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Wolff V, et al. Cannabis-related stroke: myth or reality? Stroke 2013;44:558-63.

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Subramanian Senthilkumaran MD

Duchene C, et al. Cannabis-induced cerebral and myocardial infarction in a young Takotsubo syndrome and chest pain units”>woman. Rev Neurol (Paris) 2010;166:438-42.

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?,??

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. Symp- tomatic bradycardia is a frequent presentation in the emergency department (ED), although the causes may not readily be demon- strable 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 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 ?-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 angiotensin- converting enzyme inhibitors, potassium-sparing diuretics, and Cycloox- ygenase-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 Sino- atrial 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.

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

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 hyperka- laemia. 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 Trans- plant 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 ST- elevation 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

   ? Financial support: Nil.

   ?? Conflict of interest: Nil.

   ? Disclosures: The author has disclosed no conflicts of interest.

   1416 Correspondence / American Journal of Emergency Medicine 31 (2013) 1410–1417

   levels, usually troponin I or T, serially. However, there is no certainty in the differentiation between ACS vs TTS until one resorts to an expeditious coronary arteriography, which reveals either obstructive coronary artery disease, due to a destabilized (ruptured or eroded) coronary plaque with resultant thrombosis in the former, or normal, or nonobstructive stable coronary artery disease in the latter [5].

   Can the ED physicians, staffing the CPUs, improve on the above? Perhaps they can rethink the diagnostic/management model for patients with suspected TTS and their modus operandi, along the following considerations: (1) Postmenopausal women in their 60s and 70s, without history of ACS, the same or fewer risk factors for ACS, and with a recent exposure to emotional or physical stress (persisting inquiry may be needed) deserve special attention; (2) release of specific cardiac biomarker levels from the first, second, or even third blood specimen is expected to be modest, inspite symptoms or ECG appearances, and this is frequently associated with a high brain natriuretic peptide (or N-terminal brain natriuretic peptide)/troponin I (or T) ratio [5]; (3) application of transthoracic echocardiography (ECHO) should be implemented immediately after obtaining an ECG and repeatedly thereafter, using equipment and personnel locally available in CPUs, and in contrast to what it is currently done via referral of the patient to the cardiology department (division)- controlled ECHO laboratory, with the unavoidable time delays, which results usually to ECHOs being performed, after the patient had been transferred to the catheterization suite. It is understandable that the quality of such ECHOs initially may not be on par, with what it is accomplished with our current model, but one can start with pocket- size handheld cardiac ECHO devices, which have been tried and found to be satisfactory in diagnostics [7], and immediately implement ECHO training sessions, so that what is practiced in CPUs eventually meets with currently required standards [8]. (4) A new ECG insight, which, however, needs confirmation, is that of increased prevalence of low QRS voltage in the admission ECG and/or QRS amplitude attenuation in repeat ECGs or in comparison with a potentially available previous ECG in patients with TTS [9].

   Acquired experience in CPUs with the above approach will

   undoubtedly lead to improvements in the early and timely (for management) differentiation of ACS and TTS and probably, in the future, may obviate (safely) coronary arteriography, for some patients with TTS. At least, this should be the goal.

   John E. Madias MD Icahn School of Medicine at Mount Sinai of the New York University/Cardiology Division of Elmhurst Hospital Center

   E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.06.023

   References

   DeLeon AC, Farmer CA, King G, et al. Chest pain evaluation unit: a cost-effective approach for ruling out acute myocardial infarction. Southern M J 1989;82:1083-9.

7. Gaspoz JM, Lee TH, Cook EF, et al. Outcome of patients who were admitted to a new short-stay unit to “rule-out” myocardial infarction. Am J Cardiol 1991;68: 145-9.
8. Gibler WB. Chest pain evaluation in the emergency department: beyond triage. Am J Emerg Med 1994;12:121-2.
9. Graff LG, Zun LS, Leikin J, et al. Emergency department observation beds improve patient care: Society for Academic Emergency Medicine debate. Ann Emerg Med 1992;21:967-75.
10. Bossone E, Savarese G, Ferrara F, et al. Takotsubo cardiomyopathy: overview. Heart Fail Clin 2013;9:249-66.
11. Bybee KA, Motiei A, Syed IS, et al. Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction. J Electrocardiol 2007;40:38.e1-6.
12. Panoulas VF, Daigeler AL, Malaweera AS, et al. Pocket-size hand-held cardiac ultrasound as an adjunct to clinical examination in the hands of medical students and junior doctors. Eur Heart J Cardiovasc Imaging 2013;14:323-30.
13. Expert Round Table on Ultrasound in ICU. International expert statement on training standards for critical care ultrasonography. Intensive Care Med 2011;37: 1077-83.
14. Madias JE. Transient attenuation of the amplitude of the QRS complexes in the diagnosis of Takotsubo syndrome (revised manuscript submitted to European Heart Journal: acute cardiovascular care).

    Account of antecedent diuretic treatment should also be taken

    To the Editor,

    When the differentiation of exudate from transudate is based on protein content of ascitic fluid, as was the case in the recently reported study [1], due account of the effect the preceding diuretic treatment might have on the protein concentration of ascitic fluid should also be taken [2,3]. In the context of ascites attributable to congestive heart failure, Pillay [2] documented an increase in the protein concentration when samples of ascitic fluid were reevaluated 7 to 13 days after the initiation of diuretic treatment. Evaluation of ascitic fluid protein concentration was made before and after the initiation of diuretics in 5 patients in whom pretreatment levels were 1.3 g/100 mL, 3.1 g/100 mL, 0.8 g/100 mL, 2.9 g/100 mL, 1.9 g/100 mL, and 3.6 g/100 mL, respectively. Corresponding posttreatment concentrations of ascitic fluid protein (reported as g/100 mL) amounted to 2.1, 3.2, 3.0, 3.9, and

    3.8 g/100 mL, respectively. In that study, the author made the additional observation that “In patients with long-standing cardiac failure the total proteins were remarkably high,” ranging from 3.0 g/ 100 mL to 5.1 g/100 mL in 18 patients, including 8 patients in whom the duration of cardiac failure had been ascertained to range from 6 to

    72 months. In all cases of chronic cardiac failure with ascites, temperature and erythrocyte sedimentation rate were normal. Furthermore, in the 3 patients with heart failure who died in hospital, autopsy revealed no abnormality in the peritoneum to account for the increase in ascitic fluid protein concentration. The surviving patients responded to treatment for cardiac failure, with consequent resolution of ascites [2].

    In the context of ascites attributable to decompensated liver disease, the study was composed of 27 patients who had undergone paracentesis before and after diuresis. In 25, the diuresis was drug induced, and in 2, it was spontaneous. Between the initial and final paracentesis, there was a significant (P b .001) increase in ascites total protein concentration. Of the 27 patients, 12 ultimately developed an ascites total protein concentration greater than 3.0 g/L. None of the 27 patients had experienced complications such as Spontaneous bacterial peritonitis, hepatic coma, or gastrointestinal bleeding during the period of diuresis. Accordingly, there appeared to be no explanation other than diuresis itself, to account for the increase in ascitic fluid protein concentration [2].

    In conclusion, when an interpretation of the significance of the protein concentration of ascitic fluid is made, due account should be taken of whether or not the patient has previously been on diuretics, and also of the duration of the patient’s symptoms.

    Oscar M.P. Jolobe DPhil, MB, ChB Manchester Medical Society, Manchester M13 9PL, UK E-mail address: [email protected]

    http://dx.doi.org/10.1016/j.ajem.2013.06.033

    References

    Heidari K, Amiri M, Kariman H, Bassiri M, Alimohammadi H, Hatamabadi HR. Differentiation of exudate from transudate ascites based on the dipstick values of protein, glucose, and pH. Am J Emerg Med 2013;31:779-82.

15. Pillay VKG. Total proteins in serous fluids in cardiac failure. S Afr Med J 1965;39: 142-3.
16. Hoefs J. Increase in ascites white blood cell and protein concentrations during diuresis in patients with Chronic liver disease. Hepatology 1981;1:249-54.