Copyright 2008 Society of Critical Care Medicine

Name: Copyright 2008 Society of Critical Care Medicine
Uploaded: 2017-08-10T02:14:24+00:00
Duration: PTM26S14
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Description: Copyright 2008 Society of Critical Care Medicine

Diagnosis and Management of Shock

Copyright 2008 Society of Critical Care Medicine
Objectives Identify the main categories of shock Discuss goals of resuscitation in shock Summarize principles of shock management Describe effects of vasopressor and inotropic agents Discuss the differential diagnosis of oliguria Copyright 2008 Society of Critical Care Medicine

Case Study 25-year-old with productive cough Heart rate 129/min, blood pressure 112/68 mm Hg, respirations 27/min, temperature 101.8F (38.8C) Does this patient have shock? Review case information and reveal question. It may be helpful to ask for show of hands for responses: Yes, No, Don’t know or not sure Guide discussion to defining what shock is. Challenge students with statement that shock must not be present since the blood pressure is OK. Copyright 2008 Society of Critical Care Medicine

Shock Syndrome of impaired tissue oxygenation and perfusion Mechanisms Absolute/relative decrease in oxygen delivery Ineffective tissue perfusion Ineffective utilization of delivered oxygen Review definition of shock and the mechanisms involved. Reveal figure and note that shock results from a significant disturbance of oxygen balance as explained in the Monitoring lecture. Oxygen Balance Delivery Oxygen Consumption Copyright 2008 Society of Critical Care Medicine

Case Study 25-year-old with productive cough Heart rate 129/min,blood pressure 112/68 mm Hg, respirations 27/min, temperature 101.8F (38.8C) What other clinical and laboratory findings would suggest the presence of shock? Question prompts discussion of the clinical manifestations of shock. As students offer responses, lead discussion to recognize that they fall into the following general categories: Hypoperfusion Compensatory response Specific etiology Copyright 2008 Society of Critical Care Medicine

Clinical Manifestations
Hypoperfusion/inadequate oxygenation Hypotension Altered mental status Oliguria Compensatory mechanisms Vasoconstriction Tachycardia Specific etiology Metabolic acidosis Lactate Abnormal creatinine, transaminases, etc Note that compensatory mechanisms result from neuroendocrine activation. Ask how vasoconstriction is manifested in shock. Cold, clammy skin Hypothermia Elevated diastolic blood pressure Copyright 2008 Society of Critical Care Medicine

Case Study Heart rate 129/min, blood pressure 112/68 mm Hg, respirations 27/min, temperature F (38.8C) SpO2 90% on nonrebreather mask (NRBM) Skin warm and dry Lactate 4.2 mg/dL White blood cell count 22,000/mm3 Question prompts discussion of the 4 types of shock. Distributive: sepsis, adrenal crisis, neurogenic Hypovolemic Cardiogenic Obstructive: pulmonary embolism, cardiac tamponade, tension pneumothorax Ask if the patient could have more than 1 type of shock Might have hypovolemic component with tachycardia, increased insensible fluid losses with tachypnea Point out that most shock has mixed components. What type of shock does this patient likely have? Copyright 2008 Society of Critical Care Medicine

Classification of Shock
Myopathic Arrhythmic Mechanical Cardiogenic Hypovolemic Hemorrhagic Nonhemorrhagic Septic Neurogenic Adrenal crisis Anaphylactic Distributive Discuss examples of the types of shock if not done previously. Reveal right column as each type is discussed. Massive pulmonary embolism Cardiac tamponade Tension pneumothorax Constrictive pericarditis Obstructive Copyright 2008 Society of Critical Care Medicine

Classification of Shock
Cardiac output Filling pressures Vascular resistance ScvO2 SvO2 Cardiogenic   Hypovolemic Distributive  or N  or N Obstructive Note that there are some distinct physiologic characteristics of the different types that help to understand the abnormalities and treatment approaches. Discuss findings for each type of shock by column. Note that increased vascular resistance correlates with increased diastolic pressure and decreased pulse pressure. Copyright 2008 Society of Critical Care Medicine

Case Study Blood pressure 88/40 mm Hg () Heart rate 135/min () Respirations 32/min () SpO2 90% (NRBM) Lactate 4.2 mg/dL What initial interventions are needed to treat shock in this patient? After presenting information obtained while monitoring the patient, reveal the question. Allow students to respond with specific interventions for a few minutes. Likely responses may be some of the following: Antibtiotics Cultures Intubation Fluids Vasopressor agents, etc. Guide discussion back to the definition of shock as a syndrome of impaired tissue oxygenation and perfusion as a way to approach treatment. Goal is to restore oxygenation and perfusion. Reveal next slide. Copyright 2008 Society of Critical Care Medicine

Treatment of Shock Restore tissue perfusion and oxygenation Treat specific etiology Monitor Provide supportive care Oxygen Balance Delivery Oxygen Consumption Note that the treatment of shock includes other aspects of care. Ask what interventions would treat the specific etiology of shock in this patient. Cultures Antibiotics May ask what monitoring they would institute for a patient with shock. Options might include the following: Usually arterial cannulation for blood pressure Central venous pressure Lactate ScvO2 Pulse oximetry Urine output as evidence of renal perfusion Note that restoring perfusion/oxygenation will be emphasis. Reveal figure and note that interventions involve increasing oxygen delivery or decreasing oxygen consumption. Copyright 2008 Society of Critical Care Medicine

Case Study BP 88/40 mm Hg HR 135/min RR 32/min Temperature F (38.8C) SpO2 90% (NRBM) Lactate 4.2 mg/dL What interventions would decrease oxygen consumption? First question addresses interventions that decrease oxygen consumption. Intubation, mechanical ventilation to decrease WOB Antipyretics for fever Possibly sedation or analgesia Reveal next question on interventions to increase oxygen delivery and allow discussion. Use next slide to review goals and interventions. What interventions would increase oxygen delivery? Copyright 2008 Society of Critical Care Medicine

Oxygen Delivery Determinants Blood pressure Cardiac output Oxygen content Interventions Fluids Vasoactive agents Blood transfusion Supplemental oxygen Note that these are the determinants of oxygen delivery previously discussed in lecture on Monitoring. Note that first priority is minimum blood pressure and ask what is the initial blood pressure goal in shock. MAP 65 mm Hg State that some patients may need higher MAP but ask what is the disadvantage of higher pressures. May increase myocardial oxygen demands, especially if not associated with improved perfusion Reveal next box with interventions (some probably mentioned in discussion). Ask which intervention they would use first. May answer O2 for this patient to increase hemoglobin saturation Then next intervention should be fluids. Copyright 2008 Society of Critical Care Medicine

Case Study Patient is intubated and sedated Chest radiograph  pneumonia Blood pressure 88/40 mm Hg Heart rate 135/min Hemoglobin 12 g/dL Which fluids would you administer? After reviewing case information, reveal question that addresses type of fluid. Discuss advantages and disadvantages. Isotonic crystalloids (normal saline, LR)--less expensive, requires more volume Colloids (hetastarch, albumin, gelatin)—more expensive, requires less volume, faster resuscitation Blood—scarce resource, use when oxygen carrying capacity needed When discussing blood, ask hemoglobin value would cause them to transfuse. Crystalloids Colloids Blood Copyright 2008 Society of Critical Care Medicine

Case Study Patient is intubated and sedated Chest radiograph pneumonia Blood pressure 88/40 mm Hg (MAP 56) Heart rate 135/min How much fluid is needed? Reveal question on quantity of fluid. Can ask bolus vs infusion, volumes of crystalloid compared to colloid. Emphasize that fluid is given to achieve a goal. Correction of hypotension Correction of perfusion abnormalities Ask what deleterious effects fluid resuscitation can cause. Pulmonary edema and worsening oxygenation. Reveal items below question after discussion. Fluid boluses recommended Correct hypotension then perfusion Monitor oxygenation Copyright 2008 Society of Critical Care Medicine

Case Study Normal saline solution 4 L administered Blood pressure 92/44 mm Hg (MAP 60) Heart rate 120/min SpO2 91% on 80% oxygen What is the next intervention for shock? Note new information on case—MAP is still low and oxygenation is poor after a significant quantity of fluid. Goal BP not yet reached. Reveal question. Students should offer a vasopressor as an option. Ask which drug they would choose. Reveal next slide for discussion of specific agents. Copyright 2008 Society of Critical Care Medicine

Vasoactive Agents Agents Dopamine Norepinephrine Epinephrine Vasopressin Dobutamine Others Effects Vasopressor Inotropic Vasodilator Which agent(s) is/are recommended in septic shock? Note that drugs are classified as vasoactive drugs but need to keep in mind that many have more than 1 effect. Reveal right column of effects. Briefly review some of the effects, advantages, disadvantages of the agents listed (see text) Reveal question on specific agents for septic shock. Emphasize that goals of resuscitation are most important rather than specific agent. Dopamine or norepinephrine as first line agents Epinephrine as 3rd line agent Vasopressin if refractory to other agents Dobutamine if BP adequate and still have hypoperfusion and suspected low cardiac output Copyright 2008 Society of Critical Care Medicine

Resuscitation in Severe Sepsis and Septic Shock
Supplemental O2 ± endotracheal intubation and mechanical ventilation Central venous and arterial catheterization Sedation, paralysis (if intubated), or both CVP Crystalloid <8 mm Hg Colloid 8–12 mm Hg MAP <65 mm Hg Vasoactive Agents >90 mm Hg ≥65 and ≤90 mm Hg Note that protocols using these interventions for early goal directed resuscitation have reduced mortality in septic shock. ScvO2 ≥70% <70% Transfusion of red cells until hematocrit ≥30% <70% ≥70% Goals Achieved Inotropic Agents Yes Continue to reassess No Copyright 2008 Society of Critical Care Medicine

Case Study Normal saline solution 4 L administered Norepinephrine at 0.3 g/kg/min Blood pressure 98/48 mm Hg (MAP 65) Heart rate 110/min Note new information on case—MAP better on high dose norepinephrine. Goal BP barely attained. Reveal question. Question is meant to raise issue of steroid use in septic shock. Ask when they would give steroids. Blood pressure poorly responsive to fluids and vasopressors Note that ACTH stimulation test is not recommended to determine who gets treated. What other interventions might be considered? Copyright 2008 Society of Critical Care Medicine

Management of Shock How would fluid and vasoactive agent use differ in other types of shock? Hypovolemic shock Cardiogenic shock Obstructive shock Use slide to discuss how management differs from septic shock for other forms of shock. Ask how type of fluid, quantity of fluid, choice of vasoactive agent and other therapy are different. Hypovolemic shock Type of fluid—replace type of fluid lost; blood for hemorrhage, crystalloid for vomiting, etc Similar goals for resuscitation as septic shock Vasoactive agents—only as temporizing measure while fluid resuscitation underway Cardiogenic shock Specific therapy for arrhythmia, MI with shock (PTCA) Cautious use of fluids but trial may be warranted due to altered ventricular compliance Vasoactive agents—may choose one with inotropic and pressor effects Add inotrope only when blood pressure stabilized Possible vasodilator therapy if blood pressure elevated or stabilized Obstructive shock Specific therapy dependent on etiology Fluid therapy may improve hemodynamics temporarily Vasoactive agents have minimal role Diuretics and preload reduction contraindicated Copyright 2008 Society of Critical Care Medicine

Case Study 24 hours later norepinephrine stopped Normal saline solution at 150 mL/h Blood pressure 110/60 mm Hg (MAP 77) Urine output 25 mL/h Creatinine 1.8 mg/dL, BUN 28 mg/dL Note new information on case—oliguria. Initial renal function was normal. Can ask for show of hands to answer first question. Initiate discussion on the possible etiologies of oliguria. Particularly note those that are reversible. Prerenal—decreased cardiac output, redistribution of blood flow Renal—ischemia, toxic drugs, glomerular disease, vasculitis, interstitial disease, etc Postrenal—obstruction Ask students what etiologies are most likely in this patient. Prerenal or renal Volume depletion Acute tubular necrosis from hypotension Reveal next question for discussion Assessment of volume status—may require invasive measurements Laboratory tests Next slide for laboratory test results Should fluid infusion be increased to improve urine output and renal function? What evaluations would be helpful? Copyright 2008 Society of Critical Care Medicine

Laboratory Tests Test Prerenal ATN BUN/creatinine ratio >20 10-20 Urine specific gravity >1.020 >1.010 Urine osmolality (mOsm/L) >500 <350 Urine Na (mmol/L) <20 >40 Fractional excretion of Na (%) <1 >2 Use table to review lab tests that may be helpful with prerenal suggesting need for fluids. Note that urine studies should be obtained before diuretics are given. Copyright 2008 Society of Critical Care Medicine

Management of Oliguria
Volume challenge Loop diuretic for fluid management Fluid balance Dosage adjustment of medications Avoid nephrotoxic drugs Renal replacement therapy Discuss general management techniques. Note that diuretics do not improve outcome of oliguria but may make fluid management easier. Fluid restriction may be difficult if patient needs higher preload. Copyright 2008 Society of Critical Care Medicine

Key Points Shock is characterized by impaired tissue oxygenation and hypoperfusion Types of shock are hypovolemic, distributive, cardiogenic, and obstructive Manifestations of shock result from inadequate tissue oxygenation, compensatory responses, and the specific etiology Intervention goals are adequate blood pressure and cardiac output, optimal oxygen content, and decreased oxygen demand Copyright 2008 Society of Critical Care Medicine

Key Points Initial therapy for most types of shock is volume replacement Vasoactive agents should be chosen based on desired hemodynamic effect and pharmacologic profile Reversible causes of oliguria should be excluded and intravascular volume optimized Copyright 2008 Society of Critical Care Medicine

Copyright 2008 Society of Critical Care Medicine

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