• group of signs/symptoms that form a disorder
• can be observable and measurable
• May be life-threatening
• Definition- failure of circulatory system to maintain adequate perfusion of vital organs
• Leads to anaerobic cellular metabolism and accumulated waste products
• Results in inadequate tissue perfusion with decreased oxygenation at cellular level
• Nurse’s role includes:
  – Identify the “at risk” population
  – Recognize early assessment findings
  – Initiate appropriate treatment
  

CLASSIFICATIONS OF SHOCK

• Hypovolemic- most common type, inadequate circulating blood volume.
• Cardiogenic- inadequate pumping action d/t primary cardiac muscle dysfunction
• Distributive- d/t changes in blood vessel tone that changes size of space
  

PATHOPHYSIOLOGY

• Adequate circulating blood volume depends upon three interrelated components;
• A minor impairment in one can be compensated for by the other two, but prolonged or severe impairments will lead to SHOCK.
  – Heart
  – Vascular tone
  – Blood volume
• Blood flows d/t driving force as leaves LV
• Continuous process whereby arterioles store blood and capillaries release it as needed
• Blood flow influenced by varying needs of cells located nearby
• Capillaries open on demand
• Larger blood vessels regulated by autonomic nervous system
• Sympathetic NS constricts blood vessels; parasympathetic dilates blood vessels
• Capillaries operate within own mechanisms using sphincters; different controls than autonomic nervous system
• Called: MICROCIRCULATION
  

MICROCIRCULATION

• Autonomy exists within capillaries
• No coordinated effort throughout body
• Governed by local vasoactive substances
  -sensitive to blood flow
  -adjusts moment to moment
• Capillaries meet with veins
• Veins are low pressure and have no muscles
  

MEAN ARTEIAL PRESSURE

• Represents the perfusion pressure throughout the cardiac cycle
• Used to assess perfusion of tissues
• May be calculated as:
• [(Diastolic x 2) + (Systolic x 1)] ÷ 3
• A MAP > 60 is necessary to perfuse coronary arteries, brain, and kidneys.
• Ideal for heart patients with LV disorders is 70-90

EXAMPLE: MAP

B/P = 120/60 MAP = 80

60 X 2 = 120 (plus +)
120 X 1 = 120
= 240 / 3 = 80

OTHER MECHANISMS

• Chemoreceptors located in aortic arch and carotid bodies sense decreased pH and increased PaCO2
• Tissues not receiving enough O2 maintain metabolism using anaerobic functions
• Produces lactic acid as by-product
• Respiratory rate may change
• Increased CO2 leads to increased cardiac output
• Juxtaglomerular receptor- located in kidney measures blood flow to kidney
• With lowered blood volume, renin is released
• Renin begins process leading to vasoconstriction
• ADH is released to prevent diuresis
• Leads to water conservation and increased blood volume
• If one of three components fail, others compensate
• Vasoconstriction and increased cardiac output used for decreased volume
• Two of three must adequately function
• Two or more fail---SHOCK
  

TYPES OF SHOCK

• Hypovolemic-
• Cardiogenic
• Distributive
  – Anaphylactic
  – Neurogenic
  – Septic
  

HYPOVOLEMIC SHOCK

• Most common type
• Inadequate circulating blood volume
• Caused by-
  – Hemorrhage- loss of fluid and protein
  – Burns-loss of fluids or fluid shifts
  – Dehydration- loss of fluids
  

CARDIOGENIC SHOCK

• Caused by inadequate pumping power
• 40% cardiac muscle dysfunction with 80% mortality rate
  

DISTRIBUTIVE SHOCK

• Due to changes in blood vessel tone that changes size by increasing vascular space without increasing blood volume
• Results in “relative” hypovolemia
• Fluid remains same but is redistributed
  

DISTRIBUTIVE SHOCK

• Anaphylactic-
  – Acute allergic reaction from exposure to substance client has been exposed to
  – Bee stings, snake bite, chocolate, iodine
  – Re-exposure to foreign substances leads to antigen binding to IgE on mast cells
  – Mast cells release histamine, prostagladins,etc.
  – S/S- massive vasodilation, uticaria (hives), laryngeal edema, bronchial constriction
  

DISTRIBUTIVE SHOCK

• Neurogenic-
  – Injury to spinal cord
  – Autonomic nervous system affected by loss of sympathetic vasoconstriction and smooth muscle
  – Leads to pooling of blood in veins
  – Decreased venous return to heart
  – Decreased cardiac output
  

DISTRIBUTIVE SHOCK

• Septic-
  – Sepsis is systemic response to infection
  – Begins with growth of bacteria
  – Bacteria release substances called endotoxins
  – Once released, lead to process and shock
  – Very lethal- mortality rate 20-80%
  – Most common causitive organism is gram + staph, strep, fungus
  

SEPTIC SHOCK

• Conditions predisposing clients include:
  – UTI
  – URI
  – Contaminated blood
  – Extreme ages
  – Immunosuppressed clients
  – Steroid use
  – Surgery- GU, GI
  – Invasive devices- IV, catheter
  – Men with benign prostatic hypertrophy
  

STAGES OF SHOCK

• Initial stage (early compensation stage)
• Nonprogressive stage (compensatory)
• Progressive stage (intermediate)
• Refractory stage (irreversible)
  

INITIAL STAGE

• Cardiac output is  d/t loss of actual or relative blood loss
• MAP  from baseline to < 10mm/Hg
• Compensatory mechanisms are able to maintain perfusion to tissues
• Systemic and microcirculation work together
•  aerobic metabolism with  anaerobic metabolism
• Production of lactic acid
•  C.O. results in  hydrostatic capillary pressure
• Fluid moves from interstitial to capillary to increase volume
• Vascular constriction and increase heart rate help to maintain B/P
• S/S: increase heart rate from client’s baseline or slight increase in diastolic B/P may be only manifestation
  

NONPROGRESSIVE-COMPENSATORY

• MAP  10-15 mm/Hg from baseline
• Must activate kidney and chemical mechanisms to maintain B/P
• Kidneys and baroreceptors sense  vascular volume
• Release of renin; ADH; Aldosterone; epinephrine; norepinephrine
• Systemic and microcirculation no longer work in unison

NONPROGRESSIVE

• Renin secretion begins reaction- leading to  urine output,  sodium absorption, widespread vasoconstriction
• ADH causes water reabsorption and vasoconstriction in skin
• Tissue hypoxia is present in kidneys and skin
• Anaerobic metabolism results in lactic acid production
• Acidosis (pH< 2.45)
• Hyperkalemia (K+ >5.0 mEq/l)
•  heart rate,  B/P,  urine output
• Stimulation of thirst mechanism
  

PROGRESSIVE STAGE

• Sustained decrease of MAP < 20 mm/Hg
• Tissue hypoxia has worsened
• Vital organs are hypoxic and non-vital organs become anoxic leading to ischemia
• Ischemia will lead to cell destruction and death
• Increased lactic acid production causes increased capillary permeability
• Increased blood in capillaries increase hydrostatic pressure
• Fluids moves from vascular to interstitial space
• Microcirculation reverses with pooling of blood in capillaries
• Increases vascular space
  Increased vascular space; decreased blood volume; decreased heart action—all reduces MAP
  All lead to venous pooling, decreased venous return, decreased cardiac output
  No mechanisms to change pattern at this point, therefore events become more severe
  Vital organs can tolerate this for a brief time without permanent damage
• Immediate interventions are necessary to preserve life
• Tolerance varies with individuals
• LIFE-THREATENING
• GENERALLY HAVE 1 HOUR AFTER SYMPTOMS BEGIN TO REVERSE PATTERN
  

REFRACTORY STAGE

• Vital organs experience drastic changes including cell destructin and death
• Body is unable to reverse sequence
• Metabolism is strictly anaerobic
• Underlying cause may not be more severe
• Cellular ischemia and necrosis leads to organ failure
• Therapy is ineffective---DEATH
  

EFFECTS ON BODY SYSTEMS

• Respiratory-
  tissue hypoxia leading to anoxia
  major cause of death
  ARDS (acute respiratory distress syndrome)
• Acid-base-
  – Oxygen needed for ATP production (energy)
  – Without O2 cells use anaerobic metabolism, producing lactic acid
  – Lactic acid causes cellular acidity which damages cells and decreases C.O.
  – Circulation is disrupted, blood pools, decreased venous return
  – VICIOUS CYCLE & Other Effects
  

GENERAL CLINICAL MANIFESTATIONS

• Shock had many diverse S/S
• Subjective complaints are usually nonspecific
• Observable and measurable are often conflicting
• Tachypnea-
  – Rapid, shallow respirations (tachypnea) d/t tissue hypoxia
• Tachycardia-
  – Generally pulse rate increases
  – Becomes weak and thready
  – May be unreliable due to pain, fear, anxiety
  – Be aware of clients taking beta-blockers and elderly with heart block
• Hypotension-
  – Systolic B/P indicates integrity of heart, arteries, and arterioles
  – Diastolic B/P indicates peripheral vascular resistance (vasoconstriction)
  – When diastolic falls significantly, indicates vasoconstriction in being lost as a compensatory measure
  – B/P usually falls when total blood volume is decreased by 15-20%
  – In young adults, falling B/P is a sign of late shock
  – With progression, both fall, but systolic falls more
  – Pulse pressure narrows- systolic – diastolic
  – Therefore pulse pressure is more significant in late shock than B/P
  – It parallels stroke volume- if stroke volume falls, it means volume of blood ejected is less
  – Pulse pressure may decrease before B/P and can be a more reliable indicator or severity of condition
  – Minimum of 60-70 mm Hg systolic to maintain coronary circulation
  – Must know baseline B/P to interpret findings
  – Hypotension by itself does not indicate shock
  – In early shock, systolic B/P is unreliable; may be elevated due to compensation
  – Assess strength of femoral pulses
• Level of consciousness
  – Early shock produces stimulation of SNS leading to feelings of anxiety, fear, irritability
  – Dizziness, faintness, unconsciousness (if sudden onset)
  – Apathy, confusion, restlessness, increased alertness ( if gradual onset)
  – With narcotics, must be careful not to mask situations
• Oliguria-
  – Fall in UO is often the earliest sign; one of the most sensitive indices in shock
  – However, if shock occurs suddenly, other S/S will present before urine output decreases
  – UO must be kept above 0.5 ml/kg/hr (35 ml/hr)
  

• Assess oxygenation
  – Spirometry measurements
  – Pulse oximeter
  – ABG’s
• PCO2 is key to detecting compensatory acidosis
• Rising PCO2 with low pH & bicarbonate
• Indicates respiratory assistance is needed
  

DIAGNOSIS

• Cardiac monitoring
  – EKG
• Labs
  – CBC
  – Lytes
• Body fluid cultures
  obtain culture and sensitivity (C&S) before antibiotics are started.
  

TREATMENT

• It is difficult to ascertain when shock begins. Therefore tx. Should be instituted when at least two of the following are present
  – Systolic B/P of 80 mm HG or less
  – Pulse pressure of 20 mm Hg or less
  – Pulse rate of 120 or more
• Maintain patent airway
• Supplemental O2
• Modified trendelenberg- lower extremities elevated 30-45 0, knees straight, trunk horizontal, head level with chest
  – Promotes venous return by not compressing diaphragm, mobilizes pooled blood
• REPLACE FLUIDS
  – Use IV therapy with large bore catheter or central line
  – Carefully monitor infusion of fluids
  – When UO is 60ml/hr or>, B/P is >100 systolic, or heart rate is 60-100, fluids should be tapered off
  – General rule is 3:1 : for a client’s blood loss, 3 times as much fluid should be given

  TYPES OF FLUID

• Crystalloid or balanced salt solutions:
  – D5W should not be used
  – 2/3 crystalloid solution will leave ECF to Interstitial
  – Use NS, RL, 1/2NS
• RL or NS expand volume, reduce viscosity, prevent sludging
• With liver dysfunction, using lactate will increase acidosis, so consider other fluids than RL
• Colloid solutions- contains proteins to increase osmotic pressure in ECF
  – Plasma- Fresh Frozen Plasma (FFP)- requires thawing for 15-30 min.
  – Albumin- may move into pulmonary space and contribute to ARDS
  – Dextran- can rapidly expand ECF, but interferes with type and crossmatch of blood
  – Blood products- PRBC’s or whole blood
• Fluids given in excess of normal volume should be other than blood so they can easily be removed by kidneys
  

OTHER TREATMENTS

• Monitor urinary output
  – Use indwelling catheter
  – Diuretics usually used
  – Dialysis with tubular necrosis of kidney (ATN)
  – Oliguria does not contraindicate large volumes of fluids
• Perfusion to GI will be decreased. May result in inadequate perfusion, delayed emptying, vomiting, & possible aspiration
  – Insert NG tube with suctioning
  – Assess periodically for blood
• Do not apply heat to skin, heat dilates and draws blood away from vital organs
• Heat also increases metabolism and need for more O2 & adds strain to the heart
• Do not allow to become cold- chilling requires extra energy, contributes to sludging of blood, slows heart rate, inhibits body’s reparative processes
  

MULTIPLE ORGAN SYSTEM FAILURE

• Sequential organ failure of lung, liver, and kidney, usually followed by death. 50-90% mortality. All three organs involved: 100%