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
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