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Flashcards in Cardio - Understanding HF Deck (32)
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1
Q

What is the definition of heart failure (HF)?

A

CLINICAL SYNDROME wherein the heart pumps an inadequate volume of blood to meet O2 demands of tissue and prevent fluid accumulation

2
Q

HF occurs in the face of _____ venous return (as distinguished from shock).

A

adequate/high

3
Q

What type of diagnosis is HF?

A

Common end result of many different cardiac diseases - it is NOT a primary diagnosis

4
Q

What factors determine CO?

A

HR x SV

5
Q

What factors determine SV?

A

Preload, afterload, inotropy

6
Q

What is preload?

A

Amount of blood coming back into heart during diastole

7
Q

What is afterload?

A

All forces that resist ejection from the heart in systole

8
Q

What are potential causes for L-HF due to too much afterload?

A

Systemic hypertension, congenital SAS

9
Q

What are potential causes for L-HF due to too much preload?

A

Valvular disease (mitral, aortic)

Congenital - PDA, VSD, ASD

10
Q

What are potential causes of L-HF due to not enough contractility?

A

DCM, myocarditis

11
Q

What are potential causes of L-HF due to not enough relaxation/filling?

A

HCM

12
Q

What are potential causes of R-HF due to too much afterload?

A

Pumonary hypertension, congenital PS

13
Q

What are potential causes of R-HF due to too much preload?

A

valvular disease (tricuspid), congenital tricuspid dysplasia

14
Q

What are potential causes of R-HF due to not enough contractility?

A

DCM, myocarditis

15
Q

What are potential causes of R-HF due to not enough relaxation/filling?

A

Pericardial disease (tamponade), neoplasia

16
Q

What are the clinical signs of forward (low output) HF?

A

Syncope, pallor, cyanosis, hypokinetic pulses, azotemia

(Heart is not pumping enough blood to meet demands)

17
Q

What are the clinical signs of backward (congestive) HF?

A

Pulmonary edema, pleural effusion, ascites/hepatomegaly, pericardial effusion, peripheral edema

(This is the most common manifestation of HF in animals)

18
Q

What role does the LV play in congestive HF?

A

Blood comes into LV from LA, which came from the lungs –>

Fluid accumulates in lungs –> pulmonary edema

19
Q

What role does the RV play in congestive heart failure?

A

Blood comes into RV from RA, which came from systemic circ (vena cavae) –>

Cavitary effusions –> pleural eff, ascites, pericardial eff, peripheral edema

20
Q

Where does the fluid go in DOGS with L-CHF?

A

Pulmonary edema

21
Q

Where does the fluid go in DOGS with R-CHF?

A

Ascites = major

Occ = pleural effusion, pericardial effusion, peripheral edema

22
Q

Where does the fluid go in CATS with L-CHF?

A

Pulmonary edema, pleural effusion, pericardial effusion

23
Q

Where does the fluid go in CATS with R-CHF?

A

Ascites = major

(Also pleural effusion and pericardial effusion)

24
Q

A cat with pulmonary edema only and no other issues is _____ likely to have L-CHF.

A

not

25
Q

Which of the body’s neurohormonal compensatory systems respond to HF?

A

RAAS, sympathetic system

26
Q

What activates RAAS?

A

Juxtaglomerular apparatus senses decrease in renal perfusion;

Also increased SNS tone

27
Q

What are the short-term effects of RAAS?

A

Na+/H2O retention –> increased preload

Vasoconstriction –> increased preload and afterload

28
Q

What are the long-term effects of RAAS?

A

Myocardial remodeling and fibrosis, renal and arteriolar sclerosis, cytokine activation

29
Q

What activates the SNS?

A

Baroreceptors sense a decrease in BP

30
Q

What are the short-term effects of the SNS?

A

Increased HR, increased contractility, vasconstriction –> increased preload and afterload

31
Q

What are the long-term effects of the SNS?

A

Myocardial remodeling and fibrosis, cytokein activation

32
Q

What pathophysiologic parameters can we alter pharmacologically to treat HF?

A

Increase inotropy, decrease preload, decrease afterload, optimize HR, blunt RAAS, blunt SNS

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