Optimal depth, timing and duration based on recent clinical trials (K Sunde)
Cardiac arrest is a complex disease
- several different causes (many untreatable, irreversible, extreme challenging)
- large heterogeneity
- challenges the system due to the limited/crucial time-intervals (hypoxia/extreme ischemia)
- large differences in quality of care within and inbetween systems (both during ALS and in post resuscitation care)
- very high mortality
Depth and Timing
ILCOR Statement 2003 –
Unconscious adult patients with spontaneous circulation after out-of hospital cardiac arrest should be cooled to 32-34°C for 12-24 hrs when the initial rhythm was VF.
For any other rhythm, or cardiac arrest inhospital, such cooling may also be beneficial.
Outcome, timing and adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest.
- timing, speed and duration of hypothermia had no impact on outcome!
Confounding aspects regarding early/fast cooling
- the lack of protection against a drop in core temperature is due to a larger and deeper brain injury! (link)
- If you are really “dead” you are colder and it is very easy to cool you fast! (link)
Intra-Arrest Transnasal Evaporative Cooling: A Randomized, Prehospital, Multicenter Study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness) link
Duration of TTM
Targeted Temperature Management for 48 vs 24 Hours and Neurologic Outcome After Out-of-Hospital Cardiac Arrest
Prolonged targeted temperature management in patients suffering from out-of-hospital cardiac arrest
- Cardiac arrest is complex, with large heterogeneity and very high mortality
- Large differences in quality of care within and inbetween systems
- Concerning pathophysiology and TTM: depth, speed and duration impacts on the reperfusion injury/brain injury
- We are concluding based on pragmatic trials not optimizing the intervention tested or considering the ongoing pathophysiology!
- Outcome assessment: cognitive function/QoL years after the arrest!
Haemodynamic Management During Targeted Temperature Management (Huang CH)
Multiple reasons for haemodynamic instability post-cardiac arrest
Haemodynamic Response Correlated to Outcome – Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest.
Cardiovascular Response & Haemodynamic Changes In Hypothermia Treatment
- Changes in CV β-adrenoceptor (reduced response)
- Increase in stroke volume
- Reduced intravascular volume during hypothermia is by 10– 35%
Lower heart rate is associated with good one-year outcome in postresuscitation patients (link)
Survivors Have Higher Mean Arterial Pressure (link)
Lowest value of DAP over the first 6 h after ICU admission for predicting unfavourable neurological outcome at 3 months (link)
Postresuscitation hemodynamics during therapeutic hypothermia after out-of-hospital cardiac arrest with ventricular fibrillation: A retrospective study
Inferior Vena Cava may appear congested when it’s dilated without any respiratory variation collapsed with very small diameter through the respiratory cycle, or compliant and vary through respiratory cycle. But how IVC looks like depends on how the patientis breathing, spontaneouslyvs mechanically ventilated.
During spontaneous breathing, in inspiration there is a decrease in pleural pressure, partially transmitted to the heart chambers with a decrease in Right Atrial Pressureand increase in Venous Return (the lower the RAPthe easier the venous return). Because of this decrease in RAP there is a decrease in IVC transmural pressure the size (diameter) and a decrease in size of IVC.
To give numbers, a 40% variation in spontaneouslybreathingpatients is usually associated to preload responsiveness: patient will respond to fluids (but it does not mean that he needs fluids: gives only if associated hypotension/poor perfusion).
In patients with positive pressure ventilation physiology is completely reversed: you put positive pressure in the thorax, this is partially transmitted to the heart chambers whit an increase in RAP, an increase in IVC transmural pressure and in IVC diameter. We expect a dilated and non compliant Vena Cava due to the impeded venous return, collapsible vena cava is an abnormal finding. If you observe a compliant Vena Cava n a patient on MV, changing diameter with ventilation, actually increasing diameter with insufflation due to raised pressure in thorax impeding venous return and flattening in expiration with pressure release), this means that probablythis patient has volume in the veins that can be recruited. A > 12-18% variation in mechanically ventilated patientis usually associated to preload responsiveness(Feissel et al. 2004 http://bit.ly/2Cvm6Fp; Barbier et al. 2004 http://bit.ly/2Pb8R3p).
In patients with elevated Intra-Abdominal Pressure IVC is not interpretable anymore.
The endpoint of resuscitation is improve tissue perfusion, not to increase IVC diameter. The respiratory variations in large vessels just attest that there is some stressed volume that can be recruited: is vein collapses there is room to expand a little more and by increasing the stressed volume there is an high probability to increase the venous return and cardiac output if you think this in needed.And remember: IVC measurement really simple but not make the vena cava say what it can’t say.
Pictures from Cholley B talk at #LIVES2018
It was delightful listening to Paul Mayo deliver this excellent talk based on his clinical experience.
Critical care echocardiography is a different beast to the traditional “echo lab” approach favoured by cardiology. Our environment does not lend itself well to hour long studies per patient recording every measurement.
His unit adopts a flexible approach, deploying aspects of advanced echo as needed to answer specific clinical questions. Occasionally a full study will be performed. For quality control reasons, all their TOEs (TEEs) are full studies.
NYC is staffed by 10 attending and 6 “night owls”, all of whom are competent in general critical care ultrasound. 3 of the team are competent in advanced echo.
As an example of how they apply advanced skills, All shocked patients will get VTI to estimate stroke volume. Other measurements are used selectively such as:
- E/e’ to estimate filling pressures
- Bubble studies for hypoxemia
- Quantitative studies of valve function
- Precise measurements of RV function (PASP, PADP, PAMP, RV S’, PAT, TAPSE)
- Regional wall motion abnormality assessments
- serial echoes for dobutamine or nitric oxide trials
Images are saved, and relevant findings documented in notes (except TOEs which all get a ful, report). Interesting cases are discussed at a weekly meeting.
For those training in advanced CCE, Mayo recommends ALL views and ALL measurements are performed in a specific sequence, and images rejected if they are suboptimal. Not only does it upskill the user, it brings credibility to the field and reassures our cardiology and imaging colleagues.
These were certainly useful points that all of us in the critical care and imaging community should take note of.