Arrhythmias Flashcards
Three type of heart arrhythmias
Atrial fibrillation
Superventricular tachycardia
Bradycardia
Atrial fibrillation
HB irregular and fast (350 to 600 beats per minute), not immediately life-threatening. Most common.
Superventricular tachycardia
Episodes of abnormally fast heart rate at rest. Ventricular rate generally around 100 to 200 beats per minute.
Bradycardia
Slow heart beat
Hierarchy of cardiac pacemakers
SA node - 60-100 beats/min
AV node - 40-60
Bundle of His - 40-60
Purkinje Fibres - 20-40
Cardiac conduction pathway
SA node is the natural pacemaker it releases electrical stimulant at a regular rate, rate is dictated to the bodies needs. Electrical stimulus from the SA node reaches the AV node and is delayed briefly so all contraction atrial have enough time to pump all the blood into ventricles. AV valve closes and the atria begins to refill. Conductance passes through the AV node and bundle of His into the bundle branches and purkinje Fibres.
How does electrical propagation in the heart happen?
Propagation is from cell to cell. Depolarisation in cell decays electronically to neighbour, and depolarises it to its threshold. Gap junctions allow cell to cell passage of ions allowing the threshold of neighbouring cells to be met.
What ion channels are activated during spontaneous depolarisation of SA node (threshold -40 & amp; -30mV)
if (voltage-dependent)
iT,Ca (voltage-dependent)
iL,Ca (coltage-dependent)
What ion channels are activated during depolarisation?
iKr,Ks activate
What ion channels are activated during repolarisation?
iKAch (activated by Acetylcholine)
Ventricular action potential ion channel activation
Depolarisation iNa voltage-dependent iL,Ca voltage-dependent iNa time-dependent iL,Ca time-dependent
Repolarisation
iL,Ca and iNa/Ca
iKr,Ks activates
iK1 activates
A functional change in ion transporters can lead to?
Arrhythmias
Na Ca exchanger
Na-K pump
What is an arrhythmia?
A disturbance in the rate, rhythm or pattern with which the heart contracts
Causes of arrhythmias
Coronary artery disease leaving to myocardial ischemia or infarction.
Structural changes that accompany heart failure
Many drugs
Electrolyte imbalance (K+, Na+, Ca2+)
Congenital defects
What is fibrillation?
Quivering movement due to uncoordinated contraction of individual fibrils.
What can arrhythmias produce
Vascular stasis or reduce cardiac output to the point that adequate blood flow cannot be maintained to vital organs.
Arrhythmia classification based on anatomical origin
Superventricular - originates higher up the conduction route than the ventricle.
Ventricular - originates in the ventricle.
How can ECG measure arrhythmias?
Measurement of change in the electrical field during propagation of cardiac action potential.
Arrhythmia classification based on mechanisms
Disturbance in conduction:
Conduction block, re-entry
Disturbance in impulse formation (Automaticity):
Early delayed after depolarisation (EADs), delayed after depolarisation (DADs)
AV node block causes
Reduced ventricular rate = reduced CO
Bundle of His block causes
Asystole (no ventricular contraction) or Bradycardia (reduced heart rate.)
Purkinje fibre block causes
No change in heart rate but reduces cardiac output.
Why is the refractory period important?
Prevents tetany and prevents against re-entrant arrhythmias.
Wavelength equation
Wavelength = Conduction velocity x ERP
What is the relationship between wavelength and re-entrant circuit formation?
Increase in wavelength, re-entrant circuit formation is less likely to occur.
The heart is more susceptible to re-entry and arrhythmia when?
The conduction velocity is slow and when cardiac cells spend less time in the refractory state.
What is the mechanism of re-entry
Presence of a unidirectional block within a conducting pathway, critical timing and refractory state of normal tissue that the wave-front encounter.
When conduction velocity is slowed by local damage (ischemia). The slow wave-front may find adjacent tissue no longer in the refractory period which may then propagate the signal further, becoming an arrhythmia.
What dimension does the re-entrant arrhythmia form?
Three-dimensional scroll wave. Can be confined to both single or several chambers.
Ventricular fibrillation
Life threatening, many small waves propagate throughout the ventricles.
Atrial flutter
Atrial rate 250 to 350 beats per minute, ventricular rate substantially slower
EADs and DADs triggered activity
The heart tissue is stimulated once, but results in the production of more than one conducted beats.
What is necessary for a EAD to generate?
A prolonged action potential duration (APD). If net inward currents during repolarisation (phase 3) are larger than outward currents, this can form and EAD. Can create a substrate for producing triggered beats in multiple locations, resulting in multifocal ventricular tachycardia.
Dispersion of repolaristaion and Torsades de Pointes
Heterogeneity in action potential duration (dispersion of repolarisation) results in a myocardium that is more vulnerable to multiple sites of re-entrant excitation.
Delayed afterdepolarisations
Cellular Ca2+ overload swamps SR with Ca2+. Phasic (oscilaroty) release of Ca2+ from SR via RyR2. Oscilatory depolarising inward current (NCX).
