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Heart Failure - Coggle Diagram
Heart Failure
Definition
Decreased cardiac output (CO) leads to decreased tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability
Structural or functional impairment of ventricular filling or ejection of blood resulting insufficient perfusion
Ejection Fraction
Defect in either ventricular systolic function/LV contraction (heart failure with reduced ejection fraction [HFrEF])
And (combination of both causes)
Normal LVEF
Defect in ventricular diastolic function/filling (heart failure with preserved ejection fraction [HFpEF])
Left ventricular ejection fraction (LVEF)
Classification
Setting of Left Ventricular (LV) myocardial dysfunction, left ventricular ejection fraction (LVEF)
Reduced (LVEF ≤ 40%)
Heart failure with reduced ejection function
(HFrEF)
Preserved (LVEF ≥ 50%)
Heart failure with preserved ejection fraction
(HFpEF)
Mid-range/ Borderline (LVEF 41%-49%)
Heart failure with the LVEF being in the mid range/borderline reduced EF (HFmrEF)
Heart failure with preserved ejection fraction
Earlier term (still in common usage) is diastolic heart failure
Filling of ventricles is impaired owing to abnormal relaxation or stiffness and decreased diastolic distensibility
Ejection fraction 50% or more
Patients often have left atrial hypertrophy and increased left ventricular wall thickness but do not usually have left ventricular dilation
Approximately half of all patients with heart failure
According to the clinical presentation into
Acute heart failure (Acute HF)
Chronic heart failure (Chronic HF)
Heart failure with preserved ejection fraction: borderline/mid-range ((alternative terminology is heart failure with mid-range ejection fraction)
Ejection fraction of 41% to 49%, with characteristics similar to patients with heart failure with preserved ejection fraction
Heart failure with reduced ejection fraction
Earlier term (still in common usage) is systolic heart failure
Contractility of ventricles is impaired
Ejection fraction of 40% or less
Left ventricle is typically dilated
Pathophysiology
Any interference with the normal mechanisms regulating CO may cause HF
CO depends on: (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR)
These factors affect stroke volume (SV)
Thus the equation: CO = SV × HR. Any changes in these factors can lead to decreased ventricular function and HF
The major causes of HF are divided into 2 subgroups: primary causes and precipitating causes
Precipitating causes often increase the workload of the heart, resulting in an acute condition and decreased heart function
Etiology
Long-standing hypertension is the predominant cause of heart failure with preserved ejection fraction, which is usually associated with left ventricular hypertrophy
Long-term treatment of HTN reduces the incidence of HF by 50%
Coronary artery disease and MI
Co-morbidities, such as diabetes, metabolic syndrome, advanced age, smoking, and vascular disease, contribute to the development of HF
Left-Sided Heart Failure
Left-sided HF can be
further classified as HFrEF (systolic HF),
HFpEF (diastolic HF), or a combination of the two
The most common form of HF
Heart Failure With Reduced Ejection Fraction
(Systolic Failure)
LVEF < 40%. It can be as low as 5% to 10%
LV in HFrEF loses the ability to generate enough pressure to eject blood forward through the aorta
Over time, the LV becomes dilated and hypertrophied
When the LV fails, blood backs up into the left atrium (LA), causes fluid accumulation in the lungs
Increased pulmonary hydrostatic pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli
Pulmonary congestion and edema
Heart Failure With Preserved Ejection Fraction
(Diastolic Failure)
HFpEF results from the inability of the ventricles to relax and fill during diastole
LV is generally stiff and noncompliant, resulting in high filling pressures
Decreased filling of the ventricles results in decreased SV
The eventual result of HFpEF is the same as that of HFrEF, a
reduced CO leading to fluid congestion
Right-Sided Heart Failure
Movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention)
The most common cause of right-sided HF is left-sided HF
Right-sided HF occurs when the right ventricle (RV) does not pump effectively
As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs
Over time, this increased workload weakens the RV and gradually it fails
Other causes of right-sided HF include RV infarction, pulmonary embolism, and cor pulmonale
Staging of HF
Functional
Class II (Mild)
Comfortable at rest, but symptoms of heart failure during ordinary activity
Class III (Moderate)
Comfortable at rest, but symptoms of heart failure with minimal exertion
Class I
Heart disease with no symptoms or limitations on physical activity
Class IV (Severe)
Symptoms at rest. Unable to carry on any physical activity without symptoms
Timeline
New (de novo) heart failure
Acute onset
May present suddenly as a result of acute injury (e.g. myocardial infarction)
Subacute onset
Gradual onset of symptoms
Occurs when transitioning from asymptomatic to symptomatic heart failure
Chronic heart failure
Stable
Treated heart failure with signs and symptoms unchanged for more than 1 month
Decompensated
Symptomatic deterioration of stable chronic heart failure, often requiring hospitalization
Decompensation may occur acutely owing to a precipitating event (e.g. myocardial infarction, atrial fibrillation) or subacutely
Progression
Stage B
Structural heart disease (eg, ventricular remodeling, left ventricular hypertrophy, ventricular dilation) without signs and symptoms of heart failure
Stage C
Structural heart disease (eg, ventricular remodeling, left ventricular hypertrophy, ventricular dilation) with prior or current symptoms of heart failure
Stage A
At high risk for heart failure without structural heart disease or symptoms, based on risk factors of hypertension, dyslipidemia, diabetes, and obesity
Stage D
Heart failure refractory to optimal goal-directed medical therapy
Clinical Manifestations
Acute Decompensated Heart Failure (ADHF)
JVD is the most sensitive and specific sign for elevated LV filling pressures
Auscultation of lungs: bubbling, crackles, and wheezes. Wheezing and coughing with production of frothy, blood-tinged sputum may also occur
Manifestations of pulmonary edema include acute manifestations of left HF, such as dyspnea, respiratory rate > 30 breaths/min, orthopnea, and paroxysmal nocturnal dyspnea (PND)
Patient's HR is often rapid, and an abnormal S3 or S4 heart sound may be heard
BP may be high or low. Hypotension indicates severe LV systolic dysfunction and the chance of cardiogenic shock
Pulmonary edema: acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid
Pulmonary congestion and volume overload
Chronic Heart Failure
Fatigue: earliest symptoms
Dyspnea & Shortness of breath occurs when lying down (orthopnea)
Chronic HF is a progressive syndrome characterized by reduced CO and increased venous pressure, associated with underlying molecular changes that result in the death of cardiac muscle cells
PND occurs when the patient is asleep. The patient awakens in a panic, has feelings of suffocation, and has a strong desire to sit or stand up
Dry, nonproductive cough may be the first clinical symptom
Other common signs include tachycardia; edema in the legs, liver, abdominal cavity, and lungs; nocturia; dusky skin; restlessness and confusion; angina; and weight changes
Complication & Prognosis
The decreased CO that accompanies chronic HF also results in decreased perfusion to the kidneys and can lead to anemia, renal insufficiency or renal failure
Prognosis of patients hospitalized with heart failure: very poor
Hepatomegaly may result as the liver becomes congested with venous blood
Mortality rate for patients with heart failure is approximately 50% within 5 years of diagnosis; for those with advanced heart failure, the 1-year survival rate is 50%
Complications include pleural effusion, malignant ventricular
arrhythmias, atrial fibrillation, and thromboembolic events
Diagnostic & Investigations
Chest x-ray
12-lead ECG
Serum chemistry panel, cardiac markers, BNP or NT-proBNP level, liver function tests, thyroid function tests, CBC, lipid profile, kidney d function tests, CBC, lipid profile, kidney function tests, urinalysis
Two-dimensional echocardiogram
Determine underlying cause
Nuclear imaging
History and physical examination
Cardiac catheterization
Management of Patient with HF
Use ultrafiltration to remove fluid while maintaining stability
Circulatory assist devices (IABP, VADs) help improve heart function in severe cases
Position patients with dyspnea in a high Fowler's position
Severe HF: bed rest; mild to moderate HF: limit strenuous activity
Administer O2; consider noninvasive or mechanical ventilation for severe pulmonary edema
Use ICDs for preventing sudden cardiac death, and CRT for coordinating ventricular function
Monitor heart rhythm, O2 saturation, vital signs, and urine output hourly
Implantable devices can also monitor HF patients remotely, aiding those with declining heart function or awaiting transplant
Medication Management
Morphine
Dilates vessels to reduce preload/afterload; use cautiously due to risks like respiratory depression
Positive Inotropes
Improve contractility in cardiogenic shock or low CO (e.g., dopamine, dobutamine, milrinone, digitalis). Monitor for improved CO, BP, and urine output
Vasodilators
For ADHF without hypotension. IV nitroglycerin and sodium nitroprusside reduce preload/afterload, improving CO and reducing congestion
ACE Inhibitors/ARB
Reduce afterload and inhibit remodeling (e.g., captopril, enalapril, or ARBs for those intolerant)
Diuretics
First-line for volume overload; includes thiazide (e.g., hydrochlorothiazide) and loop diuretics (e.g., furosemide). IV loop diuretics are preferred. Monitor urine output, symptoms, fluid loss, and electrolyte levels
Mineralocorticoid Receptor Antagonists (MRAs)
Potassium-sparing diuretics (e.g., spironolactone) that inhibit aldosterone, with mild diuretic effects
Nitrates
Promote vasodilation, particularly useful for myocardial ischemia
β-Blockers
Reduce SNS effects on the heart, decreasing mortality (e.g., metoprolol, bisoprolol, carvedilol). Can improve LVEF
Hydralazine/Isosorbide Dinitrate
Combination reduces mortality, improves LVEF and exercise tolerance
Digitalis (digoxin)
Enhances contractility, suppresses SNS/renin effects. Monitor renal function, serum digoxin, and potassium levels