MD Notes

creation date: 2024-12-24 19:12
modification date: Tuesday, December 24th, 2024 19:12:27
status: note
tags:

Electrocardiogram

Lead placement

Views

II, III, aVF:

  • Inferior
  • Right coronary artery, marginal branch
    I, aVL, V5, V6:
  • Lateral
  • Left coronary, circumflex & obtuse marginal
    V1, V2:
  • Septum
  • Left coronary, septal branch
    V3, V4:
  • Anterior
  • Left coronary, anterior descending, diagonal arteries

Normal values

ECG settings: 25mm/sec, 10mm/mV

Rhythm: regular P-P, R-R if ±0.06s (1.5 small box)
Heart rate:

  • If regular: 1500 / # small boxes
  • If irregular: # of complexes in 6 sec * 10
    P-wave morphology: rounded and upright
    Q-wave is < 1/3 of R wave, <0.04s

PR interval: 0.12-0.20s (3-4 small boxes)
QRS: 0.06-0.10s (1.5-2.5 small boxes)

Note: fastest electrical impulse dictates heart rate - normally SA node

Axis

Sinus Rhythms

Sinus Rhythm (Normal)

  • HR: 60-100bpm
  • P wave for every QRS
  • See Normal values above

Sinus Bradycardia

  • HR < 60bpm
  • All else normal

Sinus Tachycardia

  • HR > 100bpm
  • Complexes may come together, partially burying P waves

Sinus Dysrhythmia

  • Irregular rhythm (changing HR), can coincide with breathing
  • All else normal
  • Pathophysiology: from parasympathetic response (eg. from vagus nerve pressure) - can be from breathing, medication, etc.

Sinus Arrest

  • Pause in activity, typically constant R-R interval prior
  • Pause >6s is emergency
  • Pathophysiology: SA node stopped

Sinus Exit Block

  • Same as sinus arrest EXCEPT pause duration is multiple of R-R interval

Atrial Rhythms

Premature Atrial Complex

  • Change in P wave morphology but upright
  • Can occur frequently or occasionally
  • Pathophysiology: Early impulse occurs in atria other than SA node

Wandering Atrial Pacemaker

  • Three differently shaped P waves
  • Rhythm may or may not be regular
  • Pathophysiology: Location of impulse source moves/wanders in atria

Multifocal Atrial Tachycardia

  • Same as wandering atrial pacemaker EXCEPT HR > 100 bpm

Atrial Flutter (Aflutter)

  • Atrial depolarization denoted by series of “F” waves (no P wave)
  • Flutter rhythm documented with F:QRS ratio
  • Pathophysiology: Obstruction within atrial conduction causing series of rapid depolarization; AV node blocks extra impulses

Atrial Fibrillation (Afib)

  • Atrial activity denoted with “f” waves (no P waves)
  • f waves can be coarse (≥3mm) or fine (<3mm)
  • Irregular R-R interval
  • HR often >160bpm
  • Pathophysiology: Multiple impulses occur within atria (chaotic); AV node overwhelmed by chaotic electrical activity; HR high due to loss of cardiac output due to “quivering” atria

Junctional Rhythms

  • Impulses initiated in AV junction; affects P wave morphology based on locatino of impulse

Premature Junctional Complex (PJC)

  • Abnormal P wave (see above)
  • Often occur in bradycardic rhythms
  • Disrupts underlying rhythm by occurring early

Junctional Escape Beat

  • Same morphologically as PJC
  • Often terminate sinus arrest
  • Pathophysiology: SA impulses too slow, junction acts as backup pacemaker

Junctional (Escape) Rhythm

  • Atrial activity due to AV junction
  • HR 40-60bpm (AV junction rhythm)
  • See above for P wave morphology
    • If P wave before QrS, likely shorter than normal (<0.12s)
    • P wave can also be buried or occur after QRS

Accelerated Junctional Rhythm

  • Same as junctional escape rhythm except HR 60-100 bpm

Junctional Tachycardia

  • Same as Junctional escape rhythm except HR 100-180 bpm

Supraventricular Tachycardia (SVT)

  • Impulses above ventricles (ie. AV node or above) with HR 150+ bpm
  • Overlap of P wave and previous T wave

Ventricular Rhythms

  • Pathophysiology: Failure of faster pacemakers in heart or abnormal stimulation of ventricle resulting in faster rate of ventricular impulse

Premature Ventricular Complexes (PVC)

  • Early impulse from ventricle disrupts underlying rhythm
  • Absence of P wave and wide, bizarre QRS

Agonal Rhythm

  • HR < 20 bpm
  • No P waves and wide, bizarre QRS
  • Regular or irregular rhythm often indeterminable due to slow rate

Idioventricular Rhythm

  • HR 20-40 bpm
  • No P waves and wide, bizarre QRS

Accelerated Idioventricular Rhythm

  • HR 40-100 bpm
  • No P wave and wide, bizarre QRS

Ventricular Tachycardia (VTach)

  • HR >100 bpm
  • No P wave and wide, bizarre QRS
  • Can treat with defibrillation

Ventricular Fibrillation (VFib)

  • No P wave, no QRS
  • Heart is not beating
  • Pathophysiology: Small regions of tissue are independently depolarizing causing heart to “quiver”

Asystole

  • Total absence of electrical activity
  • Clinically dead

Ventricular Asystole

  • Asystole except P waves still present
  • Clinically dead

Pacemaker Rhythms

Atrial Pacemaker Rhythm

  • Pacing spike immediately preceding P wave
  • PR interval is from spike to QRS

Ventricular Pacemaker Rhythm

  • Pacing spike immediately preceding the QRS complex
  • May or may not have P waves

Atrioventricular Pacemaker Rhythm

  • Pacing spike immediately preceding P waves and QRS
  • PR is atrial spike to ventricular spike - referred to as AV delay, programmed by physician

Failure (Loss) to Capture

  • Presence of pacing spike but no waveform immediately following it
  • Inherent rhythm becomes present

Heart Block

First Degree Heart Block

  • Looks like sinus rhythm EXCEPT P-R interval regular and >0.20s (4 small box)
  • Typically stable; if occur during MI, should monitor

Second Degree (Mobitz) Heart Block Type I

  • Aka Wenckebach Phenomenon
  • Prolonging P-R interval from one complex to the next until QRS is non-conducted, pattern then restarts
  • P-P intervals are regular, R-R interval irregular
  • Typically stable/temporary as long as ventricular response remains “normal”

Second Degree (Mobitz) Heart Block Type II

  • Constant P-R interval with missing QRS
  • QRS can occur in specific ratio to P waves OR unpredictable
  • Can progress to third degree heart block
  • (3:1 block)

Third Degree Heart Block

  • Aka Complete Heart Block
  • Regularly occurring P waves and QRS complexes at two distinct rates
  • Pathophysiology: Disease or tissue death preventing atrial impulses from entering ventricular conduction system
  • (Red arrow pointing to buried P wave)

Bundle Branch Block

Left Bundle Branch Block (LBBB)

  • Widen QRS (>0.12s; 3 small box)
  • Dominant S wave in V1 (points down)
  • Broad monophasic R wave and absence Q wave in lateral leads (I, aVL, V5-6)
  • Prolonged R wave peak in leads V5-6

Right Bundle Branch Block (RBBB)

  • Widen QRS (>0.12s; 3 small box)
  • RSR’ in V1-3 (M-shaped QRS)
  • V1 points up
  • Wide, slurred S wave in lateral leads (I, aVL, V5-6)

Fascicular Blocks

Left Anterior Fascicular Block (LAFB)

  • Left axis deviation (positive in lead I, negative in aVF)
  • qR complex in lead I, aVL
  • rS complexes in lead II, III, aVF
  • May have prolonged QRS, increased QRS voltage in limb leads
  • Ex: LITFL

Left Posterior Fascicular Block (LPFB)

Ventricular Hypertrophy

Left Ventricular Hypertrophy

  • S wave depth of V1 + tallest R wave height in V5 or V6 is > 35mm
  • Should find evidence of left ventricular strain (ST depression or T wave inversion in left-sided leads)
  • Pathophysiology: Thickened LV wall results in prolonged depolarization (R wave peak time) and delayed repolarization (strain indicators)

Right Ventricular Hypertrophy

Ischemia, Injury, Infarction

  • Look for changes in anatomically contiguous leads (eg. II, III, aVF), should show up in more than one

Ischemia

  • Delay in repolarization resulting in:
    • ST segment depression of ≥1 mm
    • T wave inversion in two or more anatomically contiguous leads
ST depressionT inversion

Injury

  • Delayed ischemia for few minutes can worsen to myocardial injury
  • ST segment elevation of ≥1 mm in two or more anatomically contiguous leads

Infarction

  • ST elevation, T wave inversion during MI
  • Following MI, ST and T returns to normal but Q wave will remain increase duration (≥0.04s) or depth (≥ 1/3 height R wave)