Stages of shock

definition.types,stages,sign and symptoms management

1. Stages of Shock

2. To understand the physiologic responses and subsequent clinical signs and symptoms is to divide into separate stages: initial stage of shock compensatory, progressive, and irreversible.  

3. identify an initial stage of shock, changes attributed to this stage occur at the cellular level and are generally not detectable clinically. The earlier that medical management and nursing interventions can be initiated along this, the greater the patient’s chance of survival.

4. COMPENSATORY STAGE In the compensatory stage of shock, the patient’s blood pressure remains within normal limits. Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to maintaining adequate cardiac output.

5. This results from stimulation of the sympathetic nervous system and subsequent release of catecholamines (epinephrine and norepinephrine ).

6. The body shunts blood from organs such as the skin, kidneys, and gastrointestinal tract ---to the brain and heart to ensure adequate blood supply to these vital organs.

7. As a result, the patient’s skin is cold and clammy, bowel sounds are hypoactive, and urine output decreases in response to the release of aldosterone and ADH.

8. Clinical Manifestations normal blood pressure inadequate organ perfusion--------anaerobic metabolism--------lactic acid, --metabolic acidosis respiratory rate increases raises the blood pH confusion arteriolar dilation.

9. Medical Management identifying the cause of the shock, correcting the underlying disorder supporting those physiologic processes compensation maintained

10. -measures such as fluid replacement medication therapy must be initiated to maintain an adequate blood pressure and reestablish and maintain adequate tissue perfusion.

11. Nursing Management Assess those patients at risk for shock Early intervention along the continuum of shock

12. MONITORING TISSUE PERFUSION In assessing tissue perfusion, the nurse observes for changes in level of consciousness, vital signs (including pulse pressure), urinary output, skin, and laboratory values.

13. In the compensatory stage of shock, serum sodium and blood glucose levels are elevated in response to the release of aldosterone and catecholamines .

14. The role of the nurse at the compensatory stage of shock is to monitor the patient’s hemodynamic status and promptly report deviations to the physician.  

15. assist in identifying and treating the underlying disorder. administer prescribed fluids and medications, and promote patient safety.

16. REDUCING ANXIETY Providing brief explanations about the diagnostic and treatment procedures, supporting the patient during those procedures,

17. and providing information about their outcomes are usually effective in reducing stress and anxiety and thus promoting the patient’s physical and mental well-being.

18. PROMOTING SAFETY monitoring potential threats to the patient’s safety, because a high anxiety level and altered mental status typically impair a person’s judgment.

19. may now disrupt intravenous lines and catheters and complicate their condition. Therefore, close monitoring is essential.

20. PROGRESSIVE STAGE In the progressive stage of shock, the mechanisms that regulate blood pressure can no longer compensate and the MAP falls below normal limits, with an average systolic blood pressure of less than 90 mm Hg.

21. Pathophysiology all organ systems suffer from hypoperfusion at this stage, two events perpetuate the shock syndrome. the overworked heart becomes dysfunctional;

22. the body’s inability to meet increased oxygen requirements produces ischemia; and biochemical mediators cause myocardial depression.

23. Second, the autoregulatory function of the microcirculation fails in response to numerous biochemical mediators released by the cells, resulting in increased capillary permeability, with areas of arteriolar and venous constriction.

24. further compromising cellular perfusion. The relaxation of precapillary sphincters causes fluid to leak from the capillaries, creating interstitial edema and return of less fluid to the heart.

25. Assessment and Diagnostic Findings Chances of survival depend on the patient’s general health before the shock state as well as the amount of time it takes to restore tissue perfusion. As shock progresses, organ systems decompensate.

26. RESPIRATORY EFFECTS The lungs, which become compromised early in shock, are affected at this stage. Subsequent decompensation of the lungs increases the likelihood that mechanical ventilation will be needed if shock progresses.

27. Respirations are rapid and shallow. Crackles are heard over the lung fields. Decreased pulmonary blood flow causes arterial oxygen levels to decrease and carbon dioxide levels to increase.

28. Hypoxemia and biochemical mediators cause an intense inflammatory response and pulmonary vasoconstriction, perpetuating the pulmonary capillary hypoperfusion and hypoxemia.

29. Pulmonary capillaries begin to leak their contents, causing pulmonary edema, diffusion abnormalities (shunting), and additional alveolar collapse. Interstitial inflammation and fibrosis are common as the pulmonary damage progresses.

30. This condition is sometimes referred to as acute respiratory distress syndrome (ARDS), acute lung injury (ALI), shock lung, or noncardiogenic pulmonary edema..

31. CARDIOVASCULAR EFFECTS A lack of adequate blood supply leads to dysrhythmias and ischemia. The patient has a rapid heart rate, sometimes exceeding 150 bpm . Cardiac enzyme levels ( eg , lactate dehydrogenase , CPK-MB, and cTn -I) rise.

32. myocardial depression and ventricular dilation may further impair the heart’s ability to pump enough blood to the tissues to meet oxygen requirements.

33. NEUROLOGIC EFFECTS As blood flow to the brain becomes impaired, the patient’s mental status deteriorates. Changes in mental status occur as a result of decreased cerebral perfusion and hypoxia; the patient may initially exhibit confusion or a subtle change in behavior.

34. Subsequently, lethargy increases and the patient begins to lose consciousness. The pupils dilate and are only sluggishly reactive to light.

35. RENAL EFFECTS When the MAP falls below 80 mm Hg the glomerular filtration rate of the kidneys cannot be maintained, and drastic changes in renal function occur. Acute renal failure (ARF) can develop.

36. ARF is characterized by an increase in blood urea nitrogen (BUN) and serum creatinine levels, fluid and electrolyte shifts, acid–base imbalances, and a loss of the renalhormonal

37. regulation of blood pressure. Urinary output usually decreases to below 0.5/ mL /kg per hour (or below 30 mL per hour) but can be variable depending on the phase of ARF.

38. HEPATIC EFFECTS Decreased blood flow to the liver impairs the liver cells’ ability to perform metabolic and phagocytic functions. Consequently, the patient is less able to metabolize medications and metabolic waste products, such as ammonia and lactic acid.

39. The patient becomes more susceptible to infection as the liver fails to filter bacteria from the blood.

40. Liver enzymes ( aspartate aminotransferase [AST ], formerly serum glutamic-oxaloacetic transaminase [SGOT]; alanine aminotransferase [ALT], formerly serum glutamate pyruvate transaminase [SGPT]; lactate dehydrogenase ) and bilirubin levels are elevated, and the patient appears jaundiced.

41. GASTROINTESTINAL EFFECTS Gastrointestinal ischemia can cause stress ulcers in the stomach, placing the patient at risk for gastrointestinal bleeding. In the small intestine, the mucosa can become necrotic and slough off, causing bloody diarrhea.

42. Beyond the local effects of impaired perfusion, gastrointestinal ischemia leads to bacterial toxin translocation, in which bacterial toxins enter the bloodstream through the lymph system.

43. In addition to causing infection, bacterial toxins can cause cardiac depression, vasodilation , increased capillary permeability, and an intense inflammatory response with activa - tion of additional biochemical mediators. The net result is interference with healthy cells and their ability to metabolize nutrients.

44. HEMATOLOGIC EFFECTS The combination of hypotension, sluggish blood flow, metabolic acidosis, and generalized hypoxemia can interfere with normal hemostatic mechanisms. Disseminated intravascular coagulation (DIC) can occur either as a cause or as a complication of shock.

45. In this condition, widespread clotting and bleeding occur simultaneously. Bruises ( ecchymoses ) and bleeding ( petechiae ) may appear in the skin.

46. Coagulation times ( prothrombin time, partial thromboplastin time) are prolonged. Clotting factors and platelets are consumed and require replacement therapy to achieve hemostasis .

47. Medical Management there are several differences in medical management by type of shock, some medical interventions are common to all types.

48. These include use of appropriate intravenous fluids and medications to restore tissue perfusion by (1) optimizing intravascular volume, (2) supporting the pumping action of the heart, and (3) improving the competence of the vascular system.

49. Other aspects of management may include early enteral nutritional support and use of antacids, histamine-2 blockers, or antipeptic agents to reduce the risk of gastrointestinal ulceration and bleeding.

50. Nursing Management The patient in the progressive stage of shock is often cared for in the intensive care setting to facilitate close monitoring (hemodynamic monitoring, electrocardiographic monitoring, arterial blood gases, serum electrolyte levels, physical and mental status changes),

51. rapid and frequent administration of various prescribed medications and fluids, and possibly intervention with supportive technologies, such as mechanical ventilation, dialysis, and intra-aortic balloon pump.

52. Working closely with other members of the health care team, the nurse carefully documents treatments, medications, and fluids that are administered by members of the team, recording the time, dosage or volume, and the patient’s response. Additionally,

53. the nurse coordinates both the scheduling of diagnostic procedures that may be carried out at the bedside and the flow of health care personnel involved in the patient’s care.  

54. PREVENTING COMPLICATIONS If supportive technologies are used, the nurse helps reduce the risk of related complications and monitors the patient for early signs of complications.

55. Monitoring includes evaluating blood levels of medications, observing invasive vascular lines for signs of infection, and checking neurovascular status if arterial lines are inserted, especially in the lower extremities.

56. the nurse promotes the patient’s safety and comfort by ensuring that all procedures, including invasive procedures

57. and arterial and venous punctures, are carried out using correct aseptic techniques and that venous and arterial puncture and infusion sites are maintained with the goal of preventing infection.

58. Positioning and repositioning the patient to promote comfort, prevent pulmonary complications, and maintain skin integrity are integral to caring for the patient in shock.

59. PROMOTING REST AND COMFORT Efforts are made to minimize the cardiac workload by reducing the patient’s physical activity and fear or anxiety. Promoting rest and comfort is a priority in the patient’s care. SUPPORTING FAMILY MEMBERS

60. IRREVERSIBLE STAGE The irreversible (or refractory) stage of shock represents the point along the shock continuum at which organ damage is so severe that the patient does not respond to treatment and cannot survive.

61. Despite treatment, blood pressure remains low. Complete renal and liver failure, compounded by the release of necrotic tissue toxins, creates an overwhelming metabolic acidosis. Anaerobic metabolism contributes to a worsening lactic acidosis.

62. Reserves of ATP are almost totally depleted, and mechanisms for storing new supplies of energy have been destroyed.

63. Multiple organ dysfunction progressing to complete organ failure has occurred, and death is imminent. Multiple organ dysfunction can occur as a progression along the shock continuum or as a syndrome unto itself.

64. Medical management during the irreversible stage of shock is usually the same as for the progressive stage. Although the patient’s condition may have progressed from the progressive to the

65. irreversible stage, the judgment that the shock is irreversible can be made only retrospectively on the basis of the patient’s failure to respond to treatment.

66. Strategies that may be experimental ( ie , investigational medications, such as antibiotic agents and immunomodulation therapy) may be tried to reduce or reverse the severity of shock.

67. Nursing Management As in the progressive stage of shock, the nurse focuses on carrying out prescribed treatments, monitoring the patient, preventing complications, protecting the patient from injury, and providing comfort.

68. family needs to be informed about the prognosis and likely outcomes. Opportunities should be provided, throughout the patient’s    

69. care, for the family to see, touch, and talk to the patient. A close family friend or spiritual advisor may be of comfort to the family in dealing with the inevitable death of the patient.

70. Whenever possible and appropriate, the family should be approached regarding any living will, advance directive, or other written or

71. verbal wishes the patient may have shared in the event that he or she cannot participate in end-of-life decisions. In some cases, ethics committees may assist the family and health care team in making difficult decisions.  

72. Thanking you