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Cardiovascular > Heart Failure Part 1 > Flashcards

Heart Failure Part 1 Flashcards

1
Q

Complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. Characterized by signs and symptoms of reduced CO and volume overload

A

Heart Failure

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2
Q

Which patients have the highest risk of heart failure?

A

Black patients due to disparities in risk factors, socioeconomic status, and access to care

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3
Q

Which gender is more impacted by heart failure?

A

Men, slightly

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4
Q

What is the 5 year survival rate of heart failure?

A

50%
Severe disease, 1 year mortality may be as high as 40%

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5
Q

What is the MC cause of death for heart failure patients?

A

Progressive HF or sudden cardiac death

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6
Q

What 2 things related to morbidity and mortality are common with heart failure?

A
  • Hospitalization (83% hospitalized at least once)
  • Readmission
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7
Q

What are risk factors for heart failure?

A
  • CAD/atherosclerosis
  • DM
  • HTN
  • Metabolic syndrome/obesity
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8
Q

What are the most common risk factors for heart failure in men?

A
  1. Hypertension
  2. Myocardial infarction
  3. Valvular disease
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9
Q

What are the most common risk factors for heart failure in women?

A
  1. Hypertension
  2. Myocardial infarction
  3. Diabetes
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10
Q

How is heart failure classified?

A
  • Acute vs chronic
  • High vs low output
  • HF with reduced left ventricular EF vs HF with preserved EF
  • Left vs Right
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11
Q

What qualifies as acute heart failure?

A
  • Symptoms within last few days to weeks
  • Shortness of breath
  • PND
  • Orthopnea
  • RUQ pain
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12
Q

What qualifies as chronic heart failure?

A
  • Symptoms present for months
  • Fatigue
  • Anorexia
  • Abdominal distention
  • Edema

Possible to have acute exacerbation in a chronic state

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13
Q

What qualifies as high output heart failure?

A
  • Heart unable to meet the demands of the peripheral needs
  • D/t thyrotoxicosis, severe anemia, sepsis
  • Symptoms of reduced cardiac output rather than volume overload
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14
Q

What qualifies as low output heart failure?

A
  • Insufficient forward output
  • Reduced EF, hypovolemia
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15
Q

What qualifies as HF with reduced left ventricular EF (HFrEF)?

A
  • Systolic
  • EF < or equal to 40%
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16
Q

What qualifies as HF with preserved EF (HFpEF)?

A
  • Diastolic
  • EF>50%

If falls between 40 and 50% EF, symptom management depending on patient case

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17
Q

This classification of HF is referred to as systolic. It is the type of HF that efficacious therapies have been demonstrated in

A

Heart failure with reduced ejection fraction (HFrEF)

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18
Q

Also referred to as diastolic HF. Challenging diagnosis because largely of excluding other noncardiac causes of symptoms suggestive of HF. To date, no efficacious therapies have been identified

A

HFpEF

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19
Q

EF% 41 to 49

A

HFpEF, borderline. Characteristics, treatment patterns, and oucomes are similar to HFpEF

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20
Q

Which side of the heart is affected in the majority of cardiomyopathies?

A

Left

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21
Q

What does left sided HF lead to?

A
  • DOE
  • PND
  • Orthopnea
  • Fatigue

d/t poor perfusion of the body and congestion of the lungs

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22
Q

What is the most common cause of right side HF?

A

Left sided HF

Can also be caused by lung disorders, CAD, pulmonary valvular disorders, ARVC, VSD with left to right shunting

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23
Q

How does right sided HF present?

A
  • JVD
  • Hepatic congestion
  • Ascites
  • Anorexia
  • LE edema

due to R sided heart backing up into vena cava

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24
Q

What are all the symptoms of Left sided HF (based on picture)?

A
  • PND
  • Elevated pulmonary capillary wedge pressure
  • Pulmonary congestion (cough, crackles, wheezes, blood-tinges sputum, tachypnea)
  • Restlessness
  • Confusion
  • Orthopnea
  • Tachycardia
  • Exertional dyspnea
  • Fatigue
  • Cyanosis

only perfusing proximal

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25
Q

What are all the symptoms of R sided failure (based on picture)?

A
  • Fatigue
  • Increased peripheral venous pressure
  • Ascites
  • Enlarged liver and spleen
  • JVD
  • Anorexia and complaints of GI distress
  • Weight gain
  • Dependent edema

Cor pulmonale

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26
Q

What is NYHA classification used to quantify?

A
  • Functional limitation in order to estimate severity of disease
  • Assesses effort needed to elicit symptoms in HF patient
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27
Q

What are the NYHA classes?

A

I-IV

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28
Q

Is NYHA classification static or can it change?

A

It can change at any time

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29
Q

What does it mean if a patient has a NYHA classification of I?

A
  • No limitation of physical activity
  • Ordinary physical activity does not cause symptoms of HF (dyspnea, fatigue)
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30
Q

What does it mean if a patient has a NYHA classification of II?

A
  • Slight limitation of physical activity
  • Symptoms of HF develop with ordinary activity but not at rest
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31
Q

What does it mean if a patient is a NYHA classification of III?

A
  • Marked limitation of physical activity
  • Symptoms of HF with less than ordinary activity but not at rest
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32
Q

What does the American College of Cardiology Foundation/AHA staging describe?

A
  • Evolution of heart failure
  • Progressive stages that cannot change
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33
Q

How is ACCF/AHA classification helpful?

A

Helps define appropriate therapeutic approach and determine prognosis

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34
Q

What does it mean if a patient is a ACC/AHA stage A?

A
  • At risk for HF but no structural heart disease or symptoms of HF
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35
Q

What does it mean if a patient is a ACC/AHA stage B?

A
  • Structural heart disease but without signs or symptoms of HF
  • Includes NYHA class I with no prior or current signs or symptoms of HF
36
Q

What does it mean if a patient is a ACC/AHA stage C?

A
  • Structural heart disease with prior or current symptoms of HF
  • Patients in any NYHA functional class (including class I with prior symptoms)
37
Q

What does it mean if a patient is an ACC/AHA stage D?

A
  • Refractory HF requiring specialized interventions
  • Includes patients in NYHA functional class IV with refractory symptoms
38
Q

What is cardiac output the product of?

A

Heart rate and stroke volume

39
Q

What impacts the heart rate (causing an effect on the cardiac output)?

A
  • Increases with positive chronotropic agents –> atropine, beta agonists
  • Decreases with negative chronotropic agents –> beta blockers, calcium channel blockers
  • Inversely affects filling time
40
Q

What impacts stroke volume?

A
  • Inversely affected by afterload
  • Afterload directly affects ESV
  • ESV inversely affects stroke volume
  • Stroke volume is directly affected by contractility and preload due to EDV
41
Q

What impacts preload due to EDV (leading to direct impact on stroke volume)?

A
  • directly affected by filling time
  • Directly affected by venous return
42
Q

What impacts contractility (directly affecting stroke volume)?

A
  • Increases with positive inotropic agents
  • decreases with negative inotropic agents
43
Q

What impacts venous return (leading to direct impact on preload due to EDV and impact on SV)?

A
  • directly affected by blood volume and venous pressure
  • inversely affected by intrathoracic pressure
44
Q

What are neurohumoral adaptations?

A

compensatory mechanisms used by the body in an attempt to adjust for a reduction in cardiac output
* maintain systemic pressure by vasoconstriction
* restores cardiac output by increasing myocardial contractility and heart rate
* occurs in both systolic and diastolic dysfunction

45
Q

As cardiac output decreases, what does the body do to compensate?

A
  • Increases sympathetic activity
  • Vasoconstriction
  • Releases renin in response to decreased renal blood flow leading to increased angiotensin II and increased aldosterone
46
Q

What medications can be given for HF and where do they work?

A
  • Beta blockers counteract increased sympathetic activity
  • Arterial vasodilators counteract vasoconstriction
  • ACEI/ARBs counteract conversion to angiotensin II
  • Aldosterone antagonists counteract increased aldosterone release
47
Q

What is one of the first response to low cardiac output?

A
  • Activation of the SNS
  • Resulting in increased release and decreased uptake of norepinephrine to increase ventricular contractility and heart rate
  • Also leads to vasoconstriction and enhanced venous tone increasing preload
48
Q

What does increased sympathetic nervous system activity in HF do to sodium and norepinephrine?

A
  • Stimulates proximal tubular sodium reabsorption, contributing to sodium retention in HF
  • Increased release and decreased reuptake results in increase of plasma NE concentration, which correlates to severity of HF and inversely with survival
49
Q

What does HF do to the RAAS system?

A
  • RAAS system stimulated by decreased glomerular filtration and increased beta-1 adrenergic activity
  • Increases sodium reabsorption
  • Induces systemic and renal vasoconstriction
  • Can act directly on myocytes to promote pathologic remodeling via hypertrophy, apoptosis, necrosis
  • Myocytes develop more AT2 receptors, which results in cell apoptosis
50
Q

What happens to ADH in HF?

A
  • Low cardiac output –> activation of carotid sinus and aortic arch baroreceptors –> release of ADH and stimulation of thirst
51
Q

What does increased release of ADH lead to?

A
  • Increase in systemic vascular resistance
  • Water retention
  • Reduced sodium level (due to dilution via water retention and thirst)
  • Degree of hyponatemia parallels severity of HF
52
Q

What is ANP?

A
  • Atria natriuretic peptide
  • Released from atria in response to volume expansion
53
Q

How is ANP related to HF?

A

Rises early in HF

54
Q

What is BNP?

A
  • Brain natriuretic peptide
  • Released from ventricles in response to high ventricular filling pressures
55
Q

How is BNP related to HF?

A
  • Present in chronic or advanced HF
  • Reduces systemic vascular resistance and central venous pressure, while increasing natriuresis, which reduces afterload
56
Q

What are maladaptive consequences of HF?

A
  • Elevation in diastolic pressures are transmitted to the atria and pulmonary and systemic venous circulations –> pulmonary vascular congestion and peripheral edema
  • Increased afterload can depress cardiac function and enhance deterioration
  • Catecholamine-stimulated contractility and increased heart rate can worsen coronary ischemia
  • Catecholamines and antiotensin II promote myocyte loss, resulting in cardiac remodeling
57
Q

What are the 3 major determinants of the LV stroke volume?

A
  • Preload
  • Contractility
  • Afterload
58
Q

What impacts preload?

A

Venous return and end-diastolic volume

59
Q

What is contractility?

A

The force generated at any given end-diastolic volume

60
Q

What impacts afterload?

A
  • Aortic impedance
  • Vascular resistance
  • Wall stress
  • Small changes in failing heart can lead to large changes in SV
61
Q

What happens to contractility in systolic dysfunction? What does this lead to?

A
  • Reduction in myocardial contractility
  • Reduction in SV and CO
  • Which increases SNS, increasing contractility and HR
  • Which promotes salt and water retention, leading to expansion of blood volume, therefore raising end-diastolic pressure and volume
62
Q

What would patient complain of due to heart failure?

A
  • Symptoms due to low CO and fluid accumulation

Cardinal symptoms:
* Dyspnea
* Fatigue
* Fluid retnetion: lower extremity edema

63
Q

What should you include in ROS to identify source of HF?

A
  • Chest pain, flu-like symptoms, alcohol use, hx of heart murmurs
  • Family hx
  • Changes in medications (chemo, calcium channel blockers, flecainide)
  • PMH of autoimmune disorders, thyroid disease, DM, CAD, etc.
64
Q

What can be present on vital signs and volume assessment physical exam of HF?

A

Vital signs:
* Resting sinus tachycardia
* Narrow pulse pressure
* Diaphoresis
* Peripheral vasoconstriction

Volume assessment:
* Pulmonary congestion: inspiratory rales or dull breath sounds at bases
* Peripheral edema: lower extremities, scrotum, ascites
* Elevated jugular venous pressure: present if edema is due to HF

65
Q

How do you assess for LE edema?

A

Start at feet and work way proximally to see how far edema extends and don’t forget about sacral and scrotal areas

66
Q

What may be present on cardiac physical exam of HF?

A
  • Pulsus alternans
  • Precordial palpation: laterally displaced apical impulse usually indicating LV enlargement, parasternal life of RV with pulmonary HTN
  • Heart sounds: S3 gallop associated with systolic HF, S4 gallop more common in diastolic HF
67
Q

What systems should be covered in HF physical exam?

A
  • General
  • Cardiovascular
  • Respiratory
  • Abdomen
  • Skin
  • Neuro
  • Thyroid
68
Q

What is the goal of diagnostic studies in HF?

A

Confirm symptoms are due to HF
Determine cause of HF

69
Q
A
70
Q

What initial testing should be doen in HF?

A
  • Electrocardiogram
  • Chest xray
  • CBC
  • CMP
  • Coagulation studies
  • fasting blood glucose
  • Lipid panel
71
Q

why might a electrocardiogram be helpful for HF?

A
  • can detect findings that specify a cause
  • may show arrhythmia that is cause or result of HF
72
Q

Why is chest x-ray indicated in HF?

A
  • Evaluate for pulmonary edema
  • Cardiopulmonary structural abnormalities
  • Other potential causes for dyspnea
73
Q

What may be findings on chest x-ray in HF?

A
  • Pulmonary vascular congestion
  • Cardiomegaly
  • Kerley B lines
  • Pleural effusions
74
Q

What might be present on CBC of a patient with HF?

A
  • Anemia
  • Pericarditis
  • Leukocytosis
75
Q

What is important on CMP of a patient with HF?

A
  • Electrolytes
  • BUN/Cr
  • Magnesium, LFTs
76
Q

What are additional lab tests that can be considered if they will be beneficial in supporting or determining etiology of HF?

A
  • Thyroid function
  • Iron studies
  • ANA
  • Viral serology
  • Genetic testing
77
Q

What is the best test for HF evaluation?

A
  • BNP and NT-proBNP
78
Q

What is BNP and NT-proBNP?

A
  • Released from ventricles while in HF
  • Useful in supporting diagnosis and establishing severity
  • Used to exclude HF as a cause of symptoms, because it has a very high negative predictive value
79
Q

What is the normal value for BNP/pro-BNP?

A
  • BNP <100 pg/mL
  • NT-proBNP<300
80
Q

What are limitations of BNP and NT-proBNP?

A
  • Patient may present with more than one cause for dyspnea
  • Pts with severe chronic HF may have persistently elevated levels of BNP

Other causes of elevated BNP:
* ACS, LVH, valvular disease, Afib, S/P cardioversion
* Increased age, severe anemia, renal failure
* PNA, pulmonary hypertension
* Sepsis, severe burns

81
Q

What biomarkers can be helpful in HF eval?

A

Troponin I or T and BNP/pro-BNP

82
Q

Why might troponin I or T be helpful in HF evaluation?

A
  • Significant elevation indicates ischemic source for HF
  • Can be elevated with severe HF, without CAD/myocardial ischemia
83
Q

What imaging should be performed in all patients with new onset heart failure?

A
  • Echocardiography
84
Q

Wht important information can echo give you?

A
  • Info on ventricular size and function
  • LV diastolic function
  • Regional wall motion abnormalities
  • Pericardial thickening or effusion
  • Valvular disease
  • RV function and pulm pressures
85
Q

What testing is useful to exclude CAD?

A

Stress testing
* Even if normal, if no other cause identifiable, coronary angiography should be considered
* May also perform left ventriculogram during cardiac catheterization to evaluate LV function

86
Q

What additional imaging may be considered if neccessary?

A
  • Cardiac MRI
  • Cardiac CTA
  • Endomyocardial biopsy
87
Q

What is the goal of heart failure treatment?

A
  • Relieve symptoms
  • Improve functional status
  • Prevent death and hospitalizations
  • Clinical benefit of most therapies limited to HFrEF
  • HFpEF tx aimed at improving symptoms and treating comorbidities

Cardiovascular (17 decks)

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