Heart Failure: Clinical Management Flashcards

1
Q

What is heart failure?

A

inability to sustain a cardiac output sufficient to provide for their metabolic requirements are normal cardiac filling pressure

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2
Q

What are some clinical signs of inadequate cardiac output?

A
  • exercise intolerance
  • syncope
  • pallor
  • cold extremities
  • signs of hypotension (lethargy, depression)
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3
Q

Whare are some clinical signs of excessive cardiac filling pressure?

A

signs of venous congestions
- tachypnea, dyspnea (pulmonary congestion, pleural effusion)
- ascites

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4
Q

What’s the gold standard for diagnosing heart failure?

A

CXR
- cardiomegaly
- pulmonary venous congestion
- alveolar pattern

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5
Q

How does heart failure affect the preload?

A

it may increase the preload due to fluid retention

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6
Q

Which drugs would be beneficial in patients with signs of congestion?

A
  • diuretics
  • venodilators
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7
Q

How does heart failure affect the afterload?

A

sympathetic nervous system and RAAS activation –> increase in afterload

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8
Q

Which drugs would be beneficial in patients excessive afterload?

A

vasodilators

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9
Q

Which drugs would be beneficial in patients with abnormal myocardial contractility?

A

positive inotrope

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10
Q

What drugs can improve cardiac filling?

A

lusitropic drugs –> sympathomimetic agents and calcium channel blockers

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11
Q

What are some clinical signs of patients with excessive preload?

A
  • pulmonary edema (dyspnea)
  • pleural effusion (dyspnea)
  • ascites (respiratory compromise)
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12
Q

What’s the first choice in diuretics?

A

furosemide

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13
Q

If a patient is refractory to furosemide, what are the next options?

A
  • can add in thiazide or spironolactone
  • or switch to torsemide
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14
Q

What’s the MOA of furosemide?

A
  • acts at the Loop of Henle, ascending limb
  • blocks the Na/K/2Cl co transporter
  • up to 25% Na excretion
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15
Q

What’s the MOA of thiazide?

A
  • acts at the distal tubule and connecting segments
  • blocks the Na/Cl carrier – ie. inhibits sodium reabsorption
  • up to 5% Na excretion
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16
Q

What’s the MOA of K-sparing diuretic?

A
  • acts at the collecting tubules
  • aldosterone antagonist
  • up to 2% Na excretion
17
Q

What is a unique side of spironolactone in cats?

A

cutaneous adverse drug reactions

18
Q

How is spironolactone best used?

A
  • by itself it’s not a very potent natriuretic
  • best used along side a loop diuretic
  • but it’s aldosterone antagonism has benefits beyond being a diuretic
19
Q

How is thiazide best used?

A

along side with loop diuretic and K-sparing diuretic to provide “sequential nephron blockade”

20
Q

What are the 3 common complications of diuretics?

A
  1. volume depletion
  2. reduction in cardiac output
  3. electrolyte abnormalities – hypokalemia, hyponatremia
21
Q

How does hypokalemia develop in the face of diurectics?

A

the homeostatic mechanism in response to increased Na+ and water loss is more vigorous Na+ and water retention
- Na+ retention = K+ loss in the distal nephron
- therefore, hypokalemia develops, which is more common with the loop diuretics

22
Q

how does hyponatremia develop in the face of diurectics?

A

Vasopressin release
- free water retention = dilution of Na+ = hyponatremia

23
Q

How should abnormalities with diuretics be monitored?

A

baseline, and 10-14d later –> urea, creatinine, electrolyte levels

24
Q

What’s an example of a venodilator?

A

nitrate venous dilators: nitroglycerine
- cutaneous ointment
- gains tolerance quickly

25
Q

What are some complications of venodilator?

A

drop in blood pressure –> syncope, weakness, hypoperfusion
- watch in cats with hypertrophic cardiomyopathy

26
Q

How is nitroprusside used?

A

it’s a balanced vasodilator
- good for acute, ICU setting –> CRI, need to protect from light
- rapid, profound action –> need to monitor blood pressure
- gain tolerance quickly
- cyanide = metabolite, limits cumulative use

27
Q

How is angiotensin converting enzyme inhibitors (ACEi) used?

A
  • usually alongside a diuretic to minimize the effects of RAAS activation
  • not a very potent vasodilator
  • more beneficial in chronic rather than acute setting
28
Q

How is amlodipine used?

A

it’s a calcium channel blocker
- good for cats with systemic hypertension
- may be beneficial for dogs with mitral valve regurgitation
- probably given as 2nd or 3rd line vasodilator if patient refractory to ACEi or pimobendan

29
Q

How is diltiazem used?

A

calcium channel blocker
- also a lusitrope in cats
- used as an antiarrhythmic in dogs

30
Q

Which drug can be used for pulmonary vasodilation? What’s the MOA?

A

Sildenafil
- it’s the phosphodiesterase V inhibitor
- reduces pulmonary vascular resistance
- can be used in dogs with severe degenerative mitral valve disease

  • pimobendan can be used as well
31
Q

What’s the MOA of dobutamine?

A

It’s a inotrope and lusitrope
- block beta-1 receptor –>enhance myocardial contraction and rate of relaxation
- sympathomimetic agent
- only given as CRI – so in hospital use only
- high doses can lead to arrhythmia

32
Q

What’s the MOA of pimobendan?

A

Inodilator
- phosphodiesterase inhibition and calcium sensitization
- useful in DCM and DMVD
- may be helpful for cats with hypertrophic cardiomyopathy

33
Q

What’s the aim of resting respiration rate for dogs/ cats with heart failure?

A

<40 breaths per minute