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Anesthesia Oral Boards > Cardiac, Thoracic, and Vascular Anesthesia > Flashcards

Cardiac, Thoracic, and Vascular Anesthesia Flashcards

1
Q

DDx for Hypotension

A
  1. Pulmonary: Hypoxia, Hypercarbia, Tension Pneumothorax
  2. Hypovolemia: Fluid deficit, acute blood loss
  3. Cardiac: rate/rhythm abnormality, inotropic failure, myocardial ischemia, contusion, tamponade, rupture, congestive heart failure (CHF), cardiomyopathy, valvular injury
  4. Shock: hypovolemia, cariogenic, septic
  5. Surgical compression of the heart, aorta, IVC, or abdominal contents
  6. Embolus: pulmonary, air, fat, amniotic
  7. Electrolyte and hormonal abnormalities: hypoglycemia, hypocalcemia, adrenal insufficiency, ADH suppression, hypermagnesemia
  8. Anaphylaxis
  9. Deep anesthesia, drug overdose, medications (ACEs/ARBs)
  10. Hypothermia
  11. Sympathetic blockade, neuraxial block
  12. Ventilation
  13. Laparoscopy: Hypercarbia, Dysrhythmia, Increased vagal tone from excessive stretching of peritoneum, Compression of IVC, Venous Air Embolus
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2
Q

DDx of Hypertension

A
  1. Pre-existing HTN and end-organ dysfunction of brain, heart, kidney
  2. “White coat” HTN
  3. Pulmonary: Hypoxia, hypercarbia, pulmonary edema, OSA
  4. Renal: renovascular disease, renal parenchymal disease, renin-secreting tumor, polycystic kidney disease
  5. Neurologic: elevated ICP, spinal cord injury, Guillan-Barre syndrome, dysautonomia
  6. Cardiac: ischemia, stiff vessels, aortic coarctation, fluid overload
  7. Endocrine: Cushing’s syndrome, pheochromocytoma, thyrotoxicosis, hyperaldosteronism, hyperparathyroid
  8. Vascular: coarctation of aorta, vasculitis, collagen vascular disease
  9. Drugs: vasopressors, cocaine, MAOI +/- tyramine, TCAs, naloxone, glucocorticoids, contraceptive, withdrawal of anti-HTN or drugs
  10. Pain, anxiety, inadequate anesthesia,
  11. Bladder distension
  12. MH
  13. Hypothermia
  14. Electrolyte abnormalities: hypercalcemia, hypoglycemia
  15. Autonomic instability
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3
Q

PEA: H’s and T’s

A
  1. Hypovolemia
  2. Hypoxia
  3. H+ (Acidosis)
  4. Hyper- and Hypokalemia
  5. Hypoglycemia
  6. Hypothermia
  7. Toxins/Tablets
  8. Tamponade (cardiac)
  9. Tension Pneumothorax
  10. Thrombosis
  11. Trauma
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4
Q

Causes of Atrial Fibrillation/Flutter

A
  1. Severe Heart Disease
  2. Coronary Artery Disease
  3. Mitral Valve Disease
  4. Pulmonary Embolism
  5. Hyperthyroidism
  6. Cardiac Trauma
  7. Cancers of the Heart
  8. Myocarditis
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5
Q

Tx for Acute Atrial Fibrillation

A
  1. IV Diltiazem or Esmolol
  2. Start synchronized cardio version in patient with pronounced hemodynamic instability. Start with 100-200 J, then 300 J, then 360 J
  3. If A-Fib has been present for over 48 hrs, there is an increased risk of thromboembolism
    a. Consider TEE to rule out atrial thrombus
    b. Adequate anticoagulation for 3-4 weeks should be considered prior to cardio version if thrombus is present
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6
Q

Causes of Sick Sinus Syndrome

A
  1. A combination of symptoms caused by SA node dysfunction and manifested by marked bradycardia, sinoatrial block, or sinus arrest
  2. Can have associated episodes of supraventricular tachycardia; often called brady-tachy syndrome
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7
Q

S/S of Sick Sinus Syndrome

A
  • Dizziness
  • Confusion
  • Fatigue
  • Syncope
  • CHF
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8
Q

Tx of Sick Sinus Syndrome

A
  1. Atrial or dual chamber pacemaker

2. Patents are at high risk of developing PE and should be started on anti-coagulation

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9
Q

Intra-operative treatment of Acute Coronary Syndrome

A
  1. Rapid assessment of which determinants of myocardial O2 balance have been compromised (usually tachycardia)
  2. Improve patient’s hemodynamics
  3. Evaluate IV access
  4. 100% oxygen
  5. Meds (Nitroglycerin, Morphine, Beta blocker)
  6. 12-lead EKG
  7. Labs (Cardiac markers, CBC, Electrolytes, Coagulation panel)
  8. CXR
  9. Inform surgeon (cancel case or finish ASAP)
  10. Consult cardiology
  11. If unstable, consider TEE
  12. Alert the cath lab
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10
Q

What is Virchow’s Triad?

A
  1. Venous Stasis
  2. Vessel wall damage
  3. Hypercoagulability
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11
Q

Diagnosis of PE

A
  1. Pulmonary Angiography (gold standard)
    a. If renal failure, V/Q Scan (avoids IV contrast)
  2. Labs: ABG, D-Dimer (non-specific)
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12
Q

Diagnosis of Venous Air Embolus (VAE)

A
  1. Signs of Cardiac Ischemia
  2. Signs of increased pulmonary artery pressure
  3. Hypotension
  4. Acute decrease in ETCO2
    a. Increase in alveolar dead space and decrease of cardiac output
  5. Increased ETN2 (end-tidal nitrogen)
  6. Precordial Doppler: “mill-wheel” murmur
  7. Air with aspiration of a RA multi-orifice catheter
  8. TEE: right ventricular dilation or hypokinesis
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13
Q

Tx of VAE

A
  1. Lower site of air entry below level of heart
  2. Notify surgeon
  3. Secure airway and ensure adequate oxygenation and ventilation
  4. Stop N2O and place patient on 100% FiO2
  5. Flood surgical field with saline
  6. Compression of proximal vein: IJ in sitting cases
  7. Aspiration of right atrial catheter (if present)
  8. IV saline bolus
  9. Support circulation w/ vasopressor
  10. Position patient in left lateral decubitus
  11. PEEP does NOT decrease incidence of VAE
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14
Q

Diagnosis of Fat Embolism Syndrome

A
  1. Hypoxemia
  2. Neurological abnormalities: altered mental status
  3. Petechiae: occurs 12-72 hours after initial trauma or instrumentation
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15
Q

Pathogenesis of Amniotic Fluid Embolism Syndrome (AFES)

A

Immune response to amniotic fluid contents or immune reaction triggered by leukotrienes or arachidonic acid within the fluid
**NOT a mechanical outflow obstruction

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16
Q

Risk Factors for Amniotic Fluid Embolism Syndrome

A
  1. Tumultuous Labor
  2. Trauma
  3. Multiparty
  4. Advanced Maternal age
  5. C-section
  6. Increased gestational age
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17
Q

S/S of Amniotic Fluid Embolism Syndrome

A
  1. Usually presents with an abrupt onset and rapid clinical deterioration
  2. Hypoxia
  3. Bronchospasm
  4. ARDS
  5. Pulmonary Edema: Capillary leak from embolism, left heart failure, and cariogenic shock
  6. Increased pulmonary artery pressure
  7. Increased ETCO2
  8. Hypotension (cardiogenic shock)
  9. DIC
  10. AMS and seizures
  11. Fever
  12. Fetal Distress
  13. Headache
  14. Nausea and vomiting
18
Q

DDx of Amniotic Fluid Embolism Syndrome

A
  1. PE
  2. VAE
  3. Hemorrhage
  4. Anaphylaxis
  5. Transfusion reaction
  6. MI
19
Q

Diagnosis of Pericardial Tamponade

A
  1. Triad of acute tamponade
    a. Decreasing arterial pressure
    b. Increasing venous pressure
    c. Small, quit heart
  2. CVP = PAD = PAOP
  3. Pulsus paradoxus
    a. Fall of systolic pressure > 12mmHg during inspiration
  4. Kussmaul’s sign: inspiratory venous pressure remains study or increases
  5. EKG: Electrical alternans
20
Q

Pre-op preparation for Cardiac Tamponade

A
  1. Give supplemental O2
  2. Avoid positive pressure ventilation (if possible)
  3. Oliguria: reflects pre renal or intrarenal process 2/2 decreased CO and vasoconstriction
    a. Do not give diuretics
    b. Most effective treatment is pericardiocentesis
  4. Elevated PT and PTT
    a. Treat coagulopathy
    b. Have 4-6 units of PRBCs in OR before starting case
  5. Pre-meds
    a. Do NOT give anxiolytic
  6. Sympathoadrenal activation is supporting perfusion to vital organs through vasoconstriction and tachycardia
    a. Don’t give meds that decrease tachycardia
21
Q

Intra-op management of Cardiac Tamponade

A
  1. Monitors:
    a. Standard ASA
    b. Pre-induction Arterial catheter
  2. Oxygen by face mask
  3. Meds
    a. Ketamine: first choice for induction (1 mg/kg)
    i. Small increases in BP, HR, CO, myocardial oxygen demand
    ii. Direct central sympathetic stimulation and inhibition of NE uptake
    b. Etomodate: second choice
22
Q

Induction for Cardiac Tamponade

A
  1. Standard ASA monitors and arterial line
  2. Surgical team ready (gowned) with patient sterilely prepared and draped
  3. Induction w/ IV ketamine and muscle relaxant (keep spont. respiration prior to induction)
  4. Be prepared to treat circulatory collapse
  5. Management of Hypotension
    a. Vasoactive drugs
    b. Cardioactive drugs
    c. Fluid challenge
    d. Reduce inspiratory positive pressure to facilitate cardiac filling
    f. Surgical relief of tamponade is definitive treatment
23
Q

High Risk Non-Cardiac Surgical Procedures

A
  1. Cardiac Risk > 5%
    a. Aortic and other major vascular surgery
    b. Peripheral Vascular Surgery
    c. Emergency surgery
    d. Anticipated long procedures with associated fluid shifts and large estimated blood loss
24
Q

Intermediate Risk Non-Cardiac Surgery Procedures

A
  1. Cardiac Risk 1-5%
    a. Intraperitoneal and intrathoracic surgery
    b. Cardiac endarterectomy
    c. Head and neck surgery
    d. Orthopedic surgery
    e. Prostate surgery
25
Q

Low Risk Non-Cardiac Surgery Procedures

A
  1. Cardiac Risk < 5%
    a. Endoscopic procedures
    b. Superficial procedures
    c. Cataract surgery
    d. Breast surgery
    e. Ambulatory surgery
26
Q

Timing of Elective Non-Cardiac Surgery after Coronary Revascularization

A
  1. Drug Eluting Stent: 12 months
  2. Bare Metal Stent: 4-6 weeks
  3. Balloon Angioplasty: 4 weeks
27
Q

Regional Techniques for CEA

A
  1. Deep Cervical Plexus Block (CPB)
    a. Most commonly employed technique for CEA
    b. Disadvantages
    i. Diaphragmatic dysfunction (phrenic nerve block)
    ii. Greater risk of epidural, subarachnoid, vertebral artery injection
  2. Superficial CPB
    a. Lower reported complication rate compared to Deep CPB
28
Q

Indications for antibiotic prophylaxis for endocarditis

A
  1. Prosthetic cardiac valve or material
  2. Previous endocarditis
  3. Unrepaired cyanotic heart disease
  4. First 6 months after complete repair of congenital heart disease
  5. Presence of residual defects after repair of congenital heart disease
  6. Valvulopathy after heart transplant
29
Q

Diagnosis of Pheochromocytoma

A
  1. Plasma-Free metanephrines
  2. Plasma catecholamines, urine catecholamines/metanephrines, urine vanillylmandelic acid
  • *If preliminary tests equivocal, clonidine-suppression test
    • Decreases catecholamines in essential HTN, NOT in Pheo

MRI, CT

30
Q

What is optimal duration of alpha blockade pre-operatively for Pheochromocytoma?

A

10-14 days

31
Q

Drugs to avoid during a Pheochromocytoma resection

A
  1. Drugs that stimulate tumor cells and histamine release
    • Succinylcholine, morphine, atracurium
  2. Drugs that result in increased sympathetic activity
    • atropine, ketamine, ephedrine
  3. Drugs that sensitize myocardium to catecholamines
    • halothane
  4. Droperidol - associated w/ significant HTN with Pheo patients
32
Q

Compare Roller Pump vs Centrifugal CPB

A
  1. Roler Pump
    - Forward flow produced by partial compression of tubing by 2 roller heads
    - Not sensitive to preload or afterload
    - Can deliver pulsatile flow
    - Disadvantage:
    • Relatively increased damage to RBCs
    • Potential delivery to large quantities of air to patient if air entrained
    • Risk of over-pressurization to changes in afterload
    • Risk of preload occlusion leading to negative pressure-induced cavitation
  2. Centrifugal (kinetic) Pump
    - Rotational force responsible for forward flow
    - Less damaging to RBC
    - Sensitive to changes in preload and afterload
    - Will cease functioning if significant amount of air entrained
    - Disadvantages:
    • Incapable of delivering pulsatile flow
33
Q

Compare pH stat vs alpha stat

A
  1. pH Stat:
    - CO2 added to oxygenator as necessary to maintain PaCO2 of 40 mmHg and pH of 7.40
    - Primary mechanism of brain injury thought to be related to Ischemia (enhanced CBF from adding CO2 provides superior brain protection)
  2. Alpha Stat:
    • CO2 not added to oxygenator
    • Improved neurophysiologic outcomes in Adults
      • Since primary mechanism of brain injury thought to be related to embolic events rather than ischemia in Adults
34
Q

How high does ACT need to be prior to initiation of CPB?

A

480 seconds

35
Q

Causes of decreased venous reservoir at initiation of CPB

A
  1. Elevation of heart by surgeon
  2. Problems w/ venous cannula
    • Air lock
    • Inadequate diameter
    • Kinking
    • Malpositioning
    • Obstruction by thrombotic material
36
Q

When should an Intra-Aortic Balloon Pump (IABP) be inflated and deflated?

A

Inflated

  • With Aortic Valve closure (start of diastole)
  • Increases aortic diastolic pressures and augments coronary perfusion pressure
  • Timed w/ Dicrotic notch on arterial wave form & middle of T-wave on ECG

Deflated

  • Prior to Ventricular contraction
  • Promotes forward flow by reducing ventricular afterload
37
Q

Mneumonic for coming off Bypass

A

“THE VCR”

T- Temperature
H- Hemoglobin
E- Electolytes
V- Ventilator
C- Contractility
R- Rhythm
38
Q

At what temperature can a patient be weaned from CPB?

A

Esophageal/Nasopharyngeal - 37C

Rectal/Bladder - 35C

39
Q

How much Protamine is used to reverse Heparin at the end of CPB?

A

1 mg of Protamine for each 100 units of Heparin given

40
Q

What are the types of Protamine Reactions

A

Type 1: Systemic Hypotension from Rapid Injection

Type 2: Anaphylactic or Anaphylactoid Reaction

  • Antibody mediated
  • Immediate or Delayed

Type 3: Catastrophic Pulmonary Vasoconstriction w/ Systemic Hypotension

41
Q

What is the mechanism of action of Protamine?

A

Heparin (strong organic acid) combines with Protamine (strong organic base) to form a stable salt and loses its anticoagulant activity

  • Protamine has 2 active sites
    a) One neutralizes heparin
    b) One exerts mild anticoagulant effect
42
Q

DDx for Hypotension during CPB

A
  1. Inadequate pump flow at beginning of bypass
  2. Hypoxic vasodilation from initial perfusion w/ blood-free priming
  3. Vasodilation form vasoactive materials 2/2 interaction w/ foreign material in CPB machine
  4. Decreased plasma levels of catecholamines by Hemodilution

Anesthesia Oral Boards (10 decks)

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