Escolar Documentos
Profissional Documentos
Cultura Documentos
o AV bundle (His)
o left and right bundles of Purkinje fibers
Pacemaker vs Nonpacemaker
Ionic Basis of Membrane Electrical Activity
- determined by water-soluble ions Na, K, Ca
o Na and Ca primary carriers of depolarizing current
o K primary repolarizing current
- require aqueous channels to diffuse through lipid
membrane, ion-specific, voltage-gated
- Ion pumps and transporters
- movement of ions produce currents which form basis of action
potentials
Action Potentials in cardiac muscle:
- resting membrane potential = -85 to -95 mV
- caused by opening of 2 types of channels:
o fast Na channels
o slow Ca channels (slow to open, close)
Electrophysiology Review
Cardiac myocytes are electrically excitable
Resting intracellular voltage of myocardial cell= negative -90mV (SA node
is -40mV)
- high intracellular K maintained by Na/K pump
+
+
+ +
Resting state: K inside and Na outside cell (Na /K pump)
+
Action potential occurs when Na enters the cell and sets up a depolarizing
current
Stimulation of a single muscle fibre causes electrical activity to spread
across the myocardium
Electrophysiology
3 major types of cardiac muscle:
- atrial muscle
- ventricular muscle
- specialized excitatory and conductive muscle fibers
o sino-atrial node
o internodal pathways
o AV node
Pacemaker vs Nonpacemaker
ARRHYTHMIAS
A change in the normal sinus cardiac rate and rhythm
Common cause of sudden cardiac death (SCD)
Usually occurs in the presence of preexisting heart disease
Mechanisms of Arrhythmia
Abnormalities in Impulse Generation
- Automaticity
- Triggered Activity/Afterdepolarizations
Abnormalities in Impulse Conduction
- Block
- Re-entry
Both
Diagnostics: ECG
primary tool in arrhythmia analysis
timed sum of the cellular APs in atria and ventricle
12-lead ECG with long continuous recording of lead II or V1
Shows rhythm, rate, axis, presence of chamber enlargement, ischemia or
injury
Normal ECG
Normal P, Q, R, S, T, U waves
Each cycle has a P wave followed by a QRS complex = SINUS rhythm
P-P intervals and R-R intervals are approximately the same
Normal rate (60-100)
Normal axis(-30 to +100)
Additional Tests: Holter Monitoring
non-invasive
24-hour ambulatory ECG for monitoring patients over longer periods of
time
If symptoms less frequent: event recorder (30 days) or implantable loop
recorder (months)
Treatment Modalities
Antiarrhythmic Drugs
Pacemakers
- Temporary and Permanent
- Transcutaneous Pacing
Implantable Cardiac Defibrillators
Radiofrequency Ablation
Defibrillators
- Automatic External Defibrillators (AED)
Antiarrhythmics
Aim of Therapy:
1. to reduce ectopic pacemaker activity
2. to modify conduction or refractoriness in reentrant circuits to disable
the circular movement
ANTIARRHYTHMIC AGENTS
GENERALLY ALTER:
1. Diastolic potential in pacemaker cells and/or resting membrane
potential in ventricular cells (phase 4)
2. Phase 4 depolarization
3. Threshold potential
4. Action potential duration
Interval between depolarizations of a pacemaker cell =duration of action
potential + diastolic interval
Diastolic interval determined by phase 4 depolarization
Effect on Automaticity:
can slow spontaneous discharge by:
1. depressing diastolic depolarization
2. shifting threshold voltage to zero
3. hyperpolarizing resting membrane potential
affects ectopic sites more than sinus node
Class I Antiarrhythmics:
Lidocaine (Xylocaine)
low toxicity, high effectiveness in arrhythmias
associated with MI (main use: VT)
Cardiac Effects: blocks activated and inactivated Nachannels with rapid
kinetics
Toxicity: one of the least cardiotoxic drugs
- may precipitate hypotension by depressing myocardial contractility in
large doses in pts w/ heart failure
- neurologic: paresthesias, convulsions, dizziness
Class IC: Flecainide (Tambocor)
potent Na and K channel blocker
slow unblocking kinetics
very effective in suppressing premature ventricular contractions
may exacerbate arrhythmias in pts with ventricular arrhythmias + pts w/
previous MI and ventricular ectopy
oral route (100-200 mg BID), half-life 20 hrs
hepatic and renal metabolism
usually used in patients without structural heart disease
Class II Antiarrhythmics: Beta-blockers
Prototype: propranolol, esmolol
MOA:
- indirectly reduce the phase 4 slope by blocking positive chronotropic
action of norepinephrine
- Therapeutic Use: suppression of ventricular ectopic depolarizations
Beta-blocker effect on Pacemaker action potential
Effect on Reentry:
improves or depresses conduction
1. eliminate unidirectional block
2. facilitate conduction so returning wavefront reenters when cells still
refractory
3. depress conduction to transform unidirectional to bidirectional block
prolong refractoriness relative to action potential duration
Antiarrhythmics
As dosage increases, drugs also depress conduction in normal tissues,
producing drug-induced arrhythmias
Therapeutic doses may become proarrhythmic during fast heart rates,
acidosis, hyperkalemia or ischemia
Others:
Adenosine
nucleoside which occurs naturally in the body
half-life <10 seconds
Cardiac Effect:
- marked hyperpolarization
- suppression of Ca-dependent AP
- directly inhibits AV nodal conduction
Use: DOC for prompt conversion of SVT to sinus
- due to high efficacy (90-95%) and very short duration of action
- 6 - 12 mg IV bolus
Magnesium
MOA: not well known
Use:
- digitalis-induced arrhythmias if low Mg
- torsade de pointes even if Mg normal (1 g/IV)
Potassium
Hypokalemia: increased risk of EAD and DAD ectopic pacemaker activity
(digitalis)
Hyperkalemia: depresses ectopic pacemakers, SA node
Digoxin
Cardiac Glycosides
Electrical effects due mainly to:
Inhibition of Na/K ATPase at the cell membrane
Enhanced vagal tone
Actions:
Slowing the sinus node discharge rate
Prolonging AV nodal refractoriness
Main Indication:
- slow the ventricular rate in chronic AF (not very
- effective in acute setting)
Digoxin is recommended for patients with symptomatic LV systolic
dysfunction and concomitant atrial fibrillation
Narrow therapeutic range so use with caution
- Increased risk of digitalis toxicity with low K levels,
- worsening renal function, advanced age
- Toxicity: Headache, nausea/vomiting, diarrheas and arrhythmias
Clinical Application
Pharmacologic Treatment of Arrhythmias:
1. Eliminate the cause if possible
2. Make a firm diagnosis
3. Determine baseline condition
4. Evaluate need for therapy
5. Weigh benefits vs risks of therapy
Remember: Antiarrhythmics can be proarrhythmics.
Treatment Modalities
Antiarrhythmic Drugs
Pacemakers
- Temporary and Permanent
- Transcutaneous Pacing
Implantable Cardiac Defibrillators
Radiofrequency Ablation
Defibrillators
- Automatic External Defibrillators (AED)
Specific Arrhythmias
Arrhythmias
sinus arrhythmia
premature atrial contraction
premature ventricular contraction
Bradyarrhythmias
- sinus bradycardia
- sinus pause or arrest
- AV block
Tachyarrhythmias
- SVT
- atrial fibrillation
- atrial flutter
- ventricular tachycardia
- ventricular fibrillation
Sinus Node Dysfunction
One of the most common causes of pathologic bradycardia
SA node: blood supply comes from RCA (55-60%), LCX (40-45%), richly
innervated by sympathetic and parasympathetic nerves
Etiology of disease may be intrinsic or extrinsic (Table 225-1)
Includes sinus bradycardia, sinus pause/arrest
Sinus Tachycardia
AV Node Dysfunction
One of the most common cause of pathologic bradycardia
AV node: supplied by LAD and posterior descending coronary artery
Heterogenous cells with range of action potential profiles (fast and slow
pathways)
May be due to intrinsic and extrinsic causes (Table 225-2)
st
nd
Includes 1 deg, 2 deg and complete heart block
Sinus with First Degree AV Block
Sinus Arrhythmia
PR interval constant
sudden failure of conduction of P wave
Atrial Fibrillation
The most common sustained arrhythmia
Marked by disorganized, rapid and irregular atrial activation with irregular
ventricular response
Clinical Features:
- history of palpitations, easy fatigability, chest pain
- advanced age, (+) history of CHF, VHD, HPN, TIA or stroke
- PE: irregularly, irregularly cardiac rhythm
ECG:
- f waves at 350-600 beats/min with ventricular rate of 100-160
beats/min if untreated
- supraventricular complexes with irregular rhythm and NO obvious P
waves
Significance:
- Loss of effective atrial contraction (atrial kick)
- AV node blocks transmission of impulses as a protective mechanism
- Heart rate control necessary to allow proper filling of ventricles
- Thromboembolic events high risk due to circulatory stasis
MANAGEMENT:
- Determine if hemodynamically stable patient.
o Unstable patients may need cardioversion.
- Determine if acute or chronic.
o If acute, possible role for cardioversion.
o If chronic, less chance for cardioversion.
The longer patient is in AF, less chance for cardioversion since
remodelling has occurred.
Chronic Atrial Fibrillation
Goals:
- Evaluate and treat contributing factors (thyrotoxicosis, electrolyte
imbalance, pulmonary emboli, pericarditis, etc)
- Control ventricular rate
- Prevent recurrences
- Prevent thromboembolic episodes
Rate versus Rhythm Control:
- no clear benefit of one over the other
- Rate Control: Beta blockers, CCB (verapamil and diltiazem), digoxin
- Rhythm Control:
o IC (flecainide) if no structural heart disease
o III (amiodarone, sotalol) if with heart disease
Radiofrequency Ablation aimed at isolation of the pulmonary veins
- 70-85% effective in persistent and paroxysmal AF
- Alternative to pharmacological therapy in pts with recurrent AF
Maze procedure surgical interruption of circuits
Prevention of thromboembolic events
- High Risk patients (CHADS2):
o age > 65 years
o left atrial enlargement
o CAD or CHF
o prior stroke or TIA
o significant valvular heart disease
o HPN
o DM
- MUST be treated with anticoagulation (warfarin, dabigatran)
Atrial Flutter
Supraventricular Tachycardia
Narrow complex tachycardias occurring at the AV node
Most common type is AVNRT (AV nodal reentry tachycardia)
nd
th
Observed in women more than men, manifests in 2 to 4 decade of life
Occurs in patient with NO STRUCTURAL HEART DISEASE, generally welltolerated, good prognosis
Presents as palpitations, syncope, feelings of anxiety
Develops from REENTRY mechanism
Management:
- Vagal maneuvers carotid sinus massage, Valsalva, exposure of face to
ice water
- Adenosine DOC, 6-12 mg/IV; terminates SVT in 90%
- Others: verapamil, BB, digoxin
- Radiofrequency ablation
Ventricular Tachycardia
MACROREENTRANT circuit
more commonly found in the right atrium around the tricuspid valve
can be caused by incisional scars from prior atrial surgery, fibrosis
ECG: identically recurring, regular, sawtooth flutter waves