Basic:
Rate:
QTc – QT interval α to heart rate. Faster heart beats → Faster ventricles repolarize → Shorter QT interval.
I.e., “normal” QT varies with heart rate. For each heart rate, calculate an adjusted QT interval, called the:
Intervals:
“corrected QT” (QTc)
PR – 0.12 - 0.20 seconds (3 - 5 boxes) < 0.12 s High NE/E states Wolff-Parkinson-White
WPW syndrome (delta-wave)
0.12-0.20 s > 0.20 s Normal
AV nodal blocks
1st Degree AV Block
Normal ; < 0.44 s Long QT : > 0.44 s
Tip: QT > half RR interval ≈ long.
QRS – 0.04 - 0.12 seconds. (1 - 3 boxes) < 0.10 s
0.10-0.12 s > 0.12 s Incomplete BBB Normal Bundle Branch PVC Block (BBB) Ventricular rhythm Incomplete bundle branch block
3rd degree AV block with ventricular escape rhythm
A prolonged QT may predispose a type of ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte abnormalities, CNS disease, post-MI, and congenital heart disease.
Heart Arrhythmias 1. Sinus Rhythms Sinus Tachycardia Sinus Bradycardia
Rate: > 100 bpm Rate: < 60 bpm
2. Premature Contraction / Beats Atrial (PACs) Ventricular (PVCs)
Contour of P, PR interval, timing differ from normal pulse from SA node and QRS will be narrow (0.04 0.12 s) (normal impulse conduction in ventricles) Wide and bizarre QRS complex(es). a. Uniform : look alike, b. Multiform : look different
3. Supraventricular Arrhythmias
a. Atrial Fibrillation (AF) No normal P waves, Flutter wave. (No organized atrial depolarization, impulses are not from sinus), atrial activity is chaotic (irregular rate). Common, affects 2-4%, up to 5-10% if > 80 years old. Due to multiple reentry between LA and RA. b. Paroxysmal SupraventricularTachycardia (PSVT) HR suddenly speeds up, often due to PAC and the P waves are lost. Due to reentry in AV node. c. Atrial Flutter No P waves, “saw tooth” pattern at 250 - 350 bpm. Only some impulses conduct through AV node (usually every other impulse). Due to reentry in RA with every 2nd, 3rd or 4th impulse generate a QRS (others are blocked in AV node as node repolarizes). 4. Ventricular Arrhythmias a. Ventricular Fibrillation Completely abnormal. Ventricular cells are excitable and depolarizing randomly. Causes rapid drop in CO and death b. Ventricular Tachycardia Impulse originates in ventricles (no P waves, wide QRS). Due to reentry in ventricle. 5. AV Junctional Blocks a. 1st Degree AV Block PR Interval: > 0.20 s, Prolonged conduction delay in the AV node or Bundle of His.
b. 2nd Degree AV Block, Type I (Mobitz I/ Wenckebach) PR interval progressively lengthens, then impulse is completely blocked (P wave not followed by QRS). Each atrial impulse causes longer delay in AV node until one impulse (usually 3rd or 4th) fails to conduct to AV node.
c. 2nd Degree AV Block, Type II / Mobitz II is
Occasional P waves are completely blocked (P wave not followed by QRS). Conduction all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His.
d. 3rd Degree AV Block
P waves are completely blocked in the AV junction; QRS originate independently from below the junction. (Ventricles pacemaker: around 30-45 bpm, conduction through ventricles is inefficient and the QRS will be wide and bizarre.)
Axis Axis refers to the mean QRS axis (or vector) during ventricular depolarization. An abnormal axis can suggest disease such as pulmonary hypertension from a pulmonary embolism. The QRS axis is determined by overlying a circle,in the frontal plane. By convention, the degrees of the circle are as shown. A quick way to determine the QRS axis is to look at the QRS complexes in leads I and II. QRS Complexes I (L) II (R) Axis + + normal + left axis deviation + right axis deviation right superior axis deviation Diagnosing a Myocardial Infarction (MI) One way to diagnose an acute MI is to look for elevation of the ST segment. MI Location MI Lead Anterior V1 - V4 Lateral I, aVL, V5 - V6 Types of MI: Inferior II, III aVF ST (Transmural / Q wave) Non-ST (Subendocardial / Non-Q-wave) Ischemia ST depression, peaked T-waves, then T-wave ST depression & T-wave inversion inversion Infarct ST elevation & appearance of Q-waves Fibrosis ST and T-waves normalize, Q-waves persist ST normalize, but T-wave inversion persists
Heart Hypertrophy Left atrial enlargement (LAE) • •
P wave - atrial depolarization II : P > 0.04 s (1 box) between notched peaks, or
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V1 : P Neg. deflection > 1 x1 box
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Cause : LVH from hypertension.
Right atrial enlargement (RAE) • •
II : P >2.5mm, or V1/V2 : P >1.5mm
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Cause : RVH from pulmonary hypertension
Left ventricular hypertrophy (LVH) • •
R in V5 (or V6) + S in V1 (or V2) > 35 mm, or avL: R > 13 mm
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Cause: hypertension.
Right ventricular hypertrophy (RVH)
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R wave is normally small in V1, V2 because RV does not have a lot of muscle mass. But in RVH the R wave is tall in V1, V2. Right axis deviation, and V1 : R >7mm tall
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Cause: left heart failure.
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Bundle Branch Blocks (BBB) QRS complex widen because when the conduction pathway is blocked it will take longer for the electrical signal to pass throughout the ventricles.
Left Bundle Branch Blocks (LBBB) V1-V2 : Broad, deep S waves / W wave
Right Bundle Branch Blocks (RBBB) V1-V2 : “Rabbit Ears” / M wave
Bifascicular block = RBBB + left bundle hemiblock, manifest as an axis deviation, eg LAD in the case of left ant. hemiblock. Trifascicular block = bifascicular block + 1st degree heart block.
