CC | Dysrhythmia

ell Properties & Conduction** Heart cells have four properties: automaticity, excitability, conductivity, contractility [1, 2]. Conduction travels from the SA node (60–100 bpm) through the AV node (40–60 bpm), bundle of His, bundle branches, to Purkinje fibers (20–40 bpm) [1, 3]. Vagal tone slows heart rate (HR); sympathetic activity increases HR and contractility [1]. Resting potential features high internal K+, external Na+; depolarization (Phase 0) is rapid Na+ influx [1, 4]. ECG Basics & Waveforms Leads II and V1 are used for monitoring [2]. Grid: horizontally, small square = 0.04s, large = 0.20s; vertically, small = 0.1 mV, large = 0.5 mV [5]. * P Wave (0.06–0.12s): Atrial depolarization [6]. * PR Interval (0.12–0.20s): Atrial-ventricular conduction [6]. * QRS Complex (<0.12s): Ventricular depolarization; pathologic Q (>=0.03s) suggests MI [6]. * ST Segment (0.12s): Isoelectric line; elevation or depression indicates ischemia or MI [6]. * T Wave (0.16s): Ventricular repolarization [6]. * QT Interval (0.34–0.43s): Total ventricular depolarization/repolarization [6]. Dysrhythmias & Treatment * Sinus Bradycardia (<60 bpm): Regular. Symptomatic bradycardia is treated with atropine, transcutaneous pacing (TCP), or dopamine/epinephrine [7, 8]. * Sinus Tachycardia (101–180 bpm): Due to stress, fever, pain; treat the cause [8, 9]. * PSVT (151–220 bpm): Reentrant. Vagal maneuvers, rapid IV adenosine (causes brief asystole), BBs, CCBs, or cardioversion [8, 10]. * Atrial Flutter: Sawtooth F-waves (200–350 bpm). Rate controllers, cardioversion, or catheter ablation [8, 11]. * Atrial Fibrillation: Chaotic f-waves (350–600 bpm); irregular. Lost atrial kick drops CO; stasis risks thrombi/stroke [11, 12]. Rate control: metoprolol, diltiazem, digoxin. Stroke prevention: warfarin, apixaban [12]. * AV Blocks: 1st-degree: constant PR >0.20s [8, 13]. Type I (Wenckebach): progressive PR lengthening until QRS drops [8, 13]. Type II (Mobitz II): constant PR, random dropped QRS; requires pacemaker [8, 14]. 3rd-degree (complete): complete AV dissociation; needs TCP, dopamine/epinephrine, pacemaker [8, 14]. * PVCs: Early, wide (>0.12s) distorted QRS. R-on-T can trigger lethal VT/VF [14, 15]. * VT (150–250 bpm): Stable VT uses amiodarone/procainamide; pulseless VT needs CPR/defibrillation [15, 16]. * VF: Chaotic quivering; zero CO. Lethal. Needs CPR, rapid defibrillation, epinephrine, amiodarone [16-18]. * Asystole / PEA: No pulse. Needs CPR, epinephrine, and intubation [18]. Key Interventions * Defibrillation: Unsynchronized shock (Biphasic 120–200J, Monophasic 360J) for VF/pulseless VT [17, 19]. * Cardioversion: Synchronized shock on R-wave for unstable tachycardias [20, 21]. * Pacemakers: Demand pacing. Malfunctions: failure to sense (inappropriate firing), capture (no contraction), or pace (no spike) [22, 23]. Limit arm activity post-insertion to avoid lead displacement [24]. This summary encapsulates the core cellular mechanisms, normal electrocardiographic intervals, critical dysrhythmia features, and emergency clinical protocols directly from your study materials. 📚 I can compile these key dysrhythmias and emergency actions into an interactive practice quiz to help test your bedside decision-making and pattern-recognition skills.