ECG Conferences – 2012 - 2013Steven R. Lowenstein, MD, MPH

ECG Curriculum

• Inferior MI• Anterior MI• Posterior MI• ST-T depressions• ST-T elevations • Electrocardiography

of shortness of breath

• Atrial Fibrillation• Supraventricular

tachycardias• Wide complex tachycardias• Bradycardias and heart

block• Electrocardiography of

syncope• Wide, ugly QRS rhythms in

critically ill patients

46 year old female with mild, fleeting right-sided chest pain while at work. She wants to know if “everything is OK.”

Healthy 25 year old man, presented with nausea, diarrhea, dizziness

Is it Normal Sinus Rhythm?

AV

Junction

.13 sec delay

Purkinje

Cells

Atrial delay: .03 seconds

IIIII

AVF

AVR

I

AVL

Normal Sinus Rhythm

Junctional (not sinus) rhythms

II

aVF

II

aVR

25 YEAR OLD MAN WITH GASTROENTERITIS

Atrial Fibrillation

• Most irregularly irregular rhythms are atrial fibrillation.– Less frequent: Atrial flutter or MAT

• AF is the most common tachycardia encountered in clinical practice.

ATRIAL FIBRILLATION: The ECG•Irregularly irregular•No distinct, discrete p-waves

•Irregular fibrillatory f-waves (350+ beats/min)

•f-waves vary in rate, intervals, size and shape*

•Ventricular rate = 100 – 170 beats per minute•QRS complex is narrow – unless:

•Pre-existing BBB•Rate-related aberrancy•Accessory Pathway

•Exam: Pulse deficit; no S4 ; Varying S1

The irregularly irregular tachycardias

• AF: no distinct, discrete p-waves• Atrial flutter: p-waves are distinct, uniform

at a rate that is close to 300• Often slower if anti-arrhythmic drugs

• Atrial tachycardias: uniform, distinct p-waves at a slower rate (140-220)

• MAT: p-waves are distinct, but they vary in size, shape, direction (multi-form)

•In AF, electrical activity suggestive of p-waves is common

•But even where the R-R interval is long: distinct p-waves cannot be seen, and there is no uniform p-p interval

•“Fib-flutter?”

Coarse and Fine AF

• The amplitude of the f-waves correlates with duration– Coarse f-waves more common if recent onset.

• f-waves of greater amplitude also seen with atrialmuscle hypertrophy; diminishes with LA fibrosis

– Fine AF (with a quiet baseline, no obvious f-waves) often signifies AF of long duration

– Amplitude of f-waves does not correlate with left atrial size

Also on the ECG . . . . .

• Markers of other cardiac disease– Left ventricular hypertrophy– Conduction system disease– Evidence of prior myocardial infarction

85 year old female with mild dyspnea, fatigue

Atrial Fibrillation• Most common cardiac arrhythmia encountered in clinical

practice• Tied closely to advancing age• Rarely, if ever, a one-time event; it can be expected to

recur at unpredictable intervals.

•Trigger: PACs arise from atria or muscular tissue of pulmonary veins•Mechanism:•Multiple colliding re-entry wavelets•Enlarged atrium harbors fibrosis and inflammation, perpetuating re-entry•Ongoing electrical and structural remodeling

AF: Predisposing FactorsAtrial enlargement, stretchpressure overload, fibrosis

• Hypertension• Congestive Heart Failure• Other structural heart

diseases – Valvular heart disease (MS)– Cardiomyopathy

• COPD, pulmonary embolism

• Acute myocardial infarction

Other conditions• Thyrotoxicosis• Hypokalemia,

hypomagnesemia• Hypoxia• Alcohol• Obesity, metabolic

syndrome

AF: Harbingers

• Left or right atrial enlargement PACs– Hours, days, weeks or months prior to onset

of AF

Errors in ECG diagnosis of AF

• Computer & human interpretations often wrong.– f-waves are too small or too tall (p-waves)– Ventricular rate is too fast, too slow or too regular– Tremors or electrical artifacts simulate f-waves– AF is confused with sinus tachycardia, MAT,

atrial flutter, AVNRT, multiple PACs– Wide complex AF is mistaken for VT

• Missed Pes and STEMIs

What determines ventricular response?

• Normal ventricular rate is ~110 – 170

Determinants:• Intrinsic delay of AV node• Modified by:

– Balance of sympathetic –parasympathetic tone

– Drugs– Fibrosis (with aging)

• Slow ventricular response – MEDICATIONS

• Calcium channel blockers• Beta blockers• Digitalis

– Sclero-degenerative conduction disease (SSS)

– Hypothermia• Very fast response (> 200)

– ↑Sympathetic tone:• Thyrotoxicosis• Fever • Hypoxia, sepsis, GI bleeding

– Accessory pathway

70 YEAR OLD MAN WITH COPD, PRESENTS WITH 2 DAYS OF FEVER, CP, ↑COUGH, SPUTUM AND SOB; Temp was 39.8° C.

Rapid Atrial Fibrillation: Hemodynamic Consequences

• Rapid rate (shortened diastole)• Loss of regular, organized atrial systoles

(5-40% of cardiac output)• Many patients have pre-existing LV

dysfunction (hypertension, CHF)• If pronged: Ventricular dysfunction

• Tachycardia-induced cardiomypoathy– Remodeling begins in 24-48 hours if heart rate > 130

89 year old female with weakness. Unknown medical history, denies meds.

66 year old man found unconsious

AF with wide beats

• Pre-existing BBB (left or right)• Rate-related (functional) BBB

– Rate-related aberrancy below AV node– Typical pattern of BBB (usually right) at fast

rates• Pre-excitation (accessory pathway that

bypasses the AV node)

93 year old female (presented to Rose ED)

27 year-old female presents with the sudden-onset of palpitations, chest tightness, and lightheadedness approximately one hour prior to arrival … She became increasingly lethargic during her initial evaluation. BP was 88/54.

42 year old man with complaint of “fast heart beat,” mild dizziness and SOB

67 yo man with SSCP and SOB. Hx hypertension.

Review Tracings

90 year old female presented to ED with 1 day SOB and chest pain. History of CHF and CAD. BP: 144/87 Pulse: 124. Management?

66 year old female, history of multiple myeloma, DVTs, PEs. Presented with syncope, shortness of breath, mild chest pain.

38 y.o. man presented with 3 hours substernal chest pain (like “shoe on my chest”) and palpitations. At triage, BP = 115/70, then 100/80.

After electrical cardioversion

64 y.o. female has history of renal insufficiency, CHF and hypertension. Presented with 3 days of exertional dyspnea.

89 yo man with dyspnea and confusion

E.D. Management

Electrical cardioversion is treatment of choice only for:

– Hypotension or organ hypo-perfusion– Severe congestive heart failure– Active myocardial ischemia (symptomatic or

ECG)– Pre-excitation and AF

• In these circumstances, the need to restore NSR takes precedence over the need to anti-coagulate

ED Management: The non-emergent patient

• Avoid cardioversion unless anticoagulated– Conversion of AF to NSR --- by EC or drugs --- may

cause embolization of atrial thrombi unless patient has adequate anticoagulation

• Rate control (and treatment of precipitating illness) is the recommended initial treatment for all stable patients.

• After rate control, up to 50% of patients will convert to NSR “naturally” within 24 hours

Final management points• Recent-onset AF often converts to NSR

– Spontaneously or with treatment of underlying conditions

• Know how to select rate-control drugs• Only choose rhythm conversion if known < 48 hours• It is worth ordering TSH and free T4 • There is no need to admit to “rule out MI”

– Unless clinical or ECG evidence of ACS, angina• If hypotension is present with AF and moderate

ventricular response ( < 130), find another cause– PE, Acute MI, sepsis, hypovolemia

• Do not hesitate to use EC in patients who truly need it.