Check out this poor patient (ECG)

[FireMedic65]

ah yes... the almighty pulse ox... should be the first tool you use on every patient... it's a true life saver! In fact, I just might start using two, one on each hand of the patient.

[DartmouthDave]

Hello,

I had a patient yesterday (50 y/o female) with a 2 day history of general malaise, nausea, emesis and weakness. Called EMS at 0500. A BLS crew arrived to find her on the floor cover in emesis with her 14 year-old daughter by her side.

As per the PCR she was 'cold' 'pale' 'c/o numb arms' and 'weakness'. Past history of lower back pain (T#3 for pain) and mild HTN (no meds). She stated that when she got up everything 'went black'.

So, the BLS crew makes her walk to the ambulance (VS 90/60 HR 60 Temp 35) and take her to the ED (took 45 minutes). "Eventually got of the ground and walked to the ambulance." Exact quota.

On arrival a 12-lead showed ST elevation in V1 ---> V6. TNK failed and she rapidly developed Cardiogenic Shock and was medeved out for angios.

She was quite unstable (BP 50/30 (Map 45-50) EKG: ugly!). Mixed gas improved form 33% to 58% on the pressor we had. Now, what I do not get is the flight crew started Vasopressin.

Has anybody seen Vassopressin for Cardiogenic shock before???

[chbare]

Anecdotally, vasopressin would not be my agent of choice for cardiogenic shock. Then again, we are in essence robbing Peter to pay Paul when it comes to using any kind of adrenergic agent (I say vaso is adrenergic in a way; however, vaso effects are not via adrenergic receptors. Therefore, you can call me out on my statement.) in the setting of cardiogenic shock. Vasopressin is a great agent for refractory forms of distribution types of shock. Mainly because vasopression has it's own V1 & V2 receptors separate from adrenergic receptors. This is quite handy in the setting of a patient with down regulation of adrenergic receptors. The typical example being a septic patient on long term vasopressor therapy. Hence the reason some people advocate for stopping vasopressor drips on septic patients for a period of time. You may have herd the term "pressor holiday."

I digress however. Unfortunately, you are screwed regardless in the setting of cardiogenic shock. This is especially true with LV impairment. Your patient most likely lost a significant portion of their LV given the localization of the ECG changes. Not much "medically" will really help this patient. You can increase SVR or try to increase contractility with pressors; however, a dead LV is still not going to work. Was an IAPB placed? This would be a potentially viable option.

I assume a PAC/Swan was placed given your mixed gas comment? What other vales did you note (PAP, CI)?

Take care,

chbare.

[FireMedic65]

Once again a very informative post chbare. It's always a pleasure to read what you have to say

[DartmouthDave]

Hello,

I have only seen Vasso used in distributive shock and a second or third agent when things are going poorly. This is why I was perplexed by their choice of Vassopressin.

Here is some more information.

This patient had a bad metabolic acidosis due to pump failure (pH 7.1 BE -12) mixed gas of %33 and a lactate of 7.0. After some fluid and pressors we had the ABG looking better (pH 7.3 BE -10) and a mixed gas of 55% and a lactate of 5.0.

Mind you, this took awhile. We had her on Levophed of 20 mcg/min and Dopamine of 20 mcg/kg/mim and some Dobutamine 15 mcg/kg/min).

We did not have a Swan. We used the Edwards FloTrac. It connects to an arterial line and gives you much the same information that a Swan will. So, we had her in an ok position. What she needs was an angio and an IABP.

She looked grave but she was the best she could be all things considered. So, I was wondering why they hung Vasopressin at 0.03 and cranked up the pressores (Levophed 50/Dop 30/Dobutamine 30...and some IV Phenylephrine)

I followed up with the receiving hospital. Her LV was 'fried' and got numerous stents and a LVAD (Left Ventricular Assist Device...something I know very little about).

Cheers

[chbare]

I am hesitant to call somebody out on choice of pressors in such a grave situation. It sounds like your interventions helped and even cleared some of her lactate. You at least improved tissue bed perfusion and oxygenation. The LVAD and BIVAD approach is becoming quite popular. So popular in my area, I had to attend a conference on the Heartmate II and interact with a person who had this device implanted. Many people are going home on destination therapy with these devices. I know Mayo in Phoenix is very progressive with their VAD program. (closest VAD program in my area) All things considered, it sounds like the patient may have a chance.

Take care,

chbare.

[VentMedic]

We did not have a Swan. We used the Edwards FloTrac. It connects to an arterial line and gives you much the same information that a Swan will.

We are still trialing the Edwards FloTrac as it only provides calculated values off the A-line and not measured. In that respect it doesn't compare to a PA Catheter (formerly known as the Swan-Ganz). There are also some considerations for patients with other existing cardiac impairment. However, the trending data for the calculated CO can be very helpful when other lines are not available and the A-line is easier to place than a central line of some type.

When choosing the pressors for either sepsis or cardiac failure, we have to also see the degree of renal failure. The pressor vacation may not always be an option although we might try to rotate for varied receptor response. But then we tend to favor norepinephrine for its alpha and beta-adrenergic actions. CVVH capability should also be available along with the cardiac assist devices. For sepsis we can usually manage with the numbers from an RA line (central venous line) to titrate fluids, pressors and ventilator management from the SvO2.

When called to transport a patient from a local little general hospital, after viewing the patient's lab and hemodynamic/renal response to the treatment we may find the patient is headed down a path that will be out of the abilities of the initial destination. Just being a hospital with a cath lab may not be enough. We may request to divert to a facility that has more capabilities. These patients are a challenge to any IFT, either ground or flight, if the first hospital has limited capabilities. There are few things more frustrating than seeing a really sick patient get transported multiple times insearch of the right hospital or because of limited transport alternatives.

Edited September 6, 2009 by VentMedic

[DartmouthDave]

Hello,

I hope that my post did not sound judgmental. In reality, I was only irked by the BLS crew walking the patient to the ambulance and treating her as a nuisance call.

I did a quick literature search last night at work and I found a 2005 study in the American Journal of Chest Physicians that had the following conclusions;

"The use of vasopressin in CS caused, in this case series, an average increase in CI of 27.8 % and an average increase in urine output of 45.7% within the first 12 hours compared to baseline. CI decreased only when higher doses of vasopressin were used (in the range of 0.08 to 0.5 U/min)"

It also noted that Vasopressin benefits diminished after 24-48 hours.

So, considering her CO/CI wasn't the best and she had no urine output....it makes scenes.

We do have Swans. But, nobody was available to float it in. So, in a pinch the FloTrac is a nice piece of equipment. It was an interesting patient. CS is tricky.

Cheers