CARDIOGENIC, HYPOVOLEMIC, NEUROGENIC, ANAPHYLACTIC SHOCK CARDIOGENIC, HYPOVOLEMIC, NEUROGENIC, ANAPHYLACTIC

1. Summarize the generalized principles of shock and the associated pathophysiological findings. 2. Differentiate the various types of shock (hypovolemic, cardiogenic, anaphylactic, neurogenic); including the causes and pathological findings of each. 3. Identify and apply the appropriate treatment modalities for each form of shock; including pharmacological management. OBJECTIVES

SHOCK OVERVIEW All shock leads to cellular hypoxia (if not corrected) Cellular hypoxia is due to decreased perfusion or ineffective use of the oxygen provided Cellular hypoxia causes further systemic damage which can lead to SIRS and MODS (if not corrected) SHOCK OVERVIEW

The priority treatment is to remove/treat the underlying cause Most forms of shock are caused by either a decreased CO and/or decreased SVR stroke volume (preload, contractility, afterload) Systemic vascular resistance (blood viscosity, vessel tone) Distributive shock refers to all types of shock that cause massive vasodilation Septic, Neurogenic, Anaphylactic All forms of shock are progressive. Rate and method of progression depends on the type Late shock is typically irreversible. EARLY identification and treatment is key. The priority treatment is to remove/treat the underlying cause

Impaired Oxygen Consumption Anaerobic Metabolism Disruption of sodium-potassium pump Cellular edema Decreased circulatory volume Lysosomal enzyme release Activation of inflammatory and clotting cascades Leads to metabolic acidosis  lactic acid Causes a continual loop of further cellular destruction Impaired Oxygen Consumption

Impaired Glucose Consumption Ineffective glucose delivery Utilize glucose stores within the body Switch to alternate forms of fuel production Gluconeogenesis Ammonia and urea byproduct  toxic accumulation Impaired Glucose Consumption

Compensated Decompensated Irreversible Progression of Shock

Types of Shock CARDIOGENIC Causes: Acute myocardial infarction Endocarditis Dysrhythmias Pericardial tamponade Pulmonary embolism Types of Shock

Cardiogenic Shock Pathophysiology: Inability of the heart to pump adequate blood to tissues and organs Persistent Hypotension with adequate intravascular volume Hypoperfusion  activation of renin-angiotensin, sympathetic nervous system, neurohormonal compensation Compensation causes increased cardiac demand  further cardiac failure Cardiogenic Shock

Cardiogenic Shock Manifestations: Angina Dyspnea Feelings of impending doom Tachycardia Tachypnea Hypotension Jugular venous distention Pulmonary edema dysrhythmias Cardiogenic Shock

Cardiogenic Shock Signs of end-organ hypoperfusion: Cyanosis Skin mottling Faint, irregular pulses Low urine output Cardiogenic Shock

Cardiogenic Shock Treatment: Fibrinolytic drugs PCI Intra-aortic balloon pump Cardio-supportive drugs Cardiogenic Shock

HYPOVOLEMIC Causes: Hemorrhage (whole blood) Burns (plasma) Loss of interstitial fluid (emesis, diuresis, diaphoresis)

Hypovolemic Shock Pathophysiology: Hypovolemia  compensatory mechanisms Catecholamine release  increased heart rate, increased SVR Interstitial fluid moves to the vascular space Stored RBCs and plasms are released by the liver and spleen Activation of renin-angiotensin system Hypovolemic Shock

Hypovolemic Shock Manifestations: Dependent on amount of fluid/blood loss Tachycardia Poor skin turgor Increased thirst oliguria Hypovolemic Shock

Hypovolemic Shock Treatment: Crystalloid fluid resuscitation Blood products (if indicated) Vasopressors (if hypotension remains s/p fluid resuscitation) Hypovolemic Shock

Neurogenic Shock NEUROGENIC Causes: Spinal cord injuries TBI (medulla) Insulin reactions Anesthetic drugs Severe emotional stress Neurogenic Shock

Neurogenic Shock Pathophysiology: Massive vasodilation due to an imbalance between sympathetic and parasympathetic stimulation Low SVR Relative hypovolemia Normal ejection fraction Decreased central venous pressure Neurogenic Shock

Manifestations: Bradycardia Hypotension Neurogenic Shock

Neurogenic Shock Treatment: Fluid resuscitation Vasopressor therapy (if indicated) Drugs for bradycardia (if indicated) Neurogenic Shock

Anaphylactic Shock ANAPHYLACTIC Causes: Hypersensitivity reaction to an allergen… Food allergens Insect venom Pollen Medications Latex Anaphylactic Shock

Anaphylactic Shock Pathophysiology: Immediate onset Hypersensitivity reaction leads to massive vasodilation and relative hypovolemia Immune response to antigen recognition Production of mast cells, IgE Rapidly progressive if not treated immediately Anaphylactic Shock

Anaphylactic Shock Manifestations: Difficulty breathing GI cramps Airway constriction Hives Hemolysis Anxiety Anaphylactic Shock

Anaphylactic Shock Treatment: Remove underlying cause Epinephrine IV fluid replacement Corticosteroids Antihistamines Anaphylactic Shock

Adrenergic Agonists Epinephrine Norepinephrine Dopamine Dobutamine Albuterol Adrenergic Agonists

Receptor Specificity Alpha 1 Alpha 2 Beta 1 Beta 2 Vasoconstriction of blood vessels Mydriasis Alpha 2 Reduction of sympathetic outflow Relief of pain Beta 1 Increase cardiac contractility Increase heart rate Enhance impulse conduction Initiate heart beat Beta 2 Promote bronchodilation Receptor Specificity

Epinephrine Receptor specificity: Chemical class: Therapeutic uses: a1, a2, b1, b2 Chemical class: catecholamine Therapeutic uses: Delay absorption of local anesthetics Control superficial bleeding Initiate heart beat Promote bronchodilation Adverse effects: Hypertensive crisis Dysrhythmias Angina Necrosis of tissue hyperglycemia Epinephrine

Administration: Topically or injection 0.1% SQ or IM .01% IV EpiPen Epinephrine auto-injector 0.3ml solution; inject immediately Report to hospital after use IM injection to outer thigh Stored in dark @ room temperature Side effects: Palpitations, nervousness, headache, n/v

Dobutamine Receptor specificity: Chemical class: Uses: Beta 1 Chemical class: catecholamine Uses: Short term use in severe heart failure; cardiogenic shock Maintain systemic perfusion Chemical stress tests Adverse effects: Tachycardia Dysrhythmias hypertnesion Administration: IV Starting dose 0.5-1 mcg/kg/min titrate Dobutamine

Dopamine Chemical class: Receptor specificity: Uses: Adverse effects: catecholamine Receptor specificity: dose dependent Low dose – dopamine receptors Moderate dose – dopamine and beta 1 receptors High dose – dopamine, beta 1 and alpha 1 receptors Uses: Shock Heart failure Adverse effects: Contraindicated in individuals with tachycardia/dysrhythmias Angina Necrosis of tissue Administration: 2 to 5 mcg/kg/min IV continuous infusion If extravasation occurs, infiltrate area with phentolamine Dopamine

Albuterol Receptor specificity: Chemical class: Uses: Beta 2 Chemical class: Non-catecholamine Uses: asthma Adverse effects: (in large doses) Tachycardia Tremor Albuterol

Norepinephrine Receptor specificity: Chemical class: Uses: Alpha 1, alpha 2, beta 1 Chemical class: catecholamine Uses: Hypotensive states Cardiac arrest Adverse effects: Tachydysrhythmias, angina, hypertension, necrosis of tissue Administration: IV infusion only Norepinephrine