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
what is the first line treatment of Angina
B-adrenoceptor antagonists | alternative to Ca entry blockers
26
what is used to treat heart failure
low dose B-blockers (this is paradoxical) proven to improve morbidity and mortality by reducing sympathetic drive reducing increased risk of arrhythmias developing
27
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
Carvedilol
28
how should carvedilol be given
start low increasing slow to prevent worsening patients condtion
29
when is b-blocker the 1st line treatment of hypertension
only if co-morbities like angina
30
why are B-blockers given to patients with arrhytmias
block abnormal electrical activity leaving the atria and passing to ventricles to restore normal sinus rhythm
31
what are the adverse effects of B-blockers
``` bronchospasm not compensated heart failure (worsening effect) hypoglycaemia fatigue cold extremities ```
32
why can B-blockers not be given to asthmatics
block ASM B2adrenoceptors causing bronchospasm
33
why do patients on b-blockers feel fatigue
CO (B1) and skeletal muscle perfusion (B2) in exercise are regulated by B-adrenoceptors
34
how can b-blockers induce hypoglycaemia (worsen blood sugar in diabetics)
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
why do patients on B-blockers have cold extermities
loss of B2 adrenoceptor mediated Vasodilation in cutaneous vessles
36
what is a non-selective competitive antagonist of muscarinic Ach receptor on the heart
Atropine
37
what is the effect of atropine
increases HR (at all but low doses)
38
effect of low dose atropine on heart
decreases HR
39
effect of high dose atropine on heart
increase HR
40
why is the effect of atropine more pronounced on a trained athlete
trained athletes have cardiac muscle hypertrophy so increased SV (due to increased vagal tone)
41
what is the effect of atropine on arterial BP
none | resistance vessels lack parasympathetic innervation
42
what is the 1st line treatment of sever bradycardia in MI
Atropine
43
what is used to reverse cardiac arrest by blocking the effect of the parasympathetic effect on the heart
Atropine
44
when using atropine reverse cardiac arrest should a low r high dose be given
HIGH dose low dose will make things worse 300-600 mg monitoring required
45
what is an alternative to atropine to reverse cardiac arrest
glycopryrronium
46
what is used to treat anti cholinesterase poisoning to reduce excessive parasympathetic activity
atropine
47
what is a cardiac glycoside used to increase heart contractility
Digoxin
48
what is digoxin used to treat
heart failure when CO is insufficient to provide adequate tissue perfusion ventricular function curve is depressed
49
what 2 drugs have a positive inotropic effect
digoxin | dobutamine
50
what effect does digoxin have on a ventricular function curve
upward and leftward shift so SV increases at any given EDP
51
how does Digoxin increase contractility
by inhibiting sarcolemma ATPase blocking Na/K ATPase increasing intracellular Na
52
what does Ca removal from the cell to the ECF depend on
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
how does digoxin directly increase contractility
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
why is digoxin dangerous
competes with K for Na/K ATPase, effects can be dangerously enhanced by low plasma K (hypokalaemia) also very narrow therapeutic window
55
what is the direct effect of digoxin
increases vagal activity: increases parasympathetic drive/vagal activity: to slow SAN discharge, Slow AVN conduction and increase refractory period
56
what is the direct effect of digoxin
shortens AP + refractory period in arterial and ventricular myocytes
57
what happens if there is a toxic concentration of digoxin
membrane depolarisation + oscillatory afterpotentials due to Ca overload = tachycardia -> atrial fibrillation + potential death
58
when is digoxin used to treat heart failure
added to treatment in last resort in patients who haven't responded to diuretics and ACE inhibitors
59
why is digoxin given to patients with heart failure AND atrial fibrillation
increases AVN refractory period so helps prevent spreading arrhythmias to ventricles
60
what are the adverse effects of digoxin
heart block (excessive depression of AVN conduction) nausea/vomiting diarrhoea disturb colour vision
61
what is levosimendan
a calcium sensitiser that is an inotropic drug which binds to troponin C in myocytes sensitising it to Ca forms cross bridges
62
how does the calcium sensitiser levosimendan act as a vasodilator
opens K channes in vascular smooth muscle = hyper polarisation and less excitable
63
what drug is used to treat acute decompensated heart failure via IV
Levosimendan (calcium sensitiser)
64
give 2 examples of inotropic drugs that reduce peripheral resistance
amrinone and milrinone
65
how do amrinone and milrinone act as inodilators
inhibit PDE in cardiac smooth muscle cells and increase cAMP to reduce resistance in short term to improve life quality
66
what inodilator that increases cardiac contractility can trea acute heart failure by IV administration
amrinone and milrinone
67
why can amrinone and milrinene only be use in short term
shorten life by causing arrhythmias