Shock and Systemic Inflammatory

Response Syndrome

By: Bryan Mae H. Degorio, RN

Shock
- is a life threatening condition with a
variety of underlying causes.
- Characterized by inadequate tissue
perfusion that ,if untreated , results in
cell death.
- Systematic blood pressure is
inadequate to deliver oxygen and
nutrients to support vital organs and
cellular functions.
- Blalock in 1934, categorized shock into 4
etiology or causes:
a. Hematogenic
b. Neurogenic
c. Vasogenic
d. Cardiogenic
- 3 Major Factors that Regulate the
Circulatory Mechanism:
a. Preload
b. Ventricular contraction
c. Afterload
-types:
1. Hypovolemic Shock
2. Cardiogenic Shock
3. Circulatory Shock (Distributive Shock)
> Septic Shock
> Neurogenic Shock
> Anaphylactic Shock
*Obstructive Shock
-Vascular Responses
1. Central Regulatory Mechanisms
2. Local Regulatory Mechanisms
-Blood Pressure Regulation
BP= CO x TPR CO= SV x HR
>Maintained by:
a. nervous system
b. endocrine system
c. chemicals
>Maintain tissue/organ perfusion:
a. MAP= systolic BP + 2 (diastolic BP)
3
*should exceed 70-80 mmHg
-Stages of Shock
1. Compensatory Stage
>BP is maintained within normal limits
due to the effect of normally functioning
regulatory mechanisms
>s/sx:
- cold clammy skin
- oliguria
- hypoactive bowel sounds can be assessed.

>medical management:
a. identify the cause of shock
b. correction of shock
c. support of the regulatory mechanisms
>nursing management:
a. monitoring tissue perfusion
*LOC *urine output *V/S *skin *laboratory
values
 b. reducing anxiety
c. promoting safety

2. Progressive Stage
-exhaustion of the compensatory
mechanisms
- In this stage, the mechanisms that
regulate blood pressure can no longer
compensate and the mean arterial
pressure falls.
-assessment and dxtic findings:
a. respiratory effects
hypoxemia and hypercarbia

intense inflammatory response

decreased surfactant production

acute respiratory distress syndrome

(acute lung injury, shock lung, non cardiogenic

pulmonary edema)
b. cardiovascular effects
dysrhythmias
myocardial infarction
cardiac depression
c. neurologic effects
decreased cerebral perfusion
*mental status change
*behavioral change
*pupillary dilation
d. renal effects
MAP<80mmHg
acute renal failure
e. hepatic effects
decreased blood flow

less ability to perform hepatic functions

f. gastrointestinal effects
decreased blood flow

*PUD *bloody diarrhea *sepsis

g. hematologic
DIC

shock
-medical management:
a. depends on the type of shock
b. depends on the decompensation of the
organ systems
Management Common To All Types Of Shock
a. optimize intravascular volume
b. supporting the pumping action of the heart
c. improving the competence of the vascular
system
Nursing Management:
a. preventing complications
b. promoting rest and comfort
c. supporting family members
3. Irreversible Stage
-severe organ damage
-can no longer respond to treatment
-survival is less likely
-medical management:
a. same with the progressive stage
b. the use of life supporting drugs
like epinephrine and investigational
medications.
-nursing management:
a. same with progressive shock
b. moral support to the family
c. ethical issues (living will)
 Clinical Findings in the Stages of Shock
Finding Compensatory Progressive Irreversible
BP normal Systolic <80 Mechanical or
-90mmHg pharma support
HR >100bpm >150bpm erratic, asystole

Respiration >20 breaths/ min Rapid, shallow Intubation

crackles
Skin cold, clammy Mottled, Jaundice
petechiae
Urine Output decreased 0.5ml/kg/hr anuria, needs
dialysis
Mentation confusion Lethargy Coma
 Finding Compensatory Progressive Irreversible
A/B Balance Resp Alkalosis Met Acidosis Profound
Acidosis
General Management for Shock

• fluid replacement to restore

intravascular volume
• vasoactive medications to restore
vasomotor tone and improve cardiac
function
• nutritional support to address the
metabolic requirements that are
dramatically increased in shock
A. Fluid Replacement:
- Is administered in all types of shocks. The type
of fluids administered and the speed of delivery
vary, but fluids are given to improve cardiac
and tissue oxygenation.
- may include CRYSTALLOIDS (electrolyte
solutions that move freely between intravascular
and interstitial space), COLLOIDS (large-
molecule intravenous solutions) or blood
components.
 COMLICATIONS OF FLUID ADMINISTRATION
- The most common and serious side effect
of fluid replacement are cardiovascular
overload and pulmonary edema.
B. VASOACTIVE MEDICATION THERAPY
- Administered in all forms of shocks to
improve the patients hemodynamic
stability when fluid therapy alone
cannot maintain adequate MAP.
 -Vasoactive medications are
selected for their action on receptors of
the sympathetic nervous system.
- when vasoactive medications
are administered, vital sign must be
monitored frequently(at least every
15min until stable or more often if
indicated)
C. NUTRITIONAL SUPPORT -Nutritional
support is an important aspect of care for
the patient with shocks.
-Increased metabolic rates during shock
increase energy requirements. The patients in
shocks requires more than 3000 calories daily.
- The release of catecholamines early in the
shocks continuum causes glycogen stores to
the depleted in about 8 to 10 hours.
TYPES OF SCHOCK
HYPOVOLEMIC SHOCK
-most common type of shock
-characterized by decreased intravascular
volume of 15-25%
-predisposing factors:
External: Fluid Losses Internal: Fluid Shifts
a. trauma a. hemorrhage
b. surgery b. burns
c. vomiting c. ascites
d. diarrhea d. peritonitis
e. diuresis e. dehydration
f. diabetes insipidus
Manifestations:
1. Decreased Level of Consciousness
2. Tachycardia (pulse: weak and
thready)
3. Decreased B/P
4. Decreased Cardiac Output (CO=
SV x HR)
5. Decreased Urinary Output
6. Cool, Clammy Skin
PATHOPHYSIOLOGY

DECREASED IN BLOOD VOLUME

DECREASE IN VENOUS RETURN

DECREASE IN STROKE VOLUME

DECREASED IN CARDIAC OUTPUT

DECREASE IN TISSUE PERFURION

-medical management:
>goals:
a. restore intravascular volume
b. redistribute fluid volume
c. correct the underlying cause
*pharmacologic therapy
desmopressin anti-emetic
insulin anti-diarrhea
-nursing management:
a. administer O2 as ordered
b. administering blood and fluids safely
c. assess type client hydration status
d. monitor hemoglobin and hematocrit level
e. Monitor the circulatory status (HR,
arterial pressure, peripheral perfusion, and
UO.)
f. Monitor Vs and for hypotension
g. Monitor I and O, urine output, and
insert FBC as ordered
h. Monitor LOC
e. Administer small doses of narcotic
analgesic as ordered
f. Antibiotic for severely injured
g. Pressure on site- severe trauma
CARDIOGENIC SHOCK
-failure of the heart to pump blood adequately to
the circulation causing reduction in CO
-due to cardiac failure
-either coronary and non coronary
Coronary Factors Non Coronary Factors
a. myocardial a. cardiomyopathies
infarction b. valvular damage c. cardiac
tamponade
d. dysrhythmias
-signs and symptoms:
a. anginal pain
b. hemodynamic instability
c. dysrhythmias
 Decreased cardiac
contractility

Decreased stroke volume

and Cardiac output

Ineffective ventricular
emptying

Pulmonary congestion

Decreased systemic
Decreased coronary
tissue perfusion
artery perfusion
Pathophysiology
-medical management:
a. correction of underlying cause
b. initiation of first line treatment
*supplemental oxygen *vasoactive
medications
*controlling chest pain *controlling HR
*selected fluid support *mechanical
cardiac support
 c. pharmacologic therapy
*dobutamine
*nitroglycerine
*dopamine
*vasoactive meds
*anti-arrhythmic meds
d. fluid therapy
-nursing management:
a. administer IV morphine sulfate
b. administer O2
c. Prepare client for mechanical ventilation
d. administer diuretics and nitrates while
constantly monitoring the BP
e. Administer vasopressin, and postive
inotropic
f. Prepare the client for the insertion of
intraaortic balloon pump.
g. Prepare for emergency reperfusion such
as transluminal coronary angioplasty
h. Monitor blood gas
i. UO monitor
CIRCULATORY SHOCK
- is also called distributive shock
- occurs when the blood is abnormally distributed in the
vasculature

Pathophysiology:

vasodilation decreased stroke

volume

maldistribution decreased
of blood volume cardiac output

decreased tissue
decreased
perfusion
venous return
Types of Circulatory shock:
 Septic shock
 Anaphylactic shock

 Neurogenic shock

Risk Factors for Circulatory Shock

Septic shock Anaphylactic shock Neurogenic shock

Imunnosuppresion Penicillin sensitivity Spinal cord injury

Extreme ages (<1 Transfusion Spinal anesthesia
and >65) Bee sting allergy Depressant action
Malnourishment Latex sensitivity Glucose deficiency
Chronic illness
Invasive procedure
A. Septic Shock
- circulatory collapse due to infection
- due to invasive infection such as
viruses, parasites and bacteria
- Gram (-) bacteria is the most common
cause
- genito-urinary system- the most
common source of causative organism
usually after instrumentation in the
tract
- caused by the released of bacteria
toxin that directly act on the on
the blood vessel causing
vasodilation and pooling of blood ,
resulting mostly from gram
negative septicemia
- the goal of treatment is controlling
the cause of sepsis
 Manifestations:
a. The HYPERDYNAMIC PHASE
 High cardiac output with systemic vasodilatation.
 The BP remains within normal limits.

 Tachycardia

 Hyperthermic and febrile with warm, flushed skin

and bounding pulses
b. The HYPODYNAMIC or irreversible phase
 LOW cardiac output with VASOCONSTRICTION
 The blood pressure drops, the skin is cool and pale,
with temperature below normal.
 Heart rate and respiratory rate remain RAPID!

 The patient no longer produces urine.

 MEDICAL MANAGEMENT:
• Current treatment involves identifying
and eliminating the cause of infection.
• Fluid replacement must be instituted to
correct Hypovolemia
• Intravenous antibiotics are prescribed
based on culture and sensitivity.
 Nursing management:
a.Control of infection
b.Administer IV antibiotics
c. Administer O2, IV, vasoactive durgs
d.Monitor for CVP or pulmonary wedge pressure
 e. Obtain specimen for C and S
f. Assess hydration and electrolyte
imbalance

B. Anaphylactic Shock
- circulatory collapse due to massive
vasodilation from an allergic
reaction
- massive vasodilation resulting from
serious dramatic allergic reaction
causing release of histamine and
related substances for damaged
cell
 - can be due to venom, medication,
and dyes use in radiologic study

 MEDICAL MANAGEMENT:
 Treatment of anaphylactic shock
requires removing the causative
antigen, administering medications
that restore vascular tone, and
providing emergency support of basic
life functions.
 EPINEPHRINE is the drug of choice
given to reverse the vasodilatation
• Nursing management:
a. Establish a patent airway
b. Prepare for the administration
of epinephrene, benadyril,
corticosteroid
c. administer o2 and IV fluids
d. administer vasoactive drugs
C. Neurogenic Shock
-occurs due to the loss of sympathetic
tone
- an interference in the balance of the
vasoregulation influences vessels
resulting in massive vasodilation and
pooling of blood
- Aka- Primary shock
- vasodilation of both arterioles and
venules increases the reservoir
capacity thereby decreasing the
venous return
Manifestations:
a. The patient who suffers from neurogenic shock
may have warm, dry skin and BRADYCARDIA!,
poiklothermic temp.
Management:
- This involves restoring sympathetic tone,
either through the stabilization of a spinal
cord injury or in anesthesia, proper
positioning.
-nursing management:
a. elevate the head of the bed 30 degrees
( in spinal/epidural anesthesia)
b. immobilize the patient
(in spinal cord injury)
c. elastic compression stockings
d. feet elevation
e. heparin/low molecular weight heparin
f. pneumatic compression of the legs
g. passive ROM
Systemic Inflammatory
Response Syndrome
SIRS
- clinical response to a nonspecific
insult of either infectious or
noninfectious origin.
- is nonspecific and can be caused by
ischemia, inflammation, trauma,
infection, or a combination of
several insults.
SEPSIS
- is the systemic response to infection
and is defined as the presence of SIRS
in addition to a documented or
presumed infection
Epidemiology:
 500,000 – 750,000 cases annually in the United

States and rising

 Most common cause of death in non-coronary ICU

and two-thirds of cases occur in hospitalized

patients
 Increasing incidence of severe sepsis is

attributable to the aging population with chronic

diseases
 Widespread use of antimicrobial agents,

indwelling catheters, mechanical devices and

ventilators
 increase incidence

·30% mortality when shock is present

· Severe sepsis $22K/pt, $16 billion/year
Criteria for Diagnosing:
 Systemic Inflammatory Response
System(SIRS)
o Widespread inflammatory response
o Two or more of the following
 Temp > 38°C or ˂ 36°C
 Heart Rate > 90 bpm
 Tachypnea (RR > 20) or
hyperventilation (PaCoz ˂ 32
mmHg)
 WBC > 12,000 cells/mm3, < 4000
cells/mm3 or presence of >10%
immature neutrophils
 Sepsis
-SIRS + definitive source of infection
 Severe Sepsis
-Sepsis + organ dysfunction,
hypoperfusion, or hypotension
-Hypoperfusion and perfusion
abnormalities may include but not
limited to lactic acidosis, oliguria
or an acute mental state.
 Septic Shock
- Sepsis + hypotension despite fluids
-Perfusion abnormalities
a. Lactic acidosis
b. Oliguria
c. Acute AMS
 Multiple Organ System Failure
-Abnormal function of two or more
organs such that homeostasis cannot be
achieved without intervention
Pathophysiology:
Local Injury
(trauma, infection, ischemia)

Bacteria enters the damage tissue

Release of bacterial toxin

Toxin enters the blood and is circulated in the body

Damage the
Release of systemic Massive
endothelial
chemical mediators: vasodilation
cells
a. Bradykinin
b. Histamine
c. interleukin-1
Multiple organ damage
d. TNF
e. complement
Pathophysiology of SIRS

 The antigen-antibody reaction

stimulates multiple interacting
systems such as:
• Complement Cascade
• Cytokine cascades
• Arachidonic Acid Metabolites
• Cell Mediated Immunity
• Humoral Immune Mechanisms
• Clotting Cascade
 Cytokines
 Are Intercellular signaling proteins or
messengers
 More than 30 recognized
 Act through binding to specific
receptors on the target cells
triggering other cascades or its own
cascade
Pathophysiology of SIRS
 Pathophysiology of SIRS

TNF-α
 The earliest and most potent mediator in
SIRS
 It activates neutrophils, causing the
production of Interleukin-1(IL-1),
Interleukin-6 (INL-6), and Interleukin -8
(INL-8).
 It stimulates platelet activating factors
and prostaglandin,
and promotes leukocyte
or vessel cell wall adhesion.
Pathophysiology of SIRS
 IL-1 Pathophysiology of SIRS

 During an inflammatory response, it facilitates the

movement of WBCs toward the injury, ischemia, or
infected area
 It stimulates the release of arachidonic acid from
phospholipids in the plasma membranes, leading
to fever, hypotension, and decrease systemic
vascular resistance.
 IL-1 also leads to muscle protein breakdown
 IL-1 works with other cellular immunity
components to produce IL-2, which decreases
blood pressure, systemic vascular resistance, and
left ventricular ejection fraction.
 IL-2 may also increase left ventricular end diastolic
volume, cardiac output, and heart rate
 Pathophysiology of SIRS

IL-6
 Is a key messenger that can either
trigger the rest of the cascade or its
arrest
 Stimulates the release of acute
phase reactors
 Its serum levels are consistent with
the gravity of the immune reaction
 Nitric Oxide
 Nitric oxide is synthesised by inducible
nitric oxide synthase (iNOS) in the
vascular endothelium and smooth muscle
in response to pro-inflammatory cytokines
 NO is the vasoactive mediator responsible
for the fall in systemic vascular resistance
underlying the hypotension in the late
stages of SIRS and septic shock
 Pathophysiology of SIRS

Arachidonic Acid Cascade

 Thromboxane A2
• Is a potent vasoconstrictor and platelet
aggregator
• Leads to tissue ischemia from
hypoperfusion.
 Leukotrienes leads to
• ↑Capillary endothelial permeability
• Bronchoconstriction
• Activation of neutrophils
 Pathophysiology of SIRS

The Complement Cascade

 Controls the inflammatory process

• Chemotaxis
• Opsonization
• Promotion of phagocytosis
 Pathophysiology of SIRS

Clotting Cascade
 Fibrin is formed due to the injury of the
vascular endothelium
 Chemical mediators stimulate the release
of Hageman Factor and Thromboplastin
 These form clots at the site of the injury,
attempting to stabilize the site
 Fibrinolysis is activated by the coagulation
cascade, leading to mediator induced
(DIC).
 Pathophysiology of SIRS

Bradykinin
 The activation of the Hageman
Factor stimulates the release of
bradykinin
 Bradykinin creates vasodilatation and
capillary leakage, therefore volume
depletion.
 Pathophysiology of SIRS

Myocardial Depressant Factor

 Myocardial depressant factor is a

serum protein released by the
hypoperfused and ischemic cells of
the pancreas
 It decreases the velocity of
contractions of myocardial cells,
leading to decreased right and left
ventricular ejection fractions
 Pathophysiology of SIRS

Beta Endorphins

 Beta endorphins are released, by the

pituitary and hypothalamus, in
response to hypoperfusion
 They cause peripheral vasodilatation,
and decrease cardiac contractility
 Pathophysiology of SIRS

Stages of SIRS
 4 stages according to the gravity of the
situation
 Pathophysiology of SIRS

SIRS 1
Stages

 Release of proinflammatory
mediators
• These mediators create a web of
reactions designed to limit new
damage and ameliorate whatever
damage has already occurred
 Pathophysiology of SIRS

SIRS 2
Stages

 Pro-inflammatory and anti-

inflammatory mediators appear
in the systemic circulation
• Pro-inflammatory mediators recruit
neutrophils, lymphocytes, platelets,
and coagulation factors
 Pathophysiology of SIRS

SIRS 3
Stages

 Massive Systemic Inflammation

• Progressive endothelial dysfunction
occurs increasing microvascular
permeability
• Vessels lose tone and profound
vasodilatation occurs resulting in
severe shock
 Pathophysiology of SIRS

SIRS 4
Stages

 Most patients do not make it this

far --but if they do--
• A compensatory anti-inflammatory
response occurs trying to suppress
inflammation
 Clinical Picture
 The typical 2 or more of:
• Temp. >38°C or <36°C
• HR >90 bpm
• RR > 20 cpm or PaCO2 < 4.3 kPa
• WBCs
 >12 x 109/lit
 < 4 x 109/lit
 > 10% immature forms
 Symptoms & Signs of each organ sequels
 Clinical Picture

Organ Manifestations
 Cardiovascular
• Skin warm and flushed
• Widened pulse pressure
• Cardiac output is ⇑ but SVR is ⇓
• Eventually C.O. declines
exacerbating hypoperfusion
 Clinical Picture

Organ Manifestations
 Pulmonary
• Hypoxemia may be masked by
hyperventilation
• Respiratory alkalosis
• Pulmonary edema
• Respiratory failure
• Bronchoconstriction
• ARDS
 Clinical Picture

Organ Manifestations
 CNS
• Altered mental  Renal
status • Oliguria: < 500
• Confusion ml/day
• Irritability • Metabolic Acidosis
• Agitation
• Disorientation
• Lethargy
• Seizures
• Coma
 Clinical Picture

Organ Manifestations
 GIT  Blood
• Impaired motility • ⇑ or ⇓ WBCs
• ⇑ SGPT & SGOT • ⇑ PT and PTT
• Hyperbilirubinemi • ⇑ or ⇓ Platelets
a • Anemia
• Hepatic necrosis
• Hypoprothrombin
emia
• Hypoglycemia
 Investigations
 Cytokines assay (IL-6, IL-8 & TNF)
 Blood Culture
 Burn eschar biopsy with culture &
sensitivity
 Serum Procalcitonin
• The only lab test that differentiates
 SIRS (0.5 -2 ng/dl) from
 Sepsis (>2 & <10 ng/dl) from

 MOD (>10 and often >100ng/dl)

 Treatment
= Elimination of triggering factor (LPC
& LPS)
 LPS

• Antibiotics according to C&S

• Gut decontamination
 LPC through
 Prompt early surgical eschar excision
 Chemical elimination eg. Cerium Nitrate
 Treatment
 Supportive
 Medical
 Surgical
 Treatment

Supportive Therapy
 Volume replacement
 +ve inotropes & vasopressors
 Ventilation (Pressure support or PEEP)
 Nutritional Support
• Iso-Osmotic Feedings
• TPN
• PPN
• Immune Modulatory Foods such as Arginine,
Glutamine & fish oils
 Treatment

Medical
 Potent anti-oxidants
• Methylene Blue given IV
• Acetyl Cysteine
• Vitamin C
 Immune Modulators
• Ibuprofen (proved of limited value)
• Centoxin: an Ab to endotoxins
• NOSI (nitric oxide synthetase inhibtor) very
much accepted
• IL-6 blockers Experimental
 Surgical Excision
 Best option = Early excision +
coverage
 Best performed within the 1st 72
hours and after resuscitation
 Is the only way to break the circle
 Surgical Excision
 ⇓⇓ incidence of burn wound colonization

Barret et al, 2003

 Prognosis
 Death in 60% of cases of late stages &
shock in patients with no previous
history of medical conditions
 Death rate is higher if MOD develops &
is dependant on no. of organs affected
•3 organs 85%
•4 organs 95%
•5 organs 99%
Thank You