Exam 2- Cardiovascular Flashcards
Proposed benefit of Acepromazine use for treating equine laminitis
Increases blood flow to the laminae
Proposed benefit of Nitroglycerin for treating equine laminitis
Limited evidence on the benefit
Proposed benefit of Isoxsuprine for equine laminitis
Limited evidence, peripheral vasodilation
Proposed benefit of IV DMSO in treating equine laminitis
Limited evidence, anti-inflammatory & mild platelet inhibition
Proposed benefit of Pentoxifylline in treating equine laminitis
Limited evidence, hemorheologic, increases RBC membrane flexibility to increase blood flow through narrow vessels
Three hemostatics that act systemically & the evidence supporting their use
A. Aminocaproic acid- decreased fibrinolysis & post-op healing
B. Yunnan baiyao- Chinese herbs, variable evidence but suggested to increase clot strength
C. IV formalin- 81.25% cured in 4d, while <50% of untreated cows cured in 7-8d
This hemostatic can be used to treat hemorrhagic cystitis
Diluted formalin
What are two topical hemostatic agents & how do they work?
a. Silver nitrate- caustic
b. Styptic powder- anhydrous aluminum sulfate, acts as vasoconstrictor decreasing blood flow
What is “reperfusion injury” as it relates to tPA use?
a. When toxic substances that have built up in an area are released all at once
b. tPA used against clots w/ bad results= reperfusion shock & death
What ophthalmic indication is tPA used for?
a. Management of hyphema
- Injected into anterior chamber to decrease risk for glaucoma
Why is Warfarin not used therapeutically as an anticoagulant in animals?
Has a small therapeutic index, prone to drug interactions, & has an impact on the diet
Why is LMW heparin often preferred over regular unfractionated heparin? What clotting factors are affected?
a. Less likely to cause accidental hemorrhage/iatrogenic bleeding
b. Inactivates factor Xa activity, but not thrombin activity
How do aspirin & clopidogrel produce anticoagulant effects?
Aspirin- inhibits platelet function by its effects on thromboxane; interferes with cyclooxygenase, inactivating the platelet
Clopidogrel- causes anticoagulant effects through the ADP pathway; inhibits platelet function by inhibiting ADP receptors on the platelet membrane
Preference of Amlodipine vs. Enalapril in hypertension management for the dog vs. cat
Dog- Enalapril first, Amlodipine if necessary
Cat- Amlodipine first, Enalapril used in refractory cases
Epinephrine injected by different routes- why?
a. Cardiac asystole- IV or intratracheally
i. Stimulates heart & vasoconstricts, do not give intracardiac unless visualizing left ventricles
b. Anaphylaxis- IM
i. Provides a more rapid increase in plasma & tissue concentrations
c. Acute bronchoconstriction w/o hypotension- SQ
i. Rapid uptake into the system
d. Rate of absorption differs with each route of administration
i. More side effects can occur when epinephrine is absorbed too fast inappropriately
Why are vasopressors used only after more conservative measures have failed to adequately raise blood pressure?
May decrease perfusion to some tissues
This vasopressor works to raise the BP by increasing the CO, no vasoconstriction
Dobutamine
This vasopressor works by stimulating the heart & causing vasoconstriction
Epinephrine
This vasopressor works by stimulating alpha1 & beta1 receptors to create vasoconstriction & cardiac stimulation
Norepinephrine
Dopamine, when given at different doses, produces different effects, what are those?
Low dose- D1 dopamine receptors, vasodilation of renal & splanchnic vessels
Mid dose- beta1 receptor; increases heart inotropy
High dose- alpha1 receptors; vasoconstriction
This vasopressor causes vasoconstriction w/o cardiac stimulation
Phenylephrine
This vasopressor has an indirect effect by the release of NorEpi at the postsynaptic alpha & beta receptors
Ephedrine
What breed of dog may be more prone to digoxin toxicity?
Dobermans
What is considered the vasodilator of choice in pulmonary hypertension management?
Oxygen therapy
How do the pulmonary vessels differ in their response to hypoxia vs. other vessels in the body?
Hypoxia causes vasoconstriction of the pulmonary vessels to shunt blood towards healthy tissues
What drugs would be used for Left atrial enlargement w/ mild clinical signs?
Enalapril or Pimobendan
What drugs would be used for left ventricular enlargement w/ systolic impairment?
Pimobendan or Digoxin
What drugs would be used for atrial fibrillation w/ a high HR?
Digoxin or Diltiazem
What drugs would be used to treat early pulmonary edema?
Furosemide or Torsemide
What drugs would be used to treat refractory pulmonary edema?
Furosemide w/ Thiazide or Spironolactone
What drugs would be used for treating premature ventricular contractions?
Procainamide or Sotalol
Why are opioids often beneficial in pulmonary edema other than for sedation?
a. Decreased air hunger
b. Morphine- decrease preload by splanchnic vasodilation
c. Desensitizes CO2 receptors
Compare and contrast dobutamine versus dopamine as to receptors stimulated, clinical indications, existence of a “holiday”, and whether a “therapeutic window” exists.
a. Dobutamine
i. Selectively stimulates subset of β1 receptors→ increase in strength of contraction
1. Some β2 activity may also reduce afterload
ii. Normally it has minimal effects on the HR but can cause tachyarrhythmias→ monitor w/ ECG
iii. Constant IV infusion due to short plasma half-life
iv. Target to raise systolic BP 100-120mmHg
v. Accumulates in cardiac muscle→ Dobutamine holiday
b. Dopamine
i. Less selective than dobutamine
ii. Low doses stimulate β1 & dopamine receptors
1. Beta1 stimulation→ positive inotropic effects
2. Dopamine stimulation→ vasodilation of renal (dogs, not cats) & splanchnic vessels
iii. Therapeutic window relative to use in heart failure
1. Higher doses stimulate alpha receptors→ increase in peripheral vascular resistance
iv. Constant IV infusion→ short half-life
Which electrolyte abnormality predisposes to digoxin toxicity?
Hypokalemia
What benefit besides inotropy does digoxin provide for treating CHF?
Sensitizes baroreceptors → slows HR
How does renal function & body weight impact dosing digoxin?
Dose made on lean body weight; renal function affects drug elimination
When might Benazepril be preferred over Enalapril as an ACE inhibitor?
When the patient is in renal failure
How might NSAIDs interfere w/ ACE inhibitors?
Inhibit vasodilatory PG → decreases GFR → inhibits release of natriuretic PGs
Explain how an Angiotensin-converting enzyme (ACE) inhibitor, by virtue of inhibiting the conversion of angiotensin 1 to angiotensin 2, has a beneficial effect on CHF.
Less conversion of angiotensin I to angiotensin II= less vasoconstriction
Why are hydrochlorothiazide or spironolactone seldom used as a sole diuretic in congestive heart failure (CHF), yet are commonly used as adjunct diuretics with furosemide, especially when pulmonary edema occurs despite furosemide therapy?
Weak diuretics
For what group of cardiac drugs does tachyphylaxis limit the duration of their usefulness?
Nitrates
Furosemide decreases preload. What additional benefit does it provide when pulmonary edema is present?
Produces vasodilatory prostaglandins
Sodium restriction has historically been a method used in heart failure to reduce preload. What disadvantages might it however pose?
Palatability problems
May activate Renin-Angiotensin system too early
What cardiovascular drugs alter preload?
Nitroglycerine, Furosemide, Torsemide, Thiazides/hydrochlorothiazide, Spironolactone
What cardiovascular drugs alter afterload?
Amlodipine, Hydralazine, Dobutamine
What cardiovascular drugs alter preload & afterload?
Nitroprusside, ACE inhibitors, Pimobendan
In early congestive heart failure (systolic heart failure) physiologic changes occur that allow “compensated” heart failure to exist. Explain those physiologic changes and how eventually over-exaggerated responses lead to decompensated heart failure.
a. Early CHF leads to a reduced cardiac output & reduced BP.
i. Causes the activation of both the RAAS & the sympathetic NS
ii. RAAS- salt & water retention leading to excessive preload
iii. SNS- systemic arteriolar vasoconstriction leading to increased total peripheral resistance causing excessive afterload
Name the therapeutic goals in the management of hypertrophic cardiomyopathy (HCM) and what drugs we commonly use to accomplish these. Contrast the merits of diltiazem versus atenolol use in HCM.
a. Treat the underlying cause
b. Decrease the left atrial pressure
i. Oxygen
ii. Furosemide
c. Relax cardiac muscle (positive lusitropy)
i. Diltiazem
ii. Beta 1 blocker- Atenolol
iii. Nonselective beta blockers
d. Aspirin
i. Decreases risk of thromboembolism
e. Merits for treating HCM
i. Diltiazem & Atenolol→ positive lusitropy, relax the heart muscle
1. Diltiazem – calcium-channel block, q8hr dosing
2. Atenolol – beta1 block, q12hr dosing, decreases effects of catecholamines in hyperthyroidism
What cardiac drugs are useful to treat ventricular arrhythmias?
Lidocaine, Procainamide/Mexiletine, Magnesium sulphate
What cardiac drugs are useful to treat supraventricular arrhythmias?
Digoxin, Quinidine
What drugs are useful to treat both supraventricular & ventricular arrhythmias?
Amiodarone, Sotalol
What is an “escape beat” on an ECG & how does its presence impact the use of antiarrhythmics?
Escape beat= 3rd degree heart block
i- P waves not coordinated w/ QRS complex
ii- bradycardia
iii- ventricular antiarrhythmics that can cause cardiac arrest
What is the initial drug of choice in treating nearly all PVCs during hospitalization?
Lidocaine
What drug is most used to convert idiopathic a-fib to a normal sinus rhythm, & what are its main toxicities?
Amiodarone
- hepatotoxic in dogs
- causes diarrhea
What drug is most used to manage a-fib when there is underlying myocardial disease?
Digoxin
-will not convert normal rhythm, but does slow conduction at the AV node
Why do excessively high heart rates have a deleterious impact on cardiac output?
They do not allow for adequate ventricular filling to occur
What is the basic mechanism for the class I antiarrhythmics?
Sodium-channel blockade- reduce phase 0 slope & peak of action potential
Basic mechanism for class Ia antiarrhythmic
Moderate Na-channel blockade- moderate reduction of phase 0 slope, increase APD & ERP
Basic mechanism for class Ib antiarrhythmic
Weak Na-channel blockade- small reduction in phase 0 slope, reduce APD & decreases ERP
Basic mechanism for class Ic antiarrhythmic
Strong Na-channel blockade- pronounced reduction in phase 0 slope, no effect on APD or ERP
Basic mechanism for class II antiarrhythmics
Beta-blockade- blocks sympathetic activity, reduces rate & conduction
Basic mechanism for class III antiarrhythmics
Potassium-channel blockade- delay repolarization (phase 3) & thereby increase action potential duration & effective refractory period
Basic mechanism for class IV antiarrhythmics
Calcium-channel blockade- block L-type calcium-channels; most effective at SA & AV nodes; reduce rate & conduction
What treatment options exist to manage a bradyarrhythmia such as “Sick Sinus Syndrome”?
Administer a test dose of atropine & then administer propantheline
Usually requires a pacemaker sx, medical management unrewarding
