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Anesthesia Pharm > Week 10 - Pulmonary Phys and Pharm > Flashcards

Week 10 - Pulmonary Phys and Pharm Flashcards

1
Q

What is gas exchange in the lungs determined by?

A

Ventilation and Perfusion

  • appropriate matching of these two independent variables
  • gases must also be able to DIFFUSE across the alveolar membranes
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2
Q

What structures of the lungs are apart of the conducting airways?

A

Trachea

Segmental Bronchi

Non-respiratory Subsegmental Bronchi (Bronchioles)

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3
Q

What structures of the lungs are apart of the respiratory unit?

A

Respiratory Subsegmental Bronchi (Bronchioles)

Alveolar Ducts

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4
Q

What are the components of the respiratory membrane?

A
  • A layer of fluid lining the alveolus that contains surfactant
  • The alveolar epithelium, which is composed of thin epithelial cells
  • A thin interstitial space between the alveolar epithelium and the capillary membrane
  • A capillary basement membrane that fuses in places with the epithelial basement membrane
  • The capillary endothelial membrane
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5
Q

What are the three types of alveolar cells?

A

Type I: squamous cells, compose the monolayered alveolar epithelium and cover 80% of the alveolar surface area (Structure)

Type II: contain lamellar bodies that produce surfactant – decrease surface tension and prevents alveoli from collapsing

Type III: alveolar macrophages

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6
Q

What is the purpose of surfactant and what law does it use?

A

Secreted by type II alveolar epithelial cells to reduce the surface tension within the alveoli and the work of breathing
*Keeps smaller alveoli from collapsing into larger alveoli

Law of LaPlace (if two bubbles have the same surface tension, the smaller bubble will have higher pressure)

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7
Q

What factors effect the rate of diffusion in the respiratory system?

A

Fick’s Law = AxDx(P1-P2)/T

T: Thickness of the respiratory membrane – rate of diffusion is inversely proportional to membrane thickness
A: Surface area of the respiratory membrane
D: Diffusion coefficient

*Pressure difference across the respiratory membrane (difference in partial pressure of gas in alveoli and in the blood)

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8
Q

How does edema in the interstitial space and alveoli affect diffusion of respiratory gases? How about fibrosis?

A

Edema decreases diffusion of respiratory gases

Fibrosis of the lungs can also increase the thickness of some portions of the membrane decreasing diffusion of respiratory gases

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9
Q

How does emphysema affect diffusion of respiratory gases?

A

Decreases surface area – decreased gas diffusion

  • total surface area of the respiratory membrane = ~70 square meters in normal adults
  • Emphysema can cause destruction of alveolar walls and cause the total surface area to decrease by as much as five fold

*When decreased to 1/3 to 1/4 normal – exchange of gases is impaired even at rest

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10
Q

What does the diffusion coefficient in respiratory gas diffusion depend on?

A

Depends on the solubility in the membrane and inversely the square root of its molecular weight (Graham’s law)
*large molecules diffuse slower – small molecules diffuse faster

  • CO2 = 20x more soluble than oxygen
  • O2 diffuses about 2x as rapidly as nitrogen
  • N2O = 19x as diffusible as O2
  • N2O = 36x as diffusible as N2
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11
Q

How does the pressure/concentration gradient affect respiratory gas diffusion?

A

Net diffusion of gases will occur from a high concentration (pressure) area to a low concentration (pressure) area

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12
Q

What is the partial pressure of water vapor at normal body temperature?

A

47 mmHg

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13
Q

What are the normal alveolar partial pressures on room air?

A 
PO2 = 104 mmHg
PCO2 = 40 mmHg
PH2O = 47 mmHg
PN2 = 569 mmHg
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14
Q

Total body oxygen delivery is the product of what?

A

O2 content of arterial blood (CaO2) and the rate of delivery of blood to the tissues (CO)

DO2 = CO x CaO2

CaO2 = Hbg x 1.39 x SaO2 + (0.0031 x PaO2)

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15
Q

What is the equation to figure out oxygen consumption?

A

VO2 = CO x (CaO2 - CvO2)

VO2: total body oxygen consumption
CO: cardiac output
CaO2: oxygen content of arterial blood (hbg x 1.39 x SaO2 + (0.0031 x PaO2)
CvO2: oxygen content of venous blood (hbg x 1.39 x SvO2 + (0.0031 x PvO2)

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16
Q

What is the typical oxygen delivery and oxygen consumption in healthy individuals?

A

Oxygen delivery (DO2) is typically ~16 mL/kg/min

Oxygen consumption is ~4 mL/kg/min

Therefore, total body oxygen extraction fraction (OEF) is about 25% and returning oxygen (SvO2) is about 65-80%
*cellular O2 utilization is constant

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17
Q

At what oxygen extraction fraction (OEF) does cellular metabolism become anaerobic?

A

at OEF of 70% cellular metabolism becomes anaerobic and lactic acidosis

Mitochondria will metabolize aerobically at PaO2 > 2 mmHg

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18
Q

What determines oxygen consumption? What increases and decreases it?

A

It is determined by basal metabolic rate

Increased by fever, thyrotoxicosis, exercise, stress, shivering

Decreased by hypothermia, hypothyroidism, and ANESTHESIA (GA reduces O2 consumption by 10-15%; hypothermia reduces it to about 50% basal metabolic rate at 31*C)

*Estimated by the Brody Equation

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19
Q

What are the causes of hypoxemia (low PaO2) in the OR? (3)

A
  • Low inspired O2
  • Hypoventilation
  • V:Q mismatch
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20
Q

What is the normal V/Q?

What does a high and a low V/Q mean?

A

Normal V/Q = 0.8 (Alveolar ventilation/CO – 4-5 L/min)

Low: V/Q = 0 (Absolute Shunt)

  • NO ventilation (ex. atelectasis)
  • desaturated blood from right heart returns to left heart without being oxygenated

High: V/Q = infinity (Absolute Dead Space)

  • NO perfusion (ex. PE, cardiac arrest)
  • CO2 can’t be ventilated off (leads to decreased ETCO2 and increased PaCO2)
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21
Q

What are the types of dead space in the pulmonary system?

A

Apparatus dead space (mechanical)

Airway dead space (anatomic): breath which is in the mouth, pharynx, and tracheobronchial tree but doesn’t enter the alveoli
*decreased by ETT placement but not clinically relevant

Alveolar dead space: portion of breath that enters alveoli that are ventilated and not perfused (West’s zone 1)

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22
Q

How is V:Q mismatch estimated?

A

Shunt = difference in PAO2 - PaO2 (alveolar oxygenation minus arterial oxygenation)
*normal breathing RA = 5-15 mmHg difference

Dead Space = difference in PaCO2 - PACO2 (ABG CO2 minus ETCO2)
*normal = 2-10 mmHg difference

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23
Q

What are the normal A-a oxygen gradients (AaDO2)?

A

Room Air: 5-15 mmHg

  • progressively increases with age up to 20-30
  • AaDO2 in healthy elderly is ~37.5 mmHg
  • PaO2 = 102 - (age/3)
  • PaO2 range = 60 - 100

On 100% O2: PAO2 - PaO2 < 100 mmHg

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24
Q

What is the effect of increasing FiO2 for treating hypoxemia?

A
  • increasing FiO2 alone may do little to increase PaO2 if the problem is due to absolute right to left shunt (ex. PDA, atelectasis)
  • increasing FiO2 should increase PaO2 if the problem is primarily hypoventilation or increasing dead space (ex. PE)

100% FiO2 – absorption atelectasis

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25
Q

Intra-Pulmonary Pressure vs Intra-Pleural Pressure

A

Intrapulmonary: pressure within the alveoli
-negative with inspiration – positive with expiration

Intrapleural: pressure in the potential space between the inside of the chest wall and the lungs

  • lungs recoil inward and chest recoils outward
  • ALWAYS negative during normal tidal breathing
  • becomes more negative during inspiration and less negative during expiration
  • becomes positive during FORCED expiration or during Valsalva maneuver
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26
Q

Intrapleural pressure is more negative in the _____ lung and less negative in the ____ lung.

A

Intrapleural pressure is more negative in the NON-DEPENDENT lung and less negative in the DEPENDENT lung.

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27
Q

What portion of the lung has better ventilation? Better perfusion?

A

Apices of the lung have better ventilation in relation to perfusion — Higher V:Q ratio

Lower levels of the lung have better perfusion than ventilation — Lower V:Q ratio

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28
Q

How is interpretation of pulmonary function tests helpful?

A

Helps in determining causation and severity of pulmonary dysfunction

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29
Q

Define the following pulmonary function test terms: FRC, RV, and VC

A

FRC: Functional Residual Capacity (2.5 L) – lung volume at end of normal exhalation

RV: Residual Volume (1.25-2.0 L) – lung volume remaining after max exhalation

VC: Vital Capacity (3.5-5.5 L) – max volume of gas that can be exhaled following max inspiration

*Normal lung volumes in a 70kg individual

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30
Q

What do pulmonary function tests depict?

A

Depiction of forced exhalation of lung gas from TLC to RV measured as a function of time

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31
Q

What are FEV1, FVC, and FEV1/FVC?

A

FEV1: forced expiratory volume in one second – volume of gas that can be exhaled within one second of beginning a force expiration
-normal = 4 L/sec

FVC: volume of gas that can be exhaled during a forced expiratory maneuver
-normal = 5 L/sec

FEV1/FVC: ratio useful in distinguishing between obstructive and restrictive diseases

  • proportion of a person’s vital capacity that they are able to expire in the first second of expiration
  • normal = 0.8 or 80%
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32
Q

What is FEF25-75%?

A

Midmaximal expiratory flow (MMEF)

  • rate of flow occurring in a forced expiratory flow from the point where 25% of the FVC has been exhaled to the point where 75% has been exhaled
  • best test for assessing small airway disease

*Independent of respiratory effort

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33
Q

What do flow volume loops show?

A

The change in exhaled and inhaled gas flow in relation to attainable lung volumes

34
Q

What is a variable respiratory obstruction? What are the two types?

A

A lesion whose influence varies with the phase of respiration

  • Extrathoracic obstruction
  • Intrathoracic obstruction
35
Q

What is the advantage of flow-volume loops over standard spirometry?

A

their ability to differentiate the anatomic location of flow obstructions

36
Q

What phase of respiration is impaired when there is a variable EXTRAthoracic obstruction? What are some examples?

A

Inspiration is impaired – flow-volume loop will be flat on inspiration side

Examples:

  • vocal cord paralysis accompanied by inspiratory stridor
  • pharyngeal muscle weakness (residual paralysis or chronic neuromuscular disorder)
37
Q

What phase of respiration is impaired when there is a variable INTRAthoracic obstruction? What are some examples?

A

Expiration is impaired – flow-volume loop will be flat on expiration side

Examples:
-Tumors of the trachea or major bronchi

*negative pressure of inspiration keeps trachea open – positive pressure ventilation may be very difficult if ET is not passed the obstruction

38
Q

What is a fixed large airway obstruction?

A

When you have an obstruction that influences both inspiration and expiration

-flow-volume loop is flat on top and bottom

Ex: mucous plus in ETT, kinked ETT

39
Q

What are the two classifications of pulmonary diseases?

A

Restrictive: decreased lung compliance results in decreased lung volumes

  • alveolar ventilation is restricted
  • flow volume loop looks the same just smaller

Obstructive: pathologic conditions increase airway resistance which results in decrease in max rate of exhalation

  • exhalation is obstructed
  • flow-volume loop has a indented curve on expiratory flow (decreased flow)
40
Q

How are FEV1, FVC, FEV1/FVC, and compliance affected in restrictive lung disease?

A
  • Both FEV1 and FVC are decreased
  • FEV1/FVC is therefore normal or may be increased

Compliance may be as low as 0.02 L/cmH2O in severe restrictive disease

  • normal compliance in spont breathing = 0.1
  • normal in anesthetized/paralyzed = 0.05
41
Q

What are the types of restrictive lung disease?

A

Acute Intrinsic – pulmonary edema (water and solutes accumulate in interstitial tissues causing the lungs to become stiff)
*aspiration, ARDS, POPE, CHF

Chronic Intrinsic – changes in elastic tissues in the lung lead to decreased compliance
*sarcoidosis, drug induced pulmonary fibrosis (amiodarone, bleomycin)

Chronic Extrinsic – disorders of chest wall and intra-abdominal changes
*obesity, pregnancy, kyphosis, spinal cord transection, muscular dystrophies

42
Q

What are the anesthesia and surgery causes of restrictive lung disease?

A
  • Pain
  • Residual neuromuscular blockade
  • Thoracic or abdominal wound dressings
  • Positioning (lithotomy, Trendelenburg, STEEP Trendelenburg)
43
Q

What factors lead to increased risk of exaggerated post-op pulmonary dysfunction?

A
  • Dyspnea that limits activity
  • Decrease in vital capacity to less than 15 mL/kg (normal is 70 mL/kg)
  • FEV1 < 50% of predicted or <2L
  • FVC < 50% of predicted
44
Q

What is the anesthetic management of restrictive lung disease?

A
  • Preoperative treatment of reversible conditions (treat acute pulmonary infections, bronchodilators)
  • Baseline ABG, pulse ox, and PFTs (to know what to aim for)
  • Use larger ETT
  • Need to use higher inspiratory pressures
  • smaller tidal volume with higher rate (occasional “sigh” breaths with PIP 35-45 cmH2O)
  • slow inspiratory flow rates and prolong inspiration time
  • pressure control ventilation vs volume control
  • Consider PEEP
  • Consider regional (level above T10 can cause respiratory compromise)
  • Maintain neuromuscular blockade
45
Q

What is the cause of laryngospasm?

A

mediated by the superior laryngeal nerve in response to irritating glottic or supraglottic stimuli such as presence of food, blood, vomitus, or foreign body

*false cords and epiglottic body come together firmly and allow no air flow and no vocal sound

46
Q

How do you treat laryngospasm?

A
  • Forward displacement of the jaw and positive pressure ventilation with 100% O2 is often effective in breaking the spasm
  • Severe spams may require small doses (20mg-ish IV) of succinylcholine and re-intubation (may be given IM 40-60mg or by sublingual injection)
  • Hypoxia and hypercarbia decrease post synaptic potentials and brainstem output to the superior laryngeal nerve so the laryngospasm will eventually cease as hypercarbia and hypoxia develop
47
Q

What is Post Obstructive Pulmonary Edema (POPE)? What are the two types?

A

Sudden onset of pulmonary edema following upper airway obstruction

Type I: follows a sudden severe episode of upper airway obstruction
*laryngospasm during intubation or after anesthesia is the most common cause (accounts for up to 50% of cases)

Type II: develops after surgical relief of chronic upper airway obstruction

48
Q

What is the physiology of POPE?

A

High negative intrapulmonary pressure causes:

  • Increased venous return to the right ventricle
  • increases pulmonary blood flow –> elevated pulmonary capillary hydrostatic pressure
  • increased afterload and decreased ejection fraction and CO
  • Decreases pulmonary interstitial pressures
  • Increases pulmonary capillary hydrostatic pressure
49
Q

How does negative pressure pulmonary edema develop when the obstruction is relieved?

A

Forced inspiratory attempts alternated with forced expiratory attempts (Valsalva maneuver) creates an “auto-PEEP” which opposes transudation of fluid into the interstitium

Once the obstruction is relieved, unopposed venous hydrostatic pressure leads to pulmonary edema

50
Q

How do you treat POPE (Post Obstructive Pulmonary Edema)?

A

Treatment depends on severity of hypoxemia:

  • Reestablish the airway
  • Supplemental oxygen
  • Application of CPAP
  • Reintubation with application of PEEP

*usually self-limited with radiologic clearing and normalization of arterial blood gases within 48 hours

51
Q

What is obstructive lung disease? What is an example?

A

Intralumenal and extralumenal airflow obstruction results in air trapping

Chronic Obstructive Pulmonary Disease (COPD) – progressive development of airflow limitation that is not fully reversible (chronic bronchitis, emphysema, asthma)

52
Q

What is emphysema?

A

Destructive process involving the lungs parenchyma that results in loss of elastic recoil of the lungs

  • airway collapse happens during exhalation
  • increase work of breathing
  • tendency to exhale through pursed lips to provide end-expiratory pressure

Can have relatively advanced disease with preservation of PaO2 and usually don’t retain CO2

Pink Puffer

53
Q

How do the spirometry values change with emphysema?

A
  • Decreased FEV1 (when it is <40% of normal, dyspnea is seen during ADL’s)
  • Decreased FEV1/FVC
  • Decreased FEF25-75%
  • Diminished air flow at all volumes
  • Increased RV
  • Normal to increased FRC and TLC
54
Q

How does the radiograph (chest x-ray) look in emphysema?

A

Hyperlucency

Hyperinflation (flattening of the diaphragm with loss of normal domed appearance)

55
Q

What is chronic bronchitis?

A
  • Follows prolonged exposure to airway irritants
  • Characterized by hypersecretion of mucus and inflammatory changes in the bronchi
  • Copious secretions occlude airways
  • Diagnosed if a person produces sputum 2 months out of the year for 2 years in a row
  • Unlike emphysematous pts, there is a marked tendency toward decreased PaO2 early in their disease course – CO2 diffusion is also impaired (increased PaCO2)
  • Hypoxemia/Respiratory acidosis lead to pulmonary vasoconstriction and pulmonary HTN (may lead to cor pulmonale: RV hypertrophy/R axis deviation)

Blue Bloater

56
Q

How do the spirometry values change with chronic bronchitis?

A
  • FEV1/FVC is decreased
  • FEF25-75% is decreased
  • Increased RV
  • Normal to increased FRC and TLC (due to slowing of expiratory airflow and gas trapping behind prematurely closed airways)
  • Greater work of breathing at high lung volumes
57
Q

How does the chest x-ray look in chronic bronchitis?

A 
Non-specific
Bronchial wall thickening
Increased bronchovascular markings
Enlarged vessels and cardiomegaly
Scarring of tissue causes irregular bronchovascular structures
58
Q

What is asthma?

A
  • Chronic airway narrowing due to bronchial hyperactivity
  • Exacerbations
  • Pathophysiology is not completely known
  • IGE mediated
  • Increased cAMP –> Bronchodilation (sympathetic stimulation of beta 2)
  • Increased cGMP –> bronchoconstriction (parasympathetic stimulation of muscarinic)
59
Q

How does the chest x-ray look in asthma?

A

Normal cardiomediastinal contours

No pleural abnormalities

No collapse or consolidation

60
Q

What type of medications are used for bronchodilator therapy?

A

Beta 2 Agonists (albuterol, metaproterenol, and ceprenaline – relatively free of alpha 1 and beta 1 effects)

Phosphodiesterase Inhibitors; Methylzanthines (given PO or IV – aminophylline)
*inhibits breakdown of cAMP

Parasympatholytics (Ipratroprium - doesn’t have side effects that atropine has)
*blocks effect of ACh on bronchial smooth muscle

61
Q

What is the intra-operative COPD anesthetic management?

A
  • Volatiles provide bronchodilation (may attenuate regional hypoxic vasoconstriction –> R to L shunt)
  • N2O (careful of emphysematous pts with pulmonary bullae; diffusion hypoxia)
  • Opioids (extreme sensitivity)
62
Q

What are the mechanical ventilation considerations for COPD anesthetic management?

A
  • Large tidal volumes (10-15 mL/kg)
  • Slow RR (6-10)
  • Increased expiratory time
  • Avoid high PIP, especially if pulmonary bullae are present
  • PEEP may not be necessary (may impede expiratory air flow)
  • Sigh mode
63
Q

When should you consider post-op ventilation in COPD patients?

A

FEV1/FVC ratios < 0.5

Pre-op PaCO2 >50 mmHg

*higher PaCO2 needed for spontaneous respirations

64
Q

What receptors cause bronchodilation and bronchoconstriction?

A

Beta 2 –> Bronchodilation

M3 –> Bronchoconstriction

65
Q

What is parasympathetic bronchial tone?

A

Continuous partial contraction of smooth muscle fibers in the wall of bronchi and bronchioles

  • maintains airway continuously patent
  • resists rupture of airways during cough
66
Q

What is Non-Noradrenergic, Non-Cholinergic Transmitter (NANC)?

A

A neurotransmitter of the ANS that is neither ACh, norepi, or epi

Vasoactive Intestinal Peptide (VIP) and Nitric Oxide (NO) = main inhibitory transmitters thought to be responsible for airway smooth muscle relaxation

Substance P (SP) and Neurokinin A (NKA) = main excitatory transmitters and have been shown to cause neurogenic inflammation, including bronchoconstriction

67
Q

Short-acting inhaled beta 2 agonists vs Long-acting inhaled beta 2 agonists

What are each prescribed for?

A

Inhaled beta 2 agonists = mainstay of therapy for bronchospasm, wheezing, and airflow obstruction

Short-acting: prescribed for rapid relief (rescue) of wheezing, bronchospasm, and airflow obstruction
*effects seen in minutes, lasts 4-6 hours

Long-acting: prescribed for control of symptoms when rescue therapies are used greater than 2x per week
*expensive

68
Q

What are the systemic absorption side effects for inhaled beta 2 agonists?

A
  • Inhibits hypoxic vasoconstriction
  • Vasodilation leads to tachycardia (some beta 1 effects also)
  • Tremors
  • Hyperglycemia, Hypokalemia, and Hypomagnesemia

*tolerance can develop

69
Q

What is the mechanism of action of inhaled cholinergic antagonists?

A

Muscarinic 2 (M2) present on postganglionic cells and are responsible for limiting production of ACh and protect against bronchoconstriction (M2 is not the target of inhaled anticholinergics but is antagonized by them)

Muscarinic 1 (M1) and Muscarinic 3 (M3) receptors are responsible for bronchoconstriction and mucus production and are the targets of inhaled anticholinergic therapy

70
Q

What drugs are inhaled cholinergic antagonists? What are they used for?

A

Ipratropium: short acting, maintenance therapy for COPD and as rescue therapy for both COPD and asthma (not for routine treatment of asthma)

Tiotropium: long acting, been shown to reduce COPD exacerbations, respiratory failure, and mortality

Combo Therapy: Combivent or Duoneb (ipratropium/albuterol)

71
Q

What are side effects of inhaled cholinergic antagonists?

A

they are poorly absorbed so side effects are uncommon

  • dry mouth, urinary retention, and can experience pupillary dilation, blurred vision if the eyes are inadvertently exposed to the drug
  • Systemic cholinergic antagonists (atropine/glycopyrrolate) have more side effects and are not routinely used for COPD or asthma treatment
72
Q

What are the systemic beta 2 agonists?

A

Terbutaline (PO, SubQ, or IV)

Albuterol can be given IV

Epinephrine (SubQ or IV)

*greater side effects than inhaled – tremor, tachycardia, hyperglycemia, hypokalemia, hypomagnesemia

73
Q

What are the short-acting beta-adrenergic bronchodilator inhalers available in the US?

A

Albuterol

Levalbuterol

Epinephrine Injection

74
Q

What are the long-acting beta-adrenergic bronchodilator asthma inhalers available in the US?

A

Salmeterol

Formoterol

75
Q

What are the anticholinergic bronchodilators available in the US?

A

Ipratropium (Atrovent HFA)

Tiotropium (Spiriva Respimat)

76
Q

What are examples of xanthine derivatives available in the US?

A

Theophylline

Aminophylline

77
Q

What are inhaled corticosteroids used for? Side effects?

A

Asthma exacerbations and combined with long acting beta agonist for severe COPD

Glucocorticoid receptor alpha located in the cytoplasm of airway epithelial cells

Side Effects: oropharyngeal candidiasis, pharyngitis, easy bruising, osteoporosis, cataracts, elevated intraocular pressure, dysphonia, cough, and growth retardation in children

78
Q

When are systemic corticosteroids used in asthma treatment?

A

Asthma exacerbations that are either severe, with a peak expiratory flow of less than 40% of baseline, or mild to moderate exacerbation with no immediate response to short active beta agonists

PO 3-10 days with no taper

Severe COPD/Asthma may get IV therapy

79
Q

What are leukotriene modifiers and mast cell stabilizers?

A
  • Leukotrienes are potent inflammatory mediators that are released from mast cells
  • Cromolyn Sodium and Nedocromil prevent inflammation by stopping mast cells from releasing histamine
  • NOT first line treatment
  • Preventative for exercise induced asthma or as adjuncts

Zileuton causes an increase in liver enzymes and should be avoided in pts with acute liver disease or persistent elevation of liver enzymes

80
Q

What is theophylline and its mechanism of action?

A

Methylxanthine

  • phosphodiesterase inhibition by methylxanthines inhibits cAMP degradation and promotes airway smooth muscle relaxation by raising intracellular cAMP levels
  • antagonism of adenosine receptors –> methylxanthines block Ca++ activated airway smooth muscle contraction

Used for chronic persistent disease

*low therapeutic index

81
Q

What is Roflumilast?

A

Phosphodiesterase inhibitor

-type 4 PDE inhibitor, inhibits degradation of cAMP in cells of the airway (airway smooth muscle, epithelium, and inflammatory cells) and elsewhere that express the type 4 PDE isoenzyme

Promotes airway smooth muscle relaxation by increasing cAMP levels

82
Q

What anesthetics cause bronchodilation?

A

Volatiles are dose dependent bronchodilators, especially in the distal airways (treat status asthmaticus) – may inhibit hypoxic pulmonary vasoconstriction

Ketamine (smooth muscle relaxant, increases salvation)

Propofol is thought to reduce vagal tone and have a direct effect on muscarinic receptors by interfering with cellular signaling and inhibiting Ca++ mobilization

Anesthesia Pharm (18 decks)

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