Heart failure is increasingly common due to an aging population and high prevalence of contributing risk factors.
Heart failure = A clinical syndrome in which the heart's ventricles cannot pump enough blood to meet the body's needs (insufficient cardiac output).
Review:
Cardiac output,
Stroke volume,
Cardiac performance.
See cardiac cycle with
congestive heart failure
Review
blood flow through the heart
Reduced cardiac-output (CO) is due to reduced stroke volume.
Reduced stroke volume can be due to:
Systolic dysfunction, i.e., impaired contraction
Diastolic dysfunction, i.e., impaired compliance
Both scenarios can ultimately lead to increased left ventricular end diastolic pressure, which, as we'll see, can lead to pulmonary congestion.
As a clinical syndrome, heart failure is the culmination of other cardiovascular diseases, which may co-exist.
Common culprits include:
ischemic heart disease,
hypertension,
cardiomyopathies, diabetes mellitus, metabolic syndrome,
atherosclerosis, and
myocardial infarctions.
Diagnosis can rely on echocardiography, ECG, cardiac MRI, and measurement of serum B-type natriuretic peptide (BNP) levels.
S3 or S4 sounds may be heard (be aware of intertextual variation on the importance of S4 sounds and heart failure); pulmonary crackles may audible when pulmonary edema sets in.
Treatments vary, and include life-style changes and, where appropriate, addressing the causative disease(s).
Treatments to reduce symptoms include: diuretics, digoxin, and nitrates.
Long-term treatments tend to focus on lowering ventricular pressures, and include: ACE-inhibitors, angiotensin II receptor blockers (ARBs), Beta-blockers, and Aldosterone antagonists.
Device therapies include implantable cardiac defibrillators, cardiac resynchronization therapy, biventricular pacemakers, and left ventricular assist devices.
We draw a very generalized illustration of left heart failure; bear in mind that this is only representative, due to the varied causes of heart failure.
Pathophysiology:
LHF is the result of
reduced stroke volume, which
reduces systemic perfusion.
Reduced stroke volume also leads to
increased left ventricular end diastolic pressure (LVEDP); be aware that this can be the result of a variety of mechanisms, which we'll address, soon.
Increased left ventricular end diastolic pressure leads to an
increase in left atrial pressure, which, ultimately, raises
pulmonary pressures.
Increased pressures in the pulmonary vascular system "push" fluids out of vessels and into the surrounding tissues.
Pulmonary edema occurs when this fluid enters the
alveolar sacs and lung spaces.
Pleural effusions occur when the fluid accumulates between the pleural space.
Symptoms of LHF:
Dyspnea upon exertion is a common early sign; it occurs because the heart cannot increase cardiac output despite increased metabolic demands.
Orthopnea is characterized by dyspnea that occurs when lying flat, but is quickly relieved by sitting upright or standing; orthopnea occurs because the heart is unable to adjust to the redistribution of body fluids that occurs when lying flat.
Paroxysmal nocturnal dyspnea, as its name suggests, is characterized by sudden episodes of dyspnea that awaken a person after 1-2 hours of sleep, usually at night.
Sleep-disordered breathing includes obstructive sleep apnea and Cheyne Stokes Respiration; show that Cheyne Stokes Respiration is characterized by cycling periods of tachypnea or hyperpnea alternating with periods of apnea.
Other symptoms may also be present, often
reflecting reduced cardiac performance; for example, patients may experience cognitive impairments, arrhythmias, cyanosis, or thrombi formation in the heart chambers.
Heart Failure with Reduced Ejection Fraction
The ejection fraction measures how much of the blood in the ventricle was pumped out (ejected) during a contraction.
For reference, a "normal" ejection fraction is between 50% and 70%.
In Heart Failure with Reduced Ejection Fraction, the
left ventricle ejection fraction is 40% or less.
The lower ejection fraction is the result of reduced contractility of the myocardium, and is associated with
systolic dysfunction (since the left ventricle contracts during systole).
Be aware that systolic and diastolic dysfunctions may co-exist, which is why clinical focus has shifted somewhat from systolic vs. diastolic dysfunction to the ejection fraction.
Heart failure with reduced ejection fraction is particularly associated with dilated cardiomyopathies, valvular heart diseases, and myocardial infarctions.
Pathophysiology - we use dilated cardiomyopathy as an example:
Contractility is impaired, so the ejection fraction is reduced, and, via a variety of mechanisms, the left ventricular end diastolic pressure increases.
Compensatory mechanisms in HFrEF:
Several mechanisms raise blood volume and vascular resistance in attempt to increase preload and, as a result, stroke volume and tissue perfusion.
Cardiac remodeling leads to dilation and myocyte hypertrophy. These changes can ultimately lead to increased stiffness and further impair cardiac performance, and even facilitate
mitral valve regurgitation.
Reduced systemic perfusion triggers systemic and renal responses that increase blood volume and vascular resistance – recall that the renin-angiotensin-aldosterone system, the sympathetic nervous system, and the vessels themselves dynamically
regulate changes in blood flow.
However, these effects also exacerbate pulmonary hypertension and congestion in a positive feedback loop.
Thus, some long-term treatments for heart failure with reduced ejection fraction specifically target these responses (for example, ACE-inhibitors that inhibit the effects of the RAAS response).
Heart Failure with Preserved Ejection Fraction
Characterized by Left Ventricular Ejection fractions
equal to or above 50%.
It is caused by impaired relaxation and/or compliance of the myocardium, which produces diastolic dysfunction.
It is especially common in elderly people and women, and is associated with hypertrophic and restrictive cardiomyopathies, hypertension, and renal diseases.
Pathophysiology - we use a hypertrophic heart as an example:
Compliance is reduced, diastolic filling is impaired, and left ventricular end diastolic pressure is increased.
Impaired filling can lead to reduced stroke volume and cardiac output.
Prognosis
This type of heart failure often has a worse prognosis than heart failure with reduced ejection fraction, especially because it is less responsive to current treatments.
RHF is often the result of left heart failure.
Cor pulmonale: when right heart failure is isolated, it is typically due to pulmonary issues, and, therefore, is referred to as cor pulmonale.
Pathophysiology:
Right ventricular end diastolic pressure is elevated, which leads to increased pressures in the right atrium. As a result, the blood becomes "backed up" and raises systemic venous pressures.
Signs and Symptoms: RHF elevates systemic venous pressure and hepatic congestion.
Elevated systemic venous pressure and congestion leads to peripheral edema.
Elevated SVP often produces so-called "pitting edema" in the lower extremities, and congestion in the abdominal organs, especially the liver.
Hepatic portal congestion gives the liver a "speckled" or "mottled" appearance, often referred to as
"nutmeg liver;" note that hepatoportal congestion exacerbates edema.
Hepatojubular reflux is a sign of right heart failure; it is characterized by distension of the jugular veins in the neck when pressure is applied to the right abdominal quadrant (over the liver).
Pericardial and peritoneal effusions (ascites) may occur.
For references, see Heart Failure Tutorial
