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The Heart > Pharmacology of Cardiac Contractility > Flashcards

Pharmacology of Cardiac Contractility Flashcards

1
Q

two ways drugs can effect cardiac contractility

A

directly- drugs that directly affect myocardial cells, usually by controlling intracellular calcium ions via voltage gated calcium channels o intracellular Na+, affecting sodium calcium exchange

indirect drugs drugs which effect heart contractility through changing vascular tone, determining cardiac contractility through changing preload and EDV

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2
Q

examples of direct acting drugs

A

catecholamines, cardiac glycosides

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3
Q

Examples of indirectly acting drugs

A

diuretics, ACE inhibitors

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4
Q

2 main cardiac glycosides + difference between them

A

digoxin and ouabain

ouabain is shorter acting

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5
Q

basic structure of cardiac glycosides

A

sugar moiety, a steroid and a lactone ring

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6
Q

key cardiac affects of cardiac glycosides

A

cardiac slowing, reducing rate of conduction through AVN

increased force of contraction

disturbances in rhythm, especially block of AV conduction and increased ectopic pacemaker activity

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7
Q

briefly, main mechanisms of action of cardiac glycosides

A

increased vagal activity and inhibition of sodium/potassium pump

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8
Q

explain stages of the positive inotropic effect

A
  1. glycosides binds to the extracellular alpha unit of the Na+/K+ ATPase
  2. binding inhibits the pump
  3. increased intracellular sodium concentration slows extrusion of calcium by reducing the inward directed sodium gradient for the sodium calcium exchanger
  4. increased intracellular calcium stored in the SR and thus an increased amount of calcium released with each action potential
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9
Q

explain use in treatment of atrial fibrillation

A

slows the AV conduction by increasing vagal activity

increases refractory period of the AVN, increasing the interval between impulses and the ventricular rate decreases, allowing time for diastolic filling

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10
Q

main conditions treated

A

congestive heart failure, by increasing inotropic activity, meaning enough blood can be pumped round the body

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11
Q

what are used alongside cardiac glycosides + why?

A

diuretics, which decrease extracellular potassium, which means there’s reduced competition at the binding site

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12
Q

example of a catecholamine drug

A

dobutamine

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13
Q

what is dobutamine used to treat?

A

acute but potentially reversible heart failure, such as after cardiac surgery

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14
Q

dobutamine results

A

increase chronotropy and ionotropy, increasing cardiac output and cardiac oxygen consumption

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15
Q

dobutamine mechanism

A
  1. activates Gs proteins of B1
  2. eventual activation of PKA, which phosphorylates the RAD subunit of the L type calcium channel increasing open state probability. This leads to an enhanced sarcoplasmic release of calcium, increasing contractility
  3. PKA may phosphorylate troponin C, increasing calcium sensitivity
  4. phosphorylates phospholamban, activates SERCA, more calcium taken up

increases heart rate by opening ion channels responsible for pacemaker currents in the SAN

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16
Q

what are the limitations of dobutamine and adrenaline?

A

leads to an increase need for oxygen for the heart to contract

can’t be used in haemorrhage

can’t be used in myocardial infarction, where coronary arteries are blocked

can only be used for shock

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17
Q

examples of adrenoreptor antagonists

A

propranolol and atenolol

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18
Q

actions of adrenoreceptor antagonists

A

have the opposite effect to agonists, mainly reducing contractility by blocking sympathetic stimulation of beta receptors

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19
Q

another name of adrenoreceptor antagonists

A

beta blockers

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20
Q

beta blocker uses

A

used to manage abnormal heart rhythms and to protect the heart from a secondary myocardial infarction

treat hypertension

21
Q

explain propranolol and atenolol briefly

A

propanolol- blocks beta 1 and beta 2 equally, it has little effect on the heart rate at rest but reduces the effects of exercise and excitement

atenolol- beta 1 selective antagonists, used more commonly as it has fewer side effects, only targets the heart

22
Q

heart effects explained

A

blocks Gs coupled receptor, less cAMP

reduced Ca2+ entry into myocytes

decreased contractility and heart rate

decreased SERCA and Ca2+ stores

overall decreases chrontropy, inotropy, lusitropy and conduction velocity

23
Q

blood vessel effects explained

A

propranolol

inhibits Gs coupled receptor, less cAMP and PKA

PKA does not phosphorylate MLK so cannot cause smooth muscle relaxation, causing vasodilation

24
Q

arrhythmia definition

A

a group of conditions in which the heart beat is irregular, too slow or too fast

25
Q

examples of arrhythmias

A

tachycardia- heart rate is above 100 bpm

bradycardia- heart rate is below 60bpm

palpitations

26
Q

four main groups of arrythmias + examples

A

extra beats- premature atrial contractions, premature ventricular contractions

supra ventricular tachycardias- atrial fibrillation, atrial flutter

ventricular arrhythmias- ventricular fibrillation and ventricular tachycardia

bradyarrthymias- bradycardia

27
Q

what causes arrhythmias?

A

problems with the electrical conducting system of the heart

28
Q

explain atrial fibrillation

A

an abnormal heart rhythm characterised by rapid and irregular beating which becomes longer or continuous over time

thought to be due to fibrosis of the atria due to atrial dilation

29
Q

explain ventricular fibrillation

A

ventricles quiver rather then pumping normally due to disorganised electrical activity

hypoxic myocardium forms hyper irritable myocardial cells that then may act as pacemakers, stimulating the ventricles

30
Q

explain ventricular tachycardia

A

monomorphic- increased automaticity of a single point

polymorphic- abnormalities of ventricular muscle depolarisation

31
Q

what is heart block?

A

a disorder in the heart’s rhythm due to a fault in the pacemaker which causes an obstruction in the electrical conduction system of the heart

blockage normally occurs between the SAN and AVN or at or below the Bundle of His

32
Q

three types of heart block

A

first degree AV block- where electrical impulses from the cardiac atria to the ventricles pass through the AVN more slowly than normal- slowed conduction

second degree- conduction block between the atria and ventricles, block of the AVN, where one or more atrial impulses fail to conduct

third degree- complete block, where nerve impulse generated in SAN cannot propagate to the ventricles

33
Q

how does atrial fibrillation appear on an electrocardiogram?

A

absence of P wave

irregular R-R interval due to irregular conduction of impulses from the ventricles

34
Q

ventricular fibrillation on ECG

A

irregular electrical activity with no discernible pattern

no visible P waves, QRS complexes or T waves

35
Q

ventricular tachycardia on ECG

A

rate greater than 120 bpm

at least three wide QRS complexes in a row

36
Q

different heart blocks on ECG

A

1st degree- regular rhythm, elongated PR

2nd degree- irregular rhythm/increasingly prolonged, more P waves than QRS

3rd degree- regular rhythm, lack of any apparent connection between P waves and QRS complexes

37
Q

sinus rhythm definition

A

any cardiac rhythm in which depolarisation of the cardiac muscle begins at the sinus node

38
Q

5 examples of anti dysrhythmics

A

lidocaine, propranolol, amiodarone, verapamil, adenosine

39
Q

explain lidocaine use and mechanism of action

A

used for ventricular arrhythmias

binds to voltage gated sodium channels, acting as a competitive antagonist, preventing action potential generation

stabilise the excitability of over excitable cells, thus act as membrane stabilising agents

40
Q

explain propranolol and mechanism of action

A

used to treat tachycardia

binds to beta 1 adrenoreceptors and act as an antagonist, inhibiting sympathetic stimulation of the heart

also thought to act similarly to lidocaine

41
Q

explain amiodarone and mechanisms of action

A

used to treat ventricular tachycardia, ventricular fibrillation and atrial fibrillation

blocker of voltage gated potassium and calcium channels, this slows the conduction rate and prolongs the refectory period of SA and AV nodes

also acts by blocking voltage gated sodium channels and as a beta blocker

42
Q

explain verapamil and mechanisms of action

A

treats supraventricular tachycardia

calcium channel blocker, decreasing impulse conduction through the AV node, thus protecting the ventricles from atrial tachyarrhythmias- only respond to the main impulses

also block calcium channels in smooth muscle found in blood vessels, causing them to dilate and thus can be used to treat high blood pressure and angina

43
Q

explain adenosine and mechanisms of action

A

treats supraventricular tachycardia

causes transient heart block in the AVN, mediated by the A1 receptor, which inhibits adenyl cyclase, reducing cAMP and thus causing cell hyperpolarisation by increasing potassium efflux, subsequently inhibiting calcium current

44
Q

angina definition

A

chest pain or pressure usually due to not enough blood flow to heart muscle, usually due to obstruction or spasm of coronary arteries

45
Q

Vaughan Williams classification of drugs explained + examples

A

classification of cardiac drugs dependent on how they treat arrhythmias

Class I- interfere with sodium channels, lidocaine

class II- interfere with beta receptors, propranolol

class III- interfere with potassium channels, amiodarone

class IV- interfere with calcium channels, and affect AVN, verapamil, sotalol

Class V- agents work by other or unknown mechanisms, adenosine, digoxin

46
Q

use of ouabain

A

blocks sodium potassium pump, which in turn prevents the movement of calcium due to the increase in intracellular sodium reducing the activity of sodium-calcium exchanger

used to treat reversible heart failure as it increases contractility and vagal tone

47
Q

what anti muscarinic drug can also be used + explained?

A

atropine

used for bradycardia and 2nd and 3rd heart blocks

a competitive antagonist of nonselective muscarinic acetylcholine receptors, increasing firing of the SA and conduction through the AVN

oppose actions of the vagus nerve

48
Q

secondary pacemaker explained

A

if the SAN is non functional, the AVN will take over pacemaker responsibility becoming the ectopic pacemaker of the heart

49
Q

vagal tone definition

A

the continuous nature of baseline parasympathetic action that the vagus nerve exerts

The Heart (11 decks)

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