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Respiratory System > Resp Physiology > Flashcards

Resp Physiology Flashcards

1
Q

Respiration

A

The passive movement of oxygen transported to the rest of the body via the cardiovascular system. Carbon dioxide is expelled. Goal = energy production for metabolism

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2
Q

4 processes of external respiration

A
  1. Pulmonary ventilation
  2. Exchange CO2 & O2 between lungs and blood
  3. Transport O2 & CO2 by blood
  4. Exchange gases between blood and cells
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3
Q

Relationship between airflow, pressure and resistance

A

Airflow is directly proportional to pressure and inversely proportional to resistance

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4
Q

List the components of the upper respiratory system

A

mouth, nasal & oral cavity, pharynx, larynx

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5
Q

List the components of the lower respiratory system

A

trachea, R & L bronchi, lungs

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6
Q

Alveoli

A

Air filled pockets in lungs where gas exchange occurs. They are interconnected with pulmonary cavities. Alveolar walls are not muscle

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7
Q

Intrapleural fluid

A

the fluid in-between the visceral and parietal pleural membranes. About 25-30ml in a 70kg male. It is the lubrication needed to prevent friction of the layers, enabling the layers to slide past each other during respiratory movements

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8
Q

Name the pleural membranes

A

Parietal pleura = lines the interior surface of thorax (outer pleural membrane)
Visceral pleura = inner surface of lung

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9
Q

Pleurisy

A

Inflammation of the pleural sac. Causing painful breathing. Also known as pleuritis

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10
Q

Lung parenchyma

A

portion of lungs involved in gas exchange. The respiratory bronchioles and the alveoli

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11
Q

Types of cells within alveoli

A

Type I pneumocyte = alveolar surface 1 single layer thin
Type II pneumocyte = secretes surfactant
Macrophages = protect from inhaled pathogens

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12
Q

Name ALL the functions of the respiratory system

A
  • Exchange gases between the atmosphere and the blood
  • Homeostatic regulation of pH (CO2 levels)
  • Defends against pathogens inhaled & irritating epithelium substances
  • Enables speech
  • Routh for water loss & heat elimination
  • Modifies materials passing through pulmonary circulation (activates angiotensin II)
  • Participates in olfactory sense (smell)
  • enhances venous return via respiratory pump
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13
Q

What is meant by respiratory conditioning

A

Warming the air inhaled to prevent drying of the exchange epithelium and to prevent changes to the core body temp

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14
Q

How would a person feel exercising in the cold?

A

Hyperventilation of the cold air. No moistening or warming of the air inhaled so the epithelium of gas exchange will dry out causing a burning sensation

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15
Q

Describe how saline is produced.

A

NKCC brings Cl- ions into the epithelial cell from the ECF. Cl- ions are secreted by apical channels (including CFTR) into the lumen of the airways. Na+ follows into the lumen via the paracellular pathway drawn by the electrochemical gradient caused by the excess Cl-. Osmotic gradient caused from Na and Cl moving from the ECF to lumen cause H2O to follow into the lumen, creating saline .

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16
Q

Describe the disease cystic fibrosis

A

Genetic mutation causing loss of the anion channel CFTR allowing no Cl- ions to pass into the lumen. This results in less H2O moving into the lumen, so the mucus is very thick & sticky. Airways are now more susceptible to infections because bacteria gets trapped.

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17
Q

Symptoms of Cystic Fibrosis

A 
Persistent cough
Produce thick mucus 
Wheezing 
Shortness of breath 
Frequent chest infections 
Sinusitis
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18
Q

Respiratory defense system

A
  • Filtration in nasal cavity removing large particles
  • Goblet cells & mucous glands produce mucous
  • Cilia sweep debris away
  • Airway epithelial cells secrete cytokines to recruit immune cells
  • Mucus contains immunoglobulins in defense against pathogens
  • Reflex bronchoconstriction for some particles
  • Alveolar macrophages phagocytosis
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19
Q

Describe the respiratory disease pneumonia

A

Bacterial, fungi or viral. Triggers immune response & damages lung tissue. This causes the thickening of airways. It can damage alveolar walls or cause fluid build up in the alveoli

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20
Q

Symptoms of pneumonia

A 
Congestion 
Chest pain 
Difficulty breathing 
Fever
Coughing
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21
Q

Dalton’s Law

A

Total pressure = sum of partial pressures of individual gases

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22
Q

Atmospheric pressure

A

Patm = 760 mmHg at sea level

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23
Q

Partial Pressure Equation

A

Pgas = Patm x %gas in atmosphere

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24
Q

Partial Pressure in humid air equation

A

Pgas = (Patm - PH2O) x %gas in atmosphere

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25
Q

Ideal Gas Equation

A

PV = nRT

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26
Q

Boyle’s Law

A

P1V1 = P2V2

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27
Q

Pulmonary Ventilation

A

Breathing. The process of air flowing into the lungs during inspiration and out of lungs during expiration

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28
Q

Alveola Ventilation

A

Exchange of gas between alveoli & external environment

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29
Q

Respiratory Cycle

A

Consists of 1 breath in (inspiration) and 1 breath out (expiration)

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30
Q

Intra-alveolar Pressure

A

Pressure within alveoli. When it differs from atmospheric pressure, airflow will occur to equalize this difference

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31
Q

Intrapleural Pressure

A

The pressure within the pleural sac. It is usually less than atmospheric pressure (sub-atmospheric)

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32
Q

Transmural Pressure Gradient

A

There is a difference in the intrapleural pressure and the intra-alveolar pressure, creating a gradient called the transmural pressure gradient. This gradient keeps the lungs open and prevents collapse.

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33
Q

Why is the intrapleural pressure sub-atmospheric?

A

The lungs have a natural tendency to want to recoil inwards. So, after expiration at that brief second when the pressure in the lungs reaches 0mmHg, the lungs want to recoil in. The negative intrapleural pressure just outside the lung keeps it from collapsing.

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34
Q

Muscles contributing to inspiration

A

Diaphragm contracting & flattening = 60-70% of increased thoracic vol
Intercostal muscles moving rib cage = 25-40% of inspiration
Scalene muscles
Sternocleidomastoid muscles

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35
Q

Nerve stimulating the Diaphragm

A

Phrenic Nerve

stimulates the diagram to contract & flatten

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36
Q

Interstitial Space

A

Very thin layer 0.5 micro meters

separating air in alveoli from blood in capillaries. This barrier facilitates air exchange

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37
Q

Normal ventilation rate

A

12-20 breaths/min (adults)

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38
Q

Pneumothorax

A

A punctured/ injured pleural membrane. Atmospheric air flows down gradient into pleural cavity. The intrapleural pressure now = atmospheric pressure. There is no transmural gradient therefore nothing keeping the lungs open. The lungs collapse.

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39
Q

How do we fix pneumothorax injuries ?

A
  • Remove air from pleural cavity with suction pump

- seal hole to prevent air entering

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40
Q

The role of the different intercostal muscles

A

External intercostal muscles = inspiration

Internal intercostal muscles = expiration

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41
Q

Nerve control of the Respiratory System

A

Nerve supply comes from the medullary respiratory center in the brain. 2 Clusters

  • Dorsal resp group = inspiratory neurons
  • Ventral resp group = inspiratory & expiratory neurons
  • the respiratory rhythm is set by the pre-Botzinger complex located at the upper end of the respiratory medullary center
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42
Q

The role of a Spirometer

A

Asses pulmonary function. Measures how much air moves during quiet breathing and then also with maximum effort.

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43
Q

Tidal Volume

A

The volume of air that moves through the lungs during a single inspiration or expiration during quiet breathing. On ave = 500ml

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44
Q

Inspiratory Reserve Volume

A

The volume of air that can be inspired with maximum effort after tidal volume/ quiet inspiration already took place. Average = 3L

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45
Q

Expiratory Reserve Volume

A

The volume of air that can be expired with maximum effort after normal expiration already took place. Average = 1.2L

46
Q

Residual Volume

A

Volume of air in the system after maximum exhalation. Average = 1.2L

47
Q

Capacity

A

the sum of two or more volumes

48
Q

Vital Capacity

A

Represents the maximum amount of air that can be exhaled after maximum amount of effort was taken to inhale. Includes IRV + ERV + TV

49
Q

Lung Capacity

A

The amount of air in total that the lungs can hold.

TV + RV + IRV + ERV

50
Q

Inspiratory Capacity

A

Max volume of air that can be inspired after quiet breathing

51
Q

Functional Residual Capacity

A

Volume of air in the lungs at the end of normal/ quiet expiration

52
Q

Total Pulmonary Ventilation

A

Also called Minute Respiratory Volume. Volume of air moving in and out of the lungs per minute.
Ventilation rate x Tidal vol

53
Q

Anatomic Dead Space

A

Part of the inspired air that remains in the conducting airways & thus is not available for gas exchange

54
Q

Alveolar ventilation

A

Indication of how much fresh air reaches the lungs

Ventilation rate x (tidal vol - dead space vol)

55
Q

Describe what is happening during shallow rapid breathing

A

The person is drawing air in and out of the anatomic dead space without air being exchanged at the alveoli

56
Q

Dead Space Ventilation

A

Amount of air per unit time not involved in gas exchange, that stays in conducting zones.
VD = vent rate x dead space vol

57
Q

Apnea

A

Breathing stops briefly / completely

58
Q

Bradypnea

A

Slower than normal breathing

59
Q

Dyspnea

A

Short of breath, breathing is labored

60
Q

Eupnea

A

Normal breathing

61
Q

Hyperpnea

A

Breathing more deeply

62
Q

Hyperventilation

A

Deep, fast letting more air out than in

63
Q

Hypopnea

A

Partial blockage or air

64
Q

Tachypnea

A

Rapid, shallow breathing

65
Q

Influences of breathing flow

A
  1. Lung distensibility / stretch ability = compliance
  2. Airway resistance
  3. Elastic recoil
66
Q

Compliance

A

The lung distensibility. How much effort / work is needed to stretch the lungs

67
Q

Low Compliance

A

More effort is needed to stretch the lungs. The lungs require a larger transmural pressure gradient with each inspiration
eg. in patients with Pulmonary Fibrosis

68
Q

Describe the disease Pulmonary Fibrosis

A

Long exposure to pollution & or toxins triggers an inflammatory response. The alveolar macrophages secrete factors that stimulates fibroblasts to synthesize inelastic collagen fibers. Leads to a “stiff” lung causing hypertension and R heart failure.

69
Q

Describe the importance of the FEV1/FVC ratio

A

FEV1 = Forced Expiratory Volume per 1 min
FVC = Forced Vital Capacity
Indicative of restrictive / obstructive disease. Normal FEV1/FVC ratio = 80%. Lower than that indicates disease / problem

70
Q

FEV1

A

FEV1 = Forced Expiratory Volume per 1 minute. It’s the volume of air expired forcefully in a spirometry test after a deep breath in. Lower than normal FEV1 is indicative of obstructive respiratory disease

71
Q

Elastance

A

Ability to return to resting volume when stretching force is released

72
Q

What is the significance of a patient with abnormally very high compliant lungs ?

A

Their lungs have most probably lost their elastic tissue and lost their ability to recoil. It has lost all counter force to stretching thus having very high compliant lungs.

73
Q

Emphysema

A

Alveoli damage and rupture which decreases lung surface area in eg. smokers. Alveolar macrophages are activated to counter act inhaled irritants. They release elastase breaks down elastin fibers & alveoli lose elastic recoil abilities. Expiration becomes a conscious effort.

74
Q

What is elastic recoil dependent on?

A
  • Elastic connective tissue

- Alveolar surface tension

75
Q

Alveolar surface tension

A

H2O molecules are attracted to other H2O molecules by hydrogen bonding. These bonds create a force called surface tension. This “clinging” resists any force used to deform/stretch/break which is needed for lungs to stretch. Hence, higher surface tension = less compliant lungs. Surface tension reduces alveolar size promoting collapse. With increase surface tension more work is needed to expand the alveoli.

76
Q

What is the importance of surfactant

A

Surfactant lessens the effect of surface tension. Prevents collapse. Prevents pulmonary edema

77
Q

What does alveolar stability rely on?

A
  • Surfactant

- Alveolar Interdependence

78
Q

Atelectasis

A

Complete or partial collapse of the entire lung or lobe/s

79
Q

Formula for working out compliance

A

Change in Vol/Change in Pressure

Steeper slope on a graph = more compliant

80
Q

What does compliance depend on

A
  • Elastic forces of lung

- Surface tension

81
Q

Hysteresis

A

Term used to describe the difference between inspiratory and expiratory compliance

82
Q

Describe why there is a difference in ventilation at different parts of the lung.

A

Ventilation is greater at the base and smaller at the apex. Intrapleural pressure is less negative (higher) at the base at the start of inspiration. The transmural gradient is less at the base = the base is less expanded = more pressure = greater ventilation.

83
Q

Formula for ventilation rate

A

Tidal vol x Resp rate

84
Q

Perfusion of lungs

A

Vol of blood reaching pulmonary capillaries per unit time

85
Q

The significance of surfactant in newborn babies

A

The synthesis of surfactant starts at week 25 of pregnancy and finishes at week 34. Premature babies are born without enough surfactant. They have stiff lungs with low compliance at risk of collapse.

86
Q

NRDS

A

Newborn respiratory distress syndrome

Premature babies born without enough surfactant at risk of collapsing lungs.

87
Q

Poiseuille’s Law

A

Wider airways = less resistance

Rate of flow is directly proportional to viscosity and length of airway. Indirectly proportional to radius

88
Q

Describe the neural control of the different airways

A

Parasympathetic neurons causes bronchoconstriction. There is no sympathetic innervation.
Smooth muscles has B2 receptors for circulating epinephrine (bronchodilation)
Increased CO2 in exhaled air relaxes bronchiolar smooth muscle
Increased histamine release leads to bronchoconstriction

89
Q

Describe how airways are sensitive to CO2 and O2 and bloodflow

A

Bronchiolar smooth muscle = sensitive to CO2 levels. High CO2 leads to relaxation of smooth muscles = bronchodilation = more airflow allowing more CO2 out.

Greater blood supply = more O2 extracted from alveoli. Low O2 levels leads to vasoconstriction of pulmonary arterioles = less bloodflow to match the airflow.

90
Q

Work (in terms of breathing)

A

Work = energy consumed by respiratory muscles throughout the respiratory cycle. Energy needed to overcome elastic forces & airway resistance

Work = Pressure x Volume

91
Q

Describe the disease Bronchitis

A

It is triggered by frequent exposure to eg. cigarette smoke, allergens, pollution. It is a long term state of inflammation. Airways narrow from the thickening of the airways and increased mucus production.

92
Q

Describe the disease Asthma

A

Heterogenous disease. Airway inflammation. Severe constriction of small airways. Inflammation & histamine induces edema.

It is reversible therefore cannot be classified as a COPD. Compliance is not a problem here, efficient expiration is the problem.

93
Q

Symptoms of asthma

A

Wheezing
Short of breath
Chest tight
Coughing

94
Q

What is alveolar pressure comprised of ?

A

Alveolar pressure = pleural p + lung elastic recoil p

95
Q

Dynamic Compression of airways

A

Frictional resistance of the air flowing causes a decrease in driving pressure along conducting airways. Eventually the driving pressure becomes 0. This is “equal pressure point”.
Downstream P outside the airways becomes greater than the driving pressure inside. The negative pressure on the inside of the airways causes compression of the pathway. The compression of the airways increases the pressure again P1V1=P2V2 hence maintaining the driving force of the air flowing.

96
Q

Describe the spirometry graph of a patient with obstructive respiratory disease

A
  • TLC is normal
  • FRC & RV is increased due to additional air trapped in lungs after expiration (obstruction)
  • Increased RV = Decreased VC
97
Q

Describe the lung vol/pressure graph of a patient with restrictive respiratory disease

A

The graph will shift in the slope. The slope will less steep slanting to the right. More pressure is needed to achieve the same normal lung volume needed for function. There is an increase in elastic work. Resistance is unchanged. Expiration remains passive as work lies within the area of potential stored energy.
Eg. Pulmonary Fibrosis

98
Q

Describe the lung vol/pressure graph of a patient with obstructive lung disease

A

The problem is airway resistance.
Both inspiratory and expiratory work must increase to overcome additional airway resistance. Wider pressure - vol loop. If resistance is severe, the expiratory work will exceed stored potential. Expiration is no longer passive & it requires active efforts by expiratory muscles v

99
Q

4 Tissue Layers of the Respiratory Membrane

A
  • Alveolar wall (type I,II)
  • epithelial basement membrane under alveolar wall
  • Capillary basement membrane fused to epithelial basement membrane
  • Capillary epithelium
100
Q

Why is the pressure in the bronchial artery equal to the pressure of the aorta?

A

The bronchial artery has a short radius and a short length = high pressure.

101
Q

Functions of the pulmonary circulation

A
  • gas exchange
  • brings blood to alveoli
  • filter
    blood reservoir
  • metabolic functions
  • produces ACE , inactive vasoactive hormones, releases fibrinolytic substances
102
Q

Vascular Resistance

A

Anything that restricts the flow of blood

It is highly dependent on the diameter of the vessel

103
Q

State mechanisms which adjusts the vascular resistance relative to the pressure.

A
  • Capillary recruitment: the spontaneous opening of constricted capillaries due to pressure increase
  • Capillary Dilation: the capillaries that were already open will dilate
104
Q

Hypoxic Pulmonary Vasoconstriction

A

Diverting blood from an area undersupplies with oxygen and channel it to a better ventilated area/ an area with a lot of oxygen.

Caused by hypoxia or atelectasis (lung collapse)

Can cause Pulmonary Hypertension, Right Ventricular Hypertrophy, Right heart failure

105
Q

Pulmonary Arterial Hypertension

A

When the O2 undersupply becomes pathological then too many pulmonary vessels constrict. The smooth muscles become damaged. Chronic periods in this state causes pulmonary arterial hypertension (high blood pressure)

106
Q

Mountain Sickness

A

At high altitudes there’s decreased oxygen levels. Body experiences persistent hypoxia. Symptoms include hyperventilation, dizziness, headache, fatigue, short of breath. This causes high pulmonary arterial pressures and then edema.

107
Q

Pulmonary edema

A

When pulmonary fluid interstitial pressure increases from negative to positive. Fluid accumulation in the interstitial spaces and lymphatics are unable to drain effectively. Can be caused by damage to membranes of pulmonary capillaries. Left heart failure can cause capillary pressure to rise

108
Q

External respiration

A

Includes all the processes involved in exchanging oxygen and carbon dioxide with the environment

109
Q

Internal respiration

A

Intracellular reaction of oxygen with organic molecules to form carbon dioxide, water and ATP

110
Q

What are the 4 different processes of external respiration

A

1- Pulmonary ventilation, air exchange between atmosphere and lungs
2- Exchange of CO2 and O2 between lungs and blood
3- Transport of O2 and CO2 by blood
4- Exchange of gases between blood and cells

111
Q

Air conditioning of the pulmonary system

A
  • warming air to prevent changing of core temperature
  • adding water to 100% humidify the air, preventing drying of epithelium
  • filtration preventing foreign material reaching the alveoli
112
Q

Describe the relationship between ventilation and perfusion

A

They are matched. Low ventilation = low perfusion. In lungs capillaries collapse due to falling blood pressure through them. Low hydrostatic pressure at the lung apex closes capillaries.

Respiratory System (5 decks)

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