Sudden cardiac death Notes

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Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Sudden cardiac death essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Sudden cardiac death by visiting the associated Learn Page.
NOTES NOTES SUDDEN CARDIAC DEATH GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES ▪ Abrupt cessation of cardiac activity (cardiac arrest) in someone asymptomatic up until moment of arrest SIGNS & SYMPTOMS ▪ Asymptomatic DIAGNOSIS TREATMENT MEDICATIONS ▪ According to Advanced Cardiac Life Support protocols OTHER INTERVENTIONS Cardiopulmonary resuscitation (CPR) ▪ Maintains blood flow by mimicking pumping motion heart makes during a medical emergency ▪ Made based on lack of pulse BRUGADA SYNDROME osms.it/brugada-syndrome PATHOLOGY & CAUSES ▪ Condition with characteristic abnormal electrocardiogram findings → increases risk of sudden cardiac death in healthy individuals ▪ Mixture of normal, abnormal sodium channels within adjacent myocardial tissue can set up heterogenous refractory periods necessary for development of reentrant rhythms → ventricular tachycardia/ fibrillation ▪ 20% associated with SCN5A gene mutation which encodes for sodium ion channel in cell membranes of heart muscle cells RISK FACTORS ▪ Biological males, more common in Asia than North America, Europe COMPLICATIONS ▪ Ventricular fibrillation, high risk of sudden cardiac death CAUSES ▪ Inherited ▫ Autosomal dominant, variable expression OSMOSIS.ORG 127
SIGNS & SYMPTOMS ▪ Brugada pattern ▫ ECG findings, no symptoms ▪ Brugada syndrome ▫ ECG findings, symptoms of sustained ventricular tachycardia (palpitations, syncope, dyspnea, lightheadedness) DIAGNOSIS ▪ Type I ▫ Right bundle branch block pattern ▫ Gradually descending ST elevations, at least 2mm (0.2mV) in leads V1–V3 ▫ Negative T- wave in leads V1–V3 ▪ Type II ▫ Class IV antiarrhythmic can convert to a Type I Brugada pattern—often needed for diagnosis ▫ Saddle-back pattern with at least 2mm J point elevation, 1mm ST elevation (positive/biphasic T wave) LAB RESULTS Genetic testing ▪ Confirms diagnosis OTHER DIAGNOSTICS ECG ▪ Type I/II Brugada electrocardiogram pattern ▫ May present simultaneously, may be induced by certain drugs (e.g. calcium channel blockers), or may resurface due to unknown triggers TREATMENT ▪ Brugada pattern: none SURGERY Implanted cardiac defibrillator (ICD) ▪ Brugada syndrome Figure 19.1 ECG (lead V1) demonstrating Brugada waveforms type I (left) and type II (right). 128 OSMOSIS.ORG
Chapter 19 Sudden Cardiac Death Figure 19.2 Calcium channel blockers can increase the chance of developing Brugada syndrome. The condition is typically associated with right bundle branch block, which makes the heart susceptible to developing a reentrant rhythm, which in turn causes ventricular tachycardia and sometimes ventricular fibrillation. PULSELESS ELECTRICAL ACTIVITY osms.it/pulseless-electrical-activity PATHOLOGY & CAUSES ▪ Pulseless, despite electrical activity (evident on ECG) typically resulting in pulse ▪ Heart does not contract in spite of electrical activity/does not generate enough cardiac output to cause pulse ▪ Survival ~20% CAUSES ▪ Abrupt drop in preload ▪ Abrupt pump failure MNEMONIC: 6Ts & 6Hs Obstruction to blood flow Tablets/toxins (drug overdose) Cardiac Tamponade Tension pneumothorax Thrombosis (myocardial infarction) Thrombosis (pulmonary embolism) Trauma (hypovolemia - blood loss) Hypovolemia Hypoxia Hydrogen ions (acidosis) Hyperkalemia/hypokalemia Hypoglycemia Hypothermia OSMOSIS.ORG 129
SIGNS & SYMPTOMS ▪ Loss of consciousness ▪ Breathing stops DIAGNOSIS OTHER DIAGNOSTICS TREATMENT MEDICATIONS ▪ If cause unclear medicine used similar to asystole ▫ Intravenous/intraosseous line, administer epinephrine 1mg/3–5 minutes ▪ Absence of pulse ECG ▪ Organized/semi-organized electrical activity VENTRICULAR FIBRILLATION osms.it/ventricular-fibrillation PATHOLOGY & CAUSES ▪ Ventricular electrical activity disorganized to point that coordinated contraction is impossible ▪ Rapid, irregular electrical activity prevents ventricles from contracting in sync → cardiac output falls to zero ▪ Often due to tissue heterogeneity: heart cells stressed/damaged, tissues of different areas structurally, electrically different ▪ Mechanism: tissue heterogeneity in cardiac electrical system → asynchronous depolarization & contraction → inadequate blood pumped → oxygen deprivation → death ▪ Functional reentry: arrhythmia causes different areas of heart to depolarize & contract out of sync → heart non-functional CAUSES ▪ Medications causing long QT syndrome ▪ Illicit drugs (e.g. methamphetamine, cocaine) ▪ Congenital arrhythmogenic syndromes (e.g. Brugada, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, Wolff-Parkinson-White syndrome, congenital long QT syndrome) 130 OSMOSIS.ORG ▪ Electrolyte imbalances: hypokalemia, hyperkalemia ▪ Ischemia to ventricular muscle ▪ Scar tissue from previous myocardial infarction ▪ Anatomical reentry ▪ Electrocution/external electrical stimulation, such as in unsynchronized cardioversion ▪ If heart tissue stimulated during T wave upslope (in an electrocardiogram), can induce fibrillation SIGNS & SYMPTOMS ▪ Chest pains, dizziness, nausea, rapid pulse, dyspnea DIAGNOSIS OTHER DIAGNOSTICS ▪ Pulse check: no pulse ECG ▪ Absence of PQRST waves; instead, fine, coarse fibrillatory waves ▪ Electrocardiogram appears chaotic ▪ Undulating baseline
Chapter 19 Sudden Cardiac Death TREATMENT SURGERY ICD ▪ Used when cause is unpreventable ▪ Surgically implanted ▪ Constantly monitors electrocardiogram ▪ ICD recognizes ventricular fibrillation, delivers responsive defibrillating shock ▪ Doesn’t fix underlying condition; treats symptom, improves survival ▪ Primary prevention ▫ Individuals with heart failure at risk of ventricular tachycardia/fibrillation ▪ Secondary prevention ▫ Cardiac arrest survivors for whom triggers cannot be treated/prevented OTHER INTERVENTIONS Cardiopulmonary Resuscitation (CPR) Defibrillation ▪ High energy shock depolarizes large enough portion of tissue (critical mass) that sinus node can take control Electrophysiology study ▪ If individual has had previous MI/has survived cardiac arrest in whom signs are not apparent after routine, non-invasive testing ▫ Evaluate for possible ventricular tachycardia ablation Revascularization ▪ If ventricular fibrillation occurs in setting of myocardial infarction ▫ Cardiac catheterization ▫ CABG Figure 19.3 Histological appearance of fatal ventricular fibrillation demonstrating broken myocardial fibers and squared-off nuclei. OSMOSIS.ORG 131
Figure 19.4 ECG demonstrating ventricular fibrillation. 132 OSMOSIS.ORG

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Sudden cardiac death essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Sudden cardiac death by visiting the associated Learn Page.