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Anesthesia Pharm Midterm 2 > Pulmonary Physiology > Flashcards

Pulmonary Physiology Flashcards

1
Q

Gas Exchange Mechanisms

A

-determined by ventilation and perfusion of the lungs, and appropriate matching of these two independent variables

3 types of alveolar cells:

  • type I cells are squamous cells, compose the mono layered alveolar epithelium and cover 80% of the alveolar surface area
  • type II cells are thought to produce surfactant
  • type III cells are alveolar macrophages

Law of LaPlace as Pr=2T for a sphere
p=pressure inside the alveoli, r=radius, and t=surface tension trying to collapse the alveoli
**alveoli do NOT directly follow the law of laplace due to the effect of surfactant

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2
Q

Diffusion of Gas is determined by: (4) things

A
  1. Membrane thickness: thicker the membrane, slower the diffusion
  2. Surface area of the membrane: SA of lungs is massive
  3. Diffusion coefficient of the gas in the substance of the membrane
  4. the pressure difference between the two sides of the membrane.
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3
Q

Diffusion of gases: Molecular weight

A
  • Graham’s law: diffusion of a gas through a semi-permeable membrane is inversely proportional to the square root of the molecular weight of that gas
  • the larger the molecule, the slower the diffusion
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4
Q

Diffusion of gases: Distance

A
  • the greater the distance the slower the diffusion

- farther from the nerve= longer time for LA to diffuse into the nerve. distance causes a problem

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5
Q

Diffusion of gases: Pressure difference

A

-Henry’s Law: the greater the pressure difference, the greater the rate of diffusion. When we want to increase our anesthetic agents, we increase your delivered agent so more will diffuse across and deepen the anesthetic.
Really high concentration to low concentration= larger concentration gradient= faster diffusion

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6
Q

Diffusion of gases: Cross sectional area

A

-the more alveoli exposed to pulmonary blood, the more than can pick up the gas molecules, the greater the rate of diffusion.

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7
Q

Diffusion of gases: Solubility Coefficient

A

-The more soluble, the faster the diffusion (diffusion is not a friend of Fa/Fi)

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8
Q

At equal pressures, the rate of diffusion of a gas is dependent on:

A

-solubility of the gas divided by the MW
Co2 is 20 times more diffusible than O2
N2O is 19 times more diffusible than O2
N2O is 36 times more diffusible than N2

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9
Q

Oxygen Delivery

A

Total body oxygen delivery is the product of:

  • O2 content or arterial blood (CaO2) and
  • rate of delivery of blood to the tissues (CO)
DO= CO X CaO2
CaO2= Hgb X 1.39 X SaO2 + (0.0031 X PaO2)
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10
Q

If we have enough hemoglobin in the body, every 1 gram of hemoglobin can hold ______ cc of oxygen?

A

1.39 ml

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11
Q

CVO2=

A

Hb X 1.39 x SvO2 + (0.0031 X PvO2)
CvO2= oxygen content in venous blood
SVO2= venous oxygen saturation
PVO2= partial pressure of dissolved oxygen in venous blood

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12
Q

VO2=

A 
CO X (CaO2- CvO2)
VO2= total body oxygen consumption
Normal= 250 ml/min
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13
Q

In healthy individuals, oxygen delivery is about?

A

16 ml/kg/min
oxygen consumption is about 4 ml/kg/min
-therefore, total body oxygen extraction fraction (OEF) is about 25%
-and returning oxygen is about 65-80% (how much oxygen is in right side of the heart after all other body areas have been oxygenated)

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14
Q

Cellular oxygen utilization is _____________

A

constant

  • at OEF of 70% cellular metabolism becomes anaerobic and lactic acidosis
  • mitochondria will metabolize aerobically at PaO2 > 2 mmHg
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15
Q

Mixed Venous Oxygen Sat: SvO2

A

SvO2= SaO2 - { VO2/ Co X Hb x 13.9)

normal SvO2 levels between 65-80% indicate balance between O2 delivery and O2 consumption

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16
Q

Decrease in SVO2 may indicate?

A
  1. Decrease Hgb: hemolysis or hemorrhage
  2. Decrease CO: MI, CHF, hypovolemia
  3. Decrease PAO2: hypoxia, ARDs, inapp. vent setting
  4. Increase oxygen demand: fever, MH, shivering, thryoid storm, exercise, agitation
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17
Q

Increase in SvO2 suggests?

A
  1. permanently wedged SvO2 monitoring S-G catheter
  2. Decreased VO2: sepsis, hypothermia, methgb, CO poisoning, cynanide toxicity
  3. Increased CO: sepsis, burns, left to right shunt, AV fistula (paget,s cirrhosis), inotropic excess, hepatitis, pancreatitis
  4. Increased Hgb or SaO2: GA may increase SVO2 by decreasing VO2 and increase FIO2
    * *** increased SVO2 may indicate impending issues with inability to utilize oxygen
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18
Q

Oxygen consumption

A
  1. Determined by basal metabolic rate
  2. Increased by fever, thyrotoxicosis, exercise, stress, shivering
  3. Decreased by hypothermia, hypothyroidism, and ANESTHESIA
    - —- GA reduced O2 consumption by 10-15% on average
    - —- hypothermia reduces O2 consumption to about 50% BMR at 31 degrees C
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19
Q

Oxygen consumption estimated by Brody Equation

A

VO2= (IBW kg) 3/4 X 10
2-4 cc/kg/min
about 250 cc/min

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20
Q

Alevolar (A) ro Arterial (a) or A-a gradient

A

-If ventilation and perfusion were perfectly matched
PAO2- PaO2= 0
PaCO2-PACO2= 0
The difference in PAO2-PaO2 or PaCO2-PACO2 is a measure of the degree of V:Q abnormality

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21
Q

PO2 estimation

A 
PAO2= FIO2 % X 6
PaO2= FIO2 % X 5
ETCO2= average PACO2
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22
Q

A-a Oxygen Gradients (AaDO2) Normal values

A 
Breathing room air:
PAO2- PaO2 (AaDO2)= 5-15 mmHg
Progressively increases with age up to 20-30
AaDO2 in healthy elderly= 37.5 mmHg
PaO2 guessimate= 102- age/3
PaO2 range 60-100

Breathing 100% Oxygen
PAO2-PaO2 < 100 mmHg

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23
Q

Diffusion gradient for CO2

A

PaCo2-PACO2= 2-10 mmHG difference

ABG CO2 versus End tidal CO2

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24
Q

Hypoxemia

A

Causes of low PaO2

  • low inspired O2
  • hypoventilation
  • V:Q mismatch (low hemoglobin, low CO)
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25
Q

Forms of Hypoxia (4)

A
  1. Hypoemic hypoxia is secondary to inadequate arterial oxygenation
  2. Anemic hypoxia is secondary to decreased hemoglobin
  3. Circulatory hypoxia is secondary to decreased perfusion
  4. Histologic hypoxia is secondary to cellular inability to utilize oxygen
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26
Q

Treating Hypoxemia

A
  1. Increasing FIO2 alone may do little to increase PaO2 if the problem is due to absolute right to left shunt (PDA, atelectasis)
  2. Increasing FIO2 should increase PaO2 if the problem is primarily hypoventilation or increasing dead space (PE)

100% FIO2- absorption atelectasis

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27
Q

Anatomic Deadspace

A

-normally 1/2 of TV or 1 cc/lb

This is inhaled air that sits in the conducting air passages and doesn’t participate in gas exchange

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28
Q

Physiologic deadspace

A

is anatomic deadspace + alevolar deadspace.

these terms are synonomous in the healthy person

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29
Q

Pathologic Deadspace

A
  • refers to additional alveolar space which is being perfused but not ventilated.
  • In persons w/ respiratory disease, physiologic headspace may be as high as 10 X normal anatomic deadspace
  • increased V/Q ratio indicates increased headspace and may be caused by pulmonary emboli, hypotension, or ligation of a pulmonary vessel
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30
Q

Shunt

A

refers to lung that is perfused but not ventilated
-a decreased V/Q ratio indicates increased shunt and can be caused by endobronchial intubation, mucus plug, or alveolar collapse

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31
Q

Lung Compliance

A
  • compliance can be expressed as how much the volume in the lungs will increase for a given increase in alveolar pressure
  • normal lungs will expand 130 ml of volume for every 1 cm increase in water pressure or .13 L/cm H20
  • more compliant a lung is, the greater the volume that can be inspired at a lower PIP
  • less compliant lung inspires smaller volumes at higher PIPs
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32
Q

Minute ventilation

A

MV= tidal volume X respiratory rate

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33
Q

Boyle’s Law

A

P1V1=P2V2

at a constant temperature, pressure is inversely proportional to volume

34
Q

Static Compliance

A

refers to the P/V relationship when air IS NOT moving

  • static compliance decreases w/ conditions that make it difficult to inflate the lungs such as obesity, fibrosis, edema, vascular engorgement, and external compression
  • static compliance increases with emphysema which destroys lung tissue and therefore reduces the elastic recoil and results in air trapping
35
Q

Dynamic compliance

A

refers to the P/V relationship when air IS MOVING

-dynamic compliance decreases w/ airway obstruction such as foreign bodies and bronchospasm.

36
Q

Intrapulmonary pressure

A
  • pressure within the alveoli

- intrapulmonary pressure is negative w/ inspiration, positive w/ expiration

37
Q

Intrapleural pressure

A
  • pressure in the potential space between the inside of the chest wall and 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
38
Q

Apices of the lungs have better ________ in relation to ________ and V/Q?

A

better ventilation in relation to perfusion

Higher V:Q ratio

39
Q

Lower levels of the lung have better _______ in relation to ________ and V/Q?

A

better perfusion in relation to ventilation

Lower V:Q ratio

40
Q

Normal V/Q ratio

A

0.8

alevolar V/pulmonary capillary P= 4L/min / 5L/min

41
Q

Absolute Shunt

A

V/Q= zero
NO ventilation
desaturated blood from right heart returns to left heart without being oxygenated (dead space)

42
Q

Absolute dead space

A

V/Q= infinity
NO perfusion
ex= PE

43
Q

Spirometry

A

FRC: lung volume at end of normal exhalation (2.5 L)
RV: lung volume remaining after maximal exhalation (1.25-2.0 L)
VC: maximum volume of gas that can be exhaled following maximal inspiration (3.5-5L)

44
Q

FEV1

A

forced expiratory volume in 1 second
the volume of gas that can be exhaled within 1 second of beginning a forced expiration
FEV1= 4 L/sec

45
Q

FVC

A

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

46
Q

FEV1/FVC

A

ratio useful in distinguishing between obstructive and restrictive disease
-the proportion of a person’s vital capacity that they are able to expire in the first second of expiration
Normal is .8 or 80%

47
Q

Midmaximal expiratory flow (MMEF)

A

FEF 25-75%

  • 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
48
Q

Flow volume loops

A
  • normal flow volume loop looks like an upside down ice cream cone or guitar pic
  • plot the change in exhaled and inhaled gas flow in relation to attainable lung volumes
49
Q

Variable Respiratory Obstructions

A
  • a lesion whose influence varies with the phase of respiration is called a variable obstruction
  • advantage of flow-volume loop over standard spirometry is their ability to differentiate the anatomic location of flow obstructions
50
Q

Inspiration is impaired when there is a variable __________ obstruction

A

-Extrathoracic obstruction
Examples: vocal cord paralysis accompanied by inspiratory stridor, pharyngeal muscle weakness, residual paralysis, chronic NM disorders

51
Q

Variable Intrathoracic Obstruction

A

usually caused by tumors of the trachea or major bronchi
exhalation is affected
negative pressure of inspiration keeps trachea open. positive pressure ventilation may be very difficult if ET is not pass the obstruction

52
Q

Expiration is impaired when there is a variable ___________ obstruction

A

Intrathoracic obstruction

53
Q

Restrictive Pulmonary Disease

A
  • decreased lung compliance results in decrease lung volumes
  • alveolar ventilation is restricted
  • 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 total lung compliance in sport breathing pt is 0.10 L/cm H2O
  • normal in a supine anethesitzed and paralyzed pt is 0.05 L/cm H2O
54
Q

Obstructive Pulmonary Disease

A
  • pathologic conditions increase airway resistance which results in a decrease in maximum rate of exhalation
  • exhalation is obstructed
55
Q

Acute Intrinsic Restrictive Lung Disease

A
  • Pulmonary Edema
  • water and solutes accumulate in the interstitial tissues causing the lungs to become stiff
  • aspiration, ARDs, POPE, CHF
56
Q

Chronic Intrinsic Restrictive Lung Disease

A
  • Changes in elastic tissues in the lung lead to decreased compliance
  • sarcoidosis
  • drug induced pulmonary fibrosis
  • amiodarone, bleomycin
57
Q

Chronic Extrinsic Restrictive Lung Disease

A
  • disorders of chest wall and intra-abdominal changes

- obesity, pregnancy, kyphosis, spinal cord transection, MD

58
Q

Anesthesia and Surgery can cause:

A
  • pain
  • residual NM blockade
  • thoracic or abdominal wound dressings (high abdominal incisions can make for bad post op wound healing)
  • positioning (lithotomy, trend, STEEP trend)
59
Q

Increased risk of exaggerated post-operative 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 <2 L
  • FVC < 50% of predicted
60
Q

Anesthetic Management: Restrictive Lung Disease

A
  • preop treatment of reversible conditions (treat acute pulmonary infections, bronchodilators)
  • baseline ABG, pulse ox, PFTS
  • use LARGE ETT
  • need to use higher inspiratory pressures
  • —- smaller TVs w/ higher resp rate (occasional sigh breaths with PIP 35-45 cmH2O)
  • — slow inspiratory flow rate
  • — prolong inspiration time
  • — pressure control ventilation vs volume control
  • consider PEEP
  • consider Regional (level above T10 can affect respiration
  • maintain NM block
  • when in doubt DO NOT REMOVE ETT
61
Q

Laryngospasm

A
  • mediated by the superior laryngeal nerve in response to irritating glottic or supraglottic stimuli such as presence of food, blood, vomitus, or foregone body
  • false cords and epiglottic body come together firmly and allow no air flow and no vocal sound
62
Q

Treatment of laryngospasm

A
  • forward displacement of the jaw and positive pressure ventilation with 100% oxygenation is often effective in breaking spasm
  • severe spasm may require small doses (20mg IV) of succ and re-intubation– may be given IM (40-60 MG or SL)
  • hypoxia and hypercarbia decrease post synaptic potentials and brain-stem output to the superior laryngeal nerve
  • laryngospasm will eventually cease as hypercarbia and hypoxia develop
63
Q

POPE

A

Post obstructive pulmonary edema
-sudden onset of pulmonary edema following upper airway obstruction
Two types:
1. Type 1: follows a sudden severe episode of upper airway obstruction
2. Type 2: develops after surgical relief of chronic upper airway obstruction
-laryngospasm during intubation or after anesthesia is the most common cause of upper airway obstruction leading got POPE type 1 (may account for 50% of POPE 1 cases)

64
Q

High Negative Intrapulmonary Pressure

A
  • increased venous return to the right ventricle (increases pulmonary blood flow—-> elevated pulmonary capillary hydrostatic pressure. increases after load and decreased ejection fraction and CO)
  • decreases pulmonary interstitial pressures
  • increases pulmonary capillary hydrostatic pressure
65
Q

Negative Pressure Pulmonary edema may develop after the ____________ is relieved

A
  • obstruction is relieved
  • 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
66
Q

Treatment of POPE

A
  • usually self-limited with radiologic clearing and normalization of arterial blood gases within 48 hours
  • treatment depends on severity of hypoxemia
  • – reestablish the airways
  • – supplemental oxygen
  • – application of CPAP
  • – reintubation w/ application of PEEP
67
Q

Obstructive Lung Disease

A
  • intralumenal and extralumenal airflow obstruction results in air trapping
  • COPD
  • progressive development of airflow limitation that is not fully reversible
  • chronic bronchitis
  • emphysema
  • asthma
68
Q

Emphysema

A
  • destructive process involving the lung parenchyma that results in loss of elastic recoil of lungs (airway collapse happens during exhalation, increase work of breathing)
  • can have relatively advanced disease w/ preservation of PaO2, and usually do not retain CO2
  • pink puffers
  • tendency to exhale through pursed lips to provide end-expiratory pressure
69
Q

Emphysema Spirometry

A
  • decreased FEV1 (when FEV1 is < 40% of normal, dyspnea is seen during ADLs)
  • decrease in FEV1/FVC
  • decreased FEF 25-75%
  • diminished air flow at all volumes
  • increased RV
  • normal to increased FRC and TLC
70
Q

Emphysema radiographically

A
  • hyperlucency

- hyperinflation: flattening of the diaphragm w/ loss of normal domed appearance

71
Q

Chronic Bronchitis

A
  • follows prolonged exposure to airway irritants
  • characterized by hyper secretion of music and inflammatory changes in the bronchi
  • copious secretions occlude airways
  • diagnosed if a patient produces sputum 2 months out of the year for 2 years in a row
  • unlike emphysematous patients, there is a marked tendency toward decreased PaO2 early in their disease course
  • CO2 diffusion is also impaired (increased PaCO2)
72
Q

Blue Bloater

A
  • hypoxemia and respiratory acidosis lead to pulmonary vasoconstriction and pulmonary hypertension
  • may lead to for pulmonale: RV hypertrophy, R axis deviation
73
Q

Chronic Bronchitis: Spirometry

A

FEV1/FVC is decreased
FEF 25-75% is decreased
increased RV
normal to increase FRC and TLC: due to slowing of expiratory airflow and gas trapping behind prematurely closed airways
-greater work of breathing at high lung volumes

74
Q

Chronic Bronchitis X-ray

A 
-non-specific
bronchial wall thickening
increased bronchovascular markings
enlarged vessels and cardiomegaly
scarring of tissue causes irregular bronchovascular structures
75
Q

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)
76
Q

Asthmatic X-ray

A
  • normal cardiomediastinal contours
  • no pleural abnormalities
  • no collapse or consolidation
77
Q

Bronchodilator Therapy

A
  • Beta 2 agonists: albuterol, metaproterenol, and ceprenaline. Relatively free of alpha 1 and beta 1 effects
  • Phosphodiesterase inhibitors; methylzanthines (given orally or IV, inhibits breakdown of cAMP, aminophylline)
  • parasympatholytics: block the effect of Ach on bronchial smooth muscle. Ipratropium, does not have the side effects that atropine has
78
Q

COPD Anesthetic Management

A

Intra-operative: volatiles provide bronchdilation
may attenuate regional hypoxic vasoconstriction- right to left shunt
-N2O: careful of emphysematous patients with pulmonary bullae, diffusion hypoxia
-Opioids: extreme sensitivity

79
Q

COPD Anesthetic Management: Mechanical Ventilation

A
  • large tidal volumes (10-15 ml/kg)
  • slow RR (6 to 10)
  • increased expiratory time
  • avoid high PIP, especially if pulmonary bull are present
  • PEEP may not be necessary- may impede expiratory air flow
  • sigh mode
80
Q

COPD Anesthetic Management: Extubation

A
  • post-operative ventilation
  • FEV1/FVC ratios < 0.5
  • pre-op PaCO2 > 50 mmHg
  • Higher PaCO2 needed for spontaneous respirations

Anesthesia Pharm Midterm 2 (8 decks)

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