% of all cases 370 THE JOURNAL OF FAMILY PRACTICE | JULY 2014 | VOL 63, NO 7 4 EKG abNORMALITIES FIGURE 3 Case 3: 21-year-old man, light-headedness, then syncope of SCD, and 20% of cases of patients without The most concerning outcome of BS is structural heart disease.14 BS is more com- ventricular fibrillation. The estimated annual mon in men, and the mean age of diagnosis rate of cardiac events is 7.7% among patients Management is 40 to 45.15-18 who have experienced an aborted SCD, 1.9% of asymptomatic Mutations in at least 17 cardiac ion among those who have experienced syncope, patients with channel genes have been linked to BS.19 The and 0.5% in asymptomatic patients.18 type 1 Brugada SCN5A gene—a cardiac sodium channel— z Treatment. The only effective treat- pattern remains is the most commonly implicated, but ac- ment for BS is placement of an AICD; how- controversial counts for only 11% to 24% of all BS cases.15 ever, complications of AICD placement cause because the rate z Clinical features. Patients with BS may significant morbidity.6 Ten years after AICD of cardiac events present with syncope, nocturnal agonal res- placement, 37% of patients experienced inap- is low, although pirations, or ventricular arrhythmias.12 EKG propriate shocks and 29% experienced lead such events can findings include partial or complete right failure.22 Recent modifications in device pro- be fatal.
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