Impaired fluid volume

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Hi Nurse zine

can someone give me an answer to this reflective question please? Can you remember as a new graduate your pathophysiology with regards to third spacing fluid deficit? What do you think your answer might be as you learned more about it?

What is the importance of fluid volume deficit, the associated risks and complications resulting post-op after cardiac surgery that carry a life threatening risk in somepne hypotensive, dehydrated, advanced age 69 and low cardiac output and myocardial stunning

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

We are happy to help....is this for school? What do YOU think and we will jump right in.

What is myocardial stunning?

The phenomenon of myocardial stunning according to literature, is due to total coronary artery occlusion lasting anywhere from fifteen minutes or briefer (during a period that is not associated with cell death), an abnormality in regional left ventricular wall motion following reperfusion and that persists for hours or days after reperfusion. this is an assignment of interest. the cardiac system has the potential to affect many body systems such as renal and urinary systems. the patient had persistantly low cardiac output.

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

I see what you mean now....A stunned myocardium has recovery and is temporarily impaired due to insult/lack of oxygen and blood flow.

Both the hibernating and the stunned myocardium are characterized by reversible contractile dysfunction.

In hibernating myocardium ischaemia is still ongoing, whereas in stunned myocardium blood flow is fully or almost fully restored.

Both the hibernating and the stunned myocardium retain an inotropic reserve. In hibernating myocardium the increase in contractile function is at the expense of metabolic recovery whereas in stunned myocardium no metabolic deterioration occurs during inotropic stimulation. Therefore, inotropic stimulation in combination with metabolic imaging may help not only to identify viable, dysfunctional myocardium but also to distinguish between hibernating and stunned myocardium.

The therapy of hibernating myocardium is to restore blood flow to the hypoperfused tissue. Myocardial stunning per se requires no therapy at all, since by definition blood flow is normal and contractile function will recover spontaneously.

If, however, myocardial stunning is severe, involves large parts of the left ventricle and thus impairs global left ventricular function, it can be reversed with inotropic agents and procedures. In the experimental setting, antioxidant agents, calcium antagonists and ACE inhibitors attenuate stunning, most effectively when administered before ischaemia.

Doppler Tissue Imaging Quantitates Regional Wall Motion During Myocardial Ischemia and Reperfusion

Ok! so how does post operative fluid deficit occur in relation to myocardial stunning and the patient back on the ward is found hypotensive with low cardiac output and receiving Endone 10mg with 1 gram Paracetamol every 6 hours? this is off why fentanyl and morphine are not given.

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
May 13 by Honey Bee

can someone give me an answer to this reflective question please? Can you remember as a new graduate your pathophysiology with regards to third spacing fluid deficit? What do you think your answer might be as you learned more about it?

Hummm....These still sound like homework questions. Third space....where has the fluid gone? Nursing Center - CE Article

Fluid volume deficit, or hypovolemia, occurs from a loss of body fluid or the shift of fluids into the third space, or from a reduced fluid intake. Common sources for fluid loss are the gastrointestinal (GI) tract, polyuria, and increased perspiration. Fluid volume deficit may be an acute or chronic condition managed in the hospital, outpatient center, or home setting.

The therapeutic goal is to treat the underlying disorder and return the extracellular fluid compartment to normal. Treatment consists of restoring fluid volume and correcting any electrolyte imbalances. Early recognition and treatment is imperative to prevent potentially life-threatening hypovolemic shock.

http://www.ucdenver.edu/academics/colleges/medicalschool/education/degree_programs/MDProgram/clinicalcore/peri-operativecare/Documents/FluidMgmt.pdfs

Elderly patients are more likely to develop fluid imbalances.

What is the importance of fluid volume deficit, the associated risks and complications resulting post-op after cardiac surgery that carry a life threatening risk in someone hypotensive, dehydrated, advanced age 69 and low cardiac output and myocardial stunning
Check out this thread....https://allnurses.com/nursing-student-assistance/struggling-cardiovascular-system-826088.html and this thread....https://allnurses.com/nursing-student-assistance/preload-vs-afterload-887678.html

Tell me why you think about the importance of fluid volume deficit, the associated risks and complications resulting post-op after cardiac surgery that carry a life threatening risk in someone hypotensive, dehydrated, advanced age 69 and low cardiac output and myocardial stunning.

We will go from there.

Specializes in ICU.

If this patient has recently had open heart surgery, then he/she probably does have third spaced fluid. You have to ask, how much weight is this patient up from pre-op to tell you just how much fluid is third spaced. 10lbs? (typical) 20lbs? (possible) If this patient is suddenly found hypotensive on the ward, then yes, fluid resuscitation is usually the first line of defense. Perhaps just 250cc of 5% Albumin (one Plasmanate) as a fluid challenge to see if that helps the blood pressure (or perhaps a smaller amount of 25% Salt Poor Albumin or SPA). You don't want to give much more than that because depending on how stunned the heart is, it might be too much for the heart to handle. The 5% or 25% albumin is preferred over simple fluids like 0.9% normal saline because it's hypertonic, and helps pull some of that third spaced fluid back into the vascular system, rather than just adding more fluid to the problem. The surgeon on call, may opt to transfer this patient back to the ICU for more management (placing of a central line, arterial line for accurate blood pressure monitoring, and -maybe- some positive inotropes depending if the blood pressure responds or just keeps dropping). ;)

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
Ok! so how does post operative fluid deficit occur in relation to myocardial stunning and the patient back on the ward is found hypotensive with low cardiac output and receiving Endone 10mg with 1 gram Paracetamol every 6 hours? this is off why fentanyl and morphine are not given.
I'm confused...this patient is no longer in ICU?

Now I really have questions...how many days post op was this patient? Tell me the complete story or I can't help you. What is their previous cardiac history? Are they renal impaired? What was the ejection fraction pre-op? What was the EBL? How much fluid did they receive intra-op/post op?

Oxycodone and Tylenol should not do this to a patient. Are they liver impaired?

How are you sure they were volume depleted with a stunned myocardium? Several things come to my mind if this patient is extubated and post op. I think graft closure. Within post op period there is a danger of grafts closing due to competitive flow. The blood want to utilize the native coronaries and will always take the path of lesser resistance. I once knew of a case the MD placed the grafts in backwards...he should have been sued...however he continued to practice.

I also think hemorrhage...did something let go? I also think septal wall rupture from an intra-op MI.

Sepsis...I think sepsis.

why fentanyl and morphine are not given.
Used when?

Fentanyl and morphine are not used if the patient is hypotensive.

I need more details to answer your question appropriately

Female patient presented with chest and a history of unstable angina for 2 years with GORD, dyslipidaemia, obesity and a previous smoker quit 12 months ago after a 12 year history. EF = 62%. Day 5 on ward and trying to mobilise and has dizziness, light-headedness, visibly pale, warm and clammy to touch and had been started on dopamine. Also has oxycodone 5mg and 1gram paracetamol for pain 4/24. Been told for this study to focus on hypotension related to fluid volume deficit third spacing shift as patient had low cardiac output and severe acute pain. Can these answered not in public forum? Can this case be removed from public domain?

Specializes in ICU.

The first problem I see is with an EF of 62%, how is that "low cardiac output"?

Trick question! :woot:

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
Female patient presented with chest and a history of unstable angina for 2 years with GORD, dyslipidaemia, obesity and a previous smoker quit 12 months ago after a 12 year history. EF = 62%. Day 5 on ward and trying to mobilise and has dizziness, light-headedness, visibly pale, warm and clammy to touch and had been started on dopamine. Also has oxycodone 5mg and 1gram paracetamol for pain 4/24. Been told for this study to focus on hypotension related to fluid volume deficit third spacing shift as patient had low cardiac output and severe acute pain. Can these answered not in public forum? Can this case be removed from public domain?
No they can be answered fine here...but it makes no sense to me. Are you in nursing school?

AN EF of 62% is just fine for an ejection fraction. So that does not apply here.

The patient could have had a vagal response to pain when she got up. There is a possibility of volume deficit due to 3rd spacing that she has extra vascular excess and intra vascular dry. I am not sure I would jump to dopamine unless there was evidence that she had a post op cardiac event that necessitated dopamine and not fluid resuscitation or some kind.

There is something missing from the puzzle...what you are describing and told to focus on doesn't make sense.

The ONLY thing I get out of this is that she had a vagal response to severs pain that dropped her B/P that was aggravated by possible intra vascular volume depletion from 3rd spaced fluid.

CV Physiology: Arterial Baroreceptors

According to current ACC/AHA guidelines,

cut-off values for Doppler-Echocardiographic measurements of severe aortic stenosis (AS) are defined as follows: aortic valve area (AVA),1.0 cm and/or indexed for body surface are,0.6 cm/m, mean gradient 40 mmHg and peak velocity 4.0 m/s (corresponding to a peak

gradient of 64 mmHg). It is not clear in the guidelines if these criteria are mutually inclusive or exclusive but, as also stated in the guidelines, ‘When stenosis is severe and cardiac output is

normal, the mean transvalvular pressure gradient is generally greater than 40 mmHg.’ Hence, when LV function is normal, clinicians expect to see a high gradient in patients with severe AS as well as consistency between the values proposed by the guidelines. And indeed, typical reaction for the echocardiographer faced with a lower than expected gradient in a patient with severe AS on the basis of AVA would be to question the validity of the valve area calculation, since this value is derived from multiple measurements and thus more prone to error than gradient measurements. Notwithstanding these considerations, it had long been our clinical observation that many patients with severe AS on the basis of AVA calculation indeed have unequivocally low gradients (e.g.mean gradient,30 mmHg) despite a preserved LV ejection fraction (i.e. EF 50%). Hence, we hypothesized that the lower gradients were likely due to a decrease in transvalvular flow and, in a recent study of 512 consecutive patients with severe AS (indexed AVA,0.6 cm/m) and preserved EF (50%), we found that 35% had paradoxically low flows (PLF) [i.e. stroke volume index (SVi),35 mL/m].

The same patients were also observed to have a cluster of findings suggesting that they were

at more advanced stage of their disease and had a worse prognosis if treated medically rather than surgically. In the same context, Minners et al reported a series of 2427 consecutive patients with preserved LV function and AVA, 2.0 cm and found that, Corresponding author. Tel: þ 1 418 656 4767, Fax: þ 1 418 656 4562, Email: [email protected] (J.G.D.) or [email protected] (P.P.)

Published on behalf of the European Society of Cardiology. All rights reserved. &

The Author 2009.

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European Heart Journal (2010) 31, 281–289 doi:10.1093/eurheartj/ehp361 by guest on May 16, 2014 http://eurheartj.oxfordjournals.org/

Downloaded from in reference to the guidelines, 30% had the inconsistent finding of

an AVA,1.0 cm but a mean gradient, 40 mmHg. On the basis of a previous observation by Carabello (Table 1), these authors also emphasized that, based on the Gorlin formula and assuming normal cardiac output, an AVA of 1.0 cm yields a gradient of 26 mmHg and that an AVA 0.81 cm is necessary to yield a gradient 40 mmHg, thus suggesting that it is the guidelines per se that are inherently inconsistent. In a further comment, Jander observed that low flow was thus not a necessary prerequisite for inconsistently low gradients and suggested an adjustment of the AVA cut-off value for severe stenosis to 0.8 cm The same

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814220/
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