Pulm physio Flashcards
What is a pink puffer?
Emphysema (COPD) pt who is tachypneic, tripoding, skinny, pink, puffs air out, smoker. This pt is probably end stage COPD exacerbation, struggling to breath. Repeat admissions is one of the most common things in COPD and they are usually really anxious. They never actually really improve. In the hospital, we only treat sx, so we will have to send this pt home in similar circumstances. Put them o meds (narcotics?) for air hunger
What is the conducting zone?
It is responsible for bringing air into and out of the lungs (inaddition to warm, humidify, and filter the air). There is some cilia in here that help brush up some gunk. Some natural mucus here too that traps particles. Smoking kills these cilia, so the abiliity to clear the lungs becomes difficult. Mucus starts to build up because of increased inflammation and it wants compensate. This causes increased airway resistance.
What is the respiratory zone?
It is responsible for gas exchange and contains thin alveoli with a large surface area to allow for gas exchange via simple diffusion down the pressure gradient.
Beta 2 receptors (epinephrine binds here)- these dilate
Muscarinic receptors (Ach)- cause constriction
How does gas exchange occur?
Ventilation, Exchange of O2 and CO2, transport of O2 and CO2, exchange of O2 and CO2, cellular utilization
What is ventilation?
Exchange of air between atmosphere and alveoli by bulk flow. We breathe air in that has a lot of junk in it, that oxygen diffuses down its concentration gradient in the pulmonary circulation. Need to understand for vent settings
What is the exchange of O2 and CO2?
Exchange of O2 and CO2 between alveolar air and blood in lung capillaries by simple diffusion
What is the transport of O2 and CO2?
Transport of O2 and CO2 through pulmonary and systemic circulation by bulk flow
What is the exchange of O2 and CO2?
Exchange of O2 and CO2 between blood in tissue capillaries and cells in tissues by diffusion
What is cellular utilization?
Cellular utilization of O2 and production of CO2
What are pneumocytes?
cells of the lungs
What are the types of pneumocytes?
Type I alveolar cells (one cell thick and allow for simple diffusion, lungs are mostly made up of this)
Type II alveolar cells and surfactant (interspersed in between). Vascular all around the alveoli. We have alveoli ventilation.
Why do we need surfactant?
We have a tiny amount of water inside our alveoli that attract more polar molecules. Water and alveoli (both polar) now they naturally want to collapse. Surfactant is secreted by type 2 alveolar cells to reduce surface tension that is created by the tiny presence of water that gets into the lungs. Water increases surface tensions and surfactant decreases surface tension to prevent the alveoli from collaspsing.
Why is surfactant in important in neonates?
Neonatal respiratory distress syndrome. Occurs given the absence of surfactant in premature infants beccause production of surfactant does not occur until late gestation and is stimulated by the increase in cortisol secretion that occurs then. Occurs most often in premees
What is the pleural space/sac?
Made up of the visceral and parietal pleura (these are continuous with each other), there is a TINY amount of fluid that is drained by the lymphatics for lubrication to allow for lung expansion.
If fluid got into the potential, what would happen?
It would enlarge and press on the lung and eventually give us a pneumothorax
Why is atmospheric pressure important?
When the pressure in the air in higher than the pressure in the lungs, it pushes air in (inhalation). When pressure in the alveoli is greater than the pressure in the atmosphere, ait (with CO2) is pushed out of the lungs.
What is the formula for atmospheric pressure?
Q= flow rate (ex: blood flow or fluid flow)
Delta P= pressure difference (ex: between two points in a vessel)
R= resistance (ex: vascular resistance or resistance to flow)
For our purposes: delta P = Palv -Patm
What is atmospheric pressure?
Atmospheric pressure changes with altitude. We change the volume of our lungs. Inverse relationship of V and P. 760 mmHg
What is intrapleural pressure?
Pip and has a -4 mmHg where it hovers around 756 mmHg. This pressure is negative because of these opposing forces attempting to increase the intrapleural volume: elasticity (pull) of the lungs/surface tension inward and elasticity of the chest wall outward. Gas want to flow from an area of high pressure to an area of low pressure.
If atmospheric pressure drops with altitude (climbing mt everest, flying, etc) what happens?
Pressure is lower in higher altitudes. Harder to get air into lungs. Flow is going to deceases because the gradient is not as large. This is the whole concept of altitude sickness. At sea level here, it is really easy. Mt Everest (atmospheric pressure 235 mmHg).
Why do people train at high altitudes?
Body (kidneys) makes more RBCs to increase oxygen binding capacity. This is a form of blood doping.
What is intrapulmonary pressure?
Pressure inside the alveoli. 760 mmHg at rest. Usually is never equal though, because we are always breathing in and out, in and out. It acts like a vacuum. The lungs have a desire to collapse away from the chest wall (elastin). Outward pull and attachment to chest well. These opposite pulls holds everything together and short of cancel each other out (vacuum- creates a small negative space)
What happens in pneumothorax?
Intrapleural pressure (Pip)= Palv, the lungs will collapse. This can also happen by rupturing either the parietal or the visceral pleura to cause a pneumothorax. Spontaneous pneumothorax would be of the visceral pleura. Trauma pneumothorax would be the parietal pleura.
What happens during normal inspiration?
Intrapulmonary/alveolar pressure (Palv)=decreases
Intrapleural pressure (Pip) = becomes more negative/decreases (-6) because we have increased the expansive forces
Air moves DOWN its pressure gradient INTO the lungs because we dropped the pressure gradient in the lungs
What happens during normal, resting expiration?
Intrapulmonary/alveolar pressure (Palv)=increases
Intrapleural pressure (Pip)= returns to -4mmHg
Air moves DOWN its pressure gradient OUT of the lungs
What do we test to see during spirometry and PFTs?
Assessment of how lungs are functioning. Residual volume isnt measured in spirometry. This can change with disease.
They ask the patient to breathe in and out normally, then they’ll have them breath in as deep as they possibly can, then they’ll breathe normally for a little bit and then have them breathe out as much as they can, and then both at the same time. This allows for measurement of the different types of volume.
What is physiologic dead space (PDS)?
Total volume of inhaled air that is not exchanged; = anatomic + alveolar dead space, also called “Wasted Ventilation”
What happens in Ventilation and Perfusion?
Fluid in the lungs: pneumonia, etc
What are the effects of breathing pattern son alveolar ventilation?
Tidal volume has the largest impact on alveolar ventilation, because when you breathe deep, the air gets deeper into your lungs.
Tidal volume and frequency have an inverse relationship
What are the effects of breathing patterns of alveolar ventilation?
Tidal volume has the largest impact on alveolar ventilation, because when you breathe deep, the air gets deeper into your lungs.
Tidal volume and frequency have an inverse relationship
Anatomical dead= alveolar dead space and is influenced by frequency
What is compliance?
It refers to the “distensibility” of the lungs. How much can the lung expand when stretched
Greater compliance=easier to expand the lungs
Increased surfactant of the lung tissues. Pulmonary fibrosis effects this ability to stretch Pulmonary fibrosis effects this ability to stretch
What is recoil/elasiticity?
Refers to the desire for the lungs to want to “snap back” or return to original shape/size after being inflated. In emphysema, bug blebs can’t really snap back
What do obstructive airways look like?
Airways are narrows. Asthma: inflammation and bronchoconstriction. COPD= mucus and destruction of airways.
Lungs can remodel overtime to cope with airway resistance and they will stretch out a little bit. Lungs may inflame to try and overcome the obstruction- increased compliance/distensibility, but decreased recoil.
What does FEV1 look like in normal vs obstructive vs restrictive?
Obstructive- takes longer to breathe out because of decreased recoil and increased airway resistance (decrease in expiratory reserve). Usually less than 80%, because the lungs have stretched and tried to increase inspiratory, but cant get it out. FVC changes relative to FEV1
Restrictive: everything is blown out in the first second due to increases recoil
What does the alveolar capillary network look like?
What are the partial pressures of oxygen and carbon dioxide?
When we tal about oxygen, we talk about it in the sense of pressure gradients. So, venous blood, so deoxygenated blood in a sense, has about 40 mm of mercury of oxygen. It’s so low. Arterial is about 100 mm. Everything wants to go down the pressure gradient. The reason why alveoli moves into the venous blood is because you’re ging from 105 mm to 44 mm. So everything is trying to flow down, so once you have movement of oxygen down to the vneous blood, it becomes arterial blood (simple diffusion)
Glucose + O2 → CO2 + H2O + ATP = Cellular Respiration
CO2 + H2O → ←H2CO3 → ← H+ + HCO3-
What is the hemoglobin saturation curve? How do pressures relate to our actual hemoglobin saturation?
In arterial blood, we’re at 100% saturated. We’re going to use up all that oxygen we just got. We’re going to hold on to that oxygen. Well the vneous blood we’re about 80% saturated because we dropped off 20% of that oxygen at the tissues anyway. Under normal circumstances, we lose about 20%. We can modify that: left and right shift.
What would cause changes in the hemoglobin saturation curve?
Right shift: drop off 50% O2, support body tissues, oxygen binding capacity decreases
Left shift: hypothermic, vomiting, alkalotic hold onto O2, less ability to bind for CO2, oxygen binding affinity is increased
What is carbon monoxide poisoning?
Carbon monoxide has a high affinity for hemoglobin (210x that of oxygen), makes it impossible and takes up all the spaces for oxygen to bind. Even though PO2 of oxygen is 100 mm Hg in arterial blood, we’re at like 50% because that CO2 is taking away everything. So the ability for oxygen to bind is not good, because CO2 has taken all of it up. For the venous blood, the oxygen is at like 40%. We are still at 100% saturation of carbon monoxide, so it is still hanging on to all the hemoglobins and not giving us a chance to bind to any oxygen. That’s how it actually kills people.
How is CO2 present in the blood?
As dissolved CO2 (10%) in plasma and RBCs. bound to hemoglobin known as carbaminohemoglobin (25%) and as bicarbonate (HCO3-) (65%). So the bicarbonate is exchanged for chloride and it floats around in the blood plasma. Chloride does charge balance (exchanged for bicarb). Chloride shift. You don’t want them t build up a negative charge on the outside of the cell. So in certain acid base disorders, we will changes in chloride levels. CHLORIDES EXCHANGE FOR BICARB
What happens in the capilarries of the lungs?
Hydrogen binds to the hemoglobin, that hemoglobin travels back to the lungs where there’s bicarb floating around there, its able to then become carbonic anhydrase, then it is able to convert back to CO2, where it is able to exit and go to the lungs.
How does the body compensate for a V/Q mismatch?
The body can change the arteries or arterioles and the material that supply these alveoli where there is a V/Q mismatch vs how can we change ventilation for bronchial control and bronchodilation. You realize there is no oxygen there, you’re not going to direct your blood flow to that area. So the pulmonary arteries to those alveoli constrict. Reduction in ventialtion= reduction in perfusion. Improve gas exchange, how do we redirect? Really good amount of oxygen, then I want to pick that up, so I am going to dilate my arterials to that area, pick up the oxygen that’s there. So that’s where we have dilation of arteriols to areas, our arteries are able to compensate. Change ventilation when there perfusion mismatch too.
What is the medullary/ inspiratory respiratory rhythmicity center?
- Dorsal respiratory group (DRG): diaphragm and inspiratory intercostal muscles, main driver
- Ventral respiratory group (VRG): sets the basal respiratory rate at which the DRG inspires
Lung stretch receptors innervated by CN X
Muscle and joint receptors: intercostal muscles that cna detect and send signals to out brainstem
Our brain stem is our main area for respiration modulation, so we can change our breathing consciously increasing and decreasing it. So, our higher cerebral cortex can provide input into our brain stem to change our RR. Our brain stem does it without thinking too.
What are the central chemoreceptors in capillaries, the medulla, and the CSF?
In the CNS. pH and hydrogen drive the changes for our respiratory system. This CO2 gets into out CSF and crosses the blood brain barrier, it is converted into hydrogen and this is how our central chemoreceptors are actually able to sense and change our RR.
What are our peripheral common receptors?
Carotid bodies and aortic bodies. They detect that hydrogen and they relay that info back to that inspiratory center specifically and the DRG and VRG are modified by the apneustic and pneumotaxic areas of the pons which help the expiratory process
