Respiratory physiology (pie for finals) Flashcards
1
Q
Define what is meant by internal respiration ?
A
- Our body systems are made of cells
- These cells need a constant supply of oxygen (O2) to produce energy and function
- The carbon dioxide (CO2) produced by the cellular reactions must continuously be removed from our bodies
- Internal respiration refers to the intracellular mechanisms which consume O2 and produces CO2
2
Q
Define what external respiration is
A
- The term external respiration refers to the sequence of events that lead to the exchange of O2 and CO2 between the external environment and the cells of the body
- It involves four steps
3
Q
What are the 4 main steps of external respiration ?
A
- Ventilation -the mechanical process of moving gas in and out of the lungs
- Gas exchange between alveoli and blood - the exchange of O2 and CO2 between the air in the alveoli and the blood in the pulmonary capillaries
- Gas transport in the blood - the binding and transport of of O2 and CO2 in the circulating blood
- Gas exchange at the tissue level - the exchange of O2 and CO2 between the blood in the systemic capillaries and the body cells
4
Q
What are the 4 body systems involved in external respiration ?
A
- The Respiratory System
- The Cardiovascular System
- The Haematology System
- The Nervous System
5
Q
Define what ventilation is
A
The mechanical process of moving air between the atmosphere and alveolar sacs
6
Q
In terms of pressure what what condition needs to be met for ventilation to occur
A
The intra-alveolar pressure must become less than atmospheric pressure for air to flow into the lungs during inspiration.
7
Q
Define what boyles law is
A
At any constant temperature the pressure exerted by a gas varies inversely with the volume of the gas i.e. as the volume of a gas increases the pressure exerted by the gas decreases
8
Q
Before inspiration the intra-alveolar pressure is equivalent to atmospheric pressure, how is a lower pressure then achieved during inspiration ?
A
During inspiration the thorax and lungs expand as a result of contraction of inspiratory muscles and because of boyles law this increase in intra-alveolar volume containing the gas results in decreased intra-alveolar pressure
9
Q
How does movement of the chest wall expand the lungs as there is no physical connection between the lungs and chest wall?
A
Two forces hold the thoracic wall and the lungs in close opposition:
- The intrapleural fluid cohesiveness: The water molecules in the intrapleural fluid are attracted to each other and resist being pulled apart. Hence the pleural membranes tend to stick together.
- The negative intrapleural pressure: the lungs are forced to expand outwards while the chest is forced to squeeze inwards. (Across the lung wall, the intra-alveolar pressure of 760 pushes outward, while the intrapleural pressure of 756 pushes inward. This causes the lungs to stretch to fill the larger thoracic cavity. Across the thoracic wall, the atmospheric pressure of 760 pushes inward, while the intrapleural pressure of 756 pushes outward
10
Q
Describe what inspiration is
A
- Inspiration is an active process brought about by contraction of inspiratory muscles
- The chest wall and lungs stretched
- The Increase in the size of the lungs make the intra-alveolar pressure to fall
- This is because air molecules become contained in a larger volume (Boyle’s Law)
- The air then enters the lungs down its pressure gradient until the intra-alveolar pressure become equal to atmospheric pressure
11
Q
Inspiration is an active process depending on muscle contraction. What 2 muscles does it depend on and what specifically do they do ?
A
- Diaphragm (major inspiratory muscle) - increases the volume of the thorax vertically by contracting
- The external intercostal muscle - lifts the ribs and moves out the sternum by contracting
12
Q
Describe the process of expiration
A
- Normal expiration is a passive process brought about by relaxation of inspiratory muscles
- The chest wall and stretched lungs recoil to their preinspiratory size because of their elastic properties
- The recoil of the lungs make the intra-alveolar pressure to rise
- This is because air molecules become contained in a smaller volume (Boyle’s Law)
- The air then leaves the lungs down its pressure gradient until the intra-alveolar pressure become equal to atmospheric pressure
13
Q
What condition can abolish the trasmural pressure gradient needed for lung expansion and what may this result in ?
A
Pnuemothorax - this can then result in lung collapse
14
Q
What causes the lungs to recoil during expiration?
(i.e. what gives the lungs their elastic behaviour - because it is a passive process so something inherint must cause it)
A
- Elastic connective tissue in the lungs - the whole structure bounces back into shape
- But even more important is the alveolar surface tension
15
Q
What is alveolar surface tension ?
A
- It is the attraction between water molecules at liquid air interface
- In the alveoli this produces a force which resists the stretching of the lungs
16
Q
If alveoli were lined with water alone the surface tension would be too strong so the alveoli would collapse, therefore what prevents collapse of alveoli?
A
Pulmonary surfactant - it lowers alveolar surface tension by interspersing between the water molecules lining the alveoli
17
Q
What is pulmonary surfactant and what is it produced by?
A
Pulmonary surfactant is a complex mixture of lipids and proteins secreted by type II alveoli
18
Q
What does the law of LaPlace state + state the equation which deomstrates this?
A
It states smaller alveoli (with smaller radius - r) have a higher tendency to collapse
19
Q
What is a secondary factor alongside pulmonary surfactant which helps keep alveoli open ?
A
Alveolar Interdependence - if an alveolus start to collapse the surrounding alveoli are stretched and then recoil exerting expanding forces in the collapsing alveolus to open it
20
Q
This is an overview of the main opposing forces acting on the lungs
A
21
Q
What are the major inspiratory muscles of respiration ?
A
Diaphragm and external intercostal muscles
22
Q
What are the acessory muscles of inspiration (they contract only during forceful inspiration) ?
A
Sternocleidomastoid, scalenus, pectoral
23
Q
What are the muscles of active expiration ? ( they contract only during active expiration)
Note - Recall expiration is usually passive
A
Abdominal muscles and internal intercostal muscles
24
Q
Define what tidal volume is and state the average value
A
- The volume of air entering or leaving lungs during a single breath
- Average = 0.5 L
25
Define what inspiratory reserve volume is and state the average value for it
* It is the extra volume of air that can be maximally inspired over and above the typical resting tidal volume
* Average = 3.0L
26
Define what expiratory reserve volume is and state the average value for it
* It is the extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume
* Average = 1.0L
27
Define what residual volume is and state the average value
* It is the minimum volume of air remaining in the lungs even after a maximal expiration
* Average = 1.2L
28
Define what inspiratory capacity is and state the average value
It is the maximum volume of air that can be inspired at the end of a normal quiet expiration (IC =IRV + TV)
29
Define what functional residual capacity is and state the average value
* It is the volume of air in lungs at end of normal passive expiration (FRC = ERV + RV)
* Average value = 2.2L
30
Define what vital capacity is and state the average value
* It is the maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TV + ERV)
* Avergae = 4.5L
31
Define what total lung capacity is and state the average value
* It is the total volume of air the lungs can hold (TLC = VC + RV)
* Average = 5.7L
32
Lung volumes and capacities are measured using what ?
Spirometry
33
Why is it not possible to measure total lung volume using spirometry ?
Because residual volume can not be measured by spirometry, hence total lung volume cannot be measured
34
What happens to residual volume in emphysema ?
Increases due to loss of the elastic recoil of the lungs
35
Spirometry is done to measure Dynamic Lung Volumes - what are the 3 main ones it measures ?
1. **FVC =** Forced Vital Capacity (max volume that can be forciblly expelled from the lungs following a max inspiration)
2. **FEV1** = Forced Expiratory volume in one second. Volume of air that can be expired during the first second of expiration in an FVC (Forced Vital Capacity) determination.
3. **FEV1/FVC ratio.** The proportion of the FVC that can be expired in the first second = (FEV1/FVC) X 100% - Normally \> 70%
36
Measuring dyanmic lung volumes is useful in the diagnosis of what?
Obstructive and Restrictive Lung Disease
37
What are the dyanmic lung volumes results in spirometry suggestive of obstrcutive airway disease?
* FVC = low or normal
* FEV1 = low
* **FEV1/FVC % = low** (\<70%)
38
What are the dyanmic lung volumes results in spirometry suggestive of restrictive airway disease?
* FVC = low
* FVE1 = low
* FEV1/FVC % = normal
39
Resistance to flow in the airway normally is very low and therefore air moves with a small pressure gradient. What however is the Primary determinant of airway resistance?
The radius of the conducting airway
40
What causes bronchoconstriction and what causes bronchodilatation ?
* Parasympathetic stimulation causes bronchoconstriction
* Sympathetic stimulation causes bronchodilatation
41
Why is expiration more difficult than inspiration in patients obstructive airway disease e.g. Asthma, COPD etc?
Due to dyanmic airway compression:
* Dynamic airway compression causes no problems in normal people - increased airway resistance causes an increase in airway pressure upstream. This helps open the airways by increasing the the driving pressure between the alveolus and airway (i.e. the pressure downstream)
* If there is an obstruction (e.g. asthma or COPD), the driving pressure between the alveolus and airway is lost over the obstructed segment. This causes a fall in airway pressure along the airway downstream resulting in airway compression by the rising pleural pressure during active expiration
42
What does a peak flow meter estimate and what is it useful in assessing ?
It estimates peak flow rate which asseses airway function which is useful in patients with obstructive airway disease
43
How is a reading using a peak flow meter taken?
* It is measured by the patient giving a short sharp below into the peak flow meter
* The best of three attempts is usually taken
44
Decribe what is meant by pulmonary compliance
* Compliance is measure of effort that has to go into stretching or distending the lungs
* The less compliant the lungs are, the more work is required to produce a given degree of inflation
45
What is meant by decreased pulmonary compliance and give examples of causes
* Decreased pulmonary compliance means greater change in pressure is needed to produce a given change in volume (i.e. lungs are stiffer). This causes SOBOE
* Causes e.g. pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia, absence of surfactant
46
Conditions which cause decreased pulmonary compliance may cause what type of pattern on spirometry ?
A restrictive pattern
47
What is the underlying reason for increased pulmonary compliance and give the 2 main examples of causes for it
Increased pulmonary compliance is caused by loss of the normal elastic recoil of the lungs
1. Increased compliance occurs in emphysema. Patients have to work harder to get the air out of the lungs – hyperinflation of lungs
2. Compliance also increases with increasing age
48
What is the normal energy ependiture for normal work of breathing ?
3% of total energy expenditure
49
Give some examples of reasons for increased work of breathing
* When pulmonary compliance is decreased
* When airway resistance is increased
* When elastic recoil is decreased (increased pulmonary compliance)
* When there is a need for increased ventilation
50
Define what pulmonary ventilation is
* It is the volume of air breathed in and out per minute
* Pulmonary Ventilation (L) = tidal volume (L/breath) x Respiratory Rate (breath/min)
51
Define alveolar ventilation and explain why it is less than pulmonary ventilation
* It is the volume of air exchanged between the atmosphere and alveoli per minute
* Alveolar Ventilation = (tidal volume – dead space volume) x Respiratory Rate
* It is less than pulmonary ventilation because of anatomical dead space where air remains in the airways and is not available for gas exchange
52
Why is alveolar ventilation more important than pulmonary ventilation ?
This is more important as it represent new air available for gas exchange with blood
53
How do you increase pulmonary ventilation and by which way is it more advantageous to do so ?
* To increase pulmonary ventilation (e.g. during exercise) both the depth (tidal volume) and rate of breathing (RR) increase.
* Because of dead space: It is more advantageous to increase the depth of breathing
54
What 2 things does the transfer of gases between the body and atmosphere depends upon?
1. **Ventilation**: the rate at which gas is passing through the lungs.
2. **Perfusion**: the rate at which blood is passing through the lungs
55
Perfusion (blood flow) and ventilation vary from bottom to top of the lung. State how they vary
At the bottom of the lungs perfusion is much better than ventilation. The opposite is seen at the top of the lungs
56
The match between air in the alveoli and the blood in the pulmonary capillaries is not always perfect. Ventilated alveoli which are not adequately perfused with blood are considered as what?
As alveolar dead space
57
Define what the physiological dead space is
Physiological dead space = the anatomical dead space + the alveolar dead space
58
In healthy people, the alveolar dead space is very small and of little importance. When may it become a problem and why?
59
Describe how ventilation and perfusion is matched in the lungs
Local controls act on the smooth muscles of airways and arterioles to match airflow to blood flow
* Accumulation of CO2 in alveoli as a result of increased perfusion decreases airway resistance leading to increased airflow
* Increase in alveolar O2 concentration as a result of increased ventilation causes pulmonary vasodilation which increases blood flow to match larger airflow
60
What is the effect of decreased or increased pulmonary O2 on systemic arterioles ?
61
What are the 4 factors which influence the rate of gas exchange across the alveolar membrane ?
1. Partial Pressure Gradient of O2 and CO2
2. Diffusion Coefficient for O2 and CO2
3. Surface Area of Alveolar Membrane
4. Thickness of Alveolar Membrane
62
Gases move across cell membranes etc by pressure gradient, what determines this pressure gradient ?
The partial pressure of a gas determines the pressure gradient
63
Define what the partial pressure of a gas is
The pressure that one gas in a mixture of gases would exert if it were the only gas present in the whole volume occupied by the mixture at a given temperature.
64
State Daltons law of partial pressures and the equation it explains
Daltons law states the Total Pressure exerted by a gaseous mixture = the sum of the partial pressures of each individual component in the gas mixture
65
Go over this partial pressure example equation
66
How is the partial pressure of oxygen in the alveolar air (PAO2) calculated?
* Atmospheric pressure = 760
* The air in the respiratory tract is saturated with water which contributes 47 to the total pressure
* PiO2 would then = 713 x 0.21 = 150 mmHg (because atomsophere air made up of 79% N2 and 21 % O2)
* Normal arterial PCO2 = 40
Ans = PAO2 = 150 – [40/0.8] = 150 – 50 = 100 mmHg at sea level
67
Look over the partial pressure diffusion gradients for O2 and CO2, why does it not matter that the partial pressure gradient for CO2 is much smaller than the partial pressure gradient for O2?
* CO2 is more soluble in membranes than O2.
* The diffusion coefficient for CO2 is 20 times that of O2
68
* A small gradient between Alveolar PO2 (PAO2) and arterial PO2 (PaO2) is normal (ventilation-perfusion match is usually not perfect).
* A big gradient between PAO2 and PaO2 would indicate what?
Problems with gas exchange in the lungs or a right to left shunt in the heart
69
What effect does diffusion coefficient have on gas transfer across membranes?
The larger the coefficient the more effectively the gas diffuses across
70
The lungs provide a very large surface area with thin membranes to facilitate effective gas exchange. State Ficks law of diffusion
The amount of gas that moves across a sheet of tissue in unit time is proportional to the area of the sheet but inversely proportional to its thickness
71
Describe what comprises the respiratory membranes
1. **Alveoli**: Thin-walled inflatable sacs which function in gas exchange. Its walls consist of a single layer of flattened Type I alveolar cells
2. **Pulmonary capillaries** encircle each alveolus
3. **Narrow interstitial space**
72
Go over this summary
73
List the non-respiratory functions of the respiratory system
* Route for water loss and heat elimination
* Enhances venous return (Cardiovascular Physiology)
* Helps maintain normal acid-base balance (Respiratory and Renal Physiology)
* Enables speech, singing, and other vocalizations
* Defends against inhaled foreign matter
* Removes, modifies, activates, or inactivates various materials passing through the pulmonary circulation
* Nose serves as the organ of smell
74
Go over this picture showing the partial pressures of oxygen and how it follows the pressure gradient to reach the tissues
75
Define henrys law and explain what it means
* The amount of a given gas dissolved in a given type and volume of liquid (e.g. blood) at a constant temperature is proportional to the partial pressure of that gas in equilibrium with the liquid
* This means that if the partial pressure in the gas phase is increased the concentration of the gas in the liquid phase would increase proportionally
* The partial pressure of a gas in solution is its partial pressure in the gas mixture with which it is in equilibrium
76
What 2 forms is oxygen found in the blood and transported as and which is the main form of transport ?
1. **Bound to haemoglobin** in the red blood cells - 98.5%
2. Physically dissolved in the blood (very little O2 - only 1.5%)
77
How many O2 molecules can bind to one haemoglobin (Hb) molecule ?
* Each Hb molecule contains 4 haem groups
* Each haem group reversibly binds to one O2 molecule
==\> 4 O2 molecules can bind to one Hb molecule
78
Haemoglobin is considered fully saturated when all the Hb present is carrying its maximum O2 load. What is used to determine the percent saturation of haemoglobin with O2?
The PO2 is the primary factor
79
Oxygen delivery to the tissues is dependant on what 2 things and how is it calculated ?
1. Oxygen content of arterial blood
2. The cardiac output
80
The O2 content of arterial blood is determined by what and state the equation which calculates this?
The Hb concentration and the saturation of Hb with O2
81
What 3 things can impair O2 delivery to the tissues and how?
1. **Respiratory disease -** results in decreased partial pressure of inspired oxygen which decreases arterial PO2 and hence decrease Hb saturation with O2 and O2 content of the blood
2. **Heart failure -** this decreases cardiac output
3. **Anaemia** -this decreases Hb concentration and hence decreases O2 content of the blood
82
What is the name of the shape of an oxygen dissociation curve and why does it have this shape ?
* It has a **sigmoid** curve
* This is due to co-operativity - the binding of one O2 to Hb increases the affinity of Hb for O2. The curve then flattens when all sites are becoming occupied
83
What is the significance of the flat upper portion and the steep lower portion of the oxygen dissociation curve ?
* The flat upper portions means that a moderate fall in alveolar PO2 will not much affect oxygen loading (i.e. look at the curve and the normal PO2 of the pulmonary capillaries if tho PO2 dropped even moderatley, there would still be close to the same O2 delivery)
* Steep lower part means that the peripheral tissues get a lot of oxygen for a small drop in capillary PO2
84
Describe what the Bohr effect in realtion to the oxygen-dissociation curve is and state the causes of it
This is the shift of the curve to the right = for given oxygen tension there is reduced saturation of Hb with oxygen i.e. Enhanced oxygen delivery to tissues
Causes: (think '**R**aised' = **R**ight)
* raised [H+] (acidic)
* raised pCO2
* raised 2,3-DPG\*
* raised temperature
85
How does foetal haemoglobin differ in its structure and affinity for oxygen compared to adult haemoglobin ?
* Foetal haemoglobin (HbF) differs from adult haemoglobin in structure - HbF has 2 alpha and 2 gamma subunits
* HbF has a higher affinity for O2 compared to adult haemoglobin (HbA)
86
Explain the significance of the higher affinity for O2 for foetal haemoglobin in the transfer of O2 from mother to foetus
* It means O2-Hb dissociation curve for HbF is shifted to the left compared to HbA
* This would allow O2 to transfer from mother to foetus even if the PO2 is low
87
Explain the difference between O2-Hb and O2-myoglobin dissociation curves and the significance of the hyperbolic shape of the O2-myoglobin dissociation curve
* Myoglobin is present in skeletal and cardiac muscles
* One haem group per myoglobin molecule
* No cooperative binding of O2
* Dissociation curve hyperbolic
* Myoglobin releases O2 at very low PO2
* Provides a short-term storage of O2 for anaerobic conditions
* presence of myoglobin in the blood indicates muscle damage
88
What are the 3 forms CO2 is transported in the blood ?
1. As a Bicarbonate (HCO3-)
2. As Carbamino-haemoglobin
3. In a solution
89
Which of the 3 forms of CO2 transport in the blood is the main mode?
As a Bicarbonate (HCO3-)
90
Describe the bicarbonate buffer system (formation of bicarbonate)
* Carbon dioxide combines with water to form carbonic acid (H2CO3), a reaction accelerated by carbonic anhydrase
* Once carbonic acid is formed it dissociates into hydrogen and bicarbonate ions.
91
Where does the formation of bicarbonate occur ?
Inside the red blood cell
92
Considering the formation of bicarbonate what happens to the hydrogen and bicarbonate ions ?
* Bicarbonate ion diffuses out to the plasma to be exchanged for chloride ions. This is known as the **chloride shift**
* Hydrogen ions bind easily to reduced haemoglobin
93
How are Carbamino compounds formed?
* By combination of CO2 with terminal amine groups in blood proteins.
* Especially globin of haemoglobin to give carbamino-haemoglobin
94
Describe what the haladane effect is
Removing O2 from Hb increases the ability of Hb to pick-up CO2 and CO2 generated H+
95
Explain how the haladane effect works in synchrony with the Boher effect to facilitate the liberation of O2 and the uptake CO2 **at tissue level**
They work together to facilitate O2 liberation and uptake of CO2 & CO2 generated H+ at tissues by:
1. The Bohr Effect Facilitating the Removal of O2 from Haemoglobin at Tissue Level by Shifting the O2-Hb Dissociation Curve to the Right
2. In turn the haladane effect means the removal of O2 results in an increased affinity for Hb to bind with CO2 and remove it from the tissues
96
What does the haladane effect do to the oxygen dissociation curve and give examples of causes of it
It shifts the curve to the **L**eft = **L**ower O2 delivery to tissues
Causes:
Shifts to Left = Lower oxygen delivery
* HbF, methaemoglobin, carboxyhaemoglobin
* low [H+] (alkali)
* low pCO2
* low 2,3-DPG
* low temperature
97
Explain how the liberation of CO2 is facilitated at the lungs
Because at the lungs the Hb pick-up the O2 - this weaken its ability to bind CO2 and H+ ==\> facilitating the liberation of CO2
98
Go over this summary pic of CO2 transport in the blood
99
What are the 2 main controls of respiration?
The Neural & the Chemical control of Respiration
100
Describe the neural control of breathing rhythm
* Breathing rhythm is generated a network of neurons called the **Pre-Botzinger complex**.
* These neurons display pacemaker activity.
101
Where is the Pre-Botzinger complex located?
The **Medulla** - upper end of the medullary respiratory centre
102
Describe the steps of neural control which lead to insipiration (recall this is active) and then in turn expiration (recall this is passive)
1. Rhythm is generated by Pre-Botzinger complex
2. This excites Dorsal respiratory group neurones (inspiratory) causing them to fire
3. Firing leads to contraction of inspiratory muscles - inspiration
4. When firing stops, passive expiration occurs
103
Describe the neural control of active expiration ?
1. When firing of dorsal neurones occurs a second group is excited - the Ventral respiratory group neurones
2. This then in turn fires and excites internal intercostals, abdominals etc leading to active 'forceful' expiration
Note - In normal quiet breathing, ventral neurones do not activate expiratory muscles
104
The rhythm generated in the medulla is modified by what?
Neurones in the pons:
The “Pneumotaxic Centre” (PC) and
105
Where are the The “Pneumotaxic the Apneustic Centres located ?
The pons
106
How does the Pneumotaxic centre (PC) modify the rhythm generated in the medulla?
1. PC stimulated when dorsal respiratory neurones fire
2. Stimulation inhibits inspiration
107
Without PC modification of the rhythm generated by the medulla what would happen to breathing ?
Breathing becomes - prolonged inspiratory gasps with brief expiration termed **apneusis**
108
How does the apneustic centre (AC) modify the rhythm of breathing generated in the medulla ?
Impulses from the AC neurones excite inspiratory area of medulla - prolonging inspiration
109
List the stimuli which can influence the respiratory centres (neural control of breathing)
* **Higher brain centres** e.g. cerebral cortex, limbic system, hypothalamus
* **Stretch receptors in the walls of bronchi and bronchioles** – the inflation Hering-Breur reflex – guard against hyperinflation
* **Juxtapulmonary (J) receptors** - stimulated by pulmonary capillary congestion and pulmonary oedema (caused by e.g. left heart failure); also pulmonary emboli rapid shallow breathing
* **Joint receptors** – stimulated by joint movement
* **Baroreceptors**: increased ventilatory rate in response to decreased BP
* **Central chemoreceptors** - relates to chemical control
* **Peripheral chemoreceptors** - relates to chemical control
110
Describe the purpose of the Hering-Breuer reflex
Pulmonary stretch receptors are activated during inspiration - activation inhibits inspiration
111
How do joint receptors influence breathing ?
* Impulses from moving limbs reflexly increase breathing
* Probably contribute to the increased ventilation during exercise
112
List the factors which cause an increase in ventilation during exercise
* Reflexes originating from body movement
* Adrenaline release
* Impulses from the cerebral cortex
* Increase in body temperature
* Later: accumulation of CO2 and H+ generated by active muscles
113
Describe the cough reflex and state what it is in response to
Controlled by centre in the medulla
Afferent discharge stimulates:
1. short intake of breath
2. followed by closure of the larynx
3. then contraction of abdominal muscles (increases intra-alveolar pressure)
4. and finally opening of the larynx and expulsion of air at a high speed
Activated by irritation of airways or tight airways (e.g. asthma) and used to help clear airways of dust, dirt or excessive secretions
114
What receptors control the chemical control of respiration ?
Central and peripheral chemoreceptors
115
What variables are controlled to inturn inact chemical control of respiration ?
The blood gas tensions, especially CO2
116
State the location and stimuli for the peripheral chemoreceptors
The carotid and aortic bodies - these chemoreceptors sense and are stimulated by the tension of O2, CO2 & [H+] in the blood
117
State the location and stimuli for the central chemoreceptors
* Situated near the surface of the medulla of the brainstem
* Respond to the [H+] of the cerebrospinal fluid (CSF)
118
What is the ventilation response to hypercapnia (high PCO2) ?
Ventilation increases
Note - an increase in H+ ions will cause the same thing since CO2 produces H+ ions
119
120
Describe the ventilation response to hypoxia (low PO2)
* Peripheral chemoreceptors become stimulated only when arterial PO2 falls to low levels (\<8.0 kPa). Their stimulation causes an increase in ventilation
* Eventually hypoxia can become so severe that neurons are depressed and ventilation actually decreases
121
Hypoxia at high altitudes is caused by what?
Decreased partial pressure of inspired Oxygen (PiO2)
122
What is the acute response to hypoxia at high altitudes ?
hyperventilation & increased cardiac output
123
What are the symptoms of altitude sickness (acute mountain sickness)?
headache, fatigue, nausea, tachycardia, dizziness, sleep disturbance, exhaustion, shortness of breath, unconsciousness
124
List the chronic adaptations which occur due to increased altitude
1. Increased RBC production (polycythaemia) - increased O2 carrying capacity of blood
2. Increased 2,3 BPG produced within RBC - O2 offloaded more easily into tissues (right shift of oxygen dissociation curve)
3. Increased number of capillaries - blood diffuses more easily
4. Increased number of mitochondria - O2 can be used more efficiently
5. Kidneys conserve acid - decreased arterial pH
125
The H+ Drive of Respiration
* The effect is via the peripheral chemoreceptors
* H+ doesn’t readily cross the blood brain barrier (CO2 does!)
* The peripheral chemoreceptors play a major role in adjusting for acidosis caused by the addition of non-carbonic acid H+ to the blood (e.g. lactic acid during exercise; and diabetic ketoacidosis)
* Their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body (remember CO2 can generate H+, so its increased elimination help reduce the load of H+ in the body)
* This is important in acid-base balance
126
Go over this summary for the chemical factors influencing respiration
