Shock is a life-threatening condition with a variety of underlying causes. It is characterized by inadequate tissue perfusion that, if untreated, results in cell death. The nurse caring for the patient with shock or at risk for shock must understand the underlying mechanisms of shock and recognize its subtle as well as more obvious signs. Rapid assessment and response are essential to the patient’s recovery.

1. Dr.Vinoli.S.G,M.Sc(N), Ph.D (N),PGDHM
Professor,
Universal College of Nursing
SHOCK

2. INTRODUCTION
Shock is a life-threatening condition with a
variety of underlying causes. It is characterized
by inadequate tissue perfusion that, if
untreated, results in cell death. The nurse
caring for the patient with shock or at risk for
shock must understand the underlying
mechanisms of shock and recognize its subtle
as well as more obvious signs. Rapid
assessment and response are essential to the
patient’s recovery.
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3. DEFINITION
Shock can be defined as a condition in
which systemic blood pressure is inadequate
to deliver oxygen and nutrients to support
vital organs and cellular function (Mikhail,
1999).
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4. Shock is a syndrome characterized by
decreased tissue perfusion and impaired
cellular metabolism. This results in an
imbalance between the supply of and demand
for oxygen and nutrients.
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5. Classification of shock
Low blood flow
1. Cardiogenic
shock
2.Hypovolemic
shock
Maldistribution
of blood flow
1. Septic shock
2.Anaphylactic
shock
3.Neurogenic
shock
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6. PRECIPITATING FACTORS
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7. CARDIOGENIC SHOCK
• Systolic dysfunction
– myocardial infarction
– cardiomyopathy
• Diastolic dysfunction
– pericardial tamponade
• Dysrhythmias
– Bradydysrhythmias
– Tachydysrhythmias
• Structural factors
– valvular abnormality (e.g., stenosis or regurgitation)
– ventricular septal rupture
– tension pneumothorax
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8. HYPOVOLEMIC SHOCK
Absolute Hypovolemia
• External loss of whole blood (e.g.,
hemorrhage from trauma, surgery, GI
bleeding)
• Loss of other body fluids (e.g.,
vomiting, diarrhea, excessive diuresis,
diabetes insipidus, diabetes mellitus)
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9. Relative Hypovolemia
• Pooling of blood or fluids (e.g., bowel
obstruction)
• Fluid shifts (e.g., burn injuries, ascites)
• Internal bleeding (e.g., fracture of long
bones, ruptured spleen, hemothorax,
severe pancreatitis)
• Massive vasodilation (e.g., sepsis)
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10. NEUROGENIC SHOCK
• Disease to the spinal cord
• Spinal anesthesia
• Vasomotor center depression (e.g.,
severe pain, drugs, hypoglycemia,
injury)
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11. ANAPHYLACTIC SHOCK
• Contrast media
• Blood/blood products
• Drugs
• Insect bites
• Anesthetic agents
• Food/food additives
• Vaccines
• Environmental agents
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12. SEPTIC SHOCK
• Infection (e.g., urinary tract, respiratory tract,
invasive procedure, indwelling lines and catheters)
• At-risk patients:
– older adults,
– patients with chronic diseases (e.g., diabetes mellitus,
chronic kidney disease, heart failure),
– patients receiving immunosuppressive therapy,
– who are malnourished or debilitated.
• Gram-negative bacteria most common; also gram-
positive bacteria, viruses, fungi, and parasites
• Gastrointestinal.
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13. CARDIOGENIC SHOCK
• Cardiogenic shock occurs when either
systolic or diastolic dysfunction of the
pumping action of the heart results in
compromised cardiac output (CO).
• The heart's inability to pump the blood
forward is classified as systolic dysfunction.
• Diastolic dysfunction is an impaired ability
of the right or left ventricle to fill during
diastole.
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14. PATHOPHYSIOLOGY
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15. CLINICAL MANIFESTATION
Cardiovascular
• ↓ Capillary refill time
• ↑ MVO2
• Chest pain may or may not be present
Pulmonary
• Tachypnea
• Cyanosis
• Crackles
• Rhonchi
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16. Renal
• ↑ Na+ and H2O retention
• ↓ Renal blood flow
• ↓ Urine output
Skin
• Pallor
• Cool, clammy
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17. Neurologic
• ↓ Cerebral perfusion: anxiety, confusion,
agitation
• Anxiety
• Confusion
• Agitation
Gastrointestinal
• ↓ Bowel sounds
• Nausea/vomiting
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18. HYPOVOLEMIC SHOCK
Hypovolemic shock occurs when there is a
loss of intravascular fluid volume. In
hypovolemic shock, the volume is inadequate
to fill the vascular space. The volume loss may
be either an absolute or a relative volume
loss.
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19. Absolute hypovolemia results when fluid is
lost through hemorrhage, gastrointestinal (GI)
loss (e.g., vomiting, diarrhea), fistula drainage,
diabetes insipidus, hyperglycemia, or diuresis.
In relative hypovolemia, fluid volume moves
out of the vascular space into the extravascular
space (e.g., interstitial or intracavitary space).
This type of fluid shift is called third spacing.
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20. PATHOPHYSIOLOGY
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21. CLINICAL MANIFESTATION
• Increase in heart rate, CO, and respiratory
rate and depth.
• The stroke volume and PAWP are
decreased because of the decreased
circulating blood volume.
• The patient may appear anxious and urine
output will begin to decrease
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22. NEUROGENIC SHOCK
Neurogenic shock is a
hemodynamic phenomenon that can
occur within 30 minutes of a spinal cord
injury at the fifth thoracic (T5) vertebra
or above and last up to 6 weeks.
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23. PATHOPHYSIOLOGY
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24. CLINICAL MANIFESTATION
• Hypotension
• Bradycardia
• inability to regulate temperature.
(Initially, the patient's skin will be warm
Later, the patient's skin may be cool or
warm).
• absence of all voluntary and reflex
neurologic activity below the level of the
injury.
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25. ANAPHYLACTIC SHOCK
Anaphylactic shock is an acute and
life-threatening hypersensitivity
(allergic) reaction to a sensitizing
substance (e.g., drug, chemical, vaccine,
food, insect venom).
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26. PATHOPHYSIOLOGY
• Due to the causes
• massive vasodilation
• release of vasoactive mediators
• an increase in capillary permeability
• fluid leaks from the vascular space into the interstitial space
• Signs & symptoms
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27. SIGNS & SYMPTOMS
• respiratory distress, because of laryngeal edema or severe bronchospasm,
• circulatory failure, because of massive vasodilation.
• sudden onset of symptoms, including
– Dizziness
– chest pain
– Incontinence
– swelling of the lips and tongue
– Wheezing
– stridor.
• Skin changes include
– Flushing
– pruritus,
– Urticaria
– Angioedema.
• anxious and confused and feel an impending sense of doom.
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28. SEPTIC SHOCK
Septic shock is the presence of
sepsis with hypotension despite fluid
resuscitation along with the presence
of tissue perfusion abnormalities.
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29. Diagnostic Criteria for Sepsis
Infection
General Variables
• Fever (core temperature >100.9° F [38.3° C])
• Hypothermia (core temperature <97.0° F [36° C])
• Heart rate >90 beats/min
• Tachypnea
• Altered mental status
• Significant edema or positive fluid balance (>20
ml/kg over 24 hr)
• Hyperglycemia (blood glucose >120 mg/dl) in the
absence of diabetes
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30. Inflammatory Variables
• Leukocytosis (WBC count >12,000
cells/ml)
• Leukopenia (WBC count <4000 cells/ml)
• Normal WBC count with >10%
immature forms
• Elevated C-reactive protein
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31. Hemodynamic Variables
• Arterial hypotension (SBP <90 mm Hg,
MAP <70, or a decrease in SBP of >40
mm Hg)
• SvO2 >70%
• Cardiac index >3.5 L/min/m2
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32. Organ Dysfunction Variables
• Arterial hypoxemia (PaO2/FIO2 <300)
• Acute oliguria (urine output <0.5 ml/kg/hr
for at least 2 hr)
• Coagulation abnormalities (INR >1.5 or PTT
>60 sec)
• Paralytic ileus (absent bowel sounds)
• Hyperbilirubinemia (total bilirubin >4
mg/dl)
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33. Tissue Perfusion Variables
• Hyperlactatemia (>1 mmol/L)
• Decreased capillary refill or mottling
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34. PATHOPHYSIOLOGY
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35. CLINICAL MANIFESTATION
Cardiovascular
– Chest pain
– Third spacing of fluid
– ↓/↑ Temperature
– Biventricular dilation: ↓ ejection fraction
Pulmonary
– Swelling of lips and tongue
– Shortness of breath
– Edema of larynx and epiglottis
– Wheezing
– Rhinitis
– Stridor
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36. Skin
– Flushing
– Pruritus
– Urticaria
– Angioedema
– Warm and flushed → cool and mottled (late)
Neurologic
– Anxiety
– Feeling of impending doom
– Confusion
– ↓ LOC
– Metallic taste
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37. Gastrointestinal
– Cramping
– Abdominal pain
– Nausea
– Vomiting
– Diarrhea
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38. STAGES OF SHOCK
The compensatory stage
The progressive stage
The refractory (irreversible) stage
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39. COMPENSATORY STAGE
In the compensatory stage, the body
activates neural, hormonal, and biochemical
compensatory mechanisms in an attempt to
overcome the increasing consequences of
anaerobic metabolism and to maintain
homeostasis.
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40. PROGRESSIVE STAGE
The progressive stage of shock begins as
compensatory mechanisms fail. Continued
decreased cellular perfusion and resulting
altered capillary permeability are the
distinguishing features of this stage.
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41. – Altered capillary permeability allows leakage of fluid
and protein out of the vascular space into the
surrounding interstitial space.
– In addition to the decrease in circulating volume,
there is an increase in systemic interstitial edema. The
patient may have anasarca, or diffuse profound
edema.
– Fluid leakage from the vascular space also affects the
solid organs (e.g., liver, spleen, GI tract, lungs) and
peripheral tissues by further decreasing perfusion.
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42. REFRACTORY STAGE
In the refractory stage, decreased perfusion
from peripheral vasoconstriction and decreased CO
exacerbate anaerobic metabolism.
The accumulation of lactic acid contributes to an
increased capillary permeability and dilation of the
capillaries.
Increased capillary permeability allows fluid and plasma
proteins to leave the vascular space and move to the
interstitial space.
Blood pools in the capillary beds secondary to the
constricted venules and dilated arterioles.
 The loss of intravascular volume worsens hypotension
and tachycardia and decreases coronary blood flow.
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43. The patient in this stage of shock will
demonstrate profound hypotension and
hypoxemia.
The failure of the liver, lungs, and kidneys
will result in an accumulation of waste
products, such as lactate, urea, ammonia,
and carbon dioxide. The failure of one
organ system will have an effect on
several other organ systems.
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44. DIAGNOSTIC EVALUATION
• History collection
• Physical examination
• 12 lead ECG
• Continuous cardiac monitoring
• Chest X-ray
• Continuous pulse oximetry
• Hemodynamic monitoring
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45. LABORATORY STUDIES
Test Result
RBC, Hb & hematocrit Decreased
Creatine kinase Increased
Troponin Increased
BUN Increased
Creatinine Increased
Glucose Increased
Serum Electrolytes
Sodium
Potassium
Increased
Increased
Arterial blood gases Respiratory alkalosis
Metabolic acidosis
Blood cultures Growth of organisms who are in septic shock
Lactic acid Increased
Liver enzymes (ALT, AST, GGT) Increased
Urine Specific gravity Increased11/29/2019 45Vinoli.S.G

46. EMERGENCY MANAGEMENT
Initial
• Establish and maintain patent airway.
• Administer high-flow oxygen (100%) by non-rebreather mask or bag-
valve-mask.
• Anticipate need for intubation and mechanical ventilation.
• Stabilize cervical spine as appropriate.
• Establish IV access with two large-bore catheters (14-16 gauge) and
begin fluid resuscitation with crystalloids (e.g., normal saline solution).
• Draw blood for laboratory studies (e.g., blood cultures, lactate, WBC).
• Control any external bleeding with direct pressure or pressure dressing.
• Assess for life-threatening injuries (e.g., pericardial tamponade, liver
laceration, tension pneumothorax).
• Consider vasopressor therapy only after hypovolemia has been
corrected.
• Insert an indwelling bladder catheter and nasogastric tube.
• Antibiotic therapy if sepsis is suspected.11/29/2019 46Vinoli.S.G

47. Ongoing Monitoring
• Level of consciousness.
• Vital signs, including pulse oximetry,
peripheral pulses, capillary refill.
• Respiratory status.
• Cardiac rhythm.
• Urine output.
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48. Successful management of the patient in shock
includes the following:
1. Identification of patients at risk for the
development of shock
2. Integration of the patient's history, physical
examination, and clinical findings to establish a
diagnosis
3. Interventions to control or eliminate the cause of
the decreased perfusion
4. Protection of target and distal organs from
dysfunction
5. Provision of multisystem supportive care
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49. DRUG THERAPY
• dobutamine (Dobutrex)
– Positive inotropic effects
• dopamine (Intropin)
– vasopressor
• Drotrecogin alpha (Xigris)
– Anticoagulant effect by inhibiting factor Va/VIIIa
– Profibrinolytic and antiinflammatory properties
• epinephrine (Adrenalin)
– Low doses: -adrenergic agonist (cardiac stimulation,
bronchial dilation, peripheral vasodilation)
– High doses: -adrenergic agonist (peripheral
vasoconstriction)
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50. • hydrocortisone (Solu-Cortef)
– Decreases inflammation; reverses increased
capillary permeability
• norepinephrine (Levophed)
– β1-Adrenergic agonist (cardiac stimulation)
– α-Adrenergic agonist (peripheral vasoconstriction)
– Renal/splanchnic vasoconstriction
• phenylephrine (Neo-Synephrine)
– α-Adrenergic agonist
– Vasoconstriction: renal, mesenteric, splanchnic,
cutaneous, and pulmonary vessels
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51. • sodium nitroprusside (Nipride)
– Arterial and venous vasodilation
• nitroglycerin (Tridil)
– Vasodilation
• vasopressin (Pitressin [Pressyn])
– Antidiuretic hormone, nonadrenergic
vasoconstrictor
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52. • Diuretics (e.g., furosemide)
• Antibiotics as ordered
• Atropine (for bradycardia)
• Antihistamines (e.g., diphenhydramine)
• Bronchodilators: nebulized (e.g., albuterol)
• Corticosteroids (if hypotension persists)
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53. FLUID THERAPY
Crystalloids
Isotonic
• 0.9% NaCl (NSS)
• Lactated Ringer's (LR)
– Fluid primarily remains in the intravascular
space, increasing intravascular volume.
– Used for initial volume replacement in most
types of shock.
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54. Hypertonic
• 1.8%, 3%, 5% NaCl
– Fluid remains in the intravascular space, rapid
volume expansion
– May be used for initial volume expansion in
hypovolemic shock
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55. Blood/Blood Products
• Whole blood/packed red blood cells
• Fresh frozen plasma
– Replaces blood loss, increases oxygen-
carrying capability.
– Replaces coagulation factors.
– All types of shock if hemoglobin is <12 g/dl
(120 g/L) or if the patient does not respond
to crystalloids.
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56. Colloids
• Hetastarch (Hespan)
• Human serum albumin (5%, 25%), plasma
protein fraction (5% albumin in 500 ml
NSS)
• dextran
– Can increase plasma colloid osmotic pressure;
rapid volume expansion
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57. SUPPORTIVE THERAPIES
• Correct dysrhythmias
• Correct the cause (e.g., stop bleeding, GI losses)
• Use warmed fluids
• Obtain cultures (e.g., blood, wound) before beginning antibiotics
• Monitor temperature
• Control blood glucose
• Stress ulcer prophylaxis
• Minimize spinal cord trauma with stabilization
• Monitor temperature
• Identify and remove offending cause
• Prevention via avoidance of known allergens
• Premedication with history of prior sensitivity (e.g., contrast media)
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58. NUTRITIONAL THERAPY
• Protein-calorie malnutrition is one of the primary manifestations of
hypermetabolism in shock.
• Enteral nutrition should be initiated within the first 24 hours.
• parenteral nutrition is used if enteral feedings are contraindicated or
fail to meet at least 80% of the patient's caloric
• A patient in shock should be weighed daily on the same scale at the
same time of day.
• If the patient experiences a significant weight loss, dehydration should
be ruled out before additional calories are provided.
• Large weight gains are common because of third spacing of fluids.
• Serum protein, nitrogen balance, BUN, serum glucose, and serum
electrolytes are all used to assess nutritional status.
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59. NURSING DIAGNOSIS
Ineffective tissue perfusion: renal, cerebral,
cardiopulmonary, gastrointestinal, hepatic, and peripheral
related to low blood flow or maldistribution of blood as
evidenced by the following possible findings:
• Renal urinary output <0.5 mg/kg/hr; ↑ BUN ↑ plasma creatinine, ↑
BUN/creatinine ratio, ↑ urine specific gravity
• Cerebral anxiety, confusion, agitation, altered mentation, ↓ LOC ↑ ↓
temperature
• Cardiopulmonary: ↓ BP, orthostatic hypotension, tachycardia;
dysrhythmias, ↓ CVP and PAWP weak, thready pulses; flat neck veins;
tachypnea, ↓ SpO2 crackles; ↑ ventilation-perfusion mismatch, refractory
hypoxemia, respiratory failure
• Gastrointestinal: ↓ bowel sounds, paralytic ileus, hyperglycemia or
hypoglycemia
• Hepatic: ↑ liver enzymes (e.g., ALT, AST, GGT), ↑ NH3and lactate
• Peripheral: ↓ peripheral pulses, cool and clammy skin, decreased capillary
refill, pallor or cyanosis
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60. Fear; related to of condition as evidenced
by verbalization of anxiety about condition
and fear of death, or withdrawal with no
communication; restlessness; sleeplessness;
increase in heart and respiratory rate
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61. NURSING INTERVENTIONS
• Monitor vital signs, orthostatic blood pressure, mental
status, and urinary output to assess trends in patient's
condition and evaluate patient's response to treatment.
• Monitor trends in hemodynamic parameters (e.g., CVP,
PAP, PAWP) to assess patient's status and detect fluid
deficits or excesses and to evaluate patient's response to
treatment.
• Administer fluids to maintain blood pressure and cardiac
output.
• Monitor laboratory evidence of inadequate tissue
perfusion (e.g., increased lactic acid levels, decreased
arterial pH levels) to assess trends in patient's status and
evaluate patient's response to treatment.
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62. • Monitor determinants of tissue oxygen delivery (e.g., PaO2,
SpO2, ScvO2 SvO2, hemoglobin levels, cardiac output) to assess
trends in patient's status and evaluate patient's response to
treatment.
• Monitor for symptoms of respiratory failure (e.g., low PaO2,
elevated PaCO2 levels, respiratory muscle fatigue) to plan
respiratory interventions.
• Monitor fluid status, including intake and output, to evaluate
response to treatment.
• Monitor renal function (e.g., BUN, Cr levels) to evaluate
response to treatment.
• Provide oxygen therapy and/or mechanical ventilation to
maximize oxygenation and maintain SpO2 ≥90%.
• Monitor blood glucose levels, as indicated, to maintain normal
levels.
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63. • Monitor for symptoms of inadequate coronary artery
perfusion (e.g., ST changes on ECG or angina).
• Promote optimal preload to improve contractility
while minimizing heart failure (e.g., administer
nitroglycerin and maintain PAWP within prescribed
range).
• Promote coronary artery perfusion (e.g., maintain
mean arterial pressure and control tachycardia) to
prevent myocardial ischemia >60 mm Hg
• Remove stimuli precipitating neurogenic reaction to
control symptoms.
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64. • Administer antibiotics, antihistamines,
epinephrine, and antiinflammatory drugs, if
appropriate, to control symptoms.
• Monitor the patient closely for hemorrhage.
• Note hemoglobin/hematocrit level before
and after blood loss to evaluate response to
treatment.
• Administer blood products (e.g., platelets or
fresh frozen plasma) to replace lost volume.
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65. • Seek to understand the patient's perspective
of a stressful situation to validate patient's
feelings.
• Use a calm, reassuring approach.
• Listen attentively.
• Administer medications if appropriate to
reduce anxiety.
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66. • Stay with patient to promote safety and reduce
fear.
• Control stimuli for patient needs to reduce
patient's anxieties and oxygen need.
• Provide factual information concerning
diagnosis, treatment, and prognosis to reduce
patient's fear of the unknown and assist patient
in making informed decisions.
• Encourage family to stay with patient to reduce
anxiety level.
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