cardiac rhythm Flashcards
what is sinus rhythm maintained by
- entrainment and suppression of lower pacemaker
- coordinated excitation via specialised conduction system
- existence of prolonged refractory period in the myocardium
what are arrhythmias due to
disorders of impulse formation
- e.g. DAD, EAD
disorders of impulse conduction
- e.g. AV block, LBBB, reentry, dispersion of repolarization
types of reentrant arrhythmia
- atrial flutter
- atrial fibrillation
- ventricular tachycardia
- ventricular fibrillation
describe atrial flutter
- fast regular atrial rate
- p wave = sawtoothed appearance
- ignores SA node
- don’t all get through to the ventricular due to the AV node
- all the same shape P wave due to the circuit in the atria being the same over and over again
- normal QRS as when it gets through normal system
describe atrial fibrillation (AF)
- rapid disorganised atrial activation
- not all impulsed conducted to ventricles
- QRS still normal due to fast conduction system
describe ventricular tachycardia
- rapid ventricular activation
- impaired mechanical function and risk of VF
- wide QRS complexes as its not using the conduction system
- p wave absent
- rapid regular rhythm
the inactivation of Na+ channels are important in which phase of the cardiac action potential
refractory period
- longer as sodium channel takes time to repolarise back
re-entrant circuit model
- region of block e.g. scar tissue, inactive area
- usually impulse travels either side of region of block (collide & continues)
- if activation blocked down one side (unidirectional block) → spreads around & can re-enter
- vulnerability to re-entry increases w/ ↓CV or ERP
describe wavelength equation
wavelength = ERP * CV
- more likely to get a re-enttrant activation with decreased conduction velocity (CV) or decreased refractory period
gives the cell more time to repolarise
what does re-entrant activation require
- a ‘circuit’
- slow conduction and/or short ERP
- unidirectional block
- a trigger
describe wolf-parkinson white syndrome
- ventricles activated through accessory pathway
- wide QRS as its not using the fast conduction system
- delta wave, short P-R interval
rate of propagation of electrical activation determined by:
- electrical properties of myocytes
(increased coupling between increases propagation. Rate > in larger cells) - inward current during excitation
(density and status of Na+ channels)
describe how and when ectopic beats occurs
- occurs during vulnerable period (T wave)
- Na+ channels not fully reset so reduce Na+ current (slower propagation)
- repolarization non-uniform giving greater chance of local conduction block
myocardial ischaemia results in:
- slow conduction
- reduced AP duration
- non-uniform repolarization
- ectopic activations (DADs)
why does slow conduction occur in myocardial ischaemia
low ATP → ↓Na/K ATPase & reduction of gradients → partial membrane depolarisation →
(partial) inactivation of Na channels → ↓INa → ↓ rate of spread
↓ pH due to regional metabolic acidosis → ↓ gap junction coupling
describe the action potential changes in myocardial ischaemia
low ATP → ↓Na/K ATPase & reduction of gradients → hyperkalaemia shortens AP duration (IKr)
low ATP also activates IK, ATP → shortens AP duration
as this only occurs in ischemic regions, gives differences in electrical properties (AP duration, conduction velocities) = non-uniform repolarisation
describe delayed after depolarisations (DADs)
trigger for myocardial ischaemia
- impaired Ca homeostasis (due to↓Ca ATPase activity) → ↑Ca conc in SR
- may lead to episodic Ca-induced Ca release from SR → efflux of Ca via NCX
- NCX is electrogenic → activation
describe the ways in which myocardial ischaemia can result in re-entry
- slow conduction and reduced AP duration = reduced wavelength
- ectopic activations (DADs) = trigger
- nonuniform depolarisation = ↑ probability of local conduction block
consequences of VT in acute MI
VT means their rate has increased but still poor conduction. As a result, theres an increased demand for O2 but a reduced O2 supply. Causing more severe ischaemia
- positive feedback cycle
risk for VF
rhythm changes in HF
- atria dilate → increases re-entrant path lengths & promote AF
- ↑ atrial P → stimulates stretch-activated channels = currents at the wrong time
- atrial fibrosis → regional slowing of conduction
- altered expression & function of NCX (can cause DADs → re-entrant arrhythmia)
- remodeling of autonomic nervous system (influences electrical properties)
describe early after depolarizations (EADs)
- caused by prolonged action potential which enable Ica(L) to re-activate
what causes an increased AP duration
- drugs (amiodarone)
- reduced extracellular K conc (hypokalaemia)
- K+ ion channel mutations, changing current through
- Na+ ion channel mutations
