Heart Flashcards
1
Q
Quinidine
A
- Class 1A Anti-arrhythmic (delays redepolarization)
- treats both supra/ventricular arrhythmias
- increases sympathetic tone-increase HR
- alpha adrenergic antagonist: vasodilation and negative inotropy
- mostly used for horses with atrial fibrillation
- contraindications: bradyarrhythmias and heart failure
- side effects: hypotension, GI effects
2
Q
Procainamide
A
- Class 1A anti-arrhythmic (delays redepolarization)
- less autonomic effects then quinidine
- used for atrial and ventricle tachyarrhythmias
- 2nd option for ventricular tachycardia
- contraindications : bradyarrhythmias
- fewer side effects then quinidine
3
Q
Lidocaine
A
- Class 1B anti-arrhythmic
- only used for ventricular tachyarrhythmias (first option)
- does not suppress contractility or vasodilation
- high first pass effect
- lower doses in cats and horses
- contraindicated for all bradyarrhythmias
- side effects are uncommon
- only IV
4
Q
Mexiletine
A
- Class 1B anti-arrhythmic
- PO
- same as lidocaine
- can combine with class 2 or 3 to increase effect
5
Q
Propranolol
A
- Class 2 anti-arrhythmic
- non selective B-blocker
- first generation B-blocker
- highly protein bound
- caution when giving to patients with respiratory disease or diabetes
- lipophilic
6
Q
Atenolol
A
-Class 2 anti-arrhythmic
-most common
second generation
-selective B1 blocker
-longer half life then propranolol
-hydrophilic
7
Q
Esmolol
A
- Class 2 anti-arrhythmic
- selective B1 blocker
- second generation
- VERY short half life, good because we use it for emergency situation and can give a better drug later
- only IV
8
Q
Amiodarone
A
- Class 3 anti-arrhythmic
- prolongs AP and increases refractory period for ALL cardiac tissue
- also exhibits class I,II,IV, and alpha 1 effects
- LOTS of side effects: pulmonary fibrosis (most common), skin discoloration (blue skin), CNS, GI, elevation of liver enzymes, corneal microdeposits, hypothyroidism
- clinical effects are delayed for several weeks, loading dose is usually needed
- contraindication : patients with long QT syndrome
9
Q
Sotalol
A
- Class 3 anti-arrhythmic
- prolongs AP and increases refractory period in myocardial cells
- also has potent non-selective class II effects(first generation Beta-blocker)
- side effects are rare
- used to prevent sudden death in boxers with arrhythmogenic right ventricular cariomyopathy, DADs, and re-entry
10
Q
Diltiazem
A
- Class 4 anti-arrhythmic
- potent on nodal tissue
- used for supra ventricular tachyarrthythmias
- minimal vascular effects
11
Q
Amlodipine
A
- Class 4 anti-arrhythmic
- minimal cardiac effects
- used for hypertension and after load reduction
- very good vasodilator
12
Q
Furosemide
A
- loop diuretic
- less Na loss
- used for acute pulmonary edema and congestive heart failure
- causes increase in renin secretion
- always give in combination with an ACE inhibitor
- sulfonamide diuretic
- decreases reabsorption of Na and Cl in thick ascending look of H by competing for Cl site –> leads to parallel decreased of Ca reabsorption
- used in cardiac, renal, and hepatic dysfunction, pulmonary edema
- can help in treatment of hyperCa
- many routes for intake
13
Q
Torsemide
A
- loop diuretic
- longer duration and 10x more potent then furosemide
14
Q
Spironolactone
A
- K sparing diuretic
- does not work on the luminal side
- competitive antagonist of aldosterone (which wants to re-absorb Na)
- blocks aldosterone stimulated Na reabsorption therefore also blocking K + H excretion in late distal tubule (bind to its receptor on late distal tubule to increase Na, Ca, H2O excretion and decrease K loss)
- weak when given alone, needs to be given with something else to achieve sequential nephron blockade
15
Q
Mannitol
A
- osmotic diuretic
- freely filtered
- imparts H2O reabsorption
- increases blood volume, never give on CHF patients
16
Q
Digoxin
A
- cardiac glycoside
- positive inotrope
- stop giving it if DAD is present
- block Na/K pump so cell has way too much Na inside -> cell exchanges Na for Ca -> more cytoplasmic Ca for contraction
- direct stimulation of vagal nuclei causing some parasympathetic actions (slower AV)
- used for systolic myocardial failure and AF
- dose is based on lean body weight–> does not go to fat, ascitic fluid (not predictable dose response)
- renal excretion
- narrow therapeutic window
- cardiac toxicity (when 60-70% of channels are blocked); CNS; GI
- predisposition to toxicity in cases of hypoK, azotemia
- serum levels should be checked constantly
- lower therapeutic levels then before
17
Q
Dopamine
A
- synthetic catecholamine/ Beta 1 agonist
- effects alpha, B1 and DA receptors depending on doses
- -> low doses: DA for vasodilation (mostly renal)
- ->med doses: B1 for positive inotropy
- ->high doses:alpha for vasoconstriction
18
Q
Dobutamine
A
- synthetic catecholamine/ Beta 1 agonist
- mostly beta 1 effects
- no renal change in BP since both B2 and alpha receptors are stimulated in peripheral blood
- better then dopamine in patients with pump failure
19
Q
Pimobendan
A
- Ca sensitizing agent
- does not increase O2 consumption so less arrhythmias
- also phosphodiesterase III activity: also systematic and pulmonary vasodilator (inodilator)
20
Q
Nitroglycerin
A
- venodilator (nitrate forms NO, decreases intracellular Ca)
- -> very short half life because fast conversion to NO
- hepatic metabolism
- heavy, colorless, oil, explosive liquid used in demolition and mining
- topical administration
- questionable effects on the heart
21
Q
Nitroprusside
A
- venodilator (nitrate forms NO, decreases intracellular Ca) AND arterial
- -> very short half life because fast conversion to NO
- hepatic metabolism
- very effective
- VERY expensive so not used a lot
- CRI
22
Q
Hydralazine
A
- arterialdilator
- decreases GMP by unknown mechanisms
- used for acute CHF
- can cause hypotension in high doses, and sub sequential reflex tachycardia
23
Q
Sildenafil
A
- used for pulmonary artery hypertension
- NO activates guanylate cyclase -> GTP converts to cGMP -> phosphodiresterase 5 inhibitor to stop breakdown of cGMP
- increases CO by 20%
24
Q
Enalapril
A
- ACE inhibitor to minimize RAAS effects
- converted to enalaprilat by liver
- side effects: vomiting, anorexia, and diarrhea are the most common. HyperK due to decrease in aldosterone, reversible renal injury
25
Q
Benazepril
A
- ACE inhibitor to minimize RAAS effects
- converted to benazaprilat by liver
- side effects: vomiting, anorexia, and diarrhea are the most common. HyperK due to decrease in aldosterone, reversible renal injury