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Cardiovascular Pharmacology > Drugs Modifying Cardiac Rate And Force > Flashcards

Drugs Modifying Cardiac Rate And Force Flashcards

1
Q

What are the action potential phases in the nodal tissue of the heart?

A

Phase 0, 3 and 4

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2
Q

What are some of the regulatory influences in the nodal tissue of the heart?

A 
Autonomic input
Stretch
Temperature 
Hypoxia 
Blood pH
Thyroid hormones
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3
Q

What is Phase 0 in the nodal tissue of the heart?

A

The upstroke action potential in normal tissue.

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4
Q

What causes the upstroke in nodal tissue?

A

The opening of l type Ca channels. Inward leakage is depolarising giving the upstroke.

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5
Q

What is Phase 3 in nodal tissue?

A

The downstroke of action potential.

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6
Q

What brings about the down stroke in nodal tissue?

A

When the outward leakage of K+ ions begins to outweigh the inward leakage of Ca+.
The downstroke is caused by the opening of K+ channels.

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7
Q

What is Phase 4 in the nodal tissue?

A

The pacemaker potential.

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8
Q

What causes the pacemaker potential?

A

The inward leakage of background Na+, the funny current Na and K, and transpiring Ca leakage.
This builds up potential to reach the threshold.

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9
Q

What is Phase 4 in Ventricular myocytes?

A

Diastolic Potential (resting). Ventricles are related and no charge in the membrane so the potential is steady.

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10
Q

What is Phase 0 in the Ventricular myocytes?

A

Upstroke.

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11
Q

What is upstroke in the Ventricular myocytes caused by?

A

The opening of voltage gated Na+ channels.

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12
Q

What is Phase 1 in the myocytes?

A

Mediates by transient K+ outward leakage gates being opened. This has a repolarising influence. With a delay Ca+ channels open.

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13
Q

What is Plateau?

A

Ca plus enters whilst k is leaving. This creates a depolarisating activity. The opposite movement of charges holds the charge at a relatively positive value.

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14
Q

What is importance of plateau?

A

The intensity and duration is important in the cardiac force. If this is altered it can affect cardiac rhythm.

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15
Q

What is Phase 3 in Ventricular myocytes?

A

Repolarisation caused by the outward leakage of k.

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16
Q

What does noradrenaline and adrenaline act on?

A

Beta 1 adrenoceptors in cells and myocardial cells.

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17
Q

What does the binding of adrenaline/noradrenaline to beta 1 do?

A

Coupling through the Gs protein activates adenylyl Cyclase converting ATP to cAMP.

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18
Q

What is a chronotropic effect?

A

Increasing or decreasing HR.

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19
Q

How does adrenaline/noradrenaline speed up the heart rate?

A

Increasing the slope for pacemaker potential and lowering the threshold of action potential.

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20
Q

What is inatropic?

A

Heart contractility.

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21
Q

How does adrenaline/noradrenaline increase contractility?

A

Increasing phase 2 of the action potential and increasing the sensitivity of the contractile proteins to calcium.

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22
Q

What is dromotropic?

A

Conduction velocity in the AV node.

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23
Q

What effect does adrenaline/noradrenaline have on the Av node?

A

Increases conduction

Positive dromotropic

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24
Q

What is increase in automaticity causes by adrenaline/noradrenaline?

A

The tendency for non-nodal regions to squire spontaneous activity.

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25
Q

What effect does he sympathetic system have on systole?

A

Increases its duration.

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26
Q

What is a positive lusitropic effect?

A

Decrease in systole duration.

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27
Q

What does the sympathetic system do to cardiac muscle?

A

Increases it.

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28
Q

What transmitter is part of the parasympathetic system?

A

Acetylcholine

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29
Q

What does Ach act upon?

A

M2 muscarinic cholinreceptors in nodal cells.

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30
Q

What action does Ach have upon binding?

A

Gs coupled protein decreases activity of adenylyl cyclase reducing cAMP.
Also opens potassium channels causing repolarisation of the SA node.

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31
Q

How does Ach decrease HR?

A

Increasing the slope of the pacemaker potential.
Hyperpolarisation by opening GIRK channels
And increasing the action potential threshold.

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32
Q

How does Ach decrease contractility?

A

By decreasing phase 2 of the action potential and decreasing Ca entry.

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33
Q

What effect does Ach have in the conduction in the AV node?

A

It decreases it
Negative dromotropic effect.
It decreasing the activity of voltage dependent Ca channels and hyoerpolariastion by opening k channels.

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34
Q

What can parasympathetic stimulation cause?

A

Arythmias

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35
Q

What are vagal manouvers?

A

Increase in parasympathetic output?

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36
Q

When could a vagal manoeuvre be employed?

A

In atrial tachycardia, atrial flutter and atrial fibrillation.
Suppresses impisle conduction through AV node.

37
Q

What is the Valsalva manoeuvre?

A

Activates the aortic baroreceptors.

38
Q

What does massage of the carotid do?

A

Stimulates baroreceptors in the carotid sinus.

39
Q

What is the pacemaker potential modulated by?

A

The funny current (If).

40
Q

What is the funny current modulated by?

A

Hyperpolarisation and cAMP
(Hyperpolarisation activated Cyclic nucleotide gated channels)
HCN channels.

41
Q

What does blocking of the HCN channel do?

A

Decreases the slope of the pacemaker potential and reduces HR.

42
Q

What is Ivabradine?

A

Selective blocker of HCN channels.

43
Q

When would ivabradine be prescribed?

A

In angina to slow HR

44
Q

What does ivabradine do?

A

Slows HR and limits 02 consumption

45
Q

What happens during muscle contraction?

A

Ventricular action potential opens up voltage gated Ca channels causing a Ca influx into cytoplasm.
This causes the release of Ca from the sarcoplasmic reticulum.
Ca binds to troponin which allows cross bridge formation of action and myosin leading to contraction.

46
Q

What happens during muscle relaxation?

A

Repolarisation from Phase 3-4 causing the closing of l type Ca channels stopping the Ca influx.
This stops Ca release from the sarcoplasmic reticulum and so the troponin tropomysin complex can’t be shifted meaning the cross bridges between actin and myosin fail leading to relaxation.

47
Q

How does B1 adrenoceptor activation allow for cardiac contraction?

A

The increase in cAMP in the cell stimulates Protein kinase A.
Protein kinase A then phosphrylates opening the voltage gated Ca channel pumping Ca into the cell. This causes the release from sarcoplasmic reticulum.
It also increases the sensitivity of the muscle fibres to Ca enhancing contractility and increases the rate of pumping of Ca of the sarcoplasmic reticulum by phosphorylating phospholamban.

48
Q

What are the 3 b-Adrenoceptor agonists?

A

Dobutamine, adrenaline and noradrenaline.

49
Q

What if the three b-adrenoceptors agonisys is synthetic?

A

Dobutamine

50
Q

What group are the 3 b-arenorecptor agonists in?

A

Catecholamines

51
Q

What are the pharmacodynamic effects of the b-adrenoceptor agonists?

A

Increase force, rate, Co and O2 consumption

Decrease cardiac efficiency (O2 consumption means more cardiac work)

52
Q

What can the agonists of b-adrenoceptors cause?

A

Cardiac arrhythmias

53
Q

How is adrenaline given?

A

IM, SC, IV or IV infusion.

54
Q

When would adrenaline be given?

A

Cardiac arrest or anaphylaxic shock (IM)

55
Q

What affect does adrenaline have in cardiac arrest?

A

Positive inotropic and chronotropic actions.
Redistributes blood flow to heart.
Dilated the coronary arteries.

56
Q

How is Dobutamine given?

A

IV infusion

57
Q

When would Dobutamine be prescribed?

A

In acute but potentially reversible heart failure (after cardiac surgery, cardiogenic, or septic shock).

58
Q

What is beneficial about using dobutamine over other b1 agonists?

A

Causes less tachycardia.

59
Q

What does the physiological effects of B antagonists depend upon?

A

The degree to which the sympathetic nervous system is activated.

60
Q

What is an example of a non selective B anatagonist?

A

Propranolol (B1 and B2)

61
Q

What is an example of a non selective B antagonist?

A

Atenolol, bisoprolol, metoprolol

62
Q

What is an example of a non selective partial agonist b antagonist?

A

Alprenolol

63
Q

What are the pharmacodynamic effect of non selective blockers?

A

At rest there is little effect on rate, force CO and MABP (partial agonist activity will increase rate and rest but reduce in excercise)
During excercise/stress force, rate, CO will be significantly depressed which has a reduction in excercise tolerance.
Coronary diameter is marginally reduced but myocardial O2 requirement falls- better oxygenation of the myocardium.

64
Q

When can B antagonists be used?

A

In treatment of arrhythmias (stress, emotion, disease, Atrial fibrillation and supraventricular tachycardia)
Angina
Treatment of compensated heart failure
Treatment of hypertension

65
Q

In excessive sympathetic activity, what effect will beta blockers have?

A

The will decrease sympathetic drive and help restore normal sinus rhythm.

66
Q

In atrial fibrillation (AF) and supraventricular tachycardia (SVT) what do beta blockers do?

A

Delay conduction through the AV node and help restore sinus rhythm. H

67
Q

What are the adverse effects of beta blockers?

A

Bronchospasm (not to be prescribed to asthmatics)
Aggravation of cardiac failure (low dose used in compensated heart failure)
Bradycardia
Hypoglycaemia (less risk in b1 selective)
Fatigue
Cold extremities

68
Q

What is an example of a non selective muscarinic Ach reception antagonist?

A

Atropine (competitive antagonist)

69
Q

What are the pharmacodynamics of Atropine?

A

Increase HR at low doses
No effect if BP
No effect on response to exercise

70
Q

What are clinical uses of Atropine in relation to the heart?

A

First like in management of severe or symptomatic bradycardia. (Following MI).
In MI given IV at low doses (300-600 micro grams)
Glycopyrronium is an alternative.
In anticholinestrrase poisoning (stops bradycardia)

71
Q

What is Digoxin?

A

A cardiac glycoside that increases heart contractility

Inptrope

72
Q

What are inotropic drug examples?

A

Digoxin and dobutamine

73
Q

What does digoxin and other inotropic drugs do?

A

Enhance heart contractility

74
Q

What effects do heart failures and inotropes have in the Ventricular function curve?

A

Inotropes mice curve left

Heart failure goes right

75
Q

How does digoxin increase contractility?

A

By blocking the sarcolemma ATPase

Stops Ca leaving cytoplasm, release from sarcoplasmic reticulum. Contractility.

76
Q

What are the pharmacodynamics of digoxin?

A

Bonds to the a subunit of ATPase

Has complex indirect and direct actions on electrical activity.

77
Q

What are the indirect actions of digoxin?

A

Increases vagal activity
Slows SA node discharge
Slows AV node conduction increasing refractory period

78
Q

What are the direct actions of digoxin?

A

Shortens the action potential and refractory period in atrial and ventricular monocytes.
Toxic concentration cause membrane depolarisation and oscillatory afterpotentials (Ca overload)

79
Q

When would digoxin be prescribed?

A

In heart failure where symptoms exist after using ACE inhibitors and diuretics.
In heart failure with atrial fibrillation.

80
Q

What are the cardiac side effects of digoxin?

A

Excessive depression of AV node conduction (heart block)

Can cause arrhythmias

81
Q

What are the extracardiac effects of digoxin?

A

Nausea
Vomiting
Diarrhoea
Disturbance of colour vision

82
Q

What is Levosimendan?

A

Calcium sensitiser inotropic drug.

83
Q

What does levosimendan do?

A

Sensitises Troponin C to Ca+

Opens Katp channels in vascular smooth muscle causing vasodilation (reduces afterload and cardiac work)

84
Q

When would Levosimendan be prescribed?

A

Acute decompensated heart failure

IV

85
Q

What are examples of inodilator inotropic drugs?

A

Amrinone and milrinone

86
Q

What do amrinone and milrinone do?

A

Inhibits PDD in cardiac and smooth muscle cells so increase cAMP.
Increase contractility and decrease peripheral resistance.

87
Q

What are the down sides to using amrinone and milrinone?

A

Decrease survival due to increased incidence of arrhythmias.

88
Q

When are amrinone and milrinone used?

A

Acute heart failure. IV.

Cardiovascular Pharmacology (1 decks)

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