heart

Question 1

3 drug classes which influence heart rate

Answer 1

B-blockers, Ca2+ antagonists, ivabradine

Question 2

how do B-blockers reduce heart rate

Answer 2

decrease I f and I Ca

Question 3

how do Ca2+ antagonists reduce heart rate

Answer 3

decrease I Ca

Question 4

how does ivabradine reduce heart rate

Answer 4

decrease I f, spacing depolarisations

Question 5

2 drugs classes which influence contractility

Answer 5

B-blockers, Ca2+ antagonists

Question 6

effect of B-blockers on contractility

Answer 6

decrease (as less Ca2+ entry)

Question 7

how do Ca2+ antagonists reduce contactility

Answer 7

decrease I Ca

Question 8

2 classes of Ca2+ antagonists

Answer 8

rate slowing (cardiac and smooth muscle actions), non-rate slowing (smooth muscle actions - more potent)

Question 9

2 types of rate slowing Ca2+ antagonists, with examples

Answer 9

phenylalkylamines e.g. Verapamil, benzothiazepines e.g. Diltiazem

Question 10

type of non-rate slowing Ca2+ antagonists, with example

Answer 10

dihydropyridines e.g. amlodipine

Question 11

indirect effect of non-rate slowing Ca2+ antagonists on heart

Answer 11

no effect on the heart, however profound vasodilation can lead to reflex tachycardia (baroreceptors detect and cause heart rate to increase to compensate)

Question 12

2 drug types influencing myocardial oxygen supply and demand

Answer 12

organic nitrates, K+ channel openers

Question 13

how do organic nitrates (e.g. NO) and K+ channel openers increase myocardial oxygen supply

Answer 13

organic nitrates increase sGC (cGMP, promoting relaxation and K+ channel opening); both cause hyperpolarisation as K+ efflux, so more difficult to contract; both therefore increase coronary blood flow

Question 14

2 effects of organic nitrates and K+ channel openers which influence myocardial demand by reducing afterload and preload

Answer 14

vasodilation (dilate arteries), decreasing afterload, and venodilation (dilate veins), decreasing preload

Question 15

what condition are these drugs used to treat, with relation to myocardial demand and supply

Answer 15

stable angina (pain when exercising due to inadequate myocardial oxygen supply vs demand), caused by atherosclerosis

Question 16

stages of drug use for treating stable angina

Answer 16

try one and if doesn’t work, try the other -> combine drugs -> long-lasting nitrate, ivabradine, or nicorandil (K+ channel opener)

Question 17

2 features of non-selective B-blockers e.g. pindolol that make it useful at treating heart failure

Answer 17

equal affinity for B1 and B2 receptors, with intrinsic sympathetic activity (therefore helps heart failure as PSNS dominant at rest, so has mild SNS effects)

Question 18

feature of mixed B-a blockers e.g. carvedilol that make it useful at treating heart failure

Answer 18

a1 blockade gives additional vasodilator properties (so assists heart failure also as decreases vascular resistance)

Question 19

side effect of B2 blockade on heart failure

Answer 19

reduce vasodilation and increase TPR, worsening heart failure

Question 20

how do pindolol and carvediol alleviate worsening heart failure by B2 blockade

Answer 20

pindolol has some B2 stimulating effects (intrinsic sympathetic activity), carvedilol has a1 blocking effects, decreasing TPR to alleviate problem

Question 21

2 side effects of B-blockers on heart

Answer 21

worsening heart failure, bradycardia

Question 22

2 causes of worsened heart failure (cardiac output doesn’t meet tissue demand) by B-blockers

Answer 22

cardiac output reduction, increased vascular resistance (block B2 vasodilation)

Question 23

cause of bradycardia by B-blockers

Answer 23

heart block (decreased conduction through AVN)

Question 24

side effects of B-blockers on trachea and bronchioles (don’t give to asthmatics)

Answer 24

bronchoconstriction (B2 blockade)

Question 25

side effects of B-blockers on liver (don’t give to diabetics)

Answer 25

masks hypoglycaemia as B2 (and a1 in carvedilol) blockade, reducing rates of glyogenolysis and gluconeogenesis

Question 26

why do B-blockers cause cold extremities/worsening peripheral artery disease

Answer 26

vasoconstriction of cutaneous vessels by B2 blockade

Question 27

4 other common B-blocker side effects

Answer 27

fatigue, impotence, depression, CNS effects (lipophilic agents) e.g. nightmares

Question 28

2 side effects of Verapamil (Ca2+ antagonist) caused by Ca2+ channel block in heart

Answer 28

bradycardia, AV block

Question 29

side effect of Verapamil (Ca2+ antagonist) caused by Ca2+ channel block in gut

Answer 29

constipation (25% patients)

Question 30

3 side effects of dihydropyridines affecting 10-20% patients

Answer 30

ankle oedema, headache and flushing, palpitations

Question 31

which 2 side effects of dihydropyridines are also caused by nitrates and K+ channel openers

Answer 31

ankle oedema, headache and flushing

Question 32

why do dihydropyridines cause ankle oedema

Answer 32

vasodilation means more pressure on capillary vessels, plus gravity (pulls blood down)

Question 33

why do dihydropyridines cause headache/flushing

Answer 33

vasodilation

Question 34

why do dihydropyridines cause palpitations

Answer 34

vasodilation causing reflex adrenergic activation, increasing heart rate and causing palpitations