cardiovascularmedicine

Stuff relating cardiology, feel free to reblog, and follow as well as can give suggestions.

[medicaljourney]

The human heart never ceases to amaze me

[gypsyastronaut]

[miteena-deactivated20150223]

[stumblingmedstudent]

miteena:

tiny heart at 20 weeks gestation!

[thecheerfulmedic]

Online resources

Here is a list of online resources for medical students that I think are very useful. These are aimed at UK based med students but I’m sure would be very useful for everyone.

General med student revision

http://almostadoctor.co.uk

http://geekymedics.com/

http://www.fastbleep.com/

http://medrevise.co.uk

http://www.simplyrevision.org.uk

Radiology

http://radiologymasterclass.co.uk/index.html

http://radiopaedia.org/

ECG

http://www.skillstat.com/tools/ecg-simulator

http://www.learntheheart.com/ecg-review/ecg-interpretation-tutorial/introduction-to-the-ecg/

Clinical guidance and management

http://cks.nice.org.uk/ (clinical knowledge summaries and NICE guidelines)

http://patient.co.uk (especially the professional reference section)

OSCE

http://www.oscestop.com/

http://www.osceskills.com/

Paid for revision sites

pastest.co.uk

passmedicine.com

Speciality specific

http://images.rheumatology.org/

http://www.frca.co.uk/ (anaesthetics)

[post-it-note-medicine-blog]

I can never remember what the different bits are on a JVP wave so here is a way to try and remember it. It’s a bit contrived, what with Cystole and trYcuspid but silly things are easier to remember. 

C is the tricuspid valve closing and kind of bulging as it does. Imagine it over shooting ever so slightly then recoiling back into place. 

V is the atria refilling, hence why the ventricles need to prepare for the next onslaught. 

The letter refers to the bit of waveform that happened just before it. So when the atria contract they cause a bit of backflow, so the pressure in the jugular vein increases (there’s no valve into the atria, only out) causing the upswing. Then the atria relax so blood can flow into said atria, so the jugular vein empties and the pressure goes down. 

Just remember that it’s the JUGULAR VENOUS pressure. Not the right atrial pressure. They’re similar, but not the same. 

[biomedicalephemera]

Pericardium and arterial branches of the torso.

Traite d’Anatomie Descriptive. Cruvheilier, 1874.

[cardiovascularmedicine]

Patient: how'd the operation go, doc?

Doctor: omg check my FAQ pls xoxo

[itsmedventuretime]

List of Pakistani Studyblrs

in alphabetical order

@cardiovascularmedicine

@elle-studies

@fatima-khan-blog

@itsmedventuretime

@medicalmaryam

@medberry

@okaysoisthismystudyblr

@stumblingmedstudent

@stuckwidmedbooks

This list is in the making. Feel free to reblog/like/message to have your URL added to this list.

[hippano]

Here’s some cardio lecture crammed into a gif. >_> You see I DO STUDY!!

I tried to match the gif’s frame rate timing to a real resting heartbeat, so if you’re sitting at a computer this might match you! The rate for this heart is 72 bpm. (unless it’s lagging. please do not match the lagging heartbeat, only zombies do that.) 

(slowed and expanded gif here)

[thought-cafe]

A couple GIFs from Crash Course Anatomy & Physiology, because we heart you! ❤️  https://youtu.be/X9ZZ6tcxArI

[sixpenceee]

Stabbing His Own Heart

Werner Theodor Otto Forssmann, a German surgical trainee in 1929, is famous for an experiment he performed on himself. Without any direction, he put himself under local anesthetic, incised a hole in his arm and pushed a catheter all the way up his limb and shoved it into his heart. He performed the procedure on himself with two feet of cable after which he walked to the X-ray room. He was fired after this stunt, but was awarded the 1956 Nobel Prize for Medicine for developing a procedure that allowed for cardiac catheterization. (Source)

[nikolace]

All I need for work! Genius!

[md-admissions]

this diagram is a gift

[medicalmotivation-deactivated20]

A gift from the cardio gods!

[littlemissconceptions]

[logija-deactivated20160411]

studying the anatomy of the heart

[geneticist]

A heart in good condition is shown at the left, and a heart from an alcoholic is shown at the right. Excessive alcohol consumption can cause a condition known as alcoholic cardiomyopathy, in which the heart becomes enlarged and weakened.

[jewsee-medicalstudent]

Human heart in ventricular fibrillation.

Ventricular fibrillation is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. It is the most commonly identified arrhythmia in cardiac arrest patients.

While there is some activity, the lay person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography.

Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole (“flatline”). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain-dead, due to the effects of cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.

Causes of ventricular fibrillation are:

Abnormal automaticity: In the healthy myocardium, the rhythm of contraction is regulated by sinoatrial node,that acts like a pacemaker and generates the normal sinus rhythm. Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously, separated from the sinoatrial node. The product of a hypoxic myocardium can be hyperirritable myocardial cells and these may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry ventricular arrhythmia. It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.

Re-entry: The role of re-entry or circus motion was demonstrated separately by Mines and Garrey. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue.

[jewsee-medicalstudent]

Takotsubo cardiomyopathy or Broken heart syndrome. 

Takotsubo cardiomyopathy is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart and this weakening can be triggered by emotional stress, such as the death of a loved one, a break-up, or constant anxiety.

The typical presentation of takotsubo cardiomyopathy is a sudden onset of congestive heart failure associated with ECG changes mimicking a myocardial infarction of the anterior wall. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted (apical ballooning). It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name “tako tsubo”, or octopus pot in Japan, where it was first described.

Stress is the main factor in takotsubo cardiomyopathy, over 85% of cases are set in motion by either a physically or emotionally stressful event that prefaces the start of symptoms.

The treatment of takotsubo cardiomyopathy is generally supportive in nature. Since the disease is due to a high catecholamine state, patients should not be given inotropes. Treatment recommendations include intra-aortic balloon pump, fluids, and negative inotropes such as beta blockers or calcium channel blockers. In many individuals, left ventricular function normalizes within 2 months. Aspirin and other heart drugs also appear to help in the treatment of this disease, even in extreme cases.

Despite the grave initial presentation in some of the patients, most of the patients survive the initial acute event, with a very low rate of in-hospital mortality or complications.