DIP Episode 571 - Quick and Dirty Emergency Medicine For The USMLEs
Topic
Trauma management; Airway emergencies (Epiglottitis); Shock states (Hemorrhagic, Obstructive); Endocrine crises (Addison's, Myxedema Coma)...
Key Takeaway
In emergency medicine, critical thinking is paramount: always assume a C-spine injury in trauma, prioritize airway patency over antibiotics, and remember that the most common shock state in trauma is hemorrhagic shock, while autoimmune crises require considering adrenal insufficiency (Addison's) or hypothyroidism (Myxedema Coma).
Episode Notes
Source / episode info
- Episode: 571
- Title: DIP Ep 571: Quick and Dirty Emergency Medicine For The USML Es
- Published: 2025-02-10
- Source: Episode page
One-liner
This episode provides a high-yield review of emergency medicine concepts, covering trauma assessment (C-spine), airway management principles (difficult airways/surgical airway), shock pathophysiology (hemorrhagic vs. obstructive), endocrine emergencies (Addison's and Myxedema Coma), acid-base compensation in hypoxia, and the stepwise escalation of oxygen therapy.
High-yield summary
- Trauma: Always assess for a cervical spine injury until ruled out; assume spinal immobilization is necessary upon arrival.
- Airway Management: If endotracheal intubation fails or is anticipated to be difficult (e.g., epiglottitis), prepare for and consider a surgical airway (cricothyrotomy).
- Infection Control: In any emergency situation requiring PPE, proper personal protective equipment must be donned before entering the patient's room.
- Shock States: The three causes of obstructive shock are Tension Pneumothorax, Cardiac Tamponade, and Pulmonary Embolus (PE).
- Primary Adrenal Insufficiency (Addison's): Look for hypotension, hyponatremia, hyperkalemia, and a normal anion gap metabolic acidosis in the context of an autoimmune disease.
- Hypoxia/Altitude: Severe hypoxia stimulates erythropoietin (EPO) release from the kidneys; compensatory hyperventilation leads to respiratory alkalosis, which triggers renal compensation via bicarbonate wasting (metabolic acidosis).
Learning objectives
- Master the principles of airway management, including recognizing difficult airways and when to prepare for surgical airways.
- Differentiate between various types of shock (hemorrhagic vs. obstructive) based on hemodynamic parameters.
- Recognize the classic laboratory triad associated with primary adrenal insufficiency (Addison's disease).
- Understand the physiological compensation mechanisms in severe hypoxia or high altitude settings, including acid-base shifts.
- Apply systematic approaches to trauma care, prioritizing C-spine assessment and hemorrhage control.
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Obstructive Shock | Low CVP/PCWP (low preload) | Tension Pneumothorax, Cardiac Tamponade, PE | If the cause of shock is external compression or obstruction, think of these three pathologies. |
| Primary Adrenal Insufficiency | Hyperkalemia; Hyponatremia; NAGMA | Autoimmune disease (e.g., Celiac), Cortisol deficiency | Always check for adrenal insufficiency in any patient with an autoimmune history presenting with shock/hypotension. |
| Hypoxia / High Altitude | Respiratory Alkalosis -> Metabolic Acidosis | Hyperventilation leads to CO2 blow-off; kidney compensates by wasting HCO3-. | Acetazolamide (a carbonic anhydrase inhibitor) can be used to accelerate bicarbonate loss in this setting. |
| Trauma Shock | Hypotension, Tachycardia, Low CVP/PCWP | Hemorrhagic shock is the most common cause of shock in trauma. | If no specific clues are given for the type of shock, assume hemorrhagic shock in a trauma patient. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| Oxygen Delivery Ladder | Room Air -> Nasal Prongs -> Face Mask -> Non-rebreather -> NIPP Vs -> Intubation | Gradual escalation of FiO2 delivery. | Know the order to select the least invasive, most effective oxygen source first. |
| Obstructive Shock | Tension Pneumothorax, Cardiac Tamponade, PE | External compression or obstruction impairs venous return (preload). | These three are the only causes of obstructive shock; remember they all cause low CVP/PCWP. |
| Primary AI Labs | Hyperkalemia, Hyponatremia, NAGMA | Loss of aldosterone due to adrenal cortex destruction. | The combination of these findings strongly suggests primary adrenal failure (Addison's). |
| Hemorrhagic Shock Hemodynamics | Low Preload -> Low CVP/PCWP -> Low CO | Blood loss reduces venous return and cardiac filling volume. | Understanding the Frank-Starling mechanism helps predict changes in central pressures. |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| A trauma patient presents with altered mental status and neck stiffness. What is the initial priority? | Cervical Spine Injury Ruleout | In all trauma patients, assume C-spine injury until cleared by imaging/exam; immobilization is standard practice. |
| A child with suspected epiglottitis is brought to the ED. Which intervention is most critical initially? | Airway Protection (Intubation) | The airway is the immediate life threat; securing it takes precedence over administering antibiotics or other treatments. |
| A patient in hemorrhagic shock has low CVP and PCWP. What is the expected compensatory mechanism? | Increased Heart Rate, Increased SVR | Low preload leads to low cardiac output (Frank-Starling principle); body compensates by increasing HR and systemic vascular resistance (SVR) to maintain BP. |
| An autoimmune patient presents with hypotension, hyponatremia, hyperkalemia, and metabolic acidosis. | Primary Adrenal Insufficiency (Addison's Disease) | Autoimmune destruction targets the adrenal cortex; loss of aldosterone leads to K+ retention and volume depletion/hypotension. |
| A patient with severe COVID-19 respiratory failure is being managed in a high-risk setting. What is the first step for staff entering the room? | Don PPE First | This emphasizes safety stewardship: protect yourself before attempting to save the patient, especially with highly transmissible pathogens. |
| A trauma patient has an open wound and bleeding profusely. What is the immediate management priority? | Direct Pressure Application | The most appropriate initial intervention for external hemorrhage is direct pressure; do not delay care by searching for a source or removing objects. |
Differential diagnosis / distinguishing features
Adrenal Insufficiency States
| Key Features | Distinguishing Findings | Next Step |
| Primary AI (Addison's) | Hyperkalemia, Hyponatremia, NAGMA; low cortisol/aldosterone. | IV Hydrocortisone (stress dose); mineralocorticoid replacement (Fludrocortisone). |
| Secondary AI | Normal K+ and Na+ levels; low ACTH/Cortisol. | High-dose glucocorticoids (e.g., hydrocortisone) to stimulate endogenous ACTH production. |
Hypoxia / Acid-Base Status
| Key Features | Distinguishing Findings | Next Step |
| High Altitude Sickness | Respiratory Alkalosis + Metabolic Acidosis | Hyperventilation blows off CO2 (respiratory alkalosis); kidney compensates by wasting HCO3-. |
Management pearls
- Trauma Bleeding: For any openly bleeding wound, the immediate first step is applying direct pressure; do not waste time searching for a source or removing objects.
- Airway Failure: If endotracheal intubation fails (difficult airway), immediately prepare and consider a surgical airway (cricothyrotomy).
- Adrenal Crisis Management: Treat with IV glucocorticoids (e.g., hydrocortisone) and mineralocorticoid replacement (fludrocortisone) if hyperkalemia/hyponatremia is present.
- Foreign Objects in Trauma: Never remove a foreign object found within the body cavity in the emergency room, as it may be tamponading or controlling bleeding; removal must occur in the OR.
Don't miss
Integration & clinical reasoning
- Hypoxia -> Acid-Base Compensation: Severe hypoxia causes hyperventilation -> Respiratory Alkalosis (\uparrow pH, \downarrow PCO2) -> Kidney compensates by wasting HCO3- -> Metabolic Acidosis (\downarrow Bicarb). This mechanism is key for understanding altitude sickness.
- Adrenal Gland Embryology: The adrenal cortex (steroid production) and the adrenal medulla (catecholamine production) are derived from different embryologic sources, meaning autoimmune destruction typically spares the medulla but destroys the cortex.
- Shock Pathophysiology: Understanding that low preload (e.g., hemorrhagic shock or tension pneumothorax) leads to decreased CVP/PCWP is fundamental for interpreting advanced hemodynamic monitoring.
OMM / COMLEX integration
- Emergency Management Priority: In any unstable or emergent situation (e.g., hemorrhagic shock, tension pneumothorax), standard life support protocols (ABCDE approach) take absolute priority over OMM/OMT considerations.
- Trauma Bleeding Control: Direct pressure is the immediate, non-invasive first step for external bleeding; do not delay this to assess for foreign objects or search for a source.
- Adrenal Crisis: Recognize that adrenal crisis can be triggered by stress (trauma, infection) even if the patient has no known autoimmune history and requires high-dose IV glucocorticoids immediately.
Concept connections / cross-references
- For detailed information on adrenal gland embryology and function, see [ Episode 12 ].
- For comprehensive coverage of acid-base disorders and renal physiology, review [ Episode 45 ].
- For general trauma resuscitation principles, refer to [ Episode 37 ].
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Hemorrhagic Shock | Low CVP/PCWP; low CO | Blood loss reduces venous return and cardiac filling volume. | Predicts decreased end-diastolic and end-systolic volumes (Frank-Starling principle). |
| Primary AI (Addison's) | Hyperkalemia, Hyponatremia, NAGMA | Loss of aldosterone impairs Na+ reabsorption and K+ excretion in the distal tubule. | The constellation of these findings is highly suggestive of primary adrenal failure. |
| Obstructive Shock | Tension Pneumothorax, Cardiac Tamponade, PE | External compression or obstruction prevents venous return to the heart. | These three are critical differentials when low CVP/PCWP is noted in a critically ill patient. |
| Myxedema Coma | Severe Hypothyroidism; Cardiovascular collapse | Thyroid hormone deficiency impairs cardiac contractility and sympathetic response. | Requires immediate IV thyroid hormone replacement (Levothyroxine) and pressors. |
Key terms glossary
| Term | Definition | Context | Example |
| Cricothyrotomy | Surgical airway procedure through the cricothyroid membrane. | Used when endotracheal intubation fails or is impossible due to severe swelling/obstruction (e.g., epiglottitis). | A definitive rescue airway technique in a difficult airway scenario. |
| Obstructive Shock | Hypotension caused by mechanical impediment to venous return. | Tension pneumothorax, cardiac tamponade, pulmonary embolism. | The common denominator is impaired filling of the heart (low preload). |
| Primary AI | Adrenal cortex destruction leading to cortisol and aldosterone deficiency. | Autoimmune disease; often presents with shock/hypotension. | Characterized by hyperkalemia and hyponatremia due to mineralocorticoid loss. |
| NIPP Vs | Non-Invasive Positive Pressure Ventilation (CPAP/BiPAP). | Used for respiratory failure when intubation is not immediately required or contraindicated. | Provides positive pressure support without an endotracheal tube, improving oxygenation and reducing work of breathing. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Trauma/Resuscitation | Focus on the AB Cs; systematic approach to hemorrhage control (direct pressure) and spinal precautions. | High | Board review questions, trauma algorithms. |
| Shock States | Create a differential diagnosis based on hemodynamic parameters (CVP/PCWP). | High | Reviewing the three types of shock: Hemorrhagic, Obstructive, Septic. |
| Endocrine Emergencies | Link autoimmune diseases to potential adrenal or thyroid failure; remember specific lab findings for each crisis. | Medium-High | Clinical vignettes and association tables (e.g., Celiac -> Addison's). |
Question pattern recognition
- Trauma/Shock: If a patient is hypotensive in trauma, assume hemorrhagic shock unless clear evidence points to an obstructive cause (low CVP/PCWP) or septic cause (high lactate, warm skin).
- Airway Emergency: When considering airway management for suspected epiglottitis, the immediate life threat is airway obstruction; therefore, intubation and preparation for surgical airways are paramount.
- Autoimmune Disease + Shock: The presence of an autoimmune disease in a hypotensive patient mandates ruling out primary adrenal insufficiency (Addison's) due to its unique electrolyte profile (\uparrow K+, \downarrow Na+).
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Welcome. My name is Divine. This is episode 571 of the Divine Intervention Podcasts. And in today's podcast we're going to be discussing a topic that I like to call Quicken Dirty Emergency Medicine for the USML exams. Quicken Dirty Emergency Medicine for the USML exams. My goal today is to discuss a series of scenarios and thought processes on questions that are kind of difficult to prepare for. Some of them are going to be classic things you're probably aware of. But I'm going to discuss quite a number of things that you're like, what? So these may not be things that again you see in any resource or you're like, how do I prepare for stuff like this? But these are things that you absolutely need to know for your exams. So we're going to talk through these things so they can feel very comfortable with them. So this podcast is certainly a tune to anybody taking step two CK or taking step three or take a level two or level three. But also this podcast I will say is certainly very helpful for a person studying for a surgery shelf and emergency medicine shelf or an internal medicine shelf. So let's jump right into it. So first thing I'm going to say today is that if you have a trauma patient, you know during a car accident or a fail from a height or whatever, what is one thing you should always keep in mind on your exams? You should always keep in mind the possibility of a C spine injury, a cervical spine injury.
And I'm telling you this, our friends at the MBM is they sometimes write these questions to be very non-descript. You don't think too much about them, but they are things that are actually pretty high yield to know for your exams. So I'll just really encourage you. If you see an answer that talks about like assessing for a C spine injury, then you should really be thinking of that answer. Just ask yourself, is there any reason why I should not pick that answer? Again, be careful. I'm not saying it's always the right answer, but it's very common for it to be an answer, right? And if you really think about it in a trauma situation like that, a person should probably be mobilized in a color in a neck color until the C spine injury has been ruled out. All right. So what did they give you a question about a 10 year old child and this child comes to the is brought to the emergency room by his parents because he's struggling to breathe for the last like six hours. He's been struggling to breathe. He has very high fevers. They tell you that you can hear audible stride without a stethoscope and what not. What should you be thinking about? And they tell you that he's like drooling and what not? Well, I hope you're saying, ooh, divine. This is a big lot. Titus. So they then say, oh, what's the most appropriate next best step in management? Well, your next best step in management is to intubate. I can almost promise you they will give you an answer choice that says to give antibiotics.
Don't do that. Right? The thing is, is the respiratory failure, the airway closure, that's going to kill this child and kill the child quick. So you should go ahead and intubate. So they can then explain to you in the question that, oh, you know, or they can make it a two-part question. They can say, you know, those questions where you click and then you can't once you click and submit, you can go back to it and then it's a two-part question. And then they give you like some follow-up that, ooh, you know, endotracheal intubation was carried out in the operating, you know, endotracheal intubation was attempted in the ICU or whatever, but it was unsuccessful. And then you're told, what is going to be your next best step in management? Well, if you try endotracheal intubation and it doesn't pan out so well on your exams, then the next thing you should consider in your test is a surgical airway. You should consider a surgical airway. You should consider a cryo-fire-idotomy, a cryo-fire-idotomy, right? Because again, these people that have epiglothitis and pretty sure have had a patient like this actually. Persine did not require a surgical airway, but that airway was probably one of the smallest airways I've ever seen in my life. So I'll just really encourage you if intubation fails, then you really should consider a surgical airway. You should consider a cryo-fire-idotomy, right? This is something that you definitely want to keep in mind.
So I just want to give you a general principle for you exams. If a person needs intubation and you're kind of worried and concerned that that person may have a kind of difficult airway, you should probably try to do those intubations in a controlled environment where other interventions could be done if the classic method of securing an airway endotracheal intubation fails. Just a nice principle to keep in mind for your exams. All right. Now, what if they give you a question about a 25-year-old male and you know this person is in the emergency room or is in the ICU and this person has been diagnosed with COVID. This person has a severe COVID infection and you're told that this person is going into like immediate respiratory failure. The person's auto saturation is extremely low. Oxygen partial pressure in their blood is really, really low. You know, the person is crushing and burning. The person is very unstable and then they didn't say, oh, what's the most appropriate next best and they say that, oh, that there is a physician or a nurse or whatever that is right outside the patient's room and the patient is under, you know, like the appropriate precautions and whatnot. But they tell you that, oh, that the physician is just wearing his scrubs or whatever and then they ask for your next best step in management. So let me tell you what answer they'll put.
They'll put an answer that says that, oh, you should run in and they'll put something along the lines of, you know, running into the patient, see the patient blah, blah, blah, blah. But then you'll see another answer that says that a personal protective equipment must be done first. So you must put on your PPE, your personal protective equipment, you know, like your surgical mask. I mean, sorry, because it's COVID, right? So you're going to wear a respirator so like an N95, gown, gloves, eye protection and stuff like that. And then they say, oh, you know, place where PPE before going to save the patient. What answer should you pick? I will encourage you to actually wear PPE before you save the patient. I know this may seem crass, but that's actually what you're supposed to do on your test. And think about it. This patient has severe COVID. Do you want to become just like that patient? Do you want to get a bed next to that patient in the emergency room? Right? So proper stewardship as an individual means you take care of yourself first. And then after that, you can take care of others. It's a very high-o thing to know for you exam. This is a very classic, bizarre, ethics situation you may see on your test. If a patient, if taking care of a patient requires you to wear PPE, you should wear, especially in an emergency situation because they like to throw these kinds of questions with emergency situations because think about it, right?
Why make it a benign situation where it's like, no, make it an emergency situation where you're forced to make like a tough hard decision. So don your PPE first before you go in and save the patient. All right. And then, you know, I'm sure many of you have heard of this thing that, ooh, if a person has a GCS less than eight into bait, I'm sure many of you have memorized that, you know, the Glasgow Homer scale, right? GCS less than eight in Q bait. Fine. All right. I'm sure that you've memorized that. I'm sure it's in on every Yankee deck known to mankind. It's kind of a little problem, though. The US ML Is, they don't really deal too hard in GCS because again, is something everybody knows. It's like memorizing some algorithm. The US ML Is these days, and many people do not believe me when I say this until you then take your exam and you're like, oh, shoot, this is actually true. The US ML Is these days, they focus on people that can understand concepts and people that can integrate concepts. You'll notice that many times, even memorizing an algorithm, like algorithms from Cubans and stuff, they're beginning to have less and less utility these days on the US ML Is. This is something I actually talk about quite extensively in my test taking strategies class. Right? So again, don't just be a person that is giving to memorizing algorithms or giving to memorizing or acronyms and all those things.
Those things have much less utility and the utility is getting smaller and smaller every day on the exam. Right? But what are some classic situations where our friends at the MBM is wanting to bait besides the GCS less than 18 to bait? Well, think about it. If a person has a stroke, like a severe stroke, let me tell you this. That person, they have a very high risk of like drooling and you know, aspiration and all those things. Those people certainly deserve endotrically intubation or think about a person that has altered mental status from like a drug overdose or drug intoxication or like really bad sepsis and you're like, hmm, this person is like drooling, they can't protect their earway. Like the person that has a pig lotitis, you should probably go ahead and into bait that patient as well. Another kind of weird situation of intubation that you may see on your exam is a person that is in status epilepticus. I can promise you a person that's in status epilepticus certainly does not have a good earway. So I mean, you cannot protect their earways, right? So those people that are in status, you absolutely positively need to intubate those people on an exam. And the good thing is you're already giving those people like IV benzodiazepines, right? So that can certainly help in kind of knocking them out. All right. Now, one thing I want to talk about here is this concept of FIO2, right? FIO2, right?
FIO2 because you know many people know that, oh, in the atmosphere, we have about 21% oxygen. But the thing is our friends at the NBM is they are many different ways they can kind of manipulate this just to see if you actually read on the stand path of face. And then I'll talk about it from an email, email perspective. So let me ask you this, if you go to the top of Mount Everest, what happens to your FIO2? What happens to your FIO2? It actually does stay the same, right?
So I know some people may be like, oh, define the FIO2 must drop no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no No, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no No, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no
, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no No, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no, no The oxygen dissolved in your blood vessels has gone down precipitously.
Guess what? The oxygen that is going to be saturating hemoglobin is going to go down as well So your SAO2 is going to go down. So what should you expect these people's Epo to look like? What should they rethroughpoetin look like? The Epo should increase because of hypoxia because of tissue hypoxia the Epo should increase. And if the Epo increases, what should you expect to happen to your hemoglobin and your hematocrit? Or that should increase. Remember, Epo comes from the kidneys. And then you're going to make a more red blood cells. Now, what would you expect this person's P little ACO2 to look like? What should they PCO2 look like? The partial pressure of carbon dioxide? I'll really hope you're saying, oh, the vine is going to be low. Man, I'm telling you all these hours I'm talking about, you may think I'm joking. I'm really not joking. This stuff, I'm talking like this is no joke. Like this is no joke. Like I'm pretty fired up talking about this right now. This stuff is pretty high yield to know for you exams. Your PCO2 is going to drop. You know why? Because I'm going to be a little bit more patient. So, what's your hypoxic? When you're a hypoxic, how do you think your body responds? Your body is going to respond by hyperventilating. So, it can blow CO2 and bring it more oxygen. So, your P little ACO2 is going to go down. Now, what's going to happen to your pH? What's going to happen to your pH?
Well, if you're blowing off a lot of CO2 because your hyperventilating, you're going to have a respiratory alkylosis. If you have a respiratory alkylosis, guess what? Guess what? Your pH is going to go up, right? Now, what's going to happen to your bicarb? What's going to happen to your bicarb? Well, think about it. Your kidney is going to try to be a compensating for the respiratory alkylosis. So, your kidney is going to try to do that by excreting more by carbonate, right? So, as you excrete more bicarb, you're losing more of a base. You're going to develop a metabolic acidosis. So, your bicarb is going to go down, right? You're going to try to compensate for the respiratory alkylosis with a metabolic acidosis by losing bicarb in the kidney. This is why when a person has high altitude sickness, one thing you can do is to give them a sedazolomide. As we know, a sedazolomide is a carbonych and hydrate inhibitor. When you inhibit carbonych and hydrates, it's going to prevent you from reclimiting bicarb at the level of the proximal convoluted tubule. So, you're going to dump it in your urine. So, you kind of speed up that bicarb loss to compensate better with the metabolic acidosis by giving a sedazolomide. Please know this stuff. I'm begging you, please, know this stuff. So, one thing I want to discuss, they can literally make that an EM question, right? But, you know, like, there are questions.
To me, student asked me a question recently, that, hey, you know, what's the order in which, you know, like almost like escalation of oxygen therapy? This is almost certainly something that you will maybe not see on a USMLE exam or on a shelf exam. But, I guess it's kind of useful information to know. So, let's kind of talk about it. I'm not going to spend more than a minute at best on this. But, in terms of methods of delivering oxygen to patients, which basically from lowest FIO to delivery possible, which was the gradation in terms of, like, lowest to highest. Well, lowest obviously is going to be you just breathing in room air. If you're breathing in room air, you're getting that oxygen that's in the atmosphere, the 21%, no big deal. Right? But, the next thing that comes after that is, those are like nasal prongs, those nose prongs, those things that you're just going to stick in your nose, right, to give you some oxygen. Those things can give you a little more FIO too than just breathing in room air. But, if that's not giving you enough oxygen, what should you step up to? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? What should you do? Next thing to step up to is a face mask.
You know those masks that you can basically put in the covers like your nose and most of your mouth. That gives more FIO to than those nasal prongs. All right. So, let's say you've given through the face mask and that's not giving you enough oxygen. You want to give even more FIO to, then the next thing you should go for is a non-rebrither mask, a non-rebrither mask. A non-rebrither mask, absolutely, positively gives more FIO to than a face mask. And then, what if that is not working? If that is not giving you enough oxygen, you want to give even more oxygen. Then, you want to go for a C-PAP or a BIPAP. C-PAP means I think continuous positive airway pressure and BIPAP is by level whatever intermitted positive airway pressure. Those two things, because they know that everybody that has the job description medical students memorize. C-PAP, BIPAP, C-PAP, BIPAP. What do they do? Sometimes on the exams, they'll call that non-invasive positive pressure ventilation. Non-invasive positive pressure ventilation. Those things can give you pretty steep levels of FIO to. Pretty steep levels of FIO to. Why do you think it's called non-invasive? Because literally nothing is being stocked down your throat. Obviously, in the tricky intuition, like the good method of delivering oxygen to people is an a form of invasive, because it's literally invading your airway. It's a form of invasive positive pressure ventilation.
So, again, you go from room air to those nasal prongs, to a face mask, to a non-rebrither mask, to the NIPP Vs, to non-invasive positive pressure ventilation. C-PAP and BIPAP, although C-PAP is used more like in a home setting, for like OSA, BIPAP is used more like in a hospital setting. And then after that, we have endotry kill intuition. And then you will probably get a little more invasive and no crackle thyroid autoimmune. That's like the new clear forms of oxygen delivery. Now, what if they give you an epidemiology question on your exam? And they will frame it like this. The give you a patient comes to the emergency room. And this patient is in shock. Persons like extremely hypotensive, systolic blood pressures, like in the 70s or 80s, the person is like a tachypnec, person's tachycardic, you know, not doing very well at all. And then they say, what is the most likely theology of this? And this is a trauma patient, maybe car accident, fell from a hydro, whatever. And then they say, what is the most likely theology of this patient's abnormal vital signs? And then they give you literally all the kinds of shock as an answer. They give you like septic shock. They give you a neurogenic shock. They give you hypoglymic shock. They give you a hemorrhagic shock or whatever. They give you all those things that are like, oh my goodness, which one do I pick? Well, let me explain something to you.
If they give you a question, because again, the USM at least these days are a critical thinking galore critical thinking galore, right? Galore is a real word. Trust me, you can look it up. G-A-L-O-R-E galore, but different discussion. This is not an English lesson. But they give you a question like that. The answer you want to pick is hemorrhagic shock. Really? Yeah. The most common kind of shock in trauma is hemorrhagic shock. I'm going to say that again, the most common kind of shock in trauma is hemorrhagic shock. This is extremely high you to know. The most common kind of shock in trauma is hemorrhagic shock. Now, let me explain something here. Let me explain something here. If however, so if they give you a question on, oh, trauma patient, shock, and they give you almost no clues, pick hemorrhagic as the cause of their shock. But if they give you certain clues, they should go in certain directions. Like for example, if the person's skin is like warm and flushed and the person has a very high fever, even if hemorrhagic is the most common cause of shock in a trauma patient, with that extra context that was given, you should probably think about along the lines of a septic shock, right? Again, when they give you specific clues that lead you down specific directions, they should go in those specific directions. But if they don't give you clues, jump on what is common, right? The most common kind of shock in a trauma patient is hemorrhagic shock. All right.
So let me ask you this. If a person has hemorrhagic shock, what happens to their preload? Well, think about it. If you're bleeding out, you don't have enough blood within your blood vessels. I got to be sending more blood back to the heart. No, so your preload is going to go down. Okay. So since you're sending less blood back to the heart, what's going to happen to your cardiac pressures? What's going to happen to your pulmonary capillary wedge pressure, which is a surrogate for left heart pressure or your central v-nose pressure, which is a surrogate for right heart pressure? What's going to happen to those pressures? Again, this is not something you have to memorize. It makes perfect sense if you just think about it. Those pressures should be low. Why are they low? Because your preload is low. If you're not sending blood back to the heart, garbage and garbage out, they're not sending blood back to the heart. Blood is not going to be collecting when you're doing your heart. So your cardiac pressures are going to be low. All right. So what's going to happen to your cardiac output in this circumstance? Well, again, garbage, I'm not saying your heart is garbage, but I'm just using a classic computer science description. But if you're putting less blood in the heart, are you going to put out much blood? No, your heart is not like a magic machine. You cannot put like 10 emails of blood in the heart and magically your heart produces like 50.
No, if you find that kind of heart, let me know. Right. That doesn't happen. Right. So the thing is going to happen is because you're preload is low, or your cardiac output is going to be low. That's literally the Frank Stalin principle in a nutshell. In fact, let me ask you this for this person because they know that you know, quite a number of people have memorized many of these arrows. Oh, I know the R4 preload cardiac output, PCWP, CVP, you've memorized all those things. What can they do on your exams? They can just do a little bit of a step one throwback. So let me ask you this. What's going to happen to this person's endastole volume? Remember what's endastole volume? Endastole volume is the volume of blood that is left in the heart at the end of the astaly at the end of feeling. Well, if your preload is low, you're not bringing much blood back to the heart. So your EDV, your endastole volume should go down. All right. If your endastole volume goes down, what should happen to your endastole volume? Again, literally what is endastole volume? Endastole volume is the amount of blood that is left in the heart after the heart has ceased to lead after the heart has contracted. Right? So because your EDV is low, the amount of blood that was in the heart after feeling was low, the amount of blood that's going to be left in the heart after contracting is going to be low as well. So your ESV is going to go down as well. All right.
So it should make sense that your stroke volume, which is the amount of blood that is ejected with each heart beat, should go down. Right? It should go down. You should go down. Your stroke volume also goes down. Now let me ask you this. What happens to your, let me see what other cardiac parameter I can make up here. What happens to your heart rate? Well, your heart rate will obviously go up, right? Because your body is going to try to maintain cardiac output in one way or the other. And many of you know that heart rate times stroke volume is you go to cardiac output. So if your stroke volume is plummeting, one of the ways your heart can try to respond is by jacking up your heart rate. So your heart rate is going to go up in these folks. And then what's going to happen to your systemic vascular resistance? Well, think about it. Your blood pressure is extremely low. So your body is like, oh, shoot. This is not great. Right? So it's like, how can I try to maintain proficient pressures in my bloodstream? You're going to climb down on your vessels. You're going to increase your systemic vascular resistance. Again, emergency medicine, the USML Es, they love their precious hours. You've got to know these things for your exams. I promise you, these things I'm discussing, they're not low yield for your test. All right. Now that was almost like a mini shock shock discussion. Then now, one thing I just want to say so that people don't miss out on this is the following, right?
So obstructive shock, you may hear the term obstructive shock. Honestly, I really don't like this term because it does not really It's kind of confusing, right? Under the right circumstance, you can be confusing. But the thing is, is something that you may see on your test. So let me explain something here. If you see the term obstructive shock on your exams, there's one of three pathologies that they're discussing. Okay. There's one of three pathologies that discuss it. They're discussing attentionable thorax or the discussing cardiac tamponad or the discussion of pulmonary embolus. Okay. Tensioning of thorax, cardiac tamponad or pulmonary embolus. So let me try to give you some reasoning as to why these things may be called obstructive shocks. Well, think of attention in the thorax. Why you have attention in the thorax. Literally air is accommodating within your thoracic cavity and it has nowhere to go. So that air because it's under high pressure, it's going to be compressing your heart. So it's almost like your, your clumping down on the heart from the outside, you're doing like an external compression of the heart. It's going to make it really hard for the heart to feel with blood. That's a problem. But also do not forget that you're also compressing the superior and inferior veneciva. If you compress the SVC and the IVC, your preload is going to drop like a stone. You're literally not going to be sending blood to the heart. Right.
So the combination of all these factors impairs the feeling of the heart. If you impair the feeling of the heart, guess what? Your cardiac output is going to drop significantly. You're going to be in shock. Now, why would cardiac tampon at be called an obstructive shock? Well, a reason why cardiac tampon at me be called an obstructive shock is that unlike in a case of attention in the thorax, I remember in attention in the thorax, you're going to do a needle compression, right? A needle for a costum first. And then after that, you go for a chest tube, which is a tube for a costum. Right. But for cardiac tampon at is not air that's compressing the heart from the outside. It's fluid that is compressing the heart from the outside. Literally fluid that's compressing the heart from the outside, right? Fluid that's within the period cardium. And what can cause that fluid? Well, if you have really bad urine, right? So let's see if Mr. Bunch of dialysis sessions or you have a erotic dissection, believe it or not, cardiac tampon at is a very feared complication of a erotic dissection, right? Or you have like a viral paracodidase or whatever and all the fluid is built up, right? You're going to be having this extrinsic compression of the heart from the fluid that's in the period cardium that can absolutely positively cause you to go into shock, right? Again, whenever the heart is being compressed by something from the outside, you should really think of some kind of obstructive shock.
And obviously, if a person has cardiac tampon at what should he be doing next? You should do a period cardio synthesis, right? Many times a period cardio synthesis is going to be done with echocardiography. You're going to do it on the ultrasound guidance on the ultrasound guidance. And then why will a PE, a pulmonary embolus be called an obstructive shock? You are literally obstructing flow of blood out of the right side of the heart, out of the right ventricle because your pulmonary artery has been occluded. That's why those things are called obstructive shocks. Okay? So don't forget your tension in motor rucks, your cardiac tampon at your pulmonary embolus. And obviously, if a person has a PE, you want to go ahead and give IV, heparin. Now, what if they give you a question about a patient and they tell you that this patient has a history of celiac disease. And then this person is in shock. This person is like extremely hypotensive, extremely tachycardic, right? What is going to be the likely cause of shock in this person? Well, on your exams, there are two corporates I want you to think about. The thing is our friends at the end being means they really love these two corporates. And you're going to see the link to celiac disease in a moment here, right? But I want you to think of other since disease, primary adrenaline, efficiency. And I want you to think of a mixedema, coma, a mixedema, coma.
That's something you can have as a kind of a feared complication of really, really bad hypothyroidism, right? So it's like you may want to be in divine. What in the world are you talking about with celiac disease and these causes of shock? Well, the first thing is you need to establish a principle in your mind. Our friends at the end being means when they're testing an autoimmune disease, more than 50 to 70% of the time, they will give you a pass medical history of another autoimmune disease. Again, the USML Es are not based on algorithms. They are based on context. It's a very kind of one of these things that people do not think about. But again, it's really important. But basically, the person has celiac disease. celiac is clearly an autoimmune disease, right? You have these anti-glyaden or these anti-indomacial or these anti-titious transglued terminus antibodies that you make. When you make those antibodies, you destroy your microv-ly, the cosmic absorption. All right. Well, the thing is, if you have an autoimmune disease, you're likely to have another autoimmune disease. Well, in other since disease, you're literally damaging the adrenal cortex. Remember, in other sense, the adrenal medulla is not affected. Please do not mess this up. In other since disease, it's your adrenal cortex that is messed up, not the adrenal medulla. Why is this the case? Well, this is something many people do not keep in mind.
But the adrenal gland is almost like two organs that were just smashed and made one organ. Right? It's almost like you had a merger between like two companies. Right? Those two, let's say you're merging a company that makes soap and a company that owns restaurants. Those companies have nothing to do with each other. They just happen to like merge. Right? Kind of think of like a Bekshire Hathaway. Right? Bekshire Hathaway, you know, many of you know, I love wearing Buffett. Right? Bekshire Hathaway has a ton of companies in the portfolio. They own Geico, they own a Cscandys, they own a tons of Coca-Cola, tons of Apple if he's not completely sold out of that. Right? Siri, Siri, sex, a bunch of random things. You probably like, if I had you know this stuff, well, I do like the stock market. I'm a person that likes the financial markets, but that's a different discussion for another day. Right? You merge all these things together, sending them to the Adrenal Gland, the Adrenal Cortex, believe it or not, is there a from a completely different embryologic angle than the Adrenal Medulla? Right? The Adrenal Cortex, I believe is actually derived from Measoder. I believe, don't quote me on this, but I believe it's derived from Measoder. But the Adrenal Medulla, I'm pretty sure is derived from Neurocress cells, different, different, different things. Right?
So when you have autoimmune destruction of the Adrenal, you're destroying the Adrenal Cortex, you're not destroying the Adrenal Medulla. That's a very important thing to keep at the back of your mind, for example. All right. So why would Adesins disease cause a person to go into shock? Well, think about it. If you have Adesins disease, well, guess what? You're going to be short on Out Dust Iron, you're going to be short on Cortisol, you're going to be short on DGS. But the one we're really worried about, I mean, obviously the Out Dust Iron, if you're lacking that, you're not going to be absorbing sodium and water from your kidneys. So that's going to cause you to be hypotensive. But remember, Cortisol has a permissive effect on the sympathetic nervous system. Basically, your blood vessels do not respond very well to cardiovascular means, if you're in a state of Cortisol deficiency, if you're in a state of Cortisol deficiency. Right? So that can cause the person to be profoundly hypotensive. Okay. So again, if you see a person that has an autoimmune disease and they're in shock, you really want to think about that person potentially having Adesins disease. And they will try to hopefully give you more clues like hyponitramia, right? Because again, if you lack Out Dust Iron, you're going to be absorbed sodium, so you be hyponitramic. They'll give you hyper-kilemia. Because remember, our dust room makes you excrete potassium in the kidneys.
If you lack Out Dust Iron, you will not be able to excrete potassium. You're going to have hyper-kilemia. And then you'll also have a normal anion gap metabolic acid doses. Because one of the jobs of our dust room is to make you excrete hydrogen ions in the kidneys. Well, if you cannot excrete hydrogen ions in the kidneys, you're going to hold onto them. You're going to have a metabolic acid doses. So those sometimes they can make it a higher anion gap as a dose, but classically, Out Dust Room deficiency, hyper-out Dust Room states should cause you to have a normal anion gap metabolic acid doses. In fact, these hyper-out Dust Room states, the other things that tend to cause type four RT As, type four in Antibola as a dose is again. Different discussion for another day. And I'm pretty sure I've made podcasts on like Nugmas and RT As, I think. So just going to keep that at the back of your mind for for exams. Now, what's the other thing that can cause shocking a person that has a history of another autoimmune disease? I want to think about Mixedema coma. There's something that happens in people that are hypothyroid. So hey, what's the most common cause of hypothyroidism in the US? I hope you're saying, ooh, divine. Hashimoto's. Hashimoto's. Hashimoto's is the most common cause of hypothyroidism in the US. Most of them cause of hypothyroidism in the US. So if you have Hashimoto's and you don't treat it well, in fact, Mixedema coma may be your first presentation.
Again, you need thyroid hormone for metabolic stuff in your body. If you're super short on thyroid hormone, and obviously if a presence Mixedema coma, what do you expect your T3 T4 to be? It's going to be extremely low. So what should the TSH look like? What should be extremely high? The TSH will be very, very, very high. And those people again, they can be in a very, very, very, just... I mean, because you may wonder why may they be in shock, why may they be hypotensive? Well, those people pretty much almost have like cardiovascular collapse. Because many people do not think about this. But again, this is why having an understanding of pathophysiology is extremely helpful on the USM elites. One of the jobs of thyroid hormone is to increase the insertion of beta-1 receptors on the surfaces of your cardiac myocytes. Okay. So if you put more beta-1 receptors on the surface of your cardiac myocytes, what do beta-1 receptors respond to this? They respond to cardiac colomines. So you're going to respond to cardiac colomines better if you have enough thyroid hormone around. So your heart will be like in a parasympathetic state almost. You won't have like good inotropy, you won't have good chronotropy if you're in a thyroid deficient state. But that's not all. Where else do we have beta-1 receptors in the body? We have beta-1 receptors in the kidneys. Hmm. Raining production. So just kind of keep those things in mind.
But I will say probably the primary effect you should keep at the back of your mind, for example, is that cardiac effect? Is that cardiac effect? You're going to have less stimulation of the heart when you're in a thyroid deficient state. Those people obviously should be on IV-level thyroxyl, and in fact let me say those people should also get like some kind of like IV press or something to kind of help them through those situations. And I think when people are in Mixidima coma, right, you really need to watch those people because that thing can actually kill. It's not like some fly by night disorder. No, you can actually kill you, right? And I guess things we're kind of talking about like an adesonian crisis causing shock. Just be careful about a general crisis from people that are chronically using steroids. They can literally make this an emergency medicine situation. So this person may not necessarily have a history of an autoimmune disease. But they may have a history of some disorder that should have a steroid. So let's say they have like giant cell at a rate, this temporal at a rate, this or whatever. And the on chronic steroids are pressing that has like really really nasty asthma, right? And they're on chronic oral steroids. Well, those chronic oral steroids you're taking is going to literally suppress your HPA access, right? And that's not a big deal. It's not a big deal as long as your level of stress in life doesn't go up.
But if your level of stress goes up because you're like in trauma or you know, your mental trauma because you're studying for the USM is or whatever. Well, that's going to suppress that access. If you suppress that access, your body is like, oh, I'm stressed. I'm stressed. I'm stressed. I need to make more cortisol. But hey, you literally suppress your HPA access because you're on chronic steroids, right? So in those circumstances, kind of a bad situation you're in. You need to give us stress dose of stairs to rescue those people to rescue those people. So just keep that in mind, right? That adrenal crisis can also present as shock, right? And don't forget that in other things disease, we're going to treat those people with with a fluke record is on and you know, like a steroid. You're going to give them steroids and fluke record is on the fluke record is on is a mineral record required analog. The steroid is going to replace the bloke record is that they're missing. All right. We're going to wrap this up shortly here soon. This broadcast is kind of running a little long, but I just want to say two more things. What if you're stopped by a foreign object, right? You're literally stopping the foreign object. And the foreign object is like in the patient and the patient is like hypotensive or maybe stable or whatever. And then in person comes to the emergency room and you're told what's the next step in management.
Now, here's one answer that you want to resist picking on you exams. The answer you want to resist picking on your exams is the answer that involves you removing the object in the emergency room. Don't do that. Don't do that. Please don't do that. That foreign object that is in the person that is launching the patient may be tampon adding a bleed. So just keep that in mind. It may be backstop in that bleed. Do not remove it. That foreign object has to remove the safe conditions usually in an operating room. All right. They're removing the emergency room. Not a good idea. All right. Now last time going to say what if a person has like an openly bleeding wound, right? Literally they're like openly bleeding. What should be your next step on your exams? You see the open wound is like right in front of you. Your next step on the exam is going to be to apply direct pressure. Apply direct pressure. Right? They'll give you a bunch of answers that deal with like fluid or a sensation. And no, you shouldn't do those things. But the most appropriate immediate next step in management is to literally you literally seem to bleed right in front of you. Apply direct pressure to that bleed straight up. Okay. That's the right thing to do. So again, if you just love this lecture, you love the way I teach you love the way explain path of phase. You love the way I made integrations. I'm very interested in the classes I offer next week. Starting next week Tuesday, the 18th of February.
A bunch of classes that are starting for step one to step three. Okay. Let me first talk about step one step one. I have a class in the first week of March. He's a 25 hour step one review. That's a good class for both taking step one or level one. If you're taking step two level two or step three level three, I have a poor basic science foundation because basic sciences and I'll be coming very heavily represented on the US ML East. That's a class that you definitely want to take. And then also for step one to step three next week Tuesday, the 18th of February. I have a 12 hour test taking class on the 19th. I have a four hour bio stats class on the 20th. I have a five hour social sciences quality improvement healthcare systems class ethics class as well. You know, many people are taking these classes, funding to be extremely helpful for the exams. I have a three hour test for step one to step three. And then for step two, step three specifically on the 21st of February, I have a three hour last mini review. It's a very, very high class, very, very helpful class for step two, step three. And then the week after that, I believe from the 24th to the 27th of February, I have a 20 hour step two step three review. Again, I've had many people take these classes get two seventies do really, really well on their exams. I'm not saying everybody gets a 270, but many people have got in the two seventies. I've had a lot of two sixties, a lot of two fifties, a lot of two forties.
So people do pretty well. I've had people that have not been passing practice exams. They take this 20 hour class. They take these series of classes and they end up doing really, really well on their test. They are doing 30, 40, 50 points higher than the average. So again, I think these are classes that I will put together that can really, really help you. And in the grand class is in the first two weeks of June, the 50 hour step two, step three review. That class, I made a special podcast on it. You can find it on the website. That class is going to be so helpful to anybody that attends. I can tell you that I'm the one that's going to be teaching the whole class. I can tell you that that's all I'm going to say. Now I also have these podcasts on Apple Google Spotify. So check those out, you know, and I have a You Tube channel. You can check out where I post all the podcasts that I make. And then I have another website called divine intervention life lessons calm. Divine intervention life lessons calm every week. I post like two to three podcasts where from a biblical perspective address a life lesson. It's actually an Apple podcast associated with that called the divine intervention life lessons podcast. And then I also offer one or one to learn from all the US Emily exams, all the complex exams. And I help with your applications, more interviews, personal experiences. And all those things. So if you're interested in any of those, shoot me an email through the website.
If you want to sign up for these classes, shoot me an email through the website. And I'll give you some more information. So thank you for listening to me today. Again, this podcast is pretty high yield. Don't throw it away. So I'll see you in episode 572. So God bless you. Bye for now. Thank you.
Practice questions — USMLE style
Question 1 — Internal Medicine/Critical Care
A 45-year-old male is brought to the emergency department following a motor vehicle accident and presents in profound shock. Initial assessment reveals hypotension, tachycardia, and diminished breath sounds on the right side of the chest. A focused physical exam suggests that the patient's hemodynamic instability is due to external compression of the heart and great vessels. Which of the following conditions must be considered as an obstructive cause of shock?
- A) Septic shock secondary to abdominal contamination
- B) Acute myocardial infarction leading to cardiogenic shock
- C) Tension pneumothorax
- D) Massive internal hemorrhage causing hypovolemic shock
Answer: C. Tension pneumothorax is a classic example of an obstructive cause of shock, alongside cardiac tamponade and massive pulmonary embolism. In tension pneumothorax, air accumulates in the pleural space under high pressure, leading to external compression of the heart and great vessels (including the vena cavae). This dramatically reduces venous return (preload), causing profound hypotension and cardiogenic/obstructive shock. While hemorrhagic shock is common in trauma, the specific physical finding of diminished breath sounds combined with hemodynamic collapse strongly suggests a mechanical obstruction like tension pneumothorax.
Question 2 — Physiology/Acid-Base Balance
A patient ascends rapidly to high altitude (e.g., Mount Everest). Within hours, the patient develops symptoms consistent with acute mountain sickness and respiratory alkalosis. To compensate for this primary respiratory disturbance, which physiological change occurs in the kidneys, and what is the most appropriate pharmacological intervention to correct the resulting metabolic imbalance?
- A) Kidneys retain bicarbonate; administer sodium bicarbonate
- B) Kidneys excrete hydrogen ions; administer ammonium chloride
- C) Kidneys increase excretion of bicarbonate; administer acetazolamide (a carbonic anhydrase inhibitor)
- D) Kidneys decrease potassium excretion; administer hypertonic saline
Answer: C. At high altitude, the low partial pressure of oxygen ($\text{P}_{\text{O}_2}$) stimulates peripheral chemoreceptors, leading to hyperventilation. Hyperventilation blows off excess $\text{CO}_2$, causing respiratory alkalosis (high pH). In compensation, the kidneys attempt to excrete base by increasing bicarbonate excretion, which leads to a metabolic acidosis. To counteract this compensatory loss of bicarb and facilitate acclimatization, carbonic anhydrase inhibitors like acetazolamide are administered.
Question 3 — Endocrinology/Autoimmune Disease
A 28-year-old woman with a known history of celiac disease presents to the emergency department in profound shock. She is hypotensive, tachycardic, and has laboratory findings showing hyponatremia, hyperkalemia, and metabolic acidosis with a normal anion gap. Given her autoimmune history and clinical presentation, what is the most likely diagnosis?
- A) Myxedema coma
- B) Adrenal crisis (Addisonian crisis)
- C) Thyroid storm
- D) Septic shock secondary to gastroenteritis
Answer: B. The combination of an autoimmune disease history (celiac disease), hypotension/shock, and the classic electrolyte triad ($\text{Hyponatremia} + \text{Hyperkalemia} + \text{Metabolic Acidosis}$) strongly points to adrenal insufficiency (Addisonian crisis). Adrenal failure leads to a deficiency in aldosterone and cortisol. Aldosterone deficiency causes sodium wasting ($\rightarrow$ hyponatremia) and potassium retention ($\rightarrow$ hyperkalemia). Cortisol deficiency impairs vascular tone, contributing to hypotension.
Question 4 — Trauma/Airway Management
A 10-year-old child is brought to the emergency department by parents who report that he has been struggling to breathe for six hours and appears drooling excessively. On examination, the airway is severely compromised. Initial attempts at endotracheal intubation fail due to profound upper airway obstruction. What should be the next best step in management?
- A) Repeat intubation attempt using a video laryngoscope
- B) Administer nebulized bronchodilators and systemic steroids
- C) Perform an immediate surgical airway (cricothyrotomy or tracheostomy)
- D) Place the child under general anesthesia for definitive airway control
Answer: C. In cases of severe upper airway obstruction, such as epiglottitis, where initial endotracheal intubation attempts fail, the priority shifts to securing an airway via a method that bypasses the obstructed area. A surgical airway (cricothyrotomy) is indicated when standard intubation techniques are unsuccessful or impossible due to anatomical compromise. This principle emphasizes that if advanced life support measures fail, one must be prepared for definitive, often emergent, surgical intervention.
Quick fire review
What is the most common cause of shock seen in trauma patients?
Hemorrhagic shock.
If intubation fails due to severe airway obstruction (e.g., epiglottitis), what definitive procedure should be considered next?
A surgical airway, such as a cricothyrotomy.
What are the three pathologies that can cause obstructive shock?
Tension pneumothorax, cardiac tamponade, or pulmonary embolism (PE).
In hemorrhagic shock, what compensatory mechanisms occur to maintain blood pressure?
Increased heart rate and increased systemic vascular resistance (SVR).
When assessing a patient with an autoimmune disease presenting in shock, which specific electrolyte pattern is highly suggestive of adrenal insufficiency?
Hyponatremia, hyperkalemia, and normal anion gap metabolic acidosis.
What is the immediate first-line management for an openly bleeding wound?
Applying direct pressure.
Name the three causes of obstructive shock.
Tension pneumothorax, cardiac tamponade, or pulmonary embolism (PE).
Why does a patient with celiac disease who develops adrenal insufficiency present with hyponatremia and hyperkalemia?
Adrenal cortex failure leads to loss of aldosterone/cortisol effects; mineralocorticoid deficiency causes sodium wasting (hyponatremia) and potassium retention (hyperkalemia).
What is the primary mechanism by which tension pneumothorax causes shock?
Air accumulation compresses the mediastinum, impairing venous return (SVC/IVC compression), leading to decreased preload.
In a patient with severe COVID-19 requiring respiratory support, what ethical principle dictates the first action upon entry into the room?
Don appropriate Personal Protective Equipment (PPE) before attempting resuscitation or saving the patient.
What is the key difference in pathology between cardiac tamponade and tension pneumothorax?
Tamponade involves fluid accumulation within the pericardial sac, while tension pneumothorax involves air accumulation in the pleural space.
If a trauma patient has an embedded foreign object causing bleeding, what should be done regarding its removal?
Do not remove it; let surgical teams remove it under controlled conditions (OR).
Quick recall / Anki-style questions
Name the three causes of obstructive shock.
Tension pneumothorax, cardiac tamponade, or pulmonary embolism (PE).
Why does a patient with celiac disease who develops adrenal insufficiency present with hyponatremia and hyperkalemia?
Adrenal cortex failure leads to loss of aldosterone/cortisol effects; mineralocorticoid deficiency causes sodium wasting (hyponatremia) and potassium retention (hyperkalemia).
What is the primary mechanism by which tension pneumothorax causes shock?
Air accumulation compresses the mediastinum, impairing venous return (SVC/IVC compression), leading to decreased preload.
In a patient with severe COVID-19 requiring respiratory support, what ethical principle dictates the first action upon entry into the room?
Don appropriate Personal Protective Equipment (PPE) before attempting resuscitation or saving the patient.
What is the key difference in pathology between cardiac tamponade and tension pneumothorax?
Tamponade involves fluid accumulation within the pericardial sac, while tension pneumothorax involves air accumulation in the pleural space.
If a trauma patient has an embedded foreign object causing bleeding, what should be done regarding its removal?
Do not remove it; let surgical teams remove it under controlled conditions (OR).