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CARDIO > Drugs that Modify Cardiac Rate and Force > Flashcards

Drugs that Modify Cardiac Rate and Force Flashcards

1
Q

3 types of b-adrenoceptor agonists (catecholamines) that act on the heart

A

Dobuamine
adrenaline
noradrenaline

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2
Q

effect of the catecholamines(B agonists) on the heart

A

increased force, rate and CO and Oxygen consumption

decreased cardiac efficiency (oxygen consumption is increased more than cardiac work)

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3
Q

what is an adverse effect of using B1 agonsits

A

cause arrhthymias

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4
Q

what mixed (a/B) agonist is given IV and used to treat Cardiac arrests in advanced life support

A

Adrenaline

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5
Q

why is adrenaline used in short term in emergencies

A

short half life 2 mins due to uptake/metabolism

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6
Q

effect of adrenaline on cardiac arrest patients’ hearts

A

positive inotropic and positive chronotropic effect (stimulates SAN) actions B1

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7
Q

effect of adrenaline on cardiac arrest patients’ blood flow

A

redistributes blood flow to the heart (constricts blood vessels in skin, mucosa and abdomen (a1)

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8
Q

3 ways adrenaline helps cardiac patients

A

stimulates SAN increase in HR and force
redistributes blood flow to heart
dilates coronary arteries improving blood flow to heart

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9
Q

what receptor is present in coronary arteries

A

B2

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10
Q

what drug is given IM to patients in anaphylactic shock

A

adrenaline

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11
Q

what drug is given in acute heart failure that is potentially reversible (after surgery, cardigenetic, septic shock) in high dependence via IV infusion

A

Dobutamine

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12
Q

what is the half life of dobutamine

A

short (2 mins)

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13
Q

what type of agonist is dobutamine

A

selective for B1

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14
Q

what is the effect of dobutamine on the heart

A

increases force of contraction little effect in increasing HR

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15
Q

is dobutamine used in short or long term

A

only short term use

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16
Q

what do B-adrenoceptor antagonists ability to block receptors depends on

A

the degree to which sympathetic nervous system is activated

they do nothing when the sympathetic NS is inactive

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17
Q

give an example of a nonselective blocker of b-adrenoceptor

A

Propranolol

blocks both B1 and B2

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18
Q

give 3 examples of selective b-adrenoceptor blockers that block the receptor competitively

A

Atenolol
Bisoprolol
Metoprolol

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19
Q

what are non-selective partial agonists of B-adrenoceptors and give an example

A

they weakly activate receptor itself but will bock the effect of a full agonist eg. adrenaline but it itself will increase HR slightly eg. alprenolol

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20
Q

what is the effect of non-selective propranolol at rest

A

little effect on rate, force, CO, MABP

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21
Q

non-selective partial agonised activity will increase/decrease Heart rate at rest but will increase/decrease heart rate during exercise

A

increase rate in rest

decrease rate in exercise

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22
Q

what effect will non-selective propranolol have on the heart during exercise and stress

A

rate, force and CO will be significantly reduced (reduction in max exercise tolerance)

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23
Q

what is used to treat atrial fibrillation and supraventicular tachycardia

A

b-blockers

delay conduction through AVN and help restore sinus rhythm

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24
Q

what is used to treat arrhythmias (excessive symapthetic activity = tachycardia or spontaneous activation of latent cardiac pacemaker outside nodal tissue)

A

b-blockers decrease excessive sympathetic drive and help restore normal sinus rhythm

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25
Q

what is the first line treatment of Angina

A

B-adrenoceptor antagonists

alternative to Ca entry blockers

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26
Q

what is used to treat heart failure

A

low dose B-blockers (this is paradoxical) proven to improve morbidity and mortality by reducing sympathetic drive reducing increased risk of arrhythmias developing

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27
Q

name a B-blocker + a1 antagonist that causes vasodilation which reduces total peripheral resistance so heart doesn’t need to pump as forcefully given to (compensated) heart failure patients

A

Carvedilol

28
Q

how should carvedilol be given

A

start low increasing slow to prevent worsening patients condtion

29
Q

when is b-blocker the 1st line treatment of hypertension

A

only if co-morbities like angina

30
Q

why are B-blockers given to patients with arrhytmias

A

block abnormal electrical activity leaving the atria and passing to ventricles to restore normal sinus rhythm

31
Q

what are the adverse effects of B-blockers

A 
bronchospasm 
not compensated heart failure (worsening effect)
hypoglycaemia
fatigue
cold extremities
32
Q

why can B-blockers not be given to asthmatics

A

block ASM B2adrenoceptors causing bronchospasm

33
Q

why do patients on b-blockers feel fatigue

A

CO (B1) and skeletal muscle perfusion (B2) in exercise are regulated by B-adrenoceptors

34
Q

how can b-blockers induce hypoglycaemia (worsen blood sugar in diabetics)

A

B2 adrenoceptor controls release of glucose from the liver therefore there will be too much glucose output from the liver if B2 is blocked

35
Q

why do patients on B-blockers have cold extermities

A

loss of B2 adrenoceptor mediated Vasodilation in cutaneous vessles

36
Q

what is a non-selective competitive antagonist of muscarinic Ach receptor on the heart

A

Atropine

37
Q

what is the effect of atropine

A

increases HR (at all but low doses)

38
Q

effect of low dose atropine on heart

A

decreases HR

39
Q

effect of high dose atropine on heart

A

increase HR

40
Q

why is the effect of atropine more pronounced on a trained athlete

A

trained athletes have cardiac muscle hypertrophy so increased SV (due to increased vagal tone)

41
Q

what is the effect of atropine on arterial BP

A

none

resistance vessels lack parasympathetic innervation

42
Q

what is the 1st line treatment of sever bradycardia in MI

A

Atropine

43
Q

what is used to reverse cardiac arrest by blocking the effect of the parasympathetic effect on the heart

A

Atropine

44
Q

when using atropine reverse cardiac arrest should a low r high dose be given

A

HIGH dose
low dose will make things worse
300-600 mg
monitoring required

45
Q

what is an alternative to atropine to reverse cardiac arrest

A

glycopryrronium

46
Q

what is used to treat anti cholinesterase poisoning to reduce excessive parasympathetic activity

A

atropine

47
Q

what is a cardiac glycoside used to increase heart contractility

A

Digoxin

48
Q

what is digoxin used to treat

A

heart failure
when CO is insufficient to provide adequate tissue perfusion
ventricular function curve is depressed

49
Q

what 2 drugs have a positive inotropic effect

A

digoxin

dobutamine

50
Q

what effect does digoxin have on a ventricular function curve

A

upward and leftward shift so SV increases at any given EDP

51
Q

how does Digoxin increase contractility

A

by inhibiting sarcolemma ATPase blocking Na/K ATPase increasing intracellular Na

52
Q

what does Ca removal from the cell to the ECF depend on

A

Na/K ATPase by secondary active transport as the Na/Ca exchanger causes Na influx and Ca efflux
Na coming in via Na/Ca exchanger moves out via Na/K ATP tase

53
Q

how does digoxin directly increase contractility

A

you block Na/K ATPase there is increased Ca in SR as Na build up prevents Ca moving out so more Ca in SR which can be relased during Ca induced Ca release

54
Q

why is digoxin dangerous

A

competes with K for Na/K ATPase, effects can be dangerously enhanced by low plasma K (hypokalaemia) also very narrow therapeutic window

55
Q

what is the direct effect of digoxin

A

increases vagal activity: increases parasympathetic drive/vagal activity: to slow SAN discharge, Slow AVN conduction and increase refractory period

56
Q

what is the direct effect of digoxin

A

shortens AP + refractory period in arterial and ventricular myocytes

57
Q

what happens if there is a toxic concentration of digoxin

A

membrane depolarisation + oscillatory afterpotentials due to Ca overload = tachycardia -> atrial fibrillation + potential death

58
Q

when is digoxin used to treat heart failure

A

added to treatment in last resort in patients who haven’t responded to diuretics and ACE inhibitors

59
Q

why is digoxin given to patients with heart failure AND atrial fibrillation

A

increases AVN refractory period so helps prevent spreading arrhythmias to ventricles

60
Q

what are the adverse effects of digoxin

A

heart block (excessive depression of AVN conduction)
nausea/vomiting
diarrhoea
disturb colour vision

61
Q

what is levosimendan

A

a calcium sensitiser that is an inotropic drug which binds to troponin C in myocytes sensitising it to Ca
forms cross bridges

62
Q

how does the calcium sensitiser levosimendan act as a vasodilator

A

opens K channes in vascular smooth muscle = hyper polarisation and less excitable

63
Q

what drug is used to treat acute decompensated heart failure via IV

A

Levosimendan (calcium sensitiser)

64
Q

give 2 examples of inotropic drugs that reduce peripheral resistance

A

amrinone and milrinone

65
Q

how do amrinone and milrinone act as inodilators

A

inhibit PDE in cardiac smooth muscle cells and increase cAMP to reduce resistance in short term to improve life quality

66
Q

what inodilator that increases cardiac contractility can trea acute heart failure by IV administration

A

amrinone and milrinone

67
Q

why can amrinone and milrinene only be use in short term

A

shorten life by causing arrhythmias

CARDIO (14 decks)

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