Smells like team spirit

In times of crises, certain traits are desirable and some, admirable. One of those is situational awareness. What is most desired is knowing your limits and calling for help.

A competent registrar notified me of an impeding airway disaster:

  • Semi conscious patient in respiratory distress
  • Oro-pharyngeal tumour (undergoing chemo)
  • Bleeding acutely from unknown site in oropharynx or lower
  • Shocked clinically
  • The best description I can give to those who understand is "peri-arrest".
Here's the really good news though:
  • A RSI checklist had been commenced prior to my arrival
  • The airway team had been called
  • Nursing staff were ensuring all the items on afore-mentioned checklist were prepped
  • Tranexamic acid given
  • Cric kit was opened and location marked (as best we could due to oedema)
The inevitable happened and the soon GCS deteriorated as did BP. Subsequently, this followed:
  • Ketamine 
  • Unmatched blood as soon as we got it
  • Peripheral pressors 
  • Paralysis and attempt by Anesthetist
  • Continuous suctioning of blood with no view of cords
  • Bougie assisted intubation with no desats and good CO2 trace
  • Good post intubation care
The whole hospital team successfully oxygenated and ventilated this patient. I did practically nothing. Which is why I am elated. This was a triumph for systemic preparation & team sport...

... but it all started with a keen-eyed doctor with the sense to know they couldn't do it all by themselves. 


Does video make for little airway stars?

Originally posted on The Collective:

Most of us are always out for new techniques to make difficult cases easier. Videolaryngoscopy is one area of great change over the last decade. Here Andrew Weatherall looks at videolaryngoscopy as it relates to looking after the little kidlet airway. 

Seeing is believing. It can happen in a moment in sport. It’s the whole basis of magicians plying their trade.  Even people seeing mysterious circles appearing in crops want to believe.

Perhaps that impulse is why everyone wants to believe in videolaryngoscopy. And it makes sense. It’s persuasive. The view is better than your eyes alone. It must be better.

And yet … the evidence doesn’t help us back up our gut reaction. So the debate starts. It’s a pretty big debate too. Too big for here.

So let’s just talk about one bit. Let’s see where videolaryngoscopy fits in with kids.

Open Bias

I should declare an interest here. I like videolaryngoscopy. I…

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Sudden Severe SOB and ST Segment Elevation: What is the Diagnosis and Treatment?

A middle aged man with history of MI presented by EMS for the sudden onset of difficulty breathing. 

Prehospital, he was in respiratory distress and tachypneic, and was tachycardic to 130.  SpO­­­­­­­­2 was 85% on high flow oxygen.  Prehospital ECG (not available) was read as  ***ACUTE MI***  and the cath lab was activated by EMS.  

He was agitated upon arrival.  Lung exam revealed good air movement but no rales or wheezes (clear).  [Think: what does this mean?]  Heart rate was 140 bpm.  Extremities were cool. His left leg was mildly swollen compared to the right.  He was in severe shock.

The patient was intubated immediately upon arrival.  The end-tidal CO2 was low (~18 mm Hg).

The physician requested tPA to be prepared due to concern that this represented a massive PE.  It was withheld pending confirmation of the diagnosis and partially due to the uncertainty about whether he could go to the cath lab for STEMI if he received tPA. 

An ECG was recorded while a bedside ultrasound was also done:
There is sinus tachycardia.  There is inferior ST elevation with reciprocal ST depression in aVL and  in lead I, very suggestive of STEMI.  There is RV conduction delay (R'-wave in V1) with ST elevation in V1-V3 that is not suggestive of STEMI.  
Another possibility to consider is inferior and RV MI (STE in V1), with acute severe right sided failure.

Thus, the initial EKG was concerning for STEMI.

The bedside cardiac ultrasound was revealing: 

There is LV hypertrophy and a low volume LV with adequate systolic function.  The RV is hypokinetic and dilated (high volume RV).

The providers were concerned that the generous RV in the setting of respiratory distress, hypoxia, tachycardia, and unilateral leg swelling was very concerning for PE, but they felt that it did not fully explain the EKG findings.

Here is a view of the inferior vena cava:

It is dilated.  This is very suggestive of high right sided pressures.  But that by itself does not help in the diagnosis, because shock from both LV STEMI and PE would increase right sided pressures.

There was a discussion about whether this represented PE or STEMI. Treatment options were considered including TPA or cath lab activation. A second EKG was recorded:

Comment: What is going on?

Salient facts: The patient had sudden SOB with severe hypoxia and shock, but with clear lungs.  Ultrasound further confirmed this with absence of B-lines (not recorded).

Furthermore, a low end tidal CO2, though also associated with cardiac arrest, is common in patients with massive pulmonary embolism.  Because the lungs are ventilated but not perfused, the CO2 cannot be excreted through the airways and the etCO2 is low.

One might be tempted to attribute right sided failure to inferior MI with right ventricular MI and RV failure, but RV failure from RV MI does not cause hypoxia.

Acute STEMI only causes hypoxia if it results in pulmonary edema.  This patient had clear lungs.  When patients have severe pulmonary edema, the gas exchange is poor, and areas of the lung that are ventilated are OVER-perfused (causing pulmonary edema) and the end tidal CO2 (and arterial and venous pCO2) are high because the alveoli are filled with fluid.

A chest X-ray, taken 5 minutes after the ECG was recorded, confirmed clear lungs:
There is no pulmonary edema

Acute hypoxia with clear lungs and clear chest X-ray is pulmonary embolism until proven otherwise!

But another ECG showed even larger STEMI:
Sinus tach with PACs.  Now there is additional ST elevation in lateral leads, also diagnostic of STEMI.

STEMI on an ECG only tells you there is transmural ischemia.  The STE does not tell you the etiology.

In other words, the ECG may diagnose ischemia; it does not diagnose ACS.  

Rather, in less than 5% of STEMI cases, the ischemic ST elevation is caused by severe demand ischemia such as that caused by massive pulmonary embolism. 

The ECG findings were more pronounced now with ST elevation in II, III, aVF, and V4-V6. The cath lab activation was confirmed.

The patient became bradycardic and hypotensive.  tPA was given.

Another echo was done:

There is now worsening function of both ventricles.

There was no response to norepinephrine infusion nor to external pacing. He soon became pulseless and compressions were started. The resuscitation was continued for a prolonged period but the patient remained in PEA and never achieved ROSC. No autopsy was performed.

Learning Points:
1. Hypoxia with clear lungs is pulmonary embolism until proven otherwise (see other etiologies below)
2. STEMI only causes hypoxia by causing pulmonary edema
3. Massive Pulmonary Embolism can result in a STEMI ECG, identical to ACS STEMI.  (I have seen this numerous times but this is the first time I've posted one)
4. Low end tidal CO2 is typical of massive PE.  High end tidal CO2 is typical of severe pulmonary edema.
5. Shock from STEMI has unmistakably poor LV function and on bedside echo
6. RV failure from RV MI does not cause hypoxia.
7. Perhaps most important: if the differential is STEMI vs. massive PE, just give the tPA, front loaded (100 mg).  There is no contraindication to angiography and PCI for a patient who has received thrombolytics and remains in shock.  In fact, it is the therapy that is recommended therapy for patients who are in shock and need to be transferred to a PCI capable institution.

(Certainly if you know without doubt that STEMI is the diagnosis, then do not give tPA if you are at a PCI capable institution and rapid PCI can be done.)

Hypoxia with clear chest X-ray
1. Pulmonary Embolism.
2. Asthma
3. Hypoventilation (high pCO2)
4. Sepsis (pulmonary vasodilation and shunting)
5. Anatomic right to left shunt (VSD etc.)
6. Vasodilators such as nitroprusside (cause pulmonary vasodilation and shunting)

2013 STEMI Guidelines.  JACC 61(4):p. e97

5.3. Transfer to a PCI-Capable Hospital After Fibrinolytic Therapy

5.3.1. Transfer of Patients With STEMI to a PCI-Capable Hospital for Coronary Angiography After Fibrinolytic Therapy: Recommendations.  

1. Immediate transfer to a PCI-capable hospital for coronary angiography is recommended for suitable patients with STEMI who develop cardiogenic shock or acute severe HF, irrespective of the time delay from MI onset (354). (Level of Evidence: B)

Also in this section:

Angiography and PCI may be done also for:

2.  Patients with STEMI who receive thrombolytics at an outside hosptial and do not have reperfusion (as determined by EKG) should go immediately for PCI.

3.  Patients who have successful reperfusion with thrombolytics should wait 2-3 hours for their PCI.

Episode 33 – Hemoptysis

(ITUNES OR Listen Here) The Free Open Access Medical Education (FOAM) Dr. Ryan Radecki of Emergency Medicine Literature of Note reviews Gestational Age D-Dimers covering an article by Murphy and colleagues in BJOG.   The paper: The authors took blood samples from 760 healthy pregnant patients at one point during their pregnancy. They propose a continuous increase for […]