Medical Senerio IV

[Sdiver]

Originally Posted by swatsurgeon

Beck's triad is related to cardiac tamponade, not PTX
Tension PTX may reveal distended neck veins, hypotension but not muffled heard sounds.......

Aw crap, that's right. Thanks for setting me straight.
Pounding my NVTS now Sir/Doc.

[Trapper John]

Originally Posted by Sdiver

Aw crap, that's right. Thanks for setting me straight.
Pounding my NVTS now Sir/Doc.

Does this mean I can give you the nipple ring.

[docholiday161]

I know that I am chiming in a little on the late side. With both the JVD, distal edema, and the crackles at the bases; I am driven toward a cardiogenic shock secondary to CHF. Pt is obviously not perfusing but HR is not bad.

1. 15 LPM via NRB to increase SpO2. I see this as being low due to the pulmonary edema. NRB should bring the 92 to at least 97.

2. The ECG to me looks as if he is throwing multiple PVCs or wide-complex tachycardia with pulse. Pt could crash at any minute due to the irritation of the cardiac muscle.

3. Major concern for me is to increase his pressure without increasing the workload on the heart so that he can start perfusing. For this I would probably start with two large bore NS (both so a fluid challenge can be done as well as have access for follow on meds). Because of the peripheral and pulmonary edema, the pt is intravascularly dry. Meds would be Levophed 8-12 mcg/min and titrate to maintain B/P or possibly Dobutamine.

4. Also consider a Foley to have better monitoring of I/O because once his kidneys start perfusing by increasing his B/P, he should start dumping some of the fluid from his edema.

5. As for the transport decision, I like the idea of trasporting by ground to a higher EOC that could further stabilize while air assets are getting spun up.

[Sdiver]

Okay guys, I'm gonna close this one out and wrap up a few points.
Here's the diagnosis and treatment plan for this Pt.

This Pt. is having an Inferior wall MI as seen in Leads II, III and aVF, with reciprocal changes on the Lateral side as noted in Leads I, aVF and V6). This patient is in cardiogenic shock because the right ventricle has been taken out and there is no forward movement of blood through the heart. These patients are preload dependent due to Starling's Law of the heart.

-- This patient is lacking preload due to the inferior MI and his exam is consistent with RIGHT sided heart failure (JVD and swollen ankles) that is often seen in inferior MIs. He has trace crackles in his lungs, but this should not be a distractor. He needs fluids and lots of them, place on NS or Lactated ringers on a pressure infuser. This is due to Starling's Law of the heart which states that the strength of the heart's systolic contraction is directly proportional to its diastolic expansion. More fluids = more preload = more contractility = less failure.

-- This patient needs a pressor as well as he is showing signs of severe hypoperfusion. Levophed (norepinephrine) is currently the preferred pressor in all cases of hypoperfusion / shock, however not all agencies have this. Dopamine is a good alternative if that is the pressor available to you. You must improve this patient's perfusion, his heart is dying from the MI and the lack of coronary artery perfusion pressure is not helping.
http://www.nejm.org/doi/full/10.1056/NEJMoa0907118

-- Do you employ air transport? It depends on the resources the helo will bring. If the helo has a higher level of care (i.e. RN / MD or pressors like levo / anticoagulants like heparin) then this might be a good option. But remember that CPR in a helo is not an easy task. If your ground ambulance has reasonable resources, rapid ground treatment may be just as efficacious.

-- Alternatively, there is a community hospital nearby. Certainly the patient could be stabilized there, given TPA or TNK, or started on pressors and rapidly flown after it is clear that maximal therapy has been initiated to decrease the risk of in-flight cardiac arrest.

-- If pressors are to be given, IO is the best route as IO is considered equivalent to a central line.

-- O2 .... His O2 sats are at 92% on 4L via NC, would a NRB at 15L do anything for him? I've always been a big proponent for higher O2 delivery (it's due to the diver in me) but with this talk of free radicals, keeping his sats right at 92% is fine. But that doesn't mean you should completely r/o higher O2 with the type of fluids given. NS doesn't have the same O2 carrying capacity as plasma or RBCs have, so keep that in the back of your noodle.

-- Also, if this Pt. "crashes" prepare to intubate and BVM with high flow O2.


Thanks for playing, we'll have nice parting gifts for you as you leave.

**Trapper ... I'll take that nipple ring off your hands due to my above boneheaded comment, which was caught by SS.

[Trapper John]

Originally Posted by Sdiver

**Trapper ... I'll take that nipple ring off your hands due to my above boneheaded comment, which was caught by SS.

Yeee Haw! But I have a feeling I will be earning that back in the near future.

[docholiday161]

Thanks SDiver. Made me start thinking again and realizing just how rusty my reading leads is.

[Patriot007]

Originally Posted by Sdiver

-- This patient is lacking preload due to the inferior MI and his exam is consistent with RIGHT sided heart failure (JVD and swollen ankles) that is often seen in inferior MIs. He has trace crackles in his lungs, but this should not be a distractor. He needs fluids and lots of them, place on NS or Lactated ringers on a pressure infuser. This is due to Starling's Law of the heart which states that the strength of the heart's systolic contraction is directly proportional to its diastolic expansion. More fluids = more preload = more contractility = less failure.

-

With all due respect as this is your thread I disagree with the above. You are correct about Starling's Law/Curve, but it is just that, a curve. When you get to a certain preload (tank is full) contractility (pump function) actually starts to decrease. The physiology is that the cardiac muscle is stretched beyond its ideal length for function. As this patent has JVD this means that preload or central venous pressure is extremely high. This is the nitty gritty and the bottom line is nitro is contraindicated, you need an inotrope/pressor, and fluids probably aren't going to help further and may harm if the patient has JVD.

Did someone say airway?!

Bonus question before we close out this great case. Let's say the patient's mental status declines and is not protecting his airway. You are ventilating well with a BVM (good chest rise) and you are getting sats no higher than the low 80s. Breath sounds are equal but with diffuse rales (lots of fluid). Knowing that he may desat, brady and code when you attempt to intubate what small piece of equipment may be helpful to increase O2 sats before intubation, or even just keep him alive while hauling ass if you don't have RSI capabilities. (it's not an oral or nasopharyngeal airway, you are ventilating well)

[adal]

capnography?

We have also used a nasal cannula on 6lpm While performing intubation to maintain/increase sats with the procedure in conjunction with BVM.

I was gonna mention the airway. This is a perfect pt that as soon as you traditionally RSI, they code. Ketamine might be the way to go here.

Still a great discussion.

PEEP- didn't think of that because it's on all our BVM's already. Good call.

[Patriot007]

PEEP Valve correct!

I like the nasal cannula on while pre-oxygenating and leave it on while intubating. (If you can spare the O2). It's only a short time, crank that sucker up to 15 LPM and get some flow going, you won't dry out their nasal mucosa and cause harm in that time period.


It's called passive oxygenation and it increases the time your patient can be apneic before desating. It works because you are entraining the nasopharynx and airway with high flow oxygen even though you are not ventilating.

I agree Ketamine is the way to go if sedation is needed.