Tag Archives: Pulmonary Embolus

Dead Space Postscript

post·script

1 – an extra piece of information about an event that is added after it has happened

The patient in question did in fact have a massive pulmonary embolus known as a Saddle PE. Because the embolus lodged in the pulmonary artery at the bifurcation between the left and right branch, much of his lung capacity was not actively engaging in gas exchange. He was not able to offload the EtCO2 or fully oxygenate the blood. His altered state was actually a hypoxic event even though his lungs were clear and had perfect tidal volume. The EtCO2 reading was the only finding, other than skin signs and oxygen hunger, that pointed me in the right direction.

Upon turning him over to the MD at the ED I concluded my report with my findings and a differential diagnosis of PE. This bought me a raised eyebrow from the MD as a PE is a very difficult thing to diagnose without the help of a CT. That same MD seemed a little more on board with my findings when the patient flat lined ten minutes later and subsequently three more times before they pushed thrombolytics to dissolve the clot.

Later that night he was moved to the ICU and extubated the next day. He recovered with no lasting deficits yet he remained in the hospital for two more weeks as they continued to administer blood thinners and observe for any reoccurring emboli.

The bifurcation of the cherry tree is a beautiful analog for the inner vasculature of the lungs. Nutrients are carried along the trunk to the blossoms where gas exchange occurs and photosynthesis creates energy that is then carried back along the trunk. When a branch is injured the blossoms die and create a dead space. The cherry tree has the advantage of many bifurcated branches to continue the cycle – we only have one.

Dead Space

A decrease in perfusion relative to ventilation (as occurs in pulmonary embolism, for example) is an example of increased dead space.[3] Dead space is a space at which gas exchange does not take place, such as the trachea. It is ventilation without perfusion.

Saddle Pulmonary Embolus

A large thrombus lodged at an arterial bifurcation, where blood flows from a large-bore vessel to a smaller one. The ‘classic’ saddle embolus—which occurs at the bifurcation of the pulmonary arteries in fatal pulmonary embolism secondary to a centrally migrating venous embolus—is distinctly uncommon.

Segen’s Medical Dictionary. © 2011

Massive pulmonary embolism

As a cause of sudden death, massive pulmonary embolism is second only to sudden cardiac death. Massive pulmonary embolism is defined as presenting with a systolic arterial pressure less than 90 mm Hg. The mortality for patients with massive pulmonary embolism is between 30% and 60%, depending on the study cited. Autopsy studies of patients who died unexpectedly in a hospital setting have shown approximately 80% of these patients died from massive pulmonary embolism.

The majority of deaths from massive pulmonary embolism occur in the first 1-2 hours of care, so it is important for the initial treating physician to have a systemized, aggressive evaluation and treatment plan for patients presenting with pulmonary embolism.

 

 

Dead Space

dead

1 – having lost life, no longer alive

2 – having the physical appearance of death; a dead pallor

3 – not circulating or running; stagnant: dead water; dead air

 

space

1 – the infinite extension of the three-dimensional region in which all matter exists

2 – an empty area which is available to be used

dead space – a calculated expression of the anatomical dead space plus whatever degree of overventilation or underperfusion is present; it is alleged to reflect the relationship of ventilation to pulmonary capillary perfusion

Walking back into the ED room to get a signature from the nurse I’m momentarily surprised at the level of commotion surrounding the man that was my patient just a few minutes ago. I look up to the overhead monitor that displays his vitals and see the obvious cause for excitement – asystole, the most stable heart rhythm in the world, is marching across the screen and slowly erasing the beautiful complexes of normal heart beats as it fills the screen with the flat line of death. The Paramedic Intern pulls a short step stool out from the corner just as the attending MD makes the call for him to begin CPR. Well, I guess my differential diagnosis was correct, small comfort considering he’s dead now.

There’s a question in paramedicine that is useful to the Paramedic in deciding a course of action on any given call – is this person big sick or little sick? The speed at which we can determine the acuity level of any given patient helps us in determining how fast we move through the call. On occasion the first look at a patient can tell you everything you need to know in terms of acuity. As I walked into the bedroom I could see that this is one of those times. My new patient looked up at me from the bed and it’s obvious that this is big sick and I’ll be moving fast today.

The firefighters arrived just a few seconds before us so they’re still attaching the monitor  leads and trying to get a blood pressure. I know what they’ll find based on the patient’s skin signs alone. The term – pale/cool/diaphoretic – gets overused in our business but it still surprises me when I see these skin signs manifest on a patient. A man of his ethnic background would be hard pressed to look pale so the fact that he looks ashen tells me all I need to know. My first thoughts on a call like this are about extrication. I want to get this guy out of here, into my ambulance, and start driving. Everything else can be figured out on the way to the hospital but the main priority is getting him from the bedroom to the ambulance. The problem is that he’s over two hundred pounds and there are three flights of stairs between me and my ambulance.

I send my partner back to the rig for a stair chair as I start to take in the vital signs and patient history to see if I can paint a picture of the last few hours that led to this big sick presentation. It seems that he and his wife were out running some errands and he started feeling sick about an hour ago. He vomited once and now he’s presenting with an altered mental status, very low blood pressure (72/48), fast heart rate (118 bpm), clear lung sounds, and skin signs that are screaming “heart attack” at me. Of course that was until I ran the 12-lead for the second and third time. The results keep showing nothing even remotely concerning in the cardiac department. In his altered state the only intelligible uttering I can make out from him is, “I…can’t…breathe…”

I put a non-rebreather oxygen mask on him and start the trek of three flights of stairs to the ground floor and the relative comfort of my ambulance where I can start to figure this thing out. The new stair chairs with the revolving treads make quick work of the stairs while preserving our backs in the process. It seems we’re on the ground floor in just a minute or two and headed towards the ambulance.

Finally inside the ambulance, I have decent light and all of my tools at hand so I can try to analyze his condition while driving to the closest hospital. I’ve already ruled out the possibility of a STEMI (S-T elevation myocardial infarction – a.k.a. heart attack), which would require a cath-lab, so I am free to head to the nearest hospital. As I check his 12-lead a fourth time – on the right side this time, still looking for the elusive STEMI – the firefighters decide it’s a good opportunity to leave. Figures. Looks like I’m on my own on this one.

With lights flashing and the siren singing a duet with the air horn I bounce down the road while starting two IVs in my quickly fading patient. Once that’s done I set up two bags of warm saline flowing wide open to drop as much fluid on him as possible and try to keep that blood pressure out of the double digits.

I slip the non-rebreather off of his face and put on a nasal cannula that has a receptacle for reading the exhaled breath and measuring the end tidal carbon dioxide (EtCO2). I actually do a double take as the reading comes back as 8 when the normal reading should be between 35 and 45. Hell, I’ve stopped CPR and pronounced people dead with higher EtCO2 readings!

A number this low just doesn’t make sense. I listen to lung sounds again and they are still coming up clear. I check his blood sugar to rule out a DKA (diabetic ketoacidosis)  presentation and it comes up perfect. Sepsis could possibly take the reading this low and explain the presentation but not with an onset of just one hour. There’s only one other differential diagnosis that is making sense to me right now and when that flashes into my head I’m more relieved than I can admit to see the bright lights of the ED out of the back window as my partner backs us into a spot by the double doors and I prepare to give my findings to  the doctors on the other side.

In these days when science is clearly in the saddle and when our knowledge of disease is advancing at a breathless pace, we are apt to forget that not all can ride and that he also serves who waits and who applies what the horseman discovers. 

Dr. Harvey Cushing