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AGPCNP > CHF > Flashcards

CHF Flashcards

1
Q

What is heart failure?

A

Heart failure is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.
A chronic, progressive condition in which the heart muscle is unable to pump enough blood through the heart to meet the body’s needs for blood and oxygen

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2
Q

What factors contribute to cardiac output?

A

contractility
afterload
preload

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3
Q

What is contractility, and what could cause it to be impaired?

A

Actual measurement of the hearts ability to squeeze – the “force of contraction”
When inadequate this is also called “systolic failure”
Reasons the heart is not able to contract effectively:
Dead tissue doesn’t move – heart attack, cardiotoxic drugs (Adriamycin)
Abnormal heart cells (muscular dystrophy)
Excessive wall stress (dilation of the ventricle, neurohormonal activation

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4
Q

What is preload?

A

The amount of blood filling the ventricle

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5
Q

What is afterload?

A

The resistance the heart must pump against to empty the ventricle
Examples of elevated afterload include hypertension or aortic stenosis

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6
Q

Why do people get heart failure?

A 
Impaired contractility (systolic failure)
Increased afterload
Impaired filling (diastolic failure)
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7
Q

What causes HFrEF

A 
"Systolic Failure"
Impaired contractility
Myocardial infarction
Chronic volume overload
Mitral regurgitation
Aortic regurgitation
Dilated Cardiomyopathy

Increased Afterload
Aortic Stenosis
Hypertension

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8
Q

What causes HfpEF

A 
"diastolic failure"
Impaired Relaxation
Left Ventricular Hypertrophy
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
Myocardial Ischemia

Insufficient Preload
Mitral stenosis
Pericardial constriction

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9
Q

What are symptoms of heart failure?

A 
Dyspnea 
Ankle edema 
Pulmonary edema 
Fatigue 
Exercise intolerance
Orthopnea
Paroxysmal Nocturnal Dyspnea 
Weight loss
Cough
Nocturia 
Palpitations 
Depression 
Cachexia
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10
Q

What are signs of heart failure?

A 
Tachycardia 
Elevated venous pressure
Positive hepatojugular reflux
Pulmonary rales
Tachypnea
Third/fourth heart sound
Hepatomegaly
Ankle edema
Cardiomegaly
Splenomegaly
Hypotension
Pulsus alternans
Extrasystoles
Atrial fibrillation
Weight loss
Ascites
Pleural effusion
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11
Q

right sided heart failure s/s

A 
Peripheral edema
Hepatomegaly (pain?)
Jugular venous distention (with hepatojugular reflux)
Fatigue/Decreased exercise tolerance
S3/S4 Gallop
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12
Q

left sided heart failure s/s

A 
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea (PND)
Fatigue/Decreased exercise tolerance
Tachycardia/tachypnea
Pulmonary rales
S3/S4 Gallop
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13
Q

when does the S4 occur?

A

S4 occurs during the active filling of the ventricle (atrial contraction)
“Tennessee”

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14
Q

when does S3 occur?

A

S3 occurs during the passive filling of the ventricle

“Kentucky”

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15
Q

Describe NYHA Class I

A

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).

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16
Q

Describe NYHA Class II

A

Class II (Mild) – Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.

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17
Q

Describe NYHA Class III

A

Class III (Moderate) – Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.

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18
Q

Describe NYHA Class IV

A

Class IV (Severe) – Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

19
Q

Describe 2013 HF Stage A

A

Goals: heart healthy lifestyle, prevent vascular/CAD, prevent LV structural abnormalities
Drugs: ACE-I or ARB appropriate for patients with vasc disease, statins as appropriate

20
Q

Describe 2013 HF Stage B

A

NYHA Class I
Goals: prevent HF symptoms, prevent further cardiac remodeling
drugs: ACE-I or ARB as appropriate, Beta blockers as appropriate
In selected patients: ICD, revascularization or valvular surgery as appropriate

21
Q

Describe 2013 HF Stage C

A

NYHA Class II-III
HFpEF
Goals: control symptoms, improve HRQOL, prevent hospitalization, prevent mortality
strategies: ID comorbidities
Treatments: diuresis to relieve symptoms of congestion, follow guidelines driven indications for comorbidities like HTN/AF/CAD/DM

HFrEF
Goals: control symptoms, improve HRQOL, prevent hospitalization, prevent mortality
Drugs for routine use: diuretics, ACE-I or ARB, BB, aldosterone antagonists
Drugs for use in selected patients: hydralazine, ACEI/ARB, digitalis
In selected patients: CRT, ICD, revascularization surgery as appropriate

22
Q

Describe 2013 HF Stage D

A

Goals: control symptoms, improve HRQOL, reduce hospital readmissions, establish patients end of life goals

options: advanced care measures, heart transplant, chronic inotropes, temp/permanent MCS, experimental surgery or drugs, palliative care and hospice, ICD deactivation.

23
Q

What are compensatory mechanisms seen in HF?

A

Frank-Starling mechanism
Neurohormonal alterations
Ventricular hypertrophy and remodeling

24
Q

what are neurohormonal alterations

A

Adrenergic Nervous System
Baroreceptors cause an increase in heart rate, augment contractility, and vasoconstrict through α-receptors
Renin-Angiotensin-Aldoserone System (RAAS)
Renin release causes vasoconstriction, increased thirst, and augments sodium reabsorption
Increased Antiduretic Hormone (ADH)
Natriuretic Peptides
Released when ventricular myocardium is subjected to hemodynamic stress – cause excretion of sodium and water, vasodilatation, and inhibit the above hormones

25
Q

What are some reversible/precipitating causes of hypertrophy

A

Increased metabolic demands (infection, anemia, hyperthyroid, etc.)
Increased preload (excessive sodium, excessive fluid intake/administration, renal failure)
Increased afterload (pneumonia, uncontrolled hypertension, PE)
Impaired contractility (negative inotropic medications, myocardial ischemia, ethanol)
Medication non-adherence

26
Q

What are diagnostic studies to consider

A 
Chest x-ray
CBC, CMP, BNP
TSH, urinalysis
EKG
Echocardiogram
27
Q

What is BNP?

A

n-terminal-pro-BNP (nt-pro-BNP)
synthesized and secreted by the ventricular myocardium in response to increases in volume or pressure
Renally excreted
Okay for use in evaluation of dyspnea, but in general not recommended for serial measurement

28
Q

What is start for treatment of HF?

A

Good primary care – HTN and Hyperlipidemia
Treat underlying condition – valve repair/replacement, coronary artery revascularization, antihypertensives, alcohol cessation, rhythm reestablishment
Eliminate acute precipitating cause – infection, arrhythmia, salt intake, medication changes, thyroid, etc.
Treatment of heart failure symptoms
Diuretics
Vasodilators and positive inotropic drugs
Modulation of the neurohormonal response

29
Q

What should patients be educated on with new diagnosis of HF?

A

Dietary – sodium restriction, alcohol cessation, caffeine avoidance
Smoking Cessation
Exercise – may be monitored (cardiac rehab), mild-moderate intensity ~ about 60% of maximal heart rate. Should try to get within 10% of ideal body weight if obese
Daily Weights – same scale, first thing in the morning after initial urination. Need to contact provider with 2 lb weight gain in one day, or 5 lbs in one week. Can often be given a “sliding scale” to titrate their diuretic dosing.
Medications – do not miss doses or prescriptions and avoid NSAIDs, Calcium Channel Blockers, and thiazolidinediones
Vaccines

30
Q

What does diuretic do to help HF? How does it affect cardiac output? What are the most effective in treating HF?

A

With the use of diuretics it is possible to decrease the preload so that the hydrostatic pressure no longer causes pulmonary/venous congestion
Should not effect cardiac output since the Frank Starling curve has “flattened”
Most effective diuretics are the loop diuretics (furosemide, bumetanide, torsemide, ethacrinic acid)
Possible side-effects of hypokalemia, hypomagnesia, orthostatic hypotension, lethargy/drowsiness
Monitor kidney function and electrolytes

31
Q

What are vasodilators used in treating HF?

A

Venous vasodilators – nitrates
Arteriole vasodilators – hydralizine
“Balanced” vasodilators – ACE-I, ARB, hydralizine+isosorbide dinatrate
Nesiritide – recombinant BNP (intravenous drip)

32
Q

Benefits of ACEs

A

Help to break the cycle of the RAAS
Antihypertensive (afterload)
Renal protective
Indicated post myocardial infarction

33
Q

SE of ACEs

A 
Hypotension
Acute Renal Failure
Hyperkalemia
Cough
Angioedema
34
Q

Benefits of ARBs

A

Help to break the cycle of the RAAS
Antihypertensive (afterload)
Renal protective
Indicated post myocardial infarction

35
Q

SE of ARBS

A

Cough (3 versus 9%)
Angioedema
Hypotension

36
Q

what are aldosterone antagonists and what should you monitor?

A

Spironolactone and Epleronone

Monitor kidney function and potassium for risk of hyperkalemia

37
Q

talk about BB and HF

A

Initially contraindicated
Only carvedilol (β1 and β2 as well as weak α1), bisoprolol (β1), and sustained release metoprolol (β1) have been studied and approved for heart failure
Improves indices of LV function, delays progression of myocardial dysfunction, and improves survival (MERIT-HF 1999)
Monitor blood pressure and heart rate (sympathetic nervous system blockade)

38
Q

When should you consider using hydralazine and isosorbide dinitrite?

A 
Recommended for patients self-described as African Americans with NYHA class III–IV receiving optimal therapy with ACE inhibitors and beta blockers.
It can be useful in those who cannot be given an ACE or ARB because of drug intolerance, hypotension, or renal insufficiency.
39
Q

can you give nepolysin to someone on ACEI?

A

no!! not for 36+ hours, also it costs $$$$$$$$

40
Q

who should get dig?

A

positive inotrope
Digitalis – must monitor blood level (goal between 0.5 and 0.8 ng/mL )
Class II-IV despite optimal therapy should get Digoxin
Symptomatic relief, but no morbidity/mortality benefit
Indicated for atrial fibrillation

41
Q

additional treatment options

A 
Iron therapy, Sleep study, 
Cardiac Resynchronization Therapy (CRT)
Internal Cardiac Defibrillator (ICD)
Anticoagulation
Cardiac Assist Device
Cardiac Transplant
42
Q

major framingham criteria for HF

need 2 for diagnosis

A 
Paroxysmal nocturnal dyspnea 
Orthopnea 
Elevated jugular venous pressure 
Pulmonary rales 
Third heart sound
Cardiomegaly on chest x-ray 
Pulmonary edema on chest x-ray 
Weight loss ≥4.5 kg in five days in response to treatment of presumed heart failure
43
Q

Minor criteria framingham

1 major plus 2 of these = dx

A 
Bilateral leg edema
Nocturnal cough
Dyspnea on ordinary exertion
Hepatomegaly
Pleural effusion
Tachycardia (heart rate ≥120 beats/min)
Weight loss ≥4.5 kg in five days
44
Q

evaluation initial for HF

A

Complete history and physical examination
History of alcohol, illicit drugs, standard or “alternative” therapies, and chemotherapy drugs
Ability to perform routine and desired activities of daily living
Assessment of volume status, orthostatic blood pressure changes, height and weight, and calculation of body mass index
CBC, urinalysis, CMP, glucose (A1C?), lipid profile, and thyroid panel
EKG and CXR
Echocardiogram
Cardiac cath if concern for ischemia

AGPCNP (30 decks)

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