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Cardiovascular System > Session 7 > Flashcards

Session 7 Flashcards

1
Q

What is bradycardia?

A

Heart rate too slow (under 60bpm)

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2
Q

What is atrial flutter?

A

Atria beat too quickly

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3
Q

What is atrial fibrillation?

A

Irregular heartbeat due to rapid and irregular beating of the atria.

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4
Q

What is ventricular tachycardia?

A
  • Regular, fast heartbeat

- Improper electrical activity in the ventricles

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5
Q

What is supraventricular tachycardia?

A
  • Abnormally fast, regular heartbeat

- Activity abnormal in upper part of heart (AVN/SAN)

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6
Q

What is ventricular fibrillation?

A
  • Ventricles are quivering and not contracting
  • Cannot pump blood
  • Rapid and erratic heartbeat
  • CARDIAC OUTPUT NEAR 0
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7
Q

What can cause tachycardia?

A
  • Ectopic pacemaker activity
  • Afterdepolarisations
  • Atrial flutter
  • Atrial fibrillation
  • Re-entry loop
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8
Q

What is ectopic pacemaker activity?

A

When damaged myocardium becomes depolarised and spontaneously active

  • All no longer activated by SAN
  • Dominates SAN
  • Can lead to VFib
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9
Q

What are afterdepolarisations?

A

Abnormal depolarisations following an action potential

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10
Q

What are re-entry loops?

A

Electrical activity does not complete a normal circuit, but a circuit that is looping back on itself.

  • Accessory pathways
  • Conduction delays
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11
Q

What can cause bradycardia?

A

Sinus bradycardia:

  • Sick sinus syndrome
  • Fit and healthy people
  • Extrinsic factors

Conduction block:

  • AVN/BoH problems
  • AVN slow conduction due to drugs
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12
Q

What is sick sinus syndrome?

A

Intrinsic SAN dysfunction, where the depolarisation is slow.

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13
Q

What extrinsic factors can cause bradycardia?

A
  • Ca2+ channel blockers
  • Beta-blockers
    Heart beats in sinus rhythm but much slower
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14
Q

What are delayed afterdepolarisations?*

A

Abnormal action potential triggered by preceding action potential

  • Occur when action potential nearly/fully repolarised
  • Associated with high intracellular [Ca2+]
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15
Q

What are early afterdepolarisations?*

A

Abnormal action potential triggered by preceding action potential

  • Can lead to oscillations
  • More likely when action potential prolonged
  • Prolonged QT interbal
  • Common in hypokalaemia as that prolongs action potential
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16
Q

What re-entry mechanisms generate arrhythmias?*

A
  • Incomplete conduction damage
  • Excitation takes a longer route to avoid the damage, but conduction may be able to go UP the area of damage allowing conduction in the wrong way
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17
Q

Why does a complete block of conduction not generate an arrhythmia this way?*

A
  • Nothing can get through, up or down
  • Has to take the longer route as fibroblasts do not conduct
  • Nothing goes the wrong way
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18
Q

What happens when there are too many re-entrant circuits in the atria?*

A
  • AFib
  • There are many impulses in the atria rather than one rhythm from the SAN
  • Random depolarisation
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19
Q

How does this appear on an ECG?

A
  • Irregular rhythm

- No P waves

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20
Q

What is AV nodal re-entry?*

A
  • 2 pathways rather than one: 1 slow, 1 fast
  • 2 pathways = more depolarisation and therefore a re-entry loop

= SUPRAVENTRICULAR TACHYCARDIA

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21
Q

What is ventricular pre-excitation?*

A
  • There is an accessory/extra pathway that allows depolarisation from AVN to flow
  • Creates re-entry loop

= WOLFF-PARKINSON-WHITE SYNDROME

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22
Q

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

A

1) Voltage sensitive sodium channel blockers
2) B-adrenoceptor antagonists
3) Drugs blocking K+ channels
4) Drugs blocking Ca2+ channels

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23
Q

What is an example of a drug that blocks voltage sensitive sodium channels?

A

Lidocaine (IV)

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24
Q

How does lidocaine work?*

A
  • Only blocks Na+v channels when they are in an open or inactive state, so they block damaged depolarised tissue
  • Dissociates rapidly in normal tissue
  • Blocks during depolarisation but is able to dissociate in time for another AP
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25
Q

When is lidocaine used?

A
  • Following MI if patient shows signs of ventricular tachycardia (IV)
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26
Q

Why does lidocaine work?

A
  • Damaged area of myocardium may depolarise automatically
  • Open more Na+ channels
  • Prevents automatic firing
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27
Q

What are examples of B-adrenoceptor antagonists?

A

Propranolol, atenolol (beta-blockers)

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28
Q

How do they work?*

A

Block sympathetic action by acting on B1 adrenoceptors

  • Decrease slope of pacemaker potential
  • Slow conduction at AVN
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29
Q

What are beta-blockers used for?

A
  • Preventing supraventricular tachycardia (slow AVN conduction)
  • Reducing cardiac output in tachycardia
  • Reducing myocardial ischaemia due to low O2 demand
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30
Q

Why are beta-blockers often used in MIs?

A
  • MIs often cause increased sympathetic activity (eg. people become pale/sweaty)
  • This may cause arrhythmias
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31
Q

How do drugs that block K+ channels work?*

A
  • Prolong action potential by blocking the channels
  • Therefore lengthen absolute relative refractory period
    = Prevent another AP too soon
32
Q

What are the issues with K+ channel blockers?

A
  • Prolong QT interval
  • May predispose to EAD
  • Can be pro-arrhythmic
33
Q

What is an exception of K+ blockers that’s not pro-arrhythmic?

A

AMIODARONE

  • Also Ca2+ blocker and beta-blocker
  • Treat tachycardia associated with Wolff-Parkinson-White syndrome
  • Suppress ventricular arrhythmias post MI
34
Q

What are some drugs that block Ca2+ channels?

A
  • Verapamil
  • Diltiazem
    (non-dihydropiridine)
35
Q

How do they work?

A
  • Block L-type Ca2+ channels
  • Reduce slope of AP at the SAN
  • Decrease AVN conduction
  • Slow AP
  • Negative inotropy (reduced force of contraction)
  • Some coronary vasodilation
36
Q

How are non-dihydropiridine blockers different from dihydropiridine blockers?

A
  • Not effective in preventing arrhythmias
  • Act on vascular smooth muscle instead
  • Treat systemic vascular resistance and arterial pressure
37
Q

What are some examples of dihydropiridine blockers?

A
  • Amlodipine

- Nicardipine

38
Q

What is adenosine?

A
  • Drug that can be administered intravenously
  • Acts on A1 adenosine receptors at AVN
  • Enhances K+ conductance and hyperpolarises cells
    = stops heart and lets it start again
  • Gi GPCR so low cAMP
39
Q

What kind of drug is adenosine and what is it used to treat?

A
  • Anti-arrhythmic

- Terminates re-entrant SVT

40
Q

What are ACE-inhibitors?*

A

Drugs that inhibit the action of the angiotensin converting enzyme that converts angiotensin I to angiotensin II (physiologically active form)

41
Q

What is an example of an ACE-i?

A

Perindopil

42
Q

What are the actions of angiotensin II?

A
  • Acting on kidneys to increase Na+ and water reabsorption
  • Causes vasoconstriction
  • Causes aldosterone release which stimulates Na+ reabsorption
43
Q

When are ACEi used and why?

A
  • Treatment of hypertension and heart failure
  • Prevent fluid retention
  • Reduce vasoconstriction so blood is easier to pump
44
Q

Why can some people not tolerate ACEi?

A

Excess bradykinin can cause a dry cough.

45
Q

How do ACEi treat heart failure?

A
  • Decrease vasomotor tone (+ blood pressure)
  • Reduce afterload and preload of heart
  • Decrease fluid retention so reduce pulmonary oedema
    = Reduce workload of heart
46
Q

What are angiotensin II receptor blockers and when are they used?

A
  • Prevent angiotensin from binding to its receptors
  • Used in treatment of heart failure and hypertension in patients who cannot tolerate ACEi
  • AT1 receptor blockers
47
Q

What are loop diuretics?

A

Drugs that increase the amount of fluid lost in the kidneys (loop of Henle) by reducing the sodium content

48
Q

What are loop diuretics used to treat?

A
  • Heart failure
  • Hypertension
  • Congestive heart failure
  • Reduces pulmonary and peripheral oedema
49
Q

What are some diuretics?

A
  • Furosemide (loop)

- Thiazide

50
Q

How do dihydropyridine Ca2+ channel blockers act on vascular smooth muscles?

A
  • Reduce peripheral resistance
  • Prevents Ca2+ entry into smooth muscle cells
  • Reduces contraction and therefore TPR
  • Decrease workload by decreasing afterload
  • Decrease arterial blood pressure
51
Q

What are positive inotropes?

A

Drugs that increase contractility and cardiac output

52
Q

What are examples of positive inotropes?

A
  • Digoxin

- Dobutamine

53
Q

How do cardiac glycoside positive inotropes work and what are they used to treat?

A

DIGOXIN

  • Treat heart failure
  • Act by blocking Na/K ATPase
54
Q

Why are cardiac glycosides not great?

A

They make the heart work harder

  • Improves symptoms
  • Not good for long term outcomes
55
Q

What is the mode of action of cardiac glycosides?*

A
  • Block Na/K ATPase so that sodium builds up in the cell
  • Ca2+ extruded by NCX which has diminished activity due to rise in intracellular Na+
  • Rise of Na+ (main) and Ca2+ in cell SR stores
  • More Ca2+ = POSITIVE INOTROPY
56
Q

How do cardiac glycosides act on the heart rate?*

A
  • Increase vagal activity via CNS

- Higher vagal activity slows HR and AVN conduction

57
Q

When are cardiac glycosides used?

A

Heart failure treatment when there is an arrhythmia (eg. AF)

58
Q

What is dobutamine and how does it act?

A
  • Selective B1 adrenoceptor agonist

- Acts by stimulating B1 receptors at SAN and AVN on ventricular myocytes

59
Q

When are B1 adrenoceptor agonists used?

A
  • Cardiogenic shock (heart not pumping enough blood)

- Acute reversible heart failure

60
Q

What are the best treatments for heart failure?

A

ACEi, Beta blockers and diuretics
- reduce workload of heart

Cardiac glycosides will make the heart give up quicker by making it work harder

61
Q

What is angina?

A
  • Reduced oxygen supply to the heart so needs are not met
  • Limited duration so myocytes don’t die
  • Ischaemia causes chest pain (exertion)
62
Q

What is used in the treatment of angina?

A

Organic nitrates

63
Q

How do organic nitrites work?

A
  • React with thiols in vascular smooth muscles
  • Cause NO2 release
  • NO2 reduced to NO
  • NO released endogenously from endothelial cells to keep vessels open anyway (powerful vasodilator)
64
Q

What forms are used ?

A

Glycerol trinitrate spray under tongue (short acting)

65
Q

What do organic nitrites act on?

A

Veins, NOT arterioles (very little effect on arteries)

66
Q

How does nitric oxide cause vasodilation?*

A
  • NO activates guanylate cyclase in vascular smooth muscle cells
  • GTP converted to cGMP
  • Activates PKG
  • Lowers intracellular Ca2+ concentration
    = Relaxation of vascular smooth muscle
67
Q

What is the primary action of organic nitrates?*

A
  • Acts on venous system to lower preload
  • Reduces workload of heart
  • Filling less so lower force of contraction and less O2 needed (Starling’s law)
68
Q

What is the secondary action of organic nitrates?

A
  • Act on coronary collateral ARTERIES

- Improves O2 delivery to myocardium

69
Q

Why don’t organic nitrates dilate arterioles?***

A
  • Local mediators already cause full dilation
  • If bloodflow where there is no plaque is increased too, that may make situation worse
  • Dilating COLLATERALS only increases flow to ischaemic area a little
70
Q

Why do collateral arteries not make a massive contribution?

A

There are not many collaterals in end arteries

71
Q

What is used to reduce workload of heart in angina?

A
  • Organic nitrates (venodilation)
  • B-adrenoceptor blockers
  • Ca2+ channel antagonists
72
Q

What drugs are used to improve blood supply to the heart in angina?

A
  • Ca2+ channel antagonists

- Minor organic nitrates

73
Q

When are antithrombotic drugs used?

A

When there is an increased risk of thrombus formation

  • AF (stagnant blood)
  • Acute MI
  • Mechanical prosthetic heart valves
74
Q

What are anticoagulants?

A

Antithrombotic drugs that prevent venous thromboemboli

75
Q

What is heparin?

A

Anticoagulant that inhibits thrombin (IV or subcutaneous injection if fractionated)

76
Q

What is warfarin?

A

Anticoagulant given orally that antagonises Vit K action (reduces formation of Vit K dependent clotting factors)

77
Q

What are antiplatelet drugs?

A
  • Drugs that prevent clots forming on the arterial side

- Aspirin and clopidogrel (following acute MI)

Cardiovascular System (11 decks)

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