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ESA 2: Cardiovascular > Cardiovascular: Session 10 > Flashcards

Cardiovascular: Session 10 Flashcards

1
Q

What are cardiavascular drugs used to treat?

A
  • Arrhythmias
  • Heart Failure
  • Angina
  • Hypertension
  • Risk of thrombus formation
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2
Q

What can cardiovascular drugs alter?

A
  • The rate and rhythm of the heart
  • The force of myocardial contraction
  • Peripheral resistance and blood flow
  • Blood volume

Some drugs can act at more than one site

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3
Q

What can cause disturbances of cardiac rhythm?

A

Abnormality of heart rate or rhythm

  • Bradycardia
  • Atrial flutter
  • Atrial fibrillation
  • Tachycardia (ventricular tachycardia, supraventricular tachycardias)
  • Ventricular fibrillation
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4
Q

How is tachycardia caused? (arrhythmia)

A

Due to ectopic pacemaker activity

  • Damaged area of myocardium becomes depolarised and spontaneously active.
  • This Latent pacemaker region activated due to ischaemia dominates over the SA node
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5
Q

What causes arrhythmia?

A
  • Ectopic pacemaker activity
  • After depolarisation
  • Atrial flutter/atrial fibrillation
  • Re-entry loop
  • Sinus Brady cardia
  • Conduction block
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6
Q

What is the mechanism of action of an ectopic pacemaker activity in the causation of an arrhythmia?

A
  • Damaged area of myocardium becomes depolarised and spontaneously active
  • Latent pacemaker region activated due to ischaemia and dominates over SA node
  • This causes tachycardia and can lead to an arrhythmia
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7
Q

When are delayed after-deplarisation more likely to happen?

A

High intracellular Calcium

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8
Q

When are early after depolarisation more likely to happen?

A

When the action potential is prolonged. Can lead in oscillations

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9
Q

How does a longer action potential present on an ECG?

A

Long Q-T interval

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10
Q

What is the normal spread of excitation?

A
  • Splits at the branch point in two different directions

- Cancels out in the midline due to refractory period of tissue as it has already depolarised

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11
Q

What is the re-entrant mechanism for generating arrhythmia?

A
  • Incomplete conduction damage

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

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12
Q

What can lead to atrial fibrillation?

A

Several re-entrant loops in the atria leading to atrial fibrillation.

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13
Q

What can cause AV nodal re-entry?

A

Fast and slow pathways in the AV node create a re-entry loop.

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14
Q

What can cause ventricular Pre-excitation?

A

An accessory pathway between atria and ventricles creates a re-entry loop such as in owl-parkinson-white syndrome

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15
Q

What are the basic classes of anti-arrhythmic drugs?

A
  • Drugs that block voltage sensitive sodium channels
  • Antagonists of beta adreno-receptors
  • Drugs that block potassium channels
  • Drugs that block calcium channels
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16
Q

What is the mechanism of action for a voltage dependant Na+ channels?

A
  • Use dependant block. Blocks voltage gated Na+ channels in open or inactive state - therefore blocks damaged depolarised tissue.
  • Has a little effect on normal cardiac tissue as it dissociates rapidly.
  • Blocks during depolarisation but dissociates in time for the next action potential
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17
Q

How is lidocaine used in the clinical setting?

A
  • Sometimes given intravenously following Myocardial infarction if the patient shows signs of ventricular tachycardia
  • Damaged areas of the heart may be depolarised and fire automatically
  • More Na+ channels are open in depolarised tissue. Lidocaine blocks these Na+ channels and prevents automatic firing of depolarised ventricular tissue
  • Not used prophylactically following MI even in patients showing ventricular tachycardia. Tend to use other drugs
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18
Q

What is the mechanism of action of beta-adrenorecptor antagonists?

A
  • Block sympathetic action by acting at beta 1 adrenoreceptors in the heart
  • Decreases slope of pacemaker potential in SA and slows conduction at AV node. Can prevent supra ventricular tachycardias and slows ventricular rate in patients with atrial fibrillation
  • Used following myocardial infarction. Myocardial infarction causes increased sympathetic activity. They prevent ventricular arrhythmias and arrhythmia may be partly due to increased sympathetic activity
  • Also reduced oxygen demand so reduced myocardial ischaemia which is beneficial following myocardial infarction
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19
Q

What is the mechanism of action of drugs that block K+ channels?

A
  • They prolong action potential

- Lethens the absolute refractory period. in theory this prevents another Action potential occurring too soon

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20
Q

Why aren’tdrugs that block K+ channels generally used?

A

Can be also pro-arhythmic due to the prolonged action potential

21
Q

What is the exception K+ blocking drugs?

A

Amiodarone

22
Q

What is the action of amiodarone?

A
  • It is a type 3 anti-arrhythmic but has other actions in addition to blocking K+ channels
  • Beta blocker, Calcium Channel blocker
  • Used to treat tachycardia associated Wolff-parkinon-White syndrome
  • Effective for suppressing ventricular arrhythmias post myocardial infarction
23
Q

What is mechanism of action of drugs the block Ca2+ channels?

A
  • Decreases slope of action potential at SA node
  • Decreases AV nodal conduction
  • Decreases force of contraction
  • Also some coronary and peripheral vasodilation

-Dihydropyridine Ca2+ channel blockers are not defective in preventing arrhythmias but do act on vascular smooth muscle (less effect on the heart compared to verapamil)

24
Q

How does adenosine work?

A
  • Produced endogenously but can also be administered intravenously
  • Acts on alpha 1 receptors at AV node but has a very short half-life
  • Enhances K+ conductance . Hyperpolarises cells of conducting tissue
  • Anti-arrhythmic. Useful for terminating re-entrant supra ventricular tachycardia
25
Q

What is heart failure?

A

Chronic failure of the heart to produce sufficiency output to meet the body’s requirements

26
Q

What are the features of heart failure?

A
  • Reduced force of contraction or reduced filling
  • Reduced cardiac output
  • Reduced tissue perfusion
  • Oedema
27
Q

What are the type s of drugs used in the treatment of heart failure?

A

Positive inotropes to increase cardiac output

  • Cardiac glycosides
  • Beta adrenergic agonist

Drugs that reduce workload of the heart - reduce after load and preload

28
Q

What is the action of cardiac glycosides (Digoxin)?

A
  • Physiologically Ca2+ extruded via Na+/Ca2+ which is driven by Na+ moving down contraction gradient
  • Cardiac glycoside block Na+/K+ ATPase which leads to rise in intracellular Na+.
  • This leads to decrease in a activity of Na+/Ca2+ exchanger
  • Cause increase in Ca2+ intracellular so more Ca2+ stored in SR
  • Increased force of contraction
  • Cardiac glycoside also cause increase in vagal activity.
  • Action via central nervous system to increase vagal activity
  • Slows AV conduction
  • Slows heart rate
29
Q

When are cardiac glycosides used?

A

May be used in heart failure when there is an arrhythmia such as atrial fibrillation

30
Q

What is the action of beta adrenergic agonists?

A
  • Acts on beta 1 receptors

- Used in cardiogenic shock and acute but reversible heart failure

31
Q

Why can’t cardiac glycoside and beta adrenergic agonist be used long term?

A
  • Making the heart work harder is not good in the long run.

- Better to reduce workload

32
Q

Why can’t cardiac glycoside and beta adrenergic agonist be used long term?

A
  • Making the heart work harder is not good in the long run.

- Better to reduce workload

33
Q

Which Drugs reduce workload of the heart?

A
  • ACE-inhibitors
  • Diuretics
  • Beta adrenoreceptor antagonists
34
Q

What is the action of the ACE inhibitors?

A
  • Inhibit the action of angiotensin converting enzyme which is important in the treatment of heart failure
  • Prevent the conversion of angiotensin 1 to angiostensin 2
  • Decrease in vasomotor tone (decrease in blood pressure)
  • Reduce afterload of the heart
  • Reduce preload of the heart
  • Reduce work load of the heart
  • Decrease fluid retention (decrease in blood volume)
35
Q

How do diuretics reduce workload of the heart?

A

-Reduce blood volume

36
Q

What causes angina?

A
  • Occurs when O2 supply to the heart does not meet its need
  • Ischaemia of heart tissue so pain
  • Usually pain is on exertion
  • Due to narrowing of the coronary arteries due to atheromatous plaque formation
37
Q

How do you treat angina?

A

-Reduce workload of the heart (beta-adrenoreceptor blockers, Ca2+ channel antagonists, organic nitrates)
-Improve the blood supply to the heart
(organic nitrates, Ca2+ channel antagonists)

38
Q

What is the action of organic nitrates?

A
  • Reaction of organic nitrates with thiols in vascular smooth muscle causes (NO2)- to be released
  • (NO2)- is rescued to NO
  • NO is a powerful vasodilator
39
Q

How does nitric oxide cause vasodilation?

A
  • NO activates granulate cyclase
  • Increase cGMP
  • Lowers intracellular [Ca2+]
  • Causes relaxation of vascular smooth muscle
40
Q

How does NO alleviate symptoms of angina?

A

Primary

  • Action on the venous system. Venodilation reduces the venous pressure so lowers preload
  • Reduced workload of the heart
  • Heart fills less therefore force of contraction reduced
  • This lower O2 demand
  • The heart works less

Secondary Action

  • Action on coronary collateral arteries improves O2 delivery to ischaemic myocardium
  • Acts on collateral arteries not arterioles
41
Q

Why do organic nitrites preferentially act on veins?

A
  • Probably because there is less endogenous nitric oxide in veins
  • Most effective on veins>arteries
  • Little effect on arterioles
42
Q

Which heart conditions carry an increased risk of thrombus formation?

A
  • Atrial fibrillation
  • Acute myocardial infarction
  • Mechanical prosthetic heart valves
43
Q

What are the antithrombotic drugs?

A
  • Anticoagulants

- Antiplatelet drugs

44
Q

What is the mechanism of action of anticoagulants?

A
  • Heparin given intravenously which inhibits thrombin. It is used acutely for short term action
  • Fractionated heparin
  • Warfarin is given orally. It antagonises the action vitamin
  • Direct acting oral thrombin inhibitors such as digabatran
45
Q

What is the mechanism of action for antiplatelet drugs?

A

-Aspirin following acute MI or high risk of MI

46
Q

What is hypertension associated with?

A
  • Increases in blood volume (Na+ and water retention in kidneys)
  • An increase in total peripheral resistance
47
Q

What are the possible targets for treatment of hypertension?

A
  • Lowers blood volume (lower cardiac output via Starling’s laws)
  • Lower cardiac output directly
  • Lower peripheral resistance
48
Q

What are the type of drugs for Hypertension?

A
  • ACE inhibitors - Decrease Na+ and water retention by kidney and decreases total peripheral resistance (vasodilation)
  • Ca2+ channel blockers slevetive for vascular smooth muscle - vasodilation
  • Diuretics - decrease Na+ and water retention by kidney so decrease in blood volume

Not routinely used

  • Beta blockers - decreases cardiac output
  • Alpha 1 adrenoreceptor antagonist - vasodilation

ESA 2: Cardiovascular (11 decks)

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