Cardiac Rhythm and rhythm disturbance Flashcards
Conduction of heart
SA node Atria AV node bundle of his left and right bundle branches Purkinje fibers Ventircle
-Sequence of activation - from endocardial to epicardial surface
How is sinus rhythm maintained?
- suppression of lower pacemakers (av node)
- programmed excitation via the specialised conduction system
- existence of a prolonged refractory period in the myocardium
RRP and SNP ERP
RRP - stimuli greater than normal required to stimulate another AP
SNP - supernormal period - smaller stimuli than normal can generate propagated activation
ERP - cannot activate
Arrhythmia
2 main reasons this occurs
Any deviation of sinus rhythm
- disorders of impulse formation - early discharge of a pacemaker, or activity triggered by an unstable resting membrane potential in working myocardial cells - gives rise to extrasystoles (DAD, EAD)
- Disorders of impulse conduction - conduction abnormalities such as partial or complete AV block (slows heart rate), left or right bundle branch block and reentry ( these can alter time-course of ventricular activation sequence)
How can re-entrant arrhythmia be caused? and what can this lead to?
-how can this be caused?
arrhythmias can be caused by electrical stimulation during the T wave. This is normally when the ventricular myocardium is in its RRP, and excitation slowly elicits slowly propagating action potentials.
This can cause re-entrant arrhythmia - which is repeated circulation of a wave of activation in the ventricle wall giving rise to ventricular tachycardia
This can progress to ventricular fibrillation (chaotic reentrant activity in ventricles)
VF - heart loses its capacity to pump and death follows if it is not revered.
-VT and VF can occur in acute myocardial infarction, as a result of structural remodelling associated with healed myocardial infarction, in heart failure, as a result of hereditary ion channel mutations
Atrial flutter
what is it?
Is caused by a single atrial reentrant circiut and increases the atrial rate
-can cause partial AV block
Atrial fibriliation
what is it?
rapid, disorganised atrial activation, and not all impulses are conducted to the ventricles via av node
-leads to a rapid disordered ventricular rhythm
Atrial flutter and fibrillation
what can cause it?
what can it lead to
can be caused by - heart valve lesions, or congestive heart failure - common in elderly.
-significant risk of clot formation and pulmonary embolism and stroke
How does the action potential work?
Sodium and calcium are at higher concentrations outside the cell, and potassium is higher conc inside the cell
When membrane potential reaches threshold, sodium channels open and sodium flows in - rapid depolarisation
Depolarisation causes calcium channels to open
Early repolarisation - is due to outward potassium current
Plateau - balance between inward and outward
AP duration - is determined by the time of repolarisation due to potassium coming into cell
So during an action potential, sodium enters and then calcium enter the cell, and then potassium ions leave at the end.
-Action potential is a combination of the charges entering and leaving cell to make the membrane potential
Phase 0 - depolarisation phase 1 - early repolariastion phase 2 - plateau phase 3 - repolarisation phase 4 - resting state
what does the sodium calcium exchanger do?
Can change directions
Exchanges 3 sodium ions for 1 calcium ion
At the start of the action potential we get sodium ions leaving the cell, and calcium entering to get a net positive charge out of cell
At the end of the action potential we have calcium ions leaving and sodium entering, so get a positive charge going into the cell
Kinetics of channels being activated and inactivated at different membrane potentials
E.g fast sodium channel
- activation gates are shut at resting membrane potential. but open rapidly with depolarisation
- inactivation gates are open at rest and shut when the cell membrane is depolarised
- This ensures that there is a brief delay between activation and inactivation and the channel is open durign this window period of time
- this is responsible for the prolonged refractory period of the action potential
- cardiac cells cannot be reactivated durign the effective refractory period because membrane potential is -50mv and inactivation gates are closed.
Mechanism underlying re-entrant arrhythmia
This is where there is propagation of electrical activity around a region which activation is blocked because it is refractory or completely inexcitable.
- Activation arrives at the topf of region of block and propagates with equal velocity around both sides. The two waves at the bottom colide and stop. –> no reentrant arhtyhmia
- activation arrives at the top and is able to propagate around the left had side of the region of block, but not around the right hand side (path blocked). It can do a loop around the region and then reactivate it to get a reentrant circuit. This occurs if the time taken to propgate around the circuit is the same as the effective refractory period of the tissue . can get a sustained activation around the reentrant circuit
This shows that sustained reentrant activation can be set up around a region of anatomic or functional block provided
- there is a trigger
- unidirectional block
- slow conduction
Wolff parkinson white syndrome
the bundle of kent provides an accessory pathway for electrical activity to pass between atria and ventricle. This makes early activation of ventricles and then collides with the normal activation from the AV node.
ECG - wide QRS complex, short PR interval
- if get an ectopic occurs in the atria or ventricles while the tissue is in refractory period, can cause tachycardia - faintness , can lead to VF and death
- get reentry via AV node
- can get broad or narrow complex
- bad problem if have both atrial fibrilation alongside WPW because can get activation of ventricles causing ventricle fibriliation
What influences the velocity at which electrical activation spreads in heart tissues?
Electrical properties of myocytes
- cell dimension
- gap junction density
- membrane sodium channels
Inward current during excitation
-intensity of the sodium current
How does intensity of sodium current change conduction velocity
- if have more intense sodium current, then can get an increased conduction velocity
- rapid influx of sodium can move forward to next cell furhter on
- then if you get ectopic activation (e.g through bundle of kent) during the vulnerable T wave, then sodium channels are not fully reset so you will get a reduced sodium current and a reduced conduction velocity
- then could also get a non-uniform repolarisation and have an overall greater probability of local conduction block (cause the substrate for an arrythmia)
