CHAPTER 69

SHOCK
DR. E. DELAVAN PH.D. RN
NSG 5140
 SHOCK

• Shock is a syndrome characterized by:

• Decreased tissue perfusion
• Impaired cellular metabolism

• It is a whole body response – not a disease process

• All organs are affected by shock

• They either work harder to obtain oxygenation or adapt to reduced oxygen levels
 SHOCK

• Shock is categorized by the functional impairment:

• Low Flow:
• Hypovolemic – decrease in total body fluid
• Cardiogenic – direct pump failure
• Distributive:
• Septic, neurogenic and anaphylactic
• Fluids shifted from central vascular space to tissues (not returned to vascular system)
 HYPOVOLEMIC SHOCK

• Hypovolemic Shock: occurs when the intravascular fluid is lost and the remaining volume is
inadequate to fill the vascular space
• Absolute Volume losses:
• Hemorrhage
• Diabetes insipidus
• GI loss (vomiting, diarrhea)
• Diuresis
• Relative Loss:
• Fluid shift out of the vascular space into the interstitial space (tissues)
• Example sepsis or burns
TYPES OF SHOCK
 DISTRIBUTIVE SHOCK
SEPTIC SHOCK
• Sepsis is a systemic inflammatory response to infection
• Severe sepsis is complicated by organ dysfunction
• Septic shock develops due to a widespread infection causing organ failure and
dangerously low blood pressure.
 STAGES OF SHOCK

• Regardless of what action/condition starts the process, the body will first try to
compensate to ensure oxygenation for the vital organs
• Stages:
• 1. Initial
• 2. Compensatory
• 3. Progressive
• 4. Refractory
 STAGES OF SHOCK: INITIAL

• Clinical Signs:
• Usually not clinical apparent
• Metabolism changes from aerobic to anaerobic
• Lactic acid production begins
• Compensatory actions
• Increase in Heart rate (mild)
• Mild vasoconstriction
 STAGES OF SHOCK
COMPENSATORY
• Clinical Signs: • Compensatory actions by the body
• Decrease in blood pressure 10 – 15 • Increase in heart rate
mmHg • Increase respiratory rate
• Increase in lactic acid production • Kidneys reabsorb fluid
• Mild acidosis – decrease in pH and • Stimulation of thirst
hyperkalemia • Decrease in pulse pressure
 STAGES OF SHOCK
PROGRESSIVE
• Progressive shock begins as the compensatory mechanisms fail.
• More aggressive interventions are necessary to prevent the patient from developing
multisystem organ dysfunction
• Decreased cellular perfusion
• Increased anaerobic metabolism

• Altered capillary permeability

• Fluids leak into the tissue
• Less in the vascular space = hypotension
 STAGES OF SHOCK
PROGRESSIVE
• Clinical signs
• Significant decreased in blood pressure
• Fluid leaking into the alveoli = poor oxygenation
• Tachycardia – poor cardiac output
• Anoxia of non-vital organs (shunting blood to the core organs) – pallor – cyanosis in
extremities
• Hypoxia of vital organs (heart, brain kidney)
• Moderate acidosis – lactic acids level increases
• Tissue death is occurring
 STAGES OF SHOCK
REFRACTORY
• Refractory – high rate of mortality
• Exacerbation of anaerobic metabolism
• Accumulation of lactic acid
• Increased capillary permeability – venous pooling
• Hypotension
• Worsening of cardiac function
• Failure of organs
STAGES OF SHOCK
 DIAGNOSTIC STUDIES

• No one single test to determine shock

• Thorough history and physical
• Lab studies
• Hemoglobin and hematocrit
• Lactate level
• Arterial blood gases – bicarbonate level (HCO3 21 – 28 mmol/L)
• 12 lead ECG – heart rate and rhythm
• Radiology – chest x-ray or CT scan
 HYPOVOLEMIC SHOCK

• Occurs when there is too little circulating volume which prevents total body
oxygenation
• Causes include:
• Trauma
• Surgery
• Dehydration
• Internal hemorrhage (blunt trauma, GI ulcers)
 HYPOVOLEMIC SHOCK
RISK FACTORS
• Age: hypovolemic shock more common in young people from recent illness, trauma
• GI ulcers
• General surgeries
• Prolonged nausea and/or vomiting
• Use of diuretics, ASA or other NSAIDs
• Ask about fluid output
• Urine output will decrease even if intake remains normal in early stages

• Asses for obvious signs or factors: Hemorrhage, including wounds and drains
 HYPOVOLEMIC SHOCK
CARDIOVASCULAR
• Early Clinical Signs: • Late Clinical Signs:
• Decreased blood pressure • Increase in diastolic pressure =
• Increased pulse rate narrowing of the pulse pressure
• Peripheral pulses – diminished • Systole pressure will decrease and
(blocked with light pressure) cardiac output will decrease
• Peripheral pulses present with
Doppler
 HYPOVOLEMIC SHOCK: SIGNS

• Respiratory:
• Early: rate will increase – improve oxygenation
• As shock progresses – lactic acid build (anaerobic metabolism)
• Late: rate will decrease and depth will increase

• Renal (Kidney):
• Body will begin to reabsorb fluid – decrease urine production (increase water reabsorption)
• Late stage (severe) – no urine output
• Measure every hour
 HYPOVOLEMIC SHOCK: SIGNS

• Skin changes:
• Peripheral vessel vasoconstriction (more blood to vital organs)
• Early: Cool, clammy – pale mucous membranes
• Late: Skin become mottled, increased cap refill
 HYPOVOLEMIC SHOCK: SIGNS

• Central Nervous System:

• Early: May be restless or agitated, stimulation of thirst
• Late: confusion, lethargy - to somnolence and a decreased LOC
• Skeletal Muscle:
• Early: weakness and pain due to hypoxia
• Late: increasing weakness and loss of deep tendon reflexes
 HYPOVOLEMIC SHOCK
NURSING INTERVENTIONS
• Oxygen therapy
• Ensure a patent airway
• Administer oxygen and elevate
patients feet
• Head of bed no more than 30*
• Monitor pulse oximetry
• Frequent assessment q 1 - 2 hrs.
• IV therapy:
• Blood and blood products as
appropriate
• PRBC – increase volume – improve
oxygen carrying ability
• Plasma – blood product – contain
clotting factors
• IV fluid – volume (NS or LR)
 HYPOVOLEMIC SHOCK
NURSING INTERVENTIONS
• Assess for life threatening injuries
• Control external bleeding with direct pressure (trauma)
• Insert indwelling urinary catheter – strict intake and output
• Insert naso-gastric (NG) tube (if needed)
• Medications or nutrition

• Consult HCP is fluid does not being up BP

• May need vasoactive medications
 HYPOVOLEMIC SHOCK
NURSING INTERVENTIONS
• Close Monitoring
• Pulse (rate, regularity and quality)
• Blood pressure – pulse pressure
• Respiratory rate
• Skin – mucous membranes, capillary refill
• Oxygen saturation
• Mental status
• Urine output
• Treat underlying cause: Surgery
 SEPTIC SHOCK

• Sepsis and Septic Shock: complex distributive shock that usually begins as a bacterial or
fungal infection
• Can progress to a dangerous condition over a period of days
 SEPSIS

• Etiology: cause is bacterial infection – that escapes local control

• Immunological patients: fungal infections can lead to sepsis
• Increase in the number of drug resistant organisms is resulting in more cases of sepsis

• Health promotion and implementing best practices for infection control are the best
strategies for sepsis and septic shock
• Older adults are at more risk of sepsis than younger adults
 SEPSIS: INITIAL STAGE

• Stage: Local Infection:

• Infection is confined to a local area
• Immune system responds:
• Inflammatory mediators
• WBCs

• WBCs – invade infectious area = vasodilation = increased perfusion

• Results in capillary bed leakage – infectious organisms enters the blood system =
systemic infection
 SYSTEMIC INFECTION: EARLY SEPSIS

• When the pathogen enter the blood stream, it uses fuel (glucose) in the vascular system to
reproduce
• As infectious organism numbers increase – body responds with widespread inflammation

• Known as Systemic Inflammatory Respond Syndrome (SIRS)

• Inflammation leads to tissue and vascular changes which impairs oxygenation and
perfusion
 SYSTEMIC INFLAMMATORY RESPOND
SYNDROME
(SIRS)
• Clinical Signs and Symptoms:
• Mild hypotension
• Impaired oxygenation: Increased respiratory rate
• Tachycardia
• Fever – can vary from low to high grade
• Elevated WBC count
• Edema
• ** important to recognized changes in assessment and implement nursing actions =
improve patient outcomes
 SIRS: NURSING INTERVENTIONS

• Nursing Interventions
• Frequent focused assessments and vital signs
• Supplemental oxygen and fluids as needed
• Strict intake and output monitoring
• Lab – monitor WBC counts, H & H
• Notify physician
• Assess to determine site(s) of infection (urinary, respiratory extra)
• Culture and sensitivity of specimens from possible site(s) of infection
 SEPSIS

• Sepsis – a systemic inflammatory response to a suspected or documented infection

• With early sepsis you see the signs of SIRS which will worsen with time
 SEPSIS WITH SIRS

• Clinical Signs • Temperature > 101*

• Blood pressure
• Urine output
• Cap refill
• Changes in mental status
(disorientation, confusion)
• Skin pale, cool to touch
• Heart rate (tachycardia)
• Respiratory rate (tachypnea)
• WBC count > 10 X 109L
• Plasma C reactive protein levels
• Lactic acid levels
• Significant edema: positive fluid
balance
 SEPSIS WITH SIRS
NURSING INTERVENTIONS
• Within 3 hours suspected sepsis
• Measure serum lactate levels
• Obtain blood cultures (blood, urine, wound)
• Administer broad spectrum antibiotics
• If hypotensive or serum lactate level is elevated – Give IV fluid bolus NS or LR
• Frequent assessment (every 1hr)
• Frequent vital signs
• Strict intact and output (may need a urinary catheter)
• Supplement oxygen as necessary
SEPSIS BUNDLE
 SEVERE SEPSIS

• Severe Sepsis: progression of sepsis

• All the tissue are involved - hypoxia – some organs experiencing cell death
• Results in a large inflammatory response- vasodilation and blood pooling
• Blood pooling causes micro thrombi to form
• Results in hypoxia and reduced organ function
• Increasing hypoxia = anaerobic metabolism (increasing lactic acid levels) = more
toxins in the blood stream
 SEVERE SEPSIS AND SHOCK

SEVERE SEPSIS SEPTIC SHOCK

• Cardiac: tachycardia • Due to multiple micro clots – low or no
• Decrease blood pressure – widening clotting factors = hemorrhage
pulse pressure • Dramatic decrease in blood pressure,
cardiac output and pulse pressure

• Respiratory
• Depth of respirations increases and rate • ARDs – mechanical ventilator
slows = Poor oxygenation saturations • Intensive care unit care required
• CPAP or BIPAP – critical care unit
 SEVERE AND SHOCK

SEVERE SEPSIS SEPTIC SHOCK

• Skin is warm and no cyanosis is present • Cool, clammy with pallor, mottling or
– temporary (< 24 hrs.) cyanosis
• Patients may have blood oozing from
their gums or any access ports (IV sites)

• Renal: continued low output with • Extremely poor output due to

hypovolemia (anuria)
increase in serum creatinine levels, BUN
(oliguria)
 SEPTIC SHOCK

• Septic Shock: stage of sepsis when multi organ failure is evident and
uncontrolled bleeding is present
• Even with interventions death rate is > 50%
• Accompanied by severe hypovolemic shock and hypo-dynamic cardiac function
• Inability to clot because platelets were consumed earlier (clots)
• Capillary leak continues and severe hypoxia occurs – death
 SEPSIS AND SEPTIC SHOCK LAB

• Lab:
• Assess for presence of bacteria in vascular system – blood cultures
• Increasing serum lactate level
• Normal or low WBC
• used up fighting the infection – body struggling to produce more
• C reactive protein – increased initially = indicates inflammation
• Decreased indicates septic shock
• D – dimer: rises as fibrin clots is broken down
 NURSING INTERVENTIONS

• Patient requires close observation - transfer to critical care units

• Close Monitoring
• Frequent assessment – every hour
• Frequent vital signs - every 15 minutes
• Skin – mucous membranes – cap refill
• Oxygen saturation
• Mental status
• Urine output
• Mental status
 MEDICATION THERAPIES

• Oxygen therapy
• Give as needed to keep pulse oximetry > 95% - high flow oxygen devices
• Mechanical ventilator

• Drug Therapy
• IV fluid for volume – NS or LR
• Antibiotics – vancomycin, aminoglycosides, systemic PCN
• Patient are often hyperglycemic: insulin therapy
• Low dose corticosteroids – address adrenal insufficiency
• Vasoactive medications to support blood pressure
 NURSING INTERVENTIONS

• Blood transfusions as necessary

• Strict intake and output
• Basic care:
• Hygiene
• Oral care
• Turning q 2hr
• Monitoring dressings and IV sites
• Compression stockings
 LATE STAGE OF SHOCK
NUTRITION
• The body uses a lot of energy to compensate for shock, especially in the late stages
• Patient will need nutrition support early to maintain energy requirements
• Late stages patient may received nutrition via NG tube or TPN through IV access
• Nursing action:
• Monitoring daily weights
• Intake and output
• Assess serum protein levels
 LATE STAGES OF SHOCK
FAMILY SUPPORT
• Multi organ dysfunction syndrome (MODS) – 2 or more organs failure
• Mortality rate is 70%
• Nursing actions
• Support to the family
• End of life discussions
• Consideration of advanced directives
• End of life care
REVIEW
 LEARNING OBJECTIVES

• Describe key terms (bolded)

• Describe the four stages of shock (initial, compensatory, progressive and refractory)
• Identify lab and diagnostic tests for shock
• Describe the causes and risk factors for hypovolemic shock
• Identify the early signs and symptoms of hypovolemic shock
• Describe nursing interventions that would be implemented in the early stages of hypovolemic shock
• Identify the late signs and symptoms of hypovolemic shock
• Describe nursing interventions that would be implemented during the late stages of hypovolemic
shock
 LEARNING OBJECTIVES

• Describe the causes and risk factors for sepsis

• Describe the pathophysiology for SIRS, sepsis and septic shock
• Identify the early signs and symptoms of SIRS
• Describe nursing interventions that would be implemented during SIRS
• Identify the signs and symptoms of sepsis and severe sepsis
• Describe nursing interventions that would be implemented during sepsis
• Describe signs and symptoms of septic shock
• Describe the nursing intervention that would implemented during septic shock
 QUESTIONS

• Chapter 69: Practice questions at end of chapter

• Contact
• oconnec@algonquincollege.com