The "qRBBB" pattern

Presence of qRBBB in the setting of acute coronary syndrome signifies proximal occlusion of left descending coronary artery with compromise of circulation in the septal arteries supplying the bundle branches. Anterior STEMi with RBBB is associated with a higher risk of death when compared with that of patients with normal conduction. 

qRBBB with LAFBInstead of the rSR pattern (seen in RBBB), there is qRBBB pattern in V1 because the initial r wave has been knocked off by anterior wall myocardial infarction. 

Due to anterior location of the right ventricle than that of the left ventricle, activation of the right ventricular free wall can neutralize the abnormal septal forces associated with an anteroseptal MI. Therefore, in most patients with an anteroseptal infarction, abnormal Q waves in right precordial leads is mostly manifest during RBBB showing the classical qRBBB pattern, due to delayed activation of the right ventricle. 

Understanding RBBB
RBBB causes delayed depolarisation of right Ventricle as depolarisation spreads across the septum (instead of the Right Bundle) taking longer than usual. This produces characteristic ECG changes described below in the diagnostic criteria. Left Ventricle depolarisation remains normal i.e normal early part of QRS complex. 

Diagnostic Criteria 

• Broad QRS > 120 ms
• RSR’ pattern in V1-3 (‘M-shaped’ QRS complex) or a broad monophonic r wave or a qR complex
• Wide, slurred S wave in the lateral leads (I, aVL, V5-6
• Delayed intrinsicoid deflection time 

RBBB (Image from LIFTL)

RBBB often shows STD and TWI in V1-3 due to secondary depolarisation abnormalities 

Causes

• Ischemic Heat Disease
• Acute Pulmonary HTN (PE)
• Chronic Pulmonary HTN (Cor Pulmonale)
• Valvular Heart Disease
• Myocarditis
• Degenerative Diseases of conduction system
• Congenital Heart Disease
• Overdose of Na Channel Blockers
• Idiopathic
• Transient and Rate Related 

RBBB should NOT have any ST Elevation. Look for the qRBBB pattern and RBBB with LAFB (Leftward Axis, qR in lead I, aVL, rS in lead III) pattern. 

qRBBB in V1-4 with STE (Image from TheECGinAcuteMI)

Take Home:

• Remember the qRBBB pattern morphology
• RBBB should never have any ST elevation 
• When in doubt, do serial ECGs and screening bedside ECHO to look for RWMA

References and Further Reading:

1. Mishra, V., Sinha, S. K., & Razi, M. (2016). Right Bundle Branch Block: A Masquerader in Acute Coronary Syndrome. North American Journal of Medical Sciences, 8(2), 121–122. http://doi.org/10.4103/1947-2714.177347
2. 2. Widimsky P, Rohác F, Stásek J, Kala P, Rokyta R, Kuzmanov B, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: Should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33:86–95.
3. Ganesan S, Kannan K, Victor A, Selvan KT, Arun R, Majella JC, Kumar RS, Aravind A, Viswanathan N, District V. QRBBB in acute coronary syndrome: Does it matter in modern era? Angiographic correlation. Indian Heart Journal. 2015 Dec 1;67:S38.
4. Wong CK, Stewart RA, Gao W, French JK, Raffel C, White HD. Prognostic differences between different types of bundle branch block during the early phase of acute myocardial infarction: Insights from the Hirulog and Early Reperfusion or Occlusion (HERO)-2 trial. Eur Heart J. 2006;27:21–8. 
5. http://hqmeded-ecg.blogspot.co.uk/2010/01/right-bundle-branch-block-with-subtle.html
6. http://hqmeded-ecg.blogspot.co.uk/2017/04/rbbb-with-transient-st-elevation.html
7. http://hqmeded-ecg.blogspot.co.uk/2010/11/wide-complex-tachycardia-its-really.html
8. http://hqmeded-ecg.blogspot.co.uk/2014/03/elderly-woman-in-shock-ekg-from.html
9. https://emcrit.org/wp-content/uploads/2015/03/Who-to-PCI-by-Smith-and-Weingart.pdf
10. https://lifeinthefastlane.com/ecg-library/basics/right-bundle-branch-block/

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Cocaine Toxicity

Cocaine is one of the most commonly used recreational drug. It is both a CNS stimulant and a local anaesthetic.Its clinical effects and toxicity are due to sympathetic nervous system stimulation. Cocaine can be used topically, swallowed, or injected IV. 

                          

Cocaine is metabolized by plasma cholinesterase. Therefore, deficiency of this enzyme may predispose affected patients to life-threatening toxicity.  Central effects of cocaine are mediated by enhancement of excitatory amino acids and blockade of presynaptic reuptake of norepinephrine, dopamine, and serotonin. The excess of neurotransmitters at postsynaptic receptor sites leads to sympathetic activation, producing a characteristic toxidrome of mydriasis, tachycardia, hypertension, and diaphoresis, dysrhythmias, seizures, and hyperthermia. 

Like other local anesthetics, cocaine also inhibits conduction of nerve impulses by blocking fast sodium channels in the cell membrane. This can lead to QRS widening and QT-interval prolongation. 

Systemic Effects

Cardiac

• Dysrhythmias (Na/K Channel Blockade - Sinus Tachy, Wide QRS, Prolonged QTc, Rightward Axis, Brugada Pattern, Takotsubo Cardiomyopathy)
• Myocarditis
• Acute coronary syndromes
• Aortic rupture and aortic/coronary artery dissection
• Cocaine-induced chest pain (Coronary Vasospasm, also hastens atherogenesis through increased platelet aggregation, thrombogenesis)

CNS

• Seizures
• Stroke (ischemic and haemorrhages)
• Hypertension
• Spinal cord infarction
• Cerebral vasculitis
• Intracranial abscesses
• Crack dancing - Choreoathetosis and repetitive movements due to dopamine dysregulation. 
• Blindness (central retinal artery occlusion)

Other effects

• Pulmonary haemorrhage
• Pneumonitis, Asthma
• Pulmonary edema
• Acute Lung Injury
• Thermal uvulitis 
• Bowel schema and necrosis
• Splenic infarctions
• Rhabdomyolysis and AKI 
• Renal infarction 

Differential Diagnosis of Sympathomimetic Syndrome

• Anticholinergic Syndrome
• Serotonin Syndrome
• Neuroleptic Malignant Syndrome
• Alcohol Withdrawal
• Sepsis and CNS Infections
• Hypoglycaemia, Metabolic (Electrolyte Issues)
• Thyrotoxicosis
• Pheochromocytoma
• Psychosis
• Heat Stroke 

Management

• Benzodiazepines are the drugs of choice for sedation
• Antipsychotics increase QT prolongation and increase risk of ventricular dysrhythmias

• Treat Cardiac Chest Pain with aspirin and nitroglycerin, CCBs and reperfusion therapy if needed.  
• Use of β-adrenergic antagonists (“β-blockers”) in the management of cocaine-associated myocardial ischemia or infarction is controversial. 

• Sinus tachycardia - Rx with sedation, cooling, and intravenous fluid rehydration 
• Reentrant supra ventricular tachycardia /Fast atrial fibrillation or flutter - Rx with CCBs
• Wide-complex tachycardia - Rx with sodium bicarbonate (do not alkalinize above a pH of 7.55). Although Lidocaine is also a Na Channel blocker, it may be considered for use in refractory arrhythmias.
• Torsades de points - Rx with Magnesium, lidocaine, and overdrive pacing.
• Hypotension/Persistent Arrhythmias - Intravenous lipid emulsion should be considered in this scenario.

• Severe hypertension - Rx with sedation or GTN drip or Phentolamine
• Rhabdomyolysis - IV Fluids

• Seizures - BZD, Phenobarbitone (Do not Rx with phenytoin which may worsen Na Channel Blockade)

References:

1. Zimmerman JL: Cocaine intoxication. Crit Care Clin 28: 517, 2012. 
2. Phillips K, Luk A, Soor GS, Abraham JR, Leong S, Butany J: Cocaine cardiotoxicity: a
3. review of the pathophysiology, pathology, and treatment options. Am J Cardiovasc Drugs 9: 177, 2009. 
4. Lange RA, Cigarroa RG, Yancy CW, et al: Cocaine-induced coronary artery vasocon-striction. N Engl J Med 321: 1557, 1989. 
5. Hollander JE, Hoffman RS: Cocaine-induced myocardial infarction: an analysis and
6. review of the literature. J Emerg Med 10: 169, 1992. 
7. O’Leary ME, Hancox JC: Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias. Br J Clin Pharmacol 69:427, 2010. 
8. Yap YG, Behr ER, Camm AJ: Drug-induced Brugada syndrome. Europace 11: 989, 2009.
9. Arora S, Alfayoumi F, Srinivasan V: Transient left ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc 81: 829, 2006. 
10. Rangel C, Shu RG, Lazar LD, Vittinghoff E, Hsue PY, Marcus GM: Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med 170: 874, 2010. 
11. Jakkala-Saibaba R, Morgan PG, Morton GL: Treatment of cocaine overdose with lipid emulsion. Anaesthesia 66: 1168, 2011. 

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Interpreting Elevated Troponins and Types of Myocardial Infarction

Elevations of cardiac biomarkers in the blood reflect injury leading to necrosis of myocardial cells but biomarkers do not indicate the underlying mechanism of this injury. Myocardial injury can be due to ischemic and non-ischemic causes. Therefore, small amounts of myocardial injury with necrosis may be detected, which are associated with CCF, renal failure, myocarditis, arrhythmias, pulmonary embolism and percutaneous or surgical coronary procedures. Troponin elevation in these contexts should not be called as Myocardial Infarction but Myocardial Injury.

Onset of myocardial ischaemia is the initial step resulting from an imbalance between oxygen supply and demand. This can be identified from history and ECG. Possible ischaemic symptoms include various combinations of chest, upper extremity, mandibular or epigastric discomfort or an ischaemic equivalent such as dyspnoea or fatigue (in women). Pain associated with vomiting, worse on exertion, sweating is definitely worrisome. The discomfort with acute MI usually lasts 20 min. In an ideal world, the sequence should be history, physical exam, ECG and troponins. Whenever symptoms recur, it is important to repeat the ECG. If you are ordering trop troponins, you must order serial ECGs as well. remember, ECG is more of a rule in test not a rule out test for ACS.

MI is classified into various types, based on pathological, clinical and prognostic differences, along with different treatment strategies 

References:

1. Roe MT, Harrington RA, Prosper DM, Pieper KS, Bhatt DL, Lincoff AM, Simoons ML, Akkerhuis M, Ohman EM, Kitt MM, Vahanian A, Ruzyllo W, Karsch K, Califf RM, Topol EJ. Clinical and therapeutic profile of patients pre- senting with acute coronary syndromes who do not have significant coronary artery disease. The Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial Investigators. Circulation. 2000;102:1101 – 1106.
2. Bugiardini R, Manfrini O, De Ferrari GM. Unanswered questions for manage- ment of acute coronary syndrome: risk stratification of patients with minimal disease or normal findings on coronary angiography. Arch Intern Med 2006; 166:1391 – 1395.
3. Reynolds HR, Srichai MB, Iqbal SN, Slater JN, Mancini GB, Feit F, Pena-Sing I, Axel L, Attubato MJ, Yatskar L, Kalhorn RT, Wood DA, Lobach IV, Hochman JS. Mechanisms of myocardial infarction in women without angiogra- phically obstructive coronary artery disease. Circulation 2011;124:1414 – 1425. 
4. Bertrand ME, LaBlanche JM, Tilmant PY, Thieuleux FA, Delforge MR, Carre AG, Asseman P, Berzin B, Libersa C, Laurent JM. Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography. Circulation 1982;65:1299 – 1306.
5. Suwaidi JA, Hamasaki S, Higano ST, Nishimura RA, Holmes DR Jr, Lerman A. Long-term follow-up of patients with mild coronary artery disease and endothe- lial dysfunction. Circulation 2000;101:948 – 954.
6. Bugiardini R, Manfrini O, Pizzi C, Fontana F, Morgagni G. Endothelial function predicts future development of coronary artery disease: a study on women with chest pain and normal angiograms. Circulation 2004;109:2518 – 2523. 
7. Kristian Thygesen, Joseph S. Alpert, Allan S. Jaffe, Maarten L. Simoons, Bernard R. Chaitman and Harvey D. White: the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction 

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Sorting out Gabrahat (Anxiety) ~ The Common Complaint in the ED

 Gabrahat (Anxiety) is often a common complaint with many implications.

While working in Emergency Departments in India I have been surprised with what the ultimate diagnosis was when I investigated Gabrahat.

For me Gabrahat is as vague as the Horizon and I take this complaint very seriously. It is very easy for any Nurse or Emergency Physician to get framed and just label Gabrahat as Anxiety or Hysteria.

This can be the Epic Blunder of Large Proportions. 

Many times relatives who accompany the patient will Frame the Emergency Physician by saying words like “There is Tension”. What they mean to imply is Gabarahat is Stress Related.

I often relate Gabrahat to a “SENSE OF IMPENDING DOOM”. When you grade GABRAHAT in that perspective, it guides the Emergency Physician to be very Proactive and diligent.

Let me share a few blasts from the past which I have modified for the sake of Education.

Case One:

Middle Age Female comes to the ED saying that she is feeling SOB. She is hyperventilating and Diaphoretic. She says that she has been having pain all over the body and fells GABRAHAT as if something is going to happen to her.

Her vitals are stable but she continues to breathe hard and breath fast. The relatives were doing a Fine job of Framing her as hysteria.

Rapid Fire Questionnaire Labs EKG Trop and a X-ray Beta HCG UA and a BNP are ordered.

On examining the patient the only Finding is the breathing. Lorazepam given IV and Oxygen started and ABG Ordered which is showing alkalosis. Aspirin given and a bedside Glucose is Normal. She settles down but continues to breathe hard. A CTA Chest is ordered. 

There are massive shower Pulmonary Emboli. Pt gets thrombolyzed and goes to ICU.

Case Two:

A 55-year-old women comes with GABRAHAT. She says that she is afraid something is going to happen. She has no other symptom. She has no Past Psyc Issues.

Labs EKG Trop and an X-ray UA ordered. She has had a prior hysterectomy.

She had an ST Elevation MI. Went to the Cath Lab. No Symptoms at all. No Past History at all.

Case Three:

30-Year-old man came saying He had Gabrahat and felt that there was Irritation in the Chest. NO PAIN BUT ONLY IRRITATION. Exam Past History negative.

Cardiac labs CBC RFT LFT was negative so was his EKG and Xray. Against the will of the Internal Medicine Colleagues Pt admitted. 4 hour repeat EKG and Trop was placed from the ED. His EKG was normal but his Trop had become positive.

Cardiology who scheduled the patient for a cath after admitting him to CCU found a Tight Lcx Lesion which needed a Stent.

Case Four:

48 Female with Gabrahat. Second visit after discharge from the hospital. Come back saying she is afraid. No Pain, No Focus of Infection. 

CBC RFT LFT Cardiac Labs X-ray Beta HCG and UA Negative.

Says her Mind tell her Something is wrong. She has GABRAHAT.

Was admitted in a nursing home. CBC Electrolytes creatinine and SGPT was done and after overnight IV Fluids patients sent home. A CT Head done and the patient had SAH. No Neck stiffness no Eye signs. Admitted to Neurosciences ICU

The only thing that prompted a CT Head was “My Mind is telling Me. This was perceived as Hallucinations hence CT Head Ordered.

Case Five:

18 Year Old Male comes with Gabrahat with Hallucinations. He was at friends party and says “ I have gabrahat as I see a ghost”.

Tox Work up was done and it was positive for multiple substances.

Routine CBC RFT LFT EKG Trop UA and Xray with a CT Head and Tox Screen were done.

Case Six:

40 year old male comes saying that he has Gabrahat and he feels like a huge Log of wood just fell on his head and nailed his whole body vertically into the ground. Clinical Exam and Vitals were normal.

CBC LFT RFT Trop EKG Xray negative

No Neck stiffness Neuro exam normal. He kept saying I am afraid I am sinking into the ground.

CTA Aortagram ordered: He had a dissection from Thorax to iliac bifurcation.

Admitted to CVTS Sx.

Summary:

• Basic Approach should be T/P/R/BP/Pulse Ox
• I always order a CBC LFT RFT EKG Trop CXR. Looking for Rhythm abnormalities is also important. Fever can also cause Gabrahat.
• In Females in the Pregnancy Age group a HCG-UA is ordered
• If Patient has SOB I will R/O Thoracic Causes like Dissection/Pneumothorax and PE.
• If Patient has a presentation of Altered Mental Status I always order a CT Head.
• If Toxicology screen is available, I will order one.
• Co-Symptoms should guide further investigations.
• Discussing with the Relatives in key to educate them- that this is not Hysteria / Tension / Stress. Those are the diagnosis to be considered once Major Life threatening causes are ruled out.
• I have often Seen Marital Discord / Intimate Partner Abuse to be causes of GABRAHAT. So Going deeper into the history. Sitting with the patient with Privacy is the key.
• Anxiety / Panic attack also can be on the differential once Major causes are ruled out.
• Being a Compassionate Emergency Physician is the key. Communication is the answer and Competency to Care is crucial.
• GABRAHAT CAN KILL !

I want to Share a Web Review of what Non EM Experts say about GABRAHAT.

I feel a Well Trained Emergency Physician leaves no stone unturned to do the best for his/her patient

Web Review:

• http://bhj.org.in/journal/special_issue_tb/DPII_11.HTM
• http://hrelate.com/natural-remedies-for-anxiety/
• http://www.njhonline.com/1993/july_aug_93_vol_11_no_4/spider/ghabrahat.shtml

Author:

Dr. Sagar Galwankar

CEO of INDUSEM & Faculty of Emergency Medicine at University of Florida Jacksonville, Florida

@SagarGalwankar

Sagar completed his med school from the University of Pune (India). He attained Board Certified in Internal Medicine from the National Board of Examinations in India. Following this, he went on to train at the University of South Florida, USA in areas of International Health Diplomacy, Infectious Diseases and Emergency Medicine. He also holds a MPH from the University of South Florida and is a Board Certified Emergency Physician with the American Board of Emergency Medicine.

Sagar's academic and clinical career spans over a decade with experience in Education, Care and Research both in India and the USA. He has extensively published, cited and honoured for his works in International Medicine, Public Health, Infectious Diseases, Emergency Medicine and Injury Sciences. Sagar is the Founder and CEO of the INDO-US Academic Initiative for Emergency and Trauma and continue to play a defining role in establishing Emergency Medicine as a separate specialty in India.

He has had previous appointments at the University of South Florida and University of Florida in Departments of Emergency Medicine, Internal Medicine, Global Health and Mental Health. His areas of Interest include Emergency Medical Intelligence, Health Policy, Injury Medicine, International Health, Humanitarian Assistance, Quality Health Care Delivery in Emerging Economies and Global Health Diplomacy.  Sagar believes that "The role of the World's Largest and the Oldest Democracies namely India and United States is crucial for the future progress of transitional Economies and Peace across the Globe". Health is Definately an important part of this growth Story.

Originally published at beepers365.blogspot  on 11 December, 2016. Reposted with permission.

TakoTsubo Cardiomyopathy

Introduction

TakoTsubo Cardiomyopathy (TTC), also known as broken-heart syndrome, apical ballooning syndrome or stress-induced cardiomyopathy. It is a reversible cardiomyopathy characterised by transient systolic ventricular dysfunction with a clinical presentation indistinguishable from acute myocardial infarction but in the absence of significant coronary artery obstruction. This condition is frequently precipitated by sudden, stressful emotional events, occasionally due to physiologic stress such as sepsis, non-cardiac surgery, and subarachnoid hemorrhage.

The term "Takotsubo"  was coined to describe the unusual shape of the left ventricular during systole. Typically, the mid to apical segments of the left ventricle are akinetic and the spared, basal walls exhibit compensatory hypercontractility. Takotsubo is a pot with round base and narrow neck used in Japan for trapping octopuses and has a similar appearance to this apical ballooning. 

TTC occurs most commonly in postmenopausal women and has a very good prognosis. Acutely, patients are often critically ill with heart failure, arrhythmias, shock, LVOT obstruction, thromboembolism but symptoms resolve quickly and death is rare.

Pathophysiology 

The pathophysiologic basis of TTC has not been conclusively determined but several mechanisms have been proposed. The underlying histopathological findings on myocardial biopsy are distinctly different from those of coagulation necrosis seen in typical atherosclerotic epicardial artery occlusion and myocardial infarction. 

• Catecholamine overload and myocardial stunning 
• Multi-vessel coronary artery spasm with resultant ischemia and stunned myocardium 
• Spontaneously aborted myocardial infarction 
• Microvascular dysfunction and myocarditis

Clinical presentation 

TTC has been reported to account for 1-3% of all acute coronary cases. About 90% of cases reported are in post-menopausal women ages 58-75 years old.  The clinical presentation of TTC is often identical to acute myocardial infarction (AMI). Most patients with takotsubo cardiomyopathy present with typical anginal chest pain, dyspnea, ischemic changes on electrocardiogram (ECG), and elevated cardiac markers.  Emotional stress, such as news of the death of a family member, divorce, or public speaking, is implicated as the trigger in approximately two-thirds of patients. 

ECG changes and cardiac biomarkers 

The most common abnormality on the ECG is ST elevation and T-wave inversion in the precordial leads. However, there may be some population differences in presenting signs and specific ECG changes should be considered suggestive but not diagnostic of TTC. Modest elevation of cardiac biomarkers is often observed in TTC.

ECG Image (TTC) from LIFTL

Diagnosis 

Due to the dramatic clinical presentation and high suspicion for acute myocardial infarction, most patients undergo emergent coronary angiography. Typical findings in TTC are normal epicardial coronaries, mild non-obstructive atherosclerosis, or rarely coexistent coronary artery disease. Therefore, TTC is a diagnosis of exclusion which can only be made after coronary angiography. It should be on the differential diagnosis in any post-menopausal women over 50 years old presenting with chest pain and ischemic ECG changes particularly in the setting of emotional stress. Furthermore it should also be considered in critically ill patients with sudden hemodynamic compromise and/or heart failure. 

Mayo Clinic proposed diagnostic criteria in 2004 for TTC which includes four components:

(1) Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid seg- ments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present 

(2) Absence of obstructive CAD or angiographic evidence of acute plaque rupture 

(3) New electrocardiographic abnormalities (either ST-segment elevation and/or T wave inversion) or modest elevation in cardiac troponin 

(4) Absence of pheochromocytoma and myocarditis

Cardiac imaging 

Ventriculography reveals apical ballooning, with characteristic sparing of the basal segments and akinesis of the mid and apical left ventricle. However, variants of this pattern have been described. In patients with typical TTC, the wall motion abnormality usually extends beyond the distribution of a single coronary artery. 

Echocardiography can detect and measure the degree of left ventricular outflow (LVOT) obstruction and associated systolic motion of the anterior mitral valve and significant mitral regurgitation. 

LVOT obstruction is reported to occur in 25% patients and can have a major impact on acute management. In patients with hemodynamic compromise and shock, inotropes would worsen this situation and betablockers and pure vasopressor pharmacologic or mechanical support may be needed. The typical findings on cardiac MRI include the absence of delayed gadolinium hyperenhancement. This is specific to TTC and can help differentiate it from myocarditis and acute myocardial infarction in which delayed hyperenhancement is present.

Treatment 

Takotsubo cardiomyopathy has an excellent prognosis, with full and early recovery in virtually all patients. The majority of patients have normalization of LVEF within a week and all patients by 4-8 weeks. Long-term survival is similar to the general population. 

• The goals of treatment are usually conservative, supportive care. The therapy is guided by the patient’s clinical presentation and hemodynamic status. Despite the possible causal role of catecholamines in the disorder, patients who present in cardiogenic shock, and in the absence of LVOT obstruction, may be treated with inotropes. 
• Alternatively patients may derive further benefit from IABP and VADs. 
• If LVOT obstruction is present with cardiogenic shock, inotropes should be avoided and phenylphrine is the pressor agent of choice often combined with betablockade.
• Anticoagulation is reserved for those with ventricular thrombus or evidence of embolic events. 

Take Home

• Takotsubo cardiomyopathy is an acquired cardiomyopathy which is a differential diagnosis of acute coronary syndrome. 
• It is characterized by transient systolic ventricular dysfunction with regional wall motion abnormalities beyond a single vascular territory in the absence of significant epicardial coronary artery obstruction. 
• Acute emotional/ physical stressor immediately preceding the acute coronary syndrome is a common presentation. Catecholamine excess and cardiotoxicity is the most likely underlying mechanisms.
• Supportive treatment is the mainstay of therapy.

References:

1. Kurisu S, Kihara Y. Clinical management of takotsubo cardiomyopathy. Circ J. 2014. 78 (7):1559-66. 
2. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008 Mar. 155(3):408-17.
3. Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004 Dec 7. 141(11):858-65.
4. Merchant EE, Johnson SW, Nguyen P, Kang C, Mallon WK. Takotsubo cardiomyopathy: a case series and review of the literature. WestJEM. 2008. 9:104-11.