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Mervyn Singer Bloomsbury Institute of Intensive Care Medicine, University College London, UK Monitoring the adequacy of organ perfusion & function in shock.

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Presentation on theme: "Mervyn Singer Bloomsbury Institute of Intensive Care Medicine, University College London, UK Monitoring the adequacy of organ perfusion & function in shock."— Presentation transcript:

1 Mervyn Singer Bloomsbury Institute of Intensive Care Medicine, University College London, UK Monitoring the adequacy of organ perfusion & function in shock Monitoring the adequacy of organ perfusion & function in shock

2 Declarations of potential conflicts.. (Deltex) (Edwards) Oxford Optronix - free probes

3 Shock Delivery to, or utilisation of, oxygen that is inadequate to meet the cells’ metabolic needs

4 Shock - a physiological definition o hypoxic hypoxia (low PO 2 ) o circulatory hypoxia (low CO) o anaemic hypoxia (low Hb) o cytotoxic dysoxia (mitochondrial dysfunction) VO 2 DO 2 O2O2 O2O2

5 ‘Perfusion’ vs ‘Adequacy of perfusion’ Perfusion = oxygen delivery flow (macro- & microcirculation) Hb SO 2 (local PO 2 ) Adequacy of perfusion = perfusion enough to supply tissues adequately

6 Perfusion/Adequacy of perfusion o biochemical o lactate o base deficit o vascular and tissue respiratory gases o CO 2 - tissue tension o O 2 - venous, tissue, microvascular - tissue tension, saturation, VO 2 o microcirculation o mitochondrial redox status

7 Lactate o [lactate] predictive of poor outcome in …sepsis, trauma, haemorrhage o very non-specific marker of tissue hypoxia o more due to metabolic effects of epinephrine …than reduced tissue perfusion o related to ∆ muscle Na+/K+-ATPase activity …driven by epinephrine-stim’d aerobic glycolysis o high [lactate] & [epinephrine] can persist for …weeks in burn-injured patients

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9 Hyperlactataemia o.. blocked by ouabain or ß-blocker o iatrogenic causes o lactate-buffered haemofiltration o epinephrine o drugs e.g. NRTIs o non-shock causes o severe liver dysfunction o ∆ muscle protein degradation

10 Arterial base deficit = amount of base (mmol) required to titrate 1 litre of whole blood to a normal pH, assuming normal physiological values of PaO 2, PaCO 2 and temperature.

11 Arterial base deficit o ∆ H+ ion production in shock related to …..∆ hydrolysis of ATP o arterial base deficit predictive of poor outcome … in sepsis, trauma, haemorrhage o many non-hypoxic causes of metabolic acidosis o renal dysfunction o liver dysfunction o drug toxicity (e.g. cocaine) o bicarbonate loss (e.g. diarrhoea) o hyperchloraemia … n.b. starting value of base excess may ‘camouflage’

12 SUMMARY: base deficit/lactate o good early prognosticators in shock states o good early guide to therapeutic response o good sensitivity o poor specificity to shock & assessment of perfusion - many confounders (patient/iatrogenic)

13 Tissue PCO 2 o gut tonometry o sublingual capnometry

14 H+H+ local metabolic acidosis (acid buffered by tissue HCO 3 - ) HCO 3 - pCO 2 local respiratory acidosis (stagnant flow) pCO 2 Tissue PCO 2 - traditional view

15 Gutierrez G. Blood flow, not hypoxia, determines intramucosal PCO 2. Crit Care 2005; 9:149-50

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17 pHi = log HCO 3 - (0.03 x PCO 2 ) Henderson-Hasselbalch equation Tissue pCO 2 Tissue-arterial pCO 2 gap Tissue-end-tidal pCO 2 gap

18 Gastric pHi - prognosticator Low pHi related to poor outcome Doglio (CCM ‘91) Maynard (JAMA ‘93) Mythen (ICM ‘94) Low pHi related to inability to wean Mohsenifar (Ann Intern Med ‘93)

19 Gastric pHi-guided therapy?? pHi-guided Rx improved outcome in ICU subset Gutierrez (Lancet ‘92) … or doesn’t Gomersall (Crit Care Med 2000)

20 SUMMARY: tissue PCO 2 o methodological/practical issues to be resolved o marker of poor regional perfusion o relevance to other regional circulations?? o reasonable prognostic tool (as good/better than lactate/base deficit) o ability to direct therapy & improve outcome??? o much hype in the 1990s.. why so quiet now??

21 Oxygen o mixed/central venous O 2 saturation o tissue oxygen tension & saturation o oxygen consumption

22 Mixed/central venous O 2 saturation o marker of global supply/demand balance o falls in low output states e.g. heart failure o prognosticator of outcome, failure to wean… o elevated in resuscitated sepsis o microvascular shunting?? o decreased cellular utilisation?? o mixed venous vs central venous differences o one landmark ScvO 2 -targetted study (Rivers)

23 SUMMARY: mixed/central SvO 2 o PA catheter use decline.. ∆ reliance on ScvO 2 o Rivers’ study needs repeating - recently funded o Useful in global low output states o Limited in established sepsis (other than identification of low values)

24 Tissue O 2 tension o marker of local supply/demand balance o measurable with various technologies o optode, Clark electrode, NIRS, EPR oximetry.. o falls in low output states e.g. heart failure o elevated in resuscitated sepsis o studied separately in multiple tissue beds o gut mucosa, skeletal muscle, bladder, brain, kidney (animal) o brain, skeletal muscle, conjuctiva, subcutaneously (man)

25 Boekstegers et al, Shock 1994;1: Muscle tissue pO 2 in septic patients control cardiogenic shock limited infection sepsis Tissue pO 2 (mmHg)

26 Rosser et al. J Appl Physiol 1995; 79: 1878 Singer et al. Intensive Care Med 1996; 22: 324 Stidwill et al. Intensive Care Med 1998; 24: 1209 Rosser et al. J Appl Physiol 1995; 79: 1878 Singer et al. Intensive Care Med 1996; 22: 324 Stidwill et al. Intensive Care Med 1998; 24: 1209 Haemorrhage Resuscitation Hypoxaemia 21% O 2 15% O 2 10% O 2 6% O 2 Bladder tissue pO 2 falls in other shock states time (h) Bladder epithelial PO 2 (kPa) Endotoxin Control

27 o no organ-organ comparisons published o influence of inspired oxygen in shock states? o impact of volume of tissue being sampled o probe size/surface area o multi-array electrodes… Tissue O 2 tension

28 Acute response in tissue PO 2 to bolus of LPS (10 mg/kg) Time post-LPS (h) MuscleBladder Kidney Liver PO 2 (mmHg) † † † †† † †

29 o Can be relatively non-invasive o NIRS, spectrophotometry techniques … measures oxyHb (?Mb) in tissue/microvascul o porphyrin phosphorescence technique … measures microvascular PO 2 o skeletal muscle StO 2 parallels changes in human …whole body DO 2 during trauma resuscitation Microvascular O 2 tension/saturation

30 SUMMARY: tissue/microvascular O 2 o tissue PO 2 (SO 2 ) = useful marker of local supply- demand balance in non-septic shock or in early …unresuscitated sepsis o raised in resuscitated sepsis - marker of mitochondrial dysfunction o microvascular PO 2 - may provide similar info but …comparative studies needed o no outcome-related PO 2 -guided studies o research tool at present until better defined in pts

31 o Low VO 2 or poor response in VO 2 to challenge (fluid/dobutamine) = poor prognosis o Whole body ≠ regional VO 2 o How much VO 2 is coupled or uncoupled to ATP …production in shock states? Whole body/regional O 2 consumption

32 Crit Care Med 2000; 28:

33 o mainly measured sublingually o relevance of tongue to other organ beds? … but does correlate with gastric & s/l PCO 2 o prognosticator of outcome in sepsis Microcirculation

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35 o relevance to local tissue O 2 ?? o ? reactive to decreased mitochondrial utilisation c/f hyperoxia o +tive correlation between capillary O 2 extraction & degree of regional capillary stopped-flow - i.e. remaining functionally normal capillaries offload more O 2 to surrounding tissue o minimal cell death seen in sepsis o need for automated semi-quantification technique o no outcome-related microcirc’n-guided studies Microcirculation

36 SUMMARY: microcirculation o interesting research tool for assessing perfusion o applicability of tongue to other tissue beds? o pathophysiological questions - causative or 2°?? o relative infancy - not a routine clinical tool yet

37 o >90% of VO 2 used by mitochondria o >90% of ATP in most cells generated by ETC o..thus mitos play a fundamental role in shock o degree of dysfunction in established septic shock relates to poor outcome o ATP not yet measurable at bedside o redox status can be used for trend-following Mitochondrial function

38 NADH fluoroscopy & NIRS NADH NAD+ oxidised reduced

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40 Rhee P et al. Near-infrared spectroscopy: Continuous measurement of cytochrome oxidation during hemorrhagic shock. Crit Care Med 1997; 25: liver kidney muscle stomach Cyt aa 3 (%change from baseline) CO DO 2 VO 2

41 o cannot yet be quantified in vivo o good for trend-following … … ideally from normal baseline o limited use in patient who’s already critically ill Mitochondrial redox state

42 SUMMARY: mitochondrion o.. the ideal organelle to monitor the adequacy of organ perfusion o.. but, at present, no bedside mitochondrial monitor that offers more than trend following

43 SUMMARY: overall o shock is not an homogenous condition o we still lack the perfect bedside tool to assess adequacy of organ perfusion o will there ever be one? o is measuring site representative of other organ beds? o should we use an amalgam of technologies? o tool-directed outcome studies are needed

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