Rhythm Flashcards
Mechanism and impulse initiation of torsades de pointes
Triggered automaticity
EADS
Mechanism and impulse initiation of digitalis toxicity and reperfusion Vtach
Triggered automaticity
DADs
Mechanism and impulse initiation of sinus bradycardia and sinus tachycardia
Mechanism: automaticity
Impulse initiation: suppression or acceleration of phase 4
Mechanism and impulse initiation of ischemic ventricular fibrillation and AV block
Excitation
Suppression of phase 0
AP SHORTENING
INEXCITABILITY
Mechanism and impulse initiation of polymorphic VT
AP PROLONGATION , AED, DADs
REPOLARIZATION
Mechanism and impulse initiation of AF FIBRILLATION
AP SHORTENING
REPOLARIZATION
Mechanism and impulse initiation of ischemic VT/ VF
Decreased coupling
Cellular coupling
Mechanism and impulse initiation of monomorphic VT, AF
EXcitable gap and function RE-ENTRY
TISSUE STRUCTURE
Renders heart inexcitable by depolarizing the membrane potential
Hyperkalemia
Due to presence of increased Calcium load In the cytosol and sarcoplasmic reticulum
Delayed after depolarization
Causes of DADs
Digitalis glycosides
Catecholamines
Ischemia
Causes of EADS
Hypokalemia
Hypomagnesemia
Bradycardia
Drugs( class IA and Class III, phenothiazines, nonsedating antihistamines, some antibiotics)
Most common arrhythmia mechanism
RE-ENTRY
What type of Re-Entry arrhythmia has no fixed an atomic obstacle, and no fully excitable gap.
Ex AF VF
Leading circle Re-Entry
What type of Re-Entry arrhythmia has fixed anatomic structure with anterograde and retrograde limbs of the circuit
Ex
AV RE-ENTRY, ATRIAL FLUTTER, BUNDLE BRANCH REENTRY VENTRICULAR TACHYCARDIA AND VENTRICULAR TACHYCARDIA IN SCARRED MYOCARDIUM
Excitable gap Re-Entry
Or
anatomic reentry
Test used to evaluate patients with syncope when suspecting exaggerated vagal tone or vasodepression as a cause
HEAD UP TILT TESTING
HUT
Mechanism of bradyarrhythmia
Failure of impulse initiation
Or
Impulse conduction
Most common causes of pathological bradycardia
Sinus node dysfunction
AV conduction block
Only reliable therapy of bradyarrhythmia if without reversible causes
Permanent pacemaker inertion
The incidence of persistent atrial fibrillation in patientswith SA node dysfunction increases with
advanced age, hypertension, diabetesmellitus, left ventricular dilation, valvular heart disease, and ventricular pacing.
Patients with the tachycardia-bradycardia variant of SSS,similar to patients with atrial fibrillation are at risk for thromboembolism, and those at greatest risk who should be treated with anticoagulants are:
aged ≥65 years
patients with a prior history of stroke,
valvular heart disease,
left ventricular dysfunction, or atrial enlargement,
The electrocardiographic manifestations of SA node dysfunctioninclude
sinus bradycardia, sinus pauses, sinus arrest, sinus exit block,tachycardia (in SSS), and chronotropic incompetence
Sinus bradycardia is ABNORMAL if
HR<40bpm in the awake state in the absence of physical conditioning
This is alternatively defined as failure to-reach 85% of predicted maximal heart rate at peak exercise or failure to achieve a heart rate >100 beats/min with exercise or a maximal heartrate with exercise less than two standard deviations below that of an age-matched control population. Exercise testing may be useful in discriminating chronotropic incompetence from resting bradycardia
Failure to increase the heart rate with exercise is referred to as chronotropic incompetence.
The normal IHR after administration of 0.2 mg/kg propranolol and 0.04 mg/kg atropine is ____; a low IHR is indicative of SA disease.
is 117.2 − (0.53 × age) in beats/min
Drugs that may be used In AV BLOCK
Atropine 0.5 to 2 mg IV
OR
ISOPROTERENOL 1-4 ung/min IV
Transient abnormality associated with Mobitz type 1 second degree av block:
Inferior wall MI
DRUGS (digitalis, CCB, BB)
Increased vagal tone
Associated with PAROXYSMAL AV BLOCK
Mobitz Type 2 sec degree AV block
Typical site of block for Mobitz Type 2 sec degree AV block
Infranodal
Distal or infra-his conduction system