Emergency Nursing

1
Emergency Nursing

• Chapter 33 Part 2

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Clinical Signs of Pain

• Vocalization
• Depression
• Anorexia
• Tachypnea
• Tachycardia
• Abnormal blood pressure

• Pale mucous membranes
• Aggression
• Abnormal postures
• Hypersalivation
• Dilated pupils

3
Abdominal Pain

• Classic praying or play bowing position
• Hypersalivation
• Inability to lay down or sleep

4
Untreated Pain

• Causes stress
• Triggers harmful physiological changes that
  prolong recovery
• Signs not always obvious
• Monitor for absence of normal behavior

5
DIC

• Definition
• A syndrome
• The natural balance between clot formation and
  clot prevention/resolution is altered

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DIC

• Consequences
• Massive activation of coagulation
• Coagulation overwhelms bodys normal regulatory
  function
• Systemic clot formation begins on a widespread
  scale
• Clot formations will set up multiple-organ
  microthrombosis
• Subsequent multiple organ failure

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DIC

• Causes
• Vascular injury
• Severe trauma
• Severe inflammation
• Sepsis
• Toxins
• Poor perfusion

8
DIC

• Pathogenesis
• Patient commonly moves from a hypercoagulable to
  a hypocoagulable state
• Die from thrombotic or hemorrhagic episodes

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DIC

• Common physical examination findings
• Petechia
• Ecchymosis
• Cold extremities
• Abnormal mentation
• Abnormal body temperature
• Increased respiratory effort

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Treatment of DIC

• Primary goal
• Remove the stimulus initiating intravascular
  coagulation
• Treat the primary disease

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Treatment of DIC

• Secondary goal
• Prevent secondary complications
• Maintain organ perfusion
• Fluids
• Blood products
• Anticoagulants

12
Shock

• Definition
• Poor blood flow creating impaired oxygen delivery
  to the tissues

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Categories of Shock

• Compensatory or hyperdynamic
• Earliest phase of shock
• Clinical signs
• Increased heart rate and respiratory rate
• Rapid capillary re?ll time
• Brick red mucous membranes
• Bounding pulses

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Categories of Shock

• Uncompensated or hypodynamic shock
• Second phase of shock
• Blood flow is shunted vital organs (brain, heart)
  at the expense of other tissues
• Clinical signs
• Weak pulses
• Rapid heart rate
• Increased capillary refill time
• Pale mucous membranes
• Hypothermia
• Dull mentation

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Categories of Shock

• Shock can be further divided based on underlying
  cause
• Hypovolemic shock
• Distributive shock
• Cardiogenic shock
• Septic shock

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Hypovolemic Shock

• Most common form of shock
• Primary perfusion failure
• Results from a reduction in circulating blood
  volume
• Bleeding
• Dehydration
• Effusive fluid loss

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Distributive Shock

• Maldistribution of blood flow associated with
  vasodilation
• Consequent decrease in effective blood volume
• Regardless of intravascular volume or cardiac
  output
• Common causes
• Trauma
• Heatstroke
• Envenomation
• Anaphylaxis

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Cardiogenic Shock

• Associated with decreased cardiac output
• Can occur from heart failure
• Cardiomyopathy
• Valvular disease
• Cardiac arrhythmias

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Septic Shock

• Caused by massive systemic infection or primary
  infectious diseases
• Opportunistic infections can also trigger septic
  shock
• Typically associated with severe tissue damage
• Trauma
• Heatstroke
• Envenomations
• Pancreatitis

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SIRS

• Systemic inflammatory response syndrome
• Parallels septic shock
• Triggered by systemic inflammation

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SIRS

• Similar to shock in that there is an early
  hyperdynamic phase followed by uncompensated or
  hypodynamic phase
• Clinical signs
• Abnormal temperature fluctuations
• Depression
• Tachypnea
• DIC

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SIRS

• Primary treatment
• Oxygen therapy
• Aggressive fluid therapy
• Shock doses
• 90 ml/kg/hr dog
• 45-60 ml/kg/hr cat
• Fluid administration goal oriented!
• Correction of underlying problem

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Reperfusion Injury

• Cellular injury that develops as blood flow
  returns to an area or tissue previously deprived
  of perfusion
• Poor perfusion causes oxygen-starved tissues to
  develop an anaerobic metabolism and become
  depleted of cellular energy stores
• These conditions alter certain enzyme systems,
  which destabilize white blood cell membranes

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Reperfusion Injury

• Once perfusion is restored, altered enzyme
  systems generate harmful molecules called
  oxygen-free radicals
• Simultaneously, membrane-damaged white blood
  cells release inflammatory mediators that
  contribute to a reactive environment
• Oxygen-free radicals and inflammatory mediators
  cause inflammation and vessel injury leading to
  thrombosis and edema

25
Vessel Injury

• Leads to thrombosis and edema
• DIC, SIRS, and multi-organ dysfunction can
  develop