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Anesthesia Pharm Exam 3 > Pulm Pharm and Phys > Flashcards

Pulm Pharm and Phys Flashcards

1
Q

Gas exchange is determined by _______ and _______.

A

Gas exchange is determined by ventilation and perfusion of the lungs and matching of these two independent variables

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2
Q

3 Types of Alveolar Cells

A

Type I - squamous cells make up the alveolar epithelium and cover 80% of the alveolar surface area

Type II - produce surfactant

Type III - alveolar macrophages

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3
Q

Law of LaPlace

A

Pr=2T for a sphere

P - pressure inside the alveoli

R - radius of the alveoli

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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4
Q

Diffusion of gases is determined by 5 things

A

1) membrane thickness (thicker the membrane the slower the diffusion)
2) surface area (more surface area = more area to diffuse through)
3) diffusion coefficient of the gas (blood:gas coefficient, more soluble agent means faster diffusion)
4) pressure difference between the two sides of the membrane (henry’s law)
5) distance (greater the distance the slower the diffusion - more of a problem w blocks)

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5
Q

Graham’s Law

(Molecular Weight and Diffusion of Gases)

A

difusion of 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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6
Q

Henry’s Law

(Pressure difference and diffusion of gases)

A

the greater the pressure difference the greater the rate of diffusion

ie: when we want to increase our [] of anesthetic gases, we increase our delivered agent so more will diffuse across and deepen the anesthetic

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7
Q

At equal pressures, the rate of diffusion of a gas is dependent on the ________ of the gas divided by the _______ _______.

A

At equal pressures, the rate of diffusion of a gas is dependent on the solubility of the gas divided by the molecular weight.

  • CO2 is 20x as diffusable as 02
  • N2O is 19x as diffusable as 02
  • N20 is 36x as diffusible as N2
  • these principles are behind why N2O expands when we don’t want it to!*
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8
Q

Total body oxygen delivery (DO2) is the product of what 2 things?

A
  • 02 content of arterial blood (Ca02)
  • rate of delivery to the tissues (CO)

DO2 = CO x Ca02

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9
Q

Ca02 (oxygen content of arterial blood) calculation

A

Ca02 = Hgb x 1.39 Sa02 + (0.0031*Pa02)

Ca02: oxyen content of arterial blood

1.39: binding capacity of Hgb is 1.39mL 02 per gm of Hgb

Sa02: arterial oxygen saturation

0.0031: solubility of 02 in plasma (mL 02/ mmHg/100mL plasma)

Pa02: partial pressure of dissolved oxygen in arterial blood

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10
Q

Cv02 (oxygen content of venous blood) calculation

A

Cv02 = Hgb x 1.39 x Sv02 + (0.0031 x Pv02)

Cv02 - oxygen content of venous blood

Sv02 - venous oxygen saturation

Pv02 - partial pressure of dissolved oxygen in venous blood

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11
Q

VO2 calculation (total body oxyen consumption)

A

V02 = CO x (Ca02 - Cv02)

normal is 250mL/min or

2-4 cc/kg/min

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12
Q

In healthy individuals, what is oxygen delivery and consumption?

A

– Oxygen delivery (DO2) is 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%

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13
Q

Sv02 (mixed venous oxygen concentration) calculation

A
  • normal between 65-80%
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14
Q

Decreased Sv02 may indicate what 4 things?

A

- decreased Hgb (hemolysis/hemorrhage/ not enough oxygen on cells being carried around)

- decreased CO (MI, CHF, hypovolemia)

- decreased Pa02 (hypoxia, ARDS, inappropriate vent settings)

  • increased oxygen demands (fever, MH, shivering, thyroid storm, exercise, agitation)
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15
Q

Increased SV02 suggests what 4 things?

A

- permanently wedged Sv02 S-G catheter

- decreased VO2 (sepsis, hypothermia, methmeglobenmia, CO poisoning, cyanide toxicity)

- increased CO (sepsis, burns, L-R shunt, AV fistula, inotropic excess, hepatitis, pancreatitis)

- increased Hgb or Sa02 (GA may increase Sv02 by decreasing VO2 and increasing Fi02)

an increased Sv02 may indicate issues w inability to utilize oxygen

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16
Q

Oxygen Consumption

A
  • determined by basal metabolic rate, estimated by Brody Equation
  • normal is 2-4 cc/kg/min or 250cc/min
  • increased by fever, thyrotoxicosis, exercise, stress, shivering
  • decreased by hypothermia, hypothyroidism, and ANESTHESIA
  • GA reduces 02 consumption 10-15%
  • hypothermia reduces by 50% at 31 degrees C
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17
Q

A-a gradient

A

if ventilation/perfusion were perfectly matched, PA02-Pa02 = 0 and PAC02-PaCO2 = 0.

the difference in PA02-Pa02 or PACO2-PaCO2 is a measure of the V:Q abnormality

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18
Q

PO2 estimation calculation

A 
PA02 = percent Fi02 x 6 (about 120
Pa02 = percent Fi02 x 5 (105 ish)

ETCO2 = average PACO2

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19
Q

Normal A-a gradient (AaDO2) breathing room air and 100% oxygen

A

breathing room air:

PA02-Pa02 (AaDO2) = 5-15mmHg

  • progressively increases w age up to 20-30mmHg
  • AaDO2 in healthy elderly is 37.5

Pa02 guesstimate = 102-age/3 or Fi02x5

  • Pa02 range 60-100

breathing 100% oxygen:

PA02-Pa02 <100mmHg

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20
Q

Forms of Hypoxemia

A

- hypoxemic hypoxemia: 2/2 inadequate arterial oxygenation (typically low Fi02)

- anemic hypoxia: 2/2 decreased Hgb

- circulatory hypoxia: 2/2 decreased perfusion

- histologic hypoxia: 2/2 cellular inability to utilize oxygen

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21
Q

Causes of low Pa02

A
  • low inspired 02 (fi02)
  • hypoventilation
  • V:Q mismatch (low Hgb, low CO)
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22
Q

Treating Hypoxemia

A

• Increasing FiO2 alone may do little to increase PaO2 if the problem is due to absolute right to left shunt

– e.g. PDA, atelectasis

• Increasing FiO2 should increase PaO2 if the problem is primarily hypoventiation or increasing dead space

( e. g. PE).

• 100% FiO2 = absorption atelectasis (bad!)

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23
Q

Anatomic Deadspace

A

is normally 1/3 of tidal volume or 1 cc/lb. This is the inhaled air that sits in the conducting air passages and doesn’t participate in gas exchange.

ie: oropharynx, nasopharynx, trachea, 1st gen bronchi

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24
Q

Physiologic Deadspace

A

is anatomic deadspace plus alveolar deadspace. These terms are synonomous in the healthy person.

ie: deadspace in alveoli not being perfused

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25
Q

Pathologic Deadspace

A

refers to additional alveolar space which is being perfused but not ventilated. In persons with respiratory disease physiologic deadspace may be as high as 10x normal anatomic deadspace.

– An increased V/Q ratio indicates increased deadspace and may be caused by pulmonary emboli, hypotension, or ligation of a pulmonary vessel.

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26
Q

Shunt

A

refers to lung that is perfused but not ventilated (right mainstem intubation)

– A decreased V/Q ratio indicates increased shunt and can be caused by endobronchial intubation, mucus plug, or alveolar collapse

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27
Q

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 130ml of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.
  • The more compliant a lung is, the greater the volume that can by inspired at a lower PIP.
  • The less compliant lung inspires smaller volumes at higher PIPs
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28
Q

Normal lungs will expand _____mL of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.

A

• Normal lungs will expand 130ml of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.

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29
Q

Boyle’s Gas Law

A

At a constant temperature, pressure is inversely proportional to volume

  • as pressure increases, volume decreases
  • as pressure decreases, volume increases
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30
Q

static compliance

A

p/v relationship when air is NOT moving

  • decreases w conditions that make it difficult to inflate the lung, ie: obesity, fibrosis, edema, vascular engorgement, external compression (surgeons elbow)
  • increases w emphysema which destroys lung tissue as wella s reduces elastic recoil, causing air trapping
31
Q

dynamic compliance

A

P/V relationship when air IS moving

  • decreases w airway obstruction such as foreign body and bronchospasm
32
Q

Intrapulmonary pressure

A
  • pressur ewithin the alveoli
  • negative w inspiration, positive w expiration
33
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
  • this is what fills w hemo or pneumothorax
    • always negative during normal breathing*
    • becomes MORE negative w inspiration and less negative w expiration*
    • becomes positive w forced expiration/valsava*
34
Q

Is intrapleural pressure more negative in the dependent or non-dependent lung?

A
  • more nebative in the non-dependent lung
35
Q

V:Q Ratio

A

- normal V/Q: 0.8 or 4L/min / 5L/min = 0.8

- Absolute Shunt: V/Q = 0

no ventilation, desaturated blood from R heart returns to L w/o being oxygenated

Absolute Dead Space: V/Q = infinity

NO perfusion (ie: pulmonary embolus)

36
Q

FRC

A

functional residual capacity, lung volume at end of normal exhalation

  • obese = lower FRC
37
Q

RV

A

residual volume - volume remaining after maximal exhalation

38
Q

VC

A

vital capacity - max volume of gas that can be exhaled following maximal inspiration

39
Q

Normal PFT Values

A

FEV1 - 4L/sec

FVC - 5L/sec

FEV1/FVC = 4/5 = 0.8 or 80%

40
Q

FEV1

A

normal 4 L/sec

  • forced expiratory volume in 1 sec; the volume of gas that can be exhaled within one second of beginning a force expiration
41
Q

FVC

A
  • normal 5L/sec
  • volume of gas that can be exhaled during a forced expiratory maneuver
42
Q

FEV1/FVC

A

ratio used to distinguish between obstructive and restrictive diseases

  • normal = 4/5 = 0.8 = 80%
43
Q

FEF 25-75%

A

midmaximal expiratory flow (MMEF)

  • rate of flow occuring in a forced expiratory flow from the point where 25% of the FVC has been exhaled to where 75% has been exhaled
  • best test for assessing small airway disease, independent of respiratory effort!
44
Q

Extrathoracic Obstruction

A
  • inspiration is impaired
  • ie: vocal cord paralysis w inspiratory stridor, pharyngeal muscle weakness, papilloma in airway

can be overcome by using ETT

45
Q

Intrathoracic Obstruction

A
  • expiration is impaired
  • negative pressure of inspiration keeps trachea open, PPV will be difficult if ETT does not pass obstruction, often not compensated by intubation as obstruction is past carina
  • usually tumors of trachea or bronchi
46
Q
A

fixed large airway obstruction

ie: mucous plug in ETT, kinked ETT

47
Q

Restrictive Pulmonary Disease

A
  • decreased lung compliance = decreased lung volumes
  • alveolar ventilation is restricted
  • both FEV1 and FVC are decreased but FEV1/FVC ratio is normal
  • compliance as low as 0.02 L/cmH20 in severe dx (normal is 0.10)
  • types: acute intrinsic, chronic intrinsic and chronic extrinsic
48
Q

Obstructive Pulmonary Disease

A
  • pathologic conditions increase airway resistance which results in a decrease in max rate of exhalation
  • exhalation is obstructed
  • intralumenal and extralumenal airflow obstruction results in air trapping
  • ie: COPD
49
Q

Acute Intrinsic

A
  • restrictive lung disease like pulmonary edema
  • water and solutes accumulate in the interstitial tissues causing lungs to become stiff
  • aspiration, ARDS, POPE, CHF
50
Q

Chronic Intrinsic

A
  • restrictive lung dx
  • changes in elastic tissue in lung lead to decreased ompliance
  • ie: sarcoidosis, drug-induced pulm fibrosis (amiodarone, bleomycin)
51
Q

Chronic Extrinsic

A
  • restrictive lung disease
  • disorder of the chest wall and intra-abdominal changes
    ie: obesity, pregnancy, kyphosis, SCI transection, muscular dystrophy
52
Q

Indicators of Increased Risk of Post-op Pulmonary Dysfunction

A
  • dyspnea that limits activity
  • decrease in VC to <15ml/kg (normal is 70)
  • FEV1 <50% of predicted or <2 L
  • FC <50% of predicted
53
Q

Anesthetic Mgmt of Restrictive Lung Dx

A
  • treat reversible conditions preop (abx for pna, bronchodilators)
  • baseline ABG, pulse ox, PFTs
  • use large ETT (hagen-pouiselle)
  • use higher inspiratory pressures
  • smaller TV w higher rate, occasional “sigh” breaths w PIP 35-45 cmH20
  • slow inspiratory flow rate
  • prolong inspiration time
  • PC vs VC
  • consider PEEP
  • consider regional (above T10 = resp block)
  • maintain NMB
  • when in doubt, don’t pull the tube out!
54
Q

Laryngospasm

A
  • mediated by superior laryngeal nerve in response to irritating glottic/supraglottic stimuli such as food, blood, vomitus or foreign body
  • false cords and epiglottic body come together to prevent air flow and vocal sounds
  • deepening anesthetic won’t work because you can’t ventilate anyways
55
Q

Treatment of Laryngospasm

A
  • forward displacement of jaw, PPV and 100% 02
  • may need 20mg-ish of IV succx and re-intubation
  • can give 40-60 mg IM or sublingual
56
Q

POPE

A
  • post obstructive pulmonary edema
  • sudden onset of pulm edema following upper airway obstruction

Type I: follows a sudden severe episode of upper airway obstruction

Type II: 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 to POPE Type I
57
Q

High Negative Intrapulmonary Pressure

A
  • increased venous return to RV
  • increases pulmonary blood flow causing elevated pulmonary capillary hydrostatic pressure
  • increased afterload and decreased EF and CO
  • decreases pulmonary interstitial pressures
  • increases pulmonary capillary hydrostatic pressure
58
Q

How does pulmonary edema develop when an obstruction is relieved?

A
  • forced inspiratory attempts alternated w forced expiratory attempts (Valsava) creates auto-PEEP which opposes transudation of fluid in the interstitium
  • once obstruction is relieved, unopposed venous hydrostatic pressure leads to pulmonary edema
59
Q

Tx of POPE

A
  • self limited, clears within 48 hours
  • tx depends on severity of hypoxemia
  • re-establish airway (jaw thrust, chin lift)
  • supplemental oxygen
  • CPAP
  • reintubate and use PEEP
60
Q

Emphysema

A

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

– Airway collapse happens during exhalation.

– Increase work of breathing.

• Can have relatively advanced disease with preservation of PaO2 , and usually do not retain CO2 .

– “Pink Puffers”

– Tendency to exhale through pursed lips to provide end-expiratory pressure.

61
Q

Spirometry w Emphysema

A

– Decreased FEV1

• When FEV1 is < 40% of normal, dyspnea is seen during ADL’s

– Decrease in FEV1/FVC

– Decreased FEF 25-­‐75%

– Diminished air flow at all volumes

– Increased RV

– Normal to increased FRC and TLC

Radiographically you will see hyperlucency and hyperinflation (flat diaphragm)

62
Q
A

emphysema radiograph

  • hyperlucency w hyperinflation (flat diaphragm)
63
Q

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 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)
64
Q

Blue Bloater

A
  • seen in chronic bronchitis
  • hypoxemia and respiratory acidosis lead to pulmonary vasoconstriction and pulm HTN
  • may lead to cor pulmonale w RV hypertrophy and R axis deviation
65
Q

Spirometry w Chronic Bronchitis

A
  • FEV1/FVC decreased
  • FEF 25-75% is decreased
  • increased RV
  • normal to increased FRC and TLC due to slowing of expiratory airflow and gas trapping behind prematurely closed airways
  • greater WOB at high lung volumes
66
Q
A
  • chronic bronchitis x-ray
  • non specifix w bronchial wall thickening
  • increased bronchovascular markings, enlarged vessels and cardiomegaly
  • scarring of tissue scauses irregular bronchovascular structures
  • maintains curvature on diaphragm vs emphysema which is flat
67
Q

Asthma

A
  • chronic airway narrowing due to bronchial hyperactivity
  • exacerbations
  • patho not completely known, IGE mediated
  • increased cAMP = bronchodilation and sympathetic stimulation of B2
  • increased cGMP = bronchoconstriction and PS stimulation of muscarinic
68
Q
A
  • asthmatic x-ray
  • normal cardiomediastinal contours
  • no pleural abnormalities, no collapse or consolidation, unremarkable x-ray
69
Q

Beta 2 agonists

A
  • bronchodilator thearpy
  • albuterol, metaproterenol, ceprenaline
  • relatively free of a1 and b1 effects
70
Q

phosphodiasterase inhibitors

A

methylzanthines

  • oral or IV
  • inhibit breakdown of cAMP
  • aminophylline
71
Q

Parasympatholytics

A
  • block the effect of ACh on bronchial smooth muscle
  • ipratroprium (does not have the same SE as atropine, less tachycardia)
72
Q

COPD Anesthetic Mgmt

A
  • intraoperatively, volatiles provide bronchodilation and may attenuate regional hypoxic vasoconstriction (R to L shunt)
  • N20 use carefully in pts w pulmonary bulae, can cause diffusino hypoxia
  • opioids be very careful, extreme sensitivity, opioids will exacerbate breathing difficulties
73
Q

COPD and Mechanical Ventilation

A
  • large TV (10-15 mL/kg)
  • Slow RR (6-10)
  • increased expiratory time
  • avoid high PIP especially w pulmonary bullae
  • PEEP not necessary, may impede expiratory air flow
  • use sigh mode
  • extubation, use post op vent FEV1/FVC ratio of <0.5, pre-p[ PaCO2 of >50

Anesthesia Pharm Exam 3 (6 decks)

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