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CAEM Pt. 2 > Cardio Pharm & Valvular Dz > Flashcards

Cardio Pharm & Valvular Dz Flashcards

1
Q

Four main goals of treating heart disease

A

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

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2
Q

What is the cause of congestion with heart failure?

A

Result of excessively increased venous pressures

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3
Q

Clinical signs of right CHF

A

+ Ascites
+ Jugular distension
+ Pleural effusion in cats

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4
Q

Clinical sign of left CHF

A

+ Coughing associated with pulmonary edema

+/- Pleural effusion in cats

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5
Q

Three main goals with dogs with acute CHF therapy

A

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

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6
Q

Three main goals with cats with acute CHF therapy

A

1) Improve congestion (pulmonary edema and pleural effusion)
2) Improve oxygenation
3) Improve ventricular function = filling (diastole) and contraction (systole)
* Problem with ventricular relaxation

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7
Q

Which species (dogs or cats) do we want to diagnose the underlying disease with acute CHF?

A

Dogs

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8
Q

Three interventions for acute CHF

A

> > FOP

1) Furosemide
2) Oxygen
3) Pimobendan

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9
Q

MOA, route of admin, frequency of admin, and duration of effect of furosemide

A

> MOA = loop diuretic
Route = any, depends on the severity of the presentation
Duration = up to 8 hours
Frequency = patient dependent, based on respiratory rate

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10
Q

What is the number one indicator/clinical sign that pulmonary edema is worsening?

A

Increasing respiratory rate

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11
Q

What things do we want to continually monitor with furosemide use? (3)

A

1) Urine production
2) Electrolyte values
3) Renal values

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12
Q

Signs that you’ve excessively dosed an animal with furosemide (5)

A

1) Dehydration
2) Electrolyte abnormalities
3) Low cardiac output = increased CRT, weak to absent femoral pulses
4) Renal failure = azotemia
5) Hypochloremic metabolic alkalosis

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13
Q

What is the one thing you DON’T want to do when administering oxygen to the patient?

A

Stress the patient

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14
Q

MOA and effects of pimobendan

A

> INODILATOR
- Ca++ sensitizer and phosphodiesterase inhibitor (increases the amount of Ca++ available)
+ Positive inotrope = increases contractility of the heart
+ Vasodilator

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15
Q

What side effects do we see with pimobendan?

A

RARELY GI upset

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16
Q

Hydrazaline - what do we use it for and what does it do?

A

> Potent arterial vasodilator

- Used with MODERATE acute CHF cases

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17
Q

Side effects of hydrazaline use

A

Hypotension and a reflex tachycardia

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18
Q

What vasodilator do we use with severe CHF?

A

> Nitroprusside = potent mixed vasodilator

- Short half life = needs to be administered IV

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19
Q

Specific administration issue and side effects with nitroprusside

A
  • Turns to cyanide = needs to be covered from light exposure

- Side effect = hypotension

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20
Q

When do we use dobutamine? What does it do?

A

> 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
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21
Q

Side effect of dobutamine use

A

Arrhythmias

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22
Q

What therapeutic procedure do we often have to do with cats with CHF?

A

> Thoracocentesis, to drain the pleural effusion

*Isn’t effectively dealt with with diuretics

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23
Q

What sedative is helpful for nervous/stressed animals in CHF?

A

Butorphanol

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24
Q

What can happen with cats that have CHF?

A

Hypothermia - may need to warm them

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25
Q

Is FOP for acute CHF used for both dogs and cats?

A

Yes

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26
Q

Triple and quadruple therapy for treating chronic CHF

A

1) Furosemide
2) ACE inhibitor - enalpril
3) Pimobendan
4) Spironolactone

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27
Q

Three effects of ACE inhibitor use

A

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)

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28
Q

Side effects of ACE inhibitor use

A

1) Hyperkalemia
2) Renal insufficiency
3) Hypovolemia

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29
Q

Which are potent vasodilators - hydrazaline, nitroprusside, or ACE inhibitors?

A

1) Most potent = nitroprusside
2) Hydrazaline
3) Least potent = ACE inhibitors

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30
Q

What type of patient do we NOT want to administer diuretics and ACE inhibitors? Why?

A

> > 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

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31
Q

Is pimobendan contraindicated in cats with HCM?

A

No - improves diastolic (and systolic) function = improve filling of ventricles, decreases right atrial pressures

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32
Q

MOA, effects, and side effects of spironolactone

A

> MOA = aldosterone antagonist

  • Prevents myocardial fibrosis
  • Decreases Na/water retention
  • K+ sparing
  • Side effects = hyperkalemia
33
Q

Is spironolactone a diuretic?

A

NOT REALLY

34
Q

What do we do if the CHF is progressing or becoming more severe? (3)

A

1) Increase furosemide dose
2) Increase frequency of furosemide dose
3) Change route of admin of furosemide from oral –> SQ (more bioavailable)

35
Q

What two situations do we treat supraventricular arrhythmias?

A

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

36
Q

What three drugs do we use to treat supraventricular arrhythmias? What is our goal with treatment?

A

1) Ca++ channel blocker (diltiazem)
2) Beta blocker
3) Digoxin
» SLOW AV NODAL CONDUCTION TIME

37
Q

What two anti-arrhythmics do we not use in combo?

A

Beta blockers and Ca++ channel blockers

38
Q

Diltiazem MOA and effect

A

> Specific Ca++ channel blocker that works on the heart

  • Negative inotrope
  • Negative chronotrope (decrease HR)
  • Decreases AV nodal conduction time
  • Quick onset action
39
Q

Which anti-arrhythmic do we not use in patients with CHF?

A

Beta blockers

40
Q

MOA and effects of beta blockers

A
  • NOT safe with CHF
  • Negative inotrope, chronotrope (HR), lusitrope (relaxation)
  • Tx supraventricular tachycardia
  • Don’t use with diltiazem
41
Q

Side effects of beta blockers (4)

A

1) Hyperkalemia
2) Lethargy
3) Anorexia
4) Bradycardia

42
Q

MOA and effect of digoxin

A

> MOA = Na/K/ATPase inhibitor, parasympathomimetic

  • Takes 5 days to achieve levels = not for acute cases
  • Weak positive inotrope
  • Negative chronotrope
  • Narrow therapeutic range
43
Q

Common side effects of digoxin

A

GI toxicity - not for patients who aren’t eating

44
Q

What happens with digoxin with renal disease and hypokalemia?

A

Digoxin levels increase

45
Q

When do we treat ventricular arrhythmias (3)?

A

1) Patient is displaying clinical signs, Ex: syncope, low BP
2) Evidence of hemodynamic compromise
3) Risk of sudden death

46
Q

What do we use to treat ventricular arrhythmias acutely?

A

Lidocaine IV - bolus and CRI

47
Q

What can affect the efficacy of lidocaine?

A

K+ levels = if it’s too low, it won’t work

48
Q

Toxic side effects of lidocaine (3)

A
  • Nausea
  • Vomiting
  • Seizures
49
Q

What do we use to treat ventricular arrhythmias chronically in dogs? (2)

A

1) Melexitine - oral form of lidocaine

2) Sotalol - beta blocker = class III anti-arrhythmic

50
Q

What do we use to treat ventricular arrhythmias chronically in cats?

A

Beta blockers - sotalol or atenolol

51
Q

When do we treat bradyarrhythmias (3)?

A

1) Syncope
2) CHF = heart rate is too persistently slow
3) Hemodynamic compromise

52
Q

How do we treat bradyarrhythmias?

A

Place a pacemaker

53
Q

What ECG abnormalities do we see with mitral and tricuspid regurgitation?

A

Tall and/or wide P waves due to atrial enlargement

54
Q

What does tall R waves indicate on ECG?

A

Left ventricular hypertrophy

55
Q

What type of arrhythmias are common with valvular disease?

A

Supraventricular arrhythmias - narrow QRS complexes

56
Q

At what point in the cardiac cycle do we hear mitral/tricuspid regurgitation murmurs?

A

Systole

57
Q

Differential diagnoses for mitral valve regurgitation (5)

A

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

58
Q

Gross pathologic findings of endocardiosis or degenerative valve disease

A
  • 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
59
Q

Why do we see vasoconstriction and Na+/water retention with AV valve regurgitation?

A

Reduction of forward flow = slight hypotension = neurohormonal activation = activation of the RAAS

60
Q

Reasons for cough with AV regurgitation

A
  • Atrial enlargement and bronchial compression

- Atrial enlargement = increased pressure = left CHF

61
Q

Why do we see arrhythmias with AV valve regurgitation?

A

Atrial stretch = fibrosis = arrhythmias

62
Q

Diagnostics for valvular disease

A
  • 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
63
Q

Why may we see jugular pulsation with valvular disease?

A

Tricuspid valve regurgitation

64
Q

When do we treat valvular disease (4)?

A

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

65
Q

Is systolic function compromised with valvular disease?

A

No - may be dilated but is still able to contract adequately

66
Q

Goals of mitral regurgitation therapy (3)

A

> > 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

67
Q

What anti-arrhythmic therapies do we use with valvular disease? (2)

A
  • Without atrial enlargement of CHF = beta and Ca++ channel blockers
  • With significant atrial enlargement or CHF = digoxin or digoxin+diltiazem (Ca++ channel blocker)
68
Q

Clinical signs that help differentiate endocarditis from endocardiosis (3)

A

1) NEW murmur with no previous history of heart disease
2) Fever
3) Signs of systemic involvement, Ex: joint pain, moist cough, lethargy, anemia

69
Q

What valves are most commonly affected with canine endocarditis?

A

Mitral and aortic valves

70
Q

What type of dog is most commonly affected by endocarditis?

A

Larger breed dogs

71
Q

How does the animal contract endocarditis?

A

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

72
Q

Most common etiologic agents with endocarditis (4)

A

1) Staph aureus
2) E. coli
3) Beta-hemolytic Strep (common with pneumonia)
4) Rarely fungal in immunocompromised animals

73
Q

Differences between endocarditis and endocardiosis on gross lesions

A
  • Valve edges are ROUGH with endocarditis

- Endocardiosis or degenerative valve disease = valves are SMOOTH

74
Q

Clinical outcomes of endocarditis patients (6)

A

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

75
Q

What two types of arrhythmias do we see with endocarditis?

A
  • Ventricular arrhythmias because of sepsis and chemical mediators
  • Heart block = aortic node is near to the AV valves, can erode nearby
76
Q

How do we definitively diagnose endocarditis? (3)

A

1) Blood cultures
2) Echocardiography
3) Urine cultures = may help if there’s low concentration in the blood

77
Q

General goals of endocarditis therapy (4)

A

1) Treat life-threatening problems first, Ex: sepsis, arrhythmias, CHF
2) Treat bacteria infections
3) Treat chronic valvular disease and CHF
4) Supportive care

78
Q

What spectrum, concentration, route, duration, and cidal/static properties do we need with antimicrobial use with endocarditis?

A
  • 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

CAEM Pt. 2 (27 decks)

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