P502:558:594 Respiratory tree: Conducting zone Does not participate in gas exchange So oxygen that goes to the anatomic dead space is not used by the body cause it cant get to the respiratory zone If you have any pathology in the respiratory zone, then that area of pathology + your anatomic dead space becomes a separate measurement which is your physiologic dead space. Theres a difference with anatomical dead space (which is what everyone has) and physiologic dead space, which in a normal lung = anatomical dead space But a pathological lung would have a great value then the anatomical dead space P502:559:594 Pneumocytes How do ciliated cells communicate with one another? Ciliated cells communicate via gap junctions. There needs to be a coordinate movement in a particular direction. Goblet cells extend only to the terminal bronchioles (he says this in DIT) Type II cells If you have lung damage, you will have proliferation of type II cells that then become type I cells If you have a women with preeclampsia or a women with pregestational diabetes or a traumatic injury and maybe you think its of the babies best interest to deliver the baby early: maybe 36, 37 or 35 weeks. Maybe you want to check a lecithin to sphingomyelin ratio. If the value is less than 2.0 and babies lungs are not yet mature, then what would you do for the mom to mature the babys lung? Fetal lung immaturity = give the mother steroids This prevents the neonatal respiratory distress syndrome Gas exchange barrier 3 structures: Type 1 epithelial cell, basement membrane and tight junction endothelial cell comprise your diffusion barrier Anything that increases the diffusion barrier i.e. increase thickness of the diffusion barrier maybe the basement membrane gets increased maybe you have a layer of neutrophils on top of your type 1 cells so its difficult to oxygenate p503:560 bronchopulmonary segments

Right lung: More common side for inhaled foreign body Lung relations: Gastric tube cannot be inserted any further Right hand side: see barium has been aspirated into the lungs P131:139 Tracheoesophageal fistula Whats the most common type of TE fistula? Most common tracheoesophageal fistula Blind esophageal pouch (esophageal atresia, lower esophageal segment attaching to trachea) 85% of TE fistulas have this appearance Do you need to know the different lobes of the lung? Its fair game. Read it. P503:560 Diaphragm structures Know this Pt with kussmauls respiration and heavy breathing and diaphragm becomes fatigued or worn out, this will be referred to classically the shoulder Shoulder pain could be referred diaphragmatic pain P504:560 Muscles of respiration Chest wall wants to go out and lungs want to collapse During exercise or anytime you have excess respiration: i.e. exercise, kussmauls with DKA, or any respiratory distress you will use accessory muscles And sometimes you would probably even have to lean over to use these muscles for inspiration Homeless alcoholic walks into ER with aspiration pneumonia: which side would you find consolidation? Right side b/c right main stem bronchus is more vertically in line with trachea. P504:561 Physiology Prostaglandins are vascular dilators Keep a PDA open Important for maintaining renal blood flow When you give NSAIDS, you get rid of the prostaglandins and constrict renal blood flow PGs decrease bronchial tone and relax bronchi Some asthmatic pts have aspirin sensitive asthma Some asthmatics are sensitive to NSAIDS NSAIDS and aspirin can induce asthma in these patients by increasing bronchial tone Histamine causes leaky vessels So histamine in your bronchi youll have tissue edema which will narrow the lumen of your bronchi ACE from the lungs convert AG1 to AG2 P504:561 Lung volumes High yield Definition of terms Know what they mean Read it P505:562 Determination of physiologic dead space VT is the air that moves into the lung with each quiet inspiration and Not all that air is going to go into the alveoli. Some of that air is going into the dead space. How do you determine how much of your tidal volume is dead space? It will be some percentage. How do you get that percentage? Use the equation. You take arteriole CO2 minus the expired CO2 divided by arteriole CO2 If tidal volume was 500 mL If 10% of that tidal volume was your deadspace b/c you use this ratio to come up with 10%, so then your physiologic deadspace is 0.05 L or 50 mL. Do you need to memorize this equation? 4 star topic Worth learning You might be asked, you might not Lung and chest wall This diagram looks at the relationship of the dynamics of these tissues when airway pressure differs As you go up the airway pressure (x-axis), theres a propensity to go up in volume (y-axis) Where x-axis = 0 (where airway pressure is zero: we talk about atmospheric pressure) What does the chest wall want to do as it approaches, as it goes beyond airway pressure zero,? it wants to greatly increase volume. You have the chest wall that is exerting an outward pull, as airway pressure increases So the chest wall has the tendency to expand and recoil outward, but theres something thats preventing it from doing so What is it that is preventing it from doing so? The lungs. The lungs want to do the opposite. As the air pressure wants to go towards zero, the lungs want to collapse and unopposed the lungs would collapse at an airway pressure of zero, which is what you get with a pneumothorax You equalize the airway pressure by puncturing the chest wall and the lungs collapse So at zero atmospheric pressure, the lungs dont collapse. Why dont they collapse? b/c your chest wall is trying to recoil outwards. Its The balance between the two. That is what the green line is. Its the balance between the two. What else should you get from the graph. There a pinpoint place called the FRC Functional residual capacity which is the volume in the lungs after normal expiration You can at zero airway pressure, theres a certain FRC for every individual. This is the point where zero airway pressure or atmospheric pressure, the outward expansion tendency of the chest wall is balanced by the inward collapsing tendency of the lungs. So you have this ideal range of FRC The FRC is different from individual to individual. What determines what value the FRC is between individuals is? compliance. Elastic properties of both chest wall and lungs determine their combined volume. This is the green line. In patients with emphysema, the FRC will move up that straight line airway pressure zero. In emphysema the lungs wont contribute as much, so the FRC will be more like the chest wall and be more skewed towards the chest wall line. Thats why in emphysema you get the barrel chest. Huge chest, b/c the chest wall is winning. This is increased compliance, which increases your FRC. What about decreasing your lung compliance? The green line will move towards the lungs. The lungs will start to win rather than the chest wall. Decreasing lung compliance decreases your FRC. When does this happen? Pulmonary fibrosis, insufficient surfactant, and pulmonary edema. KNOW THIS. P505:562 Hemoglobin Normal adult Hg is 2 alpha and 2 beta Fetal Hg is 2 alpha and 2 gamma T form favors tissue If you want to get oxygen to the tissues you want the T form when unloading oxygen. NB: Myoglobin is not a tetramer like Hg. Myoglobin is just one globin molecule. With hemoglobin, when you bind one oxygen, you are more likely to bind the second one and more like to bind the 3rd one. This is the sigmoidal shape of the oxygen dissociation curve. In Cl-, hydrogen, CO2, 2,3BPG and temperature favor T form so favor unloading to the tissue So those things would favor unloading to the tissue If you have Hg that goes into the tissues and the tissues are working hard, i.e. muscle tissue, making a lot of CO2, you want the Hg to dump off that oxygen in the tissues. Muscles working hard will create more lactic acid and create more lactic acidosis, so theres more hydrogen ions around. So this would favor the T form over the R form. Adult Hg having this 2,3 BPG around will favor the T form and oxygen unloading The fetal Hg has a low affinity for 2, 3 BPG and will favor oxygen grabbing. This allows for oxygen exchange at the placenta. Obviously theres a purpose for fetal hemoglobin. P506:563 Oxygen-hemoglobin dissociation curve For a given oxygenation, for a given partial pressure of oxygen, you have a certain percent of your hemoglobin molecule that is saturated with oxygen to carry it. PO2 how is it measured? Its measured as a dissolved gas. When oxygen goes to the blood, some of it is bound to hemoglobin and some of it is dissolved into the blood. PO2 is a partial pressure of oxygen, which is oxygen dissolved in blood. We measure this with an ABG. ABG measures PO2 How do we measure hemoglobin saturation? Hemoglobin saturation is measured with a pulse oximeter If you look at a PO2 of a 100, its normal and above 95% of your hemoglobin is saturated. If you go down a PO2 of 75, then you have much less of your hemoglobin saturated and then going down to 60, you see the curve getting steeper and steeper Going from 80 to 60 youll have a big drop in your Hg saturation. Much bigger than you would going from 100 to 80. You drop 20 points in your PO2, but your Hg saturation is not changing that much, as compared to when you drop from 80 to 60, where you see a bigger change. When you shift the curve to the right, how will that change things? Ex. When you shift the curve to the right for PO2 of 75, you will have less saturated hemoglobin then you would compared to normal. When you shift the curve right, you have less hemoglobin saturation for a given PO2, then you normally would. What shifts the curve to the right? Elevated 23DPG, high temperature, metabolic needs You are favoring less Hg saturation. You are favoring oxygen unloading. What shifts the curve to the left? Lets talk about PO2 of 50 You will have more hemoglobin saturated at a PO2 of 50, when you shift the curve to the left, then you would when compared to normal What shifts the curve to the left? Decrease 23DPG Decreasing hydrogen ion (increase in pH) Decrease CO2 Decreasing temperature Decreasing metabolic needs High yield P506:563 Hemoglobin modifications Ferrou2 (fe2+) binds O2 better To remember. Turn the s in ferrous into a 2. What causes methemoglobin?

Methemoglobin Typically caused by drugs (e.g., nitrates) Typically caused by drugs (e.g. nitrates) If you have have a pt having an MI and pt is put on a nitric oxide infusion this is more likely to cause methemoglobin over time. Drug-induced methemoglobinemia Antimalarial drugs Chloroquine, primaquine Dapsone, sulfonamides Local anesthetics (lidocaine) Metoclopramide Nitrates (nitroglycerine) If pt comes to hospital with an MI, you might put them on a nitro drip to relieve their chest pain, while theyre waiting for their cardiac cath or waiting for resolution of their symptoms. Its commonly the case they can be on a nitro drug. So they are more likely to have increase methemoglobin level. What do you do in that case? Theres another drug that can be used to slowly lower methemologin levels. It cant be used acutely, but its an H2 blocker (cimetidine). This can be clinically useful. Maybe you have a pt you want to put on dapsone and for some reason you are worried about development of methemoglobin, you might put them on cimetidine with a dapsone. Who could be on chronic dapsone or chronic sulfonamides? AIDS pt with CD4 count less than 200 to prevent development of PCP pneumonia. Cyanide poisoning: Recall methemoglobin has a high affinity for cyanide So by using nitrites to oxidize Hg to methemoglobin, it will allow methemoglobin molecules to go throughout the body and pick up cyanide. Then you give thiosulfate to bind this cyanide to form thiocyanate which is then renally excreted. To treat, its a two step process. Nitrate then thiosulfate. Its not always done but one way to treat cyanide poisoining. Carboxyhemoglobin: Cannot be measured with a pulse oximeter. So you could be hypoxic but with a normal pulse oximeter indicating hemoglobin saturation, but youre not getting that hemoglobin to tissues. P507:564 Pulmonary circulation PAO2 = alveolar oxygen A decrease in alveolar oxygen will cause hypoxic vasoconstriction. This is different from any other tissue. Normally if you have low oxygen in a tissue, you dilate to get more oxygen there, but here you sacrifice the perfusion to the lung in order to not induce hypoxia in the rest of your body. If your lungs are chronically encountering this low alveolar oxygen, this chronic vasoconstriction consequence of pulmonary hypertension is cor pulmonale and subsequent right ventricular failure right sided heart failure You can be Limited by perfusion which is how much blood your getting into the area If you are limited by perfusion its the normal state of oxygen If you want to get more oxygen into blood, you put more blood through the lungs. So in a normal healthy lung, oxygen is perfusion limited. You see this in the right hand graph: Along the length along the pulmonary capillary, oxygen will equilibrate from your alveoli to your arteries very rapidly and very early along the pulmonary capillary The only way you get more oxygen into circulation is by increasing the blood flow through that capillary On the left hand side graph: You see normal oxygen perfusion limited During exercise you are putting more blood through the capillaries more rapidly: you can see by increasing your perfusion, you put more total oxygen into capillaries, but per instant in time, less oxygen is being put into capillaries towards the end. Fibrosis is diffusion limited If you are fibrotic or emphysematous, gas does not equilibrate by the time blood reaches the end of the capillary. You can see that in the middle diagram As you go along the length of the pulmonary capillary (middle diagram) Your arteriole partial pressure of whatever gas you are looking at, doesnt hit the alveoli partial pressure Or you can be Limited by diffusion in how quickly gases can diffuse in and out of the blood P507:564 Pulmonary hypertension: Downstream consequences of atherosclerosis, medial hypertrophy and instimal fibrosis of pulmonary arteries is you can have Cor pulmonale and righted sided heart failure can occur There are two types of pulmonary hypertension Primary If you dont have BMPR2 gene, you have excess vascular smooth muscle proliferation and this results in primary pulmonary hypertension. Know this P1#12

Secondary Due to Renal artery stenosis will cause increase resistance and increase pressure NB: Similarly there is primary or essential hypertension: which is the most common type of hypertension And theres secondary hypertension: What causes secondary hypertension? Chronic renal disease Renal artery stenosis Pheochromocytoma Course: Cyanosis and vasoconstriction causes right ventricular hypertrophy, then right sided heart failure and death from decompensated cor pulmonale. Treatment of pulmonary hypertension: P516:577 Bosentan Also ambrisentan Drugs end in sentan Pulmonary hypertension: Treatment Bosentan Prostaglandin analogue Sildenafil Dihydropyridine calcium channel blocker Prostaglandin analogue Will dilate the pulmonary arteries Sildenafil Erectile dysfunction and pulmonary hypertension treatment Dihydropyridine CCB i.e. nifedipine P508:564 PVR P = Q x R The equation for resistance, works for resistance of blood vessels and also resistance of air going through airways. What variables can you encounter that can change airway resistance? Radius Via bronchoconstriction or bronchodilation What causes bronchoconstriction of an airway? Bronchoconstriction Causes Anaphylaxis Bronchospasm Asthma Carcinoid syndrome Parasympathetic stimulation These would increase resistance in the airway 2 sympathetic stimulation increases radius of airways, decreasing resistance What can change viscosity or density of air going through the airway? A drug that can be used is helium. If you have a pt with a tumor that is compressing an airway and creating a lot of turbulent blood flow, where you are not ventilating your alveoli very well, then you can add an oxygen combined with helium. Oxygen with helium will have less viscosity/density, so oxygen can have more laminar flow There is less turbulent and so oxygen can have a more laminar blood flow and easier for oxygen to have more laminar flow P508:565 Oxygen content of blood O2 binding capacity were talking about hemoglobin % saturation of hemoglobin In your blood you have oxygen bound to hemoglobin and dissolved oxygen The dissolved O2 measured with an ABG These numbers values are not important to know. O2 content of arterial blood decreases as Hb falls Seen with fibroid patient earlier. But O2 saturation measured with pulse oximeter and arterial PO2 measured with ABG does not change. You can have hypoxia with a normal pulse Ox and normal ABG as a result of your hemoglobin falling. Alveolar gas equation Alveolar gas equation PAO2 = PIO2 PaCO2/R PAO2 = 150 PaCO2/0.8(estimate) Where does the 150 come from? This is the O2 of inspired air. There are 2 numbers that give rise to the 150 First number is 713 which is atmospheric pressure: normal atm pressure at sea level Your PiO2 is your product of two numbers: First number is air pressure and second number is FiO2 Second number is FiO2 (fraction of inspired oxygen) = 21% If you put a nasal canula on a pt and increase oxygen, that 150 would increase. If you put someone on a high altitude that 150 would decrease. As you increase your CO2 in this equation, what will happen to oxygen? As you increase your alveolar CO2, then Your alveolar oxygen will decrease As CO2 in alveoli goes down, PAO2 will go up. More clinically relevantHow do we measure oxygenation in a patient? How do we determine how successful a patient is oxygenating themselves? The first one is the A-a gradient Its your alveolar oxygen minus your arteriolar oxygen Which is normally 10 to 15 Your alveolar oxygen is measured by using your alveolar gas equation. This is why your alveolar gas equation comes into play here. What are we talking about here? We talk about difference between the oxygen in your alveoli minus the difference of the oxygen in your blood. If the difference is large, then theres a problem with the exchange. If the difference is small, then were exchanging very easily between the two. Increase in A-a gradient may occur in hypoxemia Anything that will increase barrier between type 1 pneumocytes, basement membrane, endothelial cells will increase your A-a gradient If you increase your diffusion barrier, you wont exchange gas very well. There are two other things that will increase youre A-a gradient. FiO2 Fraction of inspired O2 If this increases, this will change youre A-a gradient. b/c theres only so much oxygen you can put into blood, but you can put a lot of oxygen in your alveoli by increasing your FiO2 So increasing your FiO2, you will flood your alveoli with oxygen and your arteries wont be flooded as much with oxygen, so that will change youre A-a gradient artificially. Age As you get older, youre A-a gradient will increase slightly with age. A high A-a gradient is usually bad How do find out arterial O2? Its easy. You just check ABG But how do you get alveolar O2? You need to use the alveolar gas equation. Easier way to measure oxygenation is to use PaO2/FiO2

Measures of oxygenation: A-a gradient PaO2/FiO2 300 to 500 mmHg is normal < 300 mmHg gas exchange deficit < 200 mmHg severe hypoxia (ARDS)

The fraction of inspired O2 will be related in someway to alveolar O2. ARDS = acute or adult respiratory distress syndrome Oxygen deprivation There are 3 ways your body can get deprived of oxygen Decrease PaO2 Not get enough oxygen dissolved into blood Decrease oxygen delivery to tissues You have oxygen in blood but the oxygen doesnt get to the tissues like it should Loose blood flow P509:566 V/Q mismatch High yield Ideally, ventilation is matched to perfusion. Usually for everything you breath in, its perfused well and you have exchanged gas. Its a 1 to 1 ratio. But functionally in the lung, its not what you get. At the apex of the lung the V/Q = 3 (so you have wasted ventilation, b/c its hard for blood to get to the apex), its easy to get air into the apex and blood is heavier than air. So you have more air in the apex than you do blood. So this is wasted ventilation and is referred to as dead space. At the base of the lung you have wasted perfusion. You have lots of blood going to the base of the lung, and sooo much that you cant ventilate it enough. This is called shunting. Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung. Know this. Theres really poor perfusion at the apex. Ratios are important. If you were to measure the amount of oxygen coming out of the alveoli If the apex versus oxygen at the base of the lung, you would have less oxygen at the base of the lung coming outward during an exhalation During exhalation you have more oxygen coming out of the apex of the lung b/c you are not perfusing it very well, then would be coming out of the base of the lung. This is why tuberculosis prefers apexes of the lungs b/c it prefers higher oxygenation. Youre not pulling out all of the oxygen out, like you are at the base. With exercise (increase CO), there is vasodilation of apical capillaries, resultling in a V/Q ratio that approaches 1. During exercise V/Q ratio goes down from 3 to 1. You are no longer wasting ventilation b/c perfusion increases in that area. V/Q approaching zero is a low ventilation, a high perfusion is seen with airway obstruction. (low ventilation). Its referred to as shunting. Blood is going through this region and not getting oxygen. In shunting, a 100% oxygen does not really improve the partial pressure of oxygen in the blood b/c you are not getting oxygen there b/c you have a blockade. The reverse is true with a high ventilation and a low perfusion. So V/Q approaching infinity. This is a blood flow obstruction. Or physiologic dead space. Assuming < 100% dead space, 100% oxygen will improve PO2 b/c the perfusion will be rerouted to other areas. You will perfuse areas that are getting oxygen. So maximizing oxygen in those areas will improve the blood content of oxygen. CO2 transport NB: Oxygen is in two forms: dissolved in blood and bound to hemoglobin CO2 is transported from tissues to the lungs in 3 forms How does CO2 become bicarbonate? You see carbonic anhydrase in RBC CO2 can bind to Hg at N terminus of globin (not heme: since heme binds to Oxygen) As carbaminohemoglobin = when CO2 is bound to N terminus of globin 5% of CO2 is transported this way Dissolved CO2 is measured by an ABG P509:567 Response to high altitude (less oxygen in higher altitudes) How does your body make changes/adjustments whenever you have low oxygenation at high altitudes? Increase EPO from kidneys Some athletes will train at high altitudes to have some physiologic blood doping If you want to climb mount Everest, you might want to train at high altitudes to help your body adjust to those high altitudes You create more 2, 3 BPG to get oxygen to tissues better Cellular changes You will maximize the capability of the cells to use oxygen and you do so by increasing the amount of mitochondria in your cells Increase renal excretion of bicarbonate to compensate for the respiratory alkalosisWhy do you have respiratory alkalosis? You are breathing more You are acutely and chronically increasing ventilation So you are blowing out more CO2. So this causes respiratory alkalosis. So your body will excrete bicarbonate to compensate for this. This will take a few days for this to take place (3 to 4 days). You can augment this process with acetazolamide for altitude sickness. Chronic hypoxic pulmonary vasoconstriction results in RVH What do we call this? Cor pulmonale. This is an unwanted consequence of response to high altitude. Response to exercise PaO2 = arteriolar O2 PaCO2 = arteriolar CO2 P2#13

Virchows triad Predisposes you to coagulation and to DVTs, PEs and other emboli Stasis: Is seen in the Post-op state If you are in bed and cant go to the bathroom, you are static Increase likelihood of developing a blood clot in your leg b/c what causes venous return? Muscle contraction. You have valves in veins of the legs. The valves dont do anything. When you contract your muscles, blood goes up and doesnt go back down. If you are not contracting, then you will have stasis. Long trips Cast Pregnancy Postpartum state (laying in bed and not feel like getting up) Hypercoagulability Increase viscosity of blood Cant combine estrogen (OCPs) and smoking with a pt over 35 years old Endothelial damage NB: Postpartum: you have all 3 Estrogen excess Stasis Endothelial damage Postpartum pts Have Higher risk of acquiring DVTs and less likely to have postpartum hemorrhage. P510:568 DVTs: NB: Bilateral swollen foot/ankle would be seen in heart failure Vein could be hard and palpable (palpable cord) Measure the foot. If it looks swollen compare one side to another. Measure Calf diameter/circumference. If it is larger then do the Next step: is do an ultrasound. To diagnose a DVT is to do an ultrasound compression. Are the veins compressable. Look at veins and see if blood is flowing through there. Are the veins compressable? We are talking lower extremity duplex scan. Prevent DVTs? Can give heparin subcutaneously twice a day or 3 times a day Low molecular weight heparin can be given once or twice a day Enoxaparin is an alternative SCDs (spontaneous compression devices), these go over the calfs and inflates their pneumoatic devices and so they do the work by moving blood through the veins for you b/c you are not moving the muscles enough to do them on your own. Long-term warfarin or Coumadin will prevent DVTs DVT can embolize and cause a pulmonary embolus If you have a patent foramen ovale (PFO) then the embolus can cross over the left side of the circulation and cause a stroke. Pulmonary embolism AMS = altered mental status 3 most common things youll see in a hospitalized pt or any pt with a PE are: Tachypnea, tachycardia, AMS/confusion If you see these 3 things, you need to rule out a PE How do evaluate this? If a d-dimer is not elevated, theres probably no excess clotting somewhere in the leg or anywhere. LE = lower extremity Large Aa gradient on ABG b/c you are not perfusing your lungs very well

Pulmonary embolism: EKG changes: S1Q3T3 = Wide S in lead I Large Q Inverted T in lead III This is a common pimp question for your IM rotation You can do a CT scan PE protocol where dye is injected and youre looking for a defect in a normally highlighted vasculature This is IV contrast dye. You cant give it to who?

You cant give IV contrast dye to: Renal failure Chronic kidney disease Anybody on metformin

It could cause a contrast induced nephropathy If theyre on metformin, they need to be off of it for at least 24 hours before they can receive IV contrast dye. So sometimes you cant do the CT scan PE protocol, so in that case you go to the V/Q scan Gold standard is pulmonary angiogram Image of a normal V/Q scan The top two rows of the scan is where pt has inhaled a radionucleotide that is decaying and is highlighting the lungs (goes in the alveoli) Bottom two rows, a radioisotope has gone into the pt and goes to the lungs and is highlighting the lungs Everything is perfused and ventilated the way it should be Top two rows, everything is ventilated pretty well, you have normal ventilation But the bottom two rows, the lungs are not as high lighted clearly as they were in the previous image. You are not perfusing your lungs very well. Something is interrupting the perfusion to the lungs. This is a high probability VQ scan As a radiologist You cant say pt has a PE. All you can say is the lungs are not getting perfused and its a high probability for a PE. Diagnosis falls onto the clinician to say, given this high probability VQ scan and constellation of symptoms this pt is having a PE. One leg is larger than the other leg Pt with DVT One leg h as Purplish appearance consistent with venous congestion. If you are blocking the venous outflow with venous thrombus, then you will have venous congestion with lower extremity edema. You can diagnose this with a calf circumference. Saddle embolus straddles the bifurcation of the pulmonary arteries so that the lungs are not getting any perfusion at all. Its complete obstruction with an embolus. This causes instantaneous death. Treatment For massive PE, consider thrombolysis Thrombolytic agents TPA Streptokinase urokinase P510:567 Embolus types When do you get an air embolus? Caisson disease The bends Decompression illness Scuba diving and come up too quickly When do you get a bacterial embolus? Bacterial endocarditis P510 Obstructive lung disease You need to know the hallmark of obstructive lung disease compared to the hallmark findings of restrictive lung diseases FVC = functional vital capacity P512:570 Look at this graphically Obstructive vs restrictive lung disease High yield Left hand side In a normal lung FEV1/FVC ratio is about 80% you will get rid of a lot of volume at that 1 second mark middle diagram: obstructive lung disease FEV1/FVC ratio is < 80% Look at graph See FEV1 has increased and FVC has also increased So both of these have decreased in capacity But the ratio is most important With obstructive lung disease you have trapping of air. So you see the total lung volume is higher than it is in a normal lung. You have a lot of air you cant get out of the lungs b/c airways are collapsing prematurely. Right diagram Restrictive lung disease FEV1/FVC ratio remains normal But the absolute values of FEV1 and FVC are still decreased compared to normal lung Hallmark: You are restricted at how much air you can get into the lungs So the total lung capacity is greatly decreased TLC of normal = 6.5 L TLC of RD = 3 L You cant get air in RD TLC of OD = 8 L Trapped air in OD Chronic bronchitis Histologically you can see the hypertrophy of mucus-secreting glands n the bronchioles Reid index = gland depth divided by total thickness of bronchial wall You have your entire bronchial wall and a small portion of that should be your glands If over half of your bronchial wall is these mucus secreting glands, than obviously its mucus-secreting gland hypertrophy This is an elevated reid index >50% This is chronic bronchitis How do diagnose this? You dont need histology. Its a clinical diagnosis. Productive cough for > 3 consecutive moths in >= 2 years. Wheezing is an interesting thing b/c we usually associate it with asthma But not all wheezes is asthma Emphysema Barrel shaped chest chest wall wants to expands (lungs want to collapse) So if you can put more air into the lungs b/c the compliance of the lungs has been increased b/c the alveolar walls have been broken down, then the chest wall will be allowed to expand Therefore, Emphysema pts are barrel chested b/c they are trapping air and more air can fit into that space Carbon deposits is called Anthracosis (coal miners can get this also) There are two types of emphysema Centriacinar emphysema Just your central portion is destructed and this is caused by smoking Panacinar emphysema Is due to alpha 1 antitrypsin deficiency This is a systemic disease Will destroy your entire acini Alpha 1 antitrypsin deficiency is characterized by two things: 1) emphysema at an early age i.e. 20 or 30 year old, this is unusual. We dont normally see emphysema until theyre in their 50s or 60s. 2) liver cirrhosis Alpha 1 antitrypsin protects against elastase (the degradation of elastic fibers in the lung) It decreases the activity of elastase With alpha1 antitrypsin deficiency, you will have overactive elastase which will break down elastic tissue in lungs. This is not the same mechanism you see with cirrhosis with alpha 1 antitrypsin disease. Paraseptal emphysema a/w bullae can rupture and can result in a spontaneous pneumothorax; often seen in young, otherwise healthy males if you do an xray of the chest and you see this big large bullus pocket, looks like an air cavity, its a good chance its a bullae of bullus emphysema or paraseptal emphysema Asthma Reversibility is a hallmark of asthma If a pt has decreased FEV1/FVC ratio and you give a B2 agonist i.e. albuterol and the ratio corrects, then theres a component of asthma Theres some reversibility. And it shows theres a component of asthma. If a pt shows up with a 40 pack year of smoking, dont assume that they have chronic bronchitis or emphysema They may respond to albuterol, there may be an asthma component as well as there is bronchospasm, the muscles have to work harder and they can become hypertrophied lead to smooth muscle hypertrophy Charcot leyden crystals These are crystals a/w eosinophilic inflammation There is aspirin sensitive asthma Aspirin can trigger asthma Findings Decreased inspiratory/expiratory ratio pulsus paradoxus is when you take a deep breath and you decrease intrathoracic pressure and that causes increased blood flow into the right ventricle under certain pathological conditions, that increase blood flow can cause the ventricular septum to push over into the left ventricle, so you have decreased blood flowing into the left ventricle. So youll have decreased left ventricular output and a small drop in systolic blood pressure. If the drop in systolic BP is > 10 mmHG, this is pulsus paradoxus. Under normal circumstances you get a small drop in BP, fewer than 10 mmHg. Also seen in cardiac conditions i.e. cardiac tamponade, or pericarditis where you have restriction of the pericardial space where the heart cant expand fully, so when right ventricle fills with blood it will push the septum over to the left ventricle. Also seen in pulmonary diseases i.e. pulmonary embolism and obstructive lung disease i.e. asthma asthma is also a/w eosinophilia p2#18

Eosinophilia D NAAACP Drugs Neoplasm Allergy, asthma (Churg-straus) Addisons (adrenal insufficiency) AIN acute interstitial nephritis Collagen vascular disease Parasites (lofflers eosinophilic pneumonitis due to Ascaris lumbricoides)

DNAAACP First a is for atopic diseases i.e. allergy, asthma Churg straus is a type of vasculitis affecting the sinuses and the lungs and this leads to asthma symptoms Addisons disease (primary adrenal insufficiency) Parasites Helminthic infections: Ascaris lumbricoides, strongiloides and various hook worms. Mnemonic DNAAACP is very important and useful clinically and for USMLE. Memorize this. Treatment for asthma: P515:576 There are two main components of asthma Asthma is composed of bronchospasm and inflammation So drugs we use to treat asthma will target each of those Nonspecific beta-agonists Isoproterenol iso means same so has same effect on B1 and B2 receptors Can lead to tremor and jitteriness B2-agonists Albuterol DOC for acute exacerbation for asthma Given as a nebulizer or inhaler It does have some mild B1 agonist activity especially at higher doses So if you have a pt with prolonged asthma attack and you are giving albuterol, again again and again pt can get jitteriness and tachycardia as a result of that. Levalbuterol Its the the R-antiomer of albuterol Its a stereoisomer of albuterol It has less B1 effect So you can give it in higher doses if needed Salmeterol Not used to treat an asthma attack but used to prevent an asthma attack One potential problem with salmeterol: It can cause tolerance against B2 agonist So if you have a pt on salmeterol and they get an acute exacerbation of asthma and you need to give albuterol, the pt wont be as responsive to albuterol. Methylxanthines: Theophylline This is a drug of last resort b/c it has a low therapeutic drug index Can cause cardiotoxicity Cause tachycardia, hypotension Can cause neurotoxicity Can include seizures Antidote for theophylline overdose? Beta blockers If you have a pt with tachycardia from overdose from theophylline you want to give a beta blocker. Amenophylline Not commonly used any more Caffeine Less potent and really not used therapeutically Muscarinic antagonists: Ipratropium: Muscarinic antagonist Doesnt cause bronchodilation but it prevents bronchoconstriction Often used in combination with albuterol Cromolyn An older drug and not widely used anymore Safe drug and available over the counter. Not for asthma but for allergies as a cromo nasal spray. Blocks release of mast cells mediators i.e. histamine. Problem is that its slow acting and can take days for it to start working. Need to be given 3 times a day. So its not widely used b/c of this. Corticosteroids: These are very important Glucocorticoids Beclomethasone, prednisone Methyl prednisolone (is an important drug used for asthma) This can be given IV or orally for the treatment of asthma Inhaled corticosteroids is 1st line therapy for chronic asthma This is important to know But if you have an acute attack: you treat the broncospasm with a beta agonist i.e. albuterol. Maybe you will use ipratropium. If you have an acute attack that is severe, you can also give oral or IV glucocorticoids It doesnt make a difference in terms of efficacy if you give oral or IV (they will both work about the same) and they both will take about 4 hours to work People think, if I give the IV steroid it will work faster. But its not true. If you have a pt with an acute asthma attack and you treat them with albuterol and ipratropium and you give the steroid either IV or orally. Monitor the pt for 4 hours and see if the steroids will work. Keep giving albuterol as needed. Its usually very effective. Antileukotrienes Leukotriene inhibitors Zileuton Was discussed in the arachadonic acid pathway Zafirlukast, montelukast Are more commonly used Used to treat allergies NB: You can remember the difference between these two drugs and zileuton in that think of montelukast sounds like last, which inhibits the last step in leukotriene, which is where leukotriene attach to the receptors. A distinction between zafirlukast and montelukast Zafirlukast is FDA approved for pts 5 years of age and older Montelukast is approved for pts 1 years of age and older Its important to know the age which you can give these drugs. Its a huge hint clinically and for USMLE. Most common symptom of asthma Cough Along with recurrent wheezing, difficulty breathing when exercising and recurrent chest tightness What are the two components of an asthma attack? Inflammation and bronchoconstriction P514:575 H1 blockers Important for type1 hypersensitivity, including asthma Antihistamines 1st generation Hydroxyzine Its very sedating Toxicity: You dont want to give first generation antihistamine drugs to elderly pts b/c they will get MAD AS A HATTER They will get delirious (delirium), exacerbate dementia You want to avoid first generation antihistamines 2nd generation In high doses can be sedating i.e. cetirizine P2#22

Read it Hydroxyzine Used for sedation, itching, rash, good antihistamine You can use it as an anxiolytic or sleep aid. Hypnotic sedative drug if you need to calm someone down and you dont want to give them a benzodiazepine for some reason. P510:568 Bronchiectasis Cystic fibrosis is one of the common causes of bronchiectasis Inhaling tobacco smoke paralysis the cilia If you have a smoker that is coughing up a whole lot, they often reach for a cigarette to suppress their cough b/c it inhibits the ciliary motility Kartageners syndrome has the dynein defect where cilia are immotile Pseudomonas is a big infection these pts can get They are chronically on fluoroquinolones to address the pseudomonas P511:569 Restrictive lung disease Hallmark of a restrictive lung disease Decrease TLC Decrease lung volume (your lung is restricted at how much volume it can put in the lungs) NB: FEV1 and FVC are both decreased, but the ratio is normal. > 80% Different things that can cause restrictive lung disease Poor breathing mechanics Poor muscular effort Paralyzed b/c of polio Guillan barre syndrome can result in respiratory paralysis Poor structural apparatus Morbid obesity You have so much weight on your chest that its difficult to expand the chest wall Interstitial lung diseases Can restrict your lung capacity P511:570 ARDS (adult respiratory distress syndrome) Due to anything that can severely damage the lungs P3#25

Oxygen can be very toxic b/c it has oxygen free radicals in it Heroin overdose can cause ARDS ARDS you will get DAD and HMD As a consequence of that, it will cause more inflammatory cells and mediators and oxygen free radicals causing more damage and then it becomes a viscious cycle that you just cant stop. Look back at page 511 You have protein rich leakage into alveoli Immune system is causing all the damage and not the toxic insults Activation of coagulation cascade get DIC as a result. Look at thick diffusion barrier. See huge hyaline membrane. No oxygen will go through this thick diffusion barrier. You wont oxygenate this very well. The same process occurs with neonatal respiratory distress syndrome, but its not due to the toxic insult but its due to a surfactant deficiency P511:569 Neonatal respiratory distress syndrome If you need to deliver between 34 to 37 weeks, what do you need to do to assess the fetal lung maturity? Need to do an amniocentesis to check the lecithin to sphingomyelin ratio (L:S) If the ratio is less than 1.5 in the amniotic fluid, then you know delivering that neonate has a high likelihood of developing neonatal respiratory distress syndrome If the ratio is greater than 2.0, you are safe What if its between 1.5 to 2.0, then its a give or take and how confident you are that the lungs are mature and on gestational age and how severe the moms illness is. Treatment: Maternal steroids before birth The steroids will mature those type 2 pneumocytes more prematurily i.e. if you want to deliver a baby at 33 weeks or 34 weeks, you would give the mom steroids to mature the type 2 pneumocytes, so that when they were delivered, there is less likelihood of infant having NRDS. FYI There is no effect of maternal steroids beyond 34 weeks gestation. Up to 34 weeks and 5 days or 6 days. After 35 week marker, there is no benefit of maternal steroids. You can give it at 35 or 36 weeks, but there is no benefit. Oxygen can be very toxic. When you ventilate a pt who is a newborn or adult, you might need to increase oxygen content of air. Normal air has 21% oxygen. But the pt could be breathing 50% or 75%. But you want to lower that back down to 21% as soon as you can. Its the first thing you lower in your ventilator settings to get pt back down to normal breathing status.

Supplemental oxygen: Lower O2 back down to 21% ASAP

Treatment: If neonate is born with NRDS Give surfactant and intubate them and you shuff surfactant down their trachea and position them at 4 different directions. Give 4 different doses to fill up 4 different quandrants of the lung with surfactant. P511:569 Pneumoconiosis Coal miners There are different degrees of CWP First degree is anthracosis Pts that live in big cities that breath in the polluted air will have a mild anthracosis Pts that smoke will have a mild anthracosis And beginning stage of CWP is anthracosis If you are a coal worker, it could progress to a simple CWP Silicosis Need to know risk factors for these diseases Silica in the lung wont do anything. Its the macrophages that cause the damage and fibrosis. Does silicosis increase your risk for lung cancer? No. does CWP increase your risk for lung cancer? No what about asbestosis? yes asbestosis macrophages also cause the damage P511:569 Restrictive lung disease Sarcoidosis Lymphadenopathy is so severe that it can restrict the capacity of the lungs Goodpastures syndrome Antibasement membrane antibodies Affects the lungs and kidneys Wegeners granulomatosis Affects the lungs and kidneys To distinguish between goodpastures and wegeners: Wegeners Is an upper airway disease Drug toxicity Belomycin, busulfan, amiodarone can cause lung fibrosis and cause restrictive lung disease In amiodarone what do you have to check? TFTs b/c of Thyroid disease LFTs b/c of liver disease PFTs b/c of fibrosis See lung damaged with amiodarone toxicity Its not normal to have a nice outline of the bronchi So theres something going on with the lung parenchyma and allows the bronchi to stand out P512:570 Sleep apnea Central sleep apnea This is common in premature infants They dont have respiratory drive yet OSA You would see movement of the chest wall but air is not going anywhere. Theres no movement of air Usually due to a soft palate falling back in place, or tonsils can be swollen But classic is soft palate falling back to airway b/c youre not getting air to the lungs, lungs will get hypoxic and cause vasoconstriction, resulting in pulmonary hypertension and possibly even cor pulmonale. Pts could get excessive day time sleepiness Can be dangerous if driving or operating heavy machinery Treatment: Surgery Tonsillectomy Adenoidectomy Remove soft palate and uvula Avoid sedatives If you give alcohol or benzo to help them sleep ,it will make apnea even worst If they have excessive day time sleepiness they may need day time amphetamines i.e. modafinil For central sleep apnea Not in the case of new borns, but you can use caffeine to treat CSA. There is a respiratory effort and can help in that process. P512:571 Lung physical findings Bronchial obstruction Air cant get into the affected portion of the lung b/c bronchi is obstructed This is atelectasis Lung collapse and will pull everything towards it, so trachea will deviate towards side of the lesion Severe atelectasis is severe lung collapse is not a/w air in intrapleural space will move trachea towards side of lesion Pleural effusion In between the lung and chest wall is your pleural space That space is filling up with fluid Dont confuse pleural effusion with pulmonary edema They commonly go hand in hand. CHF, heart failure, where you have a left sided heart failure and back up of blood in the lungs, will cause both pulmonary edema and pleural effusion. But there are things that can cause pulmonary edema and dont cause pleural effusion and vice versa. Decrease breath sounds over effusion b/c there is fluid Theres dullness on percussion. Tapping like a water balloon Fremitus will be decreased Pneumonia (lobar) Tension pneumothorax Severe disease. Life threatening disease Common with trauma or puncture injuries You puncture chest wall and you puncture the lung and it creates a one way valve. So when you breath, air goes in the lung and escapes to the pleural space but its stuck there and it cant go back into the lung and back out So with each breath, you put more air in the pleural space As this happens, it will collapse the lung and push everything over. So you will have tracheal deviation away from the side of the lesion. Breath sounds will be decreased b/c you will stop filling up the lung, as it will be collapsed Hyperresonant: like a big empty bottle Could have subcutaneous emphysema All that air in the pleural space can move outwards into other tissues. Could get subcutaneous air pockets 1) hyperlucent lung field is filled with air Treatment: Need to dart the lung at the midclavicular line, 2nd or 3rd intercostal space to immediately relieve that pressure. Get that air out of there ASAP. You need to place a chest tube in. Spontaneous pneumothorax Is a collapse of the lung where you dont have this one way valve effect Air got into the pleural space for some reason and it was a one time event. Its not worsening or progressing. You have air in the thorax. This is common with bullous emphysema and common with young thin teenage males. Pneumothorax can be subtle. But you see a line, where the lung edge is. If the lung edge is not all the way to the chest wall, then that means theres air between the lung and chest wall. This is a pneumothorax. To identify a pneumothorax is there is Also suttle vascular markings going all the way out to the edge of the lung (not seen here but would be seen on a radiograph and if doesnt reach the chest wall,) could also indicate a pneumothorax. If you dont see a distinct line marking the edge of the lung, you might see vascular lining that abruptly halt and this would also indicate a pneumothorax Easier to identify on CT scan. This could be a spontaneous pneumothorax. This could be a tension pneumothorax that has not y et developed into a massive tension pneumothorax. But with a spontaneous pneumothorax at lot of times these patients just need supplemental oxygen and need to be monitored over time. Treatment of sponatenous pneumothorax Pts usually just need supplemental oxygen and need to be monitored over time Sometimes will need a chest tube if its very large But If its small, just monitor them with serial xrays to make sure its not getting larger and make sure its not getting worst. P513:571 Lung cancer Metastases to lung is most common. Presents with dyspnea, cough. SPHERE of complications Superior vena cava syndrome This is a bulk effect You have this mass in your lung and its growing. And it compresses the SVC and the SVC cant drain anymore So this is a neoplastic emergency Youll have a lot of congestion on the face, arm. Places drained by the SVC will be congested with venous blood. Pancoast tumorp572 Can result in horners syndrome Usually a unilateral phenomenon Sympathetic innervation to your face goes down to T1 and comes back up. Endocrine effects: Recurrent laryngeal symptoms If your cancer invades your recurrent laryngeal nerve Then you can get hoarseness NB: If you invasion of the cancer into the esophagus, then you will have dysphagia and potentially an inability to swallow. This is a terrible complication to have b/c you have to make a decision: this cancer is out of control Do I let this be the terminal event and stop eating and stop nutrition b/c cancer will kill me anyway, or do I get a peg tube in and get fed through stomach and continue on until cancer does something else to me inevitably. So its a hard decision to make and is heart wrenching. Another complication of lung cancer is Laryngeal invasion It can invade the larynx, then you cant breath if larynx is obstructed If you have an obstructive bronchi or larynx, what can you do to decrease the turbulent flow through that region? You can give helium. Where you replace nitrogen with helium and theres less viscosity/density of that air, so it will result in more laminar flow of the air as opposed to turbulent flow, so it can go to where it needs to go. Squamous cell carcinoma squamous is central in location Central location means towards the hilum of the lung. Not towards the periphery of the lung. a/w smoking characteristic: hilar mass arising from bronchus cavitation its paraneoplastic syndrome can be PTHrP PTHrP = PTH related peptide Works the same way will break down bone and put calcium into the serum causing hypercalcemia and trashing your phosphate. Histologically: any squamous cell can elaborate keratin pearls Squamous cells of the lung dont normally elaborate keratin, but when they are mutated and cause cancer, they might start doing so. So keratin pearls is a classic histiological finding of squamous cell cancer of wherever its coming from. Is you see a keratin pearl, then its squamous cell cancer. Adenocarcinoma: This is peripheral location Small cell Is a/w L-myc oncogene a/w smoking its called small cell b/c the nucleus to cytoplasmic ratio is very high. Very little cytoplasm, small little blue cells. Very anaplastic in appearance. a/w ectopic production of ACTH What would this cause? Cushings syndrome Is this suppresable with dexamethasone, low or high dose dexamethasone? No. Its not suppresable. ADH Will cause SIADH You have antidiuresis, which is retention of fluid, dropping of the sodium levels systemically May lead to lambert-eaton syndrome Will get weakness as a result of this Weakness improves with use You can provide a passive static resistance and when you let go of the static resistance, the muscle is improved with use. The most rapidly dividing cells are also the most responsive to chemotherapy See small blue cells Hard to identify is you see this slide and nothing else. Large cell carcinoma Carcinoid tumor

Carcinoid syndrome: Symptoms Bronchospasm and wheezing Flushing Diarrhea Right-sided heart lesions Can cause carcinoid syndrome Mnemonic BFDR Bronchospasm and wheezing Flushing Diarrhea Ride sided heart lesions Right sided valvular Right sided murmur Two most common locations for carcinoid tumor is the lung and GI tract. Its the most common tumor of the appendix, but its not the most common tumor of carcinoids. Mesothelioma Mnemonic for psammoma bodies is PSMM One of the Ms is for mesothelioma Looks like rings on a tree, concentric calcification Metastases We are talking about lung cancer metastasizing somewhere else Commonly goes to adrenal, brain, bone, and liver. What increases the risk of lung cancer? Radon A heavy gas and settles down in basements and in coal mines. P514:573 Pneumonia Lobar One or more entire lobes are involved If you have a bilateral lobar pneumonia On one lung, one lobe is involved and on the other lung, one lobe is involved then this is a huge red flag If pt looks fine, dont believe it. A bilateral lobar pneumonia is bad news. Get pt to the hospital and watch them closely. Consolidation as seen on the xray: may involve the entire lung Can start in one lobe and can sometimes go to the entire lung Bronchopneumonia Is where you Have a patchy involvement in one or more lobes See cystic cavities at the upper right hand side of the CT scan Interstitial (atypical) pneumonia) aka walking pneumonia Treatment Macrolides Azithromycin arithromycin hallmarks: Xray looks worst than the symptoms Diffuse patchy involvement seen on xray Pts do not present with fever, SOB. They might just have a cough that doesnt go away for weeks. Lung abscess Can be a cause from pts on ventilators, pts with NG tubes in will more likely aspirate. P514:574 Pleural effusions: Transudate vs exudate Also discussed in P223:248 Transudate Have high electrolyte fluid Things where you tend to lose fluid into tissues will cause a transudate of a pleural effusion CHF and nephrotic syndrome you can hold on to it b/c you Loose your oncotic pressure in capillaries, so fluid leaks out With hepatic cirrhosis, a lot of your blood proteins come from your liver i.e. your coagulation factors and albumin and when you are cirrhotic you dont make those blood proteins and thats a loss of intracapillary oncotic pressure that would normally retain fluid in the capillaries

Different causes of pleural effusions: Cause of transudate Fluid overload Pt can be on 1.5 maintenance fluid and you forget to turn it off and they have a normal diet and they drink stuff. They get fluid overload and kidneys cant handle it. They could be an elderly. This is a common error made by interns. What do you do? Where you gave too much fluid and Pt will get SOB Do a nebulizer treatment for the SOB You need to give them a diuretic to get rid of that fluid. You give them a loop diuretic. Cause of Exudate NB: What you can do with pleural effusions, is you can take an xray and you see the effusion on a PA or AP xray. You need to know if that effusion is mobile. So lay the pt down and take another xray. If the fluid layers out horizontally on a lateral film xray. Then its most likely a transudate, b/c its layering out and its mobile and its a sloshy fluid. If it doesnt layer out, it could just be a big pocket of pus, that needs to be drained. This is just a clinical pearl and not important for step1 Lymphatic pleural effusion When can you get a lymphatic pleural effusion (lymphatic fluid in your pleural space)? Your thoracic duct goes to that region Your thoracic duct carries lymphatic tissue back to your circulation. If you rupture your thoracic duct, all that lympathic fluid will go into the pleural space and cause a lymphatic pleural effusion. NB: What anesthetic is high in triglyceride, also with a milky appearance? Propofol There is a specific name of pleural effusion full of lymphatic fluid: it is called chylothorax. Why is it called a chylothorax? What else is in your lymphatic fluid? Chylomicrons (this is where triglycerides come from) You absorb triglycerides and then they go into the lymphatic fluid as chylomicrons and theyre digested into chylomicron remnants and then they go in the liver. Chylothorax is lympathic fluid in your pleural space NBWhat is hydrothorax? Its pleural fluid in the pleural space. You get water like fluid in the lymphatic space. P516:577 Expectorants Drugs that loosen up sputum and allow you to get it out is an expectorant Guaifenesin Large doses are necessary So you give guaifenesin with a cough suppressant like an opioid (an opioid i.e. dextromethorphan: rubitusin DM or mucinex DM) N-acetylcysteine Can loosen mucous plugs How? It cleaves disulfide bonds within mucous glycoproteinsin cystic fibrosis patients

N-acetylcysteine: Used as antidote for acetaminophen overdose because it regenerates glutathione What is used as an antidote for acetaminophen overdose? N-acetylcysteine Why? b/c it regenerates glutathione Glutathione is an antioxidant A third use is it can be given: it tastes terrible. It has a sulfur taste to it and smells awful. You can ingest it orally and it can help protect the kidneys against contrast induced renal nephropathy. So you can ingest it 24 hours before and 24 hours after the contrast. So if you have a pt with chronic kidney disease, you need to do a CT scan, PE protocol, where you inject dye looking for a defect in the circulation indicative of a pulmonary embolus. If you need to do this study and you have a pt with questionable kidneys, you might give them N-acetylcysteine for 24 hours before and 24 hours after the study.