LECTURE 14-17: CARDIOVASCULAR

Question 1

CO and equation

Answer 1

amount of blood pumped per min

CO = HR X SV

Question 2

SV

Answer 2

Amount of blood pumped by a ventricle per beat

Question 3

SV is affected by

Answer 3

Preload and Afterload

Question 4

Preload

Answer 4

is the amount the ventricles stretch at the end of diastole (filling phase)

Question 5

Afterload

Answer 5

pressure the ventricles must work against to pump blood out of the heart

Question 6

Heart has an intrinsic rate set by

Answer 6

SA node

Question 7

SNS is resposible for _____, innervates __ and __ nodes and also ___

Answer 7

tachycardia
SA
AV
muscle

Question 8

PSNS is responsible for ____, via ____ nerve and __ and __ nodes, and has less of an effect on ___

Answer 8

bradycardia
SA
AV
Muscles

Question 9

BP=

Answer 9

CO x peripheral vascular constriction

Question 10

what would increase in 1) force contraction 2) preload and 3) afterload do to SV

Answer 10

inc
inc
dec

Question 11

does vasoconstriction increase or decrease peripheral constriction

Answer 11

increase

Question 12

a decrease in CO causes compensation in form of

Answer 12

SNS and RAAS activation

Question 13

SNS mechanism to increase CO

and the side effects

Answer 13

1) ^HR and contrile force (B1)
2) Vasocontriction (^BP and ^ peripheral resitence)

1. tachnyarrythmia an dO2 starvation
2. ^ afterload, cyanosis

Question 14

RAAS mechanism to increase CO

Answer 14

1) Vasocontriction (^BP and ^ peripheral resitence)
2) ^ blood volume

1. ^ afterload, cyanosis
2. oedema

Question 15

Drugs we’re focussing on are

Answer 15

inotropes, vasodilators, antiarrythmias and diuretics

Question 16

+inotrope

Answer 16

improve heart contractility

Question 17

vasodilators

Answer 17

dilate BV

Question 18

diuretics

Answer 18

remove accumulated fluid

Question 19

antiarrhythmics

Answer 19

restore normal HR and rhythm

Question 20

two +ve inotropes

Answer 20

digoxin and dobutamine

Question 21

digoxin mechanism of action

Answer 21

inhibits Na-K-ATPase channel

Sodium cannot LEAVE

^ Na intracellular

Na cannot feed Na-Ca pump

Na-Ca pump inactivated

Ca builds up (calcium = contraction)

^ acxtivation of contractile proteins

decrease heart rate, more meaningful beats

Question 22

dobutamine mechanism of action

Answer 22

improves myocardial contraction by B1 agonism

Question 23

vasodilator examples (6)
AAABCN

Answer 23

1. ACE inhibitors
2. Angiotensin II receptor
3. beta blockers
4. calcium channel blockers
5. A1 antagonists
6. Nitrate

Question 24

suffix of ACE inhibitors

Answer 24

opril

Question 25

suffix of angiotensin II receptor blockers

Answer 25

sartan

Question 26

How do ACE inhibitors and angiotensinogen II receptor blockers cause vasodilation

Answer 26

by inhibiting the formation of angiotensin II (which causes vasocinstriction)

Question 27

how beta blockers cause vasodilation

Answer 27

B1 antagonism, decrease HR kinda weak as alpha more involved with blood vessels

Question 28

Calcium channel blockers and example for hypertension

Answer 28

improves blood flow and decreases afterload amlodipine

Question 29

Nitrates cause vasodilation by

Answer 29

being converted to nitric oxide

Question 30

A1 antagonism will cause vasodilation by

Answer 30

A1 antagonism, such as prazosin

Question 31

does vasoconstriction increase or decrease blood pressure?

Answer 31

increase, this is why vasodilators are used to decrease them

Question 32

what is an arrythmia

Answer 32

asynchrony between electrical stimulation and mechanical contraction

Question 33

antiarrythmic drugs

Answer 33

class I-IV digoxin

Question 34

Class I antiarrhythmic

Answer 34

sodium channel blocker

Question 35

Class II antiarrythmic

Answer 35

Beta blocker

Question 36

Class III antiarrythmic

Answer 36

potassium channel blocker

Question 37

Class IV antiarrhythmic

Answer 37

Calcium channel blocker

Question 38

example class I

Answer 38

lignocaine

Question 39

example class II

Answer 39

atenolol

Question 40

example class III

Answer 40

sotalol

Question 41

example class IV

Answer 41

diltiazem, amlodipine

Question 42

How do class III anti-arrhythmic drugs work? Give an example of this class of drug

Answer 42

During the normal heartbeat cycle, there is a rapid repolarisation with increasing K+ efflux (1 mark). When this process goes wrong, arrhythmia can result. Class III drugs are potassium channel blockers (1 mark) which prolong phase 3 repolarisation in the ventricular muscle fibres (1 mark). Examples include amiodarone, sotalol (1 mark).

Question 43

Why use diuretic

Answer 43

remove fluid accumulation (heart failure patient)

Question 44

Renal diuretics

Answer 44

1) loop diuretic 2) potassium sparring diuretic

Question 45

loop diuretic

Answer 45

- fresumide - loop of henle - Na-K-Cl channel blocker

Question 46

potassium-sparing diuretic

Answer 46

- spironolactone - collecting duct - aldosterone antagonist (aldosteron controls Na-K-ATPase pump) - pump not induced = diuresis

Question 47

osmotic diuretic

Answer 47

- mannitol - increase osmolarity in plasma

Question 48

osmotic diuretic indications

Answer 48

- cerebral oedema and glaucoma

Question 49

Briefly describe the benefit that a positive inotrope can provide to a failing heart (3 marks)

Answer 49

The body’s compensatory mechanisms to heart failure often result in a heart that is beating stronger against a high level of resistance (afterload). This is unsustainable for a failing heart. Positive inotropes improve the efficiency of myocardial contractility and therefore reduce myocardial oxygen consumption, which helps to reduce ischemic injury to the heart and arrhythmias.