Pulm Pharm and Phys Flashcards

(73 cards)

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
Pathologic Deadspace
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.
26
Shunt
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
27
Compliance
* 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
28
Normal lungs will expand \_\_\_\_\_mL of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.
• Normal lungs will expand _130ml_ of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.
29
Boyle's Gas Law
At a constant temperature, pressure is inversely proportional to volume - as pressure increases, volume decreases - as pressure decreases, volume increases
30
static compliance
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
dynamic compliance
P/V relationship when air IS moving - decreases w airway obstruction such as foreign body and bronchospasm
32
Intrapulmonary pressure
- pressur ewithin the alveoli - negative w inspiration, positive w expiration
33
Intrapleural pressure
- 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
Is intrapleural pressure more negative in the dependent or non-dependent lung?
- more nebative in the non-dependent lung
35
V:Q Ratio
**_- 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
FRC
functional residual capacity, lung volume at end of normal exhalation - obese = lower FRC
37
RV
residual volume - volume remaining after maximal exhalation
38
VC
vital capacity - max volume of gas that can be exhaled following maximal inspiration
39
Normal PFT Values
FEV1 - 4L/sec FVC - 5L/sec FEV1/FVC = 4/5 = 0.8 or 80%
40
FEV1
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
FVC
- normal 5L/sec - volume of gas that can be exhaled during a forced expiratory maneuver
42
FEV1/FVC
ratio used to distinguish between obstructive and restrictive diseases - normal = 4/5 = 0.8 = 80%
43
FEF 25-75%
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
Extrathoracic Obstruction
- inspiration is impaired - ie: vocal cord paralysis w inspiratory stridor, pharyngeal muscle weakness, papilloma in airway ***can be overcome by using ETT***
45
Intrathoracic Obstruction
- 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
fixed large airway obstruction ie: mucous plug in ETT, kinked ETT
47
Restrictive Pulmonary Disease
- 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
Obstructive Pulmonary Disease
- 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
Acute Intrinsic
- restrictive lung disease like pulmonary edema - water and solutes accumulate in the interstitial tissues causing lungs to become stiff - aspiration, ARDS, POPE, CHF
50
Chronic Intrinsic
- restrictive lung dx - changes in elastic tissue in lung lead to decreased ompliance - ie: sarcoidosis, drug-induced pulm fibrosis (amiodarone, bleomycin)
51
Chronic Extrinsic
- restrictive lung disease - disorder of the chest wall and intra-abdominal changes ie: obesity, pregnancy, kyphosis, SCI transection, muscular dystrophy
52
Indicators of Increased Risk of Post-op Pulmonary Dysfunction
- 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
Anesthetic Mgmt of Restrictive Lung Dx
- 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
Laryngospasm
- 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
Treatment of Laryngospasm
- 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
POPE
- 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
High Negative Intrapulmonary Pressure
- 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
How does pulmonary edema develop when an obstruction is relieved?
- 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
Tx of POPE
- 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
Emphysema
• 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
Spirometry w Emphysema
– 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
emphysema radiograph - hyperlucency w hyperinflation (flat diaphragm)
63
Chronic Bronchitis
* 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
Blue Bloater
- 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
Spirometry w Chronic Bronchitis
- 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
- 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
Asthma
- 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
- asthmatic x-ray - normal cardiomediastinal contours - no pleural abnormalities, no collapse or consolidation, unremarkable x-ray
69
Beta 2 agonists
- bronchodilator thearpy - albuterol, metaproterenol, ceprenaline - relatively free of a1 and b1 effects
70
phosphodiasterase inhibitors
methylzanthines - oral or IV - inhibit breakdown of cAMP - aminophylline
71
Parasympatholytics
- block the effect of ACh on bronchial smooth muscle - ipratroprium (does not have the same SE as atropine, less tachycardia)
72
COPD Anesthetic Mgmt
- 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
COPD and Mechanical Ventilation
- 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