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ESA2 > CVS Arrhythmias and Drugs > Flashcards

CVS Arrhythmias and Drugs Flashcards

1
Q

What 4 things can drugs alter in CVS?

A

Blood vol
HR
Heart rhythm
Force of contraction

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2
Q

Name some causes of tachycardia

A

Ectopic activity, AF, Aflutter, afterdepolarisations, reentry loops (e.g WPW syndrome)

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3
Q

Name some causes of bradycardia

A

Heart block 1st 2nd 3rd degree - AVN dysfunction

Sick sinus syndrome - SAN dysfunction

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4
Q

Can beta blocker cause bradycardia by affecting both SAN and AVN? What other drug can from the lecture?

A

Yes

Ca channel blockers affect both too

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5
Q

What is triggered activity?

A

Afterdepolarisations (there are early and late ones)

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6
Q

Which type of after depolarisation is more common with high intracellular Ca2+ - which drug toxicity is associated with this?

A

Delayed

Digoxin

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7
Q

Which type of afterdepolarisation is more common in AP prolonged? Why? What drug can cause this?

A

Early
Because it lengthens the QT interval which predisposes to arrhythmias
K+ channel blockers can cause this due to increasing the length of the AP

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8
Q

Describe how a re-entrant mechanism can occur in the heart and give an example of an arrhythmia caused by this?

A 
Damaged area of heart - fibrotic
Unidirectional block
Depolarisation spreads round and the wrong way through damaged area
Forms a loop
Reentry tachycardia

E.g. AF (many of these in atria)

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9
Q

Name two things can cause damage and fibrosis to the myocardium to predispose to arrhythmias?

A

Dilation (e.g. from mitral stenosis/regurg)
Necrosis (e.g. from MI)
Ischaemia (Atherosclerosis)

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10
Q

Briefly say how and AV Nodal Reentry tachycardia is formed

A

Fast and slow pathways in the AVN create reentry loop

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11
Q

Briefly say how ventricular pre excitation can occur? Which disease?

A

Accessory pathway between atria and ventricles creates a large reentry loop e.g. in wolf-parkinson-white syndrome

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12
Q

What are the 4 classes of drugs (4 areas they act)

A

I Block Na channels
II Block b adrenoceptors
III Block K+ channels
IV Block Ca2+ channels

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13
Q

Why is an ischaemic/damaged part of myocardium susceptible to tachyarrhythmias?

A

Because the NaKATPase fails and this causes the cell to spontaneously depolarise and may then act as the foci

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14
Q

What drug would you give to prevent the complication of tachyarrhythmia? Why?

A

Beta blocker

Negative chronotropic and inotropic effect - stabilises activity and prevents ventricular arrhythmias

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15
Q

How does Lidocaine work? Which tissue does it preferentially block and why? Why does it not have a big effect on normal tissue?

A

Use dependent block
Binds to open or inactivated Na channels so preferentially blocks damaged depolarised tissue - so prevents automatic firing from ventricular cells.
Little effect in normal cardiac tissue as it dissociates readily - within 1AP
Blocks during depolarisation - and dissociates in time for next AP

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16
Q

When would lidocaine be used post MI? How is it given?

A

If signs of VT

Given IV

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17
Q

Would you use it for VT in other patients not post MI?

A

No use other drugs

18
Q

What effect do b blockers have on the SAN AP?

A

Decrease the slope of the pacemaker potential and the rising phase of the AP

19
Q

What has sympathetic activity got to do with arrhythmias post MI? Which drug blocks this

A

post MI often have increased sympa activity
Increased sympa activity related to arrhythmias

B blocker

20
Q

What type of arrhythmias can b blockers prevent with their action of slowing conduction at AVN? Give an example

A

Prevent supra ventricular tachys

can slow rate in AF

21
Q

Can beta blockers help prevent both atrial and ventricular arrhythmias?

A

Yes

22
Q

How do beta blockers reduce O2 demand of tissue?

A

As it reduces workload by reducing HR and contractility

23
Q

How do K+ channel blockers (class III) work? What is the danger? What is the drug exception that is used in clinical practice?

A

Prolong AP by blocking K+ channels and prolonging the absolute refractory period
Should prevent another AP occurring too soon but in reality can be pro arrhythmic
Except amioderone - as it affects other channels not just K+ so ends up being quite helpful

24
Q

When is amioderone useful?

A

Wolff-Parkinson-White syndrome tachys

Supresses ventricular arrhythmias post MI

25
Q

What are three effects of Ca2+ channel blockers (class IV)? Give an example

A

Decreases slope of AP at SAN (reduces HR)
Decreases AVN conduction (Dromotropy)
Negative ionotropy

Verapamil

26
Q

Which type of Ca channel blockers act primarily on vascular smooth muscle (e.g. for hypertension)? Give some examples

A

Dihydropyridine Ca2+ channel blockers

Amlodipine, felodipine, nicardipine

27
Q

What role do Ca2+ channel blockers have? (Which diseases)

A

Angina/Post MI - reduce O2 demand/afterload
Anti arrhythmic
Anti hypertensive

28
Q

Which class is adenosine? What does it do? How does it work? Long or short half-life?

A

Not in a class
Binds to A1 receptors on AVN coupled to Gi GPCR
Enhances K+ conductance - hyperpolarises
Short half life
Useful for terminating reentrant SVT (supra ventricular tachy)

29
Q

Give 2 examples of ionotropes - why aren’t these generally used for HF? When would they be?

A

Glycosides = e.g. digoxin
b adrenergic agonists e.g. dobutamine

Improves symptoms but no long term outcome

AF with HF

30
Q

How does digoxin/cardiac glycosides work?

A

Blocks Na K ATPase - Increases Na in cell - reduces NCX activity, so less Ca pumped out - more Ca intracellularly therefore more taken up in to SR stores for release next time –> increased force of contraction

Increased chronotropy and ionotropy e.g. dobutamine and digoxin

31
Q

What do you target to treat HF (2)

A

Preload

Afterload

32
Q

When else would you use an inotropic agent (b adrenergic agonist)? Give an example

A

Cardiogenic shock/acute reversible HF post surgery

E.g. dobutamine - acts on beta-1 receptors

33
Q

Which drugs reduce preload and after load - useful in Hf?

A

ACE i - reduce preload by reducing blood vol by reduced Na reabsorption
reduce after load by reducing BP (by reducing vasomotor tone)

AngII antagonist can be used if ACEi not tolerated

B blockers – reduce workload of heart as said earlier

Diuretics - reduce blood vol - reduce preload

34
Q

What would you target to treat angina? Give example of types drugs that would do this

A

Reduce workload
B blocker
Ca channel blocker
Organic Nitrates (GTN)

Improve blood supply to heart
Organic Nitrates (GTN)
Ca channel blocker
35
Q

How do organic nitrites (NO) work (2)? Do they exert most of their action on the arterial or venous system? Which law of the heart do they relate to?

A

By converting to NO a powerful vasodilator Gia Guanyl Cycase (GC) producing GTP–>cGMP —> PKG —> decreases intracellular Ca in vascular smooth muscle cell = relaxation

Venous - lowers preload - reduces workload, heart fills less so less contraction (starlings law) - lowers O2 demand of myocardium

Also improve collateral flow in coronary ARTERIES (not arterioles) improves O2 delivery to ischaemia myocardium

36
Q

Why do organic nitrates act preferentially on veins?

A

Probably because less endogenous NO in veins

37
Q

Why don’t organic nitrates really work on arterioles? Why aren’t there many collateral arteries for NO to work on in the heart?

A

Because they are already fully dilated around ischaemic region

Because coronary arteries are end arteries

38
Q

Give some examples of heart conditions that are more prone to thrombus formation

A

AF
MI (thrombus can form over necroses not moving bit)
Mechanical prosthetic heart valves

39
Q

Give 4 examples of anticoagulants and how they are administers?

A

Heparin - IV
Fractionated heparin - sub cutaneous
Warfarin - Oral
Newer Oral Anticoagulant - Dabigatran - oral thrombin inhibitor

40
Q

In what emergency would you give aspirin/antiplatelet?

A

Following acute MI or high risk of MI - reduce chance of thrombus that could occlude an artery

41
Q

How would you treat hypertension (3)? How do the drugs work?

A

ACEi - reduce preload by reducing blood vol by reduced Na reabsorption, reduce after load by decreased peripheral resistant (decreased vasoconstriction)

Ca2+ channel blocker - Relaxation of smooth muscle - vasodilation reduces after load

Diuretic - reduce blood volume reduces preload

42
Q

Which other drugs can technically help hypertension but not routinely used?

A

B1 blockers - reduce CO

alpha 1 antagonist - vasodilation

ESA2 (37 decks)

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