Mastering the Art and Science of Respiratory Assessment

0:00 Critical Decisions in Respiratory Emergencies Imagine walking into a patient's room. You just got on shift. You're doing your initial rounds and you find a patient leaning over a basin coughing up blood. 0:09 Speaker 2 Yeah, that is. That's a terrifying moment for anyone. 0:11 Speaker 1 Right. And in the next 30 seconds, you have to make a decision that will basically dictate their entire trajectory of care. I mean, is that blood coming from their lungs or is it coming from their stomach? 0:22 Speaker 2 Exactly. And your ability to instantly tell the difference between, you know, frothy bright red blood and dark coffee brown blood is literally the difference between calling the pulmonary team for a massive airway hemorrhage or calling the GI team for a ruptured esophageal varix. 0:39 Speaker 1 It's massive. So welcome to a special after class Heroes deep dive. I am so glad you're here with us today. We are taking all those raw materials you've been handed in your lectures specifically for NCM 212 care of clients with problems in oxygenation, and we were figuring out how to actually use them at the bedside. 0:56 Speaker 2 Which is honestly the most critical transition you make in clinical practice. It's moving from just memorizing A textbook list of symptoms to understanding the actual underlying mechanical failures causing them. 1:08 Speaker 1 Yeah, getting past the flash cards. 1:09 Speaker 2 Exactly, because when you understand the machinery of the human body, the symptoms just become clues, right? They just point you directly to the broken part. 1:17 Speaker 1 And that ties directly into the core philosophy we operate on here. We believe nursing is a fidelity. 1:24 Speaker 2 It's a promise. 1:24 Speaker 1 Right. A steadfast, non negotiable commitment to being two things at the exact same time, technically competent and deeply compassionate. I mean, empathy is absolutely vital, but holding a patient's hand doesn't stop them from going into respiratory arrest. 1:40 Speaker 2 It really doesn't. True fidelity means having the rigorous, unshakable knowledge to keep your patient safe. You cannot have true compassion without competence. 1:48 Speaker 1 So well said, which is why today's focus on the comprehensive respiratory assessment is so incredibly vital. 1:54 Speaker 2 Yeah, because alterations and respiratory status are one of the most reliable, earliest predictors of clinical deterioration in any hospitalized patient. 2:02 Speaker 1 The lungs will tell on the rest of the body. 2:04 Speaker 2 They will. The lungs will often tell you a patient is crashing hours, sometimes a whole shift before their blood pressure drops or their heart gives out. If you know how to listen, you can intervene before it becomes a code blue. 2:17 Anatomy and Physiology of Breathing So let's build this from the ground upright. To assess a patient accurately, we need a quick foundational call back to the anatomical landscape we're exploring. I don't want to get bogged down to basic anatomy, but we do have to know the layout of the plumbing. 2:31 Speaker 2 We do. 2:32 Speaker 1 So we've got the upper airway, the nose, pharynx and larynx. And the nose isn't just an air intake, right? It's basically a climate control system. 2:40 Speaker 2 Oh, it is a highly specialized piece of HVAC equipment. I mean, the nasal mucosa is incredibly vascular, which is why it looks redder than the inside of your mouth. Makes sense. Yeah. So when cold, dry air enters the nose, that rich blood supply acts like a radiator. 2:58 It warms the air to body temperature. And the mucous membrane also humidifies that air, adding moisture so it doesn't dry out the delicate tissues deep in the lungs. 3:07 Speaker 1 And you've got those little hairs too, right? 3:09 Speaker 2 The vibrice. Yep, they act as a physical filter for large dust particles. 3:13 Speaker 1 So wait, if a patient has a tracheostomy or they are intubated, we've completely bypassed that entire HVAC system. We are just dumping cold dry room air directly into their lower trachea. 3:27 Speaker 2 Which is exactly why you see us hooking up artificial humidification and warming circuits to those patients oxygen sources. 3:34 Speaker 1 If you don't do that. 3:35 Speaker 2 If you don't, the secretions in their airway will just dry up, they turn into these thick cement like crusts and they will completely block the tube. You have to replace the physiologic function you bypass. 3:45 Speaker 1 Wow. OK, so then the air moves past the larynx, which is the intersection of the respiratory and digestive tracts, and it hits the larynx, the voice box. 3:54 Speaker 2 Right, but vocalization is almost a secondary benefit there. The primary life saving function of the larynx is protection. It's the watchdog of the. 4:01 Speaker 1 Lungs. I love that analogy. The watchdog. 4:03 Speaker 2 It fits perfectly. The larynx utilizing the epiglottis is a dynamic valve. When you swallow that valve, snap shut, sealing off the trachea so food and liquid are directed down the esophagus. 4:14 Speaker 1 And then it just springs open when you inhale. 4:16 Speaker 2 Exactly. And it also facilitates the cough reflex. So if a drop of water or a crumb gets past the epiglottis, the vocal cord spasm, the pressure builds up in the chest and it violently ejects the foreign body. 4:29 Speaker 1 So if that watchdog gets paralyzed or depressed, say by a stroke or by heavy sedation, the patient loses that protection. 4:36 Speaker 2 And they aspirate. It's that simple. 4:39 Speaker 1 Right past the watchdog we enter the lower airway, the trachea or windpipe, and this is supported by those shaved rings of cartilage. Now I always thought it was strange there aren't complete circles. I mean if their job is to keep the airway from collapsing when you take a Dee breath, wouldn't a full structural ring be stronger? 4:57 Speaker 2 Structurally maybe, but biomechanically it would be a total disaster. 5:01 Speaker 1 Really. Why? 5:02 Speaker 2 Well, think about the esophagus, the food tube. It runs vertically right behind the trachea. They actually share a wall. If the trachea were made of solid and flexible circles of bone or cartilage, every time you swallowed a large solid piece of food, it would just get stuck. 5:17 Speaker 1 Oh, because the esophagus wouldn't have any room to stretch forward. 5:20 Speaker 2 Exactly. The C shaped leaves the posterior wall of the trachea soft and flexible, so the trachea stays open during inspiration, but the esophagus can still bulge forward into that space during swallowing. 5:32 Speaker 1 Form follows function down to the millimeter that is so cool. So the trachea drops down and splits at the high list into the right and left main stem bronchi. And there is a crucial architectural difference here that we have to talk about. The right main stem bronchus is wider, shorter and much more vertical than the left one. 5:50 Speaker 2 Which has massive clinical implications for us as nurses. If a patient aspirates their own vomit or, you know, child swallows a marble, gravity in the path of least resistance mean that foreign material is almost always going to travel down the right main stem bronchus. 6:04 Speaker 1 And end up in the right lung because the left bronchus has to take a sharper, more horizontal turn to get around the heart, right? Yep. 6:11 Speaker 2 The heart takes up that space in the left. Speaking with the lungs, the right side has three lobes, upper, middle, lower, and the left side just has 2. 6:17 Speaker 1 And this whole system is wrapped in a double layered membrane called the pleura. Visceral pleura on the lungs, Parietal pleura on the chest cavity, with this tiny layer of lubricating fluid between them so the lungs can glide as they expand. 6:30 Speaker 2 Because without that fluid, every breath feels like sandpaper rubbing against your ribs. It's incredibly painful. 6:36 Speaker 1 OK, so now we have the anatomical map, but we need to briefly touch on the Physiology of how oxygen actually gets into the blood. This rests on three pillars, ventilation, diffusion and perfusion. 6:48 Speaker 2 Right, let's define these so we don't mix up the terminology. Ventilation is the pure mechanical movement, just moving air in and out. 6:54 Speaker 1 Like a bellows. 6:55 Speaker 2 Exactly like a bellows, inspiration is an active process. Your diaphragm contracts, moves down, expands the chest cavity, creates negative pressure and air gets sucked in. Expiration is usually passive. The muscles relax, the elastic lungs recoil, and the air is pushed out. 7:11 Speaker 1 OK. And then you have diffusion. 7:12 Speaker 2 Right diffusion is the microscopic chemical transfer down in the terminal alveoli, which are these tiny air sacs wrapped in a net of capillaries. Oxygen and carbon dioxide move across the alveolar capillary membrane. 7:25 Speaker 1 And they move purely based on concentration gradients. 7:27 Speaker 2 Right. Yep, From an area of high pressure to an area of low pressure. Oxygen diffuses out of the alveolus into the blood, and carbon dioxide diffuses out of the blood into the alveolus. 7:38 Speaker 1 Got it. And the third pillar is perfusion, the plumbing. 7:41 Speaker 2 The plumbing blood pumped by the right ventricle travels through the pulmonary arteries to the lungs, picks up the oxygen and comes back via the pulmonary veins to the left side of the heart to be pumped to the rest of the body. 7:52 Speaker 1 And an interesting caveat about perfusion is that not every single drop of blood going to the lungs actually gets oxygenated. 7:59 Speaker 2 No, it doesn't. About 2% of the blood pumped by the right ventricle bypasses the alveolar capillaries entirely. Furthermore, the lung tissue itself needs oxygen to survive right, which is supplied by the bronchial arteries. 8:13 Speaker 1 And that deoxygenated blood eventually drains right into the pulmonary veins, mixing with the freshly oxygenated blood. 8:19 Speaker 2 Exactly. It slightly lowers the overall oxygen saturation before it even reaches the left atrium. This is just a normal anatomic shunt. 8:28 Shunts, Dead Space, and Hypoxia Mechanisms But let's talk about abnormal shunts. Let's talk about when the whole system breaks down. I look at ventilation and profusion like a perfectly choreographed dance. The VQ ratio. 8:39 Speaker 2 I love the dance floor analogy. I like this. 8:41 Speaker 1 Yeah. So the alveolus is the dance floor, The air coming down the windpipe is 1 partner. The blood flowing through the capillary is the other partner for this dance to work. For gas exchange to happen, both partners have to arrive on the dance floor at the exact same time in the exact right amounts. 8:56 Speaker 2 And in of a healthy lung they mostly do, although gravity plays a role. I mean blood is heavy so it tends to pool in the lower dependent parts of the lungs. If you are standing up, the bases of your lungs get more perfusion than the Apis's at the top, but overall ventilation and perfusion mash up to keep you oxygenated. 9:14 Speaker 1 So what happens when a partner misses their cue? That's a VQ mismatch, and this is where I really want to push back and clarify a concept that causes a ton of confusion for students. A low VQ ratio, also known as a shunt producing disorder. 9:30 Speaker 2 OK, let's break it down. 9:31 Speaker 1 In a shunt, the blood shows up to the dance floor, but the air never arrives. There is adequate perfusion but zero ventilation. Maybe a thick mucus plug is blocking the airway, or a whole lobe of the lung is filled with inflammatory pus from pneumonia. 9:46 Speaker 2 Exactly. The alveoli are physically blocked from receiving any new oxygen. 9:50 Speaker 1 But wait, I'm confused by the mechanics of the aftermath here. If the right ventricle is still pumping perfectly fine and blood is still flowing through the rest of the healthy lungs, why is the patient suffocating? 10:01 Speaker 2 That is the $1,000,000 question. 10:03 Speaker 1 I mean, the blood is still moving, the heart is fine. Why does a shunt lead to profound hypoxia even when blood flow is totally adequate? 10:10 Speaker 2 This is a crucial concept. A shunt leads to hypoxia even when blood flow is adequate because blood bypasses alveoli without gas exchange and returns desaturated. 10:20 Speaker 1 Walk me through that visually. 10:22 Speaker 2 OK, think about the entire circuit. The right ventricle pumps dark deoxygenated blood toward the lungs. Let's say the patient has severe lobar pneumonia in their right lower lobe. The capillaries around that lobe are still wide open. Blood is rushing through them, right? 10:38 But the alveoli inside that lobe are packed full of pus and fluid. No oxygen is getting in. So that blood slides right past those diseased alveoli, drops off no carbon dioxide, and picks up 0 oxygen. It continues on its path, returning to the left atrium of the heart, just as desaturated and oxygen starved as when it started. 10:58 Speaker 1 Oh man, so now what happens when that dark unoxygenated blood mixes with the bright oxygenated blood coming from the healthy lobe? 11:05 Speaker 2 It dilutes it. 11:06 Speaker 1 Severely. 11:07 Speaker 2 Severely, it acts like an anchor on the systemic oxygen saturation. Even if the healthy parts of the lung are working at maximum capacity, they cannot over oxygenate their blood enough to compensate for the massive volume of completely unoxygenated blood pouring in from the shunted lobe. 11:22 If the amount of shunting exceeds 20% of the total blood volume, the patient develops severe life threatening hypoxia. And the terrifying thing is, just giving them supplemental oxygen often won't fix it because the oxygen physically cannot reach the blocked alveoli. 11:40 Speaker 1 I just want to pause for a second. Let that really sink in. 11:42 Speaker 2 It's a heavy concept. 11:44 Speaker 1 It makes so much sense though. It doesn't matter how fast the heart beats or how much pure oxygen you put over their face, if the blood can't touch the air the patient starves. 11:54 Speaker 2 And on the flip side of that, you have a high VQ ratio which is Dead Space. 11:58 Speaker 1 Right, so the air gives the alveolus perfectly fine, but a pulmonary embolism has blocked the blood vessel. 12:05 Speaker 2 Exactly. The air is there, but there's no blood to pick it up. Both lead to hypoxia, but through entirely different mechanical failures. 12:12 Speaker 1 Which dictates entirely different treatments. I mean, you wouldn't create a mucus plug the same way you treat a blood clot. 12:17 Visual Cues and Patient History Taking Never. And that understanding of internal mechanics directly informs how we interpret the external clues. When a patient comes into our care, we have to start translating their physical presentation into a map of what's failing inside. 12:32 Speaker 1 And this takes us to the art of the interview and symptom evaluation. Because the assessment doesn't start when you put your stethoscope in your ears. It starts the literal second you walk through the doorway. 12:43 Speaker 2 Before you even say hello, you are evaluating signs of respiratory distress. You're looking at their position. Are they relaxed in bed or are they sitting on the edge, leaning forward with their hands on their knees in the tripod position? 12:56 Speaker 1 Trying to recruit every muscle they have just to expand their chest. 13:00 Speaker 2 You're looking at their facial expression. Is their nasal flaring? Are they using accessory muscles? I mean, normally the diaphragm does all the heavy lifting, but if a patient is using their sternocleidomast asteroid muscles in their neck or the intercostal muscles between their ribs are sucking inward with every breath. 13:15 Speaker 1 That's called retractions, right? 13:17 Speaker 2 Yes, retractions. It means they are generating massive negative pressure just to pull air through narrowed or stiff Airways. 13:25 Speaker 1 Speech patterns are a massive immediate indicator too. 13:28 Speaker 2 Absolutely. Think about it. Speech requires A controlled, sustained exhalation. If a patient can tell you a long, detailed story about what they had for breakfast without stopping to breathe, their respiratory reserve is decent. But. 13:42 Speaker 1 If you ask them how they're feeling and they can only say I can't breathe in these tiny two word bursts before gasping for air, you are looking at severe impending respiratory failure. 13:52 Speaker 2 You also scan their extremities. You're looking at their fingers for clubbing. 13:56 Speaker 1 Remind us what clubbing looks like? 13:58 Speaker 2 Clubbing is where the tips of the fingers become enlarged and the angle of the nail bed gets flattened out. It's a classic sign of of chronic hypoxia. It doesn't happen overnight, it happens over months or years of the body trying to compensate for a lack of oxygen by dilating the blood vessels in the extremities. 14:13 Speaker 1 So you gather these visual clues and then you dive into the history. You're asking about childhood illnesses, asthma, allergies, immunizations, but you also have to act like a detective regarding their environment. 14:26 Speaker 2 Right. Where do they work? Do they spend 8 hours a day inhaling coal dust or silica or agricultural chemicals? 14:33 Speaker 1 And most importantly, we have to ask about personal habits, specifically smoking. But in nursing Fidelity, we don't just ask a binary question. Do you smoke yes or no? 14:44 Speaker 2 No, because that doesn't give us the data we need to assess their risk for COPD or lung cancer. We have to quantify the exposure. 14:51 Speaker 1 We calculate pack years. 14:53 Speaker 2 Pack Years is a vital standardized metric. It measures the total lifetime dose of tobacco toxins the lungs have endured. To calculate it, you just take the number of packs the patient smokes per day and multiply it by the number of years they have smoked that amount. 15:06 Speaker 1 Let's do a quick example. So if a 50 year old patient tells you they have smoked 2 packs a day since they were 30, that's 20 years of smoking. 15:13 Speaker 2 Right, so 2 packs multiplied by 20 years equals a 40 pack year history. 15:18 Speaker 1 And what if they smoke less, say half a pack a day for 20 years? 15:22 Speaker 2 Half a pack which is .5 * 20 years is a 10 pack year history. This number gives every clinician reading the chart an instant, quantifiable picture of the damage. Because smoking doesn't just cause cancer, it paralyzes the MUCO ciliary escalator. 15:38 Speaker 1 Those are the tiny, sweeping hairs lining the respiratory tract that push debris up toward the throat. 15:43 Speaker 2 Right, exactly. And it causes goblet cell hyperplasia, meaning the lungs produce way too much mucus. So you have a massive increase in mucus and the sweeping mechanism is broken. The toxins just sit there, pooling in the lungs, destroying the alveolar walls. 15:57 Speaker 1 It's a perfect storm. 15:58 Chemical Differences in Blood Origin So as we take this history, we are they're asking about their primary symptoms, dyspnea or shortness of breath, cough, chest pain. But this brings us right back to that terrifying scenario I mentioned at the very beginning of the show we need to dissect. 16:12 Speaker 2 It the bleeding patient. 16:13 Speaker 1 Right. You walk in and your patient is spitting up blood. The stakes could not be higher. If you panic, the patient panics. If you misidentify the source, you send the wrong rapid response team down the wrong clinical pathway. 16:27 Speaker 2 Distinguishing between the two sources of blood requires intense clinical vigilance because the treatments are diametrically opposed. Blood coming out of the mouth could be originating from the lower respiratory tract, which is hemocktysis, or it could be originating from the gastrointestinal tract, which is hematomesis. 16:44 Speaker 1 So let's break down exactly how to tell them apart mechanically and chemically. 16:48 Speaker 2 This is how to distinguish hemoptysis, lung origin blood from hematomesis, stomach origin blood. Let's start with hemoptysis. This is blood coughed up from the lungs. Think about the environment of the lungs. 17:00 Speaker 1 OK, it is an oxygen rich environment. 17:02 Speaker 2 Right. So when a pulmonary vessel ruptures, that blood is freshly oxygenated, making it bright red. Crucially, as that blood travels up the trachea, it gets mixed with the air sitting in the alveoli and the turbulent airflow of the cough. It also mixes with pulmonary surfactant. 17:20 Because of this, hemoptysis is almost always frothy. It's full of tiny air bubbles and chemically, if you were to test its pH, lung tissue and pulmonary secretions are alkaline. 17:30 Speaker 1 OK, so lung blood is bright red, it's frothy with air bubbles and it's alkaline. So what is the mechanism behind stomach blood? 17:37 Speaker 2 Hematomesis is blood vomited from the GI tract, usually from a bleeding ulcer or esophageal viruses. The stomach is a completely different environment. It is a highly acidic VAT designed to digest food. 17:49 Speaker 1 It's full of hydrochloric acid. 17:51 Speaker 2 Exactly. When a blood vessel bleeds into the stomach, that hemoglobin is immediately attacked by that hydrochloric acid. The acid digests and oxidizes the hemoglobin, converting it into hematin. This chemical reaction turns the blood from red to a dark brown or black color, which is why hemonymesis is universally described as having a coffee ground appearance. 18:11 Speaker 1 And the texture is different too, I imagine. 18:13 Speaker 2 Very different because it's coming from the stomach. It is frequently mixed with partially digested food particles, not air bubbles. It is never frothy and naturally it's pH will be highly acidic. 18:25 Speaker 1 I want everyone to just take a second and think about that chemical difference. 18:28 Speaker 2 It really is elegant when you break it down. 18:30 Speaker 1 I love that breakdown. Frothy, bright red and alkaline versus dark coffee ground and acidic air versus acid. Once you understand the chemistry of the environments they originate from, you don't even have to memorize the symptoms. 18:43 Assessing Chest Shape and Expansion They are just the logical outcome of the anatomy. So we've gathered the history. We've evaluated the symptoms. We've ruled out an immediate airway hemorrhage. Now it is time to actually lay our hands on the patient. It's time to set the stage for proper assessment technique, starting with inspection and palpation. 19:02 Speaker 2 Inspection of the thorax is incredibly revealing. You expose the chest, providing privacy of course, and you look at the musculoskeletal structure. You observe the skin for color, for cyanosis, for turgor. You note any asymmetry. Does one side of the chest lag behind the other when they breathe? 19:20 But the most critical structural element we assess is the chest configuration. 19:24 Speaker 1 Right, we want to know the ratio of the antero posterior diameter, meaning the depth of the chest from front to back, compared to the lateral diameter, the width of the chest from side to side. In a healthy adult, that ratio is normally 1:00 to 2:00. Your chest is roughly twice as wide as it is deep. 19:40 It's an Oval shape. 19:41 Speaker 2 But chronic respiratory disease physically deforms the skeleton over time. 19:45 Speaker 1 The most traumatic example of this is the barrel chest. 19:47 Speaker 2 Right. Yes. In a barrel chest, the anterior posterior diameter increases so much that it equals the lateral diameter. The ratio becomes 1 to 1. The chest looks perfectly round, like a barrel. This happens primarily in chronic obstructive pulmonary disease, specifically emphysema. 20:04 Speaker 1 So what's the actual mechanism there? Why does lung disease change the shape of your ribs? That seems so extreme. 20:09 Speaker 2 It comes down to elastin and air trapping. Emphysema destroys the elastin fibers in the alveolar walls. Normally those fibers are like rubber bands. You stretch them when you inhale and they naturally snap back to push the air out during exhalation. 20:24 Speaker 1 But an emphysema. 20:25 Speaker 2 An emphysema. The rubber bands snap. The alveoli lose their elastic recoil. So the patient can suck air in, but they can't push it all out. The air gets trapped. With every breath, a little more air gets stuck in the distal Airways. The lungs become chronically hyperinflated. 20:40 Speaker 1 And that pressure just pushes outward. 20:42 Speaker 2 Exactly. This constant, immense pressure of trapped air physically pushes the rib cage outward and forces the diaphragm to flatten down. Over the years, the entire Bony thorax remodels itself into that permanent hyperinflated barrel shape. 20:58 Speaker 1 The ribs are basically locked in an inhaled position. That's wild. There are other deformities too, right? You have funnel chest, also known as pectus excavatum, where the lower portion of the sternum is depressed inward, which can actually compress the heart and great vessels if it's severe enough. And you have pigeon chest, or pectuscarinatum, where the sternum protrudes outward. 21:17 And don't forget kyphoscoliosis, which is an abnormal curvature of the spine. All of these are restrictive disorders. The lungs might be perfectly healthy tissue wise, but if the Bony cage around them can't expand, ventilation fails. 21:30 Speaker 2 Which is exactly why the next step is physically measuring that expansion by assessing respiratory excursion. We need to verify that the chest can expand fully and symmetrically. If the left side expands but the right side doesn't, you might be looking at a massive pleural effusion where fluid is crushing the lung or pneumothorax with the lung has collapsed. 21:51 Speaker 1 To assess posterior excursion, you stand behind the patient. You place your thumbs on their back at the level of the 10th rib, which is around the T9 or T10 vertebrae. You grasp the lateral rib cage lightly with your hands, and you slide your thumbs medially toward the spine, just enough to pinch up a small fold of skin between them. 22:09 Speaker 2 Then you instruct the patient to inhale deeply. As they breathe in, you keep your eyes locked on your thumbs. If their chest expansion is normal and symmetric, your thumbs will move apart simultaneously and equally, and that little fold of skin between them will flatten out completely. 22:26 Speaker 1 Now, performing this posterior assessment brings up a really crucial point about technique and positioning. You can't adequately assess the posterior thorax of a patient who is lying flat on their back, sunken into a mattress. 22:38 Speaker 2 No, you'll hear nothing but the bed sheets. 22:41 Speaker 1 But even if you have them sit up on the edge of the bed, what do they do with their arms? If they just rest their hands in their lap, you're missing a massive piece of the puzzle. 22:50 Speaker 2 You are positioning is everything. This is exactly why patients are positioned with their arms crossed over the chest during a posterior thorax assessment, because it separates the scapulae and exposes more lung tissue for evaluation. 23:03 Speaker 1 Let's talk about the bio mechanics of that. Why does crossing the arms change what we can hear and feel? 23:09 Speaker 2 Think about the anatomy of the shoulder blades, the scapulae. They are large, thick, dense triangular plates of bone, and they sit directly over the upper lobes of the lungs on the posterior back. We know that bone blocks sound transmission, and it blocks the vibrations we need to feel during palpation. 23:28 If a patient is just sitting with their arms relaxed at their sides, their shoulder blades naturally retract toward the spine. They act like 2 massive Bony Shields covering a huge percentage of the posterior lung fields. If you put your stethoscope there, you are just listening to bone. 23:44 Speaker 1 But if they cross their arms. 23:45 Speaker 2 But if you instruct the patient to lean forward slightly, cross their arms tightly in front of their chest, and place their their hands on their opposite shoulders, watch what happens to their back. Those scapulae are pulled laterally. They slide away from the spine and wrap around the sides of the rib cage. 24:01 It completely opens up a massive acoustic window directly to the posterior lung tissue. 24:06 Speaker 1 I want you to really visualize pulling those Bony Shields away. 24:09 Speaker 2 It changes everything. 24:10 Speaker 1 It is such a simple maneuver, but it instantly elevates your assessment from amateur to expert. Pull the bones out of the way. 24:19 Understanding Vibrations in Lung Pathology So now that the scapulae are separated, we move deeper into palpation. We are feeling the chest wall for tenderness for masses, but primarily we are feeling for tactile fermatus. 24:30 Speaker 2 Tactile fermatus, or vocal fermatus, is the vibration you feel on the chest wall when a patient speaks. The vocal cords generate sound waves in the larynx, and those waves travel down the solid tissues of the trachea, through the bronchi, through the lung parenchyma, and out to the chest wall. 24:46 Speaker 1 The technique here is very specific. You use the palmar base of your fingers, or the ulnar aspect, the pinky side of your hands. Why those areas? 24:53 Speaker 2 Because the Bony structures in the ulnar side and the base of the fingers are highly sensitive to detecting vibratory frequencies, you place your hands symmetrically on the patient's upper back and you have them repeat a resonant phrase, usually 99 or 111. 25:08 Speaker 1 99 is a classic. 25:10 Speaker 2 It is as they speak, you move your hands down their back, comparing the vibration on the left side to the vibration on the right side. 25:16 Speaker 1 And this is where we have to dive into the physics of sound transmission, because understanding these physics is the absolute skeleton key for the rest of the respiratory exam. Sound and vibration travel differently depending on the medium they are moving through. They travel poorly through a vacuum, terribly through air, somewhat better through fluid, and best through a solid dense mass. 25:37 Speaker 2 Exactly. Air acts as an acoustic insulator. It absorbs and impedes sound waves. Solid tissue acts as a conductor. It enhances them. Normal healthy lung tissue is a matrix of microscopic air filled alveoli, so it conducts A moderate baseline amount of vibration. 25:55 Speaker 1 But pathology alters the density of the lung. 25:57 Speaker 2 Right, which drastically alters the vibration you feel. Let's look at emphysema again. 26:01 Speaker 1 In emphysema, the lungs are hyperinflated, the alveoli are destroyed and merged into massive pockets of trapped air. Because there was an enormous increase in the ratio of air to tissue, the sound waves originating from the vocal cords hit this massive wall of insulating air and get completely muffled. 26:17 Speaker 2 So a patient with severe emphysema will exhibit decreased or even absent tactile frematus. You will barely feel them saying 99. 26:27 Speaker 1 But consider the opposite extreme. What if the patient has lobar pneumonia? 26:31 Speaker 2 In lobar pneumonia, a section of the lung becomes consolidated. The infection triggers a massive inflammatory response. The alveoli in that lobe completely fill up with inflammatory exudate, pus, red blood cells, and white blood cells. 26:45 Speaker 1 So the air is gone. 26:46 Speaker 2 Completely gone. The air is completely replaced by dense, fluid filled tissue. It becomes solid, almost resembling liver tissue. Now remember our physics rule. Solid tissue conducts vibration far better than air. 26:58 Speaker 1 So it amplifies the sound. 26:59 Speaker 2 Exactly. If you place your hands over that consolidated right lower lobe and the patient says 99, the solid block of infection acts like an acoustic amplifier. The vibration bypasses the normal air insulation and transmits directly to the chest wall. You will feel a dramatic increase in vibration. 27:15 The fermatus is increased over the area of consolidation. 27:18 Speaker 1 It feels like the vibration is buzzing right into your bones. Feeling that change in density is incredible, but translating those physical changes in density into actual sounds in the next level? 27:31 Interpreting Lung Sounds and Density If we know that dense tissue vibrates differently, what does it sound like when we strike it? This brings us to percussion and auscultation. Let's start with percussion. This is arguably the hardest physical skill to master. 27:44 Speaker 2 It takes a lot of practice to get the technique right, but the concept is brilliant. Percussion involves striking the chest wall to generate a sound wave. That wave penetrates about 5 to 7 centimeters into the underlying tissue. The sound that bounces back tells you the precise density of the structures beneath. 28:01 Speaker 1 Let's breakdown the mechanics of the strike. You use your middle finger of your non dominant hand. This is called the pleximeter finger. You place it firmly flat against the patient's chest wall, specifically in the intercostal space between the ribs. You must make sure your other fingers are lifted off the skin. 28:16 If they rest on the chest they will dampen the sound wave. 28:19 Speaker 2 Then you use the tip of the middle finger of your dominant hand, the plexer. You keep your forearm stationary and you use a quick sharp relaxed flick of the wrist to strike the distal joint of the pleximeter finger. It has to be a crisp dart like motion. You strike twice, listen, and then move to the opposite side to compare. 28:38 Speaker 1 And just like with Remedus, you never percuss over bone. You map out the posterior thorax, moving side to side, avoiding those scapulae we pulled out of the way earlier. We are listening for specific ercussion notes that correspond to specific densities. Normal healthy air filled lung tissue produces a sound called resonance. 28:57 It's a loud, low pitched, hollow sound. It means there's a normal balance of air and tissue. 29:02 Speaker 2 But if there is too much air, the pitch and amplitude change. Think of a pneumothorax where air has leaked out of the lung and trapped itself in the pleural space, collapsing along. Or think of our emphysema patient with severely hyperinflated lungs. 29:15 Speaker 1 When you percuss over that trapped air. 29:17 Speaker 2 You get hyper resonance. It is a very loud lower pitched booming sound. You are essentially tapping on an air filled. 29:23 Speaker 1 On the other hand, what if we hit that lowburn pneumonia again? Or what if the patient has a pleural effusion, a massive collection of fluid between the lung and the chest wall? 29:32 Speaker 2 Then the air is gone completely, replaced by fluid or dense cellular mass. When you strike the chest over that area, the percussion note becomes dull. It is a medium pitched muffled thud like sound. You normally hear dullness if you percuss over solid organs like the liver or the heart. 29:50 Speaker 1 But if you hear a dull thud over the lung fields. 29:53 Speaker 2 It is a massive red flag indicating that the air filled space has been replaced by something solid. And if the fluid collection is extreme, like a massive hemothorax full of blood, the sound might become completely flat. A very soft, high pitched short sound, exactly like percussing your own thigh muscle. 30:09 Speaker 1 So we use our fingers to map out the zones of air, fluid and solid tissue. Then we confirm our map using the most iconic tool in nursing. 30:17 Speaker 2 The stethoscope auscultation and technique here matters just as much as percussion. You use the diaphragm of the stethoscope because we are listening for high frequency breath sounds and crucially, the diaphragm must go on bare skin. Yes, listening through a hospital gown or AT shirt is a cardinal sin of assessment. 30:34 As the patient breathes, the fabric rubs against the chest and the stethoscope. That friction creates a crackling sound that perfectly mimics adventitious lung sounds. You will end up diagnosing a cotton T-shirt with pulmonary edema. 30:48 Speaker 1 It happens all the time. 30:49 Speaker 2 It really does. The diaphragm goes firmly on the skin and you instruct the patient to breathe slowly and deeply through an open mouth. You listen to at least one full respiratory cycle, inspiration and expiration at each anatomical location. 31:03 Speaker 1 And we're listening for three categories of sound, normal breath sounds, adventitious sounds, and voice sounds. You have to know what normal sounds like before you can catch the abnormal. Normal breath sounds aren't just one continuous noise, they change depending on the diameter of the airway you are listening over. 31:18 Speaker 2 Exactly. Let's start at the periphery. Vesicular breath sounds are heard over the vast majority of the peripheral lung fields, especially out in the bases where the alveoli are, because the air is diffusing into millions of microscopic sacs. The sound is very low pitched, soft and rustling. 31:35 Speaker 1 It sounds like a gentle breeze blowing through the leaves of a tree. The inspiratory phase is much longer and louder than the expiratory phase, which is almost silent. 31:43 Speaker 2 As we move centrally toward the major bronchi, we hear broncho vesicular sounds. These are heard anteriorly around the upper sternum and posteriorly between the scapulae. The Airways are larger here, so the sound is moderate in pitch and amplitude. Inspiration and expiration are equal in duration. 32:00 Speaker 1 And finally we move up to the trachea and the larynx. Here we hear bronchial or tubular breath sounds. The trachea is a large rigid tube. The air is rushing through it at high velocity, so branchial sounds are loud, high pitched and harsh. 32:16 Speaker 2 They sound like air blowing through a hollow pipe. The expiratory phase is actually longer and louder than the inspiratory phase, but the most important thing to remember is that these harsh bronchial sounds normally belong only over the trachea and the manubrium. 32:28 Speaker 1 OK, so that's the normal layout. Soft to the bases, moderate in the middle, harsh at the top. 32:34 Crackles, Wheezes, Stridor, and Consolidation Now let's talk about adventitious sounds, the abnormal sounds superimposed on the normal breath sounds. Let's break down the physical mechanisms behind them. First crackles, historically called Rails. 32:46 Speaker 2 Crackles are discontinuous non musical popping sounds. We divide them into fine and coarse. Fine crackles originate down in the alveoli. Think about a patient with early congestive heart failure. Fluid is just starting to shift out of the capillaries and into the interstitial spaces around the alveoli. 33:04 Speaker 1 Sticky. 33:05 Speaker 2 Yes, this makes the alveoli sticky and they partially collapse during exhalation. When the patient takes a deep breath in, the negative pressure forces those sticky alveoli to suddenly pop open. That popping creates a soft, high pitched sound. Sounds exactly like taking a strand of your hair and rolling it between your thumb and index finger, right next to your ear. 33:24 Speaker 1 Coarse crackles, on the other hand, originate a little higher up in the larger bronchi and trachea. This is the sound of turbulent air colliding with larger pools of fluid or thick mucus. It's louder, lower pitched, and sounds like bubbling or gurgling. Sounds like slowly peeling a part of Velcro fastener. 33:41 You hear this in severe pulmonary edema or chronic bronchitis. 33:44 Speaker 2 Then we have wheezes. Wheezes are continuous high pitched musical squeaks. To understand wheezing, you have to think about the Bernoulli principle and the Venturi effect. In physics, when a tube narrows, the Air Force through it accelerates, causing the walls to vibrate and generate a musical pitch. 34:01 Speaker 1 It's like asthma. 34:02 Speaker 2 Right in asthma, the smooth muscle around the bronchial spasms and the airway lining swells with inflammation. The diameter of the tube shrinks drastically as the patient forces air through that narrowed Canyon. It whistles. 34:14 Speaker 1 We also have raunchy, which are deep, low pitched rumbling or snoring sounds. These usually mean there are thick, tenacious mucus plugs partially blocking the larger tracheobronchial passages. Yeah. The unique clinical feature of Rauchy is that if you instruct the patient to give a strong deep cough, they can often clear the mucus plug and the Rauchy will temporarily disappear. 34:36 Speaker 2 But there is one adventitious stomach cannot be cleared with a cough, and it should immediately trigger a mass of adrenaline spike for any nurse stridor. 34:44 Speaker 1 Stridor is a terrifying sound. 34:46 Speaker 2 It is the sound of an impending code. Stridor is a continuous, loud, high pitched crowing sound usually heard predominantly on inspiration. It is so loud you often hear it without a stethoscope. It indicates a critical narrowing or obstruction of the upper respiratory tract, the larynx, or the upper trachea. 35:03 Speaker 1 It could be a child with severe croup, a patient having an anaphylactic reaction to an antibiotic where their vocal cords are swelling shut, or someone choking on a foreign object. When you hear Strideor, the airway is closing rapidly and if you don't intervene immediately, they will arrest. 35:19 Speaker 2 It is the ultimate alarm bell. But I want to pivot back to something we discussed earlier because here is where we we hit a massive, subtle clinical red flag regarding normal sounds. OK, let's hear it. We know what crackles and wheezes mean. But sometimes an abnormal finding isn't a new sound altogether. 35:37 Sometimes it's a completely normal sound that is simply in the wrong anatomical location. We just define bronchial breath sounds. Those loud high pitched, harsh hollow pipe sounds, we establish they are completely normal over the trachea, right? 35:53 But what does it mean clinically when bronchial breath sounds are heard over the lower lung bases instead of the manumbrium where you should be hearing soft wrestling vesicular sounds, but instead you hear loud harsh bronchial breath sounds? 36:06 Speaker 1 This is one of the most vital deductions you can make in an assessment. When bronchial breath sounds are heard over the lower lung bases, it signifies consolidation such as pneumonia or heart failure. And this brings us right back to the physics of sound transmission we discussed with Tactile Freemadus. 36:21 Speaker 2 Let's explicitly connect those dots. Why does the sound change from soft to harsh just because there's fluid? 36:27 Speaker 1 Normally the lung bases are filled with air. Air is a parable conductor of sound. It acts as an acoustic filter. It naturally filters out and dampens the high frequency harsh sounds originating up in the trachea. So by the time the sound reaches the periphery of the lung, all you hear is the soft low pitched vesicular rustling. 36:46 Speaker 2 But if a patient has lobe or pneumonia, that lobe at the base of the lung is no longer an air filled filter. It is consolidated. It has become a dense solid block of inflammatory fluid, pus and cellular debris. Remember the rule solid tissue conducts sound incredibly well. 37:05 Speaker 1 Right. So it just carries the sound straight down. 37:07 Speaker 2 Exactly that. Consolidated Lurb acts exactly like a high speed acoustic cable. It takes the loud, harsh bronchial sounds originating up in the trachea and telegraphs them straight down to the base of the lung, completely unfiltered. Because the insulating air is gone, the harsh sound travels perfectly through the solid mass of infection. 37:25 Hearing bronchial sounds in the periphery means the lung tissue has solidified. 37:29 Speaker 1 I really want you to take a moment and just let that sink in. A normal sound in the wrong place is profoundly abnormal. It is a harsh tracheal breath. Sound over the base of the lung means the air is gone. It's the same physical principle behind why we check for voice sounds like bronchophony or egophony over suspicious areas. 37:48 Speaker 2 Exactly. If you asked a healthy patient to say 99, the sound is muffled and indistinct through the stethoscope because the air diffuses it. But if there is consolidation, that solid acoustic cable transmits the voice perfectly. You hear the word 99 loud and clear over the lung base. 38:06 That is bronchophane. 38:07 Speaker 1 Even more striking is whispered pectorilloquy. If the patient simply whispers 123, the normal air filled lung filters it out completely, but over a consolidated pneumonia, you will hear that whisper through your stethoscope as clearly as if they were whispering directly into your ear. 38:23 Speaker 2 Or egophony, where you ask the patient to say a long E sound. Over normal lung it sounds like D, but over consolidation the dense fluid actually distorts the acoustic frequency and the E transmits as a nasal bleeding, uh, sound. 38:37 Speaker 1 It all connects the inspection, the palpation of increased firmatus, the dullness on percussion, the bronchial breath sounds in the basses, the egg ophony. They all point to the exact same physiological reality consolidation. 38:50 X-rays, CT Scans, and Contrast Safety We have built an airtight clinical case using nothing but our hands and our ears. 38:55 Speaker 2 But our hands and ears, as incredible as they are, are just the screening tools. They tell us where the pathology is and roughly what it is. But to formulate a definitive medical diagnosis and treatment plan, we must turn to diagnostic imaging and procedures. To actually see the hidden landscape, we need to visualize the structures. 39:13 Speaker 1 The most ubiquitous starting point is the chest X-ray. It's fast, relatively inexpensive, and it provides A2 dimensional view of the major contrast between body densities. Because bone is extremely dense, it absorbs the X-rays and appears bright white. Air has almost no density, so X-rays pass right through it, making the lungs appear black. 39:31 Soft tissue and fluid fall somewhere in the middle, appearing as Shades of Grey. 39:35 Speaker 2 From a nursing standpoint, preparing a patient for a routine chest X-ray is straightforward. There is no fasting required, but the technique of the patient is critical. You must instruct them to take a very deep breath in and hold it while the image is snapped. 39:49 Speaker 1 Why is holding the breath so critical for the image quality? 39:52 Speaker 2 Because taking a deep breath forces the diaphragm to contract and move downward, pulling the lungs open to their maximum volume. This exposes the maximum amount of lung fields on the film. If they take a chalet breath, the diaphragm sits high, obscuring the lower lobes where pneumonias frequently hide. 40:09 You also have to ensure they remove any radiopaque objects, metal necklaces, underwire bras, ECG leads, because those will show up as stark white artifacts that could be mistaken for a tumor or a foreign body. 40:21 Speaker 1 But a standard X-ray has major limitations. It's a 2D shadow. If a small tumor is hiding directly behind the dense bone of a rib or the heart, the X-ray might miss it completely. If we need a highly detailed cross-sectional view of the fine tissue densities in the lungs, the mediastinum and the vascular structures, we have to escalate to a computed tomography or CT scan. 40:42 Speaker 2 ACT scanner rotates around the patient, taking hundreds of thin X-ray slices, and a computer compiles them into a highly detailed 3D map. It can define pulmonary nodules as small as a few millimeters. But ACT scan often requires the use of an intravenous contrast dye to highlight the blood vessels and vascular lesions, and the introduction of IV contrast drastically elevates the nursing implications. 41:05 Speaker 1 It completely changes our checklist. The contrast dye used in CT scans is typically an iodine based hyperosmolar solution. It is heavily processed and cleared from the body by the kidneys. Because of this, it is inherently nephrotoxic. It is toxic to the kidneys, especially if they are already compromised. 41:23 Speaker 2 So your first absolute safety check before sending a patient to CT is checking the renal function panel, specifically the blood urea nitrogen, or BUN, and the serum creatinine levels. If their creatinine is elevated, their kidneys are already failing. Hitting failing kidneys with a massive load of nephrotoxic dye can push the patient into acute, irreversible renal failure. 41:43 Speaker 1 You have to alert the physician and they might order aggressive 5 dehydration before the scan to flush the kidneys, or they might cancel the contrast altogether. 41:51 Speaker 2 Second, you must meticulously check for allergies. Because of the dye contains iodine, you specifically ask about allergies to iodine or shellfish. A mild reaction might just be hives, but a severe anaphylactic reaction while the patient is sliding into a large enclosed scanning tube is a catastrophic emergency. 42:11 But beyond allergies, there is a very specific, dangerous medication interaction that every nurse must memorize regarding contrast dye. 42:18 Speaker 1 Yes, Metformin. Metformin is a first line oral hypoglycemic medication used by millions of people with type 2 diabetes. If a patient takes metformin, it must be withheld on the day of the contrast CT scan and typically for 48 hours afterward. 42:32 Speaker 2 Let's explain the pharmacology behind that. Why is that combination so lethal? 42:35 Speaker 1 Metformin itself is not toxic to the kidneys, but it is cleared by the kidneys and a rare but fatal side effect of metformin is the buildup of lactic acid in the blood. If you give a patient IV contrast dye and the dye causes a sudden temporary drop in kidney function contrast induced nephropathy, the kidneys suddenly stop clearing the metformin. 42:57 Speaker 2 The metformin levels skyrocket in the bloodstream, which dramatically increases the risk of the patient developing severe lactic acidosis. Their blood pH drops rapidly, they become profoundly acidotic, and it carries a very high mortality rate. You prevent this entirely simply by withholding the metformin until you recheck their creatinine 48 hours later to prove their kidney survived the dye. 43:17 Speaker 1 This is what we mean by technical competence. This is fidelity. It's not just coordinating transportation to the radiology suite, it's understanding the pharmatology and Physiology deeply enough to ensure the patient survives the scan without complication. 43:30 Protecting the Airway Post-Procedure Now ACT Scan gives us a great picture from the outside looking in, but what if we need to see the inside of the airwaves with our own eyes? This brings us to a much more invasive procedure, the bronchoscopy. 43:41 Speaker 2 A bronchoscopy is a direct internal visualization of the respiratory tract. The physician inserts a flexible fiber optic scope equipped with a light and a camera through the patient's nose or mouth, down through the vocal cords, into the trachea and into the bronchae. 43:57 Speaker 1 It has both diagnostic and therapeutic purposes. Diagnostically, if ACT scan shows a suspicious mass, the physician can drive the scope right up to the tumor and use tiny forceps to bite off a tissue sample for a biopsy. Therapeutically, the patient has a massive mucus plug that is causing a severe VQ shunt. 44:16 The physician can use a scope to physically suction the plug out and instantly restore ventilation to that lobe. 44:22 Speaker 2 But sticking a tube down a conscious patient's windpipe is a violent assault on the body's natural defense mechanisms. The gag reflex and the cough reflex will fight that scope every millimeter of the way. 44:32 Speaker 1 So to make the procedure possible, the physician has to neutralize the defenses. They use a potent topical local anesthetic like lidocaine spray, and they spray it heavily onto the back of the throat, the base of the tongue, the vocal cords and the larynx. 44:46 Speaker 2 They anesthetize the watchdog. The larynx goes completely numb. The gag and cough reflexes are chemically paralyzed. This allows the scope to slide smoothly into the trachea without the patient violently coughing, bucking, or experiencing laryngeal spasm. 45:01 The procedure finishes, the scope comes out, and the patient is wheeled back to your unit. 45:06 Speaker 1 And when they get back, they are going to be miserable. They have been NPO, nothing by mouth for 8 to 12 hours before the procedure. Their mouth is dry, their throat is irritated from the scope, and the very first thing they're going to do when you walk into the room is beg you for a sip of water or ice chips. 45:23 And this is a trap. 45:24 Speaker 2 It is the ultimate test of your understanding of airway Physiology. 45:27 Speaker 1 We have to explain a critical non negotiable safety rule. Why must patients remain strictly NPO after a bronchoscopy until their cough reflex fully returns? 45:37 Speaker 2 They must remain NPO because of the impaired laryngeal protection resulting from the local anesthesia. Let's trace the mechanics of what happens if you break this rule. You feel bad for the patient, so you hand them a small cup of water. They take a drink. Normally, the moment liquid hits the back of the throat, sensory nerves alert the brain, the epiglottis slam shut over the larynx, and the water is routed safely down the esophagus into the stomach. 46:01 Speaker 1 But right now? 46:02 Speaker 2 But right now the watchdog is asleep, the larynx is completely numb, the sensory nerves cannot feel the water, and the motor nerves cannot command the epiglottis to close. 46:11 Speaker 1 So what happens to the water? 46:13 Speaker 2 The epiglottis stays wide open. The water pours straight past the vocal cords and floods directly down into the trachea and the lungs. The cough reflex is also paralyzed. The patient won't even choke or sputter. It is a silent, massive aspiration that water, along with bacteria from the mouth, pools in the alveoli. 46:31 This can instantly trigger a severe bronchospasm, acute respiratory distress syndrome, or a massive aspiration pneumonia that could easily kill them a few days later. 46:41 Speaker 1 That silence, the absence of a cough when water hits the lungs, is terrifying. 46:46 Speaker 2 It is. 46:47 Speaker 1 You withhold that water, no matter how thirsty they are, no matter how much they complain pain, until you can unequivocally prove the watchdog is awake and back on duty. You test their gag reflex gently with a tongue depressor, or you simply wait for them to demonstrate a strong, spontaneous, voluntary cough. 47:03 It takes an hour or two for the anesthesia to wear off. Withholding a pitcher of water seems like such a trivial basic nursing task, but it is a life saving intervention. It is the perfect embodiment of everything we've talked about today. 47:16 Mastering Care for Vulnerable Patients It truly is. It perfectly synthesizes our entire discussion because every single action in Exceptional Nurse Taste is anchored in a profound understanding of the underlying Physiology, from understanding the vascular climbing that makes a VQ shunt so deadly to knowing the chemical pH difference between hemoptysis and hemodomesis. 47:33 Speaker 1 From knowing the skeletal anatomy well enough to move the scapulae out of the way for auscultation, to understanding the physics of sound transmission that explain why hearing bronchial breath sounds in the bases is a harbinger of consolidation. From knowing the nephrotoxic pharmacology of contrast dye to guarding a picture of water because you understand the neurological paralysis of a topical anaesthetic. 47:56 Speaker 2 We don't just follow checklists. We anticipate, we understand what happens in the dark spaces of the body when the mechanics fail. And before we conclude this session, I want to leave you with one final provocative thought to take with you to your next clinical rotation. I want you to consider how the simple act of aging alters every single physiological mechanism we just discussed. 48:16 Speaker 1 The geriatric respiratory system is a completely different landscape. 48:19 Speaker 2 It is as a patient ages, their coastal cartilages calcify, meaning their rib cage becomes stiff and rigid, their chest wall compliance plummets. The respiratory muscles, the diaphragm and intercostals lose mass and weaken. Their alveoli naturally enlarged and lose some elastic recoil, meaning their vital capacity decreases while their residual volume trapped air increases. 48:40 But perhaps most critically, their baseline cough reflects naturally blunts and the MUCO ciliary escalator slows down. 48:46 Speaker 1 So they have a stiffer chest, weaker muscles, and a sleepy watchdog even without anesthesia. 48:51 Speaker 2 Precisely so. Think about our older adult patients. The physiological reserve they have to fight off an infection or compensate for a VQ mismatch is incredibly small. When you assess an 85 year old patient, the line between normal age-related changes and an acute life threatening deterioration becomes razor thin. 49:11 They might not exhibit massive retractions or thunderous cough when they get pneumonia because they simply don't have the muscle strength to generate them. Your assessment skills have to be exponentially sharper. Your ears have to be more tuned to the subtle adventitious sounds. Your vigilance must be absolute. 49:26 How will you adjust your technique, your interpretation and your fidelity when your patient has almost no margin for error? 49:31 Speaker 1 That is the exact question you need to carry with you on to the floor tomorrow. It changes the way you look at every single patient. It is why we keep studying, why we keep pushing past the basic memorization, and why we stay after class to master the why. 49:47 Thank you for joining us for this incredibly vital after class heroes huddle. Keep going, hero. You're not just surviving nursing or life. You're slowly becoming an after class hero. See you on the next huddle. Stay humble, say compassionate, and remember you never know when your next lesson might be the one that saves a life.