1. Move the Laryngeal Prominence (Adam's Apple) around with your free hand until your view is optimized
2. Have an assistant hold it there while you pass the tube
It’s amazing how much this can improve your view!
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The reason External Laryngeal Manipulation (ELM) is so effective is that it allows real-time visual feedback to the intubator who finds the precise direction and force required on the thyroid cartilage to optimize their laryngeal view!
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ELM not only provides enhanced laryngeal visualization, but it also brings the larynx into a more posterior position, effectively flattening the angle of the secondary curve, and decreasing the angle the endotracheal tube must travel. This makes it easier to pass the tube!
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ELM has evolved from the original technique known as “BURP”, which was introduced in the early 1990’s. BURP stands for Backwards, Rightwards, Upward, Pressure. This technique called for an assistant to blindly manipulate the thyroid cartilage in the above directions.
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The problem with BURP is that the direction and force that will optimize an intubator's view is dependent on many factors and is highly variable! So while BURP *may* improve your laryngeal view, there is also a good chance that it will worsen it!
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Ok let’s talk Cricoid Pressure. It was first described in 1961 by a British Anesthesiologist, Brian Sellick (AKA Sellick Maneuver). This theoretical technique hoped to “decrease aspiration” by pinning the esophagus between the Cricoid Cartilage and a cervical vertebral body.
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It's important to understand that Cricoid Pressure is NOT a maneuver intended to improve the intubator's view. In fact, not only have studies failed to show it’s efficacy in decreasing aspiration, but there is actually evidence that it is likely to *worsen* laryngeal view!
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So in summary use External Laryngeal Manipulation (ELM) during endotracheal intubation. It’s a much more sophisticated version of BURP that can greatly improve your laryngeal view and facilitate tube delivery. And one more thing: Cricoid Pressure is all but dead!
Here’s a great #Echo of a young lady who suddenly collapsed to the ground in Cardiac Arrest. Bystander CPR was performed and 911 was called. Paramedics shock her once for pulseless VT and get ROSC on the scene. She’s intubated, in shock, on an Epi drip.
What’s the diagnosis?
The RV is very dilated with poor systolic function. The RA is also very big. The LV is Hyperdynamic with no obvious wall motion abnormality. This appearance of Severe Right Heart Strain is common during arrest, but when it persists AFTER ROSC, you must think Massive PE!
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But the other caveat is that this Right Heart Strain could also be the result of *chronic* pulmonary hypertension.
So here’s what we did: We placed an Arterial Line & added a Norepi drip. We notified the CT techs that she needed to be next in line for an Emergent CTPA...
A 17-year-old boy was rushed to the ER by his brothers struggling to breathe...
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He was in profound respiratory distress with deep retractions breathing 40 times per minute. It turns out he was a severe asthmatic in the midst of the worst asthma attack of his young life.
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He was cyanotic and barely moving any air. His Pulse Ox registered 30% with a perfect waveform. His eyes rolled back and he lost consciousness right in front of us. He was on the brink of death...
A lot people have asked about the physiologic explanation for why the Modified Valsalva Maneuver works. I’m gonna do my best to explain it as I understand it.
Let’s start by taking a look at the body’s physiologic response to valsalva...
Narcan is the opioid antidote. It works by blocking the effects of these drugs at the receptors. So when you give it to people who have overdosed, they will typically wake up and resume breathing...
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All commercial ✈️ should carry Narcan, but if you are ever in a situation where someone has overdosed and you don’t have Narcan, you can still save their life!
I recently had a patient who presented in profound acute renal failure with a BUN of >200, creatinine of 13.5, and critical pH of 6.7, on the brink of death...
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The only reason he was still alive is because he still had a strong enough respiratory drive to blow his CO2 down to almost nothing!
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When patients go into profound metabolic acidosis, their blood bicarbonate (a base) vanishes and they compensate by blowing off CO2 (an acid).