Module 15- Shock!

1. Module 15- 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) • Critical Care

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

6. Cardiogenic Shock (cont’d) • Causes include: • myocardial infarction • cardiomyopathy • blunt cardiac injury (trauma) • severe systemic or pulmonary hypertension • cardiac tamponade • arrhythmias • valvular defects • myocardial depression from metabolic problems.

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

8. Cardiogenic Shock (Cont’d) Laboratory/ Diagnostic Studies: • Cardiac enzymes (troponin levels) • B-type natriuretic peptide (BNP) • ECG • Chest X-Ray • Echocardiogram • Heart Cathetarization (left, right or both)

9. Cardiogenic Shock (Cont’d) • Initially, what clinical condition does this sound similar to?

10. 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)

11. Cardiogenic Shock (Cont’d) Treatment (Cont’d) • Medications (depends on cause): • Aspirin • heparin • Dopamine • Norepiniphrine • dobutamine • Diuretics • Vasodilators • Amiodarone

12. PAWP Monitoring

13. IABP

14. 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

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

16. 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

17. Hypovolemic Shock (Cont’d) Causes: • Bleeding • Vomiting • Diarrhea • Diabetes insipidus • Diuresis • Third spacing

18. 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

19. Hypovolemic Shock Clinical Manifestations (Cont’d): • Decrease in stroke volume, pulmonary artery wedge pressure, and central venous pressure • Decrease in urine output, absent bowel sounds, cool, clammy skin • Anxiety, confusion, agitation

20. Hypovolemic Shock (Cont’d) Lab/ Diagnostic Tests: • Find the source of blood loss • CT, ultrasound, surgery • CBC, electrolytes, blood gases, lactate level • SpO2 • Hourly urine output monitoring

21. 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

22. Hypovolemic Shock • What is often the priority in the treatment of hypovolemic shock? • How might you recognize the development of hypovolemic shock? • What would you do about it?

23. 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

24. Neurogenic Shock (Cont’d) Clinical manifestations- • Bradycardia (from unopposed parasympathetic stimulation) • Hypotension (from massive vasodilation) • Hypothermia (due to heat loss) • Initially, skin may be warm due to vasodilation • Later, skin may be cool, depending on ambient temperature

25. Neurogenic Shock (Cont’d) Clinical Manifestations (Cont’d) • Bladder dysfunction • Paralysis below level of lesion • Bowel dysfunction

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

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

28. 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

29. 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

30. Anaphylactic Shock (Cont’d) • Fluid shift from the vascular space to the interstitial space • Respiratory distress secondary to laryngeal edema, severe bronchospasm, or circulatory failure from vasodilation

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

32. 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 (video) be needed • Fluid replacement, primarily with colloids • corticosteroids

33. From Seton. Educational use only.

34. Anaphylactic Shock • What are you worried about with a medication reaction? • What are you watching for?

35. 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

36. 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

37. Septic Shock Patho: • Invading microorganisms result in massive inflammatory response: • Causes endothelial damage, microemboli, vasodilation, increased capillary permeability, platelet aggregation, myocardial depression

38. 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

39. Septic Shock (Cont’d) Treatment- • Large amounts of fluid replacement • Vasopressor drug therapy • Corticosteroids • Antibiotics • Drotrecogin alpha (Xigris) (no longer used) • Glucose less than 150 • Stress ulcer prophylaxis with H2- receptor blockers and DVT prophylaxis

40. From Seton. Educational use only.

41. Obstructive Shock • Physical obstruction to blood flow • Causes: • Cardiac tamponade, tension pneumothorax, PE, left ventricular thrombi • Decreased cardiac output, increased afterload • Fix the underlying problem is primary treatment

42. Common Diagnostic Tests • CBC • BMP • Arterial blood gases • Blood cultures • Cardiac enzymes (cardiogenic shock) • Glucose

43. Common Diagnostic Tests (Cont’d) • DIC (Disseminated Intravascular Coagulation) screen: FSP, fibrogen level, platelet count, PTT and PT/INR, and D-dimer • Lactic Acid • Liver enzymes- ALT, AST, GGT

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

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

46. LVAD implantation (23 minutes into clip)

47. Stages of Shock Compensatory Shock- •  Mean Arterial Pressure (MAP) •  blood pressure (but adequate to perfuse vital organs) •  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

48. 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

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

50. 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