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Semester 2 Cardiovascular System > L14: Understanding arrhythmias and Action of drugs on CVS > Flashcards

L14: Understanding arrhythmias and Action of drugs on CVS Flashcards

1
Q

What are the different types of abnormalities you can have to the heart rhythm?

A 
Bradycardia
Atrial fibrillation 
Atrial flutter
Tachycardia--> Ventricular and supraventricular
Ventricular fibrillation
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2
Q

What are some of the causes of tachycardia?

A

Ectopic pacemaker activity
Afterdepolarisations–> abnormal depolarisation following AP (delayed and early)
Atrial flutter/ atrial fibrillation
Re-entry loop–> conduction delay, accessory pathway

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3
Q

How does ectopic pacemaker activity arise?

A

Damaged area of myocardium –> depolarised and spontaneously active, or latent pacemaker region activated due to ischaemia (dominates over SA node)

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4
Q

What is delayed after-depolarisations (triggered activity)?

A

Occur after repolarisation phase
More likely to happen if intracellular Ca2+ increased (activate Cl- channels or Na+/Ca2+ exchanger–> brief inward current–> threshold reached–> AP generated)

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5
Q

What is the difference between delayed after-depolarisation and early after-depolarisations?

A

Delay–> after repolarisation

Early–> During repolarisation

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6
Q

What are early after-depolarisations?

A

Interupts normal repolarisation
Occurs if prolonged AP
Leads to oscillations

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7
Q

What is the re-enterant mechanism for generating cardiac arrhythmias?

A

Occurs when point of divergence with incomplete conduction damage
Unidirectional block
Excitation (impulse) takes the long route around
Can spread through the damaged area in opposite direction (unidirectional block) leading to the formation of a circuit–> areas re-excited quickly
Damage to atria, excessive stretch–> Multiple re-entrant circuits in atria–> atrial fibrillation

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8
Q

How may re-entry occur at the AV node?

A

AV node has fast and slow pathway in AV node → common pathway at end
- Slow pathway repolarisation faster than the fast pathway
Premature beat- slow pathway activated → reaches common pathway by which time fast has recovered from refractory period
Fast pathway activated in opposite direction → Sets up circuit
Depolarisation goes round the circuit
Many depolarisations down the bundle of His etc… → ventricles activated much faster rate than normal

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9
Q

What are supraventricular tachycardias?

A

Arise above the ventricles in the atria
Atrial fibrillation
AV node re-entry

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10
Q

What causes ventricular pre-excitation?

A

Accessory pathway between atria and ventricles
Creates a re-entry route
Depolarisation from atria to ventricles without passing through AV node
Wolff-Parkinson-White syndrome

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11
Q

What are some of the causes of brachycardia?

A

Sinus brachycardia

Conduction block

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12
Q

What causes sinus brachycardia?

A

Physiological–> fit, healthy athlete
Pathological
Sick sinus syndrome (intrinsic SA node dysfunction)
Extrinsic factors–> drugs–> beta blockers, some Ca2+ channel blockers

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13
Q

What is a conduction block?

A

Problems at AV node or bundle of His

Slows conduction at AV node due to extrinsic factors –> beta blockers, some Ca2+ channel blockers

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14
Q

What are the different classes of drugs that affect the rate and rhythm of the heart?

A

1- Block voltage sensitive Na+ channels
2- Antagonist of β-adrenoreceptors
3- Block K+ channels (not used–> pro-arrhythmic)
4- Block Ca2+ channels

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15
Q

How do Na+ channel blockers (Class one) work?

A

Prevent Na+ influx and depolarisation
e.g. Lidocaine –> Local anaesthetic
Use dependent block
Blocks channel in open or inactivated state
Little effect in normal cardiac tissue as it dissociates rapidly
Help prevent ventricle tachycardia

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16
Q

What is lidocaine used for?

A

Local anaesthetic
Propholyaxis–> prevent ventricle tachycardia after MI
Damaged areas of myocardium might depolarise and fire auomatically
More Na+ channels open during depolarisation–> lidocaine blocks then preventing depolarisation
Not commonly used–> other drugs avaliable

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17
Q

How do β-adrenoreceptor antagonist (class two) work?

A

Block sympathetic action –> β1 adrenoreceptors in the heart
Decrease slope of pacemaker potential in SA node and slows conduction at AV node
Propanolol, atenolol

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18
Q

What are β-blockers used to treat?

A

Supraventricular tachycardia–> slow conduction in AV node
–> slow ventricular rate in AF
MI–> causes increased sympathetic activity–> arrhythmias–> β-blockers stop
–> also reduced O2 demand preventing ischaemia

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19
Q

What do K+ channel blockers do?

A

Theory should prolong action potential (prevent hyperpolarisation)
Lengthen the absolute refractory period
Reality–> pro-arrhythmic–> pro-long QT interval–> early after depolarisation

20
Q

What is the one K+ channel blocker that is an exception?

A

Amiodarone
Treat tachycardia
Other actions as well as K+ channel blocker
Suppression of ventricular arrhythmias
Treat tachycardia–> Wolff-Parkinson-White syndrome

21
Q

How do drugs that block the Ca2+ channels (class IV) work?

A

Decrease slope of AP at SA node
Decrease AV nodal conduction
Decrease force of contraction (negative iontropy)
Verapamil, dilitiazem (non-dihydropyridine types)

22
Q

What is the function of the dihydropyridines?

A

Ca2+ channel blockers
BUT do not prevent arrhythmias
Act on vascular smooth muscle
Amlodipine, nifedipine, nicardipine etc…

23
Q

What is the function of adenosine?

A 
Endogenously produced
Injected intravenously
Acts on alpha 1 receptors in AV node
Short half life
Enhances K+ conduction--> hyperpolarises
Anti-arrhythmic
Prevents supraventricular tachycardia
24
Q

What other drugs that act on the CVS that are not used to specifically treat arrhythmias?

A

ACHi and angiotensin II receptor blockers
Diuretics
Calcium channel antagonists
Positive inotropes
Alpha adrenoreceptor blockers and beta blockers
Antithrombotic drugs

25
Q

How do ACEi work? What are they used to treat?

A

Inhibit ACE action
Prevents conversion of AngI to AngII
Treatment of hypertension and heart failure
AngII acts on kidney–> increase Na+ absorption and H20 absorption, vasoconstrict vessels, aldosterone production
Perindopril

26
Q

How does ACEi prevent heart failure?

A 
Heart unable to provide sufficient output to meet body demand
ACEi
--> decrease vasomotor tone (↓ BP)
--> reduce afterload
--> decrease fluid retention (↓BP)
--> reduce preload 
reduce work load on heart
27
Q

What is a side effect of ACEi?

A

Dry cough

Excess bradykinin

28
Q

What are AngII receptors blockers used for?

A

Treatment of HF and hypertension
Block the receptors so AngII can’t bind
–> no vasodilation, reduced Na+ reabsorption and H2O reabsorption, no aldosterone
Losartan

29
Q

What are diuretics used for? How do they work?

A

Treatment of heart failure and hypertension
Congestive heart failure–> oedema in lungs–> difficulty breathing –> both sides of heart failing
–> Furosemide, thiazide
Act on the Loop of Henle–> Loop diuretics
Reduce oedema

30
Q

How are Ca2+ channel blockers used to treat hypertension?

A

Dihydropyridine Ca2+ channel blockers–> vascular smooth muscle
–> decrease peripheral resistance
–> decrease arterial BP
–> reduce workload of heart by reducing after load
Amlopidine, nicardipine

31
Q

What are Ca2+ blockers used to treat in the CVS?

A

Hypertension, angina, coronary artery spasms, supraventricular tachycardia
Non-dihydropyridine Ca2+ blocker–> heart
Dihydropyridine Ca2+ blockers–> vascular smooth muscle

32
Q

What are positive inotropes?

A

Drugs used to increase contractility–> CO

33
Q

What are the two types of positive inotropes?

A

Cardiac glycoside–> digoxin

β-adrenergic agonists–> dobutamine

34
Q

How do cardiac glycosides work?

A

Primary action–> block Na+/K+ ATPase
Na+ normally moves in down concn gradient whilst Ca2+ out via Na+/Ca2+ exchanger
Na+/K+ ATPase blocked –> ↑ [Na+] intracellular –> ↓ Na+/Ca2+ activity
[Ca2+] intracellular increase–> stored in SR –> increased force of contraction

Secondary action
Increase vagal nerve activity via CNS
Slow AV conduction
Slow HR

35
Q

What other conditions can cardiac glycosides be used to treat?

A

Arrhythmias in AF

36
Q

How do β1-adrenoreceptor agonists work? When are they used?

A

Stimulates β1 receptors in SA and AV node
Treat cardiogenic shock
Acute but reversible HF

37
Q

What is the problem with cardiac glycosides?

A

Relieve symptoms by making the heart contract harder
Not sustainable–> No long term benefit
Need to treat underlying cause
Reduce the workload (pre-load and after load)

38
Q

What is angina?

A

O2 supply to heart does not meet demand
Limited duration–> no death of myocytes
Ischaemia of heart

39
Q

What is used to treat angina? Why?

A

Organic nitrates
Nitrates react with thiols (-SH groups) in vascular smooth muscle causing NO2- to be released
Reduced to NO (nitric oxide) –> powerful vasodilator of VEINS
Endogenously released from endothelial cells
Exogenously delivered as GTN spray (glycerol trinitrate)–> quick short acting
Or Isosorbide dinitrate–> longer acting

40
Q

Why do organic nitrates act on veins?

A

Less endogenous nitric oxide in veins
Therapeutic dose most effective on veins
No action on arterioles

41
Q

How does nitric oxide cause vasodilation of veins?

A

NO activates Guanylate cyclase
Increase cGMP
Lowers intracellular [Ca2+]
Relaxation of vascular smooth muscle

42
Q

How does NO alleviate the symptoms of angina?

A

Primary action–> VENOdilation, lowers preload
–> reduce workload of heart–> heart fills less–> force of contraction reduced (Starlings law)–> lowers O2 demand

Secondary action–> acts on coronary collateral arteries to improve O2 delivery to tissue (NOT arterioles)–> increase blood flow to ischaemic area slightly

43
Q

In summary how is angina treated?

A

Reduce work load on heart–>

  • organic nitrates (venodilation),
  • β-adrenoreceptor blockers (block sympathetic action),
  • Ca2+ channel antagonists (reduce work load by vascular smooth muscle relaxation)

Improve blood supply to the heart–>

  • Ca2+ channel antagonists (vascular smooth muscle relaxation),
  • minor effect of organic nitrates
44
Q

Which heart diseases carry an increased risk of thrombus formation? Why?

A

Atrial fibrillation–> atria quiver but don’t fully contract, LA blood stuck in left appendage–> stasis forms clot
Acute myocardial infarction–> blood stasis–> clot forms
Mechanical prosthetic heart valves–> traps blood

45
Q

What drugs are used to prevent thrombus formation?

A

Anticoagulants–> prevents Factor Xa converting prothrombin to thrombin
Venous thromboembolisms prevented by:
–> Heparin–> inhibits thrombin, short term action (IV)
–> Fractionated heparin (subcutaneous injection)
–> Warfarin–> antagonises Vit K (oral)
–> Direct oral thrombin inhibitors such as dabigatran
Antiplatelet drugs–> aspirin, clopidogrel (given following MI) –> stops platelets aggregating

Semester 2 Cardiovascular System (21 decks)

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