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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. 
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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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