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SA Cardiovascular system > S10) Arrythmias & CVS Drugs > Flashcards

S10) Arrythmias & CVS Drugs Flashcards

1
Q

Outline, briefly, the possible action of drugs on the cardiovascular system

A

CVS drugs can alter:

  • The rate and rhythm of the heart
  • The force of myocardial contraction
  • Peripheral resistance and blood flow
  • Blood volume
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2
Q

What are arrhythmias/dysrhythmias?

A

Arrhythmias are abnormalities of heart rate or rhythm

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3
Q

Provide 5 examples of arrhythmias

A
  • Bradycardia <60 bpm
  • Tachycardia (ventricular/supraventricular) >100bpm
  • Atrial flutter
  • Atrial fibrillation
  • Ventricular fibrillation (most dangerous as there is no coordination and no output of blood to body so they can die quickly)
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4
Q

Describe four causes of arrhythmia which manifest as tachycardia

A
  • Ectopic pacemaker activity – latent pacemaker region activated due to ischaemia and dominates over SAN // damaged area of myocardium is depolarised and becomes spontaneously active
  • After depolarisations – abnormal depolarisations following the action potential
  • Atrial flutter / atrial fibrillation
  • Re-entry loop – conduction delay due to accessory pathway
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5
Q

Describe two causes of arrhythmia which manifest as bradycardia

A
  • Sinus bradycardia

I. Intrinsic SAN dysfunction

II. Extrinsic factors e.g. drugs (beta blockers, CCBs)

  • Conduction block

I. Problems at AVN / bundle of His

II. Slow conduction at AVN due to extrinsic factors e.g. drugs

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6
Q

When are delayed after-depolarisations likely to happen?

A

Delayed after-polarisations are more likely to happen if intracellular Ca2+ high = stimulate an A.P and cause ventricular tachycardia

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7
Q

When are early after-depolarisations likely to happen?

A
  • Early after-polarisations are more likely to happen if AP prolonged
  • Longer AP = longer depolarisation = longer QT (time myocardium is depolarised to polarised)
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8
Q

Describe the re-entrant mechanism for generating arrhythmias

A
  • Incomplete conduction damage (unidirectional block)
  • 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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9
Q

How does atrial fibrillation occur?

A

Atrial fibrillation arises due to several small re-entry loops in the atria

(mitral stenosis)

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10
Q

Briefly, explain how AV nodal re-entry occurs

A

Fast and slow pathways in the AV node create a re-entry loop = will go down though bundle of his and cause excitation = ventricular tachycardia

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11
Q

Briefly, explain how ventricular pre-excitation occurs

A

An accessory pathway between atria and ventricles creates a re-entry loop such as in Wolff-Parkinson-White syndrome = supraventricular fibrillation

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12
Q

There are 4 basic classes of anti-arrhythmic drugs affecting the rate and rhythm of the heart.

What are they?

A
  • Drugs that block voltage-sensitive Na+ channels
  • β-adrenoreceptors antagonists
  • Drugs that block K+ channels
  • Drugs that block Ca2+ channels
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13
Q

Describe the action of drugs which block voltage-dependant Na+ channels (Class I)

A
  • Only blocks voltage-gated Na+ channels in open/inactive state, thus preferentially blocks damaged depolarised tissue and prevents ventricular fibrillation
  • Blocks during depolarisation but dissociates in time for next action potential
  • eg. lidocane (class Ib) -> mild Na channel block
  • > slows upstoke
  • > shortens AP
  • > slows conductivity
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14
Q

In four steps, describe the action of β-adrenoreceptor antagonists (class II)

helps treat tachycardia/ atrial fibrillation = slow down heart rate

A

⇒ Act at β1-adrenoreceptors in the heart

⇒ Block sympathetic action

⇒ Decrease deploarisation/ slope of pacemaker potential in SAN

⇒ Slows conduction at AVN

eg. propranolol, atenolol

reduce effects of funny current channels, reduces CAMP being activated

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15
Q

Describe the effects of beta blockers

A

Beta blockers slow conduction in AV node:

  • Prevent supraventricular tachycardias (decrease in SNS activity)
  • Slows ventricular rate in patients with AF
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16
Q

Explain why beta blockers are beneficial following myocardial infarction

A
  • MI causes increased sympathetic activity
  • β-blockers reduce O2 demand at heart, hence reducing myocardial ischaemia
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17
Q

Describe the action of drugs that block K+ channels (class III)

A
  • Block K+ channels
  • Prolong the action potential = prolong QT intervals = pro-arrythmic
  • Lengthens the absolute refractory period
  • Preventing another action potential occurring too soon (can be pro-arrhythmic)
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18
Q

Describe the actions of drugs that block Ca2+ channels (class IV)

= antiarrythmic drugs

A
  • non-dihydropyridine = verapamil, diltiazem
  • Decreases slope of action potential at SAN
  • Decreases AV nodal conduction
  • Decreases force of contraction (negative inotropy)
  • Some coronary and peripheral vasodilation

treat hypertension, angina = decrease resistance and BP

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19
Q

What is heart failure?

A

Heart failure is the chronic failure of the heart to provide sufficient output to meet the body’s requirements

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20
Q

Identify 4 features of heart failure

A
  • Reduced force of contraction or reduced filling
  • Reduced cardiac output
  • Reduced tissue perfusion
  • Oedema
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21
Q

Which types of drugs are used in the treatment of heart failure?

A
  • Positive inotropes to increase cardiac output (not routinely used)
  • Drugs which reduce work load of the heart (afterload and preload)
22
Q

Which drugs increase myocardial contractility in the treatment of heart failure?

A
  • Cardiac glycosides
  • β adrenoreceptor agonists
23
Q

In 5 steps, explain how cardiac glycosides increase myocardial contractility

A

⇒ Ca2+ is extruded via the Na+-Ca2+ exchanger

⇒ Cardiac glycosides block Na+/K+ ATPase

⇒ Rise in [Na+]i decreases activity of Na+-Ca2+ exchanger

⇒ Causes increase in [Ca2+]i

⇒ Increased force of contraction

24
Q

Cardiac glycosides may be used in heart failure when there are arrythmias.

Describe the action of cardiac glycosides on heart rate

A
  • Action via CNS to increase vagal activity
  • Slows AV conduction
  • Slows the heart rate
25
Describe two uses of β – adrenoreceptor agonists eg dobutamine
stimulates B1 receptors present at SA node - Cardiogenic shock - Acute but reversible heart failure *e.g. following cardiac surgery*
26
Which drugs reduce the work load of the heart?
- ACE inhibitors - Diuretics - β – adrenoreceptor antagonists
27
Describe the action of ACE-inhibitors
**Prevent the conversion of angiotensin I to angiotensin II (vasoconsitriction, Na reabsoption in blood, aldosterone):** - Reduce Na+ and H2O reabsorption - Vasodilation of systemic vasculature - can increase bradykinin = dry cough =\> symptom
28
Explain why ACE inhibitors are so useful in the treatment of hypertension
- Decrease **vasomotor tone** (blood pressure) / inhibit vascocinstriction - Reduce **afterload** of the heart (easier for heart to pump around) - Decrease **fluid retention** (blood volume reduces odema) - Reduce **preload** of the heart = workload of heart
29
What is angina?
- **Angina** is a condition arising due to insufficient O2 supply to the heart for a limited duration caused by artheromatous plaque formation in the coronary arteries - It results in heart tissue Ischaemia which presents as chest pain - pain gets bad at exercise but relieved at rest
30
How does one treat angina?
- **Reduce the work load of the heart:** I. β blockers II. CCBs III. Organic nitrates - **Improve the blood supply to the heart:** I. Organic nitrates II. CCBs
31
Describe the action of organic nitrates
- **Reaction of organic nitrates with thiols** in vascular smooth muscle causes NO2- to be released - NO2- is reduced to **nitrous oxide** - NO is a powerful **vasodilator** **- venodilator** = reduce return of blood to heart = reduce 02 demand
32
How does nitrous oxide cause vasodilation?
⇒ NO activates **guanylate cyclase** ⇒ Increases **cGMP** ⇒ Lowers **[Ca2+]i** ⇒ Causes **relaxation** of vascular smooth muscle
33
In four steps, describe the primary action of nitrous oxide
**Acts on venous system (venodilation):** ⇒ Reduced venous pressure ⇒ Reduced filling → reduced contractility (Starling’s Law) ⇒ Lowers O2 demand ⇒ Reduces work load of the heart they have very little effect on arteries
34
What is the secondary action of nitrous oxide?
Acts on **coronary collateral arteries** to improve O2 delivery to the ischaemic myocardium
35
Why do organic nitrates preferentially act on veins?
**Less endogenous nitric oxide in veins:** - Most effective on veins \> arteries - Little effect on arterioles
36
Illustrate how venodilation by organic nitrates is a major contribution to their overall action
37
Illustrate how the dilation of collateral coronary arteries by organic nitrates is only a minor contribution to their overall action
38
Provide an example of an organic nitrate
Glyceryl trinitrate (**GTN spray** – sublingual)
39
Why do we need antithrombotic drugs?
To treat certain heart conditions which carry an **increased risk of thrombus formation** *e.g. atrial fibrillation (cause stroke), AMI (thromus in coronary artery), mechanical prosthetic heart valves*
40
What are the two types of antithrombotic drugs?
- Anticoagulants - Antiplatelet drugs
41
Identify some anticoagulants and describe their actions
- **IV Heparin** – inhibits thrombin / clots forming(short term) - **Oral Warfarin** – antagonises action of vitamin K / inhibits thrombus forming (long term) - Other: fractionated subcutaneous heparin, oral thrombin inhibitors **DVT (deep vein thrombosis) / atrial fibrillation -** clot breaks off and travels to the brain / clot goes into left ventricle and can cause a stroke
42
What is the most common antiplatelet drug and when is it given?
**Aspirin** – following AMI / in high risk of MI
43
What is hypertension?
**Hypertension** is the persistent elevation of blood pressure
44
What are the possible targets of hypertensive drugs?
- Lower **blood volume** - Lower **cardiac output** directly - Lower **peripheral resistance**
45
Identify 5 hypertensive drugs and describe their respective actions
- **ACE-inhibitors** – decrease Na+ and H2O retention and TPR - **CCBs** – vasodilation in vascular smooth muscle - **Diuretics** – decrease Na+ and H2O retention - **β-blockers** – decrease cardiac output (not routinely used) - **α1 adrenoceptor antagonist** – vasodilation (not routinely used)
46
role of amiodarone
blocks K channels blocks Ca channels blocks b blockers anti-arrythmic drug =\> reduce supraventicuar arrythmia
47
adenoisne (antiarrhythmic)
- produced **endogenously** - administered via **IV** - acts on a1 receptors at AV node + **short half life** - **enhances K conductance** **- alpha unit** inhibits CAMP while beta/gamma unit acts on K channels at AV node = **hyperpolarise cells** = **terminates heart** = heart can settle and **start again** - powerful but stops working quickly
48
What medication can people use if they cant use ACEi
AT1 receptor blocker treats heart failure and hypertension
49
diuretics
- treats **heart failure and hypertension** - **reduce blood volume** - **blocks Na/K/Cl** exchanger - **lose more Na** and so **lose water** in urine
50
cardiac glycoside
- treat **heart failure** (short term) - **blocks Na/K ATP ase** - **increase intracellular Na** conc so the Na/Ca exhanger doesnt work = **Ca store up in cell** = more ca can be released during AP = **increase force** of contraction
51
cardiac glycoside on heart eg digoxin
- increases vagus activity - slows down conduction at AVN - slows heart rate - used in arrhythmia and heart failure

SA Cardiovascular system (16 decks)

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