Hi all, sorry just a lowly ER doc here but I'm looking for advice on how to best approach this case.
Patient is in their 60s with chart diagnosis of diastolic heart failure but no TTE for ~10 years, not on GDMT and just on a thiazide, poorly controlled DM, HTN, prior meth use hx but in remission for > 10 years. Presents with new AFIB RVR with unclear time of onset - they were feeling unwell for ~2 weeks with worsening orthopnea, dyspnea on exertion, and mild leg swelling. No chest pain. Maybe started having palpitations / racing heart rate 3-4 days ago.
Rates 150s-160s, seen in PCP clinic and given a dose of 25 mg metoprolol tartrate before being sent to the ED. Stable hemodynamics 140s/80s, not hypoxic or in respiratory distress, just appears somewhat uncomfortable. Clinically hypervolemic with mild pulmonary edema and RLL pleural effusion (new), lower extremity edema. My POCUS showed grossly intact contractility, enlarged IVC and no pericardial effusion. Labs including TSH were normal except for elevated BNP in the 400s. No PE.
NOT on anticoagulation but CHADS2VASC 4, and I felt not a candidate for DCCV in the ED given stability and unclear time of onset.
My initial thoughts were to first attempt diuresis so I gave lasix 20 mg IV (lasix naive) with good effect but HR remained in the 150s. Ultimately decided to trial metoprolol 5 mg IV x3 to get them down to 120s and admitted to the floor for further diuresis and rate control. Started them on eliquis. Didn't get a cards consult because it was in the middle of the night.
I'm hoping to develop a more standard approach to managing AFIB RVR with CHF though I realize it's more complicated than that (HFrEF vs HFpEF, etc). Also from an ED perspective, my job is in part to get their rate under control for the floor but doing so safely.
Some really basic questions: Are BB generally well tolerated and avoid CCB universally? Consider early DCCV if adequately anticoagulated and clearly symptomatic but hemodynamically stable or await further diuresis? Would this patient be a good candidate for trialing digoxin? Amiodarone?
Thanks so much for your help!

It is almost inevitable that you will have to deal with atrial fibrillation at some point in the hospital as it is the most common arrhythmia. Generally, when I am giving a chalk talk on this subject I like to split it up into A) what medical students need to know and B) what interns need to know. Since there are a lot of non-medicine people on here, you really can probably skip to the basic management of afib (particularly afib with RVR) instead of going into the details of naming conventions, knowing where afib arises, etc.

What medical students should know

• Afib occurs when abnormal electrical activity cause the atria to quiver
• Identifying it on EKG - fibrillating baseline with no clear p wave, irregularly irregular
• Physical exam is also described as "irregularly irregular"
• Good mnemonic for common causes is PIRATES ○ Pulmonary, post-op, PE ○ Ischemia (ACS) ○ Rheumatic heart disease ○ Anemia, alcohol ○ Thyroid, toxins ○ Electrolytes ○ Sepsis
• The reason we care so much about afib = 1) risk of stroke/TIA and 2) afib with RVR
• Where do clots form? Left atrial appendage due to stagnant blood
• Risk scores = CHADSVASc and HAS-BLED to help us determine when to anticoagulate (though HAS-BLED has only been validated in warfarin from what I understand)
• Basic management is rate or rhythm control, anticoagulation, and cardioversion if needed

What medicine interns need to know

Where does afib originate from?

• LEFT atrium (as opposed to aflutter which arises from the RIGHT atrium)
• Source = pulmonary veins (still remember those from your anatomy class?)
• Why is this important? When we do an ABLATION, this is where we target to try to get rid of the afib. Aka pulmonary vein isolation. You can also do a MAZE procedure where they basically go in surgically and make tiny little cuts everywhere to stop the abnormal signals from spreading through the atrium. Sometimes they'll do this if they are doing open heart surgery for some other reason (at least from what I know). BTW anyone getting open heart surgery usually also gets left atrial appendage ligation as well to try to reduce the risk of stroke.
• One of the major risks of ablation is bleeding since you are essentially burning the heart, the EP docs usually place a temperature probe in the esophagus to make sure they aren't about to burn a hole all the way through the heart to the esophagus and create a bleeding atrio-esophageal fistula.
• Another thing to note is that when a patient starts to get a super dilated left atrium, they are basically always going to be at high risk for afib again even if you convert them to normal sinus. Imagine the pulmonary veins are now hella stretched out, they're going to be super irritated and send even more abnormal signals. So often times patients with really dilated atrium are going to be near impossible to keep in NSR.
• Oh yeah, and for atrial flutter which arises in the RIGHT atrium, the underlying issue is at the CTI (cavo-tricuspid isthmus) which is important to know because if they decide to ablate, they will do a CTI ablation.

What is the atrial rate for afib vs aflutter?

• Cardiology attendings love pimping on this all the time
• Aflutter rate is 300 bpm
• Afib rate is 400-600 bpm
• The only reasons I find this clinically useful is because if you see a HR of 150, you should highly suspect aflutter with 2:1 AV block
• Also, if you give adenosine to someone who has afib with wide QRS, indicating electrical signals may be conducting down an accessory pathway (WPW syndrome), giving adenosine will completely block their AV node and you might send the patient into vfib
• By the way, achieving rate control in aflutter is MUCH harder than in afib, not sure why though

What are the different terms for afib based on its duration?

• Paroxsymal = episodes lasting <7 days
• Persistent = episode lasting >7 days
• Long-standing persistent = episode lasting >1 year
• Permanent = basically you gave up trying to get them out of afib after trying a bunch of advanced therapies
• I want to include this because people tend to say "paroxsymal" all the time even if it's not necessarily paroxsymal, and everyone also puts "pAfib" in their notes technically ALL of these "pAfib" lol
• Otherwise this is more of a thing for medicine people to know since I don't think there's much utility in non-medicine folks to know

What is valvular vs non-valvular afib?

• Valvular = MECHANICAL VALVE REPLACEMENT or RHEUMATIC MITRAL STENOSIS
• Non-valvular = everything else
• Don't make the mistake of thinking someone with afib due to mitral regurgitation or something is "valvular" since that's not the actual definition. Also bioprosthetic valves aren't considered valvular, just mechanical ones (higher risk for clots).
• Why do we care?
• VALVULAR afib needs to be treated with warfarin. NON-VALVULAR afib can be treated with DOACs.
• Really the only reason we practice like this is because their hasn't been great trials looking at DOAC usage in the treatment of valvular afib, though there have been some small studies that showed non-inferiority to warfarin so hopefully in the future we can start just treating valvular afib the same as non-valvular afib.

What trials should you know?

• These are all pretty much LANDMARK trials and you definitely definitely need to know these
• AFFIRM - basically asked the question of whether rate control or rhythm control was better. It concluded that rate control was equivalent to rhythm control in outcomes, however there was a TREND towards higher mortality in the rhythm control group and increased adverse effects in that group. So that's why we typically start with rate control first.
• RACE II - asked whether strict rate control or lenient rate control had better outcomes (HR goal <80 vs <110) and they found that the lenient group (HR <110) had better outcomes. Therefore our goal rate for patients with afib is <110. Very important trial to know. When you have that ICU patient that is persistently in afib with RVR, just try to get them to <110. Technically they're still in RVR since any HR >100 is RVR by the way but you've hit the goal.
• EAST-AFNET4 - newer trial that came out in 2020 which showed rhythm control might be superior to rate control. I think one of the possible explanations people have for this result is that this trial used more dronedarone/flecainide/propafenone compared to amiodarone/sotalol in the AFFIRM trial. So - curious to see how this might change practice in the coming years, but for now we are still basically starting with rate control at this time.

What everyone should know (initial management)

So say you have a patient on the floor and nurse pages you, "doc, patient's HR is 150 and they feel a little lightheaded" and you get an EKG and see afib with RVR. What are your initial tools for management? In my mind, your main options to consider are going to be metoprolol, diltiazem, digoxin, esmolol, amiodarone, and cardioversion.

Cardioversion

• If patient is hemodynamically unstable, BP dropping and they are becoming obtunded, just cardiovert
• I think most people know this, but then in practice no one tells you what you have to order in order to get this done.
• If they are really truly unstable, just cardiovert. Ask the nurses to slap some pads on and do synchronized cardioversion, 200J would probably be indicated.
• If you're cardioverting a stable patient for another reason, probably reasonable to give the patient a little sedation so they don't feel the shock as much. Not sure what people's standard regimens are but 50mcg of fentanyl and like 6mg of etomidate might be reasonable to give, then shock them like 30 seconds later. 0.1mg/kg etomidate is recommended online. Some people also use midazolam but do remember that this can drop the BPs a bit. Etomidate + fentanyl has been shown to be superior to propofol + fentanyl in studies.

Loss of atrial kick

• I'm just adding this in here before we get to the medications, because sometimes patients are a little hypotensive compared to baseline but they aren't quite "unstable".
• For example, a patient who had BP 130/80 but went into RVR, now it's like 95/60 but they're still mentating fine and feeling okay, maybe a little lightheadedness or palpitations.
• One of the reasons their blood pressure dropped is because when your atrium starts to just quiver, you lose the "atrial kick" which helps get blood efficiently into your ventricle to be pumped out. So your cardiac output is going to be lower.
• This is a situation that you can try pharmacotherapy rather than cardioversion, however you may get pushback from nurses who won't be comfortable giving metoprolol with SBP in the 90s for example
• I'm just saying that this is a situation I would actually be fine giving metoprolol, because if you start to control their rates then they will actually have improved BP. If you want to be cautious you can always start with a lower dose first to see how well they tolerate it. But yeah I would try some metoprolol for this person.

Metoprolol

• Dose = 5mg IV q5min x 3 (stop once rates are controlled)
• Probably my #1 go to
• When the nurses push it you should see some kind of effect within a couple mins if it's working
• While PO metoprolol has pretty much no effect on BP, IV metoprolol CAN cause some reduction in BP
• Consider a 2.5mg dose first in really thin elderly patients
• Common mistake - if it works, make sure to give the patient an oral metoprolol tartrate dose immediately afterwards, or increase their prior dose if they were already on it. The half life of IV metop is like 10 minutes so if you don't give anything PO afterwards they are going to just go back into RVR. Give some PO metop with half life of 3-4 hours and you will help keep them rate controlled

Diltiazem

• Dose = 0.25mg/kg IV bolus (usually ~20mg), if doesn't work then 0.35mg/kg (~25mg), then escalate to gtt
• Probably the #1 go to in the ED
• Stronger AV blockade than metoprolol (probably why the ED likes to use it because it has a higher chance of controlling them)
• AVOID IN SYSTOLIC HEART FAILURE - BLACK BOX WARNING FOR INCREASED MORTALITY (likely due to its increased negative inotropy compared to metoprolol)
• If patient is started on a gtt they have to go to ICU at my institution

Digoxin

• Dose = 1mg load (0.5mg then 0.25mg q6h x2), then maintenance 0.125-0.25mg daily
• Usually only added if there is poor control with BB/CCB
• Good in hypotensive patients or patients with heart failure
• SLOW onset, will take >2 hours to kick in

Esmolol

• Dose = 500mcg/kg bolus then gtt
• Advantages are rapid titration, good in patients who you are uncertain how they will tolerate BB
• Disadvantage is that the gtt provides a lot of fluid which may eventual increase risk for volume overload

Amiodarone

• Dose = should be in an order set at your hospital, it's like a 150mg IV bolus followed by 1g IV load over next 24 hours
• It is a RHYTHM control agent, but also has some RATE control effects as well
• Good in patients who are hypotensive (a lot of times nurses page back with concern about patient's BP, but tbh I feel like whenever a patient is hypotensive in the ICU this is what we reach for)
• CAUTION, there is a risk of cardioversion so if the patient has not been on anticoagulation you want to be careful with trying amiodarone. If you cardiovert while they aren't anticoagulated you may cause clots to embolize and cause a stroke.

Some brief information on rhythm control agents

Amiodarone

• Amiodarone is still usually our go to, even though it's such an old drug
• Most effective, but most side effects
• Usually avoid in young patients (
• Remember it has CYP inhibition - meaning it will INCREASE the concentration of other drugs in your body
• Half-life is ONE MONTH (you will probably get pimped on this. Basically amiodarone gets into every cell in your body, once you stop it it's going to take a LONG time for it to come out)
• After starting, get all of the "function tests" - PFT, LFTs, TFTs and they will need to continue monitoring this as outpatient
• Typical maintenance dose is 400mg for ventricular arrhythmias, 200mg for atrial arrhythmias (like afib)

Dronedarone

• A "gentler" amiodarone with less side effects
• However, has known risk for FULMINANT hepatitis

Flecainide

Propafenone

• Class IC antiarrhythmics
• Can't be used in structural heart disease (significant valve regurgitation/stenosis, dilated chambers, scaMI, etc.)
• Pretty useful as a "pill-in-the-pocket" strategy, patients can take it as needed for when they feel symptoms

Dofetilide

Sotalol

• Only started this once in like really refractory afib
• They have to be admitted for a very specific initiation protocol with multiple repeat EKGs
• Main risk is prolonged QTc

Conclusion

I had a whole other section on new-onset atrial fibrillation but it honestly hasn't come up much in residency so you can watch a video I made about it on YouTube if you want. I think it's usually because you can't tell exactly when a patient went into afib. Basically <48 hours you can cardiovert without fear of embolizing clots, >48 hours you will need to do TEE + cardioversion to make sure no clots are present. For both you can also do 3 weeks of AC -> cardiovert -> 4 weeks AC vs indefinite based on their CHADSVASc as it has been shown that delayed cardioversion is not inferior to immediate cardioversion (RACE 7 ACWAS trial).
ANYWAYS. A quick summary for the main point of the post which is what to reach for in patients with afib with RVR.

• Metoprolol is pretty much my go to. Make sure you start PO metoprolol if it is effective
• Diltiazem is also great, it is stronger than metoprolol, but AVOID IN SYSTOLIC HEART FAILURE
• If hypotensive, consider adding digoxin or amiodarone. Digoxin will take a while to work, amiodarone has risk of cardioverting them so make sure they have been anticoagulated
• I rarely use it but esmolol gtt is an option if you aren't sure how well they will tolerate BB
• You may actually get some increase in BP after rate controlling
• If unstable, CARDIOVERT. 200J synchronized, can consider sedation in some situations but honestly if they're unstable just shock them
• Don't forget to check electrolytes and make sure they are replaced adequately

Hope this helped, let me know if you have any feedback/suggestions or other pro tips and cheers!

https://www.reddit.com/medizzy/comments/z82f8m/imagine_youre_the_healthcare_provider_fo
Quoting emmerliefje
This was a challenge! I'm a doctor in Europe, so choices may be influenced by local guidelines!
Infectious
Iodine - wound disinfection cannot be understated
Amoxicillin/clav - coverage for most common bacterial infections
Moxifloxacillin - back-up for infections that don't respond, and atypicals
Nitazoxanide - Broad-spectrum antiparasitic
Itraconazole - Broad-spectrum antifungal
Oseltamivir - Flu season without vaccines or adequate supportive care/control of chronic diseases won't be fun
Acute care/lifesavers
Insulin - a no brainer
Prednisone - for ashtma and COPD, as well as (suboptimal) control of autoimmune disease
Salbutamol - for asthma and COPD
Epinephrine im - allergic reactions, CPR, asthma
Nitroglycerine - angina/ACS
Furosemide - acute decompensated heart failure, end-stage kidney failure
Carbamazapine - for seizure control, bipolar disordedepression, alcohol withdrawal, and neuropathic pain
Painkillers
Ibuprofen - inflammatory control puts it above paracetamol in priority
Aspirin - secondary blood thinning properties make it useful
Morphine - of course
Supportive care
Ethinylestradiol/levonorgestrel - of course
Diazepam - for seizures and anxiety
Loperamide - diarrhea will surely be an important killer in low sanitation situation
Haloperidol - for nausea and supportive palliative care
Shortlist (20+)
Nadroparine - treatment and prevention of all thrombotic events (but impractical without imaging)
Meropenem - 2nd back-up broad-spectrum
Artemethelumefantrine - to treat malaria (still the world's #1 killer), if this colony is in a high risk zone
Digoxin - heart failure and serious arrhythmias (impractical without bloodtests for dosing)
Atenolol - tachycardic arythmias, heartfailure, anxiety, angina/ACS
Chronic diseases are screwed...

I first want to start off by saying THANK YOU SO, SO MUCH to everyone on here that shared their stories and graciously provided advice. It truly helped ease my anxiety and made me much more confident on this journey!
I SWORE that if I passed, I was going to make a post on here in hopes that it inspires at least one person who has the boards coming up or feels like giving up.
This is long, so apologies in advance
I graduated from an ADN program here in California in June 2021. Received my ATT beginning of August and booked it for September 2. I was studying pretty leniently (so not as seriously) leading up to August. I wanted to enjoy my summer because, you know, nursing school is a lot 🥴
1st attempt: STUDYING I solely utilized UWorld and Mark Klimek lectures on the first attempt. Much like others, I listened to those around me SWEAR by both of the materials. Everyone said, “Do a set or two of 75 randomized questions a day, read the rationales, listen to Mark K, and you should be solid!” My scores weren’t necessarily terrible (68% average) with ~400 questions left. I took one assessment with a “high chance of passing” a week prior, so I felt okay.
1st attempt: TEST DAY I think my ultimate demise was my ANXIETY. I work as a CNA at a magnet certified hospital and had a new grad job opportunity lined up at my home unit. I love my managers, coworkers, and felt pressured had I failed and couldn’t start the residency in time.
Well lo and behold, as the test went on, I just felt anxious as hell. Didn’t turn off the question counter and kept looking at it. Increasingly became frustrated when I didn’t see much SATA. Even if I did, I would dwell the MC after (thinking I got the previous SATA wrong). I spent WAY too much time analyzing the questions as “hard” or “easy”—psyching myself out THE WHOLE TIME. Got a few drag and drops (one of which was easy things like donning PPE).
Went it didn’t shut off at 75, I lost my momentum. Focused so much on, “Omg where are the SATA?” I didn’t take any breaks, just wanted to get it over with and get out. When it was finally at 145, I had a sinking feeling that I probably failed. Had a sliver of hope since one of my best friend passed in 145 the week prior. I did the PVT not too long after receiving the completion email and had the bad pop-up.
1st attempt: POST-TEST Waiting for the quick results was absolutely devastating. I think those two days were the darkest moments of my life. I didn’t leave my bed the next morning until 2:30 PM, finally eating something, and just cried, cried, cried. Paid for quick results and saw the big “FAIL”. It was no doubt the hardest pill to swallow.
Everyone around me were extremely supportive, from coworkers, boyfriend, friends, and family. I received my report and it was 1 above passing, 1 below, and rest were near passing, so I knew I wasn’t doing terrible.
I knew going for the next round, I 100% needed to pace myself, TAKE BREAKS, and just be in the moment rather than analyzing the questions I had or answered.
2nd attempt I was busy with work and mentally not prepared to take on the exam for a while—and I think that is okay. I knew the next term for the new grad residency was January, so I had time to take my next and LAST attempt. A test date shouldn’t dictate when you feel ready or feel comfortable to take it—just listen to yourself! I received my next ATT within 4 days, but still didn’t feel ready in October. I decided to enjoy all the fall/ Halloween festivities to help me mentally—and it did! ✨
2nd attempt: STUDYING I studied for no more than 4 hours, 3-4 days/week, in a month.
Last time, I crammed 8-10 hours/day within 2-3 weeks (I personally don’t recommend because it’s tiring, at least for me).
Here’s what I utilized and my final thoughts!
• UWorld: It really does contain solid questions/ rationales and great for content review. This time rather than randomizing questions, I went subject by subject, system by system. Instead of doing big blocks of 75, I did anywhere from 10-40 Q’s per set and this helped immensely. I wasn’t overwhelming myself and it was easy to review the rationales afterwards. I did all of Fundamentals, Adult Health, some Mental Health, some Maternity/Peds, and some of the prioritization. I had around ~900 questions left this time, so I did LESS.
• Mark Klimek: His lectures are pretty great in memorizing easier ways for certain subjects! For example, a SATA question asked what symptoms a person with opioid withdrawal would look like. In his lecture, anything that is not an “upper” drug (cocaine, caffeine, PCP/LSD, meth, and Adderall) is a “downer”. Withdrawal from a “downer” would make everything go “UP” = restless/agitation, irritability, etc. I recommend watching all of his lectures (maybe 1.25-1.5x speed haha). Prioritization/delegation is the most important of course!
• Simple Nursing: 1 month subscription, but free YouTube videos should be more than enough! Whatever I needed clarification on, I used Simple Nursing and Sarah from RegisteredNurseRN. Simple Nursing was great in making content that shows up on UWorld easy to remember. Pretty sure they base a lot of it from UWorld because some of the specific things they mention often was an SATA on UWorld.
• RegisteredNurseRN: My holy grail in nursing school and she did NOT disappoint when I need clarification this time either ❤️
I wanted to make sure I understood the high yield CONTENT, like endocrine, cardiac (such as HF), infection precautions, lab values, drug with narrow therapeutic range (lithium, digoxin, etc.), and the basics of maternity (amniocentesis, NST/CST, complications).
2nd Attempt: 1 DAY BEFORE EXAM I swore I wouldn’t do any studying. My bf and I went to Knott’s Berry Farm 🎡 since we have season passes and rode a few rides in the morning. Afterwards, we headed for lunch at a vegan place I’ve been eyeing. Ate the best California burrito 🌯 + Mexican style bulgogi fries ever 🌱 Then, we drove to Venice Beach and bought Dutch style bikes so we can cruise on the bike strand at the beach in front of our place. It was such a nice day! Watched a new episode of Dr. Brain (highly recommend), then went to sleep by 10:30 PM.
2nd attempt: TEST DAY My test was on 12/3 at 11 AM, so I had adequate amount of sleep when I woke up at 7:30 😇 ate breakfast, took a nice warm bath with epsom salt. I packed some snacks like water, grapes, and Lenny and Larry’s protein cookie, then headed to the test center. Blasted my favorite songs on the way and sang along. Got there 40 mins early, and just took deep breaths. Looked at the mirror and told myself I’m a badass bitch and will be walking out a nurse today 😂✨
Used the bathroom, then checked in.
My tips: - KNOW YOUR CONTENT. Know the literal BASICS of signs/symptoms and interventions. If you know this, the answers will be popping in front of you.

• Use the noise cancelling headphone provided
  
• Turn off the question counter (and time if you wanted)
  
• Before touching or beginning the exam, write on the white board things you want to remember!
  
• On the bottom, I wrote my name and “RN” after 🤍
  
• Take a break FOR SURE. I took one before my 2 hour mark since I promised that I would when I hit around 40-50. Took about 10-15 mins to eat, saved half my cookie for later, use the bathroom, and gave myself another short pep talk in the mirror LOL.
  
• Re-read the questions and go with your GUT feeling. If you aren’t 100% convinced with a potential SATA choice, DO NOT CHOOSE IT
  
• Finish a question and MOVE ON (I’m begging you).
  
• Most importantly, DON’T FOCUS ON WHETHER YOU ARE GETTING SATA BECAUSE IT MEANS NOTHING!!!
  

When it shutoff and I saw it was 76, I froze for a hot second. Like what? Me? The test itself was pretty straight forward. Yes the questions aren’t as lengthy as UWorld, but STRAIGHTFORWARD if anything. I got a good mix of questions and nothing seemed out of left field: 1 ECG, no drag and drops, no math, less than 20 SATA
I apologize for this lengthy post, but this was my raw take on my journey the last several months! Please don’t give up. We got this far, you WILL pass 🤍
I will be starting my new grad residency end of January 🥰

POTS is characterised by orthostatic intolerance. This means that patients feel significantly worse when they adopt an upright posture compared to when they are lying down. To try and find effective treatments, it is vital that we try and understand the physiology of what happens in the body when normal healthy people stand up.
When we stand up, blood in our vessels tends to get sucked down into our legs because of the effect of gravity. This means that there is less blood getting to our brain and ordinarily we would all pass out and fall because of a shortage of blood to the brain. This does not happen because two reflex mechanisms come into action which serve to maintain the blood flow to our brains. The first is regulated by stretch receptors in our blood vessels in the legs which try and constrict the best they can to prevent blood from pooling in the legs. Secondly the heart rate increases to try and maintain adequate blood flow to the brain. In some patients, the leg vessels don’t constrict as well and therefore they are not able to contribute to increasing the blood flow to the brain and therefore the body has to compensate for this by increasing the heart rate even further. As the heart rate goes up excessively the heart doesn’t have as much time to fill with blood and therefore pumps out less blood than it should which exacerbates the situation.
If we can in some way reduce the stretching of blood vessels especially in the lower limbs when we adopt an upright posture, it means that there is relatively more blood going round and less blood pooling which can improve symptoms.
Midodrine works by increasing the tone of our peripheral blood vessels and therefore reduces the likelihood of pooling of blood. It doesn’t really directly affect the heart as such but if there is more blood getting to the heart then that means that every heart beat is more effective and that can have the effect of improving orthostatic tolerance. Interestingly though this can also have an unwanted effect on the bladder. Because of the effect of the agent on tone, the bladder does not stretch as much and therefore bladder emptying is delayed.
So is there any evidence it works? Well yes but the studies are very small and therefore it is not a foregone conclusion by any means.
There was a paper in the Clinical Autonomic Research journal in 2000 (lead author: V M Gordon et al) where they found that if you gave 21 patients with POTS Midodrine before tilting them the heart rate did not go up as much.
There was another study of 53 children with POTS in the Circulation Japan journal in 2011 (Chen et al) and they found that compared to conventional therapy and even conventional therapy combined with beta blockers, the combination of conventional therapy and midodrine seemed to work much better and was associated with better symptoms control and higher rates of cure. There was another study published in Clinical Autonomic Research journal (Hoeldtke et al) who found that midodrine reduced the standing heart rate from 114/min to about 93/min.
Finally there was another interesting study which was published in the Clinical Science journal in 2014 (Amanda ross et al) which suggested that it was patients with neuropathic POTS that seemed to benefit more from midodrine than those with hyperadrenergic POTS.
We would normally start the medications at 2.5mg tablets to be taken 3 times daily. The doses can be increased after weekly intervals but most patients if they are going to gain benefit will do so at a total daily dose of less than 30 mg daily.
The times that Midodrine should be taken are important. We generally recommend that midodrine is not taken at least 4 hours before bed-time. This is because there is a risk of the blood pressure going excessively high when the patient lies down. This is known as supine hypertension. The manufacturers say that for a 10mg dose, the blood pressure can increase by 15-30 mmHg. To avoid this, dosing should avoid intake of medications for at least 4 hours before lying down. Typical times for dosing are 6.00 pm, 12.00 pm and 5.00pm.
Midodrine, like any other medication, can have side-effects but again it is important to stress that these side-effects may not affect everyone and if they happen then discontinuing the medications will result in an improvement of symptoms of side effects. I will try and list side effects that patients should look out for:
1) Cardiovascular:
Supine hypertension (most prevalent when you first start the medications or when the dose is increased). This may also be accompanied with symptoms such as chest pain, headaches, blurred vision and sometimes even palpitations. It is worth noting that many of these symptoms may also just be due to the underlying condition. It is worth saying that in my own practice if the blood pressure exceeds 180/100 whether that be lying down or standing up then I tend to discontinue it
2) Urinary retention
3) Nervous system related side effects such as; altered sensations, restlessness, excitability and irritability
4) Rash, itchy skin especially over the scalp and flushing
5) Gut related side effects such as nausea, vomiting and indigestion.
Whenever we take any medications it is important to ensure that they don’t interfere in a harmful way with other medications. Here are some medications which can interact in a harmful way with Midodrine.
1) Medications that can increase the blood pressure further. These include tricyclic antidepressants, Monoamine oxidase inhibitors, thyroid hormones, corticosteroids and sympathomimetic drugs. There is a medication that we often use in POTS because it helps fluid retention called Fludrocortisone. Although we can use both Midodrine and Fludrocortisone, they both have the effect of increasing blood pressure and especially pressure in the eyes and therefore it is important to monitor very carefully.
2) Alpha blockers can antagonise the blood pressure raising effects of the midodrine and therefore make it less effective
3) Beta blockers and Digoxin can cause the heart rate to slow down excessively when combined with Midodrine.
There are some comorbidities that the patient may be suffering from in which I would not give Midodrine at all because the risk of harm may be greater than the benefits. These comorbidities include:
1) High blood pressure especially if it is poorly controlled
2) Previous stroke
3) Organic heart disease because it can increase pressure on the heart
4) Pheochromocytoma which is a tumor that secretes hormones that can increase the blood pressure anyway
5) Thyrotoxicosis/ hyperthyroidism
6) Acute kidney injury
7) Severe kidney disease/kidney failure
8) Urinary retention and prostate disorder
9) Glaucoma
10) Proliferative retinopathy
I think it is important that before patients start the medication that they have some basic blood tests for kidney and liver function and they have these tests repeated every year. It is also patients who take midodrine have a 24 hour blood pressure monitor to ensure that their blood pressure is not being pushed too high by the medications. This should be done once a year or if the doses are being pushed up.
Please note that none of the lists in this blog are exhaustive and it is therefore vital that patients always seek counsel from their own doctors and pharmacists to get a more informed opinion.
https://drsanjayguptacardiologist.com/blog/midodrine-for-pots-dysautonomia/

I know I said I was going to do a writeup about YA Twitter drama next, but then I remembered that this is a thing that happened and I just had to post it here. I swear to god, I am not making any of this up.
This is one of those incidents that’s difficult to summarize because I honestly don’t even know where to begin. There’s so much to talk about that it’s almost overwhelming—sockpuppeting, medical fraud, false identities, and god-knows-what else all played a part in making this drama one of the biggest scandals in Tumblr history (or, at least, the biggest scandal that doesn’t involve illegally mailing body parts to people via the United States Postal Service. Don’t even ask.) Now, you may be thinking that the title probably makes more sense in context, but I can assure you that it absolutely does not. It’s just as insane as it sounds at first glance. To make it abundantly clear how nuts this whole debacle was, I should probably start by detailing Hamilton and its obsessive fandom.
Hamilton is a Broadway musical that came out a few years ago, and unless you live under a rock, you’ve probably heard someone at least mention it in passing. It’s one of the most successful shows in recent history, and it’s beloved by tumblr.com for a variety of reasons. The main, though not sole, reason is that it’s actually really good (and I say this as someone who isn’t a crazy theatre kid.) It focuses on the life of Alexander Hamilton from his arrival in the Thirteen Colonies to his death during a duel with Aaron Burr, and it’s all done surprisingly well for a musical that attempts to tell a story about the American Revolutionary War via rap battles. It’s one of the few shows in the world that can get away with including stage directions like “ELIZA BEATBOXES MATERNALLY” and still be taken completely seriously by both fans and critics.
Reason number two why Tumblr loves Hamilton is the same reason Tumblr loves the MCU and Superwholock and all the other franchises it obsesses over. There are lots of male characters and thus lots of potential slash ships (ships meaning relationships.) If you’re wondering why on Earth anyone would want to ship the Founding Fathers with one another… well, join the club. I have no idea. But some fans really liked the idea of Alexander Hamilton and [insert literally any other character] hooking up, so Hamilton the musical spawned an abundance of fan fiction and fan art featuring the signatories of the US Constitution. Keep in mind, though, that by Tumblr standards, this is not that weird. A little unusual, sure, and certainly less common than traditional fictional character shipping, but nobody’s really going to start a riot because people want John Laurens and Alexander Hamilton to have sex. This is Tumblr we’re talking about. Remember how I mentioned people mailing human body parts to one another? In comparison to those incidents, shipping the Founding Fathers is not that strange, so the rabid Hamilton fans were mostly ignored by the rest of the site. And this allowed their community to grow quite large. Nobody wanted to be the one to poke at the hornet’s nest that was the rapidly developing hive of Hamilton-obsessed fans, so they all just kind of let It be. And, in the complete absence of outside scrutiny, that community grew and grew and grew. By 2015, the amount of people who dedicated countless hours to writing Hamilton fic was far greater than anyone could have imagined.
One of the many Hamilton fics floating around on Tumblr was a piece entitled “To Scale the Blue Sky,” which was an alternate universe fanfic set in a high school. Again, taking the Founding Fathers and putting them in an American high school in the 1980s a la Clone High may sound bizarre, but that’s such a common fan fiction trope that people didn’t even question it. There are probably more high school AUs on Tumblr than there are stars in the sky at this point. The unique thing about “To Scale the Blue Sky,” though, was that it addressed an important issue affecting the LGBT community in the ‘80s: HIV and AIDS. This is a story in which Alexander Hamilton, the guy who appears on the $10 bill, gets HIV while in high school. And, ordinarily, this type of writing would have rung at least a few alarm bells; after all, fan fiction is generally not the best way to address the AIDS epidemic and the deaths resulting from its mismanagement. But “To Scale The Blue Sky” was cut some slack, partially because of who its authors were.
The main author of “To Scale The Blue Sky” was Israa, a nonbinary Chinese-Pakistani victim of sex trafficking. The other, mostly uncredited author was Israa’s wife Raj, a Catholic-Somali lesbian of color. Both were HIV+, and they ran a popular blog about how the disease impacted their lives, which was entitled hivliving. They used hivliving as a platform for activism, but also a way to share their personal experiences with various forms of trauma and discuss how being HIV+ has impacted them. They also occasionally used it to promote their fanfiction.
Unfortunately, just as hivliving was reaching the height of its popularity, Raj and/or Israa suffered some terrible, debilitating medical issue that left them in need of expensive medical treatment right away. A cash.me link was posted, and thousands of followers who credited the couple for educating them about HIV and helping them through their own diagnoses jumped at the chance to donate. And everything went exactly as planned, up until fellow Tumblr user digoxin-purpurpea noticed something was up with the cash.me.
Digoxin-purpurpea was another Hamilton fan, and she also went by the names digitalis, candiru, and cardiotoxin (this is less suspicious than it sounds; most Tumblr fanfic writers use different usernames for different fan fiction sites.) Under the blog name Cardiotoxin, digoxin-purpurpea messaged Israa and Raj shortly after the cash.me was posted, saying that she had a difficult time believing they were truly living in India, because the cash.me indicated they were within the United States. One thing led to another, and long story short, the mod of hivliving wound up making a huge confession: she didn’t live in India, and she didn’t have HIV. Israa and Raj don’t exist. The real person behind the blog, and behind “To Scale The Blue Sky,” was an American college student, Alix. That may not be her real name, but I’ll refer to her as such for the purpose of this post.
This, predictably, caused an uproar. Alix later tried to backtrack by saying that Israa and Raj were digital personas based on real people, but it later came out that not even that was true. Their lives and backstories were entirely made up just so Alix had an excuse to write HIV+ High School AU fan fiction about Alexander Hamilton without being judged too harshly for it. By pretending to be a woman with HIV+, she could deflect any questions about whether writing this type of thing is really okay by claiming that it was a coping mechanism to deal with her own disease. She also made up the additional sympathetic pieces of Israa and Raj’s tragic backstories because they made people more likely to feel bad for the couple and support them financially. Finally, their Somalian, Chinese, and Pakistani heritage allowed Alix, a white girl, to be put on lists of POC writers that she never would have been able to get onto had she not lied about her identity. Basically, Alix made up two entire people and started a HIV support blog exclusively to promote “To Scale the Blue Sky” and works like it.
Naturally, when it came out to everyone that Alix was a liar and Israa and Raj weren’t real people, a lot of fans were very upset, especially those who had donated to their bullshit cash.me. They demanded their money back, and Alix agreed to refund them, but that never actually happened. Meanwhile, other people started digging up dirt on Digoxin-purpurpea, as some people were concerned that she’d also been making things up in order to get rid of hivliving and boost her own popularity. What they found was, arguably, even stranger than a plot to reduce her competition by scrubbing hivliving from the internet—Digoxin-purpurpea was a relatively well-known author of real-person supernatural fanfiction. No, not Supernatural TV show fanfiction—I mean stories about ghosts, mermaids, and other mythical creatures, having sex with each other and real people.
At around the time Alix started asking for donations while posing as Israa and Raj, Digoxin-purpurpea was being criticized for various bizarre works she’d written, among them things like ghost!Hamilton erotica and at least one work in which Lin-Manuel Miranda, who plays Hamilton, is a cannibalistic mermaid. People quickly realized that Digoxin-purpurpea wasn’t dragging Alix for purely selfless reasons. Alix and her friends had made fun of Digoxin-purpurpea for her weird and “problematic” stories, so Digoxin-purpurpea exacted revenge by exposing Alix.
After this revelation, both Digoxin-purpurpea and Alix deleted the majority of their work, which was unsurprising, considering how much the rest of Tumblr was making fun of them. Hivliving shut down, which was to be expected, seeing as the people who ran the blog were actually one person who didn’t actually have HIV. And, finally, Tumblr learned a valuable lesson about donating to gofundmes and cash.mes without doing adequate research first. People continue to ask for money for various causes online, but Tumblr users are a lot more skeptical now, because you never know when that baby with cancer or that woman with cerebral palsy are actually just crazy Hamilton fans using medical conditions as an excuse to write stories about the Founding Fathers having unprotected sex in a high school.

overview Enlarged breast in men (gynecomastia) Enlarged breast in men (gynecomastia) Gynecomastia (mec-nuh-koh-MAS-tee-uh) is a swelling of the breast tissue in boys or men, caused by an imbalance of hormones estrogen and testosterone. Gynecomastia can affect one or both breasts, sometimes unevenly. Newborns, teenage boys, and older men can develop gynecomastia as a result of normal changes in hormone levels, although there are other causes as well.
In general, gynecomastia is not a serious problem, but it can be difficult to cope with the disease. Men and boys with gynecomastia sometimes have chest pain and may feel embarrassed.
Gynecomastia can disappear on its own. If this stops, medications or surgeries may help.
symptoms Signs and symptoms of gynecomastia include:
Breathed breast tissue Tenderness of the chest When should I see a doctor? Consult your doctor if you:
swelling pain tenderness Nipple discharge in one or both breasts
the causes Gynecomastia is triggered by a decrease in testosterone hormone compared to estrogen. The cause of this decrease can be seen in your testosterone or in a condition that increases your estrogen levels. Various things can disrupt the hormonal balance, including the following.
Natural hormonal changes Hormones, testosterone and estrogen control the development and maintenance of sexual characteristics in men and women. Testosterone controls male characteristics such as muscle mass and body hair. Estrogen controls the characteristics of the woman, including breast growth.
Most people think that estrogen is an exclusively female hormone, but also produces it. However, estrogen levels in men are too high because testosterone levels can cause gynecomastia.
Gynecomastia in infants. More than half of all male children are born with estrogen breasts to their mothers. In general, swollen breast tissue disappears within two to three weeks of birth. Gynecomastia during puberty. Gynecomastia due to hormonal changes during puberty is relatively common. In most cases, swollen breast tissue is treated within six months to two years. Gynecomastia in men. The prevalence of gynecomastia is again highest between 50 and 69 years. At least one in four men in this age group is affected. pharmaceuticals A number of drugs can cause gynecomastia. These include:
Anti-androgens for the treatment of prostate enlargement, prostate cancer and certain other diseases. Examples include flutamide, finasteride (Proscar, Propecia) and spironolactone (aldactone). Anabolic and androgenic steroids. AIDS medications. Gynecomastia can develop in HIV-positive men receiving highly active treatment called antiretroviral therapy (HAART). Efavirenz (Sustiva) is more commonly associated with gynecomastia than other anti-HIV drugs. Anti-anxiety medications like Diazepam (Valium). Tricyclic antidepressants. Antibiotics. Anti-ulcer drugs such as cimetidine (Tagamet HB). Cancer treatment (chemotherapy). Drugs for the heart such as digoxin (Lanoxin) and calcium channel blockers. Drugs of gastric motility such as metoclopramide (Reglan).
Street drugs and alcohol Substances that can cause gynecomastia are:
alcohol amphetamines marijuana heroin methadone health Various diseases can cause gynecomastia by affecting the normal hormonal balance. These include:
Hypogonadism. All conditions that interfere with normal testosterone production, such as Klinefelter syndrome or pituitary insufficiency, may be associated with gynecomastia. Aging. Hormonal changes that occur during normal aging can cause gynecomastia, especially in overweight men. You die. Some tumors, such as testicular tumors, adrenal glands, or pituitary glands, can produce hormones that alter the male-female hormone balance. Hyperthyroidism. In this condition, the thyroid gland produces too much thyroxine hormone. Kidney failure. Gynecomastia due to hormonal changes. Hepatic insufficiency and cirrhosis of the liver. Hormonal fluctuations are associated with drugs for cirrhosis associated with gynecomastia. Malnutrition and hunger If your body is not adequately nourished, the testosterone level will decrease, but the estrogen level will remain constant, which will cause a hormonal imbalance. Gynecomastia can also occur during a normal diet. Herbal products Vegetable oils, such as tea tree or lavender, used in shampoos, soaps or lotions have been associated with gynecomastia. This is probably due to their low estrogenic activity.
risk factors The risk factors for gynecomastia are:
adolescence Older Use of anabolic steroids or androgens to enhance athletic performance Certain health problems, including liver and kidney diseases, thyroid diseases, hormonally active tumors and Klinefelter syndrome complications Gynecomastia has few physical complications, but can cause psychological or emotional problems related to appearance.
prevention You can control some things to reduce the risk of gynecomastia:
Do not use illegal drugs. Examples include steroids and androgens, amphetamines, heroin and marijuana. Avoid alcohol. Do not drink alcohol or in moderation. Check your medications. Gynecomastia, where are you going?

As I mentioned before, there are only a few mirrors in the game, and mirrors obviously play an important thematic role in the game. The game itself has a mirror structure as it starts out with you acquiring followers – Huey, Quiet, etc. – and watching them leave as the game draws to a close. The game builds up to getting your revenge on Skull Face and then winds down as you deal with the effects of enacting that revenge. It opens with the hospital scene and ends with the hospital scene. It also opens within a small room zooming in on a mirror and ends in that same room with the destruction of that mirror.
This isn’t necessarily important to what I’m hoping to reveal next, but if Ishmael is an imaginary figment that mirrors Venom in appearance and actions, Skull Face seems to be a real-life mirror of Venom in appearance and intentions.
Like Ishmael, Skull Face seems to have several physical characteristics that mirror Venom. For example, his face has scarring in the same location as Venom’s shrapnel. Many scenes in the game put Skull Face and Venom in mirrored positions, most notably during the honey bee mission and the super anticlimactic car ride.
On another level, they mirror each other in their intentions. Namely, they both seek revenge against Zero, and they both promote – whether intentionally or not – nuclear proliferation.
But what if, just like Ishmael, Skull Face is just a figment? We know for certain that he appears after his death to Venom. Of course, Venom is notorious for his hallucinations. But what if they aren’t hallucinations? What if they’re figments of a broken mind?
The problem with theorizing that everything in TPP is just one big hallucination (or a VR simulation, which is really just an alternate version of the same idea) is that Skull Face appears in Ground Zeroes. And Ground Zeroes is undoubtedly real, right?
Well, maybe not. Here, again, timestamps cause some serious trouble.
Here are the time stamps from the Ground Zeroes side ops:

• Eliminate the Renegade Threat: December 3, 1974 13:18
• Intel Operative Rescue: December 7, 1974 05:31
• Classified Intel Acquisition: December 21, 1974 18:06
• Destroy the Anti-Air Emplacements: January 9, 1975 07:10

If you remember back to the “Destroy the Anti-Air Emplacements” mission, there’s a carpet bombing of the entire island at the end. And after that bombing, Miller explains the results:
“We still don’t know who sent those aircraft to strike the base. The one thing we can say is the origin was Western. Any evidence of what was going on there was reduced to ashes – along with the enemy combatants.”
So, the place is completely and utterly destroyed, “reduced to ashes.” But then where does the Ground Zeroes mission fit in there?

• Ground Zeroes Time Stamp: March 16, 1975 00:00

Ground Zeroes takes place on the island AFTER the facilities and combatants there no longer exist. Or, almost even more unbelievably, they reconstructed the entire base in pristine condition – from ashes – in just a little over 2 months. I haven’t gone back to play Ground Zeroes lately, but I don’t remember the place feeling like everything was brand new. Sure, the outer grounds were pretty ad-hoc with wooden structures, canvas tents, and chain-link fence – exactly the kind of stuff you could throw together pretty quickly. But what about the main complex?
Some quick Googling reveals an interesting study regarding how long it takes to build an apartment complex – not a military grade installation. The average is 11.7 months after getting all the paperwork taken care of. That’s in the modern era. 40+ years ago, it was likely slower. But let’s assume that it wasn’t slower. And let’s assume you’ve got a team with nearly unlimited resources and manpower at your disposal. Would that drop the construction time down by nearly 83%? I doubt it. To be honest, I doubt the concrete would even be cured enough to adequately support the structures at Camp Omega within those 2 months.
On top of this logistical problem, it would also have to be the case that whoever bombed it in the first place wasn’t watching or didn’t’ care that they had rebuilt the black site in the exact same location.
Needless to say, this timing creates a big problem – unless Ground Zeroes is just as much a part of the hallucination as the hospital scenes and the events of TPP. And why not? Why not have everything that was originally supposed to be one game be an elaborate, confused construct within someone’s mind? It would certainly give us an excellent reason to return to Camp Omega to find out what instigated all of it, to find out exactly what Camp Omega was Ground Zero for. And once we knew the actual truth, who’s to say that everything wouldn’t fall into place much like we have all seemingly come to accept the truth that there are 2 Big Bosses even though we all railed against it when we first found out?
For example, what if Big Boss went into a coma for some other reason than a chopper crash? After all, we never actually see the chopper crash – and what we do see to suggest a chopper crash is conflicted and inconsistent. In fact, Kaz, Big Boss, and Venom are supposedly in the hospital on March 16, 1975 at 1:31 PM according to Mission 46. That’s 13 hours after the beginning of the Ground Zeroes mission. Someone else can do the math to figure out how Big Boss rescues Chico and Paz, gets from Camp Omega back to Mother base, gets in a firefight, gets away, crashes into another chopper, gets rescued, makes it to a hospital, and gets resuscitated in 13.5 hours. I haven’t tried to do a point-by-point analysis of the timing of those events yet, but it feels like a stretch.
So, what if there’s another reason for Big Boss’ coma – a reason that we’d have to return to Camp Omega to discover? And what if, instead of being kept at the hospital at Cyprus, he was actually taken back to Mother Base (which was never actually destroyed)? And what if, during that coma, he overheard people like Miller and Ocelot discussing the events that were happening? And what if TPP is just his mind’s interpretation of the snippets of things he overhears?
Like, perhaps he hears about digoxin and imagines the honey bee mission, for example.
But maybe you haven’t bought into this “TPP as one big delusion” theory yet. What other evidence suggests that the events of TPP are just a figment?
Well, someone once brought up the insanely poignant fact that the ACC is the place where you return to between every mission. It’s a place that is full of representations of your comrades and plans – even from Peace Walker. It’s the hub of the game – even moreso than Mother Base itself. But ACC doesn’t just stand for “Aerial Command Center.” It stands for “Anterior Cingulate Cortex (ACC)”, and it is “related to abnormal sensory sensations such as phantom pain.” You can read the article yourself, but the anterior cingulate cortex is also responsible for a wide variety of cognitive functions. Of note, it has been posited as “a likely candidate for free will in humans” (did you choose to rescue or execute Quiet? What did you do with that lost puppy you found?). Also, “there is evidence that damage to the ACC is present in patients with schizophrenia” (a primary symptom of which is “difficulty distinguishing between what is real and what is imaginary”) and that “the area may have a role in obsessive-compulsive disorder” (how many times did we replay “Cloaked in Silence"? How much grinding have we done?). Of course, the foundation of the paper is explained in its title: “Basic Mechanisms for Phantom Pain” (the connection here should be obvious).
As much as people around here hate to look back to the trailers for clues about the final game, it’s nonetheless interesting that the Red Band Trailer refers labels the Man on Fire as “Those who ‘Don’t Exist’”. Everyone else’s introductions seem pretty literal. Code Talker is “A Wise Man denied his Homeland” and Quiet is “A Sniper deprived of her Words.”
For me, the return of Volgin as the Man on Fire (remind you of the Fury?), the statue of the Boss, a photosynthetic sniper (remind you of the End?), adversaries that can turn invisible (remind you of the Fear?), foes that can cover themselves in armor (remind you of the Pain?), and a host of other references and characters that all point back to Naked Snake’s adventures in MGS3 and Peace Walker are all just too uncanny. I mean, the bosses in TPP are all called “The Skulls” – almost as if they represent dead people or people you’ve already defeated.
Added to this, Volgin’s horse has an MSF logo on its shrapnel saddle, but why? Why not a scrap of the Shagohod or something with CCCP on it? Why even bother with the horse if he’s a magical being fueled by revenge? Volgin had nothing to do with MSF, and the Boss’ horse dies in South America and is executed by Big Boss (does the horse have such a lust for revenge?). Furthermore, the horse doesn’t appear with Volgin until after you see the statue of the Boss at the hospital on fire.
What does this all suggest? It suggests that many of the characters and villains we encounter in TPP have a symbolic meaning that points back to Big Boss’ experience. While Venom has “experienced all [Big Boss’] missions on record, and shares all [Big Boss’] knowledge and experience,” the much simpler explanation, given everything I’ve explained up until now, is that TPP is all just Big Boss’ own fragmented mind dealing with his past – possibly during a coma.

Link to Part IV: TL;DR and Sealing the Deal

Link to Intro and Part I: The General Insanity of the Hospital Scene(s)

Link to Part II: An Overarching Explanation of Hospital Scene Inconsistencies.