10/22/19

Conflict of Interest Disclosure

• Bryan E. Bledsoe, DO, FACEP, FAEMS • No conflicts of interest to disclose Early Detection of

Bryan E. Bledsoe, DO, FACEP, FAEMS Professor Emergency Medicine and Surgery (Trauma) UNLV School of Medicine Las Vegas, Nevada

Shock Shock

• A “rude unhinging” of the • Shock is inadequate tissue machinery of life. perfusion. • Samuel Gross (1862) • A clinical state of acute circulatory failure with inadequate oxygen utilization and/or delivery to the cells resulting in cellular dysoxia/.

Shock Shock

• Shock is: • Cellular and tissue hypoxia: Oxygen Glucose • Reduced oxygen delivery • Increased oxygen consumption • Inadequate oxygen utilization • Most commonly occurs due to circulatory failure. • Initially reversible if treatment provided rapidly to prevent progression to irreversible organ dysfunction.

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Shock Shock

Proteins Carbohydrates Lipids

Glucose

Shock Shock

• Oxygen: • Oxygen Transport: • Required for the majority of cellular energy • Hemoglobin-bound (97%) production derived from Krebs Cycle and Electron • Dissolved in plasma (3%) Transport Chain. • Metabolism with oxygen = aerobic metabolism • : • Metabolism without oxygen = anaerobic metabolism • Hemoglobin-bound (SpO2) • Dissolved in plasma (pO2)

Shock Shock

• What factors can affect oxygen • Metabolic oxygen demand delivery to the tissues? (MRO2): •Cardiac Output (Q) • Sum total of oxygen needed to drive various tissue metabolic •Available Hemoglobin (Hb) processes. •Oxygen Saturation (SpO2) • Metabolic oxygen delivery (DO2): • Sum total of available oxygen delivery to the tissues • Body approximately 20-30% effective in extracting circulating oxygen.

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Shock Shock

• Things that can adversely When metabolic oxygen demands exceed oxygen supply: effect oxygen delivery: • Hypoxia • Inadequate circulation • Inadequate transport medium (e.g., hemoglobin) • Cellular toxins (e.g., cyanide)

Shock Shock

32 ATP

Krebs Cycle O2

Glucose Glycolysis Pyruvate

No O2 Lactic Acid

2 ATP

Shock Shock

• Elevated lactate levels MAY be • Shock recognition must occur an indicator of hemodynamic at several levels: instability. • Examination • Current lactate monitoring • Monitoring technologies very non-specific. • Response to treatments • Experience • Numerous causes of elevated lactate levels—not all pathological.

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Shock Shock

• Causes of Shock: • Causes of Shock: • Inadequate oxygen delivery: • Inadequate nutrient delivery: • Inadequate respiration and oxygenation • Inadequate nutrient intake • Respiratory failure (mechanical, toxins) • Inadequate hemoglobin • Inadequate nutrient delivery • Inadequate fluid in the vascular system • Hemorrhage or anemia • Inadequate fluid in the vascular system • Inadequate blood movement • Hemorrhage or fluid loss (burns, vomiting, diarrhea, ) • Impaired nutrient (glucose) uptake • Inadequate blood movement • Cardiac pump failure • Impaired oxygen uptake • Biochemical poisoning (hydrogen cyanide)

Shock Shock

• Impaired oxygen uptake: • Inadequate nutrient delivery: • Cyanide: • Inadequate nutrient intake • Inhibits metal-containing • Malnutrition, GI absorption disorder enzymes (i.e., cytochrome • Inadequate nutrient delivery oxidase) • Malnutrition, hypoproteinemia • Halts cellular respiration • Inadequate fluid in the vascular system • Carbon monoxide: • Hemorrhage, fluid loss (burns, vomiting, diarrhea) • Binds to hemoglobin • Inadequate blood movement • Inhibits metal-containing • Cardiac pump failure enzymes (i.e., cytochrome • Impaired nutrient (glucose) uptake: oxidase) • Lack of insulin (Diabetes Mellitus)

Shock Shock

• Shock is a singular condition with multiple causes. • Shock types: • Hemorrhagic • Respiratory • Neurogenic • Psychogenic • Cardiogenic • Septic • Anaphylactic • Metabolic

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Shock Shock

• Distributive (66%) • : • Distributive shock: • Septic (62%) • Characterized by severe • (most common) • Anaphylactic and neurogenic (4%) peripheral . • Systemic inflammatory response • Cardiogenic (16%) • Often caused by molecules that syndrome (SIRS) mediate vasodilation • Neurogenic shock • Hypovolemic (16%) • Anaphylactic shock • Obstructive (2%) • Drug and toxin-induced shock • Endocrine shock

Vincent JL, De Backer D: Circulatory Shock. N Engl J Med 2013; 369: 1726–34

Shock Shock

• : • Cardiogenic shock: • : • Hypovolemic shock: • Intracardiac cause of cardiac • Cardiomyopathic • Reduced intravascular volume • Hemorrhagic pump failure. • Arrhythmic • Non-hemorrhagic: • Mechanical • GI losses • Skin losses • Renal losses • Third-space losses

Shock Shock

• Obstructive: • : • Extracardiac issues cause cardiac • Pulmonary vascular: pump failure (poor right • Pulmonary embolism ventricular output). • Pulmonary hypertension • Mechanical: • Te n sion p n e u m oth ora x • Pericardial tamponade • Combined

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Shock Shock

• Stages of shock: • Compensated (Pre-Shock): • The body’s compensatory • Pre-shock (compensated) mechanisms are able to maintain • Shock (decompensated) some degree of tissue perfusion. • End-organ dysfunction • Decompensated (Shock): (irreversible) • The body’s compensatory Pre-shock Shock End-organ mechanisms fail to maintain tissue dysfunction perfusion (blood pressure falls). • Irreversible (End-organ Dysfunction): • Tissue and cellular damage is so massive that the organism dies even if perfusion is restored.

Shock Shock

Organ System Compensated Shock Decompensated Shock Irreversible Shock I II III IV CNS Agitation, anxiety, lethargy AMS, encephalopathy, hypoxic- Hypoxic-ischemic injury with cell Blood loss (mL) Up to 750 750-1,500 1,500-2,000 >2,000 ischemic injury necrosis Blood loss (% Up to 11 15-30 30-40 >40 Heart Tachycar di a Tachycar di a ⋙ Myocardia ischemia, cell necrosis volume) Lungs , increased work of Acute respiratory failure Acute respiratory failure Pulse rate <100 100-120 120-140 >140 breathing Kidneys Oliguria ATN, AKI Tu bu l a r n e cr o s i s Blood Pressure Normal Normal Decreased Decreased GI Ileus, feeding intolerance, stress Pancreatitis, acalculous GI , sloughing Respiratory rate 14-20 20-30 30-40 >35 gastritis cholecystitis, GI bleed Urine output (mL/hr) >30 20-30 5-15 Negligible Liver Transaminitis, centrilobular injury Centrilobular necrosis, shock liver Hepatic failure CNS/Mental status Slightly anxious Mildly anxious Anxious Confused Hematologic Endothelial and platelet activation DIC DIC Confused Lethargic Metabolic Glycogenolysis, gluconeogenesis, Glycogen depletion, Hypocalcemia lipolysis, proteolysis hypoglycemia

Shock Shock

• Shock recognition must occur • Examination: • ITLS Primary Survey: at several levels: • Examination should be • Scene size-up. • Examination systematic. • Initial assessment. • Monitoring technologies • Avoid “freewheeling” to avoid • Rapid trauma survey or focused missing important signs and • Response to treatments exam. symptoms. • Experience • Numerous standardized • ITLS Secondary Survey protocols: • ITLS Ongoing Exam • ITLS • PHTLS • ATLS

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Shock Shock

• What is the first • What is often the second physiological factor in the physiological response to the development of shock? development of shock? • VO2 < MRO2 • Peripheral vasoconstriction • So, what are the first • What symptoms would you symptoms you would expect expect to see? to find? • Pale skin • ↑ respiratory rate • Cool skin • ↑ • Weakened peripheral pulses

Shock Shock

• As shock progresses, what • As compensatory mechanisms physiological effects are fully engage, what signs and seen? symptoms would you expect • End-organ perfusion falls to see? • What symptoms would you • Tachycardi a expect to see? • Tachypnea • Altered mental status • Pupillary dilation • Decreased urine output • Decreased capillary refill • Pale cool skin

Shock Shock

• When compensatory • Technol ogy: mechanisms fail, what signs • ECG and symptoms would you • Oximetry expect to see? • Capnography • • POC testing: • Falling SpO2 • Lactate • Bradycardia • Glucose • Loss of consciousness • Non-invasive hemoglobin • Dysrhythmias • SpCO • Death • SpHb

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Shock Shock

• Response to treatment: • Response to Treatment: • Fluid responsiveness: • Responders are those that • Every intervention performed on • Fluid responsiveness is an demonstrate physiological a trauma patient should be increase of stroke volume of 10- improvements. followed by monitoring to 15% after the patient receives • Transient responders show an determine patient response: 500 ml of crystalloid over 10-15 initial improvement followed by • Oxygen minutes. further physiological • Fluids • Indicates preload reserve deterioration. • Medications • Does not mean that patient • Non-responders show continued needs fluid. • Physical maneuvers physiological deterioration despite initial fluid .

Shock Shock

• Experience: • Medicine is very much pattern recognition. • The more patterns a provider is exposed to, the easier it is to Knowledge + Experience = Wisdom recognize the pattern. • ITLS and other standardized trauma courses are designed to improve knowledge of trauma care. • Experience comes from patient contact and management.

Shock Shock

• Early recognition of shock and • Pornography: • Shock: subsequent treatment is • “I know it when I see it.” • “I know it when I see it.” important in patient survival. • US Supreme Court Justice • Every one of us!!! • Shock recognition: Potter Stewart (1964) • Examination • Monitoring technologies • Response to treatments • Experience • You cannot treat shock until you recognize the problem!

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Shock

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