Evaluating axis from ECG (Mnemonic)

Hi everyone! We are going to learn how to determine the axis from an electrocardiogram =D

First of all, do you know which two leads should be looked at to determine whether axis is in the normal quadrant or if it is Left Axis Deviation (LAD) or Right Axis Deviation (RAD)?

Look at lead I and lead II. Sounds simple! ^__^

An upright (positive) QRS in leads I and II is normal (–30 degrees to +105 degrees).
In left-axis deviation, there is an upright QRS in lead I and a downward (negative) QRS in lead II ( +105 degrees).

How do I remember this? @_@

Thumbs up method: Lead I = Left thumb, Lead II = Right thumb.

Wait, why lead I is left thumb and lead II is the right thumb?
Because left is a smaller word and it gets the smaller number, that is, one!
Right has more alphabets and it gets the bigger number, that is, two.

Left thumb up (I) + Right thumb up (II) = Normal.
Left thumb up (I) + Right thumb down (II) = LAD.
Left thumb down (I) + Right thumb up (II) = RAD.

Mnemonic method:
Left leaves, right returns.

That’s all!
Have a splendid week everyone

Officially an MD!

Hey there fellow tumblrers! It’s been a while since I’ve been here. I’m an actual doctor now which must mean my blog must have been good for something! haha! Thankful for the #medblr community who made medical school struggles seem like a universal thing and also encourage me to step up my game.

Shout out to @medicowesome which has helpful medical whatsapp groups, practically a study group/ discussion not confined by borders which is pretty cool.

Good luck to all those out there trying to make it in whatever you’re doing! The road will be tough, keep going. I pray God eases whatever struggles you may be facing and makes that road easier for you. 

Originally posted by suburbanlumberjack

studypatches-deactivated2015092  asked:

Andddd (me again) your blog is perfect 😭 Do you have any suggestions of other blogs you follow?

Aww, thank you. That’s very sweet of you and here, enjoy your virtual heart cookie!

These are the medical blogs that I’m following, they are from all over the world:


I can’t even tell you how cool and inspiring these people are to me. They posted and reblogged some pretty interesting stuffs too.

Long time no see!

Hello Medblr Family! How is it going? 

It’s been so long since I was over here annoying you with all my posts! Haha! Well, it’s been a couple of busy months, but I’m catching up! So before I tell you about my life, first I wanted to say:

Congrats aspiringdoctors for being the most beautiful bride of the century! I wish you and the cabbage all the happinnes in the world!

And congrats to my wonderful friend md-admissions who is about to end med school! I’m sure you are gonna kick ass in your upcoming interviews.

-If I am missing any good news, please let me know!-

And now, let me share MY good news:

First, the most important one: I HAVEN’T SMOKED A CIGARRETTE IN ONE YEAR!!!!!! Yesssss I did it, baby!!!!!!! I’m going to celebrate with a lot of wine and pasta tonight :) This is the longest I’ve been without smoking, not even a little bit, I’m so proud of myself!!!

The second one: I passed step 1 (wohoooooooooooo)

And for this my friends, I wanna thank all of you. If it wasn’t for this amazing, loving, supporting, encouraging community of people all over the world, I’d have lost it. 

A couple of months ago, I posted about how this year has been awful for me. But you guys were one of the reasons I kept it together. You kept me motivated. Your positive messages and feedback made me, and continues making me so happy, everyday. And fot that, I will be forever grateful!

And I especially want to thank these beautiful, wonderful ladies, whose mnemonics, summaries and advice have literally SAVED MY ASS!

sidratimes: sweetie, your blog was the first that I followed over here, and the inspiration to make my own. The first mnemonic I learned was from you! and all your advice helped me A LOT! thanks!

usmlenotebook: i literally have your notes on my study room’s walls. Your neuro and genetics notes saved me! thanks!

medicowesome: my FA is covered with your fantastic mnemonics, you brilliant awesome lady! thanks!

And if there’s a chance we cross paths, I am going to hug you guys. You’ve been warned!!!

Ok guys, to wrap up this totally corny post, I wanted to let you know that I have a lot of stuff that I didn’t have the time to share, so I’ll be posting them the upcoming days! 

I’ll be absent for a while, meaning, I won’t be posting the following months, but if you need any help, my inbox is always open :)

I hope you guys are doing great! I FUCKING LOVE YOU ALL! 


To remember about SVT, all you need to remember is the cause and you know the symptoms and treatment!

SVT occurs due to accessory conduction pathway through the AV node.



Beta blockers

Calcium channel blockers


V - Vagal maneuvers


Ice immersion

Carotid massage

SVT: Start Vagal Treatment - - > If fails, use pharmacotherapy (ABCD drugs)

The P in Pvst reminds us that it presents with Palpitations in a hemodynamically stable patient (HR: 160-180/min)

*PVST: Paroxysmal supraventricular tachycardia

Interesting fact: In an asthmatic patient with SVT, you can’t give adenosine or beta blockers. The drug of choice in an asthmatic patient is therefore, diltiazem (A calcium channel blocker)

That’s all!


Autonomic system drugs mnemonic

Please give some tips on remembering cholinergic and adrenergic drugs.

Drugs ending in

- ine are beta agonists
(Terbutaline, ritrodine)

-sin are alpha blockers
(Prazosin, terazosin)

- olol are beta blockers
(Propanolol, metoprolol)

- alol are alpha + beta blockers (Labetalol)

- stigmine are cholinergic drugs
(Neostigmine, physiostigmine)

Tips on how to find vein or phlebotomy

Study: Know your anatomy, so if you can’t see or feel the veins, you still know where to go.

Just the anatomy of where the veins are. Sometimes you can’t see them (old people, people with dark skin) and you can’t really feel them. I’ve done some blind insertions before successfully.

Dont panic: Initially, you will find it hard, but do not get embarrassed if you miss.

Tourniquet: Tying a torniquet often helps by making the vein more swollen and prominent.

In our hospital, the patient’s relative is asked to hold with the fingers tightly around the arm instead of using torniquets.

Alternate tournique: A lil piece of the tubing (the transparent plastic tubing thats a part of the drip set)

I’ve seen people tying a glove round the arm when they don’t have a tourniquet.

Someone asked me why else is the tourniquet used.
I think the second use is stabilizing the vein by stretching the skin and underlying tissues away from the venipuncture site. If you have ever done blood collection from an elderly patient, you must know how hard it is! The lax skin makes it really difficult. So tourniquets are used in elderly even if the vein is visible just to taut the skin.

“Lift the tied tourniquet and stretch the skin and underlying tissues away from the venipuncture site. Then gently lower the tourniquet. You may be able to retract several inches of skin and tissue away from the site with this maneuver. which is especially helpful with elderly patients) who have less collagen, prolastn and elastin than younger patients) and patients who have lost a lot of weight recently.”

How else can you make the vein prominent?

Taping  the vein you’re going to prick a few times would make it more prominent.

Don’t use a bigger needle than you have to.

Look for prick marks where people have gone before.

PS: The most important thing is your safety. Never ever put the cap of the syringe first when covering it.
Because even the finest tremors can be dangerous. Slide the needle in the cap while the cap is on the table / bed whatever.

Practice: A lot.

Good luck.


In this post, we learn a mnemonic that tells us all about the inhibitors of the ETS!

The mnemonic is, “CRAP Tightens Muscle AND Produces Muscle ACHe”

Complex I inhibitors mnemonic

C - Chlorpromazine
R - Rotenone
A - Amobarbital
P - Piercidin A

Complex II inhibitors mnemonic

Tightens - Thenoyltrifluoroaceteate
Muscle - Malonate

Complex III inhibitors mnemonic

A - Antimycin A
N - Naphthoquinone
D - Dimercaprol
Produces - Phenformin
Muscle - Myxothiazole

Complex IV inhibitors mnemonic

A - Azide
C - Carbon monoxide (CO), Cyanide (CN-)
H - Hydrogen sulphide (H2S)

That’s all!


Preparing for the USMLE Step 1 exam

“How do I prepare for the USMLE Step 1 exam?” -The most requested post ever!

The essentials - Kaplan videos & notes (for basics) + Goljan book & audio + uWorld + First Aid is the general way to go for most IMG students.

Kaplan videos and notes: They are a good start. If you are time restricted, you may want to skip stuff, fast forward through it.

Pathology: Do Goljan and Pathoma. Know them cold. I had studied Goljan really well. I wish I had the time to complete Pathoma as well. The videos and concepts are awesome.

uWorld: Do it really well the first time. You are gonna get bored doing it the second time so get the concepts in the first go. Take your time if you have to.

While doing it the first time, the 2 blocks per day and 20 days scheme didn’t work for me. I got frustrated with the time constraints I had put on myself. The best I could do was 1 block per day. So give yourself 45 days, just in case you are slow with uWorld like me.

I did it in random just because I assumed studying subject-wise would get too monotonous. Subject-wise goes faster. I did it timed. You may do it untimed, tutorial, subject-wise. It doesn’t matter. Do what you are comfortable with.

First Aid: It’s your quick review book. Write uWorld notes all over it. Make it messy, draw diagrams on it. It’s the only book that’s gonna stick with you till the end of time.

NBMEs: Give as many as you can. But do them only for feedback, not for learning.

Other stuff you can do -

BRS behavioural science: I highly recommend it. You can easily do important chapters like stuff on defense mechanisms even 20 days before the exam. There are good quality, minimal in number, doable questions at the end of every chapter.

Be flexible: If you find yourself weak in any random subject, quickly Google for good sources and review the doable ones. People advice not to look into new resources a few days prior to the exam but that’s bull. Your old sources are obviously did not help you and that’s the reason you are weak in the subject… Look for new ones! I did BRS behavioural science 20 days before my step and it is one of the best decisions that I made. I tried ANKI flashcards for brain stem sections a week before. As long as you keep a balance, new resources won’t hurt you.

Flashcards: Download or make your own flashcards. It helps you revise frequently.

Other Qbanks: Yes, I had done bits of Kaplan Qbank and USMLE Rx. I had time when I started them, they helped me get what the questions are like and I did make a few notes. They did freak me out (since I got most of the questions wrong) and hence, helped me study more early in my preps. But they are not essential if you are out of time.

Doctors In Training: It’s very boring. But the worksheets do help you memorize and revise. I don’t recommend it, but I did review some of it once upon a time.

Random advice -

Be attentive during rounds: Because the USMLE will have questions on clinical stuff. If you have done your core rotations, it’s not an issue. But if you are in your basic sciences years, the only way you can get these right is by being attentive in rounds. There are very simple common clinical questions like urge incontinence on Step 1 which are not covered in First Aid. You can easily get them right. Read x-rays, especially the fracture ones.

Don’t forget to revise Kaplan and Goljan: Read a little bit of Kaplan and lots of Goljan even in your busy 2 block per day + First Aid schedule. The bain of knowledge is to forget.

Revise as much as you can before the exam: I remember antidepressants and antipsychotics being a bit foggy in my head during the step. I should have revised properly and in a more organized way before the exam.

Solving questions: The questions are scary. I made a lot of silly mistakes during the preps. I agree that the margin for error is small. You miss one word and the question goes wrong. The exam seems hard before you take it and easy after you’re done with it. Keep going. All you can do is give your best :)

Don’t delay dates too much: I delayed my exam for a month. I gave an NBME on the previous exam date. The NBME score and the test score came out to be the same. Life! xD

Social isolation: It’s normal. Friends will demand to see you, even after you’ve explained how important and hard this exam is. You will feel bad for not meeting them and have mood swings, it is okay. Don’t let it consume you. Focus. You may completely ignore the existence of any other species on the planet, it’s allowed. The good ones will stick with you anyway.

That’s all! 

Feel free to ask any questions.


Why does Digoxin toxicity result in increased automaticity?

Hey everyone!

Digitalis and other cardiac glycosides are known to cause an AV nodal delay.

Then why does too much Digoxin result in some arrhythmias that are due to increased automaticity?

Brady arrhythmias are explainable. But why tachy arrhythmias?

You see, cardiac glycosides reversibly inhibit the sodium-potassium-ATPase, causing an increase in intracellular sodium and a decrease in intracellular potassium. The increase in intracellular sodium prevents the sodium-calcium antiporter from expelling calcium from the myocyte, which increases intracellular calcium. The net increase in intracellular calcium augments inotropy.

Excessive intracellular calcium may cause delayed after-depolarizations, which may in turn lead to premature contractions and trigger arrhythmias. Cardiac glycosides shorten repolarization of the atria and ventricles, decreasing the refractory period of the myocardium, thereby increasing automaticity and the risk for arrhythmias.

That’s all!


Heart murmurs mnemonic

Hello people with a pumping heart in their chests, obviously! <3
In this post, I’ll be taking about the few mnemonics I use in relationship to murmurs.

PASS” is a good mnemonic for remembering that pulmonic and aortic stenosis give a systolic murmur.

The opposite of PASS, ie, other two valves and the other defect gives a systolic murmur too. (Mitral and tricuspid regurgitation gives a systolic murmur!)

VSD has a S so that’s systolic.

Now, the other ones - pulmonic and aortic regurgitation, mitral and tricuspid stenosis will cause diastolic murmurs :)

Here’s another mnemonic submitted by one of the readers:
For the systolic murmurs: MR. P.V. TRAPSS (Mister Per Vaginum traps? :P)
MR. P. - Mitral Regurgitation or Prolapse
V. - VSD
TR - tricuspid regurg
APS - Aortic or Pulmonary Stenosis
S - Systolic

For the diastolic murmurs: MS. PAID
MS - Mitral Stenosis
PAI - Pulmonary or Aortic Insufficiency
D - Diastolic

Here are a few more lame mnemonics I made when I was in final year! =)
I remember GDP or Gross Domestic PRoduct.
Graham Steel murmur is a Diastolic murmur associated with Pulmonary Regurgitation.
Alternatively you can remember, Graham SED PR (Graham said per rectum? xD)
For Graham Steel, Early Diastolic, Pulmonary Regurgitation.

Carrey Coombs murmur is seen in rheumatic carditis.
RCCC (Renal cell carcinoma) is diagnosed by MD and MS”, is my mnemonic.
Rheumatic carditis, Carrey Coombs, Mid diastolic, Mitral Stenosis.

Austin flint murmur is seen in aortic regurgitation.
AFAR MD” helps me remember Austin Flint, aortic regurgitation and Mid Diastolic.

I am actually not a fan of using mnemonics for concepts like murmurs. But once, I was asked to name systolic murmurs in a viva. And you know how vivas are, if you don’t answer quickly, another question is thrown at you. Luckily, I remembered this mnemonic that day and could answer quickly. That’s when I realized, it’s okay (It’s awesome, actually!) to understand all the murmur mechanisms properly when you have time to imagine at home and it’s definitely okay to use mnemonics cheaply when you don’t have time to think, that is, in time bound exams.

That’s all!

Lub dub goes my heart…


Mechanism of pulsus paradoxus in pericardial diseases like constrictive pericarditis and pericardial tamponade

Okay, so let’s begin!

Normally, during inspiration, a decrease in intrathoracic pressure is transmitted to the right heart, augmenting venous return.

What happens to the left heart?

During inspiration, expansion of the lungs and pulmonary tissues causes pulmonary blood volume to increase, which transiently decreases the flow of blood from the lungs to the left atrium and therefore, left ventricle.

Understood this? Okay, cool.

Right ventricular volume increases, pushing the interventricular septum towards the left ventricle.

This leads to an increase in left ventricular filling pressure with an unchanged or lower left ventricular end diastolic volume. (Left ventricular filling pressure? Yeah, the pressure in the ventricle as it fills with blood.)

This is a diastolic interventricular interaction which is always present.

Okay, great.

Now it get’s complex-y because we are going to talk about pericardial disease like constrictive pericarditis and pericardial tamponade.

Intrathoracic pressure changes are transmitted, normally, both to the pericardium and the cardiac chambers.

There’s a gradient between the pulmonary veins and the left ventricle (The effective filling gradient) that allows filling of blood from the pulmonary veins into the left ventricle. This remains constant during inspiration and expiration because pericardial and pleural pressure follow the intrathoracic pressures.

Understood so far? Now, let’s see what happens in constrictive pericarditis:

Anatomy fact: The pulmonary veins and a part of the left atrium are NOT covered by the pericardium.

Intrathoracic pressures are transmitted to the pulmonary veins and the portion of the left atrium not encased by the pericardium. But thepressure of the rigid pericardial bound left ventricle doesn’t vary with the intrathoracic pressure.

So, the effective filling gradient is decreased. The left ventricular volume will be reduced even more because of this.

The right ventricular diastolic pressure and volume increases like it usually does in inspiration.
This causes the interventricular septum to shift to the left even more than it used to in normal inspiration.

So basically, the inspiratory decrease in left ventricular systolic pressure results in increase in right ventricular systolic pressure.

This is known as ventricular interdependence or discordance during the respirophasic cycle. It also occurs in preicardial tamponade where fluid is present in the pericardium.

It is also why pulsus paradoxus occurs. The decreased left side effective filling gradient and the decreased left ventricular stroke volume causes the greater than normal (>10 mm Hg) decrease in aortic blood pressure when inspiration occurs.

Hope that helped clear things a little!


Hello, my favorite brainy people of the internet!
We’ll be talking about some brain tumors today.
All of the mnemonics might not work for you, so take only what you need :)

Glioblastoma Multiforme:
It is the most common malignant CNS tumor in adults. It has a butterfly appearance as it commonly crosses the corpus callosum. Areas of necrosis and hemorrhage are present. (This was asked as a MCQ in my exam!) GFAP positive.

Glioblastoma Multiforme mnemonic:
GlioBUTTERFLYoma multiforme.
G for Glioblastoma, G for GFAP.
G for gangrene (Lame way to remember about the hemorrhage and necrosis!)

A whorled appearance is seen, histopathologically. It commonly presents in women and expresses estrogen receptors. It can calcify resulting in psammoma bodies.

Meningioma mnemonic:
M flipped upside down looks like a W for whorled, women.

Psammoma body mnemonic:
Papillary carcinoma of the thyroid
Papillary renal cell carcinoma
Serous cystadenocarcinoma of the ovary

Fired egg appearance or chicken wire capillary pattern seen on histology. It commonly involves the white matter of frontal lobe resulting in seizures.

Oligodendroglioma mnemonic:
Eggs look like O.. OligOdendrOgliOma. Fried eggs leads to a fried brain. Fried brains cause seizures.

Pilocytic astrocytoma:
It’s a benign tumor of astrocytes, most common tumor in children. It involves the cerebellum (below the tentorium). Rosenthal fibers are eosinophilic, corkscrew fibers found in pilocytic astrocytoma. Pilocytic astrocytomas generally form sacs of fluid (cysts).

Pilocytic astrocytoma mnemonic:
PiloCYSTIC astrocytoma.
AstROSEcyte. ROSEnthal fibres!

Often localized to CN VIII, found in cerebellopontine angle, S-100 postitive. Histologically, shows cellular Antoni A area and paucicellular Antoni B area.

Schwannoma mnemonic:
For Schwannomas I remember the bird, “SWAN”
S-100 positive
Well circumscribed
Acoustic Schwannomas are common (More common than Trigeminal Schwannomas!)
ANtoni A and ANtoni B
Neurofibromatosis type 2 has bilateral Schwannomas.

Pituitary adenoma:
It’s a prolactinoma, most often. Derived from Rathke’s pouch. Can cause bitemporal hemianopia.

Pituitary adenoma mnemonic:
P for Prolactinoma!

Is a benign childhood tumor, derived from remnants of Rathke’s pouch. It is the most common childhood supratentorial tumor (Infratentorial is pilocytic astrocytoma, remember?) Tooth enamel like calcification is seen. Can cause bitemporal hemianopia.

Craniopharyngioma mnemonic:
C for Children, Calcification.
R for Rathkes pouch!

Ependymal cell tumors most commonly found in 4th ventricle and thus can cause hydrocephalus. Characteristic perivascular pseudorosettes seen on histology. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus.

Ependymoma mnemonic:
Epic Ependymoma. (Sounds similar, yaay!)
E for ependymal cells.
P for pseudorosettes.
I for inside the cavities of the brain (How I remember involvement of the ventricles!)
C for ciliary bodies.

Most often cerebellar, associated with von Hippel-Lindau syndrome, can produce erythropoeitin causing secondary polycythemia.

Hemangioblastoma mnemonic:
HEmangioblastoma! H for Hippel. E for EPO.

That’s all!

This post was requested by Kay =)
I covered most of them for you, lemme know which else do you need!


Case scenarios: When you don't give patients 100% O2 and why

Clinical scenario #1: Chronic lung disease patient.

The ventilatory drive of patients with chronic lung disease is primary due to their hypoxemia, rather than CO2 levels. This is because pCO2 receptors are adaptive. Chronically elevated pCO2 makes central receptors unresponsive in COPD patients. Administration of a high O2 mixture to relieve the hypoxemia is contraindicated because this removes the hypoxic drive, leading to severe hypoventilation.

Clinical scenario #2: Drug overdose where central receptors are blocked.

In morphine or heroine overdosed patients, central receptors are knocked out and the hypoxic drive is what keeps them breathing. Administration of a 100%  O2 mixture to relieve the hypoxemia is contraindicated too because this removes the hypoxic drive which kept them breathing.

Clinical scenario #3: Tracheostomy following prolonged respiratory obstruction.

Apnea in patients is due to washing out of CO2 which was acting as a respiratory stimulus. Treatment is to administer 5% CO2 in oxygen or assisted ventilation.

I know there are many such scenarios but I can’t think of any more at the moment. The basic concept in such cases is the same - understanding which receptor acts as a drive for respiration and not messing with it! Lemme know if you recall any more and we’ll add more scenarios here =)

Age of completion of ossification mnemonic
For those who forget the age at which ossification centres close, this post is for you!
Imagine the baby in a fetal position, the joints facing upwards are 18,the ones facing downwards are 16:
Elbow = 16
Pelvis = 16
Ankle = 16Shoulder = 18
Knee = 18
Wrist = 18
This diagram gives the approximate ages when the epiphyses close.

Caffeine in Migraine!

Does Caffeine play a role in therapy of migraine? Or does it cause migraine?

Asking a doctor, he said yes caffeine heals pain in migraine attack. OK yea fine. But it can cause an attack too!! This is what I found something Amazing!

Migraine is a disorder characterised by acute pulsating headache, usually restricted to one side of head. Pulsatile dilatation of cranial blood vessels is the immediate cause of pain.

But we know headache is usually caused by vasoconstriction of cranial vessels and not vasodilation!
Actually, excess vasoconstriction or vasodilation, both cause less blood to reach brain parenchyma. This makes brain tissue cry for its necessary nutrients from blood!

In migraine there’s excessive vasodilation of the vessels. So is the cause of acute pain. Caffeine constricts cranial blood vessels ( all other systemic vessels are dilated ). It is a CNS stimulant. (That’s why we have more coffee at night while studying). :p

Now here comes the point. 1-2 cups of coffee (100-200mg) heal the pain by vasoconstriction. More than this will tend to decrease blood flow and so less supply to brain tissue.
That’s why some people, who are in a habit of taking excess coffee or soft drinks, are more prone to headaches!

》 Caffeine is one of the constituents of medicines specific for treating migraine.

MIGRIL: Ergotamine 2mg, Caffeine 100mg, cyclizine 50mg tab.

VASOGRAIN: Ergotamine 1mg,  Caffeine 100mg, Paracetamol 250mg, Prochlorperazine 2.5mg tab.

PS: Remember, the moment you feel migraine symptoms, have coffee. It is the best and most effective way to heal pain, without significant side effects.

That’s all
Thanks :)