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Shock
W.Pawliuk MPH MSHEd RN CEN
Shock
 Syndrome characterized by decreased tissue perfusion
and impaired cellular metabolism
 Imbalance in supply/demand for O2 and nutrients
Shock (Cont’d)
 Classification of shock
 Low blood flow
 Cardiogenic
 Hypovolemic
 Maldistribution of blood flow
 Septic
 Anaphylactic
 Neurogenic
Low Blood Flow
Cardiogenic Shock
 Definition
 Systolic or diastolic dysfunction
 Compromised cardiac output (CO)
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
Pathophysiology of Cardiogenic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Low Blood Flow
Cardiogenic Shock
 Early manifestations
 Tachycardia
 Hypotension
 Narrowed pulse pressure
 ↑ Myocardial O2 consumption
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
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
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
Pathophysiology of Hypovolemic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Low Blood Flow
Hypovolemic Shock
 Response to acute volume loss depends on
 Extent of injury or insult
 Age
 General state of health
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
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
Pathophysiology of Neurogenic
Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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)
Maldistribution of Blood Flow
Anaphylactic Shock
 Acute, life-threatening hypersensitivity reaction
 Massive vasodilation
 Release of mediators
 ↑ Capillary permeability
Maldistribution of Blood Flow
Anaphylactic Shock (Cont’d)
 Clinical manifestations
 Anxiety, confusion, dizziness
 Tachycardia, tachypnea, hypotension
 Wheezing, stridor
 Sense of impending doom
 Chest pain
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
Maldistribution of Blood Flow
Septic Shock
 Sepsis: Systemic inflammatory response to
documented or suspected infection
 Severe sepsis = Sepsis + Organ dysfunction
Maldistribution of Blood Flow
Septic Shock (Cont’d)
 Septic shock = Presence of sepsis with hypotension
despite fluid resuscitation + Presence of tissue
perfusion abnormalities
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
Pathophysiology of Septic Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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
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
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
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
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
Compensatory(Nonprogressive) Stage of Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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
Stages of Shock
Progressive Stage (intermediate)
 Begins when compensatory mechanisms fail
 Aggressive interventions to prevent multiple organ
dysfunction syndrome
Progressive (intermediate)Stage of Shock
Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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
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
Stages of Shock
Progressive Stage (intermediate Cont’d)
 Movement of fluid from pulmonary vasculature to
interstitium
 Pulmonary edema
 Bronchoconstriction
 ↓ Residual capacity
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
Stages of Shock
Progressive Stage (intermediate Cont’d)
 CO begins to fall
 Decreased peripheral perfusion
 Hypotension
 Weak peripheral pulses
 Ischemia of distal extremities
Stages of Shock
Progressive Stage (intermediate Cont’d)
 Myocardial dysfunction results in
 Dysrhythmias
 Ischemia
 Myocardial infarction
 End result: Complete deterioration of cardiovascular system
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
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
Stages of Shock
Progressive Stage (intermediate Cont’d)
 Acute tubular necrosis/acute renal failure
Stages of Shock
Refractory Stage (Irreversible)
 Exacerbation of anaerobic metabolism
 Accumulation of lactic acid
 ↑ Capillary permeability
Stages of Shock
Refractory Stage
 Profound hypotension and hypoxemia
 Tachycardia worsens
 Decreased coronary blood flow
 Cerebral ischemia
Stages of Shock
Refractory Stage (Cont’d)
 Failure of one organ system affects others
 Recovery unlikely
Diagnostic Studies
 Thorough 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
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
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
Collaborative Care (Cont’d)
 General management strategies
 Ensure patent airway
 Maximize oxygen delivery
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
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
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
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
Collaborative Care (Cont’d)
 Nutrition is vital to decreasing morbidity from shock
 Initiate enteral nutrition within the first 24 hours
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
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
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)
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)
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
Collaborative Care
Septic Shock (Cont’d)
 Intravenous corticosteroids for patients who require
vasopressor therapy, despite fluid resuscitation, to
maintain adequate BP
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
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
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
Collaborative Care
Anaphylactic Shock
 Epinephrine, diphenhydramine
 Maintaining a patent airway
 Nebulized bronchodilators
 Endotracheal intubation or cricothyroidotomy may be
necessary
Collaborative Care
Anaphylactic Shock (Cont’d)
 Aggressive fluid replacement
 Intravenous corticosteroids if significant hypotension
persists after 1 to 2 hours of aggressive therapy
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
Nursing Assessment (Cont’d)
 Brief history
 Events leading to shock
 Onset and duration of symptoms
 Details of care received before hospitalization
 Allergies
 Vaccinations
Nursing Diagnoses
 Ineffective tissue perfusion: Renal, cerebral,
cardiopulmonary, gastrointestinal, hepatic, and
peripheral
 Fear
 Potential complication: Organ ischemia/dysfunction
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
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)
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)
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
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
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
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
Nursing Implementation
(Cont’d)
 Urine output
 Tympanic or pulmonary arterial temperature
 Skin: Temperature, pallor, flushing, cyanosis,
diaphoresis, piloerection
 Bowel sounds
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
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
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
YouTube videos of interest (cut-n-paste)
http://www.youtube.com/watch?v=xwrNsG
uquHI
http://www.youtube.com/watch?v=CbM4U
ihE1TQ
http://www.youtube.com/watch?v=-ljdPp7-
Hro
http://www.youtube.com/watch?v=9a7N9A
U1GiQ
http://www.youtube.com/watch?v=4OcrG5
eJO_0
http://www.youtube.com/watch?v=c-
qp0GdTEi8
http://www.youtube.com/watch?v=mFBQU
5B7X3o
http://www.youtube.com/watch?v=_2_CY
WiPTC0
http://www.youtube.com/watch?v=nf4fZflL
4JQ
http://www.youtube.com/watch?v=p2rEJC7
He6g
http://www.youtube.com/watch?v=h2oUFz
XpbsU

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Ppt Uma.pptx

  • 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 Cardiogenic 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  Thorough 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. YouTube videos of interest (cut-n-paste) http://www.youtube.com/watch?v=xwrNsG uquHI http://www.youtube.com/watch?v=CbM4U ihE1TQ http://www.youtube.com/watch?v=-ljdPp7- Hro http://www.youtube.com/watch?v=9a7N9A U1GiQ http://www.youtube.com/watch?v=4OcrG5 eJO_0 http://www.youtube.com/watch?v=c- qp0GdTEi8 http://www.youtube.com/watch?v=mFBQU 5B7X3o http://www.youtube.com/watch?v=_2_CY WiPTC0 http://www.youtube.com/watch?v=nf4fZflL 4JQ http://www.youtube.com/watch?v=p2rEJC7 He6g http://www.youtube.com/watch?v=h2oUFz XpbsU