4- SHOCK SIRS MODS

• Shock


  Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
• Shock


  Imbalance between supply of and demand for O2 and nutrients
• Classification of Shock


  • Cardiogenic
  • Hypovolemic
  • Neurogenic
  • Anaphylactic
  • Septic
  • Obstructive
• Cardiogenic Shock


  Systolic or diastolic dysfunction
• Cardiogenic Shock


  Systolic dysfunction is the heart's inability to pump the blood forward
• Most common cause of cardiogenic shock is MI
• Cardiogenic Shock


  Decreased filling of the heart will result in decreased stroke volume
• Cardiogenic Shock


  Low cardiac output (CO) and cardiac index
• Precipitating causes of Cardiogenic Shock

  • Myocardial infarction
  • Cardiomyopathy
  • Blunt cardiac injury
  • Severe systemic or pulmonary hypertension
  • Cardiac tamponade
  • Myocardial depression from metabolic problems
• Pathophysiology of Cardiogenic Shock

  1. Tachycardia

  2. Hypotension

  3. Narrowed pulse pressure

  4. Increased systemic vascular resistance (SVR)

  5. Increased myocardial O2 consumption
• Manifestations of Cardiogenic Shock

  • Tachypnea, pulmonary congestion
  • Pallor and cool, clammy skin
  • Decreased capillary refill time
  • Anxiety, confusion, agitation
  • Increased pulmonary artery wedge pressure (PAWP)
  • Stroke volume variation (SVV) and pulmonary vascular resistance
  • Decreased renal perfusion and urinary output
• Hypovolemic Shock


  Absolute hypovolemia: loss of intravascular fluid volume
• Causes of Absolute Hypovolemia

  • Hemorrhage
  • GI loss (e.g., vomiting, diarrhea)
  • Fistula drainage
  • Diabetes insipidus
  • Diuresis
• Hypovolemic Shock


  Relative hypovolemia: fluid volume moves out of the vascular space into extravascular space (e.g., intracavitary space)
• Pathophysiology of Hypovolemic Shock

  1. Response to acute volume loss depends on: Extent of injury, Age, General state of health

  2. Patient may compensate for up to 15% loss

  3. Loss of 15-30-5 results in SNS-mediated response
• Manifestations of Hypovolemic Shock

  • Anxiety
  • Tachypnea
  • Increase in heart rate, CO, respiratory rate and depth
  • Decrease in stroke volume, CVP, PAWP, urinary output
  • If loss is greater than 30%, blood volume is replaced
• Neurogenic Shock


  Hemodynamic phenomenon can occur within 30 minutes of a spinal cord injury at the T5 vertebra or above and can last up to 6 weeks
• Neurogenic Shock


  Results in massive vasodilation, leading to pooling of blood in vessels, tissue hypoperfusion, ultimately impaired cellular metabolism
• Manifestations of Neurogenic Shock

  • Hypotension and bradycardia
  • Inability to regulate body temperature (resulting in heat loss)
  • Dry skin
  • Poikilothermia—taking on temperature of environment
• Anaphylactic Shock


  Acute, life-threatening hypersensitivity (allergic) reaction
• Anaphylactic Shock


  Massive vasodilation, release of vasoactive mediators, increase in capillary permeability, fluid leaks into interstitial space
• Manifestations of Anaphylactic Shock

  • Anxiety
  • Confusion, dizziness
  • Sense of impending doom
  • Chest pain
  • Incontinence
  • Swelling of lips and tongue, angioedema
  • Wheezing, stridor due to laryngeal edema
  • Flushing, pruritus, urticaria
  • Respiratory distress and circulatory failure
• Septic Shock


  Sepsis: systemic inflammatory response to documented or suspected infection
• Septic Shock


  Severe sepsis: sepsis complicated by organ dysfunction
• Septic Shock


  Presence of sepsis with hypotension despite fluid resuscitation and presence of inadequate tissue perfusion resulting in hypoxia
• Pathophysiology of Septic Shock

  1. Vasodilation

  2. Maldistribution of blood flow

  3. Myocardial dysfunction, decreased ejection fraction, ventricular dilation
• Manifestations of Septic Shock

  • Increased coagulation and inflammation, decreased fibrinolysis, formation of microthrombi
  • Increase temperature, Increased HR, Increased RR, decreased BP
  • Obstruction of microvasculature, hyperdynamic state: increased CO and decreased SVR, decreased urine output
  • Tachypnea/hyperventilation, respiratory alkalosis, respiratory failure in 85% of patients, altered neurologic status, GI dysfunction, GI bleeding, paralytic ileus
• Obstructive Shock


  Develops when physical obstruction to blood flow occurs with decreased CO, caused by restricted diastolic filling of right ventricle from compression
• Obstructive Shock


  Abdominal compartment syndrome—abdominal pressure compresses inferior vena cava
• Manifestations of Obstructive Shock

  • Decreased CO, Increased afterload, Variable left ventricular filling pressure
• Stages of Shock


  • Initial
  • Compensatory
  • Progressive
  • Refractory
• Initial Stage of Shock

  Metabolism changes at cellular level from aerobic to anaerobic, lactic acid builds up and must be removed by liver, process requires O2, unavailable due to decreased tissue perfusion
• Compensatory Mechanisms in Shock

  • Neural
  • Hormonal
  • Biochemical
• Compensatory Stage of Shock

  1. Baroreceptors activate SNS in response to decreased BP, vasoconstriction while blood to vital organs maintained

  2. SNS stimulation increases myocardial O2 demands, shunting blood from lungs increases physiologic dead space, V/Q mismatch, decreased arterial O2 levels, increase in rate/depth of respirations

  3. Impaired GI motility, slowed peristalsis, risk for paralytic ileus, cool, clammy skin except septic patient who is warm and flushed

  4. Decreased blood to kidneys activates renin–angiotensin system, vasoconstriction, increased venous return to heart, stimulates release of aldosterone, increased sodium reabsorption stimulates ADH
• If cause of shock is corrected, patient recovers with little or no residual effects. If cause of shock is not corrected, patient enters progressive stage.
• Progressive Stage of Shock

  1. Decreased cellular perfusion and altered capillary permeability, leakage of protein into interstitial space, increase of systemic interstitial edema, cardiac output begins to decrease, resulting in a decrease in BP

  2. Anasarca: diffuse profound edema, fluid leakage affects solid organs and peripheral tissues, decreases blood flow to pulmonary capillaries, sustained hypoperfusion, weak peripheral pulses, ischemia of distal extremities

  3. Myocardial dysfunction results in dysrhythmias, myocardial ischemia, possible myocardial infarction, end result: complete deterioration of cardiovascular system

  4. Movement of fluid from pulmonary vasculature to interstitium, pulmonary edema, bronchoconstriction, decreased functional residual capacity

  5. Fluid moves into alveoli, edema, decreased surfactant, worsening V/Q mismatch, tachypnea, crackles, increased work of breathing

  6. Mucosal barrier of GI system becomes ischemic, ulcers, GI bleeding, risk of migration of bacteria, decreased ability to absorb nutrients

  7. Hypoperfusion leads to renal tubular ischemia, may result in acute kidney injury, worsened by nephrotoxic drugs, decreased urine output, elevated BUN and serum creatinine, metabolic acidosis

  8. Liver fails to metabolize drugs and waste, jaundice, elevated enzymes, loss of immune function, risk for DIC and significant bleeding
• Refractory Stage of Shock

  1. Exacerbation of anaerobic metabolism, accumulation of lactic acid and waste products, increased capillary permeability

  2. Profound hypotension and hypoxemia, tachycardia worsens, failure of one organ system affects others, recovery unlikely
• Diagnostic Studies


  • Thorough history and physical examination
  • Blood studies: Elevation of lactate, Base deficit
  • 12-lead ECG, continuous ECG monitoring
  • Chest x-ray
  • Continuous pulse oximetry
  • Hemodynamic monitoring
• Interprofessional Care


  • Identification of patients at risk for developing shock
  • Integration of patient's history, physical examination, and clinical findings to establish a diagnosis
  • Interventions to control or eliminate cause of decreased perfusion
  • Protection of target and distal organs from dysfunction
  • Provision of multisystem supportive care
  • Removing indwelling catheters asap, use of aseptic techniques, early ambulation, enteral feeding to preserve the integrity of the GI track, antibiotics should be given within 1 hour after being prescribed to decrease the risk of sepsis progressing to SIRS, but no before obtaining blood cultures, or any other cultures that are important to the patients cares
  • Ensure patent is responsive, ensure a patent airway, maximize oxygen delivery
  • Increase oxygen supply, optimize CO with fluid replacement or drugs, increased hemoglobin by transfusion, increased arterial oxygen with supplemental oxygen and mechanical ventilation, plan care to avoid disrupting O2 supply and demand
  • Volume expansion with isotonic crystalloids, RBCs for volume loss due to bleeding
  • Fluid responsiveness is determined by clinical assessment, vital signs, cerebral and abdominal perfusion pressures, capillary refill, neurologic status, skin temperature, urine output, passive leg raise challenge and IVC evaluation
  • Hypothermia and coagulopathy are 2 major complications of large fluid volumes, persistent hypotension after adequate fluids may require vasopressor
• Drug Therapy


  1. Vasopressor drugs (e.g., norepinephrine) to achieve/maintain MAP greater than 65 mm Hg, reserved for patients unresponsive to fluid resuscitation, continuously monitor end-organ perfusion

  2. Vasodilator therapy (e.g., nitroglycerin, nitroprusside) to decrease afterload, achieve/maintain MAP greater than 65 mm Hg, monitor hemodynamic parameters and assessment