Info: pre-excitation and tachydysrhythmia (often AVNRT) causing an earlier than normal deflection of the QRS complex called a delta wave.
Orthodromic AVNRT: Narrow QRS Complex, through AV node, treated with vagal maneuver, adenosine, verapamil, B-blockers, or amiodarone
Antidromic AVNRT: Wide QRS, atrium to ventricle through accessory pathway, treat with procainamide or amiodarone (not AV conduction dependent like adenosine, verapamil, B-blockers, digoxin), and possibly electrical cardioversion
WPW w/ AFib: Procainamide
Anesthesia: Continue antidysrhythmics, avoid events or drugs that enhance anterograde conduction of cardiac impulses through accessory pathways
Prolonged QT Syndrome
Info: Congenital and acquired versions. Abnormal depolarization allows after-depolarizations to trigger PVCs which intimate a ventricular reentry rhythm of polymorphic ventricular tachycardia (TdP). QTc exceeding 460-480msec.
Anesthesia: Isoflurane and sevoflurane prolong QT, droperidol and other antiemetics (ondansetron) prolong QT, avoid abrupt increases in sympathetic, acute hypokalemia (hyperventilation)
Under 60bpm, regular rhythm, P wave before each QRS
Tx: eliminate excess vagal tone, transcutaneous/ transvenous pacing, Atropine (0.4mg IV every 3-5min max 3mg), epi/dopamine infusions, glucagon (3mg bolus w/ 3mg/hr) if unresponsive due to B-blocker or Ca channel overdose
Sick Sinus Syndrome: dysfunction of the SA node
Nodal rhythm of 40-60bpm which can be conducted retrograde into the atria.
Tx: junctional rhythm due to myocarditis, ischemia, or digitalis toxicity should be managed by treating the underlying disorder. Atropine can be given if it becomes hemodynamically significant.
First Degree AV Block
S/S: Prolonged PR Interval Greater than 0.2sec w/ normal QRS. Sometimes due to drugs, ischemia, or increased parasympathetic
Tx: Usually asymptomatic w/ no treatment. Sometimes correct ischemia, atropine may be used but contraindicated in patients w/ significant heart disease
Anesthesia: Avoid increased vagal tone or slower AV, maintain normal K levels
Second Degree AV Block: Mobitz I (Wenckebach)
S/S: Progressive prolongation of PR interval w/ a dropped beat (absolute refractory period). May be due to ischemia, fibrosis/ calcification, or infiltrative/inflammatory disease of myocardium, or drugs (Ca channel blockers, B-blockers, sympatholytics). Usually asymptomatic.
Tx: Usually none needed. Atropine or pacing may be used.
Anesthesia: Control ventricular response. Usually no changes are needed.
Second Degree AV Block: Mobitz Type II
S/S: Complete interruption in the conduction of a cardiac impulse below the AV node (Bundle of His area). Usually symptomatic. Higher chance of profession to 3rd degree.
Tx: Transcutaneous/ transvenous pacing. Atropine for bradycardia.
Anesthesia: May need a cardiac pacemaker if it progresses to 3rd degree.
Right Bundle Branch Block
S/S: More common than LBBB without structural heart disease. Seen w/ ASD, valvular disease, and ischemic heart disease. Bifasicular block more commonly seen w/ left anterior
ECG: Widened QRS and an RSR' in V1/V2. Deep S wave in Leads I/V6
Tx: observation and elimination of contributing factors. Pacing in event of progression to 3rd degree.
Anesthesia: No major changes. Avoid significant changes in BP, arterial O2, and serum electrolytes. No prophylactic cardiac pacemaker.
Left Bundle Branch Block
S/S: Often a marker of heart disease (HTN, CAD, aortic valve disease, and cardiomyopathy). Anterior hemiblock is more likely. May be seen during tachycardia or HTN and is a sign of ischemia.
ECG: QRS over 0.12sec and no P waves in Leads I/V6
Tx: Some only have LBBB above a critical heart rate. Tx underlying condition such as ischemic heart disease, LV hypertrophy, or cardiomyopathy
Anesthesia: Pulmonary catheter may cause 3rd Degree block if RBBB occurs.
Third Degree AV Block
S/S: Complete interruption of AV conduction w/ no association between P wave and QRS complex. May signal acute inferior wall MI. Stoke-Adams attack may cause syncope. CHF may occur from bradycardia due to 3rd degree block.
ECG: Ectopic pacemaker near the AV node has a rate of 45-55bpm and a narrow QRS. An infranodal pacemaker has a rate of 30-40bpm and a wide QRS complex. Lenegre's disease is fibrotic degeneration of the distal cardiac conduction system due to aging. Lev's disease is calcific changes in more proximal conduction tissue.
Tx: Transcutaenous/ transvenous pacing.
Anesthesia: Isoproterenol may be needed to maintain HR. Antidysrhythmics may suppress the ectopic ventricular pacemaker.
Treatment of Cardiac Dysrhythmias
Abnormal physiological parameter should be corrected prior to drug therapy: Acid base levels, normal serum electrolytes, and ANS stabilization
Dose: 6mg (2nd dose may be given)
Drug of choice for termination of stable AVNRT and certain SVTs
Alpha and Beta-blocking effects that prolong the refractory period
Antidysrhythmic to tx VFib and pulseless VT
Metabolized by the liver and increases amount of warfare, quindine, procainaimide
Decrease HR and BP
Indicated in patients with presered LV function who require ventricular rate control in AFib, Aflutter, and narrow complex tachycardias above the AV node
SAs: Bradycardia, AV conduction delays, and hypotension
Contra: 2nd or 3rd degree block, hypotension, severe CHF, and reactive airway disease. NOT useful for AFib or Aflutter w/ WPW syndrome.
Ca Channel Blockers
Verapamil (2.5-5mg over 2min): slows conduction and increases refractory of the AV node. Tx narrow tachycardia (SVT) with failed vagal maneuvers and adenosine. Ventricular rate control for AFib/AFlutter
Diltiazem (0.25mg/kg over 2min): Less negative inotropic effects as verapamil and less peripheral vasodilation.
Cardiac glycoside to tx CHF and AFib
Positive inotrope, increses phase 4 depolarization time, shortens the action potential (decreasing conduction velocity through AV node and prolongs refractory period).
Na Channel Blocker
Tx: Ventricular ectopy and short bursts of VTach. Alternative to amiodarone in arrest w/ VFib or pulseless VTach
SA: CNS toxicity of tinnitus, drowsiness. Some myocardial depression and node dysfunction with other antidysrhythmics. Extensive first pass hepatic metabolism.
Dose: 1-2g over 5min.
Tx: Torsades de Pointes or Polymorphic ventricular tachycardia
Dose: 50mg/min titrated to effect
Class I Antidysrhythmic: Slows conduction, decreases automaticity, and increases refractory period.
Tx: VTach w/ pulse, Aflutter, AFib, AFib w/ WPW, and SVT resistant to adenosine and vagal (ALL w/ presered ventricular function)
SAs: hypotension, QRS prolongation
Dose: 1mg every 3/5min
Vasopressor w/ alpha and Beta effects
Peripheral vasocontrictor (not Alpha or beta)
Dose: 1mg every 3/5min
Vagolytic/ Anticholinergic: Increase HR, BP, and SVR
Dose: 1mcg/min titrated (10mcg for bronchospasm)
B1 and B2 agonist
Increased inotropy and chronotrophy
Dilates coronary vessels, but increased B1 increases cardiac oxygen demand more than supply
Tx: symptomatic bradycardia
Low (3-5 mcg/kg/min): Increases renal, mesenteric, coronary and cerebral flow through DA receptors
High (>10mcg/kg/min): Alpha stimulation causes peripheral vasoconstriction and reduction in renal flow.
Tx: sympatomatic bradycardia unresponsive to atropine.
2 chest electrodes: anterior and posterior
If given during the T wave, it could cause VTach or VFib
Start with 50-100J
Synchronized: SVT, AFlutter, and AFib and chronic/stable rate controlled AFlutter or AFib to sinus rhythm, and VTach w/ pulse
Risk: Systemic embolism, so anticoagulation is recommended if over 48 hours.
Do not place electrodes over pulse generators or ICDs.
Radiofrequency Catheter Ablation
Intracardiac electrode cathode in a large vein to produce thermal injury to destroy myocardial tissue responsible for dysrhythmias
Artificial Cardiac Pacemakers
Transcutaneous Pacing: Symptomatic bradycardia or sever conduction block requiring immediate pacing. Chest and back electrodes over areas of less skeletal mass
Implanted cardiac pacemaker: Long term treatment for sinus bradycardia and SSS
Single most important factor in determining survival from cardiac arrest due to VFib is the time between arrest and the 1st defibrillation attempt.
Delivers a shock within 15sec of dysrhythmia onset.
Surgery With Cardiac Devices
Preoperative: Determine reason for device, consult w/ cardiologist, and representative for specific device
Management: Drugs not altered by properly placed device. Electrocautery pulse should be minimized and grounding far away from the pulse generator. Avoid hyperkalemia (succinylcholine), hypokalemia (hyperventilation), arterial hypoxemia, myocardial ischemia/infarction, and catecholamine
Anesthesia: Drugs such as atropine or isoproterenol should be available is a decreased HR compromises hemodynamics.