Heart Failure Flashcards

1
Q

Cardinal clinical SYMPTOMS of heart failure

A

dyspnea

fatigue

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2
Q

Clinical SIGNS of heart failure

A

edema

rales

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3
Q

Depressed EF (<40%)

A

CAD- myocardial infarction and myocardial ischemia

Chronic pressure overload - HPN, obstructive valvular disease

Chronic volume overload - regurgitant valvular disease, intracardiac (L-R) shunting, extracardiac shunting

Chronic Lung Disease - Cor pulmonale, pulmonary vascular disorders

Nonischemic dilated cardiomyopathy - familial/genetic disorders, infiltrative disorders

Toxic/drug-induced damage - metabolic disorder, viral

Chagas disease

Disorders of rate and rhythm - chronic bradyarrhythmias and tachyarrhythmias

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4
Q

Preserved Ejection fraction (>40 - 50%)

A

pathologic hypertrophy - HCOM, HPN

aging

endomyocardial disorders
restrictive cardiomyopathy - infiltrative disorders, storage disorders

fibrosis

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5
Q

High Output States

A

metabolic disorders - thyrotoxicosis

nutritional disorders (beriberi)

excessive blood flow requirements - systemic AV shunting, chronic anemia

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6
Q

Conditions that can lead w/ a depressed EF or preserved EF

A
myocardial infarction
myocardial ischemia
hypertension
obstructive valvular disease
infiltrative disorder
metabolic disorder
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7
Q

NYHA Classification

A

Class I - px w/ cardiac disease but w/o resulting limitation of physical activity

Class II - px w/ cardiac disease w/ slight limitation of physical activity

Class III - px w/ cardiac disease w/ marked limitation of physical activity

Class IV - px w/ cardiac disease resulting in inability to carry on any physical activity w/o discomfort

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8
Q

Orthopnea

A

Results from redistribution of fluid from the splanchnic circulation and lower extremities into the central circulation during recumbency with a resultant ↑ in pulmonary capillary pressure

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9
Q

Paroxysmal Nocturnal Dyspnea

A

Refers to acute episodes of severe shortness of breath and coughing that generally occur at night d.t. INCREASED PRESSURE in BRONCHIAL ARTERIES

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10
Q

Cheyne-Stokes Respiration

A

Periodic respiration or cyclic respiration: series of APNEA, HYPERVENTILATION and HYPOCAPNIA

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11
Q

Pulmonary crackles (rales or crepitations)

A

Result from the transudation of fluid from the intravascular space into the alveoli

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12
Q

Pleural effusion

A

Result from the elevation of pleural capillary pressure and the resulting transudation of fluid into the pleural cavities

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13
Q

Hepatomegaly

A

An important sign in px with HF and may pulsate during systole if tricuspid regurgitation is present

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14
Q

Assess cardiac rhythm and determine the presence of LV hypertrophy or prior MI (absence or presence of Q-waves)

A

ECG

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15
Q

Classic Chest X-Ray Pattern In Patients with PULMONARY EDEMA

A

“butterfly” pattern of interstitial and alveolar opacities

Kerley B lines

peribronchial cuffing

evidence of prominent UPPER lobe vasculature

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16
Q

Classic Chest X-Ray Pattern In Patients with PULMONARY EDEMA

A

“butterfly” pattern of interstitial and alveolar opacities

Kerley B lines

peribronchial cuffing

evidence of prominent UPPER lobe vasculature

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17
Q

The most useful test that can provide semiquantitative assessment of LV size and function, presence or absence of valvular and/or regional wall motion abnormalities

A

2D Echo/Doppler

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18
Q

The gold standard for assessing LV mass and volumes

A

Magnetic Resonance Imaging (MRI)

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19
Q

Most useful index of LV function

A

EF (stroke volume divided by end-diastolic volume)

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20
Q

Released from the failing heart and sensitive markers for the presence of HF with depressed EF

A

B-type natriuretic peptide (BNP)

N-terminal pro-BNP (NT-proBNP)

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21
Q

Newer biomarkers that can be used for determining the prognosis of HF patients

A

soluble ST-2 and galectin-3

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22
Q

NOT routinely advocated for patients with HF but useful for assessing the need for cardiac transplantation in patients with advanced HF

A

Exercise Testing

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23
Q

Form the cornerstone of pharmacotherapy lead to attenuation of decline and improvement in cardiac structure

A

RAAS blockers

β-blockers

24
Q

• Interferes with RAAS by inhibiting conversion of angiotensin I to angiotensin II

25
Used if the px is ACE-intolerant
Angiotensin Receptor Blockers
26
Interferes with sustained activation of the adrenergic nervous system particularly B1 activation
Beta-blockers
27
Inhibits action of aldosterone on the collecting duct
Aldosterone Antagonist
28
Reduces the HR by inhibition of “funny channels” in the SA node
Ivabradine
29
Recommended to replace ACE-I in ambulatory HFrEF patients who remain symptomatic despite optimal therapy
Angiotensin Receptor Neprilysin Inhibitor (ARNI) ARB - valsartan neprilysin inhibitor - sacubitril
30
Asymptomatic LV Dysfunction (NYHA I)
ACE I or ARB B-blocker (if post MI) Aldosterone antagonist (if recent MI)
31
Symptomatic HF (NYHA II)
ACE I or ARB Diuretic (if with fluid retention) B-blocker Aldosterone antagonist
32
Worsening HF (NYHA III-IV)
``` ACE I or ARB Diuretic B-blocker Aldosterone antagonist Digoxin ```
33
End stage HF (NYHA IV)
``` ACE I or ARB Diuretic B-blocker Aldosterone antagonist Digoxin ```
34
Rapid onset or worsening symptoms/signs of HF Life threatening
Acute Decompensated Heart Failure (ADHF)
35
Acute Decompensated Heart Failure (ADHF)
peripheral edema orthopnea dyspnea on exertion usually no/minimal volume overload
36
Acute Hypertensive HF
severe dyspnea tachypnea tachycardia frank pulmonary edema
37
Cardiogenic Shock
end-organ hypoperfusion oliguria confusion cool extremities
38
First line therapy in volume overloaded patients w/ pulmonary congestion
Diuretics furosemide bumetanide
39
Initial therapy for hypertensive AHF (hypertensive emergency) decreases venous tone to optimize preload decreases arterial tone (or afterload)
Vasodilators nitroglycerin isosorbide dinitrate
40
Used for patients w/ hypotension, end-organ hypoperfusion or shock sec to myocardial pump failure
Inotropic Agents dobutamine dopamine
41
Considered for cardiogenic shock despite inotropic support
NE | high dose dopamine
42
Good perfusion and no congestion
Warm and Dry adjust oral therapy
43
Good perfusion but with congestion
Warm and Wet if HPN predominates: vasodilators and diuretics if congestion predominates: diuretics, vasodilators
44
With hypoperfusion but no congestion
Cold and Dry fluid challenge then inotropic support if still hypoperfused
45
With hypoperfusion and w/ congestion
Cold and Wet SBP >90 mmHg: vasodilators, diuretics consider inotropic agents if refractory SBP <90 mmHg: inotropic agents, consider vasopressors, diuretics when perfusion is corrected and consider mechanical circulatory support
46
Framingham Diagnostic Criteria for HF
``` MAJOR PND or orthopnea neck vein distention rales cardiomegaly acute pulmonary edema S3 gallop increased venous pressure >16 cmH20 hepatojugular reflux ``` ``` MINOR ankle edema night cough dyspnea on exertion hepatomegaly pleural effusion vital capacity decreased by 1/3 from maximal capacity tachycardia .>120 bpm ``` MAJOR or MINOR - weight loss >4.5 kg in 5 days in response to treatment 2 MAJOR or 1 MAJOR + 2 MINOR
47
MC cause of systolic dysfunction --> L sided HF
CAD
48
MC cause of diastolic dysfunction --> L sided HF
concentric LVH d.t. HPN
49
MC cause of R sided HF
L sided HF
50
Earliest cardinal symptom of L sided HF
dyspnea
51
Earliest cardinal sign of L sided HF
L sided S3
52
Most sensitive index of cardiac function
ejection fraction
53
Single most important bedside measurement to estimate volume status
JVP
54
Most important mechanism of dyspnea in HF
pulmonary congestion w/ accumulation of interstitial or intraalveolar fluid --> activates juxtacapillary J receptors
55
Cornersyone of modern therapy for HF w/ depressed EF
ACE-I/ARBS and Beta Blockers
56
Gold standard in assessing anatomy and physiology of the heart and associated vasculature
cardiac catheterization and coronary angiography