Cardiac rhythm problems Flashcards
(38 cards)
What is syncope?
Loss of consciousness with loss of tone.
How does polymorphic tachycardia present on ECG?
- Transient prolongation of the QT interval associated with non sustained VT.
I.e Long QT syndrome
What is evident in long QT syndrome?
- Family history
- Presyncope
- QT interval and VT morphology
How is long QT t wave timing different to normal sinus rhythm?
In sinus rhythm the T wave occurs around 1/3 the way between QRS complex
long QT this becomes around 1/2
What pathophysiology gives rise to long QT syndrome?
In phase 3 (repolarisation) theres a decrease Inwards K current because of Ikr and Iks
Can antihistamines induce PVT?
- Modern non-sedating antihistamines are known to inhibit potassium channels and have been implicated in VT in people with LQT syndrome.
This further increases VT risk
Given long QT syndrome what initiates VT?
EADS: Caused by prolonged APs which enable Ca channel to reactivate
What can prolong the AP?
- Drugs: Amiodarone, sotalol (Class 3 + Beta blocker), antihistamine
- Hypokalaemia (Diuretic, DnV)
- K and Na Ion channel mutations
What is amiodarone used for?
Anti-arrhythmic (prevents re-entrant arrhythmia by prolonging wavelength) But risk of LQT
Describe the mechanism of hypokalaemia induced AP prolongation:
- Hyperpolarisation (larger transmembrane K conc. grad)
- Prolonged AP depolarisation BECAUSE Ikr is dependent on Ko thus Ikr decreases as Ko decreases)
What can cause torsades de points?
Long QT (dispersion of refractoriness) + EAD triggering beat
= Reentry torsade de points
Torsade de points is an example of what?
Polymorphic ventricular tachycardia
Explain the changing axis seen in PVT? why is it not VF?
- The variable amplitude of ECF complexes with time indicates PVT and that the re-entrant path varies on a cycle to cycle basis
- NOT VF because rate is relatively constant and the QRS complexes remain identifiable and relatively ordered.
Whats happening in monomorphic VT?
Electrical activity circulates around a fixed anatomical substrate, reentry is occuring wihtin a region of functional block and is more unstable.
What can happen with PVT?
- Spontaneous termination
but - Can progress to VF
Why do after depolarisation carry a high risk of sudden cardiac death in young persons?
- EADS occur at a time when most Na channels are inactivated (vulnerable period, RRP or SNP)
- Thus most inward current because of Ca channels
= Very slow electrical propagation
Increased risk of VT and VF
What advice would you give to a patient with LQT?
- Guided by risk with QT interval
- High risk i.e prev. cardiac arrest
= Beta blockers and ICD - Lower risk = beta blockers and lifestyle mod.
What are the triggers for LQT1,2,3?
LQT1: Stress, exercise i.e swimming
LQT2: Auditory stimuli and stress
LQT3: Rest and sleep… nothing specific to avoid.
What symptoms may a patient with monomorphic ventricular tachycardia experience?
- Syncope
- Low BP
- Chest discomfort
Why does a patient with VT experience syncope, low BP and chest discomfort?
- VT leads to impaired pump / CO
- High HR = reduced filling time, poorly coordinated ventricular activation = poor mechanical coordination and hence poor pump function.
= Dec. CO = Dec. MABP
- When standing can reduce brain perfusion = syncope
Chest discomfort
- Palpations
- Impaired myocardial perfusion
- Pulmonary congesiton?
What wave morphology can be seen with monomorphic ventricular tachycardia?
- Broad complex -> Not using his-perkinje system
- High rate
- p waves hidden
Why in monomorphic VT are the QRS complexes broader and explain the abnormal morphology:
- QRS complexes are ectopic
= Slow conduction system ‘wide QRS’
Abnormal shape because of abnormal activation sequence
What are the likely causes of monomorphic ventricular tachycardia?
Re-entrant activation, requires;
- A trigger
- Unidirectional block
- Slow conduction / shortened APD
- A circuit
Anatomical or functional blocks
SLOW CONDUCTION AND UNIDIRECTIONAL BLOCK CAN OCCUR WHEN REPOLARISATION IS NOT SPATIALLY HOMOGENOUS
NB: Atria continue to activate and contract independently
What creates the monomorphic component?
- Automatic traigger within or re-entry around;
- Scar tissue etc
Circuit does not move - is stabilised or within the region of scar.
