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Advanced Principles C > Major Vascular I > Flashcards

Major Vascular I Flashcards

1
Q

What percent of cardiac output goes to the liver?

A

25%

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2
Q

What vessels supply blood to the liver?

A
  • Hepatic artery
  • Portal vein
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3
Q

What percent of the blood supply to the liver comes from the hepatic artery?

A

25-30%

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4
Q

What percent of the blood supply to the liver comes from the portal vein?

A

70-75%

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5
Q

The metabolizing cells of the liver are called _________

A

Hepatocytes

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6
Q

Hepatocytes make up what percentage of the cellular volume of the liver?

A

75-80%

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7
Q

What makes up the portal triad?

A
  • Portal vein
  • Hepatic artery
  • Bile Duct
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8
Q

Which liver zone is responsible for aerobic metabolism?

A

Periportal Zone (Zone 1) - outermost zone

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9
Q

What is Zone 3 of the liver called?
What is the function of Zone 3?

A
  • Perivenous Zone ( Zone 3)
  • Glycolysis/ Glucuronidation
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10
Q

What is the purpose of Hepatic Stellate Cells?

A

Respond to cytokines during inflammatory periods

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11
Q

Name pathological conditions that can lead to cirrhosis.

A
  • Alcoholic liver disease
  • Hep C
  • Hep B
  • Non-alcoholic steatohepatitis
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12
Q

Cirrhosis can cause the following complications:

A
  • Portal hypertension
  • Ascites
  • Peritonitis
  • Encephalopathy
  • Cardiomyopathy
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13
Q

How is compensated cirrhosis determined?

A
  • Absence of portal hypertension
  • Absence of GE varices
  • Absence of dysfunction
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14
Q

Median years of survival for compensated cirrhosis?

A

> 12 years

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15
Q

How is uncompensated cirrhosis determined?

A
  • Presences of Ascites
  • Presence of Portal Hypertension
  • Presence of Variceal Hemorrhage
  • Presence of Heaptic Encephalopathy
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16
Q

Median years of survival for uncompensated cirrhosis?

A

2 years

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17
Q

Pathology of how portal hypertension can lead to esophageal varices

A
  • Portal Hypertension causes the release of vasodilator production (NO) and angiogenic factors.
  • This will cause an increase in azygos and hemiazygos flow, leading to esophageal varices.
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18
Q

In esophageal varices, there is collateral circulation between the high-pressure __________ system and low-pressure ________ system.

A

In esophageal varices, there is collateral circulation between the high-pressure PORTAL system and low-pressure AZYGOS system.

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19
Q

Treatment to prevent initial bleed from esophageal varices.

A
  • Non-selective beta blockers (propranolol, nadolol) to decrease portal hypertension
  • Endoscopic band ligation
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20
Q

Treatment to control active hemorrhage and prevention of rebleed from esophageal varices.

A
  • Endoscopic band ligation
  • Sclerotherapy (Epi/vaso)
  • Somatostatins (Octreotide)
  • Replace PRBCs
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21
Q

How does Octreotide work?

A
  • Octreotide will cause vasoconstriction in splanchnic circulation d/t inhibition of glucagon release (splanchnic dilator).
  • Vasoconstriction will decrease blood flow → Decrease Portal Hypertension
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22
Q

What is the purpose of a Transjugular Intrahepatic Portosystemic Shunt (TIPS)?

A
  • Decompress the portal circulation in patients with portal hypertension
  • Catheter placed through jugular vein, between portal and hepatic vein
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23
Q

Indications for TIPS

A
  • Secondary prophylaxis of bleeding varices after failed medical therapy
  • Temporary relief of portal HTN while awaiting transplantation
  • Treatment of refractory ascites
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24
Q

What are the concerns and cons of TIPS?

A
  • High rate of shunt stenosis
  • Hepatic encephalopathy (↑ waste product)
  • High cost
  • Lack of availability
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25
Q

Airway considerations for cirrhosis

A
  • Recent GI Bleed → Full Stomach
  • ↓ LOC d/t encephalopathy
  • ↑ Intragastric pressure d/t ascites
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26
Q

CV considerations for cirrhosis

A
  • Alcoholic cardiomyopathy → bad pump
  • Altered intravascular volume d/t ascites, relative hypovolemia from fluid shift.
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27
Q

Pulmonary considerations for cirrhosis

A
  • ↓ FRC
  • Possible pneumonia d/t aspiration
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28
Q

Hematological considerations for cirrhosis

A
  • Coagulopathy
  • Thrombocytopenia
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29
Q

What coagulation factors does the liver produce?

A
  • Factor I
  • Factor II
  • Factor VII
  • Factors IX through Factor XIII
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30
Q

Neuro considerations for cirrhosis

A

Hepatic encephalopathy

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31
Q

Describe the volume of distribution of liver disease patients

A

Increase volume of distribution d/t ascites

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32
Q

Describe the protein binding of liver disease patients

A

Decrease protein binding → more circulating active drug

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33
Q

Describe the drug metabolism of liver disease patients

A

Decrease drug metabolism

34
Q

Describe the drug elimination of liver disease patients

A

Decrease drug elimination

35
Q

Intraoperative anesthesia considerations for TIPS procedure

A
  • Protect airway → consider RSI
  • Consider A-line/ SVV monitoring
  • Beside point of care test (chem/ blood glucose)
  • Extra supplies (cath lab)
36
Q

What substances can cause a Pulmonary Embolism (PE)?

A
  • Blood clot
  • Fat
  • Tumor cells
  • Air
  • Amniotic fluid
  • Foreign material entering the venous system
37
Q

Where do clots usually come from?

A
  • Lower extremities
  • Pelvic veins
  • Right heart
38
Q

Causes of PE

A
  • Stasis
  • Hypercoagulability
39
Q

How is dead space affected by PE?

A

Increase dead space

40
Q

How is minute ventilation affected by PE?

A

Increase minute ventilation to compensate for hypoxemia

41
Q

How is pulmonary vascular resistance affected by PE?

A

Increase PVR

42
Q

How does PE affect surfactants?

A

Loss of surfactant

43
Q

Atelectasis will occur within _______ hours of a PE, leading to potential pulmonary infarction.

A

24-48 hours

44
Q

What are the differential diagnosis of PE?

A
  • MI
  • Pericarditis
  • Pneumonia
  • Pneumothorax
  • Pleuritis
45
Q

PE Symptoms

A
  • Sudden dyspnea
  • Tachypnea
  • Pleuritic chest pain
  • Rales
  • Nonproductive cough
  • Tachycardia
  • Hemoptysis
  • Fever
46
Q

ABG diagnosis of PE

A
  • Non-specific
  • Hypoxemia
  • Hypocarbia

While hypoxemia is due to impaired oxygen exchange from V/Q mismatch, hypocapnia is a result of compensatory hyperventilation.

47
Q

EKG diagnosis of PE

A
  • Non-specific
  • ST-T changes
  • A-fib
  • Tachy
  • RBBB
48
Q

TEE diagnosis of PE

A
  • Dilated RA and RV d/t ↑ pulmonary pressure
  • Left ventricular wall abnormalities d/t poor CO
49
Q

What blood test can indicate PE?

A
  • Positive D-dimer (high levels of fibrin degradation)
  • Elevated troponin
50
Q

What test can be used to detect clots in main, lobar, and segmental pulmonary arteries?

A

Spiral CT/ VQ Study (not useful in small vessels)

51
Q

What is the gold standard used to diagnose PE?

A

Pulmonary angiogram

52
Q

In the absence of sepsis, new-onset dysrhythmias, and hypovolemia, how can PE be suspected based on blood pressure?

A
  • SBP < 90 mmHg
  • OR SBP decrease by >40 mmHg for 15 minutes
53
Q

What are prophylactic treatments for PE?

A
  • Heparin 5,000u q 12 hours
  • Early ambulation
  • Intermittent compression devices
  • Warfarin or DOAC
  • Vena cava filter (IVC Filter)
54
Q

Indications for IVC Filter

A
  • Deep vein thrombosis
  • Pulmonary embolus
  • Trauma victims
  • Immobility (Recent surgery or Delivery)
55
Q

What are the symptoms of carotid disease?

A
  • Asymptomatic bruit
  • TIA symptoms
  • Transient blindness
  • Paresthesia
  • Speech problems
  • Clumsiness of extremities
56
Q

How can carotid disease be diagnosed?

A

Duplex scan

57
Q

Carotid disease treatment

A
  • ASA therapy
  • Platelet inhibitor therapy (Clopidogrel, ticagrelor)
  • Endarterectomy
  • Stenting
58
Q

Indications for carotid endarterectomy (CEA)

A
  • Surgery within 2 weeks of ischemic event
  • Stenosis 70% or greater
  • Poor anatomy (tortuosity)
  • DAPT contraindications
59
Q

Indication for carotid stenting

A
  • Contralateral laryngeal palsy
  • Poor surgical candidate (CHF, USA, Advanced COPD)
60
Q

What are the goals of CEA and stenting?

A
  • Protect the heart
  • Protect the brain
  • Control heart rate/blood pressure
  • Ablate stress response (have beta blocker on board)
  • Awake patient at end of procedure
61
Q

Pre-operative Anesthesia Management for CEA and Stenting.

A
  • Continue Anti-anginal, anti-hypertensive, and anti-platelet meds continued
  • Discontinuation of ASA: ↑ rate of MI and TIA
  • Baseline vital signs
  • Little to no sedatives
  • Arterial line placement
  • Routine monitors
  • IV access
62
Q

Intraoperative Anesthesia Management for CEA and Stenting.

A
  • Stable hemodynamics
  • Small doses of opioids
  • Esmolol/ Cardene to control BP
  • Heparinization (100 u/kg)
63
Q

What are the problems that can occur with shunting during a CEA?

A
  • Kinking
  • Shunt occlusion against side wall
  • Air embolism
  • Injury to carotid artery
  • Impaired access due to shunt position
64
Q

What can occur from manipulating the carotid sinus?

A
  • Activation of the baroreceptor reflex
  • Sudden bradycardia and hypotension
65
Q

Treatment for baroreceptor reflex causing bradycardia and hypotension

A
  • Cessation of manipulation
  • Infiltration with Lidocaine 1%
  • Glycopyrolate IV
66
Q

What kind of block can be done for a CEA?

A

C2 to C4 Cervical plexus block

  • Anterior rami of C1 to C4 cervical roots
  • Innervatesmost neck muscles
  • Sensory innervation to anterior and lateral neck
67
Q

What is the problem with performing a cervical plexus block?

A
  • Difficult to assess the depth of the block
  • Superficial block will block sensory
  • Deep cervical plex block will block sensory/motor → phrenic nerve involvement.
68
Q

Benefits of Regional Anesthesia for CEA

A
  • Easy to monitor adequacy of cerebral perfusion
  • Consciousness
  • Greater stability of hemodynamics
  • Reduced operative site bleeding
  • Decreased cost
69
Q

Benefits of General Anesthesia for CEA

A
  • Ability to use pharmacologic cerebral protection
  • Avoid patient panic
  • Avoid phrenic nerve paresis
70
Q

What are the causes of hypertension after a CEA?

A
  • Poor control during pre-op
  • Denervation of carotid sinus baroreceptor
  • Bladder distention
  • Pain (treat w/ opioids)
71
Q

What is the cause of hyperperfusion syndrome in CEA patients?

A
  • Abrupt increase in flow d/t loss of autoregulation
  • Occurs several days after CEA
72
Q

Symptoms of Hyperperfusion syndrome

A
  • HA
  • Seizures
  • Cerebral edema
73
Q

What can cause hypotension in CEA patients?

A
  • Hypersensitive baroreceptor
  • More common after regional anesthesia
74
Q

What nerves can be affected by CEA?

A
  • Recurrent laryngeal nerve
  • Superior laryngeal nerve
  • Hypoglossal nerve
75
Q

Unilateral vs Bilateral recurrent laryngeal nerve dysfunction

A
  • Unilateral recurrent: hoarseness and impaired cough
  • Bilateral recurrent: life-threatening respiratory obstruction
76
Q

What are the effects of carotid body denervation from CEA?

A
  • Mild hypoxemia d/t impaired ventilatory responses
  • Bilateral carotid body dysfunction causes impaired response to acute hypoxia and elevated PaCO2
77
Q

What are the two types of stenting procedures used in carotid disease?

A
  • Transfemoral
  • Transcarotid
78
Q

Which type of stenting has increased stroke and death in patients over 70 years old?

A

Transfemoral

79
Q

Which type of stenting has longer fluoroscopy?

A

Transfemoral

80
Q

Which type of stenting involves reversing the flow of the carotid?

81
Q

Which type of stenting has greater surgical site complications?

Advanced Principles C (11 decks)

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