#KYJ -Wound healing Series. Part 1

What do I put on that wound?

Part 1

In this knowing your Jargon #KYJ series we look at the options for wound dressings.

Everywhere I nurse, treatment rooms and clinics have a poster helping nurses recognise different stages of wound healing and usually offering a suggestion of what dressing to use.  It's a confusing choice and often we come on shift to see that another nurse has changed to a different product.

So in this mini-series, we look at the different styles of dressing, and when they are indicated.

To get the ball rolling we must understand that wounds need 5 important things to heal.

*oxygen delivery

*nutrition (nutrients)

*moist wound bed

*warmth

*absence of infection

Oxygen / Nutrient

Oxygen and nutrients for cell growth need to be delivered to the wound systemically via the vascular network.  Arteries and arterioles deliver to the micro fine capillary beds to diffuse in to the wound.  This supports the proliferation of new tissue growth, and feeds hungry immune cells acting watch over the construction zone, preventing bacteria from colonising and initiating infection.  In diabetics and other people with poor vascular flow, there exists a chronic reduction in tissue oxygen delivery.  If the wound bed oxygen concentration should drop below an oxygen tension of 40mmHg, then wound stop healing.  They become indolent and dormant.

For oxygen to get into a wound, blood needs to be adequately drained from the wound.  In patients with heart failure (especially right heart), there is often venous engorgement/congestion.  This venous congestion (particularly in lower limbs) usually decreases the ability of blood the cycle through the wound.  Venous blood is notoriously hypoxic (without oxygen), so venous congested wounds will swell, hold and produce lots of exudate, and healing grinds to a halt.  These patients need compression bandaging or stockings to promote venous return. We have to get the oxygen right.

Moist wound bed.

Within 24-48 hours of tissue injury, fibroblast cells commence work to create a protein base to the wound bed.  It is called collagen and you could think of it as the frame or foundation of a deck verandah.  On top of the frame work, eventually the decking timber will be attached.  In wounds this construction is called granulation.

Granulation needs to take place in a moist/warm environment.  Ultimately the skin cells that form the decking need to slide (migrate) across the collagen frame to complete the surface of the wound bed (epithelialisation).  The process can take weeks, but in small wounds with close edges, the seal in just 48 hours.  The wound bed needs to be slippery.  This is where moisture comes into play. 

As nurses we need to choose a cover that maintains wound warmth (>30 deg), and traps moisture to maintain the slippery environment fibroblasts (builders) need.

Too wet and the healthy tissues in the wound swell and cease to function. Too dry and the migration, and epithelialisation can't happen.

In our next part of the series, we will look at the dressings that do this task.

Absence of infection

If a wound is colonised by pathogenic (disease causing) bacteria, it won't start repairing.  In infections, the immune system is activated to search and destroy bacteria, and using many signalling chemicals (cytokines) to aid communication between white blood cells (chemotaxis), the process of tissue repatriation ceases while active infection fighting occurs.  Infection is the enemy of wound healing.

When assessing wounds, especially chronic wounds like leg ulcers, and decubitus ulcers, get into the practice of taking a baseline bacterial culture swab.  If colonisation is present then the patient should be started on antibiotics for reduction in bacterial numbers.  A colonised wound is not an infected wound, but given moisture, time and warmth (all things a healing wound needs), that little bacterial colony becomes a rampant infection.  When wound bacteria do the dirty, they secrete toxins into the wound bed that destroys the fresh new growth, causes Vasoconstriction which reduces oxygen to the wound, and fills up the wound with excessive toxic exudate.

Wound cleaning

Warm water/saline irrigation under pressure of a 20ml syringe, and a blunt 18g needle is needed to irrigate /clean the wound.  An uninflected wound often needs very little cleaning if it is healing well (every 3-7 days).  But in infected wounds, healing is not our goal, cleaning is.  Refrain from swabbing with gauze.  This cleaning of the wound bed 1-2 times daily during active infection inhibits pus, exudate, and aids in reducing bacterial numbers.

Ok that is it for the first instalment.  A primer as it were.

Next episode we will look at the start of our wound dressing list starting with

Hydrogels, and gel based dressings.

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Hypertensive Crisis

Hypertensive Crisis

This clinical presentation is characterised by an uncontrolled high blood pressure (BP) of systolic >180mmHg leads to progressive or impending end-organ dysfunction. 

The treatment focuses on  lowering BP aggressively over minutes to hours.

Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, cerebral haemorrhage.

Cardiovascular end-organ damage may include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and/or aortic dissection. 

Renal injury, retinopathy and even Microangiopathic Haemoliyic Anaemia can also occur. 

For those being treated for essential hypertension, antihypertensives, have offered tremendous value.  The advent of crisis sits at about 1% of patients with hypertension.

Before 1950, hypertension leading to crisis demonstrated a Proor prognosis with 1-year survival rate at 20%.  Today with monitoring and a medicine cupboard full of innovative anti hypertensives, stats report  a survival rate of more than 90%.

The most common clinical presentations of hypertensive emergencies are stroke (24.5%) and pulmonary Oedema (22.5%), but CCF and cerebral encephalopathy are in high numbers.

In pregnant patients, acute hypertensive crisis usually results from severe pregnancy induced hypertension (preeclampsia).

In assessing the presentation of hypertensive crisis, the severity of the patient’s preexisting hypertension , and the duration of their HTN needs to be factored into treatment strategy.  A drug history of antihypertensives, patient compliance, use of over-the-counter (OTC) and recreational preparations such as caffeine, red bull, decongestants, Salbutamol, and , illicit drugs such as MDMA, methamphetamine and cocaine are all important, as these preps exacerbate hypertension.

The physical examination should assess whether end-organ dysfunction is present. BP should not only be measured in both the supine position and the standing position (assess volume depletion), but it should also be measured in both arms (a significant difference may suggest aortic dissection).

The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency. Evaluate for the presence of heart failure, which may be indicated jugular venous distention, crackles on auscultation, and peripheral edema. Central nervous system (CNS) findings may include changes in the patient's level of consciousness and visual fields, and/or the presence of focal neurologic signs. Abdominal masses or bruits may be noted.

Renal impairment is a likely consequence of hypertensive crisis as increasing renal vessel pressure bombards the glomerulus with more molecules of protein, causing injury.  Blood testing UECs to assess renal function is common.  A dipstick urinalysis to detect haematuria or proteinuria and microscopic urinalysis to detect red blood cells (RBCs) is an intervention we should perform at the bedside.

A full blood cell (FBC)  obtained to exclude microangiopathic anemia, and pregnancy test, and endocrine testing may be obtained.

ECG is needed if only for a baseline, and if any headache, or CNS signs are apparent , a head CT scan is considered.

One presentation is malignant hypertension.

This hypertensive emergency, always has retinal papilloedema as well as flame-shaped haemorrhages. Often there is features of LVF manifesting as pulmonary oedema which masks the initial cause.

Treatment of hypertensive crisis involves reduction of BP.

You've probably noticed that many patients have big BPs and some we treat aggressively, whereas others we tend to no be so reactive. The reality is that only a small proportion of patients will require emergency treatment. As always an important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."

We aim to identify which patients with acute hypertension have symptoms of end-organ damage.  It is these that require immediate mitigation of their hypertension. Usually IV therapy is initiated with agents like sodium nitroprusside, glyceryl trinitrate or a short acting alpha and beta-blocker, or calcium channel blockers.

The aim is to increase vessel diameter to decrease vessel pressure. Reducing afterload is the target.

With patients presenting with acutely elevated BP (systolic BP [SBP] >200 mm Hg or diastolic BP [DBP] >120 mm Hg) without symptoms and whose BP stays significantly elevated should have initiation of medical therapy and close follow-up in the outpatient or GP setting.

So crisis management is really about symptoms. 

#KYJ - Hold breath while pulling CV lines

#kYJ -  Valsalva during removal of tubes

I was sent this question:

Rob can you please explain the rationale of holding breath for 10 seconds during removal of CVC!

I understand this action minimizes risk or air embolus .... But how?

...

You may know that this is a common instruction given to patients when we remove CV lines and chest tubes.  We do it to minimise the risk of air entering the thoracic cavity when pulling out the tubes.

Ok so here is the physics.

To understand the rationale you must understand 4 concepts. 

1 Atmospheric pressure 

2 intrathoracic pressure

3 intrapulmonary pressure

4 Pascale's principle

But First, a refresher on the pressures.

All pressure (air pressure, blood pressure, intracranial pressure etc) can be measured using different pressure units.

In medicine we use 

Centimetres of water(cmH2O) or millimetres of mercury (MmHg) also called "torr" but only nerds say Torr.  Eg blood pressure might be 120/80 MmHg.

Car tyres use pounds per square inch (PSI) or kilo pascals (KPa). Eg  a full tyre may be pumped up to 36 psi or 250kpa.

Atmosphere and weather reports use Bars or pascals.

1 bar = 1000 millibars=100000 pascals.

(100 KPa or 1000hectopascals)

Thus a millibar is also a hectopascal.

It's confusing and looks like a horrible highschool maths nightmare but just know that all units of pressure can be converted into each other.

1 Atmospheric pressure is the pressure of air that we breathe.  At sea level it is 760mmHg.  If you saw it on the evening weather forecast map they would say 1013 hPa.

This atmospheric pressure is all around us and fluctuates slightly.  A tropical low might be reported at 1004hPa and a cyclone reported as 890hPa.

1013 hPa converts into 760MmHg

I will use MmHg because we are speaking in the medical context.

Just know that seal level pressure is 760. 

2.  Intrathoracic pressure is the total pressure inside your thorax.  Predominantly influenced by the changing pressure in your lungs as you breathe. This brings us to intrapulmonary pressure.

3.  Intrapulmonary pressure is the pressure inside your lungs.  As you go to breathe in, your diaphragm contracts, drops, and creates a vacuum or negative pressure change inside you lungs.  The pressure in your lungs is less than atmosphere so considered to be a relative negative pressure when compared with the atmosphere.  The change is small, only 6-8 MmHg, but enough to allow the atmosphere to rush into your lungs to equalise pressure inside.  We call this breathing in, or negative pressure ventilation. 

On inspiration

Atmospheric pressure 760

Intrapulmonary pressure 752

A relative vacuum.

Now breathing out is the opposite. I must push air pressure inside my lungs to blow air out to the world.  Diaphragm relaxes, rises and puts the lungs under higher pressure than the world.

On expiration

Atmospheric pressure 760

Intrapulmonary pressure 765+

Air rushes out.

Stay with me we have nearly answered the question.

Inside the chest wall, the pressure emulates the fluctuation of the inside of the lungs.  Thus intrathoracic pressure rises on inspiration and falls on expiration. This close relationship is described by Pascal's principle which suggests that a pressure increase in one area of a confined space (thorax) is equally transmitted across the whole confined space. I know... Boring!!! 

Back to holding your breath.

Take a big breath in now and hold it. Hold it!  Hold it!

Feels full hey?  Ok breathe normally.  

When you held your big breath (valsalva manoeuvre) you held pulmonary (and thoracic pressure) at its highest point relative to the atmosphere.

Your thoracic pressure while breath holding was perhaps 770mmHg, and thus higher than the word. It would be impossible for air to enter your lungs or chest cavity through surgical holes, because the pressure inside you was higher than atmospheric pressure.

Asking the patient to hold their breath during tube removal then makes it impossible for air to invade the hole before you seal it with an opsite or other occlusive dressing.

The pressure inside was too high.

Now the consequence of air getting in through the CVC site is an air embolism.  A very small risk, and even if air did get in it enters the venous network and bubbles flow into the right atrium.  Bubbly blood is then pumped to the lungs, where most bubbles are filtered out. 

In the context of a chest drain tube; well they are sitting in the pleural cavity not a central vein.  The tiny bit of air that can get in while pulling out a tube is insignificant and reabsorbs in a hour or so... But safe practice implores you as a nurse to take steps to avoid this introduction of air into a chest when pulling out tubes, drains and CV lines.

Just get them to hold their breath.

Pressure 

Should we reduce fever?

Fever

So I found myself banging on about kids and fever again last week in a trauma course of all platforms.

The message is slowly getting the through, but where literature focuses on efficacy of paracetamol and ibuprofen, it conclusively agrees on two key points:

1.  that these drugs should be reserved for pain and discomfort .

2.  There is no evidence that they will prevent a febrile convulsion. 

In 2010 the RACGP (college of GPs ) in Australia released a paper redefining what a fever was. Previously a patient was considered to have a fever when there core temperature rose above 37.5 degrees of Celsius. Now it is 38.0.

This was also coupled with the notion that fever should not be treated until at least 39.0. 

A common ignorance in health care providers is that at the slightest hint of a fever, some over the counter antipyretic would be given. The medical world is calling for this nonsense to cease. But it is so hard to sell this message to "out of date" parents, doctors and nurses.

Here it is - as blunt as I can put it. Stop treating fever like it is a bad thing!!

Recognise that fever is the body's normal natural response to fighting an infection.

After invasion by a virus or bacteria, phagocytes coming into contact with pathogens release signalling chemicals called pyrogens which stimulate prostaglandin release. These prostaglandins alter the body thermostat in the hypothalamus. As long as phagocytes are active in killing pathogens, they will release these chemicals to keep the temperature high. It aids in proliferation of immunity compounds and cells to the site of invasion. Fever cures infection .

Now paracetamol, and ibuprofen acting as antipyretic medicines, inhibit these prostaglandins, thereby inhibiting the natural immune response. By reducing the fever, they can mask sinister symptoms and prolong an infection

Reserve these drugs for pain and discomfort associated with illness. They don't prevent febrile convulsions, and there is NO evidence that they improve the illness. 

Just Stop treating fever!!! Fever is your friend!

Share this with your parents, colleagues and anyone you know sucked in by advertising that tries to sell a message that "Brand N" or "Brand P" is for pain and fever. 

FEVER IS YOUR FRIEND!!

This 2011 article is just another paediatric journal that refreshes the notion that antipyretics are to be reserved for discomfort.

http://pediatrics.aappublications.org/content/pediatrics/127/3/580.full.pdf

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#KYJ - Hyperkalaemia

#KYJ -  Hyperkalaemia 

High potassium in the blood.  Potassium is expressed by the chemical symbol "K".  It stands for Kalium which is the Medieval Latin word for potash, a mineral used for hundreds of years as a fertiliser, and a natural potassium salt formed millions of years ago when ancient seas dried up.  Burning plant matter in iron cauldrons (pots) yields high concentrations of potassium which in English, is termed potash.

Literally, Hyperkalaemia means high(hyper)-Potassium (Kal)-of the blood (aemia).

...

In our bodies potassium is abundant inside our cells.  It is a positively charged ion (electrolyte) termed K+.

In blood and other extra cellular fluid, it's concentration is very low relative to the high intracellular concentration.  The principle of diffusion predicts that it will leak out of our cells to balance (equilibrate) with extracellular fluid.

In converse to K+, sodium (Na+) is abundant outside cells and does the same as potassium, in that it attempts to ooze into cells. 

Normal blood potassium ranges from 3.5-5 mmol/L.  Should potassium rise beyond 5.5 then it is called Hyperkalaemia.  This is life threatening, and exerts its effects on muscle action, particularly cardiac muscle.

Elevated potassium leads to cardiac arrest. ... Badness! 

Given potassium is normally abundant inside cells, it stands to reason that when cells are damaged, destroyed and die, their potassium leaches out and increases levels in the extracellular (interstitial fluid and blood) fluid.

Under normal circumstances, your kidneys remove excess K out of your blood and some of it is transported back into cells (influx).  

Causes of Hyperkalaemia

Too much in, cell destruction or not enough excretion are the main causes.

Too much.  

When we eat foods rich in potassium, it is rapidly absorbed via our gut and enters the blood stream. It is then either transported to cells where insulin is responsible for facilitating its movement into the cell as glucose is transported into cells for energy production. 

In condition of tissue damage (burns, crush injuries and a muscle breakdown called Rhabdomyolysis), damaged cells leak massive amounts of K into the blood.  The bigger the trauma, the bigger the potassium rise.

Not enough excretion. 

If your kidneys fail, you can't excrete potassium.  It accumulates.  Remember it is continually leaking into your blood, so your kidneys need to be continually functioning to regulate potassium levels in blood.  In renal injury or failure, accumulation is swift.

Diagnosis and suspicion

Muscle weakness especially after strenuous exercise (??rhabdomyolysis)

Lethargy,

Reduced urine production

ECG abnormalities eg tall tented T waves and s widening QRS complex=badness.

Serum K (blood test) is the fastest way to definitively assess Hyperkalaemia and is part of a routine test called U&Es (Urea and Electrolytes).

Treatment

Driving kidneys to excrete is the simplest strategy.  By giving IV Normal saline, and or adding a diuretic, the patients kidneys can excrete more potassium.  The common choice is a loop diuretic like Frusemide (Lasix). Naturally these are not appropriate if the cause was renal impairment.

Insulin and glucose infusions

Insulin acts like a swipe key that open channels (gates) in the cell membranes to let glucose into cells. When this occurs, potassium molecules are moved into the cell with glucose.   Therefore an effective treatment for critically high potassium levels is an insulin infusion (with glucose).

• 10-20 units IV Actrapid insulin  and 25-50g IV glucose.
• Starts working in 20mins
• Will reduce potassium by 0.5- 1mmol/L 

Salbutamol.  

Yep you read right. Salbutamol or Ventolin either IV or Nebulised (10-20mg) causes potassium to influx very effectively. This is the preferred option in renal disease patients when diuretics are useless and mucking around with glucose and insulin is a risky gig.

Salbutamol is as quick as the insulin, 20-30 mins and strips about 1mmol/L.

Resonium

Speaking of renal patients.  A slow but relatively effective treatment for Hyperkalaemia is using oral or rectal Resonium resin.  This old school treatment binds with potassium in the bowel and facilitates its removal in faeces. 

It relies on gastric motility, so it is slow to onset, but gets the job done in the non acute patient.  It is given as a 30-45g dose usually mixed with a laxitive (to really get things moving) - sorbitol is a favourite.

When things are Critical!!

If the patient has dangerous potassium levels (>8.5) then dialysis is the game changer.

Capable of stripping K+ at a rate of 1-2mmol/L over a two hour treatment, this intensive treatment is a proven lifesaver.

So there we have it.  A very basic overview of hyperkalaemia .  I hope you enjoyed my latest #KYJ. 

#KYJ- Asthma Metered Aerosol actuations are 30% greater in quantity than the number stated on the packaging, but we don't know if it is drug or just propellant being delivered.

Introduction

Salbutamol sulphate metered inhalers are frequently observed to be able to discharge (puff) many times after the listed actuations on the product. 

This leads to confusion in patients and clinicians as to whether the device is delivering therapeutic doses of Salbutamol or just the gas propellant.  This paper reviews two common brands of salbutamol metered aerosol products to document how many total activations are possible from new.

Context 

People experiencing asthma are at risk of acute exacerbations known as flare-ups (previously "Asthma Attacks")(National Asthma Council Australia, 2015).  The pathophysiology involved frequently includes an immunoglobulin E mediated immune response to an allergen, like smoke, dust mite, foods and fragrances.  Alternatively exercise, stress and ambient temperature/humidity fluctuations may lead to a flare up (Kim and Mazza, 2011).

Regardless of aetiology,  the disease is characterised by cough, bronchiectasis, bronchospasm, and bronchiole luminal narrowing from oedema. This triad significantly causes increased work of breathing manifesting subjectively as 'shortness of breath' and chest tightness, and objectively as dyspnoea, accessory muscle use, cough and wheeze (Holgate, 2008).  

A short acting beta-2 receptor agonist (SABA) delivered as a metered aerosol (MA or "puffer"), nebuliser is common initial treatment (Asthma Foundation, 2015;Australian Resuscitation Council, 2010).  In most countries the medication of choice is Salbutamol (North America - Albuterol) often referred as "blue reliever medication".  

It is an observation by many clinicians in emergency practice, that patients using their SABA, are unaware of the correct use, correct dose and remaining drug in their MA.  Irrespective of the brand of Salbutamol, the metered aerosol delivers 100micrograms, and reports 200 doses.  Despite this, a  common observation is that long after 200 actuations, the device is capable of being discharged many more times.

This may cause concerns with those individuals that, during a flare-up, diligently self administer their SABA, believing it to be discharging drug, when it may be void of anything but propellant gas.

Some other metered aerosol products include a counter device that informs the user of doses used, or doses left. Salbutamol MA products available in Australia don't have this feature, so the user is required to keep a tally.  There is no way of knowing if the MA is drug depleted. 

Question

Despite advertising 200 metered doses, how many times will a salbutamol MA discharge before it stops actuating?

Methodology

A simple experiment was designed where six (6) metered aerosols (three of two different brands) of salbutamol  were discharged to extinction.

To minimise expiry dates, ambient temperature, atmospheric pressure or humidity being a corrupting variable, all discharges of the medication were performed on  new stock, on the same day, same time,  and at the same location.

Data

Ambient temperature was recorded at 23 degrees Celsius.  Altitude was sea level .

The brands of salbutamol sulphate included were Ventolin (GlaxcoSmithKline) expiring 4/2017 and Asmol (Alphapharm) expiring 2/2017.

The experiment was conducted at the end of September 2015 so all medication had a minimum of 16 months prior to its expiry date. 

Medication was discharged to exhaustion of propellant. One discharge per second in blasts of 10 puffs (barrages), followed by 4 shakes of the device between each barrage.

Asmol 1- totalled 276 discharges

Asmol 2- totalled 275 discharges

Asmol 3- totalled 273 discharges

Ventolin 1- totalled 272 discharges

Ventolin 2- totalled 274 discharges

Ventolin 3- totalled 274 discharges.

Results

From this small experiment it is apparent that the two brands were similar in the total number of unit discharges.  Range of variance 272-276 

Mean 274, mode 274, median 274.

It is fair to report that salbutamol sulphate metered aerosols deliver 274 +/- 2 actuations.

Discussion

Whilst it is clear that the MA devices assessed in this experiment discharge their advertised actuations, it is concerning that at a mean discharge rate of 272, this represents 72 puffs more than the reported doses.  Given this premise it was outside the scope of this study to assess the content of each discharge.

It is not known if after 200 actuations the remaining 72 puffs contain drug or just propellant gas.  A common observation in emergency departments is that a patient reports that their "puffer" is not "working" despite the apparent discharging.  This could be poor technique, out of date medication or indeed use of a MA that is drug depleted yet continues to discharge gas.  If the later is true, this represents a patient teaching opportunity, and nurses/doctors and pharmacists in a position to offer patient teaching should be informing their clients of the need to tally their MA use.

Limitations

The study was limited by a small sample of MA devices (n=6) and only two brands of salbutamol were included.  A more statistically powerful experiment could be conducted to assess a larger number of units, and include a larger number of brands.

A second limitation is that despite advertising only 200 doses on the labelling, this study did not analyse the content of each spray, so can not surmise that all sprays were delivering a full 100micrograms of salbutamol, or only the first 200 actuations.  A robust content analysis of the full 272 (+/- 2) sprays  would allow conclusions to be made as to whether manufacturers over compensate and include more than 200 metered doses, or whether, as advertised, each device only delivers 200 doses, and any excess is merely propellant.

Conclusion

Six metered aerosols of salbutamol sulphate were discharged to exhaustion to assess  quantity of actuations. All devices (n=6) discharged between 30-36% (272 +/- 2)  more times than advertised.  It is not knows if the mean 72 extra actuations contain any drug, or just propellant.

Author concludes more research and content analysis is needed, and a practice application reinforces the ongoing need for clinicians to provide education to their clients to keep tally on their salbutamol use.

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Refs

National Asthma Council of Australia

http://www.nationalasthma.org.au/handbook

Asthma Australia

http://www.asthmaaustralia.org.au

Australian Resuscitation Council.

Www.resus.org.au

HOLGATE, S. T. (2008), Pathogenesis of Asthma. Clinical & Experimental Allergy, 38: 872–897. doi:10.1111/j.1365-2222.2008.02971.x

Kim, H and Mazza, J. (2011), Asthma. Allergy, Asthma & Clinical Immunology, 7(Suppl 1):S2. 

KYJ- Takotsubo cardiomyopathy

#KYJ - Takotsubo 

It was 1976 when Sir Elton John sang those famous words..."don't go breaking my heart"; to which Kiki Dee retorted, "I couldn't if I tried".

Well Elton, a broken heart is easier than you think. Broken heart syndrome or more correctly, Takotsubo cardiomyopathy is a stress induced apical ballooning and reshaping of the left ventricle, caused by stress.  Under periods of extreme stress, brought on by tragedy, life events, loss, and anxiety inducing stimuli, the myocardium undergoes a remodelling of shape. It is induced by high concentrations of stress related hormones, eg adrenaline, norepinephrine, and cortisol, released at times of stress.  Not new, this stress induced cardiomyopathy presents as an acute heart failure that mimics an Anterior MI with typical pain, and ECG changes.  It is thought to be a silent contributor to 1.5-2.5% of ACS.  

Made up of two Japanese words, "Tako" means 'octopus' and "tsubo" means trap or pot.  Literally Takotsubo means octopus pot, and it is so called because when observed the patient's heart takes on the shape of an ancient pot that the Japanese fishermen in sea side villages, used to catch octopus for food.

It was first described in the 1990s so is really a relatively new syndrome.  It was seen women, who in their 60 & 70s, lost their husbands.  Proving to be such a stress inducing life event, a statistically significant number of widows died in the months following from what was originally called Broken hearts, then stress cardiomyopathy.  On autopsy their hearts had taken on the reshaping appearance of a Takotsubo, hence its renaming.

More?? ... 

http://m.circ.ahajournals.org/content/124/18/e460.full