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Physiology 210 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Function of Respiration

A

-Primary function of respiration is gas exchange. In mammals, gas exchange occurs in the lungs. During inspiration, air rich in O2 is inhaled in the lungs. During expiration, CO2 produced during the oxidative processes of the body is exhaled from the lungs. Both gases are transported by the blood. Therefore, both the cardiovascular system and the respiratory system are involved with supplying body cells with O2 and eliminating their waste product CO2.

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2
Q

The Respiratory Tract

A
  • Air flows through a series of air passages that connect the lungs to the nose and mouth. Inhaled air passes over a complex series of surfaces when it goes through the nose: the nasal septum and the nasal turbinates. These surfaces clean the air of big dust particles/
  • From the nose, warmed and moistened air flows through the common passages for air and food, the pharynx, and then continues through the larynx. Air finally reaches the periphery of the lungs via the trachea and bronchi
  • The lungs and the airways share the chest cavity with the heart, the great vessels, and the esophagus. The airways consist of a series of tubes that branch and become narrower, shorter, and more numerous as they penetrate into the lungs. The trachea divides into 2 main bronchi, each of which divides into lobar and segmental bronchi. The right main bronchus has 3 lobar bronchi (the right lung has 3 lobes) while the left main bronchus divides only 2 bronchi (left lung only 2 lobes) The segmental bronchi divide further into smaller branches. The smallest airways without alveoli are the terminal bronchioles.
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3
Q

Pathway/Subdivisions of the conducting airways and terminal respiratory Units.

A

Trachea –> Bronchi –> bronchioles –> terminal bronchioles –> Respiratory bronchioles –> alveolar ducts –> alveolar sacs

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4
Q

Pleura

A

-Thin cellular sheet attached to the thoracic cage interior (parietal pleura) and, folding back upon itself, attached to the lung surface

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5
Q

Visceral Pleura

A

forms two enclosed pleural sacs in thoracic cage
-pressure in the pleural space is negative
-In the pleural space there is a small amount of fluid, nothing else
-intraplueral fluid lubricates the movement of the lungs
-

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6
Q

Conducting Airways

A
  • consist of the airways from the mouth and nose openings, all the way down to the terminal bronchioles. These airways conduct air from the atmosphere to the respiratory part of the lungs
  • do not contribute to gas exchange and are thus said to compose the anatomical dead space
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7
Q

Respiratory Zone

A
  • the respiratory part of the lungs begins where the terminal bronchioles divide into respiratory bronchioles, which have some alveoli opening into their lumen.
  • Beyond the respiratory bronchioles are the alveolar ducts lined with alveoli
  • the alveolar region of the lungs is the site of gas exchange, and is called the respiratory zone.
  • because of such abundant branching of airways, the respiratory zone makes up most of the lungs
  • the smallest physiological unit of the lungs (distal to the terminal bronchioles) is the acinus
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8
Q

Functions of the Conducting Airways

4 main

A
  1. Defense against bacterial infection and foreign particles: the epithelial lining of the bronchi has hair-like projections called cilia. The epithelial glands secrete a thick substance, mucous, which lines the respiratory passages as far down as the bronchioles. Foreign particles stick to the mucous and the cilia constantly sweep the mucous up into the pharynx. This is called the MUCOCILIARY DEFENSE SYSTEM
  2. Warm and moisten inhaled air
  3. Sound and speech are produced by the movement of air passing over the vocal cords
  4. Regulation of air flow: smooth muscle around the airways may contract or relax to alter resistance to air flow.
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9
Q

Function of the Respiratory Zone

A
  • site of gas exchange between the air in the alveoli and the blood in the pulmonary capillaries.
  • there are roughly 300 mil alveoli in the human lungs, and each alveolus may be associated with as many as 1k capillaries.
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10
Q

Two types of Circulations in the Lungs

A
  1. Pulmonary circulation: brings mixed venous blood (blood that comes from differnt body organs w/ different metabolic activities) to the lungs allowing for the blood to get oxygenated, then back to the left heart
  2. Bronchial circulation: supplies oxygenated blood from the systemic circulation to the tracheobronchial tree (this circulation allows for the airways to get oxygenated.
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11
Q

Anastomosis

A
  • venous blood from the airways to the arteries. Venous blood that came from the cells or the airways mixes with oxygenated blood, goes to heart
  • slight waste
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12
Q

Three alveolar cell types

A
  1. Epithelial Type I and II cells: Alveoli are lined by epithelial type I and II cells. Together, all the alveolar epithelial cells form a complete epithelial layer seal by tight junctions. Little is known about the specific metabolic activities of type 1 cells. Type II cells produce pulmonary surfactant, a substance that decreases the surface tension of the alveoli
  2. Enothelial cells: Consitute the walls of the pulmonary capillaries. These cells may be as thing as 0.1 micron
  3. Alveolar macrophages: These removes foreign particles that may have escaped the mucociliary defense system of the airways and found their way into the alveoli.
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13
Q

Sternocleidomastoid

A

-elevates sternum.

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14
Q

External Intercostal muscles

A
  • contract, they lift the rib cage. So do the parasternal intercartilaginous muscle
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15
Q

external Oblique

A
  • contract for expiration
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16
Q

Inspiratory Muscles

A
  • Main muscle is the diapragm.
  • in addition the external intercostal muscles and the parasternal intercartilaginous muscles and neck muscles may assist. Their major contribution occurs during high levels of ventilation. Contraction of these muscles is also apparent during sever asthma and other disorders that obstruct the movements of air into the lungs.
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17
Q

Diaphragm

A
  • It is innervated by the phrenic nerves from the cervical segments 3, 4, and 5. Contraction of the diaphragm causes its dome to descend and the chest to expand longitudinally. At the same time, its contraction elevates the lower ribs because of the vertically oriented attachments of the diaphragm to the costal margins. Contraction of the external intercostal muscles also raises the ribs during inspiration. As the ribs are elevated, the anterior-posterior and transverse dimensions of the chest enlarge.
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18
Q

Expiratory Muscles

A
  • is passive during quiet breathing as a result of the recoil in the lungs and chest wall. It becomes active at higher levels of ventilation, or in pathogical states.
  • muscles involved: internal intercostal muscles and the abdominal muscles.
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19
Q

Summary of events during inspiration

A

Diaphragm and intercostal muscles contract –> thoracic cage expands –> intrapleural pressure becomes more negative (sub-atmospheric) –> transpulmonary pressure increases(dif. in pressure) –> lungs expand –> alveolar pressure becomes sub-atmospheric –> air flows into alveoli.

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20
Q

Summary of Events during expiration

A

Diaphragm and external intercostal muscles stop contracting –> chest wall moves inwards –> intrapleural pressure goes back towards preinspiratory value –> transpulmonary pressure goes back towards preinspiratory value –> lung recoil towards preinspiratory volume –> air in lungs is compressed –> alveolar pressure becomes greater than atmospheric pressure –> air flows out of the lungs

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21
Q

Spirometry

A
  • spirometer is used to measure tidal volume, vital capacity, inspiratory capacity, expiratory reserve volume, and inspiratory reserve volume
  • cannot be used to measure functional residual capacity, total lung capacity or residual volume
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22
Q

Tidal Volume (TV)

A

Amount of air inhaled or exhaled in one breath during relaxed quiet breathing
- Typical value: 500 mL

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23
Q

Inspiratory Reserve Volume (IRV)

A

Amount of air in excess of tidal inspiration that can be inhaled with maximum effort
-typical value: 3000 mL

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24
Q

Expiratory Volume (ERV)

A

Amount of air in excess of tidal expiration that can be exhaled with maximum effort
-typical value: 1,200 mL

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25
Q

Residual Volume (RV)

A

Amount of air remaining in the lungs after maximum expiration; keeps alveoli inflated between breaths and mixes with fresh air on next inspiration
-typical value: 1200 mL

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26
Q

Vital Capacity (VC)

A

Amount of air that can be exhaled with maximum effort after maximum inspiration (ERV + TV + IRV); used to assess strength of thoracic muscles as well as pulmonary function
-typical value: 4,700 mL

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27
Q

Inspiratory Capacity (IC)

A

Maximum amount of air that can be inhlaed after a normal tidal expiration (TV + IRV)
-typical value: 3,500 mL

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28
Q

Functional Residual Capacity (FRC)

A

Amount of air remaining in the lungs after a normal tidal expiration (RV +ERV)
-typical value: 2,400 mL

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29
Q

Total Lung Capacity (TLC)

A

Maximum amount of air the lungs can contain (RV + VC)

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30
Q

Functional Residual Capacity (FRC) measurement

A
  • can be measured by helium dilution. Let C1 be the helium concentration in the spirometer of volume 1 and let the subject breath of to FRC. Then, open the valve and ask the subject to breath in and out from the spirometer. After equilibrium with the subjects lungs, the conc. in the spirometer is C2. Since the total amount of helium is conserved, we have

C1 x V1 = C2 x (V1 + FRC)
–>
FRC = (C1 x V1 / C2) - V1

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31
Q

Minute Ventilation (VE)

A

-The amount of air inspired (or expired) during one minute

VE = Vt x F

Vt is the tidal volume
F is # of breaths per minute

32
Q

Alveolar Ventilation (pretty much just factoring in anatomical dead space)

A

-In a normal adult male, Vt = 500 mL, and f = 12 breath/min. Therefor, VE= 6000 ml/min. However, not all the air inhaled into the lungs reaches the gas exchanging area (respiratory zone). Some of the air remains in the conducting airways. The volume of the anatomical dead space in the adult subject is about 150 mL. This the amount of air that reaches the respiratory zone per minute and available gas exchange, the alveolar ventilation (Va) is: Va = (500-150 mL) x 12 = 4200 mL/min.

33
Q

Physiological dead space (VD)

A

-under some pathological conditions, a certain amount of inspired air, although reach the respiratory zone does not take part in gas exchange. In this case, alveoli either receive a decreased blood supply or no blood supply at all. These alveoli represent alveolar daed space. The sum of alveolar and antatomical dead space is called the physiological dead space (VD). Therefor the difference between minute and alveolar ventilation is the dead space ventilation that is wasted from the exchange point of view.

VD = VE - VA

34
Q

Types of Alveolar Ventilation

A
  • Normal Alveolar Ventilation
  • Alveolar Hyperventilation
  • Alveolar hypoventilation
35
Q

Normal Alveolar ventilation

A

VA matches CO2 and keeps PaCO2 at a constant level

36
Q

Alveolar Hyperventilation

A

-occurs when more O2 is supplied and more CO2 is removed than the metabolic rates requires (VE exceeds the needs of the body). As a consequence, alveolar partial pressures of O2 (PaO2) rises and that of CO2 (PaCO2) decreases. Note that ventilation has to be considered with respect to the metabolism so ventilation during exercise is not hyperventilation

37
Q

Alveolar Hypoventilation

A
  • a fall in the overall level of ventilation can reduce alveolar ventilation below that required by the metabolic activity of the body. Under the condition of alveolar hypoventilation, the rate at which O2 is added to alveolar gas, and the rate at which CO2 is eliminated, is lowered, so that the alveolar partial pressure of O2 (PaO2) falls and PaCO2 rises. As a results of this, the blood in the pulmonary capillary is less oxygenated and PaO2 falls below normal values. Alveolar hypoventilation may occur during severe disorders of the lungs (e.g. chronic obstructive lung disease) or when there is damage to the respiratory muscles. It can also occur when the chest cage is injured and the lungs collapse, or when the central nervous system is depressed.
38
Q

Fick’s Law

A
  • the rate of diffusion of a gas through a tissue is proportional to the tissue area and the difference in gas partial pressures b/w the 2 sides, and is inversely proportional to the tissue thickness.

Diffusion rate is proportional to:

  • surface area (50-100 m^2)
  • partial pressure gradient
  • 1/thickness (-0.2 mm)
39
Q

Diffusion of CO2 compared to O2

A

CO2 is considerably more soluble than O2, it diffuses approx. 20x more rapidly.

However the difference in PCO2 between the 2 sides of the alveolar capillary membrane is 10 times smaller than that of PO2.

40
Q

Transit Time of O2/CO2

A

-Transit time is so fast that before the blood has passed even half way , the PO2 of the blood and air have reach equilibrium

41
Q

How the pulmonary circulation differs from Systemic Circulation

A
  1. The right ventricle develops a pressure of ~25 mmHg during its systole (compared to 120 mmHg in the left ventricle)
  2. Blood pressure in the pulmonary circulation is lower than in the systemic circulation
  3. The pulmonary capillaries are thinner and contain less smooth muscle than comparable vessels in the systemic circulation
  4. Pulmonary resistance is 1/10 that of the systemic circulation
    - Low vascular resistance in the pulmonary circulation relies on the thing walls of the vascular system.
42
Q

Accommodation of Pulmonary Blood Vessels

A
  • use recruitment (previously closed vessel open as CO rises) and distension
  • increase in heart rate, but dilation of vessels increase surface area available for diffusion
43
Q

Drug (serotonin, histamine, norepinephrine)

A

cause the contraction of smooth muscle, increase pulmonary vascular resistance in the larger pulmonary arteries

44
Q

Drugs (acteylcholin, isproteranol)

A

relax smooth muscle may decrease pulmonary vascular resistance

45
Q

Reflex vasoconstriction

A

There is a reflex vasoconstriction in regions of the lungs that are poorly oxygenated. The vessel will contract so that blood is not wasted on these lower oxygenated regions.

46
Q

Nitric Oxide

A

produced by endothelial cells, relaxes vascular smooth muscle leading t vasodilation

47
Q

Effects of Gravity on Pulmonary Flow

Top: pulmonary arterial pressure

A

capillaries are compressed. Occurs only in cases of low arterial pressure or positive ventilation

48
Q

Effects of Gravity on Pulmonary Flow

Middle: Pulmoary arterial pressure > alveolar pressure >venous pressure

A

flow depends only on the difference between arterial and alveolar pressures

49
Q

Effects of Gravity on Pulmonary Flow

Bottom: Pulmonary arterial pressure > venous pressure > alveolar pressure

A

flow depends on the arterio-venous pressure difference.

50
Q

Measuring Pulmonary Blood Flow (Q) Using Ficks principle

A

-O2 consumption per minute (VO2) is = O2 taken up by the blood in the lungs in one minute.
-The (O2) in the blood entering the lungs is CvO2 and that leaving is CaO2. It then follows that :
VO2 = Q(CaO2 -CvO2)
or Q= VO2/(CaO2 - CvO2)

VO2 measured by comparing O2 in the expired gas collection in a large spirometer and O2 in inspired gas

CaO2: measured from artery
CvO2: measured via a catheter from the pulmonary artery.

51
Q

O2 Physically Dissolved in Plasma

A

The amount of dissolved gas carried by the blood is directly proportional to the partial pressure of the gas, according to Henry’s Law

  • Because O2 is relatively insoluble in H2O, the amount o O2 dissolved is very small, and linearly proportional to PO2.
  • Not enough O2 in plasma to meet metabolic needs
52
Q

Affinity of Hemoglobin

A
  • the quaternary structure of Hb determines its affinity for O2
  • the combination of the first heme in Hb with O2 increase the affinity of the second heme for O2, etc. (cooperative binding)
  • Myoglobin, found in skeletal muscle, resembles Hb but binds only one O2 molecule. The O2-myoglobin curve is hyperbolic in shape. It follows that myoglobin will release its O2 only at very low PO2
53
Q

The Bohr Effect

A
  • the shift of HbO2 dissociation curve to the right when blood CO2 or temperature increases, or blood pH decrease. Affinity decreases, so it is easier for oxygen to bind.
  • decrease in temp, increase in pH, decrease in CO2 shift it to the left
54
Q

Carbon Monoxide Poisoning

A
  • CO has an extremely high affinity for the O2 binding site in hemeglobin.
  • reduces the amount of O2 bound to hemoglobin
55
Q

Transport of CO2

A

CO2 Carried in three forms in Blood
1. Physically dissolved in blood (10%): According to Henry’s Law, CO2 from the tissues diffuse into the plasma where it is physically dissolved

  1. Combined with HB to form HbCO2 (11%): contrary to O2, that combines with the heme portion of Hb, CO2 combines with the globin portion; hence there is no competition for binding.
  2. As bicarbonate (79%): CO2 combines with H20 to produce carbonic acid (H2CO3). This reaction is very slow in plasma, but as CO2 diffuses into the erythrocytes, the reaction is aided by enzyme carbonic anyhydrase (CA).
56
Q

Haldane Effect

A

-the fact that mixed venous bllod can carry more CO2 than arterial blood can.

57
Q

Respiratory Failure

A

Occurs when the respiratory system is unable to do its job properly, due to failure of:

  1. The gas exchanging capabilities of the lungs
  2. The neural control of ventilation
  3. The neuromuscular breathing apparatus
58
Q

Arterial Hypoxia

A

Blood hypoxia refers to deficient blood oxygenation, ie. low PaO2 and low %Hb saturation. In hypoxic conditions, if PaO2 decreases below 60mmHg, O2 content in arterial and venous blood becomes lower than the normal values at sea level.

59
Q

5 general causes of Hypoxia

A
  1. Inhalation of low PO2 (at high altitude)
  2. Hypoventilation: PaO2 decreases and PaCO2 increases. It means that alveolar ventilation in relation to the metabolic CO2 production is reduced. Hypeventilation occurs due to: diseases affecting the central nervous system, neuromusclar diseases, barbiturates, other drugs and narcotics.
  3. Ventilation/perfusion imbalance in the lungs: occurs when the amount of fresh gas reaching an alveolar region per breath is too little for blood flow through the capillaries of that region
  4. Shunts of blood across the lungs: venous blood bypasses the gas exchanging region of the lungs and returns to systemic circulation, deoxygenated.
  5. O2 diffusion impairment (e.g. thickening of the alveolar-capillary membrane, or pulmonary edema)
60
Q

Voluntary and Automatic Breathing

A

Voluntary breathing - controlled by the cerebral hemispheres

Involuntary Breathing: controlled by brainstem

61
Q

If you stop ventilation voluntarily

A
  • breathing will eventually start again
  • This occurs because the arterial PCO2 has reached about 50 mmHg and arterial PO2 has reached about 70 mmHg, at which point voluntary control is over-ridden. This is called the breaking point. The over-riding of the voluntary control by the automatic control depends upon the information from the receptors sensitive to CO2 and O2 levels.
62
Q

Neuronal structures involved in involuntary control of breathing

A
  • located in the brain stem (pons and medulla)
63
Q

3 basic elements in the respiratory control system

A
  1. Sensors: these gather information about lung volume (pulmonary receptors) and O2 and CO2 content (chemoreceptors)
  2. Controllers: information from the sensors is sent to the controller, in the pons and medulla via afferent neural fibers. Once it has reached the pons and medulla, the peripheral information and inputs from higher structures of the central nervous system are integrated
  3. effectors: as a result of the integration, neuronal impulses are generated and sent via spinal motoneurons to the effectors, ie. the respiratory muscles. This results in ventilation being adjusted to the persons metabolic needs. Since the main function of the lungs is to exchange O2 and CO2 between alveolar gas and blood, whenever the demand for O2 and the production of CO2 increase (as during exercise), ventilation must increase too, to satisfy this requirement.
64
Q

Path for neuronal response w/ ventilation

A

chemoreceptors, lung and other receptors pick up change –> input to central controller (pons,medulla,other parts of brain –> output via efferent to effectors (respiratory muscles)

65
Q

Pattern of Breathing: Medulla

A
  • There are pacemaker cells in the medulla. They are mainly located into 2 groups of cells: ventral respiratory group (contains the pre-Botzinger complex) that generate the basic rhythm, and dorsal respiratory group that receives several sensory inputs. All these cells connect to inspiratory motor neurons. The ventral and dorsal groups also connect to each other
  • Respiratory neurons in the medulla generate the basic rhymicity
66
Q

Pattern of Breathing: Pons(Upper)

A
  • cells located in the rostral(upper) pons (called the pneumotaxic center) modify the inspiratory activity of the centers in the medulla. These cells “turn-off” inspiration leading to smaller tidal volume. This also leads to an increase in breathing frequency to maintain adequate alveolar ventilation
  • cutting the pneumotaxic centers causes breathing to become deep and slow (this is the same affect as cutting the vagus nerves which bring afferent information).
67
Q

Pattern of Breathing: pons (lower)

A
  • cells located in the lower pons (called the apneustic center) send excitatory impulses to the respiratory groups of the medulla, thus promoting inspiration.
68
Q

Apneuses

A
  • tonic inspiratory activity interrupted by short expirations
  • caused by removal of both the upper pons and the vagus nerves.
  • this type of breathing is seen in some severe types of brain injury
69
Q

The activity of respiratory neurons will increase if

A

PaO2 40 mmHg

70
Q

The activity of respiratory neurons will decrease

A

PaO2 > 100 mmHg or

PaCO2

71
Q

Central Chemoreceptors

A
  • located on the ventral surface of the medulla.
  • Detect the pH of the cerebrospinal fluid (CSF) surrounding them (PCO2 and pH of the CSF are influenced by those of arterial blood)
  • give rise to the main drive to breath under normal conditions
  • the sensitivity of these receptors may be easily assessed by a CO2 rebreathing test.
72
Q

Peripheral chemoreceptors

A
  • mainly sensitive to changes in PO2 but are also stimulated by increased PCO2 and decreased pH
  • located in the carotid bodies and the aortic bodies.
  • They connect with afferent fibers, which project to the dorsal group of respiratory neurons in the medulla.
73
Q

Pulmonary Vagal Receptors: 3 types of receptors in the lungs that respond to mechanical stimuli

A
  1. Pulmonary Stretch receptors
  2. irritant receptors
  3. Juxta-capillary or J receptors (C-fibres)

*Afferent fibers from all of these receptors travel in the vagus nerves. If the vagus nerve is sectioned the result is slow deep breathing.

74
Q

Pulmonary Stretch receptors

A
  • located in smooth muscles of the trachea down to the terminal bronchioles,
  • are innervated by large, myelinated fibers, and they discharge in response to distension of the lung.

-The main reflex effect of stimulating these receptor is the Hering-Breuer Inflation Reflex

75
Q

Hering-Breuer Relfex

A
  • decrease in respiratory frequency due to a prolongation of expiratory time. Other words, an increase in lung volume tends to inhibit the beginning of the next inspiratory effort (negative feedback mech.).
  • is weak in adults unless tidal volume exceeds 1Liter as in exercise, but is not noticeable in infants and animals
76
Q

Irritant Receptor

A
  • located between airway epithelial cells in the trachea down to the respiratory bronchioles
  • stimulated by noxious gases, cig smoke, cold air, and dust
  • innervated by myelinated fibers and their stimulation lead to bronchoconstriction and hypernea (increased depth of breathing).
  • may be important in the reflex bronchoconstriction triggered by histamine release during an allergic asthmatic attack.
77
Q

Juxta-Capillary receptors

A
  • located in the alveolar walls close to the capillaries
  • innervated by non-myelinated fibres and have short lasting bursts of activity
  • stimulated by an increase in pulmonary interstitial fluid, like what may occur in pulmonary congestion and edema.
  • the reflex effects caused by these receptors include rapid and shallow respiration, although intense stimulation causes apnea.
  • may play a role in dyspnea (sensation of difficulty in breathing) associated with left heart failure and lung edema or congestion

Physiology 210 (5 decks)

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