Mursenary

Hyperkalaemia ECG changes in 15 seconds. 

High levels of potassium destabilise the cardiac membrane causing arrhythmia’s which lead to cardiac arrest. This can be a real life-saving opportunity if you can catch and treat it!

Today I discovered this writer’s tactic to face her fear of rejection and failure, and it’s honestly very inspiring?! This kinda rewired my brain and I feel everyone should read and think about it.

but anyway, this lady came thru my line buying a book and the review on the front said: “few books are well written, fewer still are important, and this book manages to be both”

as i handed her the bag i was trying to say “thanks, youre all set” and instead my brain mashed up the review and i said “thanks, youre important”

there was this short pause in which i tried to figure out what the fuck id just said. she blinked and then said “oh thank you! youre important too!”

Which, actually, not such a bad thing; I’m a big guy and can come across as imposing pretty easily. The position calls can help defuse that, and also help avoid collisions.

http://gen.lib.rus.ec

http://textbooknova.com

http://en.bookfi.org/

http://www.gutenberg.org

http://ebookee.org

http://www.manybooks.net

http://www.giuciao.com

http://www.feedurbrain.com

http://oll.libertyfund.org/index.php?option=com_content&task=view&id=380

http://www.alleng.ru/ 

http://www.eknigu.com/ 

http://ishare.iask.sina.com.cn/

http://2020ok.com/

http://www.freebookspot.es/Default.aspx

http://www.freeetextbooks.com/

http://onebigtorrent.org/

http://www.downeu.me/ebook/

http://forums.mvgroup.org

http://theaudiobookbay.com/

There is quite a lot to be said about the medications we use for patients with arrhythmias. It’s easy to get lost as to what drugs do what and how, but thankfully there was a kind enough person by the name of Vaughan Williams, who actually broke them down into separate classes. Each class effects separate parts of the cardiac cycle, ultimately changing the electrical current of the heart.

Cardiac Action Potential

Before looking at the medications, we have to understand the cardiac cycle and how it actually works.

Source: x

The above chart presents the four phases of an action potential in a ventricular myocardial cell and how the electrolytes are used to cause the depolarization and repolarization of myocardial cells.

Phase 0  begins with a slight influx of sodium until it passes the potential threshold. Once past the threshold, more sodium channels will open and flood the cell, causing it the depolarize.

Phase 1 is an efflux of potassium from the cell, causing the cell to reach 0mV.

Phase 2 happens at this point. This is when calcium influx happens, prolonging the repolarization period. This period also goes by the name of an absolute refractory period for the cell, since it cannot depolarize during this time.

Phase 3 Calcium channels close again and potassium continues to efflux from the myocardial cell until the internal cell voltage returns to -90mV. Majority of potassium channels then close and the heart enters phase 4, which potassium is allowed to continue to leak into from the cell.

This process happens anywhere from 60 to 100 times per MINUTE!

Vaughan Williams Classifications

The major purpose of the medications in this class effect they way the cardiac action potential works in the cells of the heart. The drugs usually help to slow down specific phase to the heart and allow the heart to fix itself a bit.

Class I - Sodium Channel Blockers

These medications are designed to disrupt phase 0, causing a prolongation of it. There are 3 subcategories (a,b,c) that are broken down into moderate, weak, and strong.

This article won’t go into great depths, but the major goal of the class is to prolong the QRS complex and prolong or shorten QTi.

Medications include:

Lidocaine

Verapamil

Procainamide

Propafenone

Class II - Beta Blockers (-olol or -alol)

Quite commonly used out of hospital for patients with hypertension, beta blockers are actually a common antidysrhythmic. The basic pharmacology is: by blocking the beta-1 receptor sites, it prevents stimulation of the cardiac muscle to beat faster. The increase of sympathetic tone will decrease the rate the heart will beat.

Medications include:

Propranolol

Metoprolol

Carvedilol

Class III - Potassium Channel Blockers

Similar to the Class Ia medications, potassium channel blockers are used to prolong APD, which can cause a prolongation of ERP. This class of medication is commonly known to treat different ventricular dysrhythmias (Vtach or Vfib). The most common medication for this class is Amiodarone and deserves a post of its own.

It’s most common use is during CPR, when the patient is in pulses Vtach or Vfib rhythm and is then followed by a drip with ROSC is achieved. An important note to make about Amiodarone is it can take 16 weeks to leave the system.

Medications include:

Amiodarone

Sotalol 

Ibutilide

Class IV - Calcium Channel Blockers

Commonly uses for Afib with RVR and PSVT, a calcium channel blocker will prolong phase 2 of the action potion in the cell. The goal is to slow the conduction through the atrioventricular (AV) node, slowing the ventricular tachycardia that is occurring. By prolonging the ERP in the AV node, the heart is able to regulate the rate better.

Calcium channel blockers are commonly prescribed by physicians to assist in the care of such arrhythmias. One side effect of these drugs is it may drop the patient’s BP, so ensure you have an SBP >100 or a MAP >65, prior to administering the medication

Class V - Others

This is the mix bag class. These drugs do not truly fit in any category but are still highly important to mention anyways. Two of these medications are Adenosine and Digoxin.

Adenosine prevents the re-entry of a signal in a sinus rhythm, preventing SVT. A warning though is for patients that have WPW syndrome may cause an increase in heart rate instead, so make sure you’re reading the rhythm correctly.

Digoxin effects vagal tone and is seen less as an emergency drug and more as a maintenance drug for chronic heart issues. A major issue with this drug is it holds a very narrow therapeutic index. Toxicity is quite possible if given too much.

Summary

Each class works in its own way on the action potential in the cardiac conduction system. How they affect the heart greatly determines when and how the medication should be used in different medical scenarios. The point of this article is to help a bit with the pharmacodynamics involved with the medications and to hint at the situations a person in the medical field would use them?

Remember to check out my facebook page. Feel free to send suggestions for possible article ideas, it might pop up some time. Always remember that medicine is an art, just as much as a science.

So I found this and sent it to her. Because this is what they want to know: how badly is this pain affecting you? Not on a scale of “nothing” to “how I’d imagine it’d feel if bears were eating my still-living guts while I was on fire”. 

10 - I am in bed and I can’t move due to my pain. I need someone to take me to the emergency room because of my pain.

9 - My pain is all that I can think about. I can barely move or talk because of my pain.

8 - My pain is so severe that it is difficult to think of anything else. Talking and listening are difficult.

7 - I am in pain all the time. It keeps me from doing most activities.

6 - I think about my pain all of the time. I give up many activities because of my pain.

5 - I think about my pain most of the time. I cannot do some of the activities I need to do each day because of the pain.

4 - I am constantly aware of my pain but can continue most activities.

3 - My pain bothers me but I can ignore it most of the time.

2 - I have a low level of pain. I am aware of my pain only when I pay attention to it.

1 - My pain is hardly noticeable.

For example, if someone asked me how much pain I’m in at any given time, I’d say hardly any, and yet I’m apparently at a chronic 2.5, and it only goes up from there depending on the day. 

Coagulation cascade made simple.

Someone shared this with me on my surgery clerkship and I wanted to pass it forward. 

1) Everything centers around the perfect 10

2) 7 is a lucky number so I keep it to myself

3) 8 and 5 are cofactors

4) 3, 4, 6 do not exist

5) When you draw it out, it looks like a gun, and your trigger finger (TF) would go by the 7. so TF (tissue factor) goes by 7

6) You use guns and trigger fingers in war, so that’s the part effected by warfarin. The other one is heparin

7) The shorter path has the test with fewer letters (PT). The longer path has the test with more letters (PTT).

The last “rule” was told to me by someone else, but it helps me every time, so I’ll include it here:

After 4 years of volunteering in the ICU of the local hospital for respiratory diseases I’ve finally started to really understand a lot of the diagnostic procedures and the meaning of their results.

So I’ve decided to share with you some of the materials I use to study the ICU Stuff:

ABG interpretation

https://abg.ninja/abg - The site gives you a results from ABG analysis and you have to make a reading of them, then it show you if you are correct or wrong and gives you a full description why. On this site there some other very nice medical quzzes as well - Glasgow coma scale, Cranial Nerves, Basic ECG etc.

Lung function tests

http://www.ums.ac.uk/umj080/080(2)084.pdf

http://www.ics.gencat.cat/3clics/guies/184/img/–americanfamilyphysician.pdf In these PDFs the basic aproach to spirometry is described, everything you need to know when you stumble across spirometry results.

Coagulation tests

http://thrombosiscanada.ca/wp-content/uploads/2013/08/Bloody_Easy_Coag_2013.pdf

http://www.pathology.vcu.edu/clinical/coag/Lab%20Hemostasis.pdf Very consise and well writen guidelines for coagulation tests interpretations.

Chest radiology

https://lane.stanford.edu/portals/cvicu/HCP_Respiratory-Pulmoanry_Tab_2/Chest_X-rays.pdf

http://www.southsudanmedicaljournal.com/assets/files/Journals/vol_1_iss_2_may_08/how%20to%20read%20a%20cxr.pdf Basic guidelines for reading a Chest X-ray

Echography - Ultrasound Imaging

http://www.sah.org.au/assets/files/PDFs/For%20Doctors/2011-crit-care-us-heart.pdf

http://www.cardioegypt.com/cardioeg/ACSCA2014-Presentations/002001.pdf

http://www.annalsofintensivecare.com/content/pdf/2110-5820-4-1.pdf

http://www.cardiovascularultrasound.com/content/pdf/1476-7120-12-25.pdf