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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
Airway considerations for cirrhosis
* Recent GI Bleed → Full Stomach * ↓ LOC d/t encephalopathy * ↑ Intragastric pressure d/t ascites
26
CV considerations for cirrhosis
* Alcoholic cardiomyopathy → bad pump * Altered intravascular volume d/t ascites, relative hypovolemia from fluid shift.
27
Pulmonary considerations for cirrhosis
* ↓ FRC * Possible pneumonia d/t aspiration
28
Hematological considerations for cirrhosis
* Coagulopathy * Thrombocytopenia
29
What coagulation factors does the liver produce?
* Factor I * Factor II * Factor VII * Factors IX through Factor XIII
30
Neuro considerations for cirrhosis
Hepatic encephalopathy
31
Describe the volume of distribution of liver disease patients
Increase volume of distribution d/t ascites
32
Describe the protein binding of liver disease patients
Decrease protein binding → more circulating active drug
33
Describe the drug metabolism of liver disease patients
Decrease drug metabolism
34
Describe the drug elimination of liver disease patients
Decrease drug elimination
35
Intraoperative anesthesia considerations for TIPS procedure
* Protect airway → consider RSI * Consider A-line/ SVV monitoring * Beside point of care test (chem/ blood glucose) * Extra supplies (cath lab)
36
What substances can cause a Pulmonary Embolism (PE)?
* Blood clot * Fat * Tumor cells * Air * Amniotic fluid * Foreign material entering the venous system
37
Where do clots usually come from?
* Lower extremities * Pelvic veins * Right heart
38
Causes of PE
* Stasis * Hypercoagulability
39
How is dead space affected by PE?
Increase dead space
40
How is minute ventilation affected by PE?
Increase minute ventilation to compensate for hypoxemia
41
How is pulmonary vascular resistance affected by PE?
Increase PVR
42
How does PE affect surfactants?
Loss of surfactant
43
Atelectasis will occur within _______ hours of a PE, leading to potential pulmonary infarction.
24-48 hours
44
What are the differential diagnosis of PE?
* MI * Pericarditis * Pneumonia * Pneumothorax * Pleuritis
45
PE Symptoms
* Sudden dyspnea * Tachypnea * Pleuritic chest pain * Rales * Nonproductive cough * Tachycardia * Hemoptysis * Fever
46
ABG diagnosis of PE
* Non-specific * Hypoxemia * Hypocarbia ## Footnote While hypoxemia is due to impaired oxygen exchange from V/Q mismatch, hypocapnia is a result of compensatory hyperventilation.
47
EKG diagnosis of PE
* Non-specific * ST-T changes * A-fib * Tachy * RBBB
48
TEE diagnosis of PE
* Dilated RA and RV d/t ↑ pulmonary pressure * Left ventricular wall abnormalities d/t poor CO
49
What blood test can indicate PE?
* Positive D-dimer (high levels of fibrin degradation) * Elevated troponin
50
What test can be used to detect clots in main, lobar, and segmental pulmonary arteries?
Spiral CT/ VQ Study (not useful in small vessels)
51
What is the gold standard used to diagnose PE?
Pulmonary angiogram
52
In the absence of sepsis, new-onset dysrhythmias, and hypovolemia, how can PE be suspected based on blood pressure?
* SBP < 90 mmHg * OR SBP decrease by >40 mmHg for 15 minutes
53
What are prophylactic treatments for PE?
* Heparin 5,000u q 12 hours * Early ambulation * Intermittent compression devices * Warfarin or DOAC * Vena cava filter (IVC Filter)
54
Indications for IVC Filter
* Deep vein thrombosis * Pulmonary embolus * Trauma victims * Immobility (Recent surgery or Delivery)
55
What are the symptoms of carotid disease?
* Asymptomatic bruit * TIA symptoms * Transient blindness * Paresthesia * Speech problems * Clumsiness of extremities
56
How can carotid disease be diagnosed?
Duplex scan
57
Carotid disease treatment
* ASA therapy * Platelet inhibitor therapy (Clopidogrel, ticagrelor) * Endarterectomy * Stenting
58
Indications for carotid endarterectomy (CEA)
* Surgery within 2 weeks of ischemic event * Stenosis 70% or greater * Poor anatomy (tortuosity) * DAPT contraindications
59
Indication for carotid stenting
* Contralateral laryngeal palsy * Poor surgical candidate (CHF, USA, Advanced COPD)
60
What are the goals of CEA and stenting?
* 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
Pre-operative Anesthesia Management for CEA and Stenting.
* 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
Intraoperative Anesthesia Management for CEA and Stenting.
* Stable hemodynamics * Small doses of opioids * Esmolol/ Cardene to control BP * Heparinization (100 u/kg)
63
What are the problems that can occur with shunting during a CEA?
* Kinking * Shunt occlusion against side wall * Air embolism * Injury to carotid artery * Impaired access due to shunt position
64
What can occur from manipulating the carotid sinus?
* Activation of the baroreceptor reflex * Sudden bradycardia and hypotension
65
Treatment for baroreceptor reflex causing bradycardia and hypotension
* Cessation of manipulation * Infiltration with Lidocaine 1% * Glycopyrolate IV
66
What kind of block can be done for a CEA?
C2 to C4 Cervical plexus block ## Footnote * Anterior rami of C1 to C4 cervical roots * Innervates most neck muscles * Sensory innervation to anterior and lateral neck
67
What is the problem with performing a cervical plexus block?
* 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
Benefits of Regional Anesthesia for CEA
* Easy to monitor adequacy of cerebral perfusion * Consciousness * Greater stability of hemodynamics * Reduced operative site bleeding * Decreased cost
69
Benefits of General Anesthesia for CEA
* Ability to use pharmacologic cerebral protection * Avoid patient panic * Avoid phrenic nerve paresis
70
What are the causes of hypertension after a CEA?
* Poor control during pre-op * Denervation of carotid sinus baroreceptor * Bladder distention * Pain (treat w/ opioids)
71
What is the cause of hyperperfusion syndrome in CEA patients?
* Abrupt increase in flow d/t loss of autoregulation * Occurs several days after CEA
72
Symptoms of Hyperperfusion syndrome
* HA * Seizures * Cerebral edema
73
What can cause hypotension in CEA patients?
* Hypersensitive baroreceptor * More common after regional anesthesia
74
What nerves can be affected by CEA?
* Recurrent laryngeal nerve * Superior laryngeal nerve * Hypoglossal nerve
75
Unilateral vs Bilateral recurrent laryngeal nerve dysfunction
* Unilateral recurrent: hoarseness and impaired cough * Bilateral recurrent: life-threatening respiratory obstruction
76
What are the effects of carotid body denervation from CEA?
* Mild hypoxemia d/t impaired ventilatory responses * Bilateral carotid body dysfunction causes impaired response to acute hypoxia and elevated PaCO2
77
What are the two types of stenting procedures used in carotid disease?
* Transfemoral * Transcarotid
78
Which type of stenting has increased stroke and death in patients over 70 years old?
Transfemoral
79
Which type of stenting has longer fluoroscopy?
Transfemoral
80
Which type of stenting involves reversing the flow of the carotid?
TCAR
81
Which type of stenting has greater surgical site complications?
TCAR

Advanced Principles C (11 decks)

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