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SHOCK Sevgi Bilgen 2014 Students should learn; The definition of shock Types of shock and differential diagnosis Shock treatment Introduction In order to treat shock appropriately, it must first be recognized, then identify the cause In order to recognize it, it is important to understand some of the physiology of the disease process The definition of shock Shock is a physiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery Hypotension is not a requirement Shock can occur with a normal blood pressure and hypotension can occur without shock Poor tissue perfusion Results in multiple organ failure and death Basic Physiology Tissue perfusion is dependent on SVR and CO Imbalance between oxygen delivery and oxygen consumption which leads to cell death, end organ damage, multi-system organ failure, and death. Basic Physiology Oxygen Delivery = CO x arterial content of O2 Cardiac Output = HR x Stroke Volume Stroke Volume is a function Preload Afterload Myocardial Contractility Basic Physiology Understanding Shock • Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery • Sympathetic nervous system • NE, epinephrine, dopamine, and cortisol release • Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) • Renin-angiotensin axis • Water and sodium conservation and vasoconstriction • Increase in blood volume and blood pressure Understanding Shock • Cellular responses to decreased systemic oxygen delivery • ATP depletion → ion pump dysfunction • Cellular edema • Hydrolysis of cellular membranes and cellular death • Goal is to maintain cerebral and cardiac perfusion • Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow • Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms Global Tissue Hypoxia • Endothelial inflammation and disruption • Inability of O2 delivery to meet demand • Result: • Lactic acidosis • Cardiovascular insufficiency • Increased metabolic demands Multi organ Dysfunction Syndrome (MODS) • Progression of physiologic effects as shock ensues • • • • Cardiac depression Respiratory distress Renal failure DIC • Result is end organ failure Initial Patient Assessment Recognition of Shock Clinical signs and symptoms depends on the severity of the shock Early manifestations include tachycardia and cutaneous vasoconstriction Clinical Pathophysiology of Shock General / Vital signs Cardiovascular- tachycardia Skin- vasoconstriction vs. vasodilation Respiratory- increased RR Urinary- decrease urine output Neurologic- confusion, agitation Extremities- cold vs. warm Clinical Endpoints of Shock DECREASED BLOOD FLOW TO BRAIN AND HEART Restless, agitated, confused, lethargy Hypotension Tachycardia Tachypnea END-STAGE SHOCK Bradycardia Arrhythmias Death Types of shock and differential diagnosis 1.Hypovolemic shock 2.Cardiogenic shock 3.Obstructive shock 4.Distributive shock Common Causes 1.Hypovolemic shock Due to decreased circulating blood volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures 1. Hypovolemic shock Loss of blood (hemorrhagic shock) Loss of plasma Loos of fluid and electrolytes Loss of blood (hemorrhagic shock) External hemorrhage Trauma Gastrointestinal tract bleeding Internal hemorrhage Hematoma Hemothorax or hemoperitoneum Loss of plasma Burns Exfoliative dermatitis Loos of fluid and electrolytes External Vomiting Diarrhea Excessive sweating Hyperosmolar states (diabetic ketoacidosis, hyperosmolar nonketotic coma) Internal (third-spacing) Pancreatitis Ascites Bowel obstruction 2. Cardiogenic shock Due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes 2. Cardiogenic shock Dysrhythmia Tachyarrhythmia Bradyarrhythmia Pump failure (secondary to myocardial infarction or other cardiomyopathy) Acute valvular dysfunction (especially regurgitant lesions) Rupture of ventricular septum or free ventricular wall 3. Obstructive shock Due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload 3. Obstructive shock Tension pneumothorax Pericardial disease (tamponade, construction) Disease of pulmonary vasculature (massive pulmonary emboli, pulmonary hypertension) Cardiac tumor (atrial myxoma) Left atrial mural thrombus Obstructive valvular disease (aortic or mitral stenosis) 4. Distributive shock Caused by loss of vasomotor control resulting in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased SVR 4. Distributive shock Septic shock Anaphylactic shock Neurogenic shock Vasodilator drugs Acute adrenal insufficiency Clinical classification of shock Mild (<20% of blood volume lost) Moderate (20-40% of blood volume lost) Severe (>40% of blood volume lost) Mild (<20% of blood volume lost) Pathophysiology Decreased peripheral perfusion only of organs able to withstand prolonged ischemia (skin, fat, muscle, and bone). Arterial pH normal Clinical Manifestations Patient complains of feeling cold. Postural hypotension and tachycardia. Cool, pale, moist skin; collapsed neck veins; concentrated urine. Moderate (20-40% of blood volume lost) Pathophysiology Decreased central perfusion of organs able to tolerate only brief ischemia (liver, gut, kidneys). Metabolic acidosis present Clinical Manifestations Thirst Supine hypotension and tachycardia (variable) Oliguria and anuria. Severe (>40% of blood volume lost) Pathophysiology Decreased perfusion of heart and brain. Severe metabolic acidosis. Respiratory acidosis possibly present. Clinical Manifestations Agitation, confusion or obtundation. Supine hypotension and tachycardia invariably present. Rapid, deep respiration. Evaluation Airway: includes brief evaluation of mental status Breathing: If patient is conversing with you, A & B are fine. Circulation: Vitals (HR, BP). Includes placement of adequate IV access, Disability: identification of gross neurologic injury Exposure: ensures complete exam Evaluation Laboratory Hgb, WBC, platelets PT/PTT Electrolytes, arterial blood gases BUN, Cr Ca, Mg Serum lactate, mixed venous oxygen saturation (SVO2) ECG Evaluation Invazive monitoring Arterial pressure catheter CVP monitoring Pulmonary artery catheter Mixed or central venous oxygen saturation (SvO2/ScvO2) Oxygen delivery(DO2) and oxygen consumption(VO2) As indicated o Chest x-ray o Pelvic x-ray o Abd/pelvis CT o Chest CT o GI endoscopy o Bronchoscopy o Vascular radiology Treatment Identify & reverse the cause Restore tissue perfusion Restore organ function Treatment of Shock General Management • ABCDE • Airway • control work of Breathing • optimize Circulation • assure adequate oxygen Delivery • achieve End points of resuscitation Airway • Determine need for intubation but remember: intubation can worsen hypotension • Sedatives can lower blood pressure • Positive pressure ventilation decreases preload • May need volume resuscitation prior to intubation to avoid hemodynamic collapse Control Work of Breathing • Respiratory muscles consume a significant amount of oxygen • Resting ventilatory muscles will permit diversion of cardiac output to other hypo perfused organs • Tachypnea can contribute to lactic acidosis • Mechanical ventilation and sedation decrease WOB and improves survival Optimizing Circulation • Unless there are signs of intravascular volume overload initial resuscitation with IV fluids is generally indicated. • Isotonic crystalloids • Titrated to: • CVP 8-12 mm Hg • Urine output 0.5 ml/kg/hr. (30 ml/hr.) • Improving heart rate • May require 4-6 L of fluids • No outcome benefit from colloids • Vasopressor medications should be selected based on the cause of shock Maintaining Oxygen Delivery • Decrease oxygen demands • Provide analgesia and anxiolytics to relax muscles and avoid shivering • Maintain arterial oxygen saturation/content • Give supplemental oxygen • Maintain Hemoglobin > 10 g/dL • Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction End Points of Resuscitation • Goal of resuscitation is to maximize survival and minimize morbidity • Use objective hemodynamic and physiologic values to guide therapy • Goal directed approach • • • • Urine output > 0.5 mL/kg/hr. CVP 8-12 mmHg MAP 65 to 90 mmHg Central venous oxygen concentration > 70% Persistent Hypotension • Inadequate volume resuscitation • Pneumothorax • Cardiac tamponade • Hidden bleeding • Adrenal insufficiency • Medication allergy Resuscitation Fluids Blood Lactated Ringers Normal Saline Colloids Hypertonic Saline Blood Substitutes Evaluation of Treatment Assess organ perfusion Urinary output Mental Status Skin exam Vitals Which Pressor should I choose? Hypovolemic shock Fluids and Blood Cardiogenic shock Dobutamine - 1 agonist Increases squeeze and heart rate Neurogenic shock Fluids, phenylephrine, norepinephrine, look for another type of shock if it is persistent Anaphylactic shock Fluids and epinephrine Septic shock Phenylephrine- alpha agonist Increases SVR by arteriolar constriction Norepinephrine - alpha and beta agonists Dopamine Low Dose - increases renal blood supply Medium Dose - beta effects (increases heart rate and squeeze) High Dose - alpha effects (arteriolar constriction) Early versus delayed administration of norepinephrine in patients with septic shock. The 28-day mortality was 37.6% overall. Among the 213 patients, a strong relationship between delayed initial norepinephrine administration and 28-day mortality was noted. The average time to initial norepinephrine administration was 3.1¿±¿2.5 hours. Every 1-hour delay in norepinephrine initiation during the first 6 hours after septic shock onset was associated with a 5.3% increase in mortality. Twenty-eight day mortality rates were significantly higher when norepinephrine administration was started more than or equal to 2 hours after septic shock onset (Late-NE) compared to less than 2 hours (Early-NE). Mean arterial pressures at 1, 2, 4, and 6 hours after septic shock onset were significantly higher and serum lactate levels at 2, 4, 6, and 8 hours were significantly lower in the Early-NE than the Late-NE group. The duration of hypotension and norepinephrine administration was significantly shorter and the quantity of norepinephrine administered in a 24-hour period was significantly less for the Early-NE group compared to the Late-NE group. The time to initial antimicrobial treatment was not significantly different between the Early-NE and Late-NE groups. Conclusion: Early administration of norepinephrine in septic shock patients is associated with an increased survival rate. Crit Care. 2014 Oct 3;18(5):532. Bai X, Yu W, Ji W, Lin Z, Tan S, Duan K, Dong Y, Xu L, Li N. Survival and outcomes improve with early perfusion, adequate oxygenation, and identification with appropriate treatment of the cause of shock.