ITE 2020 - 2021 Flashcards

1
Q

What are 5 nerves that innervate the foot?

A

1. Posterior Tibial

2. Sural

3. Superficial Peroneal

4. Deep Peroneal (Deep Fibular Nerve)

5. Saphenous Nerve (Branch of Femoral Nerve)

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2
Q

How and where does the Sciatic Branch branch off?

List their major and minor branches

A

At popliteal fossa divides into common peroneal and tibial nerves

Common Peroneal

  • Superficial Peroneal
  • Deep Peroneal Nerves (Deep Fibular Nerve)

Tibial Nerves

  • Posterior Tibial
  • Sural Nerves
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3
Q

Identify the:

Axillary Vessels (Vein and artery)

Muscles (Tricep, Coracobrachialis) Biceps)

Nerves (Median, Musculocutaneous, Radial and Ulnar)

A
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4
Q

What is the RIFLE Criteria?

What do the define oliguria as (Include 12 and 24 hours)

A

The RIFLE criteria

(Risk, Injury, and Failure; and Loss; and End-stage kidney disease) add time frames to oliguria defining it as urine output of:

< 0.5 mL/kg for 12 hour or <400 mL pe rday

urine output < 0.3 mL/kg for 24 hours

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5
Q

What is anuria defined as?

A

Anuria is defined as urine output < 50 mL in 12 hours or urine output < 50-100 mL in 24 hours

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6
Q

List the RIFLE Criteria for:

GFR Criteria & Urinary Output Criteria for Each of the 5 phases

A

See images

Risk - Creatinine jumps 1.5x or GFR decreases 25%, UOP <0.5 mL/kg/hr for 6 hours

Injury - Creatinine jumps x2 or GFR decreases 50%, UOP <0.5 mL/kg/hr for 12 hours

Injury - Creatinine jumps x3 or Cr >4 (Acute rise in >0.5 or GFR decreases 75%, UOP <0.3 mL/kg/hr for 24 hours or Anuria for 12 hours

Loss - Persistent Failure = Complete loss of renal function >4 weeks

ESRD = Complete Loss of kidney function for >3 months

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7
Q

What is the biggest difference between HFJV and HFOV?

A

In HFJV exhalation is passive (depends on passive lung and chest-wall recoil) whereas in HFOV gas movement is caused by in-and-out movement of the “loudspeaker” oscillator membrane. Thus in HFOV both inspiration and expiration are actively caused by the oscillator, and passive exhalation is not allowed

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8
Q

What is important to remember about CO2 removal in both high-frequency jet ventilation (HFJV) and high-frequency oscillatory ventilation (HFOV)?

A

In both HFJV and HFOV, CO2 removal is inversely proportional to frequency (opposite of what we usually do in conventional ventilation modes).

This is because of the higher the frequency the lower the amplitude, which is the key to CO2 removal.

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9
Q

What are the benefits of centrifugal cardiopulmonary bypass pumps vs. roller pumps?

A

Less blood element destruction

Lower line pressures

Lower risk of air emboli

Elimination of tubing wear

Elimination of Spallation

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10
Q

What is spallation in terms of CPB (Cardiopulmonary Bypass)?

A

Spallation = The breakup of a bombarded nucleus into several parts

I.e. Creation of plastic microemboli (spallation),

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11
Q

When referencing certrifugal CPB pumps, why do they require flowmeters?

A

Centrifugal pumps require flowmeters on the arterial portion of the CPB circuit since flow can vary from alterations in pump preload and afterload.

Centrifugal pump blood flow varies depending on pump preload and afterload.

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12
Q

Are roller CPB pumps preload and afterload dependent in terms of pump flow?

A

Assuming the inflow and outflow are not occluded, roller pump flow is essentially only dependent on the speed of the rollers

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13
Q

What is the effects of electrolytes (K and Ca) on rapid NaHCO3 administration?

A

Drop in Both K and Ca

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14
Q

How does Acidosis vs. Alkalosis affect K levels?

A

In the setting of acidosis, excess hydrogen ions enter cells, resulting in the extracellular movement of potassium to maintain electrical balance, thus increasing the measured serum (K+).

Conversely, during alkalosis, extracellular potassium ions move into cells to balance the extracellular movement of hydrogen ions, resulting in decreased plasma (K+). This is the mechanism behind bicarbonate administration in the setting of severe hyperkalemia.

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15
Q

How does pH affect the ionized free calcium levels?

A

Acidosis = Hypercalcemia

Alkalosis = Hypocalcemia

Explanation:

Sodium bicarbonate can transiently lower blood calcium levels. Calcium binding to albumin is dependent on serum pH. In states of acidosis, the excess hydrogen ions displace calcium bound by albumin and thus ionized levels of calcium increase. This process is reversed in the setting of alkalosis and should be considered before administering sodium bicarbonate to a patient with pre-existing hypocalcemia.

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16
Q

Bicarbonate can cause hypotension and hypertension

List the mechanisms of why this is both possible.

A

Hypotension:

  1. Systemic acidosis causes (a) pulmonary vasoconstriction (b) increased levels of ionized calcium available for cardiac myocytes.

Administration of bicarbonate could therefore result in acute vasodilation and ventricular depression, resulting in decreased blood pressure.

Hypertension
Conversely, proponents of bicarbonate administration argue that severe acidosis can cause cardiac depression and reduced response to vasopressors (which have reduced efficacy at low pH), and thus bicarbonate administration would serve to increase blood pressure.* Additionally, a typical bolus of sodium bicarbonate contains 1,000 mEq/L of sodium, compared with 154 mEq/L in a bag of normal saline, and therefore blood pressure can transiently *increase from an acute osmotic load.

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17
Q

You just slammed 2 amps of bicarbonate in the cardiac room and you notice a patient’s pupils now are asymmetric, the patient is posturing and you have cushings triad hemodynamics.

What happened and why?

A

ICP Causing herniation

Theoretically, the Sodium Bicarbonate increase in CO2 would cause cerebral vasodilation and increased intracranial pressure, although direct clinical evidence for this has not been found.

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18
Q

What is a normal CVP?

A

2-6 mmHg

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19
Q

What is a normal PCWP?

A

6-12 mmHg

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20
Q

What is a normal Cardiac Index?

A

2.5 - 5 L / min/ m2

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21
Q

What is a normal SVR?

A

800 - 1200 dynes x sec / cm5

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22
Q

What are the 4 classes of distributive shock?

A

Distributive shock, also referred to as vasodilatory shock, can be divided into four classes

1. Septic shock

2. Anaphylactic shock

3. Neurogenic shock

4. Shock associated with adrenal crisis.

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23
Q

What are the 3 most anesthetically relevant joint manifestations of RA?

A

Several joint manifestations of RA can lead to anesthetic difficulties or complications.

  1. Atlantoaxial subluxation may make intubation more difficult and cause spinal cord trauma with neck manipulation
  2. Temporomandibular joint synovitis can limit mandibular motion
  3. Cricoarytenoid arthritis can cause hoarseness, pain on swallowing, and possible postextubation laryngeal obstruction
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24
Q

What are the most common extra articular cardiovascular complications of rrheumatoid arthritis patients?

A

Left sided regurgitant lesions (Mitral > Aortic)

Pericarditis, cardiomyopathy, myocarditis, cardiac amyloidosis, coronary artery arteritis, accelerated coronary atherosclerosis, cardiac valve fibrosis, cardiac conduction system abnormalities, aortitis with dilation of the aortic root and resultant aortic regurgitation, pericardial effusion, and vasculitis which may lead to visceral or myocardial/cerebral ischemia

Among the valvular diseases associated with RA, mitral valve disease including mitral regurgitation is the most common. Aortic valve disease, especially aortic regurgitation, is also often seen.

Stenotic valve lesions are not typically associated with RA.

Fortunately, most valvular heart disease associated with RA is generally mild.

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25
Q

What are the extra articular pulmonary manifestations of Rheumatoid arthritis?

A

Pleural effusion, pulmonary hypertension and/or pulmonary interstitial fibrosis which can cause decreased lung volumes and vital capacity (causing a ventilation-perfusion mismatch)

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26
Q

What are the neurological extraarticular manifestations of RA?

A

Neuro: Peripheral neuropathies (nerve compression, carpal tunnel, tarsal tunnel), chronic pain and keratoconjunctivitis sicca (dry inflammation of the conjunctiva and cornea).

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27
Q

What are the hematological extraarticular manifestations of RA?

A

Chronic Anemia

Thrombocytopenia

Neutropenia (Felty’s Syndrome)

Felty’s syndrome is a rare, potentially serious disorder that is defined by the presence of three conditions: rheumatoid arthritis (RA), an enlarged spleen (splenomegaly) and a decreased white blood cell count (neutropenia), which causes repeated infections.

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28
Q

What are the renal extraarticular manifestations of RA?

A

Renal: chronic renal failure possible (drugs, amyloidosis, vasculitis)

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29
Q

All diuretics will do what to urine Sodium and urine Potassium? (One exception)

A

Increase (Potassium sparing)

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30
Q

How does blood pH change with each class of diuretic?

(Carbonic Anhydrase, Loop, K Sparing and Thiazide)

A

Blood pH Decreased - Acidemia with carbonic anhydrase inhibitors, K+ sparing

Blood pH Increased - Alkalemia with loop diuretics, thiazides

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31
Q

What is the Wind Up phenomenon?

A

The wind-up phenomenon is caused by repeated stimulation of peripheral C fibers resulting in increased action potentials at the dorsal horn (spinal synapse) causing an amplified response.

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32
Q

What is the difference in allodynia and hyperalgesia?

A

Allodynia is a painful response to a non-painful stimulus. This subject was given a painful stimulus.

Hyperalgesia is an exaggerated painful response to an ordinarily painful stimulus.

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33
Q

How do you perform a Lateral Femoral Cutaneous Nerve Block?

A

The anterior superior iliac spine is an important landmark for performing a lateral femoral cutaneous nerve block.

The LFCN is best blocked where it is located between the sartorius (medial landmark) and tensor fascia lata (lateral landmark) muscles

The nerve can reliably be anesthetized by injecting 10 mL of local anesthetic approximately:

- 1-2 cm medial

- 1-2 cm inferior

to the ASIS at a depth of 0.5-1 cm from the skin.

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34
Q

What is the condition called where the lateral femoral cutaneous nerve is entraped?

A

Damage to the LFCN can lead to pain and paresthesias on the lateral upper thigh, which may extend down towards the lateral knee. This condition is called meralgia paresthetica and is most commonly caused by entrapment and compression of the nerve as it passes between the inguinal ligament and the ilium. It may also be caused by direct nerve damage, trauma, or diabetic neuropathy.

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35
Q

What are the nerve roots of the lateral femoral cutaneous nerve?

A

L2-L3

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36
Q

How does respiatory alkalosis affect serum [electrolyte]:

Calcium

Potassium

Phosphate

Explain the pathophysiology of each

A

All low

Hydrogen-potassium transporters pump hydrogen ions out of cells in the setting of alkalosis in order to restore physiologic pH. Simultaneously, potassium is pumped intracellularly to ensure electroneutrality, thus leading to hypokalemia.

Alkalosis can cause Hypophosphatemia. A rising cellular pH stimulates the glycolytic pathway, enhancing sugar-phosphate production. This triggers increased cellular uptake of phosphorus, thus decreasing serum phosphorus concentration.

Hypocalcemia is caused by increased calcium binding to negatively charged plasma proteins as the proteins release hydrogen ions to restore physiologic pH.

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37
Q

What patient types of high-risk cardiac conditions would qualify “Recommendation for IE Prophylaxis according to 2017 AHA/ACC guideline?

A
  1. Prosthetic cardiac valves including transcatheter-implanted prosthetic valves
  2. Patients with implanted prosthetic material such as annuloplasty rings and artificial chordae tendineae
  3. Patients with a history of infectious endocarditis
  4. Patients with a history of unrepaired cyanotic congenital heart disease
  5. Including cyanotic congenital disease patients with a repair, but with a residual shunt or valvular regurgitation near an implanted patch or device
  6. Patients with a history of cardiac transplantation who have a regurgitant valvular lesion due to a structurally abnormal valve
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38
Q

In addition to being a high risk patient, what procedure would qualify the need for prophylactic antibiotics to prevent infective endocarditis?

A

First, only patients who are undergoing dental procedures that “involve the manipulation of gingival tissue…periapical region of teeth, perforation of the oral mucosa, urinary mucosa is peiced in the setting of actuve UTI or colonizataion” are to be considered for prophylactic antibiotics

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39
Q

Infectious Endocarditis in cardiac transplant patients should be prophylaxed for how long post op?

Examples: (frequent central venous catheter placement, frequent endomyocardial biopsies to assess for rejection, intense immunosuppressive therapy, and because of the endothelial disruption that comes from the transplantation surgery itself.)

A

6 months

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40
Q

What is a type and screen?

A

Antibody screen:

The recipient’s serum is mixed with commercially supplied RBCs (known as screen cells) containing selected antigens commonly implicated in hemolytic transfusion reactions (other than ABO-Rh).

Antigens not represented in screen cells are unlikely to cause clinically significant hemolytic reactions.

It will detect the vast majority of antibodies that can cause a hemolytic reaction.​

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41
Q

What is a type and cross?

A

The recipient’s serum is mixed with donor RBCs.

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42
Q

What is the chance of cross matching detecting a potentially dangerous antibody that was missed by the antibody screen?

What populations are at risk for this?

A

It is possible for some patients, especially those with a history of multiple transfusions or pregnancies, to carry antibodies that would not be detected during an antibody screen.

However, the chance of cross matching detecting a potentially dangerous antibody that was missed by the antibody screen is less than 1 in 10,000.

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43
Q

What are the preservatives in:

Aminoester local anesthetics

Aminoamide local anesthetics

What is more likely to cause an allergic reaction

A

Aminoesters, which are degraded into an allergen, para-benzoic acid (PABA) = More likely for allergic reaction

Aminoamides and their metabolites are not associated with allergens and hypersensitivity reactions. It is more likely that the preservatives in the local anesthetic preparation such as methylparaben are responsible for any allergic reactions.

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44
Q

What are the autonomic changes associated with aging?

Include: Beta receptor, Alpha receptor, Autonomic activity

A

Increase in sympathetic nervous system activity

Decreased parasympathetic nervous system activity.

Decrease in beta receptor responsiveness

Maintained alpha receptor responsiveness

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45
Q

How are Carcinoid tumors diagnosed?

A

Presence of excessive amounts of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in urine.

24 hour urinary 5-HIAA (Metabolite of serotonin) of > 30 mg

Normal 5-HIAA is 3-15 mg (For reference)

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46
Q

How are pheochromocytomas diagnosed?

A

Urinary Vanillylmandelic acid (VMA) is elevated in patients with tumors that secrete catecholamines.

Norepinephrine is metabolised into normetanephrine and VMA.

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47
Q

What are the usual cardiac manifestations of carcinoid syndrome with right sided involvement?

A

Cardiac manifestations are due to fibrosis of the endocardium, primarily on the right side. Pulmonic stenosis is usually predominant. The tricuspid valve is often fixed open resulting in regurgitation.

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48
Q

What does the 11 Beta-Hydroxylase hormone do?

A

11β-hydroxylase is responsible for the conversion of 11-deoxycorticosterone to corticosterone (precursor to aldosterone) and the conversion of 11-deoxycortisol to cortisol.

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49
Q

Explain how Adenosine plays a role in arterial vs. portal vein perfusion of the liver

A

Adenosine is produced in the space of Mall surrounding the local hepatic vasculature and diffuses into the portal vein.

As portal venous blood flow decreases, the decreased flow allows the accumulation of adenosine in the hepatic vasculature.

This increased concentration of adenosine causes vasodilation of the hepatic artery and increased hepatic arterial blood flow.

As portal venous flow increases, the increased flow washes the adenosine out of the hepatic vascular system resulting in vasoconstriction of the hepatic artery.

This is known as the “adenosine wash-out hypothesis.”

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50
Q

What is the maximum effect of HABR (Hepatic Artery Buffer Response)?

A

Double the hepatic arterial blood flow

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51
Q

Liver Perfusion

What is the % of blood flow from hepatic artery vs. portal system

What is the % of oxygen of hepatic artery vs. portal system

A

The liver gets 20-25% of the cardiac output via the portal vein and the hepatic artery.

The portal vein is responsible for 75% of the blood flow while the hepatic artery is responsible for 25% of the blood flow.

However, both vascular structures each deliver 50% of the oxygen supply to the liver.

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52
Q

A decelerating flow pattern on inspiration is characteristic of which method of controlled ventilation?

A

A decelerating flow pattern on inspiration is characteristic of a pressure control breath.

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53
Q

Volume control delivers the breath to the patient as a what type of breath? Waveform

A

Volume control delivers the breath to the patient as a fixed flow breath (square waveform).

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54
Q

What spirometry pattern in seen with ascites?

FEV1/FVC

FVC

FEF25-75%

A

Tense abdominal ascites elicits an extrinsic restrictive lung disease pattern, which is indicated on pulmonary function testing by a:

Decreased forced vital capacity (FVC) (50%)

Both intrinsic and extrinsic restrictive forces lead to a decreased FVC due to a decrease in TLC.

Reduced functional residual capacity (FRC)

The FEV1/FVC ratio (90%) and FEF25-75% are generally normal (90%)

The forced expiratory volume in one second (FEV1) is usually decreased as well because of the reduced lung volumes. Since both the FEV1 and the FVC are reduced with restrictive lung pathology, the FEV1/FVC ratio is usually normal. The forced expiratory flow during the middle 50% of the FVC (FEF25-75%) is typically normal in restrictive lung disease unless small airway damage is also present from other etiologies.

Both the FEF25-75% and the FEV1/FVC ratio are measures of ventilatory capacity.

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55
Q

What is Vital Capacity?

List VC in terms of sums of different lung spaces

A

Vital capacity (VC) is the maximal amount of air that can fill the lungs and participate in gas exchange.

VC = TLC - RV

VC = IRV + ERV + TV

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56
Q

What is the FRC?

A

The amount of gas that can be forcefully and maximally exhaled from a maximal inhaled volume is the forced vital capacity (FVC).

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57
Q

What are the FVC, FEV1, FEV1/FVC, FEF25-75%, FRC, and TLC for Restrictive Lung Disease

A

FVC - Very low

FEV1 - Very low

FEV1/FVC - Normal

FEF25-75% - Normal

FRC - Very Low

TLC - Very Low

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58
Q

What are the FVC, FEV1, FEV1/FVC, FEF25-75%, FRC, and TLC for Obstructive Lung Disease?

A

FVC - Normal or slightly increased

FEV1 - Very low

FEV1/FVC - Very Low

FEF25-75% - Very Low

FRC - Normal or increased

TLC - Normal or increased

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59
Q

Normally, a patient’s FEV1 is approximately what percentage?

A

Normally, a patient’s FEV1 is approximately 75-80% of their FVC, meaning that they can exhale 75-80% of their vital capacity in one second.

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60
Q

Normal ranges for FEF25-75% are typically what percentage of the predicted value?

A

Normal ranges for FEF25-75% are typically 80-120% of the predicted value.

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61
Q

What is the FEV1/FVC ratio for Obstructive Disease?
Why is this?

A

Patients with chronic obstructive pulmonary disease (COPD) have a lower than predicted FEV1/FVC ratio. This is due to airway collapse with forced exhalation, which leads to a decreased FEV1. Therefore, a reduction in the FEV1/FVC ratio occurs as the patient’s FVC is typically unchanged or slightly increased.

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62
Q

Patients with COPD will also have a what FEF 25-75%?

What is this?

A

Patients with COPD will also have a low FEF25-75% due to small airway collapse during exhalation.

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63
Q

What is Conn Syndrome?

A

Primary Hyperaldosteronism

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64
Q

Conn Syndrome has serum levels of:

Sodium?

Potassium?

Renin?

BP?

pH?

A

HIgh Sodium –> Hypertension

Low Potassium

Low Renin

Metabolic Alkalosis (Chronic Loss of Hydrogen ions)

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65
Q

Conn Syndrome:

Preoperative management?

Intraoperative Management?

A

Preoperative management = Spirinolactose (Takes weeks), Potassium Supplementation, K sparing diuresis

Intraoperative Management- Avoid hyperventilation (Will decease K more), Cortisol eplacement with bilateral adrenalectomies for multiple aldosteronomas

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66
Q

Why would you want a faster HR for mitral regurgitation?

A

Chronic MR is typically asymptomatic in its earlier stages due to compensatory mechanisms that reduce afterload and increase left ventricular compliance, promoting forward flow. In its more severe stages, reduced ejection fraction, increased LV pressures and regurgitant volume are seen. This can be remedied by increasing heart rate to reduce systolic time, reducing afterload, and maintaining normal sinus rhythm and normovolemia.

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67
Q

A patient has an MI and found to have new MR.

What happened anatomically? What is the result.

A

Acute mitral regurgitation may also occur from posteromedial papillary muscle rupture after a myocardial infarction. This papillary muscle has a single blood supply, rendering it more susceptible to ischemia and rupture. Lastly, functional mitral regurgitation may occur from overdistended ventricles such as in dilated cardiomyopathy.

The mitral valve papillary muscles in the left ventricle are called the anterolateral and posteromedial muscles.

  1. Anterolateral muscle blood supply: left anterior descending artery - diagonal branch (LAD) and left circumflex artery - obtuse marginal branch (LCX)
  2. Posteromedial muscle blood supply: right coronary artery - posterior interventricular artery (RCA)

The posteromedial muscle ruptures more frequently because it only has one source of blood supply, hence RCA occlusion can cause papillary muscle rupture.

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68
Q

What can Midazolam do to parkinson’s patients?

A

Also, midazolam may precipitate a worsening of dyskinesias in patients with Parkinson disease.

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69
Q

What electrolyte abnormality is concerning for Digoxin toxicity and why?

A

Hypokalemia

Digoxin toxicity is more likely to occur in the setting of hypokalemia since digoxin competes with potassium for the same binding site on the Na+/K+ ATPase.

With less potassium, more digoxin is able to bind and its effects (and side effects) become more pronounced.

Digoxin toxicity is also more likely to occur in patients concurrently taking amiodarone, quinidine, or verapamil as these drugs cause an increase in serum digoxin concentration.

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70
Q

What are the 4 benefits of Digoxin?

A

Benefits:

  1. Positive inotrope improves contractility
  2. Decreases HR by slowing AV conduction through the node
  3. Sympatholytic action on baroreceptors
  4. Decreases renal sodium reabsorption (mild diuresis)
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71
Q

How does Phenytoin affect neuromuscular blockade?

A

Acute phenytoin administration potentiates the neuromuscular blockade of aminosteroid NDNBDs.

Chronic phenytoin administration increases a patient’s resistance to the effects of NDNBDs and reduces their duration of action.

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72
Q

Chronic phenytoin administration reduces the duration of action and increases the ED95 of aminosteroid NDNBDs by as much as 50%.

What are the 4 combination of multiple different mechanisms responsible for this?

A

1) Increased metabolism via cytochrome P450 enzymes induction (this may explain why there is a clear effect with the aminosteroid NDNBDs, which rely on hepatic metabolism, but not with the benzylisoquinolines which undergo hepatic-independent Hofmann elimination and ester hydrolysis)
2) Increased postjunctional acetylcholine receptor density (the weak neuromuscular blocking properties of phenytoin, see below, results in postjunctional acetylcholine receptor upregulation)
3) Decreased sensitivity at the receptor sites
4) Increased end-plate anticholinesterase activity

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73
Q

What is the enzyme and gene, respectively that is involved in Warfarin?

A

second enzyme called vitamin K reductase (encoded by the VKORC1 gene) is responsible of regenerating active (reduced) vitamin K.

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74
Q

Warfarin is metabolized by what cytochrome P450 isoform?

A

Warfarin is metabolized by the cytochrome P450 2C9 isoform (CYP2C9)

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75
Q

Warfarin is avoided in pregnancy because of?

A

Teratogenic

Warfarin must be avoided in pregnant women because it can cause abortion, fetal hemorrhage, and birth defects (nasal hypoplasia, stippled epiphyseal calcifications).

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76
Q

Of all the Vitamin K dependent factors (10, 9, 7, 2, Protein C/S) which affect PT/INR?

A

PT/INR is the method of choice to monitor warfarin therapy since it is prolonged by reduced functional levels of the vitamin K-dependent factors II, VII, and X. (1972 C/S)

Of note, not all vitamin K-dependent factors affect PT/INR (e.g. factor IX, proteins C, S, and Z do not), while reductions in some vitamin K-independent factors, such as fibrinogen and factor V, can also prolong PT/INR.

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77
Q

Can Warfarin be given during breastfeeding?

A

Warfarin is not present in milk and can be safely given to nursing mothers.

(Cannot be given during gestation as it is teratogenic)

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78
Q

Draw a Normal Flow Loop

Include:

TLC, VC, RV

Label Axis

Label Expiration and Inspiration

A
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79
Q

What flow loop is seen here?

A

A variable INTRAthoracic airway obstruction (e.g., distal tracheal tumor or mediastinal mass) produces a flow-volume loop with a plateaued EXPIRATORY curve and the flow rate is usually decreased.

During expiration, intrathoracic pressure becomes positive which further decreases the airway diameter, enhances the degree of obstruction, and impairs airflow. The inspiratory curve is usually normal since the negative intrathoracic pressure generated during inspiration helps keep the airway open.

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80
Q

What flow loop is seen here?

A

A variable EXTRAthoracic airway obstruction (e.g., vocal cord paralysis or dysfunction, proximal tracheal tumor, glottic strictures) produces a flow-volume loop with a plateaued INSPIRATORY curve and the flow rate is usually decreased.

During inspiration, the negative inspiratory pressure causes the obstruction to increase. The expiratory curve is usually normal since the positive airway pressure generated during expiration helps keep the airway open.

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81
Q

What flow loops is seen here?

A

A fixed upper airway obstruction or fixed large airway obstruction (e.g., foreign body, tracheal stenosis, large airway tumor) impairs BOTH inspiration and expiration leading to a flow-volume loop with plateaued and decreased inspiratory and expiratory flows.

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82
Q

How do you tell the difference between a Flow-Volume loop of obstructive vs. restrictrive lung disease?

A

Restrictive = Moves to the Right

Obstructive = Moves to the Left

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83
Q

What is the characteristic of thyrotoxic cardiomyopathy in terms of histological changes?

A

Triiodothyronine (T3) exerts direct effects on the myocardium and may result in thyrotoxic cardiomyopathy, characterized by fibrotic and fatty changes with lymphocytic and eosinophilic infiltration.

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84
Q

How does RV, TV, TLC< and VC change with aging?

A
RV = Increases
TV = No change

TLC = Decrease

VC = Decrease

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85
Q

What is the most common indication for retrograde cardioplegia?

A

Aortic Valve Insufficiency

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86
Q

How does nitric oxide inhaled work?

What is the half life?

How does it affect V/Q Ratios

A

Inhaled nitric oxide is an inhaled pulmonary vasodilator with an extremely short half that is used to improve pulmonary blood flow in area that are receiving ventilation.

It optimizes V/Q mismatch and also reduces pulmonary blood pressures.

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87
Q

What is the relationship between frequency, wavelengths, resolution and penetration in terms of ultrasound quality?

A

Higher frequency (shorter wavelengths) means better resolution, but worse penetration.

Lower frequency (longer wavelengths) gives better penetration but sacrifices resolution.

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88
Q

What are the 3 components of resolution of ultrasound physics?

A

Resolution is actually a very complex concept and is split into:

  1. Axial resolution
  2. Temporal resolution
  3. Lateral resolution
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89
Q

Define the 3 terms of resolution (Ultrasound Physics)

Axial resolution

A

Axial resolution is a function of the probe frequency and pulse width and represents the resolution along the vertical projection of the ultrasound beam. Resolution is improved with higher frequency, lower wavelength, and shorter pulse width.

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90
Q

Define the 3 terms of resolution (Ultrasound Physics)

Lateral resolution

A

Lateral resolution is the resolution along the horizontal axis of the ultrasound image and is a function of the beam formation. The image has both and near and far field.

The near field is columnar in shape, the length of which increases with higher frequency.

The far field results in a divergence of the beam and blurring of the ultrasound image produces.

Divergence increases with lower frequency and wider ultrasound probes.

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91
Q
# Define the ultrasound physics term:
Temporal Resolution
A

Temporal resolution is the ability of the probe to differentiate moving objects in time and is the “frame rate” of the ultrasound image.

With decreasing scan depth, temporal resolution improves.

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92
Q

What does Antithrombin 3 inactivate?

A

Antithrombin III inactivates multiple coagulant factors, most notably thrombin (factor II), factor Xa, and other factors in the intrinsic pathway (see figure below)

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93
Q

What is different about enoxaparin vs. UFH in terms of its mechanism?

A

Enoxaparin similarly binds and enhances the effects of AT3. However, the enoxaparin-induced conformational change of AT3 makes enoxaparin preferentially inhibit factor Xa

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94
Q

When is it reasonable to monitor enoxaparin with labs? (What population)

A

Monitoring may be recommended in patients with extreme BMIs (high or low), renal impairment, or in pregnant patients.

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95
Q

What is the basic pathophysiology of Malignant Hyperthermia?

A

Malignant hyperthermia-susceptible patients have RYR1 defects that, in the presence of a triggering agent (succinylcholine or any volatile anesthetic)

Cause prolonged opening of the channel which leads to sustained muscle contraction.

This produces a generalized hypermetabolic state characterized by increased CO2, lactate, and heat production which can progress to muscle cell breakdown and leads to hyperkalemia*, *rhabdomyolysis*, and their sequelae (*arrhythmias*; *liver, kidney, and other end-organ damage, and death).

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96
Q

In a suspected MH patient, what must be used in order to reduce/prevent damage to the kidneys?

A

Diuretics and Mannitol (Keep UOP 1-2 mL/kg/hr)

CK levels will rise and can cause myoglobinuria

Each 20 mg Vial of Dantrolene contains 3 grams of Mannitol

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97
Q

In a suspected MH patient, what is your dose of Dantrolene?

What is the proposed mechanism of Dantrolene?

A

Dose for Crisis: IV: Initial: 2.5 mg/kg*; monitor patient continuously and give repeat doses of *1 mg/kg* until symptoms subside or a *cumulative dose of 10 mg/kg is reached

MOA: Acts directly on skeletal muscle by interfering with release of calcium ion from the sarcoplasmic reticulum; prevents or reduces the increase in myoplasmic calcium ion concentration that activates the acute catabolic processes associated with malignant hyperthermia

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98
Q

What are the 4 most common MAOI (Mono-amine oxidase inhibitors)?

A
  1. Isocarboxazid
  2. Phenelzine
  3. Selegiline
  4. Tranylcypromine
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99
Q

What are the signs and symptoms of Serotonin Syndrome?

What is the most common criteria (name)?

A
  • Spontaneous clonus
  • Inducible clonus plus agitation or diaphoresis
  • Ocular clonus plus agitation or diaphoresis
  • Tremor plus hyperreflexia
  • Hypertonia plus temperature > 38 °C plus ocular clonus or inducible clonus

Hunter Toxicity Criteria

Serotonin syndrome results from coadministration of multiple serotonergic medications. It results in tachycardia, clonus, hyperreflexia, ataxia, and confusion.​

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100
Q

What are some S/S of Neuroleptic Malignant Syndrome?

(Hint: What do they have to take? What is S/S? Course? Muscle Tone, Reflexes, Mydriasis)

A

Neuroleptic malignant syndrome occurs in patients taking antipsychotic medication. It is characterized by muscle rigidity and altered consciousness. Both first-generation neuroleptic medications*, such as haloperidol, and *newer atypical antipsychotics have been implicated in neuroleptic malignant syndrome.

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101
Q

What is the treatment for serotonin Syndrome?

A
  1. Discontinue serotonergic agents (Fent, SSRI, Ondansetron)
  2. Supportive care
  3. Benzos (Diazepam 10-20 mg IV
  4. Cyproheptadine (Serotonergic antagonist) 12 mg PO and repeat 2 mg Q2H (Max of 32 mg / day)
  5. Dexmedeotmidine
  6. Hyperthermia (If severe, intubate sedate and paralyze)
  7. Chlorpromazine (Phenothiazine with anti-serotonergic effects 50-100 mg IM
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102
Q

What is the treatment for neuroleptic malignant syndrome?

A
  1. Agitation should be controlled with Benzodiazepines

Lorazepam 2 mg IV q5 min until agitation and muscle rigidity resolves

  1. Supportive/Fluid resuscitation
  2. Cooling measures
  3. Intubation and paralysis for severe cases, chest wall rigidity or respiratory failure

Use NON-DEPOLARIZING paralytic agent

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103
Q

What is the glucocorticoid, mineralcorticoid potency and duration of action of:

Hydrocortisone

Prednisone

Prednisolone

Methylprednisolone

Dexamethasone

Fludrocortisone

A

Hydrocortisone 1, 1, 8-10 hours

Prednisone 4, 0.8, 18-36 hours

Prednisolone 4, 0.8, 12-26 hours

Methylprednisolone 5, 0.5, 18-36 hours

Dexamethasone 25-30, 0, 36-54 hours

Fludrocortisone 10, 120, 18-36 hours

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104
Q

Can antiemetic doses of dexamethasone be used for adrenal suppression?

A

8 mg of dexamethasone is equivalent to 200 mg of hydrocortisone and will suffice to prevent adrenal insufficiency with most commonly performed surgeries

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105
Q

Why don’t we use fludrocortisone for perioperative stress dose steroids?

A

Fludrocortisone is a potent mineralocorticoid. Even in patients with symptomatic adrenal suppression, treatment with fludrocortisone is not recommended since most of the problems from adrenal suppression are secondary to both mineralocorticoid and glucocorticoid deficiency and thus both need to be supplemented.

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106
Q

What is the agent of choice for treating adrenal suppression during stressful surgeries and why?

A

Hydrocortisone is the agent of choice for treating adrenal suppression during stressful surgeries because it has a 1:1 glucocorticoid: mineralocorticoid effect. However, most current literature suggests that dexamethasone alone is appropriate for prophylaxis in patients with possible secondary adrenal insufficiency (e.g. due to steroid use).

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107
Q

When is mineralcorticoid prophylaxis appropriate?

A

Mineralocorticoid prophylaxis is most appropriate for patients with primary adrenal insufficiency (unrelated to chronic steroid use).

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108
Q

Draw the Frank Starling Curve.

What is on the X axis?

What is on the Y axis?

What are the 3 classes of medicines used to treat?

A

X axis = Cardiac Output

Y axis = EDV (Of the LV)

Classes:

  1. Diuretics
  2. Ionotropic agents
  3. Vasodilators
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109
Q

Compare the saturated vapor pressure of isoflurane, sevoflurane, and desflurane.

A

Sevoflurane = 157

Isoflurane = 240

Desflurane = 669

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110
Q

Morphine Metabolites:

What are they?

What is primary?

What is active?

What is most potent?

What are the effects of each?

A

1. Morphine - 6 - Glucuronide (Primary active metabolite)

100 fold potent, yet (CAVEAT) exhibits an equal or decreased affinity for mu-opioid receptors. Its increased potency, however, can lead to significant respiratory depression in renal failure due to accumulation from delayed excretion.

2. Morphine - 3 - Glucuronide (Minority inactive metabolite)

Nearly 300 fold lower affinity for the μ-receptors but it may have neuroexcitatory effects; myoclonus and allodynia are seen after large doses.

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111
Q

What are the 3 medication classes and specific medications used for fibromyalgia?

A
  1. Tricyclic antidepressant (e.g. amitriptyline, nortriptyline)
  2. Serotonin-norepinephrine reuptake inhibitor (e.g. duloxetine aka Cymbalta, milnacipran, venlafaxine)
  3. Alpha-2/delta calcium channel modulator (e.g. gabapentin, pregabalin)
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112
Q

What oxygen tension is required in the full term infant to close the ductus arteriosus?

A

Oxygen is the most influential factor in the closure of the ductus in the full-term infant.

The ductus arteriosus is usually functionally closed by the second day of life. In a full-term infant, a PaO2 of about 50 mmHg constricts the vessel.

Oxygen tension is not as influential in closing the preterm neonate’s ductus arteriosus

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113
Q

Draw the 4 chamber echo view

What is the distribution of coronary blood flow

A

RCA = Right heart and basal septum

Middle septum = RCA or LAD

Apical septum = LAD

Lateral wall = LAD or Circumflex

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114
Q

Draw the 2 chamber echo view

What is the distribution of coronary blood flow

A

Inferior Wall (Left) = RCA

Anterior Wall (right) = LAD

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115
Q

Draw the Long Axis of the LV view

What is the distribution of coronary blood flow

A

Posterior wall (left) = RCA or Circumflex

Anteroseptal wall (right and base) = LAD

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116
Q

Draw the echo view of transgastric Short Axis

What is the distribution of coronary blood flow

A

Notice, the distribution depends on coronary dominance

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117
Q

Rank the Bioavailability of Midazolam depending of the route

A

I SMiLN RO

  1. IV 100%
  2. SQ 96%
  3. IM 85-87%
  4. SL / Buccal 74.5%
  5. Intranasal 50-83%
  6. Rectal 18-52%
  7. Oral 15-52%
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118
Q

A full Oxygen E-cylinder contains how many Liters* and *pressure?

A

~2000 psi (1900- 2200)

660 Liters

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119
Q

A full Nitrous Oxide E-cylinder contains how many Liters and pressure?

A

1590 Liters

745 psg

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120
Q

A full Carbon Dioxide E-cylinder contains how many Liters and pressure?

A

1590 Liters

838 psi

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121
Q

A full AIR E-cylinder contains how many Liters and pressure?

A

(Appoximately Same as Oxygen)

1900 psi

620 Liters

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122
Q

A full Helium E-cylinder contains how many Liters and pressure?

A

500 Liters

1600 psi

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123
Q

What are the colors for a CO2 E cylinders in the United States?

A

Gray

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124
Q

What are the colors for a Helium E cylinders in the United States?

A

Brown

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125
Q

Draw a Normal Pressure Volume Loop indicating:

Cardiac cycle

X Axis

Y Axis

LVEDV, LVESV, CPP, AoDP, LVESP, AoSP, Contractility

A

X axis = LV Volume

Y Axis = LV pressure

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126
Q

Draw the Pressure Volume Loop for Milrinone

A
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127
Q

What is the treatment for Myxedema Coma?

A
  1. Thyroid Replacement
    - Levothyroxine preferred (TSH secretion regulation and conversion to T3)
    - Liothyronine (most potent form) can precipitate myocardial ischemia
  2. Hydrocortisone (5-10%) of patients can have adrenal insufficiency
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128
Q

The lumbar plexus gives rise to what 3 major nerves (regarding blocks)?

The sacral plexus gives rise to what 2 major nerves (regarding blocks?

A

The lumbar plexus gives rise to the femoral nerve, obturator nerve, and lateral femoral cutaneous nerve.

The sacral plexus gives rise to the posterior cutaneous nerve of the thigh and sciatic nerve.

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129
Q

The sciatic nerve provides cutaneous innervation to what locations?

A

The sciatic nerve provides cutaneous innervation to the posterior thigh and all of the leg and foot below the knee, except for a medial strip supplied by the saphenous nerve.

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130
Q

At the popliteal fossa, the sciatic nerve divides into what two nerves?

A

Tibial and common peroneal nerves

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131
Q

What are the 3 causes of auto-PEEP?

A
  1. Dynamic hyperinflation with intrinsic expiratory flow limitation: this occurs in COPD patients. COPD results in loss of elements that keep the lungs open during expiration. During exhalation, the closure of the airways results in air trapping. Applying external PEEP can help relieve this type of auto-PEEP.
  2. Dynamic hyperinflation without expiratory flow limitation: even when the airways are widely patent at the end of exhalation, if the volume delivered is too high, the exhalation time too short, or if exhalation is impeded by a blockage external to the patient (such as with blocked ETT or stuck exhalation valve) then air can get trapped. This is typically seen during rapid breathing patterns, use of high tidal volumes, when inspiration is greater than expiration, or when there is added flow resistance due to small endotracheal tubes. Removing the blockage, decreasing volume, or increasing exhalation time will help alleviate the problem.
  3. Exaggerated expiratory activity without dynamic hyperinflation: when strong expiratory muscle activity contributes to alveolar pressure at the end of the expiratory cycle there will be an end-expiratory gradient of alveolar to central airway pressure. This results in auto-PEEP phenomena even with low lung volumes.
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132
Q

Hypokalemic Periodic Paralysis

Inheritance Pattern?

A

Autosomal Dominant

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133
Q

What are the triggers for hypokalemic periodic paralysis?

A

Strenuous exercise

Excitement

High sodium

Carbohydrate meals

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134
Q

Fibrinolysis:

What is the substrate, enzyme and byproduct of clot breakdown?

A

Fibrinolysis (fibrin breakdown), a normal hematologic activity that leads to removal of thrombus when endothelium heals, is conducted mostly by the enzyme plasmin, the product of cleavage of plasminogen by tissue plasminogen activator (tPA).

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135
Q

Why do we use aminocaproic acid for Cardiopulmonary Bypass cases?

A

Fibrinolysis can be excessive and lead to bleeding, for example after cardiopulmonary bypass (cardiopulmonary bypass causes the endothelium to release tPA).

Currently available antifibrinolytic agents (aminocaproic acid and tranexamic acid) are analogs of the amino acid lysine, and as such they competitively inhibit the binding of plasmin(ogen) lysine binding sites to the lysine residues in fibrin.

In other words, they prevent the formation of the ternary complex mentioned above.

Antifibrinolytic agents have been shown to reduce total perioperative blood loss and the number of patients transfused in major cardiac, orthopedic, or liver surgery. Currently, the ASA guidelines give a recommendation to “use” such agents for prevention of bleeding in patients undergoing cardiopulmonary bypass, but only of “consider using” for other indications.

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136
Q

Other than low fibrinogen concentations, what are the two other acceptable indications for cryoprecipitate?

A

fibrinolysis, massive transfusion, and low fibrinogen concentration (definitions of “low” vary and are typically higher in pregnancy).

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137
Q

What is the mechanism of action of TXA (Tranexamic Acid)?

A
  1. Competitively inhibits activation of plasminogen (via binding to the kringle domain), thereby reducing conversion of plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and other plasma proteins, including the procoagulant factors V and VIII.

  1. Directly inhibits plasmin activity, but higher doses are required than are needed to reduce plasmin formation.
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138
Q

Going from medial to lateral, which is the correct order of neurovascular structures in the antecubital fossa?

A

Median Nerve, Brachial Artery, Radial Nerve

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139
Q

What is the largest nerve in the body unprotected, and thus is most injured during surgeries?

A

It is the largest nerve in the body that is not protected by muscle or bone, is the ULNAR NERVE

The ulnar nerve travels down the medial aspect of the upper and lower arm. It could be considered the most medial neurovascular structure in the arm at the level of the elbow, however at the level of the antecubital fossa it courses posterior to the medial epicondyle of the humerus

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140
Q

What are the components of the MELD Score?

A

MELD: “I Crush Several Beers Daily” for INR, creatinine, sodium, bilirubin, dialysis

“C DIBS” on MELD

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141
Q

What are the components of Child’s Pugh Score?

A

Childs-Pugh: “Pour Another Beer At Eleven” for PT, Ascites, Bilirubin, Albumin, Encephalopathy

142
Q

How do opioid, barbiturate, and other sedative-hypnotic medication administration shift the Ventilatory response curve?

A

Shift the VRC to the right and depress the slope, in a dose-dependent manner.

The result is a reduced minute ventilation and higher baseline PaCO2 therefore reducing minute ventilation.

143
Q

How do Volatile anesthetics shift the ventilatory response curve?

A

Volatile anesthetics at ≤1 MAC cause a rightward, parallel shift of the VRC.

Volatile anesthetics >1 MAC reduce sensitivity to elevated PaCO2, cause a rightward shift, and reduce the slope of the VRC.

144
Q

How does hypoxemia, acidosis, surgical stimulus and increased ICP shift the ventilatory response curve?

A

Surgical stimulus and heightened states of arousal (e.g. fear or anxiety) cause hyperventilation. This typically causes a leftward shift and increased slope of the carbon dioxide ventilatory response curve (VRC).

145
Q

What physiologic mechanisms is responsible for increased small airway collapse in the elderly population?

A

Increased chest wall stiffness, loss of muscle mass, flattening of the diaphragm, and increased compliance of lung parenchyma lead to several physiologic changes in elderly respiration. The volume at which small airways collapse increases with aging, such that by the mid-60s, closing capacity surpasses (increases) functional residual capacity and will eventually surpass tidal volume.

146
Q

What is the equation to determine how distance from ionization source changes from x-ray/fluoro?

A

I ∝ 1 / r2
Where: I = intensity, S = source strength, r = radius (distance from source)

Ex: Radiation intensity (exposure) with respect to distance decreases according to the inverse square law: I ∝ 1 / r^2. Accordingly, doubling the distance from a radiation source decreases exposure by a factor of 4.

147
Q

General Anesthesia resembles:

What phase of sleep pattern?

A

General anesthetic effects on the brain most resemble the naturally occurring non-rapid eye movement (NREM) sleep pattern

148
Q

General Anesthesia resembles:

What EEG findings?

A

General anesthetic effects on the brain most resemble the naturally occurring non-rapid eye movement (NREM) sleep pattern on EEG (slow-frequency, large-amplitude).

There is a transition from the low amplitude, fast-frequency pattern of wakefulness, to the high amplitude, slow-frequency EEG of NREM sleep.

149
Q

Blood PaCO2 is measured how?

A

Blood PCO2 is measured by a Severinghaus electrode using a method that builds upon the pH electrode mechanism.

Carbon dioxide from the blood sample equilibrates across a semipermeable membrane with a bicarbonate solution.

The reaction generates H+ ions and the PCO2 is determined by the degree of pH change resulting from the H+ ion generation.

150
Q

What is the equation to determine base excess?

A

Base excess (or deficit) is calculated from the measured sample pH and calculated bicarbonate concentration based on the following formula, called the Van Slyke equation. Note it is not necessary to memorize this formula for testing purposes.

BE = 0.9287 * [HCO3- – 24.4 + (pH – 7.4)]

This formula determines what is called the standardized base excess and represents serum base excess. Prior to the 1960s, whole-blood base excess was measured instead. The standardized base excess better reflects the true base excess in the extracellular fluid since it is not complicated by (and corrects for) the ability of hemoglobin to buffer acid.

151
Q

What is base excess by the definition?

What is base excess in terms of positive vs. negative?

A

The metabolic component of the acid–base balance is reflected in the base excess. This is a calculated value derived from blood pH and PaCO2. It is defined as the amount of acid required to restore a litre of blood to its normal pH (7.4) at a PaCO2 of 40 mmHg.

The base excess increases in metabolic alkalosis* and *decreases (or becomes more negative) in metabolic acidosis, but its utility in interpreting blood gas results is controversial.

152
Q

Blood PaO2 is measured how?

A

Blood PO2 is most commonly directly measured by a Clark electrode which detects the amount of current that flows between the two electrodes (amperometric).

Oxygen from the blood sample diffuses across a semipermeable membrane and is reduced at the cathode, resulting in a reaction that produces a measurable current that is directly proportional to the PO2.

153
Q

pH is measured via what physics method?

A

pH is measured via the Sanz electrode

Blood pH is directly measured using an optical absorbance technique or a pH electrode. The latter measures the potential difference between a measuring electrode (which contains the blood sample in contact with a special glass membrane permeable only to H+ ions) and a reference electrode with a stable, known pH.

154
Q

It is important to commit the following to memory:

A is measured via the Clark electrode (as per above)

B is measured via the Severinghouse electrode

C is measured via the Sanz electrode

A

It is important to commit the following to memory:

pO2 is measured via the Clark electrode (as per above)

pCO2 is measured via the Severinghouse electrode

pH is measured via the Sanz electrode

155
Q

What are some drugs that do not cross the placenta?

A

One easy pneumonic to remember drugs that do NOT cross the placenta and are also considered safe is:

He Is Going Nowhere Soon (Heparin, Insulin, Glycopyrrolate, NDNMB, Succinylcholine).

156
Q

What is the [PaO2] of the fetus in mmHg?

A

Oxygen diffuses across the placenta from the higher maternal oxygen concentration to the lower fetal concentration of about 40 mmHg

Oxygen diffuses across the placenta from the higher maternal oxygen concentration to the lower fetal concentration of about 40 mmHg. The fetal oxyhemoglobin dissociation curve is left-shifted causing it to more tightly hold onto the oxygen it receives. Carbon dioxide transfer to the maternal circulation is limited by blood flow rather than diffusion.

157
Q

Explain the concern for giving lidocaine to the mother in terms of ion trapping?

A

Because fetal blood is more acidotic than maternal blood, certain drugs such as local anesthetics will form higher concentrations of their ionized forms (Quaternary Amines) preventing the drugs from readily diffusing back across the placenta despite having a higher concentration gradient than the maternal circulation. This is termed ion trapping.

With local anesthetics, this can lead to toxic effects in the fetus such as decreased muscle tone, arrhythmias, and cardiovascular depression

158
Q

What is the dose of Atropine when used for neuromuscular blockade reversal in a pregnant patient?

A

Neuromuscular blockade reversal

IV: 15 to 30 mcg/kg administered with neostigmine

(Glyco dose is 10-15 mcg/kg for reference so its 1.5 to 2x the dose)

159
Q

What is the typical dosing of neostigmine and Glycopyrrolate for reversal of neuromuscular blockade?

A

Neostigmine Dosing

30 - 70 mcg/kg of Neostigmine depending on twitches

1-3 twitches use 50-70 mcg/kg of neostigmine

4 twitches with fade 50 mcg/kg of neostigmine

4 twitches without fade 20 mcg/kg

Glycopyrrolate Dosing

10 - 15 mcg/kg of Glycopyrrolate depending on HR

OR

200 mcg for each 1 mg of Neostigmine

160
Q

What is the dosing combination of Edrophonium and Atropine?

A

The dose delivered is 0.5 to 1 mg/kg of edrophonium and 7 to 14 mcg/kg of atropine. An edrophonium dose of 1 mg/kg should rarely be exceeded.

Note: Monitor closely for bradyarrhythmias.

161
Q

How does your Atropine dose change when using Neostigmine vs. Edrophonium?

A

IV: 15 to 30 mcg/kg administered with neostigmine

IV: 7 to 14 mcg/kg administered with edrophonium

162
Q

What two pharmacokinetics of alfentanil make it have a rapid onset?

A

high unionized fraction of alfentanil (low pKa) leads to a more rapid onset

163
Q

What two bones make up the hard palate?

A

The hard palate (maxilla and palatine bones) forms the anterior two-thirds of the roof of the mouth.

(The palatine bone is highlighted in green in the image)

164
Q

The tongue is anchored to the mandible by what muscle?

A

The tongue is anchored to the mandible by the genioglossus muscle.

When sleeping or under general anesthesia, the tongue often displaces posteriorly into the oropharynx causing upper airway obstruction

165
Q

The larynx begins and ends (superiorly to inferiorly) at what two structures?

A

larynx begins at the epiglottis, includes the thyroid cartilage and ends at the cricoid cartilage.

166
Q

What is the formula to determine ET tube depth?

A

Chula formula: ETT depth = 0.1 * [height (cm)] + 4

18 cm for under 4’9”

19 cm for 4’10” to 5’2”

20 cm for 5’2” to 5’5”

21 cm for 5’5” to 5’9”

22 cm for 5’9” to 6’1”

23 cm for over 6’1” to 6’5”

167
Q

Where does the spinal cord and dural sac end in both adults and infants?

A

In adults, the spinal cord ends at about L1-L2 (conus medullaris​) and the dural sac ends at about S1-S2

In an infant, these landmarks are shifted slightly caudad with the spinal cord ending at L3-L4 and the dural sac terminating at S3-S4.

168
Q

The lateral antebrachial cutaneous nerve is a branch of the What nerve?

It provides cutaneous innervation to what areas?

It arises from what nerve roots?

What block is needed to block it?

A

The lateral antebrachial cutaneous nerve is a branch of the musculocutaneous nerve.

It provides cutaneous innervation to the lateral half of the forearm.

It arises from C5-C6 and therefore is part of the brachial plexus and would most likely be blocked by a supraclavicular nerve block.

169
Q

Quantitatively, what is a concerning change in SSEP monitoring?

A

SSEPs are quantified by the amplitude of the signal generated and the latency of the signal, which is the time it takes for the impulse to reach the cortex. Anything that decreases the amplitude or increases the latency is concerning. This could be from direct damage to the nerve or ischemic insult.

A clinically significant decrease in amplitude is 50% from baseline and a 10% increase in latency.

170
Q

SSEPs are quantified by what?

MEP (Motor evoked potentials are used to evaluate what?

A

SSEPs are quantified by the amplitude of the signal generated and the latency of the signal, which is the time it takes for the impulse to reach the cortex.

Motor evoked potentials (MEP) are used to evaluate the integrity of the descending motor neuronal pathways.

171
Q

What is a clinically significant change in motors

A

Clinically significant change in MEP is a 50% decrease in amplitude from baseline. Latency is less important than compared to SSEPs.

172
Q

For neuromonitoring SSEP and MEP,

What is more sensitive to anesthetics?

Can you use paralytics?

A

Both SSEPs and MEPs are sensitive to volatile anesthetic agents, but this is more so with MEPs.

Unlike SSEPs, MEPs require that paralytic agents not be used, although occasionally a low dose neuromuscular blocker may be requested to minimize the background noise of the MEPs.

173
Q

What is the most resistant neuromonitoring to anesthetics?

What is the most sensitive to anesthetics?

A

BAEP (Brainstem auditory) is extremely resistant to all anesthetic techniques.

MEPs are very sensitive to and supressed by volatile agents, and total intravenous anesthesia is the preferred anesthetic if MEPs are to be used.

VEPs (Visual) are the most sensitive of the evoked potentials to volatile anesthetics.

174
Q

What are the other diseases that are associated with Lambert Eaton Syndrome?

A

Lambert-Eaton Myasthenic Syndrome (LEMS) is a paraneoplastic syndrome strongly associated with small cell carcinoma of the lung, sarcoidosis, thyroiditis, a collagen related vascular disease, or other malignancies.

175
Q

How does inspiration* / *expiration affect Intrapleural Prerssure?

How does inspiration* / *expiration affect Right Atrial Pressure?

A

As inspiration occurs, intrapleural pressure grows more negative, which leads to an increase in transmural pressure across both vena cava and right atrium.

This leads to an expansion of chamber size and facilitates venous return given the decreased pressure in the right atrium.

Simply stated, right atrial pressure falls during inspiration, creating a pressure gradient that drives an increased venous return.

Expiration leads to a more positive intrapleural pressure thus decreasing transmural pressure and decreasing chamber volume. This leads to a decreased venous return.

176
Q

What is the dose of Bivalirudin for cardiac surgery?

A

Off-pump: Initial bolus: 0.75 mg/kg, followed by continuous infusion 1.75 mg/kg/hour to maintain ACT >300 seconds (Dyke 2007).

If patient needs to go on-pump, some have recommended an additional 0.25 mg/kg bolus and increasing the i**nfusion rate to 2.5 mg/kg/hour (Angiomax Canadian product labeling 2016).

On-pump: Initial bolus: 1 mg/kg*, followed by continuous infusion *2.5 mg/kg/hour; 50 mg bolus added to priming solution of cardiopulmonary bypass (CPB) circuit.

Additional boluses of 0.1 to 0.5 mg/kg may be given to maintain ACT >2.5 times baseline ACT.

Discontinue infusion 10 to 15 minutes prior to weaning from CPB (Salter 2016).

177
Q

How long is Heparin active for?

A

Mean: 1.5 hours; Range: 1 to 2 hours

Affected by obesity, renal function, malignancy, presence of pulmonary embolism, and infections.

178
Q

What is the dose of Protamine you should give to neutralize Heparin?

A

1. 1 mg of protamine neutralizes ~100 units of heparin

Maximum single dose: 50 mg

2. Go back to see what time the Heparin was given

Because blood heparin concentrations decrease rapidly after heparin administration (half-life of heparin is ~60 to 90 minutes), may adjust the protamine dosage depending upon the duration of time since heparin administration.

For example, if 2 hours has elapsed since heparin overdose, consider administering half of the calculated initial protamine dose; this is more conservative compared to product labeling, which suggests administering half of the calculated dose at 30 minutes after heparin administration.

If patient is not bleeding, consider not administering protamine since risks may outweigh benefits of administration (Howland 2019).

179
Q

What is the ACT goal for Cardiopulmonary Bypass?

A

Classically, a goal of 480 seconds has been used. However, with improvements in bypass circuits, some providers initiate CPB at a value of 400 seconds.

180
Q

What is the treatment for Antithrombin III Deficiency?

A
  1. AT 3 concentrate
  2. FFP (2-3 Units)
181
Q

Cardiac Transplant Patients:

Who and What structure is responsible for heart rate generation?

A

Donor atrium is responsible for heart rate generation

182
Q

How does a normal heart response to a reduction in intravascular volume?

How does a transplanted heart responde to a reduction in intravascular volume?

A

Normal

In the normal innervated heart, the response to a sudden reduction in intravascular volume is an increase in heart rate and contractility.

Transplants

The initial response is an increase in stroke volume dependent on an adequate preload and not an acute increase in heart rate or contractility.

The increased contractility and heart rate is a secondary effect and is predominantly dependent on circulating catecholamine levels.

Therefore, the transplanted heart is critically preload dependent.

183
Q

What are the important anesthetic implications of heart transplant patients?

A

Anesthetic Implications

Anticholinergic agents which are indirect acting agents (e.g. atropine, glycopyrrolate, pancuronium) have minimal effect on heart rate.

The response to anticholinesterases is unpredictable.

The transplanted heart does retain its responsiveness to direct acting agents

(i.e.) isoproterenol, epinephrine, norepinephrine, dopamine, and dobutamine

184
Q

Comment on the rate of heart transplant patients after they have recovered.

A

90-110 bpm (Higher due to loss of parasympathetic tone) with less variability

185
Q

Who should receive antibiotic prophylaxis for Infective endocarditis?

Additionally, what procedures qualify?

A
  • *The list of patients who should receive prophylaxis is below:**
  • Patients with a prosthetic cardiac valve
  • Patients who have previously had IE
  • Patients with unrepaired cyanotic congenital heart disease (including palliative shunts/conduits)
  • Patients with congenital heart defects which were repaired with prosthetic material within 6 months of the procedure
  • Patients with repaired congenital heart disease with residual defects at the site, or adjacent to the site, of a prosthetic patch or device
  • Cardiac transplantation recipients who develop cardiac valvulopathy (substantial leaflet pathology and regurgitation)
  • *Of note, prophylaxis only applies to certain surgical procedures:**
  • Dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa
  • Invasive respiratory tract procedures that involve incision or biopsy of the respiratory mucosa (e.g. tonsillectomy, adenoidectomy)
  • - Infected skin, skin structure, or musculoskeletal tissue*
186
Q

What is the preferred prophylactic regimen for Infectious Endocarditis?

A

Amoxicillin 2 g given as a one time oral dose 30-60 min before the procedure.

187
Q

What are the two pathological criteria to definitively diagnose infective endocarditis alone?

A

1. Microoganisms in a vegetation

  • Culture or histological examination of a vegetation
  • Vegetation that has embolized
  • Intracadiac abscess specimen

2. Pathological lesions

- Vegetation or intracardiac abscess confirmed by histological examination showing active endocarditis

188
Q

What are the major clinical criteria of Duke’s Criteria?

A

1. Blood cultures positive for endocarditis

  • 2 separate cultures
  • Microorganisms consistent with IE from persistently positive blood cultures
  • Single positive culture for Coxiella Burnetii or Antiphase I IgG antibody titer > 1:800

2. Evidence of Endocardial Involvement

  • Echocardiogram positive for IE
  • New partial dehiscence of prosthetic valve
  • New valvular regurgitation

Note: Worsening or changing pre-existing murmur NOT sufficient

189
Q

What are the minor Duke’s criteria for infective endocarditis?

A

1. IVDU or Predisposing Heart Condition

2. Fever

3. Vasular Phenomenon

  • Emboli (Major aterial)
  • Septic Pulmonary infarcts
  • Mycotic aneurysm
  • Intracranial hemorrhage
  • Conjunctival hemorrhages
  • Janeway Lesions

4. Immunological Phenomemon

  • Glomerulonephritis
  • Osler’s Nodes
  • Roth’s Spots
  • Rheumatoid Factor

5. Microbiological evidence

  • Positive Blood culture that does not meet major criterion as noted in definitive/major role
  • Serological evidence of active infection with organism consistent with IE
190
Q

What classifies as a definitive diagnosis of infective endocarditis?

A
  1. Meets Pathological Criteria (Vegetation histology)
  2. One Major and 3 minor
  3. 5 Minor
191
Q

What is the mechanism of action of Butorphanol?

A

Butorphanol is a mixed mu-opioid receptor agonist-antagonist and a kappa-opioid receptor partial agonist

Agonist of kappa opiate receptors and partial agonist of mu opiate receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces analgesia, respiratory depression, and sedation similar to opioids

192
Q

Butorphanol Indications?

A
  1. Treating pain
  2. Postoperative shivering
  3. Neuraxial opioid-induced central pruritus

Butorphanol is a mixed mu-opioid receptor agonist-antagonist and a kappa-opioid receptor partial agonist. Its mu receptor activity makes it useful in treating pain and neuraxial opioid-induced central pruritus. Meanwhile, its kappa receptor* activity makes it a good treatment for *postoperative shivering.

193
Q

Name the Formulas for

Boyle’s Law

Charles Law

Gay-Lussac Law

A

Boyle P1V1 = P2V2

  • Boils have a high TEMPERATURE

Charles = V1 / T1 = V2 / T2

  • King Charles under PRESSURE

Gay-Lussac P1/T1 = P2/T2

  • Think of Cul de SACC (Lussac) have constant Volume of space
194
Q

Why would you want a high SVR in a patient with aortic stenosis? (Seems counter intuitive)

A

This pairs with the higher SVR goal, as the higher SVR will encourage a higher coronary perfusion pressure (diastolic blood pressure - left ventricular end-diastolic pressure) to ensure that the thick LV is adequately perfused.

An elevated SVR in the setting of AS may seem counter-intuitive, as there is an obstructive lesion in the LV outflow tract, however in cases of severe or critical AS, this stenotic aortic valve provides much greater resistance to LV outflow than any physiologic SVR that can be generated

195
Q

What are 5 classes/effects of Diphenhydramine?

A

Antihistamine (H1)

Anticholinergic activity

Inhibits serotonin reuptake

Potentiates opioid-induced analgesia

Mhave local anesthetic-like properties (intracellular sodium channel blocker).

196
Q

How does lipophilicity vs. lipophobicity opiates affect epidural effects?

A

As opioids cross the dura and enter the CSF, highly lipophilic drugs will remain primarily at the level of injection.

However, opioids with a low lipid solubility, like morphine, will diffuse greatly and have a widespread in the CSF.

When placed in the epidural space, opioids act through diffusion into the CSF. Spread of opioids is related to the hydrophilicity and lipophilicity of the opioid. Fentanyl is very lipid soluble and remains near the spinal level it is injected at, whereas morphine has a widespread in the CSF.

197
Q

What affects the onset of local anesthetics?

A

pKa and Tissue diffusibility

Lower pKa = More rapid onset of action (more RN molecules present to diffuse through the nerve sheath)

198
Q

What affects the potency of local anesthetics?

A

Lipid Solubility & Vasodilator activity

199
Q

What affects the duration of local anesthetics?

A

Protein Binding & Vasodilator Activity

200
Q

What is the acronym you can use to differentie local anesthetic characteristics

A

Local anesthetics “PLOPS”

Potency - Lipid Solubility

Onset = pKa

Potency - Lipid Solubility

201
Q

Cerebral Salt Wasting

Mechanism of Action

Volume Status

Serum [Na]

Urine [Na}

Urine Output

A

Diagnosis - Cerebral Salt Wasting

Mechanism of Action - Excess secretion of Na and Water

Volume Status - Hypovolemia

Serum [Na] - Decreased

Urine [Na} - Increased

Urine Output - Increased

202
Q

SIADH

Mechanism of Action

Volume Status

Serum [Na]

Urine [Na}

Urine Output

A

SIADH

Mechanism of Action - Water retention due to elevated ADH

Volume Status - Normovolemic or Hypervolemic

Serum [Na] - Decreased

Urine [Na] - Increased

Urine Output - Normal

203
Q

Diabetes Insipidus

Mechanism of Action

Volume Status

Serum [Na]

Urine [Na}

Urine Output

A

Diabetes Insipidus

Mechanism of Action - Free Water loss due to decreased ADH

Volume Status - Hypovolemia

Serum [Na] - Increased

Urine [Na} - Decreased

Urine Output - Increased

204
Q

Draw a graph comparing the PVR compared to lung volumes

A

In normal healthy adults, PVR is lowest when breathing at normal tidal volumes, with a nadir at functional residual capacity (FRC).

Increasing or decreasing lung volumes beyond FRC and normal tidal volumes results in an increase in PVR, creating a U-shaped curve, illustrated below.

This general relationship exists for both normal breathing and positive-pressure breathing.

205
Q

What are of the H’s and T’s of Cardiac Arrest?

A

Remember to get an:

Echo

EKG
ABG

Hypovolemia

Hypoxia

Hydrogen ions (Acidosis)

Hyper and Hypokalemia

Toxins

Tamponade

Tension Pneumothorax

Thrombosis

Trauma

206
Q

What are the timing and their respective complications associated with Subarachnoid hemorrhage?

A
  1. Re-bleeding (~24 hours after initial hemorrhage)
  2. Vasopasm (3-10 days, Peaks at 5th -10th day, Resolve 10-14 days)
  3. Hydrocephalus
207
Q

An OB Anesthesiology attending asks you:

How does a spinal work to control pain? What is your response?

A

Neuraxial fentanyl results in rapid onset of analgesia primarily through activation of mu receptors in the substantia gelatinosa in the dorsal horn of the spinal cord.

Opioids activate G-protein coupled inhibitory receptors both pre and postsynaptically to inhibit the release of excitatory neurotransmitters (presynaptic) and hyperpolarize postsynaptic neurons to inhibit neuronal transmission.

In the brain, exogenous and endogenous opioids work in the area of the periaqueductal gray matter of the midbrain and rostral ventromedial medulla and modulate descending inhibitory pain pathways.

Systemic administration, ascent in the CSF to the brain (hydrophilic opioids such as morphine), and absorption from neuraxial administration (primarily with lipophilic opioids such as fentanyl) activate these descending inhibitory pathways.

Neuraxial administration of opioids results in analgesia primarily by action in the dorsal horn of the spinal cord in the substantia gelatinosa where they inhibit release of excitatory neurotransmitters such as substance P and glutamate and inhibit afferent neural transmission to the brain from incoming peripheral pain neurons.

208
Q

What are the Gastrointestinal Effects of Glycopyrrolate?

A

Gastrointestinal

  • Anticholinergic activity leads to decreased salivary gland secretions and gastric secretions. This can lead to the side effect of a dry mouth for patients upon awakening from anesthesia.
  • Decreased gastric motility and peristalsis, which can lead to constipation.
209
Q

What are the respiratory effects of Glycopyrrolate?

A

Respiratory

  • Muscarinic receptors in the airway mucosa and bronchi are responsible for salivation and respiratory secretions. Blocking these receptors therefore inhibits these secretions, which is beneficial when performing a fiberoptic intubation.
  • Blocking muscarinic receptors in the bronchial smooth muscle leads to relaxation and decreased airway resistance.
210
Q

What are the genitourinary effects of Glycopyrrolate?

A

Genitourinary
- Blocking muscarinic receptors in the smooth muscle of the bladder causes relaxation and decreased bladder and ureter tone. This can lead to urinary retention, particularly in males with an enlarged prostate.

211
Q

What are the opthalmic effects of glycopyrrolate?

A

Ophthalmic
- Anticholinergic activity causes pupillary dilation, which could theoretically cause problems in patients with narrow angle glaucoma. It can also cause photophobia

212
Q

What are the neurological effects of anticholinergics?

A

Neurologic
- Glycopyrrolate does not cross the blood brain barrier and therefore does not have any neurologic side effects. Other anticholinergics* such as *atropine* and *scopolamine*, however, can lead to *altered mental status and hallucinations.

213
Q

You are in trauma and the patient is cold during massive resuscitation.

What are 4 detrimental effects from low body temperature in this scenario?

A

1. Including increased risk of sepsis

2. Coagulopathy

3. Irreversible bleeding

4. Acidosis

One complication of massive transfusion is the classic triad of coagulopathy, hypothermia, and acidosis. This is also called the “trauma triad of death.” These three factors are closely linked and contribute to worsening outcomes in patients receiving massive transfusions.

214
Q

Transtracheal injection of local anesthetic will block what nerve?

A

Transtracheal injection of local anesthetic will block the recurrent laryngeal nerve.

215
Q

Glucocorticoids act to produce more A and inhibit B?

A

Glucocorticoids act to produce more aldosterone and inhibit the phospholipase A2 enzyme (PLA2).

The PLA2 enzyme converts phosphatidylcholine to arachidonic acid, a precursor to prostaglandins, leukotrienes, and other proinflammatory mediators (e.g. TNF-α, interleukin-1, interleukin-6, cellular adhesion molecules).

216
Q

What is the recommended dose of Hydrocortisone?

A

The suggested dose is 200 mg IV hydrocortisone per day.

There is no commonly recommended dosing regimen (bolus vs divided doses vs infusion). Spreading doses apart or using an infusion can reduce some of the side effects, such as hyperglycemia. Steroids should be tapered once vasopressors are no longer required.

217
Q

How does respiratory rate affect the degree of citrate toxicity?

A

Hypoventilation does not increase the risk of toxicity; the reverse is true.

Hyperventilation increases the risk of citrate toxicity in a certain subset of patients because it causes a decrease in ionized calcium ions.

This is why signs of hypocalcemia can be seen in patients who have anxiety attacks and hyperventilate. In certain patients, hyperventilation will result in ionized calcium ions binding to proteins. Since citrate toxicity is actually due to hypocalcemia, anything that decreases the ionized calcium ions will increase the risk for citrate toxicity.

218
Q

Why are pediatric patients prone to citrate toxicity?

A

Pediatric patients are more likely to experience citrate toxicity. This is especially true of the neonatal population due to decreased metabolism secondary to hepatic immaturity.

219
Q

What blood product is most common with citrate toxicity?

A

Fresh frozen plasma is more likely to cause citrate toxicity compared with other blood products because more citrate is used.

220
Q

What are all the drugs used to treat bronchospasm?

A

Deepening Anesthetic (Propofol or Volataile except Desfluranae)

Beta-adrenergic agonists (Albuterol)

Epinephrine 10-20 mcg IV

Muscarinic antagonists (Glyco 0.2, atropine 0.1 - 0.5 mg),

Magnesium (Acute severe exacerbations) (off-label use): IV: 2 g as a single dose over 20 minutes (GINA 2019; NAEPP 2007); recommended as adjunctive therapy for severe life-threatening exacerbations and for exacerbations that remain severe after 1 hour of intensive conventional therapy (NAEPP 2007).

Ketamine (doses as high as60 mcg/kg/minute (3.6 mg/kg/hour) have been reported in patients with refractory bronchospasm (Youssef-Ahmed 1996)

and

Theophylline (SQ: 0.25 mg/dose; may repeat every 20 minutes for 3 doses (maximum: 0.75 mg/1-hour period)

221
Q

Why does Midazolam dosing need to be adjusted in Renal Failure?

A

Elevated blood urea (BUN) levels usually occur in the setting of decreased clearance due to renal dysfunction.

Common symptoms include fatigue, nausea, vomiting, altered mental status, and metabolic acidosis.

One of the major pharmacologic effects of uremia is decreased protein-binding of drugs. Because it is the free-fraction of a medication that exerts its physiologic effect, decreased protein binding of midazolam would cause an exaggerated effect and the dosage should, therefore, be decreased.

Additionally, premedication in any patient with an altered mental status should be avoided. Medications that are rapidly metabolized in the bloodstream, such as remifentanil and esmolol, or those that are not metabolized at all, such as volatile anesthetics, do not require a significantly decreased dosage.

222
Q

What is the gold standard for ICP monitoring?

A

Elevated Intracranial Pressure

Gold Standard:

A ventriculostomy catheter is the most cost-effective, accurate, and reliable method of monitoring intracranial pressure (ICP) and is currently the gold standard for ICP measurement.

It is also very useful in that it provides a way to drain cerebrospinal fluid (CSF), and samples for lab analysis.

223
Q

What are all the ways to measure ICP (5)?

A
  1. Intraventricular
  2. Intraparenchymal
  3. Subarachnoid
  4. Epidural (lumbar subarachnoid catheter).
  5. A non-invasive option is measuring optic nerve sheath diameter via ultrasound
224
Q

BP management for acute ischemic CVA?

A

In fibrinolysis candidates, it should be lowered if above 185 mm Hg systolic or 110 mm Hg diastolic. Treatment options include labetalol, nicardipine infusion, or clevidipine infusion. Significant blood pressure decreases should be avoided. Once blood pressure is controlled, fibrinolysis can proceed.

Following fibrinolysis for 24 hours, or during treatment, systolic blood pressure above 180 mm Hg or diastolic above 105 mm Hg can be treated with additional doses of labetalol or other antihypertensives.

For asymptomatic patients who have not undergone fibrinolysis, guidelines indicate it is reasonable to use antihypertensives to reduce blood pressure below 220 mm Hg systolic, or 120 mm Hg diastolic.

225
Q

The goal to fibrinolysis (Timing) is what time frame? What is the window?

A

The goal to fibrinolysis is 60 minutes from presentation, with a recommended cutoff of 3 to 4.5 hours from onset of symptoms.

226
Q

What % can the BP/HR increase with ketamine?

How quickly are changes seen with IV vs. IM injections?

How long do these effects last?

A

Ketamine is known as a more “stable” induction agent because it often maintains hemodynamic parameters. Ketamine is one of the only induction medications that stimulate the sympathetic nervous system. It can lead to an increase in blood pressure and heart rate, up to 30% above baseline. These changes are often seen within five minutes of intravenous injection and up to twenty minutes after an intramuscular injection. The changes often last for 20 minutes after intravenous injection and there is a wide variation in individual response.

227
Q

What are the ionotropic effects of Ketamine?

A

Inhibits reuptake of catecholamines and nitric oxide endothelial production. This results in vasoconstriction and a positive inotropic state. Additionally, ketamine acts as a vagal nerve inhibitor.

In states where the sympathetic nervous system may be exhausted, ketamine may have a negative inotropic effect. This is secondary to a depletion of catecholamines that occurs in these states. An example of this is critical illness or shock states. Given this potential, ketamine should be used cautiously in patients with decompensated ventricular failure or catecholamine depletion.

228
Q

The pathophysiology of ischemia-reperfusion injury during liver transplant is complex, however one of the mechanisms is thought to be due to?

A

The pathophysiology of ischemia-reperfusion injury is complex, however one of the mechanisms is thought to be disruption of the sodium potassium pumps secondary to decreased adenosine triphosphate and glycogen.

229
Q

What are the 3 phases of liver transplant surgery?

A

The preanhepatic stage begins with incision and ends with cross-clamping of the major vessels of the liver (portal vein, hepatic artery, inferior vena cava, or hepatic vein).

The anhepatic stage starts with cross clamping and continues until anastomosis are made and perfusion restarts – in other words from occlusion of vascular inflow to start of graft reperfusion.

The neohepatic phase begins with unclamping of the portal vein when reperfusion of the donor liver starts and continues during hepatic artery, biliary duct anastomosis, and abdominal closure.

230
Q

During an ultrasound-guided interscalene block, the probe should be moved in what direction after identifying the carotid artery?

A

During an ultrasound-guided interscalene block, the probe should be moved laterally and posteriorly after identifying the carotid artery, and the plexus is found between the anterior and middle scalene muscles.

231
Q

What is spared with an interscalene block?

A

However, the ulnar nerve (or inferior trunk) is frequently spared

232
Q

What are possible complications encountered during interscalene blocks?

A

Potential problems include phrenic nerve blocks, pneumothorax, recurrent laryngeal and vagus nerve injury, epidural, intrathecal, or intravascular injection.

233
Q

What type of syndrome is amniotic fluid embolism?

A

Amniotic fluid embolism is an anaphylactoid syndrome that is thought to result from the seeding of amniotic fluid or fetal cells in the maternal circulation causing hypoxia due to bronchospasm, pulmonary hypertension, and eventual cardiovascular collapse

Amniotic fluid embolism is sometimes referred to as ‘anaphylactoid syndrome of pregnancy’.

234
Q

Why does an Amniotic fluid embolism cause such sudden coagulopathy?

A

Amniotic fluid contains many vasoactive and procoagulant factors, the entry of this fluid into systemic circulation results in a massive inflammatory release* and eventual *disseminated intravascular coagulopathy

235
Q

Why does an amniotic fluid embolism cause such massive hemodynamic instability?

A

One of these vasoactive agents, endothelin, can cause both bronchoconstriction and pulmonary and coronary vasoconstriction and may be responsible for the initial cardiopulmonary collapse seen during the initial phases of AFE.

236
Q

What test can help diagnose amniotic fluid embolism but is often not available?

A

Tests that assess for a circulating antigen found in meconium may have some diagnostic utility, however, the test for serum sialyl Tn (STN) antigen is likely unavailable at most medical facilities. Chest radiography is typically non-specific but may demonstrate bilateral areas of increased homogeneity, similar to pulmonary edema.

237
Q

What dermatomes spinal segment coverage is needed to relieve the pain of contractions and cervical dilation?

A

T10 to L1 spinal segment coverage is needed to relieve the pain of contractions and cervical dilation

238
Q

What deratome spinal segment coverage is needed to relieve the pain of vaginal and perineal distention?

A

S2-S4 spinal segment coverage is needed to relieve the pain of vaginal and perineal distention.

239
Q

Why isn’t lidocaine and 2-chloroprocaine used for maintenance epidural anesthesia in clinical practice?

A

Lidocaine and 2-chloroprocaine are not used for maintenance epidural anesthesia in clinical practice because tachyphylaxis may develop more rapidly with these agents when compared to longer acting local anesthetics. Both bupivacaine and ropivacaine have been used and there is no evidence that one has any advantages over the other.

240
Q

What medication should you avoid giving in the presence of post partum hemorrhage with retained placenta?

A

Ergot alkaloids (e.g. methylergonovine aka Methergine) are not recommended as they may cause tetanic uterine contractions which can delay placental expulsion and make manual extraction more difficult

241
Q

What medication can help assist the OB with placenta delivery?

A

In some cases, excessive cervical and/or uterine contractions may prevent expulsion of the placenta. In these cases, nitroglycerin administration may help facilitate placental delivery.

Careful blood pressure monitoring must occur as a drop is typically seen. Intraumbilical vein injection of oxytocin with saline may be another treatment modality although the WHO states that the evidence may not be strong. Other experts recommend against this practice.

242
Q

What is normal variation/variability for fetal heart rate monitoring?

What is non-reassuring?

Decreased variability is indicative of what?

A

The variation from one beat to another can range from 5-25 BPM.

Variability in the FHR is a sign of a healthy autonomic nervous system, chemoreceptors, baroreceptors, and cardiac responsiveness.

FHR becomes non-reassuring if the variability is < 5 or > 25.

A decrease in FHR variability can be due to fetal sleep state, fetal acidosis, or maternal sedation from drugs.

243
Q

What is a sinusoidal fetal heart rate indicative of?

A

Sinusoidal FHR pattern: a smooth sine wave (no variability present).

It is rare, however, is associated with high rates of fetal morbidity and mortality. This pattern is indicative of severe fetal anemia

OR

IV administration of opioid to the mother

244
Q

A saltatory pattern consists of excessive alterations in variability (> 25 bpm) may signal what?

A

Occurrence of acute fetal hypoxia

245
Q

What mneumonic can be used when formulating a plan with congenital heart disease patients or parturients with peripartum cardiomyopathy?

A

Treatment (PANDAS M.D.)

P acemaker

A nticoagulation

N euraxial plan

D elivery
A ntibiotics
S equalae
M onitoring
D isposition

246
Q

What is the the definition of peripartum cardiomyopathy (per the National Heart, Lung, and Blood Institute?

A

(1) the development of heart failure in the last month of pregnancy or within five months of delivery (2 temporal guidelines)

(2) absence of an identifiable cause

(3) no history of heart disease prior to the last month of pregnancy

(4) left ventricular systolic dysfunction as determined by echocardiogram.

247
Q

What is the best medication for shoulder dystocia?

What if they have an epidural?

A

Nitroglycerin is the most appropriate initial drug for shoulder dystocia.

In order to assist with fetal manipulation, nitroglycerin is recommended as a fast and efficient tocolytic that resolves quickly. An appropriate dose and route is 0.4 mg sublingual. If IV dosing is needed, then 50-200 mcg IV is typical.Chloroprocaine* may also be useful for quick analgesia in patients who already have an *epidural.

In the worst cases of dystocia, the obstetrician may need to intentionally break the fetal clavicle or the anesthesiologist may need to induce general anesthesia in order to emergently deliver.

248
Q

What are the two stages of an Amniotic Fluid Embolism?

A

The characteristic cardiac signs and symptoms of AFE may be divided into 2 stages.

The early stage (1st stage) generally lasts less than 30 minutes* and is characterized by transient, often intense, pulmonary vasospasm. The resultant *right heart dysfunction can progress to fatal right heart failure. Low cardiac output then leads to ventilation-perfusion mismatch, hypoxemia, and hypotension.

The second phase of AFE is characterized by left ventricular dysfunction or failure and pulmonary edema due to the previous right heart dysfunction. Interestingly, right heart function may return close to normal during this phase. Left or biventricular failure is often fatal unless supportive care is initiated.

249
Q

What is needed to diagnose pre-eclampsia?

A

One of these states is preeclampsia which occurs in 3% to 8% of pregnancies.

The diagnosis of preeclampsia does not require proteinuria.

The diagnosis is made when the patient has elevated blood pressure during pregnancy or in the postpartum period with some degree of end-organ dysfunction.

250
Q

Why should you try to avoid ephedrine in pregnancy?

A

Ephedrine is generally avoided, particularly repeated or infusion doses, as some studies have revealed an increased risk of fetal acidosis.

251
Q

Which of the following is the MOST common cause of pregnancy-related maternal mortality in the United States?

What is the most common in the world?

A

Overall maternal mortality has increased over the last several decades in the United States, with the most common cause attributable to maternal cardiovascular conditions (34%).

Hemorrhage, hypertensive disorders of pregnancy, and anesthetic complications have declined in incidence.

Hemorrhage is the leading cause of maternal death worldwide, but only responsible for 11% of pregnancy-related deaths in the United States in 2011-2016. Also note that hemorrhage is mostly related to labor and delivery, while cardiovascular complications can occur at any time during pregnancy including the post-partum period.

252
Q

The National Institute for Occupational Safety and Health (NIOSH) recommends a maximum exposure of nitrous oxide to healthcare providers of what value?

A

The National Institute for Occupational Safety and Health (NIOSH) recommends a maximum exposure of nitrous oxide to healthcare providers of 25 parts per million.

253
Q

In the first stage of labor, maternal oxygen consumption increases by what percentage?

In the second stage of labor, maternal oxygen consumption increases by what percentage?

A

In the unmedicated parturient, oxygen demand increases by 40% in the first stage and 75% in the second stage of labor.

This increased oxygen requirement is driven by hyperventilation, the physical effort of pushing out the infant, and uterine contractility.

Epidural analgesia will mitigate this increased oxygen demand during the first and second stages of labor.

254
Q

NIOSH recommends, and other hospital accrediting groups and professional organizations support, that gases inhaled by operating room personnel contain no more than what value of volatile anesthetics?

A

NIOSH recommends, and other hospital accrediting groups and professional orga- nizations support, that gases inhaled by operating room personnel contain no more than 0.5 ppm of volatile anesthetics.

255
Q

What is your MAC goal for general crash caesarian section?

What may you need to change to?

A

1.0 to prevent awareness

May need to switch to TIVA

From induction to delivery of the infant 1.0 MAC is given to avoid maternal awareness.

After delivery, volatile anesthetics are decreased to 0.5 – 0.75 MAC and oxytocin is given concurrently to decrease the uterine relaxation and thus blood loss. Less than 0.75 MAC interfere with oxytocin’s effects and at elevated doses lead to uterine atony.

Nitrous oxide, opioids, and ketamine at less than 2 mg/kg have minimal if any effect.

256
Q

What are fetal accelerations on fetal heart monitoring defined as?

A

Fetal accelerations are defined by an abrupt increase (onset to peak < 30 seconds) with a peak of 15/min or more above fetal heart rate (FHR) baseline and a duration of 15 seconds or more from onset to return in a fetus at least 32 weeks gestation.

257
Q

What is a reactive non-stress test for OBGYN?

A

Reactive non-stress tests have ≥2 accelerations within a 20-40–minute time period.

258
Q

What is a non-reactive stress test for OBGYN?

A

A nonreactive stress test does not have sufficient FHR accelerations during a 40-minute time period.

259
Q

What medications can be considered for a pre-eclamptic crash section in addition to propofol and succinylcholine?

A

Nitroglycerin - 1.5 - 2.5 mcg/kg

Esmolol - 500 to 1000 mcg/kg

260
Q

Why does alveolar dead space decrease in the parturient?

A

Alveolar dead space is reduced during active labor secondary to a significant increase in cardiac output.

Alveolar dead space consists of alveolar units that are ventilated but not perfused; it is air that is inhaled but does not participate in gas exchange in the alveolar-capillary unit.

Because cardiac output increases 10%-40% during active labor, the parturient’s lung units are well perfused with resultant improvement in gas exchange at the level of the alveolar-capillary unit, reducing the functional alveolar dead space volume

261
Q

Why would a labor epidural decrease incidence of fetal hypoxemia?

A

Oxygen consumption during labor increases 40%-75% due to increased respiratory efforts and uterine metabolism.

Hyperventilation secondary to pain in active labor can lead to a left shift of the oxyhemoglobin dissociation curve due to alkalosis.

Between contractions, this can lead to a decreased respiratory rate, which can cause hypoxemia secondary to hypoventilation. Oxygen requirements also increase due to painful contractions. All of these factors can contribute to fetal hypoxemia.

Also catecholamines associated with labor pain may reduce uteroplacental blood flow

Said another way:

Painful uterine contractions during labor cause hyperventilation, which is followed by hypoventilation in between contractions. The detrimental effect of this “hyperventilation-hypoventilation” cycle is twofold. First, the overall respiratory status is one of hyperventilation, with hypocarbia and leftward shift of hemoglobin and reduced oxygen delivery to the fetus. Second, when hypoventilation occurs between contractions, maternal PaO2 may decrease as well. This cycle is effectively blunted by neuraxial analgesia.

Effective labor analgesia during labor can ameliorate many of these physiologic changes.

262
Q

What are the two types of cutting needles that increase PDPH risk?

What are the two non-cutting needles that cause less PDPH?

A

Pencil-point needles such as the Sprotte and the Whitacre (non-cutting) have less risk than a cutting needle such as the Quincke and Touhy (cutting)

263
Q

Why is it imperative to use therapeutic anticoagulation in pregnant women with DVT?

A

The incidence of deep vein thrombosis (DVT) in pregnancy is estimated to be 0.02 to 0.36%. Of these, 15 to 24% of women who do not receive treatment for DVT will develop a PTE which carries a 12-15% mortality rate.

If DVTs are treated, however, the incidence of PTE is reduced to 0.7 to 4.5% with a reduced mortality rate of 0.7%.

264
Q

What is the biggest risk factor for meconium aspiration?

A

By using the earliest gestational age for delivery estimation, there is a decreased risk of meconium passage and a thereby decreased chance of meconium aspiration.

Earlier gestational newborns are much less likely to pass meconium than term or postdate newborns.

The earlier gestational age decreases the likelihood of postdate delivery and significantly decreases the chances of meconium passage.

The primary risk factor for meconium passage is later gestational age.

Using the earliest gestational age for estimating delivery is recommended to help prevent meconium aspiration. Gestational age is the largest risk factor when considering the passage of meconium.

265
Q

What are the different etiologies of aortic stenosis? (List 4)

A

Congenital bicuspid aortic valve

Rheumatic

Supravalvular

Subvalvular

266
Q

Aortic Valve Area and Gradient normally?

Aortic Valve Area and Gradient to generate symptoms?

A

Normal aortic valve area is between 3.0 and 4.0 cm<strong>2</strong> with no significant pressure gradient across the valve (under resting normal cardiac output states)

Symptoms generally develop when the valve area is < 1.0 cm2 and the pressure gradient is greater than 40 mmHg

267
Q

What echocardiographic findings (Area and Gradient) would be worrisome of aortic stenosis in pregancy?

A

An aortic valve area less than 1.0 to 1.5 cm2 and a mean valve gradient of 25 to 50 mmHg generally define the group of pregnant patients with a high risk for cardiovascular complications

268
Q

How would you choose to manage left sided stenotic lesions in pregnancy (Mitral and Aortic Stenosis)?

A

SEVERE STENOSIS:

The caveat is that patients with severe or critical stenosis should probably have general anesthesia, though this is debated particularly if preparations are made for managing anticipated neuraxial hemodynamic changes.

For example, placing an arterial line before the procedure, starting a phenylephrine infusion upon spinal local anesthetic injection, and aggressively managing hypotension with phenylephrine or norepinephrine.

MILD TO MODERATE STENOSIS
In patients with less significant stenosis, neuraxial is less debated and has been thought to be relatively contraindicated due to the simultaneous decrease in preload and afterload, however, several case reports have shown successful administration.

The goals of anesthesia management are the maintenance of sinus rhythm with a normal heart rate, maintenance of intravascular volume, avoidance of aortocaval compression and avoidance of myocardial depression.

269
Q

If a woman has a history of placenta previa, the risk for placenta accreta is what percent for first, second, third, fourth, and fifth or more repeat cesarean deliveries, respectively?

A

in the subgroup of women with previa, the risk for placenta accreta was 3%, 11%, 40%, 61%, and 67% for first, second, third, fourth, and fifth or more repeat cesarean deliveries, respectively.

270
Q

What is the best time to perform non-obstetric surgery on the pregnant patient?

A

2nd trimester (13 to 26 weeks)

The first trimester is a period of rapid development and organogenesis, thus performing surgery at this time may risk teratogenesis.

In the third trimester, the size of the uterus makes abdominal surgery more difficult and the risk of preterm labor is the highest.

271
Q

What are the biggest risks of performing anesthesia of a pregnant patient

A

Preterm Labor

Low Fetal Birth weight

Fetal Loss

272
Q

What is the mortality percentage of parturients with primary pulmonary hypertension?

A

30-55%

273
Q

What is normally the general consensus about neuraxial procedures regarding the minimum platelet count?

A

While no widespread consensus exists regarding a minimum platelet count needed to ensure safety with neuraxial procedures, expert opinion suggests that a platelet count of 80,000/μL is generally sufficient for neuraxial analgesia and/or removal of a neuraxial catheter.

274
Q

What is the risk of epidural hematoma for platelet counts:

<49,000?

50k - 70k?

70k - 100k?

A

A 2017 report published in Anesthesiology calculated the risk for epidural hematoma to be

11% for a platelet count < 49,000/μL

3% for 50,000-69,000/μL

0.2% for 70,000-100,000/μL

275
Q

What coagulation factors increase during pregnancy?

What coagulation factors decrease during pregnancy?

A

Increase = 7 and Fibrinogen

Decrease = 9, 11, 13

276
Q

What pulmonary complications develop in all interscalene blocks?

What is the complication of this?

A

Ipsilateral phrenic nerve block resulting in diaphragmatic paresis occurs in 100% of patients undergoing interscalene blockade, even with dilute solutions of local anesthetics, and is associated with a 25% reduction in pulmonary function.

277
Q

Interscalene block affects the what portion of the brachial plexus?

A

Interscalene block affects the roots and trunks of the plexus.

278
Q

What muscles is the landmarks of an interscalene block?

A

The approach is to place local anesthetic between the anterior and middle scalene muscles

279
Q

What cervical landmarks are used for an interscalene block?

A

The most common level for placement is at the cricoid cartilage or C6 vertebrae level, where the cervical nerve roots C5-7 leave the spine.

280
Q

What symptoms would you expect from an intrathecal injection of medication during interscalene block?

What would the pupillary exam show and why?

A

Total spinal that would cause loss of consciousness and respiratory insufficiency or apnea.

Intrathecal injection at the cervical level would likely cause hypotension as a result of blockade of the sympathetic chain and even bradycardia as from blockade of the cardiac accelerating fibers (T1-4). Additionally, a patients with a cervical intrathecal injection would likely develop bilateral dilated non-reactive pupils. The pupillary reaction is a result of parasympathetic inhibition of the Edinger-Westphal nucleus (midbrain).

281
Q

What would decrease the likelihood of intrathecal injection during interscalene block?

A

Caudad needle direction decreases the incidence of intrathecal injection.

Additionally, if a nerve simulator is used, twitch response seen with less than 0.2 mA could occur inside the dural sleeve and lead to intrathecal spread of local anesthetic.

282
Q

What is the pathophysiology behind the Cushing Reflex?

A

Pathophysiology:

Increased ICP causes pressure on the medulla resulting in medullary ischemia.

The central vasomotor center is a critical structure within the medulla.

Upon the induction of ischemia in this region, the vasomotor center will induce activation of the sympathetic nervous system. The immediate result of this is to increase systemic vascular tone, myocardial contractility, and heart rate in an effort to improve cerebral perfusion pressure and avoid further ischemia.

The profound increase in systemic vascular tone, however, results in reflex bradycardia mediated by baroreceptors and the ultimate clinical presentation of the hypertensive and bradycardic Cushing reflex.

283
Q

What arrythmic side effects can be seen from Digoxin?

A

Early side effects from this increase in intracellular calcium include an increase in ventricular ectopy (Ectopic beats) as well as a slowing of electrical conduction through the atrioventricular node (AV nodal blockade also common)

284
Q

What is the mechanism of action of Digoxin?

A

Digoxin exerts these effects through inhibition of the sodium-potassium adenosine triphosphatase (Na/K ATPase) pump that is located in the myocardium.

This inhibition of this crucial transporter in the myocardial cell membrane results in an increase in the concentration of intracellular sodium.

This increased sodium in the myocyte decreases the activity of another membrane protein known as the sodium-calcium exchanger

Because this molecule will normally extrude a single calcium molecule from the intracellular cytoplasm in exchange for bringing three sodium molecules into the intracellular space, and increased intracellular sodium concentration will tend to increase the concentration of calcium within cardiac myocytes.

This increased intracellular calcium is the primary means by which digoxin exerts its clinical effect.

285
Q

What arrythmia is pathognomonic for digoxin toxicity?

A

In fact, atrial tachycardia with a 2:1 AV block is pathognomonic for advanced digoxin toxicity

286
Q

If you have a cardiac arrest due to digoxin, how long should you resuscitaatae them?

A

In the event of life-threatening arrhythmia or cardiac arrest that is attributed to digoxin toxicity, an antidote in the form of digoxin-specific antibody fragments does exist that directly complexes with molecules of digoxin in the patient’s plasma, effectively reducing the circulating volume of digoxin following its administration. Of note, in cardiac arrest where digoxin overdose is suspected and digoxin antibodies are administered, cardiopulmonary resuscitation should continue for at least 30 minutes to allow for adequate time for the antidote molecules to circulate.

287
Q

What is the best anatomical location to achieve a lumbar sympathetic plexus block?

A

Correct needle position at the lumbar sympathetic plexus is at the anterolateral aspect of lumbar vertebral bodies (L1-L5). The best approach is just cephalad to the middle of the L3 vertebral body due to the highest rate of successful block.

288
Q

What are the indications for a lumbar sympathetic block?

A

A lumbar sympathetic plexus block may offer significant pain relief to patients with:

1. Lower extremity complex regional pain syndrome

2. Phantom limb pain

3. Postherpetic neuralgia

4. Renal colic

5. Analgesia for first stage of labor

289
Q

Why are diuretics given during renal transplantation?

A

Given following clamping of the external iliac artery to stimulate diuresis during reperfusion.

This practice has been shown to decrease the incidence of ATN in renal transplantation

290
Q

Risk Factors for cardiac or vascular perforation during these surgeries when removing cardiac leads (ICD, Defib)? (List 4)

A

The duration of the oldest lead (generally > 5 years for implantable cardiac defibrillator (ICD) leads) due to length of endotheliazation that can develop resulting in greater incorpation of the lead into the vessel wall

Female gender (Smaller blood vessels)

BMI of less than 25 kg/m2

Te removal of ICD leads when compared to pacemaker leads. (Due to larger scar tissue formation)

291
Q

The Heart Rhythm Society (HRS) developed guidelines in 2009 that proposed indications for removal of implanted cardiac leads, whether they be from an ICD or a pacemaker.

What are they?

A

Indications included:

  1. Device or systemic infection
  2. Thrombotic complication
  3. Lead fracture causing malfunction or arrhythmias
  4. Device recall
292
Q

What are the two ways that cardiac leads can be removed?

A

Procedure Types:

  1. Explant which is typically performed on leads that have been implanted for <1 year.

These explants are typically considered low-risk and usually only require gentle traction on the lead for removal.

2. Lead extraction, and often requires the use of a specialized laser to ablate scar tissue that is holding the pertinent lead in place.

These laser lead extractions (LLE) are generally considered higher risk and require anesthetic support.

Consideration for the management of pericardial tamponade should be made prior to the procedure.

293
Q

How do you determine what is red vs. blue on ultrasound color doppler?

A

Flow that travels away from the transducer (negative Doppler shift) is depicted in blue

Flow that is traveling toward the transducer (positive Doppler shift) is depicted in red, with lighter shades of each color denoting higher velocities.

TrueLearn Insight : Color Doppler mnemonics: BART, blue = away, red = towards, and “That blew (blue) me away”

294
Q

What are the two limitations to pulse waved doppler?

A

1. Angles of blood flow to the ultrasound beam that > 20 degrees will significantly attenuate the Doppler shift and render this imaging modality inaccurate.

  1. PWD has a maximum velocity that it is able to measure that is defined by the frequency at which it sends pulses of ultrasound energy. Because this technology requires the pulse of energy to return before the next one can be sent, the greater the depth at which the sample area is being measured, the lower the velocity that is able to be measured.

Called the Nyquist limit and will typically cause imaging artifacts called aliasing at blood-flow velocities of around 1 meter/second*. Because pathologic valvular lesions may generate flows *above 5 meters/second, this imaging modality is best used to characterize flow velocities through vessels or the mitral valve, both of which are areas of relatively slow blood flow.

295
Q

How does Continuous Wave Doppler work?

A

Continuous-wave Doppler (CWD)

In order to determine the maximum velocity of blood flow through an area of relatively high flow such as a stenotic heart lesion, CWD is used.

One ultrasound crystal will continuously emit an ultrasound signal while another will continuously receive an ultrasound signal.

Because CWD does not allow for a single pulse to return before sending a second one, it is impossible to determine the precise location where a location of frequency shift (Doppler effect) may have occurred.

In exchange for this lack of spatial accuracy, CWD has an effectively unlimited Nyquist limit and no effective maximum velocity that it can measure.

This maximum velocity in itself can be incredibly useful, especially when interpreted in the context of the modified Bernoulli equation that states that the change in pressure across stenosis is equal to four times the square of the velocity across the stenosis:

ΔP = 4V^2

296
Q

Regarding EEG monitoring, when will burst suppression occur?

When will complete suppression of electrical activity occur?

A

A progressive decrease in body temperature causes a progressive decrease in power on electroencephalogram, with burst suppression occurring below 25 degrees Celsius

Complete suppression of electrical activity typically occurring below 18 degrees Celsius.

297
Q

What is the 5th position in pacemaker nomenclature?

Example: AATOA

A

Position 5 of the standard North American Society of Pacing and Electrophysiology (NASPE)/British Pacing and Electrophysiology Group (BPEG) Generic Code is used to denote multisite pacing.

In this example, position 5 is “A” denoting multisite atrial pacing, thus the most reasonable answer is that this patient has multiple atrial leads, such as in a biatrial configuration.

298
Q

What are the 5 positions of pacemaker nomenclatures and what do they mean?

A
  1. Chambers Paced (A, V, D, O is none)

Position I specifically denotes the chambers which are actively paced by the pacemaker when it determines a therapeutic pacing signal is necessary.

  1. Chambers Sensed (A, V, D, O is none)

Position II denotes the chambers which “sense” spontaneous cardiac depolarizations outside of the programmed refractory period of the pacemaker. It must be noted that the signals that are sensed can be erroneous, as can be the case when electrocautery is used during a surgery which may lead to improper pacemaker function.

  1. Response to Sensing (Triggered, Inhibited, Dual, and None)

Position III denotes the response that the pacemaker has to a sensed spontaneous cardiac depolarization. It can either immediately trigger a pacing signal as in this question’s example of AATOA for the treatment of paroxysmal atrial fibrillation, or it can inhibit a pacing signal. An example of VVI being used is in the case of an incomplete atrioventricular blockade, where the ventricular lead will not trigger a therapeutic pacing signal if it detects a ventricular beat within a predefined threshold of time.

  1. Rate Modulation (None = O, R = rate modulation)

Position IV is used to demonstrate the presence or absence of rate modulation. This is an advanced function of a pacemaker that attempts to replicate an increase in heart rate with increased physical exertion. The pacemaker will attempt to use mechanical vibration, acceleration, or minute ventilation to determine when the patient is exerting themselves, and will accordingly increase the paced heart rate if this mode is activated.

  1. Multisite Pacing (A, V, D, O is none)

Position V is used to indicate the presence of multisite pacing. The presence of biatrial or biventricular leads can be denoted by this position as denoted in the table above. The utility of these lead configurations is not fully understood, however, their presence can be shown using this position.

299
Q

What is the timeframe for administering adrenergic agents for pheochromocytoma?

A

Preoperative preparation of a patient scheduled for excision of a pheochromocytoma includes initiating adequate α-adrenergic receptor blockade (ideally 10-14 days prior to surgery) and ensuring normovolemia. Beta-blockers may be added after α-blockade in patients with persistent tachycardia, hypertension, and/or dysrhythmias.

300
Q

Why are spinals beneficial for TURP procedures? (2 reasons)

A

Spinal anesthesia provides adequate levels of analgesia that extends to the sacral nerve roots that innervate the pelvic floor, and it also relaxes the muscles of the pelvic floor which facilitates the surgeon’s approach to the prostate. When an epidural is performed for this surgery, often it will not extend to the sacral nerve roots adequately and the patient may experience painful stimuli during the surgery requiring supplemental analgesics. The use of a regional technique with monitored anesthesia care allows for an awake patient.

This facilitates monitoring for two of the most feared complications of TURP

Bladder perforation

TURP syndrome itself

301
Q

What spinal segments must be anesthetized in order to perform a TURP under spinal?

A

The desired dermatomal spinal level during a TURP procedure is T10.

The prostate* is generally innervated by the *S2 and S3 nerve roots*, while bladder sensation is supplied by the *hypogastric plexus which is formed from the T11 to L2 nerve roots.

Thus, a T10 dermatomal level is sufficient to prevent the sensation of any noxious stimuli, while at the same time allowing for monitoring of the initial signs and symptoms of bladder or prostatic capsule perforation.

302
Q

What is TURP syndrome caused from?

A

TURP syndrome arises from endovascular translocation of the cystoscopic irrigant fluid used during the procedure. If distilled water is used, the patient may become severely hyponatremic* and *hypoosmolar. Should this state be approached, hemolysis is common given the lack of plasma osmolarity, and is characteristic of this syndrome.

If a glycine-containing solution is used, glycine is biotransformed into ammonium which, in adequate concentrations, can cause blindness.

Other solutes for the irrigant solution include sorbitol, mannitol, and glucose, all of which have potential side effects if excessive volumes are absorbed into circulation.

303
Q

How does Dexamethasone affect the Cytochrome P450 pathway?

A

Medications that induce CYP-3A4 include carbamazepine, phenytoin, phenobarbital, St. John’s wort, dexamethasone, topiramate, and oxcarbazepine.

Chronic use of these medications may make premedication with commonly used benzodiazepines such as midazolam and diazepam less effective

304
Q

Preoperative peak oxygen consumption (VO2max)

Formal Exercise test

Most useful predictor of post-thoracotomy outcomes - Gold Standards

<15 mL/kg/min indicates an increased risk of morbidity and mortality

>20 mL/kg/min tend to have few complications.

His predicted postoperative FEV1 (ppoFEV1) can be determined as follows

[Preoperative FEV1] * (1 - ([% of lung resected] / 100))

DLCO

<40% indicates an increased overall perioperative risk

Warrants further workup to better risk stratify the patient

A

What are the objective measures to assess post - operative

305
Q

How does solubility of CO2 change with hypothermia? (Affects on pH and PaCO2)

A

The solubility of CO2 will increase as the patient’s temperature decreases, resulting in a relative respiratory alkalosis in a hypothermic patient as the partial pressure of CO2 above the solution decreases as more CO2 is dissolved in the serum.

This respiratory alkalosis (pH high and PaCO2 low) is not apparent when the arterial blood sample is rewarmed to 37 degrees Celsius and it is common for the arterial blood gas to appear normal.

306
Q

What is the affects of alpha stat on cerebral blood flow?

A

In alpha-stat management, cerebral blood flow is decreased as it would be any other time that a patient becomes hypocapneic (Low PaCO2 and high pH).

This decreased cerebral blood flow may result in a less cerebral embolic load than other acid-base management strategies.

The alpha-stat management strategy is primarily used in the adult cardiothoracic surgery population.

307
Q

What effect is the process of oxygen binding to hemoglobin and displacing carbon dioxide, which will result in a downward shift in the carbon dioxide dissociation curve?

A

The Haldane effect is the process of oxygen binding to hemoglobin and displacing carbon dioxide, which will result in a downward shift in the carbon dioxide dissociation curve. This facilitates the removal of carbon dioxide from the body.

308
Q

What effect is the process of carbon dioxide binding to hemoglobin causing oxygen to be displaced, which will result in a rightward shift of the oxygen-hemoglobin dissociation curve?

A

The Bohr effect is the process of carbon dioxide binding to hemoglobin causing oxygen to be displaced, which will result in a rightward shift of the oxygen-hemoglobin dissociation curve.

309
Q

What are the different waves seen in EEG monitoring?

A

TrueLearn Insight : Order in which frequency decreases and amplitude increases: BAT Drink

Beta wave: > 14 Hz, low amplitude

Alpha wave: 8-13 Hz, high amplitude

Theta wave: 4-7 Hz, high amplitude

Delta wave: 0.5-4 Hz, maximum amplitude

Gamma waves have a frequency of 25 to 100 Hz and are thought to be involved in cortical processing.

Beta waves are typically > 14 Hz in frequency and are usually found in patients who are concentrating, or sometimes in patients under anesthesia. (or sedation)

Alpha waves have a frequency of 8 to 13 Hz & found in awake patients resting with their eyes closed.

Theta waves have a frequency of 4 to 7 Hz and are also associated with sleep and sedated states.

Delta waves have a frequency of 0.5 to 4 Hz and are found in patients under deep sleep, sedation or general anesthesia.

310
Q

What is seen on the capnogram here?

A

A “double peak” appearance is commonly observed with capnography in patients with chronic obstructive pulmonary disease (COPD) who have received a single lung transplant, reflecting the difference in function of the transplanted and native lung.

A capnogram from a patient with a single lung transplantation due to chronic obstructive pulmonary disease will show a “double peak” pattern, reflecting the difference in function between the healthy transplanted lung and the diseased native lung. The rapid initial exhalation from the healthy, transplanted lung produces the first peak, while the slower rate of rise of exhaled carbon dioxide from the diseased, obstructed lung produces the second peak.

After single lung transplantation, the capnogram would be unique for each lung, if they were to be separated. The transplanted lung, assuming it is healthy, would produce an essentially normal pattern of exhalation (see Figure 1). The native lung, however, is still diseased and will show an obstructive appearance (slow, blunted upstroke, phase 2–3) and no plateau of exhalation (phase 3-4) is reached. Combined, this causes a “double peak” appearance, as in Figure 2. The first peak is from the normal (transplanted) lung, while the second peak of the tracing represents exhalation from the native, diseased lung.

311
Q

What would a ETCO2 tracing show for double lung transplant?

A

A double lung transplant in a patient with COPD should reveal a normal-appearing capnography tracing, assuming the transplanted lungs are healthy and no rejection has developed.

312
Q

What is shown here on the ETCO2 capnogram?

A

An incompetent inspiratory valve allows exhaled gas (containing CO2) to enter the inspiratory limb of the breathing circuit during expiration.

Therefore, the CO2-containing gas is inspired by the patient during the following inspiration. This extends the expiratory alveolar plateau (phase 3–4).

A decrease in CO2 occurs after the extended plateau and represents the sampling of CO2-free gas that arrived from further proximal in the inspiratory limb. Thus the inspiratory downstroke (phase 4–1) is significantly blunted and the inspiratory phase is shortened (see Figure 3). During the latter portion of inhalation, the CO2 concentration may or may not reach zero, depending on fresh gas flow (FGF).

313
Q

What ETCO2 tracing is seen here?

A

Incompent Expiratory Valve

Capnogram of incompetent expiratory valve. The capnograph shows a markedly elevated inspiratory segment that does not return to zero, representative of rebreathing of CO2. Over time, the ETCO2 will rise, but the shape of the tracing is otherwise essentially normal.

314
Q

What is the cold ischemic time for:
Heart?
Lungs?

Liver?

Pancreas?
Intestines?

Kidneys?

A

Cold ischemic time refers to the amount of time that an organ is chilled or cold and not receiving a blood supply. Cold ischemic time varies widely by organ, but in general, the sooner an organ can be transplanted, the better. Generally accepted cold ischemic times are:
Heart: 4 hours
Lungs: 4-6 hours
Liver: 6-10 hours
Pancreas: 12-18 hours
Intestines: 6-12 hours
Kidneys: 24 hours (may go up to 72 hours if placed on a perfusion pump following recovery)

315
Q

Why can hypothyroidism present with difficult airways?

A

Deposits in the tongue cause macroglossia. Coupled with a large goiter that can extend beneath the sternum, hypothyroid patients may have difficult airways.

316
Q

How can hypothyroidism present with cardiopulmonary dysfunction?

A

Cardiac function may be depressed due to decreased heart rate, contractility, and an attenuated sympathetic response that can result in congestive heart failure.

Decreased cardiac output causes reactive peripheral vasoconstriction to increase systemic vascular resistance, which clinically appears as cool, mottled extremities.

Mucopolysaccharide deposits in the pericardium can cause pericarditis, pericardial effusion, and tamponade. This can similarly occur in the pleura causing pleuritis and pleural effusion and in the peritoneum as wel

317
Q

What are the four monitoring sites are considered to be the most accurate measures of core temperature?

A

Four monitoring sites are considered to be the most accurate measures of core temperature. These include:

  • *1. Distal Esophagus
    2. Nasopharynx
    3. Tympanic Membrane
    4. Pulmonary Artery**
318
Q

What is the cellular reason why demyelinating diseases cause life threatening hyperkalemic arrest if you give succinylcholine?

A

When demyelination occurs muscle fibers receive less neural input.

With less input the muscle begins to synthesize immature acetylcholine receptors (AChR) as a compensatory mechanism.

Immature AChR have an epsilon subunit as opposed to a gamma subunit.

These receptors remain open longer and allow a larger efflux of potassium from the muscle cells.

This increases serum potassium to a greater degree than normal AChRs.

319
Q

How will you adjust your ventilatory settings for a Guillain Barre Patient?

(Spirometry)

A

Should the disease progress to the point that respiratory support is required, the patient will display a restrictive pattern of pulmonary disease. This muscular weakness will not allow the patient to make normal inspiratory or expiratory efforts and will manifest on spirometry as described above, with proportionate decreases in both FEV1 and FVC.

Change the I:E time (Increase inspiratory time) to favor Restrictive disease

This is due to the involvement of the phrenic and intercostal nerves, leading to respiratory muscle weakness and diminished ventilatory capacity.

This will manifest on spirometry as a decrease in both the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC).

This muscular weakness will not allow the patient to make normal inspiratory or expiratory efforts and will manifest on spirometry as described above, with proportionate decreases in both FEV1 and FVC.

320
Q

What is the compliance of a Guillain Barre patient?

A

It should be noted that upon intubation of this patient, their lung compliance will be normal and not in any way restricted.

Because the restrictive lung disease, in this case, is purely due to decreased innervation of the relevant muscles, there is no structural issue that impairs airflow within the lungs as with most other forms of restrictive lung disease.

321
Q

Rank the modalities to detect Venous Air Embolisms in terms of most to least sensitive.

A

MOST

TEE
Precordial Doppler

Pulmonary Artery Cathter

Transcranial Doppler

Moderate

ETN2

ETCO2

Low

Oxygen Saturation

Diect Visualization

Esophageal Stethoscope

ECG

322
Q

What does the American Heart Association state about Atropine referencing high grade AV Blocks (2nd degree Type II and 3rd degee)?

A

According to American Heart Association guidelines, “Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system).

These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with TCP or β-adrenergic support as temporizing measures while the patient is prepared for transvenous pacing.”

323
Q

What is the most common type of equipment related adverse outcome?

A

Misuse of equipment is the most likely cause of equipment related to adverse outcome.

According to a review of the anesthesia closed claims database, misuse was three times more likely to result in adverse outcome than equipment failure. This is likely due to the human component associated with misuse.

324
Q

What should be some objective criteria for determining extubation of a patient who had a thoracotomy?

A

Extubation Plan

In fact, when epidural analgesia is used during the surgery, it is reasonable to consider extubating patients with a predicted postoperative FEV1 (ppoFEV1) between 30% and 20% assuming all other variables are controlled and optimized.

These patients traditionally always remained intubated and were slowly weaned from the ventilator in the ICU, however, early extubation facilitated by the pain control provided by a thoracic epidural in these patients has been shown to decrease respiratory complications when compared to continued postoperative mechanical ventilation.

325
Q

What type of seizures have rhythmic, generalized spike pattern at a frequency of 3 Hz?

A

Absence seizures classically consist of a rhythmic, generalized spike pattern at a frequency of 3 Hz.

326
Q

What is seen on EEG during stage 2 of non-REM sleep?

A

K-complexes, commonly followed by sleep spindles, are common findings on EEG during stage 2 of non-REM sleep.

327
Q

What are EEG findings of convulsions and seizure like activity?

A

Convulsions and seizure-like activity typically present as high-voltage, rhythmic spike and slow-wave patterns on the electroencephalogram.

328
Q

What is Pregnancy Category A?

A

Category A

Control Studies show no risk to the fetus

Drugs which have been taken by many pregnant women and women of childbearing age without an increase in the frequency of malformations or other direct or indirect harmful effects on the fetus having been observed.

329
Q

What is Pregnancy Category B?

A

No human studies performed

Animal studies show no risk

330
Q

What is Pregnancy Category C?

A

No control studies have been performed in either animals or fetus

331
Q

What is Pregnancy Category D?

A

Evidence to human risk exists

Benefits may outweigh risks in certain situations

332
Q

What is pregnancy category X?

A

Control studies in both animals and humans demonstrate fetal risk

No maternal benefit in any situation

333
Q

What pregnancy category is Midazolam?

A

D

This means it should be used only in life-threatening emergencies when no safer drug is available and there exists positive evidence of human fetal risk.

334
Q

What pregnancy category is Etomidate?

A

C

335
Q

What fetal outcomes are associated with use of Midazolam in the 3rd trimester?

A

Use during the third trimester is associated with floppy infant syndrome and significant neonatal withdrawal symptoms

336
Q

How does the initial uptake and distribution of volatile anesthetics change in pregnancy?

A

The initial uptake and distribution of anesthetic medications in pregnant women vary when compared to the general population primarily through:

1. The decreased functional residual capacity

2. Decreased serum albumin concentrations respectively.

Uptake of volatile anesthetic agent is sped by the decrease in functional residual capacity, and the decreased serum albumin can lead to increased free fractions of highly protein-bound medications following their own administration.

337
Q

What are the reasons why a cirrhotic patient will develop thrombocytopenia?

A

Thrombocytopenia is a feature of cirrhosis, mostly due to hypersplenism, and also due to decreased liver synthesis of thrombopoietin (glycoprotein hormone produced by the liver and kidney which regulates the production of platelets)

In some specific liver diseases, other factors may play a role, including bone marrow suppression secondary to alcoholism or medications such as interferon, and platelet destruction from immune-mediated platelet-associated IgG (ITP)

338
Q

What are the 3 main reasons why advanced liver disease patients develop abnormalities of hemostasis?

A

1) Platelets:

Both platelet number and activity are decreased, although this is partly compensated by an increase in von Willebrand factor levels (a protein that causes platelet-platelet and platelet-collagen adhesion).

The increase in von Willebrand factor levels may be explained by a decrease in ADAMTS13 (a protease that cleaves von Willebrand factor and is synthesized in the liver).\

2) Coagulation:

Most coagulation factors are synthesized in the liver (except for thromboplastin and calcium).

Factor VIII is produced both in the liver and also endothelial cells outside the liver.

An increase in the INR in cirrhotic patients can reflect both a quantitative decrease in coagulation factors, as well as a decrease in the level of gamma-carboxylation due to decreased vitamin K.

However, liver-produced anticoagulant factors like protein C, S, Z, and antithrombin III are also decreased and the final balance between pro- and anti-coagulant factors is not necessarily reflected by the INR.

3) Fibrinolysis:

There is a decrease in hepatic clearance of t-PA (tissue plasminogen activator) as well as a decrease in the synthesis of antifibrinolytic factors like plasmin activator inhibitor-1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI).

This may lead to low-grade accelerated fibrinolysis in some patients with end-stage liver disease, however, overt DIC is not a feature of stable chronic liver disease.

339
Q

What are the hemodynamics of a cirrhotic patient in most circumstances?

What agents are great for treating this?

A

Cirrhosis hemodynamics are characterized by a hyperdynamic state

increased cardiac output

and

low peripheral vascular resistance

Rx:

1. Norepinephrine

2. Vasopressin

340
Q

List all the factors that cause a leftward shift on the hemoglobin-oxygen dissociation curve?

A

CO poisoning

Hypothermia

Hypocapnia

Alkalemia

Reduced concentrations of 2,3-bisphosphoglycerate (an enzyme formed during anaerobic metabolism which readily binds deoxygenated hemoglobin)

Hypophosphatemia

341
Q

Hyperbaric oxygen is typically used once carboxyhemoglobin levels are at what %?

A

>25%

342
Q

How does Midazolam affect HR and SVR?

A

Midazolam produces an increase in heart rate.

Midazolam produces a decrease in blood pressure due to a decrease in systemic vascular resistance.

343
Q

How does Midazolam affect the pulmonary system and airway?

A

Dose dependent decrease in ventilation.

In healthy patients, the respiratory depression is insignificant.

However, in patients with chronic obstructive pulmonary disease there is greater depression of ventilation.

Transient apnea may occur after rapid injection of large doses of midazolam especially when given with opioid medications.

Benzodiazepines also depress the swallowing reflex and upper airway activity

344
Q

What are the neurological consequences (CMRO2) of midazolam?

A

Midazolam produces a decrease in cerebral metabolic oxygen requirement (CMRO2)

With respect to CMRO2 there is a ceiling effect to decreased CMRO2 at increasing doses of midazolam.

345
Q

For a femoral nerve block, local anesthetic is deposited in between what layers?

A

Local anesthetic can then be deposited beneath the fascia iliaca or between the two layers of fascia iliaca containing the femoral nerve.

While performing an ultrasound-guided femoral nerve block, a “pop” through the fascia iliac is felt while advancing the needle just prior to the successful deposition of local anesthetic. You will have a sudden change in resistance once in this space.

346
Q

What is the half life of Apixaban (Eliquis)?

A

Half-life is 9-15 hours.

347
Q

What is the reversible agent of Apixaban (Eliquis)?

A

Reversibility: Andexanet alfa is an FDA approved antidote for apixaban.

Andexanet alfa, sold under the trade name Andexxa among others, is an antidote for the medications rivaroxaban and apixaban, when reversal of anticoagulation is needed due to uncontrolled bleeding.

It has not been found to be useful for other factor Xa inhibitors.

It is given by intravenous injection

348
Q

Rivaroxaban Half Life?

A

Rivaroxaban is also a direct factor Xa inhibitor.

Its half-life is 5-9 hours in healthier patients but can be increased to 11-13 hours in the elderly.

349
Q

Rivaroxaban most sensitive test?

A

The PT is the most sensitive test for detecting rivaroxaban but cannot accurately describe the full effects of its presence.

350
Q

Dabigatran test?

A

TT (Thrombin Time) is the most sensitive coagulation assay to determine if dabigatran is present.

351
Q

Dabigatran Half Life?

A

Dabigatran is a direct thrombin inhibitor with a half-life of 12-17 hours.