Chapter 7- Respiratory Physiology (2).ppt

ppt

1. 1
Chapter seven
Physiology of Respiration

2. Respiration
•Respiration includes two separate but related processes: cellular
respiration and external respiration
Cellular respiration:
–Intracellular metabolic processes
–Occurs within the mitochondria
–Uses O
2and produces CO
2 + ATP
External respiration:
•The exchange of O
2and CO
2between the external environment
and the cells
•It is subdivided into 4 integrated processes
2

3. 3

4. 4
Q . Discuss the functional anatomy of respiratory system
Divisions
•Respiratory system is divided anatomicallyinto:
a.Upper respiratory tract
•Nasal cavityUpperpart of trachea
b.Lower respiratory tract
•Lower part of trachea alveolar sacs (alveolar ducts + alveoli)
•Respiratory system is divided according to major function
a.Conducting zone
•For conduction of air to the lower zone
•Nasal cavity Terminalbronchioles
b.Respiratory zone
•For gas exchange (O
2and CO
2)
•Respiratory bronchioles + alveolar sacs

5. Anatomical considerations
5

6. 6

7. The Lungs
•Concave base, rest on diaphragm
•Location: within the thoracic cavity
•Protection: by the rib cage
•Right: 3 lobes -superior, middle, inferior
•Left: 2 lobes -upper and lower lobes. (accommodates heart)
•Housed in pleural cavity (the potential space b/n the 2 memb.)
•Thoracic cavity lined with parietal pleura
•Lungs covered by visceral pleura
•Both pleurae produce pleural fluid to reduce friction during
expansion
7

8. 8
•The right lung with three lobes accounts for 55%of the lung
function.
•The lungs contain about 300 million alveoli whose surface area
is >70m
2
.
•Alveoli are small outpouchings(tiny air sacs) that are final
branching of the respiratory tree and serve as a primary sites
of exchange of O
2and CO
2.
•They contain threecell types:
1. Type I pneumocytes -simple squamous epithelium lines inside,
allow rapid gas diffusion (gas exchange).

9. 9
2.Type II pneumocytes -cuboidal epithelial cells; responsible for
the production of surfactants(phospholipids + proteins),
prevent alveolar collapse
3. Type III pneumocytes -large phagocytic macrophage cells. These
cells keep alveolar surfaces sterile by removing debris and
microbes
Gas exchange occurs across the respiratory (alveolo-capillary)
membrane(0.5µm thick) —to allow rapid diffusion of gases b/n
alveolus & capillary.
Consists of fourlayers:
1. Type I & II cells of alveolus -constitutes the alveolar wall
2. Epithelial basement membrane-underlying the alveolar wall
3. Capillary basement membrane-fused to no.2
4. Capillary endothelium

10. 10

11. 11
Functions of respiratory system:
•Ventilation
•Gas exchange between alveoli and pulmonary capillaries
Non-respiratory functions:
•Water and heat loss
•Maintain normal acid–base balance
•Olfaction and phonation
•Modification of some substances that pass through lungs (like
angiotensin I)
•Enhance venous return
•Defends against microbes

12. 12
The Mechanics of Breathing
•Ventilation = movement of air into/out of alveoli
•Air flows from area of high pressure to low pressure
•Threetype of pressures are important in ventilation
1. Atmospheric (barometric) pressure
=the pressure exerted by the weight of the gas in the atm. on
objects on Earth’s surface =760 mm Hg at sea level (to
simplify=0 cmH
2O)
2. Intra-alveolar pressure (intrapulmonary pressure)
=the pressure within the alveoli =760mmHg (or 0 cmH
2O)
3. Intrapleural pressure (intrathoracic pressure)
=the pressure within the pleural sac =755mmHg (or-5cmH
2O)

13. •Respiratory muscles:
1.Diaphragm
2.External & internal intercostals muscles (lie between the ribs)
2.Accessory muscles:
Sternocleidomastoid
Scalene inneck
Pectoralis:chestmuscles
Latissimusdorsi:superficialbackmuscles
4.Musclesoftheabdominalwall
Internalintercostalsmuscles&musclesoftheabdominalwall
areexpiratorymuscles(whenitisactive).
13

14. 14
Respiratory muscles

15. 15
Direction of external and internal intercostals.

16. Inspiration
•Inflow of atm. air into the lungs
•Boyle’s Law: gas pressure is inversely proportional to volume
Enlargementof chest cavity

volume of thorax

-vePpl(-8cmH
2O)

Lung expansion

P outside (0 cmH
2O) > P inside (alveoli) (-1cmH
2O)

Air flows in
16

17. 17

18. •During inspiration:
1.Contractionofdiaphragm(onstimulationbythephrenic
nerve)movesdownward(1.5cm-7cm)
↓
verticaldiam.ofthorax
↓
Contributes70%oftheairthatentersthelungs
2.Contractionofexternalintercostals(onstimulationbythe
intercostalnerve)
↓
lateral&anteroposteriordiam.ofthorax
↓
Contributes30%oftheairthatentersthelungs
NB:Accessorymusclesareactiveduringdeepinspirations
18

19. 19
Expiration
•Outflow of air from the lungs into the atm.
reduction in chest cavity
↓
↓volume of thorax
↓
↓-vePpl(-5cmH
2O)
↓
↓lung volume
↓
P outside (0 cmH
2O) < P inside(+1 cmH
2O)
↓
Air flows out

20. 20
Passive expiration

21. 21
Active expiration

22. •During quiet passive expiration:
Elastic recoil of the chest wall and stretched lungs to their
preinspiratory size on relaxation of inspiratory muscles
•Diaphragm relaxes↓volume of the thoracic cavity
•External intercostal muscles relaxelevated rib cage falls
&↓volume of the thoracic cavity
•Active expiration(during exercise):
1.Contraction of internal intecostalsmuscles depress the ribs
2.Contraction of abdominal musclesUpward movement of
diaph.
22

23. 23
LUNG VOLUMES AND CAPACITIES
•On average, in healthy young adults, the maximum air that the
lungs can hold is about 5.7 liters in males (4.2 liters in females).
•Anatomic build, age, the distensibility of the lungs, and the
presence or absence of respiratory disease affect this total lung
capacity.
•The changes in lung volume that occur with different respi-
ratoryefforts can be measured using a spirometer

24. 24
Spirometer:
•Is a device that measures the volume of air breathed in and out
•It consists of an air-filled drum floating in a water-filled chamber.
•As a person breathes air in and out of the drum through a
connecting tube, the resultant rise and fall of the drum are
recorded as a spirogram, which is calibrated to the magnitude of
the volume change.
•The pen records inspiration as an upward deflection and
expiration as a downward deflection

25. 25

26. 26

27. •The four standard lung volumes are:
• Tidal volume (TV)
• Residual volume (RV)
• Expiratory reserve volume (ERV)
• Inspiratory reserve volume (IRV)
•TV : volume of air entering or leaving the lungs during a
single breath (500 ml)
•RV: volume of air remaining in the lungs after a maximal
expiration (1200 ml).
•ERV: extra volume of air that can be expelled after a normal
expiration (1000 ml).
27

28. 28
•IRV: extra volume of air inhaled after a normal inspiration
(3000 ml).
•The four standard lung capacities (consist of two or more
lung volumes in combination) are:
Functional residual capacity
Inspiratory capacity
Vital capacity
Total lung capacity

29. 29
•FRC: volume of air remaining in the lungs at the end of a normal
expiration (2200 ml).
(FRC=ERV + RV)
•IC: Max. volume of air that can be inspired from FRC (3500ml)
(IC=IRV + TV)
•VC: max. volume of air that can be expired after maximal
inspiration (4500 ml).
(VC=IRV + TV + ERV)
•TLC: volume of air in the lungs after a maximal inspiration
(5700 ml).
(TLC=VC + RV)

30. 30
•Two general categories of respiratory dysfunction yield
abnormal results during spirometry.
•Obstructive lung disease (e.g. asthma or bronchitis,
emphysema).
There is a difficulty in moving gas out of the lung due
to high airway resistance
•Restrictive lung disease (e.g. pulmonary fibrosis)
Replacement of delicate lung tissue with thick, fibrous
tissue
Lungs are less compliant (not expand easily) than
normal, so it is difficult to move gas into the lungs

31. Pulmonary, or minute, ventilation
•the volume of air breathed in and out in one minute.
•Pulmonary ventilation= tidal volume x respiratory rate
(ml/min) = (ml/breath) (breaths/min)
6000 ml/min =500 ml/breath x 12 breaths/min
•These values apply to conditions of normal, quiet breathing
•Tidal volume and breathing frequency (RR) increase
substantially during exercise
31

32. Dead space
= regions of the respiratory systems that contain the air but
are not exchanging gases with blood
1. Anatomical dead space:
•Airways not capable of gases exchange with the blood
•It is about 150 ml
•This volume is considered anatomic dead space b/c air within
these airways is useless for exchange.
-NB: Conducting airways do not contain alveoli to
participate in gas exchange
32

33. 2. Alveolar dead space:
•Alveoli containing air but without blood flow in the surrounding
capillaries
•In other words, these alveoli receive airflow but no blood flow;
with no blood flow to the alveoli, gas exchange cannot take
place.
3. Physiological dead space:
•anatomical dead space + alveolar dead space
•determined by measuring the amount of CO
2 in the expired air.
NB: Only 350 ml are exchanged between the atmosphere and
alveoli because of the 150 ml occupying the anatomic dead
space.
33

34. 34

35. Alveolar ventilation
•The volume of air exchanged between the atmosphere and alveoli
per minute
•Alveolar ventilation is less than pulmonary ventilation because of
dead space
Alveolar ventilation = (tidal volume –dead space volume)
x respiratory rate
Alveolar ventilation = (500 ml/breath -150 ml dead space
volume) x12 breaths/min
= 4200 ml/min
•Thus, with quiet breathing, alveolar ventilation is 4200 ml/min,
whereas pulmonary ventilation is 6000 ml/min.
35

36. Pulmonary circulation and
ventilation-perfusion ratio
Pulmonary circulation:
•Starts in right ventriclepulmonary trunkpulmonary
arteriespulmonary capillariespulmonary veinsleft atrium,
i.e. this circulation is in series with the systemic circulation.
The Pulmonary arteries:
•Conduct deoxygenatedblood from right heart to lungs to be
oxygenated
•Branch profusely, along with bronchi and ultimately feed into the
pulmonary capillary network surrounding the alveoli.
•The pulmonary veins –carry oxygenated blood from lungs to
the left atrium.
36

37. Pulmonary circulation:
•BP = 24/9 mmHg
•Pressure gradient = 7 mmHg
•Low resistance
Systemic circulation:
BP = 120/80 mmHg
Pressure gradient = 90 mmHg
High resistance
37

38. Gas Exchange
•Gas exchange at both the pulmonary capillary and the tissue
capillary levels involves simple passive diffusion of O
2& CO
2
•The diffusion of O
2and CO
2 depends on their partial pressure
gradients.
•Oxygen diffuses from an area of high partial pressure in the
alveoli to an area of low partial pressure in the pulmonary
capillary blood.
•Carbon dioxide diffuses down its partial pressure gradient from
the pulmonary capillary blood into the alveoli.
38

39. Partial pressure
•Atm.airis a mixture of gases containing 21% O
2and 79% N
2
with almost negligible percentages of CO
2, H
2Ovapor, other
gases, and pollutants.
•Partial pressure: the pressure of a specific gas in a mixture.
•Dalton’s law:
P
gas= % total gas x P
tot
•The partial pressures for oxygen (PO
2) and nitrogen (PN
2) can be
calculated:
•PO
2= 0.21 x 760 mmHg = 160 mmHg
•PN
2= 0.79 x 760 mmHg = 600 mmHg
•Altogether, these gases exert a total atmospheric pressure of 760
mm Hg at sea level.
39

40. •The total pressure is equal to the sum of the partial pressures
(=760 mmHg).
•A difference in partial pressure between capillary blood and
surrounding structures is known as a partial pressure gradient.
•It exists b/n :
-the alveolar air and pulmonary capillary blood
-the systemic capillary blood and surrounding tissues
•A gas always diffuses down its partial pressure gradient.
40

41. Partial pressures of oxygen
•As air is inspired, it is warmed and humidified as it flows through
the conducting airways.
•Therefore, water vapor is added to the gas mixture (P
H2O=
47mmHg).
•This is accounted for in the calculation of PO
2in the conducting
airways:
PO
2inspired air = 0.21 x (760 mmHg –47 mmHg) = 150 mmHg
•Alveolar PO
2is also lower than atmospheric PO
2 as a result of
humidification and the small turnover of alveolar air(100 mmHg)
41

42. •Gas exchange
systemic capillaryblood O
2tissues
CO
2
Pulmonary gas exchange
•Occurs only in the lungs
•Deoxygenated blood (from the right side of the
heart)oxygenated blood
42
Pulmonary gas exchange
alveolus O
2pulmonary capillary blood
CO
2
Tissue gas exchange

43. Systemic gas exchange
•Oxygenated blood (from left ventricle) deoxygenated blood.
•Occurs in tissues throughout the body.
43

44. 44

45. Factors affecting rate of gas exchange
•Partial pressure difference of the gases
-Rate of transfer increases as partial pressure gradient increases.
•Surface areaavailable for gas exchange
-Rate of transfer increases as surface area increases
•Thicknessof respiratory membrane
-Rate of transfer decreases as thickness increases
•Diffusion constant
45

46. Molecular Weight
•O
2has a lower molecular weightthan CO
2, O
2 diffuses faster
(about 1.2 times faster)
Solubility
•CO
2is 20 x more soluble than oxygen,therefore, it diffuses
more rapid than that of O
2(20x)
•This difference in diffusion constants is normally offset by the
difference in partial pressure gradientsthat exist for O
2and
CO
2 across the alveolar capillary membrane.
46

47. Transport of gases in the blood
1. Transport of oxygen
•Oxygen is carried in the blood intwo forms:
•Physically dissolved in plasma
•Chemically combined with hemoglobin (Hb)
i. Physically Dissolved O
2in plasma
•Only 1.5%, because oxygen is not very soluble in body fluids.
•0.003 ml O
2/100ml blood can be dissolved for each mmHg of
pressure, so normal dissolved O
2content of blood is 0.3 ml
O
2/100ml blood.
•Thus, only 15 ml of O
2can dissolve per minute in the normal
pulmonary blood flow of 5 liters/min.
47

48. •Tissue oxygen consumption at rest is 250 ml/min & 3.5 to 5.5
L/min during exercise, so need extra way to transport O
2.
48

49. ii. Chemically bound O
2
•The remaining 98.5%is transported in combination with Hb.
•PO
2is related to oxygen dissolved, not oxygen bound to Hb
•Hb, an iron-bearing protein molecule contained within the RBCs.
•If Hb not combined with O
2, it is referred to as reduced
hemoglobin, or deoxyhemoglobin; if combined with O
2, it is
called oxyhemoglobin(HbO
2):
Hb + O
2 HbO
2 (reversible)
reduced hemoglobin oxyhemoglobin
49

50. •Each gram of Hb can combine with up to 1.34 ml of oxygen.
•In a healthy individual, there are 15 g of Hb per 100 ml of blood.
•Therefore, the oxygen content of the blood is 20.1 ml O
2/100 ml
blood:
15g Hbx 1.34mlO
2= 20.1mlO
2
100ml blood g Hb 100ml blood
•P
O2determines Hb saturation
-Each Hb molecule has 4 Fe, is capable of binding to 4O.
-“Fully saturated” if 4O are bound.
-PO
2of blood (related to [O
2 dissolved]) is most important
factor determining %Hb saturation
50

51. •%Hb saturation : a measure of the extent to which the Hb pres-
entis combined with O
2, vary from 0% to 100%.
Law of mass action
•If blood PO
2is increased(i.e., in pulmonary cap.), reaction shifts
to right, get more HbO
2 (increased % Hb saturation).
•If blood PO
2 is decreased(i.e., in systemic cap.), HbO
2
dissociated, releases its oxygen, rxnshifts to left(decreased % Hb
saturation).
O
2-Hb (oxyhemoglobin ) dissociation curve:
•Is S-shaped, not linear.
•Has the lower steep and upper flat plateauportions
•Both portion of the curve have important physiological
significance.
51

52. 52

53. Plateau portion of the curve:
•60 -100 mmHg, is the PO
2range found in the alveoli.
•Normal alveolar PO
2=100 mmHg.
•Hb loads up with oxygen
•At PO
2=100mmHg , Hb fully saturated (97.5%).
•even at PO
2= 60 mmHg, Hb. is 90% saturated; the Hb
remains quite saturated with oxygen
•Thus, this portion of the curve provides a good margin of safety
for the oxygen-carrying capacity of blood.
•Therefore, even if PO
2falls to 60 mmHg (at high altitudes,
pathological conditions), body can maintain high %Hb
saturation.
53

54. Steep portion of the curve:
•0 -60 mmHg, is the PO
2range found in the cells and tissues
•PO
2 of the tissues + mixed venous blood is about 40 mmHg at
rest.
•At PO
2= 40mmHg, Hb. is 75%saturated (at PO
2= 100 mmHg,
Hb. is 97.5%saturated)
As the blood flows through the systemic capillaries, the Hb
releases 22.5%of O
2to the tissues.
•An increase in the metabolic activity of a tissue, and thus an
increase in oxygen consumption, will decrease the PO
2 in that
tissue.
-this results in a marked increase in the unloading of O
2
from Hb decreases %Hb saturation
54

55. Factors affecting transport of oxygen
1. Acidity ( pH) :
•Acidity increases (H
+
increases, pH decreases) decreases
affinity of Hb for O
2 O
2dissociates more readily from Hb.
•Therefore, an increase in acidity shifts the curve to the right.
2. Carbon dioxide:
•An increase in PCO
2also shifts the O
2–Hb curve to the right.
•CO
2 diffuses from the cells into the blood PCO
2increases in
the systemic capillaries blood decreases the affinity of Hb
for O
2 Hb unloads more O
2 at the tissue level.
•CO
2 generates H
2CO
3, the blood becomes more acidic at the
systemic capillary level
55

56. •Bohr effect–CO
2 & H
+
can combine reversibly with Hb at site
other than O
2 binding site –reduces O
2 affinity.
•The Bohr effect enhances O
2delivery to the tissue and O
2uptake in the lungs
3. Temperature
•A rise in temperature shifts the O
2–Hb curve to the right, resulting
in more unloading of O
2.
•Exercising muscles generate heat, enhances O
2release from Hb for
use by more active tissues.
4. 2,3-Bisphosphoglycerate (2,3-BPG)
•Produced by RBCs (during their metabolism)
•Production gradually increases if Hb is chronically undersaturated
(when HbO
2 is low –high altitudes, anemia, some circulatory /
respiratory diseases)
56

57. •2,3-BPG is present throughout circulation, so it
•Increases HbO
2’s ability to unload oxygen at the tissues
(helps maintain O
2 availability for tissue use)
•Bind reversibly with Hb; decreases its ability to load O
2
from alveoli (-veside of it).
•Shifts curve to right to the same degree in both the tissues
and the lungs.
57

58. 58

59. 5. Carbon monoxide (CO):
•CO is nota normal constituent of inspired air.
•It is a poisonous gas.
•Source: Incomplete combustion (burning) of carbon products
such as automobile gasoline, coal, wood, and tobacco.
•CO and O
2 compete for the same binding sites on Hb.
•Hb’saffinity for CO is 240 times that of its affinity for O
2,so it
forms carboxyhemoglobin (HbCO).
•Therefore, even small amounts of CO can tie up the Hb & make
Hb unavailable for O
2transport.
59

60. •Furthermore, formation of carboxyhemoglobin causes a leftward
shift of the oxyhemoglobin dissociation curve.
•Hb carries less oxygen & does not release this oxygen to the
tissues that need it.
•Hb concentration and PO
2 are normal, the O
2content of the
blood is seriously reduced.
•CO poisoning is particularly insidious.
Odorless, colorless, and tasteless, so an individual exposed to
CO is usually unaware of it.
It does not elicit any irritant reflexes that result in sneezing,
coughing, or feelings of dyspnea (difficulty in breathing).
It does not stimulate ventilation.
60

61. 2. Transport of carbon dioxide
•CO
2is carried in the blood in 3 forms:
•Physically dissolved
•Carbaminohemoglobin (HbCO
2)
•Bicarbonate ions
i. Physically dissolved
•depends on PCO
2, normal PvCO
2= 45 mmHg; normal PaCO
2=
40 mmHg.
•only 10% of the blood’s total CO
2content is carried this way
61

62. ii. Bound to Hb
•HbCO
2= carbaminohemoglobin
•CO
2 binds with the globinportion of Hb, not heme part.
•Reduced Hbhas greater affinity for CO
2 than HbO2(HbO
2
becomes Hb at tissues, picks up CO
2).
•30%of CO
2 in the blood is transported in this form.
iii. Transported as bicarbonate (HCO3
-
)
•The remaining 60% of CO
2is transported in the blood in the
form of bicarbonate ions.
•Taking place rapidly in RBCs, with carbonic anhydrase
catalyzing first reaction (slow in plasma)
CO
2+ H
20 H
2CO
3
-
H
+
+HCO
3
-
62

63. •HCO
3
-
is more soluble in blood than CO
2.
•RBC has HCO
3
-
-Cl
-
carrier that passively facilitates diffusion of
these ions (in opposite directions).
•Membrane is relatively impermeable to H
+
, so HCO
3
-
diffuses
alone.
•HCO
3
-
diffuses out into plasma, Cl
-
diffuses into RBC = chloride
shift
•Most H
+
that’s left behind binds to Hb (reduced Hb has greater
affinity for H
+
than HbO
2) –Hb helps keep acid-base balance
between arterial & venous blood.
•Haldane effect–removing O
2 from Hb increases its ability to pick
up CO
2, H
+
63

64. •Bohr effect & Haldane effect feed into one another
•CO
2, H
+
O
2 release (Bohr effect )
•O
2 release CO
2, H
+
loading(Haldane effect )
64

65. 65
Lungs

66. 66

67. 67

68. Neural and chemical regulation of respiration
1. Neural regulation of respiration
1. Medullary respiratory center
2. Pontine centers
68

69. 1. Medullary respiratory center
-the primary respiratory control center
-consists of several aggregations of neuronal cell
bodies within the medulla
•Dorsal respiratory group (DRG)
•Ventral respiratory group (VRG)
-provide output to the respiratory muscles
2. Pontine centers: Pneumotaxiccenter and Apneusticcenter
-Influence output from the medullary respiratory
center
69

70. 70

71. 71

72. •Cell bodies for neuronal fibers of phrenic, intercostals nerves
are in spinal cord. Impulses from medullary center terminate
there stimulate nerves for inspiratory muscles
contractioninspiration
•When neurons are not firing, inspiratory muscles relax and
expiration occurs.
•Medullary respiratory center consists of two neuronal
clusters -Dorsal respiratory group (DRG) & Ventral
respiratory group(VRG)
72

73. Dorsal respiratory group (DRG):
•In nucleus tractussolitarius; mostly inspiratory neurons,
terminate on motor neurons that supply inspiratory muscles
(initial processing station for feedback from peripheral sensors)
Ventral respiratory group (VRG)
•In nucleus retroambiguus; both inspiratory & expiratory neurons
•Both remain inactive during quiet breathing
•Called into play by DRG as ‘overdrive’ mechanism(when
demand increase).
•Especially important in active expiration. Only during active
expiration do impulses travel to expiratory muscles.
73

74. Generation of respiratory rhythm
•Generation of respiratory rhythm is comes from the pre-
Bötzingercomplex(rostral ventromedial medulla), near the
upper (head) end of the medullary respiratory center
•Neurons in this region display pacemakeractivity, undergoing
self-induced APs similar to those of the SA node of the heart.
74

75. Influences from pontine centers
•Pontine centers exert ‘fine tuning’ influences on medullary center
---> ensure normal, smooth breathing, influence timing of
switching between inspiration & expiration.
•Pneumotaxic center (upper pons) sends impulses to DRG to ‘turn
off’ inspiratory neurons, limiting the duration of inspiration.
•Apneustic center (lower pons) prevents inspiratory neurons from
being turned off, providing an extra boost to the inspiratory drive.
•Of the two, the pneumotaxiccenter dominates.
•Without pneumotaxic‘brakes’, apneusis= prolonged inspiratory
gasps with very brief interrupting expirations(can occur with
severe brain damage).
75

76. 2. Chemoreceptors
•Provide the most important input to the medullary respiratory
center
•Are sensitive to changes in PO
2, PCO
2, and pH.
•Two types: Peripheral chemoreceptors & Central chemoreceptors
1. Peripheral chemoreceptors
Carotid bodies, aortic bodies (different from the carotid sinus and
aortic arch baroreceptors)
Respond primarily to decreases in PO
2–less so to decreases in
pH, increases in PaCO
2.
When PaO
2falls below 100 mmHg, rapidresponse; below 60
mmHg–dramaticresponse (breathing rate increases)
76

77. 2. Central chemoreceptors
Near the ventral surface of the medullain close proximity to the
respiratory center.
Are sensitive to the pHof the cerebrospinal fluid (CSF)
H
+
does not cross the blood–brain barrier
CO
2 diffuses from arterial blood into the CSF.
CO
2 + H
2O H
+
+ HCO
3
-
(in CSF)
H
+
acts directly on the central chemoreceptors
Thus, increases in PCO
2 and [H
+
] stimulate breathing
(hyperventilation), and decreases in PCO
2 and [H
+
] inhibit
breathing (hypoventilation).
77

78. 78

79. Clinical correlates
Abnormalities in arterial p
O2
•Hypoxia: the condition of having insufficient O
2at the cell level.
•There are fourgeneral categories of hypoxia:
1.Hypoxic hypoxia (Hypoxemia)
•Is a decrease in arterial PO
2 inadequate Hb saturation
•caused by: 1) inadequate gas exchange 2) exposure to high
altitude or to a suffocating environment (atm. PO
2alveolar
and arterial PO
2).
79

80. 2.Anemic hypoxia
•A reduced O
2 -carrying capacity of the blood.
•It can result from:
1) a decrease in circulating RBCs
2) inadequate amount of Hb
3) CO poisoning
•In all cases of anemic hypoxia, the arterial PO
2 is normal but the
O
2content of the arterial blood is lower than normal because of
the reduction in available Hb.
80

81. 3.Circulatory hypoxia
•Is decreased O
2delivery to the tissues.
•Can be restricted to a limited area by a local vascular spasm or
blockage.
•The body may experience circulatory hypoxia in general, from
congestive heart failure or circulatory shock.
•Arterial PO
2and O
2 content are typically normal
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82. 4.Histotoxic hypoxia
•O
2delivery to the tissues is normal, but the cells cannot use the
O
2 available to them.
•The classic example is cyanide poisoning.
•Cyanide blocks cellular enzymes essential for cellular
respiration (enzymes in the electron transport system).
•Hyperoxia: an above-normal arterial PO
2oxygen toxicity
damage some cells.
•In particular, brain damage and blindness-causing damage to
the retinaare associated with O
2 toxicity.
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83. Abnormalities in arterial pco
2
•Hypercapnia:
-the condition of having excess CO
2 in arterial blood
-caused by hypoventilation(ventilation inadequate to meet
metabolic needs for O
2 delivery and CO
2 removal).
•Hypocapnia:-below-normal arterial PCO
2levels, is brought
about by hyperventilation.
•Hyperventilation occurs when a person “over breathes”.
Rate of ventilation > body’s metabolic needs CO
2is blown off
to the atm.arterial PCO
2falls
-can be triggered by anxiety states, fever, and aspirin
poisoning.
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84. •Increased ventilation is not synonymous with
hyperventilation.
•Increased ventilation that matches an increased metabolic
demand, such as the increased need for O
2 delivery and CO
2
elimination during exercise, is termed hyperpnea.
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85. Consequences of abnormalities in arterial blood gases
•Respiratory acidosis is the result of abnormal CO
2retention
arising from hypoventilation( increase in CO
2 generates more
H+)
•Causes: lung disease, depression of the respiratory center by
drugs or disease, nerve or muscle disorders that reduce
respiratory muscle ability.
•Respiratory alkalosis is the result of excessive loss of CO
2from
the body as a result of hyperventilation.
•Pulmonary ventilation increases out of proportion to the rate of
CO
2 production too much CO
2is blown off less [H+] is
formed.
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86. •Apnea :Transient cessation of breathing
•Respiratory arrest: Permanent cessation of breathing (unless
clinically corrected)
•Asphyxia: O
2 starvation of tissues, caused by a lack of O
2 in the
air, respiratory impairment, or inability of the tissues to use O
2
•Cyanosis: Blueness of the skin resulting from insufficiently
oxygenated blood in the arteries
•Dyspnea: Difficult or labored breathing (feeling of air hunger)
•Eupnea: Normal breathing
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