ECG Interpretations in Anesthesiology

Brian C. Weiford M.D., FACCPostgraduate Symposium on

AnesthesiologyApril 11, 2014

ECG Interpretations for the Anesthesia Professional

• ECG skills are valuable at every phase of the continuum of care– Preoperative: PAT clinic, etc– Intraoperative– Postoperative

Topics

• The normal ECG• Arrhythmias

– Ectopy– Supraventricular– Ventricular

• Coronary Ischemia, Injury, and Infarct• Pacemakers• Miscellaneous fun with ECGs

Components of the ECG - ReviewP – Wave: Atrial Depolarization.

• Can be positive, biphasic, negative.

QRS Complex: Ventricular Depolarization.

• Q – Wave: 1st negative deflection wave before R-Wave.

• R – Wave: The positive deflection wave.

• S – Wave: 1st negative deflection wave after R – wave.

T – Wave: Ventricular Repolarization.

• Can be positive, biphasic, negative.

Normal Sinus Rhythm with Normal ECG Normal variant Juvenile T wave pattern

From Braunwald’s Heart Disease, 7th Ed.

Sinus Arrhythmia/Dysrhythmia

Two forms of Sinus Dysrhythmia: 1) more commonly, due to respiratory variability and changes in

vagal tone

2) In elderly subjects with heart disease, and probably related to sinus node dysfunction

Sinus Bradycardia

•Sinus rate < 60 bpm, but usually not clinically significant unless < 50 bpm•Sinus rate is usually > 40 bpm in normal subjects•HR < 40 bpm can be seen commonly in normal subjects during sleep and in well-trained athletes•Sinus rate affected by numerous medications

•Beta blockers, calcium channel blockers, digoxin, antiarrhythmics, clonidine, neostigmine, etc.

•For sinus rates < 40-50 in the absence of medications:•consider sinus node dysfunction (SSS), hypothyroidism, hypothermia, ischemia, and infarction.

Sinus Tachycardia

•Most often, a physiologic reactive phenomenon (to extracardiac stimuli: e.g., hypotension, pain, fever, hypoxia, anemia, anxiety, thyrotoxicosis, etc)•Rarely, “inappropriate sinus tachycardia” observed, with elevated resting sinus rate and exaggerated acceleration of sinus rate with physiologic stimulation.

•Can be treated with radiofrequency ablation/SN modification

Sinus Tachycardia

• Age predicted maximal HR (APMHR) = 220-age

• That rate can be exceeded in intense physiologic exercise, stress, or exaggerated adrenergic stimulation

• Differentiation from supraventricular dysrhythmias (atrial tachycardia, Aflutter) can sometimes be challenging

Premature Atrial Complexes (PACs)

• A supraventricular impulse that occurs earlier than expected and originates in an atrial focus, not in the SA node

• Due to increased automaticity of an atrial focus

• Typically they are clinically insignificant– Can serve as triggers for sustained

dysrhythmias like SVT or AFib/flutter

Premature Atrial Complexes (PACs)

• Based on multiple ambulatory ECG studies, PACs are common findings in healthy subjects, being observed in:– ~15% of infants <10 days old– 13% of 10-13 year old boys– Nearly 2/3 of healthy 22-28 year old women

and > 1/2 of asx male medical students– 100% of 19-29 year old long distance runners– 100% of apparently healthy octogenarians

Wagner, Marriott’s Practical Electrocardiography, 9th ed.

PAC Generation

Courtesy of St. Jude Medical

PAC Morphology

• QRS complexes, ST segments, and T waves should be normal or unchanged from baseline.

• P wave morphology will be different than sinus P wave.

• Shorter PR intervals than sinus PR interval– Due to location of the foci– Shorter routes for

their depolarization waves

Junctional beats/escape Ectopic Atrial Rhythm

Note negatively directed P wave in II

Ectopic Atrial Rhythm

• Often transient• Can occur in individuals with and without

structural heart disease• Distinguish from sinus rhythm by

comparing P wave morphologies, P wave vector

PVC(Premature Ventricular Complex)

Frequency of PVCs in General Population

• Based on the ARIC study (of almost 16000 45-65 year olds in 4 US communities), overall prevalence was– 8% in African American males– 7% in white males– 7% in African American females– 5% in white females– In older, African American males with heart disease,

prevalence ~20%– Strong association between HTN and prevalence of

PVCsSimpson: Am Heart J 2002;143:535-40

Frequency and Significance of PVCs in General Population

• In the ARIC study, there was a more than 3x increase in coronary heart disease (CHD) mortality in subjects with PVCs

• After controlling with CV risk factors and therapy, subjects with PVCs were twice as likely to die from CHD than those without PVCs

Massing: Am J Cardiol 2006;98:1609 –1612

Quadrigeminal PVCs Actual Advertisement

Functional LBBB (with underlying sinus tachycardia and HR 115 bpm)

Atrial Fibrillation with elevated ventricular response

Note irregularly irregular and rapid R-R pattern with absence of P waves

Ventricular pacing with underlying Atrial Flutter

2nd Degree AV block (Mobitz II)

•Note predominant 2:1 association of P waves and QRS complexes•Note wide complex QRS

2nd Degree AV block

• Mobitz I (Wenckebach) 2nd degree AV block can be seen in normals and in subjects with heart disease– 2nd degree AV block present in 11% of healthy 10-13

year old boys and 40% of distance runners based on holter/ambulatory ECG studies

• QRS is prolonged 80% of the time with Mobitz II block (infranodal block—within or below bundle of His)

• 2:1 AV block can be due to to a Mobitz I or Mobitz II block mechanism

Sinus rhythm with complete heart block (in setting of acute inferior MI)

Note regular R-R intervals and lack of 1:1 association with P waves (plus ST elevation in inferior leads)

Atrial Fibrillation with complete heart block

Note absence of P waves and coarse baseline with regular R-R intervals

Note marked bradycardia, scalloped/sagging ST depression in inferior leads, flattened T waves in lateral leads, and prominent U waves in V2-3.

Digoxin effect and toxicity: complete heart block with junctional escape rhythm

WPW (underlying sinus rhythm)

From Braunwald’s Heart Disease, 7th Ed.

• Aberrant conduction of supraventricular impulses. Note association of P waves with QRS

• Refractory period of bundle branches is related to preceding R-R interval. – Long-short initiation sequence finds right bundle in

refractory period and QRS is conducted aberrantly (RBBB)

• Ashman’s phenomenon– Common cause of “pseudo VT”

Multifocal Atrial Tachycardia

•Irregularly irregular tachycardia with 3 or more distinct P wave morphologies•Important to differentiate from atrial fibrillation•Highly associated with lung disease such as COPD

From Braunwald’s Heart Disease, 7th Ed.

ECG Changes in Acute Coronary Syndromes (ACS)

• ST depression = Ischemia– Digoxin effect, Repolarization changes with LVH

• ST elevation = Injury (threatened infarction)– Pericarditis, Coronary vasospasm

• Q waves = Infarction– Pseudo Q waves

Prevalence of ECG post surgery• Based on the VISION study

– New T wave inversions most common (in 23%), but not likely clinically significant

– New ST depression of > or =1mm (in 16%)– New ST elevation of > or =1mm (in 2.3%)– New LBBB (in 0.5%)

• Three findings independently associated with 30 day mortality: ST elevation, anterior ST depression, and new LBBB

• Most new ischemic ECG changes in POD#1

Biccard: Curr Opin Anesthesiol 2014, 27:000–000

Pseudo-infarct Patterns (Q-waves in absence of MI)

• WPW• Hypertrophic CM• LVH• LBBB• RVH• LAFB• Chronic lung disease• Amyloid, sarcoid, & infiltrative

cardiomyopathies• Chest deformity• Pulmonary Embolus• Myocardial contusion• Acute CNS ischemia

• Myocarditis• Myocardial tumors• Hyperkalemia• Pneumothorax• Pancreatitis• Lead reversal• Corrected transposition• Muscular dystrophy• Mitral valve prolapse• Left/right atrial enlargement• Atrial flutter• Dextrocardia

Ischemia

Diffuse Ischemia Ischemia?

• 23 year old with hypertrophic cardiomyopathy• Note high QRS voltage Injury Pattern

Location in Acute ST-Segment elevation MI (STEMI)

• Anterior:- rS complex in V1 followed by ST segment elevation in leads V2-V4

• Anteroseptal:– abnormal Q or QS deflection in V1-V3 and sometimes V4 with ST

segment elevation• Anterolateral:

– abnormal Q waves with ST segment elevation in leads V4-V6• Lateral/High Lateral:

– abnormal Q wave in lead I and aVL with ST segment elevation• Inferior:

– abnormal Q wave in at least 2 of leads II, III, aVF with ST segment elevation

• Posterior:– initial R wave in V1-V2 >0.04s with R>S, and ST segment

depression (usually >2mm) with upright T waves.

Location

Diffuse Mild ST elevation: Pericarditis

Note PR segment depression in multiple leads, and PR elevation in aVR

Anteroseptal STEMI Inferior STEMI

Inferior STEMI (with probable RV involvement) Inferior STEMI (with probable posterior involvement)

Lateral STEMI Extensive Injury (posterior, inferior, lateral, and anterolateral)

True Posterior Injury/Infarct Criteria Extensive Injury (anteroseptal, anterolateral, lateral and inferior)

Extensive inferior and anterolateral STEMI

Acute MI with chronic LBBB

Single Chamber Pacing System

AAI Pacemaker VVI Pacemaker

Dual Chamber pacing

Real or Artifactual?

Thanks