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ECG PRACTICE CASES: PART 2 ARRHYTHMIAS Megan Chan, PGY-1 UHCMC 2015 ttp://thepracticalpsychosomaticist.com/2013/04/01/qtc-interval-prolongation-andantipsychotics-by-elysha-elson-pharm-d-mph/ 71 Y/O FEMALE WITH SOB DIAGNOSIS? WHAT CAN CAUSE AFIB? Afib with RVR (HR 140) Nonspecific ST & T wave changes ATRIAL FIBRILLATION Etiology HTN CAD Valvular heart disease Thyrotoxicosis ETOH abuse Pericarditis Post-operative state Treatment http://www.riversideonline.com/source/images/image_popup/hb7_afib.jpg Medication Rate control: beta blockers, diltiazem, digoxin Rhythm control: amiodarone, quinidine, procainamide DC-Synchronized Cardioversion Esp if associated with MI, hypotension, or pulmonary edema 43 Y/O FEMALE IN CLINIC FOR FOLLOW UP HER ECG 2 YEARS AGO DIAGNOSIS? HER ECG 2 YEARS AGO Sinus tach (HR ~100) with RBBB and a PVC HER CURRENT ECG DIAGNOSIS? New Aflutter with 2:1 conduction Old RBBB AFLUTTER http://www.medicine-on-line.com/html/ecg/e0001en_files/08.htm http://www.learntheheart.com/ecg-review/ecg-topic-reviews-and-criteria/atrial-flutter-review/ ATRIAL FLUTTER Etiology: Pulmonary disease—e.g. pulmonary HTN, PE Valvular/ischemic heart disease ETOH abuse Pericarditis Treatment: Cardioversion Medications—similar to Afib tx but don’t use quinidine or procainamide as these can decrease atrial conduction to 1:1 DC cardioversion Ablation—esp if sawtooth is down-going 67 Y/O FEMALE WITH PALPITATIONS DIAGNOSIS? SVT with LVH (Narrow complex tachycardia, HR 165) (R in I > 14, R in aVL > 12, S in V2 + R in V6 > 35) SUPRAVENTRICULAR TACHYCARDIA Pathophysiology: AV nodal reentrant tachycardia (AVNRT) 2 pathways (1 fast, 1 slow) within the AV node Common “slow-fast” AVNRT = anterograde conduction via slow pathway, retrograde conduction via fast pathway Uncommon “fast-slow” AVNRT = anterograde conduction via fast pathway, retrograde conduction via slow pathway ECG: no discernible P waves (inverted P buried within QRS complex) because the atria and ventricles activate simultaneously. Pseudo R waves in V1 or V2. ECG: inverted P wave that falls after the QRS because the atria activation is delayed Orthodromic AV reentrant tachycardia (AVRT) An accessory pathway between the atria and ventricle that conducts retrogradely ECG: P waves may or may not be discernable depending on the rate. Accessory pathway is far enough from the AV node that there is a difference in timing of activation of the atria and ventricles. AVNRT vs AVRT 2 pathways within the AV node Accessory pathway between atrium and ventricle http://en.wikipedia.org/wiki/File:AV_nodal_reentrant_tachycardia.png Common AVNRT No pseudo R waves during sinus rhythm Pseudo R waves in V1 Uncommon AVNRT P waves in yellow falling after QRS http://lifeinthefastlane.com/ecg-library/svt/ http://imgarcade.com/1/avrt-vs-avnrt-ecg/ WHAT TYPE OF SVT IS THIS? WHAT TYPE OF SVT IS THIS? Pseudo R waves Common AVNRT SUPRAVENTRICULAR TACHYCARDIA Etiology Ischemic heart disease Digoxin toxicity Excessive caffeine/amphetamine Excessive ETOH Atrial flutter with RVR WHAT IS YOUR NEXT STEP IN MANAGEMENT? SUPRAVENTRICULAR TACHYCARDIA Treatment Maneuvers to increase vagal tone and delay AV conduction to block reentry Valsalva maneuver Carotid sinus massage Breath holding Head immersion into cold water Pharmacotherapy IV adenosine = agent of choice Decreases sinoatrial and AV nodal activity IV verapamil, IV esmolol/propranolol/metoprolol, digoxin DC cardioversion if unstable or meds ineffective Prevention Digoxin = drug of choice Verapamil, Beta-blockers Radiofreqency ablation http://www.emedu.org/ecg/images/ans/2adeno_1a.jpg http://www.emedu.org/ecg/images/ans/2adeno_2a.jpg ATRIAL TACHYCARDIA WITH ADENOSINE P waves with blocked AV conduction http://www.heartpearls.com/tag/adenosine 72 Y/O FEMALE WITH PALPITATIONS DIAGNOSIS? WHAT IS YOUR NEXT STEP IN MANAGEMENT? NSR with PVC (PVC resembles LBBB because originating from right tract) PREMATURE VENTRICULAR CONTRACTIONS Etiology Variation of normal Excessive caffeine Anemia Anxiety Organic heart disease (ischemic, valvular, hypertensive) Medications (e.g. epinephrine, digitalis toxicity) Metabolic abnormalities (hypoxia, hypokalemia, acidosis, alkalosis, hypomagnesemia) Treatment None if asymptomatic. ↑ mortality if treated. However, >10 PVCs per hour ↑ risk of death in those with heart disease. If symptomatic, treat with beta-blockers and possibly ablation. 85 Y/O FEMALE ADMITTED FOR FALLS DIAGNOSIS? DIAGNOSIS? Sinus Bradycardia (HR 50) with PAC PREMATURE ATRIAL CONTRACTIONS Pathophysiology Etiology Early beat fires on it’s own from a focus in the atria Variant of normal Adrenergic excess ETOH/Tobacco Electrolyte imbalances Ischemia Infection No significance in a normal heart, but may be a precursor of ischemia in a diseased heart. REFERNCES Agabegi SS, Agabegi ED. Step up to Medicine, 3rd ed. 2013. Lippincott Williams & Wilkins. Philadelphia, PA. Gomella LG, Haist SA. Basic EKG reading. In: Clinician’s Pocket Reference. McGraw-Hill; 2007. http://flylib.com/books/en/2.569.1.27/1/. Accessed Nov 18, 2014. Longo DL, Fauci AS, Kasper DL, et al. Electrocardiography. In: Harrison’s Principles of Internal Medicine, 18th ed. 2012. McGraw Hill. New York, NY. University of Illinois at Chicago. Online ICU Guidebook. 2013. http://chicago.medicine.uic.edu/UserFiles/Servers/Ser ver_442934/Image/1.1/residentguides/final/icuguidebo ok.pdf. Accessed December 1, 2014.