Module 3 a presentation

Module 3
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
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
Maldistribution of Blood Flow
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
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
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)
(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)
(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
(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
(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
(Cont’d)
Respiratory status
Respiratory rate and rhythm
Breath sounds
Continuous pulse oximetry
Arterial blood gases
Most patients will be intubated and mechanically
ventilated
(Cont’d)
Urine output
Tympanic or pulmonary arterial temperature
Skin: Temperature, pallor, flushing, cyanosis,
diaphoresis, piloerection
Bowel sounds
(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
(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? http://www.youtube.com/watch?v=c-
v=xwrNsGuquHI qp0GdTEi8
http://www.youtube.com/watch? http://www.youtube.com/watch?
v=CbM4UihE1TQ v=mFBQU5B7X3o
http://www.youtube.com/watch?v=-ljdPp7- http://www.youtube.com/watch?
Hro v=_2_CYWiPTC0
http://www.youtube.com/watch? http://www.youtube.com/watch?
v=9a7N9AU1GiQ v=nf4fZflL4JQ
http://www.youtube.com/watch?
http://www.youtube.com/watch? v=p2rEJC7He6g
v=4OcrG5eJO_0 http://www.youtube.com/watch?
v=h2oUFzXpbsU

Module 3 a presentation

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Module 3 a presentation

Uploaded by

Copyright:

Available Formats

Module 3

W.Pawliuk MPH MSHEd RN CEN

Maldistribution of blood flow

Results in massive vasodilation leading to pooling of

Hyperdynamic state: Increased CO and decreased SVR

You might also like