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Flashcards in Quiz #1 Deck (41):
1

Tracheal Wall Layers

1. mucosa
2. submucosa
3. adventitita

2

Respiratory epithelium cell types

(i) ciliated columnar cells,
(ii) mucous (goblet) cells,
(iii) brush cells,
(iv) endocrine cells and
(v) basal (stem) cells.

Ciliated cells are the most numerous and extend through the full thickness of the epithelium. Cilia propel the mucus, produced by goblet cells and seromucous glands, toward the mouth for disposal of entrapped particles.

Goblet cells are interspersed among the ciliated cells and also extend to the full thickness of the epithelium.

Brush cells are columnar sensory cells that are present in small numbers. Brush cells and the small granule endocrine cells cannot be identified in these slides. The nuclei of basal cells are prominent along the basement membrane

3

Alveolar-arterial equation

stuff= stuff q

4

Hemoglobin Curve Shifts

Right Shifts: P50 is increased,
increased CO2, temp and 2,3 DPG, decreased pH
Decreased affinity - unloading

Left Shifts: P50 is decreased
decreased CO2, temp and 2,3, DPG, increased pH
increased affinity - loading
(fetal hemoglobin)
CO causes leftward shift - binds to hemoglobin

5

Normal Lung Pressures

PaO2 (Partial pressure of O 2 in arterial blood) = 100
PCO2 (Partial pressure of CO2 in arterial blood) = 40

PVO2 (Par. pressure of O2 in mixed venous blood) =40
PVCO2 (Par. press. of O 2 in mixed venous blood)=46

PiO2 (Partial pressure of O 2 in dry inspired air)= 160
PiCO2 (Partial pressure of CO2 in dry inspired air) = 0

PAO2

6

Oxygen content in blood - equation

O2content=
(O2​-binding capacity×%Saturation)+Dissolved O2

O2 content = (1.34 × Hb × Sao2) + (0.003 × Pao2)

7

oxygen delivery

O2 delivery = O2 content X cardiac output

8

Hypoxemia

decrease in arterial P o 2
Causes:
1) high altitude - normal Aa gradient
2) hypoventilation - normal Aa gradient

Abnormal Aa gradient:
3) R to L shunt (giving supp O2 won't help)
4) diffusion defect (fibrosis)
5) V/Q defect

9

hypoxia

decreased O 2 delivery to the tissues - impacted by either decreased CO or O2 content in blood
- could be carrying capacity or saturation
if PaO2 abnormal - hypoxemia
If PaO2 normal - could be anemia, CO poisoning, cyanide, or decreased CO (less blood flow)

10

alveolar ventilation equation

VA= RR x (TV-Dead space)

11

alveolar gas equation

PAO2= PI O2 - PaCO2/R

12

Low atmospheric O2 (high altitude)

1) peripheral chemo receptors from carotid body are stimulated
2) central medullary CO2 reflexes are depressed (increased ventilation decreases CO2)
3) Herring-Breuer are unchanged because only active under exteme conditions - if TV is changed

13

Lung location impact

both ventilation and perfusion highest but V/Q ratio is greatest at the apex of lung

Apex: V/Q>3
- lots of ventilation (compared to perfusion): high O2, low CO2

Average; V/Q = .8

Base: V/Q

14

normal ABG

pH / PCO2 / PO2 / HCO3-­ 7.4/40/100/24

15

metabolic acidosis

Increased  [H+]  or  loss  of  HCO3-­ tends  to  lower  pH CO2 will decrease via hyperventilation
lactic acidosis in shock - diabetic keto-acidosis  

pH: low
PCO2: low
HCO3: low

16

respiratory acidosis

increased CO2
COPD  or  asthma • Sleep  apnea  and   obesity   hypoventilation • Opioid  overdose • Neuromuscular   disease    
compensation - kidneys will reabsorb more bicarb

pH: low
PCO2: high
HCO3: high

17

metabolic alkalosis

H+  losses  or  HCO3-­ retention   increases  pH
w/ vomiting or NG suction
compensate by hypoventilating to increase CO2

pH: high
PCO2: high
HCO3: high

18

respiratory alkalosis

decreased CO2 from hyperventilation
compensate by retaining less bicarb

pH: high
PCO2: low
HCO3: low

19

7.5/20/100/20

Respiratory Alkalosis

20

7.24/60/50/28

Respiratory Acidosis

21

7.2/20/100/12

Metabolic Acidosis

22

7.45/45/70/35

Metabolic Alkalosis

23

Oxygen Consumption

= CO⋅([O2]a −[O2]v).

24

requirements for an efficient O2 transport system

1 It must have sufficient capacity to do the job.

2 O2 Loading and unloading must be rapid, to be complete within the RBC transit time through the pulmonary and peripheral capillaries.

3 The Po2 must be high during unloading of O2 in the tissues, to maintain a diffusional flux of O2 from the capillary to the cells.

4 It must be able to adapt to changes in acid-base balance, O2 demand, and O2 supply.

25

efficient CO2 system

1. It must have sufficient capacity to do the job.

2. Loading and unloading must be rapid, to be complete within the RBC transit time through the peripheral and pulmonary capillaries.

3. It must operate at nearly constant pH, which means only small differences in Pco2 between arterial and venous blood.

4. It must be able to adapt to changes in CO2 production (O2 consumption).

26

V/Q ratio

increases with exercise (more ventialtion relative to perfucsion)

Normal:
ventilation (air into lungs): 4L/min
perfusion (blood into lungs): 5L/min
V/Q ratio: .8

when V/Q <1, there is not enough ventilation - perfusion being wasted, blood coming into lungs but not enough O2 for it to pick up
---> extreme: V/Q = 0 ---> R to L shunt (no ventilation)
venous blood goes directly to arterial system w/o being oxygenated

SHunt will not be helped by giving 100% O2***

anatomic: heart disease and bypasses lung (VSD)
physiologic: alveoli aren't working (atelectasis)
---> hyerventilation doesnt resolve the problem because cant oxygenate, but hyperventilating does help blow off CO2 -->

When V/Q >1, there is more ventilation compared to perfusion, being wasted because plenty of O2 but not enough blood flow to lungs
---extreme: dead space, V/Q is infinite
fibrosis can destroy alveolar capillaries - so properly ventialted but cant be perfused
- pulmonary embolism is good excuse
- increased CO2 is a problem, each breath is wasted so build up of CO2
Pure dead space - no hypoxemia
- when it's unbalanced enough, the V/Q ratio will actually go down, now there is a V/Q mismatch between different regions of alveoli
giving 100% O2 WILL help w/ mismatch and dead space

27

Diffusion Limitation

Increased A-a gradient
More focus on O2 than CO2
Hypoxemia
Lung Fibrosis - causes dead space (which can cuase hypercapnia)
--> we get ventilation w/o perfusion

28

V/Q mismatch

Intermediate state between dead space and shunt
inadequate ventilation and oxygenation of blood
--->> increased RR so CO2 levels are normal
- ex: pulmonary edema
V/Q less than 1, but some normal

29

Compliance

In emphysema, increased
higher FRC, barrel shaped chest

in fibrosis, decreased
lower FRC,
intrapleural pressure is negative

30

alveoli and pressures

small alveoli have a higher collpasing pressure - surfactant helps them not collapse into larger alveoili

31

surfactant

■ lines the alveoli.
■ reduces surface tension by disrupting the intermolecular forces between liquid molecules. This reduction in surface tension prevents small alveoli from collapsing and increases compliance. ■ is synthesized by type II alveolar cells and consists primarily of the phospholipid
dipalmitoylphosphatidylcholine (dppC).
■ In the fetus, surfactant synthesis is variable. Surfactant may be present as early as gestational week 24 and is almost always present by gestational week 35.
■ Generally, a lecithin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects mature levels of surfactant.
■ neonatal respiratory distress syndrome can occur in premature infants because of the lack of surfactant. The infant exhibits atelectasis (lungs collapse), difficulty reinflating the lungs (as a result of decreased compliance), and hypoxemia (as a result of decreased V/Q).

32

Diffusion vs. perfusion limited

Perfusion limited: N20 and O2 (normal), CO2
Gas equilibrates quickly,
diffusion of the gas can be increased only if blood flow increases.

Diffusion limited: CO and O2 under strenous exercise
the gas does not equilibrate by the time blood reaches the end of the pulmonary capillary. The partial pressure difference of the gas between alveolar air and pulmonary capillary blood is maintained. Diffusion continues as long as the partial pressure gradient is maintained.

33

hemoglobin

Fetal:
■ The O2 affinity of fetal hemoglobin is higher than the O2 affinity of adult hemoglobin (left-shift) because 2,3-diphosphoglycerate (DPG) binds less avidly to the γ chains of fetal hemoglobin than to the β chains of adult hemoglobin. ■ Because the O2 affinity of fetal hemoglobin is higher than the O2 affinity of adult hemoglobin, O2 movement from mother to fetus is facilitated

34

Distribution of Pulm Blood Flow

Zone 1 (apex):
Alveolar pressure > arterial pressure > venous pressure
The high alveolar pressure may compress the capillaries and reduce blood flow in zone 1. This situation can occur if arterial blood pressure is decreased as a result of
hemorrhage or if alveolar pressure is increased because of positive pressure ventilation.

Zone 2 (middle):
Arterial pressure > alveolar pressure > venous pressure. ■ Moving down the lung, arterial pressure progressively increases because of gravitational effects on arterial pressure.
■ Arterial pressure is greater than alveolar pressure in zone 2, and blood flow is driven by the difference between arterial pressure and alveolar pressure.

Zone 3 (base):
Arterial pressure > venous pressure > alveolar pressure. ■ Moving down toward the base of the lung, arterial pressure is highest because of gravitational effects, and venous pressure finally increases to the point where it exceeds alveolar pressure.
■ In zone 3, blood flow is driven by the difference between arterial and venous pressures, as in most vascular beds

35

Lung Development - stages

Embryonic: 4-7 weeks
Lung bud Ž trachea Ž bronchial buds Ž mainstem bronchi Ž secondary (lobar) bronchi Ž tertiary (segmental) bronchi.
Endodermal tubules Ž terminal bronchioles. Surrounded by modest capillary network.
---> Errors at this stage can lead to tracheoesophageal fistula.

Pseudo-glandular: 5-17 weeks
Endodermal tubules Ž terminal bronchioles. Surrounded by modest capillary network.
---> Respiration impossible, incompatible with life.

Canalicular: 16-25
Terminal bronchioles Ž respiratory bronchioles Ž alveolar ducts. Surrounded by prominent capillary network
----> airway diameter increases, Respiration capable at 25 weeks. Pneumocytes develop starting at 20 weeks.

Saccular: 26 - birth
Alveolar ducts Ž terminal sacs. Terminal sacs separated by 1° septae.

Alveolar: 36 weeks - 8 years
Terminal sacs Ž adult alveoli (due to 2° septation). In utero, “breathing” occurs via aspiration and expulsion of amniotic fluid Ž INCREASE vascular resistance through gestation. At birth, fluid gets replaced with air Ž DECREASE in pulmonary vascular resistance.

At birth: 20–70 million alveoli. By 8 years: 300–400 million alveoli

36

Diaphragm Holes

ƒ At T8: IVC, right phrenic nerve

ƒ At T10: esophagus, vagus (CN 10; 2 trunks)

ƒ At T12: aorta (red), thoracic duct (white), azygos vein (blue) (“At T-1-2 it’s the red, white, and blue”)

37

Dead space equation

VD = VT × (Paco2 – Peco2) /Paco2

38

Compliance

Compliance—change in lung volume for a change in pressure; expressed as ΔV/ΔP and is inversely proportional to wall stiffness. High compliance = lung easier to fill (emphysema, normal aging), lower compliance = lung harder to fill (pulmonary fibrosis, pneumonia, NRDS, pulmonary edema). Surfactant increases compliance.

39

Hysteresis

Hysteresis—lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation.

40

Respiratory changes in elderly

INCREASE lung compliance (loss of elastic recoil)
DECREASE chest wall compliance ( chest wall stiffness)
INCREASE - RV
DECREASE FVC and FEV1
Normal TLC
 INCREASE ventilation/perfusion mismatch
INCREASE  A-a gradient
DECREASE respiratory muscle strength

41

CO2 Transport

In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs (Haldane effect).

In peripheral tissue, increased H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect). Majority of blood CO2 is carried as HCO3− in the plasma.

H+ is buffered inside the RBCs by deoxyhemoglobin, which acidifies the RBCs

In venous blood, CO2 combines with H2O and produces the weak acid H2CO3, catalyzed by carbonic anhydrase. The resulting H+ is buffered by deoxyhemoglobin, which is such an effective buffer for H+ (meaning that the pK is within 1.0 unit of the pH of blood) that the pH of venous blood is only slightly more acid than the pH of arterial blood. Oxyhemoglobin is a less effective buffer than is deoxyhemoglobin.