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

2. Shock- Summary- 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- Maldistribution of 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)
Ventricular assist device
Transplant (rarely)

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

10. IABP

11. 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

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

13. 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

14. Hypovolemic Shock

15. 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

16. 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

17. Neurogenic Shock-
Hemodynamic phenomenon occuring after spinal injury at T6 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

18. Neurogenic Shock

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

20. 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

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

22. 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

23. 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

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

25. 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

26. From Seton. Educational use only.

27. 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

28. Septic Shock

29. 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

30. 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

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

32. From Seton. Educational use only.

33. 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

34. 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

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

36. 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

37. Compensatory Stage of Shock

38. 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

39. Progressive Stage of Shock

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

41. Refractory- Irreversible Stage of Shock

42. 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

43. 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

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

45. 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

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

47. 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

48. 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

49. Systemic Inflammatory Response Syndrome (SIRS)
Systemic Inflammatory Response Syndrome (SIRS)- a systemic inflammatory response to a variety of insults, including infection, ischemia, infarction, and injury
Characterized by generalized inflammation of organs
Two or more of the following conditions: temperature >38.5°C (101.3 F) or <36.0°C (96.8 F); heart rate of >90 beats/min; respiratory rate of >20 breaths/min or PaCO2 of <32 mm Hg; and WBC count of >12,000 cells/mL, <4000 cells/mL, or >10 percent immature (band) forms

50. Multiple Organ Dysfunction Syndrome (MODS)
Results from SIRS
Characterized by failure of two or more organ systems such that homeostasis can not be obtained without intervention
Often culminates in ARDS
Can cause massive vasodilation and myocardial depression
Commonly manifests as changes in LOC
Acute renal failure common

51. GI tract highly vulnerable to ischemic injury secondary to shunting in early stages
At risk for ulceration and GI bleeding
Potential for bacterial translocation from GI tract to cirulation
Causes hypermetabolic state

52. Failure of coagulation system manifests as DIC
Electrolyte changes and fluid shifts
Identifying organ dysfunction video

53. Peripheral circulation Central venous pressure
A patient with a gunshot wound to the abdomen is being treated for hypovolemic and septic shock. To monitor the patient for early organ damage associated with MODS, it is most important for the nurse to assess:
Urine output
Lung sounds
Peripheral circulation
Central venous pressure

54. The development of MODS is confirmed in a patient who manifests:
Urine output of 30 ml/hr, a BUN of 65 mg/dl, and a WBC of 1120/ul
Upper GI bleeding, GCS score of 7, and a Hct of 25%
RR of 45/min, PaCO2 of 60, and a chest x-ray with bilateral patchy infiltrates
An elevated serum amylase and lipase, serum creatinine of 3.8 mg/dl, and a platelet count of 15,000/ul

56. Management of SIRS and MODS
Prognosis with MODS poor
Vigilant assessment
Prevent infection, maintain tissue oxygenation, nutritional and metabolic support, support individual failing organs

57. Pt was treated with TPA 8 months ago
At 9pm, you admit a 63 year-old with a diagnosis of acute myocardial infraction to the ED. The physician is considering the use of fibrinolytic therapy with tissue plasminogen activator (tPA, alteplase (Activase)). Which information is most important to communicate to the physician?
Pt was treated with TPA 8 months ago
Pt takes coumadin for A-fib. The INR is 1.0 today
Pt has T-Wave inversions on ECG
Chest pain has been continuous since for 38 hours

58. Note:
Questions are from Prioritization, Delegation, and Assignment (LaCharity, Kumagai, and Bartz)

59. The End!