Hypertension is a common chronic medical condition affecting over 65 million Americans. Uncontrolled hypertension can progress to a hypertensive crisis defined as a systolic blood pressure >180 mm Hg or a diastolic blood pressure >120 mm Hg. Hypertensive crisis can be further classified as a hypertensive urgency or hypertensive emergency depending on end-organ involvement including cardiac, renal, and neurologic injury. The prompt recognition of a hypertensive emergency with the appropriate diagnostic tests and triage will lead to the adequate reduction of blood pressure, ameliorating the incidence of fatal outcomes. Severely hypertensive patients with acute end-organ damage (hypertensive emergencies) warrant admission to an intensive care unit for immediate reduction of blood pressure with a short-acting titratable intravenous antihypertensive medication. Hypertensive urgencies (severe hypertension with no or minimal end-organ damage) may in general be treated with oral antihypertensives as an outpatient. Rapid and short-lived intravenous medications commonly used are labetalol, esmolol, fenoldopam, nicardipine, sodium nitroprusside, and clevidipine. Medications such as hydralazine, immediate release nifedipine, and nitroglycerin should be avoided. Sodium nitroprusside should be used with caution because of its toxicity. The risk factors and prognosticators of a hypertensive crisis are still under recognized. Physicians should perform complete evaluations in patients who present with a hypertensive crisis to effectively reverse, intervene, and correct the underlying trigger, as well as improve long-term outcomes after the episode.

F lecainide, encainide, and propafenone, all class IC antiarrhythmic drugs, have been shown to increase the pacing threshold, from 300% to more than 560%, 1-3 by modifying the action potential of the myocardial cell and interfering with the sodium channel in depressing the phase 0 repolarization. Flecainide blocks flow of the cardiac NaV1.5 sodium channel, slowing the upstroke and prolonging the cardiac action potential with minimal effect on repolarization. This drug is known to have a narrow therapeutic index.Aside from medications, hyperkalemia may result in failure of atrial and/or ventricular 4-6 pacemaker capture. The electrocardiograph in hyperkalemia often shows widening of the paced QRS complex. The increased atrial and/or ventricular pacing threshold may lead to loss of capture. 7 This is worsened by concomitant electrolyte imbalances, acid-base disorders, hypoxemia, and the intracellular-extracellular gradient.We report a case of capture loss in the setting of a combination of mild hyperkalemia and mild flecainide toxicity. Case RePoRtAn 88-year-old woman with a dual chamber (DDD) pacemaker for sick sinus syndrome presented after 3 syncopal episodes within 24 hours: 2 episodes at home and 1 witnessed in the ambulance. Medical history was significant for type 2 diabetes, hypertension, hyperlipidemia, and chronic kidney disease. Medications included flecainide 100 mg twice daily (for 5 years), metoprolol XL 200 mg daily, and aspirin.Vital signs on presentation were recorded as "irregular at a heart rate of 73 bpm," and blood pressure was 50/30 mm Hg. Physical examination was unremarkable. Admission laboratory reports showed creatinine 2.3 mg/dL, blood urea nitrogen 80 mg/dL (baseline renal function 5 months previously showed creatinine 1.1 mg/dL and blood urea nitrogen 26 mg/ dL), potassium 5.6 mmol/L (prior values ranged from 3.5 to 4.7 mmol/L), and an estimated glomerular filtration rate (GFR) 21 mL/min/1.73 m 2 (prior estimated GFR was 50 mL/min/1.73 m 2 ). Serum flecainide concentration was 1.3 µg/mL (reported therapeutic range, 0.2-1 µg/mL). 8 Monitor strips (timed 23:10) from the ambulance ( Figure 1A) demonstrate an initial sine wave with pacemaker spikes, a classic pattern for class IC toxicity. 9 The wide complex rhythm stops, and regular pacing spikes fail to capture. Intermittent capture returns (asterisk in Figure 1A), with grouped beating consistent with pacing-exit Wenckebach periodicity.Initially, there appears to be 3:2 exit Wenckebach, 4:3, and then 5:4 periodicity. A 12-lead electrocardiogram ( Figure 1B) obtained 7 hours later revealed a ventricular paced rhythm with very wide QRS complexes (240 milliseconds) and moderately peaked T waves.Flecainide was discontinued, and hyperkalemia was corrected to 4.0 mmol/L using 15 g of sodium polystyrene sulfonate and 4.65 mEq of intravenous

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