Care of the Patient in Shock

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Care of the Patient in Shock

• Becca Maddox
• N2205
• Spring 2002

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Definition

• Shock is a life-threatening condition in which
  blood flow to tissue and cells is inadequate
• Results in inadequate oxygen and nutrients to the
  cells, cellular starvation, cell death, organ
  failure and death if not treated
• Treatment must be carried out in a timely and
  appropriate manner

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Classifications of Shock

• Hypovolemic - results from severely diminished
  circulating blood volume
• Cardiogenic - as a result of cardiac dysfunction
• Anaphylactic Shock - results from
  antigen-antibody reaction that releases histamine
  into the blood stream.
• Septic Shock (systemic inflammatory response
  syndrome) - caused by widespread infection and
  invasion of microrganisms in the body
• Obstructive Shock - results from obstruction to
  blood flow
• Neurogenic shock - caused by damage or
  dysfunction of the sympathetic nervous system
  (rare)

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Classifications of Shock

• Hypovolemic - impaired tissue perfusion resulting
  from severely diminished circulating blood volume
• Hemorrhage loss of blood, plasma, body fluids as
  a result of
• surgery
• trauma
• burns
• severe dehydration (vomiting, diarrhea, DKA, DI)
• Internal, extravascular fluid loss resulting
  from third-spacing in interstitial space,
  ascites, ruptured spleen, pancreatitis,
  hemothorax
• Adrenal insufficiency

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Classifications of Shock contd

• Cardiogenic - impaired tissue perfusion as a
  result of cardiac dysfunction (most common cause
  of death from MI)
• MI (usually 40 of LV is damaged)
• Myocardial ischemia (left main artery disease,
  multivessel coronary artery disease)
• Cardiomyopathy
• Arrhythmias
• Heart failure
• Cardiac tamponade
• Acute valvular dysfunction (acute mitral
  regurgitation, aortic insufficiency)
• Papillary muscle rupture
• Other severe forms of myocardial injury (trauma)

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Classifications of Shock contd

• Anaphylactic Shock - impaired tissue perfusion
  resulting from antigen-antibody reaction that
  releases histamine into the blood stream.
  Capillary permeability increases and arteriolar
  dilatation occurs. Blood return to the heart is
  decreased dramatically.
• Contrast media
• Drug reactions
• Blood transfusion reactions
• Food allergies
• Insect bites or stings
• Snake bites

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Classifications of Shock contd

• Septic Shock (systemic inflammatory response
  syndrome) - impaired tissue perfusion caused by
  widespread infection and invasion of
  microrganisms in the body, causing vasodilation
• Obstructive Shock - impaired tissue perfusion
  resulting form obstruction to blood flow
• Pulmonary Embolus
• Aortic dissection
• Neurogenic shock - impaired tissue perfusion
  caused by damage or dysfunction of the
  sympathetic nervous system (rare)
• Trauma
• Anesthesia
• Spinal Shock

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Pathophysiology of Shock

• A mean arterial pressure (MAP) of 80 to 120 mmHg
  is needed for cells to receive the oxygen and
  nutrients needed to metabolize energy in amounts
  sufficient to sustain life.
• The body has compensatory mechanisms to assist in
  maintaining this MAP in response to changes in
  volume, pumping ability of the heart and changes
  in the vascular system.
• As long as these mechanisms are effective, the
  body can survive the changes. When these
  mechanisms fail, tissues are inadequately
  perfused and shock begins

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Compensatory Mechanisms

• Baroreceptors (pressure receptors) - located in
  the carotid sinus and aortic arch.
• Decrease in MAP causes decreased stretching of
  the baroreceptors (they lose their inhibitory
  effect on the vasomotor center)
• Sympathetic efferent activity is stimulated.
  Brain sends impulse to the adrenal glands to
  release catecholamines (epinephrine and
  norepinephrine)
• Catecholamines cause an increase in heart rate
  and vasocontriction
• Parasympathetic activity is decreased at the same
  time

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Compensatory Mechanisms contd

• Chemoreceptors - located in the aortic arch and
  carotid arteries
• receptive to oxygen changes in the blood
• regulates blood pressure and heart rate
• Kidneys - release renin which leads to the
  conversion of angiotensin I to angiotensin II, a
  potent vasocontrictor
• leads to release of aldosterone from the adrenal
  cortex which results in retention of sodium and
  water
• increase in sodium triggers release of ADH
  (antidiuretic hormone)
• ADH causes kidneys to retain water to raise blood
  volume and blood pressure

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Chain of Events

• Diminished tissue perfusion deprives cells of
  oxygen, nutrients, and therefore energy.
• Cells make ATP (energy) and store it for later
  use.
• If cells have to do this in an oxygen poor
  environment, then not as efficient. Anaerobic
  metabolism results in production of lactic acid.
• The increased acidity causes normal cell
  functions to cease.
• Cellular dysfunction is reversible at first but
  leads to organ damage if untreated

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Chain of Events contd

• Hopefully, with the drop in blood pressure and
  the decrease in oxygenated blood, the
  baroreceptors and chemoreceptors will be able to
  compensate.
• If the compensatory mechanisms cannot restore
  tissue perfusion the syndrome of shock begins
• The cell swells, the cell membrane becomes more
  permeable and fluid and electrolytes seep from
  and into the cell. Mitochondria and lysosomes are
  damaged and the cell dies.

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Chain of Events contd

• Platelets and white blood cells clump together
  and obstruct the microvasculature
• Major organs begin to malfunction as they are
  deprived of oxygen, as a result of hypoxemia and
  metabolic acidosis
• Respiratory failure, renal failure, decreased
  cerebral perfusion, and disseminated
  intravascular coagulation (DIC) may also be seen
• The earlier that medical management and nursing
  interventions can be initiated, the greater the
  chance of survival for the patient

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Stages of Shock - Compensatory

• If treated, prognosis is good
• the patients blood pressure remains in normal
  limits
• vasoconstriction, increased heart rate and
  increased contractility maintain adequate cardiac
  output
• blood is shunted away from nonessential organs
  (skin, lungs, kidneys, GI tract)
• Assessment data
• cold, clammy skin
• hypoactive bowel sounds
• decreased UOP
• confusion, combativeness (result of compensatory
  respiratory alkalosis)

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Compensatory Shock contd

• Treatment - focuses on identifying and correcting
  the cause and supporting compensatory mechanisms
  (fluids and vasoactive drugs)
• Nursing Responsibilities
• monitor for changes in LOC, skin, UOP and VS
• monitor labwork (Na and Glucose increase in
  response to release of ADH and catecholamines)
• administer fluids and medications as ordered
• promote patient safety
• report changes promptly

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Progressive Shock

• BP drops (lt 80-90 mmHg). Prognosis worsens. Even
  if the cause of the shock is reversed, the
  patient may not recover.
• Overworked heart becomes ischemic and can result
  in failure of the pumping ability of the heart
• Cellular membrane permeability increases causing
  cells to leak fluid into the interstitial
  spaces (3rd spacing) and decreasing fluid return
  to the heart
• Organ systems decompensate
• Lungs - ARDS develops leading to respiratory
  failure
• Heart - dysrhythmias, HR gt 150, chest pain, MI,
  elevated cardiac enzymes

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Progressive Shock Contd

• Brain - level of consciousness deteriorates,
  pupils may be dilated and sluggish to react to
  light
• Kidneys - acute renal failure can occur. BUN and
  Cr increase. UOP usually lt 20 cc/hr
• Liver - less able to metabolize drugs and waste
  products (ammonia and lactic acid), more prone to
  infections, SGOT (AST), SCPT (ALT) and LDH are
  elevated, patient is jaundiced
• GI - stress ulcers, GI Bleed, mucosa can become
  necrotic and slough resulting in bloody diarrhea,
  toxins are released into the blood stream that
  cause cardiac depression and vasodilation
• Hematologic System - DIC, platelets and clotting
  factors are consumed, PT/PTT are prolonged

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Progressive Shock contd

• Treatment - depends on the type of shock and its
  underlying cause
• Goal is to use fluids and medications to restore
  perfusion by
• optimizing intravascular volume
• support pumping action of the heart
• improve competence of vascular system (help
  vascular system meet demands placed on it)
• Also need to meet nutritional demands of the body
  as well as protect the GI tract

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Progressive Shock contd

• Nursing Responsibilities - requires good
  assessment skills and an understanding of shock.
  Must be able to identify significant changes in
  assessment data.
• Patient will require hemodynamic monitoring and
  EKG monitoring
• May require mechanical ventilation or IABP
  therapy (intra-aortic balloon pump)
• Requires close monitoring of changes in ABG
  results, electrolyte levels and mental physical
  status

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Progressive Shock contd

• Must make efforts to minimize cardiac workload
• reduce physical activity
• reduce fear and anxiety
• plan as much uninterrupted rest as possible
• prevent patient from becoming excessively warm or
  cold (shivering increases workload, warming
  causes vasodilation)
• Make efforts to prevent complications, protect
  from injury and provide comfort

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Irreversible Stage

• Organ damage is so severe that the patient does
  not respond to treatment and cannot survive
• BP remains low
• Complete renal and liver failure, releasing
  toxins, contributing to an overwhelming metabolic
  acidosis
• Anaerobic metabolism is creating more lactic acid
  also contributing to metabolic acidosis
• ATP reserves are used up
• The cells can no longer store ATP related to cell
  destruction
• Patient develops multi-organ failure

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Irreversible Shock contd

• Treatment - continue as with Progressive Shock
  (only determined to be irreversible when the
  patient dies)
• Nursing Responsibilities -
• Continue carrying out prescribed treatment,
  monitor the patient, prevent complications,
  protect from injury and provide comfort
• Communication with the family and supporting the
  grieving process is important

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Medical Management of Shock

• Fluid replacement to restore intravascular volume
  (Crystalloids, Colloids, Blood components)
• Vasoactive medications to restore vasomotor tone
  and improve cardiac function
• Nutritional support to address increased
  metabolic requirements

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Fluid Replacement

• Crystalloids - electrolyte solutions that move
  freely between intravascular compartment and
  interstitial spaces
• Usually give isotonic solutions - same
  concentration of electrolytes as the
  extracellular fluid (avoids wide changes in
  plasma electrolytes)
• Most commonly used are Lactated Ringers and
  Normal Saline
• Requires large amounts - for every part that
  remains in the intravascular system, 3 parts move
  to the interstitial spaces
• If a hypertonic solution is used (3 Saline),
  fluid moves from interstitial spaces to vascular
  system

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Fluid Replacement contd

• Colloids - contain molecules too large to pass
  through capillary membranes.
• Pull fluid into intravascular space by means of
  oncotic pressure (like hypertonic solutions)
• Takes less volume and acts longer
• Most common used are 5 Albumin, 6 Hetastarch
  (Hespan) and 6 Dextran solution
• Caution must be used with Dextran because it
  interferes with platelet aggregation
• Anaphylactic reactions can occur with colloids

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Fluid Replacement

• Complications of fluid therapy -
• Cardiovascular overload
• Pulmonary edema
• Monitor patient for adequate UOP, changes in
  mental status, skin perfusion and vital signs.
• Assess breath sounds frequently during fluid
  administration
• Patients may have arterial lines, CVP or
  Swan-Ganz catheter
• If CVP being monitored, should be between 4 and 12

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Vasoactive Drugs

• Used when fluid alone cannot maintain adequate
  MAP
• Drug of choice is selected according to what
  correction is needed to increase CO
• increase contractility
• cause vasoconstriction
• regulate the heart rate
• Act on receptors of the sympathetic nervous
  system
• Alpha - Vasoconstriction of Cardiorespiratory and
  GI systems, skin and kidneys
• Beta1 - increase heart rate and contractility
• Beta2 - vasodilatation of heart and skeletal
  muscles, relaxation of bronchioles

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Vasoactive Drugs contd

• Nursing Responsibilities
• Monitor vital signs q15 min while vasoactive
  drugs are being used
• Administer through a central line
• Use an IV Pump
• Titrate drip rate according to patient parameters
  (ordered by the physician)
• Do not stop drips abruptly - wean slowly while
  monitoring vital signs q15 min

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Nutritional Support

• Patients in shock can require over 3000 calories
  per day
• Release of catecholamines causes glycogen stores
  to be used up - can occur in 8-10 hours. This
  causes skeletal muscle to be broken down for
  energy.
• Start parenteral (HAF) or enteral (NGT, PEG,
  J-Tube, Duodenal tube, Dobb-Hoff) within 3-4 days
• Usually will require H2 blockers (cimetidine,
  ranitidine) to prevent stress ulcers related to
  decrease perfusion to GI tract

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Management of Specific Shock Conditions

• Hypovolemic - most common, occurs when there is a
  reduction of intravascular volume by 15 - 25
  (750-1300 ml for a 70 Kg person)
• Can occur by fluid loss or fluid shifting
• Decreased intravascular volume ? decreased venous
  return to heart and decreased ventricular filling
  ? decreased SV and decreased CO ? decrease in BP
  and inadequate tissue perfusion
• Goals are to (1) restore intravascular volume,
  (2) redistribute fluid volume, and (3) correct
  underlying cause of loss
• Unreversed hypovolemic shock progresses to
  cardiogenic shock

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Hypovolemic Shock contd

• Nursing Responsibilities
• Prevent, if at all possible, by closely
  monitoring patient who are at risk
• Safely administer fluids and meds and document
  effect
• Monitor for complications and side effects and
  report early
• Safely administer blood/blood products. Monitor
  for adverse effects
• Administer oxygen and monitor effectiveness

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Cardiogenic Shock

• Occurs when the hearts ability to pump is
  impaired. Can be coronary or non-coronary. Occurs
  most frequently in patients with MIs and
  extensive ventricular damage.
• When SV or HR decreases or become erratic, blood
  pressure drops and tissue perfusion is
  compromised
• Also, when SV decreases, ventricle does not fully
  eject volume. Pressure back up in the system to
  the lungs causing pulmonary congestion
• Patients in cardiogenic shock can experience
  chest pain and dysrhythmias
• Goals (1) limit further heart damage, (2)
  preserve healthy myocardium, (3) improve pumping
  ability

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Cardiogenic Shock contd

• Treatment
• Oxygen - monitor O2 sat and ABGs
• Morphine for chest pain - decreases workload of
  the heart by decreasing preload and afterload
• EKG and cardiac enzymes - to assess damage
• Hemodynamic monitoring - arterial line, pulmonary
  artery catheter
• Vasoactive therapy (Sympathomimetics,
  Vasodilators)
• Dopamine - low-dose (0.5 - 3 mcg/kg/min) for
  renal and mesenteric perfusion, medium-dose (4-8
  mcg/kg/min) for improving contractility and heart
  rate, high-dose causes vasoconstriction

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Cardiogenic Shock contd

• Nitroglycerin - Vasodilator. Decreases preload.
  Enhances blood flow to the heart muscle itself
  thus improving oxygen delivery. At high doses,
  causes arterial vasodilation and reduces
  afterload
• Others - dobutamine, norepinephrine, epinephrine,
  isoproterenol, amrinone
• Lasix
• Antiarrhythmics
• Sodium Bicarbonate
• Crystalloids and/or Colloids - give cautiously
• Intra-aortic balloon pump - counterpulsation.
  Balloon inflates during diastole, deflates just
  prior to systole

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Cardiogenic Shock contd

• Nursing Responsibilities
• Assist in prevention - identify patients at risk.
  Promote adequate oxygenation. Decrease workload
  of heart. Assist in preventing progression of
  shock. Assist in restoring cardiac function and
  tissue perfusion.
• Anticipate need for medications, fluids,
  hemodynamic monitoring and assist with
  implementation
• Document changes in hemodynamic and cardiac
  status and report changes promptly
• Monitor for complications and side effects - BP
  and HR changes, bleeding, tissue necrosis and
  sloughing, UOP, BUN, Cr, circulatory compromise
  with IABP

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Distributive Shock

• Category for Neurogenic, Anaphylactic and Septic
  Shock - blood volume is abnormally displaced as a
  result of massive arterial and venous dilation
  causing a relative hypovolemia
• Vasodilation caused by either a loss of
  sympathetic tone or a release of chemical
  mediators from cells
• Can initially see an increase in CO related to
  decrease in systemic vascular resistance (SVR)
  and hearts attempt to compensate
• Pooling of blood ? decreased venous return ?
  decreased SV and CO ? decreased BP ? decreased
  tissue perfusion

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Neurogenic Shock

• Occurs as a result of a loss of sympathetic tone
  - spinal cord injury, spinal anesthesia, nervous
  system damage, depressant action of medications,
  lack of glucose (insulin shock). Usually
  transient.
• Patient has warm, dry skin as opposed to cool,
  clammy skin
• Usually bradycardic as opposed to tachycardic
• Treat the cause
• Nursing Responsibilities
• Assist in prevention by positioning and
  immobilization
• Support cardiovascular and neurologic functions

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Anaphylactic Shock

• Results from an allergic reaction. Mast cells
  release potent vasodilators (histamine,
  bradykinin)
• Occurs rapidly and is life-threatening
• Treatment
• Remove causative antigen
• Restore vascular tone - Epinephrine
• Anti-histamines - Benadryl
• Bronchodilator (Aminophylline) if patient has
  histamine induced bronchospasms
• Nursing Responsibilities - Prevention!!,
  Recognition!! (sudden onset flushing, warmth,
  anxiety, itching, nasal congestion, laryngeal
  edema, bronchospasm, SOB, wheezing) Fast Action!!

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Septic Shock

• Most common - caused by widespread infection
• Mortality rate 40 - 90
• Most common causative organisms are gram-negative
  bacteria. However, can also be caused by
  gram-positive and viruses
• 2 Phases
• Hyperdynamic - high CO with vasodilation,
  hyperthermic with warm, flush skin, elevated HR
  and RR, UOP normal or increased, may have nausea,
  vomiting or diarrhea
• Hypodynamic - low CO with vasoconstriction in
  response to hypovolemia from capillary leaking,
  BP drops, skin cool and pale, temp normal or
  below, HR and RR elevated, no UOP, multiple organ
  failure

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Septic Shock contd

• Treatment - Identify and eliminate cause of
  infection
• obtain cultures
• start antibiotics (cephalosporin and
  aminoglycoside initially)
• remove potential routes of infection
• drain abscesses, debride wounds
• Crystalloid and/or colloids
• Aggressive nutritional support (If the gut
  works, use it)
• Treatment beginning to shift toward combating
  endotoxins - monoclonal antibodies (enhances
  immune function)

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Septic Shock contd

• Nursing Responsibilities
• Prevention - use aseptic technique with all
  procedures, monitor patient for signs of
  infection
• Collaborate with health care team to identify
  source of sepsis
• Reduce temperature in hyperthermic patients, but
  monitor closely for chills, shivering and
  increased O2 consumption
• Administer fluids, meds, vasoactive drugs to
  restore vascular volume
• Monitor antibiotic levels, BUN, Cr, WBC
• Monitor hemodynamic status, IO, nutritional
  status (daily wts, albumin)

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Multiple Organ Failure

• Can occur as a complication of all forms of shock
• The exact mechanism that triggers it is unknown
• Cant predict who will develop it
• Usually begins with lungs and is followed by
  liver and kidneys
• 2 patterns of presentation
• Initial episode of hypotension which is treated
  and patient seemingly responds
• If patient presents with a pulmonary insult and
  has respiratory failure, can rapidly develop MOF
  and patient only survives 2 to 4 days

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Multiple Organ Failure contd

• Other pattern occurs most often with septic
  shock
• progressive development over a month
• patient experiences respiratory failure and often
  requires ventilator
• despite apparent hemodynamic stability, patient
  exhibits a hypermetabolic state (hyperglycemia,
  hyperlactatemia, polyuria) - if can be reversed,
  mortality rate is 25-40
• infection is usually present and skin breakdown
  begins to occur

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Multiple Organ Failure contd

• severe loss of muscle mass (auto- catabolism)
  occurs
• if hypermetabolic phase cant be reversed, MOF
  progresses
• patient becomes jaundiced, has hyperbilirubinemia
  and renal failure - often requires dialysis
• patient becomes hemodynamically unstable
• Mortality rate increases to 40-60 during early
  stage of MOF and 90-100 in later stage - Patient
  usually dies in about 28 days

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Multiple Organ Failure contd

• Treatment
• control initiating event
• promote adequate organ perfusion
• provide nutritional support
• Nursing Responsibilities
• essentially the same as septic shock
• For those who survive, recovery and
  rehabilitation is a long, slow process