Heart Failure Flashcards
Cardinal clinical SYMPTOMS of heart failure
dyspnea
fatigue
Clinical SIGNS of heart failure
edema
rales
Depressed EF (<40%)
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
Preserved Ejection fraction (>40 - 50%)
pathologic hypertrophy - HCOM, HPN
aging
endomyocardial disorders
restrictive cardiomyopathy - infiltrative disorders, storage disorders
fibrosis
High Output States
metabolic disorders - thyrotoxicosis
nutritional disorders (beriberi)
excessive blood flow requirements - systemic AV shunting, chronic anemia
Conditions that can lead w/ a depressed EF or preserved EF
myocardial infarction myocardial ischemia hypertension obstructive valvular disease infiltrative disorder metabolic disorder
NYHA Classification
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
Orthopnea
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
Paroxysmal Nocturnal Dyspnea
Refers to acute episodes of severe shortness of breath and coughing that generally occur at night d.t. INCREASED PRESSURE in BRONCHIAL ARTERIES
Cheyne-Stokes Respiration
Periodic respiration or cyclic respiration: series of APNEA, HYPERVENTILATION and HYPOCAPNIA
Pulmonary crackles (rales or crepitations)
Result from the transudation of fluid from the intravascular space into the alveoli
Pleural effusion
Result from the elevation of pleural capillary pressure and the resulting transudation of fluid into the pleural cavities
Hepatomegaly
An important sign in px with HF and may pulsate during systole if tricuspid regurgitation is present
Assess cardiac rhythm and determine the presence of LV hypertrophy or prior MI (absence or presence of Q-waves)
ECG
Classic Chest X-Ray Pattern In Patients with PULMONARY EDEMA
“butterfly” pattern of interstitial and alveolar opacities
Kerley B lines
peribronchial cuffing
evidence of prominent UPPER lobe vasculature
Classic Chest X-Ray Pattern In Patients with PULMONARY EDEMA
“butterfly” pattern of interstitial and alveolar opacities
Kerley B lines
peribronchial cuffing
evidence of prominent UPPER lobe vasculature
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
2D Echo/Doppler
The gold standard for assessing LV mass and volumes
Magnetic Resonance Imaging (MRI)
Most useful index of LV function
EF (stroke volume divided by end-diastolic volume)
Released from the failing heart and sensitive markers for the presence of HF with depressed EF
B-type natriuretic peptide (BNP)
N-terminal pro-BNP (NT-proBNP)
Newer biomarkers that can be used for determining the prognosis of HF patients
soluble ST-2 and galectin-3
NOT routinely advocated for patients with HF but useful for assessing the need for cardiac transplantation in patients with advanced HF
Exercise Testing
Form the cornerstone of pharmacotherapy lead to attenuation of decline and improvement in cardiac structure
RAAS blockers
β-blockers
• Interferes with RAAS by inhibiting conversion of angiotensin I to angiotensin II
ACE - I
Used if the px is ACE-intolerant
Angiotensin Receptor Blockers
Interferes with sustained activation of the adrenergic nervous system particularly B1 activation
Beta-blockers
Inhibits action of aldosterone on the collecting duct
Aldosterone Antagonist
Reduces the HR by inhibition of “funny channels” in the SA node
Ivabradine
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
Asymptomatic LV Dysfunction (NYHA I)
ACE I or ARB
B-blocker (if post MI)
Aldosterone antagonist (if recent MI)
Symptomatic HF (NYHA II)
ACE I or ARB
Diuretic (if with fluid retention)
B-blocker
Aldosterone antagonist
Worsening HF (NYHA III-IV)
ACE I or ARB Diuretic B-blocker Aldosterone antagonist Digoxin
End stage HF (NYHA IV)
ACE I or ARB Diuretic B-blocker Aldosterone antagonist Digoxin
Rapid onset or worsening symptoms/signs of HF
Life threatening
Acute Decompensated Heart Failure (ADHF)
Acute Decompensated Heart Failure (ADHF)
peripheral edema
orthopnea
dyspnea on exertion
usually no/minimal volume overload
Acute Hypertensive HF
severe dyspnea
tachypnea
tachycardia
frank pulmonary edema
Cardiogenic Shock
end-organ hypoperfusion
oliguria
confusion
cool extremities
First line therapy in volume overloaded patients w/ pulmonary congestion
Diuretics
furosemide
bumetanide
Initial therapy for hypertensive AHF (hypertensive emergency)
decreases venous tone to optimize preload
decreases arterial tone (or afterload)
Vasodilators
nitroglycerin
isosorbide dinitrate
Used for patients w/ hypotension, end-organ hypoperfusion or shock sec to myocardial pump failure
Inotropic Agents
dobutamine
dopamine
Considered for cardiogenic shock despite inotropic support
NE
high dose dopamine
Good perfusion and no congestion
Warm and Dry
adjust oral therapy
Good perfusion but with congestion
Warm and Wet
if HPN predominates: vasodilators and diuretics
if congestion predominates: diuretics, vasodilators
With hypoperfusion but no congestion
Cold and Dry
fluid challenge then inotropic support if still hypoperfused
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
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
MC cause of systolic dysfunction –> L sided HF
CAD
MC cause of diastolic dysfunction –> L sided HF
concentric LVH d.t. HPN
MC cause of R sided HF
L sided HF
Earliest cardinal symptom of L sided HF
dyspnea
Earliest cardinal sign of L sided HF
L sided S3
Most sensitive index of cardiac function
ejection fraction
Single most important bedside measurement to estimate volume status
JVP
Most important mechanism of dyspnea in HF
pulmonary congestion w/ accumulation of interstitial or intraalveolar fluid –> activates juxtacapillary J receptors
Cornersyone of modern therapy for HF w/ depressed EF
ACE-I/ARBS and Beta Blockers
Gold standard in assessing anatomy and physiology of the heart and associated vasculature
cardiac catheterization and coronary angiography
