Unit 6 - Cardiovascular - Arrhythmia Flashcards
What causes arrhythmias?
Acquired - changes to heart muscle - damage - ischaemia - infarct Genetic - mutation - polymorphism - causing structural or ionic changes
How can a post mortem diagnose arrhythmia?
Structural abnormalities
Molecular abnormalities
- ion channel changes
Why is the duration of diastole important to allow filling of the ventricle?
Ventricles have to work harder if not stretched
- more inefficient
What do alterations in timing of the cardiac cycle lead to?
Loss of efficiency
Complete failure to pump
What is the natural prevention of arrhythmia?
Refractory period
- time in which myocyte cannot conduct or initiate action potential
- determined by voltage gated Na+ channel
What is the re-entrant circuit movement?
Action potentials not triggered by the SAN
What is WPW syndrome?
Wolff-Parkinson-White syndrome
- genetic condition
What are the effects of Wolff-Parkinson-White syndrome?
SA node impulses overwhelmed by discharges in atria and parts of the pulmonary veins - circus movement - no P waves Ventricular contraction - AC escape - idiopathic ventricular rate - irregular frequency of QRS Survivable - ventricles protected by AV node If AV node bypassed fibrillation can access the ventricle - Wolff-Parkinson-White syndrome - diagnosed by ECG - no delay at AV node
What is the treatment for Wolff-Parkinson-White syndrome?
Ablation of heart muscle
What are the classes of cardiac arrhythmias?
Classified according to the site of origin of the problem
- atrial fibrillation
- ventricular ectopic beat
Classified according to the change in heart produced
- tachycardia
- bradycardia
What are the types of cardiac arrhythmias?
Modified nodal automaticity - normal variation Ectopic pacemaker activity Delayed after-depolarisation Early after-depolarisation - long QT syndrome Re-entry Heart block
What is modified nodal automaticity?
Sinus arrhythmia - normal waxing and waning of heart rate in phase with breathing in and out - heart rate increases on inspiration - heart rate decreases on expiration Fluctuations in autonomic tone
Sinus bradycardia
- heart rate < 60 bpm during the day
- < 50 bpm when in deep sleep
Sinus tachycardia
- heart rate > 100 bpm
- rare that it is due to intrinsic sinus node factors
- causes include hyperthyroidism, fever, infection
What are ectopic foci?
Action potentials generated outside the SA node
- increased rate of depolarisation during phase 4 due to overactivity of If
- causes include sympathetic overstimulation
- dobutamine
What are delayed afterdepolarisations (DADs)?
Afterdepolarisations are depolarisations caused by excessively large inward currents carried by the Na+/Ca2+ exchanger
- if afterdepolarisations are large enough to reach threshold, premature ectopic action potentials result before the next expected normal action potential
What is the ionic cause of DADs?
The Na+/Ca2+ exchanger produces an inward current which depolarises cells
Overactivity caused by Ca2+ overload causes depolarisation
Causes
- ischaemia (low ATP compromises Ca2+ pump)
- some forms of inherited arrhythmias
- digitalis
- block of Na+/K+ exchanger
What are early afterdepolarisations (EADs)?
One cell fails to repolarise essentially resulting in prolongation of action potential
Long QT syndrome
- genetic mutations in genes encoding K+ channel subunits resulting in defective repolarisation lengthens the QT interval and can lead to arrhythmia
What is drug induced long QT syndrome (LQTS)?
Drugs with inadvertently block hERG cause aquired LQTS sometimes leading to Torsades de Points (TdP)
No one structural class of drug responsible
- antibiotics
- antihistamines
- antifungals
- antipsychotics
- GI prokinetic agents
- antiarrhythmics
Polymorphisms in genes can predispose to problems with some drugs
What is re-entry?
Essentially circus movement of cardiac action potentials
Requires
- a bifurcation
- two separate pathways of conduction which join
- an area of slow conduction and unidirectional block
Where depolarisation wavefront meet they cancel each other out
If tissue is damaged and refractory it stops a re-entrant circuit
If tissue is damaged by excitable in only the retrograde direction then depolarising wavefront may travel around and because of slowed conduction in the damaged area reaches an area no longer refractory to set up a self-sustaining circuit
What is heart block?
Major damage in the conducting system has occurred
- most striking example is block at the AV node
What is first degree AV block?
Excessive slowing of conduction through the AV node
- affecting the PQ/PR interval
What is second degree AV block?
There may be missed beats
What is third degree AV block?
There can be complete breakdown of conduction between the atria and ventricles
- here the ventricle would be driven by an intrinsic pacemaker
- ventricular escape
- much slower than normal heart rate
- 30 - 40 bpm
- bradycardia
