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36 Cards in this Set

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