Archive for the ‘Cardiology’ Category

Electrical Injury - who needs to be monitored?

Tuesday, July 6th, 2010

rbvs0210530

Electrical injury, although not a common occurence can present with significant injury. Often the extent of the injury can be under-estimated as it mostly occurs below the skin, with little more than an entry and exit wound to see.
The very fact that patients with these injuries don’t present often, can result in management challenges. These can range from resuscitation approaches, to decision making as to who needs to be monitored.

The obvious high voltage exposure, with significant burn and injury, is not really a challenge in terms of monitor/non-monitor decision making. The challenge is from that group of patients that are well, with minimal injuries. Who, if any, of these patients do we monitor?

Electrical burns have a trimodal distribution:
1. The first peak is in children. This is primarily due to behaviors such as cord biting.
2. The second peak is in adolescents who engage in risky behaviour and the third group is:
3. Those whose work involves electricity and potential exposure.

Childhood injuries are usually biting injuries, where the child will chew through an electric cord. The result will be a burn to the lips or mouth. These burns are usually bloodless and painless as the vessels have been cauterised and the nerves damaged. One of the main issues in dealing with this kind of elelctrical injury is how to approach the burn itself. These burns will result in significant contractures and current management strategies, which are controversial,  include plastics repair and/or mouth splints.
The two main questions with children are:
Do we admit all these children? and
Do we monitor them?
At one time all children were admitted, however more and more, unless there are social or other issues, children with circumoral burns can be discharged. The one thing that may occur in about 10-15%, is delayed bleeding of the labial artery. This occurs some ten days following the injury. The only treatment needed, if the child is at home and bleeding commences, is pressure over the area and representation to the emergency department.

Can we send these children home from a cardiac point of view, or do they need to be monitored?
Bailey et al (Ann Emerg Med 1995;25(5):612-17) looked at household injuries involving 120V and 240V and concluded that no ECG or monitoring was needed. This study had some limitations in that it was retrospective and didn’t look at those potential higher risk groups with loss of consciousness, tetany and passage of current through the heart.

In 2000 Bailey revisited the higher risk group(Am J Emerg Med;2000 Oct:18(16)621-5) and performed a prospective study evaluating guidelines for monitoring high risk patients. 224 children were included in this study and the criteria for 24 hours of monitoring that were tested were:
1. past cardiac history
2. loss of consciousness
3. voltage greater than 240V
4. Abnormal ECG
There was no mortality or morbidity.
Bailey has gone on to do further studies which we will discuss shortly. In children therefore there is very little reason to monitor. If you still feel uncomfortable with no monitoring, then I would still monitor the following:
1. loss of consciousness
2. past cardiac history
3. high voltage

The next group to consider is adults without a severe injury, that we are considering monitoring.

Fatovich(MJA 1991 Sept 2;155(5) 301-3) looked at who needed monitoring following household electrical injury at 240v and 50Hz. This was a small study with 50 patients, however the conclusion was clear. No monitoring was needed in patients who were asymptomatic with a normal ECG.

Bailey (Emerg Med Journ 2007 May;24(5):348-52) conducted a prospective multicentre study involving 21 emergency departments. 143 patients were enrolled with what were considered, significant factors. They were:
-transthoracic current
-tetany
-loss of consciousness
-voltage>1000V

No patient in this study developed lethal arrhythmias. The conclusion was that patients with low voltage injuries with no loss of consciousness and a normal ECG, did not need monitoring.

So lets make some sense of all of this.

In children, most low voltage injuries do not require monitoring. The exceptions would be those children with cardiac history.

In all patients with minor injuries who are asymptomatic, have been exposed to a low voltage(<240V) and have a normal ECG, monitoring is probably not required.

Peter Kas

Posted in Cardiology, Resuscitation, Trauma | 2 Comments »

ventricular tachycardia and methadone

Sunday, June 20th, 2010

A 42 year old male with a past history of IVDU and alcohol abuse and brain injury, presents with what looks like withdrawal. Current medications included methadone and earlier on the same day, he was commenced on naltraxone.

Initially he is found to be becoming progressively more agitated and having brief episodes of depressed conscious state, with improvement between. He is ‘jittery’ with myoclonic movements in the bed. On vitals, he is found to be afebrile with a fluctuating Glascow Coma Score, bradycardic, and to have a systolic blood pressure of 80mmHg, and so he is taken to a resuscitation cubicle.

Is he in withdrawal?
Is he seizing?

As I enter the resus cubicle to find out why the patient is there, I notice a wide complex tachycardia at a rate of about 230bpm. He is still moving. It is self limited after a few seconds. Then a further episode.

In between episodes we do this ECG:
img_05523

It shows a bradycardia at rate 42bpm, there are tall T waves and premature ventricular complexes. There is a hint of a sinusoidal wave form in V2-V3(but no bundle branch, so not Brugada).
Is it ischaemia?
The QTcorrected. It’s 524ms. A QT corrected of greater than 450ms is considered prolonged.

The diagnosis is; prolonged QT causing Torsades.

Here is the next ECG we take as he begins an episode.
img_0553

So now we see a bizarre wide complex tachycardia, that looks like Torsades, with very abnormal QRS complexes following and the telltale signs of of patient shaking and agitation.
It is self limiting.

We commence Magnesium infusion in this patient. His K is 3.5, so we increase that also.

He then has a further episode which is on the rhythm strip below:
img_0555

He needs cardioversion for this.
He is intubated and soon stabilises. We do one more thing and that is, get a head CT. Why do we do this? There are a small number of cases where increased intracranial pressure can cause prolonged QT. Given his history of IVDU and alcohol, we want to exclude a subdural, or other lesion.

It is normal.

Cardiology review prior to stabilisation and want isoprenaline to increase the heart rate.
Why do they want this? ………..Read on.

Let’s look at QT prolongation.

It is caused by:
-hypomagnesemia
-hypokalaemia
-hypocalcaemia
-Na channel blocking drugs, such as Type I drugs
-raised intracranial pressure
-acute coronary syndrome
-hypothermia
-hereditary causes such as Lange-Nielsen(QT and deafness) and Romano-Ward(no deafness)

Management is Magnesium and in more severe cases of recurrent Torsades an implated defibrilator.

WHAT CAUSED THE QT PROLONGATION IN THIS PATIENT?

Most probably Methadone.
It is a synthetic opioid that is metabolised by the cytochrome P450 pathway and affects Potassium ion channels.
Studies have found that it causes significant increases in the QT interval (Martell et al, Am J Cardiol 2005;95:915-918)(Krantz et al, Pharmacotherapy 2005;25:1523-1529), especially in those on a maintenance dose greater than 40mg/day.

Why was isoprenaline recommended by cardiology? Quite clever really…
We know that Torsades is caused by QT prolongation, so increasing the heart rate decreases the QT as per the following formula:
QT = 656/[1+(heart rate/100)] (Ravtaharjus’s formula)

The patient stabilised on Magnesium and Potassium, without isoprenaline and he went to an ICU bed, with a plan to manage and substitute his Methadone.

So beware the IVDU patient on methadone that presents with syncope. We often put the symptom down to the patient having used heroin or a similar drug. Do an ECG and look for a prolonged QT, although uncommon, it may have been an episode of Torsades de Pointes.

Peter Kas

Posted in Cardiology, Case Studies, Resuscitation | Comments Off

Could this be a Pulmonary Embolism?

Tuesday, June 8th, 2010

In a previous blog we looked at the following patient who presented to the emergency department:

62 year old male presents to the Emergency Department with what he calls a flare-up of his congestive cardiac failure.

He states he is short of breath. He is a frequent presenter to the department with this complaint. He has not taken his frusemide for the past 48hours. He states that he feels very tired.

He is a well looking man with normal vitals Heart sounds dual, no murmur. normal JVP, bilateral pitting oedema to mid calves. Chest clear Abdomen soft His ECG and CXR are normal Bloods including a troponin are normal.

I’m unsure of the diagnosis, but given he hasn’t taken his frusemide, I treat him with that. I am going to discharge him, however it is late at night and he lives alone, so we decide to keep him in the department overnight. In the morning, he looks well and feels better, but still lethargic, ECG is unchanged, but for some reason someone does a follow-up troponin and it is 4.

He is diagnosed with a NSTEMI and sent to cardiology.

I now ask the question could it have been a pulmonary embolism and not a NSTEMI?

Certainly if we look at this case we see that the patient had dyspnoea with a normal chest on auscultation and on chest X-ray. Hmmm…

What are the risk factors for pulmonary embolism? Well we know of the classic ones of anything affecting Virchow’s triad. There are the hereditary factors of Protein C and S deficiency as well as others and the acquired factors such as immobility, recent surgery, cancer and others.

This patient had congestive cardiac failure(CCF). Is that a risk factor? As it turns out it is. In a population based study by Helt et al (Arch Intern med. 2002;162:1245-1248), the attributable risk associated with venous thromboembolism was 9.5%. So there is an increased risk in CCF.

What about symptoms and signs? Surely they would help.

Stein et al (Chest 1991;100:598-603), looked at patients with a suspected pulmonary embolism(PE) and with no previous evidence of cardiac or respiratory disease.

He then looked at the symptoms in patients with PE(n=117) and those without PE(n=248) as follows:

Dyspnoea - 73% with PE had it, but 72% of those with no PE also had dyspnoea.

Pleuritic Pain - 66% with a PE had it, and 59% without a PE also had it.

Leg Swelling - 28% with PE had it and 22% without PE had it

None statistically significant.

Well how about signs, surely they must help?

Tachypnoea - 70% with PE had it as did 68% of those without PE

Tachycardia - 30% with PE had it as did 24% of those without PE

Deep venous Thrombosis- 11% had it in both groups

Nothing was statistically significant.

What is interesting is that 97% of patients with a PE had

DYSPNOEA

or

TACHYPNOEA

or

PLEURITIC CHEST PAIN

So be on the lookout for those.

How about the TROPONIN rise- surely a pulmonary embolism can’t cause that?

Well as it turns out it can. Although we are unsure of the pathophysiology, it is postulated that it is due to increase in right ventricular afterload and irreversible ischaemia. It is also a predictor of in-hospital death (Giannitsis et al Circulation;2000;102:211-217). It’s important to say that the troponin rose in a group of patients that had suffered at least a moderate if not a large PE.

Those with a small PE may not have a troponin rise.

So the level of troponin rise is important as a rise of >0.1 is a potential predictor of mortality, however in the above study, none of the troponins rose above 1.0.

One other important characteristic was that the troponins rose earlier, ie., within 3-5 hours, in PE.

Therefore it is important to note that although troponin can rise, it usually does not do so, to as high a level as when true cardiac ischaemia occurs.

So, how about my 62 year old gentleman - could it have been a PE? The answer is yes it could. What is against it, is the level of rise of troponin was probably too high for someone looking so well.

Could it have been a thoracic dissection?

We’ll look at that next time…….

Posted in Cardiology, Fellowship Exam, Respiratory, Resuscitation | No Comments »

How good are we at predicting ischaemic chest pain?

Monday, May 24th, 2010

lbbb-with-inferior-stemi-cropped

Here’s a case I had recently:

62 year old male presents to the Emergency Department with what he calls a flare-up of his congestive cardiac failure. He states he is short of breath. He is a frequent presenter to the department with this complaint. He has not taken his frusemide for the past 48hours.

He states that he feels very tired.

His examination is as follows:

He is a well looking man with normal vitals

Heart sounds dual, no murmur. normal JVP, bilateral pitting oedema to mid calves.

Chest clear

Abdomen soft

His ECG and CXR are normal

Bloods including a troponin are normal.

I’m unsure of the diagnosis, but given he hasn’t taken his frusemide, I treat him with that.

I am going to discharge him, however it is late at night and he lives alone, so we decide to keep him in the department overnight.

In the morning, he looks well and feels better, but still lethargic, ECG is unchanged, but for some reason someone does a follow-up troponin and it is 4.

He is diagnosed with a NSTEMI and sent to cardiology.

So the question I posed was, “How good are we at diagnosing cardiac chest pain?” and “Are there some signs or symptoms such as shortness of breath that are more important than we may initially think they are?”

Pope et al(NEJM 2000;343:1167-1170) looked at the rate of missed diagnoses of cardiac ischaemia in the emergency department.

This was a study of some 10689 patients and the conclusion was that there was a subgroup of patients more likely not to be admitted, who had ischaemia or infarction.

Those more likely to not be admitted were:

-Non-whites

-Females less than or equal to 55 years of age

-Those with shortness of breath as their only complaint

-Those patients with a normal ECG.

Chadwick et al (Ann of Emerg Med 2004;44:565-574) looked at the question of our initial diagnostic impression as clinicians and if it was adequate in excluding cardiac disease. This was a prospective registry-based study, conducted at eight hospitals. They evaluated patients where the physician’s impression was that the cause of chest pain was not cardiac. Patients had a 30 day follow-up and adverse events included STEMI, NSTEMI, going to the cath lab or death were collated.

Of the nearly 3000 patients in this study, a minimum of 2.8% a potential maximum of 6.3% of those being clinically ruled out of having ischaemic chest pain, had a cardiac event. What was interesting was that 53.2% of patients who had been labelled as non-cardiac, still had a cardiac marker workup.

Factors that were found in this study, to be significant in predicting those patients with a cardiac event were:

-Past history of coronary artery disease

-Age

-Diabetes

-Hypercholesterolaemia

-History of Congestive cardiac failure

-Feeling of ‘weakness’ correlated highly.

So beware the patient who presents with shortness of breath or weakness as complaints. Lethargy or fatigue, is especially common in the elderly, and this is the group to be most aware of the diagnosis in.

The above list is similar to the American Heart Association list, that lists the following as being important factors in the initial diagnosis:

-The nature of the presenting angina- This is critical. If a patient gives me a great story of angina, I don’t care if they have risk factors or not, they need to be assessed by cardiology as the story means everything.

-Past History of coronary artery disease

-Male

-Age

-Number of risk factors

There are also presentations that result in a lower likelihood of ischaemia and they include:

-reproducibe pain on palpation

-Positional pain

-Pleuritic pain

-Stabbing pain

-Pain radiating to the lower limbs

How good is the ECG at helping us?

We know that up to 50% of cases with acute myocardial infarction(AMI) have a normal ECG at presentation. Serials are important. What is more important is that the ECG is probably more significant than all history and examination put together and a normal ECG predicts a group of patients with a lower rate of complications.

Thomas et al (NEJM;2000:342;1187-1195) evaluated patients with acute chest pain. AMI was present in 80% of patients with ST elevation of greater than, or equal to 1 mm and in 20% of patients with ST depression or T wave inversion. With a totally normal ECG, the risk of AMI was 4%, if there was a history of coronary artery disease and the patient had chest pain and 2% if no past history.

How about other subtle presentations?

My patients will often describe the chest pain as indigestion, or they tell me that the chest pain makes them want to belch. Are these patients fine to discharge? Here are a few facts:

-About 20% of patients with an AMI describe their pain as that of ‘indigestion‘

-About 50% of patients having an AMI had belching associated with pain.

But surely, if I give them a GI cocktail(mylanta and xylocaine viscous) and the pain goes away, that should be enough? As it turns out , the GI cocktail has been found to have the same effect on ischaemia as it does on reflux(Ann of Emerg Med 1995).

So what does all this mean? Are we now going to admit everyone? No. We are still going to risk stratify. We know that despite our best efforts that we will all miss up to about 2% of cases. The purpose of this blog is to look at all those patients with more subtle presentations.

So in Summary:

-Beware the patient with shortness of breath as their only complain, especially if elderly or a diabetic, as it could be ischaemia.

-Beware the patient presenting with lethargy or weakness, especially if they are elderly, they may have ischaemia.

-Beware the diagnosis of reflux, as symptoms of belching or pain even described as that of indigestion, can be cardiac.

-Pay attention to the story. If that is a good one for angina, nothing else matters.

Next time we’ll look at the same case from the viewpoint of it potentially being a pulmonary embolism.

-

Posted in Cardiology, Case Studies | 1 Comment »

Syncope

Wednesday, March 10th, 2010

This is one of my favourite areas, as patients present very frequently with this symptom. That very fact makes syncope a challenge. It is a symptom, not a condition in itself. We have to find the cause of the syncope. We need to be experts in this area as syncope presents some 5% of all emergency department visits and comprises 6-10% of admissions.

Our role is to risk stratify patients and make sure we don’t send home those with potential sinister causes. This is not as easy as it sounds, as there are many causes.

I often hear, “… well he’s still a little hypotensive, so that was probably the cause…..” What was probably the cause? Up to 50% of patients with syncope from whatever cause will be hypotensive. Also beware hypotension in the elderly. In this age group you need to start thinking about the abdominal aortic aneurysm.

Did you know that up to 12% of patients with thoracic aortic dissection, present with syncope as their ONLY complaint? That is a little scary.

We need to differentiate those causes associated with mortality and morbidity. This means working out who has had a cardiac or neurological cause of syncope as well as differentiate syncope from seizure.

WHY IS FINDING CARDIAC CAUSES SO IMPORTANT?

-Because mortality from missed cardiac causes can reach 30%

-Because underlying heart disease, irrespective of the cause of the syncope, is associated with an increased risk of death.

WHAT ABOUT THE NEUROLOGICAL CAUSES?

-We know that patients with a neurological cause of syncope have two times the risk of a stroke, when compared to those without syncope.

TAKING A GOOD HISTORY IS THE KEY

-How did the episode occur? Was there a sudden loss of consciousness, or was there a prodrome of sweating and dizziness etc.?

-This is important as a sudden loss of consciousness with no prodrome leads us to a cardiac cause.

-Was it associated with a change in position or did it occur whilst sitting?

-Again, syncope when sitting or lying can potentially point to a more sinister cause, which includes cardiac or neurological.

-Is there a family history or cardiac disease or sudden cardiac death?

-Here we need to start talking about BRUGADA SYNDROME and thinking about those terminating arrhythmias that can occur.

-Were there other associated symptoms of chest pain, or palpitations, or vertigo or nausea and vomiting?

-Was there a headache and if so was it sudden?

-Let’s not miss the potential subarachnoid haemorrhage.

This is such an important topic. Watch the video which contains parts of a previous lecture I’ve given on this and know that the latest will be covered tis year in the lecture series.

The update at RESUS 2010 will include:

-An approach to the diagnosis of Syncope

-Syndromes such as BRUGADA, that you must learn about and cannot miss.

-A discussion of the rules in use for looking at patients with syncope, such as the San Francisco Syncope Rule and the Boston Syncope Rule.

-We’ll talk about loop recorders, and here’s a really important thing I can’t understand. Some of these loop recorders are there to catch an arrhythmia, yet for them to be activated, the patient has to hold a probe up to them when they feel a syncopal episode coming on. What?! I have never had a patient successfully do that.

-We’ll talk about tilt table testing

-We’ll also talk about some of the latest treatments and MORE!

For now enjoy the snippets of video I’ve put together on the ‘resus blog’ and I hope you’ll take the time to come and listen to some great lectures at RESUS 2010

Posted in Cardiology, Fellowship Exam, Neurology/Neurosurgery | No Comments »

Seizure, Syncope and Sudden Collapse

Sunday, September 6th, 2009

Here is a link to a GP website, where a recent video is set up. The lecture is on Syncope and its differentiation from seizures. It talks about how to risk stratify patients so that we minimise our chances of missing the cardiac cases.

Enjoy.

picture-40

Posted in Cardiology, Neurology/Neurosurgery | No Comments »

Get a resuscitation video on your mobile phone

Tuesday, June 9th, 2009

You can now get this cardiac resuscitation video in Australia by SMS’ing the word ARREST to 1995 1515

will Mr Smith survive? Get the whole video on your mobile now. The cost $4.00

Get the Flash Player to see the wordTube Media Player.



Posted in Cardiology | No Comments »

How well does Atrial Fibrillation and Electricity mix?

Tuesday, March 10th, 2009
Get the Flash Player to see the wordTube Media Player.

Hello Everyone, Greetings and Welcome.

The approach to treatment of atrial fibrillation, is still one of the most controversial areas in Emergency arrhythmia management. Is it rate control or is it rhythm control? When do you shock back to sinus, or at least attempt it? Who do you give anticoagulation to?

Given that it affects up to about 1.5% of the population, with a 10% prevalence in the >80 year old group, it is an arrhythmia you will see a lot of.

This month in ‘Medical Talk’(the latest audio CD’s for subscibers are being posted this week) one of the topics we look at is Atrial Fibrillation(AF) and its management. We look at the evidence and we look at what we do for each case.

In the video above we shock a lady with Atrial Fibrillation and Angina Pectoris.

When should you shock? Well there are some definite indications. Cardioversion is indicated in those that are haemodynamically UNstable. That can mean chest pain, hypotension, myocardial infarction, but does it? Sometimes these definitions are not so black and white.

We know that patients that have had AF for longer than 48 hours, or have an unknown duration of AF can be cardioverted following transthoracic echo ruling out right atrial thrombus. Certainly there is an indication for anticoagulating these patients for a period of up to 8 weeks after cardioversion. The reason for this is that there is up to a 5% risk of thromboembolism(Am J of Cardiol, 2000) when the AF has been going for more than 48 hours. The important thing to remember is that it won’t necessarily happen when you cardiovert, but can happen days down the track. Greater than 80% of thromboembolic events occur in the first 72 hours and 98% occur in the first 10 days.

The reason thromboembolic events may occur, is that atrial contractile dysfunction is present  for hours or weeks after cardioversion. This dysfunction is in proportion to the duration of AF prior to cardioversion.

The evidence for AF with definite duration <48 hours and the need for anticoagulation is unclear. Certainly there is no definite indication for anticoagulation. In those patients it may be more appropriate to just cardiovert.

How do we cardiovert? Biphasic is more effective than monophasic. Set the defibrillator to ‘SYNC’. If it is not synchronised and a shock is delivered on ‘T’, it may degenerate to VENTRICULAR FIBRILLATION(VF).

Use a high energy- 200Joules in Biphasic. This is a resistant arrhythmia and will probably not revert with a low energy setting, and may degenerate to VF with low energy.

Sedate the patient- ‘Propofol’ is an appropriate agent for this. Remember that it can cause hypotension, so give an appropriate amount. Delivering a shock can also be painful, so some analgesia is also good. ‘Fentanyl’ is a good analgesic, a narcotic with no deleterious haemodynamic effects; 50-100 micrograms intravenously would be fine.

Beware to attach the pads properly, and beware if the patient has a pacemaker that you attach away from the leads, although damaging these is rare.

You cardiovert the patient back into sinus rhythm- phew! The patient then asks, “So that’s it, is it doctor, I’ll never get that arrhythmia back again, is that right?” What do you tell them? We know that the probability of long term maintenance depends on two things: (i) The duration of AF prior to cardioversion and (ii) the Left atrial size. Patients may revert back in days or weeks. In fact less than 75% are still in sinus rhythm one year after cardioversion.

Atrial Fibrillation; you need to know about it. Enjoy the Blog!

Peter Kas

Posted in Cardiology | 3 Comments »