Glossary of Ch31 Pathophysiology Respiratory

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How many lungs do people have?

Questions will get much harder!
What is the point called where the trachea divides into the 2 main bronchi?
Which bronchus is more vertical?
the right bronchus
Gas exchange airways are made collectively called what?
Acini (acinus)
Respiratory bronchioles begin at aprox what level of segmental division?
The primary gas exchange unit of the resp system is what?
What is the purpose of surfactant?
It decreases surface tension in the alveoli, decreasing the risk of collapse.
What percent of the alveoli are perfused at any given point in time?
33% Lots of areas are NOT perfused normally and this is gravity dependent.
Which portion of the pleura lines the LUNG tissue?
Alveolar ventilation can be assessed by noting a pt's respiratory rate, pattern, and effort?
True or False.
False. You can't tell whats going on in the alveoli without an ABG.
Where is control of respiration managed?
In the brain stem.
Parasympathetic stimulation of the airways causes what response?
PNS causes airway constriction.
Sympathetic stimulation of the airways causes what airway response?
SNS causes airway dilation. We like that!
Histamine, serotonin, & prostaglandins stimulate what type of receptors in the airways?
Irritant receptors: located in the epithelium of the CONDUCTING airways. Sensitive to noxious stimuli and endogenous substances. There are no irritant receptors in the smaller, distal airways!
Hyperventilating can stimulate WHICH lung receptors to have WHAT effect?
Stretch receptors in the smooth muscle of the bronchi are stimulated with increased vent rate/volume and cause a reflexive decrease in rate/vol. (Hering-Breuer expiratory reflex: we probably don't need to know that name specifically).
How do central chemoreceptors monitor ventilation?
Via pH of the CSF. CO2 diffuses into the CSF and combines with H20 to form carbonic acid. This lowers the pH and stimulates the brain stem to increase rate/depth of breathing.
Which has a greater effect on respiratory rate? Hypoxia or hypercarbia? Why?
Normally, the answer is hypercarbia. CO2 crosses into brain and drops CSF pH causing increased rate/depth of breathing.
Explain why COPDers don't chronically hyperventilate.
In chronic hypercarbia, the pH sensitive central chemoreceptors become insensitive to small changes in pH. This is also affected by renal HCO3 compensation for the acidosis, which crosses blood brain barrier and increases the pH, also lessening the respiratory compensation.
Where are the peripheral chemoreceptors that support respiration? How do they work?
Aortic bodies, the aortic arch, and carotid bodies near bifurcation of carotids. These are sensitive to both pH AND pao2 (primarily pao2). Drops is pao2 cause increased rate/depth of breathing. This can be magnified if pt is hypercarbic. This system is much less sensitive to changes in pao2 then the central receptors are to change in pH. These have a lesser influence on respiration in normal people but in co2 retainers(copd) this becomes the primary respiratory drive.
Surfactant has what effect on Laplace's Law?
It reverses the effect: with decreased radius, surface tension decreases. This keeps alveoli open.
Explain distribution of ventilation and perfusion in an upright (standing) pt.
Ventilation and perfusion are greatest in the lower lobes of the lungs (lower 1/3 of lungs). The upper airway alveoli are larger and have greater residual volume therefore decreased ventilatory compliance. The upper vasculature has lower blood pressure due to gravity and is not well perfused. The opposite is true in the bases which is why they have the best V & Q.
What is a normal V/Q ratio?
What is a deadspace unit?
Give an example of a cause of this?
How is the V/Q ratio affected?
Deadspace unit is good ventilation (V) but poor perfusion (Q). Cardiogenic shock or a nice sized PE will do this--knocks out Q to a section of the alveoli. This will have a VQ ratio of >0.8 (greater than).
What is pulmonary shunting? What disease could cause this? How is the VQ ratio affected?
Shunting occurs when there is good perfusion but poor ventilation. Pneumonia or large scale alveolar collapse could cause this. As could dropping an ETT down into one bronchus and not ventilating an entire lung. This causes the VQ ratio to be <0.8
Why is the alveocapillary membrane ideal for gas exchange?
It has a large total surface area (70-100m2) and is very thin (0.5micron). The pressure gradient of PAO2 to PaO2 is large and o2 diffuses readily.
What is PHYSIOLOGIC dead space?
It is the amount of air that remains in the alveoli and tracheobronchial tree between breaths. This is part of what Dr. Obst's big long equation at the end of class describes--the difference between FI02 and PAO2. I think...
Which has the greatest effect on O2 CONTENT of the blood: hgb, pao2, or sao2?
sao2 is multiplied by a factor of 1.34 and then by the hgb level and is therefore the big player in o2 content. Pao2 makes a very small contribution by multiplying pao2 x 0.003 !
Explain the oxyhemoglobin dissociation curve in as much detail as possible.
Sorry folks, you've got to refer to p. 1099 of the text to hash this one out. I can't type a dissertation all in this little box. LOL.
Your patient is severely septic. Explain the effect of sepsis on the oxyhgb diss curve. What is ultimate clinical effect?
The curve is shifted to the right by sepsis (decreased pH, fever, elevated co2). This maximizes UNLOADING of o2 at the tissues, but makes it harder to load o2 onto the hgb at the lung.
Your patient with severe periph vasc disease is quite hypothermic intraoperatively. Why would this make you think of the oxyhgb diss curve and what effects it could have regarding their periph vasc disease?
Hypothermia shifts the curve to the left making it easier to load hgb at the lung, but decreases delivery (unloading) at the tissues. This pt already has severely compromised tissue oxygenation and now it's worse ! Warm them up CRNA !
How is CO2 transported in the blood?
CO2 in the blood readily diffuses into erythrocytes where it reacts with h20 to form carbonic acid which rapidly dissociates into H+ and HCO3-(bicarb). The H+ binds to hgb and is thus buffered. The bicarb moves back to the plasma. 60% of co2 is transported as HCO3 back to the lung.
What are carbamino compounds?
The CO2 in the blood that is not transported as HCO3 is mostly transported to lung bound to hgb or other plasma proteins. 30% of co2 goes back to lung this way.
How are hgb 02 saturation and co2 transport related?
As 02 sat decreases, hgb has increased affinity to bind and carry c02. Makes sense, eh?
What is the Haldane effect?
It describes that O2 has a greater affinity for hgb than co2 and displaces co2 at the lung. Then, when o2 is delivered to the tissues, the 02 jumps off the hgb but the co2 can now easily jump on. The key is O2's higher affinity for Hgb.
Describe the process of HYPOXIC VASOCONSTRICTION.
Alveoli that have low PAO2 stimulate vasoconstriction thereby shunting blood to better perfused lung segments. It is a compensatory mechanism. NOTE: hypercarbic acidosis can cause generalized pulmonary vasoconstriction.
What is residual volume
the volume of air that remains in the alveoli (not exchanged).
Normally 1200 cc
What is minute volume?
resps/min x TV.
varies, but aprox 7-10 lpm.
What is Tidal Volume?
The volume of expired air after one normal inspiration.
Normally aprox 500cc
What is inspiratory reserve volume?
the volume of air that could be maximally inspired ABOVE the normal TV. aprox 3000+ cc.
What is the expiratory reserve volume?
The amount of air that can be maximally expired beyond the normal TV. aprox 1000+ cc.
What is my middle name?
(I'm a Jr. too)
**this won't be on the test.
What are normal MIXED venous blood gas results?
35-40 PO2
41-57 CO2
24-28 HCO3
75% Sat
What are the major muscles of inspiration?
The diaphragm and the external intercostal muscles.
What are the accessory muscles of breathing?
The sternocleidomastoid and scalene muscles.
What are the major muscles of expiration.
There are none! But the internal intercostals and abdominal muscles help with expiration when minute volume is high.
What does elastic recoil of the lung describe?
"The tendency of the lungs to return to resting state after inspiration".
What is lung "compliance" mean?
It is a measure of lung and chest wall distensibility. It is the reciprocal of elasticity.
Explain the factors of airway resistance and what conditions may affect airway resistance.
This is determined by Poiseuille's Law and can be affected by narrowing or dilation of the bronchi, obstruction or bronchial edema (just to name a few).
What affects does aging have on breathing/ventilation?
Loss of elasticity, decreased compliance, alterations in gas exchange, increased resistance.
What is 2,3 DPG and how does it affect the oxyhgb diss curve?
2,3-diphosphoglycerate (2,3-DPG) is a substance made in the red blood cells.
Hemoglobin, the protein in the blood that carries oxygen, uses 2,3-DPG to control how much oxygen is released once the blood gets out into the tissues. The more 2,3-DPG in the cell, the more oxygen is delivered to body tissues. Conversely, the less 2,3-DPG in the cell, the less oxygen is delivered.
2,3-DPG levels are important in large blood transfusions, because stored blood quickly loses 2,3-DPG and its ability to deliver oxygen. After transfusion, the red cells rebuild the 2,3-DPG, but it takes about 24 hours to regain a normal level of 2,3-DPG and hemoglobin function.
What is the Bohr Effect?
It describes that at the tissue level CO2 levels are high (acidic)and shifts oxyhgb curve to the right causing O2 to disociate and be delivered to the tissues. Then at the lung as CO2 is excreted the pH rises and the curve swings to the left, increasing hgb affinity for O2. The key is acidity/alkalinity and curve shifting left/right.
What is FVC?
Forced vital capacity. Maximum amount of gas that can be displaced from the lung during a forced expiration.
What is FEV1?
Forced expiratory volume in one second.
What is FEV1/FVC?
Percentage of max air expired in one second, usually 80% of FVC.

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