respiration course pack part 2 (slide 55-100) Flashcards

1
Q

What is Henry’s law?
What is the O2 consumption per min?

A

-Henry’s law is the amount of dissolved gas carried by blood is directly proportional to the partial pressure of the gas
-O2 consumption per min is 300ml O2/min

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2
Q

What is essential for O2 transport?
How much O2 is bound to Hb?

A

Hemoglobin is essential for O2 transport since it allows blood to take up 65x more O2 than plasma, and it combines rapidly and reversibly with O2
-19.5% of O2 in blood is bound to Hb

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3
Q

What contributes to Po2

A

-only O2 in plasma contributes to PO2

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4
Q

What is the O2 dissociation curve shape?
What is Hb at high and low PO2

A

-sigmodal curve shape
-at high PO2 Hb is saturated (curve is more flat)
-at low PO2, Hb is deasturated to let O2 go to be available for working tissue of cell metabolism

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5
Q

What is the percent change of HbO2 at low vs high PO2?

A

-at high PO2 the chnage from 100 to 80mmhg only results in 3% HbO2 change
-at low PO2 change from 40 to 20 mmhg is 40% change

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6
Q

What does myoglobin bind to, where is it found?
What is the shape of the curve, when will it release O2?

A

-myoglobin only binds 1 O2 molecule, and it is found in skeletal muscle
-the curve shape is hyperbolic, and will only release an O2 at very low PO2

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7
Q

What is the norml amount of Hb in the blood?

A

14g/100L is the normal amount

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8
Q

What is the Bohr effect, and what happens during exercise in this process?

A

-Bohr effect is the shift of the HbO2 curve to the right when blood CO2 or temp increase, or pH decreases
-when we excercise we increase CO2 and acid production and produce heat, shifting the curve to the right, meaning when we drop PO2, and extra mount of O2 is released to be used in tissue
-makes O2 available sooner

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9
Q

What does carbon monoxide do, how does it affect the HbO2 curve?
What happens to PaO2?

A

-CO has a high O2 binding site affinity and will reduce the amount of O2 in Hb, it also shifts the HbO2 to the left decreasing amount of unloading O2 in the tissue
-in CO poisoning PaO2 remains normal so you dont know that you do not have enough O2

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10
Q

How is CO2 carried in the blood, 3 ways that it is carried?

A
  1. physically dissolved in the blood (10%)-CO2 from tissues diffuses into the plasma
  2. combined with Hb to form HbCO2 (11%)-CO2 combines with globin portion
  3. as bicarbonate (79%)-CO2 combines with H2O to produce carbonic acid, diffuses into erythrocytes with help of carbonic anhydrase then ionizes into bicarbonate (Cl- comes into cell to maintain pH)
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11
Q

What happens in lowering of PCO2?
What happens when PCO2 is higher in blood than alveoli?

A

-results in HCO3- getting transformed in to H2CO3 and further int o CO2, H2O, and HbCO2 making Hb+CO2
-there is anet diffusion from blood into alveoli which lowers the blood PCO2

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12
Q

What is the haldane effect?

A

-it is the fact that mixed venous blood can carry more CO2 than can arterial blood, creating more H2CO3 and thus more bicarbonate for CO2 to be in

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13
Q

What is the relationship between CO2 and PCO2 in the graph?
What happens if we double alveolar ventilation?

A

-it is a linear relationship
For example, if we hypoventilate and alveolar PCO2 rises, then arterial, capillary, tissue and venous CO2 also rises
-it halves alveolar PCO2, so an increase in alveolar ventilation proportionally increase CO2 removal

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14
Q

What are the reasons that can lead to respiratory failure?

A

due to failure of:
1. the gas exchanging capabilities of the lungs
2. the neural control of ventilation (the drive to breath)
3.the nueromuscular breathing apparatus (respiratory muscles and their innnervation)

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15
Q

what is hypoxia?

A

It refers to deficient blood oxygen, meaning PaO2 and Hb saturation are low

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16
Q

What are the 5 causes that can lead to hypoxia?

A
  1. inhalation of low PO2 (high altitude)
    2.hypoventilation
  2. ventilation/perfusion imbalance
    4.shunts of blood across lungs
    5.O2 diffusion impairment
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17
Q
  1. what is hypoventilation caused by?
    2.What is ventilation/perfuion imbalance caused by
A

2.hypoventilation- alveolar ventilation in relation to CO2 production is reduced (PaO2 decrease and PaCO2 increases)
3. ventilation/perfusion imbalance-amount of fresh gas reaching alveolar region is too low

18
Q
  1. what is shunt of blood caused by across lung, what is an example
    4.how is O2 diffusion impairment caused?
A

4.shunts of blood across lungs-venous blood returns to systemic circulation, deoxygenated by bypassing gas exchange region of lung
example- foramen ovule since baby in utero gets O2 from blood of mother, so when it is born the flap connecting lleft+right heart should close, if it doesnt its called shunt
5.O2 diffusion impairment-(thickening of alveolar capillary membrane)

19
Q

What is breathing controlled by, what is an example?
What controls gas exchange?

A

breathing is under voluntary (ex. hyperventilation), and involuntary control (ex. while asleep
-central nervous system controls gas exchange

20
Q

What controls voluntary and involuntary breathing?

A

-cerebral hemispheres control voluntary breathing
-brainstem controls involuntary breathing

21
Q

What parts of brainstem do involuntary control?
What are the 3 basic elements of respiratory control?

A

pons and medulla
1. sensors:gather info about lung volume and O2+CO2 content
2.controllers-info is sent here from the sensors, in the pons and medulla via afferent neural fibers
3.effectors-neuronal impulses are generated and sent via spinal motornuerons to effectors

22
Q

What are examples of sensors, central controller, and effectors

A

sensor-chemoreceptors, lung and other receptors
centrol controller-pons. medulla, etc
effectors-respiratory muscle

23
Q

What groups of cells does the medulla have?q

A

-they have pacemaker cells, that are located in the ventral respiratory group (generate basic rythm), and dorsal respiratory group that receives several sensory inputs

24
Q

What groups of cells are in upper pons?
What do these cells do?

A

-cells located here are called pneumotaxic center that modify inspirtaoty activity of the centers of medulla
-cells turn off inspiration leading to smaller tidal volume, which increases breathing frequency

25
Q

What does cutting these pneumotaxic centers do?

A

-cutting pneumotaxic centers causes breathing to become deep and slow (same effect as cutting vagus nerve)

26
Q

What groups of cells are in lower pons?
What do they send/promote?

A

-called the apneustic center
-they send excitatory impulses to the respiratory groups of the medulla, promoting inspiration

27
Q

What does removing the upper pons and the vagus nerve cause?

A

-causes apneuses which is tonnic inspiratory activity interupted by short expirations (dont have upper pons to tell you to stop breathing in)

28
Q

1.What happens when you turn off inspiration and have vagi intact vs cut?
2.What happens when you promote inspiration and have vagi intact vs cut, when there is a cut at the upper pons?
3. What happens to rhythm when you have vagi intact vs cut, when the lower pons is cut?
4. What happens when you cut at the medulla?

A

1.vagi intact- normal breathing pattern
vagi cut-slow+deep breathing pattern
2.vagi intact-slower + deeper breathing pattern
vagi cut-apnosis, large tidal breath
3.vagi intact- random pattern rhytmicity, volume is random
vagi cut-same as with vagi intact
4. with vagi intact and cut, there is no breathing

29
Q

What levels/things are detected by chemoreceptors?
What changes when one of these is changed?
What are the 2 types of chemoreceptors?

A

-PO2, PCO2, and pH in arterial blood are detected by chemoreceptors
-if these pressures or pH are changed ventilationw will also change
-central and peripheral

30
Q

Where are central chemorecptors located and what do they detect?
What do they drive?

A

-located on the ventral surface of medulla, and they detect pH of the cerebrospinal fluid (CSF)
-drives the breathing under normal conditions

31
Q

What stimulated chemoreceptors?
What happens when they are stimulated?

A

-drop in pH
-minute ventilation increases causing hyperventilation, which causes reduced PCO2 in blood, and inCSF

32
Q

WHat increases when pCO2 levels increase?

A

-minute ventilation, breathing freqeuncy, and tidal volume

33
Q

What are peripheral chemorecptors sensitve to?
Where are they located?
What part of the medulla are they project to?

A

-changed in PO2, but are also stimulated by increased PCO2 and decreased pH
-carotid bodies, and in aortic bodies which are made up of blood vessles, supporting tissue, and nerve endings of the 9th nerve (gloosopharyngela nerve) and vagus nerve (X nerve)
-the afferent fibers of these receptors project to the dorsal group of respiratory neurons in the medulla

34
Q

Where do carotid bodies send info vs aortic bodies

A

carotid bodies send info with 9th nerve
aortic bodies send info via X nerve (vagus nerve)

35
Q

What are the 3 types of pulmonary vagal receptors in the lungs that respond to mechanical stimuli?

A
  1. pulmonary stretch receptors
    2.irritant receptors
    3.juxta capillary or J recptors
36
Q

Where are pulmonary stretch receptors located?
What are they innervated by, and what do they respond to?

A

-located in the smooth muscle of the trachea down to terminal bronchioles
-they are innverated by large myelinated fibers
-they respond to the lung being distended

37
Q

What is the main refelx effect of the stretch receptors?
What does it do, and in what age is it most noticebale in

A

Hering-breuer inflation reflex- which is the decrease in respiratory frequency due to long expiratory time
-most noticeable in infants and animals

38
Q

Where are irritant receptors located?
What stimulates them?
What is innervated by and what does the stimulation lead to?

A

-Located between airway epithelial cells in the trachea down to terminal bronchioles
-they are stimulated by noxious gas, ciggarate smoke, histamine, cold air and dust
-innverated by large myelinate fibers
-stimulation leads to bronchoconstriction and hyperapnea (increased depth of breathing)

39
Q

Where are Juxta capillary receptors located?
-what are they innervated by
What are they stimulated by?

A

-in the alveolar walls close to the capillaries
-innervated by non myelinated fibers and have short bursts of activity
-stimulated by an increase in the pulmonary interstitial fluid, like what may occur in pulmonary congestion and edema

40
Q

What does JC receptor induce, what does it also play a role in?

A

-it causes rapid and shallow respiration, intense stimulation can cause apnea, and
-plays a role in dyspnea (difficulty breathing) which is associated by left heart failure and lung edema or congestion

41
Q

100How does minute ventilation increase in untrained and trainde subjects?
What does endurance training delay?

A

-increase linearly up to about 50-65% of VO2 max, then increases greater than VO2
-delays the ventilatory inflection point