ICU-Surgical Inter-departmental Grand Round Updates in Haemodynamics Support

1. ICU-Surgical Inter-departmental Grand RoundUpdates in Haemodynamics Support Speakers: Dr. OY Tam, Dr. LL Chang

2. M/78 HT / Asthma Acute abdomen, Free gas under diaphragm Emergency laparotomy Perforated rectosigmoid diverticulitis, faecal peritonitis. Hartmann’s operation performed. Intra-op required NA support.

3. Post op D1 • Warm peripheries, hypotensive, oliguric, dehydrated • DIC, ARF, severe metabolic acidosis • Faecal peritonitis with septic shock / hypovolemic shock. MODS. Post op Mx: Antibiotics, repeated fluid challenges, Nor-adrenaline and Adrenaline, CVVH, Hydrocortisone

4. Post op D2 • Condition further deteriorated despite significant fluid gain and maximal vasopressors support • Edematous, hypotensive, anuric, skin mottling • Worsening metabolic acidosis, DIC Persistent septic shock. ?volume status optimized ?pump failure Bedside TTE: hyperdynamic heart (on max vasopressors), no RWMA, small RH volume (likely fluid loss to 3rd space with intravascular volume depletion) Mx: further fluid bolus tried

5. Post op D3 • Condition still grave • Worsening clinical and laboratories parameters despite max. supportive treatment • Trial of straight leg raising  only slight improvement of SBP • Already grossly edematous • Comfort care Patient passed away on post op D5

6. Haemodynamic monitoring is essential for proper decision making in critically ill and high-risk surgical patients Yet, every haemodynamic variable has limitations and confounding factors. No monitoring device improves outcome if it’s not coupled to treatment which improves outcome.

7. Over the last thirty years… • From invasive and quantitative monitoring to less invasive and more qualitative monitoring i.e. the concept of functional haemodynamics monitoring LESS IS MORE!

8. Easy and quick to use Widely available Minimally invasive Coupled with a coherent therapeutic protocol Requirements of quality monitoring Allow us to understand the mechanisms of circulatory failure, thus enables treatment to be adapted to the circumstances

9. Haemodynamic support What are the goals? Concept of fluid responsiveness What are the tools? What are their limitations? Goal directed haemodynamics therapy

10. Shock is defined as generalized maldistribution of blood flow causing failure of delivering and/or utilization of adequate amount of oxygen resulting in tissue dysoxia. Ultimate goal of haemodynamic management is to achieve adequate organ and tissue perfusion

11. BP Targets • Most conditions with shock • MAP > 65 mmHg • Trauma patient with penetrating injury  Avoid aggressive fluid resuscitation • MAP of 40 mmHg until bleeding is controlled surgically • Trauma patient with blunt injury  no specific guideline • Traumatic brain injury without systemic haemorrhage • MAP of 90 mmHg • Cardiogenic shock • SBP > 100 mmHg if there is ST elevation Hypotension are commonly present in shock. However, it is NOT required to define shock. Signs of inadequate tissue perfusion on physical examination are required to define shock.

12. Old equipment • Right heart catheterization for bedside measurements of cardiac output and right and left filling pressures was once the gold standard of haemodynamic assessment in the field of intensive care. With time, numerous clinical studies questioned the safety and utility of PAC.

13. PAC can generate large numbers of haemodynamic variables… • Central venous pressure (CVP) • Pulmonary arterial occlusion pressure (PAOP) • Cardiac output / cardiac index (CO / CI) • Stroke volume (SV) • R ventricle ejection fraction/ end diatolic volume (RVEF / RVEDV) • Systemic vascular resistance index (SVRI) • Pulmonary vascular resistance index (PVRI) • Oxygen delivery / uptake (DO2 / VO2) However, do we really know how to interpret these complicated variables?? Erroneous interpretations lead to no clinical benefit and even harm to the patient.

14. PAC is OUT because… Increases mortality and complications • Unreliable e.g. intermittent thermodilution cardiac output determinations • Requires a high degree of skill and experience to use and interpret correctly • Some physiological variables are lacking relevance to the clinical situation • Not improve outcome • Safer, less-invasive alternatives are readily available May be useful in selected patients only!

15. What we have now… BP/P urine output PE Echocardiography Preload and fluid responsiveness Markers of inadequate tissue perfusion PiCCO / LiDCO

16. BP/P, U/O, PE • Physical signs • Arterial line - Real time, continuous measurement • Urine output • When renal perfusion is adequate urine output will exceed 0.5 ml/kg/h • Affected by use of diuretics such as lasix and dopamine • Temperature gradient between the toe and the ambient temperature correlates with cardiac index, stroke index and oxygen transport in cardiogenic shock • Low cost and low risk • Low sensitivity and specificity

17. In patients with ALI, there is a high probability that physical examination findings of ineffective circulation (capillary refill time >2 s, knee mottling, or cool extremities) are not useful for predicting low cardiac index. Prediction of haemodynamics in critically ill patients by clinical evaluation alone is inaccurate and unreliable.

18. In high-risk, hemodynamically stable surgical patients, there were no significant differences in mean BP, HR, urine output, and arterial oxygenation at any time between survivors and non-survivors, although non-survivors had higher lactate levels than survivors. Adequate resuscitation cannot be based only on normalization of vital signs.

19. Preload and fluid responsiveness • Estimates of intravascular volume based on any given level of fillingpressure do not reliably predict a patient’s response to fluid administration • In shock, low values of static measures of preload  should be immediately resuscitated with fluid with careful monitoring • Dynamic measures of fluid responsiveness are better predictors of fluid responsiveness than static parameters

20. CVP • A guide to right ventricular filling • However, preload is determined by end-diastolic volume not pressure • Without knowledge of the ventricular compliance, an isolated CVP reading is of limited value • Compliance not only varies from patient to patient but varies with time in the same patient Dynamic changes in CVP are more useful than absolute values

21. Use of CVP SHOCK Fluid challenge with 250ml of colloid over 10mins Or Straight leg raising maneuver CVP rises >7mmHg Maximally filled Further filling  pulmonary edema CVP returns to within 3mmHg of its original Value within 10mins Risk of pulmonary Edema moderate No further filling is Required CVP rises <3mmHg Underfilled Further filling Further fluid Vasopressors / Inotropes

22. Limitations of CVP • Cannot reflect actual RAP in most situations • Only valid if LV filling = RV filling • Impaired RV compliance (e.g. inferior MI, severe sepsis) • Lung disease leading to pulmonary HT • Great veins obstruction or systemic venoconstriction • TR • Elevation of ITP or IAB e.g. mechanical ventilated patients or intra-abdominal HT

23. Static preload parameters cannot accurately predict the response of CO to fluid loading Good contractility Poor contractility Preload

24. This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP orΔCVP to predict fluid responsiveness. CVP should not be used to make clinical decisions regarding fluid management.

25. Drawbacks of fluid challenge as a diagnostic approach • Ineffective fluid challenges (in up to 50% of the suspected hypovolemic patients by clinical or CVP) often lead to additional boluses, culminating in a grossly edematous patient (still hypotensive and oliguric) • Positive fluid balance is associated with a worse outcome from ALI/ARDS After acute resuscitation, additional fluid therapy may cause harm.

26. Advances in preload measures and predicting fluid responsiveness Volumetric Preload Parameters: Global End-Diastolic Volume (GEDV) and intrathoracic Blood Volume (ITBV) / PiCCO • More sensitive and specific to cardiac preload compared to the standard cardiac filling pressures CVP / PCWP as well as right ventricular end diastolic volume • Parameters are not influenced by mechanical ventilation Dynamic measurements i.e. Pulse pressure and Stroke volume variations

27. Dynamic measures of fluid responsiveness Stroke Volume Variation (SVV) Systolic pressure Variation (SPV) Pulse pressure Variation (PPV)

28. Mechanism ofDynamic measures • During inspiration, ↑ intrathoracic pressure ↓venous return, i.e., preload and ↓SV • As a result, systolic and diastolic pressures decrease and increase with a short delay after inspiration and expiration, respectively • The effect is more pronounced with hypovolemia as the ventricle is more sensitive to preload • Sensitive and specific in discriminating fluid responder and non-responder

29. Limitations • Sinus rhythm • Mechanically ventilated patients with tidal volume of at least 8ml/kg • Not reliable in ARDS patients • Alteration of vasomotor tone

30. Echocardiography Measure cardiac output base on 2D and doppler flow technique • TTE • TEE Visualization of ventricular function, valves structure, wall motion abnormalities, cardiac filling and pericardial diseases, PE, aortic dissection Provide real time guiding of fluid therapy

31. Value of echocardiography in Shock • Provides a quick and accurate assessment of structures, preload and contractility • Preload is estimated by LVEDV (cardiac dimensions, not pressures) • Measures contractility by ejection fraction Differentiate varies types of shock

32. Fluid? Vasopressor? Inotrope? Ensure adequate volume first! • Inappropriate use of vasopressor before adequate volume therapy may produce dynamic LV outflow tract obstruction non-responsiveness to vasopressor  further administration  further harm… • Use of dobutamine in septic patient  further drop in BP due to vasodilatory effect Echo is a very useful Guide to treatment!

33. TTE • Disadvantages • Operator dependent • Difficult to obtain good view in some patients (on high ventilator support, obese) • Cannot provide continuous monitoring

34. Markers of inadequate tissue perfusion In shock • Increased serum lactate • Increased base deficit • RFT and electrolytes • Decreased ScvO2 and SvO2 (tissue O2 extraction / balance between DO2 and VO2) Increased blood lactate and failure of normalization of blood lactate are associated with increased morbidity and mortality

35. Tissue O2 extraction • Low SvO2 / ScvO2 • O2 delivery is insufficient to demand  shock ?? what type of shock • High SvO2 / ScvO2 • May reflect a failure of cells to take up and utilize oxygen e.g. during sepsis ?? May also be due to numerous ddx • Normal SvO2 / ScvO2 ?? may simply reflect a combination of low CO and sepsis

36. PiCCO Utilizes any available central venous line and a PULSIOCATH thermodilution catheter with lumen for arterial pressure measurement Principle of thermodilution • Injection of cold injectate  fall in temperature in the circulation • The lower the cardiac output the lower the degree of dilution as the injectate is injected. i.e. fall in temperature will be greater

37. T injection t P t Following 3 cold saline bolus injections via the CVP line detected by the thermodilution catheter the device software can integrate this information with the arterial waveform to give a continuous display of cardiac output (response time 12s). Transpulmonary Thermodilution CV Bolus injection CALIBRATION PULSIOCATH Pulse Contour Analysis

38. PiCCO Derived values • Thermodilution Parameters • Cardiac Output CO • Global End-Diastolic Volume GEDV • Intrathoracic Blood Volume ITBV • Extravascular Lung Water EVLW* • Pulmonary Vascular Permeability Index PVPI* • Cardiac Function Index CFI • Global Ejection Fraction GEF • Pulse Contour Parameters • Pulse Contour Cardiac Output PCCO • Arterial Blood Pressure AP • Heart Rate HR • Stroke Volume SV • Stroke Volume Variation SVV • Pulse Pressure Variation PPV • Systemic Vascular Resistance SVR • Index of Left Ventricular Contractility dPmx*

39. Summary • Clinical assessment • BP, pulse, U/O • Fluid challenge • Dynamic assessment of fluid responsiveness e.g. straight leg raising, systolic pressure variation, pulse pressure variation • Laboratories parameters • Echocardiography

40. Take home messages • No monitoring device can improve patient-centered outcomes unless it is coupled to a treatment that improves outcome • Every haemodynamic variable has limitations which has to be recognized and incorporated into our practice • Trend of haemodynamic parameters is more important. Reassessment is a must in unstable patient • Multi-parametric approach may reduce the chance of erroneous decisions

41. M/66 HT / old CVA / chronic renal impairment Incidental finding of 6.4cm infrarenal AAA Elective EVAR Tight stenosis of left EIA and right CIA/EIA junction. Bilateral EIA extremely tortuous, difficult advancement of endovascular device into aorta

42. Post EVAR D0 • Hypotensive, tachycardiac, oliguric, pallor • Severe metabolic acidosis, ↑Ur / Cr, Hb 127 • Active bleeding with hypovolemic shock EOT found 500ml retroperitoneal haematoma, arterial spurter at R iliac artery. Rupture artery repaired. EBL 1L. Post op Mx: Massive fluid and blood transfusion. Nor-adrenaline. CVVH.

43. Post EVAR D1 • Remains hypotensive on high dose NA • Persistent severe metabolic acidosis despite on CVVH • Abdominal distention, scrotal hematoma, dusky bilateral lower limbs • Persistent shock as evidence by low BP, poor tissue perfusion and metabolic acidosis. EOT: bleeding from R femoral artery anastomotic site, gangrenous colon. Haemostasis. Total colectomy. Packing. EBL 2L. Post op: resumed CVVH and supportive Tx

44. Post EVAR D2 • Planned laparotomy for removal of packings and ileostomy performed C/w NSTEMI, TnT 2.9, ischemic hepatitis Mx: continued CVVH and supportive care Developed pulseless VT/VF on post EVAR D3, failed resuscitation and succumbed.

45. Take home messages • In most situations, haemodynamic instability and shock can be assessed by clinical and simple, non-invasive haemodynamic monitoring • Aim of haemodynamic monitoring is also to look for the cause of shock and give proper treatment • Ineffective treatment usually leads to further treatment which eventually causes harm to the patient • In complicated situations, echocardiography is important and can provide significant relevant information which guide treatment

46. Fluid Therapy

47. Introduction Does the timing of giving fluid resuscitation affect outcome? Does the choice of resuscitation fluid affect survival?

48. Timing • Early Goal-directed Therapy (EGDT) Rivers E et al. NEJM 2001; 345: 1368 • Randomly assigned patients with severe sepsis or septic shock to receive either 6 hrs of EGDT or standard therapy before ICU admission • Primary outcome: in-hospital mortality, APACHE II scores obtained serially for 72 hrs

50. Early Goal-directed Therapy 263 patients were enrolled, 130 to EGDT and 133 to standard therapy No significant difference in baseline characteristics In-hospital mortality: 30.5% in EGDT group and 46.5% in standard therapy group (p=0.009)