SHOCK

SHOCK

1. a life-threatening condition with many causes

   • mean arterial BP (MABP) inadequate to meet the needs of the tissue
   • the inability of the circulatory system to supply O2 and nutriets to tissues because of:
     • 1. ineffective cardiac pump
     • 2. ineffective circulatory system
     • 3. inadequate blood volume
   • demand for O2 not met by O2 delivery
     • early shock
       • respiratory alkalosis <- hyperventilation
     • late shock
       • metabolic acidosis <- accumulation of lactic acid <-anaerobic metabolism

2. systemic inflammatory response syndrome (SIRS)

   • triggered by infectious and non-infectious conditions
     • can be caused by ischemia, inflammation, trauma, infection or combination
   • non-specific
     • not always related to infection

3. multi organ dysfunction syndrome (MODS)

   • failure of more than one organ when homeostasis can not be maintained without intervention

4. Stages

   • Progessive
     • compensatory mechanisms fail
       • 1st critical dysfunction: respiratory system
         • decreased blood flow & SNS stimulation
         • pulmonary arterioles constrict
           • decreased blood flow to capillaries
             • capillary leakage
               • movement of fluid into interstitial space (bronchoconstriction
                 • alveolar edema
                 • pt develops tachypnea, crackles & increased WOB
           • ventilation perfusion mismatch
     • CO falls, BP falls
       • perfusion to the organs is compromised
         • organ failure begins
       • pt may experience chest pain, significant hypotension & arrhythmias
     • hypoperfusion to kidneys - renal tubular ischemia
       • necrosis -> acute renal failure
         • oliguria and increasing BUN & Cr
     • metabolic acidosis
       • inability to excrete acids & reabsorption of bicarbonate
     • GI
       • ischemia development
         • erosive ulcers
         • GI bleed
         • translocation of bacteria
         • decreased nutrient absorption
     • Liver
       • failure to metabolize drugs
       • ammonia and lactate
         • jaundice
     • DIC
       • consumption of platelets and clotting factors with secondary fibrinolysis
   • Compensatory
     • neural, biochemical, hormonal mechanisms
       • protect body from consequences of anaerobic metabolism and maintain BP and volume in normal limits
       • specific to underlying cause
     • GOAL: maintain Homeostasis
   • Initial
     • cellular oxygen deprivation
       • survival by producing adenosine phosphate anaerobically -> converted -> lactic acid
         • lactic acid builds up -> environment becomes acidotic and cell function ceases
           • cells swell and membranes become permeable for easy transference of fluid and electrolytes in and out of cells
           • lactic acid must be removed by blood and broken down by liver
             • requires O2; unavailable at cell level
     • Na-K pump relies on ATP to pump electrolytes in and out of cells
       • ATP produced in mitochondria
         • damage = less production of ATP
           • no improvement = cell death continues
   • Refractory
     • hypotension & hypoxia
       • multi system failure
       • accumulation of waste products
       • respiratory and cardiac arrest are inevitable

5. Types

   • Hypovolemic
     • loss of intravascular fluid volume
       • reduction in circulating volume
         • 1. fluid can move out of blood vessels and into body spaces
           • hemothorax, ruptured speen
         • 2. fluid can move into interstitial spaces
           • burns, sepsis, allergic reactions
         • 3. loss of fluid from the body
           • blood or plasma loss, fluid loss through vomiting or diarrhea
     • absolute hypovolemia
       • fluid leaves body
     • relative hypovolema
       • fluid moves into extravascular (interstitial, intracavity) space - 3rd spacing
     • clinical manifestations
       • healthy person can compensate for a sudden loss of up to 15% total blood volume
       • BP can remain normal with up to 750ml loss; can not be only sign
       • paller, cool and clammy extremities, delayed cap refill
       • increased heart rate
       • diminished urine output
       • nausea, absent bowel sounds
       • increase in resps
         • body attempts to blow off excess acid
           • respiratory alkalosis
           • altered LOC; confusion -> aggression -> stupor
       • decreased hematocrit, elevated lactate, urine specific gravity, changes in electrolytes
     • treatment
       • optimizing O2
         • dependent on cardiac output, available hemoglobin, arterial O2 sat
         • increase supply and decrease demand
       • CO
         • drug therapy or fluid replacement
       • hemoglobin
         • blood transfusion of packed RBC
       • arterial O2 saturation
         • supplemental O2 and mechanical ventilation
       • rapid IV infusion
       • strict in & outs
         • foley catheter
       • crystalloids used for volume losses up to 1500ml
         • isotonic crystalloid (RL or NS)
           • colloids
       • BP remains low: vasoconstrictors
         • act on alpha and beta receptors in peripheral blood vessels causing them to constrict and BP to increase
   • Cardiogenic
     • usually result of myocardial infarct
       • other causes: cardiomyopathies, cardiac tamponade, arrhythmias, valve disease, pericardial infection, health failure - drug toxicity
       • anterior infarction, inferior infarction, posterior infarctions
     • compensatory mechanisms
       • decreased cardiac output triggers SNS
         • SNS activation
           • increased HR and cardiac contractility (stroke volume)
             • can cause increased ischemia
           • H2O retention = increased workload on heart
           • increased SVR increase afterload = resistance for heart to pump against
           • increased demand for O2 & nutrients
           • impaired cellular metabolism
       • pts require prompt revascularization
         • angioplasty
         • CABG
           • intra aortic balloon pump
       • dilation - nitrates
       • inotropic agents - dobutamine, dopamine
         • contractility
       • pre-load morphine, diuretics, nitrates, ACE inhibitors
       • afterload ACE inhibitors, vasodilators
       • heart rate - calcium channel blockers, beta blocker
       • morphine
         • improves coronary perfusion by dilating the vessels & relieves pain and anxiety
     • mortality rate: 50-80%
   • Neurogenic
     • commonly associated with spinal cord injuries at or above T5 or closed head injury
       • results in massive vasodilation without compensation
         • from loss of SNS vasoconstrictor tone
         • leads to pooling of blood in blood vessels
         • unopposed activation of the parasympathetic nervous system leads to bradycardia
         • loss or suppression of sympathetic tone
           • decreased venous return to heart results in decreased cardiac output
             • resulting in decreased cell O2 supply, decreased tissue perfusion and impaired cell metabolism
     • rarest form
     • signs of ICP
       • vomiting
       • headache
       • changes in behaviour
       • progressive LOC, lethargy
       • neurological deficits
       • seizures
   • Anaphylactic
     • body produces IgE antibodies specfic to an antigen
       • with subsequent exposure the IgE binds to mast cells and basophils resulting in a cascade of events
         • vasodilation
         • increased vascular permeability
         • bronchoconstriction
         • increased mucous production
         • increased inflammatory mediators are recruited to sites of antigen interaction
     • treatment
       • high flow O2 via non-rebreather
       • epinephrine: 1:10,000, 0.5ml SQ/IV every 5-20 minutes depending on severity
       • diphenhydramine IM or IV
       • education on prevention of exposure and "epi-pen" use
   • Septic
     • most common form of distributive shock
     • cell walls of organisms contain endotoxins which releases inflammatory mediators
       • vasodilation
       • increased capillary permeability
         • alteration in peripheral circulation and massive dilation
     • can trigger coagulation casade
       • disseminated intravascular coagulation
       • microvascular clotting factors
       • excessive fibrinolysis
     • collaborative care
       • inotrpic therapy
       • cardio dysfunction - decreased ejection fraction
         • resulting ventricles dilating to improve stroke volume
           • pt compensates with increasing RR -> respiratory alkalosis
             • if fails, compensation develops into respiratory acidosis
               • late septic shock, mortality