Cardio Pharm & Valvular Dz Flashcards
Four main goals of treating heart disease
1) Relieving congestion
2) Improving cardiac pump function (systolic function)
3) Promoting forward flow = vasodilation
4) Reducing the amount of work on the heart = vasodilation and decrease SVR
What is the cause of congestion with heart failure?
Result of excessively increased venous pressures
Clinical signs of right CHF
+ Ascites
+ Jugular distension
+ Pleural effusion in cats
Clinical sign of left CHF
+ Coughing associated with pulmonary edema
+/- Pleural effusion in cats
Three main goals with dogs with acute CHF therapy
1) Relieve congestion
2) Improve oxygenation
3) Improve cardiac output (systolic function) by increasing pump function and promoting forward flow (vasodilation)
* Problem pushing the blood forward
Three main goals with cats with acute CHF therapy
1) Improve congestion (pulmonary edema and pleural effusion)
2) Improve oxygenation
3) Improve ventricular function = filling (diastole) and contraction (systole)
* Problem with ventricular relaxation
Which species (dogs or cats) do we want to diagnose the underlying disease with acute CHF?
Dogs
Three interventions for acute CHF
> > FOP
1) Furosemide
2) Oxygen
3) Pimobendan
MOA, route of admin, frequency of admin, and duration of effect of furosemide
> MOA = loop diuretic
Route = any, depends on the severity of the presentation
Duration = up to 8 hours
Frequency = patient dependent, based on respiratory rate
What is the number one indicator/clinical sign that pulmonary edema is worsening?
Increasing respiratory rate
What things do we want to continually monitor with furosemide use? (3)
1) Urine production
2) Electrolyte values
3) Renal values
Signs that you’ve excessively dosed an animal with furosemide (5)
1) Dehydration
2) Electrolyte abnormalities
3) Low cardiac output = increased CRT, weak to absent femoral pulses
4) Renal failure = azotemia
5) Hypochloremic metabolic alkalosis
What is the one thing you DON’T want to do when administering oxygen to the patient?
Stress the patient
MOA and effects of pimobendan
> INODILATOR
- Ca++ sensitizer and phosphodiesterase inhibitor (increases the amount of Ca++ available)
+ Positive inotrope = increases contractility of the heart
+ Vasodilator
What side effects do we see with pimobendan?
RARELY GI upset
Hydrazaline - what do we use it for and what does it do?
> Potent arterial vasodilator
- Used with MODERATE acute CHF cases
Side effects of hydrazaline use
Hypotension and a reflex tachycardia
What vasodilator do we use with severe CHF?
> Nitroprusside = potent mixed vasodilator
- Short half life = needs to be administered IV
Specific administration issue and side effects with nitroprusside
- Turns to cyanide = needs to be covered from light exposure
- Side effect = hypotension
When do we use dobutamine? What does it do?
> SEVERE CHF = when you may not have enough time for pimobendan to start working
- MOA = B-1 (positive inotrope) and A-1 agonist
- Minimal B-2 activity
- Short half life = needs to go IV
Side effect of dobutamine use
Arrhythmias
What therapeutic procedure do we often have to do with cats with CHF?
> Thoracocentesis, to drain the pleural effusion
*Isn’t effectively dealt with with diuretics
What sedative is helpful for nervous/stressed animals in CHF?
Butorphanol
What can happen with cats that have CHF?
Hypothermia - may need to warm them
Is FOP for acute CHF used for both dogs and cats?
Yes
Triple and quadruple therapy for treating chronic CHF
1) Furosemide
2) ACE inhibitor - enalpril
3) Pimobendan
4) Spironolactone
Three effects of ACE inhibitor use
1) Inhibits Na+/water retention by decreasing aldosterone production
2) Cause vasodilation (helps block the RAAS activation due to dehydration)
3) Decreases remodeling (fibrosis and scarring of vasculature and the myocardium)
Side effects of ACE inhibitor use
1) Hyperkalemia
2) Renal insufficiency
3) Hypovolemia
Which are potent vasodilators - hydrazaline, nitroprusside, or ACE inhibitors?
1) Most potent = nitroprusside
2) Hydrazaline
3) Least potent = ACE inhibitors
What type of patient do we NOT want to administer diuretics and ACE inhibitors? Why?
> > DEHYDRATED patients = vasoconstricting the efferent arteriole of the kidney + dehydration/hypovolemia = double decrease in GFR = can cause renal failure
- Administer them once they’re drinking or rehydrated
Is pimobendan contraindicated in cats with HCM?
No - improves diastolic (and systolic) function = improve filling of ventricles, decreases right atrial pressures
MOA, effects, and side effects of spironolactone
> MOA = aldosterone antagonist
- Prevents myocardial fibrosis
- Decreases Na/water retention
- K+ sparing
- Side effects = hyperkalemia
Is spironolactone a diuretic?
NOT REALLY
What do we do if the CHF is progressing or becoming more severe? (3)
1) Increase furosemide dose
2) Increase frequency of furosemide dose
3) Change route of admin of furosemide from oral –> SQ (more bioavailable)
What two situations do we treat supraventricular arrhythmias?
1) Animals displaying clinical signs as a consequence of the arrhythmias
2) Evidence of hemodynamic compromise = poor BP due to high HR or compromised CO
What three drugs do we use to treat supraventricular arrhythmias? What is our goal with treatment?
1) Ca++ channel blocker (diltiazem)
2) Beta blocker
3) Digoxin
» SLOW AV NODAL CONDUCTION TIME
What two anti-arrhythmics do we not use in combo?
Beta blockers and Ca++ channel blockers
Diltiazem MOA and effect
> Specific Ca++ channel blocker that works on the heart
- Negative inotrope
- Negative chronotrope (decrease HR)
- Decreases AV nodal conduction time
- Quick onset action
Which anti-arrhythmic do we not use in patients with CHF?
Beta blockers
MOA and effects of beta blockers
- NOT safe with CHF
- Negative inotrope, chronotrope (HR), lusitrope (relaxation)
- Tx supraventricular tachycardia
- Don’t use with diltiazem
Side effects of beta blockers (4)
1) Hyperkalemia
2) Lethargy
3) Anorexia
4) Bradycardia
MOA and effect of digoxin
> MOA = Na/K/ATPase inhibitor, parasympathomimetic
- Takes 5 days to achieve levels = not for acute cases
- Weak positive inotrope
- Negative chronotrope
- Narrow therapeutic range
Common side effects of digoxin
GI toxicity - not for patients who aren’t eating
What happens with digoxin with renal disease and hypokalemia?
Digoxin levels increase
When do we treat ventricular arrhythmias (3)?
1) Patient is displaying clinical signs, Ex: syncope, low BP
2) Evidence of hemodynamic compromise
3) Risk of sudden death
What do we use to treat ventricular arrhythmias acutely?
Lidocaine IV - bolus and CRI
What can affect the efficacy of lidocaine?
K+ levels = if it’s too low, it won’t work
Toxic side effects of lidocaine (3)
- Nausea
- Vomiting
- Seizures
What do we use to treat ventricular arrhythmias chronically in dogs? (2)
1) Melexitine - oral form of lidocaine
2) Sotalol - beta blocker = class III anti-arrhythmic
What do we use to treat ventricular arrhythmias chronically in cats?
Beta blockers - sotalol or atenolol
When do we treat bradyarrhythmias (3)?
1) Syncope
2) CHF = heart rate is too persistently slow
3) Hemodynamic compromise
How do we treat bradyarrhythmias?
Place a pacemaker
What ECG abnormalities do we see with mitral and tricuspid regurgitation?
Tall and/or wide P waves due to atrial enlargement
What does tall R waves indicate on ECG?
Left ventricular hypertrophy
What type of arrhythmias are common with valvular disease?
Supraventricular arrhythmias - narrow QRS complexes
At what point in the cardiac cycle do we hear mitral/tricuspid regurgitation murmurs?
Systole
Differential diagnoses for mitral valve regurgitation (5)
1) Chronic/degenerative mitral valve disease
2) Dilated cardiomyopathy and stretching of the valve
3) Vegetative endocarditis
4) Congenital mitral dysplasia
5) Secondary to hypertension
Gross pathologic findings of endocardiosis or degenerative valve disease
- Diffuse thickening of the valve
- Thickening of chordae tendinae, may stretch or rupture
- SMOOTH surface to the valves
- Curling of the valve leaflets
- Ventricular dilation and atrial enlargement based on regurgitated blood flow
- Tears in the atrial endocardial surface
Why do we see vasoconstriction and Na+/water retention with AV valve regurgitation?
Reduction of forward flow = slight hypotension = neurohormonal activation = activation of the RAAS
Reasons for cough with AV regurgitation
- Atrial enlargement and bronchial compression
- Atrial enlargement = increased pressure = left CHF
Why do we see arrhythmias with AV valve regurgitation?
Atrial stretch = fibrosis = arrhythmias
Diagnostics for valvular disease
- History: cough, small breed and middle aged dogs
- PE = auscult murmur
- Thoracic rads
- Echocardiography
- Arrhythmias on ECG
+/- Systemic complications found on CBC and chem = renal and lyte values
Why may we see jugular pulsation with valvular disease?
Tricuspid valve regurgitation
When do we treat valvular disease (4)?
1) When CO is compromised, Ex: signs of hypotension, > 1/3 abnormal or premature complexes
2) Evidence of CHF
3) Electrically stable - ventricular arrhythmias
4) Underlying disease associated with sudden death, Ex: v-tach
Is systolic function compromised with valvular disease?
No - may be dilated but is still able to contract adequately
Goals of mitral regurgitation therapy (3)
> > Reduce left atrial size
1) Cause diuresis to reduce LA pressure on bronchi with ACE-I and furosemide
2) Decrease BP and encourage forward flow with ACE-I and vasodilators (amlodipine, hydralazine)
+/- With CHF = add pimobendan to increase systolic function and vasodilation
What anti-arrhythmic therapies do we use with valvular disease? (2)
- Without atrial enlargement of CHF = beta and Ca++ channel blockers
- With significant atrial enlargement or CHF = digoxin or digoxin+diltiazem (Ca++ channel blocker)
Clinical signs that help differentiate endocarditis from endocardiosis (3)
1) NEW murmur with no previous history of heart disease
2) Fever
3) Signs of systemic involvement, Ex: joint pain, moist cough, lethargy, anemia
What valves are most commonly affected with canine endocarditis?
Mitral and aortic valves
What type of dog is most commonly affected by endocarditis?
Larger breed dogs
How does the animal contract endocarditis?
1) Stems from a previous wound or infection, Ex: mouth with stems, skin wound, pneumonia, GI , urogenital tract
2) Roughened endocardial surface causes platelet aggregation around the bacteria on the valve
3) Has the ability to embolize and spread bacteria
Most common etiologic agents with endocarditis (4)
1) Staph aureus
2) E. coli
3) Beta-hemolytic Strep (common with pneumonia)
4) Rarely fungal in immunocompromised animals
Differences between endocarditis and endocardiosis on gross lesions
- Valve edges are ROUGH with endocarditis
- Endocardiosis or degenerative valve disease = valves are SMOOTH
Clinical outcomes of endocarditis patients (6)
1) Death from septicemia
2) Valvular insufficiency (both AV and semilunar)
3) Valvular stenosis (semilunar)
4) R or L CHF
5) Thromboembolic events to the liver, spleen, brain, extremities, or myocardium
6) Other disorders = DIC, sterile polyarthritis
What two types of arrhythmias do we see with endocarditis?
- Ventricular arrhythmias because of sepsis and chemical mediators
- Heart block = aortic node is near to the AV valves, can erode nearby
How do we definitively diagnose endocarditis? (3)
1) Blood cultures
2) Echocardiography
3) Urine cultures = may help if there’s low concentration in the blood
General goals of endocarditis therapy (4)
1) Treat life-threatening problems first, Ex: sepsis, arrhythmias, CHF
2) Treat bacteria infections
3) Treat chronic valvular disease and CHF
4) Supportive care
What spectrum, concentration, route, duration, and cidal/static properties do we need with antimicrobial use with endocarditis?
- BROAD spectrum = need to cover gram +/-
- Bacteriocidal with sepsis
- HIGH concentrations delivered parenterally for the first 5-10 days
- LONG duration = at least 4 weeks
- Adjust if needed, after starting empirical treatment, after getting the C&S results
