Basic respiratory Physiology Flashcards
Which muscles are involved in inspiration? Which are involved in expiration?
diaphragm (normal inspiration)
strap muscles: all scalenes (normal inspiration) and sternocleidomastoid (deep inspiration)
external intercostals
large back muscles, some paravertebral muscles, muscles of shoulder girdle, and pectoralis muscles (maximal effort)
Expiration:
The muscles of expiration include the:
Normal expiration is passive Internal intercostals (depending on level the names can change a bit, but just remember any intercostal that’s not the external intercostal is involved in expiration) Abdominal muscles
Explain vital capacity:
Finally, to take the largest breath you possible can you need to take a normal tidal volume, plus your inspiratory reserve volume and then blow it all out all the way down to your residual volume (this is the vital capacity)
Why is lung volume never zero?
Because the chest wall’s outward force, the lung volume is never zero or even all the way down to residual volume (unless there’s a pneumothorax, in which case the chest can outwardly recoil and the lung inwardly recoil unopposed).
90% of airway resistance occurs where? And what are these airways?
In the conducting airways. These airways include the very large cartilaginous airways and the non-cartilaginous conducting airways including “terminal” bronchioles.
The bronchioles at the distal end of the conducting airways do not have _________ support and have the highest proportion of ___ muscle. This is also the area most affected by ______, and constriction of these airways can increase airway resistance profoundly. COPD can have both ______ and ______ involvement, increasing resistance at both areas.
The bronchioles at the distal end of the conducting airways do not have cartilaginous support and have the highest proportion of smooth muscle. This is also the area most affected by asthma, and constriction of these airways can increase airway resistance profoundly. COPD can have both bronchiole and alveolar involvement, increasing resistance at both areas.
In the larger airways, resistance is a result of the balance between laminar and turbulent flow. The Reynold’s number describes the balance between the two types of flow. In general, and always true with air, laminar flow will have less resistance than turbulent flow.
True
You absolutely need to know the difference between laminar and turbulent flow, and the factors that affect their contributions to resistance. So tell me about flow in the large conducting airways and where _____ is greatest.
In the large conducting airways, flow tends to be turbulent. Turbulence is greatest near branching points in the airway and any deformities (tumors, etc). The balance between laminar and turbulent flow is described by the Reynold’s number.
What determines if flow will be turbulent as it relies to density and speed of flow? What does the reynold’s number have to do with that? What does helium have to do with this?
you do need to know that the higher the density and faster the flow, the more likely flow will be turbulent. A Reynold’s number greater than 2,000 (or 2,300 if you want to be technical) means that the flow will be primarily turbulent.
decreasing density with low density heliox can decrease the work of breathing for people with very turbulent airflow.
Explain Poiseuille’s Law:
In asthma, there is a loss of radius in small conducting airways as described above, creating an increased pressure drop for a given flow, therefore increasing resistance. Poiseuille’s Law describes pressure changes for laminar flow (which would be expected in bronchioles) and the equation is:
Pressure drop = (8 X viscosity X length of airways X flow rate) / (π X radius^4)
Therefore according to Poiseuille’s Law: at a given flow rate, resistance will increase with decreasing radius, increasing length of airways and viscosity.
Describe the The Law of LaPlace
Laplace-describes the pressure within the alveoli, assuming that alveoli behave anything like bubbles.
Pressure = (wall tension X wall thickness X2) / radius
So, for an alveoli, less pressure is required to open an alveoli when the wall tension is lower (like adding surfactant) or the radius is larger (avoiding atelectasis). The Law of LaPlace
For air to flow into the lungs, what must happen?
For airflow into the lungs, the pressure in the alveoli must be more negative than the pressure in the atmosphere.
The largest breath you can take and exhale is ____. At which lung volume or capacity would pleural pressure be most negative? Why?
Vital capacity (starting point is TLC). TLC. Why? Because if one was to take the largest breath they could take, you need to generate even more negative pleural pressures, to create even more negative alveolar pressures, to increase airflow.
What is the alveolar gas equation?
pAO2 = [FiO2 X (atmospheric pressure – vapor pressure of water)] – pCO2/RQ
What does elevation do to PAO2 and PaO2? Why?
Increasing the elevation will decrease the atmospheric pressure, meaning your pAO2 will be lower at a given FiO2 because that vapor pressure of water does not change. This means that the pAO2 (alveolar) will decrease and therefore also the paO2 (arterial). This should all be very much review.
The next step is to understand how a decreased paO2 (from a low pAO2) will cause an increased CSF pH. Carotid/aortic? 4th ventricles? Carbonic anhydrase? Respiratory quotient?
When paO2 drops, oxygen sensing receptors in the carotid and aortic bodies send signal back to the brainstem to increase respiration.* As ventilation increases due to hypoxia, paCO2 drops. The drop in paCO2 causes a net movement of H+ from the CSF into the plasma (just as the opposite is true when the pCO2 is high), therefore increasing the CSF pH.* The decreased H+ (increased pH) in the CSF means that the medullary chemoreceptors (in the 4th ventricle)* will result in less ventilation and partially offset the increased ventilation (driven by the peripheral oxygen sensors), but the overall effect will be increased ventilation, decreased paCO2, and increased CSF pH. Remember that the blood brain barrier is impermeable to H+ and HCO3-, but not CO2. Therefore, a net movement of CO2 from the CSF to the plasma will cause the CSF to become alkalotic.
How is CO2 formed in the CSF? It’s our old friend carbonic anhydrase, that you’ll hear more about in the renal section. The H+ and HCO3- form H2CO3 and then H2O and CO2.* The CO2 dissolves down its concentration gradient from the CSF and into the plasma and is reformed into bicarb and H+ in the red blood cell.*
The respiratory quotient should not change in this setting. The RQ is the production on CO2 (VCO2) divided by the consumption of oxygen (VO2).* In normal situations the VCO2 is 200 mL/min and the VO2 is 250 mL/min, thus the RQ would be 0.8.*
Which of the following is not a cause of hyperventilation:
A. Arterial hypoxia
B. Metabolic acidosis
C. Intracranial hypertension
D. Normal sleep
The correct answer is: D: Normal sleep
As described above, arterial hypoxia causes increased ventilation through stimulation of peripheral chemoreceptors in the carotid and aortic bodies. Also as described above, metabolic acidosis with production of H+ go on to cause trapping of H+ (by way of CO2) in the CSF, thus increasing medullary chemoreceptor output. Central etiologies of hyperventilation include anxiety, pain, fear, high intracranial pressures, drug effects, cirrhosis, among others. With normal sleep, one’s pCO2 increases because CO2 responsiveness decreases, but peripheral hypoxic drive remains intact. Volatile anesthetics depress CO2 responsiveness and hypoxic drive.
Look at photo on #9 basic resp phys: it talks about the body’s response to CO2
Line A demonstrates that as CO2 increases, ventilation also increases. Line B has the same responsiveness per unit change in CO2 (slope) as line A, but requires a higher CO2 level for the same ventilation. This describes most ventilation depressants, which shift the curve to the right and is true for sedative doses of opioids, as well as anesthetic doses of barbituates, benzodiazepines, and far less so ketamine. The final line, C, is even more right shifted, but also has less response to a given rise in CO2 and is severely blunted. This describes very high dose opioids and volatile anesthetics at 1 MAC.
What is dead space? What is shunt?
Dead space is ventilation without perfusion and shunt is perfusion without ventilation. True dead space would be ventilation without any perfusion at all and true shunt would be perfusion without any ventilation.
Ventilation and perfusion are best matched in which lung zone? where is that? Higher VQ means what? Keep in mind that lower numbered ribs are more:
that ventilation and perfusion are best matched in West Zone 3**-the bottom of the lung. and least matched near the apex, where there’s increased dead space. Therefore the higher the V/Q, the worse the mismatch is and the greater the dead space.
Lower numbered ribs are more cephalad
PA pressures higher in lower or higher parts of the lung?
Higher in lower parts
A patient’s end-tidal CO2 decrease while the paCO2 increase, which of the following is an explanation:
A. Decreased cardiac output B. Pulmonary embolism C. COPD D. ARDS E. Answers A & B F. Answers A, B, & C G. All of the above
G: All of the above
A decreasing end-tidal CO2 (ETCO2) and increasing paCO2 means that there has been an increase in dead space, or said another way, there is now ventilation without perfusion. This question did not give a time period in which this occurs, but if it happened intraoperatively, likely only decreased cardiac output (CO) and pulmonary embolism (PE) could cause this. With decreased CO, there is less perfusion and more areas where alveolar pressure is greater than pulmonary precapillary pressure are present, therefore increasing dead space. In fact the absence of ETCO2 is a fairly good indictor that the patient had a cardiac arrest, and decreased ETCO2 is not all that bad for hypotension either. With a PE, perfusion is prevented, but ventilation continues unobstructed. There is a change in alveolar architecture in COPD that can lead to areas of decreased perfusion as well as dynamic hyperinflation with resultant high alveolar pressures due to the obstructive lung disease. ARDS can have profound vasoconstriction to ventilated areas of the lung (and lack of hypoxic pulmonary vasoconstriction to unventilated portions). ARDS develops over hours typically, whereas COPD takes years to decades.
After placing an otherwise healthy patient on mechanical ventilation, dead space:
A: Increases to approximately 50% of tidal volume
Under normal circumstances, a healthy person will have 2/3rds of their tidal volume contribute to ventilation, and 1/3rd to dead space. Dead space is categorized as either anatomic dead space or alveolar dead space. With mechanical ventilation (not accounting for the artificial airway even), alveolar dead space will increase. Why? Perfusion is more or less the same (well, read the advanced cardiopulmonary section and then see if you still agree with that statement) but alveolar pressure is now positive, meaning that the areas where alveolar pressure is greater than perfusion pressure has increased.
A patient has a paCO2 of 30 mm Hg and an ĒTCO2 of 20 mm Hg, what is the percent dead space:
That was a pretty simple question, I admit, but I wanted to showcase the dead space equation and not wrap it up in an unrelated explanation. The equation is:
% Dead Space = (PaCO2 – ĒTCO2)/(PaCO2)
The ETCO2 that you get on your anesthesia machine is not the same thing that you’re using for this equation. For this, ĒTCO2 really means the pCO2 from all expired gasses, not the end-tidal (that’s what the little line above the E means). That being said, if you use the ETCO2 from your anesthesia machine you’ll get a rough estimate.
