Heart failure Part 1 Flashcards
Etiology of HF
o 60-70% CAD – ischemic heart disease (most common cause of LV systolic dysfunction)
o idiopathic, dilated cardiomyopathy
o Valvular heart disease – declined except for calcific aortic stenosis
o Hypertensive heart disease
• Congenital
• Viral myocarditis – coxsackie A, B; influenza A, B
• Toxins – etOH, Adriamycin, cocaine
• Endocrine – hypo/hyperthyroid
• Nutritional
o Restriction/obstruction to ventricular filling
• RV infarct
• Constrictive pericarditis
• Mitral stenosis
• Atrial myxoma
o Thryotoxicosis, AV fistula, beriberi
Stages in evolution of heart failure - objective
o A: HF risk factors, no heart disease, no symptoms
• HTN, DM, CAD (post-MI or revascularization) PVD, CVA, fx, exposure to cardiac toxins
• Excessive etOH, metabolic syndrome, obesity
o B: Heart disease, LV dysfunction, no symptoms
• Prior MI, LVH or reduce LVEF, asymptomatic valvular disease
o C: Prior or current HF symptoms
• Known structural heart disease
• SOB, fatigue, reduced exercise tolerance
o D: Refractory HF symptoms
• Marked symptoms at rest despite maximal medical therapy, recurrent hospitalizations
• LV assist devices, heart transplants, recurrent exacerbations
NYHA Functional Classification Clinical Stages
o Class I
• No limitation of physical activity
• No symptoms with ordinary exertion
• One year mortality 5-10%
o Class II
• Slight limitation of physical activity
• Ordinary activity causes symptoms
• One year mortality 15-30%
o Class III • Marked limitation of physical activity • Less than ordinary activity causes symptoms • Asymptomatic at rest • One year mortality 15-30%
o Class IV
• Inability to carry out physical activity without discomfort
• Symptoms at rest
• One year mortality 50-60%
Echocardiogram evaluation of HD
o Specific causes of HF
• Hypertensive heart disease – concentric ventricle hypertrophy
• Ischemic heart disease – wall motion abnormality
• Hypertrophic heart disease – significant cardiac silhouette, thickened wall, small ventricular cavity
• Infiltrative heart disease – amyloidosis, speckled pattern of muscle
• Primary valvular heart disease
o Distinguish systolic heart failure from diastolic heart failure
Systolic HF
at least 50% cases
• Decreased stroke volume, increased ventricular filling pressure
• EF 40%s - mild reduction; 30%s moderate reduction, 20%s severe reduction
• Hypoperfusion with impaired ventricular emptying
• Weak, fatigued, reduced exercise tolerance
• DOE, orthopnea, PND (paroxysmal nocturnal dyspnea)
• LVEF = SV/EDV
Diastolic HF
- SOB, DOE, Pulmonary edema
- Inability of LV to relax/fill; increased resistance to ventricular filling; decreased compliance or increased stiffness
- Decreased ventricular diastolic capacity
- Restrictive/constrictive pericarditis, hypertensive/hypertrophic cardiomyopathy
- Impaired ventricular relaxation – acute ischemia, myocardial fibrosis, amyloidosis
High output HF
- Hyperthyroidism, anemia, pregnancy, AV fistula, beriberi (Vit B1), Paget’s
- High CO but low EF
Low output HF
- Ischemic heart disease, HTN
* Dilated cardiomyopathy, valvular and pericardial disease
Acute vs chronic HF
- Acute: due to acute MI, ruptured papillary muscle, MR, AI, toxins
- Chronic: multivalvular disease of dilated cardiomyopathy, progresses slow, edema, weight gain
Neurohormonal responses to HF
• SNS
• RAAS
• Decreased renal perfusion
• Increased renin, Angiotensinogen, A1
• AngI → AngII via ACE
o Increases BP by vasoconstriction, stimulates adrenal gland release of aldosterone
o Na and H2O retention – increased preload, congestive symptoms, volume expansion
• AngII – vasoconstrictor, increases PVR – increases afterload
• Arginine vasopressin – AVP or ADH
o Stimulation of thirst leads to increased TBW and hyponatremia (dilutional)
o Increases preload – salt and water retention
- Cytokine activation
- Altered renal physiology
- LV remodeling
Precipitating causes of HF
o Noncompliance with diet – 25-50%
• To much Na
• Too many calories
• Too many stimulants – tea, coffee, colas
o Noncompliance with meds – 25-50%
• Too costly
• Side effects
o Meds worsen HF – CCB, Beta blockers, NSAID, antiarrhythmics
o Infection – 20%
• Fever, tachycardia, increases metabolic demands, hypoxia
o Anemia
• Increased oxygen needs of tissues
• Increased cardiac output
o Thyrotoxicosis/Pregnancy – high cardiac output state
o Arrhythmias – 20-30%
• Tachyarrhythmias – decrease diastolic filling time, leading to ischemia
• Bradycardia
o Others:
• Physical over exertion
• Fluid excess – transfusion/volume overload
• Environmental – stress
• Worsening HTN, MI – ischemia/infarction
• PE
• Hypothyroid
• etOH
• Valvular heart disease worsening (MS, AS, MR, AI)
• Pericardial disease
S/S of HF
o Decreased atrial perfusion to organs and venous congestion (liver, lungs) leads to dyspnea (most common)
o Exercise intolerance, orthopnea, paroxysmal nocturnal dyspnea (PND), nocturnal angina dt pulmonary congestion and increased LA pressure
• PND increases likelihood of heart failure 2 fold
o Weakness, fatigue not specific for HF
o Pulmonary edema
o Hepatomegalia – passive congestion with increased LFTs, altered coagulation studies, ascites, increased abdominal girth, peripheral and sacral edema
o JVD – CVP can be elevated in volume overload
• Prominent in cardiac tamponade and COPD (lung hyperinflation)
o S3, S4
• S3 gallop increased likelihood of heart failure 11 fold
o LV failure
o Orthopnea, PND
o Tachypnea, wheezing, crackles, decreased breath sounds
o Dullness to percussion over pleural effusions
o RV failure
Pulmonary edema
crackles in lungs
• Transudation of fluid from pulmonary capillaries into alveolar spaces and interstitium
• May wheeze or cough – frothy, pink fluid
• Possible cyanotic and acidotic
RV failure
- Peripheral/sacral edema
- Hepatomegalia
- Ascites
- Increased JVD, HJR
CXR in HF
- Cardiomegalia
- Pulmonary edema with central peripheral infiltrates
- Increased size of vessels in upper portion of lungs
- Pleural effusions
- Transudate blunts angles and gutters
