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CVRS > 2.2 CVS Pharmacology (1 + 2) > Flashcards

2.2 CVS Pharmacology (1 + 2) Flashcards

1
Q

What are the aims of CVS drug therapy? (5)

A
  • Enhance systolic function
  • Enhance diastolic function
  • Ensure optimal cardiac rate and rhythm
  • Optimise distribution of fluid within the circulation
  • Counteract effects of detrimental neurohormonal activities
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2
Q

What cardiac functions can be manipulated pharmacologically?

A

Heart rate
Heart rhythm
Cardiac muscle contractility

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3
Q

What is the effect of noradrenalin on cardiac muscle cells?

A

Inhibits phosphodiesterase
cAMP not broken down
Increased action of protein kinase A
Increased [Ca2+]i

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4
Q

Describe ion handling in cardiac myocytes

A
  • Ca2+ influx balanced by efflux via Ca2+/Na+ exchange
  • Na+ extruded in exchange for K+ by the Na+/K+/ATPase
  • Changes in [Na+]i affect [Ca2+]i
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5
Q

List the targets for drugs acting on cardiac muscle

A

1) Receptors (e.g. M2, B1 adrenoreceptors)
2) Ion channels (e.g. fast Na+ channels, slow Ca2+ channels, K+ channels)
3)Cardiac muscle cell enzymes (e.g. Na+/K+ ATPase, PDE)

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6
Q

What are the effects of a sustained increase in HR?

A
  • Increased myocardial O2 consumption
  • Reduced time for ventricular filling
  • Reduced time for coronary blood flow
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7
Q

List the drugs that slow HR (negative chronotropes)

A
  • Muscarinic (M) receptor agonist
  • Drugs that act centrally to increase vagal tone - cardiac glycosides
  • 𝛃 adrenoceptors antagonists
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8
Q

List the drugs that increase HR (positive chronotropes)

A
  • Muscarinic receptor antagonists
  • 𝛃 adrenoceptor agonists
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9
Q

Describe the use of B adrenoceptor antagonists as drugs that slow heart rate

A

Particularly effective in hearts driven by high sympathetic tone

Also reduces the force of contraction of ventricular muscle (which may have negative effects)

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10
Q

Describe when B adrenoceptor agonists may be used as drugs that increase heart rate

A

Non-selective agonists increase heart rate more than B1-selective drugs

Causes vasodilation (particularly in skeletal muscle) B2 effect

Used in emergency of complete (3rd degree) cardiac block

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11
Q

Describe when muscarinic receptor antagonists as drugs that increase heart rate might be used

A

Premedication for anaesthesia and surgery, particularly when vagal stimulationn and slowing of the heart is a potential problem

Treatment of bradycardia (incomplete heart block)

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12
Q

What are the actions of the 4 classes of commonly used antidysrhythmic drugs?

A

Class I: Block voltage-dependant Na+ channels
Class II: Antangonise 𝛃 adrenoceptors
Class III: Unknown mechanism
Class IV: Inhibits Ca2+ channels

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13
Q

Describe class I antidysrhythmic drugs

A

Block voltage-dependant Na+ channels
-Decreased rate and magnitude of depolarisation
-Reduced conduction in non-nodal tissues (e.g. purkinje fibres)

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14
Q

Describe class II antidysrhythmic drugs

A

Antagonise 𝛃 adrenoceptors
-Reduce excessive sympathetic tone that may cause arrhythmias

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15
Q

Describe Class III antidysrhythmic drugs

A

Mechanism not yet understood
-Involves blockade of K+ channels involved in cardiac repolarisation
-Emergency use in vet med

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16
Q

Describe class IV antidysrhythmic drugs

A

Reduce plateau current, shorten action potential, negative isotropic effect

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17
Q

List the types of drugs that increase cardiac muscle contractility (positive isotropes)

A

Cardiac glycosides
Phsophodiesterase (PDE) inhibitors
Benzimidazole derivatives
Sympathomimetric drugs

18
Q

Explain how cardiac glycosides increase muscle contractility

A

Glycoside inhibits Na+/K+ exchange
Increased [Na+]i
Decreased Na+/Ca2+ exchange
Increased [Ca2+]i
Increased force of contraction

19
Q

Explain how PDE inhibitors increase muscle contractility

A

PDE inhibited
Increased cAMP
Increased force of contraction

20
Q

Explain how benzimidazole derivatives increase mucle contractility

A

Increases Ca2+ sensitivity of cardiac myofibrils
Inhibits types III cAMP-phosphodiesterase

21
Q

What is vascular tone maintained by?

A

Balance between opposing actions of neurotransmitters, hormones, and mediators that have vasoconstrictor and vasodilator properties

22
Q

Which mediators have vasoconstrictor properties?

A

Noradrenaline / Adrenaline (𝛃 adrenoceptors)
Prostacyclin (PGl2)
NO
Atrial natriuretic peptide (ANP)

22
Q

Which mediators have vasoconstrictor properties?

A

Noradrenaline / Adrenaline (𝛂 adrenoceptors)
ATP
Angiotensin II
Vasopressin (ADH)
Endohelin
TxA2
ADP

23
Q

What mediators have vasodilator properties?

A

Noradrenaline / Adrenaline (𝛃 adrenoceptors)
Prostacyclin (PGl2)
NO
Atrial natriuretic peptide (ANP)
Adenosine

24
Q

Why is the sympathetic system important in the vasculature?

A

Can control contraction/dilation of blood vessels
Helps contribute to arterial BP control

25
Q

What targets for drugs acting on the vasculature are there?

A

Membrane receptors
Cell membrane ion channels
Smooth muscle cell enzymes
Enzymes generating or inactivating vasoconstrictors/dilators

26
Q

What do arterial dilators act on? How do these work?

A

Arterioles
Reduce afterload
Cause an increase in SV
Decreases myocardial O2 consumption
Eventually decreases preload

27
Q

What do venodilators act on? How do these work?

A

Veins
Reduce preload by β€˜trapping’ blood in the venous circulation

28
Q

What are the three targets for drugs which interfere with natural vasoconstrictors?

A

Sympathetic nervous system
RAAS
Endothelin-I

29
Q

What vasodilator drugs act on the symapthetic system?

A

Ξ±1-selective agrenoreceptor agonists

30
Q

How do Ξ±1-selective agrenoreceptor agonists work?

A

Act on venous and arteriole circulation
Best response where sympathetic tone to blood vessels is high
Fall in vascular tone is usually short lived

31
Q

What is renin?

A

Proteolytic enzyme
Secreted by specialised cells in the kidney

32
Q

What is the stimulus for renin release?

A

Renal sympathetic nerve stimulation
Reduced pressure in afferent arteriole
Reduced [NaCl] in distal tubules

33
Q

What is ACE?

A

Angiotensin Converting Enzyme
Non-specific carboxypeptidase that also breaks down bradykinin

34
Q

Where is ACE found?

A

Endothelial cells of lung capillaries

35
Q

What is angiotensin II?

A

One of the most potent vasoconstrictor agent known

36
Q

How does angiotensin II work?

A
  • Enhances salt and water retention (acts via aldosterone)
  • Acts on cardiac muscle to cause hypertrophy (promotes protein synthesis to make heart grow)
  • Increases release of norepinephrine from sympathetic nerves
37
Q

At what points can RAAS be influenced by drugs?

A

Renin release
ACE
AT1 receptors

38
Q

What drugs affect renin release?

A

𝛃-antagonists block renin secretion

39
Q

What is the RAAS

A

Angiotensinogen -(Renin)-> Angiotensin I -(ACE)-> Angiotensin II

40
Q

How is angiotensin production controlled?

A

By controlling renin release:
- reduced glomerular filtration
- Reduced [Na] in distal tube
- 𝛃 antagonist
- 𝛃 agonist

ACE inhibitors

AT1 antagonists

CVRS (18 decks)

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