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Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
Hemodynamic Stabilisation In Septic Shock
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Hemodynamic Stabilisation In Septic Shock

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  • Perfusion becomes dependent on pressure below a certain mean arterial pressure because autoregulation in various vascular beds can be lost. Supplement goal such as blood pressure with the assessment of global perfusion such as blood lactate concentrations Dopamine increases mean arterial pressure and cardiac output due to an increase in stroke volume and heart rate Norepinephrine increases mean arterial pressure due to vasoconstrictive effects Norepinephrine causes little change in heart rate and less increase in stroke volume compared to dopamine Dopamine causes more tachycardia and may be more arrhythmogenic
  • Arterial catheter placement in an emergency department is typically not possible or practical. Vasopressin is a direct vasoconstrictor without inotropic or chronotropic effects and may result in decreased cardiac output and hepatosplanchnic flow. Most published reports exclude patients from treatment with vasopressin if the cardiac index is < 2 or 2.5. Low doses of vasopressin may be effective in raising blood pressure in patients refractory to other vasopressors, although no outcome data are available.
  • Dobutamine is the first-choice inotrope for patients with measured or suspected low cardiac output in the presence of adequate left ventricular filling pressure (or clinical assessment of adequate fluid resuscitation) and adequate mean arterial pressure. The goal of resuscitation should be to achieve adequate levels of oxygen delivery or avoid flow dependent tissue hypoxia. “Two large prospective clinical trials that included critically ill ICU patients who had severe sepsis failed to demonstrate benefit from increasing oxygen delivery to supranormal levels by use of dobutamine.” P. 863
  • Transcript

    • 1. Hemodynamic Stabilisation in Septic shock Dr. T.R.Chandrashekar Intensivist K.R. Hospital Bangalore
    • 2.
      • Shock is defined as a life-threatening, generalized maldistribution of blood flow resulting in failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia .
      • Hypotension [SBP < 90 mmHg, SBP decrease of 40 mmHg from baseline, or mean arterial pressure (MAP) < 65 mmHg], while commonly present, should not be required to define shock .
      • Shock requires evidence of inadequate tissue perfusion on physical examination .
      Shock
    • 3. Septic shock
      • The definition underscore a few points
      • 1) Blood flow at a adequate pressure (MAP)> 65mmHg
      • Shock can still occur with a normal perfusion.
      • Delivery and utilisation of O2 at cellular level-abnormalities are the hall mark of septic shock.
    • 4. Septic shock Macrocirculation Perfusion with adequate oxygen Microcirculation Improper delivery and utilisation Mitochondrial dysfuction Microcirculatory and Mitochondrial Distress syndrome (MMDS) MMDS = sepsis +genes+ therapy + time Adequate perfusion pressure MAP>=65mmHg Adequate oxygen delivery CO x Hb x SPO2 x 1.34 + .003 x PaO2
    • 5. Macro-Circulation
    • 6. Optimisation of Macrocirculation
      • Assessment
      • Clinical
      • Hypotension
      • Tachycardia
      • Altered mental status
      • Delayed capillary refill
      • Decreased urine output
      • Cool skin
      • Cold extremities
      • Hemodynamic parameters
      • Organ perfusion
      • Goals
      • HEMODYNAMCS
      • CVP = 8–12 mm Hg
      • MAP > = 65 mm Hg
      • CI >=2.5- 3 L/min/m2
      • O2 DELIVERY
      • Arterial Hgb SpO2 > 93%
      • ScVO2 > =70 mm Hg
      • Blood Lactate Conc < 2 mM/L
      • Hematocrit >=30%
      • ORGAN PERFUSION
      • CNS - improved sensorium
      • Skin - warm, well perfused
      • Renal - Urine output >=0.5ml/kg/hr
    • 7. Hemodynamic Truths
      • Tachycardia is never a good thing
      • Hypotension is always pathological
      • There is no normal cardiac output
      • CVP is only elevated in disease
      • Peripheral edema is of cosmetic concern
    • 8. Volume Vessel tone Heart function If shock is prolonged, mechanisms of shock are combined Physiologic Classification of Acute Circulatory Insufficiency Fluids / blood Vasopressors Inotropes
    • 9.
      • The question “Will my patient respond to fluids?” cannot be accurately answered by any ‘preload’ parameter
      • Principles of Volume challenge
      • To test Starling’s law the fluid needs to be given quickly – the faster it is given the less that is needed
        • It makes no sense to test “preload” responses over long periods of time (eg Kumar et al 2004)
      • The type of fluid is not critical if given quickly enough
      • There needs to be a change in CVP to know that Starling’s Law has been tested
    • 10. PRELOAD assessment-Volume
      • To look at CVP/ PAOP
      • Always CVP is in relation to CO
      Volume responsive Volume unresponsive Preload OK Failing Heart Add dopamine or dobutamine
    • 11. Volume SV Decreased contractility Right atrial volume
        • The actual value of the CVP is determined by the interaction of Cardiac function and return function
      return function cardiac function
    • 12. PRELOAD assessment
      • Attempts to assess EDV through surrogate measures
        • CVP, Ppao, LV end-diastolic area, RV EDV, intrathoracic blood volume
      • A fluid challenge and flow response remain the gold standard for assessing fluid responsiveness
      • The functional range of CVP/Pra is small so that technical factors are important
        • Importance of leveling
        • Transmural pressure
        • Position on waveform
    • 13. CO Preload Fluid Responsiveness is a dynamic parameter that reflects the degree by which the CO responds to changes in preload “ Will my patient respond to fluids?”
    • 14. Dynamic (functional) parameters
              • SPV / dDown, PPV, SVV, RSVT, Others
      • ‘ RULE OF THUMB’
      • (in the absence of any confounding factors )
      • If SPV > 10 mmHg (or 10%), SVV>10%, PPV>13% --- probable significant volume responsiveness (may indeed signify hypovolemia!)
      • Spontaneously breathing patients
      • Passive leg raising test
      MV PATIENTS
    • 15.
      • Fluid resuscitation may consist of natural or artificial colloids or crystalloids
          • No evidenced-based support for one type of fluid over another
            • Crystalloids have a much larger volume of distribution compared to colloids
            • Crystalloid resuscitation requires more fluid to achieve the same endpoints as colloid
            • Crystalloids result in more edema
      Fluid Therapy: Choice of Fluid Grade C Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
    • 16.
      • Fluid challenge in patients with suspected hypovolemia may be given
          • 500 - 1000 mL of crystalloids over 30 mins
          • 300 - 500 mL of colloids over 30 mins
          • Repeat based on response and tolerance
          • Input is typically greater than output due to venodilation and capillary leak
          • Most patients require continuing aggressive fluid resuscitation during the first 24 hours of management
      Fluid Therapy: Fluid Challenge Grade E Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
    • 17. SHOCK MAP < 65mmHg Oliguria (<0.5ml/Kg/hour) Clinical signs of tissue hypoperfusion
      • 1) Clinical approach
      • HR/BP
      • Peripheral perfusion
      • Impact of volume loading
      • Urine output
      2) CVP/SvcO 2 3) Echocardiography should preceed any CO monitoring First step Second step Third step Fourth step Predominant RVF or global F PAC catheter Predominant LVF any CO monitoring
    • 18. Mixed/central venous O 2 saturation
      • marker of global supply/demand balance
      • falls in low output states e.g. heart failure
      • prognosticator of outcome, failure to wean…
      • elevated in resuscitated sepsis
        • microvascular shunting??
        • decreased cellular utilisation??
      • mixed venous vs central venous differences
      • one landmark ScvO 2 -targetted study (Rivers)
    • 19. 75% Factors that influence mixed and central venous SO 2 _ + Hypothermia Anesthesia  PaO2  Hb  Cardiac output  PaO2  Hb  Cardiac output Stress Pain Hyperthermia Shivering  VO2  DO2  DO2  VO2
    • 20. Mixed/central SvO 2
      • PA catheter use decline .. ∆ reliance on ScvO 2
      • Useful in global low output states
      • Limited in established sepsis
      • (other than identification of low values)
    • 21. SvO2 closely correlates with ScvO2
    • 22. The major problems with the interpretation of ScvO2
      • Like the CO, a low SvO2 tells you that something is wrong, but not what is wrong and what should be done about it (fluids? inotropes?).
      • When the SvO2 is normal or high -one cannot assume that all is well (e.g., CO normal) since in septic patients the ScvO2 may be elevated due to an abnormally low O2 extraction.
    • 23. Insert CVP/SvcO 2 SvO2 >70% SvO2 <70% Sepsis? Repeat Fluid challenge 250ml/ 5mins Haemodynamic improvement ? Consider global/right ventricular failure Echocardiography that preceeds cardiac output monitoring Yes Continue until normal values obtained No Vasopressors Hypovolaemic/ Haemorrhagic/ cause? No response Continue until normal values obtained Haemodynamic improvement Repeat fluid challenge (250ml/5mins) or transfusion if necessary. Echocardiography that preceeds CO monitoring CVP N or low CVP high CVP low
    • 24. How to differentiate between Contractility vs Vasomotor tone
      • Echocardiography
      • Cardiac output monitoring
    • 25. INTERPRETATION OF CARDIAC OUTPUT Do we have a problem ?
      • Arterial hypotension
      • Tachycardia
      • Oliguria
      Increase in cardiac output FLUIDS ? Do we need to measure cardiac output ? DOBUTAMINE ? Faster information ?
    • 26. Why/when would I want to measure CO or SV in shock?
      • Failure hemodynamic management based on clinical signs and CVP-ScvO2; this should always direct to echocardiography
      • Echocardiography should, ideally, always preceed CO monitoring
      • CO monitoring shoud be a PAC catheter in case of RV dysfunction while any CO monitoring, less invasive than PAC, should be favored for LV dysfunction
    • 27.  
    • 28. The way I do
      • After adequate fluid resusciation
      • Start with nor adrenaline then add dobutamine- looking at contractility and SVR
      • If MAP <65 mmHg
      • Add adrenaline or contemplate
      • Vasopressin or phenylephrine
    • 29.
      • Initiate vasopressor therapy if appropriate fluid challenge fails to restore adequate blood pressure and organ perfusion
          • Vasopressor therapy should also be used transiently in the face of life-threatening hypotension, even when fluid challenge is in progress
      • Either norepinephrine or dopamine are first line agents to correct hypotension in septic shock
          • Norepinephrine is more potent than dopamine and may be more effective at reversing hypotension in septic shock patients
          • Dopamine may be particularly useful in patients with compromised systolic function but causes more tachycardia and may be more arrhythmogenic
      Vasopressors Grade E Grade D
    • 30.
      • Low dose dopamine should not be used for renal protection in severe sepsis
      • An arterial catheter -Vasopressors
          • Arterial catheters provide more accurate and reproducible measurement of arterial pressure
          • Vasopressin may be considered in refractory shock patients that are refractory to fluid resuscitation and high dose vasopressors
          • Infusion rate of 0.01-0.04 units/min in adults
          • May decrease stroke volume
      Vasopressors (cont) Grade B Grade E Grade E
    • 31.
      • In patients with low cardiac output despite adequate fluid resuscitation, dobutamine may be used to increase cardiac output
          • Should be combined with vasopressor therapy in the presence of hypotension
      • It is not recommended to increase cardiac index to target an arbitrarily predefined elevated level
          • Patients with severe sepsis failed to benefit from increasing oxygen delivery to supranormal levels by use of dobutamine
      Inotropic Therapy Grade E Grade A
    • 32. Hemodynamic Patterns with Prognostic Value
      • A lower heart rate at the onset of disease is predictive of survival.
      • Normalization within 24 hours of either tachycardia or elevated cardiac index is associated with survival. Persistence of hyperdynamic state increases likelihood of death.
      • A low ejection fraction and ventricular dilatation are also associated with survival. This perhaps reflects Frank-Starling compensation of sepsis induced myocardial depression.
    • 33.
      • Even with the ‘best’ parameters it is not always easy to make the right decision.………
    • 34. Micro- Circulation
    • 35.  
    • 36. “… Our understanding of hemodynamic mechanisms (in distributive shock) depends not so much on the total volume of blood that flows past the aortic valve or the cardiac output as on the amount of blood delivered to the exchange sites. Even though cardiac output may be substantial, if that blood flow does not arrive at the exchange sites, the ultimate metabolic detriment is no different from low cardiac output without shunt flow.” Weil MH, Shubin H (1971) Adv Exp Med Biol 23:13-23.
    • 37. Why the microcirculation is important in shock .
        • It is where oxygen exchange takes place.
        • It plays a central role in the immune system.
        • During sepsis and shock it the first to go and last to recover.
        • Rescue of the microcirculation = resuscitation end-point.
    • 38. Shunting model of sepsis O 2 lactate CO 2 v a Implication : that active recruitment of the microcirculation is an important component of resuscitation. Ince C & Sinaasappel M (1999) Crit Care Med 27:1369-1377
    • 39.  
    • 40. Spronk P, Zandstra D, Ince C (2004) Critical Care 8:462-468 Sepsis is a disease of the microcirculation
    • 41. Mitochondrial Dysfunction in Cell Injury Increased cytosolic Ca 2+ , oxidative stress, lipid peroxidation Mitochondrial PermeabilityTransition Cytochrome c and other pro-apoptotic proteins Apoptosis Robbins & Cotran Pathologic Basis of Disease: 2005
    • 42. Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP Na pump Influx of Ca 2+ H 2 0, and Na + Efflux of K + ER swelling Cell swelling Blebs Clumping chromatin Anaerobic glycolysis Glycogen pH Lipid deposition Detachment of ribosomes Protein synthesis
    • 43. Pump failure or mitochondrial dysfunction Hemodynamic failure Pump failure Mitochondrial dysfunction Hemodynamic and mitochondrial failure Energy failure BE - Lactate Volume test VO 2  Lactate  VO 2  Lactate  Dobutamine test VO 2  Lactate  VO 2  Lactate 
    • 44. Microcirculation assessment
      • Tissue perfusion
      • Gastric tonometry
    • 45. Orthogonal polarization spectral (OPS) imaging
    • 46. Capillary flow in sepsis
    • 47. Microcirculation Recruitment Manoeuvres Ince C (2005) Critical Care 9:S13-S19 Correct pathological flow heterogeneity, microcirculatory shunting and restore autoregulatory dysfunction by control of inflammation, vascular function and coagulation. Avontuur (1997) Cardiovas Res 35:368-376. Siegmund M (2005) Inten Care Med 31:985-992 . Open the microcirculation and keep it open by support of the pump, fluids, vasodilators and restricted use of vasopressor agents. : Boerma (2005) Acta Anaesthesiol Scand. 49(9):1387-90. Spronk (2001) The Lancet 360:1395-1396 Siegemund (2006) Intensive Care Med
    • 48. Sublingual OPS imaging in a patient with septic shock after pressure guided volume resuscitation. the same patient after subsequent nitroglycerin 0.5 mg ivbolus Nitroglycerin promotes microvascular recruitment in septic and cardiogenic shock patients Spronk, Ince, Gardien, Mathura, Oudemans-van Straaten, Zandstra DF. (2002) The Lancet 360:1395-1396.
    • 49.
      • Conclusions
      • Distributive shock has a bad prognosis with difficult to define hemodynamics end-points.
      • 2) It causes a distributive defect at the apillary level of the microcirculation causing functional shunting of weak microcirculatory units.
      • 3) It is the reason why distributive shock cannot be adeqautely monitored by systemic hemodynamic parameters.
      • 4) OPS/SDF en tissue capnography provide an integrative evaluation of the functional state of the microcirculation.
      • 5) Microcirculatory Recruitment Maneuvres are affective in correcting distributive shock
    • 50. Take home thoughts
      • Time is important-EGDT
      • Energy failure may be due to primitive hemodynamic inade q uacy and/or mitoc h ondrial dysfunction
      • Prolonged energy failure leads to irreversible mitoc h ondrial d y sfunction (necrosis - apoptosis
      • Once MMDS starts shock becomes irreversible
      • First optimise macrocirculation
    • 51. Some “ Pretty Good ” Cardiovascular Management Goals
      • Fluid resuscitation to keep a CI > 2.5 l/min/m 2 with a Ppao < 20 mm Hg
      • Add inotropic support if unable to sustain CI within this Ppao limit
      • Vasopressors to maintain a mean arterial pressure > 65 mm Hg
      • If measures of organ perfusion available (urine output,  PCO 2 , tissue blood flow, Serum lactate, base deficit ) use them to guide response to therapy.
      • Trends may be more important than absolute values
    • 52. THANK YOU

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