Cardiac rhythm problems Flashcards
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.
Why do some patients have epidsodes of VT?
Episodes of ischeamia
How does ischeamia lead to VT?
- Trigger (DADs b/c ischeamia)
+ Unidirectional block
+ Slow conduction (shortened APD)
+ A circuit
Why do DADs occur in ischeamia?
- No oxygen = Decreased ATP
= Reduced Ca re-uptake
= Ca sparks
= High iCa
= NCX works
= Na in -> threshold met and depolarisation
Why does slow conduction occur in ischemia? VIP
- Low ATP
- Na/K gradients reduced b/c Na/K ATPase not working
- Partial membrane depolarisation
- Inactivation of Na channels
- Reduced gap junction coupling (low pH due to regional metabolic acidosis)
How is the AP changed in myocardial ischeamia? VIP
- Na/K ATPase reduced
- iNa reduced
- Hyperkalaemia shortens AP duration (Ko increases Ikr)
- Activation of Ik,ATP channels shortens AP duration
IN ISCHEAMIC regions hence in-homogenous electrical properties.
How do you treat monomorphic ventricular tachycardia?
- Ant–arrhythmic drugs.
- Ca channel blocker but effects everything so decreased BP S/E
- Sedate and defib heart
- Ablation if meds dont work
What features of an ECG are consistent with an acute infarct?
- ST segment elevation
- T wave inversion
Suggests acute MI
Where does V1 look?
LAD territory (anterior infarct)
Whats the most common ectopic trigger for reentrant arrhythmia immediately after MI?
DADs
- Impaired Ca homeostasis and ischeamic myocytes.
What other factors can contribute to electrical instability following post MI?
- Increased cardiac SNS
- Effects of aberrant wall motion on stretch activated channels
i.e ischeamic wall mechanical function impaired
i.e Wall thinning and expansion during systole in the infarct region while rest of LV is thickening
Why are ectopic beats more likely to occur in the 24hrs post MI?
- Ischeamic myocytes in the region of the ifnarct and border zone are electrically active, though highly unstable
- During the 24hrs affected cells either die or the ischeamia is resolved.
Re-perfusion of an infarct region increases acute electrical instability.
What is the likely cause of ventricular tachycardia following acute MI?
- Re-entrant electrical activation associated with the ischeamia.
- # Na/K ATPase inhibition, Na and K conc. changes. Rises in Ca. Metabolic acidosis
- Slow conduction
- Reduced APD
- Non-uniform repolarisation
- EADs which generate ectopic activation
How can MI lead to rhythm disturbances?
- Acute MI the onset of ventricular tachycardia may lead to a positive feedback situation in which rhythm becomes totally irregular and ventricular fibrillation occurs.
- Inc HR = Inc. O2 demand & reduced diastolic perfusion time (supply demand compromised)
- Inc HR impairs ventricular performance, falling CO and MABP in addition to the causes of initial ischeamia
- Extending ischeamic region and making it more likely VT->VF
What creates the variable amplitude in QRS complexes during ischeamia?
When it transitions to polymorphic ventricular tachycardia. (assuming rate is constant and QRS are identifiable otherwise VF)
In acute ischeamia theres a region of functional block not scar yet. Thus re-entrant path can vary cycle to cycle basis. (more unstable than monomorphic VT)
Spontanoues reversion to sinus rhythm can occur or -> VF
