Prescribed Drugs And ECGs

Question 1

Describe the normal ventricular action potential

Answer 1

Baseline - slow leaky Na channel 
Upstroke - voltage gated Na channel
Down blip - voltage gated K leaving
Plateau - K still leaving but Ca in through L type CC
Downstroke - CC close so just K leaving

Question 2

Describe the pacemaker cell action potential

Answer 2

Initial up - T type Ca open so Ca in
Upstroke - L type Ca open so Ca in
Downstroke - K channel open so K out
Baseline - slow leaky Na channel

Question 3

What happens to the ECG when Na channels are blocked and why

Answer 3

Reduced rate and rise of ventricular cell action potential
Wide QRS
Elevated R in AVR
+/- RBBB
VT and VF can occur due to the slowed conduction resulting in re-entrant circuits

Question 4

Which drugs inhibit fast Na channels

Answer 4

CVS: class 1a/c antiarrythmics, propranolol, verapamil
Psych: carbamezapine, amitriptyline, citalopram
Illicit: cocaine
Amantadine
Antihistamine
Antimalarials (chloroquine)

Question 5

Describe the ECG in hyperkalaemia

Answer 5

Peaked T wave
Small, broad P
Wide QRS
Prolonged PR

Question 6

Describe the ECG changes when calcium channels are blocked

Answer 6

Pacemaker cells slow/unable to initiate a cardiac impulse - sinus brady +/- av blocks
You may get ventricular escape rhythms - wide QRS

Question 7

Name some calcium channel blockers

Answer 7

Nifedipine
Amlodipine
Verapamil
Diltiiazem

Question 8

What can nifedipine do to an ECG

Answer 8

Reflex tachycardia

Question 9

What does blocking the K channel do to an ECG

Answer 9

Prolongs the action potential (delayed repolarisation) = QT prolongation. This can lead to TdP
Delayed repolarisation minimises the difference of charge across the membrane = depolarisation can happen again early = early afterdepolarisation. This can lead to re-entry and polymorphic VT
U wave is often prominent in precordial leads

Question 10

Why do you get VT with K channel blocking drugs

Answer 10

The delay in repolarisation leads to a reduced difference in charge across the membrane. This can lead to early afterdepolarisations which then lead to re-entry tachycardia

Question 11

which drugs block the K channel

Answer 11

CVS: antiarrhythmics 1a/1c/3
Psych: tricyclics, citalopram, antipsychotics (chlorpromazine, haloperidol, olanzapine)
Antihistamine
Antimalarials
Antibiotics: ciprofloxacin, clarithromycin, erythromycin

Question 12

What does digoxin do to an ECG

Answer 12

Digoxin toxicity: Atrial tachycardia with AV block (due to increased vagal tone causing AVN depression). Can lead to ventricular ectopics
Digoxin effect: Flat/inverted T and ST depression and Short QT

Question 13

How does digoxin work (ions and channels)

Answer 13

Blocks NaKATPase
Intracellular Na rises
Intracellular Ca rises
Positive inotropic effect

Question 14

Action of sympathetics on the heart (receptor and ions)

Answer 14

B1 receptor

Increase permeability to Na and Ca to increase excitability therefore increased conduction

Question 15

What are the action of parasympathetics on the heart (receptor and effect)

Answer 15

Muscarinic receptors
Reduce atria exciteability
Slow the conduction to the ventricles

Question 16

B blockers do what to an ECG

Answer 16

Bradycardia
+/- AV block (long PR often first sign)
+/- prolong QT - sotalol
+/- wide QRS - propranolol

Question 17

Why would you end up with TdP, VT or VF in B blocker OD

Answer 17

Sotalol and propranolol prolong the QT interval due to blocking the K channel

Question 18

If you block the sympathetic system what ECG changes might you see

Answer 18

Bradycardia

AV block

Question 19

What do sympathomimetics do to an ECG

Answer 19

Sinus or atrial tachycardia

+/- ventricular dysarrhythmias in high dose

Question 20

What do anticholinergics do to an ECG

Answer 20

Sinus and atrial tachycardia

Premature ventricular beats

Question 21

Name some drugs with an anti cholinergic effect

Answer 21

Antihistamines
Atropine
TCAs
Antipsychotics eg clozapine

Question 22

What do cholinomimetics do to an ECG

Answer 22

Bradycardia

AV block

Question 23

What HR would you expect with the various escape rhythms

Answer 23

AVN: 40-60bpm
Ventricular: 20-40bpm

Question 24

Which drugs prolong your QT interval

Answer 24

CVS: antiarrhythmics 1a/1c/3, sotalol
Psych: TCAs, citalopram, antipsychotics (haloperidol, chlorpromazine, olanzapine)
Antihistamines
Antimalarials
Antibiotics (clarythromycin, erythromycin, ciprofloxacin)

Question 25

How is TdP treated immediately

Answer 25

IV MgSO4 2g over 10 minutes Or 4ml 50% Mg

Question 26

Compare PMVT and TdP

Answer 26

PMVT: multiple ventricular foci and therefore QRS morphology is constantly changing, it is a wide complex tachycardia, AV dissociation TdP: PMVT + QT prolongation needed for diagnosis. QRS twists around the isoelectric point

Question 27

What can often be the first sign of CCB or Bblocker toxicity

Answer 27

Prolonged PR interval (even in absence of bradycardia)

Question 27

What ion channel does propranolol effect in OD and what is the result

Answer 27

Fast sodium channels | QRS widening with a positive R wave in AVR

Question 28

What ion channel does sotalol block in toxicity and what is the result

Answer 28

Potassium channels | QT prolongation which can lead to TdP

Question 29

What channels are effected in TCA OD and what is the result?

Answer 29

Muscarinic - sinus tachy Fast Na - wide QRS (lead to VT) + Tall R in AVR K - QT prolongation

Question 30

Other than ECG changes how might someone with TCA toxicity present

Answer 30

Anticholinergic toxidrome Hypotension Seizures

Question 31

How is TCA toxicity managed

Answer 31

IV sodium bicarb an hyperventilate | + activated charcoal, benzo’s for seizures, fluids for hypotension