Perfusion Confusion Understanding Shock Syndrome Prepared

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Perfusion Confusion Understanding Shock Syndrome

• Prepared by
• Gerald Glotfelty EMT-P I/C
• Wayne County Community College Detroit Michigan

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Physiology of HypoperfusionShock

• Inadequate tissue perfusion
• Inadequate delivery of O2 and nutrients to the
  body tissues,
• Inadequate elimination of metabolic waste.

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AP of Perfusion

• Perfusion O2 , nutrient, delivery and CO2
  elimination requires four things.
• 1. A properly beating heart.
• 2. Adequate transport medium, blood and
  hemoglobin.
• 3. An intact functioning vessel system.
• 4. A functioning respiratory system.

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Physiology of CirculationThe Pump

• Stroke volume X Heart rate Cardiac Output.
• Preload will Stroke volume Cardiac
  output
• Frank Starling Effect

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Physiology of Circulationthe Vessels

• 600,000 miles of vessels containing 5-6 liters of
  blood
• Vessel tone is controlled by the sympathetic and
  parasympathetic nervous system.
• Pre-capillary sphincters control blood flow
  through the capillaries in response to O2 demand
  of the tissue.
• Preload is dependant on constant peripheral
  vascular resistance.

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Physiology of CirculationBlood

• Container (vessels) must be full of blood at all
  times.
• Hemoglobin must be present in adequate amount and
  be free to carry O2, nutrients and CO2

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Pathophysiolgy of ShockSeven Stages of Cell
Death

• 1. Normal cell
• 2. Hypoxia intracellular ischemia occurs
  anaerobic metabolism begins lactic acid
  builds up in cell leading to metabolic
  acidosis causes the sodium potassium pump
  to fail.
• 3. Ion shift occurs Sodium rushes into the cell
  bringing water with it.

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Seven stages of cell death, continued

• 4. Cell swelling occurs.
• 5. Mitochondrial swelling occurs production of
  ATP ceases.
• 6. Intracellular disruption releases lysosomes,
  cell membrane begins to break.
• 7. Cell destruction begins leading to tissue
  death.

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Stages of Shock Classic Shock Syndrome

• 1. Compensated - body is able to compensate
  and maintain tissue perfusion.
• 2. Progressive - body begins to loss its ability
  to compensate - inadequate perfusion begins.
• 3. Irreversible - Cell and tissue damage result
  in multi-system organ failure leading to
  death.

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Classifications of Shock

• 1. Hypovolemic shock (classic shock)
• Classic shock is the most common. It is the
  standard used to compare other forms of shock in
  differential diagnosis.
• Hemorrhagic / Blood loss
• Dehydration / Fluid loss
• 2. Obstructive Shock
• Pulmonary Embolism / Blocked pulmonary
  circulation
• Tension Pneumothorax / Increased intrathoracic
  pressure
• Cardiac Tamponade / Pressure on myocardium.
  Decreased preload.

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Classifications of Shock, continued

• 3. Cardiogenic Shock
• Heart (pump) Failure (40 of Myocardium damaged
  by AMI)
• 4. Distributive Shock
• Neurogenic / Spinal cord injury , drug overdose
  or poisoning which affects nervous systems
  ability to maintain vascular tone leading to
  vasodilation.
• Anaphylactic / Vasodilation and fluid shifting
  from capillary to cell. Leads to micro clotting
  (hives) and smooth muscle contraction
  (brochospasm)
• Septic / vasodilation and fluid shifting due
  to overwhelming infection.

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Hypovolemic Shock

• Shock resulting from fluid loss blood plasma,
  or body water.
• Hemorrhagic blood loss. (classic shock)
• Dehydration fluid loss.
• Third spacing Shifting of plasma from blood
  vessels to interstitual spaces. May be caused by
  dehydration or sepsis.

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Hemorrhagic Shock

• Compensated Stage
• Mechanism Volume depletion due to bleeding.
• Body detects decrease in cardiac output.
• Sympathetic nervous system is stimulated
  releasing epinephrine and norepinehrine to
  stimulate alpha and beta receptors.
• Alpha Vasoconstriction Beta
  bronchodilation and cardiac
  stimulation.

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Hemorrhagic (Classic) Shock CompensatedSigns
and Symptoms
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Hemorrhagic (Classic) Shock Progressive

• Progressive Stage
• Mechanism Kidneys release anti-diuretic hormone
  which increases vasoconstriction by closing the
  capillary sphincters, greatly reducing peripheral
  circulation.
• Increased hypo-perfusion causes increase in
  metabolic acid build up

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Hemorrhagic (Classic) Shock ProgressiveSigns
and Symptoms
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Hemorrhagic (Classic) Shock Irreversible

• Mechanism
• Compensatory mechanisms fail.
• Pre-capillary sphincters open releasing metabolic
  acids, micro-emboli and other wastes into
  circulation.
• Cell damage, organ failure and death occur.

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Hemorrhagic (Classic) Shock IrreversibleSigns
and Symptoms
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Differential Diagnosis of Hypovolemic
ShockUnique Signs and Symptoms

• Mechanism Dehydration Hypovolemia due to fluid
  loss.
• Skin Sweating absent, Poor skin turgor (tenting)
  Pediatric patients may cry without tears have
  sunken fontanels.
• Other Thirst (except in elderly with impaired
  thirst mechanism.)

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Differential Diagnosis Obstructive
ShockUnique signs and symptoms

• Mechanism Pulmonary Emboli
• Mental status Anxiety, feeling of impending
  doom.
• Skin Pallor to cyanosis around mouth and nose.
• Other Chest pain, lung sound may be clear,
  possible syncope, cardiac dysrhthmia, (PVCs and
  A-Fib ) common can lead to sudden cardiac arrest.

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Obstructive Shock, continuedUnique Signs and
Symptoms

• Mechanism Cardiac Tamponade or Tension
  Pneumothorax.
• Skin Cyanosis first around mouth and nose,
  spreads to extremities.
• Pulse Paradoxical Pulse (pulse drops on
  inspiration) narrowed pulse pressure.
• Respiration Sudden sharp chest pain and acute
  dyspnea in COPD pt with ruptured bleb. Clear
  lung sounds.
• Other Distended neck and hand veins. Tension
  Pneumothorax unequal breath sounds. Cardiac
  Tamponade distant heart tones.

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Differential Diagnosis Cardiogenic ShockUnique
Signs and Symptoms

• Mechanism Heart (pump) failure drop in cardiac
  output.
• Skin Cyanosis
• Pulse May be bradycardic, tachycardic or within
  normal limits .
• Respiration's Diminishing breath sounds
  progressing to wheezing and crackles. Patient
  complains of increasing dyspnea. Coughs up
  white or pink tinged foamy sputum.
• Other Pulmonary edema left heart failure /
  Pitting edema right heart failure

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Differential Diagnosis Distributive
ShockNeurogenic Shock

• Mechanism Neurogenic shock Vasodilation.
• Skin Areas of vasodilation, at first become
  warm pink and dry. Later with pooling mottling
  of dependant areas, pallor and cyanosis to upper
  surfaces.
• Pulse Highly variable depending on injury or
  action of drug / poison May be abnormally slow
  or abnormally fast will usually not be normal.
• Respiration severely compromised Becoming slow,
  shallow, with abnormal patterns. Patient may
  loose stimulus to breath.
• Other Hypothermia, Pulmonary edema may occur
  with drug or poisoning.

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Distributive Shock continued,Anaphylactic Shock

• Mechanism Anaphylaxis, severe allergic reaction.
• Skin Hives, itching, possible petechia.
  Flushing (urticaria), pallor or cyanosis.
• Blood pressure abrupt fall in cardiac output.
• Respiration Rapid shallow, dyspnea with stridor,
  wheezing , crackles, leading to respiratory
  arrest.
• Other Swelling of mucous membranes / pulmonary
  edema.

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Distributive Shock, continued,Septic Shock

• Mechanism Overwhelming infection.
• Skin Varies from flushed pink (if fever is
  present) to pale and cyanotic. Purple blotches
  possible, peeling of skin, general or at palms
  and soles of feet.
• Blood pressure Early Cardiac output increases
  but toxins prevent increase in blood pressure.
  Late drop in blood pressure, hypotension.
• Respiratory Dyspnea with altered lung sounds.
• Other High fever, (except in some elderly and
  very young patients).
• Late sign Pulmonary edema

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General Treatment of Shock

• Assure airway
• Administer oxygen
• Assist ventilations if necessary.
• Position patient to assist perfusion. (elevate
  head and shoulders if pulmonary edema.)
• Keep patient warm.
• Perform a Focused history and physical.
• Adjust O2, Gain IV access, ECG monitor, Pulse
  Oximetry.

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Advanced Care Hypovolemic Shock

• Large bore IV Minimum 18 gage
  
  Preferably 14 or 16 gage
• Use blood tubing if available or macro tubing
  apply pressure to bag to speed infusion
• Fluid Replacement Lactated Ringers or Normal
  Saline (Make sure fluids are warm
• Need 3 liter fluid to replace 1 liter blood loss,
  titrate fluid infusion to the B/P.

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Treatment of Obstructive Shock Tension
Pneumothorax

• High flow oxygen nonrebreather mask
• Needle Decompression 12 or 14 gauge over needle
  catheter inserted, between second and third ribs
  at midclavicular line upper edge of third rib.
• Removal of occlusive dressing over sucking chest
  wound.
• May need to intubate patient and provide positive
  pressure ventilation.

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Treatment Obstructive Shock Cardiac Tamponade

• Notify receiving hospital ASAP.
• Pericardiocentesis needs to be performed in
  hospital.
• Fluid bolus may help (20ml / kg body weight)
  should seek medical control advise before bolus
  administration.
• Priority should be given to rapid transport.

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Treatment of Obstructive Shock Pulmonary Emboli

• Supportive treatment.
• High flow oxygen
• Monitor cardiac rhythm.
• Follow treatment specific algorithms for cardiac
  dysrhythmia.

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Treatment of Distributive ShockNeurogenic

• Monitor and manage respiratory and cardiac
  systems. Bradycardia is common, manage with
  atropine.
• If drug / poison induced contact poison control
  and medical control for treatment guidance. 2 mg
  Naloxone for narcotic O/D
• If lungs sound are clear fluid challenge (200 ml)
  bolus. Neurogenic shock is self limiting so
  massive fluid replacement is not needed.
• Pulmonary edema with hypotension should be
  managed with Dopamine titrated to maintain the
  blood pressure.

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Treatment of Distributive ShockAnaphylaxis

• Mild reaction with wheezing, manage with
  bronchodilator if blood pressure is above 70
  systolic.
• Severe with hives, airway/cardiovascular effects,
  manage with 0.3-0.5 mg 11000 Epinephrine.
• Benadryl 10-25 mg slow IV or 25-50mg IM. may be
  used if reaction is mild or Epinephrine is
  contraindicated ( patient over 40 with cardiac
  history in past year.)
• Hypotension after treatment with Epinephrine or
  Benadryl. Manage B/P with
  dopamine start at 5-10mcg /kg/min. titrate to
  effect.

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Treatment Distributive ShockSeptic

• High flow oxygen, Intubate and ventilate if
  necessary.
• IV bolus with Crystalloid solution. (200ml)
• Hypotension after bolus administration manage
  with dopamine 5-10 mcg/kg/min. titrated to
  effect.
• PVCs are common, treat with oxygen.

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Cardiogenic Shock

• General High flow Oxygen,
• IV Normal saline, use macro tubing set, 18 gage
  if possible, at KVO rate.
• Monitor rate /rhythm If hypotension is related
  to heart rate treat rate.
• Bradycardia Sinus /Atropine, all other use
  pacer if available.
• Tachycardia Narrow complex / Adenosine,
  unconscious or severely decompensated, cardiovert
  (sedate first if conscious)
• Wide complex tachycardia Treat with lidocaine,
  Defibrillation, or if conscious sedate and
  cardiovert.
• Hypotension not related to heart rate should be
  treated with Dopamine.
• Patients on oral diuretics should be fluid
  challenged prior to Dopamine administration
  monitor respiratory effects.

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Summery

• Shock is a syndrome.
• Golden minute principleno more than 10 min on
  scene, Rapid diagnosis and field stabilization is
  critical.
• Golden hour principle Shock must be stopped
  within one hour of cause.
• Treat during transport when ever possible.