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36 Cards in this Set
- Front
- Back
Shock Definitions
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Low BP causing inadequate organ perfusion and oxygenation
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Shock clinical manifestations
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Skin is pale, cold, sweaty
Pulse is rapid, weak, thready Blood pressure low (It must be hypotension) Respiratory rate increased Altered mental status (anxiety, apprehension, coma) Decreased urine output |
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Shock in essence is due to either
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decreased CO or blood is not distributed in the right way.
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Shock stages are
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Stage I - Compensated shock
Stage II - Decompensated shock Stage III - Irreversible |
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Shock Reflex responses
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Increased sympathetic activity
Catecholamine secretion Vasoconstriction Increased pulse Increased cardiac output |
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Compensatory mechanism to shock
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Blood redistributed to vital organs (, heart, brain, kidney)
Blood shunted away from skin, gut, and muscles. All these fail in late stage of shock |
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Cellular Hypoxia in shock
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Inadequate substrate delivery
Anaerobic metabolism Increased lactate production Acidotic state |
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Pulmonary function under shock
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Respiratory alkalosis
Impaired oxygenation Respiratory acidosis |
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Renal function Shock
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Oliguria
Renal Vasoconstriction Decreased renal blood flow Acute renal failure Ischemic cellular injury |
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Shock class 1 characteristic
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Minimal tachycardia
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Class II shock characteristics
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Tachycardia, tachypnea
Subtle CNS findings (anxiety) |
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Class III shock chracteristics
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Marked tachycardia, tachypnea, altered mental status
Fall in systolic blood pressure(SBP) |
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Class IV shock characteristics
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Marked tachycardia, decreased SBP
Depressed mental status No urine output Skin cold and pale |
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Hemorragic shock characteristics
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Etiology is rapid blood loss
Blood loss may be internal or external Decreased circulating blood volume |
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Hemorragic shock causes
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Traumatic
Gastrointestinal bleeding (esophageal varices) Vascular (Abdominal Aortic Aneurysm) Pregnancy (ectopic, placenta previa, placental abruption) |
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Hemorragic shock Pathophysiology
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Rapid blood loss
Decreased venous return Reduced ventricular filling pressures Decreases stroke volume, CO Hypotension |
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Hemorragic shock clinical manifestations
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Clinical manifestations
Skin is pale Increased pulse, respiratory rate Decreased BP Altered mental status |
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Hemorragic shock treatment
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Restore intravascular volume
Intravascular fluids Blood Identify and treat cause |
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Hypovolemic Shock
characteristics |
Fluid or electrolyte losses
Pathophysiology same as hemorrhagic Common etiologies Severe vomiting and diarrhea Diabetes mellitus Burns |
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Septic shock early manifestation
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(increased CO) warm shock
Vasodilatation Skin warm and flushed Hyperdynamic Altered mental status Fever |
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Septic shock late phase
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Late phase (decreased SV, CO) cold shock
↓ cardiac output, blood pressure ↓ urine output Peripheral vasoconstriction Mortality rate in septic shock is ~ 45% |
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Septic shock Tx
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Oxygen/ventilation
Fluids Antibiotics Removal/drainage of infection Inotropic/vasoconstrictive agents |
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Neurogenic Shock
caused by |
Spinal cord trauma
Loss of sympathetic tone Vasodilatation Decreased preload and CO Bradycardia (unusual in shocks)* |
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Neurogenic Shock Clinical presentation
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Decreased blood pressure
Spinal trauma Bradycardia |
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Neurogenic Shock
Tx |
Fluids with caution
Vasopressor ( alpha-adrenergic activity) |
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Cardiogenic Shock
characteristics |
Decreased pumping ability of the heart causing inadequate perfusion to tissues
Over 40% of the myocardium must be affected or ischemic to go to cardiogenic shock Can occur with cardiac trauma, cardiomyopathy |
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Cardiogenic shock leads to myocardium damage leading to
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↓ contractility
↓ ejection fraction ↓ CO ↑ ventricular filling pressures cardiac chamber dilatation ventricular failure systemic hypotension, pulmonary edema |
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Cardiogenic shock cellular eventsCascade of events -
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endogenous substances (myocardial depressant factor, bradykinin, leukotrienes, etc)
inhibits cardiac function increases myocardial depression worsening shock |
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Cardiogenic shock Clinical presentation
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Hypotension
Cool, diaphoretic skin Cyanosis, SOB Altered mental status |
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Cardiogenic Shock
Tx |
Myocardial preservation (rapid revascularization)
Best treatment is prevention Oxygen Fluid challenge Cardiac monitoring Vasopressors, inotropes |
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Anaphylactic Shock
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Severe allergic reaction
Immunologically mediated systemic vasodilation Type I hypersensitivity reaction IgE mediated Release of histamine from basophils and mast cells |
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Anaphylactoid reaction
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- not immune mediated, direct release of mediators (histamine, leukotriene C4, tryptase, prostaglandins
) |
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Anaphylactic Shock
characteristics |
Diffuse vasodilation
Increased capillary permeability Increased secretions from mucous membranes Increased bronchial smooth muscle tone Distributive shock |
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Anaphylactic Shock Etiologies
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Drugs (PCN, sulfonamides)
Foods (nuts, shellfish) Toxins (bee, snake venom) Latex Animal sera (tetanus antitoxin) |
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Anaphylactic Shock Symptoms
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Increased HR, low BP
Urticaria, pruritis, erythema, angioedema (>90% have skin involvement) SOB, wheezing, airway obstruction Facial/pharyngeal/laryngeal edema Eyes tearing, itching |
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Anaphylactic Shock Treatment
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Epinephrine
Oxygen/airway support/B agonists Antihistamines, H1 and H2 blocking agents |