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Cardiovascular System > Lecture 9.2: Action of Drugs on the CVS > Flashcards

Lecture 9.2: Action of Drugs on the CVS Flashcards

1
Q

What Conditions are Cardiovascular Drugs used to Treat? (5)

A
  • Arrhythmias
  • Heart Failure
  • Angina
  • Hypertension
  • Risk of Thrombus Formation
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2
Q

What Factors are Cardiovascular Drugs able to alter? (4)

A
  • The rate and rhythm of the heart
  • The force of myocardial contraction
  • Peripheral resistance and blood flow
  • Blood volume
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3
Q

Drugs influence the Heart in different ways: Inotropy

A
  • Contractility
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4
Q

Drugs influence the Heart in different ways: Chronotropy

A
  • Heart Rate
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5
Q

Drugs influence the Heart in different ways: Dromotropy

A
  • Electrical Conduction
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6
Q

Drugs influence the Heart in different ways: Lusitropy

A
  • Relaxation
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7
Q

What is the key cellular event in muscle contraction?

A

An increase in intracellular Calcium (Ca2+)!!

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8
Q

Cardiac Muscle Contraction and Relaxation (8 Steps)

A

1) Rapid depolarisation occurs when fast‐.
opening Na + channels in the sarcolemma
open and allow an influx of Na + ions into the
cardiac muscle cell (Na + channels close)
2) A plateau phase occurs during which Ca 2+
enters the cytosol of the muscle cell from
sarcoplasmic reticulum and also from outside
the cell through slow‐opening Ca2+ channels
in the sarcolemma
3) Within the cell, Ca2+ binds to troponin
4) This triggers the cross‐bridge binding that
leads to the sliding of actin filaments past
myosin filaments
5) The sliding of the filaments produces cell
contraction
6) At the same time that the Ca2+ channels
open, K+ channels, which normally leak small
amounts of K+ out of the cell, become more
impermeable to K+ leakage
7) Re-polarisation occurs as K + channels open
and K + diffuses out of the cell. At the same
time, Ca 2+ channels close
8) A refractory period follows, during which.
concentration of K + and Na + are actively
restored to their appropriate sides of the.
sarcolemma by Na +/K + pumps

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9
Q

Bradycardia

A

Abnormally Slow Heart Rate

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10
Q

Tachycardia

A

Abnormally Fast Heart Rate

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11
Q

Atrial Flutter

A

It occurs when a short circuit in the heart causes the upper chambers (atria) to pump very rapidly

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12
Q

Atrial Fibrillation

A

The atria beat irregularly

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13
Q

Ventricular Tachycardia

A

It occurs when the lower chamber of the heart beats too fast to pump well and the body doesn’t receive enough oxygenated blood

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14
Q

Supraventricular Tachycardias

A

Supraventricular tachycardia (SVT) is as an irregularly fast or erratic heartbeat (arrhythmia) that affects the heart’s upper chambers (atria)

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15
Q

Ventricular Fibrillation

A

The ventricles beat irregularly

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16
Q

Inappropriate Sinus Tachycardia

A

Characterised by a sinus heart rate inexplicably higher than one hundred beats per minute (bpm) at rest

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17
Q

Ectopic Pacemaker Activity

A

An excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart

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18
Q

Afterdepolarisations

A
  • Abnormal depolarisations following the action
    potential
  • Anything which prolongs the duration of the
    action potential can allow afterdepolarisations
    to occur
  • Can cause a premature AP to fire
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19
Q

Re-Entry Loop

A
  • Reentry describes a self-sustaining cardiac
    rhythm abnormality (several of these can lead
    to AF)
  • In reentry, the action potential propagates in a
    circus-like closed loop manner
  • Conduction Delay
  • Accessory Pathway
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20
Q

What is Wolff-Parkinson-White Syndrome?

A
  • A relatively common heart condition that
    causes the heart to beat abnormally fast for
    periods of time
  • The cause is an extra electrical connection in
    the heart
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21
Q

Pathophysiology of Wolff-Parkinson-White Syndrome

A

An extra electrical pathway between your heart’s upper chambers (atria) and lower chambers (ventricles) causes a rapid heartbeat (tachycardia)

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22
Q

What are the basic classes of anti-arrhythmic
drugs? (4/5 Classes)

A
  • Class I: Drugs that block voltage-sensitive
    sodium channels
  • Class II: Antagonists of β-adrenoceptors
  • Class III: Drugs that block potassium channels
  • Class IV: Drugs that block calcium channels
  • Class V: Drugs that don’t fit the first 4 classes
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23
Q

Class I Anti-Arrhythmic Drugs: Mechanism? Examples?

A
  • Only blocks voltage gated Na+ channels in
    open or inactive state
  • Dissociates rapidly in time for next AP
  • Typical example is the local anaesthetic
    lidocaine
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24
Q

When is Lidocaine Used? Why does it work?

A
  • Sometimes used following MI if patient shows
    signs of ventricular tachycardia
  • Damaged areas of myocardium may be
    depolarised and fire automatically
  • More Na+ channels are open in depolarised
    tissue
  • Lidocaine blocks these Na+ channels
  • Prevents automatic firing of depolarised
    ventricular tissue
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25
Q

Class II Anti-Arrhythmic Drugs: Mechanism? Examples?

A
  • Block sympathetic action
  • Act at β1-adrenoreceptors in the heart
  • Decrease slope of pacemaker potential in SA
  • Examples: propranolol, atenolol (β-blockers)
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26
Q

When is β-blockers Used? Why does it work?

A
  • Used following an MI
  • MI causes increased sympathetic activity,
    arrhythmias may be partly due to increased
    sympathetic activity
  • β-blockers prevent ventricular arrhythmias
  • Also reduces O2 demand (thus reduces
    myocardial ischaemia)
  • β-blockers slow conduction in AV node (thus
    prevent supraventricular tachycardias)
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27
Q

Class III Anti-Arrhythmic Drugs: Mechanism? Examples?

A
  • Prolong the action potential, mainly by blocking
    K+ channels
  • This lengthens the absolute refractory period
  • Prevents another AP occurring too soon (in
    theory)
  • Amiodarone, sotalol, dofetilide, and ibutilide
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28
Q

Why are Class III Anti-Arrhythmic Drugs often not used?

A
  • Not generally used because they can be also
    be pro-arrhythmic
29
Q

What is the Class III Anti-Arrhythmic Drug that is NOT pro-arrhythmic?

A

Amiodarone

30
Q

What is Amiodarone used to treat?

A

Used to treat tachycardia associated with
Wolff-Parkinson-White syndrome (re-entry loop
due to an extra conduction pathway)

31
Q

Class IV Anti-Arrhythmic Drugs: Mechanism? Examples?

A
  • Drugs that block Ca2+ channels
  • Decreases slope of pacemaker action potential
    at SA node
  • Decreases AV nodal conduction
  • Decreases force of contraction (negative
    inotropy)
  • Also cause some coronary and peripheral
    vasodilation
32
Q

Dihydropyridine vs Non-Dihydropyridine Ca2+ Channel Blockers?

A
  • Dihydropyridine: predominantly peripheral
    vasodilatory actions, block calcium channels
    located in the muscle cells of the heart and
    arterial blood vessels, thereby reducing the
    entry of calcium ions into the cell
  • Non-Dihydropyridine: significant SA and AV
    node depressant effects and possible
    myocardial depressant effects with lesser
    amounts of peripheral vasodilation
33
Q

Adenosine as an Anti-Arrhythmic Drug: Where is it produced?

A

Produced Endogenously

34
Q

Adenosine as an Anti-Arrhythmic Drug: How does it work?

A
  • Acts on A1 receptors at AV node
  • Enhances K+ conductance
  • Hyperpolarises cells of conducting tissue
  • Stops heart momentarily & resets the
    rhythm
35
Q

What is Heart Failure?

A

Chronic failure of the heart to provide sufficient output to meet the body’s requirements

36
Q

What are some Common Features of Heart Failure? (4)

A
  • Reduced force of contraction
  • Reduced cardiac output
  • Reduced tissue perfusion
  • Oedema – from back pressure
37
Q

What does the Frank–Starling Law state?

A

The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant

38
Q

What are the 3 Types of Drugs used to Treat Heart Failure?

A
  • β-Adrenergic Agonists (+ve inotropes increase
    cardiac output)
  • Cardiac Glycosides (+ve inotropes increase
    cardiac output)
  • ACE Inhibitors (reduce work of heart)
39
Q

How do ACE Inhibitors work?

A
  • Inhibit the action of angiotensin converting
    enzyme (prevent conversion of angiotensin I to
    angiotensin II)
  • Aldosterone acts on the kidneys to increase
    Na+ and water reabsorption
  • Decrease vasomotor tone (↓ blood
    pressure)
  • Reduce after-load of the heart
  • Decrease fluid retention (↓ blood volume)
  • Reduce preload of the heart
  • Reduce work load of the heart
40
Q

Why is is important that ACE-Inhibitors prevent the conversion of angiotensin I to angiotensin II?

A
  • Angiotensin II is also a vasoconstrictor
  • Thus increases vasomotor tone (increased BP)
41
Q

What other type of drugs have a similar effect as ACE-Inhibitors?

A

Angiotensin II Receptor Blockers (ARBs)
E.g. Losartan

42
Q

Examples of ACE-Inhibitors (3)

A
  • Benazepril
  • Ramipril
  • Lisinopril
43
Q

How do β–adrenoceptor antagonists (β-blockers) work?

A
  • Beta blockers work by blocking the effects of
    the hormone epinephrine, also known as
    adrenaline
  • Act as Diuretics (as adrenaline increased water
    reabsorption, blocking it means more urine
    output)
  • Reduce blood volume
  • Cause the heart to beat more slowly and with
    less force, which lowers blood pressure
44
Q

How do Cardiac Glycosides work?

A
  • They increase myocardial contractility
    (ionotropy) and output force of the heart
  • They do this by acting on the cellular sodium-
    potassium ATPase pump
  • Block Na+/K+ ATPase
  • Increase in Na+ concentration inside the
    cells leads to an inhibition of the Na+/ Ca2+
    exchanger
  • Increase Ca2+ concentration inside cardiac
    myocytes
  • Positive inotropic effect
  • Increased force of contraction
45
Q

What else are Cardiac Glycosides used to treat?

A

Atrial Fibrillation

46
Q

Examples of Cardiac Glycosides

A

Digitoxin (derivatives of foxglove)

47
Q

What is the Action of Cardiac Glycosides on Heart Rate?

A
  • Chronotropy
  • Cardiac glycosides also cause increased vagal
    activity
  • Action via central nervous system
  • Slows AV conduction
  • Slows the heart rate
48
Q

How do β–adrenoreceptor agonists work? What are they used to treat?

A

increase myocardial
contractility and speed of relaxation

49
Q

What is Angina (Myocardial Ischaemia)?

A
  • Occurs when O2 supply to the heart does not
    meet its need
  • Chest Pain
  • Usually pain with exertion
  • Due to narrowing of the coronary arteries,
    atheromatous disease
50
Q

Treating Angina: What Drugs work to reduce the work load of the heart?

A
  • ACE inhibitor / ARB
  • β-adrenoceptor blockers
  • Ca2+ channel antagonists
  • Organic nitrates
  • If channel blockers (slow pacemaker)
51
Q

Treating Angina: What Drugs work to improve the blood supply to the heart?

A

Ca2+ channel antagonists

52
Q

Treating Angina: What Drugs reduce Cholesterol?

A

Statins

53
Q

Treating Angina: Surgery

A
  • Angiography
  • +/- stents
  • Revascularise
54
Q

Action of Organic Nitrates

A
  • Reaction of organic nitrates with thiols (-SH
    groups) in vascular smooth muscle causes
    nitrite (NO2-) to be released
  • NO2- is reduced to NO
  • NO is a powerful vasodilator
  • Venodilation reduces venous pressure and
    the return of blood to the heart
  • This reduces the work of the heart
55
Q

Examples of Organic Nitrates (3)

A
  • Glyceryl Trinitrate (GTN)
  • Isosorbide Mononitrate (ISMN)
  • Isosorbide Dinitrate
56
Q

How does NO cause Vasodilation?

A
  • NO activates guanylate cyclase
  • Increases cGMP
  • Lowers intracellular [Ca2+]
  • Causes relaxation of vascular smooth muscle
57
Q

How does this vasodilation (due to NO) help alleviate symptoms of Heart Failure?: Primary Action

A
  • Action on venous system venodilation lowers
    preload
  • Reduces work load of the heart
  • Heart fills less therefore force of contraction
    reduced (Starling’s Law)
  • This lowers O2 demand
58
Q

What is Preload?

A

Preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole

59
Q

How does this vasodilation (due to NO) help alleviate symptoms of Heart Failure?: Secondary Action

A
  • Action on coronary arteries improves O2
    delivery to the ischaemic myocardium
  • Acts on collateral arteries rather than arterioles
60
Q

What conditions carry an increased risk
of thrombus formation? (3)

A
  • Atrial Fibrillation
  • Acute Myocardial Infarction
  • Mechanical Prosthetic Heart Valves
61
Q

Antithrombotic Drugs: Anticoagulants (target clotting cascade) Examples (4)

A
  • Heparin (given intravenously)
  • Fractionated Heparin (subcutaneous injection)
  • Fondaparinux
  • Warfarin (given orally)
62
Q

How does Heparin work?

A
  • Inhibits thrombin
  • Used acutely for short term action
63
Q

How does Warfarin work?

A
  • Blocks activation/recycling of vitamin K (vitamin
    K epoxide reductase complex 1 inhibitor)
  • This Inhibits synthesis of hepatic clotting
    factors II, VII, IX and X
  • Can be used long term
64
Q

Antithrombotic Drugs: Novel Oral Anticoagulants (NOAC) Examples (2)

A
  • Thrombin Inhibitor (Dabigatran)
  • Factor Xa Inhibitors (Apixaban, Rivaroxaban)
65
Q

Antithrombotic Drugs: Antiplatelet Drugs Examples (3)

A
  • Aspirin (following acute MI/high risk of MI)
  • Dipyridamol (phosphodiesterase inhibition)
  • Clopidogrel (inhibits ADP dependant platelet
    aggregation)
66
Q

Mineralocorticoid Receptor Antagonists MoA

A
  • Decrease the aldosterone effect by binding to
    the mineralocorticoid receptor inhibiting
    aldosterone
  • This leads to higher levels of potassium in
    serum and increased sodium excretion
  • Resulting in decreased body fluid and lower
    blood pressure
67
Q

Examples of Mineralocorticoid Receptor Antagonists

A

Spironolactone and Eplerenone

68
Q

I(f) Channel Blockers MoA

A

Cardiovascular System (19 decks)

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