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Flashcards in Pulm Deck (73):

Explain the anatomy of the lungs and their division into lobes and bronchopulmonary (BP) segments

Right lung:
Upper middle lower lobe, oblique and horizontal fissures
Left lung: upper and lower lobes, separated by oblique fissure; also has lingula
*fissure = double fold of pleura

BP segments: ~10 in each lung that represent further divisions of the lobes, each BP served by tertiary bronchus, pulmonary artery, and vein


What are the impressions on the medial surface of the lung and what are they created by?

Right lung:
cardiac impression
groove from azygos vein
groove from SVC
groove from esophagus

Left lung:
cardiac impression and cardiac notch
grooves from aortic arch
groove from L subclavian artery
groove from descending aorta
impression from lower esophagus


Describe the development of the respiratory system. What clinical abnormalities can occur?

1) Ventral diverticulum develops off of the foregut early on in embryology
divides and forms trachea + 2 lung buds
lung buds evaginate into pleural cavities and become covered in the visceral pleura (visceral and parietal pleura meet at the roots of the lungs at the blood vessels)

2) Tracheoesophageal fistula
most common - esophagus ends in blind pouch, lower part of esophagus forms fistula with trachea
polyhydramnios (Excessive amniotic fluid) bc fetus cannot swallow


What are pleural reflections and recesses?

Reflection - parietal pleura turns back on itself
Recess - reflection is at an acute angle so lung doesnt enter this area during quiet breathing --> parietal pleura touching parietal (no visceral involved)

*2 intercostal spaces of recess (from 10th to 12th ribs) -- acts as reserve space


Describe the articulation of the ribs and movement during inspiration

Ribs: 12 bones, articulate with vertebral column posteriorly and terminate as costal cartilage
head --> 2 vertebral bodies (corresponding + one above)
tubercle --> transverse process

Ribs 2-6: anterior posterior expansion
axis through head and tubercle; anterior ends of ribs move up, sternum moves anteriorly --> "pump handle" (caused by external intercostal muscles)

Ribs 7-10: transverse expansion
axis through head of rib and sternocostal joint
lateral shaft of rib elevates --> "bucket handle" (caused by contraction of the diaphragm and inferior displacement of the liver)


Using Boyle's Law, describe the different stages of respiration and the muscles involved

*Boyle's law: pressure and volume inversely related

1) At rest: intrapleural pressure ALWAYS negative (lung and chest wall pulling in opposite direction)
alveolar pressure = atmospheric pressure --> no gas exchange

2) Inspiration: Increase the volume in thoracic cavity --> Decreases pressure --> air rushes in bc of pressure differential
intrapleural pressure more negative, muscular contraction (External intercostals + diaphragm) > elastic recoil --> thoracic cavity enlarges
abdominal muscles and internal intercostals are relaxed

3) Expiration: decrease volume in thoracic cavity --> increased intrathoracic pressure --> air rushes out
intrapleural pressure less negative, elastic recoil increased and decreases alveolar volume, thereby increasing alveolar pressure, abdominal muscles and internal intercostals contract if need be
alveolar pressure > atmospheric pressure --> air flows out of alveoli


Explain how cardiac function is linked to pulmonary function

Deep breath --> lowers intrathoracic pressure --> dilates great veins --> increases venous return to the heart

Expiration (also laughing, coughing) --> increased intrathoracic pressure --> impedes venous return (thats why face flushes, veins become more prominent)


What is the function and innervation of the diaphragm? What is paradoxical movement?

Function: anything requiring change in intrathoracic or intraabdominal pressure
eg breathing, phonation, laughing, singing, coughing, sneezing, urination, defecation
*works with pelvic diaphragm to change intraabdominal pressure

Innervation: phrenic nerve (bilaterally)
unilateral loss of the phrenic nerve - diaphragm doesnt descend during inspiration, is instead forced superiorly


What is the nerve supply to the lungs?

More specifically, what is the innervation of bronchial smooth muscle?

1) Afferent - on vagus nerve, feedback on pain, pressure, stretch in the pulmonary veins
Sympathetic - postganglionic thoracic splanchnics, innervate smooth muscle and blood vessels
Parasympathetic - preganglionic, synapse on small ganglia on bronchial tree; innervate smooth muscle

2) Vagus - parasympathetic constriction
epinephrine (from adrenal medulla)- sympathetic beta2 adrenergic dilation


What happens during open (sucking) pneumothorax? What happens during tension (positive pressure) pneumothorax?

1) Open (sucking) pneumothorax
open chest wound --> air enters pleural cavity --> negative intrapleural pressure lost --> collapse of lung --> reduced venous return to the heart
Inspiration: mediastinum shifts --> compresses opposite lung
Expiration: mediastinum and unaffected lung shift back to normal position, but venous return further affected by distortion of vena cavae

2) Tension (positive pressure) pneumothorax
valve-like chest wound --> air enters pleural cavity --> negative intrapleural pressure lost --> lung collapses --> reduced venous return to the heart
Inspiration: mediastinum shifts --> compresses opposite lung
Expiration: valve opening closes --> air cannot escape --> increases intrathoracic pressure --> unaffected lung is still compressed
and venous return further affected by both increased pressure and distortion of vena cavae

*pneumothorax lowers Pa02 bc it creates a shunt V/Q defect


What is hemothorax?

Hemothorax- blood in the thoracic cavity, blood may not clot, since liquid is not compressible it makes the lungs smaller and smaller
blood can come from lung, thoracic wall arteries, heart, abdominal structures, or intercostal vessels


What is the structure and function of mucosa?

Wet epithelium + lamina propria (adjacent epithelial tissue)

Epithelium - pseudostratified columnar, has cilia and goblet cells produce saliva, can also have intraepithelial lymphocytes which migrated from lamina propria
basement membrane
Lamina propria - loose connective tissue with blood vessels, nerves, and lots of lymphatic vessels (called MALT- defense mechanism)


Define the conductive vs respiratory parts of the respiratory system

Conducting: nose and nasal cavity --> nasopharynx --> pharynx --> larynx --> trachea --> primary, secondary, tertiary bronchii --> bronchioles (end is terminal bronchioles)
function: warm, moisten, clean inspired air

Respirating: respiratory bronchioles --> alveolar ducts --> alveolar sacs --> lined with alveoli (have alveolar pores in the walls)
function: gas exchange


What are the cells in olfactory mucosa?

How do you differentiate from respiratory epithelium?

Olfactory mucosa - on roof of nasal cavity
1) olfactory receptor cells - responsible for sense of smell, secretion (by Bowman's glands in the lamina propria) that dissolves odor molecules -- impulse carried by olfactory nerves
2) sustentacular cells - support and nourish olfactory receptor cells
3) basal cells - stem cells that replace both receptor and sustentacular cells

3 layers of cells, much thicker, and no goblet cells


Describe the protective mechanisms of the respiratory tract

sneeze reflex sensory: V1 and V2 (ophthalmic and maxillary, trigeminal)
cough: vagus nerve


What are the 3 layers of trachea and bronchii?

1) Mucosa - epithelium + basement membrane + lamina propria with BALT (lymphatic tissue- defense mechanism)
2) Submucosa with serous (pink) and mucous (frothy white) glands and lymphoid tissue
3) Adventitia of connective tissue - hyaline cartilage (keeps airway open) and smooth muscle (regulates diameter of airways)


What are the cells in the respiratory epithelium?

1) Goblet cells - produce mucous which traps foreign particles
2) ciliated cells - move mucous with trapped foreign material --> mucociliary escalator (mucous swallowed or spit out once it reaches pharynx)
3) Basal cells - stem cells replace goblet and ciliated cells, can also sense environment
4) DNES/K cells - secrete vasoactive substances into lamina propria
*bowman's glands in CT below epithelium (ie lamina propria) - secretion for dissolving odor


What is the difference between a pulmonary lobule and acinus?

Lobule - tissue served by terminal bronchiole

Acinus - tissue served by respiratory bronchiole


What comprises the blood air barrier?

Type I pneumocyte of alveoli - squamous cell where gas exchange occurs
Continuous capillary endothelium
shared basement membrane between the two epithelia

interstitial tissue away from blood-air interface, dont want any fluid leakage


What is the function of Type II pneumocytes?

dome shaped cells in alveolar wall, contain lamellar bodies that discharge surfactant into alveolar lumen - reduces surface tension and prevents alveolar collapse during expiration, contributes to elastic recoil of lung, also has defense functions
can maybe also proliferate to replace Type I (where gas exchange occurs) and Type II


What is the function of alveolar dust cells?

Macrophages that travel through alveolar pores to phagocytose foreign matter that escaped the mucous blanket
enter lymphatics and go through multiple lymph nodes to drain the hilar lymph nodes --> see black lymph nodes at hilum of the lung
also secrete antitrypsin inhibitor (when you want elastase and want to break down elastic fiber)


What is the pathology of emphysema?

Destruction of tissue distal to terminal bronchioles - elastic fibers in interstitial tissue are destroyed --> air passages cannot remain open --> gas exchange compromised and surface/diffusion area decreases

normally elastase (which makes new elastic breaks down elastic fiber), inhibited by antitrypsin
in emphysema, toxins suppress antitrypsin --> elastase produced in excess --> elastic fibers destroyed --> airways cant stay open


What are the major physiologic and nonphysiologic contributors to body acid load?

1) Metabolism of fats and carbohydrates --> H2C03 (carbonic acid)
*C02 is volatile acid, expired via respiration

Metabolism of protein --> H2PO4- (phosphoric and sulfuric acids)
*non-volatile acids, have net negative charge
buffered by renal HC03- retention, H+ secretion

2) Pathophysiologic
ketoacids (starvation, DMII)
salicylic acid (Aspirin)
lactic acid


What happens during respiratory acidosis?

What is compensation rule #1 for acute respiratory acidosis?

Compensation rule #2 for chronic respiratory acidosis?

Decreased pH, increased PC02 in blood

Rule #1: Up 1 for 10
[HC03-] increases 1 meq/l per 10 mm Hg rise in PC02 above 40

Rule #2: Up 4 for 10
[HC03-] increases 4 meq/l per 10 mm Hg rise in PC02 above 40


What happens during respiratory alkalosis?

What is compensation rule #3 for acute respiratory alkalosis?

Compensation rule #4 for chronic respiratory alkalosis?

Increased pH, decreased PC02 in blood

Rule #3: Down 2 for 10
[HC03-] decreases 2 meq/l per 10 mm Hg decrease in PC02 below 40

Rule #4: Down 5 for 10
[HC03-] decreases 5 meq/l per 10 mm Hg decrease in PC02 below 40


Why is there limited capability of compensation in metabolic acidosis?

initially Kussmaul breathing lowers PC02 bc of increased tidal volume --> increases pH
but lowering PC02 --> lowers renal HC03- reabsorption --> decreases plasma [HC03-] --> decreases pH again


Why is there limited capability of compensation in metabolic alkalosis?

initially reduced ventilation raises PC02 --> Decreases pH
but raising PC02 --> increases renal H+ secretion --> increases HCO3- reabsorption and generation --> increases plasma [HC03-] --> increases pH again


What is negative pressure breathing?

What is positive pressure ventilation?

1) Negative pressure breathing: alveolar pressure alveolar pressure (mechanical ventilator)


How is the gradient for negative pressure breathing generated?

Muscles of inspiration contract --> intrapleural pressure becomes more negative --> transmural pressure difference increases (inside alveolar pressure - outside intrapleural pressure) --> alveoli all passively expand (bc of structural interdependence, alveoli are tethered together) --> alveolar volume increases --> alveolar pressure decreases --> air rushes in

*alveolar pressure needs to be less than atmospheric pressure for this to occur


Why is intrapleural pressure negative even when no inspiratory muscles are contracting?

lung holds chest wall in because of inward elastic recoil of alveoli (wants to decrease volume)

chest wall holds alveoli open because of outward elastic recoil (wants to increase volume)


For the transpulmonary pressure-lung volume curve:
1) what is the slope? What 2 factors affect the slope?
2) explain how and why the inhalation and exhalation curves are different
3) How do emphysema and fibrosis affect the pressure-volume curve?

1) Slope = change in volume / change in pressure = compliance;
steeper slope --> more compliant;
Compliance increased by surfactant (decreased surface tension) and decreased elastic recoil (easier to inflate)

2) "hysteresis" - For a given pressure, lung volume lower during inspiration vs expiration;
difference is due to the energy required during inspiration to recruit and inflate additional alveoli

3) Fibrosis shifts the curve to the right --> less compliance, decreased diffusion of gases, increased alveolar elastic recoil;
Emphysema shifts the curve to the left --> more compliance. destroys alveolar septal tissue and decreases elastic recoil that opposes lung expansion


What properties impact the elastic recoil of the lung?

Tissue elastic forces (eg elastin is more compliant/distensible, important at low and normal lung volumes) - 1/3 total lung elasticity

Fluid air surface tension - 2/3


Given constant surface tension, what prevents smaller alveoli from collapsing into larger ones due to pressure gradient?
What happens if these factors are not present?

1) mechanical interdependence - if one alveolus were about to collapse, increased stress on other alveoli would hold it open bc they are tethered together
2) surfactant - lowers surface tension of alveoli --> reduces lung elastic recoil and stabilizes alveoli against collapse

Decrease in surfactant during hypoxia, in neonates -- decrease in surfactant increases surface tension --> small alveoli collapse into larger ones --> decreased gas exchange --> V/Q mismatch, hypoxemia, cyanosis;
lack of surfactant --> Decreases lung compliance --> harder to inflate the lungs --> increases the work of breathing -> dyspnea (shortness of breath)
*decreases FRC


Where in the bronchial tree is the resistance the highest?

Resistance is inversely proportional to radius^4 (larger airways have smaller resistance)

resistance highest in medium bronchii/airways

smallest airways have highest individual resistance but they are parallel --> their resistances are added as reciprocals --> overall have very low resistance


Describe the dynamic compression of airways

Increased resistance to airflow during forced expiration

positive intrapleural pressure > atmospheric pressure thus intrapleural pressure > alveolar pressure --> pressure outside airway > pressure inside airway --> small airways may compress or collapse bc of inherent recoil


What are the main determinants of the cross sectional areas of the airways?

elastic recoil of the lung
lung volume
bronchial smooth muscle tone


What is the equal pressure point hypothesis?

Equal pressure point where transmural pressure gradient = 0 (intrapleural pressure = alveolar pressure)
during forced expiration - equal pressure point moves down towards smaller airways --> dynamic compression increases --> airways begin to collapse


Explain the action of the diaphragm on the chest wall and abdomen.

What happens during diaphragmatic paralysis?

1) Diaphragm contracts downward and pushes down on abdomen --> displaces abdomen wall outwards
*only diaphragm is used during quiet breathing

Contraction creates zone of apposition (since fibers are apposed to inner aspect of lower rib cage) --> lifts and expands the lower rib cage --> causes lower chest wall to expand (lateral displacement)

2) Diaphragm does not contract, abdomen wall moves inward
chest wall still moves outward because of external intercostal muscles


What are the accessory muscles, when are they used, and what is their function?

accessory muscles inactive in normal breathing, recruited during high levels of ventilation or when inspiratory pump abnormally loaded (eg edema)
1) Sternocleidomastoids- pull up sternum, expand upper rib cage in anteroposterior direction
2) Scalenes- expand upper rib cage during inspiration


What is the function of the abdominal muscles in ventilation?

Contraction of abs --> inward displacement of abdominal wall --> increase in intraabdominal pressure --> diaphragm moves up(cranially) --> decreases lung volume and increases pleural pressure
used for expiration, cough generation


Describe diaphragm force-length and force-velocity relationships

1) Force-length: generate maximal force at 125% of L0 (resting length)
as diaphragm length decreases (eg lung hyperinflation in COPD), force generation decreases
2) Force-velocity: greater force generation at slower velocity of contraction
as demand increases - curve shifts up and to the right as muscle fibers are recruited (more force for given velocity) --> more ventilation


Define the characteristics of respiratory muscle fiber types

50%+ of respiratory muscles are Type I fibers - slow twitch, fatigue resistant (high oxidative), active at quiet breathing
remainder are Type II - fast-twitch, fatigue sensitive, activated at high frequencies


Describe the determinants of diaphragmatic fatigue. How is it detected? How is it measured?

Diaphragm fatigue when exposed to high inspiratory loads which require Type II fibers, when they cannot generate sufficient contractile force to sustain adequate airflow
Detected through paradoxical motion of chest wall and abdomen
Transdiaphragmatic pressure = P abdomen - P pleural


Describe anatomy of pulmonary circulation. What happens if you increase pulmonary blood pressure?

1) Pulmonary circulation thinner walls and less smooth muscle --> less resistance and more distensible --> lower pressure and more compressible

3) If you increase pulmonary BP --> increase blood flow --> decrease pulmonary vascular resistance


Describe differences in pulmonary and systemic circulation

LV workload, metabolic demand, mean arterial pressure more than for RV - has to go against gravity and control blood flow in different tissues (Eg during exercise)
Pulmonary circulation - pressure is lower, dont need to redistribute blood bc its all going to the alveolar-capillary units


What is hypoxic pulmonary vasoconstriction?

Local vasoconstriction with alveolar hypoxia or atelactasis --> increasing vascular resistance --> increased pulmonary arterial pressure --> decreased blood flow --> diverts venous blood flow away from poorly ventilated areas --> prevents lowering of arterial P02
*not a strong response bc v little smooth muscle in pulmonary circulation


Describe the effect of gravity on the zones of the lung.

How does V/Q change throughout zones of the lung?

1) Gravity affects perfusion
Zone 1 - no perfusion, alveolar dead space bc PA>Pa
Zone 2- Pa>PA>Pv
Zone 3- Pa>Pv>PA
pressure and perfusion greater in gravity dependent (lower) regions of the lung

2) V/Q highest at apex, decreases as you go down lung;
apex has highest P02, lowest PC02 since gas exchange is most efficient at apex


What is pulmonary edema? Describe causes and consequences

1) Fluid that should be in blood is let out into the interstitium; occurs when lymphatic drainage of the lung is overwhelmed (can remove up to 10x as safety factor)-- then leaks into the alveoli

2) Causes:
Increased capillary permeability (bc toxins, acute respiratory distress)
Increased Pcap (bc increased left atrial pressure which increases pulmonary vein and capillary pressure eg mitral stenosis)
Decreased Pif (bc upper airway obstruction)
Decreased blood plasma colloid oncotic pressure (bc protein starvation, renal problems)
Lymphatic insufficiency

3) Consequence: impaired gas transfer; diffusion of oxygen decreases


What is the A-a gradient? What is its function?

Alveolar-arterial 02 difference; assesses the integrity of the alveolar-capillary unit and used to determine physiological cause of hypoxemia

Needs to be low so that gas exchange can happen (02 from alveoli --> capillary)
should be 15 --> problem with gas exchange (high respiratory effort to achieve oxygenation)


What is ventilation, perfusion, and the V/Q ratio?

ventilation - delivering 02 to the alveoli, removing C02
amount of air that reaches alveoli
*key determinant of PaC02
perfusion - pulmonary blood flow to capillary, brings C02 that diffuses into alveoli, takes up 02
amount of blood that reaches alveoli
V/Q ratio - ventilation/perfusion ratio
*V/Q mismatch major cause of hypoxemia


Describe V/Q mismatch in pneumonia

In pneumonia (asthma, COPD), some alveoli are filled with gunk and thus consolidated--> normal perfusion but low ventilation--> no gas exchange in damaged alveoli --> Pa02 decreases --> hypoxemia
PaC02 increases (hypercapnia)

A-a gradient increases
V/Q ratio decreases

*can administer supplemental 02 to fix hypoxemia, this does NOT work in a shunt


Describe V/Q mismatch in a shunt vs dead space:
-A-a gradient effect
-V/Q ratio

1) Shunt (anatomical or physiological) --> perfusion without ventilation - desaturated blood bypasses oxygenation at alveolar-capillary level;
alveoli equilibrates with venous blood: decreased PA02, increased PAC02;
gas exchange impaired --> low Pa02, low PaC02 (even though C02 excretion is impaired, compensate by hyperventilating to diffuse C02 and lower levels);
increased A-a gradient, refractory to oxygen therapy,
low V/Q eg asthma, pulmonary edema

2) Dead space (anatomic or physiological)--> ventilation without perfusion;
alveoli equilibrates with inspired air: increased PA02, decreased PAC02;
gas exchange impaired --> low Pa02, high PaC02;
increased A-A gradient;
high V/Q eg pulmonary embolism
*highER V/Q leads to increased Pa02 since there is some blood flow


What is the acute and chronic impact of metabolic acidosis on peripheral and central chemoreceptors

1) Acute metabolic acidosis
low pH triggers strong peripheral chemoreceptor drive
compensation: increased ventilation to decrease PaC02
creates downhill C02 gradient where C02 from CSF diffuses into arterial blood
this increases CSF pH --> reduces central chemoreceptor drive (thinks there is alkalosis)

2) Chronic (over several hours)
HC03 lost from CSF
CSF pH drops --> activates central chemoreceptors

*central chemoreceptor main sensor for C02


What is hypoxic drive? What causes it?

1) Normal respiration driven by level of C02 in the arteries (Detected by peripheral and central chemoreceptors)

hypoxic drive - body uses oxygen peripheral carotid body chemoreceptors to regulate respiration (not central chemoreceptors)

2) Hypoventilation --> lower Pa02 --> hypoxic drive once Pa02 desensitize C02 receptors --> Rely on hypoxic drive to breathe
increasing 02 removes hypoxic drive and they get worse


Describe the respiratory control system in the brainstem

Central respiratory controller in brainstem (medulla + pons)
-rostral 1/3 = PRG pneumotaxic center - inhibits inspiration in order to transition from inspiration to expiration; increases respiratory rate
-caudal 2/3 = apneustic center - prolongs inspiration
-medulla = spontaneous rhythm generation
DRG - inspiratory neurons; coordinates inspiration
VRG- inspiration and expiration; Pre-Botzinger complex for generation of respiratory rhythm (respiratory pacemaker) and Botzinger complex for expiration


Describe the ventilatory response to exercise. How is Pa02, PaC02, and arterial pH affected during exercise?

Phase I: increase in ventilation in anticipation of exercise
Phase II: gradual increase in breathing due to muscle afferents sending signal to central network
Phase III: steady state bc ventilation is matched to increased 02 consumption and metabolic rate (below anaerobic threshold)

*exercise increases V/Q ratio
recruitment of previously closed capillaries and distension/dilation of open capillaries --> increases surface area of blood into which 02 can diffuse

No change in mean Pa02, PaC02, or pH


Describe the sensory feedback provided by the following classes of vagal mechanoreceptors:
1) stretch
2) irritant
3) J

1) stretch- slow-acting in smooth muscle of airways, can decrease breathing rate (Hering-Breur reflex) by turning off inspiration when set lung volume met

2) Irritant- rapidly adapting for noxious chemicals in epithelial cells lining airways- causes constriction in bronchial smooth muscle and increase in breathing rate

3) J- in alveolar walls, can sense edema (ie increases in interstitial fluid volume) and produce rapid breathing/dyspnea if there is blockage eg PE


What factors affect rate of diffusion? (per Fick's law)

Increased diffusion with:
increased surface/cross-sectional area
increased diffusivity coefficient
decreased thickness of barrier
decreased molecular weight
increased partial pressure difference


What is perfusion limited transfer? What is diffusion limited transfer?

1) Perfusion limited - blood partial pressure equilibrates with alveolar partial pressure within amount of time blood is in pulmonary capillary (.75 sec)
eg 02, C02 - can equilibrate within 0.25 sec
2) Diffusion limited - equilibration does not occur within time blood is in capillary eg CO bc it is strongly bound to Hb
physiological diffusion limitation can be mucous, inflammation,e dema


How is 02 transported by blood?

1) Combined with Hb - 99%
2) dissolved in blood - 1%, incapable of fulfilling 02 demand


What is the significance of the shape of the oxyhemoglobin dissociation curve?

Sigmoidal curve, plateaus above P02 =80 (bc of allosteric affect)
In plateau- large decreases in P02 only lead to small decreases in 02 content - more wiggle room for moderate hypoxia; facilitates transport and delivery of 02 to tissues
In steep part at lower P02 - facilitates offloading of 02 to tissues


How is 02 unloading affected by:
23 BPG

What is the significance of these factors?

1) pH - lower pH shifts curve right (towards unloading 02)
2) temp - higher temp shifts curve right (give more 02)
3) 23BPG - shifts curve right (23BPG makes you want to release 02 bc it favors the T conformation of Hb; high altitude releases BPG)

Tissues have lower pH, higher temp, higher pC02 --> all help unload 02 from Hb


How is C02 transported by blood?

1) dissolved in blood - 10%
2) combined with amino acids - 10% (as carbaminohemoglobin)
3) as bicarb - 80% (catalyzed by carbonic anhydrase)

20x soluble in blood plasma and RBCs than 02


What is the Haldane effect?

Greater levels of oxyhemoglobin (Hb02) shift curve to the right (offload C02 at the lungs)
Greater levels of deoxyhemoglobin shift curve to the left (load C02 to take C02 from tissues) --> deoxygenation of blood increases ability to carry C02


What is the Bohr effect?

At low P02 - substantial amount of deoxyHb in RBCs --> deoxy Hb accepts H+ ions --> facilitates release of 02

decrease in pH --> shifts dissociation curve to the right --> hemoglobin releases oxygen load


What is obstructive disease? What is restrictive disease?
How do they affect TLC, RV, FEV1, FVC, and FEV1/FVC?

Obstructive disease eg asthma, emphysema, old age - hard to get air out bc you have narrowed airways (mucous, constriction due to irritation and inflammation) and thus increased airway resistance and decreased air flow and lung recoil--> increased work of breathing
increased RV
increased TLC
decreased FEV1
decreased FVC

*FVC=total amount of air exhaled during forced breath


Explain the effort independent section of the expiratory part of the flow volume curve

After hitting peak expiratory flow, expiration becomes effort independent bc of dynamic compression

transmural = Palveolar - Pintrapleural
When Pintrapleural > Palveolar (during forced expiration) --> transmural pressure becomes negative --> airways collapse through dynamic compression


How is perfusion matched to the increased ventilation during exercise?

Why does arterial PC02 not rise?

1) Exercise --> Increased cardiac output --> increased pulmonary blood flow --> opens pulmonary capillaries that are normally closed and non-perfused --> increases perfusion for gas exchange (optimal 02 loading/C02 unloading)

2) venous PC02 increases bc of increased C02 produced by muscle, but is blown off by hyperventilating lungs --> so arterial P02 does not change


Where would aspirated peanut go if standing/sitting? Supine?

Standing/sitting - posterior basal segment of right lower lobe
Lying down - superior segment of right lower lobe


What factors influence turbulent flow? Where is it most commonly seen?

Likelihood of turbulent flow increases with:
increased radius
increased velocity
increased density
decreased viscosity
most common in higher airways eg mouth, trachea where velocity has to be faster bc there are fewer airways


How do you differentiate bronchioles from bronchii? What special cells are in the smallest bronchioles?

1) Bronchiole is


At what lung volume are lung and chest elastic recoil equal and opposite?

at FRC - maximizes recruitment of large airways and minimizes compression of small airways
optimal point for perfusion


What factors influence vascular resistance?

R=(8*viscosity*length) / (pi*radius^4)