Pocus and deresuscitation
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Part of the joint International Fluid Academy and World Society of Abdominal Compartment Syndrome workshop at the Emirates Critical Car Conference 2018
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Pocus and deresuscitation
- 5. • Too much/little • Interactions • Appropriate timing Drug • Pharmacokinetics • Pharmacodynamics • Toxicity Dosing • Appropriate duration • Treat until responseDuration • MonitoringDe-escalation
- 11. POCUS and and fluid management A BETTER WAY
- 13. @PARADicmSHIFT
- 15. 1 When to start fluids When to stop fluids When to start fluid removal 2 3 When to stop removal 4
- 17. Core Echocardiography LV function and size RV function and size IVC
- 19. RV function
- 22. Lung ultrasound •B-lines yes/no •Effusions yes/no Basic •B-line quantification Advanced
- 26. Misc Advanced echocardiography Portal vein pulsatility Intra-renal Doppler Tissue
- 30. Diastology
- 44. Summary Too much fluid is detrimental Knowing ‘when is too much’ is crucial Intergrated, multimodal POCUS examination can aid decisions at all stages
- 45. 7th #IFAD2018Reviewing recent advances in fluid management and haemodynamic and organ function monitoring in critical care All specialties welcome! @Fluid_Academy www.fluidacademy.org International FluidAcademy Day The Netherlands Amsterdam
- 46. Key References Four phases of intravenous fluid therapy: a conceptual model - https://academic.oup.com/bja/article/113/5/740/2920186 Transthoracic echocardiography: an accurate and precise method for estimating cardiac output in the critically ill patient - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5465531/ www.Thinkingcriticalcare.com Development of a fluid resuscitation protocol using inferior vena cava and lung ultrasound - https://www.ncbi.nlm.nih.gov/pubmed/26475100 Diastolic dysfunction in anaesthesia and critical care - https://academic.oup.com/bjaed/article/16/9/287/1743688 IntrarenalVenous Flow:AWindow Into the Congestive Kidney Failure Phenotype of Heart Failure? - http://heartfailure.onlinejacc.org/content/jhf/4/8/683.full.pdf
Editor's Notes
- These are some of the organisations and societies I contribute to. I have no financial confliction of interests to declare. Perhaps my most important declaration of interest is the fact that I use point-of-care ultrasound in my daily practice.
- A little reminder that ultrasound as we know it today was developed from SONAR technology used in submarines. The use of soundwave as a way of imaging has come a long way since then. Early machines had patients submerged in baths of water and look nothing like the devices we know today. Ultrasound and water/fluids have gone hand in hand and today, Im going to revisit this relationship.
- You’ve heard it already today and I’ll re-emphasise this key message. Fluids are drugs.
- Like all drugs they have got their specific indication and contra-indication. My colleagues have told you about the various considerations that you must play attention to when prescribing fluids.
- The harm of associated with excessive fluid is well known. It’s a scenario I’m sure we are all familiar with.
- It affects all organ systems of the body and not just the obvious cardiovascular and respiratory system. I would like to focus your attention on the hepatic and renal system as I will come back to these later in my lecture.
- Let’s remind ourselves of the 4 phases of fluid management – the ROSE concept. Resuscitation, Optimisation, Stabilisation and de-Escalation
- Much of ICU research has focused on the rescue and optimisation phase of the 4 phases. There has been less attention paid to the the later stages. Perhaps it is because of the misconception that if you get the first few 2 stages right, the remaining stages becomes less of an issue.
- In the orginal paper, the authors suggested various forms of monitoring that you could use according to the various phases. Note that cardiac echo/doppler is primarily thought to be for these first 2 phases. Note that ultrasound of the other organs isn’t mentioned and there is precious little suggested help in the later 2 phases.
- With that all in mind, I am going to tell you about how I/we can potentially use point-of-care ultrasound with regards the fluids with emphasis on the later stages. It is impossible to talk about everything that POCUS can offer so I am just going to focus on the big headlines.
- This is just one of the many papers/statements which has pushed the fact that the ability to use point-of-care ultrasound should be a core competency of the intensivists.
- Every single practicing intensivisits out there should have the ability to perform focused examination of the heart, lung and so on by the bedside to aid decision making and devise management strategies.
- I will show you that POCUS has a role in all the phases of fluid management.
- You’ve seen this before, but essentially, the 4 phases are about asking these 4 questions. When to start fluids When to stop fluids When to start fluid removal When to stop fluid removal I’m going to focus on the last 2
- Ultrasound/Echocardiography has the ability to tell us when to stop our fluid resuscitation – i.e. stop giving fluids. We need to know when the glass is getting full. It also helps us to decide when we may have overshot and hence need to start taking off fluid – either by diuretics or renal replacement therapy
- Lets talk about basic or core echocardiography. This skill can be acquired and maintained by the average intensivists. I am NOT talking about advanced echocardiography. We are talking about focused examination. In this case, we are going to assess LV function and size. RV function and size. The inferior vena cava.
- These are some of the standard views of the echocardiography. PSSX, PSLX, A4C, Subcostal. Focusing on the LV, from these views we can get an idea of its size and systolic function. Is it grossly dilated? Is it grossly impaired? Or is it very empty which is what you would be looking for if you are considering giving fluids.
- With regards to the right ventricle. You can again get an idea of its size and function just by eye-balling it. The RV base should be about 2/3s that of the LV in the apical 4 chamber view. But I personally like the TAPSe measurement – Use M-mode over the tricuspid annulus and measure how much it moves forward. The magic number is 1.6cm or 16mm.
- You could also look at how the two ventricles interact with each other especially how the septum which separated the LV and the RV behaves. Compare these two images. Normal on the left side of the screen. Look at the right sided image, Notice how the septum bows into the left ventricle as RV pressure exceeds the LV.
- Subcostal view of the IVC. Examination of the IVC – strongly advocated in most resuscitative protocols. 2 parameters are measured – absolute diameter and the degree of collapse during the respiratory cycle. If the IVC is small and collapsing, the patient will probably be fluid responsive. BUT doubts have arisen, it is not as straight forward as we thought. We are not sure how to inteprete, where to measure, how to measure (m-mode, collapse). Caution is advised.
- Onto lung ultrasound. We are going to focus on the B-lines and effusions. Most ppl are comfortable recognizing pleural effusions on ultrasound and indeed the use of ultrasound to guide the draining of the effusion. This is widely accepted as gold standard practice. B-lines and A-lines are perhaps less well known and established in critical care practice. B-lines represent fluid in the interstitium and at the very basics could be interpreted as the equivalent of crackles on auscultation.
- This is a normal ultrasound scan of the lung. Rib shadows here and here. Hortizontal A-lines which are reverberation artifacts from the pleura line. Notice the occasional vertical streak on the side of that rib shadow. That’s a B-line. You are allowed 2 per rib space.
- So you’ve seen a normal ultrasound scan of the lung, compare these two images. I’m sure you can appreciate how different they are compared to the last slide. Notice that there are much more vertical B-lines. They are so numerous that they almost coalesce. So if you see these images throughout the lung field, you may have overfilled the patient and its time to move to fluid removal.
- These are effusions. They are so much easier to pick out compared to that of plain radiographs. The specificity and sensitivity of ultrasound in diagnosis pleural effusions outperforms those of clinical examination and plain radiographs.
- Onto more advanced and perhaps experimental techniques. Things that are perhaps in the future compared to the modalities that I’ve already described to you. I would emphasise that all these scans provide that extra bit of information to put together when devising your fluid strategy. They do NOT replace clinical acquiment and history. It does not replace the need or ability to bring all the information together to devise our fluid strategy.
- I’m sure you are all familiar with the use of the passive-leg raise test to test for fluid responsiveness. This is an important test not just an important test in deciding when to give fluid but also it can also tell you when to stop giving fluid – when there is no longer a response increase in cardiac output.
- You can use a variety of cardiac output monitors with your PLR. But I would advocate the use of echo ultrasound like this paper here which uses the velocity time integral to measure cardiac output.
- To measure the cardiac output, you need these two views – the PSLX and the apical 5 chamber view. From the PSLX, you get the diameter of the aortic outflow tract and in the 5 chamber view, you can measure the velocity of the blood in the outflow tract.
- Diastolic function is defined as/describes the filling of the heart during diastole. This means how good the myocardium is at relaxing and complying (blood filling up the heart). Between 30% and 50% of patients with chronic heart failure have preserved LV systolic function.
- Again, there are various measures of diastolic dysfunction but here are just two Doppler-based assessments. In patients with sinus rhythm, conventional pulsed wave (PW) Doppler of trans-mitral blood flow reveals a biphasic waveform. The initial (E) wave represents early, passive LV filling and the following (A) wave results from active atrial contraction. The relationship of these peak velocities is known as the E/A ratio. Tissue Doppler imaging (TDI) uses a low-pass filter to exclude blood flow and measure tissue velocity, and it can be used to measure the velocity of longitudinal displacement of the LV basal wall as it relaxes and fills in diastole. TDI at of the mitral annulus reveals a waveform that is similar in shape to the E and A waves, the corresponding peak velocities are known as e prime (e′) and a prime (a′).
- A bigger image of the E A wave
- TDI showing the e’ and a’ wave
- You can then put the two together to grade the degree of diastolic dysfunction according to these patterns or you can utilize the ratio of E to e’. If E is conceptualized as LA/LV driving pressure and e′ is the increase in LV volume, then E/e′ represents the relationship between LV pressure and volume change—or, known as elastance, with its reciprocal being compliance. TDI data are important because they are independent of loading conditions and are easy to obtain so they have considerable utility in critically ill patients. E/e’ ratio < 8 corresponds to normal filling pressure.
- POCUS examination of the portal vein seems to be getting more widely discussed. But just to introduce the concept, the normal portal vein waveform normally shows gentle undulations. During RV failure, higher right heart filling pressures are transmitted back to the hepatic veins and sinusoids, which reduce the compliance of these vessels, thus resulting in a more pulsatile waveform. This finding has been clearly associated with elevated right atrial pressure, tricuspid regurgitation, and RV failure and has also been described in cirrhotic and normal thin (body mass index <20 kg/m2) patients, probably reflecting low abdominal and hepatic acoustical damping. Conceptually, in the right clinical context, PV pulsatility therefore represents the indirect consequence of RV failure. In this short paper, the authors describe the changes of in portal vein pulsatility as right heart failure and overload were treated. Notice the marked marked pulsatility before treatment got commenced and notice how it all levels off as the patient got better.
- Along the same concepts of portal vein pulsatility is the use of doppler studies to study renal blood flow. This is a fascinating concept where arterial and venous flow to the kidneys can be studied in a point-of-care fashion.
- Using these concepts, this table just summarises the findings from the more advanced/experimental techniques I talked about, and that of the well-known IVC.
- As a quick mention, you can use ultrasound to detect tissue oedema such as this case.
- Take home message, the strength of POCUS is that you can examine a number of modalities in order to formulate the appropriate fluid strategy together with clinical examination and history.
- Individually, all these modalities have their strength and weakness. The analogy of the blindmen asked to describe an elephant. You only get the true picture by bringing all the pieces of information together.
- The combined use of heart, lung and abdominal ultrasound has been pooled to construct RESUSCITATIVE fluid protocols such as RUSH. Heart lung abdominal to describe the pump, tank and pipes.
- And also the SESAME protocol by colleagues in Paris.
- As mentioned at the start, there is little work on protocols to help deresuscitation – this is one of the first and few. I suspect as our understanding and utilisation of US increases, such protocols will become more common.
- So to summarise, Too much fluid is harmful A lot of work has focused on giving fluid compared to when to stop giving or indeed removing fluid I hope to have at least show you that POCUS examination is not only useful for the early stages of fluid resuscitation but may also have a role in guiding fluid removal.