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CVS * > S7 Understanding Arrhythmias and the Action of Drugs on CVS > Flashcards

S7 Understanding Arrhythmias and the Action of Drugs on CVS Flashcards

1
Q

What can cause tachycardia?

A
  • ectopic pacemaker activity
  • after depolarisations
  • atrial flutter
  • re-entry loops
  • sinus tachycardia
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2
Q

What can cause bradycardia?

A
  • sinus bradycardia

* conduction block

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3
Q

What are the abnormalities in heart rate/rhythm (arrhythmias)?

A
  • bradycardia
  • atrial flutter
  • atrial fibrillation
  • tachycardia (supraventricular/ventricular)
  • ventricular fibrillation
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4
Q

What are cardiovascular drugs used to treat?

A
  • arrhythmias
  • heart failure
  • angina
  • hypertension
  • risk of thrombus formation
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5
Q

When are delayed after-depolarisations more likely to happen?

A

More likely to happen if intracellular Ca2+ is high

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6
Q

What are delayed after-depolarisations depolarisations?

A

Abnormal depolarisations that occur before the next depolarisation should occur (if they reach threshold, it triggers an earlier action potential) causes ventricular tachycardia

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7
Q

What are early after-depolarisations? What can it lead to?

A

Abnormal depolarisation leads to production of an action potential before repolarisation is complete

Can lead to oscillations

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8
Q

When are early after-depolarisations likely to happen? When does someone have this?

A

More likely to happen is the action potential is prolonged

If they have a longer QT interval

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9
Q

What is re-entry?

A

When a propagating impulse fails to die out after normal activation of the heart so it persists to re-excite the heart after the refractory period has needed - leads to arrhythmias

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10
Q

What normally happens to the impulses in the spread of excitation?

A

Reach a point where they cancel out

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11
Q

What happens if there is incomplete conduction damage?

A

Excitation can take a long route to spread the wrong way through the damaged area, setting up a circuit of excitation

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12
Q

What does a re-entrant mechanism arise from in the AV node?

A

The slow and fast pathways in the AV node

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13
Q

How can re-entrant circuits lead to atrial fibrillation?

A

You can get multiple small re-entry loops in the atria

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14
Q

How does ventricular pre-excitation occur? What is this syndrome called?

A

An accessory pathway between the atria and ventricles creates a re-entry loop

Wolff-Parkinson-White syndrome

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15
Q

What are the 4 classes of anti-arrhythmic drugs?

A
  1. Drugs that block voltage-sensitive sodium channels
  2. Antagonists of beta-adrenoreceptors
  3. Drugs that block potassium channels
  4. Drugs that block calcium channels
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16
Q

What is an example of a drug that blocks voltage-dependent Na+ channels (class I)? How does it work?

A

Lidocaine (anaesthetic)

Blocks voltage-gates Na+ channels in the open/inactivated states so blocks damaged depolarised tissue and has little effect in normal cardiac tissue due to it’s quick dissociation (in time for next AP in normal tissue)

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17
Q

When is lidocaine used following a MI? How is it given?

A

If the patient has ventricular tachycardia

Intravenously

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18
Q

What does lidocaine prevent?

A

Prevents automatic firing of depolarised ventricular tissue (damaged) by blocking Na+ channels

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19
Q

What are some examples of beta-adrenoreceptor antagonists (class II)?

A

Propranolol
Atenolol

(Both are beta blockers)

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20
Q

What do beta-adrenoreceptors do?

A

Blocks sympathetic action by acting on beta-1 adrenoreceptors and decreases the slope of the pacemaker potential in the SA node and slows conduction at the AV node

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21
Q

What can beta-blockers be used for?

A
  • prevents supraventricular tachycardia by slowing conduction in the AV node so slows the ventricular rate of patients with atrial fibrillation
  • used after myocardial infarction
  • reduces the oxygen demand
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22
Q

What do drugs that block K+ channels (class III) do?

A

They prolong the action potential by blocking K+ channels and hence lengthen the absolute refractory period to prevent another AP from occurring too soon

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23
Q

What is the disadvantage of drugs that block K+ channels?

A

They produce a prolonged QT interval which is pro-arrhythmic rather than anti-arrhythmic

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24
Q

What is the K+ channel blocker drug that is used? What is is usually used to treat?

A

Amiodarone (has other actions as well as blocking K+ channels)

Treat tachycardia associated with Wolff-Parkinson-White syndrome (re-entry lop due to extra conduction pathway) and effective for suppressing ventricular arrhythmias post MI

25
What are some drugs that can block Ca2+ channels in the heart?
Non-dihydropyridine types: verapamil and dilitiazem
26
What do non-dihydropyridine type Ca2+ channel blockers do?
* decrease the slope of the AP at the SA node * decrease AV nodal conduction * decrease force of contraction (negative inotropy)
27
Where do dihydropyridine Ca2+ channel blockers act?
Act on vascular smooth muscle
28
How is adenosine produced usually?
Produced endogenously at physiological levels but can be administered intravenously
29
What does adenosine act on?
Alpha-1 receptors at the AV node (but have a short half life)
30
What does adenosine do?
* enhances K+ conductance (hyperpolarises cells of conducting tissue) * anti-arrhythmic - terminates re-entrant supraventricular tachycardias
31
What do ACE inhibitors do?
* inhibit action of angiotensin converting enzyme * prevents conversion of angiotension I into angiotensin II * involved in treatment of hypertension and heart failure
32
What is a disadvantage of ACEi?
Can cause a dry cough due to excess bradykinin (ACE breaks down bradykinin)
33
What is the advantage of inhibitor production of angiotensin II?
Angiotensin II increases reabsorption of Na+ and water in kidneys meaning an increase in blood volume and lead to vasoconstriction. So inhibiting this means less reabsorption so decreased blood volume and increased vasodilation.
34
What is the benefit on the heart of decreasing blood pressure (deceasing vasomotor tone) and blood volume (decreasing fluid retention)?
* blood pressure - reduces afterload of the heart * blood volume - reduces preload of the heart Both of these reduce the work load of the heart
35
What type of drug has similar affects of ACEi? When are these used?
Angiotensin II receptor blockers (ARBs) e.g. losartan Used if a patient can’t tolerate ACEi due too the dry cough
36
What heart issues are diuretics used to treat?
Treat heart failure and hypertension Loop diuretics are useful in congestive heart failure (fluid building up around the heart) - increase loss of Na+ and water from the kidneys
37
What is the advantage of vascular smooth muscle Ca2+ channel blockers in heart problems?
* decrease peripheral resistance * decrease arterial blood pressure So reduce workload of heart by reducing afterload
38
What do positive inotropes do?
Increased contractility and cardiac output
39
What are the two types of positive inotropes?
* cardiac glycosides | * beta-adrenergic agonists
40
What is a type of cardiac glycoside?
Digoxin
41
What do cardiac glycosides block?
Na+/K+ ATPase
42
How do cardiac glycosides work to increase contractility?
1. Na+/K+ ATPase is blocked by cardiac glycosides 2. Leads to a rise in intracellular Na+ conc. 3. This rise leads to decreased activity of the Na+-Ca2+ exchanger 4. So increase in intracellular Ca2+ conc. (more Ca2+ is stored in SR) 5. This leads to an increased force of contraction
43
What is the action of cardiac glycosides on heart rate? When can they be used in heart failure?
1. Increases vagal activity (via CNS) 2. This slows the AV conduction 3. Which slows heart rate If there is an arrhythmia like atrial fibrillation
44
What is an example of a beta-adrenoceptor agonist? What does it stimulate?
Dobutamine (a selective beta-1 adrenoceptor agonist) Stimulates beta-1 receptors at the SA node, AV node and ventricular myocytes
45
When are beta-adrenoceptors used?
* cardiogenic shock | * acute but reversible heart failure e.g. after cardiac surgery
46
Why would you not use cardiac glycosides as a long term treatment for heart failure?
It makes the heart conduct faster, but this isn’t good in the long run
47
When does angina occur?
When oxygen supply to the heart doesn’t meet it’s need - results in pain with exertion and ischaemia of heart tissue (chest pain)
48
How can you treat angina?
With organic nitrates
49
What is the effect of NO on veins? Why do they act preferentially on veins?
Vasodilation of veins (venodilation) Because there is less endogenous nitric oxide in veins?
50
How does NO cause vasodilation of veins?
1. NO activates guanylate cyclase 2. This leads to an increase in cGMP 3. This lowers the intracellular Ca2+ conc 4. And so causes relaxation of vascular smooth muscle
51
How does dilation of smooth muscle vasculature help alleviate angina symptoms?
* venodilation lowers preload so workload of heart is decreased so heart fills less so reduced force of contraction (Starling’s Law) and so oxygen demand of heart is lowered * action of coronary collateral arteries improves oxygen delivery to ischaemic myocardium
52
Why don’t organic nitrates work by dilating arterioles?
Because in the ischaemic region, the arterioles are already fully dilated and if you increase the dilation of the normal arterioles will have a negative impact
53
What types of drugs do you use to treat angina by reducing the workload of the heart?
* organic nitrates (venodilation) * beta-adrenoreceptor blockers * Ca2+ channel antagonists
54
What types of drugs do you use to treat angina by improving the blood supply to the heart?
* Ca2+ crabbed antagonists | * minor effect of organic nitrates
55
Which heart conditions carry an increased risk of thrombus formation?
* atrial fibrillation * acute myocardial infarction * mechanical prosthetic heart valves
56
What are the two types of antithrombotic drugs?
* anticoagulants | * antiplatelet drugs
57
What is a type of antiplatelet drug?
Aspirin
58
What anticoagulants prevent venous thromboembolism?
* heparin (via IV) * fractionated heparin (subcutaneous injection) * warfarin (orally)

CVS * (17 decks)

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