Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M1 > Brandon Ong's M1 Anki Deck__3. Physiology__C. Respiratory System > Flashcards

Brandon Ong's M1 Anki Deck__3. Physiology__C. Respiratory System Flashcards

1
Q

What is inspiration?

A

Expansion of chest cage → ↓ pleural pressure → ↓ alveolar pressure to -1cm → air flows into lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is expiration?

A

Elastic recoil of lungs or compression of pulmonary cavities in forced expiration → ↑ pleural pressure → ↑ alveolar pressure to +1cm → air flows out of lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What affects work of breathing?

A
  1. ↓ compliance → ↑ work of breathing
  2. ↑ airway resistance → ↑ work of breathing
  3. ↑ respiratory demand → ↑ work of breathing (↑ 50x in exercise)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is compliance of lungs?

A

<img></img><div>- Measures stretchability of lungs & chest wall</div><div>- Transpulmonary pressure reflects compliance</div><div>   - Norm: ↑ 1cm transpulmonary pressure → ↑ 200ml alveolar volume</div>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What determines lung compliance?

A
  1. Elastic forces of lung tissue
  2. Surface tension elastic force
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the factors affecting alveolar collapse?

A

<img></img><div>- Surfactant helps to reduce surface tension elastic force</div>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can disrupt normal ventilation?

A
  • Pregnancy 3rd trimester:<div>   - ↑ intraabdominal pressure → ↓ diaphragm movement → ↓ lung vol & compliance</div><div>- Pneumothorax or pleural effusion</div><div>   - Expansion of pleural space → intrapleural pressure cannot fall enough to give inspiration</div>
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a tension pneumothorax and how is it treated?

A
  1. Fascia in chest wall develops 1-way valve, allowing air to enter but not exit
  2. Air in pleural space develops high pressure and displaces mediastinal structures towards side of normal lung, distorting great vessels, compromise blood flow

Treatment: needle thoracostomy to relieve pressure, converts tension pneumothorax into normal pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical signs of tension pneumothorax?

A

<img></img>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is airway resistance controlled?

A
  • Bronchodilation: sympathetic nerves/hormone (epinephrine on β2 adrenergic receptors)
  • Bronchoconstriction: parasympathetic by vagus nerve (acetylcholine)
  • Local secretory factors can trigger bronchoconstriction
       - Eg pollen causes mast cells to release histamine & slow-reacting substance of anaphylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can result from narrowing of bronchi & bronchioles?

A

Obstructive diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can bronchodilate asthmatic airways?

A

β2 adrenergic agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the protective functions of the upper respiratory tract?

A
  1. <font>Mucus</font>(secreted by goblet cells): moistens inspired air and traps small particles
  2. <font>Cilia</font>(from nose to terminal bronchioles): beat to move mucus towards pharynx where it is swallowed or coughed out
  3. <font>Upper respiratory passages:</font>warm, humidify, filter air
  4. <font>Cough reflex:</font>foreign matter/irritation of airways (esp carina) → rapid inspiration, closure of epiglottis & vocal cords → forced expiration at high pressure → expel foreign matter
  5. <font>Sneeze reflex:</font>similar to cough reflex but apply to nasal passageways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens in asthma?

A
  • Excessive mucus accumulation
  • Airway swelling
  • Due to immune response
       - Steroids can regulate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can defective ciliary movement result in?

A

Infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the danger of artificial respiration?

A
  • Bypasses protective mechanisms of upper respiratory tract
  • Can lead to ventilator-associated pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the functional volumes of ventilation?

A

<img></img>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the variations of the functional volumes of ventilation?

A
  • In exercise, tidal volume recruits IRV & ERV to increase ventilation
  • Ability to ventilate depends on:
       - Chest wall integrity (eg kyphosis - humpback)
       - Lung resistance/elasticity/collapse
       - Other restrictions (eg abdominal pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is minute respiratory volume and what are possible variations?

A
  • Tidal vol x Respiratory rate
  • Norm: 0.5L x 12 breaths/min = 6L/min

<div>- Deviations:<br></br></div>

<div>&nbsp; &nbsp;- Hyperventilation</div>

<div>&nbsp; &nbsp;- Hypoventilation</div>

<div>&nbsp; &nbsp;- Tachypnea (increased rate of breathing)</div>

<div>&nbsp; &nbsp;- Dyspnea (distressful sensation of breathing)</div>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is max expiratory flow?

A
  • Rate of expiration is limited: beyond a limit, increased pleural pressure in expiration collapses bronchioles, increasing airway resistance and opposing expulsion of alveolar air
  • Max expiratory flow greater when lungs are filled: in enlarged lung, bronchioles held open by taut elastic pull of lung structural elements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is spirometry used for and what are its values?

A
  • Used to measure functional volumes of ventilation
  • <font>FVC</font>(forced vital capacity): maximum inspiration then maximum forced expiration
  • <font>FEV1:</font>forced vital capacity in 1st second
  • Norm: FEV1/FVC = 80% (ie 80% of air is exhaled in 1st second)
  • Decreased FEV1/FVC in obstructive diseases (greater airway resistance)
  • No change in restrictive diseases (poorer compliance, lungs cannot expand)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the rate of alveolar ventilation?

A
  • Rate at which new air reaches gas exchange areas of lung (alveoli, alveolar sacs, alveolar ducts, respiratory bronchioles)
       - Key to gas exchange in lungs
  • VA = Respiratory rate x (Tidal vol - Physiologic dead space)
  • Norm VA = 12 breaths/min x (0.5L-0.15L) = 4.2 L/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the types of dead space?

A
  • <font>Anatomic dead space:</font>air filling conducting passages where gas exchange does not occur (nose, pharynx, trachea), expired first on expiration
  • <font>Physiologic dead space:</font>anatomic dead space + air ventilating nonfunctional/partially-functional alveoli (eg due to poor perfusion)
  • Normally, all alveoli functional, anatomic dead space = physiologic dead space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the characteristics of adult pulmonary circulation?

A
  • Low pressure: pulmonary artery = 24/8mmHg (vs 120/80 of aorta)
  • High-flow: highly compliant pulmonary arteries receive whole RV stroke volume
  • Lungs serve as blood reservoir
  • CO affects pulmonary blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

When do pulmonary vessels constrict?

A
  • Constrict when alveoli PO2 decreases (esp below 73mmHg)
       - Opposite of systemic vessels which dilate during hypoxia
       - Local vessels of poorly-ventilated alveoli constrict, directing bloodflow to elsewhere where gas exchange is more effective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens to pulmonary vessels during exercise?

A
  • During exercise, 4x-7x extra blood flow accommodated by:
       - Increasing no of open capillaries
       - Capillary distension
       - Increase in pulmonary arterial pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the effect of gravity on pulmonary circulation?

A
  • Significant since pulmonary artery pressure only 24/8mmHg
  • 15mmHg of lungs above heart, 8mmHg below
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the zones of blood flow in lungs?

A

<img></img>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the characteristics of fetal pulmonary circulation?

A
  • Lungs collapsed, oxygenation via placenta
  • Blood entering RA from IVC (from umbilical vein) directed through foramen ovale into LA
  • Blood entering RA from SVC directed into RV → pulmonary art → through ductus arteriosus into desc aorta
  • At birth:
       - Lungs expand and are perfused
       - Umbilical artery & veins obliterated
       - Foramen ovale closes, ductus arteriosus constricts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a pulmonary embolism and how is it treated?

A
  • When embolus (blood clot), fat globule or air bubble lodges in pulmonary artery (severity depends on significance of artery occluded)
       - Large embolus results in acute respiratory distress due to major decrease in blood oxygenation
       - Blockage of artery supplying bronchopulmonary segment results in pulmonary infarction

Treatment: t-PA, streptokinase, embolectomy (heparin & warfarin too slow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the clinical signs of pulmonary embolism?

A

<img></img>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How long does blood take to flow through pulmonary capillaries?

A
  • Blood passes through pulmonary capillaries in 0.8s
       - With ↑ CO, blood passes through in 0.3s
  • Blood normally stays in capillaries 3x longer than necessary for oxygenation, can fully oxygenate even in shorter exposure time during exercise
  • In healthy people, rate of blood flow does not limit oxygenation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the pulmonary capillary pressure?

A

7mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How are the alveoli kept dry?

A
  • Due to hydrostatic & osmotic pressure of capillaries & interstitial fluid: mean filtration pressure = +1mmHg outwards
       - Slight continual flow of fluid from capillaries to interstitial space
  • Pulmonary lymphatic pump maintains slight negative pressure in interstitial spaces
       - Negative pressure keeps alveoli dry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the safety factor preventing pulmonary edema?

A

Pulmonary capillary pressure must rise from 7mmHg to 28mmHg (acute) or 40mmHg (chronic) to cause pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the basis for gas exchange?

A

Diffusion from area of high partial pressure to low partial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is partial pressure proportional to?

A

Conc of dissolved gas
- Gas complexed w hemoglobin does not exert partial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What must be fulfilled in order for gas exchange to occur?

A
  1. Alveoli must be ventilated by air
  2. Alveoli must be perfused by blood
  3. Diffusion must be efficient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is solubility of a gas and partial pressure related?

A

Greater solubility of gas → more amt of dissolved gas at particular partial pressure
- Solubility of CO2 > solubility of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why is alveolar air humidified?

A

Prevent damage to respiratory epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Why is alveolar air only partially replaced by atmospheric air with each breath?

A

Prevent sudden changes in blood gas conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does alveolar PO2 & PCO2 change with rate of ventilation?

A
  • Alveolar PO2 increases w rate of ventilation
       - Upper limit = 149mmHg due to dilution with water vapour as air is humidified
  • Alveolar PCO2 decreases w rate of ventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is normal expired air comprised of?

A

Combination of dead space air & alveolar air
- Gas conc between alveolar air & humidified atmospheric air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the normal partial pressures?

A

<img></img>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the factors affecting gas exchange and what problems can arise from them?

A
  1. Thickness of respiratory membrane
       - Edema fluid ↑ thickness
       - Fibrosis ↑ thickness
  2. Surface area of respiratory membrane
       - Emphysema (alveoli coalesce) ↓ SA
       - Infection fills alveoli w WBC → ↓ SA
  3. Diffusion coefficient: CO2 more soluble in blood, diffuses faster
  4. Partial pressure difference of gas
       - ↓ PO2 at high altitude
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What affects the thickness of the respiratory membrane?

A

Increased thickness decreases diffusion efficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What affects the surface area of the respiratory membrane?

A

Emphysema (alveoli coalesce) decreases surface area. Infection fills alveoli with WBC, leading to decreased surface area.

48
Q

What is the diffusion coefficient of CO2?

A

CO2 is more soluble in blood and diffuses faster than O2.

49
Q

What is the partial pressure difference of gas?

A

Partial pressure of O2 decreases at high altitude.

50
Q

What is the ventilation/perfusion ratio and what does it show?

A

It provides a quantitative understanding of the imbalance between air ventilation and blood perfusion.

51
Q

What causes non-optimal VA/Q ratio?

A

Various factors including physiological shunts and dead spaces.

52
Q

What are the normal non-optimal VA/Q ratios?

A

Normal physiologic dead space: VA/Q = 2.5. Normal physiologic shunt: VA/Q = 0.6.

53
Q

What are the causes of pathological anomalies of VA/Q ratio?

A

Physiologic shunt: air trapped in unventilated alveoli; collapsed alveoli, edema, inflammation. Physiologic dead space: damaged alveolar walls & pulmonary capillaries, pulmonary embolism, poor cardiac output.

54
Q

How does lung fibrosis cause physiologic shunts & dead spaces?

A

Fibrous tissue seals off ventilation of perfused alveoli, forming a shunt, and seals off capillaries in ventilated tissue, forming dead space.

55
Q

How does COPD due to smoking cause physiologic shunts & dead spaces?

A

Obstruction of bronchioles results in unventilated alveoli, forming shunts. Emphysema destroys alveolar walls & capillaries, forming dead space.

56
Q

How is O2 diffused between blood and interstitial fluid?

A

O2 in blood rapidly unloads until equilibrium is reached. Interstitial PO2 = 40mmHg = Blood PO2.

57
Q

What affects interstitial PO2?

A

Interstitial PO2 rises with increased blood flow and falls with higher metabolic rates.

58
Q

What affects intracellular PO2?

A

Intracellular PO2 ranges from 5-40mmHg, depending on the distance between capillaries and cells.

59
Q

How is O2 transported in blood and what affects it?

A

1% of O2 is dissolved; 99% is bound to hemoglobin in RBC. The amount carried depends on PO2 and [Hb].

60
Q

Does fetal hemoglobin or HbA have a higher affinity for O2?

A

Fetal hemoglobin has a higher affinity for O2.

61
Q

What does the O2 dissociation curve represent and what is its shape?

A

It relates the proportion of hemoglobin saturated with O2 against blood PO2, with a sigmoid shape.

62
Q

What are the blood PO2 & SpO2 levels in different scenarios?

A

Refer to the provided image for specific values.

63
Q

What is the tissue O2 buffering effect of hemoglobin?

A

Hemoglobin stabilizes tissue PO2 due to its sigmoid curve, maintaining almost constant tissue PO2.

64
Q

What is the significance of very low or high atmospheric O2?

A

Alveolar PO2 < 60mmHg leads to rapid SpO2 drop, causing hypoxia. Hyperbaric O2 can lead to acute oxygen poisoning.

65
Q

What does a shift in the O2 dissociation curve mean and what factors do so?

A

A rightward shift indicates Hb has a lower affinity for O2. Factors include increased H+, temperature, and 2,3-BPG.

66
Q

What is carbon monoxide poisoning, what are its symptoms and how can it be treated?

A

CO displaces O2, forming carboxyhemoglobin. Symptoms include disorientation & unconsciousness. Treatment: administer pure O2.

67
Q

How is CO2 diffused between blood and interstitial fluid and what are their PCO2 values?

A

CO2 diffuses 20x faster than O2. Interstitial PCO2 = 46mmHg, Venous PCO2 = 45mmHg, Arterial PCO2 = 40mmHg.

68
Q

What affects interstitial PCO2?

A

Decreased blood flow and increased metabolism raise PCO2.

69
Q

How is CO2 transported in blood?

A

7% dissolved CO2, 23% Hb-CO2, 70% as HCO3-. CO2 enters RBCs and is catalyzed to H+ and HCO3-.

70
Q

What is the respiratory exchange ratio?

A

Fat metabolism: 0.7, Carbohydrate metabolism: 1.0. A ratio of 0.7-1.0 indicates a mix of fat and carbohydrates.

71
Q

What is the Haldane effect?

A

Binding of O2 to Hb displaces CO2 and HCO3-, doubling the amount of CO2 released in lungs and picked up in tissues.

72
Q

What are the normal arterial and venous blood pH?

A

Arterial blood: pH 7.41, Venous blood: pH 7.37.

73
Q

What causes acidosis and alkalosis?

A

Acidosis: high metabolic activity, poor tissue perfusion. Alkalosis: hyperventilation.

74
Q

Why is CO2 the main regulator of respiration?

A

PCO2 is directly affected by pulmonary ventilation and not buffered, making it a primary regulator.

75
Q

How do the medulla (central) chemoreceptors sense PCO2?

A

Changes in blood PCO2 reflect in interstitial fluid and CSF, stimulating the respiratory center in the medulla.

76
Q

What are the peripheral chemoreceptors and how do they work?

A

They measure arterial PO2. Carotid bodies and aortic bodies transmit impulses to the medulla, especially when PO2 < 60mmHg.

77
Q

What are the principles behind the control mechanism of respiration?

A

Ventilation changes to restore normal arterial PCO2, PO2, pH, with sensors in the chemoreceptors and control in the brainstem.

78
Q

What are the parts of the brainstem respiratory centre and what do they do?

A

Dorsal respiratory group: inspiratory signals. Pneumotaxic centre: controls inspiratory ramp. Ventral respiratory group: provides forced inspiration & expiration.

79
Q

What is the Hering-Breuer Inflation Reflex?

A

A protective mechanism preventing excessive lung inflation by switching off the inspiratory ramp.

80
Q

How does exercise control respiration?

A

Motor impulses stimulate the respiratory centre, increasing ventilation before PCO2 rises.

81
Q

What respiratory causes induce dyspnea?

A

Alveolar PCO2 rises above 60-75mmHg; hypoxia triggers dyspnea to a lesser extent.

82
Q

What can cause depression of respiration?

A

Brain edema, overdose of anesthesia or sedatives, narcotic drugs.

83
Q

What is Cheyne-Stokes breathing?

A

A lag in response of the respiratory centre, leading to alternating overventilation and underventilation.

84
Q

What respiratory causes induce dyspnea?

A

Alveolar PCO2 rises above 60-75mmHg. Hypoxia triggers dyspnea to a lesser extent.

85
Q

What is Cheyne-Stokes breathing?

A

Lag in response of respiratory centre due to slow transport of blood from lungs to brain during cardiac failure. Overventilation and underventilation occur alternately.

Overbreathing blows off too much CO2; underbreathing causes CO2 to accumulate.

86
Q

What is CO2 narcosis?

A

Excessive PCO2 > 80mmHg (lethargy) or 120mmHg (anesthesia/death) depresses rather than stimulates respiration due to depression of CNS.

87
Q

What is N2 narcosis?

A

Breathing ↑↑ PN2 in compressed air during diving results in anesthesia, loss of coordination, and coma.

88
Q

What is decompression sickness?

A

During deep diving, N2 dissolves into tissues, especially fat. Upon rapid ascent, N2 bubbles out, blocking vessels.

To joints: joint pain; to CNS: deafness, impaired vision, paralysis.

89
Q

What is O2 toxicity?

A

Free radicals from many hours of 80-100% O2 irritate respiratory passages. 4-6atm 100% O2 exhibits CNS toxicity, causing muscle twitching and convulsions.

90
Q

What are the effects of hypoxia & hypercapnia?

A

Depressed mental activity and coma, reduced muscle work capacity, cellular death, cyanosis due to >5g/dL deoxygenated Hb.

91
Q

What is hypoxia & hypercapnia?

A

Hypoxia: lack of O2. Hypercapnia: excess CO2.

92
Q

What is the compensatory response for hypoxia & hypercapnia?

A

Circulatory reserve: ↑ CO, ↑ local blood flow (autoregulation). Erythropoetic reserve: ↑ Hb, ↑ RBC. Chemical reserve: ↑ BPG → ↓ Hb-O2 affinity. Ventilatory reserve: ↑ ventilation.

93
Q

What is the treatment for hypoxia & hypercapnia?

A

Hypoxia & hypercapnia: artificial ventilation. Hypoxia but no hypercapnia: give O2.

94
Q

Why must 100% O2 not be given for too long?

A
  1. Normally, inhaled N2 (75%) is water insoluble, providing volume to keep alveoli inflated even when O2 is transported away by blood. 2. Inhaled 100% O2 can be completely transported away by blood, especially when the patient stops breathing. 3. Dramatic ↓ volume of gas inside alveoli → alveolar collapse. 4. ↑ surface tension with ↓ in alveolar radius worsens collapse.
95
Q

What are the acute effects of high altitude changes?

A

O2 saturation decreases significantly. Hypoxic stimulation of receptors results in hyperventilation. Hyperventilation blows off too much CO2 → respiratory alkalosis. Hypoxia + respiratory alkalosis: drowsiness, headache, fatigue, etc.

96
Q

What is the process of acclimatization to high altitude changes?

A
  1. Within 2-3 days, respiratory centre loses most sensitivity to PCO2 changes, excess ventilatory loss of CO2 no longer inhibits respiration. 2. Low oxygen levels can drive system to much higher ventilation, improving hypoxia. 3. Initial alkalosis corrected by increased renal excretion of bicarbonate and reduced excretion of H+, restoring pH balance, further reducing inhibitory effect of low PCO2 on respiration.

Secondary polycythemia: hypoxia stimulates EPO production in kidneys → ↑ RBC → hematocrit ↑ from 45% to 60%, blood Hb ↑ from 15 to 20 g/dL. Increased 2,3-BPG in RBCs: ↓ RBC affinity for O2, release more O2 to tissues. Increased pulmonary diffusing capacity: capillary expansion & ↑ pulmonary BP → improve V/Q mismatch (especially in upper lung).

97
Q

What is asthma?

A
  1. IgE binding to allergens and mast cell release of histamine, bradykinin, slow-reacting substance of anaphylaxis. 2. Causing: spastic contraction of smooth muscle in bronchioles, edema, secretion of mucus in airway.
98
Q

What is COPD?

A

COPD (chronic obstructive pulmonary disease): emphysema + bronchitis.

Emphysema (excess air in lungs): inhalation of irritants (especially cigarette smoke) → erosion of alveolar walls; destruction of elastic fibres → decreased surface area of alveoli. Chronic bronchitis: thick, abundant mucus accumulation in bronchioles → inflammation of bronchioles → long-term cough.

99
Q

What are the causes of obstructive disease?

A

Asthma, COPD, emphysema, chronic bronchitis.

100
Q

What are the general characteristics of obstructive disease?

A

Air trapping & barrel chest: in inspiration, -ve intrapleural pressure pulls lungs open; in expiration, +ve intrapleural pressure collapses airway. Ventilation defect: mucus plugs narrow airways, increasing resistance and work of respiration, causing hypoventilation. V/Q defect: physiologic shunt develops, air to perfused alveoli blocked by mucus. Diffusion defect: reduced alveolar surface area. Hypoxia: develops due to above.

101
Q

What are the causes of dyspnea?

A

Cardiac cause: pulmonary edema, increased work of breathing (left heart failure, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea). Respiratory cause: hypoxia/hypercapnia (COPD, asthma, cancer, infection, pulmonary embolism). Anemia: caused by hypoxia/hypercapnia. Metabolic acidosis: compensation via hyperventilation. Neuromuscular: eg motor neuron disease, myasthenia gravis affecting diaphragm.

102
Q

What are the differences between obstructive and restrictive disease?

A

Refer to the provided image.

103
Q

What are the types of respiratory failure?

A

Type 1: hypoxemia, PO2 < 60mmHg, PCO2 normal due to hyperventilatory compensation. Type 2: hypoxemia & hypercapnia, PCO2 > 45mmHg, CO2 retention.

104
Q

What are the stages of COPD?

A

Early stage: pink puffers. Late stage: blue bloater.

105
Q

What is early stage COPD and what are its effects?

A

Emphysema predominates, diffusion more problematic than ventilation. O2 exchange more problematic than CO2 exchange as CO2 diffuses faster.

Effects: hypoxemia triggers hyperventilation (hence pink puffers), blow off excess CO2. Type 1 respiratory failure (hypoxemia). Respiratory alkalosis.

106
Q

What is late stage COPD and what are its effects?

A

Bronchitis predominates, hypoventilation and V/Q mismatch more problematic than diffusion. Work of breathing increases significantly, beyond what patient can sustain, patient cannot hyperventilate to compensate.

Effects: Type 2 respiratory failure (hypoxemia & hypercapnia, hence blue bloater). Cyanosis (bluish coloration) & pallor. Respiratory acidosis. Hyperinflated lungs (barrel chest): inspiration easier than expiration as increased intrathoracic pressure collapses alveoli during expiration. Pulmonary hypertension, RHS heart failure, edema: hypoxemia causes pulmonary vasoconstriction.

107
Q

How is obstructive disease treated?

A
  1. Bronchodilators (eg albuterol, β2 adrenergic agonists). 2. Fluids: thin out mucus (cardiac problems contraindicate). 3. Steroids: reduce inflammation & bronchoconstriction. 4. Carbonic anhydrase inhibitors: help treat alkalosis if it does not resolve after treatment of ventilation problem. 5. Mechanical ventilation: for late stage COPD.
108
Q

What caution must be taken with O2 therapy?

A

In patients with type 2 respiratory failure, patients have gotten used to high PCO2, respiratory system driven by PO2. Giving O2 may cause ↓ stimulus to breathe, patient stops breathing.

Similarly, patients must also be weaned off ventilator slowly.

109
Q

What are the causes of restrictive disease?

A

Pulmonary fibrosis, pulmonary edema, atelectasis, pneumonia, tuberculosis.

110
Q

What is pulmonary fibrosis?

A

Replacement of elastic lung tissue by fibrous, non-elastic tissue which does not fill up (TLC, RV ↓). Fibrous tissue resists collapse during expiration, resistance not changed. Exhalation easier, FEV1 decreases less than FVC.

X-ray: reticular, nodular opacities.

111
Q

What is atelectasis?

A

Collapse of alveoli due to obstruction or lack of surfactant. If lung is rigid due to fibrotic tissue, alveoli cannot collapse.

Instead, negative pressure within alveoli causes alveoli to fill completely with edema fluid. Collapse of lung reduces blood flow via pulmonary vessels, most blood routed to ventilated lung, V/Q only moderately compromised.

112
Q

What is pulmonary edema?

A

Interstitium filled with fluid: rigid & less expandable. Edema washes out surfactant: decreasing compliance; causing alveolar collapse.

113
Q

What is pneumonia?

A

Infection of alveoli: consolidation of lung (air replaced by fluid & cellular debris).

114
Q

What is tuberculosis?

A

Infected lesions walled off by fibrous tissue to form tubercle.

  1. Causes fibrosis and reduced functional use. 2. ↑ work of breathing. 3. ↓ VC (vital capacity). 4. ↓ respiratory membrane surface area. 5. ↑ thickness of pleura. 6. V/Q mismatch.
115
Q

What are the general characteristics of restrictive disease?

A

Ventilation defect: hypoventilation due to shallow breaths. V/Q defect: physiologic shunt: perfused alveoli not ventilated due to filling with edema or sealing off by fibrous tissue. Physiologic dead space: if capillaries damaged/sealed off by fibrous tissue. Diffusion defect: thickened alveolar membrane (in fibrosis), edema fluid, cell debris, inflammatory exudate (in pneumonia) act as barriers to diffusion. Hypoxia: develops due to above. Hypercapnia: only in severe fibrosis.

116
Q

How is restrictive disease treated?

A

Short term: O2 therapy can help hypoventilation, diffusion & shunting defects, but not dead space. Pulmonary edema: sit up, encourage gravity to work; avoid vigorous exercise. Hypoxia & hypercapnia: mechanical ventilation.

117
Q

How does pulmonary blood pressure affect blood flow?

A

When capillary pressure < alveolar pressure, capillaries close and no blood flow. During exercise, pulmonary pressure increases, blood flow to all parts of lung increases to zone 3 blood flow.

M1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions