Presentation on theme: "Shock Scott G. Sagraves, MD, FACS Assistant Professor"— Presentation transcript:
1Shock Scott G. Sagraves, MD, FACS Assistant Professor Trauma & Surgical Critical CareAssociate Director of TraumaUHS of Eastern Carolina
2Objectives Define & classify shock Outline management principles Discuss goals of fluid resuscitationUnderstand the concepts of oxygen supply and demand in managing shock.Describe the physiologic effects of vasopressors and inotropic agents
3Goals Review hemodynamic techniques in the ICU Introduce the concept of the cardiac cycleReview of the pulmonary artery catheter parametersUtilize the presentation to analyze clinical cases and to feel comfortable with pa-c parameters.
4“A momentary pause in the act of death.” -John Collins Warren, 1800s Shock:“A momentary pause in the act of death.”-John Collins Warren, 1800s
5Hypotension In Adults: systolic BP 90 mm Hg mean arterial pressure 60 mm Hg systolic BP > 40 mm Hg from the patient’s baseline pressure
6DefinitionSHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand.
7“Hypoperfusion can be present in the absence of significant hypotension.” -fccs course
8Pathophysiology ATP + H2O ADP + Pi + H+ + Energy Acidosis results from the accumulation of acid when during anaerobic metabolism the creation of ATP from ADP is slowed.H+ shift extracellularly and a metabolic acidosis develops
9PathophysiologyATP production fails, the Na+/K+ pump fails resulting in the inability to correct the cell electronic potential.Cell swelling occurs leading to rupture and death.Oxidative Phosphorylation stops & anaerobic metabolism begins leading to lactic acid production.
10Why Monitor? Essential to understanding their disease Describe the patient’s physiologic statusFacilitates diagnosis and treatment of shock
11History1960’slow BP = shock; MSOF resulted after BP restored1970’sSwan & Ganz - flow-directed catheterthermistor cardiac output1980’sresuscitation based on oxygen delivery, consumption & oxygen transport balance.
28LVSWI = (MAP-PAOP) x SVI x 0.0136 Stroke WorkLVSWI = (MAP-PAOP) x SVI xnormal =VSWI describe how well the ventricles are contracting and can be used to identify patients who have poor cardiac function.ventricular stroke work = pressure x vol. ejected
30DefinitionsO2 Delivery - volume of gaseous O2 delivered to the LV/min.O2 Consumption - volume of gaseous O2 which is actually used by the tissue/min.O2 Demand - volume of O2 actually needed by the tissues to function in an aerobic mannerDemand > consumption = anaerobic metabolism
31Rationale for Improving O2 Delivery InsultTissue HypoxiaDemands are metIncreased DeliveryIncreased Consumption
32Critical O2 Delivery VO2I DO2I The critical value is variable & is dependent upon the patient, disease, and the metabolic demands of the patient.DO2I
33Oxygen CalculationsArterial Oxygen Content (CaO2)Venous Oxygen Content (CvO2)Arteriovenous Oxygen Difference (avDO2)Delivery (O2AVI)Consumption (VO2I)Efficiency of the oxygenation of blood and the rates of oxygen delivery and consumption
34Arterial Oxygen Content CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x )If low, check hemoglobin or pulmonary gas exchange
35Arteriovenous Oxygen Difference avDO2 = CaO2 - CvO2Values > 5.6 suggests more complete tissue oxygen extraction, typically seen in shock
36Oxygen Delivery (DO2I) O2AVI = CI x CaO2 x 10 Normal values suggests that the heart & lungs are working efficiently to provide oxygen to the tissues.< 400 is bad sign
37If VO2I < 100 suggest tissues are not getting enough oxygen Oxygen ConsumptionVO2I = CI x (CaO2 - CvO2)If VO2I < 100 suggest tissues are not getting enough oxygen
40Resuscitation Goals CI = 4.5 L/min/m2 DO2I = 600 mL/min/m2 VO2I = 170 mL/min/m2NOT ALL PATIENTS CAN ACHIEVE THESE GOALSCritically ill patients who can respond to their disease states byspontaneously or artificially meeting these goals do show abetter survival.
50Treatment - Hypovolemic Reverse hypovolemia vs. hemorrhage controlCrystalloid vs. ColloidPASG role?Pressors?
51ResuscitationTransport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial.Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.
52Fluid Administration 1 L crystalloid 250 ml colloid crystalloids are cheaperblood must supplement eitherFFP for coagulopathy, NOT volumeWatch for hyperchloremic metabolic acidosis when large volumes of NaCl are infusedNO survival benefit with colloids
53Role of PASG?Houston - Higher mortality rate in penetrating thoracic, cardiac traumaNo benefit in penetrating cardiac traumaRole undefined in rural, blunt traumaSplinting role
54Cardiogenic Shock Cause Signs defect in cardiac function cardiac output PAOP SVR left ventricular stroke work (LVSW)
55Coronary Perfusion Pressure Coronary PP = DBP - PAOPcoronary perfusion = P across coronary a.GOAL - Coronary PP > 50 mm Hg
56The Failing HeartImprove myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient.Fluids first, then cautious pressorsRemember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure)If inotropes and vasopressors fail, intra-aortic balloon pump
58SIRS - Distributive Shock Prompt volume replacement - fill the tankEarly antibiotic administration - treat the causeInotropes - first try DopamineIf MAP < 60Dopamine = g/kg/minNorepinephrine = titrate (1-100 g/min)R/O missed injury
59Adrenal Crisis Distributive Shock CausesAutoimmune adrenalitisAdrenal apoplexy = B hemorrhage or infarctheparin may predisposeSteroids may be lifesaving in the patient who is unresponsive to fluids, inotropic, and vasopressor support. Which one?
61Endpoints?ACS CoT ATLS - restoration of vital signs and evidence of end-organ perfusionSwan-guided resuscitationC.I. 4.5, DO2I 670, VO2I 166Lactic Acid clearanceGastric pH
62Summary Type PAOP C.O. SVR HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE or N varies OBSTRUCTIVE
63Vasopressor Agents?Augments contractility, after preload established, thus improving cardiac output.Risk tachycardia and increased myocardial oxygen consumption if used too soonRationale, increased C.I. improves global perfusion
66Dobutamine -agonist 5 - 20 g/kg/min potent inotrope, variable chronotropecaution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension
67Norepinephrine Potent -adrenergic vasopressor Some -adrenergic, inotropic, chronotropicDose g/minUnproven effect with low-dose dopamine to protect renal and mesenteric flow.
68Epinephrine - and -adrenergic effects potent inotrope and chronotropedose g/minincreases myocardial oxygen consumption particularly in coronary heart disease
69AmrinonePhosphodiesterase inhibitor, positive inotropic and vasodilatory effectsincreased cardiac stroke output without an increase in cardiac stroke workmost often added with dobutamine as a second agentload dose = mg/kg g/kg/min dripmain side-effect - thrombocytopenia
73GSW24 year old male victim of a shotgun blast to his right lower quadrant/groin at close range.Hemodynamically unstable in the field and his right lower extremity was cool and pulseless upon arrival to the trauma resuscitation area.