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Wellen's Syndrome involves an ECG pattern representing a significant major coronary artery stenosis. More specifically, a Left Anterior Descending(LAD) artery stenosis. In most cases this is proximal, but it may be mid or distal LAD. It actually represents a reperfusion of the vessel and is one more reason to perform serial and painfree ecgs. If not recognised and treated, it can result in up to 75% of patients having an anterior wall myocardial infarction within days/weeks. How to Recognise the Pattern? The peculiarity of this ECG pattern is that it may not appear when the patient has pain. In fact the only finding when the patient has chest pain, may be a small negative deflection at the end of V1 and V2 . The T waves become deeply inverted when the patient is pain free and represents a reperfusion of the myocardium. Cardiac enzymes will be normal in most cases or mildly elevated. Below are the two key ecg patterns in Wellens'.  What is Pseudo-Wellens'?It is a mimic. Pseudo-Wellens’, is a similar pattern to Wellens’, but results from other ECG abnormalities such as abnormal T waves, due to left ventricular hypertrophy(LVH). We cannot diagnose Wellens' Syndrome in a patient with left ventricular hypertrophy. The biphasic waveforms are a direct result of the left ventricular hypertrophy, and represent a T wave change associated with the enlarged heart. So if there is LVH we cannot diagnose Wellens’ Syndrome on ECG. The patient may however still have ischaemia, so beware. One more thing that is different in Pseudo-Wellens’, is that the changes are more lateral i.e.., V3-V6, whereas in true Wellens’ they are at V2-V3. The ECG below is a very good example of the ‘pseudo’ pattern. The biphasic waveforms are due to left ventricular hypertrophy. They are also more lateral than the true Wellens.  Other mimics also existSubstance abuse such as cocaine and other stimulants as well as cannabis can also result in a mimic pattern. Examples of these mimics are shown below. Even though we may consider them as mimics, our first priority always is to rule out ischaemia first. The diagnosis of a pseudo-Wellens' is a diagnosis of exclusion. A patient presenting after taking cocaine and showing the pseudo-Wellens' pattern:  A patient with excessive cannabis use, showing a pseudo-Wellens' pattern: 
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A 90 yo patient with multiple co-morbidities and mild dementia presents with chest pain. The patient is haemodynamically stable. An ECG is done and there is concern over the rate. Look at the ECG. What is the diagnosis?  Is it SVT? Is it Torsades? What do you do next? .........Move away from the patient..... ie., do nothing. Let's see why. Let's go back to the clinical picture. The patient is haemodynamically stable and looks well. Now back to the ECG: It is a narrow complex EXTREME tachycardia. Notice lead III. It is not the same as the others. One lead cannot refuse to show the tachycardia whilst all the others are. In fact lead III here is the underlying rhythm. The rest of the ECG is artifact. Remember that if the ventricle is beating at above 300 beats per minute in an adult patient, it will very soon convert to ventricular fibrillation. Clinically at a rate of 350 or so, the patient will not be stable, as the ventricle doesn't have time to fill properly, so the blood pressure will be impaired. What is the artifact caused by? Artifacts can be external, relating to line current. They can also be internal relating to tremor or shivering. They can also be caused by other devices such as deep brain stimulators ( which are usually there to control tremor). An ECG was redone and is shown below. The artifact is gone and the patients underlying rhythm is there.  Don't be fooled by the mimics. To read more on this and see more examples like the one below go to the blog on 'A Patient with Wide Complex Tachycardia' 
A 6 week old baby is brought into the ED with Shortness of Breath and Diaphoresis when feeding.
The ECG is shown below. What are the abnormalities shown? Take a minute to look at it. Then watch the video below as we go over the diagnosis. 
What are the abnormalities?
Here are some hints:
. . . Here is the diagnosis...... ALCAPA Watch the 2 minute video below. ​ This is a section taken directly from the cardiac bootcamp course. Members can go to Paediatric ECGs section for more examples and videos. A 35 year old woman, who is a known intravenous drug user, is admitted with septic shock secondary to bacterial endocarditis. She is acidotic and hypotensive. Her ECG is shown.  Crinion D et al. Circulation. 2020(1) Answer the following 3 questions: Can you recognise this sign?
The Spiked Helmet Sign Is this an acute myocardial infarction?
No This is a STEMI mimic. It does however occur in critically ill patients. If your hospital had no cath lab, would you thrombolyse?
Beware with the spiked helmet sign. You have to look beyond the heart for the cause. Always, when you see this sign get a cardiology opinion, certainly prior to thrombolysis and look for the ST elevation beginning before the QRS, which gives this diagnosis. See the details below. This certainly looks like ST elevation, but is actually a mimic. If you look at the complexes, the upward shift starts before the onset of the QRS complex. There is a dome-and-spike pattern, similar to a Prussian military helmet. This has been called the 'Spiked Helmet Sign'. It is a STEMI mimic and usually found in critically ill patients with no cardiac pathology. In one case series by Littmann(2), 8 patients with this sign were presented. None had a cardiac illness and 6 of the 8 patients died. In some cases, the sign was only after intubation and it is postulated that the mechanism for this ST elevation is related to repetitive epidermal stretch due to an acute elevation in intra-thoracic or intra-abdominal pressure. Below is another example.  So remember the helmet sign. It is usually present in critically ill patients. Think of sepsis, or abdominal conditions ie., think beyond cardiac.
References
He had been lifting a box of shopping from the floor to a table when he collapsed. A colleague had heard a thud and entered the room to find the patient unresponsive on the floor with what sounds like agonal breathing. His colleague initiated CPR and called for the ambulance. On arrival the patient was found to be responsive but confused and complaining of chest pain. He was transferred to the emergency department promptly. En route he was noted to be hypotensive, tachycardic, mildly hypoxic and tachypnoeic. His blood sugar was noted to have been 5.6mmol/L. He was given 500mls crystalloid en-route which settled the tachycardia. On arrival he was still a little disorientated but able to give a history, he remained hypoxic on room air but corrected with modest supplemental oxygen. He had a systolic blood pressure of 100mmHg, and complained of chest pain that was bruising in nature. The collateral history suggested that he went pale then blue just prior to collapse, but the patient had no memory of the events. The CPR had been brief at about 3 mins before he spontaneously started to breathe normally and recovered from his cyanosis. He had no prodrome and the only history of note was of Klinefelter Syndrome for which he received monthly testosterone injections. The initial differential was quite broad but essentially required differentiating cardiovascular from neurological causes of collapse in the first instance. The lack of prodrome, sudden nature of the collapse, rapid recovery with no postictal period and cyanosis all point towards a cardiorespiratory event. His ECG is shown:  The ECG shows sinus rhythm with a partial right bundle branch block and T wave inversion in lead III, with S1Q3T3. Members go to the section on ECG changes in PE to find out more. Bedside echo showed a very dilated right ventricle. It was concluded that he had suffered a massive pulmonary embolism and cardiac arrest. The subsequent CPR had converted the massive PE to a submassive PE. Given that he was relatively stable at this point he was taken to CT for a CTPA. The CT is shown below.  The CTPA shows total occlusion of the left pulmonary trunk the right lower lobar vessel is patent otherwise the right pulmonary tree was occluded.
He was given tenectaplase peripherally and low molecular weight heparin and referred to ICU His symptomatic hypoxia resolved over the next few hours and his echo at 24 hrs post thrombolysis was normal. Issues raised by the case:
Klinefelter syndrome (trisomy 47XXY) is treated with testosterone therapy. Ester based testosterone products are known to cause erythrocytosis and raised haematocrit which is associated with venous thromboembolism. This patient had a mildy raised haematocrit of 0.58. Is thrombolysis beneficial? The European Society of Cardiology 2008 guideline concluded “Randomized trials have consistently shown that thrombolytic therapy rapidly resolves thromboembolic obstruction and exerts beneficial effects on haemodynamic parameters. In an early small trial, an 80% increase in cardiac index and a 40% decrease in pulmonary arterial pressure was observed after 72 h of streptokinase treatment. In the Plasminogen Activator Italian Multicenter Study 2, serial angiograms revealed that 100 mg of recombinant tissue plasminogen activator (rtPA) induced a 12% decrease in vascular obstruction at the end of the 2 h infusion period, whereas no change was observed in patients receiving heparin. The effect of rtPA was associated with a 30% reduction in mean pulmonary arterial pressure and a 15% increase in cardiac index. One of the largest thrombolysis trials demonstrated a significant reduction in mean RV end-diastolic area on echocardiography 3 h after treatment with rtPA.” Yep. The authors of this paper also noted that the myocardial infarction contraindications should be considered relative contraindications in the unstable submassive PE patients. Peripheral vs local thrombolysis? Again the European Cardiology Society Guideline- “Direct local infusion of rtPA via a catheter in the pulmonary artery (at a reduced dosage) was not found to offer any advantages over systemic intravenous thrombolysis. This approach should generally be avoided, as it also carries an increased risk of bleeding at the puncture site.” A 52 yo male presents with atypical chest pain for 3-4 hours. He has had a vague feeling of chest heaviness for the whole day and has had an episode of palpitations. His only past medical history is of hypertension. Examination is normal, with dual heart sounds and no reproducible chest pain on palpation. Lungs are clear and abdo is soft. An ECG is done as shown below. Which of the following diagnoses does this represent?: (a) STEMI (b) Ischaemia (c) Pericarditis (d) Benign Early Repolarisation  ANSWER
This is not a straightforward ECG, as few of them are. My diagnosis and the diagnosis we gave this patient was pericarditis. The patient did very well on standard pericarditis treatment. Below is my thinking, plus also view the image below this:
 Learn about Pericarditis
The stages of pericarditis How to differentiate it from BER and ischaemia and more... A 68 year old male is brought into resus with chest pain and diaphoresis. The patient rapidly loses consciousness and is in cardiac arrest, with the rhythm strip shown below. CPR was rapidly commenced and the team went into resus mode.  This week we look at a few pearls that come straight out of the 'Cardiac Arrest Pearls' part of the Cardiac Bootcamp Course. Some of these may surprise you..... The Pulse Check During the rhythm check during CPR someone checked the pulse. During the rhythm check someone checked the pulse. Can we rely on the pulse to guide further resuscitative efforts?
We must stop relying on the pulse. Old ATLS teaching was it that a carotid or femoral pulse being present, meant that the systolic blood pressure was at least 70mmHg. Studies have shown that our ability to detect a pulse and the accuracy of the reading are unreliable. Also the blood pressure with a pulse present can be less than 60mmHg Deakin et al BMJ 2000 Sept 16;321(7262):673-674 CPR CPR is everything and distinguishes between NO FLOW(no CPR) and LOW FLOW(CPR). At best we will achieve 50% of normal cardiac output (yes, that's with the best CPR we can perform). It's not great, but it again reinforces the need to continue CPR and not interrupt it. The QUALITY OF CPR IS DEFINED BY:
AIRWAY Everyone is obsessed with "getting the tube in". In resuscitations, the airway is simple, unless there are compelling reasons to; do not intubate until ROSC is achieved. Intubation confers no benefit over supraglottic airway. SOME POINTS ON AIRWAY
All Patients should be intubated as soon as possible following a cardiac arrest: True/False? ANSWER
FALSE The studies in out of hospital cardiac arrest showed that intubation conferred no benefit over BVM or supraglottic airway. In in-hospital cardiac arrests, those patients intubated within the first 15 minutes of cardiac arrest, had a worst outcome. ADRENALINE The use of 1 mg of adrenaline which initially came from canine models, was introduced at this time and has been a major part of all resuscitations since then. The clinical significance of adrenaline is uncertain. It’s been shown to give no improvement and even to decrease survival to hospital discharge and decrease the rate of favourable neurological outcomes. Steil in the multi-centre OPALS study demonstrated no improvement in neurologically intact survivors to hospital discharge when using advanced life-support. We know that high-dose adrenaline doesn’t improve outcomes. Jacobs, further randomised 601 cardiac arrest patients and found a significantly improved likelihood of achieving return of spontaneous circulation(ROSC) in the adrenaline group. There was a trend to increased survival to discharge in this group, unfortunately the study was underpowered. Everyone should get 1mg of Adrenaline right? Giving 1mg of adrenaline to a heart that has just resumed beating, can have dire consequences. The effect of markedly increased afterload against which a weak heart must beat, can result in a rapid loss of circulation. The adrenaline dose must be titrated to achieve adequate coronary and cerebral perfusion. Our aim should be to achieve a coronary perfusion pressure of above 15 – 20 mmHg. This equates to diastolic blood pressure of 25 – 35 mmHg, which has been shown to provide adequate cerebral perfusion pressure. Monitoring with an arterial line is the only way to do this accurately. As I have discussed at several EMCORE conferences, the aim is to locate the femoral artery with ultrasound during the first rhythm check pause and to then pass the catheter during the second rhythm check. This requires practice and coordination of the team. If you don’t have an arterial line, don’t trust the pulse check, or the electrical wave form. Use the cardiac ultrasound to verify whether the heart is beating or not. In the FEEL study it was found the 38% of patients with asystole on the ECG, had coordinated cardiac motion on echo. It was further found that 58% of those in PEA had coordinated cardiac motion seen when the heart was visualised. Hypothesize what might happen with the massive alpha effects of giving 1 mg of adrenaline to these hearts. Keep the dose small if the heart is beating.  Wide complex tachycardias can be a little scary. Bootcamp Members can go to the VT section and review wide complex tachycardias. Also a New section has just been added on monomorphic and polymorphic ventricular tachycardias. This week we look at two simple cases. The key is is to pick the right treatment. The wrong treatment may simply not work, but worst than that, it may kill your patient. CASE 1 A 32 yo male is brought into the emergency department from the methadone clinic across the road. It appears that he has been having short bursts of seizure activity. He has no other past history apart from IVDU and he is on the methadone program. An ECG is performed as shown below. See what you think.  He soon begins to have 'seizure' activity. You attach him to a monitor and the following rhythm strip is obtained.  What is the diagnosis? (a) Monomorphic Ventricular Tachycardia (b) Polymorphic Ventricular Tachycardia (c) Torsades de Pointes ANSWER
This is Torsades de Pointes The definition of Torsades de Poines is a polymorphic ventricular tachycardia in a patient with prolonged QT interval. This patient had a very prolonged QT secondary to hi Methadone. The patient receives one shock and reverts to sinus rhythm. You wish to start medication to prevent the patient from going back into this polymorphic ventricular tachycardia. Which one of these would you use? (a) Procainamide (b) Amiodarone (c) Magnesium (d) All of the Above ANSWER
The answer is (c) Magnesium. DO NOT use Amiodarone or Procainamide as these may prolong the QT interval even further. CASE 2 An 85 yo male presents with palpitations and pre-syncope. He has a past history of hypertension and had an AMI 5 years ago. His cardiac examination is normal and he is neurologically intact. You perform an ECG, shown below:  What is the diagnosis? (a) Monomorphic Ventricular Tachycardia (b) Polymorphic Ventricular Tachycardia (c) Torsades de Pointes ANSWER
Monomorphic Ventricular tachycardia This is non-sustained; defined as < 3 complexes or < 30seconds. You decide to treat the patient to prevent a recurrence. What would you use? (a) Potassium (b) Amiodarone (c) Magnesium (d) All of the Above ANSWER
Amiodarone can be used here. Procainamide is an alternative, however in patients with poor left ventricular ejection fraction, it can worsen heart failure. A 19 yo male presents to the emergency department with palpitations. He has a narrow complex tachycardia on the monitor at a rate of 155 beats per minute. He has some left sided chest discomfort which this is pinpoint, sharp and totally reproducible. He states that he has had this for the last 2 days following working out at the gym. An ECG is done and you diagnose SVT. You discuss what SVT means with the patient and progress to vagal manoeuvres, which don't revert the patient. You then discuss the use of Adenosine with the patient. The patient reverts with a single dose of Adenosine. The post reversion ECG is shown below. What does it show?  What is the Diagnosis? (a) Anterior ST elevation Infarction (b) Pulmonary Embolism (c) Brugada Syndrome (d) Lead misplacement (e) Arrhythmogenic Right Ventricular Dysplasia ANSWER
(d) Lead misplacement The ECG shows a RBBB pattern in V1 with inverted T waves in V1-2. The p waves are the key here. The p wave in V1 is inverted and biphasic in V2. This indicates that these two leads are placed too high. A 65 yo male is brought in by ambulance. He has had chest pain for the previous 3 hours. He is diaphoretic and looks unwell. His BP is 71/50 and he is speaking in single words, with saturations of 90% on a non-rebreather. His chest examination has widespread crepitations. He has no relevant past medical history. Hi ECG is shown below:  You diagnose a probable LAD occlusion and that the patient is in cardiogenic shock. Your hospital doesn't have a Cath lab and so you decide to thrombolyse. However, you also need to sort out the cardiac failure and the blood pressure. GTN is not an option to dilate due to the cariogenic shock. You decide on CPAP for the breathing but need to support the blood pressure. What do you use?
Some Important Comments in the LiteratureIs one Pressor better than the other? Perhaps another question to ask is if one pressor, although efficacious in the short term lead to worst outcome? By this I mean, something that may work well right now, but lead to worst outcomes a week or two down the track when the patient is out of the emergency department. The Cochrane Review first published findings in 2016 of Vasopressors in hypotensive shock and said" “We found no evidence of substantial differences in total mortality between several vasopressors. Dopamine increases the risk of arrhythmia compared with norepinephrine and might increase mortality. Otherwise, evidence of any other differences between any of the six vasopressors examined is insufficient.” Cochrane Database of Systematic reviewsTarvasmaki et al, in an observational study in Critical Care (2016) 20:208 found that patients on Adrenaline had a worst survival and an increased 90 day mortality compared to other vasopressors. However the study didn't prove causality and a prospective trial is needed. In a comparison of Dopamine and Noradrenaline in the treatment of shock, De Baker et al (NEJM 2010;362(9):779) found that although not significant, there was a trend towards a higher death rate when Dopamine was used. There were certainly a significant number of adverse events such as arrhythmias, when Dopamine was used. In a sub-group analysis in this same study they found that in cariogenic shock, Noradrenaline was superior to dopamine in terms of reduction in mortality. This was the case of the 65 yo male in CARDIOGENIC SHOCK. The optimal treatment for this patient would have been to start NorAdrenaline and then add Dobutamine, especially as there was no previous history of heart disease. Milrinone may be a substitute in patients with known poor ejection fraction ie., known significant heart failure. The key is to start with Noradrenaline. A quick review of the Medications available
α1 = vascular(arterial) smooth muscle β1 = Heart: Increases rate and force of contraction β2 = Bronchial Smooth muscle dilatation INOPRESSORS: Adrenaline and NorAdrenaline Adrenaline (αβββ) Non-selective adrenergic agonist: acts on α and β receptors. At low doses, acts on β2 receptors causing vasodilation. At higher doses its effect on α1 and β1, resulting in positive inotropy and vasoconstriction( of peripheral vasculature and pulmonary arterial and venous circulation). It is both a chronotrope and an inotrope It's use is mostly in anaphylaxis and cardiac arrest as other drug combinations have been found to be better for both septic and cariogenic shock. NorAdrenaline(αααβ) It acts on vascular α1 adrenergic receptors, causing vasoconstriction and thus increasing systolic and diastolic blood pressures. It has chronotropic and inotropic effects by acting on on cardiac α1 receptors. It can cause tachycardia and increase myocardial oxygen demand. It may also have a direct toxic effect on cardiac cells. It is the first line management of septic shock and may be used with other medications. INODILATORS: Dobutamine and Milrinone Dobutamine (αββ) Dobutamine, a synthetic catecholamine, acts on β1 receptors increasing cardiac contractility. It also has α1 and β1 effects on peripheral vasculature resulting in vasodilatation at lower doses, thus increasing cardiac output. At doses above 5mcg/kg/min it can result in vasoconstriction. It is usually used with an inopressor in cariogenic shock. A meta-analysis, showed Dobutamine to be associated with higher in-hospital mortality and readmission rates for heart failure exacerbation when compared to nesiritide therapy. Higher doses of dobutamine is not preferred in patients with recent myocardial ischemia, as it can increase myocardial oxygen demand and induce tachycardia. Milrinone It is a Phosphodiesterase Type 3 inhibitor(PDE3) used inotropic agent in patients with cardiogenic shock. It inhibits PDE3, which results in more calcium ions entering the myocardial cell, increasing cardiac contractility. It also acts on peripheral and pulmonary vasculature leading to vasodilatation as well as inotropic effect. It does not act on the beta adrenergic pathway. Another feature of the mechanism of action of milrinone is that the same intracellular processes is activated in smooth muscle cells of the peripheral and pulmonary vasculature, leading to a net vasodilatory effect in addition to its positive inotropic effect. In a sub-group analysis of the OPTIME-CHF trial, it was found to increase mortality in patients with heart failure of ischaemic origin. Conclusion: Think about the medications you are using in cardiogenic shock. Start with Noradrenaline and then add to that. In most cases it will be Dobutamine. |
AuthorDr Peter Kas 
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