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Hemodynamic Stabilisation in Septic shock Dr. T.R.Chandrashekar Intensivist K.R. Hospital Bangalore
[object Object],[object Object],[object Object],Shock
Septic shock ,[object Object],[object Object],[object Object],[object Object]
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
Macro-Circulation
Optimisation of Macrocirculation  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hemodynamic Truths ,[object Object],[object Object],[object Object],[object Object],[object Object]
Volume Vessel tone Heart  function If shock is prolonged, mechanisms of shock are combined Physiologic Classification of  Acute Circulatory Insufficiency Fluids / blood Vasopressors Inotropes
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
PRELOAD assessment-Volume  ,[object Object],[object Object],Volume responsive Volume unresponsive Preload OK Failing Heart Add dopamine or dobutamine
Volume SV Decreased contractility Right atrial volume ,[object Object],return function cardiac function
PRELOAD assessment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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?”
Dynamic (functional) parameters ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],MV  PATIENTS
[object Object],[object Object],[object Object],[object Object],[object Object],Fluid Therapy: Choice of Fluid Grade C Dellinger, et. al.  Crit Care Med 2004, 32: 858-873.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Fluid Therapy: Fluid Challenge Grade E Dellinger, et. al.  Crit Care Med 2004, 32: 858-873.
SHOCK MAP < 65mmHg Oliguria (<0.5ml/Kg/hour) Clinical signs of tissue hypoperfusion ,[object Object],[object Object],[object Object],[object Object],[object Object],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
Mixed/central venous O 2  saturation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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
Mixed/central SvO 2 ,[object Object],[object Object],[object Object],[object Object]
SvO2 closely correlates with ScvO2
The major problems with the interpretation of ScvO2 ,[object Object],[object Object]
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
How to differentiate between  Contractility vs Vasomotor tone ,[object Object],[object Object]
INTERPRETATION OF CARDIAC OUTPUT Do we have a problem ? ,[object Object],[object Object],[object Object],Increase in cardiac output FLUIDS ? Do we need to measure cardiac output ? DOBUTAMINE  ? Faster information ?
Why/when would I want to measure CO or SV in shock? ,[object Object],[object Object],[object Object]
 
The way I do ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],Vasopressors Grade E Grade D
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Vasopressors  (cont) Grade B Grade E Grade E
[object Object],[object Object],[object Object],[object Object],Inotropic Therapy Grade E Grade A
Hemodynamic Patterns with Prognostic Value ,[object Object],[object Object],[object Object]
[object Object]
Micro- Circulation
 
“… 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.
Why the microcirculation is important in shock . ,[object Object],[object Object],[object Object],[object Object]
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
 
Spronk P, Zandstra D, Ince C (2004) Critical Care 8:462-468 Sepsis is a disease of the microcirculation
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
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
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  
Microcirculation assessment ,[object Object],[object Object]
Orthogonal polarization spectral (OPS) imaging
Capillary flow in sepsis
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
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.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Take home thoughts ,[object Object],[object Object],[object Object],[object Object],[object Object]
Some “ Pretty Good ”  Cardiovascular Management Goals ,[object Object],[object Object],[object Object],[object Object],[object Object]
THANK YOU

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Hemodynamic Stabilisation In Septic Shock

  • 1. Hemodynamic Stabilisation in Septic shock Dr. T.R.Chandrashekar Intensivist K.R. Hospital Bangalore
  • 2.
  • 3.
  • 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
  • 6.
  • 7.
  • 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.
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  • 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?”
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  • 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.
  • 22.
  • 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.
  • 25.
  • 26.
  • 27.  
  • 28.
  • 29.
  • 30.
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  • 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.
  • 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.
  • 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.
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  • 51.

Editor's Notes

  1. 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
  2. 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 &lt; 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.
  3. 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