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Objectives
Unit III (d) Shock and its
management
Edition:
Akash Samuel
Nursing Instructor
BSN, RN
Acknowledgement:
Tanzeel Ul Rahman
Nursing Instructor
BSN, RN, M.Phil Public health
• Define shock.
• Identify physiological responses to shock
• Explain Clinical manifestations, and general
management of different stages of shock
• Identify treatment goals of client with shock
• Describe general management strategies for
shock
• Explore different types of shock

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Objectives
Shock
• Explore hypovolemic shock its pathophysiology,
medical management and nursing management Definition:
• Explore Cardiogenic shock its pathophysiology,
medical management and nursing management Clinical conditions that result in cellular
• Explore neurogenic shock its pathophysiology, medical hypoperfusion are often referred to as shock
management and nursing management states. Which results in inadequacy to deliver
• Explore anaphylactic shock its pathophysiology,
medical management and nursing management oxygen and nutrients to support vital organs
• Explore septic shock its pathophysiology, medical and cellular function.
management and nursing management
• Explain MODS

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Pathophysiology Physiological responses to

shock
• Shock begins with cardiovascular system • Hypoperfusion → hypoxia → anaerobic
failure cellular respiration → lactic acidosis →
• Alterations in at least one of four metabolic acidosis → cell death →
components: progressive organ dysfunction
– Blood volume • Hypercoagulability – increasing viscosity
– Myocardial contractility of blood
– Blood flow • Activation of the inflammatory response
– Vascular resistance – vasoactive mediators i.e. histamine

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Stages of shock
Three stages of shock.
• Stage I (Compensated or Non-progressive).
• Stage II (Decompensated or Progressive).
• Stage III (Irreversible)
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Stage I (Compensated or Non-
progressive)
The body activates compensatory mechanisms in an effort
to maintain circulatory volume, blood pressure, and
cardiac output.
Vasoconstriction, increased heart rate, and increased
contractility of the heart contribute to maintaining
adequate cardiac output. This results from stimulation of
the sympathetic nervous system and subsequent release of
catecholamines (epinephrine and norepinephrine). Patients
display the often-described “fight or flight” response The
body shunts blood from organs such as the skin, kidneys,
and gastrointestinal tract to the brain, heart, and lungs to
ensure adequate blood supply to these vital organs.
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Medical Management in
Stage 1
Medical treatment is directed toward
• Identifying the cause of the shock
• Correcting the underlying disorder

• Non specific measures such as fluid

replacement and medication therapy can
initiated to maintain an adequate BP and tissue perfusion

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Nursing Management in Stage Stage II (Decompensated or

Monitoring Tissue Perfusion
1 Progressive)
• The nurse observes for changes in
– level of consciousness,
– vital signs( Report BP lower than 90 mm Hg and pulse
• Compensatory mechanisms begin to fail,
pressure less than 30 mm Hg) metabolic and circulatory derangements
– urinary output, skin, and laboratory values (eg, base
deficit and lactic acid levels). In the compensatory become more pronounced, and the
stage of shock, serum sodium and blood glucose levels inflammatory and immune responses may
are elevated
• Administer prescribed fluids and become fully activated.
medications, and promote patient safety.
• Oxygen administration
• Hemodynamic monitoring
• Reduce anxiety

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Clinical Manifestations of Clinical Manifestations of Stage

•
Stage II
Respiratory Effects
II
• Renal Effects
– Respirations are rapid and shallow. – ARF, increased BUN and Creatinine
– Crackles are heard over the lung fields. – Low urine output
– Acute respiratory distress syndrome – Acid base and electrolyte imbalance
• Cardiovascular Effects • Gastrointestinal Effects
– Dysrhythmias and ischemia. – Stress ulcers in the stomach, putting the patient at risk for GI bleeding
– Heart rate is rapid, sometimes exceeding 150 bpm. • Hematologic Effects
– chest pain – Disseminated intravascular coagulation (DIC)
– Week pulse – Ecchymoses, petechiae
– Low BP • General
• Neurologic Effects – Anxiety or agitation/restlessness
– changes in behavior or agitation and confusion. – Bluish lips and fingernails
– Subsequently, lethargy increases, and the patient begins to lose – Dizziness, lightheadedness, or faintness
consciousness – Pale, cool, clammy skin
– Dizziness, Light headedness or faintness – Profuse sweating, moist skin

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Medical Management in Medical Management in

Stage II Stage II
• Depends on the type of shock
• Supporting the respiratory system
• Preventing Complications
• Optimizing intravascular volume • Promoting Rest and Comfort
• Supporting the pumping action of the heart
• Enteral nutritional support, aggressive hyperglycemic • Supporting Family Members
control with IV insulin
• Antacids, histamine-2 (H2) blockers, or antipeptic agents to
reduce the risk of GI ulceration and bleeding.
• The patient should not be warmed too quickly, and
warming blankets should not be applied, because they can
cause vasodilation and a subsequent drop in BP.

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Stage III (Irreversible)

In the final, irreversible stage, cellular and tissue
injury are so severe that the patient’s life is not
sustainable even if metabolic, circulatory, and
inflammatory derangements are corrected.
At this point, full-blown multisystem organ
dysfunctionsyndrome (MODS) may become
evident.
• The judgment that the shock is irreversible can be
made only retrospectively on the basis of the
patient’s failure to respond to treatment.

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Stage IV: Refractory Systemic Inflammatory Response

Syndrome (SIRS)
• Prolonged inadequate tissue perfusion • Widespread systemic inflammatory
– Unresponsive to therapy response
– Dysrhythmias
• Associated with diverse disorders
– Pulmonary edema
– Infection
– Respiratory Distress Syndrome (RDS)
– Trauma
– Cerebral changes
– Shock
– Renal decreased GFR
– Pancreatitis
– Contributes to multiple organ dysfunction and
death – Ischemia
• Most frequently associated with sepsis

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Goal of Shock Treatment General Management Strategies of

Goal of treatment are to reestablish adequate
organ perfusion and oxygenation and to
lessen the inflammatory response as quickly
as possible.
• opportunity that increases the likelihood
of patient survival occurs when
aggressive therapy begins within 6 hours
of identifying a shock state, especially
septic shock
Shock
• Support of the respiratory system with
supplemental oxygen and/or mechanical
ventilation to provide optimal oxygenation
• 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 often dramatically increased
in shock

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General Management Strategies of General Management Strategies of

Shock Shock
Fluid Replacement
• The fluids administered may include crystalloids • Vasoactive Medication Therapy
(electrolyte solutions that move freely between – These medications help increase the strength
intravascular and interstitial spaces), colloids of myocardial contractility, regulate the heart
(large-molecule IV solutions), and blood
rate, reduce myocardial resistance, and initiate
components (packed red blood cells, fresh frozen
plasma, and platelets). vasoconstriction
• Complications of fluid replacement:
– cardiovascular overload and pulmonary edema.
– Abdominal compartment syndrome

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General Management Strategies General Management

of Shock Strategies of
Nursing Considerations while using vasoactive Shock
agents:
• Vital signs must be monitored frequently (at least
every 15 minutes until stable • Nutritional Support
• administered through a central venous line, • Parenteral or enteral nutritional support should
because infiltration and extravasation of some be initiated as soon as possible
vasoactive medications can cause tissue necrosis
• An IV pump or controller should be used .
• should never be stopped abruptly, because this
could cause severe hemodynamic instability

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Types of shocks Hypovolemic shock

• Hypovolemic shock Hypovolemic shock is a result of inadequate
– Hemorrhagic shock circulating blood volume, The extracellular
• Cardiogenic shock body fluid is found in one of two
• Distributive shock compartments: intravascular (inside blood
i. Neurogenic shock vessels) or interstitial (surrounding tissues).
ii. Anaphylactic shock Hypovolemic shock occurs when there is a
iii. Septic shock reduction in intravascular volume by 15% to
-Obstructive Shock 30%, which represents a loss of 750 to 1500
mL of blood in a 70-kg person

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Etiology

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Assessment Medical Management

• Treatment of the Underlying Cause
– Hemorrhaging, efforts are made to stop the bleeding. This
• History or active bleeding may involve applying pressure to the bleeding site or
• ABG’s surgical interventions.
– If the cause of the hypovolemia is diarrhea or vomiting,
• Lactate Levels medications to treat diarrhea and vomiting
• CBC (Hb, HCT)
• Coagulation profile
• BSL

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Medical Management
• Fluid and Blood Replacement Nursing Management
– Large bore IV access or central Venous access
– Fluid replacement • Continuously telemetry
• Sodium chloride 0.9% infusion
• Ringer lactate infusions • Prevent from hypothermia
– Plasma Expanders • Rapid infusion therapy
– Blood transfusion
• Surveillance of transfusion induced
– Antibiotic therapy
anaphylactic reactions and complications
• Pharmacologic Therapy
• Vasoactive medicines, antiemetic’s, antidiarrheal

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Cardiogenic Shock

• Definition:
Cardiogenic shock, which results from
loss of contractility of the heart, is an
extreme form of heart failure.

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Causes of Cardiogenic Shock

Cardiogenic Shock
• Either coronary or non coronary. Pathophysiology
• Left ventricular damage from myocardial
infarction
• Papillary muscle rupture
• Ventricular septal rupture
• Cardiomyopathy
• Cardiac tamponade
• Acute myocarditis
• Valvular disease
• Dysrrhythmias

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Medical Management of
Cardiogenic Shock
• Correction of Underlying Causes
• Initiation of First-Line Treatment
– Oxygenation
– Pain Control
– Hemodynamic Monitoring
– Laboratory Marker Monitoring
– Fluid Therapy
• A fluid bolus should never be given rapidly, because rapid
fluid administration in patients with cardiac failure may
result in acute pulmonary edema.

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Medical Management of
Cardiogenic Shock
• Pharmacologic Therapy
– Dobutamine.
– Nitroglycerin.
• Angiography
– Dopamine. • Angioplasty
– Epinephrine and • CABG
norepinephrine
– Furosemide
– Antiarrhythmic medications
Mechanical Assistive Devices
– IABP
– TPM
– PPM

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Nursing Management
• Preventing Cardiogenic Shock
• Telemetry continuously( hemodynamic
monitoring)
• Administering Medications and Intravenous
Fluids
– Prevent for both fluid deficit and overload.
• Maintaining Intra-Aortic Balloon Counter
pulsation
• Enhancing Safety and Comfort
– Proper positioning
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Distributive shock or Circulatory
shock
• The mechanism underlying all distributive
shock states is vasodilation that causes pools in
peripheral blood vessels.
i. Neurogenic shock:- Vasodilation results from
a loss of sympathetic innervation to the blood
vessels.
ii. Anaphylactic shock and septic shock,
vasodilation results from the presence of
vasodilating substances in the blood.
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Neurogenic Shock Clinical manifestations

• Neurogenic shock results from loss or • hypotension with bradycardia, rather
disruption of sympathetic tone, most than the tachycardia
often due to severe cervical or upper • dry, warm skin rather than the cool, moist
thoracic spinal cord injury. skin seen in hypovolemic shock.

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Medical Management Nursing Management

• Stabilization of a spinal cord injury or, in
the instance of spinal anesthesia
• Fluid replacement
• Vasoconstrictors
• External Pacing (for bradycardia)
• Assessment
• Anti-embolism stockings and elevating the
foot of the bed may minimize pooling of
blood in the legs.
• The nurse must check the patient daily for
any lower extremity pain, redness,
tenderness, and warmth
• Administration of heparin as prescribed
• Passive ROMs

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Mechanism of anaphylaxis
Anaphylactic shock
• IgE-mediated anaphylaxis:- immune response
• Anaphylaxis is an allergic reaction to a to a specific antigen.
specific allergen that evokes a life- • 1st time immune system is exposed to the
threatening hypersensitivity response. antigen, a very specific IgE antibody is formed
Anaphylaxis may be either and circulates in the blood.
immunoglobulin E (IgE)– or non–IgE • When 2nd time exposure to this antigen occurs,
mediated. the antigen binds to this circulating IgE, which
then activates the immune system, triggering
the release of chemical mediators that initiate
anaphylaxis.

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Mechanism of anaphylaxis Pathophysio of Anaphylaxis

• Non-IgE responses (anaphylactoid reactions):- occur • The antibody–antigen reaction causes the white
without the presence of IgE antibodies. blood cells (WBCs) to secrete chemical mediators
• 1st time the person is exposed to the antigen. that cause
• Systemic vasodilation
• rapid onset of hypotension
Direct activation of mediators causes this • Increased capillary permeability
response. Anaphylactoid reactions are • Bronchoconstriction
commonly associated with NSAIDs, including aspirin. • Coronary vasoconstriction
• Urticaria (hives).
• cardiac

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Medical Management

• Removing the causative antigen

• IV access
• Telemetry continuously
• Oxygen therapy if indicated
• Corticosteroids ( Solucortif = hydrocortisone)
• Antihistamines (Avil = Phenarimine injection)
• Intubation or mechanical ventilation
• Inotropes

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Nursing Management
• Monitor the patient’s response to the treatment.
• Providing care to relieve dermatological
manifestations.
• Evaluated for allergies and future risk for
anaphylaxis.

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Septic Shock
• Septic shock, the most common type of
circulatory shock, is caused by widespread
infection
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Clinical Menefestatins
In the early stage of septic shock
• BP may remain within normal limits (or hypotensive but responsive to fluids).
• Heart and respiratory rates elevated.
• High cardiac output with vasodilation.
• Hyperthermia (febrile) with warm, flushed skin, bounding pulses.
• Urinary output normal or decreased.
• Gastrointestinal status compromised (eg, nausea, vomiting, diarrhea, or decreased
bowel sounds).
• Subtle changes in mental status.
As sepsis progresses
• Low cardiac output with vasoconstriction
• BP drops
• Skin cool and pale
• Temperature normal or below normal
• Heart and respiratory rates rapid
• Anuria and multiple organ dysfunction progressing to failure
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Medical Management in Septic
Shock
• Blood, sputum, urine, and wound drainage specimens
are collected to identify and eliminate the cause of
infection.
• Potential routes of infection are eliminated (IV lines
rerouted if necessary). Abscesses are drained and
necrotic areas debrided.
• Fluid replacement is instituted.
• Broad-spectrum antibiotics are started. Recombinant
human activated protein administered to patients with
end-organ dysfunction and high risk of death.
• Aggressive nutritional supplementation (high protein) is
provided. Enteral feedings are preferred
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Nursing management of Septic
Shock
• Identify patients at risk for sepsis and septic shock.
• Carry out all invasive procedures with correct aseptic
technique after careful hand hygiene.
• Monitor IV lines, arterial and venous puncture sites, surgical
incisions, trauma wounds, urinary catheters, and pressure
ulcers for signs of infection.
• Reduce patient’s temperature when ordered for temperatures
higher than 40C (104F) or if the patient is uncomfortable by
administering acetaminophen
• Administer prescribed IV fluids and medications.
• Monitor hemodynamic status, fluid intake and output, and
nutritional status.
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Obstructive Shock Obstructive Shock (Cont.)

• Physical impairment to adequate
circulatory blood flow
• Causes
• Clinical manifestations
– Chest pain
– Dyspnea
– Jugular venous distension
– Hypoxia Figure 12-9. Obstructive shock

– Cause-dependent findings

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Management of Obstructive Multiple Organ Dysfunction

Shock Syndrome (MODS)
• Multiple organ dysfunction syndrome
• Treat the cause (MODS) is altered organ function in
– Cardiac tamponade (pericardiocentesis) acutely ill patients that requires medical
– Tension pneumothorax (thoracentesis) intervention to support continued organ
function. It is another phase in the
progression of shock states.

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Multiple Organ Dysfunction

Multiple Organ Dysfunction
Syndrome (MODS)
• Clinical manifestations
• Pulmonary dysfunction.
• Renal dysfunction
• Liver dysfunction
• Cardiovascular dysfunction
• Hematologic dysfunction.
• Neurologic dysfunction
Syndrome (Cont.)
– Tachypnea/hypoxemia
– Petechiae/bleeding
– Jaundice
– Abdominal distension
– Oliguria → anuria
– Tachycardia
– Hypotension
– Change in level of consciousness

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Multiple Organ
Shock, Sepsis, and MODS
Dysfunction Syndrome
(Cont.) • Patient outcomes
• Management – Improved tissue perfusion
– Control infection • Alert, oriented
• Antibiotics • Normotensive
– Provide adequate tissue oxygenation • Warm, dry skin
• Maintain 88% to 92% arterial oxygen saturation • Adequate urine output
• Maintain hemoglobin above 7 to 9 g/dL • Normal hemodynamics
– Restore intravascular volume • Lab values within normal limits
• Aggressive fluid resuscitation • Absence of infection
• Isotonic crystalloids • Intact skin
– Support organ function

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References
• Smeltzer, S.C.C., Bare, B.G., Hinkle, J.L. and Cheever,
• K.H. eds., 2010. Brunner & Suddarth's textbook of medical-
surgical nursing (Vol. 1). Lippincott Williams & Wilkins.
• Grossman, S., Porth, C.M., Conelius, J., Gerard, S.O., Moriber,
N., O'Shea, E.R. and Wheeler, K., 2014. Porth's
pathophysiology: Concepts of altered health states.
• Reference: Morton,P. G., & Fontaine, D. K. (2013).
Essentials of critical care nursing: Wolters Kluwer
Health/Lippincott Williams & Wilkins.
• Sole, M.L., Klein, D.G., Moseley, M.J., Brenner, Z.R. and
Powers, J., 2009. Introduction to critical care nursing. 5th
Edition St. Louis, Mo.: Saunders,

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