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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
CAT Tachypnea Dyspnea Lethargy Syncope What type of HF is this?
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
26
DOG ``` Tachypnea Cough Dyspnea Exercise intolerance Syncope ``` What type of heart failure is this?
Congestive Signs could be due to left or right.. this is likely left because there is no abdominal distention
27
DOG ``` Exercise intolerance Weakness or collapse Lethargy Depressed mentation Pallor Hypothermia ``` What type of heart failure is this?
Low output heart failure -signs in the cat would be similar
28
What are the three main goals of heart failure therapy?
Relieve congestion Improve cardiac output Prevent progression (cardioprotection)
29
How can congestion be relieved when treating heart failure?
Decreased ventricular filling - decreased blood volume (preload) —> diuretics/dietary sodium restriction/venodilators - increase forward flow Abdominocentesis/throacocentesis
30
How can you improve cardiac output in systolic dysfunction?
Increase ventricular contractility—> positive inotropic drugs Decrease afterload —> arteriodilators
31
How can you improve cardiac output for diastolic dysfunction?
Need to improve ventricular relaxation and decrease heart rate
32
T/F: sinus tachycardia is a compensatory mechanism in HR to improve cardiac output
True
33
What is the consequence to a pathological tachyarrhythmia during heart failure?
Heart rate is too high —> diastole time is too short —> EDV falls —> SV falls —> CO falls
34
What is the consequence of pathological bradyarrhythmia during heart failure?
HR too low —> ventricles are to ejecting blood into arteries frequently enough to maintain BP and meet body’s metabolic requirements
35
What are the classes of cardiovascular drugs?
``` Diuretic ACE inhibitors Vasodilator Positive inotropes Anti-arrhythmics Cardioprotective ```
36
What is the first choice drug for CHF and what is its MOA?
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
How can you administer Furosemide?
Oral IV IM SC (off label)
38
What is the dose for acute/emergency CHF of furosemide ?
Dog: 2-4mg/kg IV or IM +/- CRI Cat: 1-3mg/kg IV or IM +/- CRI
39
What are the the expected/adverse effects of furosemide and hydrochlorothiazide?
Expected: polyuria and polydipsia Adverse: - volume depletion and pre-renal azotemia - electrolyte imbalances - renal failure - ototoxicity - dermal ulcerations
40
What drug has better bioavailability and longer duration than furosemide, often used as an adjunct therapy in refractory CHF?
Torsemide
41
What is the MOA of hydrochlorothiazide?
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
What is the potassium sparing diretic?
Spironolactone
43
What is the MOA of spironolactone?
Aldosterone receptor antagonist
44
Why use spironolactone in CHF patients?
As add on to furosemide in patients that are becoming hypokalemic (potassium sparing) Cardioprotective (anti-fibrotic effects)
45
What are the ACE inhibitor drugs?
Benazepril | Enalapril
46
What is the MOA of enalapril and benazepril?
ACE inhibitors | -inhibit conversion of angiotensin I to angiotensin II
47
What are the uses of ACE inhibitors in heart failure?
Inhibit chronic effects of RAAS—> decreased afterload due to vasodilation Cardioprotective by helping to prevent myocardial fibrosis
48
What are adverse effects of ACE inhibitors?
Systemic hypotension Impaired renal function GI upset
49
When is use of ACE inhibitors contraindicated?
Dehydrated or hypotensive patients Caution in renal disease and with concurrent NSAID use —> decreased perfusion pressures and low GFR
50
What is the MOA of nitroglycerin and nitroprusside ?
Increase production of nitric oxide -> vasodilation
51
T/F: nitroglycerin and nitroprusside are given topically, usually on the inner surface of pinna
False Only nitroglycerin is given topically Nitroprusside is a potent and rapid arterio-and vasodilator —> is CRI and must be closely monitored
52
Nitroglycerin is primarily a arterio- or venodilator?
Venodilator (reduce preload)
53
What is the MOA of hydralazine ?
Potent arteriodilator | Interferes with cellular calcium metabolism in smooth muscle
54
What is the indication for hydralazine?
For severe/life-threatening pulmonary edema if nitroprusside is not an option Oral
55
What is the MOA amlodipine?
Arteriodilator | Calcium channel blocker
56
What is the main use of amlodipine?
Chronic treatment of systemic hypertension (cats and dogs) Adjunct therapy in refractory CHF
57
What is the MOA of sildenafil?
Pulmonary arteriodilator | Inhibit phosphodiesterase 5
58
What is the main use of sildenafil?
Moderate to severe pulmonary hypertestion
59
What is the MOA of pimobendan?
“Inodilator” Calcium sensitization —> increase contractility phosphodiesterase 3 inhibitor —> vasodilator
60
What is the main use of pimobendan ?
Canine HF due to degenerative valve disease/ dilated cardiomyopathy Inodilator
61
What is the MOA of dobutamine ?
B1 agonsit | —> inotropic
62
When do you use dobutamine?
Severe HR and cardiogenic shock | -when there is lack of response to other drugs
63
What is the MOA of diltiazem?
Class IV | Calcium channel blocker
64
What are the uses of diltiazem ?
Atrial fibrillation Supraventricular tachycardia (SVT) Can be used to improve myocardial relaxation in hypertrophic cardiomyopathy
65
What is the acute (emergency) dose of diltiazem ?
0.1mg/kg IV slow over 5mins
66
What drug slows conduction through the AV node and is used in conjunction to diltiazem to control heart rate in AF and SVT ?
Digoxin -cardiac glycoside
67
What is the MOA of lidocaine?
Class I | Sodium channel blocker
68
What is the main used of lidocaine IV?
Suppress VPC and ventricular tachycardia
69
What is the actue(emergency) dose of lidocaine?
Dog: 2mg/kg IV slow over 2-3mins Cat: 0.2mg/kg IV slow
70
What is used for chronic management of ventricular tachycardia?
Mexiletine (PO) | Class I sodium channel blocker
71
What is the MOA of sotalol?
Class III potassium channel blocker Beta blocking effects -typically used for chronic management of ventricular tachycardia and other complex ventricular ectopic
72
What is the MOA of amiodarone ?
Class III potassium channel blockers
73
What are the uses of amiodarone?
Post cardioversion of AF | Refractory ventricular tachycardia
74
What are the cardioprotective drugs?
Beta blockers ACE inhibitor Aldosterone antagonist
75
What does chronic sympathetic stimulation do to cardiac muscle?
Fibrosis Apoptosis Necrosis
76
When are beta blockers contraindicated
Acute heart failure Use cautiously in patients with ventricular systolic dysfunction
77
What non pharmacologic methods can you use in treatment of heart failure?
Supplemental oxygen Thoracocentesis /abdominocenesis Mechanical ventilation
78
What diets should you recommend to patients in heart failure?
Complete and balanced with high quality protein and moderate sodium restriction is possible
79
What is the cause of cardiac cachexia?
Loss of lean body mass - increased inflammatory cytokines - decreased appetite/intake —> omega fatty acids are beneficial —>inflammatory
80
T/F: mild azotemia is relatively common in patients with CHF
True -often pre renal -> from diuretic or decreased CO Mild elevations in BUN/CREA do not warrant a reduction in diuretic dose
81
CHF is a chronic condition that usually progresses to death, what is the exception to this?
If the underlying disease is reversible, CHF will resolve

RUSVM SAM 1 (26 decks)

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