Reminder to myself: When I purchased Dr. Weingart’s awesome Resuscitation Crisis Manual, I received a PDF copy which I placed on my smart phone. Be sure to review the Massive Pulmonary Embolus checklist in the Manual.
So first I more or less transcribed Dr. Swaminathan’s talk. Doing this helps me fix the information in my mind. And Dr. Swaminathan’s explanations of his clinical reasoning is as valuable as the show notes.
Massive pulmonary embolus is defined as a PE with hemodynamic compromise or signs of end organ malperfusion.
This is the severe end of the PE spectrum where seconds and minutes matter and we have to make rapid decisions.
[In this case a 73 year old man arrives by EMS from a rehab facility] who was at that facility after a trimalleolar ankle fracture-dislocation and had a repair done.
He syncoped on transfer from bed to chair and when he came to he complained of shortness of breath.
EMS reports from the field that he is hypotensive and tachycardic with a lot 02 sat.
And on arrival he’s got vital signs with a heart rate of 153; a BP of 80/43; oxygen sat is 94% on a non-rebreather and a respiratory rate of 32.
He’s pale and he is clearly working hard to breathe.
When I take the non-re-breather off his sats drop to 73% and he feels like he is going to die.
And both in retrospect and at the time this case seemed really straight forward.
No real diagnostic dilemma here: Massive PE. That is clearly what’s going on and that means lytics.
But pulling the trigger on lytics without backup from imaging can sometimes be hard.
It’s nice to do some bedside stuff to further convince yourself that that is what you are dealing with and then pull that trigger.
On exam, the patients lungs were clear and this really narrowed the diagnosis down.
There are only a couple of things that cause shortness of breath or low 02 sats with clear lungs.
That list to me is:
- Pericardial tamponade
- Metabolic acidosis from things like aspirin overdose and DKA
- Pulmonary hypertension
- and, of course, PE
Now you can also throw pneumothorax in the mix because maybe it’s too loud [in the environment] or you’re getting transmitted breath sounds. And some people say that carbon monoxide can have that similar appearance.
This patient looks far to sick to go to CT at this point and so a quick ultrasound can help us parse some of these things out if we’re not sure.
We did a RUSH exam* and there was no pericardial effusion so pericardial effusion is out.
*Link is to The RUSH Exam 2012: Rapid Ultrasound in Shock in the Evaluation of the Critically Ill Patient
There is good lung sliding so pneumothorax is out.
There is no free fluid in the abdomen so blood loss is unlikely.
And when we looked at the heart again, we saw clear signs of RV strain and the RV was larger than the LV.
A quick ECG shows sinus tach with right heart strain* so MI was less likely as well.
* Link is to A crashing patient with an abnormal ECG that you must recognize. Written by Pendell Meyers, with edits from Steve Smith from Dr. Smith’s ECG Blog.
All of this information can be gathered in a short amount of time. It took us four maybe five minutes to get all this stuff done.
And with all this information behind us, I was pretty sure we were dealing with a massive PE if I wasn’t 100% sure before.
The American College of Chest Physicians, ACEP, AHA, and the European Society of Cardiology all recommend giving systemic lytics to massive pulmonary embolism.
It is nice to have a consensus.
Dr. Swaminthan then discusses what dose of thrombolytic should be given and he reviews some points to consider. [3:46 – 4:12]. The right dose is not as clear.
Let’s go back to our patient.
We held fluids in this patient even though he was hypotensive because we know that IV fluids can worsen the RV distention and that can lead to worsening left ventricular outflow tract obstruction leading to worsening hypotension.
Instead we started the patient on norepinephrine to get a reasonable blood pressure.*
*The chapter on Massive Pulmonary Embolism from the Resuscitation Manual gives the following suggestions:
For a norepinephrine infusion, use hospital protocol or start with 4 mg in 50 mL at 5 mL/hr (scale up for 100 mL or 250 mL dilutions).
Doses of medications for stabilization
- norepinephrine 1-30 mcg/min (may increase to 1 mcg/kg/min with caution)
- inotropic epinephrine 0.01-0.08 mcg/kg/min
- dobutamine 1-20 mcg/kg/min
- nitric oxide 10-40 ppm
Returning now to Dr. Swaminathan’s talk:
This patient was healthy except for a bit of hypertension but clearly on the older side.
So we decided to go with the smaller dose, the 50 mg of alteplase over about an hour.
As we were giving the thrombolytic I remembered that Josh Farkas had a nice discussion about targeted lysis in pulmonary embolism.*
*PulmCrit: Controlled Thrombolysis of Submassive PE
And he recommended getting a fibrinogen level. You can use this to predict the risk of hemorrhage as well as guiding our subsequent administration of heparin.
The patient’s fibrinogen was just over 100 which is a bit on the lower side. And we communicated that information to our ICU team and held heparin at that point.
We should not be giving heparin and the thrombolytics together. It is just a matter of when to start the heparin. [See Dr. Farkas post above if you’re interested in reading more on this point.]
Over the next hour the patient appeared more stable. They appeared less tachypneic and so we went to CT for confirmation and then up to the Unit.
The patient did great. He got discharged back to rehap about a week later. And at that time they were back to baseline function.
[Dr. Swaminatham briefly discusses the use of catheter based thrombolytics (5:30 – 6:06). The interventional radiologists the doctor discussed this case with all agreed that this patient was too sick (the peri-hemodynamic collapse sick) for interventional radiology (IR). Give the systemic lytic therapy if you think the patient can tolerate them and then when the patient is more stable then call in IR to consider those catheter based lytics.]
What follows next are the show notes from Dr. Swaminatham’s portion of EM Quick Hits 1:
Priorities in massive pulmonary embolism management
- Massive PE is a true life threat. These patients will die and will die quickly if you don’t act; so get moving.
- You don’t need a CT to pull the trigger on treatment – think about what else could cause the clinical scenario and master POCUS to quickly eliminate these causes and gain supporting evidence of PE (see Rob Simard’s video POCUS Cases 1 – POCUS for PE) [Note to myself: Dr Simard’s video is awesome–when I review this post I need to also watch the video.]
- If the patient has PE with hemodynamic compromise or collapse, consider thrombolytics but don’t forget the other things; start a vasopressor for hemodynamic support and avoid fluids whenever possible.
- We don’t know the right dose of lytics so tailor to the patient in front of you. If the patient is in cardiac arrest, use 50mg alteplase or tenecteplase as an initial dose.
The resources below are from the EM Quick Hits 1 Massive Pulmonary Embolus show notes.
REBEL EM: The Critical Pulmonary Embolism Patient
PulmCrit: Controlled Thrombolysis of Submassive PE
Wan S et al. Thrombolysis compared with heparin for the initial treatment of pulmonary embolism: a meta-analysis of the randomized controlled trials. Circulation 2004; 110(6): 744-9.
Wang C et al. Efficacy and safety of low dose recombinant tissue-type plasminogen activator for the treatment of acute pulmonary thromboembolism: a randomized, multi center, controlled trial. Chest 2010; 137(2): 254-62.