1. Emergency Nursing CHAPTER 33 PART 2

2. 2 Clinical Signs of Pain  Vocalization  Depression  Anorexia  Tachypnea  Tachycardia  Abnormal blood pressure  Pale mucous membranes  Aggression  Abnormal postures  Hypersalivation  Dilated pupils

3. 3 Abdominal Pain  Classic “praying” or “play bowing” position  Hypersalivation  Inability to lay down or sleep

4. 4 Untreated Pain  Causes stress  Triggers harmful physiological changes that prolong recovery  Signs not always obvious  Monitor for absence of normal behavior

5. 5 DIC  Definition  A syndrome  The natural balance between clot formation and clot prevention/resolution is altered

6. 6 DIC  Consequences  Massive activation of coagulation  Coagulation overwhelms body’s normal regulatory function  Systemic clot formation begins on a widespread scale  Clot formations will set up multiple-organ microthrombosis  Subsequent multiple organ failure

7. 7 DIC  Causes  Vascular injury  Severe trauma  Severe inflammation  Sepsis  Toxins  Poor perfusion

8. 8 DIC  Pathogenesis  Patient commonly moves from a hypercoagulable to a hypocoagulable state  Die from thrombotic or hemorrhagic episodes

9. 9 DIC  Common physical examination findings  Petechia  Ecchymosis  Cold extremities  Abnormal mentation  Abnormal body temperature  Increased respiratory effort

10. 10 Treatment of DIC  Primary goal  Remove the stimulus initiating intravascular coagulation  Treat the primary disease

11. 11 Treatment of DIC  Secondary goal  Prevent secondary complications  Maintain organ perfusion  Fluids  Blood products  Anticoagulants

12. 12 Shock  Definition  Poor blood flow creating impaired oxygen delivery to the tissues

13. 13 Categories of Shock  Compensatory or hyperdynamic  Earliest phase of shock  Clinical signs  Increased heart rate and respiratory rate  Rapid capillary refill time  Brick red mucous membranes  Bounding pulses

14. 14 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

15. 15 Categories of Shock  Shock can be further divided based on underlying cause  Hypovolemic shock  Distributive shock  Cardiogenic shock  Septic shock

16. 16 Hypovolemic Shock  Most common form of shock  Primary perfusion failure  Results from a reduction in circulating blood volume  Bleeding  Dehydration  Effusive fluid loss

17. 17 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

18. 18 Cardiogenic Shock  Associated with decreased cardiac output  Can occur from heart failure  Cardiomyopathy  Valvular disease  Cardiac arrhythmias

19. 19 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

20. 20 SIRS  Systemic inflammatory response syndrome  Parallels septic shock  Triggered by systemic inflammation

21. 21 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

22. 22 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

23. 23 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

24. 24 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. 25 Vessel Injury  Leads to thrombosis and edema  DIC, SIRS, and multi-organ dysfunction can develop