Module 15A- Shock!

1. Module 15A- Shock! John Nation, RN, MSN From the notes of Nancy Jenkins, RN, MSN

2. Shock- Summary- • Lewis p. 1772-1798, 1738-1746 • Types of Shock • Stages of Shock • Management of Shock • Nursing Interventions • Systemic Inflammatory Response Syndrome (SIRS) • Multiple Organ Dysfunction Syndrome (MODS)

3. Shock Defined Shock- Clinical syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply and demand for oxygen and nutrients • Put simply, not enough oxygen and not enough nutrients for body

4. Types of Shock- Low blood flow- • Cardiogenic shock • Hypovolemic shock Maldistribution of blood flow- • Neurogenic shock • Anaphylactic shock • Septic shock

5. Etiology and Pathophysiology Cardiogenic shock- • Occurs when systolic or diastolic dysfunction of the pumping of the heart causes decreased cardiac output • Cardiac output= stroke volume x heart rate • Causes include myocardial infarction, cardiomyopathy, blunt cardiac injury (trauma), severe systemic or pulmonary hypertension, cardiac tamponade, arrhythmias, valvular defects,and myocardial depression from metabolic problems.

6. Cardiogenic Shock

7. Cardiogenic Shock (Cont’d) Clinical Manifestations: • Tachycardia • Hypotension • Narrowed pulse pressure • Tachypnea • Pulmonary congestion • Cyanosis • Cool, clammy skin • Confusion/ agitation • Decreased capillary refill time

8. Cardiogenic Shock (Cont’d) Treatment- • Restore blood flow to myocardium- early PCI! • Thromboyltic therapy, angioplasty, stenting, emergency revasularization, valve replacement • Hemodynamic monitoring PAWP • Intraaortic balloon pump (IABP) 50. IABP • Ventricular assist device VAD video • Transplant (rarely)

9. Cardiogenic Shock (Cont’d) Treatment (Cont’d) • Medications: aspirin, heparin, dopamine, norepiniphrine, diuretics, vasodilators

10. PAWP Monitoring

11. IABP

12. Cardiogenic Shock (Cont’d) • Mortaliaty rate of 80-90% when caused by acute MI • Prior MI, increasing age, and oliguria are associated with worsening outcomes

13. Hypovolemic Shock- • Loss of intravascular fluid volume • Volume inadequate to fill the vascular space • Categorized as absolute or relative hypovolemia

14. Hypvolemic Shock (Cont’d) Absolute hypovolemia- • Results from fluid loss via hemorrhage, gastrointesinal (GI) loss (vomiting, diarrhea), fistula drainage, diabetes insipidus, hyperglycemia, or diuresis Relative hypovolemia- • Results from fluid moving out of the vascular space and into the extravascular space- aka third spacing

15. Hypovolemic Shock

16. Hypovolemic Shock (Cont’d) Clinical Manifestations- • Depend on extent of injury, age, general health status • Decrease in venous return, preload, stroke volume, and cardiac output • Increase in heart rate, increase in respiratory rate • Decrease in stroke volume, pulmonary artery wedge pressure, and urine output

17. Hypovolemic Shock (Cont’d) Treatment- • Stop source of fluid loss • Restore circulating volume • 3:1 rule- 3 ml of isotonic crystalloid for every 1 ml of estimated blood loss

18. Neurogenic Shock- • Hemodynamic phenomenon occuring after spinal injury at T5 or above • Usually within 30 minutes of injury, can last up to 6 weeks • Causes massive vasodilation without compensation secondary to the loss of sympathetic nervous system vasoconstrictor tone • Can also be caused by spinal anesthesia

19. Neurogenic Shock

20. Neurogenic Shock (Cont’d) Clinical manifestations- • Bradycardia (from unopposed parasympathetic stimulation) • Hypotension (from massive vasodilation) • Hypothermia (due to heat loss)

21. Neurogenic Shock (Cont’d) Early Signs- • Blood pools in venous and capillary beds • Skin warm and pink • Pulse slow and bounding • Decreased BP • Decreased temperature • Decreased MAP

22. Neurogenic (Cont’d) Late Signs- • Skin pale and cool

23. Neurogenic Shock (Cont’d) Treatment- • Depends on the cause • If spinal cord injury, promote spinal stability • Vasopressors and atropine for hypotension and bradycardia (respectively) • Fluids administered cautiously • Monitor for hypothermia

24. Anaphylactic Shock • Acute and life-threatening allergic reaction (hypersensitivity) reaction • Can be caused by drugs, chemicals, vaccines, food insect venom • Causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability • Fluid shift from the vascular space to the interstitial space • Respiratory distress secondary to laryngeal edema, severe bronchospasm, or circulatory failure from vasodilation

25. Anaphylactic Shock (Cont’d) Clinical Manifestations- • Anxiety, confusion • Dizziness • Chest pain • Incontinence • Swelling of lip and tongue • Wheezing, stridor • Flushing, pruritus, and uticaria • angioedema

26. Anaphylactic Shock (Cont’d) Treatment- • Epinephrine is the drug of choice • Diphenhydramine used to block massive release of histamine • Maintain patent airway • Nebulized bronchodilators (albuterol) • Intubation or cricothyroidotomy may be needed • Fluid replacement, primarily with colloids • corticosteroids

27. From Seton. Educational use only.

28. Septic Shock Septic shock- Presence of sepsis with hypotension, despite fluid resuscitation, with decreased tissue perfusion Sepsis- systemic inflammatory response to an infection • Over 750,000 clients diagnosed with severe sepsis annually and 28% to 50% die

29. Septic Shock

30. Septic Shock (Cont’d) Course- • Septicemia (initially bacteremia) causes inflammatory cascade • Commonly caused by gram negative bacteria • If gram positive infection (Staphylococcus and streptococcus), up to 50% mortality rate

31. Septic Shock (Cont’d) Clinical Manifestations- • Increased or decreased temperature • Biventricular dilations causing decreased ejection fraction • Hyperventilation, respiratory alkalosis, respiratory acidosis, crackles, ARDS • Decreased urine output • Skin warm and flushed, then cool and clammy • Altered LOC • Paralytic ileus, GI bleeding •  & WBC,  platelets,  lactate,  glucose,  urine specific gravity,  urine Na, positive blood cultures

32. Septic Shock (Cont’d) Treatment- • Large amounts of fluid replacement • Vasopressor drug therapy • Corticosteroids • Antibiotics • Drotrecogin alpha (Xigris) • Glucose less than 150 • Stress ulcer prophylaxis with H2- receptor blockers and DVT prophylaxis

33. From Seton. Educational use only.

34. Diagnostic Tests • RBC, hemoglobin, hematocrit • Arterial blood gases • Blood cultures • Cardiac enzymes (cardiogenic shock) • Glucose • DIC (Disseminated Intravascular Coagulation) screen: FSP, fibrogen level, platelet count, PTT and PT/INR, and D-dimer • Lactic Acid • Liver enzymes- ALT, AST, GGT

35. Diagnostic Tests (Cont’d) Electrolytes- • Sodium level increased early, decreased later if hypotonic fluid administered • Potassium decreased, then increased later with cellular breakdown and renal failure

36. Common Nursing Diagnoses • Decreased cardiac output • Altered tissue perfusion • Fluid volume deficit • Anxiety • Fear

37. LVAD implantation (23 minutes into clip)

38. Stages of Shock Compensatory Shock- •  Mean Arterial Pressure (MAP) •  blood pressure •  cardiac output • Sympathetic nervous system (SNS) stimulation causes vasoconstriction. Blood flow to heart and brain maintained, while blood flow to the kidneys, GI tract, skin, and lungs is diverted • Decreased blood flow to kidneys causes activation of renin-angiotensin system, leading to sodium retention and potassium excretion • In this stage the body is able to compensate for changes in tissue perfusion

39. Compensatory Stage of Shock

40. Progressive Shock • Altered capillary permeability (3rd spacing) • Alveolar and pulmonary edema, ARDS,  PA pressures •  cardiac output,  coronary perfusion, can cause arrhythmias and MI • Acute tubular necrosis • Jaundice,  ALT,AST GGT • DIC • Cold, clammy skin

41. Progressive Stage of Shock

42. Refractory Stage • Anaerobic metabolism- lactic acid build-up • Increased capillary blood leak • Profound hypotension, inadequate to perfuse vital organs • Respiratory failure • Anuria • DIC • hypothermia

43. Refractory Stage of Shock

44. Collaborative Care Successful management involves: • Identifying at risk clients • Integration of client’s medical history, assessment findings to establish diagnosis • Interventions to address cause of decreased perfusion • Protection of organs • Multisystem supportive care

45. Collaborative Management (Cont’d) • Start with ABCs! Ensure patent airway and oxygen delivery • Volume expansion and fluid administration cornerstone of treatment of septic, hypovolemic, and anaphylactic shock • Primary goal of therapy is correction of decreased tissue perfusion • Hemodynamic monitoring, drug therapy, circulatory assist

46. Nursing Implementation Health Promotion- • Identify at risk clients • Prevent shock (monitoring fluid balance, good hand washing to prevent infection, community education and health promotion)

47. Interventions (Acute) • Assess neurologic status- check LOC every hour or more often • Monitor heart rate/ rhythm, BP, central venous pressure, pulmonary artery pressure, cardiac output • Trendelenburg position not supported by research and may compromise pulmonary function and increase ICP • Monitor EKG for dysrhythmias, S3 or S4 heart sounds

48. Interventions Assessment (Respiratory)- • Respiratory rate and effort • Pulse oximetry • ABGs for acid/base balance • Intubation/ ventilation

49. Assessment- • Hourly urine output • If less than 0.5 ml/kg/hour, may indicate inadequate kidney perfusion • BUN and creatinine • Temperature • Capillary refill • Monitor skin for pallor, flushing, cyanosis, diaphoresis, piloerection

50. Assessment (Cont’d)- • Check bowel sounds • If NG tube present, check drainage for blood • Passive ROM and oral care • Talk with client, even if sedated or intubated