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Y1 - CVS > Arrythmias And Actions Of Drugs On The CVS > Flashcards

Arrythmias And Actions Of Drugs On The CVS Flashcards

1
Q

What is Bradycardia?

A

Slow heart rate
Less than 60bpm

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2
Q

What is atrial flutter?

A

When atria beat faster but regularly compared to the ventricles (like 4 atria contractions per 1 ventricular contraction)

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3
Q

What is atrial fibrillation?

A

When atrial electrical contraction/activity is chaotically irregular

Irregularly irregular

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4
Q

What is Tachycardia?

A

Fast heart rate
Over 100bpm

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5
Q

What are the 2 types of Tachycardia?

A

Ventricular tachycardia
Supraventricular tachycardia

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6
Q

What is ventricular fibrillation?

A

Irregularly irregular contractions/electrical activity of the ventricles

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7
Q

What is the definition of an arrhythmia?

A

Any deviation from the normal rhythm of the heart

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8
Q

What are the 2 types of arrhythmias?

A

Tachyarrythmias
Bradyarrythmias

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9
Q

What are some of the different causes of Tachyarrythmias?

A

Ectopic pacemaker activity
Early after depolarisations
Atrial flutter/atrial fibrillation
Re-entry loop

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10
Q

How does Ectopic pacemaker activity cause a Tachyarrythmia/tachycardia?

A

Damaged area of myocardium becomes depolarised and spontaneously active (rapidly depolarises)

Ischaemic damage can cause a region which depolarises faster than the SAN to form

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11
Q

How can early after depolarisations cause Tachycardia/tachyarrythmia?

A

Triggered activity (abnormal depolarisations following an action potential) cause more AP to be fired than should be

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12
Q

What type of tachycardia can Atrial flutter/atrial fibrillation cause?

A

Supraventricular tachycardia

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13
Q

How do re-entry loops cause tachycardia?

A

Either a conduction delay
or
Accessory pathway

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14
Q

What are the 2 causes of Bradyarrythmias?

A

Sinus bradycardia
Conduction block

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15
Q

What is sick sinus syndrome?

A

Cause of sinus bradycardia
Where the SAN doesn’t depolarise quickly enough

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16
Q

What type of drugs can cause sinus bradycardia?

A

Beta blockers
Somme Ca2+ channel blockers

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17
Q

How do Conduction blocks occur causing bradycardia?

A

Problems at AVN or bundle of his causing slow conduction
Slow conduction due to factors like Beta blockers and some Ca2+ channel blockers

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18
Q

The prolonged duration of what increases the chances of Early After Depolarisations (EAD)?

What interval on an ECG indicates a longer AP?

A

Action potentials

Longer QT interval = longer AP

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19
Q

What condition of the blood can increase chances of EADs and why?

A

Hyperkalaemia

Takes longer for ventricles to repolarise due to less steep gradient of K+
This prolongs the action potential making it more likely for EADs

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20
Q

What type of tachycardia is likely to develop when AP/QT interval is longer?

A

Ventricular tachycardia

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21
Q

What are Delayed after-depolarisations? (Triggered activity)

A

An action potential that occurs after repolarisation

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22
Q

What makes Delayed after-depolarisations more likely to happen?

A

High Intracellular [Ca2+]

Possibly involves Na+/Ca2+ exchanger

If threshold reached AP triggered

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23
Q

What is the re-entrant mechanism for generating arrhythmias?

A

A unidirectional conduction block (incomplete conduction damage)
Allows for conduction to only flow one way through or decreases speed of conduction, meaning there isn’t a point where impulses cancel out
Produces constant loop to be set up (excitation travels the wrong way)

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24
Q

What is AV Nodal Re-entry?

A

Fast and slow pathways in the AVN create a re-entry loop

Causes ventricles to contract early (Supraventricular tachycardia)

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25
Q

What causes Ventricular Pre-excitation?

A

Accessory pathway for electrical impulses between atria and ventricles creating a re-entry loop

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26
Q

What is a condition which has an accessory pathway between atria and ventricles?

A

Wolff-Parkinson-White syndrome

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27
Q

How can the re-entrant mechanism cause atrial fibrillation?

A

Several re-entry loops form in atria

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28
Q

What are the 4 basic classes of anti-arrhythmic drugs?

A

I. Block VOltage gated sodium channels
II. Antagonists of B-adrenoreceptors
III. Drugs that block K+ channels
IV. Drugs that block Ca2+ channels

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29
Q

What is an example of a drug which blocks Voltage gated Na+ channels? (Class I)

A

Local anaesthetic lidocaine

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30
Q

What type of arrhythmia is Lidocaine used to treat?

A

Ventricular Tachycardia

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31
Q

How is Lidocaine administered to treat Ventrcular Tachycardia?

A

Intravenously

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32
Q

What state are the VGSCs in when Lidocaine blocks it and why is this useful?

A

Only blocks Open or Inactivated channels so preferentially blocks damaged depolarised tissues

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33
Q

How does Lidocaine treat ventricular tachycardia?

A

Blocks the damaged areas of myocardium’s Voltage gated Na+ channels preventing these areas from firing automatically

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34
Q

What is another name for drugs that are B-adrenoreceptor antagonists?

A

Beta blockers

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35
Q

What are the names of some Class II B-adrenoreceptor antagonists (Beta blockers)?

A

Propranolol
Bisoprolol
Atenolol

36
Q

How do Beta blockers act to prevent Supraventricular tachycardia?

A

Act on B1 receptors in heart
Slows down the funny current from reaching threshold in the SAN (HCN channels)

Slows conduction at AVN by reducing VG Ca2+ activity in the AP upstroke

37
Q

Why are Beta blockers often used following MI?

A

MI leads to increased sympathetic activity of the heart

So Beta blockers often given to reduce this activity preventing ventricular arrhythmias
It makes the heart not work so hard decreasing its O2 demand minimising further ischaemic damage

38
Q

Which stage of the action potential does Class III K+ channel blockers affect?

A

Repolarisation

39
Q

What affect do Class III antiarrhythmics have on the heart?
(Amiodarone)

A

Lengthens the Absolute refractory period
HOWEVER
Prolongs the action potential (prolong QT interval) so can be PRO-arrhythmic

40
Q

What is a Class III anti-arrhythmic that blocks K+ that is the exception which is used and why?

A

Amiodarone

Has other affect like Beta blocking as well as blocking K+ channels

Treats Wolff-Parkinson-White syndrome

41
Q

What are the 2 types of Ca2+ channel blockers?

A

Non Dihydropyridine Ca2+ channel blockers

Dihydropyridine Ca2+ channel blockers

42
Q

What is the type of Ca2+ channel blocker which acts as an anti-arrhythmic drug affecting heart rate and rhythm?

A

Non Dihydropyridine Ca2+ channel blockers
Like a Phenylaklyamine like Verapamil

43
Q

What are some examples of Ca2+ channel blockers that act as Class IV anti-arrhythmics?

A

Phenylalkylamine = Verapamil
Benzothiazapine = Diltiazem

44
Q

How do Ca2+ channel blockers affect the heart?

A

Decreased influx of Ca2+ into cells

Decreases speed of upstroke of AP at SAN
Decreases AVN Conduction (both above have -Ve chronotropic effect)
Decreases force of contraction (-Ve inotropic effect)

45
Q

What do Dihydropyridine Ca2+ channels work on if they don’t prevent arrhythmias?

A

Vascular smooth muscle

46
Q

What type of receptor is the Alpha 1 adrenoreceptor?

A

G protein coupled receptor

47
Q

How does adenosine act to treat arrhythmia?

A

Acts on A1 receptors at AVN

Enhances K+ conductance causing hyperpolarisation

Temporarily stops the heart allowing the APs to re align

48
Q

What is an example of an ACE-inhibitor?

A

Perindopril
Enalapril
Lisonopril
Ramipril

49
Q

How does the ACE inhibitor Perindopril act to treat hypertension and Heart failure?

A

Prevents conversion of Angiotensin I to Angiotensin II

Prevents Angiotensin II s effects of increasing Na+ and water reabsorber and its acton as a Vasoconstrictor

50
Q

What is the goal of ACE inhibitors in treating heart failure and how do they acheive this?

A

Reduce how hard the heart has to work

Decrease vasomotor done (dec BP) reducing afterload

Decrease fluid retention (dec blodo vol) reducing preload

51
Q

What is afterload?

A

Pressure the heart must work against to eject blood during systole

52
Q

Why might someone not be able to tolerate ACE-inhibitors?

A

Can cause a dry cough

53
Q

What can be given to patients who cant tolerate ACE inhibitors?
(Have a dry cough, why do they have this?)

A

Angiotensin II receptor blockers

Losartan

Due to Bradykinin accumulating as a result of inhibiting ACE being inhibited

54
Q

How do Diuretics treat heart failure and hypertension ?

A

Reduce Na+ and water retention
Helps reduce pulmonary and peripheral oedema

55
Q

What is the name of a drug that can treat congestive heart failure which is a loop diuretic?

A

Furosemide

56
Q

How do the Dihydropyridine Ca2+ channel blockers help reduce workload of the heart?

A

Act on vascular smooth muscle
Decreases peripheral resistance
Decreases arterial BP
Which reduces the afterload

57
Q

What are some Dihydropyridine Ca2+ channel blockers (act on vascular sm)?

A

Amlopidine
Nicardipine

58
Q

What 2 types of drugs are positive inotropes?
(Increase contractility of the heart)

A

Cardiac glycosides
B-adrenergic agonists

59
Q

What do both Cardiac glycosides and the B-adrenergic agonist Dobutamine do?

A

Block Na+/K+ ATPase leading to stronger contractions

60
Q

What is an example of a cardiac glycoside?

A

Digoxin

61
Q

How does the cardiac glycoside digoxin act to increase strength of heart contraction?

A

[Na+] in cell inc due to Na+/K+ ATPase being blocked by Digoxin
Means activity of Na+/Ca2+ exchanger decreases since gradient of Na+ decreases so [Ca2+] in cell INCREASES
More Ca2+ in cell = STRONGER contraction

62
Q

Why are cardiac glycosides not normally used to treat heart failure?

A

Only normally improve symptoms but not long term outcome because the heart is being made to work harder

63
Q

What affect do cardiac glycosides have on the heart?

A

Increased vagal activity on heart
Slows AV conduction
Slows heart rate

64
Q

When are cardiac glycosides like Digoxin used as a form of treatment for heart failure?

A

Only when the heart failure is accompanied by arrhythmia since into an anti-arrhythmetic

65
Q

How does the B-adrenoreceptor agonist Dobutamine act on the heart?

A

Stimulates B1 receptors at SAN and AVN and on myocytes in ventricles

Can be used to help restart heart

66
Q

What receptors does the Beta blocker Propranolol act on?

A

Non selective so on B1 and B2

67
Q

What affect does Propranolol have on the body?

A

-Ve chronotropic affect on heart (B1)
-Ve Isotropic affect on heart (B1)
Bronchoconstriction can happen (B2)

68
Q

Bisoprolol is often used when a patient is asthmatic when the heart is too fast, why is this the case?

A

Its cardio selective so only affects B1 receptors
Means that bronchoconstriciton is less likely

69
Q

What is an example of an alpha adrenoreceptor antagonist and what receptor does it work on?

A

Prazosin (doxazosin too)
On A1 receptor

70
Q

What is Prazosins mechanism of action as an A1 adrenoreceptor antagonist?

A

Inhibits Noradrenalines action on the A1 receptors of vascular smooth muscle causing VASODILATION

71
Q

What is Angina?

A

When O2 supply to the heart does meet its requirements so some ischaemia of the heart occurs causing pain

72
Q

When do you normally feel the pain with stable angina?

A

Upon exercise/exertion due to increase O2 demand of heart

73
Q

How do organic nitrates cause venous dilation?

A

Organic nitrate forms NO2-
This is reduced to NO (nitric oxide)

74
Q

What blood vessels do organic nitrates/NO (nitric oxide act on?

A

Powerful vasodilator of veins

Likely due to less endogenous nitric oxide in veins

75
Q

On a basic level how does Nitric oxide cause vasodilation of veins?

A

Reduces Intracellular [Ca2+] causing the vascular sm to relax

76
Q

How does the action of nitric oxide causing vasodilation of veins help treat angina?

A

Lowers central venous pressure
Reduces the PRELOAD since less blood returns to the heart (heart fills less so doesn’t contract as hard)
This lowers the hearts demand for Oxygen

Has minimal action on coronary collateral arteries improving O2 supply to heart

77
Q

What are the 2 general principles to treating angina?

A

Reduce workload of heart
Improve blood supply to the heart

78
Q

How can the workload of the heart be decreased to treat angina?

A

Organic nitrates (venodilation)
B-adrenoreceptor blockers (propranolol or bisoprolol)
Ca2+ Channel antagonists (Amlopidine, nicardipine, verapamil and Diltiazem)

79
Q

How can the blood supply to the heart be increased to treat angina?

A

Ca2+ channel antagonists
(Minor affects of organic nitrates)

80
Q

What heart conditions increase risk of thrombus formation?

A

Atrial fibrillation
Acute myocardial infarction
Mechanical prosthetic heart valves

81
Q

What are the anticoagulants that prevent venous thromboembolism?

A

Heparin (inhibits thrombin)
Warfarin (inhibits action of vitamin K)

82
Q

What are 2 anti platelet drugs and when are they typically given?

A

Aspirin
Clopidogrel

Following acute MI or people with high risk of MI

83
Q

What is the definition of a supra-ventricular tachycardia?

A

Tachycardia which arises as a result of problems in the atria or AV node

84
Q

What is the definition of ventricular tachycardia?

A

Tachycardia which arises as a result of problems in the bundle of His, Purkinje fibres or the ventricular myocytes

85
Q

What is the key difference between early after depolarisations and delayed after depolarisations?

A

EAD when an action potential is fired during repolarisation (Hyperkalaemia cause)
DAD when an action potential is fired after repolarisation (High Intracellular Ca2+ cause)

Y1 - CVS (21 decks)

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