Cardiac arrhythmias Flashcards
Brady and Tachy cardia
Arrhythmias are disturbances in the rate or sequence of cardiac electrical activation
Bradycardia (under 60 beats/min) –> decrease in cardiac output, hypotension, ht failure and dizziness, syncope, palpitations
Tachycardia (over 100/min– palpitations, impairment of cardiac output, hypotension, heartfailure, ischemia, and (chest pain, palp, dizziness, syncope)
Arrhythmias
Arrhythmia: no rhythm or abnormal rhythm
Bradyarryhthmia: abnormal bradicardia (normal- bradycardia during rest or sleep)
Tachyarrhythmia: abnormal Tachyarrhythmia (normal- exercise or stress)
Tachycardias
Supraventricular Tachycardia: (SVT)- Abnormal tachycardia which requires participation of either atrial or AV nodal tissue, when chaotic –atrial fibrillation and not supraventricular tachycardia
Ventricular Tachycardia: VT- abnormal tachycardia originating in the ventricle or His-purkinje system, VT does not require invovlement of either the atrium or the AV node, when chaotic referred to a Ventricular fibrillation and not ventricular tachycardia
Disorders of heart rhythm arise as a consequence of either
Alteration in impulse formation, alteration in impulse propagation
Normal impulse formation
intrinsic automaticity of specialized cardiac cells, pacemaker cells
The site of fastest intrinsic automaticity in the heart determines the heart rate (normally Sinus node (60-100), AV node (50-60), Hispurkinje (30-40) Normal gradient of automaticity,
Normal gradient of automaticity–normal rhythm originates in the sinus node
Failure of faster structure may–> automatic tissue to exhibit automaticity at slower rate (Escape rhythms or pacemaker. Subsidary escape pacemakers provide redundancy in the conduction system–> protect from catastrophic bradycardia
Ionic basis of normal automaticity
most myocardial cells (working myocytes) maintain a very negative and static resting membrane potential (around -90 mV) and lack intrinsic automaticity
Specialized cells in the sinus node and AV node have a higher diastole membrane potential (-60) –exhibit spontaneous gradual diastolic depolarization
Pacemaker current (If) slow inward Na potential, slow inward Ca current, progressive declike K efflus, inward Na current due to the NaCa exchanger
high resting membrane potential keeps most Fast Na channels in the Inactived state (requries dependence on slower Ca current to mediate depolarize and slower AP upstroke)
Overdrive suppression
Faster automatic sites normally preempt subsidary slower potential pacemaker,
Mechanism: in spontaneous cells, hyperpolarizing current of the NAKAtpase, is offset by the funny channel
In passively activated subsidiary slower pacemaker cells, If is much smaller leading to net hyperpolarization, hyper polarization–> leads to slow recovery after overdrive of pacemaker cells by faster foci
Regulation of normal Automaticity (Sinus node)–heart rate is closely regulated by autonomic tone to match cardiac output to metabolic demand, normal automaticity is regulated at a cellular level by the interplat of 3 factors (Rate of diastolic depolarization (If) faster depolatization–faster rate), (Max negative diastolic potential, More neg–slower rate) Threshold potential (More negative–faster rate, less negative slower rate)
Autonomic regulation of heart rate
Sympathetic Effects on Automaticity: SN rate is augmented by sympathetic tone. Beta stimulation– increasing the open probablity of the pacemaker Current If, increases rate of diastolic depolarization, makes threshold more negative–easier to trigger the Ca currnent
Parasympathetic effects: SN is depressed by Parasympathetic tone, decreases the open probablity of pacemaker current channel If, makes threshold potential less negative, increases probablity of Ach sensative K channels, being open at rest more negative membrane potential
Parasympathetic tone dominates at rest so if you knock it out SN intrinsic rate is faster
Electronic interactions
Adjacent myocytes are coupled by low resistance gap junctions.
During diastole, cells have differing potentials, current may bleed from one cell to the other following the potential gradient
less negative pacemaker cells will become more negative withle more negative working cells become less negative
Escape ryhthems
Sinus node maintains control of normal rhythm because of the normal Gradient of Automaticity
A failure of Sinus node automaticity is often moderated by emergence of normally suppressed secondary pacemakers in the AV node or infranodal conduction system
An escape rhythm arising in the AV node (junctional escape) has a narrow QRS without a preceding P wave and a slower rate
An escape rhythm arising in the Infranodal tissue (ventricular Escape) will have a wide QRS
Cellular Tachycardia Mechanism
Enhanced Automaticity: increase in rate of tissue (normally capable of pacemaker activity)
Abnormal Automaticity: abnormal impulse formation or automaticity in tissue not normally capable of pacemaker activity . cell injury, loss of normal strongly negatively resiting membrane potential.
Triggered Activity: single or repetitive cell activity following a prior AP. Due to oscillations in membrane potential, can be triggered by antecedent Tachychardia/ rapid pacing or prior pauses/bradycardia
Triggered activity
Early Afterdepolarizations (EADs): membrane oscillations within the AP either in plateau (phase 2) or during repolarization (phase3), Promoted by conditions which prolong the Action potential (Long QT)
Related to inward Ca current in Phase 2 or reactiviation of fast Na current in phase3
Clinical mechanism of Torsades de pointes VT, precipitated by QT prolonging drugs
Delayed afterpolarization (DADs): membrane oscillations occuring after completion of Full Repolarization, promoted by conditions which lead to high intracellular calcium, promoted by catecholamines and inhibited by Ca channel blockers, clinical mechanimsm of idopathic VT (VT in the normal heart), mechanism of Digitalis toxicity
Altered impulse propagation
Conduction block: occurs when a propagating wavefront encounters tissue which is unexcitable, permantent or fixed (all impulses fail to propagate), intermittent (ability to conduct is variable and changes over time), functional (block may be present only at critical rates which are faster than tissue refractory period will accomodate)
Block within the conduction system: (pathologic block can occur at multiple levels in the normal conduction system), Block in the AV node or His bundle can result in interruption of the AV conduction (1st degree delay without failure of conduction), (2nd degree some but not all beats fail to conduct), (3rd degree no propogation from atrium to ventricular)
Block in the right or left bundle branches (doesnt interrupt AV conduction but results in abnormal sequence of ventricular activation reflected in bundle branch block
unidirectional block and reentry
reentry represents abnormal endless loop myocardial propogation and is the primary mechanism of tachycardias
Reentry occurs inmyocardial tissue composed of many myocytes working in sequence
Normal propagation is constrained to a single activation of each myocytes due to a wall of refractory tissue preventing the wavefront from looping back on itself
however in presence of abnormal conduction, conduction block and slowed conduction, wave front may turn around on itself and form a self perpetuating loop of activity
Requirement for reentry- 2 distinct paths for propagation, slowed conduction (in at least one path, unidirectional block (tissue capable of conduction in one but not the opposite direction),
