Shock; Invasive Hemodynamics

VFlutter

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A 84 y/o male patient presents to a rural ER after an outpatient endoscopy the previous day with complaints of shortness of breath and fatigue/malaise. Initial chest x-ray reveals infiltrates, questionable aspiration. While obtaining labs the patient begins to c/o substernal chest pain then develops hypotension. Initial cardiac enzymes negative and 12 lead shows possible ischemic changes but no definitive STEMI. Patient has history of CAD and prior MI with a stent a couple years ago. On Plavix/ASA which was held 3 days prior to procedure. Patient is placed on Dopamine drip and transferred by ground, 1hr drive, to your ICU.

Upon arrival patient is clearly in shock, mottled, and in respiratory distress. Levophed is initiated and dopamine weaned off. Patient is intubated. After intubation patient has increasing pressor requirements and worsening acidosis despite multiple liters of fluid boluses. The decision is made to place a Swan.

Below is the hemodynamic review for the next day. Listed at the bottom are the current drips. The blood pressures are retrieved from the latest NIBP, so they are just a snap shot in time. The patient had an arterial line and the average pressures were a little lower.

1. Differentiate the type of shock
2. Comment on the medical treatment. What was beneficial, what was not, what else could have been done.
3. Explain the pathophysiology and pharmacology of what is going on.
4. What would you anticipate for this patient? Anything you want to see done?

Levo = Levophed. Dbx = Dobutrex. Hydral = Hydralazine IV push.

 

VentMonkey

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A 84 y/o male patient presents to a rural ER after an outpatient endoscopy the previous day with complaints of shortness of breath and fatigue/malaise. Initial chest x-ray reveals infiltrates, questionable aspiration. While obtaining labs the patient begins to c/o substernal chest pain then develops hypotension. Initial cardiac enzymes negative and 12 lead shows possible ischemic changes but no definitive STEMI. Patient has history of CAD and prior MI with a stent a couple years ago. On Plavix/ASA which was held 3 days prior to procedure. Patient is placed on Dopamine drip and transferred by ground, 1hr drive, to your ICU.

Upon arrival patient is clearly in shock, mottled, and in respiratory distress. Levophed is initiated and dopamine weaned off. Patient is intubated. After intubation patient has increasing pressor requirements and worsening acidosis despite multiple liters of fluid boluses. The decision is made to place a Swan.

Below is the hemodynamic review for the next day. Listed at the bottom are the current drips. The blood pressures are retrieved from the latest NIBP, so they are just a snap shot in time. The patient had an arterial line and the average pressures were a little lower.

1. Differentiate the type of shock
2. Comment on the medical treatment. What was beneficial, what was not, what else could have been done.
3. Explain the pathophysiology and pharmacology of what is going on.
4. What would you anticipate for this patient? Anything you want to see done?

Levo = Levophed. Dbx = Dobutrex. Hydral = Hydralazine IV push.

 

VentMonkey

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Waiver: I am not an ICU nurse, and have limited experience in this environment, however, enjoy the aspects of critical care, and look forward to some input from other regarding this case presentation. I will give it my best shot, so here it goes...

1. I an going to say that this patient's initial lab values seem to be in line with that of a patient in cardiogenic shock.

2. I think switching this patient's pressor from Dopamine, to Levophed, and then adding Dobutamine as a secondary adjunct to their probable failure helped augment their pump problem. I also think intubating was the right call, and noted "inflitrates" mentioned; to me this screams ARDS until proven otherwise. Is there an Fio2/ PAO2 ratio somewhere? Repeat 12 leads would be nice, or even one repeated to see if there were any other changes, or where exactly we are seeing inschemia present (e.g., is it seen in the anteroseptal leads leading us to perform a right sided 12 lead in the event the patient had suffered a PWMI). Obviously, the Dopamine proved non-beneficial, as it has for some time, hence the reason for switching over to the Levo.

The "initial" cardiac enzymes are nice, however, my understanding is that it does in fact take time for changes, and elevation in certain cardiac markers to develop; repeats are needed for this gentleman.

3. Given this patient's previous history, and co-morbidities, he is at a very high risk for developing an AMI, even if presenting with vague complaints of fatigue, and malaise without clear cut "classic" MI symptoms, or patterns on an ECG. To my knowledge, Dopamine is falling more and more out of favor in place of Norepinephrine, and even though it was initially pigeon-holed as "leave em dead", we are beginning to realize it was often a matter of improper dosing. It's primary role as an effective pressor will augment this patient's lack of perfusion given his shock state.

The Dobutamine will augment contractility to this patient's heart, which also lead me down the cardiogenic shock path. I'm not too familiar with Hydralazine in this setting, but would love to hear others input, and reasoning for it's utilization, and effectiveness.

4. I would like to see a recent set of lab values to include a repeat set of cardiac enzymes, base deficits, and the most recent ABG done prior to transport.

The patient's outcome is poor at best. His age, and co-morbidities alone are a huge factor in his recovery. The most recent CXR would also be helpful to see if there were any further developments, changes, or clear cut "patchy inflitrates" seen on a recent CXR.

Again, this to me is sounding like a cardiogenic shock, and not his PCWP also to be elevated. I look forward to input, insight, and the diagnosis of this case.

Also, what was his endoscopic procedure for?
 
OP
VFlutter

VFlutter

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The patient was initially on 5 of PEEP at 40% fi02 but was increased to 8 of PEEP after fi02 increased to 60%. Copious frothy sputum was noted in ET tube.

Initial 12 lead showed biphasic T waves in the Anterior leads and inverted T waves in Lateral.

Repeat chest x rays were read as various things including Inflitrate/edema/consolidation.

Initial Troponin, taken around the onset of chest pain, was negative. Subsequent were 26 the 178.

Based off his CVP alone would you give this patient fluids? Notice any correlation between his Stroke Volume and CVP? What happens to his Stroke Volume after fluid boluses? Is he fluid optimized?

What happens to his CI after the doses of Hydralazine? Why?

Besides medical therapy is there anything else that could improve the situation?

I know this is probably out of most peoples comfort zone but I will give it a little more time for more responses.
 

TXmed

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I think my computer isnt showing me all the information because ventmonkey mentioned some things i couldnt see.

but ill give it a go.

1. yes the infiltrates do make you suspect of ARDS but since you were able to keep him oxygenated with an Fio2 of 60% and PEEP of 8 probably not severe, im gonna lean to cardiogenic shock with LV failure.

2. his CVP was fine throughout, dopamine wouldnt be the best. starting levo + dobutamine and titrating down the levo was good as dobutomine is a vasodilator with a narrow window to make a difference. You brought down his SVR while maintaining good BP which helps the heart. Milirone ?

3. his wedge pressures are up so definite edema which is injuring his lungs. your goal sho(uld be to increase Mean Airway Pressure (MAP), PEEP is good to start with but consider adjusting rise time or if in volume mode your I:E ration and RR instead of just Fio2 %. MAP is a fickle beast as it can lower your Mean Arterial Pressure(MAP). If the patient began having a low BP consider using higher PEEP and reducing your TV to 4ML/kg of IBW and increase RR and allow for permissive hypercapnia ETCO2 of 45-65 and permissive hypoxia SPo2 of greater than 88% but try for 92%

4. I am intrigued by the hydralazine usage as its a a vasodilator, possibly to reduce afterload and help cardiac output? which is why you reference CI ?

5. If you felt the need for another fluid bolus consider Albumin.

6. IABP candidate or impella.

7. have patient in semi-fowlers position.

i really wanna see ABG's.
 

VentMonkey

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I think my computer isnt showing me all the information because ventmonkey mentioned some things i couldnt see.

but ill give it a go.

1. yes the infiltrates do make you suspect of ARDS but since you were able to keep him oxygenated with an Fio2 of 60% and PEEP of 8 probably not severe, im gonna lean to cardiogenic shock with LV failure.

2. his CVP was fine throughout, dopamine wouldnt be the best. starting levo + dobutamine and titrating down the levo was good as dobutomine is a vasodilator with a narrow window to make a difference. You brought down his SVR while maintaining good BP which helps the heart. Milirone ?

3. his wedge pressures are up so definite edema which is injuring his lungs. your goal sho(uld be to increase Mean Airway Pressure (MAP), PEEP is good to start with but consider adjusting rise time or if in volume mode your I:E ration and RR instead of just Fio2 %. MAP is a fickle beast as it can lower your Mean Arterial Pressure(MAP). If the patient began having a low BP consider using higher PEEP and reducing your TV to 4ML/kg of IBW and increase RR and allow for permissive hypercapnia ETCO2 of 45-65 and permissive hypoxia SPo2 of greater than 88% but try for 92%

4. I am intrigued by the hydralazine usage as its a a vasodilator, possibly to reduce afterload and help cardiac output? which is why you reference CI ?

5. If you felt the need for another fluid bolus consider Albumin.

6. IABP candidate or impella.

7. have patient in semi-fowlers position.

i really wanna see ABG's.
Milrinone from what I was taught/ know, while its M.O.I. may mirror Dobutamine, is given more so in the NICU setting; perhaps a CHD infant? Good point and consideration, though.

Another great point you mention was this patient being a candidate for either IABP, or impella placement. Could you elaborate?

What's your rationale for Albumin? I haven't even thought of this. Fascinating.

I await yours and others input, and hope more join this thread with their spin on this complex scenario.
 

MonkeyArrow

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Milrinone from what I was taught/ know, while its M.O.I. may mirror Dobutamine, is given more so in the NICU setting; perhaps a CHD infant? Good point and consideration, though.
Milrinone is very common (first line) for our (adult) advanced heart failure patients.
 

VentMonkey

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Milrinone is very common (first line) for our (adult) advanced heart failure patients.
Good to know, thanks. Still fairly new to critical care medicine, though it does seem to mirror most medicine in general in that there's almost always "more than one way to skin a cat".
 

TXmed

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To my understanding (i could be wrong), Milirinone has more vasodilatory effects and is "easier" on the heart.

IABP is becoming more popular with all cardiogenic shock not just relating to a STEMI or transplant. it can greatly improve blood flow, and reduce myocardial work. blood flow is really what we are trying to accomplish. the first BP was 129/80 but with a SVR >4400, this patient has a good pressure but blood flow is reduced. i am not sure at what SVR the kidneys and other organs have trouble perfusing. impella is a solid alternative but doesn't increase coronary perfusion like a IABP will. so an augmented BP on a IABP will be like 75/55 but its fine because they will have the blood flow of someone with a BP of 120/80.

Albumin helps in regulating all of the bodies osmotic pressure. something CHFers have a hard time with. the OP gave 1L of NS and stated several other liters were given prior (i would have given LR). this fluid will only stay in the vascular space for a short time 30min-1hr. then it is 3rd spaced or pee'ed out (hopefully). Albumin will pull this excess fluid back into the vasculature where it can help. it is great for burns, liver failure, cardiac patients and sometimes trauma. but it is expensive and not routinely used for transport medicine unfortunately.
 

VentMonkey

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Awesome follow up, great breakdown, thanks!
 
OP
VFlutter

VFlutter

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ABG on 15L NRB was..
7.22 ph
34 pc02
48 p02
17 hc03
-7.7 base excess
79 sa02

Sv02 (Mixed venous) was p02 of 30 with sat of 52%

Milrinone (Primacor) is a very useful inotrope however it is not used nearly as much as Dobutrex. I think many practitioners are just not as familiar with it and its dosing.

Patient was consider for IABP and Impella, which would have helped greatly, but was felt not to be a candidate.

IABP would have reduced afterload and helped increase cardiac output. Impella would have directly increased cardiac output but would not have increase perfusion to his coronaries.

I will put a more detailed response when I am not at work.
 

VentMonkey

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Great stuff, Chase. I love learning from knowledgeable sources. A lot of nurses are on a whole different level of thinking than the average "street" paramedic when it comes to their form or critical thinking and differential diagnosis.

I assume this was the initial ABG reading as it was on 15 lpm NRB. Clearly this gas reveals a metabolic acidosis with a PaO2 (<) 60, indicating respiratory failure, and the need to intubate. I am surprised I am not seeing a mixed acidosis though it is very possible I am missing something.

I understand you have more to come, and await further follow up. A repeat ABG after intubation, preferably the latest would be of interest to me. Also, if there is a PaO2/ FiO2 ratio available, that would be cool and help confirm my suspicions of ARDS, and it's level if severity.

Again, great case presentation. This gets me thinking, and a reason I love this forum!

I do hope other paramedics aside from myself and TXmed chime in as well.
 

E tank

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I'd like to get in on this, but I can't open the CC summary for the patient. Any other way to see it besides the link in the OP?
 

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