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APEX Study Guide > Unit 1: Respiratory > Flashcards

Unit 1: Respiratory Flashcards

1
Q

Which muscles tense and relax the vocal cords?

A

CricoThyroid: “Cords Tense”

ThyroaRytenoid: “They Relax”

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2
Q

What muscles abduct and adduct the vocal cords?

A

Posterior CricoArytenoid: “Please Come Apart”

Lateral CricoArytenoid: “Let’s Close Airway”

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3
Q

Describe the sensory innervation of the upper airway

A

Trigeminal: V1 (nares, anterioer 1/3 of septum); V2 (turbinates, septum); V3 (anterior 2/3 of tongue)

Glossopharyngeal: posterior 1/3 of tongue, soft palate, oropharynx, vallecula, anterior side of epiglottis

Superior Laryngeal: Internal branch (posterior side of epiglottis to level of vocal cords); External branch (no sensory)

Recurrent Laryngeal: below vocal cords to trachea

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4
Q

How does recurrent laryngeal nerve injury affect the integrity of the airway?

A

Bilateral Injury:

  • acute – respiratory distress (unopposed action of cricothyroid muscles)
  • chronic – no respiratory distress

Unilateral: no respiratory distress

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5
Q

How does superior laryngeal nerve injury affect the integrity of the airway?

A

Bilateral: hoarseness and no respiratory distress

Unilateral: no respiratory distress

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6
Q

What are the 3 airway blocks? Identify the key landmarks for each one.

A

Glossopharyngeal Nerve Block: palatoglossal arch at the anterior tonsillar pillar

Superior Laryngeal Nerve Block: greater cornu of hyoid

Transtracheal Nerve Block: circothyroid membrane

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7
Q

What are the 3 paired and 3 unpaired cartilages of the larynx?

A

Unpaired: epiglottis, thyroid, cricoid

Paired: corniculate, arytenoid, cuneiform

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8
Q

What is the treatment for laryngospasm?

A
  • 100% FiO2
  • Remove noxious stimulation
  • Deepen anesthesia
  • CPAP 15-20
  • Open the airway (head extension, chin lift)
  • Larson’s maneuver
  • SUX
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9
Q

How to the respiratory muscles function during the breathing cycle?

A

Contraction of inspiratory muscles reduces thoracic pressure and increases thoracic volume — example of Boyle’s Law

Inspiration: diaphragm increases superior/inferior dimension – external intercostals increase AP diameter – accessory muscles are sternocleidomastoid and scalene muscles

Exhalation: usually passive - driven by recoil of chest wall – abd musculature assist in active exhalation

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10
Q

What is the difference between Minute Ventilation and Alveolar Ventilation?

A

Minute Ventilation (Ve): amount of air in a single breath multiplied by number of breaths per minute — Ve = Vt x RR

Alveolar Ventilation (VA): only measures the fraction of Ve that is available for gas exchange (removes anatomic dead space from minute ventilation equation) — VA = (Vt - Anatomic dead space) x RR

  • directly proportional to CO2 production
  • indirectly proportional to PaCO2
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11
Q

What are the four types of dead space?

A

Anatomic Vd – air confined to the conducting airway (nose/mouth to terminal bronchioles)
Alveolar Vd – alveoli that are ventilated but not perfused (reduced pulmonary blood flow - decreased CO)
Physiologic Vd – anatomic Vd + alveolar Vd (anything that increases anatomic or alveolar Vd)
Apparatus Vd – Vd added by equipment (facemask, HME, limb of circle system if incompetent valve present)

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12
Q

What does the alveolar compliance curve tell you?

A

Alveolar ventilation is a function of alveolar size and its position on the alveolar compliance curve

  • best ventilated alveoli are the most compliant (steep slope of the curve)
  • poorest ventilated alveoli are the least compliant (flat portion of the curve)
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13
Q

What does the V/Q ratio represent?

A

V/Q ratio = ratio of ventilation to perfusion (minute ventilation / CO)

  • normal Mv = 4 L/min
  • normal CO = 5 L/min
  • normal V/Q ratio = 0.8
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14
Q

What are the different V/Q mismatch scenarios?

A

If V/Q ratio >0.8 – moves toward dead space
If V/Q ratio <0.8 – moves toward shunt

-dead space = V/Q of infinity
shunt = V/Q of 0

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15
Q

What are the West zones of the lung?

A

Zone 1: PA > Pa > Pv — dead space - ventilation w/o perfusion

Zone 2: Pa > PA > Pv — waterfall - normal physiology

Zone 3: Pa > Pv > PA — shunt - perfusion w/o ventilation

Zone 4: Pa > Pist > Pv > PA — pressure in the interstitial space impairs ventilation and perfusion

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16
Q

What is the alveolar gas equation?

A

Alveolar Oxygen = FiO2 x (Pb - PH2O) - (PaCO2/RQ)

Pb = atmospheric pressure
PH2O = 47 mmHg
RQ = 0.8 (respiratory quotient)
  • tells us that hypoventilation can cause hypercarbia and hypoxemia – also explains how supplemental O2 reverses hypoxemia, but does nothing to reverse hypercarbia
  • Alveolar oxygen in healthy pt breathing room air at sea level ~105.98 mmHg
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17
Q

What is the A-a gradient? What factors affect it?

A

The difference between alveolar oxygen (PAO2) and arterial oxygen (PaO2)

  • helps diagnose the cause of hypoxemia by quantifying the amount of venous admixture
  • it is less than 15 mmHg

Increased by high FiO2, aging, vasodilators, right to left shunting, and diffusion limitation

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18
Q

What are the five causes of hypoxemia? Which ones do supplemental O2 reverse?

A
  • Reduced FiO2 (normal A-a gradient) — Yes
  • Hypoventilation (normal A-a gradient) — Yes
  • Diffusion Limitation (increased A-a gradient) — Yes
  • V/Q Mismatch (increased A-a) — Yes
  • Shunt (increased A-a) — No, no way for O2 to access the pulmonary capillary
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19
Q

What are the five lung volumes? What are the reference values for each?

A

Inspiratory Reserve Volume - 3000 mL (volume of gas that can be forcibly inhaled after a tidal inhalation)
Tidal Volume - 500 mL (volume of gas that enters and exits the lungs during tidal breathing)
Expiratory Reserve Volume - 1100 mL (volume of gas that can be forcibly exhaled after a tidal exhalation)
Residual Volume - 1200 mL (volume of gas that remains in the lungs after a complete exhalation)
Closing Volume - ~30% age 20 ~55% age 70 (volume above residual volume where the small airways begin to close)

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20
Q

What are the five lung capacities? What are the reference values for each?

A
  • Total Lung Capacity - 5800 mL (IRV+TV+ERV+RV)
  • Vital Capacity - 4500 mL (IRV+TV+ERV)
  • Inspiratory Capacity - 3500 mL (IRV+TV)
  • Functional Residual Capacity - 2300 mL (RV+ERV) – lung volume at end expiration
  • Closing Capacity - variable (RV+CV) – absolute volume of gas contained in the lungs when the small airways close
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21
Q

What factors influence functional residual capacity (FRC)?

A

Conditions that Reduce – tend to reduce outward lung expansion and/or reduce lung compliance

  • when FRC is reduced, intrapulmonary shunt (zone III) increases
  • PEEP acts to restore FRC by reducing zone III

COPD or any condition that causes air trapping increases FRC

*FRC cannot be measured by conventional spirometry – includes residual volume

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22
Q

What tests can measure FRC?

A

Measured indirectly by:

  • nitrogen washout
  • helium wash in
  • body plethysmography
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23
Q

What increases closing volume?

A

CLOSE-P:

  • COPD
  • Left ventricular failure
  • Obesity
  • Surgery
  • Extreme age
  • Pregnancy
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24
Q

What is the equation for oxygen-carrying capacity? What is normal?

A

CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)

Normal = 20 mL O2/dL

*how much O2 is carried in the blood

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25
Q

What is the equation for oxygen delivery? What is normal?

A

DO2 = CaO2 x Cardiac Output x 10

Normal = 1000 mL O2/dL

*how much O2 is delivered to the tissues

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26
Q

What factors shift the oxyhemoglobin dissociation curve to the LEFT? (8)

A

Left Shift = Higher Affinity – Left = Love
-occurs in lungs

  • Decreased Temp
  • Decreased 2-3-DPG
  • Decreased CO
  • Decreased [H+]
  • Increased pH
  • Increased HgbMet
  • Increased HgbCO
  • Increased HgbF
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27
Q

What factors shift the oxyhemoglobin dissociation curve to the RIGHT? (5)

A

Right Shift = Decreased Affinity — Right = Release
-occurs near metabolically active tissue

  • Increased Temp
  • Increased 2,3-DPG
  • Increased CO
  • Increased [H+]
  • Decreased pH (acidosis)
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28
Q

What are the mechanisms of CO2 transport in the blood?

A

Venous blood transports it to the lungs -> excreted into atmosphere

Mechanisms of CO2 Transport:

  • bicarbonate = 70%
  • bound to hgb = 23%
  • dissolved in plasma = 7%
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29
Q

What is the Hamburger Shift?

A

When RBC releases HCO3 into the plasma, Chloride is transported into the RBC to maintain electroneutrality

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30
Q

What is the Bohr Effect?

A

Describes O2 carriage

  • increase CO2 and decreased pH cause erythrocyte to release O2
  • it is the cells way of asking hgb to release oxygen to support aerobic metabolism
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31
Q

What is the Haldane Effect?

A

Describes O2 carriage

  • increased O2 causes the erythrocyte to release CO2 (occurs in the lungs)
  • deoxygenated (venous) blood can carry more CO2 than oxygenated (arterial) blood
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32
Q

What are the three primary causes of hypercapnia? Provide an example of each

A
  • Increased CO2 Production: sepsis, overfeeding, malignant hyperthermia, intense shivering, prolonged seizure activity, thyroid storm, burns
  • Decreased CO2 Elimination: airway obstruction, increased dead space, increased Vd/Vt, ARDS, COPD, respiratory center depression, drug overdose, inadequate NMB reversal
  • Rebreathing: exhausted soda lime, incompetent unidirectional valve in circle system, inadequate fresh gas flow in mapleson circuit
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33
Q

What are the four areas of the respiratory center in the brain?

A

Medullary Respiratory Centers:

  • dorsal respiratory center (active during inspiration –respiratory pacemaker)
  • ventral respiratory center (active during expiration)

Pontine Respiratory Centers:

  • pneumotaxic center - upper pons (inhibits DRC) – strong stimuli = rapid shallow breaths; weak stimuli = slow deep breaths
  • apneustic center - lower pons (stimulates the DRC
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34
Q

Describe the location and function of the central and peripheral chemoreceptors

A

Central Chemoreceptors:

  • located in the medulla
  • responds to H+ concentration in the CSF
  • H+ in CSF = function of the PaCO2 in the blood – PaCO2 = primary stimulus to breathe

Peripheral Chemoreceptors:

  • located in carotid bodies (nerves of Hering -> Glosopharyngeal n.)
  • located in aortic arch (Vagus n.)
  • respond to decreased O2, increased CO2, and increased H+
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35
Q

What reflex prevents over inflation of the lungs?

A

Hering-Breuer inflation reflex

-Lung inflation >1.5L -> CNX -> Inspiratory Off Switch -> Central Respiratory Activity -> Phrenic n. -> Inspiration Stops

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36
Q

What is hypoxic pulmonary vasoconstriction?

A

Minimizes shunt by reducing blood flow through poorly ventilated alveoli

  • low alveolar PO2 = the trigger that activates it
  • effect begins almost immediately and reaches its full effect after 15 min
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37
Q

What things impair hypoxic pulmonary vasoconstriction? What is the consequence of inhibition?

A
  • Halogenated anesthetics > 1-1.5 MAC
  • Phosphodiesterase inhibitors
  • Dobutamine
  • Vasodilators

Consequence = anything that inhibits it increases shunt (perfusion w/o ventilation)

*IV anesthetics do NOT inhibit

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38
Q

What does the diffusing capacity for carbon monoxide (DLCO) tell us?

A

It is used to assess how well the lung can exchange gas
-normal = 17-25 mL/CO/min/mmHg

Using Fick’s law of diffusion, the DLCO tells us two key characteristics about alveolar-capillary interface –> surface area and thickness
*anything that reduces alveolar surface area (emphysema) and/or increases thickness (pulm fibrosis or pulm edema) reduces DLCO

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39
Q

How is tobacco smoke harmful?

A
  • Increases SNS tone
  • Increases sputum production
  • Increases carboxyhemoglobin concentration
  • Increases the risk of infection
40
Q

What are the short and intermediate term benefits of smoking cessation?

A

Short Term does NOT reduce risk of postop pulmonary complications, but short term benefits include:

  • SNS stimulating effects of nicotine dissipate after 20-30 min
  • P50 returns to near normal in 12 hours (CaO2 improves)

Intermediate term:

  • return of normal pulm function requires at least 6 weeks (airway function, mucociliary clearance, sputum production, pulm immune function)
  • hepatic enzyme induction subsites after 6 weeks
41
Q

How are Pulmonary Function Tests affected in obstructive disease?

A
  • FEV1: normal or decreased if gas trapping
  • FVC: normal or decreased if gas trapping
  • FEV1 to FVC Ratio: decreased
  • REF 25-75%: decreased
  • Residual Volume: normal or increased in gas trapping
  • FRC: normal or increased if gas trapping
  • Total Lung Capacity: normal or increased if gas trapping
42
Q

How are Pulmonary Function Tests affected in restrictive disease?

A
  • FEV1: decreased
  • FVC: decreased
  • FEV1 to FVC Ratio: normal
  • REF 25-75%: normal
  • Residual Volume: decreased
  • FRC: decreased
  • Total Lung Capacity: decreased
43
Q

Which of the pulmonary flow loops belongs to each:

  • normal
  • obstructive disease
  • restrictive disease
  • fixed obstruction
A

Obstructive: i.e. COPD

Restrictive: i.e. Pulm Fibrosis

Fixed Obstruction: i.e. Tracheal Stenosis

  • extrathoracic = abnormal during inspiration
  • intrathoracic = abnormal during expiration
44
Q

What is the treatment for acute bronchospasm?

A
  • 100% FiO2
  • Deepen anesthetic (volatile agent, propofol, lidocaine, ketamine)
  • Inhaled beta-2 agonist (albuterol)
  • Inhaled anticholinergic (ipratropium)
  • Epinephrine 1 mcg/kg IV
  • Hydrocortisone 2-4 mg/kg IV (takes several hrs to take effect)
  • Aminophylline
  • Helium-Oxygen reduces airway resistance (decreases Reynold’s number)

*Montelukast is NOT used in treatment of acute bronchospasm

45
Q

What is alpha-1 antitrypsin deficiency? What is the treatment

A
  • Alveolar elastase is a naturally occurring enzyme that breaks down pulmonary connective tissue – enzyme is kept in check by alpha-1 antitrypsin (produced in liver
  • When there is a deficiency alveolar elastase can wreak havoc on pulmonary connective tissue – leads to panlobular emphysema
  • Liver transplant is the definitive treatment
46
Q

What is the goal and mechanical ventilation strategies for a pt with COPD?

A

Goal = prevent barotrauma and reduce air trapping

  • Low tidal volume (6-8 mL/kg IBW)
  • Increased expiratory time to minimize air trapping
  • Slow inspiratory flow rate optimizes V/Q matching
  • Low levels of PEEP are ok (as long as air trapping doesn’t occur)
47
Q

What is restrictive lung disease characterized by?

A

Decreased lung volumes and capacities

Decreased compliance

Intact pulmonary flow rates

48
Q

What are examples of acute and chronic intrinsic lung diseases?

A

Intrinsic Lung Disease affect lung parenchyma

Acute: aspiration, negative pressure pulm edema

Chronic: pulm fibrosis, sarcoidosis

49
Q

What are examples of extrinsic lung diseases?

A

Extrinsic Lung Disease affects areas around the lungs

Chest Wall/Mediastinum: kyphoscoliosis, flail chest, neuromuscular disorders, mediastinal mass

Increased Intraabdominal Pressure: pregnancy, obesity, ascites

50
Q

What are the risk factors for aspiration pneumonitis?

A
  • Trauma
  • Emergency Surgery
  • Pregnancy
  • GI obstruction
  • GERD
  • Peptic ulcer disease
  • Hiatal hernia
  • Ascites
  • Difficult airway management
  • Cricoid pressure
  • Impaired airway reflexes
  • head injury
  • Seizures
  • Residual NMB
51
Q

What are the pharmacologic prophylaxis of aspiration pneumonitis?

A
  • Antacids: sodium citrate, sodium bicarb, magnesium trisilicate
  • H2 Antagonists: ranitidine, cimetidine, famotidine
  • GI Stimulants: metoclopramide
  • PPIs: omeprazole, lansoprazole, pantoprazole
  • Antiemetics: droperidol, ondansetron
  • routine use of these as prophylaxis for pts NOT at risk for aspiration is NOT recommended
  • anticholinergics as prophylaxis is NOT recommended
52
Q

What is Mendelson’s syndrome?

A

A chemical aspiration pneumonitis – first described in OB pts receiving inhalation anesthesia

Risk Factors = Gastric pH <2.5 and Gastric volume >25 mL (0.4 mL/kg)

53
Q

What is the treatment of aspiration?

A
  • Tilt head down or to the side (1st action)
  • Suction upper airway
  • Lower airway suction is only useful for removing particulate matter (not helpful for chemical burn from gastric acid)
  • Secure airway to support oxygenation
  • Apply PEEP to reduce shunt
  • Admin bronchodilators to reduce wheezing
  • Admin lidocaine to reduce neutrophil response
  • Steroids probably won’t help
  • Antibiotics are only indicated if the patient develops a fever or an increased WBC count >48 hrs
54
Q

What is the pathophysiology of flail chest? How is it treated?

A
  • It is a consequence of blunt chest trauma w/ multiple rib fractures
  • Key characteristic = paradoxical movement of chest wall at site of fractures
  • Inspiration (negative intrathoracic pressure) = injured ribs move inward and collapse affected region
  • Expiration (positive intrathoracic pressure) = injured ribs move outward and affected region doesn’t empty

Treatment = epidural catheter or intercostal nerve blocks

55
Q

What is pulmonary hypertension? What are causes? What is the goal of anesthetic management?

A

Pulmonary HTN = mean PAP >25

Causes: COPD, left-sided heart disease, connective tissue disorders

Goals: optimize PVR

56
Q

What increases Pulmonary Vascular Resistance?

A
  • Hypoxemia
  • Hypercarbia
  • Acidosis
  • SNS stimulation
  • Pain
  • Hypothermia
  • Increased intrathoracic pressure (PEEP, atelectasis, mechanical ventilation)
  • Drugs (nitrous oxide, ketamine, desflurane)
57
Q

What decreases Pulmonary Vascular Resistance?

A
  • Increased PaO2
  • Hypocarbia
  • Alkalosis
  • Decreased intrathoracic pressure
  • Preventing coughing/straining
  • Spontaneous ventilation
  • Drugs (inhaled nitric oxide, nitroglycerin, phosphodiesterase inhibitors, prostaglandins PGE1 and PGI2, Calcium channel blockers, ACE inhibitors)
58
Q

What is the pathophysiology of carbon monoxide poisoning?

A
  • Carbon monoxide reduces the oxygen carrying capacity of blood (left shift)
  • It latches to the oxygen binding site on hgb w/ an affinity 200x that of O2
  • Oxidative phosphorylation is impaired and metabolic acidosis results
  • a co-oximeter (not pulse ox) measures CO
  • pts take on a cherry red appearance (not cyanosis)
  • SNS stimulation may be confused w/ light anesthesia or pain

*if soda lime is desiccated, then volatile anesthetics can produce CO (Des > Iso&raquo_space;> Sevo)

59
Q

What is the treatment of carbon monoxide poisoning?

A

100% FiO2 until CoHgb is less than 5% or for 6 hours

Hyperbaric oxygen if CoHgb >25% or pt is symptomatic

60
Q

What are the absolute indications for one lung ventilation?

A
  • Isolation of one lung to avoid contamination (infection, massive hemorrhage)
  • Control of distribution of ventilation (bronchopleural fistula, surgical opening of major airway, large unilateral lung cyst, life threatening hypoxemia due to lung disease)
  • Unilateral bronchopulmonary lavage (pulmonary alveolar proteinosis)
61
Q

What are the relative indications for one lung ventilation?

A
  • Surgical exposure (high priority): thoracic aortic aneurysm, pneumonectomy, thoracoscopy, upper lobectomy, mediastinal exposure
  • Surgical exposure (low priority): middle and lower lobectomy, esophageal resection, thoracic spinal surgery
  • Pulmonary edema s/p CABG or robotic mitral valve surgery
  • Severe hypoxemia due to lung disease
62
Q

How does anesthesia in the lateral decubitus position affect the V/Q relationship in the nondependent and dependent lung?

A

Nondependent Lung:

  • moves from flatter region (less compliant) to an area of better compliance (slope)
  • ventilation is optimal in this lung

Dependent Lung:

  • moves from the slope to the lower, flatter area of the curve (less compliant)
  • perfusion is best in this lung (effect of gravity)
  • reduction of alveolar volume contributes to atelectasis

*net effect is ventilation is better in nondependent lung and perfusion is better in dependent lung – creates V/Q mismatch and increases risk of hypoxemia during OLV

63
Q

How do you manage hypoxemia during OLV?

A
  1. 100% FiO2
  2. Confirm DLT position with bronchoscope
  3. CPAP 2-10 cmH2O to nondependent (non-ventilated) lung
  4. PEEP 5-10 cmH2O to dependent (ventilated) lung
  5. Alveolar recruitment maneuver
  6. Clamp pulmonary artery to the non-dependent lung
  7. Resume two lung ventilation

*if hypoxia is severe it is prudent to resume two lung ventilation promptly

64
Q

What are the five indications for the use of a bronchial blocker?

A

Indicated for pts requiring lung separation who:

  • children <8 yo (smallest DLT = 26F for 8-10 yo)
  • require nasotracheal intubation
  • have a tracheostomy
  • have a single lumen ETT in place
  • require intubation after surgery and you want to avoid changing DLT to a single lumen at the end of the case
65
Q

How can the lumen of the bronchial blocker be used during OLV?

A
  • Insufflate oxygen into the non-ventilated lung
  • Suction air from the non-ventilated lung (improves surgical exposure)

*do NOT use to ventilate or suction blood, pus, or secretions from non-ventilated lung

66
Q

What is mediastinoscopy and why is it performed?

A

Performed to obtain biopsy of the paratracheal lymph nodes at the level of the carina

Helps the surgeon stage the tumor before lung resection

67
Q

What are the potential complications of mediastinoscopy? What is the most common?

A
  • Hemorrhage (#1 most common)
  • Pneumothorax (#2 most common)
  • Thoracic aorta -> hemorrhage and reflex bradycardia
  • Innominate artery -> decreased carotid blood flow and cerebral blood
  • Vena cava -> hemorrhage
  • Trachea -> airway obstruction
  • Thoracic duct -> chylothorax
  • Phrenic and recurrent laryngeal nerve injury
68
Q

Where should you place the pulse ox and NIBP for mediastinoscopy?

A

Pulse Ox on right upper extremity
-if scope compresses innominate artery -> waveform dampens or disappears

NIBP on left upper extremity
-if scope compresses innominate artery -> BP reading on left arm won’t be affected (allows BP measurements even if artery is compressed)

69
Q

Describe the Mallampati score

A

Assesses the oropharyngeal space — Remember PUSH

Class I: Posterior pillars, Uvula, Soft palate, Hard palate
Class II: __, Uvula, Soft palate, Hard palate
Class III: ___, ___, Soft palate, Hard palate
Class IV: ___, ___, ___, Hard palate

70
Q

Describe the inter-incisor gap. What is normal?

A

Patient’s ability to open the mouth directly affects ability to align the oral, pharyngeal, and laryngeal axes
-small inter-incisor gap creates a more acute angle between oral and glottic openings, increasing difficulty of intubation

Normal = 2-3 finger breaths or 4cm

71
Q

What is the thyromental distance? What values suggest an increased risk of difficult intubation?

A

Thyromental distance helps estimate size of submandibular space
-tip of thyroid cartilage to tip of mentum

Laryngoscopy may be more difficult if TMD is less than 6cm (3 fingerbreadths) or greater than 9cm

72
Q

What is the mandibular protrusion test? What values suggest an increased risk of difficult intubation?

A

Assesses function of temporomandibular joint
-ask pt to sublux the jaw and the position of the lower teeth compared to the position to the top

Class 1: pt can move LI past UI and bite the upper lip
Class 2: pt can move LI in line with UI
Class 3: pt cannot move LI past UI Increased risk of difficult intubation

73
Q

What conditions impair atlanto-occipital joint mobility?

A
  • Degenerative joint disease
  • Rheumatic arthritis
  • Ankylosing spondylitis
  • Trauma
  • Surgical fixation
  • Klippel-Feil
  • Down syndrome
74
Q

What is the Cormack and Lehanne score?

A

Helps measure the view we obtain during direct vision laryngoscopy

Grade I through Grade IV

75
Q

What are the five risk factors for difficult mask ventilation?

A

BONES

  • Beard
  • Obese (BMI >26)
  • No teeth
  • Elderly (age >55)
  • Snoring
76
Q

What are the 10 risk factors for difficult tracheal intubation?

A
  • Small mouth opening
  • Palate is narrow with a high arch
  • Long upper incisors
  • Interincisor distance <3cm
  • Mallampati class III or IV
  • Mandibular protrusion test class 3
  • Poor compliance of submandibular space
  • Thyromental distance <6cm or >9cm
  • Neck is thick and short
  • Limited AO joint mobility (can’t touch chin to chest or extend neck)
77
Q

What are the six risk factors for difficult supraglottic device placement?

A
  • Limited mouth opening
  • Upper airway obstruction
  • Altered pharyngeal anatomy (prevent seal)
  • Poor airway compliance (requires excessive PIP)
  • Increased airway resistance (requires excessive PIP)
  • Lower airway obstruction
78
Q

What are five risk factors for difficult invasive airway placement?

A
  • Abnormal neck anatomy (tumor, hematoma, abscess, hx of radiation)
  • Obesity (can’t ID cricothyroid membrane)
  • Short neck (can’t ID cricothyroid membrane)
  • Limited access to cricothyroid membrane (halo, neck flexion deformity)
  • Laryngeal trauma
79
Q

What are the EBP guidelines for preop fasting?

A

2 hours = Clear Liquids
4 hours = Breast Milk
6 hours = Nonhuman Milk, Infant Formula, Solid Food
8 hours = Fried or Fatty Foods

*ingestion of clear liquids 2 hours before surgery reduces gastric volume and increases gastric pH

80
Q

What is angioedema?

A

Result of increased vascular permeability that can lead to swelling of the face, tongue, and airway

Airway obstruction is an extreme concern

81
Q

What are two common causes of angioedema? What is the treatment of each?

A

Anaphylaxis – treat with Epi, antihistamines, and steroids

ACE Inhibitors or C1 Esterase Deficiency – treat with icatibant, ecallantide, FFP, or C1 esterase concentrate

82
Q

What is Ludwig’s angina?

A

Bacterial infection characterized by a rapidly progressing cellulitis in the floor of the mouth

  • inflammation and edema compress the submandibular, submaxillary, and sublingual spaces
  • most significant concern is a posterior displacement of the tongue resulting in complete, supraglottic airway obstruction
83
Q

What is he best way to secure the airway in a pt with Ludwig’s angina?

A

With the patient awake

  • awake nasal intubation
  • awake tracheostomy
84
Q

What are the 4 types of oropharyngeal airways? Which are best for fiberoptic intubation?

A
  • Guedel (what’s at UIHC)
  • Berman
  • Williams (for blind orotracheal intubation or fiberoptic intubation)
  • Ovassapian (for fiberoptic intubation)
85
Q

When is a nasopharyngeal airway contraindicated?

A
  • Cribriform plate injury (risk of brain injury): LeFort 2 or 3 fracture, Basilar skull fracture, CSF rhinorrhea, Raccoon eyes, Periorbital edema
  • Coagulopathy (risk epistaxis)
  • Previous transsphenoidal hypophysectomy
  • Previous Caldwell-Luc procedure
  • Nasal fracture
86
Q

What is the maximum recommended cuff pressures for and ETT and LMA?

A

ETT < 25 cmH2O

LMA < 60 cmH2O

87
Q

What is the largest size ETT that can pass through each LMA size?

A 
Size 1 : 3.5 ETT
Size 1.5 : 4.0
Size 2 : 4.5
Size 2.5 : 5.0
Size 3 : 6.0
Size 4 : 6.0
Size 5 : 7.0
88
Q

What is the maximum recommended peak inspiratory pressures for an LMA-Unique, LMA-Proseal, and LMA-Supreme?

A

LMA-Unique = < 20 cmH2O

LMA-ProSeal = < 30 cmH2O

LMA-Supreme = < 30 cmH2O

89
Q

What are the five indications for the Bullard Laryngoscope?

A

Bullard laryngoscope = rigid, fiberoptic device used for indirect laryngoscopy

  • Small mouth opening (minimum = 7mm)
  • Impaired cervical spine mobility
  • Short, thick neck
  • Teacher Collins syndrome
  • Pierre-Robin sequence
90
Q

When is the best time to use an Eschmann introducer (Bougie)?

A

When a grade 3 view is obtained during laryngoscopy (grade 2 is the next best time)

*During a grade 4 view, the likelihood of successful intubation is unacceptably low

91
Q

What is the proper placement of the lighted stylet?

A

When lighted stylet is in the trachea, the light has to travel through less tissue, so you’ll observe a well-defined circumscribed glow below the thyroid prominence

-when it is in the esophagus - more diffuse transillumination of the neck without circumscribed glow

92
Q

What are two indications for retrograde intubation?

A

Unstable cervical spine (most common use)

Upper airway bleeding – can’t visualize glottis

*use when intubation has failed but ventilation is still possible

93
Q

What are the pros and cons of awake extubation?

A

PROS:

  • airway reflexes intact
  • ability to maintain airway patency
  • decrease risk of aspiration

CONS:

  • increased CV and SNS stimulation
  • increased coughing
  • increased intracranial pressure
  • increased intraoccular pressure
  • increased intraabdominal pressure
94
Q

What are the pros and cons of deep extubation?

A

PROS:

  • decreased CV and SNS stimulation
  • decreased coughing

CONS:

  • airway reflexes are ineffective
  • increased risk of airway obstruction
  • increased risk of aspiration
95
Q

When is the best time to use an airway exchanger catheter? What can you do with it?

A

It is a long, thin, hollow tube that maintains direct access to the airway following tracheal extubation
-Common device used to manage extubation of the difficult airway

You can also:

  • measure EtCO2
  • Jet ventilation (via luer-lock adapter)
  • oxygen insufflation (via 15mm adapter)

APEX Study Guide (13 decks)

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