CVS drugs

Question 1

Name two main causes of arrhythmias

Answer 1

1. Ectopic pacemaker activity 2. Afterdepolarisations

Question 2

How are ectopic beats developed?

Answer 2

Ischemic myocardium depolarises spontaneously

*dominates SA node

Question 3

Why do afterdepolarizations occur?

Answer 3

Anything prolonging AP -> triggers premature AP

Question 4

What causes re-entry loops?

What’s the difference between an incomplete and a complete block?

Answer 4

Ischemic myocardium blocks AP from being conducted properly -> follows an alternate depolarising pathway/”re-entry” loop -> arrhythmia

Incomplete: AP can travel through ischaemic myocardium one way
Complete: can’t travel through at all

Question 5

What is Wolff Parkinson White Syndrome?

Answer 5

Accessory pathway between heart’s upper - lower chambers via bundle of KENT (around tricuspid)

Question 6

Name the 5 classes of antiarrhythmic drugs

Answer 6

Drugs blocking: VGNa+ channels, K+ channels, Ca2+ channels, b blockers

Other:
adenosine - lowers HR
magnesium - relaxes myocytes
HCN channel blockers

Question 7

One example of a drug blocking Na+ channels

*what condition might it be given for?

Answer 7

Lidocaine

*slow AP upstroke, given in ventricular tachycardia

Question 8

How do B adrenoceptor antagonists work in pacemaker cells and the myocardium and what does this prevent?

Answer 8

Block NA -> less steep pacemaker potential and reduce FOC

• prevents ventricular arrhythmias and atrial tachycardia (slows AV node conduction)
• reduces myocardium O2 requirement

Question 9

Example of beta blocker

Answer 9

“olol” suffix: propanolol

Question 10

Why do drugs blocking K+channels work? Name one exception and a syndrome where this drug can be used

Answer 10

Less repolarisation prolongs the AP -> can be pro arrhythmic

Amiodarone WPW syndrome (has ca2+ channel and b-blocking activity)

Question 11

Why do drugs blocking the Ca2+ channels work in the heart and in vascular smooth muscle? Name an example

Answer 11

Slows excitability of SA node and conductibility of AV node
*slowing calcium influx/AP upstroke in pacemaker cells

Vasodilates sm muscle (lowers BP)
*Reduces calcium influx, i.e verapamil

Question 12

How does adenosine work and how is administered? Which receptors does it interact with?

Answer 12

Acts on A1: increases K+ conductance -> cell goes into hyperpolarisation -> temporarily stops to reset rhythm

*AV pacemakers can’t transmit excess atrial systoles into more ventricular systoles

Question 13

What will happen to Starling’s Curve in heart failure?

Answer 13

X: End diastolic volume Y: Stroke Volume

Shifts right and reduces in height

*despite increases in end-diastolic volume heart cannot pump out a stronger SV

Question 14

How do positive inotropic drugs increase the CO? Name 2 examples

Answer 14

B-agonists that increase FOC e.g: adrenaline, dobutamine

Question 15

Name an example of a cardiac glycoside and 2 main things it can do for the heart

Answer 15

Digoxin: blocks Na+/K+ ATPase
+ve inotropic: Increase FOC

Blocks Na+/K+ ATPase -> Na+ accumulates in cell -> deactivates Na/Ca exchanger -> intracellular calcium accumulates

Question 16

What is one reason you might prescribe an Angiotensin II receptor blocker over an ACE inhibitor?

Answer 16

Inhibiting ACE causes cough

ACE breaks down bradykinin which normally leads to sm muscle contractions in bronchioles/COUGH

Question 17

Why does angina occur and what often occurs alongside it?

Answer 17

Heart receiving inadequate O2

*i.e atheromatous plaques, to compensate heart tries to increase HR and FOC which shortens diastole and increases O2 demand

Question 18

What are the primary and secondary actions of NO?

Answer 18

Primary: venodilation lowers preload - FOC- O2 demand

Secondary: Vasodilation to collateral arteries improves O2 delivery to ischemic myocardium

Question 19

2 heart conditions that have an increased risk of thrombus formation

Answer 19

Acute MI: plaque rupturing causes clots and blocked arteries

AF: atrial quivering - blood stasis and clots

Question 20

3 anticoagulant drugs

Answer 20

Heparin, Warfarin, Novel oral anticoagulants (NOAC)

Question 21

What is the mechanism of Warfarin? What are the possible cons of using it? What should you check in a patient before administering them warfarin?

Answer 21

Antagonizes Vitamin K (a cofactor for 2,7,9,10)

Internal bleeding, narrow therapeutic window, other drug interactions

Check patients INR