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Y2 Pharmacology and Therapeutics > Drugs and the cardiovascular system: The heart > Flashcards

Drugs and the cardiovascular system: The heart Flashcards

1
Q

What is the primary pacemaker of the heart and how does it carry out its function

A

Cells of the sinoatrial node (SAN)
They have no true resting potential and generate regular, spontaneous action potentials
The depolarising current is carried into the cell by relatively slow Ca2+ currents
There are no fast sodium channels and currents in SAN cells

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2
Q

Which channels are involved in action potential generation in the SAN

A

If - hyperpolarization-activated cyclic nucleotide–gated (HCN) channels

Ica (T or L) – Transient T-type Ca++ channel or Long Lasting L-type Ca++ channel

IK – Potassium K+ channels

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3
Q

What are the changes made with sympathetic and parasympathetic system to regulate heart rate

A

Sympathetic - ↑ cAMP, ↑ If + Ica

Parasympathetic - ↓ cAMP, ↑ IK

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4
Q

Describe the mechanism that is involved in regulating contractility

A
  1. Action potential enters from adjacent cells
  2. Voltage-gate Ca2+ channels open and Ca2+ enters the cell
  3. Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR)
  4. Local release causes Ca2+ spark
  5. Summed Ca2+ sparks creates a Ca2+ signal
  6. Ca2+ ions bind to troponin to initiate contraction
  7. Relaxation occurs when Ca2+ unbinds from troponin
  8. Ca2+ is pumped back into the sarcoplasmic reticulum for storage
  9. Ca2+ is exchanged with Na+
  10. Na+ gradient is maintained by Na/K ATPase
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5
Q

What is the free Ca2+ in a cardiac twitch produced by

A

Depolarization-induced influx of Ca2+ current (ICa) through the L-type channels (20–25%)

The release of Ca2+ through the RyRs (75–80%)

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6
Q

Describe the mechanisms regulating myocardial oxygen

demand (HR increase)

A

Myocyte contraction is the primary determinant of myocardial oxygen demand

Increase in HR -> more contractions

Increase in afterload or contractility -> greater force of contraction

Increase in preload -> small increase in force of contraction

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7
Q

Which drugs influence heart rate and what do they do

A

β-blockers – Decrease If and Ica

Calcium antagonists – Decrease Ica

Ivabradine – Decrease If

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8
Q

Which drugs influence contractility and what do they do

A

β-blockers – Decrease contractility

Calcium antagonists – Decrease Ica

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9
Q

What are the two classes of calcium antagonists and give examples

A

Rate slowing (cardiac and smooth muscle actions)
Phenylalkylamines (e.g. Verapamil)
Benzothiazepines (e.g. Diltiazem)

Non-rate slowing (smooth muscle actions - more potent)
Dihydropyridines (e.g. amlodipine)

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10
Q

What is the effect of non-rate slowing calcium antagonists on the heart

A

No effect on the heart. Profound vasodilation can lead to reflex tachycardia

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11
Q

Which drugs influence oxygen supply/demand and how do they work

A

Organic nitrates e.g. NO
Potassium channel opener

NO promotes K+ channel opening, and therefore efflux and hyper polarisation
Also promotes relaxation
Increases coronary blood flow and therefore increases preload and afterload

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12
Q

What two different effects of nitrates/potassium channel openers influence preload and afterload

A 
Vasodilation = ↓ afterload
Venodilation = ↓ preload
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13
Q

Which drugs are used to treat stable angina

A

1st - beta blocker/calcium channel blocker
2nd - combination or switch
3rd - long-acting nitrate, ivabradine, nicorandil

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14
Q

What are the side effects of non-selective beta blockers

A

Worsening heart failure
CO reduction
Increase vascular resistance
Bradycardia
Heart block - decreased conduction through AV node
Cold extremities
(fatigues, impotence, depression, CNS effects)

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15
Q

What are the side effects of beta blockers that block beta 2 receptors

A

Beta 2 receptor blockade will reduce vasodilation and increase TPR which can worsen heart failure.

Pindolol will have some beta 2 stimulating effects due to ISA or carvedilol with alpha 1 blocking effects can decrease TPR and alleviate this problem.

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16
Q

Why are cold extremities a side effect of beta blockers

A

Cold extremities
Loss of β2 receptor mediated cutaneous vasodilation in
extremities

17
Q

What are the side effects of verapamil

A

Bradycardia and AV block (Ca2+ channel block)

Constipation (Gut Ca2+ channels) – 25 % patients

18
Q

What are the side effects of dihydropyridine

A

Ankle Oedema – vasodilation means more pressure on capillary vessels
Headache / Flushing – vasodilation
Palpitations
Vasodilation/reflex adrenergic activation (from the reflex sympathetic response)

19
Q

What are the aims of rhythm disturbances treatment

A

Reduce sudden death
Prevent stroke
Alleviate symptoms

20
Q

How are arrhythmias classified based on site of origin and give examples of drugs used for each

A

Supraventricular arrhythmias (e.g. amiodarone, verapamil)

Ventricular arrhythmias (e.g. flecainide, lidocaine).

Complex (supraventricular + ventricular arrhythmias) (e.g. disopyramide).

21
Q

What is the Vaughan Williams classification

A

Mechanism of classifying anti-arrhythmic drugs.
Class I - Sodium channel blockers
Class II - Beta adrenergic blockade
Class III - prolongation of depolarisation
IV - Calcium channel blockers

22
Q

What is adenosine used for

A

Anti-Arrhythmics
Used intravenously to terminate supraventricular tachyarrhythmias (SVT).
Its actions are short-lived (20-30s) and it is consequently safer than verapamil.

23
Q

What is verapamil used for and what is the mechanism of action

A

Reduction of ventricular responsiveness to atrial arrythmias

Depresses SA automaticity and subsequent AV node conduction

24
Q

What is amiodarone used for

A

Supraventricular and ventricular tachyarrhythmias (often due to re-entry)

Used for arrhythmias when other drugs are ineffective or contraindicative

25
Q

What is digoxin used for

A

Atrial fibrillation and flutter lead to a rapid ventricular rate that can impair ventricular filling (due to decreased filling time) and reduce cardiac output.

Digoxin via vagal stimulation reduces the conduction of electrical impulses within the AV node. Fewer impulses reach the ventricles and ventricular rate falls.

26
Q

What are the adverse effects of digoxin

A

dysrhythmias (e.g. AV conduction block, ectopic pacemaker activity)

27
Q

Hypokalaemia (usually a consequence of diuretic use) lowers the threshold for digoxin toxicity. Why?

A

-

28
Q

What is phase 4 in heart rate regulation

A

The spontaneous depolarization (pacemaker potential) that triggers the action potential

29
Q

What influences the myocardial oxygen supply

A

Coronary blood flow

Arterial oxygen content

30
Q

What influences myocardial oxygen demand

A

Heart rate
Preload
Afterload
Contractility

31
Q

Which drugs can be used to alleviate side effects of beta blockers

A

Non-selective beta blockers that have equal affinity for b1 and b2 receptors e.g. pindolol
Intrinsic sympathetic activity

Mixed beta-alpha blockers
e.g. Carvedilol
Alpha blockade gives additional vasodilator properties

32
Q

What is the mechanism of action for cardiac glycosides such as digoxin

A
  1. Inhibition of the Na-K-ATPase
  2. Results in increased intracellular Ca2+ via effects on Na+/Ca2+ exchange
  3. Leads to a positive inotropic effect
  4. Central vagal stimulation causes an increased refractory period and reduced rate of conduction through the AV node
33
Q

What is the mechanism of action for amiodarone

A

Complex action probably involving multiple ion channel block

34
Q

What are the adverse effects amiodarone

A

Amiodarone accumulates in the body (t½ 10 - 100days)

Photosensitive skin rashes
Hypo- or hyper-thyroidism
Pulmonary fibrosis

Y2 Pharmacology and Therapeutics (34 decks)

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