Shock and its management

detail description of shock and its management

1. SHOCK AND ITS MANAGEMENT Ms. SAHELI CHAKRABORTY 2 ND YEAR MSC NURSING RINER

2. Objectives :- From today’s class we are going to learn about- Definition of shock. Incidence and Etiology of shock. Pathophysiology of shock Stages of shock and management in each stages of shock. Compensatory mechanism Diagnostic evaluation and complications of shock. First aid management, nursing management of shock.

3. INTRODUCTION Shock is a complex, life threatening condition or syndrome characterized by inadequate blood flow to the tissues and cells of the body and resulting in cell death. Rapid assessment and prompt treatment is necessary to improve the patient’s recovery.

4. DEFINITION Shock is a pathological state in which group of symptoms occurs characterized by- decrease tissue perfusion, impaired cellular metabolism , increase oxygen and nutrient demand to the tissues, results in cell death.

5. INCIDENCE OF SHOCK: Shock is common in both gender. Children and old age group more prone to shock. 80% of mortality rate is caused by shock. The incidence of septic shock in ICU has a upward trend across recent years in INDIA with an estimated mortality of >50%

6. ETIOLOGY OF SHOCK :- 1. Reduced blood volume- Injury Internal bleeding Burns Chronic illness Severe vomiting Dehydration Severe diarrhoea Anaphylaxis

7. 2. Acute heart conditions:- Heart attack Arrhythmias Coronary thrombosis Ruptured aortic aneurysm 3. Other causes: Pulmonary embolism. Severe infection Sepsis Severe pain Poisoning Myocardial infarction Spinal Injuries.

8. PATHOPHYSIOLOGY OF SHOCK There are 3 types of changes occurs in shock. Cellular changes. Vascular responses Blood pressure regulation.

9. Cellular changes: Due to etiological factor Cells lack an adequate blood supply Deprived of oxygen and nutrients Energy production through anaerobic metabolism Low energy yields from nutrients and an acidotic intracellular environment Normal cell function ceases The cells swells and the cell membrane becomes more permeable , allowing electrolyte and fluids to seep out of and into the cell.

10. Contd.. Impairment in Na-K pump, damage of mitochondria and cell structures, and death of the cell occurs. This state is called as shock state. catecholamine, cortisol , glucagon and inflammatory cytokines and mediators are released in response to stress. Hyperglycemia occurs and insulin resistance to mobilize glucose for cellular metabolism. Gluconeogenesis , glycogenolysis Depletion of glycogen stores. Increased proteolysis and eventual organ failure.

11. Vascular responses: Local regulatory mechanism, autoregulation . Stimulate vasodilation or vasoconstriction in response to biochemical mediators released by the cell. The substance triggers an action at a cell site or travels in the blood stream. Need for oxygen and nutrients. Deprived oxygen and nutrient in the cell. Decreased tissue perfusion. Shock.

12. Blood pressure regulation: When blood pressure drops, catecholamine releases from the adrenal gland. Increased heart rate Vasoconstriction Restore blood pressure and respiratory rate. Meanwhile catecholamine activates the renin angiotensin and aldosterone mechanism. Conversion of angiotensin I to angiotensin II and thus results in vasoconstriction. Angiotensin II activates the aldosterone . Release of ADH by the pituitary gland.

13. Retention of sodium and water Increase blood volume and blood pressure. Continues to drop blood pressure and blood volume Decrease oxygenation to the tissues. Hypo perfusion to the tissues and vital organs. Multisystem organ failure.

14. STAGES OF SHOCK: A convenient way to understand the physiological responses and subsequent clinical signs and symptoms of shock is to divide the continuum into separate stages. It include the following: Compensatory stage Progressive stage Irreversible stage

15. COMPENSATORY STAGE: In this stage BP remains in normal limits. Vasoconstriction, increased heart rate, increased contractility of the heart contribute to maintaining adequate cardiac output. Patient displays the ‘fight or flight’ response. The body shunts blood from skin, kidneys, GI tract to the brain, heart and lungs; to maintain the adequate blood supply. Skin becomes cool, clammy, hypoactive bowel sounds and urine output decreases in response to ADH and aldosterone .

16. Pathophysiology of compensatory stage: Initial stage: Lack of oxygen supply to the tissues. Inadequate tissue perfusion Tissue hypoxia Mitochondria unable to produce the ATP Cell membrane damage because of hypoxia, leakage of cell content to extracellular fluid. Tissue performs anerobic respiration Formation of pyruvic acid and lactic acid Systemic metabolic acidosis.

17. Compensatory stage: Employment of physiological mechanism including neural, hormonal and biochemical mechanism in an attempt to reverse the condition. The baroreceptor in the arteries detect hypotension. Stimulation of adrenaline and nor-adrenaline as well as there is a stimulation of sympathetic nervous system. That results in vasoconstriction Increase heart rate, contractility of the heart, increase cardiac output and increased blood pressure.

18. Shunting of blood from other organ to ensure adequate blood supply. Cold, clammy skin, hypoactive bowel sound, decrease urine output in response to ADH

19. Clinical manifestation of compensatory stage of shock: Normal BP. Inadequate organ perfusion. Build up of lactic acid produces metabolic acidosis. Rapid respiratory state. Increase blood carbondioxide level and blood pH level Respiratory alkalosis Changes in blood status. Confusion.

20. Medical and nursing management: Monitoring tissue perfusion: Check for level of consciousness, vital signs, pulse pressure. Check urine output. Laboratory values ( eg . Base deficit and lactic acid level) should be checked. The nurse should monitor the patient’s hemodynamic status. Administer prescribed fluids and medications Promote patient safety

21. The nurse should report a systolic BP less than 90mmHg or a drop in 40mmHg from baseline. Pulse pressure should be monitored. Continuous central venous oxymetry should be checked. Reducing anxiety : patient and their families often become anxious and apprehensive when they face major threat to health and well being. Brief explanation of the patient’s health should be given. Use gentle therapeutic touch. Speak in a calm reassuring voice and also help ease the patient’s concern.

22. Promoting safety: The nurse must be vigilant for potential threats to the patient’s safety because a high anxiety level and altered mental status impair judgement. Close monitoring and frequent reorientation intervention are essential.

23. Progressive stage of shock In the second stage of shock the mechanism that regulate blood pressure can no longer compensate, and the mean arterial pressure falls below normal limits. Patients are clinically hypotensive, systolic blood pressure less than 90mmHg or a decrease in systolic blood pressure of 40mmhg from baseline.

24. Pathophysiology of 2 nd stage of shock: Decrease cardiac output Tissue hypoperfusion Cells switch from aerobic to anerobic metabolism Lactic acid production Cell function ceases and swells Membranes becomes more permeable Electrolyte and fluid seep in and out of the cell Sodium build up and potassium leak out. Damage of mitochondria Cell death.

25. Clinical manifestation Of 2 nd stage of Shock: Respiratory effects: Subsequent decompensation of the lungs increases. Rapid and shallow respiration Crackles present Decrease pulmonary blood flow causes arterial oxygen levels to decrease and carbon dioxide level to increase. Hypoxemia and released chemical mediator causes intense inflammatory response and pulmonary vasoconstriction.

26. Pulmonary capillary hypoperfusion . Pulmonary capillary begins to leak, causing pulmonary edema and additional alveolar collapse. Acute lung injury. Acute respiratory distress syndrome. 2. Cardiovascular effects: Dysarrhythmias and ischemia. Rapid heart rate. The patient may complaints of chest pain and even suffer a MI Levels of cardiac enzyme increases Impairs the heart’s ability to pump the blood. B-type Natriuretic peptide (BNP) increases due to over distension of the ventricle

27. 3. Neurologic effects: Changes in mental status occur with decreased cerebral perfusion, hypoxia. Agitation Confusion Lethargy increases Loss of consciousness 4. Renal effects: Acute renal failure Increase BUN and serum creatinine level Fluid and electrolyte shift. Acid base imbalances Decrease urinary output less than 30 ml/kg/hour.

28. 5. Hepatic effects: Decrease blood flow to the liver Impairment in phagocytic and metabolic function Impairment in gluconeogenesis and glycogenolysis . The patient become more susceptible to infection as the liver fails to filter the blood Increase level of bilirubin Jaundice Elevated liver enzyme level

29. 6. GI Effects: Stress ulcer due to GI ischemia Risk for GI bleeding Bloody diarrhoea as necrosis of the mucosa. Ischemia results in increase bacterial toxins which results in cardiac depression, vasodilation and an intense inflammatory response with activation of additional biochemical mediators.

30. 7. Hematologic effects: Hypotension Sluggish blood flow Coagulation system imbalance DIC occur as a complication of shock Bruises and bleeding Prolonged coagulation time

31. Medical and Nursing Management : Preventing complication: The nurse should monitor the early signs of complication Blood level of medication should be checked. Check the neurovascular status if arterial lines are inserted. Maintain correct aseptic technique VAP should be prevented. Frequent oral care. Follow aseptic suction technique

32. Turning and elevating the head at least 30 degree to prevent aspiration Positioning of the patient Promoting rest and comfort Efforts are made to minimize the cardiac workload by reducing the patient’s physical activity and treating pain and anxiety Promote rest to the patient Maintain temperature because elevated temperature may increase the metabolic rate and thus increases the workload of the heart. Avoid blankets to prevent vasodilation

33. c. Supporting family member The family member should be informed about the patient’s status. Families need advice from the health care team to get some rest.

34. C. IRREVERSIBLE STAGE:- In this stage of shock organ damage are more prominent. Patient does not respond to treatment BP remains low Renal and liver failure occurs. Metabolic acidosis due to release of necrotic tissue toxin. Depletion of ATPase energy supply Respiratory system fails. Patient will be on ventilator support. Multiple organ dysfunction occurs. Death is imminent.

35. Medical and Nursing Management: Antibiotic therapy Immunomodulation therapy Monitor patient and prevent complication, provide comfort to the patient. Reassurance should be given The family must be informed about the prognosis of the patient. Counselling with all members of the health care team and family member promotes better understanding about the patient’s condition.

36. COMPENSATORY MECHANISM Posture: A patient in acute circulatory failure falls down. Patient should lie flat on the floor or in head down position to improve circulation towards heart. Contraction of skin vessels: Contraction of arterioles and venules of the skin is usual to improve the blood supply. Application of heat to the skin should be avoided.

37. 3. Insensitivity: A much collapse patient has little pain. Large quantities of pain relieving drugs are not effective in this stage unless given by intravenous route. 4. Urinary secretion: These are diminished to conserve fluid in the body but it is also a sign that tissue perfusion is inadequate. 5. Heart rate accelerates: It is an attempt to ensure that remaining fluid is circulated as early as possible to provide sufficient oxygen to the tissues.

38. 6. Subnormal temperature: It helps in reduction in the requirement of the tissues for the diminishing amount of oxygen available.

39. Diagnostic evaluation History collection Physical examination 12 lead ECG X ray chart. Continuous pulse oxymetry Continuous cardiac monitoring Hemodynamic monitoring Laboratory investigation. CBC Decrease hemoglobin Decrease hematocrit Decrease/increase WBC Decrease/increase glucose Decrease/increase potassium Decrease calcium Increase lactate.

40. COMPLICATION Multiple organ dysfunction syndrome Acute respiratory distress syndrome Acute renal failure Gastrointestinal ulceration DIC Death

41. First Aid Management Of Shock Reassure the patient. Place the patient in supine position with head low and turned to one side except in case of head injury. Loosen the clothing around the neck, chest and waist Give the patient seeps of water if the patient is thirsty Never use hot water bag or massage the limbs

42. Check pulse, respiration and level of consciousness. Stop the haemorrhage. Transfer the patient to the hospital immediately.

43. NURSING MANAGEMENT: Maintain airway, breathing, circulation of the patient. Continuous monitoring of the vital sign. Provide supplemental oxygen therapy to the patient. In severe cases put the patient in mechanical ventilator. Monitor for ABG values, Check for urine output Maintain nutritional status of the patient Administer prescribed medication to the patient Give psychological support to the patient and family.