Acute shock?

[RxBoy]

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Female mid 50s, obese, HTN, hx latex allergy admitted for abdominal pain .

CT scan consistent with infected bowel and large abdominal abscess.

Surgeon boards for ex lap, bowel resection, and abdominal washing.

Preop: Pt stable, A-line placed, 2 large perpherial IVs in place. Preop labs normal.

pt taken to OR.

Pt induced, intubated w/o difficulty. VS/UO stable through first hour of case with minimal blood loss.

As surgeon drains/washes out abdominal abscess pt becomes unstable.

Over next 3 minutes HR increases to 130s, BP tanks to 70/40s, SpO2 decreases to upper 80s, EtCO2 decreases from 30s to lower 20s. No UO.

Volatile turned down, 500 cc bolused, 100 mcg epi given... Minimal response... pt continues to deteriorate.

Knowing acute shock in the anesthetized patient falls in 1 of these 4 categories or combination:

Obstructive (possible PE/tamponade/ect.)
Distributive (possible sepsis/anaphylaxis)
Hypovolemia (no acute blood loss but pt already hypovolemic and other conditions will excerbate the hypovolemia)
Cardiogenic (intraop MI/acute valvular changes)


How do you proceed to treat and quickly diagnosis the cause of shock? If you order a lab what are you looking for or if you want to place extra line/another monitor what is your rationale?

 

[PMPMD]

.

 

[sevoflurane]

.

 

[sevoflurane]

Over next 3 minutes HR increases to 130s, BP tanks to 70/40s, SpO2 decreases to upper 80s, EtCO2 decreases from 30s to lower 20s

Sounds like a PE or Tension Pneumo. Pretty rapid decrease.

The answer to your question lies in the clinical scenario and information available.

Bilateral breath sounds? Peak pressures? Tidal volume changes?
EKG with new tombstones? New rip roaring murmur?
What does the patient look like? What does his pulse feel like? What's going on in the surgical field? Did you just hang blood or products or just start an antibiotic or gave some rocuronium? Response to fluids? TEE/PAC/..is the CVP down to 5 from 16?. ABG/AA-gradient. You can always get an intraop XRAY while you are temporizing.

As a general rule, I start with the ventilator and work my way back to the patient.

 

[sevoflurane]

If all you have is an a-line... look at systolic pressure variations and Delta P.

Sometimes, helpful in determining the effectiveness of a fluid bolus.

 

[RxBoy]

OK its too tough to continue a hypothetical scenario... So I'll actually present a real case I encountered helping out another resident (I'll edit my original post too).

Female mid 50s, obese, HTN, hx latex allergy with infected bowel.

boarded for ex lap, bowel resection, and abdominal washout:

MORE details:

Preop: Pt stable, A-line placed, 2 large perpherial IVs in place. Preop labs normal.

pt taken to OR.

Pt induced, intubated w/o difficulty. VS/UO stable through first hour of case with minimal blood loss.

As surgeon drains/washes out abdominal abscess pt becomes unstable.

Over next 3 minutes HR increases to 130s, BP tanks to 70/40s, SpO2 decreases to upper 80s, EtCO2 decreases from 30s to lower 20s. No UO.

Volatile turned down, 500 cc bolused, 100 mcg epi given... Minimal response... pt continues to deteriorate.

No central line access yet so no CVP. No new murmur appreciated (tough in a noisy OR), breathe sounds equal but due to body habitus and environment unable to appreciate whether clear vs. junky or distant vs. baseline. Peak pressures are bit higher, volume same (VC).

Pt not cynotic, no appreciable physical changes, nothing noted on surgical field except working near abscess. No excessive blood loss.

No blood products or recent administration of medications. Only products given Sux/Vec/fentanyl/prop/sevo/ 500 cc hespan/ and nothing but NS hanging.

Send off ABG: PaO2/FiO2>200. pH=7.25, PaCO2 50 (EtCO2 was 24), BE-6. K/Ca normal.

Give another 500 cc NS bolus with full blown 1 mg epi IV, pt still unstable. Surgeon stop operating. EtCO2 goes to 0, radial A-line goes flat after ABG draw, EKG still shows sinus tachy, surgeon can still feel aorta pulsating. (at this point attending/resident ask nurse to call anesthesia stat overhead). A bunch of us arrive, radial pulse on opposite hand extremely faint. NIBP not picking up reading.

What next?

 

[RxBoy]

If all you have is an a-line... look at systolic pressure variations and Delta P.

Sometimes, helpful in determining the effectiveness of a fluid bolus.

I love SPV, I would take A line over CVP for fluid responsiveness any day. It noticed it works well with pulse oximeter waveforms too.

 

[G0S2]

Ive seen this many times. Opening up an abscess can quickly lead to bacteremia and sepsis.

 

[seinfeld]

what does the echo show? Physical exam on the obese not very helpful. Fluids , fluids fluids, central line to check CVP as this could help dx obstructive vs distributive.

 

[dhb]

Give another 500 cc NS bolus with full blown 1 mg epi IV, pt still unstable. Surgeon stop operating. EtCO2 goes to 0, radial A-line goes flat

You don't arrest in five minutes from sepsis.
Something is impeding cardiac output:
-decreased venous return from clamp/surgeon pushing on the IVC
-blood loss: from the aorta in the retroperitoneum?
-tension pneumothorax
-massive PE
-myocardial infarction

 

[RxBoy]

More Details:

Switch to hand ventilate against a near closed APL with a return of EtCO2 and TV in 300s, pulse ox waveform poor but in the upper 80s, NIBP finally registers a pressure 70s/40s. 1 resident works on giving fluids, one starts a central line, another works on vent. 2 Attendings directing staff.

Portable TEE on its way. Stat chest xray tech enters.

Questions:
What is your DD?

How could a TEE be used to determine low SVR state vs. low preload state vs. cardiogenic shock causing acute CHF?

What chest xray findings would one want to look for?

Can a ultrasound probe be used to detect a large PTX?

 

[dhb]

Can a ultrasound probe be used to detect a large PTX?

Even a small one

 

[IgM]

I love these threads. I don't know enough yet to contribute anything useful (except I heard that you can use PVP as an analog of CVP and it correlates extremely well... just hook up the IV to the CVP transducer!... but maybe everyone already heard that too), but I just want you to know that future CA-1s like me are out here reading and trying to learn from it, so definitely keep it coming. Thanks for posting

 

[RT2MD]

I love these threads. I don't know enough yet to contribute anything useful (except I heard that you can use PVP as an analog of CVP and it correlates extremely well... just hook up the IV to the CVP transducer!... but maybe everyone already heard that too), but I just want you to know that future CA-1s like me are out here reading and trying to learn from it, so definitely keep it coming. Thanks for posting

What (s)he said...
👍👍👍

 

[RxBoy]

Even a small one

Very nice.. I am not sure if its common knowledge but very few attendings at my institution know about U/S and ptx. If you don't, this 10 minute will save your ***** one day and probably your pt's life. All anesthesiologists should be familiar with this:

[YOUTUBE]http://www.youtube.com/watch?v=fntJ7GLjCSU[/YOUTUBE]

As for this case, I only knew about this reading in hindsight. There was an U/S literally right next to us which we used to quickly mark the RIJ because the carotid pulse was so weak.

In any case it would of only R/O a ptx. Stat Cxray (with we immediate read on the portable xray machine monitor) did not show any obvious pneumothorax, pleural effusions, or pulmonary congestion.

 

[cincincyreds]

So what was cause of the hypotension ultimately? Preload, afterload, contractility, rate, or rhythm? Sounds like a fun case in the middle of the night.

 

[RxBoy]

So what was cause of the hypotension ultimately? Preload, afterload, contractility, rate, or rhythm? Sounds like a fun case in the middle of the night.

It actually turned out to be very interesting. But where's the fun with no discussion 😴... Feel free to discuss:

DD?

How could TEE be used to determine low SVR state vs. low preload state vs. cardiogenic shock causing acute CHF? something I also only learned in hindsight

 

[PMPMD]

It actually turned out to be very interesting. But where's the fun with no discussion 😴... Feel free to discuss:

DD?

How could TEE be used to determine low SVR state vs. low preload state vs. cardiogenic shock causing acute CHF? something I also only learned in hindsight

TEE can assess volume status of the chambers, contractility, RWMAs.

 

[PMPMD]

It actually turned out to be very interesting. But where's the fun with no discussion 😴... Feel free to discuss:

DD?

How could TEE be used to determine low SVR state vs. low preload state vs. cardiogenic shock causing acute CHF? something I also only learned in hindsight

Some kind of allergic rxn? You said hand ventilation was difficult (closed APL) = bronchospasm? Did something with latex get in there?

 

[G0S2]

See any veggies on the valves (large abdominal infectious process)? Evidence of pulmonary edema, valve dysfunction?

 

[RxBoy]

How could TEE be used to determine low SVR state vs. low preload state vs. cardiogenic shock causing acute CHF? something I also only learned in hindsight

Per Miller:

"Transesophageal Echocardiography During Life-Threatening Hypotension

Ultimately, hypotension has only two possible causes: inadequate cardiac output or inappropriately low systemic vascular resistance. TEE is remarkably well suited for addressing this differential diagnosis. During severe hypotension, qualitative TEE estimates of ventricular filling and function serve as practical guides for the administration of fluids, inotropes, and vasopressors. An experienced observer can differentiate severe ventricular dysfunction from other life-threatening causes of hypotension. In severe LV failure, ventricular filling (as assessed by end-diastolic area) is increased and ejection is decreased, whereas in inappropriately low systemic vascular resistance, ventricular filling is usually normal or slightly decreased and ejection is markedly increased. Hypovolemia is easily recognized as a marked decrease in ventricular filling and a marked increase in ejection. Although inappropriately low systemic vascular resistance, severe aortic regurgitation, severe mitral regurgitation, and ventricular septal defects can manifest the same LV filling and ejection pattern on the TG SAX cross section, distinguishing these causes of hypotension is not difficult with the use of other cross sections and color Doppler."

 

[psychbender]

How could TEE be used to determine low SVR state vs. low preload state vs. cardiogenic shock causing acute CHF? something I also only learned in hindsight

One can check out the LV in multiple views (TG short axis mid-pap, mid-esophageal four-chamber, etc) to get an idea of left-sided function. Are the walls thickening and moving appropriately, but nearly touching in systole? If so, likely low LV preload, with good LV function. Are the walls barely thickening or moving, resulting in a very low EF? If so, acute LV failure (also check out the mitral valve, LV failure may worsen mitral regurgitation by spreading the valve annulus, leading to acute increases in LA pressures, translating to increased pulmonary pressures, and right heart dysfunction). Also check out the RV, looking for RV dilation, TR, and free wall movement (a better indicator of RV function than the septal wall, which can be affected by several non-RV factors). Additionally, the probe can check out the IVC, and measure the diameter and response to respiration to estimate CVP (diameter <1cm, responds to respiration = CVP<10; diameter >2.5, no respiratory variation = CVP>20).

 

[psychbender]

Blast, you were faster than me.

 

[NotThatOne]

OK its too tough to continue a hypothetical scenario... So I'll actually present a real case I encountered helping out another resident (I'll edit my original post too).

Female mid 50s, obese, HTN, hx latex allergy with infected bowel.

boarded for ex lap, bowel resection, and abdominal washout:

MORE details:

Preop: Pt stable, A-line placed, 2 large perpherial IVs in place. Preop labs normal.

pt taken to OR.

Pt induced, intubated w/o difficulty. VS/UO stable through first hour of case with minimal blood loss.

As surgeon drains/washes out abdominal abscess pt becomes unstable.

Over next 3 minutes HR increases to 130s, BP tanks to 70/40s, SpO2 decreases to upper 80s, EtCO2 decreases from 30s to lower 20s. No UO.

Volatile turned down, 500 cc bolused, 100 mcg epi given... Minimal response... pt continues to deteriorate.

No central line access yet so no CVP. No new murmur appreciated (tough in a noisy OR), breathe sounds equal but due to body habitus and environment unable to appreciate whether clear vs. junky or distant vs. baseline. Peak pressures are bit higher, volume same (VC).

Pt not cynotic, no appreciable physical changes, nothing noted on surgical field except working near abscess. No excessive blood loss.

No blood products or recent administration of medications. Only products given Sux/Vec/fentanyl/prop/sevo/ 500 cc hespan/ and nothing but NS hanging.

Send off ABG: PaO2/FiO2>200. pH=7.25, PaCO2 50 (EtCO2 was 24), BE-6. K/Ca normal.

Give another 500 cc NS bolus with full blown 1 mg epi IV, pt still unstable. Surgeon stop operating. EtCO2 goes to 0, radial A-line goes flat after ABG draw, EKG still shows sinus tachy, surgeon can still feel aorta pulsating. (at this point attending/resident ask nurse to call anesthesia stat overhead). A bunch of us arrive, radial pulse on opposite hand extremely faint. NIBP not picking up reading.

What next?

Dropping in EtCO2 and wide gap between PaCO2 & EtCO2 suggest that something is impairing CO2 from pulmonary vasculature to the vent:
1) Massive PE
2) Tension pneumothorax
3) Flash pulmonary edema
4) Mucus plug
5) Bronchospasm
6) ...

 

[RxBoy]

So the conclusion:

Once central line access established, attending sticks TEE probe in, immediately scan for obvious abnormalities (tamponade/disection/severe valvular dysfunction) and get to the transgastric SAX. Attending yells tanks empty fill'er up. Residents begin to pound fluid in and slowly LV expands. VS become more stable.

So what was the cause? Still unsure at this point until I inadvertently diagnosis the etiology.

As I setup the lining of the central line, I attach blood tubing. Figure pt needs volume fast, so hang a bag of hespan. One squeeze of blood tubing and pt has total HD collapse again! We look at the TEE and low and behold the LV shrivels like a worm. Immediately disconnect hespan tubing. Again peak pressures increase but now we know why. Hand bag to break the spasm. Slowly work in another 300 mcg of epi and pt condition returns. Reconnect fresh tubing with NS and start low dose epi drip and pt VS rock solid. Draw a tryptase level. Surgery commences uneventfully.

Pt transferred to ICU. Patient weaned off epi by night. C/S allergist who sets up outpatient appointment. Tryptase lab for our institution is about a 5 day turn around because its a send out lab. Levels come back are through the roof.

So why didn't 1 mg of epi fix the problem initially? I have no idea. My theory is that I could only assume 500 cc of that stuff floating around must of took awhile for to burn out a massive mast degranulation. It was a slow reaction first time around, it took 10 to 20 minutes to develop. 2nd time around it was immediate. Pt must of had a severe allergy because 30 cc or so whatever was in one pump caused another severe HD collapse.

So I did a quick literature search after that case... Found this interesting case report that was VERY similar to our case:

http://www.anesthesia-analgesia.org/content/101/6/1709.full

Makes me wonder if the pt truly had a latex allergy or was it just hespan and someone assumed it was latex.

Moral of the story: Never assume anything... Even our rescue agents can be the biggest offenders. Anaphylasis to ANYTHING should always be near the top of the DD in an unexplained HD collapse.

What lupus is to medicine, anaphylaxis is to anesthesia. It can present so many different ways and if you don't think about it you'll never diagnose it. Only difference is anaphylaxis will kill you in minutes.

 

[RxBoy]

Some kind of allergic rxn? You said hand ventilation was difficult (closed APL) = bronchospasm? Did something with latex get in there?

Nice pickup.

One can check out the LV in multiple views (TG short axis mid-pap, mid-esophageal four-chamber, etc) to get an idea of left-sided function. Are the walls thickening and moving appropriately, but nearly touching in systole? If so, likely low LV preload, with good LV function. Are the walls barely thickening or moving, resulting in a very low EF? If so, acute LV failure (also check out the mitral valve, LV failure may worsen mitral regurgitation by spreading the valve annulus, leading to acute increases in LA pressures, translating to increased pulmonary pressures, and right heart dysfunction). Also check out the RV, looking for RV dilation, TR, and free wall movement (a better indicator of RV function than the septal wall, which can be affected by several non-RV factors). Additionally, the probe can check out the IVC, and measure the diameter and response to respiration to estimate CVP (diameter <1cm, responds to respiration = CVP<10; diameter >2.5, no respiratory variation = CVP>20).

Excellent... Exactly what we saw.

 

[OB1🤙]

TEE is the nuts.

It isn't the first maneuver I'd do in cardiovascular collapse, but you can pretty precisely calculate SVR with TEE. It would have been interesting to see what it was in your case.

As you know, SVR=(MAP-CVP)*80/CO

MAP and CVP are on the monitor, if no CVP use IVC size/resp variation to estimate. CO can be calculated from the HR x area x VTI in either the LVOT or the PA, whichever you can get a more accurate diameter of.

 

[Mman]

I love SPV, I would take A line over CVP for fluid responsiveness any day. It noticed it works well with pulse oximeter waveforms too.

Most of the literature uses Pulse Pressure Variation, not Systolic Pressure variation. Either that or Stroke Volume Variation.

But anyways, relying on your eye to pick it up on the monitor is not useful. Clinically significant differences exist that are not detectable to the naked eye in the OR. A recent article (I think in A&A) suggested PPV < 8% definitely doesn't need volume and > 13% definitely does need volume and between 8 and 13 is a gray area. But can you really pick up a difference of 5% of pulse pressure variation by eyeballing it? I don't even need to dig up the research to know that you can't. By the time you can see it easily on the monitor, you are so far behind the 8 ball you've already missed your chance to intervene in a timely manner.

And I wouldn't even bother looking at the pulse ox waveform. Lots of variables between the pulse ox trace on your monitor and a realistic measurement of cardiac output responsiveness to fluid.


Gotta use something like a Lidco or a Vigileo (calculate SVV or PPV off the a-line) or something like esophageal doppler or some bioimpendance device calculating cardiac output and stroke volume.

 

[Planktonmd]

When you have an acute hemodynamic collapse like the one described you should treat the possible etiologies empirically without wasting too much time on the differential.
Meaning: You have a sudden hypotension, with decrease of ETCO2 (low cardiac output), and decrease of SPO2 (most likely caused by low perfusion but we don't have an ABG yet).
You start treating all the possible causes: Listen to chest, if there is bilateral BS and airway pressure did not change dramatically then tension pneumo is unlikely and you concentrate on increasing cardiac output and increasing SVR simultaneously regardless of the etiology, this means you give fluids and Epi and if there is no response you give vasopressin.
Once the patient is more stable you start your investigative work, but wasting time on diagnostic work (TEE, ABG, Labs...) instead of resuscitating a patient who is about to arrest is not a great idea IMHO.

 

[RxBoy]

Most of the literature uses Pulse Pressure Variation, not Systolic Pressure variation. Either that or Stroke Volume Variation.

I think SPV is very valuable. This is a pretty good study: http://www.anesthesia-analgesia.org/content/78/1/46.long

I can easily pick up a 12 mm Hg change, although its not a true delta down because I don't constantly change from apnea to ventilation. With my monitor I setup P1,P2,P3 (corresponds to each transduced tracing) all be displayed even though only P1 displays. Then I set it to combined P tracings and it gives me a giant A-line tracing.

I agree though PPV is near impossible to measure and vigileo with SVV would be the most accurate measurement. Maybe in the next 10 years all the new anesthesia machine will have one integrated.

As for plethysmographic changes, you would be surprised:
http://www.ncbi.nlm.nih.gov/pubmed/17525584

Yeah, its no vigileo but its still an extra tool in your arsenal.

 

[gtb]

Once the patient is more stable you start your investigative work, but wasting time on diagnostic work (TEE, ABG, Labs...) instead of resuscitating a patient who is about to arrest is not a great idea IMHO.

Seriously good advice.

 

[RxBoy]

Once the patient is more stable you start your investigative work, but wasting time on diagnostic work (TEE, ABG, Labs...) instead of resuscitating a patient who is about to arrest is not a great idea IMHO.

Agreed especially if rapidly deteriorating or solo.

Our pt had multiple hands on deck, 2 were resuscitating and VS were holding up. The dx workup never interferred with resuscitating efforts. We just didn't want to pound fluids if it was a pump problem. Its not like we were twiddling our thumbs waiting for the TEE.

And the whole point of my post wasn't to prove what superstars we are.... I thought it was a good learning case. Maybe I was wrong.

 

[leviathan]

Agreed especially if rapidly deteriorating or solo.

Our pt had multiple hands on deck, 2 were resuscitating and VS were holding up. The dx workup never interferred with resuscitating efforts. We just didn't want to pound fluids if it was a pump problem. Its not like we were twiddling our thumbs waiting for the TEE.

And the whole point of my post wasn't to prove what superstars we are.... I thought it was a good learning case. Maybe I was wrong.

Great case, I enjoyed it. I've heard about delta PP from 3 different intensivists that I've worked with. Another good one for volume status I've been told about is looking at the responsiveness of the IVC to inspiration (on echo). Any opinions on that one?

 

[Planktonmd]

And the whole point of my post wasn't to prove what superstars we are.... I thought it was a good learning case. Maybe I was wrong.

No, you were not wrong, the case was good and it is very helpful to discuss these cases where each anesthesiologist should have a preformulated plan of action.
Acute hemodynamic collapse under anesthesia is something we should always be prepared for.

 

[IlDestriero]

No, you were not wrong, the case was good and it is very helpful to discuss these cases where each anesthesiologist should have a preformulated plan of action.
Acute hemodynamic collapse under anesthesia is something we should always be prepared for.

Absolutely. The difference between a superstar veteran and the average Joe punter is that the superstar always has a plan for disaster ready to go. You have to think things through, review the literature for important updates, have ACLS/PALS algorithms memorized, common DDx. I can't tell you how many times over the last decade I've seen experienced anesthesiologists floundering in common disaster scenarios. Some is the adrenaline, anxiety, terror, etc. but if you have well rehearsed plans on the top of your head and ready to go, you can do what needs to be done immediately, get your help, products, crash cart, TEE, etc. called for, and then work on the DDx and how to confirm and manage the likely cause(s).
I don't think a lot of people think through these things much after passing the oral boards, and that could make the difference between a good and bad outcome.
Nice case.

 

[Mman]

I think SPV is very valuable. This is a pretty good study: http://www.anesthesia-analgesia.org/content/78/1/46.long

I can easily pick up a 12 mm Hg change, although its not a true delta down because I don't constantly change from apnea to ventilation. With my monitor I setup P1,P2,P3 (corresponds to each transduced tracing) all be displayed even though only P1 displays. Then I set it to combined P tracings and it gives me a giant A-line tracing.

I agree though PPV is near impossible to measure and vigileo with SVV would be the most accurate measurement. Maybe in the next 10 years all the new anesthesia machine will have one integrated.

As for plethysmographic changes, you would be surprised:
http://www.ncbi.nlm.nih.gov/pubmed/17525584

Yeah, its no vigileo but its still an extra tool in your arsenal.

I understand that people have looked into pulse ox waveforms and systolic pressure variation, but the volume of literature supporting pulse pressure variation and stroke volume variation is at least an order of magnitude greater. I mean there are outcomes studies comparing fluid management based off pulse pressure variation. Decreased hospital length of stay, etc. Eyeballing the aline or pulse ox waveform to determine fluid responsiveness is akin to seeing if the patient is blue to determine oxygenation. Sure, it can work, but we have waaay better ways of doing things.

My hierarchy for determining volume responsiveness

1) LVEDV on TEE
2a) PPV or SVV from noninvasive monitors, usually the Lidco. I'm not a fan of esophageal doppler despite the fact it has the largest volume of literature supporting it's use because it is finnicky and hard to get quality data from.
2b) PA cath
3) CVP (as in measure how it responds to a volume challenge, not just a static number)
4) eyeballing the pulse ox or a-line waveforms and using clinical judgment

 

[cincincyreds]

Cool case. So I guess the answer is decreased afterload from the hesban allergy.