Cardiac arrhythmias Janusz Witowski Department of Pathophysiology Poznan University of Medical Sciences
A 68-year old man presents to the emergency department late one evening complaining of increasing shortness of breath, dizziness, and the sensation of his "heart racing." On admission, his heart rate is 160 bpm, blood pressure 100/50 mm Hg, respirations 26 breaths per minute, and oxygen saturation is 88% on room air. Patient reports that his symptoms started abruptly earlier that day and have steadily become worse. He reports a history of long-standing hypertension and coronary artery disease. Crackles are present in the bases of both lungs. Peripheral pulses are diminished and irregular. ECG shows a narrow QRS complex tachycardia with an irregularly irregular rhythm and the absence of sinus P waves.
Electrical conduction system of the heart 1 m/s 0.05 m/s 4 m/s
Sinoatrial node action potentials Klabunde RE. Cardiovasc Physiol Concepts; Lippinctt Williams Wilkins 2011
Ventricular myocyte action potentials Klabunde RE. Cardiovasc Physiol Concepts; Lippinctt Williams Wilkins 2011
Sinoatrial vs. ventricular action potentials Sinoatrial Low conduction safety coefficient Activation threshold:- -40 mv No true resting potential; spontaneous depolarization instead (Na + - and Ca ++ -mediated) Blocking: Calcium channel blockers (Verapamil) Potential amplitude: 55 mv Ventricular High conduction safety coefficient Activation threshold: -60 mv True resting potential at -90 mv (K + -mediated) Blocking: Sodium channel blockers (Tetrodotoxin) Potential amplitude: 115 mv
Overdrive suppression SA node (rate 60-100 per min) Atrial foci (inherent rate 60-80 per min) Junctional foci (inherent rate 40-60 per min) Ventricular foci (inherent rate 20-40 per min) Suppression by the SA node of other than physiological pacemaker sites The highest frequency of SA nodal firing supresses all foci with a slower inherent pacing activity Increased hyperpolarizing currents offset the depolarizing current (I f ) Klabunde RE. Cardiovasc Physiol Concepts; Lippinctt Williams Wilkins 2011
Mechanisms of controlling automaticity Normal Decreased threshold voltage Through changing: threshold voltage resting potential intensity of the depolarizing current (I f ) Increased membrane diastolic potential Increased slope of phase 4 depolarization Gaztanaga L et al. Rev Esp Cardiol 2012; 65:174
Sympathetic and parasympathetic effects on action potentials Norepinephrine: Increases the pacemaker current (I f ) and the slope of phase 4 Acetylcholine: Supresses the pacemaker current (I f ) and decreases the slope of phase 4 Klabunde RE. Cardiovasc Physiol Concepts; Lippinctt Williams Wilkins 2011
Tachyarrhythmias Increased SA node automaticity Increased automaticity Ectopic automaticity Triggered activity Incomplete blocks and re-entry Abnormal impulse formation Abnormal impulse conduction Decreased SA node automaticity Conduction blocks Bradyarrhythmias
Causes of altered automaticity Mechanism Bradycardia Tachycardia Autonomic activity Vagal Sympathetic Endocrine activity Hypothyroidism Hyperthyroidism Electrolyte balance Hyperkalaemia Hypokalaemia Ischaemia Hypoxia - Drugs Beta-blockers Calcium-channel-blockers Atropine
Ectopic activity Ectopic foci: Abnormal pacemaker sites Can cause additional beats In the absence of overdrive suppression, they can generate escape rhythms that are generally slower than those produced by the SA node Klabunde RE. Cardiovasc Physiol Concepts; Lippinctt Williams Wilkins 2011
Triggered activity Initiated by oscillations of the myocyte membrane potential Depolarization occurs during or immediately after a preceding action potential Likely to happen when the duration of the action potential is abnormally long (long Q-T syndrome) Cells contract twice, although they have only been activated once Occur during late phase 2 or phase 3 Occur in late phase 3 or early phase 4
Mechanisms of afterdepolarizations EADs: excessive prolongation of the action potential; associated with bradycardia DADs: spontaneous leak of calcium from endoplasmic reticulum during diastole resulting from calcium overload and/or ryanodine receptor dysfunction Lin H et al. PACE 2008;31:1048
Potential causes of afterdepolarizations Slow heart rate (bradycardia, complete heart block) Mechanical stretch Hypokalaemia Hypoxia Acidosis Hypocalcaemia Hypomagnesaemia Antiarrhythmic drugs Antidepressants
Conduction blocks Occur at the AV node, bundle of His, or bundle branches In a complete block, a pacemaker site distal to the block will become the new pacemaker Secondary pacemakers have slower intrinsic rates (30-50 impulses/min) AV blocks will lead to ventricular bradycardia In a bundle branch block, the ventricles will still be driven by the SA node, but the sequence and timing of ventricular depolarization will be altered
First-degree heart block Impulses are slowed, but they all successfully reach the ventricles P-R interval increased > 0.2 second Every P wave followed by a QRS complex Rarely causes symptoms or problems
Second-degree heart block Some impulses from the atria cannot pass through the AV node Not all P waves are followed by a QRS complex Manifestation varies from no symptoms to syncope and hypotension
Third-degree heart block Conduction through the AV node completely blocked QRS complexes originate from secondary pacemakers (slow escape rhythms) QRS complexes are not preceded by P waves Dissociation and asynchrony of atrial and ventricular activity Symptoms include syncope, dyspnoea, chest pain, sudden death Treatment with implantable pacemakers
Re-entry Repetitive propagation of the wave of activation, returning to its site of origin to reactivate that site Pre-requisites for re-entry: 1. The presence of two conduction pathways. 2. A unidirectional block (conduction block in one direction, but not the other) 3. Conduction time around the circuit greater than the refractory period in the circuit to enable the recovery of the refractory tissue Gaztanaga L et al. Rev Esp Cardiol 2012; 65:174
Sinus-node dysfunction (Sick sinus-node syndrome) Idiopathic degeneration with age (replacement of nodal tissue with fibrotic tissue) Pharmacological agents (β-blockers, calcium channel blockers, digoxin) Infiltrative disease (sarcoidosis, amyloidosis, hemochromatosis) Hypothyroidism Neurologic disorders Electrolyte imbalance (potassium) Dizziness Disorientation Syncope
Atrial fibrillation Mechanism: Enhanced automaticity in multiple atrial foci Re-entry in multiple aberrant circuits Main underlying causes: Cardiac disease Pulmonary disease Hyperthyroidism Regularity: Irregular Rate (beats/min): 100-220 Onset: Sudden Gradual (if in chronic AF) Link M. NEJM 2012; 367:1438 P:QRS relationship: No P waves Fibrillatory waves No relationship to QRS
Underlying causes of atrial fibrillation Gutierrez et al. Am Fam Physician 2011; 83:61
Implications of atrial fibrillation Increased ventricular response Tachycardia Shorter fill time Reduced coronary circulation Tachycardia-mediated cardiomyopathy Loss of coordinated atrial contraction Decreased diastolic filling Decreased cardiac output Blood stasis and atrial clot formation Thromboembolism Stroke Increased morbidity and mortality Gutierrez et al. Am Fam Physician 2011; 83:61
Ventricular fibrillation Polymorphic VT with various sites of activity throughout the ventricle ECG tracing of differing morphologies and shape Washington Heart Rhythm Associates; http://washingtonhra.com
Causes of ventricular fibrillation-induced cardiac arrest Cardiac Myocardial ischemia or infarction Cardiomyopathies Valvular defects Myocarditis Pericarditis Mechanical or electrical heart injury Drug-induced QT prolongation Channelopathies
Causes of ventricular fibrillation-induced cardiac arrest Respiratory Bronchospasm Aspiration Pulmonary embolism Metabolic Electrolyte imbalance Drugs Poisoning Neurologic Intracranial haemorrhage Ischaemic stroke Seizures