Lecture 13 Respiratory System Part 2 Flashcards
daltons law
total pressure of gas mixture is the sum of each gas partial pressure
percent of O2 in air
21%
pressure at sea level
760 mmHg
pressure H2O in wet air
47 mmHg
PO2 in wet air vs dry air - include calculations
- wet = .21(760-47) = 150mmHg
- dry = .21(760) = 159 mmHg
- not a large difference
at sea level
- atmospheric pressure
- PO2 in air
- PO2 in alveoli
- PO2 arterial
- 760mmHg
- 159 PO2 in air
- 105 PO2 in alveoli (large decrease because O2 is removed so quickly in lungs)
- 100 PO2 arterial
- think of PO2 alveoli as pressure pushing O2 into blood vessels of lungs
affect of altitude on air pressure
increased altitude decreases air pressure
arterial PO2 at 10k and 20k
- 10k = 65mmHg
- 20k = 35mmHg
henry’s law aka 3 factors effecting gas movement
- solubility of gas in liquid (CO2 is more soluble)
- partial pressure of gas (this is the determining factor)
- temperature - more can be dissolved in cold liquid
dissolve/free O2
- what is it a good measure of
- amount in blood
- what does it depend on
- 3ml/100ml
- very little and depends on PO2
- good measure of lung function
total O2 content
- what does it depend on
- amount in blood
20ml/100ml
- depends on hematocrit
why do we intubate/ventilate people
- ventilation only increases hemoglobin saturation from 97-100%
- increases dissolved O2 which can be used by cells
- cells cannot use bound O2
increase in hemoglobin saturation from intubation/ventilation
97 to 100%
not much!
PCO2 pressure in veins and arteries - specific numbers
- veins = 46mmHg
- arteries = 40 mmHg
what happens if pressure in pulmonary circulation is too high
- high pressure –> fluid leaves capillaries causing pulmonary edema –> short of breath and cant lay down
ventilation perfusion matching - how is this opposite of systemic circulation
- pulmonary capillaries and arteries dilate in more ventilated area of lungs (more O2 means more O2 to be absorbed by more blood)
- in systemic circulation, more O2 means the area has enough blood –> vasconstriction –> blood shunting to other areas where blood is needed
apex vs base of lungs - ventilation vs perfusion
- apex = overventilated and under perfused
- based = underventilated and overperfused
hemoglobin structure
- 4 polypeptides 2 alpha and 2 beta
- 1 heme group on each polypeptide
heme group structure and 6 bonds
- porphoryin ring with a metallic ion in the center
- in this case Fe
- 4 bonds to N to attach to prophoryin ring, 1 attaches to polypeptide, 1 attaches to oxygen
oxyhemoglobin and deoxyheomglobin, what type of iron
- oxyhemoglobin when O2 attached, deoxyhemoglobin when no O2 attached
- Fe2+ ferrous ion
oxyhemoglobin saturation - definition and normal value
oxyhemoglobin / total hemoglobin - normally 97%
methemoglobin - what type of iron, mechanism to make i able to carry oxygen
- Fe3+, cannot bind to O2
- methemoglobin reductase to convert Fe3+ to Fe2+
carboxyhemoglobin
- CO bound, bond is 200x stronger than oxygen
anemia
- low hemoglobin
polycythemia - definition and absolute vs relative
- relative = transient, could be due to dehydration
- absolute = more RBC made due to hypoxia, high altitude, infection, smoking
erythropoietin
- hormone made by kidneys to increase RBC production in red bone marrow
oxygen dissociation curve and importance of plateau
- x axis = PO2, y axis = oxyhemoglobin saturation
- plateau means that life at high elevation is supported
Bohr effect and relation to increased metabolism
- as pH decreases and more acidic graph shifts right and hemoglobin affinity is lowered
- increased metabolism = more acid produced adn more O2 reelased
temperature, oxygen dissociation curve, and increased metabolic activity
- high temp = curve shifted to the right, affinity for oxygen decreases
CO2, oxygen dissociation curve, and increased metabolic activity
-high CO2 shifts curve to the right, lowers oxygen affinity, CO2 produced during metabolism so more O2 released
2,3 DPG - where does it come from, what conditions cause it, mechanism and affect on hemoglobin
- intermediate in glycolysis/anaerobic respiration
- binds to beta polypeptide and causes change that decreases O2 affinity so more O2 released
fetal hemoglobin
- 2 alpha and 2 gamma
- 2,3 DPG cannot bind to gamma so it has higher affinity for O2
- this way O2 is transferred from maternal to fetal blood
sickle cell anemia
- hemoglobin type and affect
- sickle cell crisis
- heterozygous vs homozygous for trait
- hemoglobin S due to 1 amino acid change
- during hypoxia the hemoglobin polymerize causing sickle shaped RBC that have a shorter life span and cannot fit through blood vessels
- sickle cell crisis = wide spread ischemia and whole body pain
- heterozygous = sickle cell trait, occasional crisis
- homozygous = sickle cell disease, many crisis and constant need for blood transfusions
thalassemia and 2 types
- common in mediterranean people
- alpha/beta thalassemia based on if alpha/beta polypeptide cannot be made properly
myoglobin and comparison to hemoglobin
- only found in muscle
- higher affinity for O2 and only releases O2 when O2 is very low
- only carries 1 O2 vs the 4 that hemoglobin carries
different forms of CO2 in body and percentage distribution
- dissolved 20%
- carbaminohemoglobin 10%
- bicarbonate 70%
CO2 and bicarbonate chemical equation
CO2 + H2O –> carbonic anhydrase enzyme catalyzes reaction –> carbonic acid –> freely dissociates to H+ and bicarbonate ion
why CO2 is a volatile acid
- can be released /exhaled
chloride shift
- in tissues
- CO2 produced in tissues –> enters RBC and becomes bicarbonate –> bicarbonate leaves RBC and goes into blood and Cl- goes in so RBC is electrically neutral
reverse chloride shift
- in lungs
- bicarbonate enters RBC to be converted to CO2 –> Cl exits RBC so that RBC is electrically neutral
le chatliers principle
- for a reaction that can occur in both directions, reaction moves from higher concentration to lower concentration
acid production and 2 systems that maintain pH
- produced by metabolic reactions
- kidneys/renal system release H+ in urine
- respiratory system and bicarbonate buffering gets ride of H+ as CO2
respiratory acidosis and causes
- hypoventilation (high CO2 concentration) –> H+ builds up
- caused by opioids and heroin which decrease breathing rate
respiratory alkalosis and causesa
- hyperventilation, low CO2 and H+
metabolic acidosis and 2 causes
- high H+ due to metabolic causes –> high CO2 in blood –> brain increases rate of breathing
- diabetes - lots of acidic ketone bodies made, cause s kussmal breathing that is tachypnea and hyperpnea
- bicarbonate loss through diarrhea so H+ cannot be buffered
metabolic alkalosis
- too much bicarbonate so not enough H+ in blood
3 respiratory control centers
- rhythmicity center in MO
- pneumotaxic and apneustic center in pons
rhythmicity center - 2 type of neurons and function
- inspiratory neurons innervate LMN that control inspiratory muscles like diaphragm
- expiratory neurons inhibit inspiratory neurons
- exhalation is passive
apneustic center
- excites inspiratory neurons causing inhalation
pneumotaxic center
- inhibits apneustic center ultimately leading to exhaation
peripheral chemoreceptor location, what is monitored, and through what nerve is information sent
- located in aortic and carotid bodies
- monitors blod CO2, H+, and O2
- sends information to rhythmicity cente via vagus nerve
central chemoreceptors - location
- located in MO
describe connection between other parts of the brain and rhythmicity center
- other parts of brain send info to rhythmicity center explaining why thoughts, emotions, and visual information can cause changes in breathing rate
voluntary breathing - what parts of the brain are involved
- frontal cortex sends commands directly to LMN
- autonomic responses can override voluntary breathing control
blood brain barrier - can H+ and CO2 pass through?
- CO2 can pass through but H+ cannot
central chemoreceptor vs peripheral chemoreceptor - how do they detect hypoventilation and how long does it take
- peripheral: stimulated by H+
- central - stimulated by CO2 which crosses blood brain barrier and is then converted to H+
- central has a larger affect but takes a longer amount of time
total minute volume - definition and normal amount
- amount of volume exhaled in a minute
- tidal volume * breath per minute
- 4L/minute
PCO2 range and link to rhythmicity cente r
PCO2 = tight range of 40mmHg +- 2
- rhythmicity center tries to regulate this amount in the blood
effect of PCO2 vs PO2 on ventilation - describe the graph
- overall PCO2 has a much larger effect
- as PCO2 rises total minute volume gradually then steeply rises
- total minute volume only increases when PO2 is very low and even then it doesnt increase that much
hypoxic drive - when does it occur and what is the mechanism
- PO2 = 70mmHg = 10k altitiude
- carotid bodies respond directly to low O2
why is there greater sensitivity to CO2 then O2
- high CO2 = high H+ = acidic and protein denaturation
