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
What are some reversible/precipitating causes of hypertrophy
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
What are diagnostic studies to consider
``` Chest x-ray CBC, CMP, BNP TSH, urinalysis EKG Echocardiogram ```
27
What is BNP?
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
What is start for treatment of HF?
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
What should patients be educated on with new diagnosis of HF?
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
What does diuretic do to help HF? How does it affect cardiac output? What are the most effective in treating HF?
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
What are vasodilators used in treating HF?
Venous vasodilators – nitrates Arteriole vasodilators – hydralizine “Balanced” vasodilators – ACE-I, ARB, hydralizine+isosorbide dinatrate Nesiritide – recombinant BNP (intravenous drip)
32
Benefits of ACEs
Help to break the cycle of the RAAS Antihypertensive (afterload) Renal protective Indicated post myocardial infarction
33
SE of ACEs
``` Hypotension Acute Renal Failure Hyperkalemia Cough Angioedema ```
34
Benefits of ARBs
Help to break the cycle of the RAAS Antihypertensive (afterload) Renal protective Indicated post myocardial infarction
35
SE of ARBS
Cough (3 versus 9%) Angioedema Hypotension
36
what are aldosterone antagonists and what should you monitor?
Spironolactone and Epleronone | Monitor kidney function and potassium for risk of hyperkalemia
37
talk about BB and HF
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
When should you consider using hydralazine and isosorbide dinitrite?
``` 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
can you give nepolysin to someone on ACEI?
no!! not for 36+ hours, also it costs $$$$$$$$
40
who should get dig?
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
additional treatment options
``` Iron therapy, Sleep study, Cardiac Resynchronization Therapy (CRT) Internal Cardiac Defibrillator (ICD) Anticoagulation Cardiac Assist Device Cardiac Transplant ```
42
major framingham criteria for HF | need 2 for diagnosis
``` 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
Minor criteria framingham | 1 major plus 2 of these = dx
``` 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
evaluation initial for HF
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