SHOCK

Shock is a serious medical condition where the tissue perfusion is insufficient to meet
demand for oxygen and nutrients. This is the body's response to poor tissue perfusion
and oxygenation. When compensation or interventions are infective and shock
progresses, extensive hypoxia and lead to the complication of multiple organ
dysfunction syndrome.

Pathophysiology
Adequate blood volume, an effective cardiac pump and effective vasculature are
necessary to maintain blood pressure and tissue perfusion.
The main trigger leading to the recognizable picture of shock is sustained decrease in
mean arterial pressure (MAP) that results from decreased cardiac output, decreased
circulating blood volume or expansion of the vascular bed( ineffective vasculature).
A decrease in mean arterial pressure below the client's baseline values is detected
immediately by baroreceptors in the aortic arch and carotid sinus. This information is
transmitted to brain centres, which stimulates compensatory mechanisms which
ensure continued blood flow and oxygen delivery to vital organs while limiting blood
flow to less vital areas, thus causing physiologic changes and clinical manifestation of
shock.
Here if the event that led to the initial decrease in mean arterial pressure is stooped or
halted at this point then compensatory mechanisms can return the body to normal
perfused and oxygenated state even without external intervention. However, if the
initiating events continue and mean arterial pressure decrease further, some tissues
start functioning under anaerobic condition thus leading to increased production of
lactic acid levels and other harmful metabolites that have generalized tissue damage,
effects and depress cardiac activity.
When such conditions continues for long periods without prompt intervention, the
resulting acid base balance, electrolyte imbalance and increased levels of toxic
metabolites cause cell damage in vital organs that is to say multiple organ dysfunction
syndrome occurs that could lead to death.

Shock occurs in stages as follows:

Initial stage of shock( Early Stage)

This occurs when any condition that causes mean arterial pressure to decrease from
the client's baseline level by less than 10mmHg . Here, active compensatory
mechanisms are so effective at returning mean arterial pressure to normal levels that
oxygenated blood flow to all vital organs is maintained. Cellular changes in this stage
are decreased aerobic metabolism and increased anaerobic metabolism with
production of lactic acid, although overall cellular metabolism is still aerobic,
compensation through vascular constriction, increased heart is effective and both
cardiac output and mean arterial pressure are maintain.
Signs and symptoms of shock are difficult to detect at this point because vital organ
function is not disturbed.
Compensatory Stage
This stage is characterized by the employing physiological, neural, hormonal and bio –
chemical compensator mechanisms in an attempt to reverse the condition and
maintain mean arterial pressure and supply needed oxygen to the vital organs.
The kidneys and baroreceptors sense an ongoing decrease in mean arterial pressure,
thus this leads to the release of renin, antidiurectic hormone (ADH), aldosterone,
epinephrine and norepinephrine.
Kidney compensation occurs through the renin angiotensin aldosterone system
(RAAS), that leads to decrease in urine output, increased sodium and water re-
absorption and wide spread vasocontriction. Further more, ADH is secreted by the
posterior pituitary gland that increases water re-absorption in the kidney and causes
blood vessels constriction in the skin and other less vital tissues areas.
As a result of acidosis, the person begins to hyperventilate in order to rid the body of
carbondioxide which indirectly act to acidity the blood and by removing it, the body is
attempting to raise the pH of the blood.
Therefore together, these actions attempt to compensate for shock by maintaining the
volume in the central blood vessels. Stopping the conditions that started the shock and
providing supportive interventions can prevent the shock from progressing and reverse
the effects at this stage.

Progressing stage of shock (Intermediate)

In this stage, compensation mechanisms are functioning but no longer able to deliver
sufficient oxygen, even to vital organs. The compensatory mechanisms use large
amounts of oxygen in certain tissues, which worsens the problem of general
inadequate oxygenation an build up of toxic metabolites. This is a life threatening
emergency, because vital organs can tolerate this situation for only a short time before
being damaged permanently.

Irreversible stage (Refractory stage)

This occurs when too much cell death and tissue damage results from too little oxygen
reaching the tissues. Thus vital organs have failed and shock can no longer be
reversed. Brain damaged and cell death have occurred. Death will occur imminently.

Shock has different types which is caused or brought about by different conditions or
diseases as follows:
Hypovolemic shock
This occurs when too little circulating blood volume causes a mean arterial pressure to
decrease so that the body's total need for tissue oxygenation is not met. Most common
conditions leading to hypovolemia are hemorrhage which can both internal or external
and dehydration.
Hypovolemic shock caused by external hemorrhage is common after trauma, wounds,
surgery, while internal hemorrhage occurs with blunt trauma, gastrointestinal ulcers
and poor control of surgical bleeding.
Both internal and external hemorrhage can be caused by inadequate clotting which
can be due to; hemophilia, liver disease, malnutrition, bone marrow suppression,
cancer and anticoagulation therapy.
Hypovolemia as result of dehydration can be caused by vomiting, diarrhea, heavy
diaphoresis, diuretic therapy, diabetes insipidus, hyperglycemia, nasogastric suction.

Cardiogenic shock
This occurs when the actual heart muscle is unhealthy and contraction is directly
impaired, that is to say direct pump failure, which can be due to; myocardial infarction,
cardiac arrest, ventricular dysrhythmias. All these conditions decrease cardiac output
and afterload, thus reducing mean arterial pressure.

Distributive shock
This is caused by a loss sympathetic tone, blood vessels dilation, poor of blood in
venous and capillary beds, and increased blood vessels permeability (leak). All of
these factors decrease mean arterial pressure and may be induced neurogenically or
chemically( which is divided in septic and anaphylactic shock).
Neurogenic shock which is the rarest form of shock is caused by injury and disease to
the spinal cord. It can also be due to spinal anesthesia, deep general anesthesia, and
vasomotor center depression and thus sudden loss of autonomic reflexes below the
injury level.
Septic shock is due to over whelming infection like urinary tract, respiratory tract,
invasive procedures, at risk patients like those with HIV/AIDS, and chronic conditions
leading to vasodilation. The microorganism like bacteria produce endotoxins which
produces adverse biochemical, immunological and occasional neurological effects
which are a harmful to the body.
Anaphylactic shock on the other hand is due to severe anaphylactic reaction to an
allergen or antigen like drugs, insect bites, foods, vaccines which causes the release
of histamines that cause to wide spread vasodilation, that lead to hypotension and
increased capillary permeability.

Obstructive shock
This is due to conditions that affect the ability of the normal heart muscle to pump
effectively which include cardiac tamponade, arterial stenosis, pulmonary embolus,
pulmonary hypertension, thus blood flow is obstructed thus impeding circulation and
thus result in circulation arrest.

Through assessment and history taking the clinical manifestations can be got as
follows:
In the early stage of shock the following can be observed:
• Restlessness, confusion
• Increase in pulse pressure and respiratory pressure
• Diaphoresis
• Cool, clammy skin ( warm, flushed skin in septic shock)
• Normal or decreased blood pressure
• Decreased urine output
 • Thirst, dry mucus membrane
• Respiratory alkalosis
• Hypokalemia

While in the late stage, shock presents as or has the following clinical manifestations:
• Shallow respiration
• Decreased blood pressure
• Increased pulse pressure
• Oliguria or anuria
• Hypokalemia
• Edema
• Cool, clammy skin due to constriction of peripheral blood vessels
• Cool mottled skin
• Hypothermia
• Lethargy
• Decreased bowel sounds
• Cyanosis
• Dilated pupils

Diagnosis
No single laboratory finding confirms or rules out the presence of shock, though
changes in laboratory may support the diagnosis of hypovolemia shock, like:
Arterial blood gas values (abnormal)
pH decreases
Partial pressures of oxygen decreases while the partial pressures of carbondioxide
increases.
Further more, an electrocardiogram and electrocardiograph can be used to diagnose.

Treatment
This is focused on recovery of the shock, restoring fluid volume, and preventing
ischemic complications through supportive therapies as follows:
Oxygen therapy
This is very useful whenever shock is present, which can be administered by mask as
prescribed by the physician.
Further still, intravenous(IV) therapy where colloids are commonly used for volume
replacement during hypovolemia. IV colloidal therapy is used to restore plasma
volume and colloidal osmotic pressure.
Worth to note, is monitoring of the patient with shock. This is a major nursing
responsibility in caring for a client with shock by monitoring his or her vital signs and
level of consciousness. The vital signs to be monitored could be pulse rate, respiratory
rate, oxygen saturation, blood pressure, and skin and mucous colour.

Drug therapy
The client should be give drugs like vasoconstricting agents like intropin that increase
cardiac output, tissue perfusion and oxygenation. Further more, the client should be
given clients that enhance myocardial contractility.

Nursing concerns and diagnosis

 Fluid volume deficit related to excessive vascular loss, inadequate intake or
replacement evidenced by tachycardia, decreased pulse volume and pressure
and decreased concentrated urine.

Intervention
Restore intravascular volume to reverse the sequence of events leading to
inadequate tissue perfusion. This can be done through administering:
• Whole blood and blood products.
• Colloidal solutions for example albumin, plasma protein factors.
• Fluids like normal saline, lactated ringer's solution, and 5% dextrose.

Further more, using vasoactive medications to restore and improve cardiac function
like:
Sympathomimetics
• Amrinone
• Dobutamine
• Epinephrine
Vasoconstrictors
• Norepinephrine (Levophed)
Worth to note is that, nutritional support to address the metabolic requirements that
are often dramatically increased in shock.
Practice strict sepsis

 Knowledge deficit related to disease process evidenced by the family

verbalizing, we do not understand what happened what to our brother

Intervention
Teach the patient and family about the condition and make sure they verbalize that
they have understood.

References
Smeltzer and Bare., 2004., Brunner and suddarth's Textbook of Medical – surgical
Nursing. 10th Ed. Philadelphia. Lippincott william and wilkin. Chapter 56

Udan JQ., 2002., Medical – Surgical Nursing, Concepts and clinical application. 1st Ed.
Erimita, Manila. Philippines