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- 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
Right Bundle Branch
- 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.
Left Bundle Branch
- 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
Mechanisms of Tachydysrhythmias
- 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
- Normal P wave before QRS
- Tx: Underlying condition, B-blocker, supplemental O2, avoid vagolytic drugs
Premature Atrial Beats (PACs)
- 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.
Supraventricular Tachycardia (SVT)
- 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
Multifocal atrial Tachycardia
- 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)
- 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 Ventricular Contractions (PVCs)
- 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
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.
- 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.
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)
- 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.
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).
- 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.
- 150/200 J
- 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.