Other Flashcards
Electrical cardioversion/defib mechanism
- Shock delivered to critical mass of myocardium → atrial myocyte AP = coordinated alteration of membrane potential → refractory state
o SA node regain control of rhythm
Success in terminating arrhythmia with electric shock depend on
o Amount of E delivered
o Path of current vs position of heart
Position paddles/patches at level of atrium
o Transthoracic impedance: ↑ impendance → ↓ probability of successful shock
Determined by: chest conformation, water/fat content, pulmonary volume, size/position of paddles
Synchronized cardioversion mechanism
Premature activation of all potentially receptive areas to terminate tachyarrhythmia and convert to sinus rhythm
Indications
o Used with patients with pulse
o Unstable patients
o Unsuccessful chemical cardioversion
SVT, Afib, Aflutter, Vtach with pulse, unstable reentrant tachycardia
Shock delivery with cardioversion
o Synchronous mode: time shock delivery to peak of R wave
Absolute refractory period
Prevent shock delivery at T wave peak
After shock, default back to asynchronous mode
o Most arrhythmias stopped w 1 or 2 shocks
Vulnerable period of ventricles
T wave peak
* Impulse reach ventricles during repol = electrical heterogeneity → ↑ risk of Vfib
* R on T phenomenon
Cardioversion vs defib
requires < E vs defibrillation
1st shock: 1-2J/kg
Subsequent shocks: ↑ output until conversion occurs or max output fails to terminate arrhythmia
Heart disease do not ↑ E required for cardioversion
Indications for defib
- Treatment for immediate life threatening arrhythmia w/o pulse
- Technique to terminate ventricular fibrillation
Pulseless Vtach, Vfib, Cardiac arrest due to/resulting in Vfib
Considerations defib
o Electrolyte imbalances: corrected before shock
o Ensure adequate O2
o Avoid opioids → effect on vagal tone
Prone to maintenance/reoccurrence of Afib
complications Defib
- Vfib induction: shock to synchronized to R wave
o Should be rapidly treated w high E asynchronous shock - General anesthesia
- Skin burns
- Thromboembolic events
Defibrillator devices
multifct devices
o Monitoring + external pacing capabilities
Synchronous/asynchronous mode
o ECG tracing, amount of energy
o Monophasic shocks: current of 1 polarity
o Biphasic shocks: direction is reversed near halfway point of electrical cycle
Require less E + higher success rate
Define overdrive suppression
Driving a PM cell faster than its intrinsic rate
Mechanism of overdrive supp
o ↑Na+ enters the /unit of time
o ↑activation of Na+/K+ pump → Na+ efflux → hyperpolarization
↓ depolarizing If current
o If activity of driving PM stops → pause to allow ↓[Na+]
↑rate or longer suppression → greater ↑ in pump activity → longer pause
Degree of overdrive suppression depends on
membrane potential
At ↑ membrane potential (less negative) → ↓ Na+ channels available → ↓ Na+ influx → ↓ activation of Na+/K+ pump
At ↓ membrane potential (normal values) → ↑ Na+ channels available → ↑ Na+ influx → ↑ activation of Na+/K+ pump = ↑ overdrive suppression
Overdrive suppression in normal heart
- Usually SA node > subsidiary PM
o Intrinsic slope of phase 4 is faster → ↑ automatic rate
Overdrive suppression w/ SVTs
o SA node can be suppressed by SVTs
Less susceptible since depol is mostly dependent on ICaL
* ↓Na+ enter during depol upstroke
* Accumulation of intra [Na+] and activation of Na+/K+ pump occur to a lesser degree
Diseased SA node in SSS can be much more easily suppressed
Abn automatic cells and overdrive suppression
lack of overdrive suppression
Gap phenomenon
- Ability of premature impulse to propagate through AV node, while other “less premature” fail to reach ventricles
o 2 levels: proximal = shorter refractory period and distal = longer refractory period
o Premature impulses can travel proximal region, but are blocked at distal level - Gap phenomenon = impulse with a shorter coupling interval
o Proximal level during relative refractory period → delayed conduction
o Distal level have time to recover → conduct impulse
Supernormal conduction
- Conduction of an impulse at an unexpected time
o Short period during repolarization where excitation is possible with a subthreshold stimulus
At the end of phase 3 (end of T wave) - Availability of fast Na+ channels
- Proximity of membrane potential to threshold potential
o Smaller stimulus than normal required to depol
Conduction is better earlier in the cycle than expected
Normal QRS morphology or ↓aberrancy
Duration of supernormal phase
constant even with RR changes
Larger proportion of AP at faster HR
Supernormal conduction associated with
o APC during sinus rhythm with BBB
o Narrow and wide QRS alternans during SVT
o Narrow QRS during Afib with BBB
Physiologic mechanisms of supernormal conduction
a) Supernormal excitability in phase 3
b) Diastolic phase 4 depolarization: rapid conduction
c) Gap phenomenon (see previous)
d) Dual AV nodal pathways: early APC propagate through slow pathway
e) Peeling back refractoriness: shorter absolute AV node refractory period by VPC or JPC
f) Shorter refractoriness from changing preceding cycle length: proportional to length of cycling interval
g) Summation of subthreshold impulses
h) Wendensky facilitation: multiple impulses on blocked site → block is overcome → multiple stimuli summate and reach distal site → conduction
i) Bradycardia dependent blocks
j) Wenckebach phenomenon in BB
Def: Effective inter-sinus interval
time between conducted sinus impulses
Def: Escape capture bigeminy
bigeminal rhythm with an escape beat followed by captured beat
When does escape capture bigeminy occurs
marked difference between escape interval and effective inter-sinus interval
o Sinus interval longer > escape interval
SA node dz → low intrinsic rate
Sinus rhythm associated with accelerated junctional rhythm
o Rare
Forms of escape capture bigeminy
atrial or ventricular capture bigeminy
o Most commonly in Hi w SSS or 2AVB
Requirementsof escape capture bigeminy
o Effective inter-sinus interval > sum of escape interval + refractory period
o Escape complex: do not alter SA node cycle (no retrograde conduction
o Intermittent block of sinus impulse at sinus or AV level
Mechanisms of escape capture bigeminy
o SA block
Sinus impulses occur just after recovery period of VPC (shaded)
* Normal conduction if relatively late
* Aberrant conduction if early after VPC
If PP interval ↓ and become < escape rhythm interval → rhythm is abolished
o AV block
Starts with a dissociated beat
3:2 AVB→ block permit AV node to escape resulting in dissociated beat
o Reversed reciprocal rhythm
Starts with a dissociated beat
2nd impulse conducted from SA node
* 1st degree AVB present
* Conduct retrogradely by accessory pathway
o Negative P wave in ST segment
o Depol SA node → delay next impulse
o Postpone next sinus impulse
3rd impulse: AV node escape from delay of sinus impulse
Mechanism of atrial echo beat
VPC conducted retrogradely to atrium → provoke atrial impulse conducted via normal pathway (AV node, His Purkinje system)
o AV node: particularly if dual pathways
Antegrade along slow pathway = long PR
Retrograde along fast pathway
Since long PR → atria recovered from previous depolarization
o Accessory pathway: WPW, concealed bypass tract
* Occurs when pacemaker and intact ventriculoatrial conduction
o Can result in bigeminal rhythm
Factors necessary for re-entry
o Circuit: path followed by electrical impulse during re-entry
Size and shape: determined by conduction velocity + myocyte refractory period
* Size must = or > length of re-entry
* Cycle length = refractory period x conduction velocity
2 branches: α and β
* α: antegrade conduction
* β: retrograde conduction
* If same conduction velocity: impulse meet at the end and block in single wavefront
o Unidirectional block in a branch of the circuit
o Slow conduction velocity in a branch of the circuit
o Appropriate cycle length
o Trigger
