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BMS317 - Pharmacology > LECTURE 14-17: CARDIOVASCULAR > Flashcards

LECTURE 14-17: CARDIOVASCULAR Flashcards

1
Q

CO and equation

A

amount of blood pumped per min

CO = HR X SV

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2
Q

SV

A

Amount of blood pumped by a ventricle per beat

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3
Q

SV is affected by

A

Preload and Afterload

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4
Q

Preload

A

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

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5
Q

Afterload

A

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

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6
Q

Heart has an intrinsic rate set by

A

SA node

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7
Q

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

A

tachycardia
SA
AV
muscle

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8
Q

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

A

bradycardia
SA
AV
Muscles

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9
Q

BP=

A

CO x peripheral vascular constriction

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10
Q

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

A

inc
inc
dec

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11
Q

does vasoconstriction increase or decrease peripheral constriction

A

increase

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12
Q

a decrease in CO causes compensation in form of

A

SNS and RAAS activation

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13
Q

SNS mechanism to increase CO

and the side effects

A

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

  1. tachnyarrythmia an dO2 starvation
  2. ^ afterload, cyanosis
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14
Q

RAAS mechanism to increase CO

A

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

  1. ^ afterload, cyanosis
  2. oedema
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15
Q

Drugs we’re focussing on are

A

inotropes, vasodilators, antiarrythmias and diuretics

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16
Q

+inotrope

A

improve heart contractility

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17
Q

vasodilators

A

dilate BV

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18
Q

diuretics

A

remove accumulated fluid

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19
Q

antiarrhythmics

A

restore normal HR and rhythm

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20
Q

two +ve inotropes

A

digoxin and dobutamine

21
Q

digoxin mechanism of action

A

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

22
Q

dobutamine mechanism of action

A

improves myocardial contraction by B1 agonism

23
Q

vasodilator examples (6)
AAABCN

A
  1. ACE inhibitors
  2. Angiotensin II receptor
  3. beta blockers
  4. calcium channel blockers
  5. A1 antagonists
  6. Nitrate
24
Q

suffix of ACE inhibitors

A

opril

25
Q

suffix of angiotensin II receptor blockers

A

sartan

26
Q

How do ACE inhibitors and angiotensinogen II receptor blockers cause vasodilation

A

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

27
Q

how beta blockers cause vasodilation

A

B1 antagonism, decrease HR

kinda weak as alpha more involved with blood vessels

28
Q

Calcium channel blockers and example for hypertension

A

improves blood flow and decreases afterload

amlodipine

29
Q

Nitrates cause vasodilation by

A

being converted to nitric oxide

30
Q

A1 antagonism will cause vasodilation by

A

A1 antagonism, such as prazosin

31
Q

does vasoconstriction increase or decrease blood pressure?

A

increase, this is why vasodilators are used to decrease them

32
Q

what is an arrythmia

A

asynchrony between electrical stimulation and mechanical contraction

33
Q

antiarrythmic drugs

A

class I-IV
digoxin

34
Q

Class I antiarrhythmic

A

sodium channel blocker

35
Q

Class II antiarrythmic

A

Beta blocker

36
Q

Class III antiarrythmic

A

potassium channel blocker

37
Q

Class IV antiarrhythmic

A

Calcium channel blocker

38
Q

example class I

A

lignocaine

39
Q

example class II

A

atenolol

40
Q

example class III

A

sotalol

41
Q

example class IV

A

diltiazem, amlodipine

42
Q

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

A

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).

43
Q

Why use diuretic

A

remove fluid accumulation (heart failure patient)

44
Q

Renal diuretics

A

1) loop diuretic
2) potassium sparring diuretic

45
Q

loop diuretic

A
  • fresumide
  • loop of henle
  • Na-K-Cl channel blocker
46
Q

potassium-sparing diuretic

A
  • spironolactone
  • collecting duct
  • aldosterone antagonist (aldosteron controls Na-K-ATPase pump)
  • pump not induced = diuresis
47
Q

osmotic diuretic

A
  • mannitol
  • increase osmolarity in plasma
48
Q

osmotic diuretic indications

A
  • cerebral oedema and glaucoma
49
Q

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

A

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.

BMS317 - Pharmacology (22 decks)

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