The Respiratory System (2) Flashcards
1
Q
What are some secondary functions of the respiratory system?
A
Regulation of blood pH, speech, defense against pathogens, smell
2
Q
What is the trachea?
A
Trachea is the tube covered by c-shaped bands of cartilage for structural rigidity (to prevent encroachment of oesophagus) .
3
Q
How many secondary bronchi are there in the lungs?
A
There are 3 secondary bronchi in the right lung and 2 on the left.
4
Q
How does pulmonary oedema affect external respiration?
A
Pulmonary oedema is caused by the excessive accumulation of fluid in the lungs, leading to impaired gas exchange; a poor rate of diffusion.
5
Q
What are goblet cells?
A
Goblet cells secrete mucus in the conducting zone to trap foreign particles.
6
Q
What are ciliated cells?
A
Ciliated cells propel the mucus up the glottis to be swallowed or expelled in a process called the mucus escalator.
7
Q
What prevents the collapse of bronchioles, considering their absence of cartilage?
A
Smooth muscle
8
Q
What are the pores of Kohn?
A
The pores of Kohn permit airflow between adjacent alveoli (collateral ventilation).
9
Q
State the 3 types of alveolar cells.
A
Type I, type II and alveolar macrophages
10
Q
What are type I alveolar cells?
A
Type I alveolar cells make up the wall of alveoli, consisting of a single layer of epithelial cells.
11
Q
What are type II alveolar cells?
A
Type II alveolar cells secrete surfactant. Surfactant reduces surface tension in alveolar walls, preventing alveolar collapse.
12
Q
What are alveolar macrophages?
A
Alveolar macrophages remove foreign particles.
13
Q
What surrounds the lungs?
A
The pleural sac
14
Q
State the 3 layers of the pleura.
A
The visceral pleura, the interpleural space, the parietal pleura
15
Q
What difference in pressure drives external respiration?
A
The difference between intra-alveolar pressure and atmospheric pressure drives external respiration.
16
Q
What is the relative pressure of intrapleural pressure?
A
-4mmHg, compared to the 760mmHg of atmospheric pressure.
17
Q
What causes the negative pressure in intrapleural spaces?
A
Negative pressure in intrapleural spaces is due to the elasticity in the lungs and thoracic wall. The lung recoils inward, while the thoracic wall recoils outward, this creates a vacuum, and hence sub-atmospheric pressure. (the surface tension of intrapleural fluid holds the wall and lungs together)
18
Q
What is FRC?
A
FRC is functional residual capacity. This is the volume of air in lungs between breaths, at rest. At this point, intra-alveolar pressure=atmospheric pressure, the volume is about 2.2L.
19
Q
What is pneumothorax?
A
Pneumothorax is a punctured lung. In emergencies, a large-bore needle is inserted into the 2nd intercostal space at the midclavicular line to relieve pressure.
20
Q
What is ventilation?
A
Air flow
21
Q
What are some sources of resistance in air flow?
A
The radius of airways and mucus
22
Q
Define transmural.
A
Across a wall.
23
Q
State the muscles of inspiration.
A
Principal: external, internal, innermost intercostals and diaphragm
Secondary: sternocleidomastoid and scalenus (elevated sternum and ribs respectively)
24
Q
State the muscles of expiration.
A
Passive: recoil of lungs
Active: internal intercostals, rectus abdominis, external oblique, internal oblique, transversus abdominis (depresses ribs).
25
How do type II pneumocytes (alveolar cells) affect the compliance of the lungs during pulmonary ventilation?
Type II pneumocytes produce surfactant to decrease the surface tension of alveoli, increasing the ease of expansion.
26
What is EE?
total Energy Expenditure
27
What COPD?
Chronic obstructive pulmonary disorder, resistance makes it so that EE is 30% dedicated to breathing instead of the typical 3%.
28
State the function of a spirometer?
A spirometer is used to measure the volume and flow of air during inhalation and exhalation.
29
What is the total lung capacity of a healthy young adult male?
5.7L
30
Define pulmonary minute ventilation.
Pulmonary minute ventilation is the total volume of air entering and leaving respiratory system every minute. 6L/min
31
Why is alveolar ventilation less than pulmonary ventilation?
Pertaining to anatomic dead space, air in these areas are left unused by the body. About 150mL of air is useless in this way every breath.
32
State the average alveolar minute ventilation.
4.2L/min
33
What is perfusion?
Blood flow
34
Why is oxygen toxicity dangerous?
Excess concentrations of oxygen in the blood leads to oxygen toxicity because oxygen free radicles form, these are highly reactive particles which damage cell structures.
35
How is perfusion in capillaries surrounding alveoli and ventilation regulated when ventilation is low?
At a low ventilation, CO2 is high, local airway smooth muscle is relaxed, and airways are dilated, ventilation is increased. Due to the low amount of O2, local pulmonary-arteriolar smooth muscle is contracted, increasing vascular resistance, in this way perfusion is redirected to areas in the lung where O2 is more readily available, since perfusion to the lungs is limited. The opposite occurs at a high ventilation.
36
Where is ventilation and perfusion highest, and thus the ventilation-perfusion ratio the lowest?
At the bottom of the lungs
37
What are the 2 classifications of pulmonary disease?
Obstructive: increased airway resistance
Restrictive: Reduced compliance
38
What are some examples of obstructive pulmonary disease?
Emphysema, bronchitis, asthma
39
What are some examples of restrictive pulmonary disease?
Fibrosis, scoliosis, amyotrophic lateral sclerosis (ALS), ankylosing spondylitis
40
What is the FEV1.0/FVC ratio?
The FEV1.0/FVC ratio (forced expiratory volume in 1st second/forced vital capacity) is a pulmonary function test. A normal ratio is above 80%, below is an abnormal result, indicating an obstructive lung disease.
41
What are the characteristics of the different types of obstructive airway disease?
I = airway hyper-reactivity (allergies), mucous thickening, smooth muscle spasms
II = inflammation of airway walls, excessive mucous production
III = irreversible condition, caused by destruction of alveolar walls (by trypsin) and elastic fibers, in essence, excessive lung compliance. Caused by smoking or genetic lack of α anti-trypsin production.
42
Describe the characteristics of diffuse interstitial lung disease.
This disease arises from over 130 disorders, it is caused by reduced elasticity and overall compliance of lungs and thoracic wall. Increased work of breathing. Weight loss may be presented in patients. In 66% of cases, there is no known cause.
43
State Fick's law.
V(gas)=A/T × D⋅(ΔP)
V(gas)=rate of diffusion
A=surface area in lung
T=thickness of alveolar wall
D=diffusion constant
S=gas solubility
MW=molecular weight
D is directly proportional to S/(MW)^0.5
44
Compare the diffusion rates of CO2 and O2.
CO2's diffusion rate is 2 times that of O2.
45
How long does blood spend in the alveolar capillaries (how much time is allowed for gas exchange)?
At rest 0.75s is allowed, during physical activity, this can be as little as 0.25s, which is the duration required for normal equilibration.
46
What is pulmonary oedema? State its causes and treatment.
Pulmonary oedema is the accumulation of fluid in interstitial spaces or alveoli, it is a restrictive respiratory disease. It impairs diffusion and increases work of breathing.
It may be caused by left heart failure, where fluid accumulates in capillaries, increasing capillary pressure, resulting in fluid leakage to the lungs. Also at high altitudes, the same can occur due to pulmonary vasodilation. It is treated by administering O2 and diuretics.
47
Define diuresis.
Diuresis is the increased production and excretion of urine.
48
Define tidal volume.
Tidal volume is the amount of air inhaled or exhaled in a normal breath.
49
What expiratory reserve volume?
ERV is the approximate 1.2L of air remaining in the lungs after tidal volume is exhaled, this is to prevent alveolar collapse.
50
What is residual volume?
RV is the volume of gas left in the respiratory system after exhaling maximally.
51
What is vital capacity?
VC is a measure of the maximum volume of gas in the respiratory system that can be exchanged with each breath.
52
In what form do blood gases contribute to circulating partial pressures?
Blood gases only contribute to circulating partial pressures when dissolved.
53
How much O2 is in the blood? In what states?
PaO2 = 100mmHg, for a total of 200 mLO2.L^-1
1.5% in plasma and 98.5% bound to Hb.
54
In what state is CO2 transported in the blood?
10% dissolved, 30% bound to Hg, 60% as HCO3-
55
Describe the reaction between CO2 and H2O.
CO2 + H2O =(carbonic anhydrase) H2CO3 + H+ + HCO3-
56
Define hypoxia.
The state of insufficient cellular O2.
57
Define haemoglobin saturation.
Hemoglobin saturation (SpO2/SaO2) refers to the percentage of hemoglobin binding sites occupied by oxygen in the blood.
58
State the cause and symptoms of hypoxic hypoxia.
Causes: low PaO2 (hypoxemia), leading to a low % Hb saturation, leading to inadequate gas exchange, occurs at low pressures (high altitudes)
Symptoms: cyanosis, <70%SaO2
59
State the cause and symptoms of anaemic hypoxia.
Causes: low total blood O2 content, normal PaO2, low circulating RBCs, low RBC Hb content, CO poisoning (24 times more affinity than O2)
Symptoms: HbCO causes pale, pink skin
60
State the cause and symptoms of circulatory hypoxia.
Causes: low supply of oxygenated blood, normal O2 content, normal PaO2
Symptoms: vessel blockage, congestive heart failure
61
State the cause and symptoms of histotoxic hypoxia.
Causes: O2 delivery to tissues is normal, but cells are unable to use it
Symptoms: cyanide poisoning (blocks enzymes for respiration)
62
Define hyperoxia.
Hyperoxia is above-normal arterial O2, O2 toxicity
63
What is the effect of hyperoxia on a healthy person?
No major effect
64
What is the effect of hyperoxia on a diseased person?
At a high PaO2, hyperoxia is dangerous as increased dissolved O2 can damage brain (causing blindness)
When dissolved O2 is the main driver of ventilation, decreased peripheral chemoreceptor sensitivity is risked.
65
Describe the characteristics of hypercapnia.
Hypercapnia is characterised by excess PaCO2. Occurs due to hypoventilation. Occurs with most lung diseases. Occurs in conjunction with PaO2.
66
Describe the characteristics of hypocapnia.
Hypocapnia is characterised by decreased PaCO2. Occurs due to hyperventilation. Occurs due to anxiety and fear. It does not have an affect on PaO2. May occur due to hyperpnea.
67
Define hyperpnea.
Hyperpnea is increased ventilation to match metabolic demand.
68
What are the respiratory control centers in the brain stem, and what do they consist of?
The pons respiratory center consists of the pneumotaxic center and apneustic center.
The medullary respiratory center consists of the dorsal and ventral respiratory group.
69
How do chemoreceptors control external respiration?
Chemoreceptors detect changes in PO2 and PCO2.
70
How do pulmonary stretch receptors control external respiration?
Pulmonary stretch receptors using the Hering-Breuer reflex. They sense the inflation and deflation of the lungs.
71
How do irritant receptors control external respiration?
Irritant receptors detect dust and pollutants to trigger coughing/sneezing.
72
Localise the peripheral chemoreceptors.
Carotid bodies (near baroreceptors in carotid sinus) and aortic bodies (on aortic arch)
73
State the function of the peripheral chemoreceptors.
Peripheral chemoreceptors respond to low PaO2 (<60mmHg). They also respond to high PaCO2 and H+. Aortic bodies rarely respond to low total arterial O2 content, which is important in anaemia and CO poisoning.
Peripheral chemoreceptors provide around 20% of respiratory drive.
74
Localise the central chemoreceptors.
Medulla
75
State the function of central chemoreceptors.
Central chemoreceptors respond to H+ in the CSF, which is derived from PaCO2, this is because circulating H+ can not cross the blood brain barrier. This provides 80% of respiratory drive.
76
Define alkalosis.
Alkalosis is characterized by the buildup of excessive alkali in the body.
77
How is external respiration adapted at high altitudes (low Pa)?
Hyperventilation due to low PaO2 acting on carotid body peripheral chemorecptors.
78
What can hyperventilation result in?
Hyperventilation may result in respiratory alkalosis, as when CO2 clearance increases, blood pH increases.
79
What preventative measures does the body take against alkalosis?
To prevent alkalosis, the kidneys excrete HCO3- ions, more acid remains in the blood and alkalosis is reversed. pH comes to be normal within 3 days.
80
Why may ventilation occur after alkalosis is prevented after hyperventilation?
It is likely due to an increased sensitivity of the carotid bodies to PaO2.
81
Define polycythaemia (erythrocytosis).
Polycythaemia is characterised by a high concentration of RBCs (and Hb) in the blood.
82
What does erythropoietin stimulate?
Erythropoietin stimulates RBC production in the bone marrow.
83
What are the consequences of polycythaemia?
Hypoxemia at high altitude stimulates the kidneys to release erythropoietin (EPO) after approximately 8 hours. EPO stimulates reticulocyte maturation and release as well as erythropoiesis. So, despite low PaO2 and Hb saturation (due to O2-Hb dissociation curve), O2 content may be normal or elevated.
It does however cause elevated blood viscosity, increasing cardiac work and hypertrophy, which leads to uneven blood flow distribution.
84
How do altitude adaptations affect levels of 2,3-bisphosphoglycerate?
Increased 2,3-BPG is seen.
85
Why do endothelial cells release up to 10 times more NO in persons habituated in high altitudes?
NO release is a compensatory response to hypoxia, it induces vasodilation. This is because endothelia nitric oxide synthase (eNOS) is upregulated.
86
What are some acute symptoms of altitude sickness?
Headaches, loss of appetite, nausea, insomnia, vomiting, dyspnea. Begins around 6 hours on arrival and severity is maximised on day 2/3. It is exacerbated at night.
87
Why may pulmonary/cerebral oedema occur at high altitudes?
It is caused by hypoxia-induced pulmonary vasoconstriction, leading to increased capillary permeability and high-protein fluid leakage into the lungs. Fluid accumulation may occur in the cranial cavity. Its symptoms are determined because cyanosis, ataxia, confusion, loss of consciousness and severe headache ensue.
88
What are some problems with respiration at depth (underwater)?
Gas cavities in the lung and middle ear are compressed with descent and may over-expand with ascent. Gas solubility =(dp) partial pressure, leading to excess gas absorption.
89
What is narcosis?
Narcosis is a state of stupor.
90
What is decompression sickness caused by?
During rapid ascent, Pb falls. N2 becomes less soluble and is brought out of solution, bubbles are formed. Gas embolus may lead to tissue ischaemia (avascular necrosis). At the myelin sheath, nerve conduction is impaired, dizziness/paralysis ensues. Lung tissue rupture. Deafness. Painful joints.
91
What are methods for prevention of decompression sickness?
Slow ascent, N2 replacement by He, exhalation during ascent. May be treated by recompression.
92
Define the 2 ventilatory thresholds.
VT1 occurs at a work-rate of 140W and a VO2 of 2.1 Lmin^-1. This is the commencement of the lactate threshold. VT2 occurs at 260W and 3.4 Lmin^-1 respectively.
93
What are factors that affect the ventilatory response to exercise?
Reflexes originating from body movements, epinephrine release, body temperature, impulses from cerebral cortex (voluntary).
