Cardiac Arrhythmias A Guide For Medical Students William Beaumont Hospital Department of Emergency Medicine

In evaluating arrhythmias - Rate - Is it fast or is it slow If slow – is there group to group beating Rhythm - Is it regular, irregular or irregularly irregular? P waves - Are they present? QRS - Is it narrow or wide?

Sinus Bradycardia What is it? What causes it? When do you treat it? How do you treat it? Answers in next slide

Sinus Bradycardia A sinus rhythm with normal intervals and a rate less than 60 bpm Normal variant, beta blocker overdose, dig, hypothermia, hypothyroidism, brady-tachy syndrome, and SA node ischemia Requires treatment only if there is evidence of hypoperfusion Two treatment options Pacing: transvenous or transcutaneous Atropine 0.5 mg IVP

Sinus Tachycardia A sinus rhythm faster than 100 bpm Etiology - usually a physiologic response to a stressor Volume depletion / low stroke volume Hypoxia Systemic pathology: fever, anemia, hyperthyroidism Drugs Treatment - treat the underlying cause

PACs MAT Atrial Fibrillation, atrial flutter SVT Atrial Arrhythmias PACs MAT Atrial Fibrillation, atrial flutter SVT

Multifocal Atrial Tachycardia Diagnosis requires the presence of three distinct p waves in a narrow complex tachycardia Almost always associated with pulmonary disease Less often due to hypokalemia or hypomagnesemia Treat the underlying disorder – usually hypoxia Unlike the other atrial tachyarrhythmias, cardioversion is of no value in MAT

MAT Rule of Threes 3 different p waves, 3 different pr intervals and 3 different r to r intervals

Causes of A-fib Cardiovascular - CAD, HTN, CHF, myopathy, myo-, endo- and pericarditis, infiltrative disease, valvular, congenital Metabolic - thyroid, electrolytes Pulmonary - pulmonary HTN, PE Toxic - cocaine, ETOH (holiday heart), beta agonists Sepsis Idiopathic

ECG Rules for A-fib Regularity - irregularly irregular Rate - atrial rate usually > 350 Controlled - ventricular rate < 100 RVR - ventricular rate > 100 P wave - none discernable, may be f waves QRS - less that 0.12 seconds (easy dx). If > 0.12 sec must rule out VT (which is usually more regular)

A-fib with RVR A fib with ventricular rate > than 100-120 bpm Patients usually symptomatic requiring rapid tx Unstable – cardioversion Stable - control rate with calcium channel blockers, beta blockers or digitalis

A-fib treatment Recognize the underlying cause A rate under 120 in an asymptomatic patient generally requires no emergent treatment Unstable patients with acute rapid a-fib should receive synchronized cardioversion with 50-100 J Treatment otherwise depends on the duration

Treatment of A-fib Less than 48 hours duration Cardioversion is indicated in any unstable patient, synchronized if possible, with 50-100 J May also be used electively in symptomatic but stable patients Pharmacologic cardioversion may be attempted with procainamide, amiodarone or ibutilide

Treatment of A-fib > 48 hours Longer duration predisposes the patient to atrial clot formation and failure of conversion Rate control with diltiazem, beta blockers or digitalis Do not attempt cardioversion unless emergently indicated Anticoagulation and arrangement for echo

Atrial Flutter Patients usually with cardiac or pulmonary dz Conduction through the AV node may be at a 2:1, 3:1, 4:1 or 5:1 rate Whenever you see a ventricular rate close to 150 you should consider a flutter Frequently is a transient rhythm which may degenerate into a-fib or convert to sinus

Treatment of A-flutter Hemodynamically unstable - immediate synchronized cardioversion Hemodynamically stable Vagal manuevers – if no carotid bruits Adenosine - will not terminate the atrial tachycardia, but may allow flutter waves to become more apparent Dig, beta blockers or calcium channel blockers for AV nodal blockade to slow the ventricular rate

SVT AV nodal reentrant tachycardia Usually you see a regular, narrow complex tachycardia without p waves Treatment – adenosine, beta blockers, calcium channel blockers, digoxin

Is it SVT, afib, aflutter, sinus tach? SVT – HR around 150s Is it SVT, afib, aflutter, sinus tach?

Preexcitation syndrome Wolf-Parkinson-White syndrome AV re-entrant tachycardia (accessory pathway) Short PR interval, delta waves Treat like PSVT if the QRS is narrow If the QRS is wide or if afib is present, use amiodarone or procainamide (slow the atrial rate and increase conduction through the AV node) Avoid ABCD – adenosine, beta blockers, calcium channel blockers, dig – if WIDE QRS

Narrow complex WPW

Wide complex WPW

Atrioventricular Blocks First Degree Second Degree - Type I Second Degree - Type II Third Degree

Second Degree AV Blocks Group to group beating Second degree blocks are partial blocks Two types Type I, Mobitz I or Wenckebach - transient Type II, Mobitz II or Classic - often degenerates into 3rd degree heart block

Second Degree Type I Decremental Conduction: Grouped beats with progressively longer PR intervals until an impulse is not conducted (a p without a QRS) Usually narrow QRS Generally requires no treatment – atropine, temporary pacing if symptomatic May be associated with inferior MI

Second Degree Type II Conduction fails suddenly, without a change in the PR interval This is not a benign rhythm, is chronic and often progresses to a complete heart block Is associated with anteroseptal MI May have wide QRS

Second Degree Type II No pharmacologic treatment – atropine has no effect on the His-Purkinje system so not helpful and may worsen the conduction ratio Emergency treatment - transcutaneous or transvenous pacing

Third Degree Block Complete block - there is total AV Dissociation None of the atrial impulses are conducted through to the ventricles (P and QRS are independent, P-P and R-R intervals constant An escape rhythm from a focus below the block will drive the ventricles If the escape rhythm originates in the AV junction, the ventricular rate will be in the range of 40-60 and the QRS less than 0.12 If the escape is generated from the ventricles, the rate will be in the range of 20-40 with a wide QRS

Third Degree Block Although patients may be asymptomatic, transcutaneous or transvenous pacing is warranted Autonomic drugs such as atropine will have no effect on ventricular rate Type I antiarrhythmics should be avoided (they may suppress the escape rhythm)

Ventricular Arrhythmias PVCs V tach V fib

Premature Ventricular Contractions Generally benign, but may be a consequence of a pathology, esp if multifocal More concerning causes include hypoxia, ischemia, MI, toxins/drugs, acidosis or alkalosis, hypokalemia

Ventricular Tachycardia Results from a dysrhythmia originating at or below the bundle of His Has a wide QRS complex (>0.12 second) May be monomorphic or polymorphic

Monomorphic V-tach Morphologically consistent QRS complexes Most common form of v-tach Seen primarily with cardiac ischemia Also seen in cardiomyopathy, valvular disease, electrolyte imbalance, myocarditis

Polymorphic V-tach QRS complexes vary in structure and amplitude Predominantly caused by CAD Associated with more severe disease

Torsades de pointes A specific form of polymorphic v-tach Associated with prolonged QT May be due to drugs (tricyclics), electrolyte imbalance (hypo K, Mg or Ca), or subarachnoid hemorrhage

Treatment of Ventricular Tachycardias Unstable - immediate cardioversion 100 – 200 – 300 – 360 Stable - amiodorone 150 mg IVP or lidocaine 1 mg/kg and prepare for elective cardioversion If torsades de pointes – magnesium 1-2g IV

Ventricular Fibrillation An irregularly irregular rhythm with no p waves or definite QRS complexes

Treatment of V Fib Defibrillate Adult 360/360/360 joules Children 2 joules/kg Epinephrine 1 mg IVP q 3-5 min (0.01 mg/kg) Amiodarone, Lidocaine, Magnesium

Osborne Waves Not a true arrhythmia, but an EKG abnormality suggestive of underlying pathology Seen primarily in hypothermia, < 35.6 degrees May also be seen in other conditions, such as hypercalcemia or brain injury Also called J-waves, Camel backs, hathooks

Osborne Waves - Hypothermia

Osborne Waves - Hypercalcemia

Brugada Syndrome Genetic disease - autosomal dominant Mutation in the gene that controls the Na channel Characteristic ECG – ST segment elevation V1-V3 no signs of ischemia short QT interval Most common cause of sudden death in young males with no underlying cardiac disease Prevalence for Asians Cause of death – polymorphic V tach or V fib Treatment – no medicine will prevent AICD to abort lethal arhythmias

Diagnostic Criteria Type I is the only ECG criterion that is diagnostic of Brugada syndrome. (see figure). Definitive diagnosis - type 1 ST-segment is observed in >1 right precordial lead (V1 to V3) and one of the following: documented ventricular fibrillation (VF) polymorphic ventricular tachycardia (VT) a family history of sudden cardiac death at <45 years old coved-type ECGs in family members inducibility of VT with programmed electrical stimulation syncope nocturnal agonal respiration.

Brugada Syndrome

Now for some cases…

82 yo male with hx HTN c/o weakness dizziness SOB BP 100/50 HR 155 What does the EKG show? What is the treatment? EKG = a fib with RVR A-adenosine B-beta blockers C-ca channel blocker D-dig

35 yo female c/o palpitations, near syncope, occasional episodes of rapid HR What does the EKG show What medicines should be avoided in this patient? EKG= WPW avoid adenosine, beta blockers, ca channel blockers, dig

65 yo male with COPD c/o SOB, wheezing and pedal edema What does the EKG show? What is the treatment? EKG=MAT Treat the COPD

91 yo female c/o weakness and syncope. What does the EKG show 91 yo female c/o weakness and syncope. What does the EKG show? What is the treatment? EKG= 3rd degree block

What does the monitor show? What is the treatment? 26 yo medical student presents with N,V altered mental status. She has not been eating well. She is on Erythromycin for a URI. Her K=2.1 Mg=1.0 (nl=1.8-3.0) She collapses in the ER and is placed on a monitor. What does the monitor show? What is the treatment? Monitor = torsades treatment = IV magnesium

48 y/o F presents lightheaded after walking 48 y/o F presents lightheaded after walking. She just started metoprolol. What does the ecg show? What is the treatment? Ecg = SB no rx if stable, pacing or atropine if unstable

42 y/o F presents with palpitations and DIB. What does the ecg show 42 y/o F presents with palpitations and DIB? What does the ecg show? How could you differentiate the rhythm? Ecg = SVT, could give adenosine to differentiate SVT, afib, aflutter

You are working in the EC. The nurses come get you for this rhythm You are working in the EC. The nurses come get you for this rhythm. It appeared 45 min after giving thrombolytics for AMI. Previously it was NSR. What is this? What should you do? Ecg= idioventricular rhythm, do nothing for AMI thrombolytics as it is transient, other circumstances treat if unstable

86 y/o M c/o weakness and DIB. What rhythm is this on the monitor? What should you worry about? Are you going to treat this? Wenckebach, inferior mi, treat with pacing/atropine if unstable

61 y/o M with CP, palpitations, and dizziness. What is the ecg show 61 y/o M with CP, palpitations, and dizziness. What is the ecg show? What do you want to do? Ecg = VT, cardiovert if there is a pulse and unstable or symptomatic

What should you do (besides soil yourself)? So you cardioverted the previous rhythm and now this is on the monitor… What is this? What should you check? What should you do (besides soil yourself)? Vfib, pulse, defibrillate

24 y/o pregnant F presents with 3 days of vomiting… What does the ecg show? What is the treatment of choice? Ecg = ST, fluids, the p waves are clearly seen in lead III

52 y/o M who is homeless and found sleeping in an alley 52 y/o M who is homeless and found sleeping in an alley. What does the ecg show? What is the treatment? Osborne waves, re-warming, check electrolytes

45 y/o M with CKD on HD presents with palpitations and DIB after missing dialysis. What does this ecg show? What should you do to treat this? Hyperkalemia, calcium, bicarb, D50/insulin, kayexalate plus fluids and potentially lasix or albuterol

Had enough yet? The End