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ACVECC 2024 > Cardiovascular pharmacology > Flashcards

Cardiovascular pharmacology Flashcards

1
Q

What is considered first line in treating systemic hypertension in dogs?

A

ACEi
e.g. benazepril, enalapril

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2
Q

MOA for ACEi as an anti-hypertensive

A

1) Inhibition of conversion of ATI to ATII => vasodilation, venodilation + reduced plasma volume
2) Decrease proteinuria by causing preferential efferent arteriole constriction
3) Decrease metabolism of bradykinin (vasodilatory agent)

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3
Q

Main adverse effects of ACEi

A

1) Worsen GFR & renal function (due to preferential dilation of efferent arteriole -> reducing glomerular filtration pressure)
Contraindicated in: dehydration, high diuretic therapy usage, severe azotemia
2) Hyperkalaemia through aldosterone inhibition (low clinical relevance)

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4
Q

What are the differences between ARBs (angiotensin receptor blockers) and ACEi?

A

1) ARBs block ability of ATII from activating its receptors regardless of how it’s formed
2) Do not affect bradykinin metabolism

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5
Q

Name an ARB that can be considered a monotherapy in cats with significant proteinuria

A

Telmisartan

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6
Q

Side effects of ARBs

A

Few reported but similar to ACEi

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7
Q

Indication for use of spironolactone

A

1) Anti-hypertensive in hyperaldosteronism
2) potassium sparing diuretic

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8
Q

MOA spironolactone:

A

1) Aldosterone antagonist - bliocking its effects in DCT and CT
- blocks Na + water reterntion
- potassium + acid scretion
2) blocks pro-inflam effects from chronic exposure
3) prevents fibrosis and vascular remodelling (esp. in glomerulus) from chronic exposure

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9
Q

Adverse effect of spironolactone

A

Hyperkalaemia occasionally when used with ACEi, ARBs or beta-blockers

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10
Q

What is the first line anti-hypertensive in cats?

A

Amlodipine besylate.
- a second agent such as ACEi or ARB can be added if refractory

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11
Q

MOA of amlodipine and nicardipine

A

Calcium Channel Blocker - dihydropyridine family: selective for decreasing Ca influx in vascular smooth muscle cells => vasorelaxation + decrease SVR

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12
Q

Side effect of amlodipine

A

1) reflex bradycardia
2) weakness, lethargy
3) reduced appetite
4) increase intraglomerular pressure -> damage to glomerulus + worsen proteinuria

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13
Q

Why is amlodipine not recommended as a lone tx for SHT in dogs?

A

Preferential afferent arteriolar dilation > efferent arteriole
- increase intraglomerular pressure
- damage glomerulus + worsen proteinuria
Concurrent ACEi usage, offsets this effect

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14
Q

What is the mechanism of sympathetic system activation causing SHT?

A
  • alpha-1 activation causing vasoconstriction
  • beta-1 activation: increased HR + contractility
  • Na + water retention
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15
Q

MOA for prazosin and phenoxybenzamine

A

alpha-1 receptor antagonist: promotes vascular smooth muscle relaxation
- adjunct role in SHT management
Main indication: pheochromocytoma

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16
Q

Side effect of alpha-1 antagonists

A
  • excessive hypotension
  • GIT upset
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17
Q

MOA of atenolol and propanolol

A

beta-antagonist (atenolol = beta-1 selective)
- decrease HR + contractility
- decrease renin release + SVR
Cats: adjunct SHT management in hyperT
Dogs: adjunct refractory SHT management secondary to pheochromocytoma (reflex tachycardia control)

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18
Q

Adverse effect of beta-antagonists

A
  • bradycardia
  • hyperkalaemia
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19
Q

What is labetalol

A

Injectable adrenergic antagonist (alpha and beta)
Indication: acute severe hypertension - promote vasodilation + prevent reflex tachycardia

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20
Q

MOA hydralazine

A

Unclear: alters smooth muscle intracellular Ca metabolism => smooth muscle relaxation + decrease SVR

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21
Q

Side effects of hydralazine

A
  • excessive + irreversible hypotension
  • reflex tachycardia
  • Na/water retention
  • GIT upset
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22
Q

MOA of sodium nitroprusside

A

Release of NO: acts of vascular smooth muscle -> decrease intracellular Ca influx + activation of actin/myosin chains + overall contractile force => potent smooth muscle relaxation, decrease vascular tone + SVR

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23
Q

Why is nitroprusside ideal in hypertensive crisis?

A

Injectable, short-half life allows close titration

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24
Q

Side effects of nitroprusside

A
  • concern for cyanide and thiocyanate toxicity after high doses for prolonged periods (signs: metabolic acidosis, depression, stupor, seizures)
  • patients with liver/renal insufficiency more predisposed
  • dramatic hypotension
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25
Q

What can be considered as a substitute for nitroprusside?

A

Nitroglycerine IV: another arteriolar vasodilator
- no concern for cyanide toxicity

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26
Q

MOA of fenoldopam

A

Selective dopamine-1 receptor agonist:
- peripheral + renal vasodilation
- natriuresis
- increase GFR
Further investigation needed for cats & dogs, but first line hypertensive crisis medication in humans (IV, short acting)

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27
Q

MOA of pimobendan (4)

A

Inodilator (positive inotrope + arteriovenous dilation)
1) Calcium sensitisation
- increases binding site affinity for the regulatory site on tropinin C
2) PDE III inhibition
- increase in cAMP in cardiac myocytes -> increase Ca sequestration during diastole + Ca influx in systole (more healthy hearts)
- arterial and venous dilation: increases cAMP and cGMP in vascular smooth muscle -> increase intracellular storage of Ca -> relaxation as less Ca available for contraction
- anti-thrombotic: anti-platelet aggregation through inc. cAMP (maybe)
3) Suppress NO - more contractility, anti-inflam (?)
4) positive lusitropy: enhance left ventricular isovolumetric relaxation

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28
Q

How is pimobendan different from traditional positive inotropic drugs?

A

Does not depend on catecholamines => does not increase myocardial oxygen dependent.
Does not increase intracellular Ca, only sensitisation => does not induce arrhythmias.

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29
Q

When to use pimobedan in cats?

A

Cats in CHF with
- refractory pulmonary oedema
- L ventricular systolic dysfunction
- significant pleural effusion
- azotaemia
Try to avoid in cats with severe LVOTO

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30
Q

Adverse effects of pimobendan

A

GIT (inappetence, vomiting, diarrhoea)
Lethargy

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31
Q

Pharmacokinetics of pimobendan

A
  • Hepatic dimethylation to active metabolite
  • highly protein bound
  • 95% fecally excreted, 5% renal
    Dogs:
  • Oral: max. conc. in 1 hour, increase in systolic function 2-4 hours, lasts for up to 8 hours
  • IV inotropic effect within 5 minutes
    Cats:
  • longer elimination half life
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32
Q

Most effective site of diuretic actions in the kidneys?

A

Loop of Henle: large amount of filtrate delivered to this site + lack of efficient rebasorptive regions distal to this.

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33
Q

MOA of furosemide

A

Loop diuretic: inhibits Na-K-2Cl co-transporter on APICAL membrane of epithelial cells of TAL of loop of Henle
=> dec. Na and Cl re-absorption -> dissipates medullary osmotic gradient
=> inc. distal delivery of Na promotes kaliuresis through Na-K exchange
=> block Cl influx in macula densa: inhibits tubuloglomerular feedback -> avoid antidiuretic counter-regulation in response to tubular loss of solutes

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34
Q

Advantage and disadvantage of torsemide

A

+ve: Loop diuretic
Longer half life (once daily dosing)
Higher bioavaiability
Stronger diuretic effect (5-20x)
-ve: high rate of renal adverse events

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35
Q

Mechanism for decreased furosemide responsiveness

A

1) compensatory increase distal Na reabsorption
=> combining with distal nephron diuretic such as thiazide may help
2) intermittent rebound Na retention
=> CRI or freqent admin may help
Novel: combine with hypertonic saline for refractory CHF: maintain diuresis, less neuro-humoral actival, preserve renal fn.

36
Q

MOA of thiazide diuretics

A

Inhibits NaCl co-transporter on apical membrane of the distal tubule
- Anticalciuretic effects: for Ca containing uroliths
- Combined with furosemide when tolerance is suspected

37
Q

Pharmokinetics of furosemide

A

Onset of action: 5 min
Peak effect: 30min
Duration: 120-180min
Secreted from blood into tubule lumen using an organic ion transport in the PCT

38
Q

List 3 situations where furosemide therapy may need to be increase:

A

1) poor CO -> reduced renal perfusion
2) concurrent NSAID therapy: competition with other organic anions
3) severe hypoalbuminemia: degree of furosemide bound to albumin in circulation

39
Q

MOA of Spironolactone

A

Competitively antagonise aldosterone binding to its receptor on the late DT and collecting ducts => inc. Na, Ca and water excretion + dec. K+ loss

40
Q

What is the main classification system for anti-arrhythmics?

A

Vaughan Williams classification system: grouped by major ion channel or receptor effects

41
Q

What is the main drawback of Vaughan Williams classification?

A

Some medications may work on multiple receptors or channels.

42
Q

Common characteristics of class I anti-arrhythmics:

A

1) Inhibits fast Na channels
2) ↓ slope of phase 0

43
Q

What determines subclassification for class I AAs?

A

1) Relative potency of Na channel effects
2) Activated/inactivated channel blockade
3) Effects on other channels/receptors

44
Q

Example of class IA anti-arrhythmic:

A

Procainamide

45
Q

Why can class IA drugs have proarrhythmic effects?

A

1) moderate blockade of rapid component of rectifier potassium current (outward K+ flow during plateau phase of AP)
2) depression of conduction veloctiy predisposing to intramyocardial re-entry

46
Q

Which tissues is procainamide effective in?

A
  • atrial and ventricular myocardium
  • accessory atrioventricular pathways
  • retrograde fast atrioventricular nodal pathways
47
Q

Why is procainamide considered first tx of choice for atrial tachyarrhythmias?

A

Because 1) it prolongs retrograde atrioventricular nodal (AVN) pathways 2) anti-cholinergic effects => increase ventricular response rate => more rapid AVN conduction 3) slowing of atrial tachycardia rate

48
Q

Adverse effects of procainamide

A

More in humans and cats > dogs
Acute effects in humans: rash and fever Late effects in humans: arthralgia, myalgia and agranulocytosis
GIT adverse effects
Systemic lupus erythematosis (rare)

49
Q

Examples of class IB anti-arrhythmics:

A

Lidocaine
Mexiletine

50
Q

Characteristics of class IB AAs

A
  • Inhibits fast Na channel in open and inactivated state (rapid onset-offset kinetics)
  • Use-dependent agents: act on rapidly depolarising tissue
  • Blocks the steady-state component of the fast sodium current (INA)
  • selectively suppress automaticity and slow conduction velocity in ischemic and diseased ventricular myocardium
51
Q

First line in treating canine VT

A

Lidocaine

52
Q

Advantages of lidocaine

A

minimal hemodynamic effects, sinoatrial and AVN effects at standard doses

53
Q

What conditions predispose a patient to lidocaine toxicity

A

Conditions that reduce hepatic blood flow and hence clearance e.g. heart failure, hypotension, severe hepatic disease

54
Q

Why is lidocaine not effective orally?

A

Due to its first pass effect

55
Q

Adverse effects:

A

Cats MUCH more sensitive
Otherwise predominant:
- GI (vomiting, nausea)
- Lethargy
- Tremor, seizures (tx with diazepam)

56
Q

Pharmacology of mexiletine

A

Protein bound
Eliminated by renal excretion
Use and adverse effects similar to lidocaine

57
Q

What are class IC anti-arrhythmics?

A
  • Potent blockade of open state of fast sodium channel
  • Greater effect as depolarisation rate increases (use dependence)
  • Prolongs effective refractory periods in atrial, ventricular tissues and atrioventricular pathways
58
Q

Examples of class IC:

A

Propafenone
Flecainide
Side effect: GIT

59
Q

Mechanism for class II anti-arrhythmics:

A

Beta-blockers
Treats SVT and VT
Indirect effects on stabilizing the cardiac cell membrane by reducing catecholamine secretion and associated catecholamine-induced arrhythmias.
Beta blockade will also result in decreased myocardial contractility and myocardial oxygen consumption.

60
Q

First choice of AA control of SVT or VT in cats and dogs with subaortic stenosis

A

Atenolol

61
Q

Why are beta-blockers inferior in treatment of SVT in dogs compared to diltiazem?

A

Dose required to prolong AV node conduction can cause severe drop in LV contractility
Often used in combination with class I or III drugs

62
Q

When are class II AAs contraindicated?

A
  • Sinus nodal dysfunction
  • AV nodal conduction disturbances
  • Pulmonary disease (especially non-specific or high doses)
  • CHF
  • Extremely low dose in patients with myocardial dysfunction
63
Q

Why is atenolol preferred over propanolol?

A

beta-1 selectivity and longer half life

64
Q

Metabolism and elimination of atenolol

A

water soluble, renal elimination

65
Q

Metabolism and elimination of metoprolol

A

Hepatic metabolism and elimination

66
Q

Mechanism of class III

A

Blocks repolarising K+ current => prolonged AP duration + effective refractory period

67
Q

Why are most class IIIs (except amiodarone) pro-arrhythmic

A

Blocks rapid and not slow component of repolarising K+ current => risk of early afterdepolarisation (especially at slower HR)

68
Q

The pro-arrhythmic effects of class IIIs are enhanced by (5)

A

Hypokalaemia
Bradycardia
Intact female
Increasing age
Macrolide antibiotic

69
Q

Mechanism of sotalol

A

Non-selective beta blocker and inhibition of fast repolarising K+ current
- beta more at lower doses
- class III more at higher doses

70
Q

Indications of sotalol

A

Used in SVT and VTs
- Boxers with familial VT
- GSD with inherited ventricular arrhythmia (combined with mexiletine)

71
Q

Why is the negative inotropic effects of sotalol less than propanolol?

A

Due to enhanced Ca entry during AP plateau as AP is prolonged

72
Q

Pharmacokinetics of sotalol:

A
  • Hydrophilic, non-protein bound
  • 100% renal excretion
73
Q

Mechanism of amiodarone:

A

Broadest spectrum: exhibits effects of all 4 AA classes (more effective)

74
Q

Indications of amiodarone:

A

Life-threatening VT or SVT, not responding to other therapy

75
Q

Side effects of amiodarone:

A

MANY:
- Vomiting, anorexia
- Hepatopathy
- Thrombocytopenia
NB: most common IV formulation (Cordarone) can be deadly in dogs due to the solvents used.

76
Q

Mechanism of class IV anti-arrhythmics:

A

Calcium channel blockers
- Slows AV nodal conduction
- Prolongs effective refractory period of nodal tissue
- Use dependence (more effect at faster stimulation rate)
- Voltage dependence (more effect in depolarised fibres)

77
Q

Indications and contraindications for class IV AAs:

A

Indications: atrial tachyarrhythmia
Contraindicated in: wide complex tachyarrhythmias

78
Q

Indications for diltiazem:

A

Atrial fibrillation: Slows AV nodal conduction while maintaining good hemodynamic profile
- minimal neg inotropic effects compared to verapamil

79
Q

Adverse effects of diltiazem:

A

Hypotension, bradyarrhythmia
Sustained release formulation has more side effects in cats: vomiting, inappetence, hepatopathy

80
Q

Mechanism of digoxin:

A

Enhances central and peripheral vagal tone:
- slows sinus nodal discharge rate
- prolongs AV node refractory
- shortens atrial refractory

81
Q

Indications fo digoxin:

A

Atrial fib: in combination with diltiazem, more effective than either agents alone

82
Q

Adverse effects of digoxin:

A

Low therapeutic index, watch for digoxin toxicity: GIT, neuro effects, arrhythmia, vision problems

83
Q

Which patients are more predisposed to digoxin toxicity?

A

1) renal dysfunction
2) hypokalaemia
3) advanced age
4) chronic lung dz
5) hypoT

84
Q

Indications for magnesium sulfate:

A
  • First line for Torsades de Pointes
  • Refractory VT or arrhythmias due to hypomagnesemia
85
Q

Adverse effects of Mg sulfate

A

1) CNS depression
2) Hypotension
3) Bradycardia
4) Hypocalcemia
5) QT prolongation

ACVECC 2024 (1 decks)

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