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1st Year - Cardiology > Pharmacology 1 - Drugs Affecting Cardiac Rate and Force > Flashcards

Pharmacology 1 - Drugs Affecting Cardiac Rate and Force Flashcards

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1
Q

What causes phase 4 of the action potential in nodal tissue of the heart?

A

Increased Na+ influxDecreased K+ efflux

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2
Q

What causes phase 0 of the action potential in nodal tissue of the heart?

A

Increased Ca2+ influx

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3
Q

What causes phase 3 of the action potential in nodal tissue?

A

Increased K+ efflux

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4
Q

What transmits Na and K movement during phase 4?What switches this on? (nodal tissue)

A

The funny current - Hyperpolarisation-activated and cyclic nucleotide gated channels (HCN channels)Hyperpolarisaiton (Very negative)

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5
Q

What causes stage 3 of the action potential in nodal tissue?

A

Repolarisation caused by K+ efflux (delated rectifier potassium channel)

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6
Q

What causes phase 0 of the action potential in cardiac myocytes?

A

Fast Na+ influx

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7
Q

What causes phase 1 of the action potential in cardiac myocytes?

A

Transient K+ efflux

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8
Q

What causes phase 2 of the action potential in cardiac myocytes?

A

Ca2+ influx, also a small bit of Na+ influx and NCX1 operating in reverse direction (Normally brings 3 Na in and expels 1 Ca but now brings 1 Ca in and pumps 3 Na out)

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9
Q

What causes phase 3 of the action potential in cardiac myocytes?

A

K+ efflux

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10
Q

What is the difference between noradrenaline and adrenaline?

A

Noradrenaline is a post-ganglionic neurotransmitter where as adrenaline is a hormone

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11
Q

In terms of the sympathetic system on the heart, what receptor is stimulated and where are these located?

A

B1 adrenoceptorNodal cellsMyocardial cells

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12
Q

What protein does B1 adrenoceptors use and what enzyme is activated?

A

Gs proteinsadenylyl cyclase

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13
Q

What does adenylyl cyclase do? (B1 adrenoceptor)

A

Converts ATP to cAMP

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14
Q

What does activation of B1 adrenoceptors cause? (8)

A

Increased heart rateIncreased contractilityIncreased conduction velocity in AV nodeIncreased automaticityDecreased duration of systoleDecrease in cardiac efficiencyIncreased activity of the Na+/K+/ATPaseIncreased mass of cardiac muscle

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15
Q

What causes an increased heart rate due to sympathetic stimulation? (2)

A

Mediated by the SA node and due to an increase in the slope of phase 4 depolarisation (caused by enhanced If and Ica) and reduction in the threshold for AP initiation caused by enhanced Ica

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16
Q

What causes the positive inotropic effect due to sympathetic stimulation?

A

Increase in phase 2 of the cardiac action potential in atrial ad ventricular mycoses and enhanced Ca2+ influx and sensitisation of contractile proteins to Ca2+

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17
Q

What cause an increased conduction velocity in the heart?

A

Enhancement of If and Ica

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18
Q

Why is increased activity of the Na+/K+ATPase important in sympathetic stimulation of the heart?

A

For depolarisation and restoration of function following generalised myocardial depolarisaiton

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19
Q

What happens to the stroke volume due to sympathetic stimulation?

A

It increases along with contractility (Frank-starling curve)

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20
Q

What receptor does the parasympathetic system controlling the heart stimulate?G protein?What effect does this have on what enzyme?What other effect does it have?

A

M2 muscarinic cholinoceptors mainly in nodal cellsThrough GiDecreases activity of adenylyl cyclaseOpens potassium channels (GIRK) to cause hyper-polarisation of SA node (mediated by Gi B gamma subunits)

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21
Q

What effects does parasympathetic stimulation have on the heart? (3)

A

Decreased heart rateDecreased contractilityDecreased conduction in AV node

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22
Q

What 3 factors cause the decreased heart rate due to parasympathetic stimulation?

A

Decreased slope of pacemaker potential due to a reduction in the funny currentOpening of GIRK = hyper polarisationIncrease in threshold for AP due to reduced ICa2+

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23
Q

Where does decreased contractility due to para. stimulation effect?

A

Atria only

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24
Q

What causes decrease contractility due to para. stimulation?

Study These Flashcards
A

Decrease in phase 2 of action potential and decrease in Ca2+ entry

25
How can parasympathetic stimulation predispose to arrhythmias?
Predisposes to arrhythmias in the artier as AP duration is reduced ad correspondingly the refractory period (predisposes to re-enterant arrhythmias)
26
What can vagal manoeuvres be attempted to treat?
Atrial tachycardia - increases parasympathetic output therefore suppressing impulse conduction through the AV node
27
2 typesof vagal manouvres and what they do?
Valsalva manoeuvre - activate aortic baroreceptors by breathing techniquesMassage of bifurcation of the carotid artery to stimulate baroreceptors in the carotid sinus
28
What activates HCN channels (the funny current)?
HyperpolarisaitoncAMP
29
How does Ivabradine work?What is it used to treat?
It is a selective blocker of HCN channels meaning it slows heart rate by decreasing the slope of the pacemaker potentialAngina - by slowing the heart, O2 consumption is reduced
30
how many different types of HCN channels are there?what is the most common type in the heart?
4HCN4
31
What is the process by which cardiac smooth muscle contracts?
During Phase 2 of ventricular AP, opening of voltage-activated Ca2+ channels occursThis causes Ca2+ influx that causes Ca2+ induced Ca2+ release from the sacroplasmic reitculum This causes cross bridges between actin and myosin due to Ca2+ binding to troponin
32
What is the process by which cardiac smooth muscle relaxes?
Repolarisation in phase 3 to phase 4 causes voltage activated Ca2+ channels to close Ca2+ influx ceases and ca2+ efflux occurs by NCX1Ca2+ dissociates from troponin = cross bridges break
33
How does B1-adrenoceptor activation modulate cardiac contractility`/
It activates adenylyl cyclase which converts ATP to cAMPcAMP activates PKA which phosphorylates the voltage phosphorylate the voltage activated Ca2+ channels causing them to be open for longer, it also increases the sensitivity of the cotnractile proteins making them more sensitive to Ca2+It also phosphorylates the phospholamban on tCa2+ATPase meaning that it pumps Ca2+ back into the sarcoplasmic reticulum quicker meaning the heart relaxes quicker(activation of M2 blocks these effects)
34
What are examples of B-adrenoceptor agonists for the heart? (3)
DobutamineAdrenalineNoradrenaline
35
What effect do B-adrenoceptor agonists have on the heart?
They increase its force, rate and cardiac output (+ O2 consumption)
36
What are 2 disadvantages of B-adrenoceptor agonists?
They decrease cardiac efficiencyThey can cause arrhythmias
37
Clinical uses of adrenaline (B-adrenoceptor) on the heart?
Used during cardiac arrest and anaphylactic shock to redistribute blood to the heart and for its positive inotropic and chronotropic effect
38
Use of dobutamine (B-adrenoceptor) on the heart?
on acute but potentially reversible heart failure e.g. following cardiac surgery or septic shock
39
What is an example of a non-selective b-adrenoceptor?
Propranolol
40
What is an example of a selective B1-adrenoceptor?
Atenolol, bisoprolol, metoprolol
41
What does the effect o B-adrenoceptor blockade depend upon?
The degree to which the sympathetic nervous system is activated
42
What effect do B-adrenoceptors have?
Little or no effect at rest but during exercise rate, force and CO are greatly depressed
43
Clinical uses of B-adrenoceptors?
Treatment of arrhythmias related to excessive sympathetic activity (MI, heart failure)AF and SVT (b-blockers delay conduction through the AV node)AnginaCompensated heart failureHypertension (no longer first line unless co-morbidities are present)
44
What is a B-adrenoceptor that has additional alpha 1 antagonist activity that is used to treat heart failure?
Carvedilol
45
Adverse effects of B-blockers?
BronchospasmAggravation of cardiac failure BradycardiaHypoglycaemia (release of glucose from the liver is controlled by B2-adrenoceptors)FatigueCold peripheries
46
Example of a non-selective muscarinic ACh receptor antagonist?What does this do?
AtropineIncreases the HR in normal subjects (no effect on BP as resistance vessels lack a parasympathetic innervation, no effect upon response to exercise)
47
Clinical use of atropine?
First line in management of severe, or symptomatic bradycardia, particularly following MI
48
What is the origin of digoxin?
Foxglove components
49
What effect does digoxin have on the heart?
Increases contractility of the heartSlows SA node dischargeSlows AV node conduction
50
What is digoxin used to treat?
IV in acute heart failure and oral in chronic heart failure when optimal use of other drugs fails to control symptoms (particularly indicated if AF is also present)AF
51
How does dioxin work?
It blocks the Na+K+ATPase therefore increasing the intracellular concentration of Ca2+ which binds to the sarcoplasmic reticulum causing increased contractilityIt also increases vagal activity causing a slowing of the SA node discharge and AV node conduction increasing refractory time
52
What ion change is particularly dangerous with digoxin?
Hypokalaemia
53
Unwanted effects of digoxin?
Excessive depression of AV node conduction = heart blockCan cause arrhythmiasNausea/ vomitingDiarrhoeaDisturbances in colour vision
54
What is a calcium-sensitiser drug?
Levosimendan (calcium-sensitisers)
55
How does levosimendan work?
It binds to troponin C in cardiac muscle sensitising it to the action of Ca2+Additionally opens ATP channels in vascular smooth muscle causing vasodilation (reduces afterload and therefore cardiac work)
56
What is levosimendan used to treat?
Acute decompensated heart failure (IV)
57
Aside from digoxin and levosimendan, what is another 2 examples of inotropic drugs?
Amrinone and milirinone (inodilators)
58
How does amrinone and milirinone work?
Inhibit phosphodiesterase (PDE) in cardiac and smotth muscle cells and hence increases [cAMP]i - increases myocardial contractility, decreases peripheral resistance but worsens survival (perhaps due to incidence of arrhythmias)
59
What is amrinone and milirinone used to treat?
Acute heart failure (IV)

1st Year - Cardiology (25 decks)

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