Cardiac rhythm problems

Question 1

What is syncope?

Answer 1

Loss of consciousness with loss of tone.

Question 2

How does polymorphic tachycardia present on ECG?

Answer 2

• Transient prolongation of the QT interval associated with non sustained VT.

I.e Long QT syndrome

Question 3

What is evident in long QT syndrome?

Answer 3

• Family history
• Presyncope
• QT interval and VT morphology

Question 4

How is long QT t wave timing different to normal sinus rhythm?

Answer 4

In sinus rhythm the T wave occurs around 1/3 the way between QRS complex

long QT this becomes around 1/2

Question 5

What pathophysiology gives rise to long QT syndrome?

Answer 5

In phase 3 (repolarisation) theres a decrease Inwards K current because of Ikr and Iks

Question 6

Can antihistamines induce PVT?

Answer 6

• 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

Question 7

Given long QT syndrome what initiates VT?

Answer 7

EADS: Caused by prolonged APs which enable Ca channel to reactivate

Question 8

What can prolong the AP?

Answer 8

• Drugs: Amiodarone, sotalol (Class 3 + Beta blocker), antihistamine
• Hypokalaemia (Diuretic, DnV)
• K and Na Ion channel mutations

Question 9

What is amiodarone used for?

Answer 9

Anti-arrhythmic (prevents re-entrant arrhythmia by prolonging wavelength) But risk of LQT

Question 10

Describe the mechanism of hypokalaemia induced AP prolongation:

Answer 10

• Hyperpolarisation (larger transmembrane K conc. grad)
• Prolonged AP depolarisation BECAUSE Ikr is dependent on Ko thus Ikr decreases as Ko decreases)

Question 11

What can cause torsades de points?

Answer 11

Long QT (dispersion of refractoriness) + EAD triggering beat
= Reentry torsade de points

Question 12

Torsade de points is an example of what?

Answer 12

Polymorphic ventricular tachycardia

Question 13

Explain the changing axis seen in PVT? why is it not VF?

Answer 13

• 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.

Question 14

Whats happening in monomorphic VT?

Answer 14

Electrical activity circulates around a fixed anatomical substrate, reentry is occuring wihtin a region of functional block and is more unstable.

Question 15

What can happen with PVT?

Answer 15

• Spontaneous termination
  but
• Can progress to VF

Question 16

Why do after depolarisation carry a high risk of sudden cardiac death in young persons?

Answer 16

• 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

Question 17

What advice would you give to a patient with LQT?

Answer 17

• Guided by risk with QT interval
• High risk i.e prev. cardiac arrest
  = Beta blockers and ICD
• Lower risk = beta blockers and lifestyle mod.

Question 18

What are the triggers for LQT1,2,3?

Answer 18

LQT1: Stress, exercise i.e swimming

LQT2: Auditory stimuli and stress

LQT3: Rest and sleep… nothing specific to avoid.

Question 19

What symptoms may a patient with monomorphic ventricular tachycardia experience?

Answer 19

• Syncope
• Low BP
• Chest discomfort

Question 20

Why does a patient with VT experience syncope, low BP and chest discomfort?

Answer 20

• 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?

Question 21

What wave morphology can be seen with monomorphic ventricular tachycardia?

Answer 21

• Broad complex -> Not using his-perkinje system
• High rate
• p waves hidden

Question 22

Why in monomorphic VT are the QRS complexes broader and explain the abnormal morphology:

Answer 22

• QRS complexes are ectopic
  = Slow conduction system ‘wide QRS’

Abnormal shape because of abnormal activation sequence

Question 23

What are the likely causes of monomorphic ventricular tachycardia?

Answer 23

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

Question 24

What creates the monomorphic component?

Answer 24

• Automatic traigger within or re-entry around;
• Scar tissue etc

Circuit does not move - is stabilised or within the region of scar.

Question 25

Why do some patients have epidsodes of VT?

Answer 25

Episodes of ischeamia

Question 26

How does ischeamia lead to VT?

Answer 26

- Trigger (DADs b/c ischeamia) + Unidirectional block + Slow conduction (shortened APD) + A circuit

Question 27

Why do DADs occur in ischeamia?

Answer 27

- No oxygen = Decreased ATP = Reduced Ca re-uptake = Ca sparks = High iCa = NCX works = Na in -> threshold met and depolarisation

Question 28

Why does slow conduction occur in ischemia? VIP

Answer 28

- 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)

Question 29

How is the AP changed in myocardial ischeamia? VIP

Answer 29

- 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.

Question 30

How do you treat monomorphic ventricular tachycardia?

Answer 30

- Ant--arrhythmic drugs. - Ca channel blocker but effects everything so decreased BP S/E - Sedate and defib heart - Ablation if meds dont work

Question 31

What features of an ECG are consistent with an acute infarct?

Answer 31

- ST segment elevation - T wave inversion Suggests acute MI

Question 32

Where does V1 look?

Answer 32

LAD territory (anterior infarct)

Question 33

Whats the most common ectopic trigger for reentrant arrhythmia immediately after MI?

Answer 33

DADs - Impaired Ca homeostasis and ischeamic myocytes.

Question 34

What other factors can contribute to electrical instability following post MI?

Answer 34

- 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

Question 35

Why are ectopic beats more likely to occur in the 24hrs post MI?

Answer 35

- 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.

Question 36

What is the likely cause of ventricular tachycardia following acute MI?

Answer 36

- 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

Question 37

How can MI lead to rhythm disturbances?

Answer 37

- 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

Question 38

What creates the variable amplitude in QRS complexes during ischeamia?

Answer 38

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