Supraventricular tachycardia Notes


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Atrial fibrillation

Atrial flutter

NOTES NOTES SUPRAVENTRICULAR TACHYCARDIA GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES ▪ Abnormally fast heart rhythms due to inappropriate electrical activity in upper portion of heart, atria/atrioventricular (AV) node ▪ Ventricles contract > 100 beats per minute, pathology originates above ventricles ▫ Ventricles protected by gating at AV node CAUSES ▪ Reentry conductive loops ▪ Increased automaticity ▪ Triggered activity RISK FACTORS ▪ Cardiac: coronary artery disease, heart failure ▪ Non-cardiac: chronic obstructive pulmonary disease (COPD), pulmonary embolism, alcohol abuse, hyperthyroidism DIAGNOSIS LAB RESULTS ▪ Electrolytes, thyroid stimulating hormone levels OTHER DIAGNOSTICS ▪ ECG TREATMENT ▪ See individual disorders MEDICATIONS ▪ Calcium channel blockers, beta blockers, anticoagulants SURGERY ▪ Catheter ablation SIGNS & SYMPTOMS ▪ Palpitations, chest pain, anxiety, dyspnea, syncope, lightheadedness OSMOSIS.ORG 133
ATRIAL FIBRILLATION PATHOLOGY & CAUSES ▪ Rapid, irregular (no discernible rhythm) heart rate ▪ Progression ▫ Paroxysmal: intermittent rhythm, may revert back to sinus rhythm spontaneously ▫ Persistent: > seven days, requires intervention to convert back to sinus rhythm ▫ Permanent: long-standing atrial fibrillation, cardioversion unsuccessful CAUSES ▪ Disorganized waves of atrial depolarization, exact mechanisms not well understood ▫ Regular impulses of sinus node overwhelmed by rapid electrical discharges from various sources (automatic foci, multiple reentry phenomena) ▫ Arise from left more than right atrium RISK FACTORS ▪ Old age: affects 4% 60–70, 14% > 80 ▪ Obesity, diabetes mellitus, excessive alcohol consumption, genetic predisposition ▪ Cardiovascular disease: heart failure, hypertension, coronary artery disease, non-rheumatic mitral regurgitation, mitral valve prolapse, rheumatic heart disease, damaged atrial myocytes ▪ Increased catecholamine levels ▪ Lung disease ▪ Hyperthyroidism COMPLICATIONS ▪ Thromboembolic events, heart failure, hypotensive shock 134 OSMOSIS.ORG SIGNS & SYMPTOMS ▪ May be asymptomatic ▪ Dyspnea, fatigue, palpitations, lightheadedness, weakness, chest pain, hemodynamic shock DIAGNOSIS LAB RESULTS ▪ Thyroid stimulating hormone (TSH) levels: exclude hyperthyroidism DIAGNOSTIC IMAGING Transthoracic echocardiogram ▪ Evaluate atrial, ventricular size; valvular disease; left ventricular function; pericardial disease Transesophageal echocardiogram ▪ Evaluate for atrial thrombi OTHER DIAGNOSTICS ECG ▪ Absent P waves ▪ Irregularly timed QRS complexes (irregular R-R intervals) ▪ No sawtooth wave in atrial fibrillation
Chapter 20 Supraventricular Tachycardia TREATMENT MEDICATIONS Anticoagulation ▪ E.g. warfarin, dabigatran, apixaban, rivaroxaban ▪ CHA2DS2-VASc/CHADS2 score ▫ Estimate risk of stroke in non-rheumatic atrial fibrillation; higher score = greater risk of stroke ▫ Score 0 (biological male)/1 (biological female): low risk, no anticoagulation recommended ▫ Score 1 (biological male): moderate risk, consider anticoagulation ▫ Score ≥ 2: high risk, anticoagulation recommended ▫ See table of scores OTHER INTERVENTIONS Rhythm control ▪ Restore sinus rhythm via cardioversion Electrical cardioversion ▪ Defibrillator for synchronization Catheter ablation ▪ Destruction of heart regions responsible for abnormal impulses Rate control ▪ < 100 beats per minute ▪ Beta blockers (preferably β1 selective) ▪ Non-dihydropyridine calcium channel blockers (e.g. diltiazem, verapamil) ▪ Digoxin Chemical cardioversion ▪ Administer antiarrhythmic medication ▪ Class Ic antiarrhythmics ▪ Class III antiarrhythmics ▪ Maintenance of sinus rhythm after cardioversion ▫ Class Ic antiarrhythmics ▫ Class III antiarrhythmics OSMOSIS.ORG 135
Figure 20.1 An ECG demonstrating atrial fibrillation. ATRIAL FLUTTER PATHOLOGY & CAUSES ▪ Atria depolarize regularly at very high rates (200–350bpm), appear to flutter TYPES Typical atrial flutter (AKA Type 1 flutter) ▪ More common ▪ Single reentrant circuit, right atrium ▪ Isthmus-dependent: reentry circuit crosses cavotricuspid isthmus ▪ Circles tricuspid annulus (ring), usually counterclockwise (viewed from below) ▪ Cavotricuspid isthmus tissue propagates signal slower than surrounding tissue → circuit loops → slows propagation → surrounding tissue exits refractory period Atypical atrial flutter (AKA Type 2 flutter) ▪ Less common 136 OSMOSIS.ORG ▪ Isthmus-independent ▪ Reentrant circuit develops in either atrium ▪ Associated with variety of reentry loops (common after incomplete atrial ablation procedures, right atrial surgical scars) CAUSES ▪ Reentrant electrical signal from either atrium ▪ Reentrant signal loops back on itself → overrides normal sinus rhythm → establishes endless loop of stimulation ▪ Underlying disease (e.g. heart failure, valvular disease, hypertension, pulmonary disease) → heart cells less electrically stable → alters refractory periods → increased risk of reentrant circuits ▪ Reentrant circuits initiated by premature atrial contraction (PAC) → partial premature contraction, normal tissue relaxes → wave of stimulation propagates → normal tissue
Chapter 20 Supraventricular Tachycardia contracts, premature tissue recovers → chance of reentrant circuit, stimulation wave doubles back on itself RISK FACTORS ▪ Diseases that change atrial heart cell properties → differing electrophysiological properties in adjacent areas → reentry circuit ▪ Ischemia, fibrosis, previous myocardial infarction, heart failure, high blood pressure, diabetes, valvular heart disease, obstructive sleep apnea COMPLICATIONS ▪ Heart failure, thromboembolic events, atrial fibrillation SIGNS & SYMPTOMS ▪ Palpitations, tachycardia, fatigue ▪ Pain/tightness/discomfort in chest ▪ Heart failure ▫ Exercise intolerance ▫ Difficulty breathing at night/while lying flat ▫ Edema of legs, abdomen DIAGNOSIS DIAGNOSTIC IMAGING Echocardiogram ▪ Evaluate size of right, left atria, ventricles ▪ Detect pericardial/valvular heart disease ▪ Decreased ejection fraction (% of blood pumped by heart per contraction) LAB RESULTS ▪ Serum electrolytes ▪ Renal function ▪ Thyroid stimulating hormone (TSH) levels: exclude hyperthyroidism OTHER INTERVENTIONS ECG ▪ Typical P waves absent ▪ Typical atrial flutter: P waves, saw tooth shape (F waves) localised to leads II, III, aVF ▪ Atypical atrial flutter: atrial activity (sawtooth waves/otherwise) may occur anywhere, dependent on reentrant circuit location ▪ Ventricular rate usually 1/2 atrial flutter rate (even ratios 2:1, 4:1 more common than odd, 3:1, 5:1) ▪ 1:1 atrial: catecholamine excess, presence of accessory bypass tract/class 1A, 1C antiarrhythmic drug therapy Figure 20.2 An electrocardiogram demonstrating atrial flutter with a 3:1 AV nodal block. The atrial trace demonstrates a characteristic sawtooth pattern. OSMOSIS.ORG 137
Figure 20.3 An electrocardiogram demonstrating atrial flutter with a 3:1 AV nodal block. The atrial trace demonstrates a characteristic sawtooth pattern. TREATMENT MEDICATIONS ▪ Anticoagulants (reduce chance of clot formation), beta blockers/calcium channel blockers (control rates of ventricles) SURGERY Radiofrequency catheter ablation ▪ Cavotricuspid isthmus no longer able to carry electrical signal, prevents reentry OTHER INTERVENTIONS Electrical cardioversion ▪ Depolarize atrial tissue, resynchronize contraction 138 OSMOSIS.ORG
Chapter 20 Supraventricular Tachycardia ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA (AVNRT) PATHOLOGY & CAUSES ▪ Heart rate disturbance due to accessory pathway in/near AV node ▪ Electric conduction splits into two pathways → forms loop ▫ Alpha pathway: slow conduction, short refractory period ▫ Beta pathway: fast conduction, long refractory period RISK FACTORS ▪ Biologically-female individuals → 75% of cases, emotional stress → alcohol use disorder, hyperthyroidism, electrolyte disturbances SIGNS & SYMPTOMS ▪ Palpitations, transient chest pain, bouts of transient tachycardia, transient hypotension, (pre)syncope TYPES Slow-fast/“typical” AVNRT ▪ Anterograde conduction to ventricles via slow pathway (alpha) ▪ Retrograde to atria conduction via fast pathway (beta) ▪ Depolarization down both pathways → reaches end of beta pathway first → signal splits ▫ Travels to ventricles → contraction ▫ Travels up alpha pathway → meets slow signal → signals cancel each other out ▪ Depolarization wave from premature beat reaches AV node → refractory fast (beta) pathway → signal initially down alpha pathway only → splits ▫ Travels to ventricles → contraction ▫ Travels up beta pathway → signal travels down alpha pathway, beta pathway comes out of refractory period → signal reaches end of alpha pathway →splits back up beta pathway Fast-slow/”atypical” AVNRT ▪ Anterograde conduction via fast pathway, retrograde conduction via slow pathway DIAGNOSIS LAB RESULTS ▪ Thyroid function ▪ Serum electrolytes OTHER DIAGNOSTICS ECG ▪ Tachycardia 140–280bpm ▪ Absent P waves ▪ P waves immediately before/after QRS complex ▪ P waves inverted/retrograde ▪ R’ waves (small secondary R waves) TREATMENT MEDICATIONS ▪ Adenosine, beta blockers, calcium channel blockers to slow AV node conduction OSMOSIS.ORG 139
OTHER INTERVENTIONS Radiofrequency catheter ablation ▪ Definitive treatment ▪ Ablation of slow alpha pathway Slow AV node conduction ▪ Vagal maneuver (carotid sinus massage/ Valsalva maneuver) → activates vagus nerve Figure 20.4 Illustration depicting path of electrical conduction in AV node during slow-fast AVNRT. Figure 20.5 An ECG demonstrating typical (slow-fast) AVNRT. R waves are best seen in lead V1. 140 OSMOSIS.ORG

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