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E2 Flashcards

1
Q

What is the most common problem with divers and why does it occur?
What law is this a result of?

A

Expansion on ascent due to failure to exhale during ascent
Boyle’s Law (P1V1=P2V2)
Tx!: recompression, life support

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2
Q

What are 3 things that can happen due to compression on descent?

A

mask squeeze (unique to descending), ear drum rupture, middle ear squeeze

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3
Q

What is Boyle’s law?

A

P1V1=P2V2; gas volume decreases in direct proportion to applied pressure when temperature remains constant

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4
Q

What is Dalton’s law?

A

each gas in a mixture exerts a partial pressure that is in proportion to its concentration; Ptotal= Pnitrogen + Poxygen + PH2O + Pother

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5
Q

This condition in divers occurs when you have too much O2. Can cause alveolar & endothelial membrane damage. Use ______ Law to determine what concentration of O2 you should have in your tanks to prevent this.

A

oxygen toxicity; Dalton’s Law; mixtures of tank gas with helium and decreased O2 help prevent

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6
Q

occurs in divers when there is an increase in amount of dissolved N2 in lipid membranes of CNS & in blood; acts as anesthetic and affects divers similarly to EtOH

A

Nitrogen Narcosis/Toxicity; “Rapture of the Deep”; prevent by substituting helium for nitrogen gas in tank

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7
Q

caused by too rapid rise to the surface leading to creation of nitrogen bubbles in places such as blood vessels, heart, joints, brain, etc.

A

Decompression sickness, bends, or caisson’s disease; Tx!= immediate recompression w/ gradual drop in pressure to allow gas to dissolve slowly

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8
Q

the most common mechanism of injury in diving (hyperbaric conditions) is ______

A

barotrauma (caused by creation of pressure differentials during descent and ascent during diving)

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9
Q

the acute increase in ventilation at high altitudes (hypobaric conditions) is the result of ______, as sensed by what? These are stimulated when?

A

(acute) hypoxia; peripheral chemoreceptors, stimulated when PAO2 is less than 60 mmHg

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10
Q

what are some ways the body acclimates to altitude?

A

hyperventilation; increased hematocrit and blood volume–increasing blood viscosity (increases load on heart); increased EPO production by kidneys leads to RBC production; increased capillary growth in tissue; plasma volume decreases (due to hyperventilation and reduced water intake)

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11
Q

Describe acute mountain sickness (AMS)

A

from 5 hours to 5 days after reaching 8000 ft or higher. Headache, nausea, weakness, insomnia, dyspnea. Fluid retention, treated w/ diuretic. Least severe. Symptoms decrease over days.

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12
Q

Describe High Altitude Cerebral Edema (HACE).

A

more serious than AMS; ataxia & inability to walk cardinal signs; swelling can cause brain ischemia & herniation

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13
Q

Describe High Altitude Pulmonary Edema (HAPE).

A

most serious of all altitude pathology, highest mortality; most often in young athletic males; mandates return to lower altitude immediately; cardinal sign is hemoptysis–coughing up blood

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14
Q

What are the signs of infant respiratory distress syndrome (IRDS)? What is another name for the disorder?

A

tachypnea, grunting, nasal flaring, subcostal retractions, cyanosis (not always); looks like frosty beer mug on film; aka hyaline membrane disease

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15
Q

What is RDS?

A

a surfactant deficiency; leads to alveolar collapse and impaired gas exchange

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16
Q

What cells secrete surfactant? At what gestational stage?

A

Type 2 pneumocytes beginning around 24 weeks gestation

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17
Q

What are risk factors for RDS?

A

prematurity; male & Caucasian; infant of diabetic mother; patent ductus arteriosus; previous baby w/ RDS

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18
Q

IRDS differential

A

1) Transient Tachypnea of Newborn (TTN) aka Retained Fetal Lung Fluid (at risk: C-section; failure of fetal lung fluid to be reabsorbed, failure of Na channel reversal)
2) Congenital Pneumonia (elevated WBC; maternal fever, prolonged rupture of membranes)
3) Spontaneous Pneumothorax (at risk from difficult deliveries/birth trauma; large for age)
4) Congenital Diaphragmatic Hernia (see on films; decreased breath on left & heart sounds)

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19
Q

more and more air accumulates in the pleural cavity w/ each breath

A

tension pneumothorax; medical emergency, accumulating air puts pressure on organs of the chest

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20
Q

there is air in the pleural cavity, but it does not accumulate w/ each breath

A

non-tension pneumothorax

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21
Q

pneumothorax w/o any blunt force trauma or medical procedure

A

spontaneous pneumothorax; two types: primary (w/o any existing lung pathology) & secondary (arising due to lung disease such as COPD)

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22
Q

pneumothorax arising due to blunt force trauma or medical procedure

A

non-spontaneous pneumothorax; two types: traumatic (blunt force trauma, GSW, knife wound, car accident) & iatrogenic (trauma due to medical procedure ex: pacemaker insertion)

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23
Q

______ is a partial or total collapse of lung; which way will mediastinum shift?

A

atelectasis; mediastinum shifts toward side of collapse (as opposed to in pneumothorax shifts away from side with air)

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24
Q

inflammation of the pleural cavity; results in severe sharp chest pain with each breath

A

pleurisy/pleuritis
visceral layers insensitive to pain; parietal pleural innervated by somatic afferent and intercostal nerves–perceives pain; viral infections most common cause

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25
Q

What part(s) of the airway does gas exchange occur?

A

respiratory bronchioles, alveolar ducts and alveolar sacs

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26
Q

complete absence of spontaneous ventilation

A

apnea

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27
Q

difficulty of breathing that the individual is aware of

A

dyspnea

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28
Q

increased depth (volume) of breathing w/ or w/o increased frequency

A

hyperpnea

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29
Q

decreased RR

A

bradypnea

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30
Q

rapid rate of breathing

A

tachypnea

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31
Q

dyspnea which occurs when lying flat, causing person to have to sleep propped up or sitting in a chair

A

orthopnea

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32
Q

What is lung compliance?

A

softness of lung; C=V/P

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33
Q

Hydrostatic pressures use what units? What about partial pressure units?

A

hydrostatic pressures= cm H2O

partial pressures= mmHg

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34
Q

the amount of gas present in the lungs when your mouth is open & respiratory muscles are relaxed; defined by the equilibrium situation in which the elastic recoil forces of the lung and chest wall are equal and opposite

A

functional residual capacity (FRC) of the lung

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35
Q

elastic recoil forces in the lung:

the chest wall tends to _____ and the lung tends to _____

A

chest–expand; lung–collapse

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36
Q

lung elastic recoil forces are the result of:

A

1) lung tissue elastic recoil & 2) surface tension forces; ST is the main contributor

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37
Q

a _____ is a vascular pathway in which there is no gas exchange

A

shunt; ex: blood comes from right side of heart and goes through lung w/o undergoing gas exchange (this is called right-to-left shunt)

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38
Q

What is the main component of surfactant? What is the primary surface tension lowering surfactant?

A

90% phospholipids, 10% protein; DPPC (dipamitoyl phosphatidyl choline)

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39
Q

What cells secrete surfactant?

A

type II alveoli cells

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40
Q

What is the major role of surfactant? Where does it interact?

A

lower surface tension; positions itself at gas-liquid interface

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41
Q

Are inspiration and expiration active/passive processes? What muscles are involved?

A

inspiration: active; main mover= diaphragm; external intercostal muscles lift ribs; accessory muscles not involved in quiet breathing but can be used in exercise, coughing, sneezing, or disease
expiration: passive; driven by elastic recoil of lung; diaphragm relaxes
forced exhalation: internal intercostal muscles; abdominal muscles; during exercise or hyperventilation

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42
Q

What is transmural pressure?

A

pressure difference inside and outside a given system; in lungs: alveolar pressure minus pleural pressure

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43
Q

What drives exhalation?

A

elastic recoil forces of the lungs

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44
Q

pleural pressure is always ______ in quiet breathing; why?

A

negative; so the alveoli do not collapse

-during forced expiration, will become positive, pushes air out of lungs

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45
Q

Describe process of inhalation/exhalation with relevance to various pressures in alveoli, intrapleural space, transmural, and atmospheric.

A
  • All pressures are relative to atmospheric pressure which is denoted as 0 cmH2O.
  • Transmural pressure is the difference in alveolar and pleural pressures.
  • Air flow occurs when there is a pressure difference.
  • Air will flow to the location of lower pressure.
  • To fill the lungs w/ air, the alveolar pressure lowers from 0 cmH2O to a negative #
  • When exhale, pressure in alveoli increases, driving airflow outside of body
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46
Q

What is specific compliance?

A

Accounts for size differences in people; specific compliance = compliance/FRC

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47
Q

How is compliance measured? What is the equation for total pulmonary compliance?

A

measured by spirometry; 1/total C= 1/lung C + 1/chest wall C (this is unique to lungs!)

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48
Q

What protein is deficient in emphysema? What is a risk factor in the disease?

A

alpha-1-antitrypsin; smoking

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49
Q

tissue destruction (often in emphysema); increased breakdown of structural proteins

A

alveolar simplification–loss of entire alveoli

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50
Q

most common subtype of emphysema; affects central portion of secondary pulmonary lobules around central respiratory bronchioles, typically in superior lungs/lobes; spreads peripherally

A

centrilobular (centriacinar) emphysema; assoc. w/ long-term smoking, occupational exposure

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51
Q

subtype of emphysema that destroys entire alveolus uniformly; predominantly in lower half of lungs

A

panacinar (panlobular) emphysema; often in pts. w/ homozygous alpha-1-antitrypsin deficiency or who abuse Ritalin

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52
Q

What effect would each of the following factors have (increase/decrease) on compliance (and PV curve)?
Fibrosis, Emphysema, Age, Surfactant (loss of), Obesity, Surgical Removal of One Lung

A
  • fibrosis, obesity, & loss of surfactant decrease compliance (shift PV curve right)
  • In surgical removal of one lung, shifts, right (dec. C)
  • emphysema & age increase compliance (shift PV curve left) due to loss of elastic fibers
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53
Q

Where is the greatest airway resistance? Why is this?

A

The largest airways (bronchus) bc there are fewer in number; total resistance of airways arranged in parallel is = to the sum of reciprocal Rs

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54
Q

Where is the greatest flow velocity? Why?

A

the large airways (bronchus); turbulent flow here; higher resistance

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55
Q

Describe passive exhalation.

A
  • At end inspiration, all muscles are relaxed.
  • Elastic recoil forces of lung cause alveoli pressure to be positive
  • relax diaphragm, volume of thoracic cage decreases (pleural pressure increases but remains negative)
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56
Q

Describe forced exhalation.

A
  • abdominal muscles push gut up against diaphragm
  • pleural pressure becomes positive
  • alveolar pressure positive (w/ pressure drop along airway)
  • issue in pts w/ soft airways (emphysema–diminished elastic recoil)
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57
Q

during forced exhalation, at some point the pressure outside the airway is greater than the pressure inside, from that point on, airway subjected to collapsing transmural forces; what is it called and why is it not an issue in normal airways?

A

“dynamic compression;” airways are reinforced by cartilage rings that resist collapse

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58
Q

How does Bernouilli’s effect take place in the airways? How is this counteracted?

A

faster the airflow, the lower the pressure exerted on the inside of the airway walls; the lower the pressure inside, promotes collapse; airflow is fastest in the large airways, which is why they have cartilaginous rings to prevent collapse

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59
Q

What is the tethering of airways? What happens in emphysema and asthma pts?

A
  • aka radial traction; refers to action of lung tissue on airway walls, tending to hold them open;
  • if there is a loss of tethering & airway size decreases, velocity of flow increases (and airways are more likely to collapse)
  • emphysema: use forced exhalation; air moves faster; have loss of radial traction and tissue loss; high tendency of airway collapse
  • asthma: causes airway constriction; increased flow velocity, lower pressure in airway

**collapsed units are perfused but not ventilated–acting as shunts impairing gas exchange

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60
Q

volume of air inspired or expired w/ each breath

A

tidal volume (TV)

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61
Q

air a person breathes but is not used for gas exchange; fills respiratory passages such as nose, pharynx, trachea

A

dead space volume

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62
Q

volume of air in lungs that cannot be exhaled/pushed out of lungs; volume of air left in lungs after a forced exhalation

A

residual volume (RV)

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63
Q

volume of air in lungs after maximal inspiratory effort

A

total lung capacity (TLC)

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64
Q

amount of air that can be exhaled during a forced exhalation

A

forced vital capacity (FVC)

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65
Q

amount of air exhaled in first second of a forced exhalation

A

forced expiratory volume in 1 second (FEV1)–should be 80% of FVC

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66
Q

volume of air in lung when lung and chest wall have equal recoil force; volume of gas left in lungs after a normal expiration, all lung muscles are relaxed

A

functional residual capacity (FRC); FRC= ERV+RV

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67
Q

maximal amount of air which can be inhaled or exhaled by a person

A

vital capacity

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68
Q

What values cannot be directly measured by spirometer?

A

RV, FRC, & TLC (anything involving RV!)

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69
Q

What is a way to measure FRC? any limitations?

A
  • helium dilution technique; cannot measure FRC for pts w/ emphysema or COPD (high airway resistance); for these pts, use body box plethysmography
  • introduce known amount of He into bag, let patient breathe in/out until equilibriated, then measure pressure of He
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70
Q

What happens to FRC as a person ages? Supine vs. standing? Pregnancy or obesity? Lung resection? Emphysema and COPD? Kyphoscoliosis?

A

FRC= ERV+RV

  • aging increases FRC because there is an increase in compliance & decrease in elastic recoil of lung
  • standing: guts pull diaphragm down, increasing FRC
  • supine: guts push up on diaphragm, decreasing FRC
  • pregnancy & obesity: decrease FRC (mass pushes up on diaphragm)
  • Lung resection: decreased FRC
  • Emphysema/COPD: have larger RV’s, cannot empty lungs efficiently, therefore, increased FRC (have larger thoracic cages)
  • kyphoscoliosis: underventilation of lungs, decrease RV & FRC
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71
Q

List the obstructive diseases. What are they characterized by?

A 
CCABE- high airway resistance
cystic fibrosis (CF), COPD, asthma, bronchitis, emphysema
COPD= bronchitis + emphysema
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72
Q

List the restrictive diseases. What are they characterized by?

A

WPASS- low lung compliance (increased stiffness of lungs & increased lung recoil)
Wegener’s granulomatosis, pulmonary fibrosis, asbestosis, silicosis, sarcoidosis

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73
Q

Compare normal FEV1/FVC values to those in obstructive and restrictive disease. Describe what happens to both variables. What about slope of FEF25-75%?

A

normal FEV1/FVC ratio = 0.80
obstructive= less than 0.70 (both FEV1 & FVC decrease, but FEV1 decreases significantly)
restrictive = normal or higher than normal value (both FEV1 & FVC decrease)
slope of FEF25-75% is decreased for both restrictive and obstructive disease

74
Q

FEV1 is an estimate of airway _____. The larger the FEV1, the ______ the ______.

A

estimate of airway resistance; larger the FEV1, the lower the resistance–why can diagnose pulmonary diseases (very low FEV1 indicative of obstructive disease–high airway resistance)

75
Q

Describe the shift in PV loops of obstructive and restrictive diseases. Why does this occur?

A

obstructive: shifts left toward larger volumes bc lung tissue is more compliant; expiratory flow rate is decreased (from airway collapse on exhalation)
restrictive: shifts right toward smaller volumes bc lung is stiffer (less compliant)

76
Q

What happens to PEF in obstructive and restrictive diseases?

A

Peak expiratory flow…
obstructive- decreases; expiration is low & prolonged bc of high compliance & dynamic collapse
restrictive: decreases; lungs are stiffer, only small volume is inhaled and expired quickly

77
Q

What are the shapes of obstructive vs. restrictive disease on flow vs. volume graphs?

A 
obstructive= pointed w/ scooping/concavity; slope is lower than normal 
restrictive= witch hat
78
Q

What is the methacholine challenge test used for? Describe key steps/factors. What are some exceptions to results?

A

Used to detect hyperreactive airways. Sensitive test for asthma.
-five stages; inhale progressive concentrations of methacholine; after each stage, pt performs spirometry; when there is 20% reduction in FEV1, test is terminated & considered positive for hyperactive airway; pt given bronchodilator for recovery
-[methacholine] required to produced 20% reduction in FEV1 = PC20
-PC20 of less than 8mg/mL suggest clinically important airway hyperactivity
-if drop in airway is less than 20% after 5 stages, challenge test is negative for hyperactivity
Exceptions:
1) Pts w/ COPD, who smoke, or have allergic rhinitis will test positive (and may not have asthma)
2) asthma pts taking anti-inflammatory drugs may test negative
3) pts whose asthma is triggered by specific agents (cold, allergens) may test negative

79
Q

In the methacholine challenge test, when comparing values, do you use the baseline or control values?

A

control

80
Q

Describe what happens in fixed and intra vs. extrathoracic variable obstructions and their corresponding changes on flow-volume graphs.

A
  • fixed: affects both forced inspiration & forced exhalation; both decreased on flow volume graph
  • variable intrathoracic: constriction of airway during forced exhale, mostly affects expiration; top portion of graph decreased
  • variable extrathoracic: airway gets compressed, mostly affects inspiration: bottom portion of graph decreased
81
Q

Where is pleural pressure greatest? Why is there a difference in pleural pressures in the thorax?

A

bc of gravity, uniform effect of pleural pressures is distorted by the pressures generated by the weight of the lung. At bottom of thorax, gravity presses lung tissue against the chest wall & pleural pressure is less negative. Pleural pressure is most negative at the uppermost part of the thorax and least negative in the lowermost part of the thorax.

82
Q

True/False: all alveoli are inflated to the same size

A

False; due to the gradient of pleural pressures, alveoli at different locations are inflated to different sizes
-alveoli inflation lowest at bottom of lung where transmural (inflating) pressure is least

83
Q

Which part of the lung is ventilated most?

A

the lowest part; whether upright, supine, etc; whichever part is lowest will be most ventilated; this is caused by gravity

84
Q

What does alveolar ventilation rate depend on?

A

respiratory rate, tidal volume, and dead space volume

85
Q

volume of air left in conducting airways

A

anatomical dead space

86
Q

volume of air left in unperfused alveoli

A

alveolar dead space; very small in normal adult; useful measure of lung disease & ventilation-perfusion mismatch

87
Q

What is physiological dead space?

A

the sum of alveolar dead space and anatomical dead space

88
Q

What are the assumptions made in Bohr’s method of measuring physiological dead space?

A

1) the content of CO2 in the atmosphere is negligible
2) all expired CO2 comes from alveoli
3) all the CO2 comes from alveoli which are both ventilated & perfused, and none from dead space

therefore, if there is more dead space, it will contribute less CO2

89
Q

What are factors that increase physiological dead space?

A

ventilators, snorkels, tubes; phys. dead space strongly elevated in pulmonary embolism (or lung units w/ high V/Q ratio)

90
Q

Alveolar ventilation is proportional to what?

A

volume of CO2 & inversely proportional to PCO2; also proportional to metabolic rate (and temperature)

91
Q

Describe hypoventilation.

A

VA (alveolar vent.) is decreased; alveolar & arterial PCO2 increase; this lowers blood pH, causes respiratory acidosis (if CO2 production constant)

92
Q

Describe hyperventilation.

A

VA (alveolar vent.) is increased; alveolar & arterial PCO2 decrease; this increases blood pH, causes respiratory alkalosis; eliminating/breathing out more CO2 from body (if CO2 production constant)

93
Q

When looking at blood gas values for respiratory function, what do you use?

A

ARTERIAL blood gas values; NEVER venous- they do not tell you anything about respiratory function

94
Q

low partial pressure of oxygen in arterial blood

A

hypoxemia

95
Q

high partial pressure of carbon dioxide in arterial blood

A

hypercapnia

96
Q

What affects partial pressure of a gas?

A

the amount of dissolved gas ONLY
once O2 and CO bind w/ Hemoglobin, they do not exert PP; when CO2 reacts to form carbonic acid or bicarb, it does not exert PP anymore

97
Q

PO2 is _____ proportional to dissolved oxygen content. if 0.3 vol% O2 in plasma =PaO2 =100mmHg, then 0.6 vol% = ?

A

directly proportional; 200 mmHg

98
Q

What are the ways oxygen is held in blood?

A

1) dissolved in plasma; solubility = 0.003 ml O2; CO2 solubility = 20x O2 (0.06 ml)
2) bound to hemoglobin

99
Q

Which way will the reaction shift (oxygen binding w/ hemoglobin) at…

1) high altitude
2) breathing 100% oxygen
3) breathing high pressure (hyperbaric) oxygen
4) under hypoxic conditions

A

1) left
2) right
3) right
4) left

100
Q

Describe transport of O2 from alveoli to tissue using hemoglobin.

A

Oxygen (humidified air) enter alveolus. O2 diffuses down partial pressure gradient into plasma, raising PO2 in plasma. O2 associates w/ Hb for transport (in RBC). During transport, O2 dissociates from Hb, dissolves in the plasma, diffuses out of the blood vessel and reaches the target tissue as dissolved O2.

When O2 delivered to a tissue, it is dissolved gas that moves out–this lowers PO2 in plasma and causes Hb to release O2.

**All moving down partial pressure gradients.

101
Q

What are chemical properties of CO that make it detrimental to health?

A

1) it reduces O2 transport by occupying O2 binding sites; has 200x affinity for Hb; partial pressure of CO is 0 in blood
2) raises affinity of the remaining O2 binding sites for O2 (have higher affinity for O2 & makes unloading only happen when PO2 very low)

102
Q

maximal amount of oxygen Hb is capable of carrying; does not include dissolved oxygen

A

oxygen capacity

  • decreased in anemia and CO poisoning
  • increased in polycythemia
103
Q

What measures Hb saturation? What are limitations?

A 
pulse oximeter; 
anemia (does not tell you HOW MUCH Hb there is, just its saturation w/ O2);
CO poisoning (does not tell you what Hb is saturated w/)
104
Q

condition that occurs when the lungs cannot remove all the CO2 the body produces

confusion, fatigue, lethargy, SOB, sleepiness

A 
respiratory acidosis
excess CO2 (hypercapnia) causes blood to bceome too acidic; CO2, when dissolved in plasma becomes carbonic acid, which dissociates to produce H+
105
Q

condition that occurs when CO2 is removed too quickly from lungs (due to hyperventilation)

dizzy, light-headed, numb hands/feet; severe cases may cause seizures

A

respiratory alkalosis

106
Q

What values are used to assess pulmonary function? Why?

A

ABGs! arterial blood gases bc CO2 and O2 content in arterial blood is determined primarily by lungs

venous blood has been exposed to peripheral vascular beds where gas exchange w/ tissues alters gas concentrations

107
Q

definition: partial pressure of oxygen when Hb is 50% saturated

A

P50; normal P50 = PaO2 about 26 mmHg

108
Q

What are some variables that can cause shifts in the hemoglobin curve?

A

temperature, [H+], CO2, DPG, CO, O2 saturation

109
Q

What occurs in exercising tissues and is reflected in the oxyhemoglobin graph?

A

high [H+]; increased temperature; high PCO2; all cause HbO2 curve to shift to right (favor unloading of oxygen)

110
Q

Explain the role of 2-3 DPG (BPG).

A

lowers the affinity of Hb for oxygen. DPG production accelerated at high altitudes and in persistent hypoxia.
-can be degraded in stored blood (blood banks must monitor levels)

111
Q

Compare/contrast fetal hemoglobin to adult.

A

Fetal Hb’s affinity is much greater for O2 than adults (has a lower P50 value). Oxygen sat curve is left shifted for fetal Hb.
Fetal Hb is unable to interact w/ 2,3 DPG, accounting for this difference (adult Hb alone would have higher affinity if DPG levels did not reduce it)

112
Q

What is erythropoesis?

A

an adaptation to chronic hypoxemia; generation of new RBCs; takes 2-3 weeks; increases hematocrit & O2 carrying capacity of blood; increases blood volume and viscosity of blood- additional workload on heart (polycythemia–elevated hematocrit)

113
Q

How is CO2 transported in blood? What is the main form of transport?

A

1) dissolved in plasma
2) as bicarb (HCO3-)– main form of transport (85%)
3) bound to Hb (carbamino)

114
Q

What is Hambruger (chloride) shift?

A

Cl- ions move into (or out of if in lungs) RBCs to maintain electroneutrality when CO2 is moving via diffusion…
In tissues: CO2 diffuses into RBC and is converted quickly through steps to H+ & HCO3-; H+ is buffered by Hb, & HCO3- leaves RBC and is transported in plasma. Cl- moves into cell to maintain electroneutrality
In lungs: Hb gains O2, displaces H+, driving reaction of H+ & HCO3- back to H2O and CO2; HCO3- in plasma reenters RBC and Cl- in lungs moves out; HCO3- picks up H+ giving rise to carbonic acid which dissociates to CO2 which dissociates into alveoli

115
Q

Where is carbonic anhydrase located? Where are H+ ions generated (from this reaction)?

A

Both are in the RBC; also where Hb is located, so Hb can buffer H+ and minimize change in pH from H+

116
Q

What is the PCO2 if you mix 2 blood samples w/…
sample 1) 100 ml & PCO2 44 mmHg
sample 2) 100 ml & PCO2 46 mmHg

A

mixture= 45mmHg; because of the linear relationship between PCO2 & CO2 blood content, you can just average the two together

117
Q

What is the PO2 if you mix 2 blood samples w/…
sample 1) 100 ml & PCO2 100 mmHg
sample 2) 100 ml & PCO2 40 mmHg

A

between 50 and 60 mmHg; there is a nonlinear relationship between PO2 and O2 blood content; you cannot simply average the PO2 numbers; must first find the two oxygen contents and then find their average and corresponding PO2

118
Q

What are some non-respiratory functions of the lungs?

A

1) defense mechanism: alveolar macrophages engulf bacteria, foreign particles; can activate immune cells
2) air-conditioning: nasal muscosa & turbinates heat and humidify air as it reaches the tracheobronchial tree
3) olfaction: detect odors and hazardous substances
4) filtration, removal of particles: remove particles; entire respiratory tract (to the bronchioles) lined w/ cilia that move mucus upwards (mucociliatory escalator)\
5) blood filter: capillaries can trap clots, gas bubbles, fat cells, emboli (& stop them from going to heart or brain)
6) blood reservoir: can shift blood from lungs into systemic vessels
7) metabolism of circulating substances: endothelial cells in lung vasculature involved in metabolism of vasoactive substances in circulation

119
Q

pulmonary arteries carry _____ blood, while pulmonary veins carry _____ blood

A

pulm arteries= deoxygenated

pulm veins= oxygenated

120
Q

Compare pulmonary blood vessels to systemic vessels.

A

pulm capillaries have very thin walls and low vascular resistance, soft & easily distended;
pulm vessels offer less resistance to blood flow, lower intravascular pressures than those in systemic vessels;
presence of anastomoses in pulm vessels

121
Q

Where is perfusion greatest in the lungs?

A

greatest in lowest part of lung; least in top part; resistance to blood flow decreases as you go to the bottom of the lung

122
Q

Patients on positive pressure ventilator with PEEP increase perfusion in what types of zones?

A

zone 1; PA is positive during mechanical ventilation; high alveolar pressure causes collapse of pulmonary capillaries increasing zone 1;
hemorrhage or general anesthesia also increase zone 1

123
Q

all fluids flowing through a non-distensible tube in laminar flow encounter resistance to flow; in the pulmonary circulatory system this describes

A

PVR (pulmonary vascular resistance)

124
Q

What is cor pulmonale?

A

right heart failure; pulmonary vascular smooth muscle contracts throughout the lung, resistance is increased, and workload on right heart is increased

125
Q

Explain vasoconstriction in the lungs.

A

an increase in PVR: pulmonary vascular smooth muscle contracts/vasoconstricts in low PO2 (hypoxia induced) to divert blood away from area of low PO2 to distribute it to well-ventilated areas.

126
Q

What happens to PVR during exercise? Why?

A

decreases bc recruitment & distension
1) opening of previously closed arteries
2) increase in radius of existing blood vessels
(both occur at same time)

127
Q

What happens to PVR during the following:
a- removal of one lung
b- breathing at high altitude
c- mechanically ventilating lung w/ positive pressure
d- severe hypoxia
e- exercise

A 
a- decrease PVR in remaining lung
b- increase PVR
c- increase PVR
d- increase PVR
e- decrease PVR
128
Q

this type of pulmonary edema is caused by an increase in capillary pressure

A

hydrostatic/cardiogenic edema;
usually occurs in left heart failure; no change in Kf or sigma
characteristic Kerley B lines on film; cardiomegaly
use echocardiogram to diagnose

129
Q

type of pulmonary edema in which there is an increase in the permeability of the vessel wall that separates blood from the tissue

A

permeability edema (non-cardiogenic)
capillary wall is more porous/permeable to fluid or protein & vascular fluid exits vascular space bc the membrane is compromised
-principle disorder in ARDS
-Kf change

130
Q

severe form of lung injury marked by persistent lung inflammation & increased capillary permeability; usually observed after some form of insult to lung (infection or inhalation of toxin)

symptoms: breathlessness; dry cough; chest pain; rapid, shallow breathing

A

ARDS- adult respiratory distress syndrome

also have diffuse alveolar damage & pulmonary edema

131
Q

What is diffusion dependent on? When all variables held constant, what is the major determinant?

A

surface area, thickness of barrier, diffusion constant, and gradient of partial pressure;
difference in partial pressure is major determinant of rate of diffusion**

132
Q

Gas exchange is dependent on what factors…

A

partial pressure gradient
thickness & properties of membrane
alveoli surface area

133
Q

What does perfusion-limited refer to? What is an example of a perfusion limited gas?

A

O2 uptake is perfusion-limited: limited by how much blood flows into the pulmonary capillary;
the amount of gas that gets taken up is determined by how much blood you pump through the capillary; if you want to deliver more O2 to the body, you just pump more blood through the lung
other gases perfusion-limited: N2O & CO2

134
Q

What does diffusion limited mean? What gas is diffusion limited?

A

uptake of the gas is limited by the ability of the membrane to transfer it by diffusion

ex: CO; CO is diffusion limited due to its high affinity for Hb
- in lung disease, O2 transport often switches from perfusion limited to diffusion limited

135
Q

What is the DLCO test?

A

pulmonary function test to measure how well pts lungs exchange gases; based of principle PCO= 0 everywhere in blood; compare values to normal values; gas uptake determined by Fick’s law

136
Q

What is DLCO and what is it proportional to?

A

diffusing capacity; measure of conductance of the lung to a gas (efficacy of diffusion of the alveolar membrane)
proportional to area of alveolar capillary membrane,
inversely proportional to thickness of alveolar capillary membrane

137
Q

What will increase/decrease DLCO? (look at histo slides for reference)

A

DLCO reduced by obstructive (bc alveolar simplification and loss of capillary structures) & restrictive (bc thickened capillary membrane) diseases
-DLCO increased in alveolar hemorrhage (blood/Hb comes into alveoli), polycythemia (increase in Hb), obesity, shunts

NO change in DLCO: neuromuscular disease, chest wall deformitites, sometimes asthma & bronchitis

138
Q

What are the chemoreceptors we possess and what do they detect?

A

central- in brain- detect CO2
peripheral- in neck (aortic and carotid)- detect H+ mainly, CO2 (bc they contribute to H+ changes), & O2 if it drops below 60 mmHg

139
Q

What is the principle controller of ventilation?

A

PaCO2 (acting through central chemoreceptors)

140
Q

What does CSF lack? Why is this important?

A

does not have hemoglobin; buffering capacity is limited; H+ ions detected immediately

141
Q

How do central and peripheral chemoreceptors adapt?

A

central: central chemoreceptors detect increases/decreases in pH once CO2 is converted and transmit signals to respiratory component to increase/decrease alveolar ventilation
peripheral: they don’t!

142
Q

Describe the hypoxic stimulation of ventilation.

A

mediated only by peripheral chemoreceptors (just in carotid bodies); very fast in onset, does not adapt; occurs when PaO2 falls below 60mmHg

143
Q

What is the most powerful stimulus known to influence respiratory components? What is it mediated by?

A

H+ concentration in arterial blood; mediated by peripheral chemoreceptors

144
Q

Describe respiratory drive in lung disease patients.

A

Patients w/ low V/Q mismatch have hypoxemia & hypercapnia. Acidosis eventually compensated for by renal compensatory mechanism. Pt relies on hypoxic stimulus (peripheral chemoreceptors) to drive ventilation. Giving such a pt supplemental O2 will raise PaO2, relieve hypoxic drive, and may depress ventilation

145
Q

Describe the respiratory control centers.

A

located in the medulla

1) dorsal respiratory groups: mostly inpiration; control rhythmicity; get signals from chemoreceptors
2) ventral respiratory groups: inspiration & expiration; control muscles of upper airways (regular diameter during breathing)

146
Q

What are the apneustic and pneumotaxic centers? Where are they?

A

Located in pons;
apneustic center- continually sends neural impulses to DRG & VRG; referred to as “normal respiration cut-off switch”
apneustic breathing- respiratory cycle holds in inpiration which is periodically interrupted by expiration
pneomotaxic center- prevents apneusis; enhances and fine-tunes rhythmicity of breathing

147
Q

What are the hallmarks of congenital central hypoventilation syndrome (CCHS)?

A

central pattern generator is inoperative; rare congenital disorder; insensitivity of chemoreceptors to CO2, O2, and pH; no automatic control of respiration, voluntary breathing intact; issue when they sleep and conscious activity ceases- require permanent tracheostomy and connection to mechanical ventilation

148
Q

Examples of things that depress/increase ventilation.

A
  • alcohol and some drugs decrease ventilation
  • stimulants (caffeine, cocaine, meth) increase ventilation
  • fever increases ventilation
  • deep hypothermia depresses ventilation
  • pain and panic can increase ventilation
149
Q

type of breathing in which 10-30s of apnea is followed by gradual increase in volume and frequency of breathing until another period of apnea occurs

A

Cheyne-Stokes breathing; **crescendo to crescendo pattern; in pts of heart failure or brain damage
PCO2 of pulmonary blood changes in advance of PCO2 of respiratory neurons; however, respiration corresponds to PCO2 in brain where ventilation occurs

150
Q

breathing pattern characterized by rhythmic but deep respiration movements which alternate w/ long respiratory pauses at approx. regular intervals

A

Biot’s respiration; in meningitis patients or cerebral circulation; damage to respiratory center from trauma, stroke, opioids

151
Q

absence of airflow due to an occlusion in upper airway that lasts about 10 seconds

A

obstructive sleep apnea; often in obese people; upper airway blocked by too much fat around pharynx- pharyngeal muscles do not contract properly

  • can also happen if enlarged tonsils, deviated septum, large tongue, etc
  • thoracic effort will be continuous even if airflow stops
152
Q

pattern of breathing w/ normal deep inspiratory cycle interchanged w/ complete cessation of breathing

A

central sleep apnea; typically caused by problems w/ how brain controls breathing rather than occlusion of airway;
airflow and thoracic effort diagrams will match

153
Q

hyperventilation, gasping, deep & labored respiration, often in diabetic ketoacidosis, kidney failure, diabetic coma, or high acidosis

A

Kussmaul’s respiration

fast, pointed on airflow diagram

154
Q

What are the 2 pumps in the pulmonary system?

A

1) heart pumping blood into lung

2) chest wall pumping air into lung

155
Q

when there is V but no Q, this is…

A

dead space

156
Q

When there is Q but no V, this is…

A

a shunt; pure mixed systemic venous blood

157
Q

Describe low V/Q units.

A

under-ventilated but still perfused
act in shunt-like manner
increase A-a gradient
result of many partially obstructive and restrictive diseases

158
Q

Where does all CO2 come from?

A

ventilated and perfused alveoli

159
Q

Where is the highest V/Q ratio?

A

top of the lungs

160
Q

Which area has the highest V? Q? Why?

A

bottom part of lungs has highest V and Q due to gravity

161
Q

Why was the single lung transplant successful in pulmonary fibrosis but unsuccessful in emphysema patients?

A
  • in fibrosis pt, most of ventilation goes to new transplanted lung (other lung is stiff & has high recoil), & V/Q matching in transplant lung is ok
  • in emphysema pt, diseased lung is more compliant, so ventilation will go there; emphysema is also accompanied by tissue destruction and loss of pulmonary vascular bed, so perfusion will greater in transplanted lung… transplanted lung is underventilated & overperfused: a SHUNT; emphysematous lung has high V, low Q: contributes to dead space
162
Q

What determines PCO2 in an alveolar unit?

A

V/Q

Q brings CO2 in, V carries CO2 out

163
Q

What is PACO2 when…

1) there is V but no Q (V/Q= infinity)
2) there is Q but no V (V/Q=0)

A

1) 0 mmHg (same as room air)

2) 46 mmHg (same as venous blood-perfusion ok but no ventilation)

164
Q

PACO2 is _____ to V/Q; PAO2 is _____ to V/Q

A

PACO2: inversely proportional
PAO2: proportional

165
Q

What is PAO2 when…

1) there is V but no Q (V/Q= infinity)
2) there is Q but no V (V/Q=0)

A

1) 150 mmHg (same as moist room air)

2) 40 mmHg (same as venous blood)

166
Q

What treatment reverses hypoxic pulmonary vasoconstriction?

A

nitric oxide–vasodilator; causes smooth muscle relaxation

167
Q

total blockage, where V/Q= 0

A

absolute intrapulmonary shunt (true shunt)

168
Q

low V/Q mismatch is said to be a

A

shunt-like state

169
Q

What are the hallmarks of low V/Q mismatch?

A

large/high A-a difference, hypoxemia, and hypercapnia

-common in obstructive lung disease

170
Q

What are local lung level compensation mechanisms to low V/Q mismatch?

A
  • low PO2 causes local vascular contraction
  • low PCO2 causes airways to constrict locally

also have compensatory mechanism largely at play mediated by chemoreceptors to increase ventilation

171
Q

How does a shunt vs. low V/Q mismatch respond to 100% O2?

A

shunt: little affect/relief

low V/Q: significant change

172
Q

Where is the A-a gradient the largest?

A

at the top of the lungs

173
Q

a _____ is a blood flow through the lung that has no access to O2

A

shunt

174
Q

What are 5 causes for hypoxemia?

A

1) breathing air with low PO2 (high altitude)
2) hypoventilation- not exhaling as much CO2 (hypercapnia & hypoxemia), normal A-a gradient
3) shunts- large A-a gradient; little PaO2 change when administered O2
4) low V/Q mismatch- marked increase in PaO2 when administered 100% O2
5) diffusion problem (uncommon)

175
Q

What causes high V/Q ratios?

A

1- pulmonary embolism!!!

2- lung geometry and gravity

176
Q

Discuss PE and high V/Q

A

area of lung affected becomes dead space; right heart must work harder to force cardiac output through remaining parts of lung;
if PE is blood clot–immune response is elicited-local inflammation, pain, etc; may act on neighboring alveoli & airways and alter capillary permeability, causeing edema, destroy surfactant, and may cause alveolar collapse or atelectasis
-embolus causes blood to be diverted to another unit; respiration control system increases ventilation until PCO2 back to normal

177
Q

The conventional ventilator uses…

A

active inhalation, passive exhalation

178
Q

What ventilator does active inhalation and active exhalation?

A

high frequency oscillator?

179
Q

What ventilator is easiest on lungs and good for diseased patients?

A

high frequency jet ventilator

180
Q

What does ventilation refer to? What is the equation for it?

A

ventilation is how much CO2 is in the body; MV= RRxTv; MV directly impacts amount of CO2 in body

181
Q

how is oxygenation controlled? How can you increase it?

A

oxygenation controlled by mean airway pressure (MAP); can increase MAP by increasing PEEP

182
Q

How are total compliance, lung compliance, and chest wall compliance measured?

A

total: spirometry
lung: esophageal balloon technique
chest wall: total compliance equation

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