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Shock

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Shock

• Shock is characterized by an inadequate


supply of oxygen and nutrients to cells
from impaired tissue perfusion and, if
untreated, results in death. Adequate
blood flow to the tissues and cells requires
the following components:
– Adequate cardiac pump
– Effective vasculature of circulatory system
– Sufficient blood volume
• When one component is impaired, blood
flow to the tissues is threatened or
compromised.
• Without treatment, inadequate blood flow
to the tissues results in poor delivery of
oxygen and nutrients to the cells, cellular
starvation, cell death, organ dysfunction
progressing to organ failure and eventual
death.
Normal Cellular Function
• Energy metabolism occurs within the cell, where nutrients
are chemically broken down and stored in the form of
adenosine triphosphate (ATP).
• Cells use stored energy to perform necessary functions,
such as active transport and muscle contraction.
• ATP can be synthesized aerobically or anaerobically.
• Aerobic metabolism use bigger amounts of ATP than
anaerobic metabolism and thus is a more efficient and
effective way of producing energy.
• Anaerobic metabolism results in the accumulation of the
toxic end product lactic acid, which must be removed from
the cell and transported to the liver for conversion into
glucose and glycogen.
Pathophysiology

• When the body is in shock, cells do not receive enough


oxygen or nutrients and must produce energy through
anaerobic metabolism.
• Energy production is lower and acidotic, because of
these changes normal cell function ceases.
• The cell start to swell and the cell membrane is more
permeable, allowing electrolytes and fluids to seep out of
and into the cell.
• cell structures, primarily the mitochondria, are damaged;
and death of the cell results.
Vascular Responses

• Oxygen attaches to hemoglobin in red blood cells and is


carried to the body cells. The amount of oxygen that is
delivered to cells depends on blood flow to a specific
area and on blood oxygen concentration.
• This process of circulation is facilitated through a
vasculature consisting of arteries, arterioles, capillaries,
veins and venules. The vasculature can dilate or
constrict based on central and local regulatory
mechanisms.
• Local regulatory mechanisms (autoregulation) stimulate
vasodilation or vasoconstriction in response to
biochemical mediators released by the cell.

Blood Pressure Regulation

• An adequate blood pressure is necessary for effective


tissue perfusion.
• Blood pressure is regulated through a complex
interaction of neural, chemical and hormonal feedback
systems that affect cardiac output and peripheral
resistance.
• Cardiac output is determined by stroke volume (the
amount of blood ejected at systole) and heart rate.
• Peripheral resistance is determined by the diameter of
the arterioles.
This relationship is expressed in
the following equation:
Formula for Estimating Mean
Arterial Pressure (MAP)
MAP = systolic BP = 2(diastolic
BP)
3

Example: Patient’s BP = 125/75 mm


Hg

MAP = 125 + (2 x
75)
3
The MAP is the average
MAPpressure at which blood
= 92 (rounded to moves
nearestthrough the
vasculature. 1/10)
MAP should exceed 70 to 80 mm Hg for cells to receive enough oxygen
and nutrients to live.
Stages of Shock

• In this stage the client’s blood pressure remains within


normal limits.
• Vasoconstriction, increased heart rate and increased
contractility of the heart contribute to maintain adequate
cardiac output as result of epinephrine and
norepinephrine release.
• The “fight or flight” response is activated and shunts
blood from organs such as the skin, kidneys and
gastrointestinal tract to the brain and heart to ensure
adequate blood supply to the vital organs.
• The client’s skin is cold and clammy, bowel sounds are
hypoactive and urine output decreases in response to
the release of aldosterone and ADH.
Clinical Manifestations

• The client shows numerous clinical signs indicating inadequate


organ perfusion.
• The result is anaerobic metabolism and a build up of lactic acid,
producing metabolic acidosis.
• The respiratory rate facilitates removal of excess carbon dioxide but
raises the blood pH and often causes a compensatory respiratory
alkalosis.
• The alkalotic state causes mental status change, such as confusion.
• If treatment begins in this stage of shock, the prognosis for the client
is good.
Management

• Identify the cause of shock.


• Correct the underlying disorder.
• Initiate fluid replacement and medication therapy to
maintain an adequate blood pressure.
• Reestablish and maintain adequate tissue perfusion.
• Early intervention is needed to improve the client’s
prognosis therefore the nurse should recognize clients at
risk for shock.
Management

• Monitoring Tissue Perfusion


• Observe for changes in:
– Level of consciousness
– Vital signs (including pulse pressure)
– Urinary output
– Skin
– Laboratory values

• In the compensatory state of shock, serum sodium and


blood glucose levels are elevated in response to the
release of aldosterone and catecholamines.
Nursing Management

• Monitor the client’s hemodynamic status and report


abnormalities to the physician.
• Administer prescribed fluids and medications and
promote client safety.
• Vital signs are key indicators of the client’s hemodynamic
status.
• Pulse pressure correlates well to stroke volume and is
calculated by subtracting the diastolic measurement from
the systolic measurement; the difference is the pulse
pressure.
• The pulse pressure should be 30 to 40 mm Hg and a
narrowing or decreased pulse pressure is an earlier
indicator of shock.
Progressive Stage
• In this stage the mechanisms that regulate blood pressure
can no longer compensate and the MAP falls below
normal limits.
• The heart is overworked and becomes dysfunctional and
the body is unable to meet increased oxygen requirements
which result in ischemia and myocardial depression. This
leads to failure of the cardiac pump; even of the underlying
cause of the shock is not of cardiac origin.
• Capillary perfusion is further compromised by arteriolar
and venous constriction. Fluid starts to leak from the
capillaries, creating interstitial edema and less fluid return
to the heart. The client’s prognosis worsens.
Clinical manifestations

• Respiratory Effects
• Cardiovascular Effects
• Neurologic Effects
• Renal Effects
• Hepatic Effects
• Gastrointestinal Effects
• Hematologic Effects
Management

• Management is based on the degree of


decompensation in the organ systems.
• Use of appropriate intravenous fluids and medications to
restore tissue perfusion by (1) optimizing intravascular
volume, (2) supporting the pumping action of the heart
and (3) improving the competence of the vascular system.
• close monitoring -Hemodynamic monitoring,ECG,ABG,
Evaluating serum electrolyte levels,Physical and mental
status changes
• Intervention with supportive technologies, such as
mechanical ventilation, dialysis and intra-aortic balloon
pump.

Irreversible Stage

• The irreversible (or refractory) stage of shock -organ


damage is so severe that the client does not respond to
treatment and cannot survive. Despite treatment, blood
pressure remains low.
• Complete renal and liver failure creates an overwhelming
metabolic acidosis.
• Anaerobic metabolism contributes to a worsening lactic
acidosis.
• Multiple organ dysfunction progressing to complete
organ failure has occurred and death is imminent.
Management

• Medical management during the irreversible stage of


shock is usually the same as for the progressive stage.
• The nurse focuses on carrying out prescribed
treatments, monitoring the client, preventing
complications, protecting the client from injury and
providing comfort.
• Families should be encouraged to express their wishes
concerning the use of life-support measures.
Clinical Findings in Stages of Shock
ASSESSMENT

Finding Compensatory Progressive Irreversible


Blood Systolic <80-90 Require
pressure mmHg mechanical or
pharmacologic
support
Heart rate >100 bpm >150 bpm Erratic or
asystole
Respiratory >20 Rapid, shallow Requires
status breaths/min respirations; intubation
crackles
Skin Cold, clammy Mottled, Jaundice
petechiae
Urinary output Decreased 0.5 ml/kg/hr Anuric, requires
dialysis
Mentally Confusion Lethargy Unconscious
Acid-base Respiratory Metabolic Profound
balance alkalosis acidosis acidosis
HYPOVOLEMIC SHOCK

Risk Factors for Hypovolemic Shock


External: Fluid Losses Internal: Fluid Shifts
Trauma Hemorrhage
Surgery Burns
Vomiting Ascites
Diarrhea Peritonitis
Diuresis Dehydration
Diabetes insipidus
Modified Trendelenburg
CARDIOGENIC SHOCK
CIRCULATORY SHOCK
Risk Factors for Circulatory Shock
Septic Shock Anaphylactic Shock Neurogenic Shock

Immunosuppression Penicillin sensitivity Spinal cord injury

Extremes of age Transfusion Spinal anesthesia


(<1 yr and >65 yr) reaction
Malnourishment Bee sting allergy Depressant action
of medications
Chronic illness Latex sensitivity Glucose deficiency

Invasive procedures
Sepsis
Pathogenesis of Sepsis

Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med.
Treatment
Algorithm

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med.

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