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A Change of Pace: Sudden Hypotension
DIAGNOSTIC DILEMMA Thomas J. Marrie, MD, Section Editor
A Change of Pace: Sudden Hypotension Neal Yuan, MD,a Rabih M. Geha, MD,a Nelson B. Schiller, MDb Departments of aMedicine and bCardiology, University of California, San Francisco.
PRESENTATION A hospitalized patient was ready to go home when he developed a problem that proved unrelated to the illness for which he had been admitted. The 78-year-old man first presented after 2 weeks of dysuria and suprapubic pain. He had a history of chronic urinary incontinence and recurrent urinary tract infections. These were ascribed to a prostatectomy for prostate cancer. An artificial urinary sphincter had been placed to treat incontinence and reduce the frequency of infections. His medical history also included heart failure with mildly reduced ejection fraction and sick sinus syndrome, for which he had a dual-chamber pacemaker. He was admitted to the medicine service for a Proteus mirabilis lower urinary tract infection, and his symptoms diminished significantly after a 7-day course of intravenous antibiotics. On the day of the patient’s expected discharge, his supine blood pressure decreased precipitously from 110/70 mm Hg to 80/50 mm Hg. His heart rate decreased from 70 to 65 beats/min. He remained afebrile and was oxygenating well on room air. Although the patient reported that he was lightheaded, he denied constitutional symptoms, dysuria, urinary frequency, flank pain, nausea, chest pain, palpitations, or shortness of breath. He was in no apparent distress and was warm to the touch. His mental status was intact, his lungs were clear to auscultation, and his heart rate was regular and disclosed no murmurs, rubs, or gallops. He had no elevation in his jugular venous pressure, no evidence of edema, and no abdominal or flank tenderness.
ASSESSMENT The patient was given 2 L of intravenous crystalloid without improvement in his blood pressure. Repeat laboratory studies revealed that his creatinine level was newly elevated at 1.2 mg/dL from his baseline of 0.8 mg/dL. New Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to Neal Yuan, MD, 505 Parnassus Ave, Room 987, San Francisco, CA 94143-0119. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2017 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjmed.2017.03.026
elevations also were noted in his brain natriuretic peptide level, which had increased to 2562 pg/mL from 238 pg/mL on admission (normal, <100 pg/mL), and his serum troponin level, which was documented at 0.12 ng/mL (normal <0.10 ng/mL). The remainder of his laboratory values, including electrolyte levels, complete blood count parameters, and lactate level, remained within normal limits. A chest x-ray showed prominence of the pulmonary vasculature and interstitial edema. An electrocardiogram (ECG) revealed new right ventricular pacing compared with the ECG obtained on admission, which demonstrated sinus rhythm with premature atrial complexes (Figure). The patient remained hypotensive and was transferred to the intensive care unit. One concern was that his genitourinary hardware was the source of an untreated infection. He was given antibiotics that covered a broader spectrum of microorganisms and norepinephrine was started for blood pressure support. His central venous oxygen saturation was 75%. Computed tomography with contrast of the chest, abdomen, and pelvis revealed bilateral effusions and diffuse anasarca but no radiographic evidence of infection. An echocardiogram was ordered to evaluate for newly decompensated congestive heart failure. The patient’s ECG changes warranted consultation with the electrophysiology service. Interrogation of his pacemaker revealed a low battery, which had activated a battery-preserving setting called the “elective replacement interval.” This setting had switched the pacemaker mode from one that sensed and paced the right atrium and ventricle (DDD) to one that sensed and paced only the right ventricle (VVI). In addition, although the patient had been previously paced <1% of the time, his native heart rate had now spontaneously decreased below the pacemaker’s threshold of 65 beats/min, thereby triggering right ventricular lead pacing.
DIAGNOSIS The patient’s pacemaker was deactivated, restoring his native sinus rhythm. His blood pressure abruptly normalized so that he was weaned from his inotropic support. In this
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The American Journal of Medicine, Vol 130, No 7, July 2017
Figure (A) The ECG obtained on admission showed sinus rhythm with premature atrial complexes. (B) The ECG was repeated after right ventricular pacing.
way, right ventricular pacing was implicated as the cause of his hypotension (Video, available online). Review of a recent prior transthoracic echocardiogram ordered for the patient disclosed left ventricular diastolic dysfunction, moderate mitral regurgitation, and a dilated right ventricle with severe tricuspid regurgitation. These conditions made him particularly sensitive to both the atrioventricular and ventriculoventricular dyssynchrony that results from right ventricular pacing. Large randomized controlled trials have shown that patients with right ventricular pacing have higher rates of heart failure hospitalization and mortality when compared with those in sinus rhythm.1,2 Most evidence implicates ventriculoventricular dyssynchrony as the major contributor. Small studies examining the effects of better coordinated atrioventricular synchrony have found that correcting atrioventricular dyssynchrony, although able to reduce
mitral regurgitation, has not produced significant differences in clinical end points.3-5 To address the detrimental effects of right ventricular pacing, cardiac resynchronization therapy is pursued in select patients. Researchers who carried out a systematic review of dozens of clinical trials concluded that cardiac resynchronization therapy results in a greater likelihood of patients’ heart failure symptoms improving by at least 1 New York Heart Association (NYHA) class and in reductions in heart failure hospitalization and all-cause mortality.6 Current American College of Cardiology and American Heart Association guidelines make a strong recommendation for cardiac resynchronization therapy in patients with heart failure who have a left ventricular ejection fraction of 35% or less; sinus rhythm; NYHA class II, III, or ambulatory IV symptoms that are treated with guideline-directed medical therapy; left bundle branch block; and a QRS duration of 150 ms
Yuan et al
Sudden Hypotension
801
Table American College of Cardiology/American Heart Association Class I, IIa Recommendations for Cardiac Resynchronization Therapy in Systolic Heart Failure7 Class I; should be performed Patients with LVEF 35%, sinus rhythm, LBBB, QRS duration 150 ms, NYHA class II, III, or ambulatory IV symptoms on GDMT Class IIa; reasonable to perform Patients with LVEF 35%, sinus rhythm, LBBB, QRS duration 120-149 ms, NYHA class II, III, or ambulatory IV symptoms on GDMT Patients with LVEF 35%, sinus rhythm, non-LBBB pattern, QRS duration 150 ms, NYHA class III/ambulatory class IV symptoms on GDMT Patients with LVEF 35%, on GDMT, undergoing new or replacement device placement with anticipated requirement for significant (>40%) ventricular pacing Patients with atrial fibrillation, LVEF 35%, and on GDMT if they require ventricular pacing or otherwise meet CRT criteria and AV nodal ablation or pharmacologic rate control will allow w100% ventricular pacing with CRT Class IIb; may be considered Patients with LVEF 30%, ischemic heart failure, sinus rhythm, LBBB, QRS duration 150 ms, NYHA class I symptoms on GDMT Patients with LVEF 35%, sinus rhythm, non-LBBB pattern, QRS duration 120-149 ms, NYHA class III/ambulatory class IV symptoms on GDMT Patients with LVEF 35%, sinus rhythm, non-LBBB pattern, QRS duration 150 ms, NYHA class II symptoms on GDMT ACC ¼ American College of Cardiology; AHA ¼ American Heart Association; AV ¼ atrioventricular; CRT ¼ cardiac resynchronization therapy; GDMT ¼ goal-directed medical therapy; LBBB ¼ left bundle branch block; LVEF ¼ left ventricular ejection fraction; NYHA ¼ New York Heart Association.
or more.7 Weaker recommendations extend the use of cardiac resynchronization therapy to patients with these characteristics but no left bundle branch block and to patients with combinations of traits that include factors such as a QRS duration of 120 to 149 ms, planned insertion of a new or replacement device and an anticipated high (>40% of beats) ventricular pacing requirement, a less severe NYHA symptom class, or atrial fibrillation (Table). Although most of the evidence is derived from patients with severe systolic heart failure, recent research has begun building a stronger case for cardiac resynchronization therapy in pacemaker-dependent patients without a severely reduced left ventricular ejection fraction, such as the patient presented in this case.8,9
3.
4.
5.
6.
7.
MANAGEMENT The patient’s pacemaker was reprogrammed to a lower heart rate pacing threshold so that he could maintain his native sinus conduction. Because he had rarely required ventricular pacing previously and was unlikely to require prolonged ventricular pacing in the future, cardiac resynchronization therapy was not pursued. Antibiotics were discontinued.
References 1. Wilkoff BL, Cook JR, Epstein AE, et al; Dual Chamber and VVI Implantable Defibrillator Trial Investigators. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA. 2002;288:3115-3123. 2. Sweeney MO, Hellkamp AS, Ellenbogen KA, et al; MOde Selection Trial Investigators. Adverse effect of ventricular pacing on heart failure
8.
9.
and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation. 2003;107:2932-2937. Rossi R, Muia N Jr, Turco V, Sgura FA, Molinari R, Modena MG. Short atrioventricular delay reduces the degree of mitral regurgitation in patients with a sequential dual-chamber pacemaker. Am J Cardiol. 1997;80:901-905. Shinbane JS, Chu E, DeMarco T, et al. Evaluation of acute dual-chamber pacing with a range of atrioventricular delays on cardiac performance in refractory heart failure. J Am Coll Cardiol. 1997;30:1295-1300. Capucci A, Romano S, Puglisi A, et al. Dual chamber pacing with optimal AV delay in congestive heart failure: a randomized study. Europace. 1999;1:174-178. McAlister FA, Ezekowitz J, Hooton N, et al. Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction: a systematic review. JAMA. 2007;297:2502-2514. Tracy CM, Epstein AE, Darbar D, et al; American College of Cardiology Foundation; American Heart Association Task Force on Practice Guidelines; Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2012;126:1784-1800. Yu CM, Chan JY, Zhang Q, et al. Biventricular pacing in patients with bradycardia and normal ejection fraction. N Engl J Med. 2009;361: 2123-2134. Curtis AB, Worley SJ, Adamson PB, et al. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J Med. 2013;368: 1585-1593.
SUPPLEMENTARY DATA Supplementary video accompanying this article can be found in the online version at http://dx.doi.org/10.1016/j. amjmed.2017.03.026.
A Change of Pace: Sudden Hypotension Neal Yuan, MD,a Rabih M. Geha, MD,a Nelson B. Schiller, MDb Departments of aMedicine and bCardiology, University of California, San Francisco.
PRESENTATION A hospitalized patient was ready to go home when he developed a problem that proved unrelated to the illness for which he had been admitted. The 78-year-old man first presented after 2 weeks of dysuria and suprapubic pain. He had a history of chronic urinary incontinence and recurrent urinary tract infections. These were ascribed to a prostatectomy for prostate cancer. An artificial urinary sphincter had been placed to treat incontinence and reduce the frequency of infections. His medical history also included heart failure with mildly reduced ejection fraction and sick sinus syndrome, for which he had a dual-chamber pacemaker. He was admitted to the medicine service for a Proteus mirabilis lower urinary tract infection, and his symptoms diminished significantly after a 7-day course of intravenous antibiotics. On the day of the patient’s expected discharge, his supine blood pressure decreased precipitously from 110/70 mm Hg to 80/50 mm Hg. His heart rate decreased from 70 to 65 beats/min. He remained afebrile and was oxygenating well on room air. Although the patient reported that he was lightheaded, he denied constitutional symptoms, dysuria, urinary frequency, flank pain, nausea, chest pain, palpitations, or shortness of breath. He was in no apparent distress and was warm to the touch. His mental status was intact, his lungs were clear to auscultation, and his heart rate was regular and disclosed no murmurs, rubs, or gallops. He had no elevation in his jugular venous pressure, no evidence of edema, and no abdominal or flank tenderness.
ASSESSMENT The patient was given 2 L of intravenous crystalloid without improvement in his blood pressure. Repeat laboratory studies revealed that his creatinine level was newly elevated at 1.2 mg/dL from his baseline of 0.8 mg/dL. New Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to Neal Yuan, MD, 505 Parnassus Ave, Room 987, San Francisco, CA 94143-0119. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2017 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjmed.2017.03.026
elevations also were noted in his brain natriuretic peptide level, which had increased to 2562 pg/mL from 238 pg/mL on admission (normal, <100 pg/mL), and his serum troponin level, which was documented at 0.12 ng/mL (normal <0.10 ng/mL). The remainder of his laboratory values, including electrolyte levels, complete blood count parameters, and lactate level, remained within normal limits. A chest x-ray showed prominence of the pulmonary vasculature and interstitial edema. An electrocardiogram (ECG) revealed new right ventricular pacing compared with the ECG obtained on admission, which demonstrated sinus rhythm with premature atrial complexes (Figure). The patient remained hypotensive and was transferred to the intensive care unit. One concern was that his genitourinary hardware was the source of an untreated infection. He was given antibiotics that covered a broader spectrum of microorganisms and norepinephrine was started for blood pressure support. His central venous oxygen saturation was 75%. Computed tomography with contrast of the chest, abdomen, and pelvis revealed bilateral effusions and diffuse anasarca but no radiographic evidence of infection. An echocardiogram was ordered to evaluate for newly decompensated congestive heart failure. The patient’s ECG changes warranted consultation with the electrophysiology service. Interrogation of his pacemaker revealed a low battery, which had activated a battery-preserving setting called the “elective replacement interval.” This setting had switched the pacemaker mode from one that sensed and paced the right atrium and ventricle (DDD) to one that sensed and paced only the right ventricle (VVI). In addition, although the patient had been previously paced <1% of the time, his native heart rate had now spontaneously decreased below the pacemaker’s threshold of 65 beats/min, thereby triggering right ventricular lead pacing.
DIAGNOSIS The patient’s pacemaker was deactivated, restoring his native sinus rhythm. His blood pressure abruptly normalized so that he was weaned from his inotropic support. In this
800
The American Journal of Medicine, Vol 130, No 7, July 2017
Figure (A) The ECG obtained on admission showed sinus rhythm with premature atrial complexes. (B) The ECG was repeated after right ventricular pacing.
way, right ventricular pacing was implicated as the cause of his hypotension (Video, available online). Review of a recent prior transthoracic echocardiogram ordered for the patient disclosed left ventricular diastolic dysfunction, moderate mitral regurgitation, and a dilated right ventricle with severe tricuspid regurgitation. These conditions made him particularly sensitive to both the atrioventricular and ventriculoventricular dyssynchrony that results from right ventricular pacing. Large randomized controlled trials have shown that patients with right ventricular pacing have higher rates of heart failure hospitalization and mortality when compared with those in sinus rhythm.1,2 Most evidence implicates ventriculoventricular dyssynchrony as the major contributor. Small studies examining the effects of better coordinated atrioventricular synchrony have found that correcting atrioventricular dyssynchrony, although able to reduce
mitral regurgitation, has not produced significant differences in clinical end points.3-5 To address the detrimental effects of right ventricular pacing, cardiac resynchronization therapy is pursued in select patients. Researchers who carried out a systematic review of dozens of clinical trials concluded that cardiac resynchronization therapy results in a greater likelihood of patients’ heart failure symptoms improving by at least 1 New York Heart Association (NYHA) class and in reductions in heart failure hospitalization and all-cause mortality.6 Current American College of Cardiology and American Heart Association guidelines make a strong recommendation for cardiac resynchronization therapy in patients with heart failure who have a left ventricular ejection fraction of 35% or less; sinus rhythm; NYHA class II, III, or ambulatory IV symptoms that are treated with guideline-directed medical therapy; left bundle branch block; and a QRS duration of 150 ms
Yuan et al
Sudden Hypotension
801
Table American College of Cardiology/American Heart Association Class I, IIa Recommendations for Cardiac Resynchronization Therapy in Systolic Heart Failure7 Class I; should be performed Patients with LVEF 35%, sinus rhythm, LBBB, QRS duration 150 ms, NYHA class II, III, or ambulatory IV symptoms on GDMT Class IIa; reasonable to perform Patients with LVEF 35%, sinus rhythm, LBBB, QRS duration 120-149 ms, NYHA class II, III, or ambulatory IV symptoms on GDMT Patients with LVEF 35%, sinus rhythm, non-LBBB pattern, QRS duration 150 ms, NYHA class III/ambulatory class IV symptoms on GDMT Patients with LVEF 35%, on GDMT, undergoing new or replacement device placement with anticipated requirement for significant (>40%) ventricular pacing Patients with atrial fibrillation, LVEF 35%, and on GDMT if they require ventricular pacing or otherwise meet CRT criteria and AV nodal ablation or pharmacologic rate control will allow w100% ventricular pacing with CRT Class IIb; may be considered Patients with LVEF 30%, ischemic heart failure, sinus rhythm, LBBB, QRS duration 150 ms, NYHA class I symptoms on GDMT Patients with LVEF 35%, sinus rhythm, non-LBBB pattern, QRS duration 120-149 ms, NYHA class III/ambulatory class IV symptoms on GDMT Patients with LVEF 35%, sinus rhythm, non-LBBB pattern, QRS duration 150 ms, NYHA class II symptoms on GDMT ACC ¼ American College of Cardiology; AHA ¼ American Heart Association; AV ¼ atrioventricular; CRT ¼ cardiac resynchronization therapy; GDMT ¼ goal-directed medical therapy; LBBB ¼ left bundle branch block; LVEF ¼ left ventricular ejection fraction; NYHA ¼ New York Heart Association.
or more.7 Weaker recommendations extend the use of cardiac resynchronization therapy to patients with these characteristics but no left bundle branch block and to patients with combinations of traits that include factors such as a QRS duration of 120 to 149 ms, planned insertion of a new or replacement device and an anticipated high (>40% of beats) ventricular pacing requirement, a less severe NYHA symptom class, or atrial fibrillation (Table). Although most of the evidence is derived from patients with severe systolic heart failure, recent research has begun building a stronger case for cardiac resynchronization therapy in pacemaker-dependent patients without a severely reduced left ventricular ejection fraction, such as the patient presented in this case.8,9
3.
4.
5.
6.
7.
MANAGEMENT The patient’s pacemaker was reprogrammed to a lower heart rate pacing threshold so that he could maintain his native sinus conduction. Because he had rarely required ventricular pacing previously and was unlikely to require prolonged ventricular pacing in the future, cardiac resynchronization therapy was not pursued. Antibiotics were discontinued.
References 1. Wilkoff BL, Cook JR, Epstein AE, et al; Dual Chamber and VVI Implantable Defibrillator Trial Investigators. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA. 2002;288:3115-3123. 2. Sweeney MO, Hellkamp AS, Ellenbogen KA, et al; MOde Selection Trial Investigators. Adverse effect of ventricular pacing on heart failure
8.
9.
and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation. 2003;107:2932-2937. Rossi R, Muia N Jr, Turco V, Sgura FA, Molinari R, Modena MG. Short atrioventricular delay reduces the degree of mitral regurgitation in patients with a sequential dual-chamber pacemaker. Am J Cardiol. 1997;80:901-905. Shinbane JS, Chu E, DeMarco T, et al. Evaluation of acute dual-chamber pacing with a range of atrioventricular delays on cardiac performance in refractory heart failure. J Am Coll Cardiol. 1997;30:1295-1300. Capucci A, Romano S, Puglisi A, et al. Dual chamber pacing with optimal AV delay in congestive heart failure: a randomized study. Europace. 1999;1:174-178. McAlister FA, Ezekowitz J, Hooton N, et al. Cardiac resynchronization therapy for patients with left ventricular systolic dysfunction: a systematic review. JAMA. 2007;297:2502-2514. Tracy CM, Epstein AE, Darbar D, et al; American College of Cardiology Foundation; American Heart Association Task Force on Practice Guidelines; Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2012;126:1784-1800. Yu CM, Chan JY, Zhang Q, et al. Biventricular pacing in patients with bradycardia and normal ejection fraction. N Engl J Med. 2009;361: 2123-2134. Curtis AB, Worley SJ, Adamson PB, et al. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J Med. 2013;368: 1585-1593.
SUPPLEMENTARY DATA Supplementary video accompanying this article can be found in the online version at http://dx.doi.org/10.1016/j. amjmed.2017.03.026.