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SHOCK

SHOCK OBJECTIVES
Upon completion of this chapter/lecture, the learner should be able to:
1. Define the four types of shock.
2. Describe the path physiologic changes as a basis for the signs and
symptoms of shock.
3. Discuss the nursing assessment of the patient in shock.
4. Based on assessment data, identify nursing diagnoses and expected
outcomes associated with patient in shock.
5. Plan appropriate interventions for the patient in shock.
6. Evaluate the effectiveness of nursing interventions for patients in shoe

INTRODUCTION

Classification and Etiology


Shock is a syndrome resulting from inadequate perfusion of tissues, leading
to a decrease in the supply of oxygen and nutrients required to maintain the
metabolic needs of cells. When the supply of oxygen and nutrients cannot
meet the demand to sustain normal cellular metabolism, the body responds
initially by activating intrinsic compensatory mechanisms to improve
perfusion, especially in areas of high demand such as the brain, heart, and
lungs. When compensatory mechanisms fail to-restore adequate perfusion, a
cascade of cellular abnormalities can result in total organ dysfunction and,
eventually, death

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Numerous classification systems have been used to define shock either by
causes or by the underlying path physiologic effects. One such system
classifies shock syndromes according to the underlying pathology:
Etiology Underlying pathology

Hypovolomic - hemorrhage - whole blood loss


- burns - plasma loss
Cardiogenic - myocardial infraction - loss of cardiac contractility
- dysrrythmia - reduced cardiac output
- blunt cardiac injury - loss of cardiac contractility

Obstructive - Cardiac tamponade - compression of the heart with


obstruction of a trial filling
- tension pneumothorax mediastinal shift with obstruction
of atrial filling
- tension hemothorax combination of above
distributive - Neurogenic shock -Venous pooling- maldestribution
of blood
- Anaphylactic shock -Shunting in microcirculation and
in later stage- decrease in venous
resistance.
- Septic shock -Poor distribution of blood

HYPOVOLEMIC SHOCK
The most common shock syndrome to affect a trauma patient is caused by
hypovolemia. Hypovolemia a decrease in the amount of circulating blood
volume may result from a significant loss of whole blood because of
hemorrhage. It may also result from the loss of the semi permeable integrity
of the cellular membrane leading to leakage of plasma and protein from the
intravascular space to the interstitial space,

CARDIOGENIC SHOCK
Cardiogenic shock is a syndrome that results from ineffective perfusion
caused by inadequate contractility of the cardiac muscle. Some of the causes
of cardiogenic shock are myocardial infarction, blunt cardiac injury, mitral
valve insufficiency, dysrhythmias, and cardiac failure.

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OBSTRUCTIVE SHOCK
Obstructive shock results from an inadequate circulating blood volume
because of an obstruction or compression of the great veins, aorta,
pulmonary arteries, or the heart itself. Cardiac tamponade may compress the
heart during diastole to such an extent that the atria cannot adequately fill
leading to a decrease in stroke volume. A tension pneumothorax may also
lead to an inadequate stroke volume by diplacing the inferior vena cava and
obstructing venous return to the right atrium.

DISTRIBUTIVE SHOCK
The fourth category of shock is distributive shock, which is a shock
syndrome resulting from either poor distribution of blood flow or blood
volume. Examples of shock because of a change in the distribution of blood
volume are neurogenic and anaphylactic shock. Neurogenic shock may
occur as a result of injury to the spinal cord in the cervical or upper thoracic
region.

PATHOPHYSIOLOGY AS A BASIS FOR SIGNS AND


SYMPTOMS
Shock is a syndrome that involves all cells and their chemical and metabolic
balance. The consequences of inadequate tissue perfusion can be described
organ by organ. The body responds to shock by initiating compensatory
mechanisms as specific organ systems are affected. Untreated, shock can
progress to irreversible stages as the body's own compensatory mechanisms
fail to restore perfusion and as organ systems become unable to maintain
homeostasis. Some of the compensatory mechanisms and their responses
follow.

Vascular Response
As blood volume decreases, the peripheral blood vessels vasoconstriction as
a result of sympathetic stimulation via inhibition of the baroreceptors. The
arterioles constrict to increase total peripheral resistance and, ultimately,
blood pressure. The venous capacitance system vasoconstricts to improve
venous return to the right atrium

Cerebral Response
As shock progresses, the primary goal of the body is to maintain perfusion
of the brain, heart, and lungs. Consequently, blood flow to these centers is
preserved while blood flow to other organs, such as the liver, bowel, skin
and to some extent, the kidneys, may be compromised.

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Sympathetic stimulation (compensatory vasoconsinction) has little effect on
cerebral and coronary vessels, but the brain and heart can auto regulate
blood flow based on the needs of the tissues.' Therefore, the brain and heart
are preferentially perfused during early and intermediate stages of shock. If
the blood pressure drops below 50 mm Hg and cerebral ischemia ensues, the
collection of carbon dioxide in the brain's vasomotor center will stimulate
the central nervous system ischemic response. This response yields further
stimulation of the sympathetic nervous system. Alterations in level of
consciousness may indicate cerebral ischemia.

Renal Response
Renal ischemia activates the release of rernin, an enzyme stored in the
kidneys' juxtaglomerular cells of the arterioles. When the kidneys do not
receive an adequate blood supply, renin is release into the circulation.
Renin causes angiotensinogen, a normal plasma protein, to release
angiotensin 1. Angiotensin2 is then formed from angiotensin 1; the
conversion to angiotensin II is enhanced by the angiotensin-converting
enzyme (ACE) from the lungs where the majority of the conversion takes
place.
The effects of angiotensin II are:
• Vasoconstriction of arterioles and some veins
• Stimulation of the sympathetic nervous system
• Retention of water by the kidneys
• Stimulation of the release of aldosterone from the adrenal cortex (sodium
retention hormone)
As powerful as the renin-angiotensin mechanism is, it does take
approximately 10 to 60 minutes to fully activated Decreased urinary output
may be a sign of renal hypoperfusion

Adrenal Gland Response


When the adrenal glands are stimulated by the sympathetic nervous system,
there will be an increase in the release of catecholamines (epinephrine and
norepinephrine) from the adrenal medulla. The epinephrine stimulates
receptors in the heart to increase the force of cardiac contraction and
increase the heart rate in order to improve cardiac output and. ultimately,
improve blood pressure and tissue perfusion.

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Hepatic Response
The liver can store the body's excess glucose as glycogen. As shock
progresses, glycogenolysis is activated by epinephrine to break down
glycogen into glucose. In a compensatory response to shock, hepatic vessels
constrict to redirect blood flow to other vital areas.

Pulmonary Response
The patient in shock may have tachypnea for two reasons: to maintain acid-
base balance and to maintain an increased supply of oxygen for cells to
produce energy.

Irreversible Shock
Untreated shock, or shock in progressive and/or irreversible stages, will
eventually cause compromises in most body systems. For example,
prolonged hypovolemia will cause a decrease in arterial pressure since there
is inadequate venous return, inadequate cardiac filling, and decreased
coronary artery perfusion, since coronary arteries are perfused during
diastole and diastolic pressure eventually falls, there will be decrease in
coronary artery perfusion with a subsequent decrease in myocardial
contractility.
The membranes of the lysomes break down within cells and release
digestive enzymes that cause intracellular damage.

NURSING CARE OF THE PATIENT IN HYPOVOLEMIC SHOCK

Assessment
A patient who arrives in the ED in profound shock because of trauma will
require simultaneous assessment and intervention
HISTORY
Refer to Initial Assessment, for a description of general information that
should be collected regarding every trauma victim.

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PHYSICAL ASSESSMENT
Inspection
• Determine level of consciousness (LOC):
A patient's LOC may progressively deteriorate. Restlessness, anxiety, or
confusion may occur in shock as cerebral perfusion is diminished. After 30
to 40% of the blood volume is lost, the patient may be unresponsive to
verbal and/or painful stimuli. A loss of greater than 40% of the total blood
volume generally leads to unconsciousness.
• Assess breathing effectiveness and rate of respirations
• Identify obvious sources of external bleeding
• Assess skin color
Patient may be ashen or pale especially around the mouth: mucous
membranes may be pale
• Observe external jugular veins and peripheral veins for distention or
flattening
• Inspect the chest, abdomen, and extremities for signs of obvious bleeding,
fractures, or major tissue injury

Auscultation
• Obtain blood pressure
Because of vasoconstriction and low cardiac output, auscultated blood
pressures may be difficult, obtain A Doppler Ultrasonic Flow Meter may
assist with blood pressure measuremen
• Auscultate breath sounds
Bleeding into the thoracic cavity may lead to diminished or even absent
breath sounds.
• Auscultate heart sounds
Heart sounds may sound distant or muffled if blood collects in the
pericardia] sac.
• Auscultate bowel sounds
The absence of bowel sounds may indicate intra-abdominal bleeding patients
in profound shock.

Percussion
Percuss chest and abdomen
Dullness of the chest or abdomen may indicate the presence of blood. Early
identification of sources of internal blood loss is essential.

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Palpation
• Palpate carotid pulse
• Palpate peripheral pulses
• Palpate skin temperature and degree of diaphoresis

DIAGNOSTIC PROCEDURES
Radiographic Studies
• Chest radiograph to determine the presence of a hemothorax or
pneumothorax and to assess the size of the mediastinum. Widening of the
mediastinum may indicate injury to the aorta or other mediastinal vessels.
• Pelvis radiograph to locate fractures, which may result in significant blood
loss because of disruption of pelvic veins.
• Femur radiograph, if fracture is suspected

Laboratory Studies
• Venous blood sample for typing Baseline levels of the patient's
hemoglobin, hematocrit, serum osmolarity, electrolytes. BUN, creatinine
and serum lactate should be obtained.
• Urinalysis including specific gravity
• Arterial PH, PaO2, PaCO2 and base deficit

Planning and Implementation


Refer to Initial Assessment, for a description of the specific nursing
interventions for patients with compromises to airway, breathing,
circulation, and disability.
* Adminster oxygen via a nonrebreather mask at a flow rate sufficient to
keep the reservoir bag inflated during inspiration; usually requires a flow
rate of at least 12 liters/minute and may require 15 liters/minute or more.
Oxygen is essential for the patient in shock. Oxygen via a nonrebreather
mask can deliver up to 100% with a snug fit of the mask around the nose and
mouth. For the patient who requires bag-to-mask or bag-to-tube ventilation,
oxygen must be delivered via a device with an appropriate oxygen reservoir.
* Control any uncontrolled external bleeding
Rapid control of bleeding is essential to prevent the progression of shock.
Control major external bleeding by direct pressure.

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* Prepare for surgery if control of internal bleeding is indicated
Prepare the patient for immediate transportation to surgery after appropriate
interventions for stabilization have been instituted
• Initiate intravenous replacement of fluids
Prior to the administration of blood or colloid solutions, initiate an isotonic,
electrolyte-balanced, crystalloid solution via two large-bore 14- 16-gaugc
intravenous catheter, lactate Ringer's solution is a "near-physiologic"
solution that is similar to the body's extracellular fluid. Normal saline (0.9%)
is considered the second fluid of choice for a hypovolemic patient
An initial bolus of 1 to 2 liters of lactated Ringer's solution may be given to
adult patients as rapidly as possible.
-The use of large-bore, short catheters, short intravenous tubing, and a rapid
infusor device will contribute to rapid infusion. It is important to observe the
patient's response to the bolus. by measuring blood pressure and heart rate as
well as listening to breath sounds.
• Initiate blood replacement
Patients who do not adequately respond to a crystalloid fluid bolus are
potential candidates for blood volume replacement.
• Type-specific and cross matched blood
Type-specific and crossmatched blood is the ideal, but may take longer to
procure.
• Type-specific blood
Type-specific blood is usually available within minutes from blood banks.
• Type O-negative packed cells
O-negative is considered the universal donor
• O-positive packed cells
If O-negative packed cells are scarce, type O-positive packed cells are
sometimes used for male patients .since the risk of their plasma having anti
D antibodies is remote (85% of white population and 95% of black
population is Rh positive
- Fresh frozen plasma (FFP). Cryoprecipitate (Factor VIII). And/or platelete
administration may be considered when coagulopathy studies are known."
• Administer blood through a filtering device designed to trap any clots.
• Infuse blood through an intravenous line using normal saline
• Warm fluids to 39 "C (102.2°F) to prevent hypothermia*
• Consider auto transfusion for a patient with a hemothorax
•Continue or consider application of a pneumatic antishock garment (TASG)
• Position patient with legs elevated

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• Insert a gastric tube
- Gastric distension may lead to vomiting and/or aspiration.
• A urinary catheter provides for bladder drainage, allows for frequent
monitoring of urinary output, and is necessary for any shock patient who is
being prepared for surgery. Suspected injury to the urethra is a
contraindication to catheterization through the urethra.
• Attach leads and monitor the patient's cardiac rate and rhythm
• Attach a pulse oximeter to monitor the patient's arterial oxygen saturation
• Peripheral vasoconstrictors are contraindicated in a hypovolemic patient,
but may be considered in patients who present in neurogenic shock with no
other injuries causing hypovolenua.

Evaluation and Ongoing Assessment


Additional evaluations include:
• Monitoring urinary' output for response to fluid resuscitation and for
overall renal function. The ability of the kidneys to form urine is a reflection
of the patient's overall perfusion status.
• Collaborating with other trauma team members as diagnostic studies and
physical assessment identify the cause and source of hemorrhage
• Monitoring temperature to determine hypothermia. Hypothermia in the
patient with hemorrhagic shock has serious sequel including:
• Decreased tissue extraction of oxygen from hemoglobin
• Impaired cardiac contractility and decreased cardiac output
• Coagulopathies because of disruption of cellular enzymatic function,
platelet disturbances, and increased fibrinolysis

SUMMARY
Shock is a syndrome resulting from inadequate perfusion of tissues leading
to a decrease in the supply of oxygen and nutrients required to maintain the
metabolic needs of the body. The four types of shock are hypovolemic.
cardiogenic, obstructive, and distributive. Hypovolemic shock is the most
common shock in trauma patients, results from an inadequate intravascular
blood volume. The organs and certain structures of the body respond to
shock in a compensatory fashion. If compensatory mechanisms fail and/or
treatment is not initiated, organ, tissue, and cellular ischemia ensue.
Adherence to the six phases of the trauma nursing process allows for an
organized approach to the assessment and management of compromises to
airway, breathing, and circulation.