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ANESTHESIA PRACTICE 3 > ANESTHESIA FOR HEPATIC DISEASE > Flashcards

ANESTHESIA FOR HEPATIC DISEASE Flashcards

1
Q

what are the functional units of the liver?

A
  • lobule

* acinus

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2
Q

name the 8 segments of the liver

A
  • I – posterior caudal segment
  • II – lateral segment
  • III – left anterior lateral segment
  • IV – medial segment
  • V – anterior medial segment
  • VI – right anterior lateral segment
  • VII – posterior lateral segment
  • VIII – posterior medial segment
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3
Q

describe the large vascular capacity of the liver

A
  • 25-30ml blood/100gm tissue
  • 10-15% of total blood volume
  • (70% venous)
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4
Q

how much blood flow does the liver receive per minute?

A

total hepatic blood flow = 1200-1400ml/min

* 100ml/min/100gm tissue

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5
Q

what percentage of total cardiac output does the liver see?

A

25% of cardiac output

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6
Q

what percentage of hepatic blood flow does the portal vein receive? from what organs?

A

portal vein received 70-80% of hepatic blood flow

  • intestine (60%)
  • stomach (20%)
  • pancreas (10%)
  • spleen (10%)
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7
Q

what percentage of hepatic blood flow does the hepatic artery receive?

A

20-30%

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8
Q

blood from the superior mesenteric vein is filtered primarily through which lobe of the liver?

A

right lobe

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9
Q

blood from the splenic, gastric, and inferior mesenteric veins is filtered primarily through what lobe of the liver?

A

left lobe

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10
Q

describe the hepatic acinus

A

functional microvascular unit, cluster of parenchymal cells formed about a vertical axis, consisting of:

  • terminal portal venule
  • hepatic arteriole
  • bile duct
  • lymph vessels and nerves
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11
Q

describe hepatic blood flow

A

high flow, low resistance

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12
Q

describe the liver as a blood reservoir

A
  • normal blood reservoir of 450ml (10% TBV)

* expandable to 0.5-1.0L (CHF)

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13
Q

describe lymph flow in the liver

A
  • sinusoids are permeable to fluids and proteins
  • contain half of all lymph in body
  • ascites forms from high hepatic vascular pressure (e.g., cirrhosis, liver disease)
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14
Q

describe the hepatic artery buffer system

A

hepatic artery blood flow increases with decreases in portal vein flow to maintain pressure in liver

  • hepatic artery can perfuse the entire liver
  • dependent on systemic arterial pressure
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15
Q

describe hepatic compliance

A

highly compliant

  • 2-3ml/mmHg for each 100g of liver weight
  • raising venous pressure by 1mmHg results in an increase of 40-50ml
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16
Q

define hepatic volumes for unstressed and stressed hepatic compliance

A
  • unstressed (0mmHg): 210-250ml
  • stressed (8mmHg): 300-350ml
  • capacitance is about 600-1000ml
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17
Q

intrinsic regulation of hepatic flow is maintained by what two mechanisms?

A
  • autoregulation

* metabolic control

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18
Q

how does autoregulation maintain intrinsic hepatic flow?

A

hepatic artery vasoconstriction

* myogenic response to smooth muscle stretch

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19
Q

how does metabolic control maintain intrinsic hepatic flow?

A
  • arterial hypoxemia
  • decreased blood pH (acidosis, hypercarbia)
  • hyperosmolarity
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20
Q

extrinsic regulation of hepatic blood flow is maintained by what two mechanisms?

A
  • neural control

* humoral factors

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21
Q

how does neural control maintain extrinsic regulation of hepatic flow?

A
  • sympathetic stimulation of vagus and splanchnic nerve decreases blood flow
    • 500ml can be expelled in seconds
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22
Q

how does epinephrine help to maintain extrinsic regulation of hepatic flow?

A

epinephrine – initial vasoconstriction via alpha receptors, then vasodilation via beta-receptors

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23
Q

how does glucagon help to maintain extrinsic regulation of hepatic flow?

A

glucagon is a long-lasting arterial vasodilator

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24
Q

how does angiotensin II help to maintain extrinsic regulation of hepatic flow?

A

angiotensin II produces profound vasoconstriction

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25
Q

how does vasopressin (ADH) help to maintain extrinsic regulation of hepatic flow?

A

vasopressin produces marked splanchnic vasoconstriction

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26
Q

how does anesthesia affect hepatic blood flow?

A
  • all anesthetics and techniques that decrease cardiac output will produce a proportional decrease in total hepatic blood flow
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27
Q

how does controlled ventilation affect hepatic blood flow?

A
  • controlled ventilation will decrease portal venous flow
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28
Q

how does regional anesthesia affect hepatic blood flow?

A
  • regional anesthesia will decrease hepatic blood flow in parallel with systemic BP
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29
Q

how does controlled hypotension affect hepatic blood flow?

A
  • controlled hypotension with sodium nitropresside will not alter hepatic blood flow due to an increased portion of blood flow to the portal vascular bed
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30
Q

how does the site of surgery affect hepatic blood flow?

A

the site of surgery effects hepatic blood flow, with upper abdominal surgery decreasing flow up to 60%

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31
Q

which inhalation anesthetic has the least effect on hepatic blood flow? the most?

A
  • least –sevoflurane

* most – halothane (almost linear sharp decrease in HBF as MAC level increases)

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32
Q

describe the metabolic function of the liver

A
  • protein metabolism – except gamma globulin
  • produces albumin
  • production of all coagulation factors – except factor III, IV, VIII
  • amino acid metabolism
  • carbohydrate metabolism
  • nutrient metabolism
  • fat metabolism
  • bacterial filtering
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33
Q

what is the normal range for serum albumin?

A

3/5-6g/dl

* serum albumin is a reliable predictor of chronic liver disease

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34
Q

which coagulation factors are vitamin K dependent?

A

II, VII, IX, X

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35
Q

which coagulation factors are non-vitamin K dependent?

A

V, XI, XII, XIII, fibrinogen

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36
Q

what test is a good indicator of acute hepatic dysfunction, as well as vitK dependent coagulation factor deficiencies?

A

PT (prothrombin time)

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37
Q

why must liver function be significantly impaired before coagulation decreases?

A

only 20-30% of normal levels needed for adequate coagulation

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38
Q

describe amino acid metabolism in the liver

A
  • deamination of amino acids in process of energy production
  • removal of ammonia in form of urea
    • impaired in both acute and chronic hepatic disease
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39
Q

describe carbohydrate metabolism in the liver

A

“glucose buffer system”

  • storage of large amounts of glycogen – converted to glucose as needed
    • glycogen stores exhausted by NPO in 24hr
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40
Q

describe the deleterious effects of impaired liver function in terms of nutrient metabolism

A

in pts with impaired liver function, glucose loads are poorly tolerated, and blood glucose can rise several-fold –> diabetes

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41
Q

the majority of cholesterol synthesized in the liver is converted to what?

A

bile salts, secreted in bile

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42
Q

what cells in the liver are responsible for phagocytosis of bacteria that enter through the intestines?

A 
Kupffer cells (macrophages)
* liver can trap all but less than 1% of bacteria before it passes into systemic circulation
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43
Q

describe fat metabolism in the liver

A
  • oxidation of fatty acids for energy
  • synthesis of cholesterol and phospholipids
  • major source of acetyl-CoA
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44
Q

how much bile is produced by hepatocytes daily?

A

~500ml

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45
Q

how much bile can the gallbladder hold?

A

35-50ml of concentrated bile

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46
Q

how is the secretion of bile triggered?

A
  • fat in duodenum triggers cholecystokinin release from duodenal mucosa
  • cholecystokinin reaches gallbladder through circulation – stimulates gallbladder contraction
  • bile released into small intestine
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47
Q

describe the mechanism of fat solubilization by bile

A
  • bile contains bile salts, bilirubin, cholestorol

* bile salts act as detergent, solubilizing fat to be absorbed

48
Q

describe the formation of bilirubin

A
  • breakdown of hemoglobin (RBCs)
  • heme released converted to free, unconjugated bilirubin (lipid soluble), bound to albumin
  • conjugated in liver (hydrophilic), secreted into bile
  • 300mg produced daily
49
Q

how does jaundice progress?

A
  • results from accumulation of bilirubin in extracellular fluids
  • skin coloration (yellow-green) visible with plasma bilirubin = 3x normal value
  • result of increased Hgb breakdown or obstruction of bile duct
50
Q

what form of bilirubin are hemolytic and obstructive jaundice associated with?

A
  • hemolytic jaundice – unconjugated (indirect) bilirubin

* obstructive jaundice – conjugated (direct) bilirubin

51
Q

describe how drugs affect bile formation

A
  • all narcotics increase common bile duct pressure (fentanyl >morphine >demoral)
  • attenuated by NTG, nalonone, atropine and glucagon
52
Q

define drug biotransformation

A

conversion of lipophilic substances to excretable metabolites
* enzymatic responses

53
Q

describe the two phases of biotransformation

A
  • phase I – oxidation, cytochrome P450, >90%

* phase II – conjugation w/ glucuronic acid to increase water solubility for biliary excretion

54
Q

what factors affect drug metabolism?

A
  • HBF, protein binding, intrinsic hepatic clearance

* enzyme inducing compounds

55
Q

which liver enzyme lab test is a good indicator of hepatitis?

A 
alanine aminotransferase (ALT) – primarily found in liver
* 5-40 IU/L
56
Q

which liver enzyme lab test is a good indicator of biliary disease or blockage?

A 
alkaline phosphatase (ALP) – primarily found in bile ducts
* 13-39 IU/L
57
Q

how is serum albumin assessed for liver function?

A

albumin levels are decreased in chronic liver disease (cirrhosis)

58
Q

how is coagulation assessed for liver function?

A

PT –assesses extrinsic pathway of clotting cascade, namely factor VII and is associated with acute liver disease

59
Q

what is the normal range for PT?

A

9-12, 10-15sec

60
Q

what factors will affect PT?

A
  • liver disease
  • coumarin therapy
  • heparin therapy
  • VitK deficiency
  • Factor VII deficiency
61
Q

what effects will low serum albumin levels have? what is the normal range for serum albumin?

A
  • reduced intravascular osmotic pressure
  • vascular leaking leading to edema and ascites
  • range: 3.9-5.0g/dl
62
Q

coumadin interferes with which coagulation factors?

A

VitK dependent factors: II, VII, IX, X

63
Q

tissue factor is which coagulation factor and is the sole factor in the extrinsic pathway?

A

VII

64
Q

trace the intrinsic pathway to factor X

A

XII –> XI –> IX –> VIII

65
Q

a deficiency of what intrinsic pathway factor leads to hemophilia B/christmas disease?

A

IX

66
Q

a deficiency of what intrinsic pathway factor leads to hemophilia A and von willebrand disease?

A

VIII

67
Q

elevated unconjugated (indirect) bilirubin is an indicator of what?

A

problem upstream of bilirubin excretion

* hemolysis, hepatitis, cirrhosis can be suspected

68
Q

elevated conjugated (direct) bilirubin is an indicator of what?

A

problem with bilirubin excretion

* bile duct obstruction by gallstones or cancer can be suspected

69
Q

what are the ranges for total, direct, and indirect bilirubin?

A
  • total bilirubin – 0.2-1.5mg/dl
  • direct (conjugated) – 0.0-0.03mg/dl
  • indirect (unconjugated) – 0.2-0.8mg/dl
70
Q

how is hepatitis A transmitted?

A

via fecal/oral route, contaminated shell fish is common route

71
Q

how does hep A manifest?

A

clinically manifests as acute viral hepatitis:

  • fever
  • jaundice
  • painfully enlarged liver
72
Q

how is hep B transmitted?

A
  • blood transfusion
  • needle sticks
  • sexual contact
  • across the placenta
73
Q

how does hep B manifest?

A
  • clinically manifests as acute with development to fulminant hepatitis and rapid liver destruction
  • 10% develop chronic hepatitis (asymptomatic or chronic)
  • complications: primary hepatocellular carcinoma or cirrhosis
74
Q

is there a vaccination for hep B?

A

yes. should be taken by healthcare workers who are at high risk of potentially contracting it through contaminated needle sticks

75
Q

how is hep C transmitted?

A

same as hep B

  • blood transfusion
  • needle sticks
  • sexual contact
  • across the placenta
76
Q

how does hep C manifest?

A

clinically manifests as acute hepatitis

77
Q

how does hep C progress?

A
  • 50% of pts will get chronic
  • 20% will develop cirrhosis
  • increased risk of developing hepatocellular carcinoma
78
Q

describe hep D

A
  • co-infection acquired with hep B

* acute infection that can progress to fulminant hepatitis or cirrhosis

79
Q

describe hep E

A
  • spread by fecal/oral route due to contaminated water or poor hygiene
  • rarely found in US
80
Q

what are the anesthetic considerations for hepatitis?

A
  • assessment of coagulation preoperatively, tx with FFP if indicated
  • glucose monitoring
  • maintain near normal HBF, avoid hypercarbia
  • drug metabolism may be affected – prolonged effect
81
Q

what effects will benzodiazepines have on pts with severe hepatic dysfunction?

A
  • prolonged and more intense effect

* should be avoided as a pre-med w/ severe hepatic failure

82
Q

how will opioids affect pts with hepatic dysfunction?

A
  • morphine, alfentanil – prolonged effect

* fentanyl, sufentanil – not so much

83
Q

what effect will non-depolarizing muscle relaxants have on pts with hepatic dysfunction?

A
  • hepatic dysfunction = hypoproteinemia

* less drug bound to protein, prolonged effect

84
Q

what muscle relaxants are a better choice for hepatic dysfunction?

A

cis and atracurium

  • metabolized by plasma esterases
  • best choice if reversal is planned
85
Q

describe cirrhosis

A
  • chronic disease of liver characterized by distortion of the normal hepatic structure or scarring caused by cellular destruction
  • interference with intrahepatic circulation and gradual failure of liver function
86
Q

describe cholelitiasis

A

formation of calculus (stones) in gallbladder, caused by cholesterol crystal precipitation

87
Q

describe cholecystitis

A

inflammation of gallbladder caused by gallstone in cystic duct that connects to hepatic duct

88
Q

anesthetic considerations for pts presenting for cholecystectomy

A
  • may present with recent history of N/V
  • considered full stomach – RSI
  • opioids may constrict sphincter of oddi preventing flow of contrast dye from common bile duct
89
Q

what complications should be considered when administering blood to pts with hepatic dysfunction?

A
  • 1u PRBCs contains ~ 250mg bilirubin – increases with age of transferred unit
  • an elevation of unconjugated bilirubin can lead to seizures and brain damage (Kernicterus)
  • pts with hepatic disease/hyperbilirubin get newest PRBCs possible
90
Q

where do malignant tumors of the liver generally arise from?

A
  • parenchymal cells – hepatocarcinoma (80-90%)

* bile duct epithelium – cholangio-carcinoma

91
Q

what percentage of malignant tumors of the liver have underlying cirrhosis (primarily alcoholic in origin)

A

75%

92
Q

what is the most common source of hepatic tumors?

A

metastasis from another site

93
Q

what is the treatment for hepatic tumors?

A

chemotherapy and/or surgery if the tumor is isolated to a lobe or segment

94
Q

what are the anesthetic considerations for hepatic resection?

A
  • large bore IV access
  • a-line monitoring
  • CVP monitoring
  • epidural catheter for post-op pain management
  • keep pt relatively hypovolemic during resection phase to minimize venous engorgement of liver/blood loss
  • T&C for at least 6u blood
95
Q

describe portal hypertension

A

a sustained elevation of pressure in the portal vein above the normal level of 6-12cmH2O (8-16mmHg)

96
Q

how does portal hypertension manifest clinically?

A
  • increased resistance to blood flow in liver (decreased outflow), increased splanchnic arterial flow (increased inflow) = overflow of portal circulation
97
Q

what comorbidities present with portal hypertension?

A
  • development of collateral channels/varices in attempt to circumvent hepatic obstruction
  • splenomegaly caused by back pressure in portal system – partly responsible for accumulation of ascites in abdomen
98
Q

what causes portal HTN in the hepatic vein (posthepatic portal HTN)?

A
  • Budd-Chiari syndrome
  • right heart failure
  • restrictive cardiomyopathy
  • constrictive pericarditis
99
Q

what causes portal HTN in the liver (intrahepatic portal HTN)?

A

cirrhosis

100
Q

what causes portal HTN in the portal vein (prehepatic portal HTN)?

A

thrombosis

101
Q

what is the morbid clinical manifestation of portal HTN?

A

GI bleeding

* bleeding of varices esp in esophagus means that hepatic obstruction and portal HTN are severe

102
Q

what is the treatment for GI bleeding/portal HTN?

A
  • temporarily stop the hemorrhage

* attempt to decompress portal venous circulation

103
Q

what are the anesthetic considerations for GI bleeding/portal HTN?

A
  • may require large volume blood transfusion

* pt may already be coagulopathic from liver disease = high mortality rate

104
Q

describe transjugular intrahepatic portosystemic shunt (TIPS)

A
  • used as a way to decompress portal circulation and buy time in course of underlying liver disease
  • often used as a bridge to liver transplant
105
Q

what anesthetic plan is used for TIPS?

A

GA in the interventional radiology suite

106
Q

describe ascites

A
  • accumulation of serous fluid in the peritoneal cavity
107
Q

what are the anesthetic considerations for draining ascites?

A
  • abdominal viscera are compressed

* decompression allows expansion of large venous reservoir causing hypovolemia and potentially severe hypotension

108
Q

describe arterial hypoxemia relative to ascites

A
  • PaO2 values of 60-70mmHg common in pts with ascites = supplemental O2
  • probably due to impaired movement of diaphragm, right-to-left intrapulmonary shunting as a result of portal HTN, smoking, COPD
109
Q

what is the treatment for ascites?

A
  • drug-induced diuresis with spironolactone

* max diuresis of ascitic fluid not to exceed 1L/d for fear of hypovolemia

110
Q

how is removal of ascites fluid managed?

A
  • requires venous volume expansion – IV fluids, usually colloids, to prevent/minimize hypotension
  • good IV access important – may have to administer large amounts of fluid quickly
111
Q

what are the normal values for PT, PTT, activated clotting time, and thrombin time?

A
  • PT – 10-12sec
  • PTT – 25-35sec
  • activated clotting time –90-120sec
  • thrombin time –9-11sec
112
Q

what is the primary treatment of coagulopathy?

A

FFP

113
Q

in addition to FFP, what may be required to bring coagulopathic pt PT to within 3sec of normal preoperatively?

A

cryoprecipitate and platelets

114
Q

what is the greatest fear of massive blood loss in the coagulopathic pt?

A

breakdown of the clotting process (fibrinolysis)

115
Q

how does encephalopathy (hepatic coma) manifest?

A
  • mental confusion/ obtundation
  • asterixis –flapping motion of hands at wrist caused by loss of extensor tone
  • fetor hepaticus – fruity odor of the breath
116
Q

what are the causes of encephalopathy?

A
  • cerebral intoxication caused by intestinal contents that have not been metabolized by the liver
  • protein breakdown products from GI bacteria
  • ammonia (normally converted to urea by the liver)
117
Q

how is encephalopathy treated?

A
  • protein restriction
  • antibiotics to restrict gut bacteria (neomycin)
  • reduce diuretic therapy
  • treat hypokalemia
  • restrict sedatives, tranquilizers

ANESTHESIA PRACTICE 3 (5 decks)

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