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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
Normal Tidal Volumes
500 mL
26
Normal inspiratory reserve volume
3,000 mL
27
Normal end residual volume
1,100 mL
28
Normal residual volume
1,200 mL
29
Define FEV1 and the normal value
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
30
Define forced vital capacity and its normal value
Volume of air exhaled after a maximum inhalation Male = 4.8 L Female = 3.7 L
31
FEV1 to FVC ratio normal value and use
75 - 80% predicted value Used to distinguish between restrictive and obstructive <70% = obstructive normal with restrictive
32
Forced expiratory flow at 25-75% vital capacity is:
aka Mid maximal expiratory flow rate Measure airflow in the middle of FEV Normal: 100 +/- 25% predicted value
33
What is FEV25-75% used to indicate?
Small airway disease - most sensitive indicator Usually reduced with obstructive Usually normal with restrictive
34
Maximum voluntary ventilation is:
Endurance test Max volume of air inhaled and exhaled over 1 minute Normal Male= 140-180L Normal Female = 80-120L
35
Another name for FEV 25-75%
Mid maximal expiratory flow rate (MMEF)
35
Another name for FEV 25-75%
Mid maximal expiratory flow rate (MMEF)
35
36
Postop pulmonary comp risk factors: patient
age > 60 ASA > 2 CHF COPD Cigarette smoking (>40 pack years
37
Postop pulmonary comp risk factors: procedure
aortic > thoracic > upper abdominal ~ neuro ~ peripheral vascular > emergency general anesthesia duration of surgery > 2 hours
38
Postop pulmonary comp risk factors: diagnostic testing
albumin < 3.5 g/dL -indicates poor nutritional status
39
Factors NOT shown to increase postop pulmonary comps
mild/moderate asthma arterial blood gas analysis pulmonary function testing
40
Smoking: respiratory effects
increase risk for pulmonary disease decreased mucociliary clearance airway hyperactivity reduced pulmonary immune function
41
Smoking: CV effects
leads to CV disease carbon monoxide -> decreased DO2 catecholamine release coronary vasoconstriction decreased exercise healing
42
Smoking: effects
impaired wound healing
43
Smoking: short term effects of stopping
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
Smoking: intermediate term effects of stopping
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
What is the best way to reverse anesthesia-induced atelectasis?
Alveolar recruitment methods
46
How do you perform an effective alveolar recruitment method?
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
Most common ABG finding in asthma
respiratory alkalosis with hypocarbia
47
What does an elevated PaCO2 in an asthmatic suggest?
Air trapping -> respiratory muscle fatigue -> impending respiratory failure
48
What EKG changes may occur in a patient with asthma?
Right axis deviation due to RV strain and increased workload from increased PVR
49
Is tracheal intubation the first choice in a patient with asthma?
No! Use regional, mask, or LMA if appropriate. If tube, consider deep extubation.
50
What drugs can be given to decrease airway reactivity on extubation?
Opioids Lidocaine 1-1.5 mg/kg 1-3 mins prior to extubation
51
Ventilator settings in asthmatic
Limit inspiratory time Prolong expiratory time Tolerate moderate permissive hypercapnia
52
What drugs do you avoid in an asthmatic?
Histamine releasing drugs: Sux, atracurium, morphine, meperidine, etc.
53
What is the role of H1 and H2 antagonists in the patient with asthma?
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
List differential diagnoses concerning intraop bronchospasm and wheezing.
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
How does bronchospasm present?
Wheezing Decreased breath sounds Increased peak inspiratory pressure with normal plateau pressures (decreased dynamic pulmonary compliance) Increased alpha angle on capnograph (expiratory upslope)
56
How do you treat bronchospasm?
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
Describe the pathophysiology of COPD.
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
Describe the acid base changes with COPD
Respiratory acidosis due to chronic elevation of PaCO2 Metabolic alkalosis (compensatory) due to reabsorption of bicarbonate
59
What results if you restore PaCO2 to normal using mechanical ventilation in a patient with COPD?
Risk of severe alkalosis due to amount of bicarb in blood not changing Reduced O2 unloading and apnea result
60
How is chronic bronchitis diagnosed?
Presence of cough and sputum for more than 3 months in a span of 2 years
61
What lung changes occur with chronic bronchitis?
hypertrophied bronchial mucus glands chronic inflammation air flow is limited during exhalation
62
Why does erythrocytosis result from chronic bronchitis?
RBCs are overproduced in compensation of V/Q mismatch and hypoxia. Increased blood viscosity and myocardial work result.
63
How does chronic bronchitis lead to cor pulmonale?
Chronic hypoxemia and hypercarbia -> pulmonary HTN -> RV strain and right axis deviation -> cor pulmonale
64
What happens to left heart function as a result of chronic bronchitis?
It is normal (normal PAOP)
65
What is the most efficient drug to improve pulmonary hypertension and erythrocytosis in chronic bronchitis?
Oxygen
66
How does chronic bronchitis affect the liver?
A weakened right heart causes back pressure on the liver that leads to congestion and ascites
67
What lung changes occur with emphysema?
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
What O2 and CO2 changes occur in emphysema?
Normal or slightly reduced PaO2 Normal or decreased PaCO2 (hyperventilation) Late disease -> increased PVR due to hypoxemia and hypercarbia -> right heart failure
69
What protein deficiency can cause emphysema?
Alpha-1 antitrypsin deficiency
70
How does Alpha-1 antitrypsin deficiency cause emphysema?
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
What lung spirometry changes occur in COPD?
Increased: RV, FRC, TLC Decreased: FEV1, FEV1/FVC ratio, FEF 25-75%
72
What FEV1/FVC ratio after bronchodilator therapy is diagnostic of COPD?
<70%
73
What are the recommended ventilator settings in COPD?
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
What can happen if using N2O in a patient with COPD?
Can rupture pulmonary bleb -> pneumothorax
75
Three characteristics of restrictive lung disease:
Decreased lung volumes and capacities Decreased compliance Intact pulmonary flow rates
76
Two spirometry tests diagnostic of restrictive lung disease:
FEV1 and FVC <70%
77
Ventilator settings for restrictive lung disease:
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
Three potential problems of aspiration:
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
What is Mendelson's syndrome?
Chemical aspiration pneumonitis first described in OB patients. Characterized by gastric pH <2.5 and gastric volume > 25 mL
80
Pharmacologic prophylaxis of aspiration:
Antacids: sodium bicarb, sodium citrate, magnesium trisilicate H2 antagonists: ranitidine, cimetidine, famotidine GI stimulants: metoclopramide PPIs: omeprazole, pantoprazole, lansoprazole Antiemetics: ondansetron, droperidol
81
Is routine use of prophylaxis against aspiration recommended?
No
82
Diagnosis of aspiration:
Hallmark = hypoxemia dyspnea, tachypnea, cyanosis, tachycardia, htn
83
Aspiration treatment includes:
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
When are antibiotics indicated for aspiration?
Only if WBCs are increased or if the patient develops a fever >48H after the incident
85
Hallmark characteristics of a pneumothorax include:
Hypoxemia Increased airway pressures Tachycardia Hotn Increased CVP POC Ultrasound = absence of lung sliding
86
How does a tension pneumothorax affect hemodynamics?
Increased intrathoracic pressure compresses mediastinal structures and decreases venous return, cardiac output, and BP
87
What is the emergency treatment for a tension pneumothorax?
14g angiocath insertion at -2nd intercostal space at mid-clavicular line -4th or 5th intercostal space at anterior axillary line
88
What drugs can be given via ETT?
NAVEL - narcan, atropine, vasopressin, epinephrine, lidocaine
89
Normal vital capacity:
65-75 mL/kg
90
Normal inspiratory force:
75-100 cm/H2O
91
Normal PaO2:
>72 mmHg
92
Normal A-a gradient:
<10-15
93
Normal PaO2 at 100% O2:
>400 mmHg
94
Normal A-a gradient at 100% FiO2:
<100 mmHg
95
What EKG characteristics are present in Wolf-Parkinson-White?
Delta wave caused by ventricular preexcitation Short PRI <0.12s Wide QRS Possible T wave inversion
96
Why does a delta wave appear on the EKG in Wolf-Parkinson-White syndrome?
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
Describe the MOA of adenosine:
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
Discuss the concentration effect:
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
What two components make up the concentration effect?
1. Concentrat"ing" effect 2. Augmented gas inflow effect
100
Discuss the concentratING effect:
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
Discuss tidal breathing pressure changes:
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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