1. Right-sided Heart Failure
1.1. Cor Pulmonale
1.1.1. (COPD) Chronic Obstructive Pulmonary Disease
1.1.2. Obstructive Sleep Apnea
1.1.3. Pulmonary Hypertension
1.1.4. Pulmonary Embolization
1.2. Decompensated HF
1.2.1. Hypertrophy
1.2.1.1. Decrease lumen size
1.2.1.2. fails to increase contractility
1.2.2. Exacerbation of HR
1.2.2.1. Increase oxygen demand
1.2.2.2. Decrease contractility
2. Restrictive Cardiomyopathy
2.1. Cardiac muscle becomes stiff
2.1.1. Infiltration with abnormal cell/substances
2.1.2. Excessive deposition of metabolic by-products
2.1.3. Direct fibrosing injury
2.2. During Diastole (cannot relax properly) inadequate filling of the heart with blood
2.2.1. Atria becomes dilated/enlarged
2.2.2. Increased pulmonary and sysemic congestion
2.2.3. Increases HR, Heart is unable to adequately increase CO
2.3. Systolic function normal
2.4. slight ventricular dilation or thickening
3. Risk factors (objective)
3.1. Metabolic Syndrome
3.2. Obesity
3.3. Sedentary lifestyle
3.4. Hereditary risk for HF
3.4.1. Family History of cardiomyopathy
3.5. Coronary artery disease
3.6. Diabetes mellitus
3.7. Hypertension
4. Pathophysiologic mechanisms
4.1. Compensatory mechanism decreased Cardiac Output
4.1.1. Decreased cardiac output (CO)
4.1.1.1. Compensation to CO
4.1.1.1.1. Activation of sympathetic NS
4.1.1.1.2. Activation of Renin-anginotensin-aldosterone system
4.1.1.1.3. Increased Antidiuretic horomone release
4.1.1.1.4. Increase Atrial natriuretic peptide/brain natriuretic peptide (BNP) release
4.1.2. Decreased perfusion
4.1.3. Decreased stroke volume (SV)
4.1.3.1. Compensation to increase SV
4.1.3.1.1. Increase cardiac output
4.1.3.1.2. Increase Afterload and Preload
4.1.3.1.3. Prevent the development of symptoms
4.1.3.1.4. Cardiac remodeling (Hypertrophy)
4.1.4. Increases pulmonary vessel pressures
4.2. Neurohormonal mechanisms
4.2.1. Increase Heart rate
4.2.2. Arterial and venous (vasoconstriction) maintain BP
4.2.3. Increase Blood volume; Increase ventricular filling
4.3. Frank-Starling mechanism
4.3.1. Increased venous return
4.3.2. Greater ventricular filling
4.3.3. Increased stroke volume
5. Development of signs and symptoms
5.1. Increases left ventricular end-diastolic pressures (LVEDP) and atrial pressure
5.1.1. Increase pulmonary capillary pressure
5.1.2. Transduation of fluid
5.1.3. pulmonary edema
5.1.4. Dyspnea
5.2. Right ventricular dysfuction dysfuction increased venous congestion
5.2.1. Jugular venous distention
5.2.2. Increased hydrostatic pressure
5.2.2.1. transduation of fluid from capillaries
5.2.2.2. Peripheral edema
5.2.3. Hepatic congestion
5.2.3.1. Liver injury (congestive hepatopathy)
5.2.3.2. Cirrhosis
5.3. Acute kidney injury
5.3.1. Inadequate blood pressure
5.3.2. decrease renal perfusion
5.3.3. progressive chronic disease (cardiorenal syndrome)
5.4. Inability to supply blood to other areas
5.4.1. Confusion
5.4.2. Fatigue
5.4.3. Diaphoresis
6. Classification of Heart Failure
6.1. Stage A= At risk for heart failure w/o any symptoms or structural heart disease
6.2. Stage B= Patients have structural heart disease but do not exhibit symptoms of heart failure
6.3. Stage C= Patients with structural heart disease who currently experience or have previously experienced symptoms of heart failure
6.4. Stage D= Patients with advanced heart failure who exhibit severe symptoms and are often hospitalized despite optimal medical therapy.
6.5. New York Heart Association Functional
6.5.1. Class I= No limitation of physical activity
6.5.2. Class II= Slight limitation of physical activity
6.5.3. Class III= Marked limitation of physical activity
6.5.4. Class IV= Severe limitation
6.6. Ejection fraction
6.6.1. Preseved Ejection Fraction (HFpEF)
6.6.1.1. Inadequate relaxtion and filling
6.6.1.2. normal myocyte contractility
6.6.1.3. Perseved EF despite low SV
6.6.1.4. LVEF> or equal to 50%
6.6.2. Midrange Ejection Fraction (HFmrEF)
6.6.2.1. Known in Europe as HF with mildly reduced EF
6.6.2.2. LVEF between 41% and 49%
6.6.3. Reduced Ejection Fraction (HFrEF)
6.6.3.1. Ischemic heart disease
6.6.3.2. dilated cardiomyopathy
6.6.3.3. Mitral insufficiency
6.6.3.4. EF is dimminished
6.6.4. HF with improved EF (HFiEF)
6.6.4.1. LVEF was previously < equal to 40%, but on follow up assessment is betteEF (>40 %)
6.7. Areas affected
6.7.1. Left sided HF anormalities
6.7.1.1. Left ventricle
6.7.1.2. aortic valve
6.7.1.3. mitral valve
6.7.2. Right sided HF abnormalities
6.7.2.1. Right ventricle
6.7.2.2. tricuspid valve
6.7.2.3. pulmonic valve
6.7.3. Left and Right occuring at the same time
6.7.3.1. Biventricular
7. Assessment and Exam findings
7.1. Left sided HF
7.1.1. S3 heart sound (low-pitched sound in early diastole)
7.1.2. Cyanosis (poor perfusion)
7.1.3. Crackles or Rales lungs sounds
7.2. Right sided HF
7.2.1. Jugular venous distention
7.2.2. Hepatojugular reflux
7.2.3. Hepatosplenomegaly
7.2.4. Ascites
7.2.5. Symmetric and /or pitting lower-extremity edema
7.2.5.1. Volume overload
7.2.5.2. Skin induration
7.2.6. S4 Heart sounds
8. Diagnosis
8.1. Clinical Evaluation
8.1.1. Signs and symptoms of Congestion
8.1.1.1. Left sided symptoms
8.1.1.1.1. Fatique
8.1.1.1.2. Dyspena
8.1.1.1.3. Exercise intolerance
8.1.1.1.4. Cough
8.1.1.1.5. Pulsus alternans (alternating strong and weak pulses)
8.1.1.2. Right sided symptoms
8.1.1.2.1. Dyspena
8.1.1.2.2. Fatique
8.1.1.2.3. Nausea
8.1.1.2.4. Abdominal Distention
8.1.2. Fluid retention and/or hypoperfusion
8.1.3. Impairment functional capacity
8.1.4. Percipitating factors casue exacerbation to increase cardiac workload
8.1.5. Family history of cardiac disease
8.2. Evidence of cardiac dysfunction
8.2.1. Echocardiography evidence of cardiac dysfunction
8.2.2. Cardiac catheterization
8.3. Laboratory test/imaging studies
9. Patient education
9.1. Lifestyle modifications
9.1.1. Weight loss
9.1.1.1. weight monitoring if >5 lb weight gain, consult a physician
9.1.1.2. Exercise contraindicated if decompensating )
9.1.2. Restriction of sodium to 3g/day
9.1.3. Restriction of fluids to 1.5-2 liters per day in volume overload/edema
9.1.4. Cessation of smoking and alcohol consumption
9.1.5. Avoid illicit drug use
9.2. Avoid drug that trigger exacerbation
9.2.1. NSAIDs
9.2.2. Thiazolidinediones
9.2.3. Antidepressants (tricyclic)
9.2.4. Trimethoprim-sulfamethoxazole (increase patassium when taken with drugs for HF)
9.2.5. Nondihydropyridine calcium channel blockers
9.2.6. Phosphodiesterase-3
9.2.7. Cardiotoxic chemotherapy
9.2.8. Antiarrhythmics (class 1C and dronedarone) negative inotropic effect
9.2.9. Dipeptidyl peptidase-4 inhibitors (alogliptin, saxagliptin)
9.2.10. Tumor necrosis factor-alpha inhibitors
9.3. Keep immunizations current
9.3.1. Pneumococcal polysaccharide vaccine
9.3.2. Annual influenza vaccine
10. Effects on Systems
11. Diagnostic tests
11.1. Echocardiography
11.2. Electrocardiography (ECG)
11.2.1. Evaluates for evidence of current ischemia
11.2.2. Detects abnormalities in cardiac rhythm and conduction
11.2.3. Show evidence of cardiomyopathy or prior MI
11.2.3.1. Increased QRS voltage in leads 1 and aVL
11.2.3.2. Q waves
11.2.3.3. St- and T-wave abnormalities
11.3. Transthoracic echocardiography (TTE) with Doppler imaging
11.3.1. Measures ejection fraction and assesses cardiac anatomy
11.3.2. Detects abnormalities in valves, myocardium, and pericardium
11.4. Cardiac magnetic resonance imaging (CMR)
11.4.1. Detects damaged myocardium
11.4.2. Fibrosis
11.4.3. Detects Myocardium infarction (acute and chronic)
11.4.4. Detects infiltrated and inflammatory disease
11.5. Multigated acquistion scan (radionuclide ventriculography)
11.5.1. Most accurate way to assess ejection fraction
11.5.2. Obtain baseline assessment of ventricular function
11.5.3. Monitor cardiotoxicity of anthracyclines (chemotherapy)
11.6. Cardiopulmonary exercise testing (CPET)
11.6.1. Detect ischemic heart disease
11.6.2. Assess appropriatness of advanced treatment such as transplantation
11.6.3. Assess maximal oxygen uptake (VO2) to estimate the severity of myocardial dysfunction
11.7. Chest X-ray
11.7.1. ABCDE finidings on CXR
11.7.1.1. A: alveolar edema (batwing)
11.7.1.2. B: Kerley B lines
11.7.1.3. C: Cardiomegaly
11.7.1.4. D: dilated upper lobe vessels
11.7.1.5. E: pleural effusion
11.7.2. Pulmonary edema
11.7.3. Pulmonary vascular congestion
11.7.4. Cephalization of vessels
11.8. Cardiac catheterization
11.9. Laboratory test evaluation
11.9.1. Cardiac markers
11.9.1.1. BNP/N- terminal pro BNP (NT-proBNP) levels
11.9.1.1.1. BNP >400 pg/mL
11.9.1.1.2. Pro-BNP
11.9.1.1.3. Variation in subpopulation
11.9.1.1.4. Noncardiac elevated levels
11.9.1.2. Troponin
11.9.1.2.1. Determined presence of acute coronary syndrome
11.9.1.2.2. Obtained in the emergency setting of acute decompensated heart failure
11.9.2. Additional lab studies
11.9.2.1. CBC
11.9.2.1.1. Anemia casuses high-output (Cardiac Failure)
11.9.2.1.2. Hemoglobin <8mg/dl impaired delivery of oxygen
11.9.2.2. BUN and creatinine
11.9.2.2.1. >20 prerenal failure worse prognosis
11.9.2.2.2. Increased BUN increased mortality
11.9.2.2.3. Increase of >0.3 mg/dL in creatinine increased mortality
11.9.2.3. Electrolytes
11.9.2.3.1. Hyponatremian worse prognosis
11.9.2.3.2. Sodium <137 mEq/l decrease survival
11.9.2.4. Bilirubin
11.9.2.4.1. Elevated total bilirubin worse prognosis (congestive hepatopathy)
11.9.2.5. Albumin
11.9.2.5.1. Hypoalbuminemia worse prognosis
11.9.2.6. Lipid panel
11.9.2.6.1. Increase Lipids
11.9.2.6.2. Increase risk for atherosclerotic cardiovascular disease.
11.9.2.7. Serum aminotransferase levels
11.9.2.7.1. reflects liver function
11.9.2.8. Thyroid function test
11.9.2.8.1. Hyperthyroidism
11.9.2.8.2. Hypotheroidism
11.9.2.8.3. these can lead to or contirbute to severe heart failure
11.9.2.9. Fasting glucose and hemoglobin A1c
11.9.2.9.1. Diabetes mellitus is a common comorbidity
12. Medications/Treatments
12.1. Etiology testing
12.1.1. Cardiac stress tset can assess functional impairment due to coronary heart diseae
12.1.1.1. Exercise ECG testing completed with treadmill exercise
12.1.1.2. Radionuclide myocardial perfusion imaging (rMPI) completed with exercise or pharmacologic stress
12.1.1.3. Stress echocardiograghy completed with exercise or pharmacologic w/o radiation exposure
12.1.2. Coronary angiography Gold standar for diagnosing coronary artery stenosis
12.1.2.1. Measures CO, the dgree of left ventricular dysfunction, LV end diastolic pressure
12.1.2.2. Invasive procedure that carries risk of arrhytmias, storke, and atheroemboli
12.1.2.3. Diagnostic as well as therapeutic procedure (revascularization can be done)
12.1.3. Endomyocardial biopsy
12.1.3.1. Invasive procedure with risk
12.1.3.1.1. Cardiac tamponade
12.1.3.1.2. Perforation
12.1.3.1.3. Thrombus formation
12.1.3.2. Performed to influence the management and the information provided outweighs the risk
12.1.4. Right heart (pulmonary artery) catheterization
12.1.4.1. Measures intracardiac pressures
12.1.4.2. Directs eligility for advanced therapies
12.1.4.3. Consider if HF is due to
12.1.4.3.1. Constrictive percarditis
12.1.4.3.2. Restrictive cardiomyopathy
12.1.4.3.3. Congenital heart disease
12.1.4.3.4. High-output state
12.1.4.4. Advanced HF
12.1.4.4.1. Left- and right-sided filling pressures are persistently high
12.1.4.4.2. Decreased cardiac index (< or equal to 2.2 l/min/m2)
12.2. Consultation Cardiologist
12.2.1. Advanced therapies w Cardiologist
12.2.1.1. ICD (implantable cardiverter defibrillator)
12.2.1.2. Cardiac resynchronization therapy (CRT)
12.2.1.3. Coronary revascularization
12.2.1.3.1. Percutaneous transluminal coronary angioplasty
12.2.1.3.2. Coronary artery bypass surgery
12.2.1.4. Mechanical circulatory support
12.2.1.4.1. Inotropic therapy
12.2.1.4.2. Short term MCS
12.2.1.4.3. Durable MCS long trem therapy
12.2.1.5. Cardiac transplantation
12.3. Medication
12.3.1. Loop Diuretics
12.3.1.1. Furosemide 20‒40 mg 1–2 times daily
12.3.1.2. Bumetanide 0.5‒1 mg 1–2 times daily
12.3.1.3. Torsemide 10–20 mg daily
12.3.2. Thiazides
12.3.2.1. Chlorothiazide 250‒500 mg 1–2 times daily
12.3.2.2. Chlorthalidone 12.5‒25 mg daily
12.3.2.3. Hydrochlorothiazide 25 mg 1–2 times daily
12.3.2.4. Indapamide 2.5 mg daily
12.3.2.5. Metolazone 2.5 mg daily
12.3.3. ARNIs
12.3.3.1. Sacubitril-valsartan (24mg/26mg, 49mg/51mg twice daily)
12.3.4. ACEi
12.3.4.1. Lisinopril (2.5-5mg) daily
12.3.4.2. Ramipril 1.25‒2.5 mg daily
12.3.4.3. Enalapril 2.5 mg daily
12.3.5. ARBs
12.3.5.1. Losartan 25‒50 mg daily
12.3.5.2. Valsartan 20‒40 mg twice daily
12.3.5.3. Candesartan 4‒8 mg daily
12.3.6. MRA
12.3.6.1. Spironolactone 12.5‒25 mg daily
12.3.6.2. Eplerenone 25 mg daily
12.3.7. SGLT2 inhibitors
12.3.7.1. Dapagliflozin 10 mg daily
12.3.7.2. Empagliflozin 10 mg daily
12.3.8. Beta-1 adrenergic blocker
12.3.8.1. Metoprolol XL12.5‒25 mg daily
12.3.8.2. Carvedilol 3.125 mg twice daily
12.3.8.3. Bisoprolol 1.25 mg daily
12.3.9. Mineralocorticoid receptor antagonists
12.4. Management of acute or exacerbation HF
12.4.1. Lasix/Loop diuretic
12.4.2. Morphine (for ACS)
12.4.3. Nitroglycerin
12.4.4. Oxygen
12.4.5. Position or Prop up the patient
13. Contributing factors
13.1. Underlying causes
13.1.1. Renal Failure
13.1.1.1. Electrolyte abnormalities
13.1.1.1.1. Hyperkalemia: potassium binders can be given to those with hyperkalemia while on renin-angiotensin inhibitor.
13.1.1.1.2. Severe hyponatremia (sodium ≤ 120 meq/L):
13.1.2. Valvular heart disease
13.1.3. Myocarditis
13.1.4. Pericardial disease
13.1.5. Myocardial infarction
13.1.6. Left ventricular hypertrophy
13.1.7. Hemochromatosis
13.1.8. Amyloidosis
13.1.8.1. Amyloidosis: Tafamidis, a transthyretin stabilizer, is an option for amyloid cardiomyopathy with class I–II symptoms
13.1.9. Chemotherapy or cardiotoxic drugs
13.1.9.1. Cancer-related cardiomyopathy: ARB/ACEi and β-blockers given in EF < 50% to reduce progression
13.1.10. Arrhythmias
13.1.10.1. Bradyarrhythmia
13.1.10.2. Tachyarrhythmias
13.1.10.2.1. Atrial fibrillation (AF) with HF symptoms: Consider AV nodal ablation or cardiac resynchronization therapy if with rapid ventricular rates despite optimized medical therapy.
13.2. Compliance with medical therapy
13.3. Presence of comorbidities
13.3.1. Hypertension
13.3.1.1. Optimize guideline-directed medical therapy up to maximally tolerated dose.
13.3.1.2. The following drug classes are generally avoided or used with caution
13.3.1.2.1. Direct-acting vasodilators
13.3.1.2.2. Calcium channel blockers
13.3.1.2.3. Alpha-blockers
13.3.1.2.4. Centrally acting alpha-agonists
13.3.2. Obstructive SA
13.3.2.1. Perform sleep study in those in whom sleep disorder is suspected.
13.3.2.2. Continuous positive airway pressure (CPAP) recommended in those confirmed with OSA
13.3.3. Type 2 diabetes mellitus
13.3.3.1. SGLT2i is recommended.
13.3.3.2. Avoid thiazolidinediones.
13.3.3.3. Optimize glycemic control.
13.3.4. Plumonary HTN
13.3.4.1. Manage the underlying cause.
13.3.4.2. Pulmonary vasodilators may be of benefit.
13.3.5. Iron deficiency
13.3.5.1. IV iron therapy is indicated in HFrEF.
13.3.5.2. Erythropoietin-stimulating agents are not recommended.