Cardiac Rhythm problems

Question 1

Twin - died from ventricular fibrilation suddenly (Long QT syndrome)
-what are some questions we would want to know?

Answer 1

-want to know what she was doing before she died - because the different types of long QT can be triggered by different things

Question 2

what is syncope

Answer 2

loss of tone and conciousness (faint)

Question 3

What does loratadine do?

Answer 3

• antihistamine for nasal congestion
• can exasberate the QT elongation
• these can inhibit potassium channels, and can induce VT in people with LQT syndrome - K channels help with repolarisation however if you block these then will prolong the AP more
• increases risk of VT due to prolonged AP

Question 4

Explain Long QT syndrome

Answer 4

• may be a problem with L type Caclium channles or sodium or potassium channels
• this can prolong the action potential, giving these channels time to reactivate and then they can become depolarisated again while the action potential is still occuring
• if this is big enough, it can depolarise ventricles early leading to a premature ventricular contraction
• However if some neighbouring cells are ready for a depolarisation, and some cells are not, then the wave of depolarisation can propgate through the cells that are ready and get blocked by the not ready cells, and then when those cells become ready, the wave can go around and depolarise those cells whcih can cause a re-entrant circuit which leads to reentrant tachycardia
• causes torstade de points
• can resolve, or can cause palpatations, syncope, dizziness, cardiac death

Question 5

What can cause VT initiation when there is already a long QT interval

Answer 5

Drugs (amiodarone (prolongs AP by inhibiting potassium currents) , sotalol, antihistamine, …)
• Reduced extracellular potassium concentration (hypokalaemia – decreased [K+]o decreases IKr) (e.g vomiting, diuertics, diahorrhea)
• Potassium ion channel mutations which lead to reduced effectiveness of delayed rectifier IK : LQT1 [IKs] & LQT2 [IKr]
• Sodium ion channel mutations that affect inactivation of INa (LQT3)

Question 6

Different types of QT syndrome and what they are triggered by
and what to avoid

Answer 6

• ong QT1 syndrome - often event occurs during exercise and stress
• long QT2 syndrome - when someone yells at you, load noises and stress
• long QT3 - person dies at night (sodium channel) - rest and sleep
• avoid these triggers
• history helps add to ECG

Question 7

Why is it torstades de pointes

and what can happen

Answer 7

because there is no fixed anatomical substrate that the reentrant circuit is circulating around , the reentry is occurring within a region of functional block

• more unstable than monomorphic VT
• could resolved back to sinus rhythm or could progress to VF

Question 8

What advice would you give someone with Long QT syndrome?

Answer 8

Prior cardiac events-beta blockers and a implatable cardioverter defibrillator

No prior events - beta blocker and lifestyle modificaiotsn

-E.g avoid triggers of cardiac events and medications (in slide above for specific QT syndromes)

Question 9

How to describe monomorphic tachycardia on an ECG?

Answer 9

• ecg - monomorphic tachycardia, broad complex, regular

Question 10

Why does patient have syncope, low BP and chest discomfort with VT

Answer 10

• heart not pumping as well due to VT, and not enough time to fill ventricles due to increase HR
• reduce CO, reduce BP - reduced perfusion to brain - syncope
• Chest discomfort - palpitations, imparied myocardial perfusion, pulmonary congestion due to poor LV pump

Question 11

Why is there prolonged QRS complex?

Answer 11

QRS complexes are ectopic

• these originate somewhere in ventricle and spread, hence this is not using the fast conduction system so is a relatively slow process so has a wide QRS
• also has an abnormal QRS shape due to abnormal activation sequence

Question 12

What are most common causes of the the arrhythmia (previous MI, and now has VT)

Answer 12

need a trigger, substrate, unidirection flow, AP length of ERP, circuit

-the circuit does not move and is resatabalised around or withint the region of the scar

Question 13

How can you get an MI with current ischaemia

Answer 13

Slow conduction - low ATP, na/k ATPase reduced, NA/K gradients reduced, partial membrane depolarisation, inactivaiton of sodium channles, reduced gap junction coupling due to metabolic acidosis
AP duration shortened
-na/k atapase reduced, transmembrane potassium gradient reuced, hyperkalemia - shorteneds AP duration, - elad to inhomogenous electrical properties - can get regions of block and re-entry pathways
DADs - cannot pump calcium out of cell and into SR as well due to reduced ATP, leads delayed after depolarsiation

Question 14

What do we do for person with VT?

• fibrilation
• low BP
• kidney

Answer 14

• dont want VF - want him in resuscitation area - can monitor and resusitate
• hypotension - treat rhythm disturbance to treat this
• troponin measurement
• kidney - give drugs if there is renal impairment (creatinine)
• defibrillate - sedate this person
• lifestyle behaviours- longterm care
• external defibrillator i drug deosnt help
• could do a left ventricular gram
• cut out anurysm of heart
• ablation of re-entrant circuits after percutaneous electrical mapping or implanation of an external defibrillator may be considered where VT is refractory to drug treatment

short term - stop rhythm distrubance, investigate other conditiosn (e.g kidney)
-long term - target and prevent arrhythmia

Question 15

What features on an ecg are suggestive of an acute MI

Answer 15

ST segment elevation, T wave inversion

Question 16

how do we get DADs in myocardial infarction

Answer 16

The reduction of ATP concentration that occurs as a result of reduced oxygen delivery impairs Ca2+ removal from the cell because:
• reduced sarcolemmal Ca2+ ATPase & Na+/K+ ATPase activity leads to reduced Ca2+ removal both directly and via Na+/Ca2+ exchange.
• Intracellular [Ca2+] is increased with respect to normal during diastole.
• Resultant spontaneous release of Ca2+ from the overloaded SR generates cyclic calcium transients that transiently increase the extrusion of Ca2+ via the Na+/Ca2+ exchanger.
• Due to the electrogenic properties of the exchanger, inward current is generated that depolarizes the cell membrane.
• If this process generates SR calcium release of sufficient magnitude, electrical threshold for the sarcolemmal membrane may be reached and a DAD will occur.
Impaired calcium homeostasis in myocardial ischaemia leads to elevated intracellular Ca2+ concentration in diastole
• This may lead to episodic calcium- induced Ca2+ release from SR
• Increased efflux of Ca2+ via sodium calcium exchanger
• Due to the stoichiometry of the sodium calcium exchanger membrane is depolarized and this may trigger activation (DADs)

Question 17

what else can cause electrical instability in the heart with an MI?

Answer 17

Other factors that can contribute to electrical instability after MI are:
• the increased cardiac sympathetic activity that commonly occurs under these circumstances and
• possible effects of aberrant wall motion on stretch-activated channels.
• aberrant LV wall motion occurs because the mechanical function of the
ischaemic region is impaired.
• for instance, wall thinning and expansion can occur during systole in the infarct region in the presence of wall thickening over the rest of the LV.

Question 18

why are ectopic beats more likely to occur in the 24 hours after an MI?

Answer 18

• Ectopic electrical activation (and reentrant arrhythmias) are most likely to occur in the first 24 hours after MI, because ischaemic myocytes in the region of the infarct and border zone are electrically active, though highly unstable.
• Over the 24 hours post-infarction, the affected cells either die or the ischaemia is resolved.
• NOTE: reperfusion of an infarcted region (as is now common clinically immediately after MI) increases acute electrical instability.

Question 19

why do we get VT?

READ REST OF PROBLEM SLIDES

Answer 19

The short run of VT during C is almost certainly due to reentrant electrical activation associated with the ischaemia.
• During acute ischaemia cellular homeostasis is perturbed in the affected region of the heart producing conditions that markedly increase the probability of reentrant arrhythmia.
• Internal ATP concentration decreases and the Na+/K+ ATPase is inhibited.
• As a result, both [K+]o and [Na+]i rise (along with the rise in [Ca2+]i).
• Ischaemia also leads to regional metabolic acidosis.
• These changes give rise to: (i) slow conduction (ii) reduced APD (iii) nonuniform repolarisation, and (iv) after-depolarisations which generate ectopic activation
The short run of VT during C is almost certainly due to reentrant electrical activation associated with the ischaemia.
• During acute ischaemia cellular homeostasis is perturbed in the affected region of the heart producing conditions that markedly increase the probability of reentrant arrhythmia.
• Internal ATP concentration decreases and the Na+/K+ ATPase is inhibited.
• As a result, both [K+]o and [Na+]i rise (along with the rise in [Ca2+]i).
• Ischaemia also leads to regional metabolic acidosis.
• These changes give rise to: (i) slow conduction (ii) reduced APD (iii) nonuniform repolarisation, and (iv) after-depolarisations which generate ectopic activation

Question 20

What does slow QRS mean?

Answer 20

=electrical activation is propagating slwoely not through the fast conduction system but through the renetrant circuit