Gas Exchange
Equation for minute ventilation
Minute ventilation= tidal volume x frequency Brain senses CO2 going up, so diaphragm goes up and intercostals come up and out to breathe. Intrapleural pressure goes down with increased volume.
Where is there more blood flow in the lung?
More blood flow at base of lung Alveoli at top pulled apart (like a slinky) and only move a little. At bottom of lung, alveoli can expand and recoil much more. This allows for much more ventilation
Where does gas exchange begin?
No gas exchange until reach respiratory bronchioles: above this is the anatomical dead space and below this is physiological dead space (start to plug up alveoli with consolidation and transudate or exudate)
HMD (hyaline membrane disease)
Occurs from lack of surfactant. This makes it very hard to breathe and physicians need to replace surfactant (wont ask specific questions about this for exam)
Vital capacity (VC)
Peak inspiration to peak expiration
Atelectasis
alveoli collapse Causes physiologic dead space, but can still have blood flow though
Expiratory reserve volume
exhale until you cannot anymore
Pulmonary injury
for example: aspiration pneumonia or a disease that affects surfactant production and distribution Leads to adult respiratory distress syndrome (ARDS): stiff lungs. Need surfactant to maintain normal lung compliance and function.
Trachea
has unique pseudostratified columnar epithelium with goblet cells for protection
Inspiratory capacity
max inspiration. Volume taken in above Tidal Volume
Residual volume
the gas that is left in lungs after you have a full expiration During expiration, alveoli get smaller and start to recoil to resting state, but surfactant keeps them from collapsing. If *deficiency in surfactant*, there is a *change in residual volume* and *alveoli become stiffer*.
want hemoglobin to load and unload O2 to tissues in periphery
want hemoglobin to load and unload O2 to tissues in periphery
Upper airway function
warms, cleans, and humidifies air
Esophageal balloon:
Measures esophageal pressure changes to calculate alveoli pressure changes. Also shows compliance
Hemoglobin Saturation Curve Manipulation
(As O2 partial pressure goes up, Hgb becomes saturated around 100%). More O2 is getting to alveolus because of increased tension and causes greater saturation. Different hemoglobins have different curves As you saturate and desaturate, curve can be manipulated by temperature, pH, 2,3-DPG from glycolysis, and anerobic metabolism (produce ATP). The curve gets you a lot of information, but can be deceiving.
Functional residual capacity (FRC)
*Functional residual capacity (FRC): expiratory reserve volume (ERV) + residual volume (RV)* Have FRC at end of full expiration In a diseased lung, phagocytes attempt to clean abnormal cells, but damage alveoli in the process. This causes the lung to resemble a floppy bang and become overly compliant (don't recoil in resting state). This starts to change FRC.
Gas Trapping
*occurs in the lower airways* In a nutshell the term "air-trapping" refers to air that, well ... gets trapped in your lungs! Basically what happens, is that a person with an obstructive lung disease (like asthma), inhales a volume of air, but cannot exhale it easily or completely. The resulting sensation is often perceived as a feeling of chest heaviness or breathlessness. This uncomfortable symptom can vary in intensity from mild to debilitating and usually lasts until the lungs decompress to their baseline state. In the most severe cases, as in severe emphysema, air- trapping tends to get progressively worse and the lungs never fully decompress. The hallmark of Emphysema, COPD and Severe Asthma, air- trapping occurs when mucus and/or inflammation obstructs the inside of air passages preventing the inhaled air from being easily exhaled. The condition can also occur when the airways themselves loose their elasticity (their ability to recoil) and/ or through the loss of alveolar attachments that stint the alveoli open from the outside. This type of destruction of the airways is seen in both emphysema and in chronic severe asthma (the former usually caused by cigarette smoking).
2,3-DPG and Hemoglobin
2,3-DPG involved in glycolytic pathway and Krebs cycle: where mitochondria produce ATP for electron transport chain (ETC) *2,3-DPG allows Hgb to release more oxygen so decreases O2 level* *Hemoglobin also unloads oxygen more readily in presence of acid*
Room air composition
21% O2 and 80% N
A left shift on hemoglobin saturation curve
A left shift will increase oxygen's affinity for hemoglobin. In a left shift condition (alkalosis, hypothermia, etc.) oxygen will have a higher affinity for hemoglobin. SaO2 will increase at a given PaO2, but more of it will stay on the hemoglobin and ride back through the lungs without being used. This can result in tissue hypoxia even when there is sufficient oxygen in the blood.
a right shift on hemoglobin saturation curve
A right shift decreases oxygen's affinity for hemoglobin. In a right shift (acidosis, fever, etc.) oxygen has a lower affinity for hemoglobin. Blood will release oxygen more readily.vThis means more O2 will be released to the cells, but it also means less oxygen will be carried from the lungs in the first place.
Ventilation is a function of the tidal volume and rate of ventilation
Alveolar O2 content can be determined by using the frequency of breaths, the O2 content in the air, humidity and the volume of air inhaled. The volume of anatomical dead space needs to be subtracted as does physiologic dead space. Anatomic dead= space is relatively fixed in volume Physiologic dead space= can increase with different disease states, etc.
ventilation must match perfusion
Alveoli are the sight of CO2 and O2 exchange Must match ventilation and perfusion
Zones of West
Because of the resistance of blood vessels lying above the level of the heart, there is more blood flow at the base of the lungs than the apex. The alveoli are more inflated at the top of the lungs than at the bottom. Upper alveoli have more air flow than lower alveoli and alveoli at the apex are more rounded and open in space, while the alveoli at the base are more stretched. There is more blow flow going to the areas of the lung with more ventilation. This is an attempt to match ventilation and perfusion in order to ensure that the blood going through the lungs is properly oxygenated. When an area of the lung is damaged, blood vessels can vasoconstrict and shunt blood away from the damaged or infected area. This is called an *inter-pulmonary shunt* and this ensures continued ventilation- perfusion matching. Pulmonary embolisms will prevent blood flow, in which case ventilating that area of the lung is useless. Patient will need a clot buster to break up the embolism.
Tidal volume
Breathe air in and out: tidal volume (roughly 500 ml) *Amount of air with each breath/ the amount of gas that moves with each breath* Out of 500ml, it is spread out over the entire lung and through the trachea, bronchi, and alveoli. Roughly *150ml is dead space* (*only 350 ml get to alveoli*) *Alveolar ventilation*= 350 ml but tidal volume is still 500ml *Expand tidal volume by taking in more air or exhaling more air*
What is compliance?
Compliance: given change in volume for given change in pressure. With less surfactant, more difficult to inflate lungs and takes more pressure, so lung less compliant.
Normally, Hgb is 16-18 and saturated. If the patient bleeds and Hgb becomes 4 (very low), can still be 100% saturated on pulse oximeter even though tissue not getting enough O2
Example of MVA: Patient in the field has volume loss and medics replace volume with saline. The patient has high lactate from hypoxia. Even though volume was increased, they need blood to maintain o2 carrying capacity *can have stat of 100% but need enough hemoglobin to deliver O2*
Fetal hemoglobin
Fetus Hgb has higher affinity for O2 than mom's Hgb, so fetus grabs mom's O2 After birth the neonate starts to breathe on its own and Hgb becomes normal
Fetal Hemoglobin
Fetus depends on mom's oxygen (on her hemoglobin) Fetus has greater affinity for O2 so pulls Hgb from mom, so it is important to make sure mom has enough O2 when pregnant (shift to the left)
What makes pulmonary surfactant?
From *type 2 alveolar cells*: "Conditioner like": Surfactant makes alveoli distensible and breaks water surface tension and allows alveoli to expand and relax more readily. *Loss of surfactant* leads to *decreased lung compliance*. Surfactant in alveoli (lower airway is site of gas exchange): *Fick Principle*: high dissipation goes to low dissipation (example: a wave of water will try to dissipate and seek its lowest level). *Pressure is also important*. In alveoli, air rushes in and based on oxygen concentration, gets through. If CO2 concentration is high in pulmonary vasculature, it will diffuse into alveoli and exchange will occur. CO2 and O2 gases mix at the alveolar level (ignore nitrogen for now).
Pressure Volume Loop
From algebra we remember y=mx +b. Lung volume is represented as y and pressure is represented by x (slope) If lung compliance decreases, have to create a greater pressure change to inhale (example: low surfactant level)-> this causes the work of breathing to increase and surface area in curve to decrease Change in volume for change in pressure gives you compliance Small pressure change for large volume change (very compliant) Large pressure change for small change in volume (not compliant)
Where does gas exchange occur?
Gas exchange occurs within the lower airways, primarily the alveoli. Often called the "business end" of respiration. Blood entering the lungs via the pulmonary artery is deoxygenated. It becomes oxygenated when the capillaries pass through the alveoli and reenters the heart via the pulmonary vein with oxygenated blood.
Hemoglobin Molecule
Hemoglobin: 2 alpha and 2 beta chains Partial pressure and concentration of oxygen at alveoli are important because they determine how much oxygen will get through alveolar membrane into red blood cells and bind hemoglobin (Hgb). Plasma does not have a lot of 02 dissolved in it. In blood, O2 binds Hgb quickly and increases its affinity. In the periphery, the Fick Principle applies. CO2, a tissue by-product is increased in the vasculature and O2 depleted. At the alveoli, CO2 leaves and O2 enters and Hgb unloads O2 in tissues.
methemoglobinemia
If Hgb doesn't bind O2, it is called methemoglobinemia. This causes extreme SOB and because there is blood flow (but no oxygen), it can be fatal
pH affect on hemoglobin saturation curve
If add acid to blood, decrease Hgb's affinity for O2 (so release more o2). Decreasing the pH, more acidic, shifts the hemoglobin saturation curve to the right. Tissue metabolism produces CO2 (when combusts carbon) and binds to water to produce carbonic acid. Carbonic acid splits into H+ and bicarbonate molecule. Tissue Metabolism Bohr Effect: As H+ goes up, pH goes down and hemoglobin's affinity for O2 decreases. Under normal pH of 7.4, Hgb attached to less O2. At pH of 6.9, holding onto more O2 because less saturated. Is this good or bad? If patient becomes more acidemic, they begin to breathe faster to blow out more CO2 and get rid of acid. The pH goes from 6.9 to 7.4. If tissue hypoxia: permissive acidemia helps unload O2. *We have to know when to let a patient be acidotic and when to push bicarbonate* If the Hgb is normal, but the pH goes up, a carbopedal spasm can occur from hyperventilation. Give an give o2 mask and sedative to treat. *Hyperventilation: not increasing breathing frequency, but breathing fast enough that your Co2 levels drop and increasing the pH, more basic blood*.
residual volume vs. air trapping
It's important to note, that while air-trapping is abnormal, there is always a small amount of air that remains in the lungs after you exhale completely... even if have totally healthy lungs. This is known as residual volume. Without this residual air, your lungs would collapse into themselves and you would not be able to overcome the resistance required to re-inflate them.
How many lobes on the right and how many lobes on the left
Lungs are not homogenous (2 lobes on left and 3 on right)
Difference in shape between mainstem bronchi
Right main stain bronchus wider than left bronchus (can accidently intubate this or get food stuck there)
Sickle cell disease
Sickle cell disease causes a defect in hemoglobin, which forms a C shape. This sickle cell Hgb can't bind O2 and can't get through capillaries. This is very painful and cause a spleen infarction.
what determines the compliance?
Surfactant determines the compliance More surfactant, more compliant Less surfactant, less compliant This is because the surfactant breaks the surface tension in the lung. You can think of surfactant as a detergent.
Temperature's effect on Hgb
Temperature does effect physiology: Colder environments: As you decrease the temperature you shift the curve to the left. O2 released less and holds onto it more. The higher the temperature, the higher the unloading O2. Metabolism slows down in the cold so body doesn't need as much O2. Example of Hypothermia: After heart surgery, inducing hypothermia is cardioprotective, but people were becoming brain dead,etc because other organs weren't getting enough O2. Want to warm person so will unload O2 more. Conclusion: Temperature matters!! Also evaluate the patient based on age and get pulse ox, heart and respiratory rates, temperature (oral or rectal), and blood pressure
Normal Respiration
The act of inspiration (the act of inhaling) is an active process. It requires the use of certain muscles (in this case the diaphragm) to make the process work. What happens, is that the diaphragm muscle(which is a dome shaped muscle in your abdomen), contracts and pulls down making room for the lungs to expand within the chest cavity. The expansion of the lungs creates a vacuum within them, allowing air to be drawn in. As the lungs fill with air, stretch receptors tell the brain when equilibrium has been reached and inspiration terminates. Expiration is (or should be)totally passive. Under normal circumstance there are no muscles used during the act of expiration. The whole system works pretty much like an inflatable balloon. You have to "work" to blow up the balloon, but to deflate it, you just let it go and the air escapes by itself. Ah, but if you have swollen airways or thick mucus in them, or if your balloon is made out of cardboard or stiff plastic instead of rubber, it then becomes much harder for that balloon to deflate on it's own. People who have obstructive lung diseases have to actually work harder to breath, because they have to literally "push" or force the air out of their lungs to make room for the next breath. This requires the use accessory muscles that you wouldn't normally use to breath, and that extra muscle expends more energy, which makes you more tired and even more short of breath.
Remember respiration occurs only at the cellular level.
The air that is inspired is NOT 100% O2, but will be a mixture of O2 and CO2. When measuring the rate of breaths you are measuring the *ventilation rate*. Respiration occurs only at the cellular level. With build up of fluid, fibrosis, etc. there is less volume for gas exchange to occur. Damage to the alveoli membrane causes blood to mix with the surfactant. This cause a bloody sputum to be coughed up.
premature birth and surfactant
There is a special circulation in utero where lungs are bypassed (right ventricle pumps blood to ductus arteriosus instead of lungs), so surfactant is not utilizable in utero in the premature baby. Premature babies have less compliance and surfactant production problems. Important from birth to enhance lung function and compliance, so we need surfactant for our whole lives.
How to evaluate respiratory function
To evaluate respiratory function: 1. Listen to breath sounds: Rales (snap, crackle, pop), Wheezes (sounds like singing on expiration), and Rhonchi (sounds like tube with water in it). 2. Looking at patient: Normally breathing or SOB? Child Drooling? Color of patient? If gray/blue color, represents cyanosis. 3. How fast they are breathing: premature baby breathes at 60 times per minute because cannot expand lungs 4. Put on pulse oximeter 5. Get a chest x-ray: Look for symmetrical trachea, heart size and apex, costal angles, menisci, rib cage, and trachea clarity. These lungs are flattened and overinflated, Small lines around bronchi -> heart vessels "juicy" and induce more blood flow which increases vascularity.
visceral pleura covers what and parietal covers what?
Visceral pleura covers lungs and parietal pleura that covers chest wall
Components of surfactant
Water is a dipole, which has both + and - ends. Water molecules like to stick together (because of van der wals forces), but surfactant gets in between the molecules' bonds in order to decrease adherence and thus decrease surface tension. Example: You have a glass table and a glass of iced tea that is wet. It is hard to pick the glass up so you have to slide glass off edge of table to pick it up. This is due to surface tension. SURFACTANT BREAKS SURFACE TENSION
Alveoli are managed by the pressure changes which occur during ventilation
We can control the PEEP. Higher pressures open more alveoli, while lower pressures leave more closed
Hemoglobin saturation curve
When oxygen gets into bloodstream, it will bind to tetramer of Hgb and this exponentially creates an s shaped curve called *hemoglobin saturation curve* *Measuring saturation*: this binding of oxygen to Hgb causes a stoichemetric change in the molecule, which changes amount of light absorbed. If Hgb has a lot of O2 bound, it looks pink. If less O2 bound, starts to look darker and turn blue. Hgb absorbs more light as becomes more deoxygenated and pulse ox starts to drop. As 02 goes up, Hgb becomes saturated.
Total lung volume
peak of inflation to trough of having no gas in lungs at all Example: take in deep breath and exhale as fast as you can: this measures peak flow. If the tracheal bronchial tree is working well: gas comes out quickly and therefore isn't constricted. If constricted, you cannot exhale as fast
