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Interventions for Clients in Shock

Interventions for Clients in Shock. Shock. Can occur when any part of the cardiovascular system does not function properly for any reason Begins with abnormal cellular metabolism that occurs when too little oxygen is delivered to tissues. Review of tissue perfusion.

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Interventions for Clients in Shock

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  1. Interventions for Clients in Shock

  2. Shock • Can occur when any part of the cardiovascular system does not function properly for any reason • Begins with abnormal cellular metabolism that occurs when too little oxygen is delivered to tissues

  3. Review of tissue perfusion • Organ perfusion is related to mean arterial pressure (MAP). Because the cardiovascular system is a closed but continuous circuit, the factors that influence MAP include the following: • Total blood volume • Cardiac output • Size of the vascular bed • Total blood volume and cardiac output are directly related to MAP — increases in either total blood volume or cardiac output usually raise MAP. Decreases in either total blood volume or cardiac output eventually lower MAP. • The size of the vascular bed is inversely (negatively) related to MAP — increases in the size of the vascular bed lower MAP, and decreases raise MAP

  4. Processes of Shock • Initial stage (early shock) • Nonprogressive stage (compensatory stage) • Progressive stage (intermediate stage) • Refractory stage (irreversible stage)

  5. Multiple Organ Dysfunction Syndrome • Cell damage is caused by the massive release of toxic metabolites and enzyme. • Metabolites trigger small clots to form that block tissue oxygenation and damage more cells, continuing the devastating cycle.

  6. Hypovolemic Shock • Occurs when low circulating blood volume causes a mean arterial pressure decrease; the body’s oxygen need is not met • Caused by external hemorrhage; common after trauma and surgery or reduction in levels of clotting factors (Continued)

  7. Hypovolemic Shock (Continued) • Caused by internal hemorrhage as occurs with blunt trauma, gastrointestinal ulcers, and poor control of surgical bleeding

  8. Cardiogenic Shock • Actual heart muscle is unhealthy and pumping is directly impaired. • Cardiac output and afterload are reduced, thus reducing mean arterial pressure.

  9. Distributive Shock • Caused by loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased blood vessel permeability • Neural-induced distributive shock • Chemical-induced distributive shock (Continued)

  10. Distributive Shock (Continued) • Anaphylaxis • Sepsis • Capillary leak syndrome

  11. Obstructive Shock • Shock is caused by problems that impair the ability of the normal heart muscle to pump effectively. • Heart is normal but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle.

  12. Physical Assessment/Clinical Manifestations • Cardiovascular changes • Pulse • Blood pressure • Oxygen saturation • Skin changes • Respiratory changes • Renal and urinary changes • Central nervous system changes • Musculoskeletal changes

  13. Interventions • Reverse the shock. • Restore fluid volume. • Prevent complications through supportive and drug therapies. • Nonsurgical management includes oxygen therapy, fluid replacement, and monitoring.

  14. Drug Therapies • Vasoconstrictors, such as dopamine, epinephrine, norepinephrine, phenylephrine • Agents that enhance contractility • Agents that enhance myocardial perfusion

  15. Collaborative Management of Septic Shock • Manifestations of the first phase: unique to septic shock and often opposite from those seen with all other types of shock • Cardiovascular changes • Respiratory changes • Skin changes: in the hyperdynamic phase of septic shock, the skin is warm with no cyanosis evident

  16. Interventions for Septic Shock • Focus on correcting conditions causing shock and preventing complications. • Give oxygen therapy. • Drug therapy: antibiotics and anticoagulants, clotting factors and blood products, activated protein C, and antibodies, such as interleukin-1, interleukin-6, and tumor necrosis factor

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