Shock Presentation Definition, etiology, types and management

This is a presentation on shock, it's different types ,causes and management

1. SHOCK MANAGEMENT
PRESENTATION
BY
DR AMINU BELLO
DIRECTOR SCHOOL OF
NURSING KATSINA

2. Shock
•Syndrome characterized by decreased tissue
perfusion and impaired cellular metabolism
–Imbalance in supply/demand for O2 and nutrients

3. Shock (Cont’d)
•Classification of shock
–Low blood flow
•Cardiogenic
•Hypovolemic
–Maldistribution of blood flow
•Septic
•Anaphylactic
•Neurogenic

4. Low Blood Flow
Carcinogenic Shock
•Definition
–Systolic or diastolic dysfunction
–Compromised cardiac output (CO)

5. Low Blood Flow
Cardiogenic Shock (Cont’d)
•Precipitating causes
–Myocardial infarction
–Cardiomyopathy
–Blunt cardiac injury
–Severe systemic or pulmonary hypertension
–Cardiac tamponade (Obstructive)
–Myocardial depression from metabolic problems

6. Pathophysiology of Cardiogenic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

7. Low Blood Flow
Cardiogenic Shock
•Early manifestations
–Tachycardia
–Hypotension
–Narrowed pulse pressure
–↑ Myocardial O2 consumption

8. Low Blood Flow
Cardiogenic Shock (Cont’d)
•Physical examination
–Tachypnea, pulmonary congestion
–Pallor; cool, clammy skin
–Decreased capillary refill time
–Anxiety, confusion, agitation
•↑ in pulmonary artery wedge pressure
•Decreased renal perfusion and UO

9. Low Blood Flow
Hypovolemic Shock
•Absolute hypovolemia: Loss of intravascular
fluid volume
–Hemorrhage
–GI loss (e.g., vomiting, diarrhea)
–Fistula drainage
–Diabetes insipidus
–Hyperglycemia
–Diuresis

10. Low Blood Flow
Hypovolemic Shock (Cont’d)
•Relative hypovolemia
–Results when fluid volume moves out of the
vascular space into extravascular space (e.g.,
interstitial or intracavitary space)
–Termed third spacing

11. Pathophysiology of Hypovolemic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

12. Low Blood Flow
Hypovolemic Shock
•Response to acute volume loss depends on
–Extent of injury or insult
–Age
–General state of health

13. Low Blood Flow
Hypovolemic Shock (Cont’d)
•Clinical manifestations
–Anxiety
–Tachypnea
–Increase in CO, heart rate
–Decrease in stroke volume, PAWP, UO
•If loss is >30%, blood volume is replaced

14. Maldistribution of Blood Flow
Neurogenic Shock
•Hemodynamic phenomenon that can occur
within 30 minutes of a spinal cord injury at the
fifth thoracic (T5) vertebra or above and can
last up to 6 weeks
•Results in massive vasodilation leading to
pooling of blood in vessels

15. Pathophysiology of Neurogenic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

16. Maldistribution of Blood Flow
Neurogenic Shock (Cont’d)
•Clinical manifestations
–Hypotension
–Bradycardia
–Temperature dysregulation (resulting in heat loss)
–Dry skin
–Poikilothermia (taking on the temperature of the
environment)

17. Maldistribution of Blood Flow
Anaphylactic Shock
•Acute, life-threatening hypersensitivity
reaction
–Massive vasodilation
–Release of mediators
–↑ Capillary permeability

18. Maldistribution of Blood Flow
Anaphylactic Shock (Cont’d)
•Clinical manifestations
–Anxiety, confusion, dizziness
–Tachycardia, tachypnea, hypotension
–Wheezing, stridor
–Sense of impending doom
–Chest pain

19. Maldistribution of Blood Flow
Anaphylactic Shock (Cont’d)
•Clinical manifestations
–Swelling of the lips and tongue, angioedema
–Wheezing, stridor
–Flushing, pruritus, urticaria
–Respiratory distress and circulatory failure

20. Maldistribution of Blood Flow
Septic Shock
•Sepsis: Systemic inflammatory response to
documented or suspected infection
•Severe sepsis = Sepsis + Organ dysfunction

21. Maldistribution of Blood Flow
Septic Shock (Cont’d)
•Septic shock = Presence of sepsis with
hypotension despite fluid resuscitation +
Presence of tissue perfusion abnormalities

22. Maldistribution of Blood Flow
Septic Shock (Cont’d)
•Mortality rates as high as 50%
•Primary causative organisms
–Gram-negative and gram-positive bacteria
–Endotoxin stimulates inflammatory response

23. Pathophysiology of Septic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

24. Maldistribution of Blood Flow
Septic Shock
•Clinical manifestations
–↑ Coagulation and inflammation
–↓ Fibrinolysis
•Formation of microthrombi
•Obstruction of microvasculature
–Hyperdynamic state: Increased CO and decreased
SVR

25. Maldistribution of Blood Flow
Septic Shock (Cont’d)
•Clinical manifestations
–Tachypnea/hyperventilation
–Temperature dysregulation
–↓ Urine output
–Altered neurologic status
–GI dysfunction
–Respiratory failure is common

26. Stages of Shock
Initial Stage
•Usually not clinically apparent
•Metabolism changes from aerobic to
anaerobic
–Lactic acid accumulates and must be removed by
blood and broken down by liver
–Process requires unavailable O2

27. Stages of Shock
Compensatory Stage (Nonprogressive)
•Clinically apparent
–Neural
–Hormonal
–Biochemical compensatory mechanisms
•Attempts are aimed at overcoming
consequences of anaerobic metabolism and
maintaining homeostasis

28. Stages of Shock
Compensatory Stage (Nonprogressive)
•Baroreceptors in carotid and aortic bodies
activate SNS in response to ↓ BP
–Vasoconstriction while blood to vital organs
maintained
•↓ Blood to kidneys activates renin–
angiotensin system
–↑ Venous return to heart, CO, BP

29. Compensatory(Nonprogressive) Stage of
Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

30. Stages of Shock
Compensatory Stage (Nonprogressive Cont’d)
•If perfusion deficit corrected, patient recovers
with no residual sequelae
•If deficit not corrected, patient enters
progressive stage

31. Stages of Shock
Progressive Stage (intermediate)
•Begins when compensatory mechanisms fail
•Aggressive interventions to prevent multiple
organ dysfunction syndrome

32. Progressive (intermediate)Stage of Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

33. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Hallmarks of ↓ cellular perfusion and altered
capillary permeability:
•Leakage of protein into interstitial space
•↑ Systemic interstitial edema

34. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Anasarca (severe generalized edema)
•Fluid leakage affects solid organs and peripheral tissues
•↓ Blood flow to pulmonary capillaries

35. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Movement of fluid from pulmonary
vasculature to interstitium
•Pulmonary edema
•Bronchoconstriction
•↓ Residual capacity

36. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Fluid moves into alveoli
•Edema
•Decreased surfactant
•Worsening V/Q mismatch
•Tachypnea
•Crackles
•Increased work of breathing

37. Stages of Shock
Progressive Stage (intermediate Cont’d)
•CO begins to fall
•Decreased peripheral perfusion
•Hypotension
•Weak peripheral pulses
•Ischemia of distal extremities

38. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Myocardial dysfunction results in
•Dysrhythmias
•Ischemia
•Myocardial infarction
•End result: Complete deterioration of cardiovascular
system

39. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Mucosal barrier of GI system becomes
ischemic
•Ulcers
•Bleeding
•Risk of translocation of bacteria
•Decreased ability to absorb nutrients

40. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Liver fails to metabolize drugs and wastes
•Jaundice
•Elevated enzymes
•Loss of immune function
•Risk for DIC and significant bleeding

41. Stages of Shock
Progressive Stage (intermediate Cont’d)
•Acute tubular necrosis/acute renal failure

42. Stages of Shock
Refractory Stage (Irreversible)
•Exacerbation of anaerobic metabolism
•Accumulation of lactic acid
•↑ Capillary permeability

43. Stages of Shock
Refractory Stage
•Profound hypotension and hypoxemia
•Tachycardia worsens
•Decreased coronary blood flow
•Cerebral ischemia

44. Stages of Shock
Refractory Stage (Cont’d)
•Failure of one organ system affects others
•Recovery unlikely

45. Diagnostic Studies
•Through history and physical examination
•No single study to determine shock
–Blood studies
•Elevation of lactate
•Base deficit
–12-lead ECG
–Chest x-ray
–Hemodynamic monitoring

46. Collaborative Care
•Successful management includes
–Identification of patients at risk for shock
–Integration of the patient’s history, physical
examination, and clinical findings to establish a
diagnosis

47. Collaborative Care (Cont’d)
•Successful management includes
–Interventions to control or eliminate the cause of
the decreased perfusion
–Protection of target and distal organs from
dysfunction
–Provision of multisystem supportive care

48. Collaborative Care (Cont’d)
•General management strategies
–Ensure patent airway
–Maximize oxygen delivery

49. Collaborative Care (Cont’d)
•Cornerstone of therapy for septic,
hypovolemic, and anaphylactic shock =
volume expansion
–Isotonic crystalloids (e.g., normal saline) for initial
resuscitation of shock

50. Collaborative Care (Cont’d)
•Volume expansion
–If the patient does not respond to 2 to 3 L of
crystalloids, blood administration and central
venous monitoring may be instituted
•Complications of fluid resuscitation
–Hypothermia
–Coagulopathy

51. Collaborative Care (Cont’d)
•Primary goal of drug therapy = correction of
decreased tissue perfusion
–Vasopressor drugs (e.g., epinephrine)
•Achieve/maintain MAP >60 to 65 mm Hg
•Reserved for patients unresponsive to other therapies

52. Collaborative Care (Cont’d)
•Primary goal of drug therapy = correction of
decreased tissue perfusion
–Vasodilator therapy (e.g., nitroglycerin
[cardiogenic shock], nitroprusside [noncardiogenic
shock])
•Achieve/maintain MAP >60 to 65 mm Hg

53. Collaborative Care (Cont’d)
•Nutrition is vital to decreasing morbidity from
shock
–Initiate enteral nutrition within the first 24 hours

54. Collaborative Care (Cont’d)
•Nutrition is vital to decreasing morbidity from
shock
–Initiate parenteral nutrition if enteral feedings
contraindicated or fail to meet at least 80% of the
caloric requirements
–Monitor protein, nitrogen balance, BUN, glucose,
electrolytes

55. Collaborative Care
Cardiogenic Shock
•Restore blood flow to the myocardium by
restoring the balance between O2 supply and
demand
•Thrombolytic therapy
•Angioplasty with stenting
•Emergency revascularization
•Valve replacement

56. Collaborative Care
Cardiogenic Shock (Cont’d)
•Hemodynamic monitoring
•Drug therapy (e.g., diuretics to reduce
preload)
•Circulatory assist devices (e.g., intra-aortic
balloon pump, ventricular assist device)

57. Collaborative Care
Hypovolemic Shock
•Management focuses on stopping the loss of
fluid and restoring the circulating volume
•Fluid replacement is calculated using a 3:1
rule (3 ml of isotonic crystalloid for every 1 ml
of estimated blood loss)

58. Collaborative Care
Septic Shock
•Fluid replacement (e.g., 6 to 10 L of isotonic
crystalloids and 2 to 4 L of colloids) to restore
perfusion
•Hemodynamic monitoring
•Vasopressor drug therapy; vasopressin for
patients refractory to vasopressor therapy

59. Collaborative Care
Septic Shock (Cont’d)
•Intravenous corticosteroids for patients who
require vasopressor therapy, despite fluid
resuscitation, to maintain adequate BP

60. Collaborative Care
Septic Shock (Cont’d)
•Antibiotics after obtaining cultures
(e.g., blood, wound exudate, urine, stool,
sputum)
•Drotrecogin alfa (Xigris)
–Major side effect: Bleeding

61. Collaborative Care
Septic Shock (Cont’d)
•Glucose levels <150 mg/dl
•Stress ulcer prophylaxis with histamine (H2)-
receptor blockers
•Deep vein thrombosis prophylaxis with low-
dose unfractionated heparin or low-
molecular-weight heparin

62. Collaborative Care
Neurogenic Shock
•In spinal cord injury: Spinal stability
–Treatment of the hypotension and bradycardia
with vasopressors and atropine
–Fluids used cautiously as hypotension is generally
not related to fluid loss
–Monitor for hypothermia

63. Collaborative Care
Anaphylactic Shock
•Epinephrine, diphenhydramine
•Maintaining a patent airway
•Nebulized bronchodilators
•Endotracheal intubation or cricothyroidotomy may be
necessary

64. Collaborative Care
Anaphylactic Shock (Cont’d)
•Aggressive fluid replacement
•Intravenous corticosteroids if significant
hypotension persists after 1 to 2 hours of
aggressive therapy

65. Nursing Assessment (Cont’d)
•ABCs: Airway, breathing, and circulation
•Focused assessment of tissue perfusion
–Vital signs
–Peripheral pulses
–Level of consciousness
–Capillary refill
–Skin (e.g., temperature, color, moisture)
–Urine output

66. Nursing Assessment (Cont’d)
•Brief history
–Events leading to shock
–Onset and duration of symptoms
•Details of care received before hospitalization
•Allergies
•Vaccinations

67. Nursing Diagnoses
•Ineffective tissue perfusion: Renal, cerebral,
cardiopulmonary, gastrointestinal, hepatic,
and peripheral
•Fear
•Potential complication: Organ
ischemia/dysfunction

68. Planning
•Goals for patient
–Assurance of adequate tissue perfusion
–Restoration of normal or baseline BP
–Return/recovery of organ function
–Avoidance of complications from prolonged states
of hypoperfusion

69. Nursing Implementation
•Health Promotion
–Identify patients at risk (e.g., elderly patients,
those with debilitating illnesses or who are
immunocompromised, surgical or accidental
trauma patients)

70. Nursing Implementation (Cont’d)
•Health Promotion
–Planning to prevent shock
(e.g., monitoring fluid balance to prevent
hypovolemic shock, maintenance of handwashing
to prevent spread of infection)

71. Nursing Implementation (Cont’d)
•Acute Interventions
–Monitor the patient’s ongoing physical and
emotional status to detect subtle changes in the
patient’s condition
–Plan and implement nursing interventions and
therapy

72. Nursing Implementation (Cont’d)
•Acute Interventions
–Evaluate the patient’s response to therapy
–Provide emotional support to the patient and
family
–Collaborate with other members of the health
team when warranted

73. Nursing Implementation (Cont’d)
•Neurologic status: Orientation and level of
consciousness
•Cardiac status
–Continuous ECG
–VS, capillary refill
–Hemodynamic parameters: central venous
pressure, PA pressures, CO, PAWP
–Heart sounds: Murmurs, S3, S4

74. Nursing Implementation (Cont’d)
•Respiratory status
–Respiratory rate and rhythm
–Breath sounds
–Continuous pulse oximetry
–Arterial blood gases
–Most patients will be intubated and mechanically
ventilated

75. Nursing Implementation (Cont’d)
•Urine output
•Tympanic or pulmonary arterial temperature
•Skin: Temperature, pallor, flushing, cyanosis,
diaphoresis, piloerection
•Bowel sounds

76. Nursing Implementation (Cont’d)
•Nasogastric drainage/stools for occult blood
•I&O, fluid and electrolyte balance
•Oral care/hygiene based on O2 requirements
•Passive/active range of motion

77. Nursing Implementation (Cont’d)
•Assess level of anxiety and fear
–Medication PRN
–Talk to patient
–Visit from clergy
–Family involvement
–Comfort measures
–Privacy
–Call light within reach

78. Evaluation
•Normal or baseline, ECG, BP, CVP, and PAWP
•Normal temperature
•Warm, dry skin
•Urinary output >0.5 ml/kg/hr
•Normal RR and SaO2 ≥90%
•Verbalization of fears, anxiety

79. THANK YOU VERY MUCH FOR
YOUR ATTENTION.