Lecture 4: Respiratory Flashcards
(134 cards)
1
Q
What is the difference between respiration and ventilation?
A
Ventilation is the movement of air in and out of the lungs.
Respiration is the exchange of gases.
2
Q
What is the ventilation perfusion ratio? Where is it high and low?
A
It is the ratio of alveolar ventilation relative to pulmonary blood flow.
Starting from the top of the lungs, it is high, at 2.1.
In the middle, it goes to 1.
At the bottom of the lungs, it goes to 0.3.
3
Q
When is the work of breathing? Inspiration or expiration?
A
Inspiration.
4
Q
What are the two mechanisms that expand and contract our lungs?
A
Movement of the ribcage using the intercostal muscles. (elevation and depression of the ribs to increase and decrease anterposterior diameter of the chest cavity)
Contraction and relaxation of the diaphragm to adjust the chest cavity volume. (- to lengthen or shorten the chest cavity)
5
Q
What is the key limiting factor for all people in terms of exercise?
A
It is our cardiometabolic limits, not our lungs.
6
Q
During NORMAL expiration, what occurs?
A
Relaxation of the diaphragm.
Elastic recoil of both the lungs and chest wall.
7
Q
During HEAVY expiration, what occurs?
A
Relaxation of the diaphragm.
Use of abdominal & intercostal muscles.
8
Q
During HEAVY inspiration, what occurs?
A
Contraction of the diaphragm.
Use of external intercostals, sternocleidomastoid, anterior serrati, and scaleni muscles.
9
Q
What king of pressure does inspiration generate? What pressure are our lungs at relative to the environment?
A
Negative pressure. Air is sucked into our lungs because the pressure INSIDE is LOWER than outside.
Inside pressure is 754mm Hg usually.
10
Q
Why do people with lung disease seem more tired?
A
Breathing is energy intensive.
11
Q
describe a lung
A
elastic structure that collapses like a balloon and expels all its air through the trachea whenever there is no force to keep it inflated.
12
Q
Where is the lung attached to the chest wall?
A
At the hilum from the mediastinum.
13
Q
Which parietal surface is found directly on the lungs?
A
Visceral pleural surface lining.
14
Q
Which pleural surface is found on the thoracic cavity?
A
Parietal pleural surface lining.
15
Q
What maintains the suction between the two pleural surfaces?
A
pleural fluid, which is continually suctioned into the lymphatic channels. It helps create a seal, similar to a drop of water between two glass surfaces.
16
Q
What does pleural pressure usually measure at?
A
-5 to -7.5 cm H2O.
17
Q
when does alveolar pressure = 0
A
when the epiglottis is open (no airflow)
18
Q
During inspiration, what occurs to alveolar pressure?
A
It falls by approximately 1cm H2O.
19
Q
What does the change in alveolar pressure during inspiration cause?
A
Negative pressure, usually sucking in 500 mL of air into the lungs, AKA our tidal volume.
20
Q
During expiration, what occurs to alveolar pressure?
A
It increases by approximately 1cm H2O back to its original pressure.
21
Q
What is trans-pulmonary pressure? How do I measure it?
A
Difference between alveolar pressure and pleural pressure.
22
Q
What is recoil pressure? what is it equal to?
A
It is a measure of the elastic forces in our lungs that collapse our lungs at the end of inspiration. equal to trans-pulmonary pressure.
23
Q
What two fibers make up the elasticity of our lung?
A
Elastin and Collagen.
24
Q
where are collagen and elastin and what state are they in
A
they are interwoven among the lung parenchyma (thin wall of alveoli). and they are in a kinked, elastically contracted state.
25
What happens to our lung fibers as our lung expands?
They start stretching and unkinking, exerting the elastic force that makes expiration easy relative to inspiration.
26
What does poor lung compliance mean?
It means our lungs are stiff, so it requires more effort INSPIRING to generate the elastic force that makes expiration easy.
In other words, people with poor lung compliance have difficulty INSPIRING.
27
What two mechanisms determine our lung's elastic force?
The lung fibers themselves (elastin and collagen)
Surface tension within the alveoli.
28
Which mechanism generates most of the elastic recoil in expiration?
Surface tension = 2/3.
The elastic force due to tissues (elastin and collagen) are responsible for only 1/3.
29
Why do we care that alveolar fluid interacts with air instead of more water?
The surface tension is generated when air meets water. The water has a stronger attraction for other water molecules if it meets air.
30
describe the difference between a saline filled lung and a air filled lung
saline filled will have :
- no air-water interference
- no surface tension
- only elastic forces at work
- very little transplural pressure required to expand
-3x force needed to exapnd the air filled lung
31
Clinical Question: What is a pneumothorax and the two kinds?
Pneumothorax: Collection of air in the chest OUTSIDE of the lung, causing lung collapse.
Primary pneumothorax: Occurs without apparent cause in the absence of lung disease.
Secondary pneumothorax: Occurs in the presence of existing lung pathology.
Special: A tension pneumothorax is created via one-way valves made from an area of damaged tissue, so the lungs slowly get squeezed. Leads to decreasing spo2 and low BP.
32
What makes surfactant in the lungs? What is surfactant?
Type II alveolar epithelial cells.
Surfactant is an agent that reduces the surface tension of water.
Note: laundry detergent is also a type of surfactant.
33
When do babies start making surfactant?
6-7 months of gestation, or 24-28 week which is when their type II alveolar epithelial cells develop.
Note: A baby's lungs are usually fully developed around 32-36 weeks.
34
What is the key differences between a restrictive lung disease and an obstructive lung disease?
Restrictive lung diseases show reductions in all lung capacity measurements, such as VC, FRC, TLC, and FVC.
Obstructive lung diseases show a marked decrease in the ability to expire.
35
Name some restrictive lung diseases.
Idiopathic pulmonary fibrosis (IPF)
Non-specific interstitial pneumonia (NSIP)
Cryptogenic organizing pneumonia (COP)
Sarcoidosis
Acute interstitial pneumonia (AIP)
36
Name some common obstructive lung diseases.
Emphysema
Asthma
Chronic bronchitis
Note: COPD refers to most of the obstructive diseases. Also, these are all NON-reversable.
37
What disease do I commonly see barrel chest in?
Emphysema
38
What is the average tidal volume? (In terms of what we learned class-wise)
500 mL
39
What do capacity measurements include that reserve volumes do not for lung measurements?
Any reserve volume measurement does NOT include tidal volume.
Any capacity is a combination of 2 or more things.
Example: Functional vital capacity is the addition of Inspiratory reserve volume (IRV) + Tidal Volume (TV) + Expiratory reserve volume (ERV)
40
What is minute ventilation? The normal average?
The volume of air we breathe in one minute.
It is normally 6L, which is 12 breaths/min X 500 mL/breath. AKA breathing rate x tidal volume.
41
How much dead space is in our tidal volume?
150mL
42
What two things make up dead space?
Anatomic dead space and physiologic dead space.
Anatomic dead space = trachea and the parts of the airway that are not alveoli. (very tippy top of lungs, no alveoli)
Physiologic dead space = the parts of the alveoli that have bad perfusion. (well ventilated but poorly perfused)
43
What is the main disadvantage with shallow breathing relative to minute ventilation?
Overventilation of the dead space.
Shallow breathing with high respiratory rate commonly does not exceed the dead space, since our tidal volume is decreased per breath.
44
What are the main disadvantages with deep breathing in regards to minute ventilation?
Tiring of the intercostal muscles.
Inadequate exhalation of CO2.
45
How do we measure alveolar minute ventilation?
It is the difference between our total minute ventilation and our dead space minute ventilation.
46
Clinical: How do we check if someone has an obstructive lung disease? What do we measure, and at what point is it clinically significant?
We measure FEV1/FVC, which is the forced expiratory volume in 1 second divided by the functional vital capacity. In other words, it is how much I can exhale in a single second relative to my total lung capacity - the dead space in my lungs.
Example: My Predicted FEV1 is 4L. My actual FEV1 is 3L. I would say that I am at 75% of predicted.
Ideally, we want 80%, but if you go down to 60%, then we consider that concerning.
Note: Asthma is one of the few reversible lung diseases, whereas chronic ones are not.
47
What kind of rings does my trachea have? Why?
Cartilage, to help prevent collapse.
48
What is a key difference between my bronchi and trachea?
My bronchi have LESS cartilage, therefore they can expand and contract more.
49
What keeps my bronchioles expanded?
Rigidity of their walls + transplumonary pressure. This is the same pressure that also keeps alveoli expanded.
50
Why are bronchi and bronchioles the site of narrowing in obstructive lung diseases?
They are mainly made of smooth muscle, which contracts. The obstructive lung diseases can cause excessive contraction.
51
When does the conducting zone end?
After the 16th division within the bronchioles.
52
When does the respiratory zone begin?
At the 17th division within the bronchioles, where alveoli start appearing on the bronchioles.
53
Clinical: What is significant about the respiratory zone in regards to particulates?
Air moves very slowly in this zone, so particulates tend to just settle here and stay. This is the reason things like coal dust or asbestos can cause gradual lung symptoms.
54
Where is the resistance to air flow the greatest?
Large bronchioles and bronchi.
55
What contributes to air flow resistance the most when we are diseased?
Smaller bronchioles contribute the most because they are easily occluded by muscle contractions in their wall or edema in their walls or mucus in their lumens.
56
What does sympathetic stimulation of the lungs cause? Main NT responsible?
Bronchial dilation via both NE and epi but MAINLY epi.
Note: Epi has greater stimulation of BETA adrenergic receptors. In case it gets confusing, we use epi pens when someone has anaphylaxis, not norepi. Epi will dilate our lungs, whereas norepi will not.
57
What does parasympathetic stimulation of the lungs cause? Main NT responsible?
Bronchial constriction via Ach, which cause mild to moderate constriction, but if someone has constriction already, it can worsen it.
Note: We use atropine to block Ach in these sorts of cases.
58
What kind of cells line our airways that are involved in inflammation? What do they release and when?
Mast cells.
Releases histamine and SRS-A (slow reacting substance of anaphylaxis, aka a trio of leukotrienes!)
They release these in allergies, pollen, allergic asthma, sudden cooling/drying of the airways.
59
What is the pulmonary circulation that contains oxygenated blood?
It is the high pressure, low flow circulation originating from the aorta. Supplies the lungs with blood via the bronchial arteries off the thoracic aorta.
Note: Less pressure than aortic pressure.
60
How does blood from the lungs reenter the heart? Where does it reenter?
Blood from the lungs to the heart via the pulmonary veins, which enter at the left atrium.
61
What is the pulmonary circulation that contains deoxygenated blood?
It is the low pressure, high flow circulation originating from the pulmonary artery heading to the lungs. Deoxygenated blood goes via the pulmonary artery to the arterial branches to the alveolar capillaries, where CO2 is removed and O2 is added. It then goes to the pulmonary veins back to the left atrium.
62
Describe the location of the pulmonary artery.
5cm beyond the base of the RV, sitting under the arch of the aorta.
63
Describe the characteristics of the pulmonary artery.
It bifurcates to supply blood to both lungs.
It is much THINNER than the aorta, only 1/3 thickness.
It has very short arterial branches.
It has large diameters but a thin wall, giving it very large compliance and the ability to accommodate the stroke volume of the RV.
64
What are the usual pulmonary systolic and diastolic pressures for the pulmonary artery?
Remember that the pulmonary artery is low pressure, high flow.
Systolic = 25 mm Hg
Diastolic = 8 mm Hg
Our lungs must receive the same amount of blood as our entire body in the same amount of time, so they need to flow faster.
65
Describe the process to measure pulmonary pressure.
Pulmonary Capillary Wedge pressure is measured via insertion of a swan-ganz catheter into a peripheral vein, going to the RA, then the RV, then the pulmonary artery.
66
What does elevated PCWP or diastolic pulmonary artery pressure indicative of?
Pulmonary edema when it is > 20 mm Hg (Normal is 8mm Hg)
It is also highly suggestive of left-sided heart failure.
67
What is the difference between perfusion and ventilation?
Perfusion = the amount of blood going through the lungs.
Ventilation = the amount of air going through the lungs.
68
For hydrostatic pressures, where is it greatest and lowest in my lungs?
Pulmonary arterial pressure is greatest at the bottom of the lungs. There is more blood at the bottom of the lungs, similar to more water at the bottom of a glass, not at the top. It is typically 8 mm Hg GREATER than the PAP at the level of the heart.
PAP is lowest at the top of the lungs. It is typically 15 mm Hg LOWER than the PAP at the level of the heart.
69
What are the 3 zones of blood distribution in my lungs at rest? Describe their blood flows.
Superior to Inferior:
Zone 1: no blood flow during the cardiac cycle.
Zone 2: Intermittent blood flow only during systole of pulmonary arterial pressure.
Zone 3: Continuous blood flow because capillary pressure > alveolar air pressure.
70
How does zone 2 of my lung adapt during exercise from rest?
Because blood flow to my lungs increases 7-8x, the zone 2 distribution converts to zone 3, which has continuous blood flow.
71
Why does pulmonary artery pressure only marginally increase during exercise?
Even with increased CO (cardiac output), the PA pressure only increases a little because:
Our body opens 3x more capillaries
Each capillary gets distended to increase blood flow 2x
72
What forces contribute to fluid leaking out of a capillary?
Inside: Hydrostatic (+7)
Outside: Interstitial colloid osmotic pressure (-14)
Negative interstitial fluid pressure (-8)
AKA 29 mm Hg outward force.
73
What forces contribute to fluid staying inside of a capillary?
Inside: Plasma colloid osmotic pressure (-28)
AKA 28 mm Hg inward force.
74
Does fluid flow in or out of a capillary normally? What system captures it if it flows out?
Slight pressure of 1 mm Hg forcing fluid out.
Our lymphatic system normally collects the fluid.
75
What two factors cause pulmonary edema?
Any factor that increases fluid filtration OUT of the capillaries.
Any factor that impedes pulmonary lymphatic drainage.
AKA what fills up my lungs with fluid and what prevents me from draining the fluid.
76
What are the MCCs of pulmonary edema?
Increased pulmonary venous pressure.
Increased pulmonary capillary pressure (Left-sided heart failure and mitral valve disease)
Damage to pulmonary capillaries (pneumonia)
Breathing in noxious substances (chlorine or sulfur dioxide gas)
77
What factors does diffusion of a gas depend on?
Solubility of gas in fluid.
Cross-sectional area of fluid.
Distance
Weight (constant)
temperature (constant)
78
What is the Rate of Gas Diffusion formula?
Diffusion is proportional to (deltaP x A x S)/d x sqrt(MW)
delta P = partial pressure difference between two ends of the diffusion.
A = cross sectional area
S = solubility
d = distance of diffusion
MW = molecular weight of gas (constant)
79
What has a higher diffusion coefficient than oxygen?
Carbon dioxide (20x greater)
80
What is the major limitation of the movement of gases?
Tissue water!
81
How do we increase our oxygen diffusing capacity?
Open up dormant capillaries
Dilate existing capillaries
This results in increased SA for our blood to interact, so our V/Q ratio is matched better.
82
What affects the thickness of our membranes for gas diffusion?
fibrosis
83
What affects the surface area of our membranes for gas diffusion?
Lung removal
Coalesence of alveoli (aka they clump together)
Fluid in the interstitial space
84
When is PCO2 40 mm Hg and 46 mm Hg?
How is it related to the changes in PO2?
Starting at the alveoli, it begins at 40 mm Hg, stays the same as it goes through the arterial blood vessels to the skeletal muscles. At the skeletal muscles, it goes up to 46 mm Hg, and stays at 46 mm Hg until it gets back to the alveoli.
Note: the partial pressure of oxygen follows the same steps and changes from 100 mm Hg to 40 mm Hg at the muscle. You can imagine that the partial pressure of CO2 must increase since muscles use up oxygen and release CO2. At the same point, using up oxygen results in a lower PO2.
85
Why does PO2 change much more than PCO2?
The solubility of CO2 is much higher than O2, so it needs less of a pressure change.
86
What is a physiologic shunt? When/where does it occur?
It is when VA/Q is below normal.
This implies inadequate ventilation, since VA is low.
This is a result of some venous blood going to the capillaries before it gets oxygenated.
This occurs at rest at the bottom of the lungs. This is due to air not reaching the bottom of the lung.
Note: Disappears during exercise.
87
What is physiologic dead space? When/where does it occur?
It is when VA/Q is greater than normal.
It implies wasted ventilation, since VA is way too high.
This is a result of more oxygen available than venous blood to absorb it.
This occurs at rest at the top of the lungs. This is due to having insufficient blood to match the amount of oxygen present.
Note: Disappears during exercise.
88
What kind of disease cause physiologic shunts in our lungs? What is the physiological basis?
Obstructive diseases, such as COPD, Bronchial obstruction due to smoking/emphysema, and emphysema.
Because our bronchioles are obstructed, everything past it is unventilated. This means VA is extremely low, so VA/Q is below normal.
89
What can cause a physiologic dead space in our lungs?
Destruction of alveolar walls but ventilation still occurs. This means we have wasted ventilation since VA is still normal, but Q (perfusion) drops a lot because there is no blood flow with broken walls.
90
How much of our tidal volume does physiologic dead space make up during rest? During exercise?
1/3 at rest (aka around 150 mL)
1/5 at exercise (aka still around 150 mL), but our tidal volume goes to about 1L instead of 500 mL)
91
When is our dead space to tidal volume ratio the lowest? What does this imply?
It is lowest at exercise, which is when alveolar ventilation (VA) is uniform to perfusion (Q). AKA when VA/Q is uniform.
92
Would I expect a large or small V/Q mismatch in people with lung disease?
I would expect high, because their dead space to tidal volume ratio is increased at rest and cant decrease when exercising.
AKA they probably have bad bronchioles that increase the dead space, and they cant breathe as much because their lungs are stiff.
93
What is the common Alveolar - arterial pressure difference?
5 - 10 mm Hg
94
What changes in alveolar and arterial pressures would I expect in someone with airway disease?
Reduced PaO2 (Reduced partial pressure of oxygen in arteries)
Increased P(A-a)O2, so either an increase in alveolar pressure or a reduction in arterial pressure or both.
Note: Scar tissue increases arterial pressure (a)
Chest wall damage increases alveolar pressure (A)
95
If I have inefficient gas exchange, do I need to ventilate more or less to get rid of CO2?
More.
96
How does PO2 change in my blood going from a pulmonary artery to a pulmonary vein?
It goes from 40 mm Hg to 104 mm Hg as it gets oxygenated.
97
Describe the change in PO2 in my blood beginning at my systemic venous blood all the way back to my systemic venous blood.
Systemic venous blood enters my pulmonary capillaries to get refilled with oxygen, going from 40 mm Hg to 104 mm Hg.
From the pulmonary capillaries, it gets mixed with some pulmonary shunt blood to get to 100 mm Hg as it enters the systemic arterial blood.
As the systemic arteries distribute blood to my systemic capillaries, my organs take the oxygen, bringing my PO2 back down to 40 mm Hg. The blood then enters my systemic venous blood again.
Repeat!
98
If my cells need more oxygen than normal, what change would I expect in my PO2?
It would decrease even more, since oxygen is being used up.
99
What is tissue PO2 a balance between?
The rate of O2 getting to my tissues.
The rate at which O2 is being used by my tissues.
100
Based on the oxygen dissociation curve, when does hemeglobin have the worst affinity for oxygen?
At extremely low pressures and saturations, which is right when it leaves my tissues that just used up all the O2.
101
Based on the oxygen dissociation curve, what is the hemeglobin saturation, approximate PO2 and O2 carrying capacity of venous blood?
75% saturation.
40 mm Hg PO2.
15% carrying capacity.
102
Based on the oxygen dissociation curve, what is the hemeglobin saturation, approximate PO2 and O2 carrying capacity of arterial blood?
90-100% saturation.
80-120 mm Hg PO2.
18-20% carrying capacity.
103
What is O2 carrying capacity?
The measure of how much oxygen blood can carry. It is dependent on hemoglobin.
At max, you can carry around 20 mL O2/ 100 mL blood.
104
What is the typical a-VO2 difference in blood?
5 mL/100 mL blood
105
What shifts an oxygen dissociation curve to the right?
Lower pH, which is caused by:
Increased hydrogen ions
Increased CO2
Increased temperature
Increased BPG (molecule that intereferes with hemeglobin affinity)
106
What is CO2 mainly transported as in the blood?
Bicarbonate, HCO3-
107
What is a chloride shift?
It is when chloride enters a blood cell as bicarbonate leaves it.
108
What enzyme converts carbon dioxide and water to carbonic acid?
Carbonic anhydrase
109
What is the general equation for bicarbonate?
H2O + CO2 <=> H2CO3 <=> H+ + HCO3-
110
Do we have a lot of hydrogen ions in our blood?
No. We have a pH of 7.4, so we have like 0.0000004 for the concentration.
111
What is an acid? A Base?
Acids are ions or molecules that liberate/produce an H+.
Bases are ions or molecules that absorb/accept an H+.
112
What does it mean when an acid is strong?
Highly likely to dissociate their H+, aka HCl becomes H+ and Cl- very easily.
113
What pH range is alkalotic vs acidotic?
Alkalosis = > 7.4
Normal = 7.4
Acidosis < 7.4
114
What 3 things regulate our pH?
Chemical acid-base buffer systems of body fluids.
Respiratory regulation of acid base balance.
Renal control of acid-base balance.
115
What is the most important buffer in the chemical acid-base system?
Bicarbonate, which is a base that can accept a hydrogen ion.
116
If I add acid to the blood, which way does the equation shift?
To the left, away from bicarbonate and towards water and CO2.
117
If I increase [HCO3-] in the blood, what happens to pH?
Increased pH, towards alkalosis.
Bicarb is a base, so we become more basic.
118
What regulates [HCO3-]?
Kidneys
119
What regulates PCO2?
Lungs via respiration.
120
Define metabolic acidosis and alkalosis.
Metabolic acidosis is caused primarily by a DECREASE in [HCO3-]
Metabolic alkalosis is caused primarily by an INCREASE in [HCO3-]
121
Define respiratory acidosis and alkalosis.
Respiratory acidosis is caused by an INCREASE in PCO2.
Respiratory alkalosis is caused by a DECREASE in PCO2.
122
What are the other buffer systems of the blood?
Phosphate and Hemoglobin, which both function as bases also.
123
How do the lungs affect blood pH?
We can ventilate more, which will increase how much CO2 we breathe out. Eliminating CO2 also eliminates H+.
124
How do the kidneys affect blood pH?
The kidneys control how much [HCO3-] we excrete. By excreting it, we lower the amount of base in our blood, so we lower the pH.
The kidneys also control how much H+ is secreted, so the more H+ we secrete, the more acid we secrete.
125
What are some conditions/diseases that can affect blood pH?
Any disease that affects our respiration or kidney absorption of H+/excretion of [HCO3-].
Common examples:
Respiratory obstructions, pneumonia, emphysema, COPD.
126
How do we compensate for respiratory acidosis?
Metabolically, aka we use our buffers and our kidneys to reduce our [HCO3-] excretion.
127
What are some causes of respiratory alkalosis?
Psychoneurosis and high altitudes.
Both cause us to breathe more.
Note: respiratory alkalosis is not very common.
128
What is metabolic acidosis? Causes?
All other types of acidosis besides those caused by excess CO2 in the blood.
Causes:
Chronic renal failure
Diarrhea
Diabetes Mellitus
Ingesting acids (methyl alcohol => formic acid, acetylsalicyclics aka aspirin)
129
What are the 4 physiological phenomena that cause metabolic acidosis?
Failure of the kidneys to excrete metabolic acids.
Formation of excess metabolic acids.
Addition of metabolic acids via ingestion/infusion.
Loss of base from body fluids.
130
What are the causes of metabolic alkalosis?
Administration of any diuretic besides a carbonic anhydrase inhibitor.
Excess aldosterone: Extensive Na+ reabsorption
Vomiting of gastric contents: Usually causes net loss of acid.
Ingestion of alkaline drugs (such as sodium biarb)
131
What kind of graph helps us visualize metabolic vs respiratory corrections?
PCO2 Isobar graph or davenport diagram.
132
What are the steps to determinge metabolic/respiratory acidosis/alkalosis?
Determine current pH to determine acidosis vs alkalosis.
Determine if [HCO3-] is high or lower, as well for PCO2.
Whichever one matches the current pH state, the compensation would be the opposite.
133
Where is the cardiorespiratory center of the brain
Medulla Oblongata.
134
Where are the 3 major groups of neurons for acid/base?
Dorsal respiratory group next to the medulla.
Ventral respiratory group next to the medulla.
Pneuotaxic.
