- StudyBlue
- Wisconsin
- University of Wisconsin - Madison
- Physiology
- Physiology 335
- Altschafl/lokuta/strang
- Exam 4 Respiratory Phys
Exam 4 Respiratory Phys
Physiology 335 with Altschafl/lokuta/strang at University of Wisconsin - Madison
About this deck
By: Nora Thompson
Textbook:
Vander's Human Physiology: The Mechanisms of Body Function with ARIS (HUMAN PHYSIOLOGY (VANDER))
Created: 2011-12-19
Size: 42 flashcards
Views: 96
Textbook:
Vander's Human Physiology: The Mechanisms of Body Function with ARIS (HUMAN PHYSIOLOGY (VANDER))Created: 2011-12-19
Size: 42 flashcards
Views: 96
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Functions of Resp system
-Regulate H+ ion concentration (pH) in coordination w/ kidneys
-Form speech sounds (homeostasis on hold)
-Defends microbes
-Influences arterial conc. of hormones
-Traps/dissolves blood clots arising from systemic veins (from legs...)
Ciliary Elevator
-Microscopic
-Brings particles back up the trachea and out of lungs
-Smoking kills cilia
Bronchioles
-Regulate airflow like arterioles regulate blood flow
Respiratory bronchiole
-exchange
-branch into alveoli
Alveoli
-Main site of gas exchange
-70 sq. Meters of SA
-efficient with gas exchange
protective mechanisms in lungs
-constriction of bronchioles
-macrophages in airways/alveoli [injured by cigarettes]
Type 1 and 2 alveolar cell
-Type 1: flat epithelial cells, line alveoli
-Type 2: interspersed, produce surfactant, immune function
Muscles of Inspiration
-Diaphragm
External intercostals
Scalenus
Muscles of expiration [active]
-Internal intercostals
-abdominals
functional residual capacity (FRC)
-volune in lungs after an exhale when respiratory muscles are relaxed
-lungs LIKE to be smaller when exhaled
-Pressure of IP space is negative compared to atmosphere, keeps lung inflated against chest wall
P atm at sea level
760 mmHg
Inspiration: Palv < Patm (driving force for airflow is negative)
Expiration: Palv > Patm
As chest wall expands
-Pip more negative
-Ptp more positive
-Palv decreased (compared to Patm)
Pneumothorax
-puncture of lung/alveoli, ATM air enters ip space (Pip from - to 0)
-Ptp is eliminated
-Lung collapses, chest wall recoils out
-Often unilateral
-can happen with air from lung OR air from outside
Expiration
-Pip Increases
-Ptp decreases
-elastic recoil
-Palv < Patm
-air out
Boyle's law
-when volume of a space gets larger, pressure in that space gets lower
Compliance
-stretchability
-high compliance = easy inhale
-fibrous tissue (collagen) decreases compliance (Cystic fibrosis)
-Surfactant Increases COmpliance
-Equation: change in lung volume/Ptp (Palv-Pip)
-Less compliance, need more Ptp to breathe
Surfactant
-detergent (hydrophobic and hydrophilic)
-Desrupts H2O binding
-regular water droplet has strong hydrogen bonding forces that pull it together
-If only H2O was in lungs, alveoli would be pulled closed
-Deep breath = strech of type 2 cells = up surfact
2 determinants of Compliance
1) stretchability of lung tissues (elastic CT)
2) surface tension @ air/water interfaces with alveoli
minute ventilation
freq x TV = MV
Alveolar ventilation
freq x (TV-DS) = AV
-Change in TV has more effect than change in frequency in AV
dead space
-airways that do not permit gas exchange with blood
Dalton's law
-Total atmospheric pressure @ sea level: 760 mmHg
-N2 = 79%
-O2 = 21%
-CO2 = ~0%
Henry's law
-Gasses dissolve evenly so their partial pressures are equal in liquid and surrounding air
ex: alveoli and blood
-Dissolved gas = Pgas x Sol coefficient (.03)
-diffusion happens quickly at first
-amount of gas dissolved is proportional to P of gas
Gas exchange between alveoli and blood
-THIN LAYER
-equilibration depends on thin layer
-Diffusion problems:
Cystic Fibrosis
Pneumonia
Congestive heart failure
O2 dissolved vs. bound to hemoglobin
-Systemic Arterial Blood:
197 Bound to Hb
3 Dissolved
=98% saturation
-Systemic venous blood
150 bound to Hb
1.2 dissolved
=75% saturation
O2 bound = Red
No o2 Bound = blue/dark red
O2 is transported in blood in 2 forms
-Dissolved in Plasma & RBC cytosol
-Reversibly combined with hemoglobin in RBCs
Key features of Hb saturation/PO2 curve
1) plateau protects you if alveolar PO2 falls
2) Steep part helps you unload O2 at tissues QUICKLY
3) Sigmoid shape due to cooperative binding of O2
(as more O2 binds, Hb has higher O2 affinity -- explains PO2=0 --> PO2=60)
What Causes dissociation curve to the R
High:
-Blood PCO2
-H+ conc.
-Temp
-DPG conc.
-Hb saturation
-with more of these, Hb has a lower affinity for O2
*DPG important in high altitudes
Transport of CO@ and H+ ions in blood
Begin: 100% CO2 produced in cell
Dissolved CO2 --> Plasma
a) 10% CO2 dissolves in plasma/RBCs
b) 30% Binds to hemoglobin (CO2 + Hb -> HbCO2)
c) 65% --> HCO3-
CO2 + H2O --> H2CO3 --> HCO3 + H+ (Binds to Hb)
-Reaction occurs in nRBCs
Chloride Shift
-HCO3 made in RBCs moves into plasma
-Bicarb OUT chloride IN
-PCO2 in cells = 46
-PCO2 in plasma = 40
Carbonic Anhydrase
-Made from Rxn of CO2 + H2O
-made in RBCs
H+ transport in tissues/lungs
-Small amount of H+ generated in blood remains free
-explains why venous blood is higher in acidity than arterial
CO2 and H+ transport @ the lungs
A) Chloride Shift: HCO3 into RBC, Cl Out
B) HCO3- + H+ --> H3CO3-
C) H2CO3- --> H2O + CO2
D) HbCO2 --> Hb + CO2
*Underlined CO2 are dissolved in plasma
*CA released from reaction C
Hypoventilating
-Increased PCO2
-Increased H+
-Respiratory Acidosis (Increased arterial H+ due to increased PCO2)
Hyperventilating
-decreased PCO2
-Decreased H+ in arteries
Respiratory Alkalosis
Hypoxia
-deficiency of O2 at tissue level
-exposure of decreased PO2 @ high altitude = hypoxic hypoxia
-Emphysema is major cause of hypoxia (less SA for gas exchange)
Acclimitization to high altitudes
1) Peripheral chemoreceptor increase ventilation
2) Erythropoiten (fron kidney) stimulate RBC production
3) DPG increases, shift curve to R, helps O2 unloading at tissues
4) Increased Sk. muscle capillaries
5) Plasma vol. down, increased conc. RBC/Hb
Peripheral Chemoreceptors
-monitor PO2 and H+
-Carotid and Aortic Bodies
-Stimulated by:
down arterial PO2
Up arterial H+
metabolic acidosis
respiratory acidosis
= INCREASED VENTILATION
Effect of O2 level of ventilation
-peripheral chemoreceptors
-only in emergencies (not minute to minute)
Effect of CO2 level on ventilation
-CO2 determines how deeply/quickly you breathe
-Both CENTRAL and peripheral chemoreceoptors
-modulator of non emergency ventilation
-Hyper/hypo ventilation defined by CO2 status
-CO2 less affected by diffusion problems in alveoli
Effect of Plasma H+ level on vent
-Metabolic H+ is under peripheral detection
(metabolic acidosis)
-H+ from CO2 is under peripheral AND central detection
Inputs that affect ventilation during exercise (to respiratory center)
-motor cortex & skeletal muscle (proprioceptic reflex)
-Joints
-Up plasma epi/potassium
-Conditioned response
-Up temperature
-Down PO2, Up PCO2, H+ (MAYBE?) via chemoreceptors
About this deck
By: Nora Thompson
Textbook:
Vander's Human Physiology: The Mechanisms of Body Function with ARIS (HUMAN PHYSIOLOGY (VANDER))
Created: 2011-12-19
Size: 42 flashcards
Views: 96
Textbook:
Vander's Human Physiology: The Mechanisms of Body Function with ARIS (HUMAN PHYSIOLOGY (VANDER))Created: 2011-12-19
Size: 42 flashcards
Views: 96
About StudyBlue
STUDYBLUE makes things that make you better at school.
Things like online flashcards with photos and audio.
Things like personalized quizzes and friendly reminders about when (and what) to study next.
Think of it as a digital backpack™: access to all of your study materials online and on your phone.
STUDYBLUE exists to make studying efficient and effective for every student, for free. Join us.
“I have been getting MUCH better grades on all my tests for school. Flash cards, notes, and quizzes are great on here. Thanks!”
Kathy
Kathy