Shock.ppt

Presented By.
Mr. Pradeepsingh B
Asst. Professor
HOD of Medical Surgical Nursing

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Presented By
Mr. Pradeepsingh B
HOD of Medical surgical Nursing

2. Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Shock
Syndrome characterized by decreased tissue perfusion
and impaired cellular metabolism
Imbalance between the supply and
demand for O
2and nutrients
shock

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Shock
Classification of shock
Low blood flow
Cardiogenic
Hypovolemic
Maldistribution of blood flow
Septic
Anaphylactic
Neurogenic

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Low Blood Flow
Cardiogenic Shock
Definition
Systolic or diastolic dysfunction
Compromised cardiac output (CO)

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Low Blood Flow
Cardiogenic Shock
Precipitating causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems

6. Pathophysiology of
Cardiogenic Shock
Fig. 67-2
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Low Blood Flow
Cardiogenic Shock
Early manifestations
Tachycardia
Hypotension
Narrowed pulse pressure
↑Myocardial O
2 consumption

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Low Blood Flow
Cardiogenic Shock
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

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

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Low Blood Flow
HypovolemicShock
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
Fig. 67-3
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Low Blood Flow
HypovolemicShock
Response to acute volume loss depends on
Extent of injury or insult
Age
General state of health

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Low Blood Flow
HypovolemicShock
Clinical manifestations
Anxiety
Tachypnea
Increase in CO, heart rate
Decrease in stroke volume, PAWP, UO
If loss is >30%, blood volume is replaced

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Maldistributionof Blood Flow
NeurogenicShock
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
Can be in response to spinal anesthesia
Results in massive vasodilation leading to
pooling of blood in vessels

15. Pathophysiology of
Neurogenic Shock
Fig. 67-4
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Maldistributionof Blood Flow
NeurogenicShock
Clinical manifestations
Hypotension
Bradycardia
Temperature dysregulation
(resulting in heat loss)
Dry skin
Poikilothermia(taking on the
temperature of the environment)

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Maldistributionof Blood Flow
Anaphylactic Shock
Acute, life-threatening hypersensitivity reaction
Massive vasodilation
Release of mediators
↑Capillary permeability

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Maldistributionof Blood Flow
Anaphylactic Shock
Clinical manifestations
Anxiety, confusion, dizziness
Sense of impeding doom
Chest pain
Incontinence

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Maldistributionof Blood Flow
Anaphylactic Shock
Clinical manifestations
Swelling of the lips and tongue, angioedema
Wheezing, stridor
Flushing, pruritus, urticaria
Respiratory distress and circulatory failure

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

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Maldistributionof Blood Flow
SepticShock
Septic shock = Presence of sepsis with hypotension
despite fluid resuscitation + Presence of tissue
perfusion abnormalities

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Maldistributionof Blood Flow
SepticShock
Mortality rates as high as 50%
Primary causative organisms
Gram-negative and gram-positive bacteria
Endotoxin stimulates inflammatory response

23. Pathophysiology of Septic Shock
Fig. 67-5
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Maldistributionof Blood Flow
SepticShock
Clinical manifestations
↑Coagulation and inflammation
↓Fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Hyperdynamic state: Increased CO and decreased SVR

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Maldistributionof Blood Flow
Septic Shock
Clinical manifestations
Tachypnea/hyperventilation
Temperature dysregulation
↓Urine output
Altered neurologic status
GI dysfunction
Respiratory failure is common

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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 O
2

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Stages of Shock
Compensatory Stage
Clinically apparent
Neural
Hormonal
Biochemical compensatory mechanisms
Attempts are aimed at overcoming consequences of
anaerobic metabolism and maintaining homeostasis

28. Compensatory Stage of Shock
Fig. 67-6
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Stages of Shock
Compensatory Stage
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

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Stages of Shock
Compensatory Stage
Impaired GI motility
Risk for paralytic ileus
Cool, clammy skin from blood
Except septic patient who is warm and flushed

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Stages of Shock
Compensatory Stage
Shunting blood from lungs increases physiologic dead
space
↓Arterial O
2levels
Increase in rate/depth of respirations
V/Q mismatch
SNS stimulation increases myocardium O
2demands

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Stages of Shock
Compensatory Stage
If perfusion deficit corrected, patient recovers with no
residual sequelae
If deficit not corrected, patient enters progressive stage

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Stages of Shock
Progressive Stage
Begins when compensatory mechanisms fail
Aggressive interventions to prevent multiple
organ dysfunction syndrome (MODS)

34. Progressive Stage of Shock
Fig. 67-7
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Stages of Shock
Progressive Stage
Hallmarks of ↓cellular perfusion and altered capillary
permeability:
Leakage of protein into interstitial space
↑Systemic interstitial edema

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Stages of Shock
Progressive Stage
Anasarca
Fluid leakage affects solid organs and
peripheral tissues
↓Blood flow to pulmonary capillaries

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

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

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

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

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

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

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Stages of Shock
Progressive Stage
Acute tubular necrosis/acute renal failure

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Stages of Shock
Refractory Stage
Exacerbation of anaerobic metabolism
Accumulation of lactic acid
↑Capillary permeability

45. Refractory Stage of Shock
Fig. 67-8
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Stages of Shock
Refractory Stage
Profound hypotension and hypoxemia
Tachycardia worsens
Decreased coronary blood flow
Cerebral ischemia

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Stages of Shock
Refractory Stage
Failure of one organ system affects others
Recovery unlikely

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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

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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

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Collaborative Care
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

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Collaborative Care
General management strategies
Ensure patent airway
Maximize oxygen delivery

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

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Collaborative Care
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

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Collaborative Care
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

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Collaborative Care
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

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Collaborative Care
Nutrition is vital to decreasing morbidity from shock
Initiate enteral nutrition within the first 24
hours
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

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Collaborative Care
Cardiogenic Shock
Restore blood flow to the myocardium by restoring
the balance between O
2supply and demand
Thrombolytic therapy
Angioplasty with stenting
Emergency revascularization
Valve replacement

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

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Collaborative Care
HypovolemicShock
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)

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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

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Collaborative Care
Septic Shock
Intravenous corticosteroids for patients who require
vasopressor therapy, despite fluid resuscitation, to
maintain adequate BP

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

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Collaborative Care
Septic Shock
Glucose levels <150 mg/dl
Stress ulcer prophylaxis with histamine (H
2)-receptor
blockers
Deep vein thrombosis prophylaxis with low-dose
unfractionated heparin or low-molecular-weight
heparin

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Collaborative Care
NeurogenicShock
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

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

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Collaborative Care
Anaphylactic Shock
Aggressive fluid replacement
Intravenous corticosteroids if significant
hypotension persists after 1 to 2 hours of aggressive
therapy

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Nursing Assessment
ABCs: Airway, breathing, and circulation

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Nursing Assessment
Focused assessment of tissue perfusion
Vital signs
Peripheral pulses
Level of consciousness
Capillary refill
Skin (e.g., temperature, color, moisture)
Urine output

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Nursing Assessment
Brief history
Events leading to shock
Onset and duration of symptoms
Details of care received before hospitalization
Allergies
Vaccinations

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

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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

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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)

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Nursing Implementation
Health Promotion
Planning to prevent shock
(e.g., monitoring fluid balance to prevent hypovolemic
shock, maintenance of handwashing to prevent spread
of infection)

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Nursing Implementation
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

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Nursing Implementation
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

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Nursing Implementation
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, S
3, S
4

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

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

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

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Nursing Implementation
Assess level of anxiety and fear
Medication PRN
Talk to patient
Visit from clergy
Family involvement
Comfort measures
Privacy
Call light within reach

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Evaluation
Normal or baseline, ECG, BP, CVP, and
PAWP
Normal temperature
Warm, dry skin
Urinary output >0.5 ml/kg/hr
Normal RR and SaO
2≥90%
Verbalization of fears, anxiety