Physiology 🫁 Flashcards

1
Q

What is the definition of respiration?

A
  • It is the transport of O2 from atmosphere to the tissue.
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2
Q

What happens in the tissues? “Concerning respiration”

A
  • In the tissues, oxidation of food stuffs occurs with liberation of energy & CO2.
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3
Q

What are the phases of respiration?

A

Respiration can be divided into:

I. External respiration which consists of:
1-Pulmonary ventilation or renewal of the air in the lungs from atmospheric air

2- Exchange of gases between the alveolar air and venous blood in the capillaries around the alveoli.

II. Respiratory function of the blood:
It is the carriage of O2 and CO2 by the blood.

III. Internal respiration:
- It is the utilization of the atmospheric oxygen in oxidation of food stuffs with production of the energy required for body activities.

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4
Q

What is a Physiological anatomy of the respiratory system?

A

The respiratory system consists of:

  1. The air passages and lungs. “Conducting zone and respiratory zone”
  2. Respiratory muscles which change the volume of the thoracic cavity and their nerve supply.
  3. Nerve center controlling respiration.

❖The air passages are divided into two functional zones, the conducting zone and the respiratory zone.

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5
Q

What is the conducting zone of the respiratory system?

A

This part includes the nose, nasopharynx, larynx, trachea and the two main bronchi (one for each lung), the smaller bronchioles till the respiratory bronchioles.

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6
Q

What are the characteristics of the wall of the conducting zone of the respiratory system?

A

The walls the conducting part are thick and do not allow gas exchange.

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7
Q

What are the functions of the conducting zone?

A

CC HF RN

  1. Conducting air into the respiratory zone
  2. Air conditioning
  3. Humidification
  4. Filtration
  5. Protective reflexes
  6. Non-respiratory function
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8
Q

What is the conditioning function of the conducting zone?

A

Inspired air reach the respiratory zone at a temperature of 37 °C to maintain a constant internal body temperature. The mucosa of the nose, mouth and pharynx has a large surface area and a rich blood supply. This adds heat to cold air or removes heat from hot air.

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9
Q

What is the humidification function of the conducting zone? “So as to avoid injury of the respiratory zone”

A
  • Air is saturated with water vapour to protect delicate lung tissue from dryness.
  • This humidification occurs by the trans-capillary fluid filtration in the mucous membrane.
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10
Q

What is the filtration function of the conducting zone?

A
  • The air conducting part filters air from particles and bacteria.
  • Large particles, larger than 4-6 microns are trapped by hairs at the entrance of the nose.
  • Small particles are trapped by mucous secreted from the goblet cells in the epithelial lining of the passage.
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11
Q

What are the protective reflexes of the conducting zone?

A
  • These reflexes remove foreign bodies & irritant substances from the respiratory passage. They include sneezing reflex and cough reflex.
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12
Q

What are the non-respiratory functions of the conducting zone?

A
  • Smell: by olfactory epithelium of the nose.
  • Phonation: the larynx is adapted to act as a vibrator; the vibrating element is the vocal cord. When air passes, it vibrates the vocal cord and produces sound.
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13
Q

What is a Respiratory zone and what are the characteristics of its walls?

A
  • It consists of respiratory bronchioles “Belong to respiratory zone note conducting zone” , alveolar ducts, air sacs and alveoli.
  • The membrane separating blood in pulmonary capillaries and air in alveoli is very thin. So, gas exchange occurs free and rapid.
  • The alveoli are packed together by elastic connective tissue which makes them one unit.
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14
Q

What is pulmonary ventilation and in what way does it occur?

A
  • It is renewal of air in the lung alveoli from the atmospheric air by movement of air in (inspiration) followed by its movement out (expiration).
  • This occurs in cycles called “respiratory cycles”.
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15
Q

what does each respiratory cycle consist of?

A

Inspiration, expiration and expiratory pause

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16
Q

What is the definition of inspiration and what is its duration?

A
  • It is an active process during which the thoracic cavity increases, lungs distend and air rushes in the lungs
  • Its duration is l.3 sec. in normal quiet breathing.
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17
Q

What is the definition of expiration and what is its duration?

A
  • It is a passive process during which the thoracic cavity decreases, lungs recoil and air rushes out of the lungs.
  • It is slightly longer than inspiration. Its duration is about 1.7 seconds in normal quiet breathing.
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18
Q

what is the definition of the expiratory pause and what is its duration?

A
  • A period of rest present after expiration in normal quiet breathing.
  • Its duration is about 0.7 second.
  • It is absent in rapid respiration as in muscular exercise.
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19
Q

What is the total duration of respiratory cycle?

A

1.3 + 1.7 + 0.7 = 3.7 sec.

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20
Q

What is the respiratory rate in adults and children?

A
  • about 16/minute.

- In children respiratory rate is about 25/minute

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21
Q

What is the definition of normal inspiration?

A
  • It is an active process that occurs as a result of contraction of the diaphragm and external intercostal muscles.
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22
Q

What is a muscle that is responsible for 75% of respiration?

A

The diaphragm

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23
Q

What does the contraction of the diaphragm lead to and what supplies the diaphragm?

A

▪ Contraction of diaphragm leads to its descend from 1.5 cm.

▪ It is supplied by phrenic nerve (AHCs of cervical 3,4,5).

“C3,4,5 keep the diaphragm alive”

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24
Q

What does the contraction of external intercostal muscles lead to and what are they supplied by?

A
  • Their contraction pushes the sternum outward causing increase the antero-posteriror diameter of the chest and elevates and everts the ribs causing increasing the transverse diameter. They are supplied by intercostals nerves (AHCs of thoracic 1-10).
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25
Q

What is the mechanism of normal inspiration?

A
  • Contraction of the diaphragm and external intercostal muscles increases all diameters of the chest and the lungs follow the chest passively “pressure is distributed”. This causes increased volume of the lungs & decreased the intrapulmonary pressure by about -2mm Hg (below the atmospheric pressure) resulting in rush of 500 ml air into the lungs (Tidal volume).
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26
Q

What is the definition of normal expiration?

A
  • It is a passive process that occurs as a result of relaxation of the diaphragm and external intercostal muscles.
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27
Q

What is the mechanism of normal expiration?

A

This relaxation decreases all diameters of the chest and lung recoils by its elasticity. This increases the intrapulmonary pressure to about + 2 mmHg (above the atmospheric pressure) resulting in rush out of 500 ml air (tidal volume).

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28
Q

What is forced inspiration?

A

It is an active process that occurs as a result of:

a) Forceful contraction of the diaphragm and external intercostal muscles.
b) Contraction of other thoracic muscles which are called (accessory muscles of respiration). They include: Sternocleiomastoid, serratus anterior, scaleni muscles, pectoralis minor and latismus dorssi muscles.

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29
Q

What is the mechanism of forced inspiration?

A
  • Contraction of all these muscles causes marked increase of the dimensions of the chest & marked decrease in the intrapulmonary pressure to -20 mmHg causing rush of large volumes of air in.
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30
Q

What is forced Expiration?

A

It is an active process that occurs as a result of:

a) Relaxation of the diaphragm and external intercostal muscles.
b) Contraction of muscles of forced expiration (abdominal muscles and internal intercostal muscles)

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31
Q

What is the mechanism of forced expiration?

A
  • This causes marked reduction of the dimensions of the chest & marked increase in the intrapulmonary pressure to + 30 mmHg causing rush of large volumes of air out.
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32
Q

What are the factors that affect pulmonary ventilation?

A

1) Resistance of the respiratory passage.
2) Pressure relationship in the thoracic cavity.
3) Surfactant.
4) Pulmonary compliance.

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33
Q

What describes the resistance of the respiratory passages?

A

Poiseuille’s law

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34
Q

What is poiseuille’s law?

A

where: R = 8 η l / πr 4

R = resistance
η = viscosity of the inspired gas 
l = length of the airway
r = radius of the airway
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35
Q

What are the factors that change airway resistance?

A

A. Contraction or relaxation of bronchial smooth muscle “Altering radius”

B. Lung volume “Altering radius”

C. Viscosity or density of inspired gas “Altering viscosity”

D- Bronchial Mucosa

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36
Q

How does contraction or relaxation of bronchial smooth muscles affect airway resistance?

A

■ Changes airway resistance by altering the radius of the airways.

(1) Parasympathetic stimulation, irritants, and the slow-reacting substance of anaphylaxis (asthma) constrict the airways, decrease the radius, and increase the resistance to airflow.
(2) Sympathetic stimulation and sympathetic agonists (isoproterenol) dilate the airways via β2 receptors, increase the radius, and decrease the resistance to airflow.

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37
Q

What is diurnal variation of the autonomic nervous system regarding airway resistance?

A
  • The autonomic nervous activity shows “diurnal variation” in which the sympathetic activity reaches its maximum in the afternoon period whereas the parasympathetic activity is maximum in the late evening & early morning.
  • This is why attacks of bronchial asthma are most common at late times of the day.
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38
Q

How does the lung volume affect the airway resistance?

A

■ alters airway resistance because of the radial traction exerted on the airways by surrounding lung tissue.

(1) High lung volumes are associated with greater traction and decreased airway resistance. Patients with increased airway resistance (e.g., asthma) “learn” to breathe at higher lung volumes to offset the high airway resistance associated with their disease.
(2) Low lung volumes are associated with less traction and increased airway resistance, even to the point of airway collapse.

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39
Q

How does viscosity or density of inspired gas affect airway resistance?

A

■ changes the resistance to airflow.

■ During a deep-sea dive, both air density and resistance to airflow are increased.

■ Breathing a low-density gas, such as helium, reduces the resistance to airflow.

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40
Q

How does bronchial mucosa affect airway resistance?

A
  • The presence of secretion (mucus) or an increase in the thickness of the mucosa (mucosal edema) increases the airway resistance as in bronchial asthma.
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41
Q

what are the pressures in the thoracic cavity?

A

A. Intra pulmonary pressure.
B. Intra pleural pressure.
C. Intrathorathic pressure.

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42
Q

What is the definition of intrapulmonary alveolar pressure? And what is it connected with?

A
  • It is the pressure inside the lung alveoli, with the atmosphere
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43
Q

What are the values of the intra- pulmonary alveolar pressure?

A
  • Before the start of inspiration, it equals zero (i.e., equal to atmospheric pressure).
  • During normal inspiration, It is equals -2 mmHg (i.e., 2 mmHg below the atmospheric pressure). This is due to contraction of the diaphragm and external intercostal muscles that increases all dimensions of the chest.
  • At the end of inspiration, pressure becomes atmospheric (zero) again. This is due to rush of about 500 ml air (tidal air) air that fills the lungs at the end of inspiration.
  • During normal expiration: the intrapulmonary pressure increases to about +2 mmHg (i.e., 2 mmHg above the atmospheric pressure). This is due to relaxation of the diaphragm and external intercostal muscles that decreases all dimensions of the chest cavity. This forces 500 ml of air out of the lungs helped by its elasticity. Thus, pressure returns zero again at the end of expiration.

N.B.: in forced respiration, the alveolar pressure follows the same course of change BUT at different values during forced inspiration (where it reaches -20 mmHg) and during forced expiration (where it reaches +20 mmHg).

“‏كلام فاضي كله”

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44
Q

What is the anatomy of pleura?

A
  • Each lung is enclosed in a double-walled sac called “pleura”. Both layers of the pleura are formed of serous membrane.
  • The part of the pleura that lines the thoracic cavity is called “parietal pleura”. It is reflected at the hilum of the lung to cover firmly the outer surface of the lung as “visceral pleura”.
  • Between the two layers of pleura, there is an extremely narrow “pleural cavity” or “pleural sac”.
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45
Q

What is the pleural cavity filled with and what is its function?

A
  • This cavity (sac) is filled with “pleural fluid”, which is serous fluid secreted by pleura. This fluid acts as lubricant to reduce friction between the two layers during respiratory movements. So, it causes lung to slide on the chest wall & resists their separation. Thus, lungs follow passively movement of chest wall.
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46
Q

What is intrapleural pressure?

A

It is the pressure in the pleural cavity (sac).

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47
Q

What are the values of intrapleural pressure?

A

Normal values of I.P.P. (usually a negative pressure):

▪ - 3 mmHg at the end of normal expiration.

▪ - 6 mmHg at the end of normal inspiration.

▪ -30 mmHg in forced inspiration with closed glottis (Muller’s experiment).

▪ +40 mmHg in forced expiration with closed glottis (Valsalva’s maneuver).

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48
Q

What are the causes of negativity of intrapleural pressure? “Lack of air tendency”

A
  1. Lack of air in the pleural cavity.
  2. Continuous tendency of the lung to recoil AGAINST tendency of chest wall to expand. Both lungs and chest wall have a “relaxation volume” at which they are neither stretched nor compressed. This relaxation volume is 0.6 L for the lungs and 3.5 L for the chest wall. However, at the end of normal expiration (when respiratory muscles are relaxed), the volume of both lung and chest wall equals 2.2 L (functional residual capacity). Thus, lungs continuously tend to recoil (from 2.2 to 0.6) and chest wall tends continuously to expand (from 2.2 to 3.5).

“Easy”

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49
Q

What happens of air is introduced into the intrapleural cavity?

A
  • If air is introduced into the pleural sac (in pneumothorax), the negativity of I.P.P. is lost, the lung collapses and the chest is expanded.
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50
Q

What is responsible for the elastic properties of the lungs?

A
  • The elastic tissue in the bronchial wall and the interstitial tissues of the lungs.
  • The arrangement of the muscle fibers of the bronchi and bronchioles in a network. So that, on contraction, the bronchial tree not only becomes constricted but also shortened in length (recoils).
  • The surface tension of the fluid lining the alveolar walls.
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51
Q

What is the significance of the negativity of intrapleural pressure?

A

Negative pressure is a suction force so:

  1. It helps expansion of the lung during inspiration and prevents its collapse during expiration.
  2. Responsible for the negativity of intrathorathic pressure which helps:
    a. Expansion of the lung.
    b. Venous return to the heart: This is called “respiratory pump”. During normal and more during forced inspiration; the intrathorathic pressure becomes negative lead to suction of more blood from the extrathorathic vein increasing venous return and cardiac output.
    c. The negative intrathorathic pressure helps lymphatic flow in the thoracic duct through the thoracic cavity.
    d. Helps pulmonary blood flow.
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52
Q

what does a surfactant line and what is its function in brief?

A

■ lines the alveoli and reduces surface tension by disrupting the intermolecular forces between liquid molecules. This reduction in surface tension prevents small alveoli from collapsing and increases compliance.

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53
Q

What synthesizes the surfactant and what is it primarily consisting of?

A

■ is synthesized by type II alveolar cells and consists primarily of the phospholipid dipalmitoyl phosphatidylcholine (DPPC).

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54
Q

When is surfactant synthesized in the fetus?

A

■ In the fetus, surfactant synthesis is variable. Surfactant may be present as early as gestational week 24 and is almost always present by gestational week 35.

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55
Q

What reflects mature levels of surfactant?

A

■ Generally, a lecithin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects mature levels of surfactant.

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56
Q

What causes neonatal respiratory distress syndrome and what does the infant experience during it?

A

■ Neonatal respiratory distress syndrome can occur in premature infants because of the lack of surfactant. The infant exhibits atelectasis (lungs collapse), difficulty reinflatingthe lungs (as a result of decreased compliance), and hypoxemia (as a result of decreased V/Q).

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57
Q

What are the functions of surfactant? “Immunity and decreasing surface tension”

A
  1. It decreases the surface tension of the fluid lining the alveoli through:
    a) It scatters among the fluid molecule decreasing the attraction between them.
    b) It also spreads over the fluid preventing air-fluid interface.

This decreased surface tension:

▪ Helps lung expansion during inspiration esp.
▪ Protects against pulmonary edema as it decreases the filtration forces for the fluid from pulmonary
capillaries into alveoli.

▪ Prevents lung collapse during expiration.
▪ Decreases the work of breathing needed.

  1. Surfactant activates alveolar macrophages.
  2. It has a bacteriolytic effect, making the bacteria susceptible to alveolar macrophages.
  3. The phospholipids of surfactant may act directly on T-lymphocytes cell membrane to prevent excess immune response.
  4. It assists ciliary movement in upper respiratory tract (so, helps to remove any particles and mucus away from air passage).
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58
Q

What is the types of respiratory distress syndrome?

A

Infant RDS (hyaline membrane disease)

Adult respiratory distress syndrome (ARDS)

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59
Q

What is the definition of infant RDS?

A

is a deficiency of surfactant in infants

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60
Q

Why does infant RDS happen?

A
  • In fetal life, surfactant is not produced in sufficient amounts until about the eighth month. Thus, premature babies lacking sufficient surfactant are born with collapse alveoli.
  • Because of the high surface tension, plasma fluid leaks into the alveoli producing pulmonary edema.
  • Due to “glistening membrane” appearance, the condition is also called “hyaline membrane disease”.
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61
Q

What are the characteristics of RDS in infants?

A
  • RDS is a fatal condition. It is more sever and more common in infants with low plasma level of thyroid hormone. Thyroid hormone increases the size and number of lamellar bodies in type II alveolar cells.
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62
Q

How is RDS in infants treated?

“Ready O2 or surfactant or helping in the synthesis of the surfactant”

A
  • RDS babies can be saved by mechanical ventilators that keep them alive until their lung can manufacture sufficient surfactant. Otherwise, bovine or synthetic surfactant can be administrated.
  • When premature delivery (before 8 months) is life-saving for the mother, elective caesarean section may result in baby with collapsed lungs. It is better in this condition to inject the mother with cortisol hormone which is essential for surfactant formation.
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63
Q

What is adult RDS?

A

Acute lung injury.

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64
Q

What causes acute RDS?

A

A- Bloodstream (sepsis): develops from injury to the pulmonary capillary endothelium, leading to interstitial edema and increased lymph flow.

B- Airway (gastric aspirations): direct acute injury to the lung epithelium increases permeability of the epithelium followed by edema.

C- Cigarette smoking decreases surfactant. It leads to destruction of type II alveolar cells.

D- After cardiac surgery during which the pulmonary circulation is interrupted, alveolar epithelium fails to secrete surfactant.

E- Long-term inhalation of 100% O2.

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65
Q

what are the harmful effects of respiratory distress syndrome?

A

In respiratory distress syndrome, the lung becomes stiffer and compliance decreases. This greatly increases the work of breathing. Also, a more negative pressure is required to maintain a given lung volume.

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66
Q

What is the equation that describes compliance?

A

C = Δ V/P

C = compliance (mL/mm Hg) ,V = volume (mL), P = pressure (mm Hg)

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67
Q

What is compliance?

A
  • the extent to which the lung expands for each unit increase in its transmural pressure.
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68
Q

What is transmural pressure?

A
  • For the lungs, transmural pressure = intrapulmonary pressure – intrapleural pressure. It is called “transpulmonary pressure”.
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69
Q

What is the normal compliance of the lungs in the average adult human?

A
  • approximately 200 ml/cm of water pressure. That is every time, the transpulmonary pressure increase by one centimeter of water, the lungs expand 200 milliliters.
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70
Q

What are the types of pulmonary compliance?

A

Two types of pulmonary compliance can be measured:
1- Static pulmonary compliance.
2- Dynamic lung compliance.

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71
Q

How is static pulmonary compliance estimated?

A
  • Can be estimated from static (relaxation) pressure – volume curve of the whole respiratory system (pressure is recorded after the muscles of respiration are relaxed).
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72
Q

Describe the relaxation pressure - volume curve at FRC

A
  • The relaxation pressure of the lung and chest wall equals zero when the lung volume is equal to functional residual capacity (FRC) which is the volume of the lung and chest wall at the end of normal expiration. Thus, FRC is the relaxation volume of the total respiratory system. At this volume, lung tendency to recoil and chest tendency to expand balance.
  • At the FRC volume, the curve of the lung alone shows +ve pressure (as the lung tends to collapse to reach its relaxation volume which is about 0.6 L) whereas the curve of chest wall alone shows –ve pressure (as the chest wall tends to expand to reach its relaxation volume which is about 3.5 L).
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73
Q

Describe the relaxation pressure-volume curve at volumes higher than FRC.

A
  • At volumes higher than FRC, the relaxation pressure of total respiratory system is positive “instead of zero” mainly due to recoil tendency of the lung “strong” (as chest wall is approaching its relaxation volume). “Weaker”
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74
Q

Describe the relaxation pressure-volume curve at volumes lower than FRC.

A
  • At volumes lower than FRC, the relaxation pressure of total respiratory system is negative mainly due to expansion tendency of the chest wall (as lungs are approaching their relaxation volume).
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75
Q

How can dynamic lung compliance be estimated?

A
  • Can be estimated from pressure – volume curve of the lungs recorded during the respiratory cycle (pressure is recorded in steps during inspiration and expiration).
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76
Q

what can be concluded from the dynamic lung compliance curve?

A
  • The compliance of the lung is more during expiration (BZA) than during inspiration (AXB).
  • This is known as “hysteresis” (i.e., forward path is different from the reverse path).
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77
Q

What determines the lung compliance?

“Only lung compliance not the whole respiratory system”

A
  • The compliance of the lung is determined by the diagonal line (BYA) connecting the two ends of the curve (average lung compliance).
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78
Q

What are the factors affecting compliance?

A
  1. Factors in the lung:
    - It is affected by elastic forces of the lung (1/3 of compliance) and surface tension of the fluid lining the alveoli (2/3 of the compliance).
  • Lung compliance is decreased in pulmonary congestion, pulmonary fibrosis and pulmonary edema whereas it is increased in emphysema. (CFE - E)
  1. Factors in the chest wall:
    - It is affected by the elastic properties of the thorax caused by elasticity of the muscles, tendons and connective tissues in the chest wall.
  • Chest wall compliance is decreased in case of:
  • Deformities of spine
  • Arthritis of vertebra.
  • Skeletal muscle disease e.g. poliomyelitis
  • Obesity.
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79
Q

What are the changes in lung compliance?

A

Emphysema and fibrosis

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80
Q

How does emphysema change lung compliance?

A
  • often caused by smoking, results in destruction of the alveolar septa and capillaries. Therefore, lung compliance is increased and the tendency of the lungs to collapse is decreased. Therefore, at the original FRC, the tendency of the lungs to collapse is less than the tendency of the chest wall to expand. The lung–chest wall system will seek a new, higher FRC so that the two opposing forces can be balanced; the patient’s chest becomes barrel-shaped, reflecting this higher volume. “Easy”
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81
Q

How does fibrosis change lung compliance?

A
  • Fibrosis has increased collagen fiber deposition, which increases the tissue component of elastic recoil. Therefore, lung compliance is decreased and the tendency of the lungs to collapse is increased. Therefore, at the original FRC, the tendency of the lungs to collapse is greater than the tendency of the chest wall to expand. The lung–chest wall system will seek a new, lower FRC so that the two opposing forces can be balance. “Easy”
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82
Q

What is work of breathing and what is its value?

A
  • During normal quiet respiration, work is done only during inspiration whereas expiration is entirely a passive process. At rest, work of breathing is about 1-2% of the total body energy expenditure. Even during heavy exercise, work is only about 3-5% of the total energy expenditure of the body.
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83
Q

What is the work of breathing divided into?

A

1- Compliance work (elastic work) (65% of total work)
2- Tissue resistance work (7% of total work)
3- Airway resistance work (28% of total work)

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84
Q

What is compliance work? And how could it be calculated?

A
  • It is the work required to expand the lung against its elastic force.
  • This can be calculated as follow:
    Compliance work = volume x pressure needed to inflate this volume
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85
Q

What is tissue resistance work?

A
  • It is the work required to overcome the resistance of non-elastic tissue of the lungs and thoracic cage.
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86
Q

What is airway resistance work and what is the major factor affecting it?

A
  • It is the work required to overcome airway resistance during the movement of air into the lung.
  • The major factor, affecting airway resistance is the diameter of the passage ways. The larger the diameter of the airway, the less work done.
87
Q

What are the conditions associated with increased work of breathing?

A

1- Decreased elasticity (fibrosis) - Lung congestion (heart failure).

2- Increased tissue resistance work:

  • Diseases affecting thoracic cage e.g. kyphoscoliosis.
  • Muscle disease.

3- Increased airway resistance work:

  • Obstruction of air way.
  • Chronic bronchitis.
  • Asthma.
88
Q

What separates the air in the alveoli from the blood in the capillaries? And what is its composition?

A
  • A very thin respiratory membrane which consists of:

1) Layer of fluid lining the alveoli and containing surfactant that reduce the surface tension of the alveolar fluid.
2) Single layer of thin alveolar epithelial cells.
3) An epithelial basement membrane.
4) A very thin interstitial space between the alveolar epithelium and the capillary membrane.
5) Capillary basement membrane.
6) Capillary endothelial membrane.

89
Q

What are the properties of the respiratory membrane that helps in gas exchange?

A

Thickness of the respiratory membrane

Surface area “inc in exercise”

90
Q

What is the relation between the rate of diffusion and thickness of the membrane?

A
  • The rate of diffusion of gases through the membrane is inversely proportional to the thickness of the membrane.
91
Q

What is the thickness of the respiratory membrane?

A
  • the overall thickness of the membrane is 0.6 μm.
92
Q

What are the factors that increase of the thickness of respiratory membrane?

A
  • Any factor that increases the thickness to more than two to three times normal (such as pulmonary edema and pulmonary fibrosis can interfere with exchange of gases.
93
Q

What is the relation between the surface area and rate of gas diffusion?

A
  • The greater the surface area, the more will be the rate of gas diffusion.
94
Q

What is the total surface area of the respiratory membrane in normal adult?

A

60 m2

95
Q

What are the factors that decrease surface area of respiratory membrane?

A

❑ Removal of an entire lung will decrease surface area to 1⁄2 normal.

❑ Emphysema: a condition in which the walls of the alveoli become over distended causing many alveoli to coalesce together with dissolution of alveolar walls. Therefore, the total surface area by loss of the alveolar walls.

96
Q

What are the properties of respiratory gases that help in gas exchange?

A

A. Pressure gradient

B. Lipid solubility and molecular weight (MW) of gases

97
Q

What is the partial pressure of oxygen in alveolar air, arterial blood vessels and venous blood vessels respectively?

A

100 100 40

98
Q

What is the partial pressure of carbon dioxide in alveolar air, arterial blood vessels and venous blood vessels respectively?

A

40 40 46

99
Q

What is the direction of diffusion of gases according to pressure gradient?

A
  • According to the pressure gradient, O2 diffuses from the alveoli into the capillaries and CO2 diffuses from the capillary to the alveoli.
100
Q

What Is the relation between lipid solubility and the molecular weight to the rate of gas diffusion?

A
  • All respiratory gases are highly lipid soluble. The rate of gas diffusion is directly proportional to the solubility and inversely proportional to the MW of the gas.
101
Q

What is the solubility and molecular weight of carbon dioxide and oxygen?

A
  • The solubility of CO2 is 24 times greater than that of O2.

- The MW of CO2 is 44 and 32 for O2. So, CO2 diffuses about 20% slower than O2 due to its high MW.

102
Q

What is the diffusion coefficient?

A

It is a constant which measures the amount of dissolved gas diffusing through a membrane when concentration gradient is one unit.

103
Q

What is the diffusion rate of carbon dioxide in relation to oxygen and nitrogen?

A
  • The net result is that the diffusion rate of CO2 through the respiratory membrane is about 20 times that of O2. Oxygen diffuses twice as rapidly as nitrogen.
104
Q

What describes diffusion of gases?

A

Diffusion is described by Fick’s law of diffusion as follow: V gas = A × D ( P1-P2) / T

Where,

Vgas = rate of gas diffusion across a membrane.
A = Surface area of the membrane. 
D= Diffusion coefficient.
T= Thickness of the membrane.
P1-P2 = Pressure gradient along which gas diffusion occurs.
105
Q

What is a diffusion capacity?

A
  • It is the volume of a gas that diffuses through the membrane each minute for a pressure difference of 1 mmHg.
106
Q

What is the diffusion capacity for O2 and CO2 under resting conditions?

A
  • The diffusion capacity for O2 under resting condition is about 20ml./ min./ mmHg. The diffusion capacity for CO2 is 400 ml./min./mmHg (20 times that of O2).
107
Q

What is the diffusion capacity of oxygen and carbon dioxide during muscular exercise?

A
  • This capacity increases during muscular exercise to 80 ml./min./mmHg for O2 and 1200 ml./min./mmHg for CO2.
108
Q

What causes the increase in the diffusion capacity of gases during exercise?

A
  • This increase is due to increase surface area of blood for O2 to diffuse and better ventilation/perfusion ratio (all zone 3) (see below).
109
Q

What is perfusion limited situation?

A
  • situation in which the substance equilibrates between the capillary and interstitium.
110
Q

What is diffusion limited situation?

A
  • situation in which the substance does not equilibrate between the capillary and interstitium.
111
Q

What is unique about carbon monoxide and what is its clinical importance?

A
  • Carbon monoxide is a unique gas in that it typically doesn’t equilibrate between the alveolar air and the capillary blood. Thus, it is a diffusion-limited gas. This is taken advantage of clinically, and the measurement of the uptake of CO in mL/min/mm Hg is referred to as the diffusing capacity of the lung (DLCO). DLCO is an index of the lung’s structural features.
112
Q

What is the definition of ventilation perfusion ratio?

A
  • This is the ratio between alveolar ventilation “air that reaches the alveoli” and pulmonary blood flow per minute.
113
Q

What is the normal alveolar ventilation in adults and what is that normal total perfusion?

A
  • The normal alveolar ventilation in an adult is about 4 L / min. and the total perfusion (the blood flow through the lungs) is equal to the cardiac output of the right ventricle (about 5 L/min). So, V/P ratio is about 0.8.
114
Q

What changes the V/P ratio?

A
  • This ratio differs from one part of the lung to another. This is due to effect of gravity on both pulmonary ventilation and pulmonary blood flow. Thus, these differences appear in erect posture and disappear in recumbent position.
115
Q

How does gravity affect pulmonary ventilation in resting position of the shift (FRC)?

A
  • In relaxation (resting) position of the chest (i.e., FRC):

❑During standing, under the effect of gravity, the weight of lung in relaxation (resting) position keeps the upper parts of the lung more stretched than the lower parts. So, upper parts contain more air in resting position than the lower ones.

❑ Also, because of gravity, I.P.P. is more negative at the apex and less negative at the base. Since the negativity of I.P.P acts as expanding pressure, the upper lung zones have larger resting volumes than the lower ones.

116
Q

How does gravity affect pulmonary ventilation when ventilation starts?

A
  • When ventilation starts in standing position, most of tidal volume is shifted to the lower lung zones which are of low volumes (i.e., more compliant). The upper lung zones receive only small ratios of tidal air.
117
Q

How does gravity affect pulmonary perfusion?

A
  • Gravity also affects the pressure in the pulmonary blood vessels. The lung is 30 cm high causing a difference in pressure of about 30 cm H2O or 23 mm Hg. The blood pressure is less at the top and more at the base.
  • Thus, normally in standing position the blood flow at the upper lung zones is considerably less than that of the lower lung zones.
118
Q

What can be concluded from the effect of gravity on both pulmonary ventilation perfusion?

A
  • both ventilation and perfusion is less in the upper lung zones than in the lower. But, since the blood has a higher density than the lung tissues, changes in perfusion is much greater than changes in ventilation per unit distance down the lungs.
119
Q

What are the zones of the lung according to the relationship between alveolar pressure, pulmonary artery pressure, pulmonary venous pressure?

A

Zone I
Zone II
Zone III

120
Q

What is the position of the zone I and what are its characteristics?

A
  • Present at the apex of the lung.
  • It is hypoperfused (blood flow is little). This is due to high alveolar pressure which compresses the pulmonary vessels. PA > Pa > Pv.
  • V/P ratio = 3.3.
121
Q

What are the characteristics of a zone II?

A
  • The blood flow starts to increase as: Pa > PA > Pv

- The pulmonary vessels are now partly open. The blood flow increases gradually from the top to the bottom of this zone.

122
Q

What is the position of the zone III and what are its characteristics?

A
  • Present at the bottom of the lung.
  • It is hyperperfused. i.e., Pa > Pv > PA. So, the blood vessels are continuously opened.
  • V/P ratio = 0.6.
123
Q

in which zone does poor gas exchange occur?

A
  • Poor gas exchange occur when the alveolar air flow is either inadequate or excessive in relation to the blood flow i.e., in zone I and zone III.
124
Q

How does the long compensate for for gas exchange in zone I and zone III?

A
  • To compensate for this poor gas exchange, the following local autoregulatory mechanisms contribute to match alveolar air flow and blood flow
125
Q

What are the local autoregulatory mechanisms done to match alveolar air flow and blood flow?

A

I. Pulmonary vessels

II. Respiratory air way

126
Q

What are the local autoregulatory mechanisms done by pulmonary vessels to match alveolar air flow on Blood flow?

A

❑ Low PO2 causes V.C of pulmonary blood vessels and decrease in pulmonary blood flow.

❑ While, high PO2 causes V.D. of pulmonary blood vessels and increase in pulmonary blood flow.

❑ This helps to redistribute blood flow from areas poor in O2 to areas rich in O2 producing normal V/P ratio

127
Q

What are the local autoregulatory mechanisms done by the respiratory airway to match alveolar air flow on Blood flow?

A

❑ High CO2 level dilates the airways and increases airflow in the alveoli.

❑ While low CO2 level constricts the airways and decrease airflow in the alveoli.

❑ This helps to match alveolar air with the pulmonary blood flow.

128
Q

What are the changes that occur in V/Q ratio?

A
  1. V/Q ratio in airway obstruction

■ If the airways are completely blocked, then ventilation is zero. If blood flow is normal, then V/Q is zero, which is called a shunt.

■ There is no gas exchange in a lung that is perfused but not ventilated. The PO2 and PCO2 of pulmonary capillary blood (and, therefore, of systemic arterial blood) will approach their values in mixed venous blood.

■ There is an increased A–a gradient.

  1. V/Q ratio in pulmonary embolism

■ If blood flow to a lung is completely blocked (e.g., by an embolism occluding a pulmonary artery), then blood flow to that lung is zero. If ventilation is normal, then V/Q is infinite, which is called dead space.

■ There is no gas exchange in a lung that is ventilated but not perfused. The PO2 and PCO2 of alveolar gas will approach their values in inspired air.

129
Q

What are the forms of oxygen in blood?

A

Physical solution (Dissolved Oxygen)

Chemical combination

130
Q

What is the dissolved oxygen in blood and what is its function?

A
  • Oxygen dissolves in blood and this dissolved oxygen exerts a pressure. Thus, PO2 of the blood represents the pressure exerted by the dissolved gas, and this PO2 is directly related to the amount dissolved.
131
Q

What does each 100 ml of arterial blood and Venous blood contain of physically dissolved oxygen?

A
  • Each 100 ml of arterial blood contains 0.3 ml of O2 dissolved physically in plasma.
  • Each 100 ml of venous blood contains only 0.13 ml of dissolved O2.
132
Q

What is the significance of dissolved oxygen?

A
  • Although it is small amount but it has the following significance:

a) It reflects and determines the O2 tension in the blood.
- At O2 tension 100 mmHg (arterial blood), the amount of O2 dissolved is 0.3 ml, while at O2 tension 40mm Hg (venous blood), the amount of O2 dissolved is 0.13ml.

b) It determines the rate and direction of oxygen flow.
- At the systemic capillary, it is the dissolved oxygen that diffuses to the tissues. when dissolved oxygen decreases, PO2 also decreases, and oxygen is released from Hb. Oxygen comes off Hb and dissolves in the plasma to maintain the flow of oxygen to the tissues.

“As a compensatory mechanism”

133
Q

What is oxygen in chemical combination?

A
  • More than 98% of the O2 is bound to hemoglobin of the red blood cells.
134
Q

What is hemoglobin?

A
  • It is an oxygen carrying pigment. Each molecule consists of: Globin and heme
135
Q

What is globin and heme respectively?

A

1) Globin: a protein composed of four polypeptide chains. There are many types of polypeptide chains according to their amino acid sequence. e.g., alpha-chain, β-chain, γ- chain, and δ-chain.
2) Heme: Four organic pigment molecules containing a single ferrous ion in the center of each molecule. Each ferrous ion can combine with one molecule of O2.

136
Q

How many molecules of o2 does each of hemoglobin add myoglobin bind to respectively?

A

4 - 1

137
Q

What are the characteristics of the reaction between hemoglobin and oxygen?

A
  • The reaction is reversible and rapid.
  • The reaction is oxygenation not oxidation. i.e., the iron in the heme remains in the reduced form “Fe++ or ferrous iron”.
  • The combination of Hb and O2 occurs in steps and each step accelerates the next one.
138
Q

What is the oxygen content of the blood? And what does it depend on?

A
  • It is amount of O2 present in chemical combination with Hb in 100 ml of blood.
  • It depends on hemoglobin content and O2 tension.
139
Q

What is the oxygen capacity of the blood and what does it depend on?

A
  • It is the amount of oxygen present in chemical combination with Hb in 100 ml of blood when it is fully saturated.
  • In normal subjects, Hb content is about 15 gm % and each gram of Hb can combine with 1.33 ml O2.
    O2 capacity = 15 x 1.33 = 19.95 ml (about 20 ml O2 / 100 ml.)
  • Oxygen capacity depends upon Hb content “Not oxygen tension as we measure the max”. So, It is decreased in anaemia.
140
Q

What is the percentage of saturation of hemoglobin with oxygen?

A

This equal = O2 content/O2 capacity * 100

141
Q

What is the percent of saturation of hemoglobin in arterial blood under normal conditions?

A
  • Under normal condition, the Hb of systemic arterial blood is only 97% saturated with O2. This is due to addition of venous blood from bronchial and coronary veins to the arterial blood which is called physiological shunt.
142
Q

What is the coefficient of o2 utilization?

A
  • It is the % of the blood that gives its oxygen as its passes through the tissue capillaries.
143
Q

what is the equation used to calculate the coefficient of oxygen utilization?

A
  • It equals oxygen content in arterial blood minus oxygen content in Venus blood divided by oxygen content in arterial blood
144
Q

What is the normal value for utilization coefficient in rest and in Muscular exercise?

A
  • The total quantity of oxygen bound with Hb in normal arterial blood is approximately O2 content in arterial blood 19.5 ml/100 ml blood.
  • On passing through tissue capillaries, this amount is reduced to about 14.5 ml /100 ml blood. Thus, during rest about 5 ml of O2 is utilized by the tissues by each 100 ml of blood.
  • The normal value for utilization coefficient is approximately 25%. In muscular exercise, It is increased to 75%.
145
Q

What is the hemoglobin oxygen disassociation curve?

A
  • The hemoglobin–O2 dissociation curve is a plot of percent saturation of hemoglobin as a function of PO2.a.

At a PO2 of 100 mm Hg (e.g., arterial blood): hemoglobin is 100% saturated b.

At a PO2 of 40 mm Hg (e.g., mixed venous blood): hemoglobin is 75% saturated.

146
Q

What is the shape of the oxygen disassociation curve?

A

sigmoid or S shape.

147
Q

What is the cause of the sigmoid shape of oxygen hemoglobin dissociation curve?

A
  • This is because the combination of O2 with the haem groups of the Hb occurs in steps as the affinity of haem to O2 is increased after the haem group is oxygenated.
148
Q

What is a physiological significance of the curve?

A
  • The upper flat part plateau This enables persons living at high altitudes or with lung disease to get enough O2 from this blood.
  • Middle curved part slope This satisfies the tissues needs during rest.
  • lower vertical part steep as occurring in muscular exercise.
149
Q

What does the upper flat plateau show?

A

This part shows that:
❑ At O2 tension (100 mmHg.), % Hb saturation is 100%.
❑ At O2 tension (80 mmHg), % Hb saturation is 93 %.
❑ At O2 tension (60 mmHg), % Hb saturation is 90%.

“Slight decrease”

  • So, decrease O2 tension from 100 to 60 mmHg causes decrease of % Hb saturation from 100% to 90% (i.e., only 10%).
  • The functional significance of the flat part of the curve is that the arterial O2 saturation does not change much until PO2 has decreased to about 60 mmHg.
150
Q

What does the middle curved part of the curve show?

A
  • At O2 tension (40 mm Hg), the % Hb saturation is 70%. So, decrease O2 tension from 100 to 40 mmHg, causes decrease of % Hb saturation from 100% to 70% (i.e., 30% decrease of % O2 saturation which are given to the tissues during rest).
151
Q

What does the lower vertical part of the curve show?

A
  • With further decrease of O2 tension (below 40 mmHg), there is marked decrease in the % Hb saturation (i.e., more O2 supply to the tissues)
152
Q

What is the significance of Venus oxygen reserve?

A
  • It is the oxygen that remains in venous blood after supplying the tissues.
  • This reserve equals 14 ml O2 i.e., 70% during rest.
  • This reserve is utilized during emergency e.g., muscular exercise.
153
Q

What does shifting in a hemoglobin oxygen dissociation curve to the right or to the left mean?

A
  • Shift to right: Hb gives more O2 to tissues even under high O2 tension.
  • Shift to left: Hb gives less O2 to the tissue even under low O2 tension.
154
Q

What shifts the hemoglobin oxygen dissociation curve to the right?

A

The following factors shift the curve to the right:

1) Increased CO2(Bohr effect).
2) Increased hydrogen ion (decrease pH). “Acidosis”
3) Increased temperature.
4) Increased 2,3-bisphosphoglycerate (2,3-BPG). “Produced by anaerobic glycolysis”

155
Q

What shifts hemoglobin oxygen dissociation curve to the left?

A
  • Stored blood loses 2,3-bisphosphoglycerate, causing a left shift in the curve, while hypoxia stimulates the production of 2,3-bisphosphoglycerate, thereby causing a right shift.
  • Carbon monoxide (CO) has a greater affinity for Hb than does oxygen. CO shifts O2– Hb dissociation curve to the left.

“CoHB & HBF”

156
Q

What is myoglobin and where is it present?

A
  • It is an iron containing pigment.

- It is present in slow twitch (red) skeletal and cardiac muscle fibers.

157
Q

What has a higher affinity for oxygen, hemoglobin or myoglobin?

A
  • It has higher affinity for O2 than Hb. So, Its O2 dissociation curve is shifted to the left of Hb dissociation curve.
158
Q

What is the function of myoglobin?

A

It acts as O2 store

  • In skeletal muscle: During muscular exercise, the muscle blood supply is compressed by muscle contraction and then Myoglobin provide O2 to the muscles.
  • In cardiac muscle: During diastole, when the coronary blood flow is greatest, the Myoglobin can load up with O2. This stored O2 can be released during systole, when the coronary arteries are squeezed and closed by the contracting myocardium.
159
Q

What is the amount of carbon dioxide in arterial blood?

A

In arterial blood each 100 ml carries 48-52 ml CO2. This large amount is carried in two forms

“While it has a maximum of 20 ml of oxygen”

160
Q

What are the forms of carbon dioxide in arterial blood?

A

❑ Physically dissolved (5%): in the plasma and RBCs. “2.5 ml”

❑ Chemically combined (95%): in two forms
1- Carbamino compounds (6%)
2- Bicarbonate ions (89%)

161
Q

What are carbamino compounds?

A
  • It is the combination of CO2 with the terminal amino group of polypeptide chains of blood proteins as Hb “in RBCs” and plasma protein “in plasma” .
    R NH2 + CO2 —————-> R NH COOH
162
Q

How are bicarbonate ions formed?

A
  • CO2 combines with water to form carbonic acid. Carbonic acid being a weak acid dissociates into bicarbonate ion (HCO3-) and H+ ion.

CO2 + H2O ————> H2CO3 ——–> H+ + HCO3-

  • This reaction occurs more rapidly in the presence of carbonic anhydrase enzyme which that present in RBCs and absent from plasma.
163
Q

What is the importance of Arterial carbon dioxide?

A
  • It represents a store for strong base (NaHCO3) it is called “alkali reserve”.
  • At the pulmonary capillaries, as O2 combines to Hb, its affinity to CO2 decreases and it releases the CO2 that diffuses into the alveoli.
164
Q

Transport of CO2 from the tissues to the lungs in venous blood. H+ is buffered by hemoglobin (Hb–H).

A

Okay!

165
Q

What is tidal carbon dioxide?

A
  • it is the amount of CO2 added by the tissues to the blood

- It equals 5ml. “55ml/100ml in venous blood”

166
Q

How is carbon dioxide transported in venous blood?

A

same way as the CO2 in the arterial blood.

167
Q

What are the forms of carbon dioxide in venous blood?

A

▪ Physically dissolved: in plasma 10%.

▪ Carbamino compounds: formed by combination of CO2 with terminal amino group of blood proteins 20%.

▪Bicarbonate: 70%.

168
Q

What results from the disassociation of carbonic acid?

A
  • As a result of dissociation of H2CO3 the released H ions helps unloading of oxy- Hb. “Shift oxygen disassociation curve to the right”
  • H+HbO2 → H.Hb+O2.
  • due to released HCO3, HCO3 becomes much greater in RBCs than in plasma, thus many of bicarbonate ions diffuse to plasma.
  • The inside of RBCs gains more positive charge, this attracts chloride ions from plasma to enter the RBCs in exchange.
169
Q

What are the results of chloride shift?

A

✓ Increased bicarbonate content of both plasma & RBCs.

✓ Increase Cl in RBCs and its decrease in plasma.

✓ water shift: shift of water from plasma to RBCs to maintain osmotic equilibrium.

✓ Hematocrit value of venous is about 3% greater than that of arterial blood due to increase RBCs volume by water shift.

170
Q

What generates respiration?

A
  • Respiration is generated by the activity of respiratory centers.
171
Q

What is the definition of a respiratory center?

A
  • They are poorly defined collection of neurons which are located in the brain stem.
172
Q

What are the types of respiratory centers?

A
  • medullary and pontine centers.
173
Q

What are the medullary centers in the brain stem?

A

Dorsal Respiratory Group (DRG) (Mainly inspiratory)

Ventral Respiratory Group (VRG) (inspiratory & expiratory “mainly”)

174
Q

What is the site of the DRG?

A
  • The dorsal respiratory group of neurons extends in dorsal region of the medulla. Most of its neurons are located within the nucleus of the tractus solitarius.
175
Q

What is the function of DRG?

A

❑ DRG has the property of intrinsic periodic firing “at regular intervals” . Thus, the basic rhythm of respiration is generated mainly in DRG.

❑ The neurons of the medullary inspiratory center are connected with the motor neurons of the diaphragm present in cervical segments (3,4,5) of the spinal cord and motor neurons of intercostal muscles present in the upper thoracic segments (1-10) by descending respiratory tract which run in the spinal cord.

❑ The nervous signals discharged by DRG begin weakly and increases steadily in a ramp manner (inspirtory ramp signal) for about 2 seconds then, it ceases abruptly for approximately the next 3 seconds causing relaxation of inspiratory muscles and produce expiration.

176
Q

What is the site of VRG?

A
  • Located in each side of the medulla, anterior and lateral to the dorsal respiratory group of neurons.
177
Q

What are the functions of VRG?

A

❑ The neurons of the ventral respiratory group remain almost totally inactive during normal quiet respiration, since expiration is a passive process.

❑ They become active only during forced expiration.

178
Q

What are the Pontine centers found in the brainstem?

A

A) Pneumotaxic center

B) Apneustic center

179
Q

What is the site of pnemotaxic center?

A

It is located in the upper pons, transmitting signals to the inspiratory area.

180
Q

What are the functions of pneumotaxic center?

A

❑ The primary effect of this center is to control the “switch-off” point of the inspiratory ramp, i.e., limit respiration, thus controlling the duration of the filling phase of the lung cycle and regulates the respiratory rate.

181
Q

What is the site of apneustic center?

A
  • It is located in the lower 1/3 of pons.
182
Q

What is the function of apneustic center?

A
  • It continuously sends excitatory impulses to the medullary DRG center. Therefore, it tends to prolong the time span of the inspiration.
183
Q

What is the mechanism of inspiration?

“From the very start”

A

Mechanism of inspiration:

  • continuous excitatory impulses from the apneustic center to the DRG send excitatory impulses to motor neurons of inspiratory muscles.
  • Impulses in the phrenic & intercostal nerves cause contraction of the diaphragm & external intercostal muscles with subsequent increase in all diameters of the thorathic cavity and expansion of the lung.
  • The intrapulmonary pressure decreases to -2 mmHg and air rushes in.
184
Q

What is the mechanism of expiration?

“From the very start”

A
  • Inhibitory impulses from both the pneumotaxic center mainly and (Herring-Breuer inflation reflex) from lung suppress the spontaneous activity of DRG and apneustic center. Therefore, inspiration is terminated & expiration starts passively.
  • The intrapulmonary pressure increases to +2 mmHg and air rushes out.
185
Q

What are herring-Breuer reflexes initiated by?

A
  • They are initiated by certain receptors in the lung parenchyma and the wall of the bronchioles.
186
Q

What are herring-Breuer reflexs?

A

There are two reflexes:

1) Inflation reflex
2) Deflation reflex

187
Q

When is inflation reflex done and what is its function?

A
  • Inflation of the lungs at the end of normal inspiration stimulates stretch receptors.
  • These receptors send afferent inhibitory impulses along the vagus to inhibit apneustic center and inspiratory center. So, inspiration stops & expiration occurs.
188
Q

When is deflation reflex number and what is its function?

A
  • Excessive deflation of the lung at the end of deep expiration stimulates deflation receptors that send inhibitory impulses to the expiratory center. So, expiration is inhibited and inspiration is produced.
189
Q

What are the factors that regulates the activity of respiratory centers?

A

Respiratory centers are under the control of:
A) Nervous factors. “Kinda in specific cases”
B) Chemical factors. “In rest” “the most imp”

190
Q

What is the Nervous regulation of respiratory centers?

A

i) Impulses from other nerve centers “rather than RESP. Centers”
ii) Afferent impulses from different systems

191
Q

Where do the impulses from other nervous centers to regulate the respiratory centers come from?

A
  1. Cortex

2. Hypothalamus and Limbic system

192
Q

Where do the afferent impulses from different systems to regulate the respiratory centers come from?

A

1) Respiratory system:

  • From upper airway
    a) Nose (Sneezing reflex) “dep ins. Then forced exp.”
    b) Pharynx (Deglutition apnea)
  • From lower airway and lungs
    a) Stretch receptors:
    b) Irritant receptors
    c) C- receptors

2) Cardiovascular system: “in cases of increased VR and ABP”

a. Harrison’s reflex:
b. Effect of arterial blood pressure (ABP):

193
Q

What are examples of cases in which impulses come from the cortex to regulate the activity of respiratory centers?

A

❑ Voluntary hyperventilation.
❑ Voluntary Apnea.

‘Both are limited”

194
Q

What are examples of cases in which impulses come from the hypothalamus and limbic system to regulate the activity of respiratory centers?

A

❑ Pain.
❑ Temperature.
❑ Emotions.

“Mild to moderate inc while severe dec”

195
Q

What is sneezing reflex?

A
  • It is a protective reflex that expels out foreign material from nasal cavity. “By trigeminal nerve”
196
Q

What is a description of deglutition apnea?

A
  • Breathing is inhibited during 2nd phase of deglutition (pharyngeal phase). This prevents aspiration of food into the airways during swallowing.

“By glossopharyngeal nerve”

197
Q

What are the types of receptors in the lungs and airways?

A
  • Receptors in the lungs and airway are of 3 types:
  1. Stretch receptors:
  2. Irritant receptors
  3. C- receptors
198
Q

What are the characteristics of stretch receptors in LRT?

“In between smooth muscles of the airway“

A
  • They are mechanoreceptors.
  • They are slowly adapting receptors.
  • These receptors are responsible for Herring-Breuer inflation and deflation reflexes.
199
Q

What are the characteristics of irritant receptors in LRT?

“ Free nerve endings in between epithelium”

A
  • They respond to irritant stimuli which may be: chemical stimuli (as histamine & PGS) or mechanical stimuli as (aspiration of foreign body).
  • They are rapidly adapting receptors
  • which are responsible for several reflexes resulting in cough, bronchoconstriction, and mucous hypersecretion.

“ Respiration is affected during eating, sneezing and the cough”

200
Q

What are the characteristics of C-receptors of LRT?

A
  • they were previously termed J receptor signifying juxta pulmonary capillary receptors.
  • These receptors are stimulated by: chemical stimuli (as histamine, bradykinin, serotonin and some prostaglandins) and mechanical stimuli (as interstitial

pulmonary edema).
- Activation of these receptors causes laryngeal closure and apnea followed by rapid shallow breathing.

201
Q

What is Harrison’s reflex?

A
  • Increased venous return to right side of the heart leads to an increase in the respiratory rate.
202
Q

What is the significance of Harrison’s reflex?

“By vagus”

A
  • This increase in ventilation helps oxygenation and removal of CO2 from the excess venous return. This helps to maintain V/P ratio constant.

“VR & RR are friends”

203
Q

What is the effect of arterial blood pressure on respiratory rate?

A

❑ If ABP increases above normal: This will increase the rate of discharge of inhibitory impulses from arterial baroreceptors in the walls of aortic arch and carotid sinus. Impulses are transmitted along sinus nerve (branch from 9th cranial nerve) and aortic nerve (branch from 10th cranial nerve) to the medullary centers. This causes inhibition of respiration.

204
Q

What is adrenaline apnea?

A
  • It is temporary stoppage of respiration on injection of large dose of adrenaline.

“As if it tightens the bronchioles”
“Of course it doesn’t, this is just a mnemonic”

205
Q

What does intravenous administration of adrenaline in large dose produce?

A
  • V.C. which increase ABP. This stimulates arterial baroreceptors in the aortic arch and carotid sinus leading to inhibition of R.C.
206
Q

What is ventilation mainly regulated by at rest?

A
  • At rest, ventilation is mainly regulated according to the level of metabolism “the main controller of RR” which produces changes in partial pressures of O2, CO2 and H+ concentration in the arterial blood.
207
Q

What is the main regulator of respiration in terms of chemical regulation?

A
  • CO2 “more specifically the main controller of RR” (the major metabolic end product) is the principal chemical factor that regulates ventilation.
208
Q

What responds to changes in the pressure of O2 and CO2 and H+?

A
  • Chemoreceptors are receptors that respond to changes in the concentration of O2, CO2, and H+ in their environment.
209
Q

What are the types of chemo receptors?

A
  • central and peripheral
210
Q

What are central chemoreceptors sensitive to?

A
  • They are sensitive to the pH of the cerebrospinal fluid (CSF). Decreases in the pH of the CSF “indirect indication of CO2 levels” produce increases in breathing rate (hyperventilation). “To wash excess CO2”
211
Q

Does carbon dioxide cross the blood brain barrier and what happens after it crosses this barrier?

A

▪ H+ does not cross the blood–brain barrier as well as CO2 does.

a) CO2 diffuses from arterial blood into the CSF because CO2 is lipid-soluble and readily crosses the blood–brain barrier.
b) In the CSF, CO2 combines with H2O to produce H+ and HCO3. The resulting H+ acts directly on the central chemoreceptors.

212
Q

Where are peripheral chemoreceptors In the carotid and aortic bodies located?

A

■ The carotid bodies are located at the bifurcation of the common carotid arteries.

■ The aortic bodies are located above and below the aortic arch.

213
Q

What stimulates peripheral chemoreceptors?

A

❑ Decreases in arterial PO2: “Main stimulant”
PO2 must decrease to low levels (<60 mm Hg) before
breathing is stimulated.

❑ Increases in arterial PCO2: “mild stimulation”
■ stimulate peripheral chemoreceptors and increase breathing rate.

■ potentiate the stimulation of breathing caused by hypoxemia. “Potentiation each other so that they produce an effect”

■ The response of the peripheral chemoreceptors to CO2 is less important than the response of the central chemoreceptors to CO2 (or H+).

❑ Increases in arterial [H+]
■ stimulate the carotid body peripheral chemoreceptors directly, independent of changes in PCO2.

214
Q

Compare between central chemoreceptors and peripheral chemoreceptors according to:

Site
Connection
Stimulus

A

Site:
- Present in medulla oblongata.

  • Present in Carotid bodies and Aortic bodies. “Connected to RC by buffer nerves”

Connection:
- Direct connection to the inspiratory centers. “Near it”

  • Connect the resp. centers in M.O. via sensory nerve fibers “buffer nerves”

Stimulus:
- Very sensitive to changes in CO2 level in the blood (↑ PCO2).

  • Sensitive to ↓in arterial PO2 and pH and ↑ in PCO2.