16. RBBB Diagnostic criteria 1 QRS ≥ 0.12 s with slurring in the mid-final portion of the QRS. 2 V1: rsR′ pattern with a slurred R wave and a negativeT wave. 3 V6: qRs pattern with S-wave slurring and a positive T wave. 4 aVR: QR with evident R-wave slurring and a negative T wave. 5 T wave with polarity opposite to that of the slurred component of the QRS.
17. Partial or first-degree RBBB In this case, activation delay of the ventricle is less delayed. The QRS complex is 0.1–0.12 s in duration, but V1 morphology is rsR′ or rsr′.
19. Diagnostic criteria 1 QRS ≥ 0.12 s, sometimes over 0.16 s, especially with slurring in the mid-portion of the QRS. 2 V1: QS or rS pattern with a small r wave and a positive T wave. 3 I and V6: a single R wave with its peak after the initial 0.06 s (delayed intrinsicoid deflection). 4 aVR: a QS pattern with a positive T wave. 5 T waves with their polarity usually opposite to the slurred component of the QRS complex. LBBB
20.
21. Diagnostic criteria 1 QRS complex duration < 0.12 s. 2 ÂQRS deviated to the left (mainly between –45° and –75°). 3 I and aVL: qR, in advanced cases with slurring especially of the descending part of R wave. 4 II, III and aVF: rS with SIII > SII and RII > RIII. 5 S wave seen up to V6. LAHB
22. Diagnostic criteria 1 QRS complex duration < 0.12 s. 2 ÂQRS shifted to the right (between +90° and +140°). 3 I and aVL: RS or rS pattern. 4 II, III and aVF: qR morphology. 5 Precordial leads: S waves up to V6. Must first exclude (on clinical or other grounds) other causes of right axis deviation such as cor pulmonale, pulmonary heart disease, pulmonary hypertension, etc., because these conditions can result in the identical ECG picture! (A) An example of left posterior hemiblock. (B) The ECG of same patient some days before. The sudden appearance of ÂQRS shifted to the right confirms the diagnosis of LPH LPHB
23. (A) Right bundle branch block plus left anterior hemiblock and, the following day, (B) right bundle branch block plus left posterior hemiblock
54. (A) An example of left anterior hemiblock. (B) SI SII SIII pattern. See in this case SII > SIII and there is S in lead I.
55.
56.
57.
58.
Editor's Notes
Let’s consider reentry, another mechanism that can cause impulse conduction disorders. Reentry is the most common mechanism for tachyarrhythmias.
Like automaticity, triggered activity involves the leakage of positive ions into a cell, resulting in new action potentials. However, unlike automaticity, Triggered Activity is not consistently spontaneous. It may be either a single or repetitive firing of a myocardial cell, or group of cells, caused by re-excitation. Ion leakages that occur late in Phase 3 or early in Phase 4 (after cell recovery has begun) are called afterdepolarizations, or late potentials. Afterdepolarizations can be the ‘trigger’ that cause ventricular tachyarrhythmias.
Early afterdepolarizations, which occur in Phase 3 of the action potential, are responsible for pause-dependent triggered activity. Early after-depolarization may be caused by: a. Low potassium blood levels b. Slow heart rate c. Drug toxicity (ex. quinidine causing the Torsades de Pointes type of VT) Late afterdepolarizations, which occur in late Phase 3 or Phase 4 of the action potential, are responsible for catechol-dependent triggered activity. Delayed after-depolarization may be caused by: a. Premature beats b. Increased calcium blood levels c. Increased adrenaline levels d. Digitalis toxicity
ERP - Effective Refractory Period (also known as the “Absolute Refractory Period”) Occurs in Phases 0, 1, 2 and early Phase 3. During ERP an impulse of any strength cannot initiate depolarization because the impulse follows the initial depolarization too closely. The Na+ channels are inactive and can not be opened no matter how much the membrane is stimulated to depolarize. Without the limits ERP places on depolarization, the heart would beat so rapidly that it would be unable to fill and eject blood efficiently. Many antiarrhythmic drugs alter the ERP, thereby altering cellular excitability. Drugs that prolong the ERP can be effective in abolishing reentry currents responsible for some tachyarrhythmias.
RRP - Relative Refractory Period RRP is that period following the effective or absolute refractory period during which a cardiac cell can be stimulated to depolarize, but only by a stronger stimulus or impulse than is normally required for depolarization. In responding to high intensity stimuli, the impulse occurring during RRP typically conduct more slowly than normal and with aberrancy. Additionally, serious, life-threatening rhythm disorders can arise if a depolarization occurs within certain areas of the RRP. This is known as the R on T phenomenon.
Reentry refers to an electrical impulse continuously traveling an electrical loop within the myocardium. The depolarization wave-front reenters areas that have just been repolarized, creating a circular, continuous series of depolarizations and repolarizations. The following anatomic and physiologic properties create a reentrant loop: Two parallel conduction pathways around a central obstacle (A and B in above figure). Conducting tissue connects the pathways at both ends. One of the pathways (A) conducts more slowly than the other The other pathway, (B), exhibits unidirectional block, usually in the form of a substantially longer refractory period than the other pathway
To put it briefly: The tissue that forms the block and pathways for a reentry circuit is called the substrate A premature impulse (such as a Premature Ventricular Contraction, or PVC) serves as a trigger Substrate + Trigger results in reentry *Note: A substrate may develop due to scar tissue from various forms of heart disease.
For reentry to occur, the following events must take place: A premature impulse occurs in the reentrant circuit at a time when Pathway A (with the short refractory period) is ready to accept the impulse, and Pathway B (with the long refractory period) is still repolarizing from the previous depolarization. The impulse slowly travels through Pathway A and reaches Pathway B just as Pathway B completes it repolarization and is no longer refractory, which means it is ready to accept a stimulus. The impulse travels through Pathway B in a retrograde direction and reenters Pathway A. The impulse is conducted antegrade through Pathway A, and the circuit continues. Reentry does not display a “warm up” or “cool down” period.
There are many causes of rhythm disorders. Some of which include: Congenital, which are usually present at birth, but can develop through a lifetime Heart Disease Drug or chemically induced Some secondary causes of arrhythmias are: Electrolyte imbalances Endocrine disorders (hyperthyroidism, hypothyroidism and adrenal insufficiency, among others) Temperature (hypo/hyperthermia)
Neurocardiogenic Syncope is when a neurological disorder causes the inhibition of an electrical impulse. The brain keeps the impulse from being formed. Hypersensitive Carotid Sinus Syndrome (CSS) is a disease of the carotid sinus, a dilated portion of the carotid artery that has pressure-sensitive receptors that regulate heart rate and blood pressure. CSS is an extreme reflex response to carotid sinus stimulation and usually results in bradycardia and/or vasodilation. It can be induced by, among other things, a tight collar, shaving, head turning, exercise, and, of course, carotid sinus massage. Vasovagal syncope is a neurally mediated transient loss of consciousness and can be triggered by prolonged standing, fear, mental anguish, physical pain or anticipation of trauma or pain. The most common symptoms are dizziness, blurred vision, weakness, nausea, sweating, and abdominal discomfort.
Bradyarrhythmias can be categorized by the following: 1. Those caused by abnormalities of impulse formation: Sinus Arrest / Sinus Pause Sinus Bradycardia Brady / Tachy Syndrome 2. Those caused by abnormalities of impulse conduction: Exit Block (where the impulse is formed by the sinus node, but blocked immediately upon exit – no P-wave is formed) 1 st Degree AV Block 2 nd Degree AV Block 3 rd Degree AV Block Bi / Tri Fascicular Block
The first bradyarrhythmia we will consider is Sinus Arrest.
Sinus bradycardia occurs when the SA node fires at an abnormally slow rate.
Now, we’ll look at Third-Degree AV Block
Sinus Arrest occurs when there is a pause in the rate at which the SA node fires. With sinus arrest, there is no relationship between the pause and the basic cycle length.
SA exit block occurs when the SA node fires, but the impulse does not conduct to the pathways that cause the atrium to contract. In SA exit block there is a relationship between the pattern and the basic cycle length (because the sinus node continues to fire regularly), of approximately two, but less commonly three or four times the normal P-P interval.
Let’s now consider Sinus Bradycardia: a slow heart rate normally classified as being anything <60 BPM. Sinus Bradycardia is caused by abnormalities of impulse formation.
Let’s now consider Sinus Bradycardia: a slow heart rate normally classified as being anything <60 BPM. Sinus Bradycardia is caused by abnormalities of impulse formation.
