notes by dr Claudio Italiano
Sometimes the clinic makes us run into the patient with severe heart pump deficiency, ie the one with a 25% ejection fraction, where the heart hardly moves, with a very depressed kinetics. Since the heart is still a pump, its activity as it happens with other pumps, resides in the ability to suck up liquids and pump them away. If a heart is insufficient, that is, it does not have sufficient strength to aspire, then a bottleneck of liquids is determined, which we technically call "stasis". Well, because the liver is "aspirated" from the heart, in the sense that the suprahepatic veins discharge into the right atrium through the vena cava system, if there is stasis, even the liver in the resent and goes into suffering: stasis liver. In most patients the clinical picture is dominated by the signs and symptoms of right-sided heart failure rather than those of hepatopathy. The stigmata of chronic liver disease, such as palmar erythema, spider telangiectasia and caput medusae are rare.
The patient with heart failure has obliged
orthopedic decubitus, ie to breathe better he
is forced to spend his time remaining sitting with
his feet dangling, out of bed.
Portal area sinusoidal and vascular
congestion. In the other picture: congestion
of central lobular vein
- Stasis liver in the acute phase: it catharsises due to blockage of the center
of the liver lobules, due to lack of venous discharge in the suprahepatic veins,
a condition that can arise acutely in the course of myocardial infarction with
insufficiency of pump on the right or sudden occlusion of the suprahepatic veins
themselves or for compressive facts; the liver becomes swollen, filled with
blood with the glissoniana dilatata.
- Stable liver in the subacute phase: it is a slower and longer-lasting process
that causes damage to the other regions of the lobule, from the central vein to
zones 2 and 3, due to stasis prolonged over time, with fatty degeneration of
hepatocytes; in this phase you can have the "nutmeg" look for biliary congestion.
- Chronic phase stasis liver up to the confirmed picture of cardiac cirrhosis
- Discomfort in the upper right quadrant
- Hepatomegaly
- Marcala hepatomegaly (> 5 cm below the right rib margin)
- Jaundice
- Peripheral edema
- Ascites
- Pleural effusion
- Splenomegaly
The painful symptomatology located in the right upper quadratic is due to the
distention of the hepatic capsule and is mediated by the phrenic nerve. The
liver can restore its normal size as fibrosis develops during the course of
hepatic congestion, but it is never reduced in size. Hyperbilirubinemia and
jaundice appear due to liver failure and inability of the liver to detoxicate
substances from the body, including the metabolism of bilirubin.
Hyperbilirubinemia is due in part to the unconjugated bilirubin which is formed
as a result of tissue infarcts, especially the pulmonary infarcts. In this case
jaundice may be prolonged due to the inability of the hypoxic liver to cope with
the bilirubin load. Jaundice, however, increases with repeated repeated relapses
of congestive heart failure. In the case of tricuspid regurgitation there is a
palpable systolic pulsation above the liver related to the transmission of
atrial pressure to the hepatic vein.
Splenomegaly is common, but other features
of portal hypertension are usually absent, except in severe cardiac cirrhosis
associated with constrictive pericarditis. The presence of ascites is most
likely related to the increase in pressure and permeability in the sinusoids and
to the increase in lymph loss rather than the presence of cirrhosis. This is
responsible for a high protein content in the ascitic fluid (with a high serum
albumin gradient / ascitic fluid). The presence of peripheral edema and pleural
effusion probably reflects heart disease rather than concomitant hepatic
congestion. Ischemic hepatitis. secondary to a low cardiac output, it may be not
evident from a clinical point of view. A state of hypotension is not always
documented and left heart failure can be subtle. Diagnosis is often based on
abnormal results at biochemical examinations and for a high suspect index.
Fulminant hepatic failure with asterisks and coma, which complication of
circulatory failure is rare, usually appears after two or three days of
circulatory failure. The serum concentration of aminotransferase can exceed 1000
U / l. The prognosis is unfavorable: half of the patients die because of the
underlying heart disease.
Bromosulphthalein retention test (BSP):
• Is the most sensitive test of hepatic dysfunction in congestive heart failure
and may be the only liver test impaired in this condition, but it is not
widespread.
• Is altered in over 80% of patients and is related to the increase in central
venous pressure
• 20-75% of bilirubin is observed in 20-75% of patients with congestive heart
failure. Inertia is usually mild during congestive heart failure with a serum
bilirubin concentration typically less than 4.5 mg / dl;
• serum bilirubin levels may drop rapidly following improvement of liver
congestion reaching normal levels in 3-7 days;
• serum bilirubin levels may not return to normal values for months after
congestion resolution in patients with prolonged congestive heart failure. This
may be due to covalent bonds of bilirubin conjugated with albumin to form
bilirubin which has a prolonged half-life of 21 days
• in congestive heart failure that is stable without decompensation,
aminotransferases are only elevated in 5-30% of patients. Levels are usually 2-4
times higher than the normal upper limit
• remarkably high levels (more than 10 times the normal upper limit) are
observed in patients with acute, severe and chronic congestive heart failure,
with hypotension or shock.
• AST tends to be higher than ALT because the hepatocytes are richer than AST.
The increase in the concentration of AST generally appears earlier than the
increase in ALT.
• a moderate increase in AST may also be due to myocardial infarction, a rather
common clinical picture.
• Increases in alkaline phosphatase levels are rare in congestive heart failure.
When present they are usually mild and do not exceed twice the upper normal
limit. The mechanism responsible for the increase of alkaline phosphatase during
hepatic congestion is unknown. Both pressure-induced intrahepatic biliary
obstruction and liver dysfunction may play a role.
• When regenerative lobular hyperplasia complicates congestive heart failure the
only abnormality in liver function tests is an increase in alkaline phosphatase
• an increase in prothrombin time is observed in over 180% of patients with
congestive heart failure; prolongation of prothrombin time is more common in
acute and chronic congestion. In acute congestion, prothrombin time can rapidly
increase to twice normal values, does not respond to vitamin K administration,
and can return to normal values very rapidly after congestion resolution.
• serum albumin is moderately reduced in 30-50% of patients with congestive
heart failure. Lower albumin levels are observed in patients with ascites and
edema
• a low serum albumin level may be partly due to the reduction of hepatic
synthesis and partly to the dilution effect secondary to fluid retention.
• suspect cardiac cirrhosis in a patient with documented tricuspid regurgitation
and absence of abnormal liver pulsation
• cardiac cirrhosis should also be suspected in case of:
severe mitral stenosis
constrictive pericarditis
prolonged or recurrent severe congestive heart failure
passive congestion of the boundary, but clinically severe with a small liver.
splenomegaly and ascites
Treatment of liver congestion should be sufficient to solve the primary problem, which is heart failure. Clinical improvement of cardiac function can be achieved after definitive treatment of heart failure, for example after valve replacement, pericardiotomy for constrictive pericarditis or after correction of a congenital anomaly.