Shock And its Management For BSN. .pptx

Shock Definition
Types
Management
Important terms

1. Unit III (d) Shock and its management AHSAN ELAHI BSN, RN, M.Phil Public health , ICN,ICU 1

2. 2 Objectives Define shock. Identify physiological responses to shock Explain Clinical manifestations, and general management of different stages of shock Identify treatment goals of client with shock Describe general management strategies for shock Explore different types of shock

3. 3 Objectives Explore hypovolemic shock its pathophysiology, medical management and nursing management Explore Cardiogenic shock its pathophysiology, medical management and nursing management Explore neurogenic shock its pathophysiology, medical management and nursing management Explore anaphylactic shock its pathophysiology, medical management and nursing management Explore septic shock its pathophysiology, medical management and nursing management Explain MODS

4. 4 Shock Definition: Clinical conditions that result in cellular hypoperfusion are often referred to as shock states. Which results in inadequacy to deliver oxygen and nutrients to support vital organs and cellular function.

5. 5 Pathophysiology Shock begins with cardiovascular system failure Alterations in at least one of four components: Blood volume Myocardial contractility Blood flow Vascular resistance

6. 6 Physiological responses to shock Hypoperfusion → hypoxia → anaerobic cellular respiration → lactic acidosis → metabolic acidosis → cell death → progressive organ dysfunction Hypercoagulability – increasing viscosity of blood Activation of the inflammatory response – vasoactive mediators i.e. histamine

7. 7 Stages of shock Three stages of shock. Stage I (Compensated or Non-progressive). Stage II (Decompensated or Progressive). Stage III (Irreversible)

8. 8 Stage I (Compensated or Non-progressive) The body activates compensatory mechanisms in an effort to maintain circulatory volume , blood pressure , and cardiac output. Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to maintaining adequate cardiac output. This results from stimulation of the sympathetic nervous system and subsequent release of catecholamines (epinephrine and norepinephrine). Patients display the often-described “fight or flight” response The body shunts blood from organs such as the skin, kidneys, and gastrointestinal tract to the brain, heart, and lungs to ensure adequate blood supply to these vital organs.

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10. 10 Medical Management in Stage 1 Medical treatment is directed toward Identifying the cause of the shock Correcting the underlying disorder r e placeme n t and medication t herapy Non specific me a s ures su c h a s f l u i d can initiated to maintain an adequate BP and tissue perfusion

11. 11 Nursing Management in Stage 1 Monitoring Tissue Perfusion The nurse observes for changes in level of consciousness, vital signs( Report BP lower than 90 mm Hg and pulse pressure less than 30 mm Hg) urinary output, skin, and laboratory values (eg, base deficit and lactic acid levels). In the compensatory stage of shock, serum sodium and blood glucose levels are elevated Administer prescribed fluids and medications, and promote patient safety. Oxygen administration Hemodynamic monitoring Reduce anxiety

12. 12 Stage II (Decompensated or Progressive) Compensatory mechanisms begin to fail, metabolic and circulatory derangements become more pronounced, and the inflammatory and immune responses may become fully activated.

13. Clinical Manifestations of Stage II Respiratory Effects Respirations are rapid and shallow. Crackles are heard over the lung fields. Acute respiratory distress syndrome Cardiovascular Effects Dysrhythmias and ischemia. Heart rate is rapid, sometimes exceeding 150 bpm. chest pain Week pulse Low BP Neurologic Effects changes in behavior or agitation and confusion. Subsequently, lethargy increases, and the patient begins to lose consciousness Dizziness, hedaec 14

14. 14 Clinical Manifestations of Stage II Renal Effects ARF, increased BUN and Creatinine Low urine output Acid base and electrolyte imbalance Gastrointestinal Effects Stress ulcers in the stomach, putting the patient at risk for GI bleeding Hematologic Effects Disseminated intravascular coagulation (DIC) Ecchymoses, petechiae General Anxiety or agitation/restlessness Bluish lips and fingernails Dizziness, lightheadedness, or faintness Pale, cool, clammy skin Profuse sweating, moist skin

15. 15 Medical Management in Stage II Depends on the type of shock Supporting the respiratory system Optimizing intravascular volume Supporting the pumping action of the heart Enteral nutritional support, aggressive hyperglycemic control with IV insulin H istamine-2 (H2) blockers, or antipeptic agents to reduce the risk of GI ulceration and bleeding. The patient should not be warmed too quickly, and warming blankets should not be applied, because they can cause vasodilation and a subsequent drop in BP.

16. 16 Medical Management in Stage II Preventing Complications Promoting Rest and Comfort Supporting Family Members

17. 17 Stage III (Irreversible) In the final, irreversible stage, cellular and tissue injury are so severe that the patient’s life is not sustainable even if metabolic, circulatory, and inflammatory derangements are corrected. At th i s po i nt, fu l l - b lown m u l t i s yst e m dysfunction syndrome (MODS) may evident. o r gan bec o me

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19. 19 Stage IV: Refractory Prolonged inadequate tissue perfusion Unresponsive to therapy Dysrhythmias Pulmonary edema Respiratory Distress Syndrome (RDS) Cerebral changes Renal decreased GFR Contributes to multiple organ dysfunction and death

20. 20 Systemic Inflammatory Response Syndrome (SIRS) Widespread systemic inflammatory response Associated with diverse disorders Infection Trauma Shock Pancreatitis Ischemia Most frequently associated with sepsis

21. 21 Types of shocks Hypovolemic shock – Hemorrhagic shock Cardiogenic shock Distributive shock Neurogenic shock Anaphylactic shock Septic shock -Obstructive Shock

22. 22 Hypovolemic shock Hypovolemic shock is a result of inadequate circulating blood volume, The extracellular body fluid is found in one of two compartments: intravascular (inside blood vessels) or interstitial (surrounding tissues). Hypovolemic shock occurs when there is a reduction in intravascular volume by 15% to 30%, which represents a loss of 750 to 1500 mL of blood in a 70-kg person

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25. 25 Assessment History or active bleeding ABG’s Lactate Levels CBC (Hb, HCT) Coagulation profile

26. Medical Management Treatment of the Underlying Cause Hemorrhaging, efforts are made to stop the bleeding. This may involve applying pressure to the bleeding site or surgical interventions. If the cause of the hypovolemia is diarrhea or vomiting, medications to treat diarrhea and vomiting 26

27. Medical Management Fluid and Blood Replacement Large bore IV access or central Venous access Fluid replacement Sodium chloride 0.9% infusion Ringer lactate infusions Plasma Expanders Blood transfusion Antibiotic therapy Pharmacologic Therapy 9/21/2 – 17 V asoactive m e C d o p i y r c i g i h t n © e 2 s 1 7 , b y a T n a n z t e i e l e U m l R a e h m t a i n c ' s, anti d iarr h e a l 34

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29. 29 Cardiogenic Shock Definition: Cardiogenic shock, which results from loss of contractility of the heart, is an extreme form of heart failure.

30. 30 Causes of Cardiogenic Shock Either coronary or non coronary. Left ventricular damage from myocardial infarction Papillary muscle rupture Ventricular septal rupture Cardiomyopathy Cardiac tamponade Acute myocarditis Valvular disease Dysrrhythmias

31. Cardiogenic Shock Pathophysiology 31

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33. 33 Medical Management of Cardiogenic Shock Correction of Underlying Causes Initiation of First-Line Treatment Oxygenation Pain Control Hemodynamic Monitoring Laboratory Marker Monitoring Fluid Therapy A fluid bolus should never be given rapidly, because rapid fluid administration in patients with cardiac failure may result in acute pulmonary edema.

34. 34 Distributive shock or Circulatory shock The mechanism underlying all distributive shock states is vasodilation that causes pools in peripheral blood vessels. Neurogenic shock :- Vasodilation results from a loss of sympathetic innervation to the blood vessels. Anaphylactic shock and septic shock , vasodilation results from the presence of vasodilating substances in the blood.

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37. 37 Neurogenic Shock Neurogenic shock results from loss or disruption of sympathetic tone, most often due to severe cervical or upper thoracic spinal cord injury.

38. 38 Clinical manifestations hypotension with bradycardia, rather than the tachycardia dry, warm skin rather than the cool, moist skin seen in hypovolemic shock.

39. 39 Anaphylactic shock Anaphylaxis is an allergic reaction to a specific allergen that evokes a life-threatening hypersensitivity response. Anaphylaxis may be either immunoglobulin E (IgE)– or non–IgE mediated.

40. 40 Pathophysio of Anaphylaxis The antibody–antigen reaction causes the white blood cells (WBCs) to secrete chemical mediators that cause Systemic vasodilation rapid onset of hypotension Increased capillary permeability Bronchoconstriction Coronary vasoconstriction Urticaria (hives). cardiac

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42. Medical Management Removing the causative antigen IV access Telemetry continuously Oxygen therapy if indicated Corticosteroids ( Solucortif = hydrocortisone) Antihistamines (Avil = Phenarimine injection) Intubation or mechanical ventilation Inotropes 57

43. 43 Nursing Management Monitor the patient’s response to the treatment. Providing c a r e t o rel i e v e dermato l o g ical manifestations. Ev a l u a t ed f or a l le r g i es and fu t ure r isk f or anaphylaxis.

44. Septic Shock Septic shock , the most common type of circulatory shock, is caused by widespread infection 44

45. 45 Obstructive Shock Physical impairment to adequate circulatory blood flow Causes Clinical manifestations Chest pain Dyspnea Jugular venous distension Hypoxia Cause-dependent findings

46. Obstructive Shock (Cont.) Figure 12-9. Obstructive shock 46

47. 47 Management of Obstructive Shock Treat the cause Cardiac tamponade (pericardiocentesis) Tension pneumothorax (thoracentesis)

48. 48 Multiple Organ Dysfunction Syndrome (MODS) Multiple organ dysfunction syndrome (MODS) is altered organ function in acutely ill patients that requires medical intervention to support continued organ function. It is another phase in the progression of shock states.

49. 49 Multiple Organ Dysfunction Syndrome (MODS) Pulmonary dysfunction. Renal dysfunction Liver dysfunction Cardiovascular dysfunction Hematologic dysfunction. Neurologic dysfunction

50. 50 Multiple Organ Dysfunction Syndrome (Cont.) Clinical manifestations Tachypnea/hypoxemia Petechiae/bleeding Jaundice Abdominal distension Oliguria  anuria Tachycardia Hypotension Change in level of consciousness

51. 51 Multiple Organ Dysfunction Syndrome (Cont.) Management Control infection Antibiotics Provide adequate tissue oxygenation Maintain 88% to 92% arterial oxygen saturation Maintain hemoglobin above 7 to 9 g/dL Restore intravascular volume Aggressive fluid resuscitation Isotonic crystalloids Support organ function

52. 52 Shock, Sepsis, and MODS Patient outcomes Improved tissue perfusion Alert, oriented Normotensive Warm, dry skin Adequate urine output Normal hemodynamics Lab values within normal limits Absence of infection Intact skin

53. 53 References Smeltzer, S.C.C., Bare, B.G., Hinkle, J.L. and Cheever, K.H. eds., 2010. Brunner & Suddarth's textbook of medical- surgical nursing (Vol. 1). Lippincott Williams & Wilkins. Grossman, S., Porth, C.M., Conelius, J., Gerard, S.O., Moriber, N., O'Shea, E.R. and Wheeler, K., 2014. Porth's pathophysiology: Concepts of altered health states. Re f e r e n c e : Mo r ton, Esse n ti a ls of cri t i c al ca r e n ursi n g : W ol t ers P . G ., & Fontai n e, D . K. ( 201 3 ) . Kl u wer Health/Lippincott Williams & Wilkins. Sole, M.L., Klein, D.G., Moseley, M.J., Brenner, Z.R. and Powers, J., 2009. Introduction to critical care nursing. 5th Edition St. Louis, Mo.: Saunders,