Quiz #1 Flashcards
Tracheal Wall Layers
- mucosa
- submucosa
- adventitita
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
Alveolar-arterial equation
stuff= stuff q
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
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
Oxygen content in blood - equation
O2content=
(O2-binding capacity×%Saturation)+Dissolved O2
O2 content = (1.34 × Hb × Sao2) + (0.003 × Pao2)
oxygen delivery
O2 delivery = O2 content X cardiac output
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
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)
alveolar ventilation equation
VA= RR x (TV-Dead space)
alveolar gas equation
PAO2= PI O2 - PaCO2/R
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
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
normal ABG
pH / PCO2 / PO2 / HCO3- 7.4/40/100/24
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
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
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
respiratory alkalosis
decreased CO2 from hyperventilation
compensate by retaining less bicarb
pH: high
PCO2: low
HCO3: low
7.5/20/100/20
Respiratory Alkalosis
7.24/60/50/28
Respiratory Acidosis
7.2/20/100/12
Metabolic Acidosis
7.45/45/70/35
Metabolic Alkalosis
Oxygen Consumption
= CO⋅([O2]a −[O2]v).
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.
efficient CO2 system
- It must have sufficient capacity to do the job.
- Loading and unloading must be rapid, to be complete within the RBC transit time through the peripheral and pulmonary capillaries.
- It must operate at nearly constant pH, which means only small differences in Pco2 between arterial and venous blood.
- It must be able to adapt to changes in CO2 production (O2 consumption).
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
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
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
Compliance
In emphysema, increased
higher FRC, barrel shaped chest
in fibrosis, decreased
lower FRC,
intrapleural pressure is negative
alveoli and pressures
small alveoli have a higher collpasing pressure - surfactant helps them not collapse into larger alveoili
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).
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.
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
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
Lung Development - stages
Embryonic: 4-7 weeks
Lung bud trachea bronchial buds mainstem bronchi secondary (lobar) bronchi tertiary (segmental) bronchi.
Endodermal tubules terminal bronchioles. Surrounded by modest capillary network.
—> Errors at this stage can lead to tracheoesophageal fistula.
Pseudo-glandular: 5-17 weeks
Endodermal tubules terminal bronchioles. Surrounded by modest capillary network.
—> Respiration impossible, incompatible with life.
Canalicular: 16-25
Terminal bronchioles respiratory bronchioles 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 terminal sacs. Terminal sacs separated by 1° septae.
Alveolar: 36 weeks - 8 years
Terminal sacs adult alveoli (due to 2° septation). In utero, “breathing” occurs via aspiration and expulsion of amniotic fluid INCREASEvascular resistance through gestation. At birth, fluid gets replaced with air DECREASEin pulmonary vascular resistance.
At birth: 20–70 million alveoli. By 8 years: 300–400 million alveoli
Diaphragm Holes
At T8: IVC, right phrenic nerve
At T10: esophagus, vagus (CN 10; 2 trunks)
At T12: aorta (red), thoracic duct (white), azygos vein (blue) (“At T-1-2 it’s the red, white, and blue”)
Dead space equation
VD = VT × (Paco2 – Peco2) /Paco2
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.
Hysteresis
Hysteresis—lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation.
Respiratory changes in elderly
INCREASElung compliance (loss of elastic recoil)
DECREASEchest wall compliance (chest wall stiffness)
INCREASE - RV
DECREASE FVC and FEV1
Normal TLC
INCREASE ventilation/perfusion mismatch
INCREASE A-a gradient
DECREASErespiratory muscle strength
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.
