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Cardiology > Drugs modifying cardiac rate and force > Flashcards

Drugs modifying cardiac rate and force Flashcards

1
Q

What phases of the action potential are in normal tissue as well as in cardiac muscle cells?

A

Phase 0, 3, 4

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2
Q

What is phase 4 in normal tissue cells?

A

Pacemaker potential

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3
Q

What conductance governs upstroke?

A

opening of voltage gates calcium channels

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4
Q

Why isn’t the action potential bigger than it is?

A

During the time that the voltage gated calcium channels are opening, there is also background current which act against the calcium channels. Also voltage gated potassium channels begging to open but more slowly than the calcium channels

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5
Q

What causes downstroke?

A

Delayed rectifier potassium current. When this channel opens it allows potassium to leave the call meaning the repolarisation can occur.

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6
Q

What is the role of the background sodium current (Ib)

A

Allows a trickle of sodium into the cell, contributes to depolorisation

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7
Q

What is the role of transient calcium current (Icat)?

A

The channel opens briefly unlike long calcium current it occurs around threshold andgives the final kick in the pacemaker potential allowing the threshold to be reached and opening thr iCAL channel.

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8
Q

What is the role of the funny current?

A

Allows sodium ions to move into the cell. Activated at end of action potential by hyperpolarisation so they turn on t the most negative membrane potential.

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9
Q

What occurs in phase 0?

A

Action potential comes along and ventricular muscle is activated. Promptly opens voltage gated sodium channels

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10
Q

What occurs in phase 1?

A

After peak of action potential, brief period of repolarisation.
-current that opposes it is the transient outward potassium current which opens very briefly.

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11
Q

What occurs in phase 2? (plateau phase)

A

permits calcium entry over a long period of time to drive contraction. Stops the heart beating too rapidly.

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12
Q

What occurs in phase 3?

A

2 K conductances which activate and bring the membrane potential down to diastolic/resting membrane potential.

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13
Q

What happens with the stimulation of noradrenaline/adrenaline?

A
  • noradrenaline activates B1 adrenocenptors
  • Then undergo Gs protein coupling
  • this activates adenylyl cyclase
  • this increases cAMP levels
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14
Q

What is the result of stimulation with noradrenaline/adrenaline?

A
  • positive inotropic effect (increased muscular contractions)
  • positive dromotropic effect (increased conduction velocity in AV node)
  • increased automaticity
  • Positive lusitropic effect (decreased duration of systole)
  • increased activity of Na+/K+ ATPase
  • increased mass of cardiac muscle
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15
Q

What occurs in parasympathetic stimulation?

A
  • acetylcholine activates M2 muscarinic cholinoreceptors
  • coupling in Gi protein
  • decreases adenylate cyclase activity
  • and reduces cAMP
  • also opens K channels to cause hyperpolarisation of SA node.
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16
Q

What is the result of parasympathetic stimulation?

A

-negative chronotropic effect (decreased HR)
-decreased slope of pacemaker potential
-negative inotropic effect (decreased contractility)
-negative dromotropic effect (decreased conduction in AV node)
(force of atrial contraction decreases but force of ventricular contraction remains the same)

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17
Q

What are HNC channels?

A

Hyperpolorised activated cyclic nucleotide gated channels. They are channels mediated by hyperpolorisation and cyclic AMP

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18
Q

What occurs if the HNC channels are blocked?

A

the pacemaker potential slope decreases and heart rate is decreased

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19
Q

What drug can be used to block HNC channels?

A

Ivabradine . It increases the interval between action potentials causing HR to slow

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20
Q

What can this drug be used in?

A

Angina. It decreases HR which means less oxygen is required which reduces the pain in angina.

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21
Q

what are the stages of muscle contraction?

A
  • ventricular action potential
  • opening of voltage gated Ca+ channels
  • Ca+ influx into cytoplasm
  • Ca+ released from SA
  • Ca+ binds to troponin and shifts tropomyosin out of the actin cleft
  • cross bridge formation resulting in contraction
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22
Q

What are the stages in muscle relaxation?

A
  • repolarisation in phase 3 to phase 4
  • voltage gated Ltype Ca+ channel closes
  • Ca+ influx ceases. Ca leaves the cell by the Na+/Ca+ exchanger 1
  • calcium is no longer released from SR
  • Ca+ dissociates from troponin
  • cross bridges break resulting in relaxation
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23
Q

how does b1 receptor activation modulate cardiac contractility?

A
  • cAMP activates protein kinase A which has 3 roles:
    1) Decrease in duration of systole. When phospholambam phosphorylates it increases activity of ATPase. Calcium is more rapidly pumped from cytoplasm into the Sarcoplasmic Reticulum.
    2) Sensitises contractile proteins to calcium contributing enhanced contractility in stimulation.
    3) Phosphorylates the L type channel which increases the opening property leading to increased force of contraction.
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24
Q

name 3 b-1 agonists

A

dobutamine, adrenaline and noradrenaline (catecholamines)

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25
Q

What does adrenaline do that is beneficial in cardiac arrests?

A
  • positive inotropic and chronotropic actions
  • redistribution of blood flow to heart (reduces peripheral circulation)
  • dilation of coronary arteries
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26
Q

When is dobutamine used?

A

acute but potentially reversible heart failure. eg following cardiac surgery, or cardiogenic/septic shock

27
Q

What do non selective b blockers block?

A

B1 and B2 adrenoceptors equally

28
Q

Give an example of a non selective adrenoreceptor

A

alprenolo

29
Q

What do selective B blockers block?

A

B1 adrenoceptors

30
Q

Give three examples of selective B blockers

A

atenolol, bisoprolol and metoprolol

31
Q

What are the advantages of selective and partial agonists?

A

They have a mild stimulatory effect on the heart however since they’re weak they can block the effects of full agonists like adrenaline so they’re basically acting as antagonists.

32
Q

What do B blockers to to heart rate?

A

They block the effects of noradrenaline so decrease HR

33
Q

What do b blockers do during exercise and stress?

A

reduce rate, force and CO

34
Q

What do B blockers do during rest?

A

have no effect on HR and CO

35
Q

What do B blockers with partial agonists do during exercise and rest?

A

they slightly increase rate during rest but decrease rate during exercise

36
Q

What happens when B2 adrenoceptors are initiated?

A

Relaxation of vessels and reduced blood supply to the heart.

37
Q

What do non selective B blockers do?

A

They block B2 adrenoceptors and thereby reduce rate, force and CO to coronary vessels which allows it to better oxygenate the myocardium

38
Q

What are some clinical uses of B blockers?

A
  • treatment of arrythmias
  • treatment of angina
  • treatment of compensated heart failure
  • treatment of hypertension
39
Q

How do B blockers help arrhythmias?

A

Increased sympathetic activity can lead to tachycardia or spontaneous activity of Latent pacemakers activated which can cause stress induced arythmias. B blockers can help by blocking B1 adrenoceptors.

40
Q

How do B blockers help VF and supraventricular tachycardia?

A

Suppression of impulse conduction from atria through Av nodes to ventricles can help stop spread of electrical activity. B blockers delay conduction through AV node and restore sinus rhythm.

41
Q

How do B blockers help in heart failure?

A

Sympathetic system becomes greatly activated in heart failure. Arrhythmia can occur due to too much sympathetic stimulation of heart.
So therefore a low dose of B blocker is beneficial in heart failure alongside other medication to aid in the heart failure.

42
Q

What is the B blocker of choice for treating Heart failure and why?

A

Carvedilol. It is a B blocker and also blocks a1 adrenorecpetors.

43
Q

What do a1 adrenoceptors do upon activation?

A

When a1 adrenoceptors are activation cause vasoconstriction, increasing total peripheral resistance so increase the work the heart has to do to get CO. So by blocking the a1 adrenoreceptors you’re reducing the work the heart has to do

44
Q

What are the adverse effects of B blockers?

A
  • bronchospasm
  • Aggravation of cardiac failure
  • bradycardia
  • hypoglycaemia
  • fatigue
  • cold extremities
45
Q

What drug blocks all muscarinic receptors?

A

Atropine

46
Q

What does atropine do?

A

Increases HR in normal individual by blocking the parasympathetic system

47
Q

Who does atropine have more of an effect on and why?

A

Athletes as they have increased parasympathetic tone.

48
Q

What does the level of effect of atropine depend on?

A

degree of parasympathetic tone

49
Q

What are the effects of atropine at very low doses?

A

Has a paradoxical effect and decreases HR.

50
Q

What is the recommended starting dose for atropine?

A

300-600micrograms

51
Q

When is atropine used?

A
  • severe or symptomatic bradycardia especially post MI

- anticholinesterase poisoning

52
Q

What is Digoxin?

A

A cardiac glycoside that increases contractility of the heart

53
Q

How does digoxin work?

A

Blocking Na/K ATPase means less sodium out of cell. This means no sodium to pump in via Na/Ca exchanger so build up of calcium in cell. This extra calcium goes to SR. This increase of calcium in SR causes increased calcium induced calcium release which leads to increased contractility

54
Q

Does digoxin have a high or low therapeutic range?

A

low

55
Q

What are the indirect effects of digoxin on the heart?

A
  • slows SA node discharge

- slows AV node conduction, increases refractory period

56
Q

What are the direct effects of

A

-shortens the action potentials and refractory period in atrial and ventricular myocytes.

57
Q

When is digoxin used?

A

Used as an add on drug when other drugs dont help reduce symptoms in heart failure.

58
Q

What are the most serious cardiac effects of digoxin?

A
  • excessive depression of AV node

- propensity to cause arrythmias

59
Q

What does levosimendan do?

A

sensitise the contractile apparatus to calcium in order to generate greater force

60
Q

How does levosimendan do this?

A

Increases cross bridge formation between actin and myosin
Also opens a potassium channel which cause a vascular smooth muscle cells to hyperpolarise which moves the membrane potential away from threshold and thereby relaxing the smooth muscle cell lowering peripheral vascular resistance.

61
Q

When is levosimendan used?

A

acute decompensated heart failure

62
Q

What are amrinone and milirone?

A

Inodilators which increase heart force and decrease peripheral resistance.

63
Q

When are amrinone and milirone used?

A

When no other treatment works because they increase frequency of cardiovascular disease rather than reducing it.

Cardiology (32 decks)

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