Flashcards in Respiratory Anatomy and Physiology Deck (21):
What are the large airways of the conducting zone? Small airways of the conducting zone? What does the respiratory zone consist of? What is the role of the conducting zone? Another name for it? What is the role of the respiratory zone? What is the role of alveolar macrophages? How far down do cartilage and goblet cells extend? How far down do pseudostratified ciliated columnar cells extend? What are the cells like after that? How long do these cells go on? After that? How far down do airway smooth muscle cells extend? How far down do cilia extend?
CONDUCTING: Warm, humidify, and filter air (no gas exchange=anatomical dead space)
Nose, pharynx, larynx, trachea, and bronchi
bronchioles that further divide into terminal bronchioles
RESPIRATORY: Gas exchange
Resp. bronchioles, alveolar ducts, alveoli
Alveolar macrophages: clear debris and immune response
Beginning of terminal bronchioles, then to cuboidal to resp. bronchioles, then simple squamous to alveoli
What are type I pneumocytes like? Type II? What are their functions? What are club/clara cells like? Function?
97% of alveolar surface. Squamous. Line alveoli. Gas exchange
Cuboidal and clustered. precursors to type I and type II cells. Secrete surfactant
Nonciliated. Low columnar/cubidal. Secrete cmponent of surfactant, degrade toxins, reserve cells.
What incr. collapsing pressure? Decreases it? When in resp. cycle do alveoli collapse? Waht is this called? What is the role of surfactant? What is it composed of? When does synth begin in utero? When is maturity reached? Lab result?
Surface tension incr. collapsing pressure.
Incr. radius decreases it.
During expiration (decr. radius)
Decrease surface tension
Week 26-week 35
Lecithin to sphingomyelin > 2.0.
What are the lobes of the right lung? Left lung? Where will an inhaled foreign body enter? Why? While supine? While upright? What is the relation of the pulm. artery to the bronchus at the lung hilum on each lung? What are the fissures in each lung?
Enter into the right inferior lobe b/c the right bronchus is wider and more verticle.
upright: lower portion
Supine: upper portion
RALS (Right: anterior, Left: Superior)
Where do the Esophagus, Aorta, thoracic duct, azygous vein, vagus nerve, and IVC penetrate the diaphragm (what level)? What innervates the diaphragm? What can cause pain to it? Where is the pain felt? Where do the carotids bifurcate? trachea? abdom aorta?
T8: IVC=vena cava (8 letters)
T10: oesophagus (10 letters), vagus nerve (10 letters)
T12: aortic hiatus (12 letters)
T-1-2 its the red (aorta), white (thoracic), blue (azygos vein)
I (IVC) ate (8) ten (10) eggs (esoph) at (aorta) twelve (12)
C3,4,5 keeps the diaphragm alive
Blood/air in peritoneum leads to shoulder and trapezius ridge pain
Carotids: C4 (bifourcation)
Abdom Aorta: L4
What is IRV? TV? ERV? RV? IC? FRC? VC? TLC?
IRV? inspiratory reserve volume: volume that could still be inhaled after a normal inhalation
TV? Tidal volume=normal breath
ERV? Expiratory reserve volume: volume that could still be exhaled after a normal exhalation
RV? Residual volume: air still left in airway after ERV is exhaled
IC? Inspiratory capacity: TV + IRV
FRC? Functional residual capacity: ERV + RV
VC? Vital capacity: IRV + TV + ERV
TLC? Total lung capacity: IRV + TV + ERV + RV
What is the equation to determine physiologic dead space? What does it consist of? What portion of lung contributes most to it?
VD= VT x (PaCO2 - PECO2)/PaCO2
PECO2=expired air PCO2
Volume of inspired air that does not participate in gas exhange
Anatomic dead space plus alveolar dead space
Apex of lung has the most alveolar dead space.
What is minute ventilation? Alveolar ventilation? How are they calculated?
Minute (VE): Total volume of gas entering lungs per minute
VE=VT x RR
Alveolar (VA): Total volume f gas per unit time that reaches alveoli
VA= (VT-VD) x RR
What is elastic recoil? What occurs at FRC? Explain compliance. When is it incr. Decr?
Tendency for lungs to collapse inward and chest wall to spring outward
At FRC, these forces are balanced and system pressure is 0, while intrapleural pressure is negative which prevents pneumothorax. PVR is at a minimum.
Compliance: Change in volume per change in pressure.
Decr: pulmonary fibrosis, pneumonia, pulmonary edema
Incr: Emphysema, normal aging
What are the two states of hemoglobin? What things induce each one? What do they do to the dissociation curve? Where in the body do these states occu?
Taut (deoxy): Low affinity for O2
Relaxed (oxygenated): high affinity for O2
Oxygen binding leads to relaxed state
Cl-, H+, CO2, 2,3-BPG, and temperature favor taut form leading to a right shift of curve
Taut in Tissue
Relaxed in resp. tract
What is methemoglobin? What is its binding pattern like? What does ferrous mean? Ferric? How does methemoglobinemia present? How is it treated? How is it induced? What can it be used to treat?
Oxidized form of Hb that does not bind O2 as readily but readily binds CN
Reduced=ferroUS=two of US=Fe2+
Induced by nitrites followed by thiosulfate=can treat CN poisoning
Also induced by benzocaine
Cyanosis and chocolate colored blood
What is carboxyhemoglobin? What binding pattern does it cause? Dissociation curve effects? Tissue oxygenation effects? Treatment?
Hb bound to CO instead of O2
Decr. O2 binding capacity but with left shift leading to decr. unloading in tissues
CO binds wiht 200x greater affinity
100% O2 and hyperbaric O2
What does the O2 content of blood consist f? What is the normal binding capacity of 1 g f Hb? What is a normal amount of Hb? At what levels of deoxygenated Hb does cyanosis result? What is a normal total O2 binding capacity? What happens to Hb conc, % sat, PaO2 (dissolved O2), and total O2 content in CO poisoning, anemia, and polycythemia?
O2 content = (O2 binding capacity x % sat) + PaO2
1 g Hb can bind 1.34 mL O2
Normal Hb level is 15 g/dL
Cyanosis=>5 g deoxy Hb
O2 binding capacity=20.1 mL O2/dL
What are the resistance and compliance of pulm. circulatin like? What effects do PO2 and PCO2 exert on it? What gases are perfusion limited? Diffusion limited? In what circumstances? What is the equation to calculate diffusion? What decreases diffusion and how?
Low resistance, high compliance
PO2=Decreases leads to vasoconstriction
PCO2=increases leads to vasoconstriction
O2 (normal health), CO2, N2O
O2 (emphysema, fibrosis)
Diffusion: Vgas=A/T x Dk (P1-P2)
A=Area (increases diffusion)
Dk (P1-P2)=difference in pressure (incr. diffusion)
Emphysema decreases area
Fibrosis increases thickness
What does PVR equal (equation)? What does resistance equal (equation)?
n=viscosity, l=length, r=radius
What is the alveolar gas equation? What are the given values for this equation? How is each variable calculated? What is the A-a gradient? What is a normal one? What might increase it? Causes?
PAO2=PIO2 - PaCO2/R
PAO2=150mmHg (at sea level room air) -PaCO2/ (CO2 produced/O2 consumed)
A-a gradient=PAO2-PaO2=10-15 mmHg
May be increased in hypoxemia (shunting, V/Q mismatch, fibrosis)
What is hypoxemia? What are some normal gradient causes for this? Incr gradient causes? What is hypoxia? Causes? What is ischemia? Causes?
HYPOXEMIA: Decr. PaO2
Normal gradient: high altitude, hypoventilation (opiates)
Incr. gradient: V/Q mismatch, diffusion limitation, right to left shunt.
HYPOXIA: Decr. O2 delivery to tissue
ISCHEMIA: loss of blood flow
Impeded arterial flow
decr. venous drainage.
What are the 3 lung zones? what are the pressures like in each? What is the V/Q ratio like in each? How do V and Q differ in each? What happens during exercise? What would cause V/Q=0? infinity? How will 100% O2 affect these conditions?
Zone 1=apex=PA>Pa>Pv, so the pressure of the alveoli shuts down perfusion (higher than Pa)
Ventilation and perfusion are decreased but Q is much more decr. than V resulting in an Incr. V/Q (wasted ventilation)
Zone 2=middle=Pa>PA>Pv leading to blood flowing through alveoli and picking up plenty of air and leaving through veins
Zone 3=base=Pa>Pv>PA. Blood doesn't flow as much through alveoli so there is not as much ventilation.
V and Q are increased but Q is much more incr. leading to a decr. V/Q (wasted perfusion)
Exercise: Incr. CO leads to incr. vasodilation of apical capillaries leads to a V/Q ratio of almost 1 at apex.
V/Q=0 during an airway obstruction (shunt). Will not improve with oxygen
V/Q=infinity during a blood flow obstruction. Will improve with Oxygen.
What are the 3 forms of circulating CO2? What percentage does each make up? How are they formed/interconverted? Explain the Haldane effect. Exlpain the Bohr effect.
Carbaminohemoglobin or HbCO2 (5%)=CO2 bound to globin leading to taut form
Dissolved CO2 (5%)
CO2 enters an RBC. If it binds to Hb, it forms HbCO2
It can combine with water and form H2CO3 through carbonic anhydrase. It will then dissociated into HCO3 and H+. HCO3 can then be shuttled out through an exchange with Cl-
Haldane: In lungs, oxygenation of Hb leads to the dissociation of H+ from Hb leading to more H+ in the RBC which favors the formation of H2CO3 which favors formation of CO2 and H2O which allows CO2 to be released.
Bohr effect: In peripheral tissue, incr. H+ from tissue metabolism shifts the dissociation curve to the right, making it more like to give up O2.
Describe the various changes that occur in response to high altitude.
Decr. atmospheric pressure leads to decr. PaO2 which leads to incr. ventilation which leads to decr. PaCO2
There is a chronic incr. in ventilation
Incr. EPO leads to incr. hematocrit and Hb
2,3-BPG increases so that tissues get more O2
Cellular changes (Incr. mitochondria)
Incr. renal excretion of HCO3 to deal with resp. alkalosis (incr. ventilation)
Chronic hypoxic pulmonary vasoconstriction results in RVH.