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Atropine resistant bradycardia and hyperkalemia: our experiences
Correspondence / American Journal of Emergency Medicine 31 (2013) 1410–1417 [15] Wolff V, et al. Cannabis-related stroke: myth or reality? Stroke 2013;44:558–63. [16] Duchene C, et al. Cannabis-induced cerebral and myocardial infarction in a young woman. Rev Neurol (Paris) 2010;166:438–42. [17] Singh NN, Pan Y, Muengtaweeponsa S, Geller TJ, Cruz-Flores S. Cannabis-related stroke: case series and review of literature. J Stroke Cerebrovasc Dis 2012;21: 555–60.
Atropine resistant bradycardia and hyperkalemia: our experiences☆,☆☆
Subramanian Senthilkumaran MD Department of Emergency & Critical Care Medicine, Sri Gokulam Hospitals & Research Institute, Salem-636004, Tamil Nadu, India E-mail address: [email protected] Suresh S. David MS Department of Emergency Medicine, Christian Medical College and Hospital, Vellore, India Rishya Manikam MD Department of Emergency Medicine, University Malaya Kuala Lumpur, Malaysia
To the Editor, We read the report of Srivali et al [1] with great interest and wish to share our experiences with atropine-resistant bradycardia. Symptomatic bradycardia is a frequent presentation in the emergency department (ED), although the causes may not readily be demonstrable during the early phase of management. Invariably, atropine is administered to treat such cases, and many respond well. However, a few continue to have persistent symptomatic bradycardia and are often referred for temporary cardiac pacing. Bradycardia secondary to hyperkalemia is a frequently overlooked electrocardiographic (ECG) finding [2]. Here, we wish to share some of the clinical characteristics of 55 cases of symptomatic bradycardia referred to our ED over a period of 2 years. None were on β-blockers, verapamil, digoxin, or any poisoning. In this population, maximal dosage of atropine failed to enhance the heart rate significantly in 11. The mean age of nonresponders was 52.3 years (SD, 10.3) with male preponderance and was similar to those who responded to atropine. Heart rate at presentation varied from 30 to 48, and the initial ECG findings were junctional rhythm in 5, sinus rhythm in 4, and nonspecific in 2 others. Serum potassium level varied from 6.4 to 8 with a median of 6.8 mEq/dL. Of 11, 9 improved within 10 to 15 minutes after commencement of antihyperkalemic therapy. Urgent hemodialysis was carried out in 2 patients (4%). Discharge diagnoses was “adverse drug effect” and attributable to angiotensinconverting enzyme inhibitors, potassium-sparing diuretics, and Cyclooxygenase-2 inhibitors in 8, 2, and 1, respectively. Hyperkalemia causes various ECG changes including shortening of QT interval to asystole. However, these patterns may not correlate clinically or with the serum potassium levels [3]. Absence of ECG changes despite markedly elevated serum potassium [4] was noticed in patients with renal insufficiency. Therapeutic agents have been noted to be a major cause for hyperkalemia in 35% to 75% of hospitalized patients [5], and some of them were on a combination of angiotensin-converting enzyme inhibitors with potassium-sparing diuretics or potassium supplements. Hyperkalemia reduces myocardial excitability, suppresses Sinoatrial node activity, and blocks the conduction at the Atrioventricular node, which eventually attenuates the response to atropine. Slade et al [6] reported 2 cases of atropine-resistant bradycardia due to hyperkalemia and suggested rapid bedside assessment of potassium by arterial blood gas analyzer in the ED and ensure early intervention. From the point of patient safety, hyperkalemia needs to be investigated, in those receiving hyperkalemia-prone therapeutic agents, and considered at as a bedside investigation, if the pulse rate reduces significantly. Hyperkalemia may also manifest without ECG changes. Therefore, timely recognition and intervention not only avoid referral but also avert expensive pacemaker therapy. Interestingly, the etiology for predilection toward hyperkalemia and the frequent absence of ECG changes in such individuals warrant further exploration. Emergency physicians shall remember that bradycardia is not always a primary cardiac issue and, hence, consider or suspect hyperkalemia for bradyarrhythmia, if not responding to atropine or failure to capture the beat, in the absence of other demonstrable causes. ☆ Financial support: Nil. ☆☆ Conflict of interest: Nil.
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Ponniah Thirumalaikolundusubramanian MD Department of Internal Medicine, Chennai Medical College and Research Center, Irungalur, Trichy, India http://dx.doi.org/10.1016/j.ajem.2013.06.020 References [1] Srivali N, Ratanapo S, Cheungpasitporn W, Chongnarungsin D, Bischof EF. Hyperkalemia-induced pacemaker dysfunction. Am J Emerg Med 2013;31:879–80. [2] Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalaemia. Am J Emerg Med 2000;18:721–9. [3] Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008;3:324–30. [4] Aslam S, Friedman EA, Ifudu O. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients. Nephrol Dial Transplant 2002;17:1639–42. [5] Stevens MS, Dunlay RW. Hyperkalemia in hospitalized patients. Int Urol Nephrol 2000;32:177–80. [6] Slade TJ, Grover J, Benger J. Atropine-resistant bradycardia due to hyperkalaemia. Emerg Med J 2008;25:611–2.
Takotsubo syndrome and chest pain units☆ To the Editor, Patients presenting with suspected takotsubo syndrome (TTS) are mostly evaluated by emergency department (ED) physicians, except if such illness occurs in the already hospitalized patients, admitted for a diverse array of medical/surgical conditions or in the setting of diagnostic and therapeutic procedures or perioperatively. Because the most prevalent presenting symptom of patients with suspected TTS is chest pain, which is indistinguishable from the one experienced with an acute coronary syndrome (ACS), such patients may be admitted and observed in chest pain units (CPUs) [1-4]. Such CPUs staffed by ED physicians, with available prompt consultation by a cardiologist at the discretion of the ED physicians, provide for admission, observation, and triage of patients with chest pain, most of whom do not have ACS but noncardiac chest pain. Some of the patients presenting with chest pain turn out to have TTS, and such occurrences are being identified with accelerating frequency [5]. The crux of the matter, in reference to differential diagnosis of ACS and TTS, is to distinguish anterior STelevation myocardial infarction (a subtype of ACS) from TTS because the former requires expeditious referral for coronary revascularization, with thrombolysis and preferably percutaneous coronary intervention, whereas the latter is managed currently with nonspecific supportive (based on symptoms) therapies [5]. Patients with both syndromes show ST-elevations primarily in precordial electrocardiographic (ECG) leads in their admission ECG, but this diagnostic modality does not appear to differentiate between the 2 [5,6]. What is being currently done, besides obtaining a targeted history and performing a focused physical examination, is to record the ECG and sample for blood biomarker
☆ Disclosures: The author has disclosed no conflicts of interest.
Atropine resistant bradycardia and hyperkalemia: our experiences☆,☆☆
Subramanian Senthilkumaran MD Department of Emergency & Critical Care Medicine, Sri Gokulam Hospitals & Research Institute, Salem-636004, Tamil Nadu, India E-mail address: [email protected] Suresh S. David MS Department of Emergency Medicine, Christian Medical College and Hospital, Vellore, India Rishya Manikam MD Department of Emergency Medicine, University Malaya Kuala Lumpur, Malaysia
To the Editor, We read the report of Srivali et al [1] with great interest and wish to share our experiences with atropine-resistant bradycardia. Symptomatic bradycardia is a frequent presentation in the emergency department (ED), although the causes may not readily be demonstrable during the early phase of management. Invariably, atropine is administered to treat such cases, and many respond well. However, a few continue to have persistent symptomatic bradycardia and are often referred for temporary cardiac pacing. Bradycardia secondary to hyperkalemia is a frequently overlooked electrocardiographic (ECG) finding [2]. Here, we wish to share some of the clinical characteristics of 55 cases of symptomatic bradycardia referred to our ED over a period of 2 years. None were on β-blockers, verapamil, digoxin, or any poisoning. In this population, maximal dosage of atropine failed to enhance the heart rate significantly in 11. The mean age of nonresponders was 52.3 years (SD, 10.3) with male preponderance and was similar to those who responded to atropine. Heart rate at presentation varied from 30 to 48, and the initial ECG findings were junctional rhythm in 5, sinus rhythm in 4, and nonspecific in 2 others. Serum potassium level varied from 6.4 to 8 with a median of 6.8 mEq/dL. Of 11, 9 improved within 10 to 15 minutes after commencement of antihyperkalemic therapy. Urgent hemodialysis was carried out in 2 patients (4%). Discharge diagnoses was “adverse drug effect” and attributable to angiotensinconverting enzyme inhibitors, potassium-sparing diuretics, and Cyclooxygenase-2 inhibitors in 8, 2, and 1, respectively. Hyperkalemia causes various ECG changes including shortening of QT interval to asystole. However, these patterns may not correlate clinically or with the serum potassium levels [3]. Absence of ECG changes despite markedly elevated serum potassium [4] was noticed in patients with renal insufficiency. Therapeutic agents have been noted to be a major cause for hyperkalemia in 35% to 75% of hospitalized patients [5], and some of them were on a combination of angiotensin-converting enzyme inhibitors with potassium-sparing diuretics or potassium supplements. Hyperkalemia reduces myocardial excitability, suppresses Sinoatrial node activity, and blocks the conduction at the Atrioventricular node, which eventually attenuates the response to atropine. Slade et al [6] reported 2 cases of atropine-resistant bradycardia due to hyperkalemia and suggested rapid bedside assessment of potassium by arterial blood gas analyzer in the ED and ensure early intervention. From the point of patient safety, hyperkalemia needs to be investigated, in those receiving hyperkalemia-prone therapeutic agents, and considered at as a bedside investigation, if the pulse rate reduces significantly. Hyperkalemia may also manifest without ECG changes. Therefore, timely recognition and intervention not only avoid referral but also avert expensive pacemaker therapy. Interestingly, the etiology for predilection toward hyperkalemia and the frequent absence of ECG changes in such individuals warrant further exploration. Emergency physicians shall remember that bradycardia is not always a primary cardiac issue and, hence, consider or suspect hyperkalemia for bradyarrhythmia, if not responding to atropine or failure to capture the beat, in the absence of other demonstrable causes. ☆ Financial support: Nil. ☆☆ Conflict of interest: Nil.
1415
Ponniah Thirumalaikolundusubramanian MD Department of Internal Medicine, Chennai Medical College and Research Center, Irungalur, Trichy, India http://dx.doi.org/10.1016/j.ajem.2013.06.020 References [1] Srivali N, Ratanapo S, Cheungpasitporn W, Chongnarungsin D, Bischof EF. Hyperkalemia-induced pacemaker dysfunction. Am J Emerg Med 2013;31:879–80. [2] Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalaemia. Am J Emerg Med 2000;18:721–9. [3] Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008;3:324–30. [4] Aslam S, Friedman EA, Ifudu O. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients. Nephrol Dial Transplant 2002;17:1639–42. [5] Stevens MS, Dunlay RW. Hyperkalemia in hospitalized patients. Int Urol Nephrol 2000;32:177–80. [6] Slade TJ, Grover J, Benger J. Atropine-resistant bradycardia due to hyperkalaemia. Emerg Med J 2008;25:611–2.
Takotsubo syndrome and chest pain units☆ To the Editor, Patients presenting with suspected takotsubo syndrome (TTS) are mostly evaluated by emergency department (ED) physicians, except if such illness occurs in the already hospitalized patients, admitted for a diverse array of medical/surgical conditions or in the setting of diagnostic and therapeutic procedures or perioperatively. Because the most prevalent presenting symptom of patients with suspected TTS is chest pain, which is indistinguishable from the one experienced with an acute coronary syndrome (ACS), such patients may be admitted and observed in chest pain units (CPUs) [1-4]. Such CPUs staffed by ED physicians, with available prompt consultation by a cardiologist at the discretion of the ED physicians, provide for admission, observation, and triage of patients with chest pain, most of whom do not have ACS but noncardiac chest pain. Some of the patients presenting with chest pain turn out to have TTS, and such occurrences are being identified with accelerating frequency [5]. The crux of the matter, in reference to differential diagnosis of ACS and TTS, is to distinguish anterior STelevation myocardial infarction (a subtype of ACS) from TTS because the former requires expeditious referral for coronary revascularization, with thrombolysis and preferably percutaneous coronary intervention, whereas the latter is managed currently with nonspecific supportive (based on symptoms) therapies [5]. Patients with both syndromes show ST-elevations primarily in precordial electrocardiographic (ECG) leads in their admission ECG, but this diagnostic modality does not appear to differentiate between the 2 [5,6]. What is being currently done, besides obtaining a targeted history and performing a focused physical examination, is to record the ECG and sample for blood biomarker
☆ Disclosures: The author has disclosed no conflicts of interest.