NLE Emergency & Critical Care Nursing — Shock, Sepsis & Multi-Organ DysfunctionConcept Map

Related concepts

Concept connections

• Shock: Inadequate Tissue Perfusion→Four Classes of ShockShock is classified by its underlying mechanism; all classes converge on the same final pathway of failing perfusion
• Four Classes of Shock→Hypovolemic ShockLoss of circulating volume (hemorrhage, dehydration, burns, third-spacing); preload falls, cardiac output falls
• Four Classes of Shock→Cardiogenic ShockPump failure despite adequate volume; cardiac output falls while filling pressures rise; pulmonary congestion results
• Four Classes of Shock→Distributive ShockProfound loss of vascular tone causes blood pooling; normal volume cannot maintain perfusion; includes septic, neurogenic, and anaphylactic subtypes
• Distributive Shock→Septic ShockVasodilation and capillary leak driven by overwhelming infection; most common and lethal form of distributive shock; requires rapid sepsis bundle implementation
• Distributive Shock→Neurogenic ShockLoss of sympathetic tone after spinal cord injury above T6; distinctive for bradycardia with hypotension (not tachycardia like other shocks)
• Distributive Shock→Anaphylactic ShockIgE-mediated massive histamine release; causes vasodilation, capillary leak, and bronchospasm; requires immediate IM epinephrine
• Four Classes of Shock→Obstructive ShockMechanical obstruction blocks blood flow (tension pneumothorax, tamponade, massive PE); requires mechanical relief, not just fluids and drugs
• Shock: Inadequate Tissue Perfusion→Stages of Shock ProgressionAll shock progresses through four predictable stages; treatment window narrows at each step; early intervention in compensatory stage is most effective
• Stages of Shock Progression→Initial StagePerfusion drops at cellular level; cells shift to anaerobic metabolism; lactic acid accumulates; no visible clinical signs yet; biochemical changes only
• Stages of Shock Progression→Compensatory StageBody activates protective reflexes; sympathetic activation produces tachycardia, vasoconstriction, increased RR; blood pressure often maintained (false reassurance); MOST TREATABLE stage
• Stages of Shock Progression→Progressive StageCompensation fails; blood pressure falls; tissue ischemia worsens; acidosis severe; altered mental status; organs begin failing; aggressive intervention can still save but margin is thin
• Stages of Shock Progression→Refractory StageCellular and organ damage is irreversible; patient does not respond to any therapy; death follows despite maximal support
• Septic Shock→SIRSSIRS (≥2 of: fever/hypothermia, tachycardia, tachypnea, abnormal WBC) is a precursor to sepsis; can be triggered by infection or non-infectious insults
• Septic Shock→SepsisSepsis is life-threatening organ dysfunction from dysregulated response to infection; septic shock is sepsis with circulatory collapse requiring vasopressors and elevated lactate despite fluids
• Septic Shock→Sepsis BundleHour-1 bundle of interventions (lactate, blood cultures, antibiotics, fluids, vasopressors) is the evidence-based protocol that saves lives; each hour of delay increases mortality
• Sepsis Bundle→Blood Cultures Before AntibioticsCritical sequencing: obtain cultures first, then antibiotics; cultures drawn after antibiotics are far less useful for identifying pathogen
• Sepsis Bundle→Rapid Crystalloid Resuscitation30 mL/kg IV push is standard first-line fluid resuscitation; goal is to restore perfusion and reduce lactate; done before vasopressors
• Sepsis Bundle→Vasopressor InitiationNorepinephrine is first-line vasopressor; started only if hypotension persists after fluid resuscitation; goal MAP ≥65 mmHg
• Septic Shock→Multi-Organ Dysfunction SyndromeUntreated or late-treated septic shock is the most common cause of MODS; prolonged hypoperfusion triggers systemic inflammation and cascading organ failure
• Shock: Inadequate Tissue Perfusion→Multi-Organ Dysfunction SyndromeMODS is the progressive consequence of severe shock; failure of ≥2 organ systems; mortality increases steeply with each additional failing organ
• Multi-Organ Dysfunction Syndrome→Organ Failure SequenceTypical sequence: lungs (ARDS) first, then kidneys (AKI), liver, coagulation, GI, cardiac; progression is not always linear but reflects cumulative hypoperfusion injury
• Shock: Inadequate Tissue Perfusion→Disseminated Intravascular CoagulationDIC is a complication of severe shock and sepsis; widespread clotting activation consumes platelets and factors, producing simultaneous thrombosis and bleeding
• Disseminated Intravascular Coagulation→Laboratory Findings in DICProlonged PT and aPTT, low platelets, low fibrinogen, and elevated D-dimer are hallmark findings; reflect both consumption of factors and activation of fibrinolysis
• Disseminated Intravascular Coagulation→DIC TreatmentCornerstone is correcting the underlying cause (treating infection in sepsis); supportive care replaces consumed components with FFP, cryoprecipitate, and platelets
• Nursing Management & Priority Interventions→Airway & OxygenationFirst priority in all shock: ensure patent airway, adequate oxygenation, and prepare for ventilatory support; hypoxia worsens tissue perfusion
• Nursing Management & Priority Interventions→Circulation SupportPosition most patients supine with legs elevated to promote venous return and improve preload; exception is cardiogenic shock with pulmonary congestion (more upright position)
• Nursing Management & Priority Interventions→Volume & Vasoactive Drug TitrationRapid crystalloids through large-bore access; vasoactive drugs titrated to MAP ≥65 mmHg; therapy choice depends on shock class (fluids for hypovolemic, inotropes for cardiogenic, vasopressors for distributive)
• Nursing Management & Priority Interventions→Perfusion MonitoringHourly assessment of urine output (≥0.5 mL/kg/hr), lactate trend, mental status, skin perfusion, and hemodynamic parameters; trends are more important than isolated values
• Nursing Management & Priority Interventions→Class-Specific Therapy MatchingCritical nursing judgment: match therapy to the identified shock class; fluids for hypovolemia, inotropes for cardiogenic, vasopressors + fluids for septic, epinephrine for anaphylactic, mechanical relief for obstructive
• Compensatory Stage→Early Warning SignsRising respiratory rate and narrowing pulse pressure are among the earliest reliable warnings of inadequate compensation; recognition at this stage enables intervention before blood pressure falls
• Hypovolemic Shock→Volume Replacement TreatmentCrystalloids (normal saline or lactated Ringer's) plus blood products for hemorrhage; treatment includes source control (stop the bleeding, replace fluids)
• Cardiogenic Shock→Inotrope & Vasodilator TreatmentDobutamine or other inotropes support failing pump; vasodilators or cautious diuresis reduce afterload; aggressive fluid loading (which helps hypovolemic shock) can worsen cardiogenic shock
• Anaphylactic Shock→Epinephrine IMPriority drug is epinephrine 0.3 to 0.5 mg IM (1:1000 solution); given IM not IV for safer absorption; followed by IV access, antihistamines, and corticosteroids
• Obstructive Shock→Mechanical ReliefTension pneumothorax requires needle decompression and chest tube; tamponade requires pericardiocentesis; massive PE requires thrombolysis or embolectomy; fluids alone will not restore perfusion
• Neurogenic Shock→Bradycardia ExceptionUnique feature: bradycardia + hypotension + warm dry skin; every other shock is tachycardic; recognition of this distinctive pattern guides appropriate treatment (fluids, possibly atropine)
• Prevention of MODS→Early Shock RecognitionRecognizing shock in compensatory stage (before hypotension) enables early intervention; waiting for blood pressure to fall means intervening in progressive stage with narrowed treatment window
• Prevention of MODS→Rapid Fluid Resuscitation30 mL/kg crystalloid bolus is standard; restores circulating volume, improves organ perfusion, and reduces lactate; critical for preventing progression to MODS
• Prevention of MODS→Timely Antibiotics in SepsisEach hour of antibiotic delay in septic shock increases mortality; broad-spectrum coverage must start within 1 hour of recognition; cultures drawn first but do not delay antibiotics
• Prevention of MODS→Source ControlIdentifying and treating the infection source (imaging, cultures, possible drainage/surgery) is essential; antibiotics alone cannot cure an undrained abscess or remove infected tissue

Diagrams