Abnormal Cardiac Conduction & Rhythm

• 60-100bpm
• 60% Right coronary artery
• 40% Left circumflex artery
• Sympathetic and parasympathetic innervation

• 85-90% Right coronary Artery
• 10-15% Left circumflex coronary artery
• Sympathetic and parasympathetic innervation

• Thin bundle of fibers coursing down the RV and branching at the RV apex
• More vulnerable to interruption due to late branching
• Blood from the left anterior descending coronary a.

• Branches into left anterior superior fascicle and left posterior inferior fascicle (less vulnerable to interruption).
• Blood from the left anterior descending coronary a. 
• Left posterior inferior fascicle also receives good from the posterior descending coronary artery and is more difficult block.

• Time between atrial and ventricular depolarization
• 0.12-0.2 sec

• Ventricular depolarization
• 0.05-0.1 sec

• Ventricular depolarization to ventricular repolarization
• T wave should be the same direction as QRS

• 1. Increased Automaticity in normal conduction tissue or in an ectopic focus
• 2. Re-entry of electrical potential through abnormal pathways
• 3. Triggering of abnormal cardiac potentials due to after-depolarizations.

• Irregular sinus rhythm 
• Bainbridge reflex: normal variation during inspiration (+HR) and expiration (-HR)

• Common SVT dysrhythmia w/ MI
• 100-160bpm
• Normal P wave before QRS
• Tx: Underlying condition, B-blocker, supplemental O2, avoid vagolytic drugs

• Ectopic foci in atria
• Dx: early, abnormally shaped P wave w/ variable PR interval, NOT followed by a compensatory pause
• Tx: avoid sympathetic stimulation and eliminate drugs that may induce PACs. 
• Suppressed with Ca Channel blockers or Beta-blockers.

• 160-180bpm 
• Initiated at or above AV node
• Usually paroxysmal (unlike sinus tachycardia)
• AV nodal re-entrant tachycardia (AVNRT) is most common
• Tx: vagal maneuver, adenosine, B-blocker, Ca channel blocker
• Adenosine: rapid onset and offset
• Anesthesia: avoid sympathetic, electrolyte imbalance, and acid-base disturbance
• 3x more in women
• Polyuria due to increased ANP from increased atrial pressures

• Irregular rhythm
• P wave with 3 or more morphologies and variable PR intervals. 
• Tx: underlying condition (methylxanthine toxicity, acute exacerbation of chronic lung disease, CHF, sepsis, metabolic/ electrolyte abnormalities). Bronchodilators (for lungs), O2, and magnesium (2g over 1hr), Verapamil. B-blockers (cardioversion has NO EFFECT)

• 250-350bpm
• Sawtooth "F waves"
• Tx: cardioversion (often less than 50J)
• Initial goal: ventricular rate control with amiodarone, diltiazem, verapamil)

• Loss of AV synchrony and rapid heart rate associated with dysrhythmia
• No discernable P waves
• Rapid ventricular response seen w/ accessory tracts (wide QRS)
• Thromboembolic event likely causing a stroke due to stasis of blood and atrial thrombi formation
• Tx: Electrical cardioversion (100-200J), amiodarone, propafenone, ibulitide, sotalol
• Ventricular control: B-blockers, Ca channel blockers, and digoxin
• Often underlying HTN and ischemic heart disease
• IV heparin is most common preoperative drugs
• Anesthesia: close monitoring of Mg and K concentrations

• Premature wide QRS complex, no P wave, ST segment and T wave inversion, and compensatory pause. 
• R on T phenomenon in vulnerable period at the middle third of T wave
• Tx: underlying cause, defibrillator present, B-blockers
• Progression to ventricular tachycardia: amiodarone, lidocaine, and other antidysrhythmics. 
• Associated: ischemia, valve disease, cardiomyopathy, prolonged QT, electrolyte abnormalities,

• Usually 150-200bpm
• Regular rhythm, Wide QRS, no P waves
• Torsades de pointes (polymorphic ventricular tachycardia) from prolonged QT
• Tx: cardioversion, amiodarone (150mg over 10 min), procainamide, sotalol, and lidocaine, Beta blockers, Ca channel blockers, acid base/ electrolyte disturbance

• Irregular ventricular rhythm, no BP or CO
• Tx: Electrical defibrillation (3-5 min) is the only method capable of generating a CO, followed by 1mg of epinephrine or 40units vasopressin
• DDx: hypoxia, hypovolemia, acidosis, hypokalemia, hyperkalemia, hypoglycemia, hypothermia, drug/ toxins, cardiac tamponade, tension pneumothorax, ischemia, pulmonary embolus, hemorrhage.

• 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

• 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. 
• Tx: electrolyte correction (Mg or K), B-blocker, cardiac pacing, ICD implant
• 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.

• 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

• 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.

• 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.

• 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.

• 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.

• 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.

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)
• Alpha Agonist
• Drug of choice for termination of stable AVNRT and certain SVTs
• Rapid injection followed by 20ml bolus
• SA: facial flushing, dyspnea, and chest pressure. 
• Contra: Sick sinus syndrome, 2nd&3rd degree blocks

• Dose: 150/300mg
• 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.

• 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).

• Dose: 1-1.5mg/kg
• 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

• Dose: 40units
• Peripheral vasocontrictor (not Alpha or beta)
• Antidiuretic hormone

• 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
• Moderate (5-7mcg/kg/min): Beta effects predominate
• 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.

• Monophasic/biphasic
• 150/200 J
• Do not place electrodes over pulse generators or ICDs.

Intracardiac electrode cathode in a large vein to produce thermal injury to destroy myocardial tissue responsible for dysrhythmias

• 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.

• 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.