SHOCK

Transcript

1 SHOCK

2 La diagnosi di shock conclamato è per lo più facile, più complicato può essere individuare gli aspetti clinici iniziali (riconoscimento e valutazione dello stadio dello shock). SEGNI PIU FREQUENTI: - PA massima < 90 mmhg o diminuzione di 40 mmhg dai livelli basali - diuresi < 0,5 ml/kg/h - riduzione del flusso ematico periferico: cute fredda, umida, cianotica - alterazione dello stato di coscienza - tachicardia, tachipnea DATI DI LABORATORIO: Acidosi metabolica Aumento acido lattico DIAGNOSI

3 Shock: è una condizione di insufficient oxygen transport and perfusion Inadeguato apporto e trasporto di ossigeno. Riduzione della perfusione tessutale. ipossia cellulare Limita l apporto di ossigeno Riduce la funzione cardiaca. Inadeguato volume circolante IPOVOLEMICO Inadeguata funzione cardiaca CARDIOGENO Vasodilatazione periferica e alterata distribuzione del flusso ematico DISTRIBUTIVO Ostruzione extracardiaca al flusso ematico OSTRUTTIVO

4 CLASSIFICAZIONE - SHOCK IPOVOLEMICO : emorragico deplezione di liquidi - SHOCK CARDIOGENO : miogeno meccanico aritmico - SHOCK DISTRIBUTIVO : settico anafilattico neurogeno spinale - SHOCK OSTRUTTIVO : tamponamento cardiaco tromboembolia polmonare pneumotorace

5 Sepsi Almeno due segni+infezione Temperatura >38 C o <36 C Frequenza cardiaca >90 bpm Frequenza respiratoria >20 atti/min or PaCO2 <32 torr (<4.3 kpa) Globuli bianchi >12,000 o <4,000 cells/mm3 or >10% bands Sepsi Severa Sepsi associata a disfunzione d organo, ipoperfusione, o ipotensione. Le alterazioni di perfusione includono ma non sono limitate a: acidosi lattica, oliguria e alterazione stato mentale* Shock Settico Sepsi con ipotensione (SBP<90), nonostante adeguata infusione di liquidi e modificazioni della perfusione *.

6 MONITORAGGIO NELLO SHOCK SEGNI VITALI: - frequenza cardiaca - frequenza respiratoria - stato della coscienza (G.C.S.) - temperatura cutanea ECG al monitor MONITORAGGIO EMODINAMICO: -PA -PVC: ALTA (>12 cm di H20 ) cardiogeno, ostruttivo, settico ( faase ipodinamica) NORMALE ( 5-12 cm di H20) neurogeno, spinale, settico (fase iperdinamica) BASSA (<5 cm di H20 ) ipovolemico, anafilattico, neurogeno, settico (fase iperdinamica) -CWP: 8-18 mmhg miglior riempimento V sn con maggiore gettata cardiaca > 18 mmhg congestione polmonare fino ad edema

7 FUNZIONALITA RENALE: diuresi oraria ( 0,5-1 ml/kg/h; 30 ml/h) FUNZIONE RESPIRATORIA E METABOLICA: EGA e saturazione O2 ESAMI DI LABORATORIO: -emocromo - elettroliti, funzionalità renale - lattati - enzimi sierici - coagulazione -glicemia - prove crociate ECOCARDIOGRAMMA ED ECOGRAFIA ADDOMINALE RX TORACE TAC ULTERIORI INDAGINI SECONDO IL QUADRO CLINICO (SCINTIGRAFIA POLMONARE, ANGIOGRAFIA,...)

8 Goals of Shock Management Resuscitation - resuscitare To re-animate or revive Physiologically Restore normal blood volume, BP, organ perfusion Cellular level Restore balance between O2 utilization and cellular function Resuscitation = Reversal of shock

9 DO2crit V O 2 DO2 QUANDO SI REALIZZA UN DEFICT DI OSSIGENO SI OSSERVA UN AUMENTO DEL METABOLISMO ANAEROBIO ACIDO LATTICO SE IL DEFICIT E PROLUNGATO DEPOSITI ATP E ALTERAZIONE FUNZIONAMENTO POMPE IONICHE DI MEMBRANA DANNO CELLULARE

10 Cardiac output + N - A B C D + N - SVR Modificata da Fry DE: SIRS and MODS: Biologic dominio effect. Pag 24 in Multiple Organ Faikure. Pathophisiology, Prevention, and Therapy. Baue et al Ed

11 TREATMENT OF SHOCK ENHANCING PERFUSION/OXYGEN DELIVERY CO= Cardiac output (MAP-CVP) SVR Arterial O 2 content Vasopressors Oxygen delivery = HR X SV X Hb X S0 2 X ,0031 x pao 2 Inotropes Transfuse Partially dependent on FIO 2 and pulmonary status Fluids

12 E P Rivers, H B Nguyen, S Havstad, MC Tomlanovich: EARLY GOAL DIRECTED THERAPY IN THE TREATMENT OF THE SYSTEMIC INFLAMMATORY RESPONSE SYNDROME WITH GLOBAL TISSUE HYPOXIA: AN OUTCOME EVALUATION. Chest, Oct, 2000 prospective randomized trial 233 adult patients with SIRS and a systolic blood pressure <90 mmhg after a 20 cc/kg fluid challenge, or (2) SIRS criteria and a lactate level >4 mmol/l randomized to a treatment(115) or control group (118). The treatment group received a 6 hours of hemodynamic optimization consisting fluid management to a central venous pressure (CVP)> 8-12 mm Hg, vasopressors if required to a mean arterial pressure (MAP)< 65 mm Hg and efforts to increase systemic oxygen delivery or decrease in systemic oxygen utilization if the central venous oxygen saturation (Scv02) was< 70% compared to standard care in the control group. In-hospital mortality and 28 day mortality was 40.7% and 48.6% in the control group versus 25.2% and 32.3% in the treatment group, respectively, (both p=0.017). In the treatment group, the duration of mechanical ventilation and length of hospital stay were 1.4 days (p=0.001), 3.8 days (p=0.040) less than the control group.

13 EARLY GOAL DIRECTED THERAPY During the first 6 hours of resuscitation, the goal of initial resuscitation of sepsis-induced hypoperfusion should include all of the following as one part of a treatment protocol: Central venous pressure 8-12 mmhg ( mmhg in ventilated patient) Mean arterial pressure 65 mmhg Urine output 0,5 ml/kg/hr Central venous (superior vena cava) or mixed venous oxygen (SvO2) saturation 70 % Resuscitation Fast rate Slow rate % survival None Modificated by Rivers N J Eng 2001 Time

14 Rivers E, Nguyen B, Havstad S, et al: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001, 345: patients (130 randomly assigned to early goal-directed therapy and 133 to standard therapy). mortality was 30.5 percent in the group early goal-directed therapy and 46.5 percent in the group standard therapy (P=0.009). The patients assigned to early goal-directed therapy had a significantly higher mean (±SD) central venous oxygen saturation (70.4±10.7 percent vs. 65.3±11.4 percent), a lower lactate concentration (3.0±4.4 vs.. 3.9±4.4 mmol per liter), a lower base deficit (2.0±6.6 vs.. 5.1±6.7 mmol per liter), and a higher ph (7.40± vs ±0.12) than the patients assigned to standard therapy (P 0.02 for all comparisons). R. Phillip Dellinger,, et al Crit Care Med 2004 Vol.32, N 3;

15 VENOUS CAPACITANCE CIRCUIT Portion of the circulatory system contains 80% of the intravascular volume Decrease in effective circulating blood volume and MAP caused by: Decreases in venous tone Increases in venous vascular capacitance NORMAL INCREASED VENOUS CAPACITANCE Decreased effective blood volume Decreased MAP

16 Vasodilatation A-V shunting CAPILLARY LEAK SYNDROME Maldistribution of flow Increased capillary permeability + interstitial edema EDEMA Decreased oxygen extraction Primary defect of oxygen utilization at cellular level

17 COME: : l infusione l di liquidi può consistere nella somministrazione di colloidi o di cristalloidi, attualmente non ci sono evidenze che supportano l impiego di un tipo di fluido rispetto l altrol Colloidi in E, Cristalloids in NA Il carico idrico può essere dato con un flusso di ml per cristalloidi or ml per colloidi in circa 30 min ripetibili in base alla risposta (aumento( della pressione ematica output urinario) ) e tolleranza (evidenze( di overload intravascolare)

18 INOTROPIC AND VASOPRESSOR DRUGS THERAPY When an appropriate fluid challenge fails to restore adequate blood pressure and organ perfusion, therapy with vasopressor agents should be started. Either norepinephrine or dopamine is the first choice vasopressor agent to correct hypotension. In patient with low cardiac output despite adequate fluid resuscitation, dobutamina may be used to increase cardiac output R. Phillip Dellinger, et al for the Surviving Sepsis Campaign Management Guidelines Committee Crit Care Med 2004 Vol.32, N 3; There is no high level evidence to recommend one catecholamines over another It should be combined with vasopressth

19 Dose Azione Simolaz. cardiaca Vasocost. Vasodil. Portata cardiaca Dopamina O.5-25 µg/kg min 400mg/250ml α-β-dopamin Norepinefrina µg/kg min 4mg/250ml α1-β / Fenilefrina µg/kg min 10mg/250ml α / ++++ / Efedrina 5/25 mg α-β Vasopressina U/min 200U/250ml α ++++ Epinefrina µg/kg min 1mg/250ml α-β Dobutamina µg/kg min 250mg/250ml β Isoproterenolo µg/kg min 1mg/250ml β / ++++

20 FLUID THERAPY RESUSCITATION MAINTENANCE Crystalloid Colloid ELECTROLYTES NUTRITION 1. Replace acute loss (hemorrhage, GI loss, 3 rd space etc) 1. Replace normal loss (IWL + urine+ faecal) 2. Nutrition support

21 Volemia: Difficile da quantizzare nel paziente critico Quale parametro da seguire per il riempimento? Cristalloidi vs Colloidi

22 Goals of volume and fluid replacement for critically ill patients Achieve and mantain normovolemia and hemodynamic stability Optimize oxygen delivery and oxygen consumption Restore fluid homeostasis in different fluid compartments Ensure adequate plasma Collid Osmotic Pressure Improve microcirculatory perfusion Ensure appropriate inflammatory response and endothelial cell-leukocyte leukocyte interactions Year book of Intensive care and emergency medicine; 2000:

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24 Electrolyte composition meq/l ICF ECF Plasma Interstitial Na K Ca 2+ Mg 2+ Cl - HCO 3 - HPO 4 2- SO 4 2- Organic acid Protein

25 Fluid infusion CRISTALLOIDS COLLOIDS ICF ECF Plasma ICF ECF Plasma

26 Crystalloids vs Colloids: : THE FACTS AMOUNT OF FLUIDS REQUIRED Crystalloids Colloids

27 BLOOD VOLUME Colloids Cristalloids TIME Wang et al. J Surg Res 50:

28 EDEMA Impaired gas exchange Limited oxygen availability Impaired wound healing Gut dysfunction Cutaneous lesions Decubitus ulcers

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30 BMJ 1998;316: ( 28 March ) Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: : a systematic review of randomised trials Gill Schierhout,,,, Ian Roberts

31 HEMODYNAMIC MONITORING

32 ARTERIAL PRESSURE SKIN PERFUSION URINE OUTPUT MENTAL STATUS CLINICAL ASSESSMENT CARDIAC OUTPUT AND SvO2 LACTATE TISSUE PO2 (?) PgCO2 OVERALL ASSESSMENT

33 OXYGEN DELIVERY FLUIDS (BLOOD, COLLOIDS, CRYSTALLOIDS)

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35 Hypervolemia with concurrent renal failure and volume overload poses a special management problem. Since diuretics cannot be relied on to reduce the expanded extracellular-fluid volume, hemodialysis, hemofiltration,, or peritoneal dialysis must be used J Am Soc Nephrol 12; 2001

36 Age HIGH RISK GROUPS Abuse Traumatic Injury Drug therapy Invaded Device Spaghetti Syndrome

37 Recombinant Hum Activated Protein C EG-DT Initial Resuscitation Fluid Therapy Vasopressors And Inotropic Therapy SOURCE CONTROL Diagnosis and antibiotic therapy Steroids Glucose control Modified from Bone Chest 1992 MOST: multiple organ support therapy Modificata da Bone et al: Definition for sepsi and orgain failure and guidelines for the use of innovative theraphies in sepsi.chest 1992;101: Respiratory Support

38 CARDIAC OUTPUT = HR X SV Intravascular volume Heart Arteriolar bed CO X SVR = PA CHANGES IN MANY ELEMENTS REGULATE BP AND PERFUSION RESISTANCE CIRCUIT Capillary exchange network Venules Venous capacitance circuit Decreased peripheral resistance Decreased arterial blood pressure Increased peripheral resistance Decreased venous return Decreased EDV Decreased SV Decreased arterial blood pressure Heart rate Contractility Loading conditions