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

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
Carcinogenic 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

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

Low Blood Flow
• 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

Neurogenic Shock (Cont’d)
– Hypotension
– Bradycardia
– Temperature dysregulation (resulting in heat loss)
– Dry skin
– Poikilothermia (taking on the temperature of the
environment)

Anaphylactic Shock
• Acute, life-threatening hypersensitivity
reaction
– Massive vasodilation
– Release of mediators
– ↑ Capillary permeability

Anaphylactic Shock (Cont’d)
– Anxiety, confusion, dizziness
– Tachycardia, tachypnea, hypotension
– Wheezing, stridor
– Sense of impending doom
– Chest pain

– Swelling of the lips and tongue, angioedema
– Wheezing, stridor
– Flushing, pruritus, urticaria
– Respiratory distress and circulatory failure

Septic Shock
• Sepsis: Systemic inflammatory response to
documented or suspected infection
• Severe sepsis = Sepsis + Organ dysfunction

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

• Mortality rates as high as 50%
• Primary causative organisms
– Gram-negative and gram-positive bacteria
– Endotoxin stimulates inflammatory response

Pathophysiology of Septic Shock

Septic Shock
– ↑ Coagulation and inflammation
– ↓ Fibrinolysis
• Formation of microthrombi
• Obstruction of microvasculature
– Hyperdynamic state: Increased CO and decreased
SVR

– 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

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

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
• Anasarca (severe generalized edema)
• Fluid leakage affects solid organs and peripheral tissues
• ↓ Blood flow to pulmonary capillaries

Stages of Shock
• Movement of fluid from pulmonary
vasculature to interstitium
• Pulmonary edema
• Bronchoconstriction
• ↓ Residual capacity

Stages of Shock
• Fluid moves into alveoli
• Edema
• Decreased surfactant
• Worsening V/Q mismatch
• Tachypnea
• Crackles
• Increased work of breathing

Stages of Shock
• CO begins to fall
• Decreased peripheral perfusion
• Hypotension
• Weak peripheral pulses
• Ischemia of distal extremities

Stages of Shock
• Myocardial dysfunction results in
• Dysrhythmias
• Ischemia
• Myocardial infarction
• End result: Complete deterioration of cardiovascular
system

Stages of Shock
• Mucosal barrier of GI system becomes
ischemic
• Ulcers
• Bleeding
• Risk of translocation of bacteria
• Decreased ability to absorb nutrients

Stages of Shock
• Liver fails to metabolize drugs and wastes
• Jaundice
• Elevated enzymes
• Loss of immune function
• Risk for DIC and significant bleeding

Stages of Shock
• 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
• 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

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

• General management strategies
– Ensure patent airway
– Maximize oxygen delivery

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

• 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

• 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

• 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

• Nutrition is vital to decreasing morbidity from
shock
– Initiate enteral nutrition within the first 24 hours

• 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
• 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
• Intravenous corticosteroids for patients who
require vasopressor therapy, despite fluid
resuscitation, to maintain adequate BP

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

Collaborative Care
• 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
• 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)

• 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

• 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

• 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

• Respiratory status
– Respiratory rate and rhythm
– Breath sounds
– Continuous pulse oximetry
– Arterial blood gases
– Most patients will be intubated and mechanically
ventilated

• Urine output
• Tympanic or pulmonary arterial temperature
• Skin: Temperature, pallor, flushing, cyanosis,
diaphoresis, piloerection
• Bowel sounds

• Nasogastric drainage/stools for occult blood
• I&O, fluid and electrolyte balance
• Oral care/hygiene based on O2 requirements
• Passive/active range of motion

• 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

THANK YOU VERY MUCH FOR
YOUR ATTENTION.

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