SEARCH RESULTS FOR: Ventricular-Fibrillation

Ventricular Fibrillation

Ventricular Fibrillation: Pathogenesis and clinical findings Channelopathies (diseases of ion channels such as Brugada syndrome) Abnormalities in ion channel (Na+ , K+, Ca2+) permeability & channel opening/closing Impaired cardiomyocyte depolarization & repolarization Replacement of cardiac tissue with nonconductive fibrous tissue Structural damage (cardiac surgery or genetic conditions like arrhythmogenic dysplasia) Authors: Jared McCormick, Shuvam Prasai, Sergio F. Sharif Reviewers: Brett Edwards, Dave Nicholl, Angela Kealey*, Jason Waechter*, Vikas Kuriachan* * MD at time of publication Hypoglycemia Impairment in ATP- dependent processes Disruption in cardiomyocyte action potential propagation ↓ Oxygen delivery & ischemia Cardiac hypoperfusion Drugs (antiarrhythmics, QT prolonging antipsychotics, etc.) Direct alteration of ion channel function Disruption in the ion gradients of cardiac cells At-risk patient (altered impulse conduction) Impairment & damage to cardiac tissue ↓metabolic activity & blood flow Hypothermia Electrolyte imbalances (K+ , Mg2+, Ca2+ etc.) Abnormal extracellular ion concentrations ↑ ectopic activity & self-sustaining conduction loops further disrupt normal pathways Major ischemia & necrosis of cardiac tissue Myocardial infarction** (one of the most common causes of V-Fib) Abnormal rhythm Impairment in ion channel activation & recovery Ventricular fibers contract erratically instead of in unison Atrial fibrillation** & rapid conduction to ventricles Accessory pathway (pathways bypassing normal conduction pathways in the heart) ECG shows disorganized activity without identifiable QRS/T waves & obscured P waves* Ventricular Fibrillation (V-fib) Heart rhythm disorder where the ventricles fibrillate (quiver) & fail to contract effectively *Obscured P waves No heart rate ↓ATP & disruption in Na⁺/K⁺-ATPase Pump Cerebral hypoxia (ischemia driven brain injury) Uncoordinated contraction & no cardiac output (V-fib is non-perfusing) No blood pressure ↑ Creatinine kinase indicating cell damage Ion imbalances & intracellular Ca2+ influx Depolarization induced glutamate release Global hypoperfusion (widespread ↓ in blood flow to tissues & organs) Ca2+ toxicity & widespread neuronal cell damage & death Death Multi-system organ failure due to ↓ perfusion Clinical cardiac arrest (cessation of cardiac activity)** Inadequate blood flow & widespread ischemic injury** ↑ Lactate dehydrogenase indicating ischemia **See corresponding Calgary Guide slides ↑ Troponin indicating myocardial injury Legend: Published Feb 10, 2014; updated Oct 19, 2025 on www.thecalgaryguide.com Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications