SHOCK

Introduction

Shock is a life threatening condition. It is characterized by inadequate tissue perfusion that if

untreated results in cell death. The supply of oxygen to tissues is essential in the maintenance of
life and this can be ensured when circulatory system is functioning normally. Historical
background; In 1923 Walter and Canner first worked for all conditions of shock.

Definition

Shock can be defined as a condition in which systemic blood pressure is inadequate to deliver
oxygen and nutrient to supply to vital organs and cellular functions. Shock is defined as a failure
of circulation to supply adequate oxygen to the tissues. Significance of shock: shock affects ali
the body systems. It may develop slowly or rapidly depending upon the underlying causes.
During shock body struggles to survive, caliing on all its haemostatic mechanism to restore
blood flow and tissue perfusion. Therefore any patient with any disease state may be at risk of
developing shock. Nursing care of patient with shock requires ongoing systemic assessment.
Many interventions required in caring for the patient with shock call for close collaboration with
other members of health care team and a physician's order. The nurse must anticipate such orders
which need to be executed with speed and accuracy.

Causes Of Circulation Failure

Circulation may fail from

1. Sudden malfunction of heart

This may occur as a result of

• Coronary artery occlusion with acute myocardial ischemia.

• Trauma with structural damage to heart.

• Toxemia-viral or bacterial.

.. Effects of drugs.

2. Deficient oxygenation of blood in lungs

Amongst many causes the following are the most important.

• Post operative atelectasis

• Thoracic injuries particularly of chest , i.e. pneumothorax, crushing and laceration of lung
• Obstruction of puimonary artery by an embolus.

• Disturbances of lung function following surgery and anesthesia.

3. Reduction in blood volume ( oligaemia and hypovolemia )

This may occur from loss of

• Whole blood - hemorrhage (internal or external).

. Plasma - this is particularly significant in burns.

• Water and electrolytes which occurs from peritonitis, intestinal obstruction, paraiytic
iieus, acute dilation of the stomach, severe diarrhoeas and vomiting.

4. Miscellaneous

There are number of other conditions that may iead to

shock state with low blood pressure.

• Faintneq,s.

• Acute anaphylaxis.

• Acute adrenal deficiency (Addison's disease).

• Over dosage of drugs e.g. analgesics like pethidine.

• Following therapy with beta blocking agents.

• Noxious stimuli such as pain, if severe will cause vasodilatation particularly of splenetic
vessels with pooling of blood in the area. This is the mechanism of primary shock.

Compensatory Mechanism

Whatever the cause of sudden collapse there are certain compensatory physiological mechanism
which occur.

• Posture: A patient in acute circulatory failure falls down; he should lie flat on the floor or
better in head down position so that circulation can be improve towards heart.

• Contraction of skin vesseis; Contraction of arterioles and venules of the skin is usual so
as to conserve the blood supply to the more vital organs. The application of heat dilates the skin
vessels thereby aggravating the condition and shouid not be used.
• Insensitivity: A much collapsed patient usually has little pain. Large quantities of pain
relieving drugs are unnecessary and are ineffective because they cannot be absorbed unless given
by intravenous route.

• Urinary secretions: These are diminished to conserve fluid in the body but it is also a sign
that tissue perfusion is inadequate.

• Heart rate accelerates: It occurs in most forms of circulatory failure with the important
exception of faint. It is an attempt to ensure that remaining fluid is circulated as rapidly as
possible thereby providing sufficient oxygen to tissues.

• Subnormal temperature: This reduces the requirements of the tissues for the diminishing
amount of oxygen available. The core temperature actually is rising. The difference between the
two is a measure of the degree of shock. All these compensatory mechanisms are temporary in
their beneficial effects and if the condition of circulation is restored to normal without delay
irreversible changes set in.

Pathophysiology

Lack of oxygen supply and nutrient in cells

Cells produce energy through anaerobic

metabolism to produce ATP

Low energy yielding from nutrients and produces

acidic intracellular environment

Normal cell function affected, cells swells and cell membrane become more permeable, allowing
fluid and electrolytes to move out and into the cells

Sodium potassium pump impaired due to this

Cell structure damage

Ultimately death of cells

Stages of shock

There are 4 stages for shock

1. Initial stage

2. Compensatory stage
3. Progressive (or) (decompensate)

4. Refractory (Irreversible)

1) Initial stage

During this stage

Inadequate perfusion

Cellular hypoxia

Mitochondria becomes unable to produce ATP

Due to the lack^of oxygen and the cell membranes becomes damaged.

Leakage to the extracellular fluid

Cell performs anaerobic respiration

Build up of lactic and pyruvic acid

Systemic metabolic acidosis

The process of removing these components from the cells by the liver requires oxygen (Which is
absent?)

2) Compensatory stage

This stage is characterized by the body employing physiological mechanisms including neural
hormonal and bio-chemical mechanism in an attempt to reverse the condition In the
compensatory stage of shock, the patient’s blood pressure remains within normal limits.
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). The patient
displays the often-described “fight or flight” response. The body shunts blood from organs such
as the skin, kidneys, and gastrointestinal tract to the brain and heart to ensure adequate blood
supply to these vital organs. As a result, the patient’s skin is cold and clammy, bowel sounds are
hypoactive, and urine output decreases in response to the release of aldosterone and ADH (Anti-
diuretic hormone).

Clinical manifestation

 Normal blood pressure.

 Metabolic acidosis.
 Respiratory alkalosis
 Deep rapid respiration
 Flat neck vein
 Changes in LOG (Level of Consciousness).
 Irritability.
 Restlessness, dilated reactive pupil.
 Tachycardia bounding pulse.
 Dry warm skin.

Medical management

Medical treatment is directed toward identifying the cause of the shock correcting the underlying
disorder measures such as

• Fluid replacement and medication therapy.

Must be initiated to maintain the adequate BP and re establish and maintain adequate tissue
perfusion.

3. Progressive stage (de-compensating)

In the progressive stage of shock, the mechanisms that regulate blood pressure can no longer
compensate and the Mean Arterial Pressure (MAP) falls below normal limits, with an average
systolic blood pressure of less than 90 mm Hg.

Although all organ systems suffer from hypoperfusion at this stage, two events perpetuate the
shock syndrome. First, the overworked heart becomes dysfunctional; the body’s inability to meet
increased oxygen requirements produces ischemia; and biochemical mediators cause myocardial
depression
This leads to failure of the cardiac pump, even if the underlying cause of the shock is not of
cardiac origin. Second, the auto regulatory function of the microcirculation fails in response to
numerous biochemical mediators released by the cells, resulting in increased capillary
permeability, with areas of arteriolar and venous constriction further compromising cellular
perfusion. At this stage, the patient’s prognosis worsens. The relaxation of precapillary
sphincters causes fluid to leak from the capillaries, creating interstitial edema and return of less
fluid to the heart. Even if the underlying cause of the shock is reversed, the breakdown of the
circulatory system itself perpetuates the shock state, and a vicious circle ensues.

Clinical manifestations

 Confusion
 Dilated, sluggish pupil.
 Thirst, rapid shallow breathing.
 Tachycardia, cool moist skin.
 Slow capillary refill, muscle weakness.
 Hypotension.

Managements
To restore the perfusion by following Method:-
• Optimizing intravascular volume
• Supporting the pumping action of the heart
• Improving the competence of the vascular system
• Supporting the respiratory system

4) Refractory (irreversible)
At this stage the vital organs have failed and the shock can no longer be reversed. Brain damage
and cell death will occur, death of the person will occur immediately

Clinical manifestations

• Unconsciousness, absence of reflexes.

• Dilated sluggish pupil, severe thirst.

• Acute respiratory distress syndrome, Disseminated intravascular coagulation.
Bradycardia.

• Cyanosis.

• Absence of bowel sounds.

• Immune system collapse.

• Anuria.

Management

Management same like progressive stage

Classification of shock

Shock can be classified according to the etiology and can be described as

1. Hypovolemic shock.

2. Cardiogenic shock.

3. Circulatory shock or distributive shock

a. Septic shock.

b. Obstructive shock

c. Neurogenic shock.

d. Anaphylactic shock

1)Hypovolemic shock

This is the most common type of shock, due to insufficient circulatory volume. In hypovolemic
shock there is decrease in circulatory volume to level that is inadequate to meet body's need for
tissue oxygenation. This occurs when there is loss in the intravascular fluid upto 15% to 25%.
This would represent a loss of 750 to 1300 ml of blood in a 70 kg person. Common causes of
shock are: exercise, fluid loss from circulatory system

e.g. bleeding, burns, and blood loss from Gastro Intestinal or severe diarrhoea.
Pathophysiology

Decreased blood volume

Decreased venous return

Decreased cardiac output Decreased tissue perfusion

2) Cardiogenic shock

It is caused by the failure of heart to pump an adequate amount of blood to vital organs. This will
lead to reduction in cardiac output. After due damage of heart muscles, heart's ability to contract
and pump blood is impaired and the supply of oxygen is inadequate for the heart and muscles. It
can be the result of myocardial infarction. Other causes include arrhythmias, cardiomyopathy,
congestive heart failure, and cardiac valve problems.

Pathophysiology

Decreased cardiac contractility

Decreased stroke volume and cardiac output

Pulmonary congestion decreased tissue perfusion decreased coronary artery perfusion volume

Decreased cellular metabolism

3) Circulatory shock or distributive shock

In this there is no blood loss but the shock is due to the dilation of the blood vessels. This
displacement of blood causes a relative hypovolemia because not enough blood returns to heart
which leads to subsequent inadequate tissue perfusion. The varied mechanisms leading to the
initial vasodilatation in circulatory shock is subdivided into septic shock. It is the most common
type of circulatory shock and caused by wide spread infection due to sepsis called by an
overwhelming infection leading vasodilatation. E.g. Infections by bacteria. They release toxins
which produce adverse biochemical, immunological and neurological effects. The most common
causative organism of septic shock is gram negative bacteria.

It is sub divided into

a. Septic shock.

b. Obstructive shock.

c. Neurogenic shock.

d. Anaphylactic shock.
Pathophysiology

Vasodilatation

Mai distribution of blood volume

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased tissue perfusion

a. Septic Shock

It is secondary to infections by micro organisms

Vasodilation

Maldistribution of blood volume

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased tissue perfusion

b. Obstructive shock

Obstruction of blood flow results from cardiac arrest. E.g. Cardiac tamponade, pneumothorax,
pulmonary embolism, and aortic stenosis.

c. Neurogenic shock

This is a very uncommon type of shock. It is most often seen in patients who have had and
extensive spinal cord injuries. The loss of autonomic and motor reflexes below level of injury
results in loss of sympathetic control. This leads to relaxation of vessels and peripheral dilation
and hypotension. This is characterized by warm and dry skin, bradycardia, rather than other type
of shock.
Pathophysiology

Spinal trauma or anaesthesia

Inhibit the sympathetic nerve stimulation

Psychic trauma

Fainting

Spinal cord injury

Loss of function below the level of injury

Venous vasodilation

Decrease venous return

Decreased stroke volume

Decreased cellular oxygen supply

Anaphylactic shock

Anaphylactic shock is caused by severe reaction to an allergen, antigen, drug or foreign protein.
When a patient who has already produced antibodies to a foreign substance develops a systemic
antigen antibody reaction. Antigen antibody provides mast cells to release vasoactive substance
such as histamine or bradykinin that cause vasodilatation

Pathophysiology

Due to antibody responses

Release of histamine

Vasodilatation

Increased capillary permeability

Severe broncho constriction

Decreased oxygen supply and utilization

Inadequate tissue perfusion.

Risk factors

Immunosuppressants, invasive procedures and psychological trauma.

Diagnosis of shock

Diagnosis of shock is essential for proper treatment and management. An accurate history and
assessment of patient symptoms must be done before commencing treatment.

• Conducts head to toe examination for signs of shock.

• Assess neurological status of the person by assessing the level of consciousness.

• Assess the cardiovascular status. Blood pressure varies with the stages of shock.

• Assess for renal status. Anuria and renal failure can occur.

• Assess for integumentary status. Check for skin color,

cold and clammy skin, cyanosis.

• Assess gastro intestinal status. Hypoactive bowel sounds.

• Assess for the metabolic status. Metabolic acidosis will be there.

Diagnostic studies

Blood studies reveals overly acidic blood PH with low circulatory carbon dioxide, blood pressure
monitoring

First Aid In Case of Shock

Principles Involved In First Aid

1) Remove the cause of accident from near the causality. If possible remove the causality
from danger such as burning house, room with poisonous gases.

2) Handling the patient with due care and attention to reduce pain and to prevent worsening
of the condition.

3) Constant observation should be provided to the causality to identify failure of breathing,

bleeding and then to take appropriate measures to treat problems.

4) Using material available at hand.

5) Clear the crowd around the causality.

6) Take the help of the bystanders to give first aid.

7) Reassure the causality.

8) Transport the causality to the doctor as early as possible.

First aid in shock

• Reassure the causality.

• Lay him down on his back comfortably with head low and turned to one side except in
case of head injury.

• Loosen the clothing around the neck, chest and waist.

• Keep the causality warm.

• Give him sips of water if he is thirsty. Never give any alcoholic drinks.

• Never use hot water bag or massage the limbs.

• Arrest hemorrhage by adequate measures.

• Check pulse, respiration and level of consciousness.

• Transport the causality to the hospital immediately.

Treatment Of Shock

Pharmacological interventions.

1) Hypovolemic shock

• Volume expanders

• Desmopression (in case of diabetes)

• Antidiarrhoeal agents for diarrhoea

2) Carcinogenic shock

• Volume expanders

• Positive cardiac ionotropics

• Vasodilators

• Vasoactive and antiarrythmia medication

3) Distributive shock
• Volume expanders

• Positive cardiac ionotropics

• Vasoconstrictors

4) Obstructive shock

• Volume expanders

5) Septic shock

• Broad spectrum antibiotics

6) Neurogenic shock

• Hypoglycemia - glucose is rapidly administered.

Management Of Shock

• Administration of intravenous fluids, blood products, and medication. They are helpful in
treating shock.

These inciude

• Crystailoids: these are used for intravenous fluid replacement in early stages of shock
.e.g. ringer's solution and normal saline most commonly used.

• ionotropic agents: like dopamine, dobutamine and epinephrine to improve

myocardial'contractility, adequate cardiac output and improve tissue perfusion.

• Vasodilators: nitroglycerine, sodium nitroprusside used to dilate the coronary arteries.

• Diuretics: these are used to treat oliguria and increase urine output.

• Antibiotics: used to treat septic shock because they are bactericidal.

• Antihistamines: epinephrine used in anaphylactic shock.

• Steroids: used to decrease fluid shifts out of vasculature by stabilizing capillary walls.

• Sodium bicarbonate: it is used to treat metabolic acidosis that occurs as shock progress.

• Bronchodilators: like atropine, aminophyline, used to relieve bronco constriction in case

of anaphylactic shock.
Nursing Management in Case Of Shock

• Maintain ABC of the patient.

• Provide supplemental oxygen therapy to the patient.

• Do not deliver more than 2 It. of oxygen per minute if person has history of chronic
pulmonary diseases.

. Monitor for ABG value to assess the patient response to oxygen therapy.

• Continuous monitoring of vital signs should be done.

• Check for urine output of the client.

• Maintain nutritional status of the patient. Administer prescribed medication to the patient.

• Give psychological support to the patient and the relatives.

Nursing Diagnosis In Case Of Shock

1. Fluid volume deficit related to hemorrhage.

Nursing interventions:

Monitor the signs and symptoms of internal bleeding. Check for blood pressure.

Give comfortable position.

Keep the patient warm and monitor temperature hourly. Administer intravenous fluids as
ordered.

Monitor urine output. ^

• Administer oxygen as ordered.

2. Decreased cardiac output related to ineffective cardiac function.

Nursing interventions:

• Administer IV fluids

• Monitor urine output.

• Monitor blood pressure and pulse rate.

• Administer ionotropic agents to correct ventricular function.

3. Risk for infection related to interruption of skin integrity from invasive procedures.

Nursing interventions

• Take precautions to prevent nosocomial infections.

a) Wash hands frequently.

b) Use aseptic techniques.

c) Monitor sites of insertion for signs of infection.

d) Change the intravenous catheter every three days.

e) Provide indwelling catheter care frequently.

1) Monitor for white blood cell count for elevation greater than 10,000 cells per mm3.

Altered nutrition less than body requirement related to decrease oral intake.

Nursing interventions:

• Monitor daily weight and identify weight loss.

Consult nutritionist for recommendations about diet.

• Check for gastric residuals every 4 hourly; notify the physician if it is greater than 100
ml.

• Monitor for hematocrit, hemoglobin to assess the adequacy of nutritional replacement.

5. Altered peripheral tissue perfusion related to edema from stasis of blood in the
capillaries and vasoconstriction.

Nursing interventions:

• Monitor the extent of fluid retention.

. Monitor daily weight of the patient.

• Determine the severity of edema.

• Watch for elevation in central venous pressure.

• Check signs and symptoms of fluid overload.

Prevention of Shock Preoperative measures

Circulatory collapse should be assessed by strenuous measures if at all possible. Preoperatively
the patient should be as fit as possible and from the point of view from circulatory system.

• His blood should be adequate in quantity and volume.

• His tissues should be adequately hydrated.

• He should be mobile so that there should be no stagnation in the circulatory system.

• Patient should be kept warm on his journey from ward to theatre.

Post operativeiy ^

• Fluid and electrolyte replacement should be done with normal saline, dextrose 5%,
plasma and rest and relief from the pain continues.

• Gentle handling by nursing staff will help in prevention of shock.

• Diuretics like mannitol an osmotic diuretic which is neither absorbed in the renal tubules
nor metabolized. If oliguria persists frusemide can be given. Dopamine can be given to improve
blood pressure.

Complications

a. ARDS- (acute respiratory distress syndrome)

In case of septic shock patient may go for ARDS or Die - disseminated intravascular coagulation
due to ineffective perfusion and decrease venous return

b. Multiple Organ Failure

Due to inadequate tissue perfusion and decreased venous return multiple organ failure occurs.