CHF is a heart that fails when it is unable to eject blood delivered to it by the venous system. The inferior vena cava (IVC) empties blood into the right atrium (RA), and the pulmonary vein empties blood into the left atrium (LA).
Epidemiology
CHF is the most common hospital admission diagnosis for those >65 years of age.
Types of CHF include:
a. LHF (most common type).
b. RHF.
c. biventricular heart failure (LHF and RHF).
d. high-output heart failure (HOF; least common heart failure).
Blood builds up behind the failed ventricle.
a. In LHF, blood backs up into the lungs (pulmonary congestion).
b. In RHF, blood builds up in the systemic venous system (vena cava and its tributaries).
C. LHF
In LHF, the LV cannot efficiently eject blood into the aorta (Ao), causing blood to backup into the lungs (“blood builds up behind the failed heart”).
a. Causes an increase in the LVEDV and left ventricular end-diastolic pressure (LVEDP; hydrostatic pressure)
b. Backup of blood into the lungs produces pulmonary edema
Pathogenesis of LHF.
a. Decrease in LV contraction
(1) Decreased LV contraction defines systolic heart failure (SHF).
(a) SHF is the most common type of LHF.
(b) Some clinicians use the term systolic dysfunction rather than SHF.
(2) Causes of SHF include:
(a) ischemia caused by atherosclerosis of the CAs (most common cause of SHF).
(b) post–myocardial infarction (MI), myocarditis, and dilated cardiomyopathy.
b. Noncompliant LV (stiff ventricle) with impaired relaxation
(1) Noncompliant LV with impaired relaxation defines diastolic heart failure (DHF).
(a) Increased LVEDP (not volume)
(b) Some clinicians use the term diastolic dysfunction rather than DHF.
Causes of DHF include:
(a) concentric LVH due to primary HTN is the most common cause of DHF.
(b) other causes include AV stenosis, HCM, and restrictive cardiomyopathy
(amyloidosis or glycogenosis).
Gross and microscopic findings in LHF
a. Lungs are heavy and congested and exude a frothy pink transudate (edema) on the cut
surface or in the airways.
b. Alveoli are filled with a pink-staining fluid and alveolar macrophages (MPs) often contain hemosiderin (“HF,” heart failure cells).
(1) Presence of hemosiderin implies that the pulmonary capillaries ruptured under
pressure and red blood cells (RBCs) entering the alveoli were phagocytosed by
alveolar MPs.
(2) Excess iron in the macrophage binds to ferritin, which degrades into hemosiderin
(rust-colored granules with hematoxylin and eosin stain or blue with Prussian blue
stain), producing a rust-colored sputum
4. Clinical and laboratory findings in LHF include:
a. difficulty with breathing (dyspnea).
(1) Definition: In dyspnea, the patient has difficulty with breathing because she or he
cannot take a full inspiration.
(2) Interstitial fluid stimulates the juxtacapillary (J) receptors that are innervated by the
vagus nerve, the latter inhibiting the patient from taking a full inspiration.
b. pulmonary edema.
(1) An increase in LVEDV and pressure leads to a backup of blood into the pulmonary veins and pulmonary capillaries.
(a) When pulmonary capillary hydrostatic pressure is greater than the oncotic pressure (OP), fluid (a transudate) enters the interstitial space and then the alveoli, producing pulmonary edema
(b) Peribronchiolar edema narrows the small airways and produces expiratory wheezing (called cardiac asthma).
(2) Bibasilar (base of the lungs) inspiratory crackles (rales) are present.
(a) Inspiratory crackles are caused by air expanding alveoli filled with fluid.
(b) Rust-colored sputum. Hemorrhage into the alveoli from increased hydrostatic pressure in the pulmonary capillaries results in the phagocytosis of the extravasated RBCs by alveolar MPs. The MPs break hemoglobin down into hemosiderin (called heart failure cells).
Chest radiograph findings in LHF include:
(a) congestion in the upper lobes (early finding).
(b) perihilar congestion (“bat-wing configuration” or “angel-wing configuration”;
(c) fluffy (“ground glass”) alveolar infiltrates.
(d) Kerley B lines (septal edema
(e) air bronchograms (air is visible in the small airways because fluid surrounds the airways).
c. left-sided S3 (first cardiac sign of LHF) and S4 heart sounds . Excess fluid in the LV produces the S3 heart sound, and the increased left-ventricular end-diastolic pressure produces the S4 heart sound.
d. functional MV regurgitation. Stretching of the MV ring by the increased LVEDV causes a regurgitant murmur. This is why it is called functional MV regurgitation. When the LVEDV is normalized with treatment, the murmur disappears.
e. paroxysmal nocturnal dyspnea (PND).
(1) Definition: PND refers to a choking sensation that occurs at night when the patient is supine.
(2) Without the effect of gravity, fluid from the interstitial space moves into the vascular compartment.
(3) This increases venous return to the right side of the heart and then to the failed left side of the heart.
(4) The failed left heart cannot handle the excess load, and blood backs up into the lungs, producing dyspnea and pulmonary edema.
(5) Dyspnea is relieved by standing or placing pillows under the head (called pillow orthopnea).
(a) Both standing and raising the head on pillows increase gravity, which reduces venous return to the heart (decreases preload).
(b) The number of pillows that causes symptomatic relief should be quantitated (e.g., three-pillow orthopnea is worse than one-pillow orthopnea).
f. Serum B-type natriuretic peptide (BNP) is increased.
(1) Definition: BNP is a cardiac neurohormone secreted from the ventricles when they are stretched because of volume overload
(2) BNP is useful in:
(a) diagnosing LHF (BNP increased).
(b) excluding LHF (BNP normal).
(c) predicting survival (remains high; bad prognostic sign).
(3) Serum atrial natriuretic peptide (ANP) is also increased in LHF because of left atrial dilation.