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Module 15A- Shock!. John Nation, RN, MSN From the notes of Nancy Jenkins, RN, MSN. Shock-. Summary- Lewis p. 1772-1798, 1738-1746 Types of Shock Stages of Shock Management of Shock Nursing Interventions Systemic Inflammatory Response Syndrome (SIRS)

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module 15a shock

Module 15A- Shock!

John Nation, RN, MSN

From the notes of Nancy Jenkins, RN, MSN



  • Lewis p. 1772-1798, 1738-1746
  • Types of Shock
  • Stages of Shock
  • Management of Shock
  • Nursing Interventions
  • Systemic Inflammatory Response Syndrome (SIRS)
  • Multiple Organ Dysfunction Syndrome (MODS)
shock defined
Shock Defined

Shock- Clinical syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply and demand for oxygen and nutrients

  • Put simply, not enough oxygen and not enough nutrients for body
types of shock
Types of Shock-

Low blood flow-

  • Cardiogenic shock
  • Hypovolemic shock

Maldistribution of blood flow-

  • Neurogenic shock
  • Anaphylactic shock
  • Septic shock
etiology and pathophysiology
Etiology and Pathophysiology

Cardiogenic shock-

  • Occurs when systolic or diastolic dysfunction of the pumping of the heart causes decreased cardiac output
  • Cardiac output= stroke volume x heart rate
  • Causes include myocardial infarction, cardiomyopathy, blunt cardiac injury (trauma), severe systemic or pulmonary hypertension, cardiac tamponade, arrhythmias, valvular defects,and myocardial depression from metabolic problems.
cardiogenic shock cont d
Cardiogenic Shock (Cont’d)

Clinical Manifestations:

  • Tachycardia
  • Hypotension
  • Narrowed pulse pressure
  • Tachypnea
  • Pulmonary congestion
  • Cyanosis
  • Cool, clammy skin
  • Confusion/ agitation
  • Decreased capillary refill time
cardiogenic shock cont d1
Cardiogenic Shock (Cont’d)


  • Restore blood flow to myocardium- early PCI!
  • Thromboyltic therapy, angioplasty, stenting, emergency revasularization, valve replacement
  • Hemodynamic monitoring PAWP
  • Intraaortic balloon pump (IABP) 50. IABP
  • Ventricular assist device VAD video
  • Transplant (rarely)
cardiogenic shock cont d2
Cardiogenic Shock (Cont’d)

Treatment (Cont’d)

  • Medications: aspirin, heparin, dopamine, norepiniphrine, diuretics, vasodilators
cardiogenic shock cont d3
Cardiogenic Shock (Cont’d)
  • Mortaliaty rate of 80-90% when caused by acute MI
  • Prior MI, increasing age, and oliguria are associated with worsening outcomes
hypovolemic shock
Hypovolemic Shock-
  • Loss of intravascular fluid volume
  • Volume inadequate to fill the vascular space
  • Categorized as absolute or relative hypovolemia
hypvolemic shock cont d
Hypvolemic Shock (Cont’d)

Absolute hypovolemia-

  • Results from fluid loss via hemorrhage, gastrointesinal (GI) loss (vomiting, diarrhea), fistula drainage, diabetes insipidus, hyperglycemia, or diuresis

Relative hypovolemia-

  • Results from fluid moving out of the vascular space and into the extravascular space- aka third spacing
hypovolemic shock cont d
Hypovolemic Shock (Cont’d)

Clinical Manifestations-

  • Depend on extent of injury, age, general health status
  • Decrease in venous return, preload, stroke volume, and cardiac output
  • Increase in heart rate, increase in respiratory rate
  • Decrease in stroke volume, pulmonary artery wedge pressure, and urine output
hypovolemic shock cont d1
Hypovolemic Shock (Cont’d)


  • Stop source of fluid loss
  • Restore circulating volume
  • 3:1 rule- 3 ml of isotonic crystalloid for every 1 ml of estimated blood loss
neurogenic shock
Neurogenic Shock-
  • Hemodynamic phenomenon occuring after spinal injury at T5 or above
  • Usually within 30 minutes of injury, can last up to 6 weeks
  • Causes massive vasodilation without compensation secondary to the loss of sympathetic nervous system vasoconstrictor tone
  • Can also be caused by spinal anesthesia
neurogenic shock cont d
Neurogenic Shock (Cont’d)

Clinical manifestations-

  • Bradycardia (from unopposed parasympathetic stimulation)
  • Hypotension (from massive vasodilation)
  • Hypothermia (due to heat loss)
neurogenic shock cont d1
Neurogenic Shock (Cont’d)

Early Signs-

  • Blood pools in venous and capillary beds
  • Skin warm and pink
  • Pulse slow and bounding
  • Decreased BP
  • Decreased temperature
  • Decreased MAP
neurogenic cont d
Neurogenic (Cont’d)

Late Signs-

  • Skin pale and cool
neurogenic shock cont d2
Neurogenic Shock (Cont’d)


  • Depends on the cause
  • If spinal cord injury, promote spinal stability
  • Vasopressors and atropine for hypotension and bradycardia (respectively)
  • Fluids administered cautiously
  • Monitor for hypothermia
anaphylactic shock
Anaphylactic Shock
  • Acute and life-threatening allergic reaction (hypersensitivity) reaction
  • Can be caused by drugs, chemicals, vaccines, food insect venom
  • Causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability
  • Fluid shift from the vascular space to the interstitial space
  • Respiratory distress secondary to laryngeal edema, severe bronchospasm, or circulatory failure from vasodilation
anaphylactic shock cont d
Anaphylactic Shock (Cont’d)

Clinical Manifestations-

  • Anxiety, confusion
  • Dizziness
  • Chest pain
  • Incontinence
  • Swelling of lip and tongue
  • Wheezing, stridor
  • Flushing, pruritus, and uticaria
  • angioedema
anaphylactic shock cont d1
Anaphylactic Shock (Cont’d)


  • Epinephrine is the drug of choice
  • Diphenhydramine used to block massive release of histamine
  • Maintain patent airway
  • Nebulized bronchodilators (albuterol)
  • Intubation or cricothyroidotomy may be needed
  • Fluid replacement, primarily with colloids
  • corticosteroids
septic shock
Septic Shock

Septic shock- Presence of sepsis with hypotension, despite fluid resuscitation, with decreased tissue perfusion

Sepsis- systemic inflammatory response to an infection

  • Over 750,000 clients diagnosed with severe sepsis annually and 28% to 50% die
septic shock cont d
Septic Shock (Cont’d)


  • Septicemia (initially bacteremia) causes inflammatory cascade
  • Commonly caused by gram negative bacteria
  • If gram positive infection (Staphylococcus and streptococcus), up to 50% mortality rate
septic shock cont d1
Septic Shock (Cont’d)

Clinical Manifestations-

  • Increased or decreased temperature
  • Biventricular dilations causing decreased ejection fraction
  • Hyperventilation, respiratory alkalosis, respiratory acidosis, crackles, ARDS
  • Decreased urine output
  • Skin warm and flushed, then cool and clammy
  • Altered LOC
  • Paralytic ileus, GI bleeding
  •  & WBC,  platelets,  lactate,  glucose,  urine specific gravity,  urine Na, positive blood cultures
septic shock cont d2
Septic Shock (Cont’d)


  • Large amounts of fluid replacement
  • Vasopressor drug therapy
  • Corticosteroids
  • Antibiotics
  • Drotrecogin alpha (Xigris)
  • Glucose less than 150
  • Stress ulcer prophylaxis with H2- receptor blockers and DVT prophylaxis
diagnostic tests
Diagnostic Tests
  • RBC, hemoglobin, hematocrit
  • Arterial blood gases
  • Blood cultures
  • Cardiac enzymes (cardiogenic shock)
  • Glucose
  • DIC (Disseminated Intravascular Coagulation) screen: FSP, fibrogen level, platelet count, PTT and PT/INR, and D-dimer
  • Lactic Acid
  • Liver enzymes- ALT, AST, GGT
diagnostic tests cont d
Diagnostic Tests (Cont’d)


  • Sodium level increased early, decreased later if hypotonic fluid administered
  • Potassium decreased, then increased later with cellular breakdown and renal failure
common nursing diagnoses
Common Nursing Diagnoses
  • Decreased cardiac output
  • Altered tissue perfusion
  • Fluid volume deficit
  • Anxiety
  • Fear
stages of shock
Stages of Shock

Compensatory Shock-

  •  Mean Arterial Pressure (MAP)
  •  blood pressure
  •  cardiac output
  • Sympathetic nervous system (SNS) stimulation causes vasoconstriction. Blood flow to heart and brain maintained, while blood flow to the kidneys, GI tract, skin, and lungs is diverted
  • Decreased blood flow to kidneys causes activation of renin-angiotensin system, leading to sodium retention and potassium excretion
  • In this stage the body is able to compensate for changes in tissue perfusion
progressive shock
Progressive Shock
  • Altered capillary permeability (3rd spacing)
  • Alveolar and pulmonary edema, ARDS,  PA pressures
  •  cardiac output,  coronary perfusion, can cause arrhythmias and MI
  • Acute tubular necrosis
  • Jaundice,  ALT,AST GGT
  • DIC
  • Cold, clammy skin
refractory stage
Refractory Stage
  • Anaerobic metabolism- lactic acid build-up
  • Increased capillary blood leak
  • Profound hypotension, inadequate to perfuse vital organs
  • Respiratory failure
  • Anuria
  • DIC
  • hypothermia
collaborative care
Collaborative Care

Successful management involves:

  • Identifying at risk clients
  • Integration of client’s medical history, assessment findings to establish diagnosis
  • Interventions to address cause of decreased perfusion
  • Protection of organs
  • Multisystem supportive care
collaborative management cont d
Collaborative Management (Cont’d)
  • Start with ABCs! Ensure patent airway and oxygen delivery
  • Volume expansion and fluid administration cornerstone of treatment of septic, hypovolemic, and anaphylactic shock
  • Primary goal of therapy is correction of decreased tissue perfusion
  • Hemodynamic monitoring, drug therapy, circulatory assist
nursing implementation
Nursing Implementation

Health Promotion-

  • Identify at risk clients
  • Prevent shock (monitoring fluid balance, good hand washing to prevent infection, community education and health promotion)
interventions acute
Interventions (Acute)
  • Assess neurologic status- check LOC every hour or more often
  • Monitor heart rate/ rhythm, BP, central venous pressure, pulmonary artery pressure, cardiac output
  • Trendelenburg position not supported by research and may compromise pulmonary function and increase ICP
  • Monitor EKG for dysrhythmias, S3 or S4 heart sounds

Assessment (Respiratory)-

  • Respiratory rate and effort
  • Pulse oximetry
  • ABGs for acid/base balance
  • Intubation/ ventilation
  • Hourly urine output
  • If less than 0.5 ml/kg/hour, may indicate inadequate kidney perfusion
  • BUN and creatinine
  • Temperature
  • Capillary refill
  • Monitor skin for pallor, flushing, cyanosis, diaphoresis, piloerection
Assessment (Cont’d)-
  • Check bowel sounds
  • If NG tube present, check drainage for blood
  • Passive ROM and oral care
  • Talk with client, even if sedated or intubated
systemic inflammatory response syndrome sirs
Systemic Inflammatory Response Syndrome (SIRS)

Systemic Inflammatory Response Syndrome (SIRS)- a systemic inflammatory response to a variety of insults, including infection, ischemia, infarction, and injury

  • Characterized by generalized inflammation of organs
  • Two or more of the following conditions: temperature >38.5°C (101.3 F) or <35.0°C (95.0 F); heart rate of >90 beats/min; respiratory rate of >20 breaths/min or PaCO2 of <32 mm Hg; and WBC count of >12,000 cells/mL, <4000 cells/mL, or >10 percent immature (band) forms
multiple organ dysfunction syndrome mods
Multiple Organ Dysfunction Syndrome (MODS)
  • Results from SIRS
  • Characterized by failure of two or more organ systems such that homeostasis can not be obtained without intervention
  • Often culminates in ARDS
  • Can cause massive vasodilation and myocardial depression
  • Commonly manifests as changes in LOC
  • Acute renal failure common
GI tract highly vulnerable to ischemic injury secondary to shunting in early stages
  • At risk for ulceration and GI bleeding
  • Potential for bacterial translocation from GI tract to cirulation
  • Causes hypermetabolic state
Failure of coagulation system manifests as DIC
  • Electrolyte changes and fluid shifts
  • Identifying organ dysfunction video

A patient with a gunshot wound to the abdomen is being treated for hypovolemic and septic shock. To monitor the patient for early organ damage associated with MODS, it is most important for the nurse to assess:

  • Urine output
  • Lung sounds
  • Peripheral circulation
  • Central venous pressure
the development of mods is confirmed in a patient who manifests
The development of MODS is confirmed in a patient who manifests:
  • Urine output of 30 ml/hr, a BUN of 65 mg/dl, and a WBC of 1120/ul
  • Upper GI bleeding, GCS score of 7, and a Hct of 25%
  • RR of 45/min, PaCO2 of 60, and a chest x-ray with bilateral patchy infiltrates
  • An elevated serum amylase and lipase, serum creatinine of 3.8 mg/dl, and a platelet count of 15,000/ul
management of sirs and mods
Management of SIRS and MODS
  • Prognosis with MODS poor
  • Vigilant assessment
  • Prevent infection, maintain tissue oxygenation, nutritional and metabolic support, support individual failing organs

At 9pm, you admit a 63 year-old with a diagnosis of acute myocardial infraction to the ED. The physician is considering the use of fibrinolytic therapy with tissue plasminogen activator (tPA, alteplase (Activase)). Which information is most important to communicate to the physician?

  • Pt was treated with TPA 8 months ago
  • Pt takes coumadin for A-fib. The INR is 1.0 today
  • Pt has T-Wave inversions on ECG
  • Chest pain has been continuous since for 38 hours

Questions are from Prioritization, Delegation, and Assignment (LaCharity, Kumagai, and Bartz)