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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

L-type 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 (5)

A

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

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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 (4)

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
What can be considered as a substitute for nitroprusside?
Nitroglycerine IV: another arteriolar vasodilator - no concern for cyanide toxicity
26
MOA of fenoldopam
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)
27
MOA of pimobendan (4)
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
28
How is pimobendan different from traditional positive inotropic drugs?
Does not depend on catecholamines => does not increase myocardial oxygen dependent. Does not increase intracellular Ca, only sensitisation => does not induce arrhythmias.
29
When to use pimobedan in cats?
Cats in CHF with - refractory pulmonary oedema - L ventricular systolic dysfunction - significant pleural effusion - azotaemia Try to avoid in cats with severe LVOTO
30
Adverse effects of pimobendan
GIT (inappetence, vomiting, diarrhoea) Lethargy
31
Pharmacokinetics of pimobendan
- 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
32
Most effective site of diuretic actions in the kidneys?
Loop of Henle: large amount of filtrate delivered to this site + lack of efficient rebasorptive regions distal to this.
33
MOA of furosemide
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
34
Advantage and disadvantage of torsemide
+ve: Loop diuretic Longer half life (once daily dosing) Higher bioavaiability Stronger diuretic effect (5-20x) -ve: high rate of renal adverse events
35
Mechanisms for decreased furosemide responsiveness (4)
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. 3) decreased ECV, decreased GFR -> filtration, not reaching its site of action 4) counter regulatory mechanisms - natriuretic peptides, ADH counteraction
36
MOA of thiazide diuretics
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
Pharmokinetics of furosemide
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
List 3 situations where furosemide therapy may need to be increase:
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
MOA of Spironolactone
Competitively antagonise aldosterone binding to its receptor on the late DT and collecting ducts => inc. Na, Ca and water excretion + dec. K+ loss
40
What is the main classification system for anti-arrhythmics?
Vaughan Williams classification system: grouped by major ion channel or receptor effects
41
What is the main drawback of Vaughan Williams classification?
Some medications may work on multiple receptors or channels.
42
Common characteristics of class I anti-arrhythmics:
1) Inhibits fast Na channels 2) ↓ slope of phase 0
43
What determines subclassification for class I AAs?
1) Relative potency of Na channel effects 2) Activated/inactivated channel blockade 3) Effects on other channels/receptors
44
Example of class IA anti-arrhythmic:
Procainamide
45
Why can class IA drugs have proarrhythmic effects?
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
Which tissues is procainamide effective in?
- atrial and ventricular myocardium - accessory atrioventricular pathways - retrograde fast atrioventricular nodal pathways
47
Why is procainamide considered first tx of choice for atrial tachyarrhythmias?
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
Adverse effects of procainamide
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
Examples of class IB anti-arrhythmics:
Lidocaine Mexiletine
50
Characteristics of class IB AAs
- 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
First line in treating canine VT
Lidocaine
52
Advantages of lidocaine
minimal hemodynamic effects, sinoatrial and AVN effects at standard doses
53
What conditions predispose a patient to lidocaine toxicity
Conditions that reduce hepatic blood flow and hence clearance e.g. heart failure, hypotension, severe hepatic disease
54
Why is lidocaine not effective orally?
Due to its first pass effect
55
Adverse effects:
Cats MUCH more sensitive Otherwise predominant: - GI (vomiting, nausea) - Lethargy - Tremor, seizures (tx with diazepam)
56
Pharmacology of mexiletine
Protein bound Eliminated by renal excretion Use and adverse effects similar to lidocaine
57
What are class IC anti-arrhythmics?
- 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
Examples of class IC:
Propafenone Flecainide Side effect: GIT
59
Mechanism for class II anti-arrhythmics:
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
First choice of AA control of SVT or VT in cats and dogs with subaortic stenosis
Atenolol
61
Why are beta-blockers inferior in treatment of SVT in dogs compared to diltiazem?
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
When are class II AAs contraindicated?
- 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
Why is atenolol preferred over propanolol?
beta-1 selectivity and longer half life
64
Metabolism and elimination of atenolol
water soluble, renal elimination
65
Metabolism and elimination of metoprolol
Hepatic metabolism and elimination
66
Mechanism of class III
Blocks repolarising K+ current => prolonged AP duration + effective refractory period
67
Why are most class IIIs (except amiodarone) pro-arrhythmic
Blocks rapid and not slow component of repolarising K+ current => risk of early afterdepolarisation (especially at slower HR)
68
The pro-arrhythmic effects of class IIIs are enhanced by (5)
Hypokalaemia Bradycardia Intact female Increasing age Macrolide antibiotic
69
Mechanism of sotalol
Non-selective beta blocker and inhibition of fast repolarising K+ current - beta more at lower doses - class III more at higher doses
70
Indications of sotalol
Used in SVT and VTs - Boxers with familial VT - GSD with inherited ventricular arrhythmia (combined with mexiletine)
71
Why is the negative inotropic effects of sotalol less than propanolol?
Due to enhanced Ca entry during AP plateau as AP is prolonged
72
Pharmacokinetics of sotalol:
- Hydrophilic, non-protein bound - 100% renal excretion
73
Mechanism of amiodarone:
Broadest spectrum: exhibits effects of all 4 AA classes (more effective)
74
Indications of amiodarone:
Life-threatening VT or SVT, not responding to other therapy
75
Side effects of amiodarone:
MANY: - Vomiting, anorexia - Hepatopathy - Thrombocytopenia NB: most common IV formulation (Cordarone) can be deadly in dogs due to the solvents used.
76
Mechanism of class IV anti-arrhythmics:
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
Indications and contraindications for class IV AAs:
Indications: atrial tachyarrhythmia Contraindicated in: wide complex tachyarrhythmias
78
Indications for diltiazem:
Atrial fibrillation: Slows AV nodal conduction while maintaining good hemodynamic profile - minimal neg inotropic effects compared to verapamil
79
Adverse effects of diltiazem:
Hypotension, bradyarrhythmia Sustained release formulation has more side effects in cats: vomiting, inappetence, hepatopathy
80
Mechanism of digoxin:
Enhances central and peripheral vagal tone: - slows sinus nodal discharge rate - prolongs AV node refractory - shortens atrial refractory
81
Indications fo digoxin:
Atrial fib: in combination with diltiazem, more effective than either agents alone
82
Adverse effects of digoxin:
Low therapeutic index, watch for digoxin toxicity: GIT, neuro effects, arrhythmia, vision problems
83
Which patients are more predisposed to digoxin toxicity?
1) renal dysfunction 2) hypokalaemia 3) advanced age 4) chronic lung dz 5) hypoT
84
Indications for magnesium sulfate:
- First line for Torsades de Pointes - Refractory VT or arrhythmias due to hypomagnesemia
85
Adverse effects of Mg sulfate
1) CNS depression 2) Hypotension 3) Bradycardia 4) Hypocalcemia 5) QT prolongation

ACVECC 2024 (14 decks)

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