CPS- physiology quiz 2 (gas exchange, gas transport, ventilation/perfusion)

dalton's law-

equation-

- the pressure exerted in each individual gas in a space is independent of the pressure of other gases in the mixture

- partial pressure= % total gas * total pressure

inspired partial pressure-

equation-

- accounts for dilution of dry gas

- (total pressure - 47) * % of gas

what is the difference between bulk flow and diffusion?

bulk flow- movement of air due to partial pressure gradient; does not have a choice where it goes; O2 and CO2 move through circulatory system this way

diffusion- occurs by random molecular motion in the pulmonary capillaries and systemic capillaries

what are 3 reasons why the alveolar partial pressure of oxygen and carbon dioxide DO NOT change much over the course of a normal breath?

1. alveolar volume is much larger than pulmonary capillaries

2. so when O2 diffuses into the alveolus, the alveolar PO2 and PCO2 do not really change

3. alveolar PO2 and PCO2 determine arterial PO2 and PCO2 in a perfect gas-exchanging lung (mixed venous PO2 will increase to equal alveolar PO2 and mixed venous PCO2 will decrease to equal alveolar PCO2)

3 things that alveolar PO2 is determined by?

1. pulmonary blood flow

2. oxygen consumed by tissues

3. oxygen brought in by inspiration

3 things that alveolar PCO2 is determined by?

1. pulmonary blood flow

2. oxygen produced by tissues

3. amount of CO2 expired

what 3 things determines alveolar PO2 and PCO2?

1. alveolar ventilation

2. amount of pulmonary blood flow

3. level of metabolism (O2 consumption and CO2 production by the tisses)

hyperventilation-

what does the equation indicate?

- increase in alveolar ventilation will decrease the arterial and alveolar PCO2 below 35-45 range, increase arterial and alveolar PO2

- the alveolar PCO2 is INVERSELY proportional to alveolar ventilation

if you double alveolar ventilation, what happens? will alveolar O2 double too?

- the alveolar PCO2 will decrease and cut in half

- no because PO2 is already at the highest (150)

hypoventilation-

- a decrease in ventilation will increase the arterial PCO2 above 35-45 range, and decrease the alveolar and arterial PO2

- If arterial PCO2 goes above 45, then you are hypoventilating

alveolar air equation estimates ?

what is the equation?

- the partial pressure of oxygen in the alveoli

- PAO2= FIO2 - PaCO2/R

Partial pressure of oxygen in the alveoli equation-

PAO2= FIO2 (PB-PH2O) - PaCO2/R

PAO2= FIO2 (PB-PH2O) - PaCO2/R

what does each variable mean?

PAO2- partial pressure of oxygen in the alveoli

FIO2- fraction of inspired oxygen

PB- barometric pressure (760 mmHg)

PH2O- partial pressure of water vapor in inspired air (around 47)

PaCO2- partial pressure of carbon dioxide in arterial blood (assumed to be same as alveoli)

R= respiratory quotient (ratio of CO2 produced to oxygen consumed)

fick's law of diffusion describe? make up most of?

- describes the factors affected the volume of gas diffusing across a barrier per unit of time

- the lung diffusing capacity (Vgas)

what is the Vgas equation?

2 characteristics?

Vgas= (surface area diffusivity P1-P2) / thickness

1. emphysema decreases surface area

2. pulmonary edema increases the thickness of alveolar capillary membrane and reduces diffusing capacity

diffusivity-

2 characteristics?

- proportional to the solubility / square root of MW

1. solubility is 24 times greater for CO2 then O2

2. Square root of MW is 1.17 times greater for CO2 then O2

how does emphysema decrease he diffusing capacity of the lung?

by decreasing the surface area by destroying the barrier walls

what are 4 ways that pulmonary edema decreases the diffusing capacity of the lung?

1. increases the thickness of the alveolar capillary membrane

2. increases the difference between alveolar and arterial PO2

3. decreases arterial PO2

4. decreases the lung diffusing capacity

what are 5 ways that pulmonary fibrosis decreases the diffusing capacity of the lung?

1. has extra connective tissue

2. increases the difference between arterial and alveolar PO2

3. reduces diffusing lung capacity

4. decreases diffusivity of oxygen

5. decreases arterial PO2

what does decreased diffusing capacity of the lung mean?

what are 3 consequences?

- means there is less efficiency at transferring oxygen from the air to the bloodstream

1. low blood oxygen levels

2. increased shortness of breath

3. increased death in certain lung diseases

shunt-

determinant of alveolar gases?

2 characteristics?

- ventilation is blocked off, but blood still flows because PO2 is 100 mmHg (basically the blood is being shunted away from the lungs because there is no oxygenation taking place or elimination of CO2)

- mixed venous blood

1. V/Q ratio is zero

2. right lung has low V/Q

alveolar dead space-

determinant of alveolar gas?

2 characteristics?

- the alveolus that is ventilated but not perfused

- inspired air

1. V/Q ratio is infinity

2. left lung has high V/Q

what 4 things happen in the right lung of a shunt-like state?

what is the result?

1. narrowed airways

2. increased resistance

3. decrease ventilation

4. airflow goes with least resistance, so it will go to the left lung

result: low V/Q ratio

what 2 things happen in the left lung of a ventilation/ perfusion relationship

what is the result?

1. problem with blood flow, so it will go to the right lung

2. high resistance

result: high V/Q ratio

What is the effect of a high ventilation-perfusion ratio on alveolar PO2 and PCO2?

alveolar PO2- increase

alveolar PCO2- decreased

what are 4 relationships of Ventilation/ Perfusion?

1. High V/Q in left lung

2. low V/Q in right lung

3. high V/Q does NOT make up for low V/Q

4. consequence of V/Q mismatch: decrease in arterial PO2 and increase in arterial PCO2

what is the physiologic shunt equation?

what is the difference between anatomic shunt and absolute intrapulmonary shunt?

physiologic shunt= anatomic shunt + intrapulmonary shunt

- anatomic shunt: refers to the bronchial circulation that returns to the left side of the heart withOUT passing through the pulmonary circulation

- absolute intrapulmonary shunt: refers to the blood passing through pulmonary circulation

2 characteristics of absolute intrapulmonary shunt?

1. absolut shunt: V/Q= 0

2. shunt-like state: low V/Q

what is the equation for fraction of cardiac output perfusing unventilated alveoli?

Qs/Qt (shunt blood flow / total blood flow)

shunt equation for blood flow?

Qt - Qs

Shunt Equation: Oxygen content for normal V/Q units?

(Qt - Qs) * Cc'O2

Shunt Equation: Oxygen content for shunt V/Q units?

Shunt Equation: Oxygen content for delivering oxygen to the systemic capillaries?

- Qs CvO2 (shunt blood flow mixed venous blood)

- Qt CaO2 (total blood flow arterial oxygen content)

final shunt equation?

what is 1 major note about this?

Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2)

- arterial oxygen content is decreased by shunt and will always be less than end-capillary oxygen content of normal V/Q units

What causes hypoxic pulmonary vasoconstriction and what is its physiologic function?

- cause: decreased alveolar PO2

- Functions: 1. HPV increases resistance to blood flow to hypoventilated alveolus 2. blood flow is diverted away from hypoventilated alveolus to vetter-ventilated alveolus

what stimulates bronchodilation? hypoxic pulmonary vasoconstriction?

- increasing PO2 in airways

- decreasing alveolar PO2

what are 3 ways to test for V/Q mismatch?

1. physiologic shunt- shunt equation (anatomic or intrapulmonary: absolute shunt or shunt-like states)

2. physiological dead space- Bohr equation

3. alveolar-arterial PO2 difference

what is the physiological dead space equation?

anatomical dead space + alveolar dead space

2 characteristics about alveolar dead space?

equation?

1. normal expired PCO2 decreases because CO2 is not being added to the alveoli, since there is no perfusion

2. normal= 40 mmHg

equation: physiological dead space - anatomic dead space

in the bohr equation, what happens when alveolar dead space is present?

alveolar dead space increases the difference between arterial and mixed expired PCO2

Bohr Equation ?

VdCO2/Vt = (PaCO2-PeCO2)/PaCO2

What are the potential causes of a difference between the alveolar and arterial PO2? explain.

1. V/Q mismatch- PO2= 68; anatomic dead space is the reason alveolar and arterial pressures are not the same

2. shunt- PO2= 40

3. diffusion impairment- PO2= 80

How is the ventilation-perfusion ratio normally distributed in the top and bottom of the lung?

- top of the lung: high V/Q, less ventilation, less perfusion

- bottom of the lung: low V/Q, more ventilation, more perfusion

what are 2 ways that the V/Q ratio changes from the bottom of the lung to the top?

1. 2 extremes: mixed venous blood on the LEFT and inspired air on the RIGHT

2. High V/Q: high PO2 and low PCO2 because there is more ventilation, which adds oxygen unless there is blood flow because blood flow takes blood away

How much oxygen is normally carried of physically dissolved in the blood?

1.5% is physically dissolved oxygen (NOT bound to hemoglobin)

98.5% is carried oxygen bound to hemoglobin

oxygen transport equation?

Total blood oxygen content = physically dissolved oxygen (1.5%) + oxygen bound to hemoglobin (98.5%)

hemoglobin equation?

why is it reversible?

Hb + O2 -> <- HbO2

- because the hemoglobin wants to load oxygen in the pulmonary capillaries and unload the capillaries in systemic circulation, so it can go into the tissues

what is the equation for oxygen-carrying capacity of the blood?

hemoglobin concentration * 1.34 = maximum amount of oxygen that can be carried in blood bound to hemoglobin

what does percent saturation measure?

what is the equation?

the proportion of a hemoglobin that is binding to oxygen; basically how much O2 is binding to hemoglobin

oxygen bound to Hb / oxygen-carrying capacity (ex: if 2 oxygens are bound to the heme group, then 50% saturation. If 3 O2 are bound, then 75% saturation)

what is the primary determinant of % saturation? explain

blood PO2- the more O2 available, the more likely that an O2 will bind to a heme.

- more UNBOUND PO2= more PO2

- more PO2= increased % saturation (BOUND O2)

what are 4 secondary factors that influence % saturation?

2 characteristics?

1. CO2 2. hydrogen ion 3. 2,3-BPG 4. increased temperature

1. all bind to globin subunits

2. reduce affinity of oxygen for heme groups

what contributes to partial pressure?

what does NOT contribute?

- contributes: UNBOUND/ dissolved O2

(the O2 that is surrounding hemoglobin)

- does not contribute: bound O2

what does the oxyhemoglobin dissociation curve state? explain.

- as PO2 increases, % saturation increases

- if PO2 increases, then there is more oxygen in the blood, which means there is a higher likelihood of binding to hemoglobin

oxygen content of the blood equation-

percent saturation rearranged

Oxygen bound to Hb = percent saturation * oxygen-carrying capacity

describe loading oxygen in the lung: physically dissolved oxygen

- at 37 C, 1 mL blood contains 0.00003 mL O2 / mm Hg PO2 and 100 mL contains 0.003 mL O2

- arterial blood: 0.003 mL O2 = 0.003 mL O2 / 100 mL blood PO2 100 mm Hg

- total blood oxygen: 19.58 ml O2 / 100 mL blood + 0.3 ml O2 / 100 mL blood = 19.88 mL O2 / 100 mL blood

describe loading oxygen in the lungs: oxygen-carrying capacity

step 1: oxygen carrying-capacity equation

step 2: oxygen-carrying capacity * % saturation

step 3: add in physically dissolved oxygen

step 4: oxygen bound to HB + arterial blood = total blood oxygen content

describe how oxygen moves in the lungs? (3)

1. as mixed venous blood passes through the pulmonary capillaries, oxygen diffuses down the partial pressure gradient and into the blood

2. this causes the pulmonary capillary PO2 to increase and more O2 binds to HB (increase % saturation)

3. at the end of pulmonary capillaries, the PO2 will rise to 100 mmHg and the % saturation will be about 97%

describe the oxygen movement in the tissues

- as oxygenated blood passes through the systemic capillaries, the PO2 is greater than 60 mmHg, which results in dissolved O2 to be released into the tissues and hemoglobin releases O2

What is the significance of the flat and steep portions of the oxyhemoglobin dissociation curve?

- flat- constitutes a safety factor, as the arterial PO2 can decrease to 60 mmHg and the % saturation is still about 90%

- steep- necessary for hemoglobin to release O2 to the tissues as the PO2 decreases

explain the oxyhemoglobin dissociation curve:

1. decrease in PO2 means a decrease in oxygen content- when you stop breathing or not breathing enough, alveolar PO2 decreases so the O2 content decreases

2. increase in PO2 does NOT mean increase in oxygen content- PO2 of arterial blood is at 100 mmHg, and gives off supplemental O2, which increases arterial PO2, but NOTHING happens to the % saturation because it is already as high as it can be.

What conditions shift the oxyhemoglobin dissociation to the right?

1. increase in hydrogen ions- decreases pH, decrease in % saturation

2. increase in blood temperature- decrease in % saturation, hemoglobin releases O2

3. mixed venous blood- PO2 decreases, hemoglobin releases O2, decrease in % saturation, PCO2 increases

4. added 2,3-BPG - occurs when O2 is low and pressure is high, hemoglobin releases O2

how does metabolism play a role in mixed venous blood?

1. CO2 is being created, so PCO2 increases

2. an increase in PCO2= pH decreases because H ions are being creases and blood temperature increases

3. these increasing means that systemic capillary oxyhemoglobin dissociation curve shifts right and aids in the release of oxygen to the tissues

what are 3 conditions that shift the oxyhemoglobin dissociation curve to the left?

1. decrease in hydrogen ions- increases pH, increases % saturation

2. decrease in blood temperature- increase in % saturation, hemoglobin increases O2

3. No 2,3-BPG - Hemoglobin holds on to oxygen for too long and does not release it, so this shifts left and decreases the PO2

How does carbon monoxide affect oxygen transport?

1. CO binds very tightly to heme and prevents O2 from binding (decreased oxygen content)

2. Does not move tissues, so they attach themselves to the heme group, and starves the O2 for it to eventually die off

How does anemia affect oxygen transport?

1. reduces hemoglobin concentration

2. reduces oxygen-carrying capacity

3. reduces arterial oxygen content

Anemia does NOT affect: % saturation and arterial and alveolar PO2 are NORMAL

what percentages is carbon dioxide being transported in the blood?

Physically dissolved → 5-10%

Carbamino compounds → 5-10%

Bicarbonate --> 80-90%

3 ways carbon dioxide moves in the systemic capillaries?

1. arterial blood passes through the systemic capillaries, and there is a partial pressure gradient for CO2

2. this causes CO2 to diffuse from the tissues and into the systemic capillaries- increasing PCO2

3. some CO2 remains dissolved, some binds to globin, and most forms bicarbonate in the RBC, then distributes itself equally between RBCs and plasma

2 ways carbon dioxide moves in pulmonary capillaries?

1. As mixed venous blood goes through the pulmonary capillaries, there is a partial pressure gradient driving the diffusion of CO2 into the alveoli, where it can be expired.

2. This makes the PCO2 in the pulm cap decrease, which makes the hemoglobin subunit release CO2, and then the carbonic anhydrase reaction to shift to the LEFT, forming free CO2 which can then diffuse into the alveoli.

rate and depth of breathing determined by?

the respiratory centers in the medulla in response to an input

respiratory center function:

sends burst of action potentials to the inspiratory muscles to determine the rate of breathing

depth of breathing determined by ?

the frequency of the burst of action potentials and by the # of motor units of respiratory muscles recruited

what does NTS sense?

site of what?

- termination of vagus and glossopharyngeal nerves

- integration of inputs that can relax the altered cycle of inspiration and expiration

DRG location? consist of?

2 function:

- located in the NTS

- mostly inspiratory neurons

1. primary generator of basic rhythm of respiration

2. primary projection site of afferent nerves

VRG consist of?

function:

- inspiratory and expiratory cells

1. drive either spinal respiratory neurons (intercostal and abdominal muscles) or accessory muscles of respiratory innervated by vagus nerves

what does the pneumotaxic center limit?

duration of inspiration

irritant receptors-

1. lies between airway epithelial cells

2. stimulated by noxious gases, cigarette smoke, inhaled dusts, cold air

Juxtacapillary receptors-

detects?

location?

- endings of nonmyelinated C fibers

- detects a rise in interstitial pressure/ pulmonary capillary volume (ex: pulm edema)

- alveolar walls, close to capilaries

what does stimulation of J receptors cause?

what happens if stimulation is decreases?

what activates J receptors?

- rapid, shallow breathing (ex: pulm embolism)

- decreased stimulation causes apnea

- Engorgement of pulmonary capillaries and increased interstitial fluid volume

what are the joint and muscle receptors a part of?

stimulus to ventilation during exercise

where are arterial chemoreceptors located?

what are they stimulated by?

- bilaterally in carotid bodies and aortic bodies

1. increased PCO2

2. decreased PO2

3. decreased pH

what are 4 effects of arterial chemoreceptors?

1. hyperapnea- increase rate and depth of breathing

2. vasoconstriction

3. bronchoconstriction

4. dilation of upper airway

what is a direct and indirect effect of arterial chemoreceptors?

direct- decreased heart rate

indirect- increased heart rate and lung inflation

arterial baroreceptors effects: (2)

1. increased blood pressure causes brief apnea and bronchodilation

2. decreased blood pressure causes hyperventilation

what are the 3 Pain and temperature receptors:

1. somatic pain- hyperventilation

2. visceral pain- hypoventilation

2. heating of skin- hyperventilation

how do chemoreceptors of a negative feedback loop regulate gas exchange? (3)

1. by maintaining the rate and depth of breathing

2. what changes between breaths

3. sends action potentials to the medulla

chemoreceptors-

what are the regulated variables in arterial blood and CSF?

- the control of breathing in a negative feedback loop

- variables in arterial blood- PO2, PCO2, pH

- variables in CSF- PCO2 and pH

what does arterial and central chemoreceptors increase and decrease?

arterial: increase PCO2, decrease PO2 and decrease pH

central: increase PCO2, decrease pH in CSF because hydrogen ions do not cross the blood-brain barrier

what are the 2 steps of how the regulated variables are kept normal?

1. the medulla receives increased action potential frequencies from the chemoreceptors

2. actions potentials are sent to the respiratory muscles, which affect the rate and depth of breathing

3 influences of higher centers on ventilation? explain

1. voluntary influence- the highest influence, means you can override the autonomics (if you want to hyperventilate you can)

2. speech, singing, and wind instrument

3. emotion

explain the alveolar ventilation and PaCO2 line graph:

Increase in arterial PCO2 generally leads to an increase in ventilation, while a decrease in PCO2 leads to a decrease in ventilation

how are Sleep, narcotics, and deep anesthesia affected in the CO2 response curve?

result?

- they depress the response to CO2

- decrease ventilation

what stimulates both arterial and central chemoreceptors as CO2 crosses the blood-brain barrier?

- in between breaths, small increase in alveolar and arterial PCO2

what are peripheral chemoreceptors stimulated by?

1. decrease PO2

2. decrease pH

3. increase PCO2

what do central receptors respond to? cause? what do they not?

-respond to: increased PCO2 and decreased pH (increase H+ ions)

- not respond to: hypoxia

- increased PCO2 causes slow buildup of CO2 in CSF

what can pass through the blood-brain barrier? what cannot pass through?

- pass: CO2

- cannot pass: hydrogen ions and bicarbonate ions

what do central chemoreceptors establish?

most of the steady-state ventilatory response to ELEVATED CO2

what is most important in short-term transient responses to CO2?

arterial chemoreceptors

what does CO2 lead to?

what leads to that?

1. CO2 leads to high production of H+ ions

2. high H+ concentration leads to increase in minute volume (the rate and depth of breathing)

why is it hard to separate the response to hydrogen ion from the response to carbon dioxide?

where does this response come from?

- because there is a carbonic anhydrase in the CSF that causes an increase in hydrogen ins when CO2 increases

- arterial chemoreceptors

what are the 8 steps in the response to hydrogen ions?

1. increased production of non-CO2 acid (meaning hydrogen does not result from CO2- lactic acid)

2. decreased arterial pH: does NOT stimulate central chemoreceptors bc hydrogen ions do not pass through barrier

3. increased firing of arterial chemoreceptors: only arterial bc H+ ions too slow across barrier

4. increased respiratory muscle contractions

5. increased alveolar ventilation: directly affects CO2, which directly affects H ions, which can influence the alveoli

6. decreases alveolar PCO2

7. decreased arterial PCO2

8. return to arterial pH toward normal

explain the response to hypoxia graph (4):

1. response arises from arterial chemoreceptors ONLY (carotid bodies more than aortic) - not central

2. insensitive response at normal arterial PO2

3. sensitive response at lower arterial PO2

4. response to hypoxia is potentiated at high arterial PCO2