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Respiratory Flashcards

1
Q

50% decrease in airflow, >10 seconds, more than 15 seconds/hour of sleep, results in 4% decrease in O2 sats

A

hypopnea

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2
Q

Snoring, complete or partial obstruction of the airway during sleep + frequent episodes of apnea or hypopnea

A

Obstructive sleep apnea

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3
Q

Obesity, awake arterial hypercapnia, insufficient alveolar impairment indecent of any other pulmonary disease

A

Obesity hypoventilation syndrome

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4
Q

Obesity, awake arterial hypercapnia, insufficient alveolar impairment indecent of any other pulmonary disease

A

Obesity hypoventilation syndrome

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5
Q

What is hepatopulmonary syndrome?

A

Hypoxemia due to liver disease

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6
Q

What are the defining characteristics of hepatopulmonary disease?

A
  1. Presence of portal hypertension
  2. Increase Aa gradient
  3. Intrapulmonary vasodilation
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7
Q

Bronchoconstriction pathway

A

PNS- vagal stimulation
released Ach acts on M3 to stim Gq
phospholipase C is activated
converts PIP2 to IP3
IP3 stims Ca release from sarcoplasmic reticulum
bronchoconstriction results

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8
Q

How is bronchoconstriction from PNS stimulation turned off

A

IP3 phosphatase deactivates IP3 to IP2

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9
Q

How do mast cells promote bronchoconstriction:

A

Coughing, allergy, or infection activate IgE, cytokines, and complement -> amplification of allergic response

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10
Q

Do non-cholinergic C-fibers promote bronchodilator or bronchoconstriction?

A

bronchoconstriction

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11
Q

Identify Mast Cell mediators and their respective receptors

A

Histamine -> Histamine 1
Prostaglandins D2 and F2 -> Thromboxane-specific prostanoid receptor
Leukotrienes C4, D4, and E4 -> CysLT1
Platelet activating factor -> PAF
Bradykinin -> Bradykinin 2

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12
Q

Name C-fiber mediators and their respective receptors:

A

Substance P -> Neurokinin-2
Neurokinin A -> GCRP
Calcitonin gene related peptide

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13
Q

Bronchodilation pathway due to Circulating Catecholamines

A

B2 Receptors activated by circulating catecholamines
Gs protein activated
adenylate cyclase activated
cAMP activated
cAMP and protein kinase A reduce Ca release from sarcoplasmic reticulum
smooth muscle contraction decreased
bronchodilation results

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14
Q

How is bronchodilation from circulating catecholamines turned off

A

Phosphodiesterase 3 deactivates cAMP by converting it to ATP

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15
Q

NO and bronchodilation

A

potent smooth muscle relaxant
vasoactive intestinal peptide released onto airway smooth muscle by non-cholinergic PNS nerves
NO production increased
stimulates cGMP
smooth muscle relaxation and bronchodilation result

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16
Q

Two ways B2 Agonists cause bronchodilation:

A

B2 stim -> increased cAMP -> decreased iCa+2

Stabilizes mast cell membranes -> decreased mediator release

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17
Q

B2 agonist examples and side effects

A

Albuterol, salmeterol, metproteronol

tachycardia, dysrhythmias, hypoK, hyperglycemia, tremors

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18
Q

How do anticholinergics promote bronchodilation:

A

Antagonize M3R -> decrease IP3 -> decrease iCa+2

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19
Q

Two ways inhaled corticosteroids cause bronchodilation:

A

Stimulate intracellular steroid receptors

Regulate inflammatory protein synthesis (results in decreased airway inflammation and decreased airway hyperresponsiveness

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20
Q

Cromolyn and bronchodilation

A

Mast cell membrane stabilizer
(blocks cytokines, leukotrienes, histamine)?

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21
Q

Leukotriene modifier MOA

A

Inhibit 5-lipooxygenase enzyme (decreased leukotriene synthesis)

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22
Q

Three ways methylxanthines work and give an example

A

Theophylline

Inhibit PDE -> increase cAMP
Increase endogenous catecholamine release
Inhibit adenosine receptors

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23
Q

Define static lung volumes

A

How much air the lungs can hold at one time

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24
Q

Define Dynamic lung volumes

A

How quickly air can be moved in and out of the lungs over time

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25
Q

Normal Tidal Volumes

A

500 mL

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26
Q

Normal inspiratory reserve volume

A

3,000 mL

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27
Q

Normal end residual volume

A

1,100 mL

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28
Q

Normal residual volume

A

1,200 mL

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29
Q

Define FEV1 and the normal value

A

Forced Expiratory Volume in 1 second
Volume let out in 1 second after a maximum inhalation
-depends on patient effort
-declines with age

normal= >80% predicted value

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30
Q

Define forced vital capacity and its normal value

A

Volume of air exhaled after a maximum inhalation
Male = 4.8 L
Female = 3.7 L

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31
Q

FEV1 to FVC ratio normal value and use

A

75 - 80% predicted value
Used to distinguish between restrictive and obstructive
<70% = obstructive
normal with restrictive

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32
Q

Forced expiratory flow at 25-75% vital capacity is:

A

aka Mid maximal expiratory flow rate

Measure airflow in the middle of FEV

Normal: 100 +/- 25% predicted value

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33
Q

What is FEV25-75% used to indicate?

A

Small airway disease - most sensitive indicator
Usually reduced with obstructive
Usually normal with restrictive

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34
Q

Maximum voluntary ventilation is:

A

Endurance test
Max volume of air inhaled and exhaled over 1 minute
Normal Male= 140-180L
Normal Female = 80-120L

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35
Q

Another name for FEV 25-75%

A

Mid maximal expiratory flow rate (MMEF)

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35
Q

Another name for FEV 25-75%

A

Mid maximal expiratory flow rate (MMEF)

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35
Q
A
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36
Q

Postop pulmonary comp risk factors: patient

A

age > 60
ASA > 2
CHF
COPD
Cigarette smoking (>40 pack years

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37
Q

Postop pulmonary comp risk factors: procedure

A

aortic > thoracic > upper abdominal ~ neuro ~ peripheral vascular > emergency

general anesthesia
duration of surgery > 2 hours

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38
Q

Postop pulmonary comp risk factors: diagnostic testing

A

albumin < 3.5 g/dL
-indicates poor nutritional status

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39
Q

Factors NOT shown to increase postop pulmonary comps

A

mild/moderate asthma
arterial blood gas analysis
pulmonary function testing

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40
Q

Smoking: respiratory effects

A

increase risk for pulmonary disease
decreased mucociliary clearance
airway hyperactivity
reduced pulmonary immune function

41
Q

Smoking: CV effects

A

leads to CV disease
carbon monoxide -> decreased DO2
catecholamine release
coronary vasoconstriction
decreased exercise healing

42
Q

Smoking: effects

A

impaired wound healing

43
Q

Smoking: short term effects of stopping

A

carbon monoxide t1/2 = 4-6 hours
P50 returns to near normal in 12 hours
short term cessation not effective in reducing pulmonary complications

44
Q

Smoking: intermediate term effects of stopping

A

Pulmonary function return takes at least 6 weeks. Includes:
airway function
mucociliary clearance
sputum production
pulmonary immune function
hepatic enzyme induction subsides after 6 weeks

45
Q

What is the best way to reverse anesthesia-induced atelectasis?

A

Alveolar recruitment methods

46
Q

How do you perform an effective alveolar recruitment method?

A

Peak airway pressure 30 cm H2O required to initially reopen atelectatic region
Then increase PIP to 40 cm H2O for 8 seconds
Apply method to open alveoli, then apply PEEP to keep open

46
Q

Most common ABG finding in asthma

A

respiratory alkalosis with hypocarbia

47
Q

What does an elevated PaCO2 in an asthmatic suggest?

A

Air trapping -> respiratory muscle fatigue -> impending respiratory failure

48
Q

What EKG changes may occur in a patient with asthma?

A

Right axis deviation due to RV strain and increased workload from increased PVR

49
Q

Is tracheal intubation the first choice in a patient with asthma?

A

No! Use regional, mask, or LMA if appropriate.
If tube, consider deep extubation.

50
Q

What drugs can be given to decrease airway reactivity on extubation?

A

Opioids
Lidocaine 1-1.5 mg/kg 1-3 mins prior to extubation

51
Q

Ventilator settings in asthmatic

A

Limit inspiratory time
Prolong expiratory time
Tolerate moderate permissive hypercapnia

52
Q

What drugs do you avoid in an asthmatic?

A

Histamine releasing drugs:
Sux, atracurium, morphine, meperidine, etc.

53
Q

What is the role of H1 and H2 antagonists in the patient with asthma?

A

An H2 antagonist (ranitidine and famotidine) allows for unopposed H1 stimulation which can lead to bronchospasm.
However, an H2 antagonist may be used in GERD-induced asthma.

54
Q

List differential diagnoses concerning intraop bronchospasm and wheezing.

A

Mechanical obstruction of ETT (biting, kinked, secretions, cuff overinflation)
Light anesthesia (coughing + straining -> decreased FRC)
Bronchospasm
Acute asthmatic attack
Pulmonary embolism
Pulmonary edema
Pulmonary aspiration
Endobronchial intubation
Pneumothorax

55
Q

How does bronchospasm present?

A

Wheezing
Decreased breath sounds
Increased peak inspiratory pressure with normal plateau pressures (decreased dynamic pulmonary compliance)
Increased alpha angle on capnograph (expiratory upslope)

56
Q

How do you treat bronchospasm?

A

100% FiO2
Deepen anesthetic (volatile agent, propofol, lidocaine, ketamine)
Short acting inhaled B2 agonist (albuterol)
Inhaled ipratroprium
Epinephrine 1 mcg/kg IV
Hydrocortisone 2-4 mg/kg IV (doesn’t treat acute, prevents problems later)
Aminophylline (theophylline not great for acute)
Heliox to reduce airway resistance

57
Q

Describe the pathophysiology of COPD.

A

Loss of lung elasticity = decreased recoil -> air trapping -> increased residual volume

Reduced airway rigidity -> airway collapse during exhalation -> air trapping

Increase gas velocity through narrow airways -> decreased pressure in airways -> airway collapse -> air trapping

Secretions -> airflow obstruction and bronchospasm

58
Q

Describe the acid base changes with COPD

A

Respiratory acidosis due to chronic elevation of PaCO2
Metabolic alkalosis (compensatory) due to reabsorption of bicarbonate

59
Q

What results if you restore PaCO2 to normal using mechanical ventilation in a patient with COPD?

A

Risk of severe alkalosis due to amount of bicarb in blood not changing
Reduced O2 unloading and apnea result

60
Q

How is chronic bronchitis diagnosed?

A

Presence of cough and sputum for more than 3 months in a span of 2 years

61
Q

What lung changes occur with chronic bronchitis?

A

hypertrophied bronchial mucus glands
chronic inflammation
air flow is limited during exhalation

62
Q

Why does erythrocytosis result from chronic bronchitis?

A

RBCs are overproduced in compensation of V/Q mismatch and hypoxia. Increased blood viscosity and myocardial work result.

63
Q

How does chronic bronchitis lead to cor pulmonale?

A

Chronic hypoxemia and hypercarbia -> pulmonary HTN -> RV strain and right axis deviation -> cor pulmonale

64
Q

What happens to left heart function as a result of chronic bronchitis?

A

It is normal (normal PAOP)

65
Q

What is the most efficient drug to improve pulmonary hypertension and erythrocytosis in chronic bronchitis?

A

Oxygen

66
Q

How does chronic bronchitis affect the liver?

A

A weakened right heart causes back pressure on the liver that leads to congestion and ascites

67
Q

What lung changes occur with emphysema?

A

Enlargement and destruction of airways distal to the terminal bronchioles

Decreased surface area for gas exchange results -> dead space increases

Pulmonary capillary beds are destroyed -> contribute to pulmonary htn due to same amount of blooding traveling to smaller amount of vessels

68
Q

What O2 and CO2 changes occur in emphysema?

A

Normal or slightly reduced PaO2
Normal or decreased PaCO2 (hyperventilation)

Late disease -> increased PVR due to hypoxemia and hypercarbia -> right heart failure

69
Q

What protein deficiency can cause emphysema?

A

Alpha-1 antitrypsin deficiency

70
Q

How does Alpha-1 antitrypsin deficiency cause emphysema?

A

Alpha-1 antitrypsin deficiency is an enzyme made in the liver. Alpha-1 antitrypsin usually blocks alveolar elastase breakdown in pulmonary connective tissue. Deficiency allows overactivity of breakdown and results in destruction of pulmonary connective tissue -> pan lobular emphysema

71
Q

What lung spirometry changes occur in COPD?

A

Increased: RV, FRC, TLC
Decreased: FEV1, FEV1/FVC ratio, FEF 25-75%

72
Q

What FEV1/FVC ratio after bronchodilator therapy is diagnostic of COPD?

A

<70%

73
Q

What are the recommended ventilator settings in COPD?

A

Vt 6-8 mL/kg IBW
Slow inspiratory flow
PEEP to maintain airway patency in alveoli (prevent atelectasis)
Increase expiratory time -> minimize air trapping and auto-PEEP
Caution volume cycled ventilation -> higher PIP from less time to get same volume of gas in)

74
Q

What can happen if using N2O in a patient with COPD?

A

Can rupture pulmonary bleb -> pneumothorax

75
Q

Three characteristics of restrictive lung disease:

A

Decreased lung volumes and capacities
Decreased compliance
Intact pulmonary flow rates

76
Q

Two spirometry tests diagnostic of restrictive lung disease:

A

FEV1 and FVC <70%

77
Q

Ventilator settings for restrictive lung disease:

A

Minimize barotrauma
-smaller Vt (6 mL/kg IBW)
-faster RR (14-18 breaths/min)
-PIP < 30 cm H2O
-prolonged inspiratory time (I:E ratio 1:1)

78
Q

Three potential problems of aspiration:

A

Airway obstruction due to gastric contents entering airway
Bronchospasm/impaired gas exchange due to chemical burn of airway and lung parenchyma from gastric contents
Bacterial infection due to entry of infectious material (infection does not always occur)

79
Q

What is Mendelson’s syndrome?

A

Chemical aspiration pneumonitis first described in OB patients.
Characterized by gastric pH <2.5 and gastric volume > 25 mL

80
Q

Pharmacologic prophylaxis of aspiration:

A

Antacids: sodium bicarb, sodium citrate, magnesium trisilicate

H2 antagonists: ranitidine, cimetidine, famotidine

GI stimulants: metoclopramide

PPIs: omeprazole, pantoprazole, lansoprazole

Antiemetics: ondansetron, droperidol

81
Q

Is routine use of prophylaxis against aspiration recommended?

A

No

82
Q

Diagnosis of aspiration:

A

Hallmark = hypoxemia
dyspnea, tachypnea, cyanosis, tachycardia, htn

83
Q

Aspiration treatment includes:

A

First action - tilt head down or to side
Upper airway suction to remove debris
Lower airway suction only to remove debris; not useful for chemical burn due to gastric acid
Secure the airway, support oxygenation
PEEP to reduce shunt
Bronchodilators to decrease wheezing
IV Lidocaine to reduce the neutrophil response

84
Q

When are antibiotics indicated for aspiration?

A

Only if WBCs are increased or if the patient develops a fever >48H after the incident

85
Q

Hallmark characteristics of a pneumothorax include:

A

Hypoxemia
Increased airway pressures
Tachycardia
Hotn
Increased CVP
POC Ultrasound = absence of lung sliding

86
Q

How does a tension pneumothorax affect hemodynamics?

A

Increased intrathoracic pressure compresses mediastinal structures and decreases venous return, cardiac output, and BP

87
Q

What is the emergency treatment for a tension pneumothorax?

A

14g angiocath insertion at
-2nd intercostal space at mid-clavicular line
-4th or 5th intercostal space at anterior axillary line

88
Q

What drugs can be given via ETT?

A

NAVEL - narcan, atropine, vasopressin, epinephrine, lidocaine

89
Q

Normal vital capacity:

A

65-75 mL/kg

90
Q

Normal inspiratory force:

A

75-100 cm/H2O

91
Q

Normal PaO2:

A

> 72 mmHg

92
Q

Normal A-a gradient:

A

<10-15

93
Q

Normal PaO2 at 100% O2:

A

> 400 mmHg

94
Q

Normal A-a gradient at 100% FiO2:

A

<100 mmHg

95
Q

What EKG characteristics are present in Wolf-Parkinson-White?

A

Delta wave caused by ventricular preexcitation
Short PRI <0.12s
Wide QRS
Possible T wave inversion

96
Q

Why does a delta wave appear on the EKG in Wolf-Parkinson-White syndrome?

A

WPW bypasses the AV node and forfeits the slowing of conduction at the node. Therefore, the impulse travels through the AV node and accessory pathway at the same time, leading to early arrival at the ventricle characterized by the upsloping delta wave.

97
Q

Describe the MOA of adenosine:

A

Adenosine is an endogenous nucleoside that slows AV node conduction. Stimulation of the cardiac adenosine-1 receptor causes K efflux -> hyper polarizes the cell membrane -> slow AV node conduction

98
Q

Discuss the concentration effect:

A

higher concentration of inhalation anesthetic delivered to the alveolus (FA), the faster the onset of action, aka over pressuring. (only relevant for nitrous oxide)

99
Q

What two components make up the concentration effect?

A
  1. Concentrat”ing” effect
  2. Augmented gas inflow effect
100
Q

Discuss the concentratING effect:

A

nitrogen is primary gas in lungs when breathing room air
nitrous oxide is ~34 times more soluble in blood than nitrogen
when N2O is introduced in lungs, the volume of N2O going from the alveolus to the pulmonary blood is much higher than the nitrogen moving in the opposite direction
this leads to alveolus shrinkage and relative increase in FA due to reduced alveolar volume

101
Q

Discuss tidal breathing pressure changes:

A

Transpulmonary pressure = always positive (keeps airway open)
Intrapleural pressure = always negative (keeps lungs inflated)
Alveolar pressure = slightly negative during inspiration and slightly positive during expiration

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