Cardiovascular Modulators

Question 1

what is cardiac remodelling?

Answer 1

changes in heart, e.g. fibrosis making it less efficient at pumping blood around body

Question 2

name effects of cardiac remodelling

Answer 2

reduced contractility, reduced filling therefore reduced CO

Question 3

what is the effect of reduced CO

Answer 3

activation of compensatory mechanisms e.g. symp NS, RAAS activation. aim to increase BP therefore CO and tissue perfusion

Question 4

what are the consequences of Symp NS activation?

Answer 4

tachycardia (B1) and vasoconstriction (a2) to increase perfusion. Tachycardia not good longterm as heart already not working well so now even harder. will need more O; progression of remodelling. vasoconstriction increases TPR, worsens progression

Question 5

describe the RAAS

Answer 5

kidneys detect low BP therefore secrete renin. renin cleaves angiotensinogen to produce An1. converted to An2 in lungs by ACE. causes release of ADH and Aldosterone to increase Na therefore water absorption, increasing blood volume.

Question 6

consequences of the RAAS

Answer 6

good initially but in heart failure already back up of fluid in system as stuck in heart. can cause pulmonary oedema

Question 7

what are the 3 aims of treatment of CV disease?

Answer 7

improve cardiac function - + inotrope increases contractility, increase filling and vasodilation
prevent progression - inhibit RAAS, prevent water retention
treat heart failure - diuretics to prevent fluid accumulatiuon

Question 8

what are the 5 classes of drugs

Answer 8

positive inotropes, endocrine modulators, diuretics, vasodilation, anti-arrhythmic drugs

Question 9

name 2 + inotropic drugs

Answer 9

pimobendan and dobutamine

Question 10

describe the properties of Pimobendan

Answer 10

given oral/ IV in emergency. increases contractility, causes vasodilation and anti-remodelling. more rapid effect IV. phosphodiesterase inhibitor, increases cAMP and Ca sensitiser. used for acts and dogs

Question 11

describe the properties of Dobutamine

Answer 11

= catecholamine. mainly stimulates B1 receptors (heart) cf Pimobendan. given as CRI. potent inotrope and high doses can cause arrhythmias and tachycardia. down regulation of receptors after 24h so no longer use. Used in shock

Question 12

endocrine modulators - ACE inhibitors. describe properties

Answer 12

e.g. benazepril, ramipril. less production of An2 thus aldosterone and ADH release so reduces Na therefore water retention, reduces remodelling and fibrosis (pre and afterload) also potent vasodilator so watch BP and kidney perfusion

Question 13

aldosterone inhibitors

Answer 13

e.g. spironolactone. anti-remodelling and fibrosis. weak K sparing diuretic. antagonist of aldosterone receptor. prevents progression

Question 14

give examples of diuretics

Answer 14

furosemide, torasamide, thiazides, amiloride

Question 15

what are common signs of CHF?

Answer 15

increased resp rate and possible coughing (pulmonary oedema)

Question 16

describe the properties of furosemide

Answer 16

most important drug for treatment of CHF = loop diuretic ascending limb. blocks NaKCl symporter. inhibits reabsorption of 25% Na. less water reabsorption so reduces atrial pressure (preload) can give IV/ IM/ SC/ PO. also causes venodilation IV so removes preload. Give IV then PO once stabilised. mobilises oedema so removes fluid in lungs (breathe less)

Question 17

describe adverse effects of furosemide

Answer 17

reduction in volume will activate RAAS so dont’ use too early in treatment of heart failure as compensation increases work heart needs to do. give free access to water and monitor electrolytes and kidney function

Question 18

describe properties of torasemide

Answer 18

loop diuretic but more potent and longer duration of action. use if F not working but monitor electrolytes and kidney function. anti-aldosteronergic effect; pevents fibrosis

Question 19

thiazides

Answer 19

given PO. act in DCT, inhibit Na and Cl absorption. not as potent as F. part of sequential nephron blockade

Question 20

amiloride

Answer 20

k sparing. inhibits Na absorption DCT and collecting duct which occurs as compensation at expense of K. weakest diuretic and used in combo with thiazide

Question 20

when are vasodilators used

Answer 20

in patients with systemic hypertension to prevent progression of disease. If hypertension is caused by something else this must be addressed.

Question 21

what is the treatment of choice for systemic hypertension in dogs?

Answer 21

Ace inhibitor

Question 22

cats?

Answer 22

Amlodipine - ca channel blocker

Question 23

name some vasodilators

Answer 23

nitroglycerine, hydralazine, nitroprusside

Question 24

what is the result of venodilation?

Answer 24

reduced preload

Question 25

arteriodilation?

Answer 25

reduced afterload

Question 26

what is the main adverse effect of these drugs?

Answer 26

massive reduction in BP. must be closely monitored (hospitalisation)

Question 27

name an anti-arrhythmic drug

Answer 27

atenolol

Question 28

describe the features of atenolol

Answer 28

used when there is obstruction of ventricular outflow (B blocker), reduces heart rate and contractility so don’t use in CHF. reduces inapt tachycardia, prolongs diastole so improves outflow.

Question 29

what drugs are used in dilated cardiomyopathy?

Answer 29

benazepril and Pimobendan

Question 30

how would you treat degenerative valvular disease?

Answer 30

no treatment

Question 31

how would you manage heart failure

Answer 31

minimise stress and poss give O. dogs give furosemide, pimobendan, ACE inhibitor and Spironolactone.
cats give same + anti-coagulation.
drain any pleural effusion

Question 32

what is decompensation?

Answer 32

worsening of symptoms of heart failure

Question 33

how would you manage decompensation?

Answer 33

increase dose of furosemide, optimise doses of other drugs and possibly add more diuretics. add dobutamine if in cardiogenic shock.