Cardiac Arrhythmias: Sinus, Atrial & Junctional Rhythms

Sinus Rhythms

• Normal Sinus Rhythm: A normal heartbeat pattern. Characterized by consistent P waves preceding each QRS complex.

• Sinus Bradycardia: Heart rate below 60 bpm. P waves precede QRS complexes.

• Sinus Tachycardia: Heart rate above 100 bpm. P waves precede QRS complexes.

• Sinus Arrest: The SA node stops pacing completely, resulting in a flatline on the ECG for more than 3 seconds.

Atrial & Junctional Rhythms

• Sinus Arrhythmia: Heart rate varies with breathing patterns. Normal variation.

• Atrial Fibrillation: Multiple chaotic electrical signals from the atria. No discernible P waves; erratic baseline, irregular heart rhythm. Atrial rate of 350-450 bpm.

• Atrial Flutter: Extremely irritable signals from the right atrium. Atrial rate of 250-300 bpm, with a distinct saw-tooth pattern of F waves. Rhythm is still regular.

• Junctional Rhythms: The junctional foci take over and form a rhythm, sometimes replacing the normal sinus rhythm. Consecutive beats.

Junctional Escape Beats

• Pathology: Sinus pause, junctional foci take over and create a singular beat, then returns to normal sinus rhythm. A pause is noted then immediate resumption of beats, otherwise the rhythm is the same

• Sinus Pause: Inverted or hidden P wave with normal sinus rhythm.

Premature Atrial Contractions (PACs)

• Etiology: Increased sympathetic stimulation; caffeine, cocaine; adrenergic stimuli;hyperthyroidism;digoxin;alcohol; etc.

• Pathology: Irritable foci in the atria causing QRS complexes to appear sooner than expected.

Atrioventricular Reentrant Tachycardia (AVRT)

• Etiology: Males. Accessory pathway (Bundle of Kent) allows impulses to sneak from atria to the ventricle. Early ventricular depolarization.

• Pathology: The Bundle of Kent is an accessory pathway that allows impulses to slip past the AV node, leading to rapid, irregular heartbeats.

Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

• Etiology: Females. AV node possesses two pathways; impulses circle within the AV node creating a loop circuit, where the atria and ventricles are just passageways in this feedback loop.

• Pathology: AV Node possesses two pathways allowing impulses to continue looping in the AV node, causing rapid, irregular heartbeats.

Multifocal Atrial Tachycardia

• Etiology: COPD; Elderly; CAD; Valvular disease; HTN; Cor pulmonale; Digoxin toxicity; decreased K+ and Mg+.

• Patho: Shifting pacer site in the heart from the SA node to two or more atrial pacer sites. This leads to different P wave morphologies.

Ventricular Rhythms

• Asystole: Absence of ventricular depolarization. Essentially a flatline on the ECG.

• Premature Ventricular Contractions (PVCs): Irritable ventricular foci cause earlier-than-expected ventricular depolarization - producing a wide QRS complex.

• Ventricular Tachycardia: Three or more PVCs in a row. Rate 150-250 bpm.

• Sustained VT: >30 seconds

• Non-sustained VT: <30 seconds

• Ventricular Fibrillation: Multiple chaotic depolarizations of ventricular fibers, leading to no pulse - cardiac arrest.

Other Cardiac Rhythms

• Ventricular Flutter: Single ventricular foci fires at rates of 250-350 bpm, with a sinusoidal wave pattern that closely resembles tachycardia.

• Torsades de Pointe: Drug-induced long QT; congenitally prolonged QT interval; characterized by twisting appearance of the QRS complex.

Atrioventricular Blocks

• First-Degree Block: Delay between atrial and ventricular depolarisation, PR interval > 0.2 seconds but not medically significant.

• Mobitz Type I (Wenckebach): Progressively lengthening PR intervals, followed by a dropped QRS complex.

• Mobitz Type II: Regular PR intervals, but occasional dropped QRS complexes.

• Third-Degree Block: Complete dissociation between atrial and ventricular depolarization, no communication between atria and ventricles.

Hypertrophy

• Left Atrial Hypertrophy: Mitral valve stenosis, hypertension, heart failure. Thickness of the atrium >2.5mm.

• Right Ventricular Hypertrophy: Stressor; infarction; heart failure. Right ventricle wall thickness increases, depolarizing toward V1, generating a sizeable R wave.

• Left Ventricular Hypertrophy: Stressor; infarction; heart failure. Left ventricle thickens; larger QRS deflections in precordial leads, such as V1-V6.

Myocardial Ischemia & Infarction

• Right Bundle Branch Block: Delays ipsilateral ventricular depolarization, resulting in wide bunny ear QRS complex in V1/V2.

• Left Bundle Branch Block: Delays the ipsilateral ventricular depolarization, creating a wide curved bunny ear QRS complex in V5/V6; QRS duration >0.12 seconds.

• Angina Pectoris (Stable/Unstable): Decreased coronary blood flow (ischemia); ST segment depression; inverted T waves.

• Myocardial Infarction: Complete blockage of a coronary artery. ST elevation >1.5 mm (women), >2 mm (men) in 2 contiguous leads; Anterior/Anteroseptal/Inferior/Lateral.

Posterior Wall MI

• Pathology: ST depressions in V1/V2. (inverted T waves may accompany this). This suggests ischemia, potentially infarction on the posterior wall.

Overview of different heart rhythms like sinus bradycardia/tachycardia, atrial fibrillation/flutter, and junctional rhythms. Covers ECG characteristics: P waves, QRS complexes, heart rate variations. Includes sinus arrhythmia and arrest.