การอบรมว ทยาศาสตร พ นฐานทางศ ลยศาสตร เร อง นพ.ส ณฐ ต โมราก ล ภาคว ชาว ส ญญ ว ทยา คณะแพทยศาสตร โรงพยาบาลรามาธ บด มหาวทยาลยมหดล

Transcription

1 การอบรมว ทยาศาสตร พ นฐานทางศ ลยศาสตร เร อง นพ.ส ณฐ ต โมราก ล ภาคว ชาว ส ญญ ว ทยา คณะแพทยศาสตร โรงพยาบาลรามาธ บด มหาวทยาลยมหดล

2 Distributive shock Severe sepsis and Septic shock Anaphylactic shock Neurogenic (spinal) shock Endocrinologic Adrenal crisis

3 Classification of Shock

4 Poiseuille s s Law Tissue V P in R P out V = ΔP/ / R

5 Poiseuille s s Law CVP MAP V = ΔP/ R MAP CVP = CO x SVR CO BP = CO x SVR Tissue

6 Autoregulation Blood flow Arterial pressure

7 Poiseuille s s Law Tissue V P in R P out V = ΔP/ R

8 Distributive shock brain gut kidney heart

9 Septic Shock

10 Septic Shock The natural history of the SIRS. JAMA 1995, 273:

11 Spectrum of Sepsis SIRS Sepsis Severe Sepsis Septic Shock :Infection :Inflammatory response :Plus organ :Plus hypotension to a variety of severe plus SIRS dysfunction (adequate fluid clinical insults. This resuscitation) syndrome is clinically recognized by > 2: Temp T >38 C or <36 C Heart rate >90 /min RR>20 /min WBC >12,000 or <4000 cells/mm 3

12 Spectrum of Sepsis

13 Inflammatory Responses to Sepsis

14 Procoagulant Response in Sepsis

15 SIRS Sepsis Severe Sepsis Septic Shock Systemic hemodynamic alterations Decreased vascular tone Hypovolemia Absolute (increased permeability) Relative (blood pooling) Myocardial dysfunction Systolic Diastolic

16 SIRS Sepsis Severe Sepsis Septic Shock Systemic hemodynamic alterations Oxygen delivery Oxygen consumption Regional blood flow alterations Tissue Hypoxia Microvascular blood flow alterations Leak, dilated, occluded Constricted, DIC.. Decreased flow

17 Microvascular blood flow alterations Sublingual microcirculation was visualized By using orthogonal polarization spectral imaging technique Backer DD, Vincent JL et al. Am J Respir Crit Care Med; 2002: 166:

18 Management of Septic Shock Initial resuscitation and infection management Hemodynamic support and adjunctive therapy Other supportive therapy of severe sepsis and Other supportive therapy of severe sepsis and septic shock

19 Management of Septic Shock Initial resuscitation and infection management Hemodynamic support and adjunctive therapy Other supportive therapy of severe sepsis and Other supportive therapy of severe sepsis and septic shock

20 Initial resuscitation and infection management Initial resuscitation (first 6 hrs) Diagnosis Antibiotic therapy Source identification and control

21 Initial resuscitation and infection management Initial resuscitation (first 6 hrs) Diagnosis Antibiotic therapy Source identification and control

22 Diagnosis Obtain appropriate cultures before starting antibiotics Do not significantly delay antimicrobial administration i ti

23 Antibiotic therapy Begin intravenous antibiotics as early as possible and always within the first hour of recognizing severe sepsis and septic shock Broad spectrum: one or more agents active against likely bacterial/fungal pathogens and with good penetration into presumed source

24 Source identification and control A specific anatomic site of infection should be established as rapidly as possible and within first 6 hrs of presentation

25 Initial resuscitation and infection management Initial resuscitation (first 6 hrs) Diagnosis Antibiotic therapy Source identification and control

26 Oxygen delivery Oxygen consumption

27 Oxygen Oyge Delivery e RBC Stroke Volume Vl Heart trt Rate 1.34 x Hb x SaO 2 Preload Afterload Volume Contractility Inotrope Vasoactive x PaO 2 Oxygen

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29 Assessment of regional and global perfusion

30 CO x CO CvO 2 CO x CO CaO 2 Tissue Vo 2

31 Fick Principle VO 2 = CO x (CaO 2 CvO 2 ) VO 2 = CO x 1.34x Hb x (SaO 2 SvO 2 ) CO = VO 2 PAC 1.34x Hb x (SaO 2 SvO 2 ) CVC

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34 Standard d therapy in ED

35 Goal Directed Therapy

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38 Mortality and causes of in hospital death

39 Timing of Intervention

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44 Initial resuscitation (first 6 hrs) Begin resuscitation immediately in patients with hypotension or elevated serum lactate > 4 mmol/l; do not delay pending ICU admission

45 Initial resuscitation (first 6 hrs) Resuscitation goals CVP 8 12 mm Hg Mean arterial pressure 65 mm Hg Urine output 0.5 ml/kg/hr Central venous (superior vena cava) oxygen saturation >70% or mixed venous >65%

46 Initial resuscitation (first 6 hrs) If venous oxygen saturation ti target tis not achieved Consider further fluid Transfuse packed red blood cells if required to hematocrit of >30% Dobutamine infusion, maximum 20 μg/kg/min

47 Management of Septic Shock Initial resuscitation and infection management Hemodynamicsupport and adjunctive therapy Other supportive therapy of severe sepsis and septic shock

48 Hemodynamic support and adjunctive therapy Fluid therapy Steroids Vasopressors Inotropic therapy Recombinant human activated protein C

49 Fluid therapy Fluid resuscitate using crystalloids or colloids Target a CVP of > 8 mm Hg (> 12 mmhg if mechanically ventilated) Use a fluid challenge technique while associated with a hemodynamic improvement

50 Fluid therapy Give fluid challenges of 1000 ml of crystalloids or ml of colloids over 30 mins. More rapid and larger volumes may be required in sepsis induced induced tissue hypoperfusion Rate of fluid administration should be reduced if cardiac filling pressures increase without concurrent hemodynamic improvement

51 Frank Starling law SV (CO) Have I optimized Preload? Preload Volume

52 Preload d& Cardiac filling fll pressure LV Preload LVEDV LVEDP LAP PAP RVP RAP

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54 Fluid Challenge

55 Fluid Challenge Test Guided by CVP PCWP Infusion After bolus < 2 < 3 continue > 5 > 7 stop 2 < < 5 3 < < 7 Wait After10min > 2 > 3 stop < 2 < 3 continue

56 Fluid Therapy The validity of CVP in patients with sepsis

57 Inability of CVP and PAOP to assess changes in Preload Kumar et al, Crit Care Med 2004, 32(3)

58 Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge hll Osman et al, Crit Care Med 2007, 35(1)

59 Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge hll Osman et al, Crit Care Med 2007, 35(1)

60 Heart Lung interaction ti SV SVV SVV Increase intrathoracic pressure Decrease venous return of RV/LV Decrease LV preload Decrease LV SV Preload Volume

61 From Arterial At lpressure to SV S k l i d i db d i i h d h Stroke volume is derived by determining the area under the curve of the sysytolic part of the arterial pressure

62 Stroke Volume Variation by Pulse Contour Analysis SVV = SVmax SVmin SVmean

63 Pulse Pressure variation & Systolic Pulse Pressure variation & Systolic Pressure Variation

64 Pulse Pressure variation & Systolic Pulse Pressure variation & Systolic Pressure Variation

65 Echocardiography

66 Fluid Therapy Which are the goal of fluid therapy? Capillary refill time Pulse pressure variation Stroke volume variation Collapsity index of IVC CVP Rarely PCWP

67 Vasopressors Maintain MAP > 65 mm Hg Norepinephrine and dopamine are the initial vasopressors of choice Epinephrine, phenylephrine, or vasopressin should not be administered i das the initial iti vasopressor in septic shock

68 Vasopressors Use epinephrine as the first alternative agent in septic shock when BPis poorly responsive to norepinephrine or dopamine Do not use low dose dopamine In patients requiring vasopressors, insert an arterial catheter as soon as practical

69 Inotropic therapy Use dobutamine in patients with myocardial dysfunction as supported by elevated cardiac fll filling pressures and low cardiac output Do not increase cardiac index to predetermined supranormal levels

70 Dopamine Dopamine Receptor Effects (μg/kg/min) activation < 5 DA 1 vasodilation in the renal and 1 mesenteric beds 5 10 β 1 increasing cardiac contractility and heart rate > 10 α 1 arterial vasoconstriction and an increase in BP

71 Dopamine Dopamine (μg/kg/min) / MAP CO HR SVR PCWP < >

72 Dopamine Tachycardia and arrhythmogenesis Immunologicand metabolic effects diminishes cyclic adenosine monophosphate (camp) inhibits proliferation in lymphocytes Dopamine allows lymphocyte apoptosis Inhibits immunoglobulins, cytokines,,growth hormone and thyroid stimulating hormone (TSH) production

73 Dopamine Septic patients with compromised cardiac function or cardiac reserve Limit by side effects and dose

74 Norepinephrine

75 Norepinephrine NE MAP CO HR SVR PCWP (μg/kg/min) ± ± +1 +1

76 Norepinephrine Potent α adrenergic d i agonist with ihless pronounced β adrenergic agonist Increases MAP by vasoconstriction, with a small increase in CO and SV Filling pressures are either unchanged or modestly increased Norepinephrine is more potent than dopamine and may be more effective at reversing hypotension in septic shock patients

77 Norepinephrine Norepinephrine i can have detrimental effects on renal hemodynamics in patients with hypotension and hypovolemia, with a potential ti for renal ischemia Norepinephrine has a greater effect on efferent than afferent renal arteriolar resistance and increases the filtration fraction, urine output and renal function in adequately resuscitated patients with hyperdynamic septic shock

78 Epinephrine

79 Epinephrine Epinephrine (μg/kg/min) MAP CO HR SVR PCWP < 0.06 ± >

80 Epinephrine potent α adrenergic and β adrenergic agent increases MAP by increasing i both cardiac index and peripheral vascular tone It increases heart rate, and has the potential to induce tachyarrhythmias, ischemia, and hypoglycemia increases oxygen delivery, but oxygen consumption may be increased as well

81 Epinephrine i Decrease regional blood flow, particularly in the splanchnic circulation Lactate levels can be increased Its use should be limited to patients who fail to respond to traditional therapies for increasing or maintainingblood pressure

82 Dobutamine Dobutamine is a racemicmixture i of two isomers, D isomer with β1 and β 2 adrenergic effects, and L isomer with β 1 and α1 adrenergic effect predominant effect is inotropic via stimulation of β1,, with a variable effect on BP chronotropic effect in addition when the heart rate is disproportionately t high, it increases the systemic vasodilation, worsening the hypotension

83 Dobutamine Dobutamine has a coadjuvant role with the vasopressors in septic shock The final goal of this mixture is to improve the cardiac index and mixed venous oxygen saturation

84 Other supportive therapy Blood product administration MV of sepsis induced induced ALI/ARDS Sedation, analgesia, and NMBA Glucose control Renal replacement Bicarbonate therapy Deep vein thrombosis prophylaxis Stress ulcer prophylaxis

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