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It's mid morning in the emergency department. An 81 yo male presents to triage with chest pain. The pain started last evening ie., 14 hours previously and is still present. The pain is described as a pressure pain with some radiation into the jaw area. There is no diaphoresis, no dyspnoea and no distress. There is minimal past medical history. An ECG is done. Take a moment to look at it. QUESTION: What does it show?  ANSWER: There is an INFERIOR infarct. In most cases this is due to a RIGHT CORONARY ARTERY occlusion but in a small number of cases a left circumflex artery occlusion can also cause this. A right coronary occlusion is most likely as when the following are present:
The patient gets ASPIRIN and you prepare to give GTN. QUESTION: Should you give GTN? What ECG should you perform before this?  ANSWER: We know that up to half of all patients with an inferior infarction will develop RIGHT VENTRICULAR infarction. Right Ventricular infarction is associated with a greater than two-fold increase in mortality as well as an increased risk of arrhythmias and high grade AV-nodal blocks. Patients with a right ventricular infarction, are preload dependant ie., if we drop the preload, by giving a dilator such as GTN, they drop their blood pressure significantly. If you do give them GTN without looking at the Right Ventricular leads, they need IV fluid pushed, to improve the preload and they may need inotropes. In a RIGHT VENTRICULAR INFARCTION the following are present on the ECG
ST elevation in RV4 has a 100% sensitivity and an 87% specificity and 92% predictive accuracy in diagnosing right ventricular myocardial Infarction. BEWARE: In up to 50% of patients with a Right Ventricular Infarction the ST Elevation may disappear after about 12 hours. If there is no right ventricular ST elevation, but the patient decompensates following nitrates, suspect it.  Right Ventricular Leads What occurs in Right Ventricular Infarction?Why are patients preload dependant and why do they drop their blood pressure? With a right ventricular infarction, the right ventricle cannot pump properly and the right ventricular volume and end-diastolic pressure of the right ventricle are high. Due to the pump failure, the left ventricle is not receiving a sufficient amount of blood, but now the right ventricle with it's increased volume also displaces the septum towards the left ventricle, decreasing its volume even further.. Anything that decreases preload ie., diuretics nitrates, beta blockers, morphine, can significantly decrease blood pressure. These patient may then require IV fluids and inotropic support. POSTERIOR Myocardial InfarctionUp to 20% of inferior infarctions will present as a posterior infarction. This represents a significantly larger area of infarction. The diagnosis is made by performing a posterior lead ECG ie leads V7-9. Some clues of a posterior infarction on the normal ECG include:
 Posterior Leads There are no posterior changes in leads V7-9 OUTCOMEThe patient was transferred out for catheterisation and diagnosis. A 100% right coronary artery occlusion was stented. QUESTION: Could we have given thrombolytics? Time from symptom onset, is a marker of downstream myocardial damage. Usually late presentations(>12 hours) are referred for percutaneous coronary intervention, although not always. Three studies (references given below) a worth reading here:
My approach is that given that the patient was stable and had presented more than 14 hours following symptom onset, transfer for PCI was appropriate. If there was no cath lab and there would be a significant delay in treatment, I would discuss thrombolysis with the Cardiologist. Rescue plasty could always occur later. All Cardiac Bootcamp Self Study Course Members should review the topic 'Subtle Ischaemic Changes', in the syllabus, especially changes in aVL. How to set up Right Sided and Posterior ECG Leads REFERENCES
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This week I am putting on a 30 minute webinar on The Approach to the patient with Syncope. Date: Thursday July 22nd at 3.00pm (Melbourne Time) Here is the Zoom link: https://us02web.zoom.us/j/87324913445?pwd=VkwwcHhjdHZJd09JT2N3c214RDVKdz09 Before the Webinar Try your hand at these few ECGs.The ECG has a < 5% yield but is still the highest yield of all investigations we can do in the syncope patient. It's importance cannot be understated, as cardiac causes of syncope have the highest mortality and morbidity of all causes. Below are 7 ECGs of patients that present with syncope ECG 1: A 30 yo male presents with his third episode of syncope. He was waiting for a bus and felt a brief episode of palpitations then found himself on the ground. He has no past medical history by states that his father died suddenly of unknown causes. He has had a cardiac workup during a previous presentation, which included monitoring, serial troponins and an echocardiogram, which were all normal. What does the ECG show?  ECG 2A 78 yo male is brought in by ambulance following a fall at home. He has no memory of the incident. He states that he was making a cup of tea, felt dizzy and then found himself on the floor of his kitchen. He couldn't get up and called for help. His wife called the ambulance. What does his ECG show? What probable definitive treatment will he need?  ECG 3A 56 yo male presents with a syncopal episode. He had momentary dizziness, but no shortness of breath or palpitations or chest pain. What does the ECG show and what caused his syncopal episode?  ECG 4A 56 yo woman has presented to the emergency department following a brief syncopal episode. The patient had no chest pain, or palpitations. Following the ECG and serial normal troponins, the patient was discussed with the senior as a possible discharge. The senior wanted cardiology called and an admission. What was missed? What is the diagnosis?  ECG 5A 38 yo greek man is brought in by ambulance as he collapsed, whilst playing soccer. He has no past medical history and has had some previous episodes of palpitations in the past. He is well and wishes to go home. What does the ecg show? What waveform is shown in leads V1 and V2?  ECG 6A 28 yo woman presents with palpitations and a syncopal episode. She is haemodynamically stable and looks well. There has been a history of syncope. What is the diagnosis? What is the treatment, or even more precisely, what medications can't we give?  ECG 7A 32 yo male is brought into the emergency department with a diagnosis of seizures. He has had several small seizures according to his partner. He is on the methadone program. His ecg is shown, what is the diagnosis? Is there a reason related to the ecg that could describe the seizures?  Try all of these. Join the zoom webinar this week. If you can't
A well looking woman in her late twenties presents complaining of palpitations. She has had a past medical history of bigeminy, for which she is on metoprolol and magnesium. She presents complaining of palpitations different to the ones she normally has with her bigeminy. She is well looking, afebrile, with a blood pressure of 142/70 and a normal respiratory rate. A Venous Blood Gas shows a potassium of 3.3mmol/L. Her ECG is as below. What is the Diagnosis and how would you Manage this patient?  ECG INTERPRETATION It is a wide complex tachycardia. The rate is about 1`50bpm and I think I can see 'p' waves in lead I. In a well young person, we might assume it's SVT. Could it be VT? It could be. The patient is young so SVT with aberrancy is probably most likely. However we need to be a little bit careful with that. Ventricular bigeminy can lead to arrhythmias. The patient is stable and looks well, so we have some time to think. IS IT VENTRICULAR TACHYCARDIA? We know that 80% of wide complex tachycardias are Ventricular Tachycardia(1). There are well known rules that we can use. Let's see what happens if we use them. BRUGADA CRITERIA(2) The Brigade Criteria are 92% sensitive and 65% specific, so not perfect. There are 4 parts:
The Vereckei Criteria have similar sensitivity to Brugada. Let's apply Vereckei:
Griffith Criteria having about the same sensitivity, but rule in SVT. It’s all too complex. In the real world cardiologists reviewing these eggs can’t agree. WHAT IF WE ASSUMED IT WAS SVT AND GAVE ADENOSINE? If it's ventricular tachycardia, apart from a particular kind of ventricular tachycardia, then nothing would happen, as Adenosine blocks the AV node and Ventricular tachycardia comes form the Ventricles. You wouldn't harm the patient unless it were an irregular wide rhythm (ie., AF with WPW) We need a simple solution to working this out. We need a solution that you can apply when you’re woken at 2 o’clock in the morning. MY 3 STEP APPROACH
What would I do in this case? Given the patient is stable and looks well, I would try a vagal manoeuvre, either the 'REVERT' technique, or the 'Reverse Vagal Manoeuvre'. If these were not successful, I would advise the patient on the side effects of Adenosine and try Adenosine. If the blood pressure dropped at any point I would prepare for cardioversion, but would give a small dose of Metaraminol, as this sometimes reverts SVT. Always check the POTASSIUM in any arrhythmia A final word about bigeminy. I recently wrote a blog on this topic on resus.com.au titled ‘Is Bigeminy Benign?‘ The bottom line is that we normally don’t need to do anything for these patients, as ectopics are a normal physiological response. HOWEVER:
 What if we had a way to predict PEA/Asystolic Cardiac Arrest, a few minutes before it happened? Would that be helpful?.... Perhaps. PEA and asystolic cardiac arrests have a very poor outcome. The rate of survival in out of hospital arrests is less than 2%. In hospital, survival is higher, at about 30%(1). Having this knowledge may or may not change the outcome, but I think it gives us a significant advantage, at least in our mental preparation. In a recent research paper by Do et al in Resuscitation(2), they identified a right ventricular strain pattern that preceded hypoxic pulseless electrical activity cardiac arrest. STUDY DESIGN: What they did. This was a retrospective cross sectional study at two tertiary care hospitals. They looked at in hospital cardiac arrests due to PEA/Asystole
Right Ventricular strain pattern The most common terminal morphology(67% of cases) was a RBBB in V1, which progressed from an increasing RV delay as shown below:  Definite Right Ventricular strain(RVS) pattern was defined as having the above progressive morphological changes in lead V1 and either no intraventricular conduction delay or terminal intraventricular conduction delay (ie., incomplete RBBB) and two or more of the following occurring simultaneously:
Results
ECG Patterns identified  Conclusion
Next time we are monitoring a patient and see the gradual Right ventricular delay pattern, indicative of right ventricular failure, we should get ready as up to about half of these patients may have a PEA/Asystolic arrest in the next few minutes. REFERENCES
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AuthorDr Peter Kas 
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