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RUSVM SAM 1 > Congestive Heart Failure > Flashcards

Congestive Heart Failure Flashcards

1
Q

What is heart failure?

A

Syndrome in which the heart is unable to meet the metabolic needs of tissues, DESPITE adequate venous return

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2
Q

What are the two types of heart failure?

A

Congestive heart failure

Low output heart failure

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3
Q

What is the difference between congestive and low output heart failure?

A

Congestive heart failure-> cardiac malfunction resulting in increased pulmonary/systemic venous pressures (“backward” or “wet”)

Low output heart failure -> severe ventricular dysfunction resulting in arterial hypotension and poor tissue perfusion (“forward” or “cold”)

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4
Q

T/F: In heart failure, end diastolic pressure is lower than normal

A

False

There are increased ventricular filling pressures

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5
Q

If you have increased, left sided ventricular filling pressure you will get _________ congestion

A

Pulmonary

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6
Q

If you have increased, right sided ventricular filling pressure you will get _________ congestion

A

Systemic

-> effusion in peritoneum or pleural cavity

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7
Q

What are consequences of decreased cardiac output?

A

Hypoperfusion

Arterial hypotension

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8
Q

CO = ___________x_________

A

CO= stroke volume x heart rate

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9
Q

Stroke volume = ___________ - ___________

A

SV =End diastolic volume - End systolic volume

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10
Q

What three factors regulate stroke volume?

A

Preload, afterload, and contractility

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11
Q

What is preload?

A

Amount of stretching of ventricular myocytes prior to contraction, determined by amount of blood filling the ventricle

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12
Q

When preload increases, the force of contraction _______________

A

Increases

Therefore increased preload —> increased stroke volume

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13
Q

What is afterload??

A

Tension acting on ventricular myocytes after the onsite of myocyte shortening, determined by the degree of arterial tone

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14
Q

T/F: when afterload increases, stroke volume increases

A

False

When afterload increases, stroke volume decrease

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15
Q

What in inotropy?

A

Inherent ability of cardiomyocyte to contract

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16
Q

One of the primary way the body comespates for decreased CO is making and pumping more blood. How does this contribute to worsening cardiac dysfunction?

A

More blood —> larger EDV —> increased SV —> increased CO

Increased afterload to overcome —> more back up in heart —> more congestion

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17
Q

What are the acute responses to decreased cardiac output?

A

Decreased stretch in baroreceptors —> increase SNS

—> INCREASE HR
—> VASOCONSTRICTION
—> INCREASE CONTRACTILITY

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18
Q

What is the chronic response to decreased cardiac output?

A

Decreased renal blood flow—> RAAS activation

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19
Q

T/F: chronically activation of angiotensin II can worsen heart fialure

A

True

—> increased vasoconstriction and increased water retention and stroke vol

Increased afterload and increased preload —> more congestion

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20
Q

What are two ways the heart can change in response to hemodynamic overload?

A

Concentric hypertrophy -> thickened muscle wall
-in response to pressure overload

Eccentric hypertrophy -> stretching
-in response to volume overload

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21
Q

As heart disease worsens, hydrostatic pressure in the pulmonary and/or systemic system continues to rise and eventually fluid in intersitial space overcomes lymphatic causing what type of heart failure?

A

Congestive

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22
Q

If ventricular contractility is markedly depressed, cardiac output will be too low to maintain adequate tissue perfusion and arterial BP may also fall causing what type of heart failure?

A

Low output heart failure

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23
Q

What type of heart failure is more common and why?

A

Congestive heart failure more common because body prioritizes maintenance of normal arterial pressure over maintenance of normal venous pressure

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24
Q

What are the 6 mechanisms of heart failure?

A
  1. Myocardial systolic dysfunction
  2. Myocardial diastolic dysfunction
  3. Volume overload
  4. Pressure overload
  5. High output states
  6. Rhythm disturbances
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25
Q

CAT

Tachypnea
Dyspnea
Lethargy
Syncope

What type of HF is this?

A

Congestive Heart failure

These signs are consistent with left or right CHF

  • Dyspnea is more pronounced in left
  • Abdominal distention would be seen in right
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26
Q

DOG

Tachypnea 
Cough 
Dyspnea 
Exercise intolerance 
Syncope

What type of heart failure is this?

A

Congestive

Signs could be due to left or right.. this is likely left because there is no abdominal distention

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27
Q

DOG

Exercise intolerance 
Weakness or collapse 
Lethargy 
Depressed mentation  
Pallor 
Hypothermia

What type of heart failure is this?

A

Low output heart failure

-signs in the cat would be similar

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28
Q

What are the three main goals of heart failure therapy?

A

Relieve congestion

Improve cardiac output

Prevent progression (cardioprotection)

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29
Q

How can congestion be relieved when treating heart failure?

A

Decreased ventricular filling

  • decreased blood volume (preload) —> diuretics/dietary sodium restriction/venodilators
  • increase forward flow

Abdominocentesis/throacocentesis

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30
Q

How can you improve cardiac output in systolic dysfunction?

A

Increase ventricular contractility—> positive inotropic drugs
Decrease afterload —> arteriodilators

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31
Q

How can you improve cardiac output for diastolic dysfunction?

A

Need to improve ventricular relaxation and decrease heart rate

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32
Q

T/F: sinus tachycardia is a compensatory mechanism in HR to improve cardiac output

A

True

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33
Q

What is the consequence to a pathological tachyarrhythmia during heart failure?

A

Heart rate is too high —> diastole time is too short —> EDV falls —> SV falls —> CO falls

34
Q

What is the consequence of pathological bradyarrhythmia during heart failure?

A

HR too low —> ventricles are to ejecting blood into arteries frequently enough to maintain BP and meet body’s metabolic requirements

35
Q

What are the classes of cardiovascular drugs?

A 
Diuretic 
ACE inhibitors 
Vasodilator 
Positive inotropes 
Anti-arrhythmics
Cardioprotective
36
Q

What is the first choice drug for CHF and what is its MOA?

A

Furosemide

Inhibit Na/K/Cl cotransporter in thick ascending loop of Henle —> increase Na, K, Cl, Mg, Ca, H, NH4+, and HCO3- secretion —> water secretion

37
Q

How can you administer Furosemide?

A

Oral
IV
IM
SC (off label)

38
Q

What is the dose for acute/emergency CHF of furosemide ?

A

Dog: 2-4mg/kg IV or IM +/- CRI

Cat: 1-3mg/kg IV or IM +/- CRI

39
Q

What are the the expected/adverse effects of furosemide and hydrochlorothiazide?

A

Expected: polyuria and polydipsia

Adverse:

  • volume depletion and pre-renal azotemia
  • electrolyte imbalances
  • renal failure
  • ototoxicity
  • dermal ulcerations
40
Q

What drug has better bioavailability and longer duration than furosemide, often used as an adjunct therapy in refractory CHF?

A

Torsemide

41
Q

What is the MOA of hydrochlorothiazide?

A

Inhibits Na/Cl cotransporter in the distal tubule, which results in incresed renal excretion of sodium, chloride, and water

-also increase K, Mg, and phosphate

42
Q

What is the potassium sparing diretic?

A

Spironolactone

43
Q

What is the MOA of spironolactone?

A

Aldosterone receptor antagonist

44
Q

Why use spironolactone in CHF patients?

A

As add on to furosemide in patients that are becoming hypokalemic (potassium sparing)

Cardioprotective (anti-fibrotic effects)

45
Q

What are the ACE inhibitor drugs?

A

Benazepril

Enalapril

46
Q

What is the MOA of enalapril and benazepril?

A

ACE inhibitors

-inhibit conversion of angiotensin I to angiotensin II

47
Q

What are the uses of ACE inhibitors in heart failure?

A

Inhibit chronic effects of RAAS—> decreased afterload due to vasodilation

Cardioprotective by helping to prevent myocardial fibrosis

48
Q

What are adverse effects of ACE inhibitors?

A

Systemic hypotension
Impaired renal function
GI upset

49
Q

When is use of ACE inhibitors contraindicated?

A

Dehydrated or hypotensive patients

Caution in renal disease and with concurrent NSAID use —> decreased perfusion pressures and low GFR

50
Q

What is the MOA of nitroglycerin and nitroprusside ?

A

Increase production of nitric oxide -> vasodilation

51
Q

T/F: nitroglycerin and nitroprusside are given topically, usually on the inner surface of pinna

A

False

Only nitroglycerin is given topically

Nitroprusside is a potent and rapid arterio-and vasodilator —> is CRI and must be closely monitored

52
Q

Nitroglycerin is primarily a arterio- or venodilator?

A

Venodilator (reduce preload)

53
Q

What is the MOA of hydralazine ?

A

Potent arteriodilator

Interferes with cellular calcium metabolism in smooth muscle

54
Q

What is the indication for hydralazine?

A

For severe/life-threatening pulmonary edema if nitroprusside is not an option

Oral

55
Q

What is the MOA amlodipine?

A

Arteriodilator

Calcium channel blocker

56
Q

What is the main use of amlodipine?

A

Chronic treatment of systemic hypertension (cats and dogs)

Adjunct therapy in refractory CHF

57
Q

What is the MOA of sildenafil?

A

Pulmonary arteriodilator

Inhibit phosphodiesterase 5

58
Q

What is the main use of sildenafil?

A

Moderate to severe pulmonary hypertestion

59
Q

What is the MOA of pimobendan?

A

“Inodilator”
Calcium sensitization —> increase contractility

phosphodiesterase 3 inhibitor —> vasodilator

60
Q

What is the main use of pimobendan ?

A

Canine HF due to degenerative valve disease/ dilated cardiomyopathy

Inodilator

61
Q

What is the MOA of dobutamine ?

A

B1 agonsit

—> inotropic

62
Q

When do you use dobutamine?

A

Severe HR and cardiogenic shock

-when there is lack of response to other drugs

63
Q

What is the MOA of diltiazem?

A

Class IV

Calcium channel blocker

64
Q

What are the uses of diltiazem ?

A

Atrial fibrillation

Supraventricular tachycardia (SVT)

Can be used to improve myocardial relaxation in hypertrophic cardiomyopathy

65
Q

What is the acute (emergency) dose of diltiazem ?

A

0.1mg/kg IV slow over 5mins

66
Q

What drug slows conduction through the AV node and is used in conjunction to diltiazem to control heart rate in AF and SVT ?

A

Digoxin -cardiac glycoside

67
Q

What is the MOA of lidocaine?

A

Class I

Sodium channel blocker

68
Q

What is the main used of lidocaine IV?

A

Suppress VPC and ventricular tachycardia

69
Q

What is the actue(emergency) dose of lidocaine?

A

Dog: 2mg/kg IV slow over 2-3mins

Cat: 0.2mg/kg IV slow

70
Q

What is used for chronic management of ventricular tachycardia?

A

Mexiletine (PO)

Class I sodium channel blocker

71
Q

What is the MOA of sotalol?

A

Class III potassium channel blocker
Beta blocking effects

-typically used for chronic management of ventricular tachycardia and other complex ventricular ectopic

72
Q

What is the MOA of amiodarone ?

A

Class III potassium channel blockers

73
Q

What are the uses of amiodarone?

A

Post cardioversion of AF

Refractory ventricular tachycardia

74
Q

What are the cardioprotective drugs?

A

Beta blockers
ACE inhibitor
Aldosterone antagonist

75
Q

What does chronic sympathetic stimulation do to cardiac muscle?

A

Fibrosis
Apoptosis
Necrosis

76
Q

When are beta blockers contraindicated

A

Acute heart failure

Use cautiously in patients with ventricular systolic dysfunction

77
Q

What non pharmacologic methods can you use in treatment of heart failure?

A

Supplemental oxygen
Thoracocentesis /abdominocenesis
Mechanical ventilation

78
Q

What diets should you recommend to patients in heart failure?

A

Complete and balanced with high quality protein and moderate sodium restriction is possible

79
Q

What is the cause of cardiac cachexia?

A

Loss of lean body mass

  • increased inflammatory cytokines
  • decreased appetite/intake

—> omega fatty acids are beneficial —>inflammatory

80
Q

T/F: mild azotemia is relatively common in patients with CHF

A

True

-often pre renal -> from diuretic or decreased CO
Mild elevations in BUN/CREA do not warrant a reduction in diuretic dose

81
Q

CHF is a chronic condition that usually progresses to death, what is the exception to this?

A

If the underlying disease is reversible, CHF will resolve

RUSVM SAM 1 (26 decks)

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