SEMINAR ON SHOCK

Submitted By, Submitted To,

Mrs Gayathri . R Mrs Salini

IstYear M.Sc. Nursing Senior Lecturer

Upasana College Of Upasana College Of
Nursing, Kollam Nursing, Kollam

Submitted On:09.11.18

INDEX

1
1. Introduction [3]

2. Definition [4]

3. Shock & it’s significance [4-5]

4. Causes of circulation failure [5-6]

5. Compensatory mechanism [6-8]

6. Conditions precipitating shock [9-10]

7. Stages of shock [10-15]

8. First aid in case of shock [30]

9. Nursing diagnosis in case of shock [31-33]

10.Prevention of shock [33-34]

Complications

11.Promoting home and

12.Community based car e [34-35]
13.Conclusion [35-36]

14.Bibliography [36-37]

2
INTRODUCTION

All living cells in the human body require oxygen in order to efficiently

convert glucose into energy. In order for cells to receive oxygen, there needs to

be adequate blood flow throughout the body so that oxygen- rich blood can

deliver oxygen to the tissues and cellular respiration can occur. When there is

impedance in the body’s ability to perfuse blood to the tissues, shock may

occur. Shock is a life threatening condition with a variety of underlying causes.

It occur when there is circulatory failure throughout the entire body, which

results in cellular damage and can lead to multiple organ failures if not treated

immediately.

Blood pressure is a major determinate in the perfusion of tissues because there

needs to be pressure in order to push the blood through the capillaries of this

tissue. Blood pressure is determined by two factors; resistance to flow and

cardiac output. Resistance to flow is determined by length and width of the

vessels, as well as the viscosity of the blood. Cardiac output is determined by

the heart rate & stroke volume [amount of blood pumped out on each beat].

There are several factors that affect the body’s blood pressure and they are

placed into four categories with several sub categories.

Historical background: In 1923 Walter and Canner first worked for all

conditions of shock

3
DEFINITION

o Shock can best be defined as condition in which tissue perfusion is

inadequate to deliver oxygen and nutrients to support vital organs and
circular function. [Hameed
, Arid & Cohn , 2003]
o Shock is defined on a complex life threatening conditions characterized
by inadequate blood supplied to the tissues & cells of body.
[Brunner &
Siddharth]
o In medicine critical condition that is brought on by a sudden drop in
blood flow through the body. The circulatory system fail to maintain
adequate blood flow, sharply curtailing the delivery of oxygen and
nutrients to vital organs.
o It is defined on a clinical syndrome resulting from gross impairment of
tissues perfusion & wide spread cellular dysfunctions caused by
diminished O2 delivery.
[K.V Krishnardan]

SHOCK & ITS SIGNIFICANCE

Shock affects all body system. It may develop slowly or rapidly

depending upon the underlying cause’s adequate blood flow to the tissues and
cells requires the following components: adequate cardiac pump effective
vasculature or circulatory system and sufficient blood volume. If one
component is impaired, perfusion to the tissues is threatened or compromised.
Without treatment, inadequate blood flows to the tissues results in poor delivery
of oxygen and nutrients to the cells, cellular starvation, cell death, organ
dysfunctions progressing to organ failure and eventual death during shock the
4
body struggles to survive, calling on all its homeostatic mechanisms to restore
blood flow. An insult to the body can create a cascade of events result in poor
tissue perfusion. Therefore, almost any patient with any disease state may be at
risk for developing shock.

Nursing care of person with shock requires on-going systematic assessments.

Many of the interventions require in caring for patients which shock call for
close collaboration with other members of the health care team and rapid
implementation of physician order. Nurses must anticipate orders, because these
orders 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.
 Toxaemia-viral or bacterial.
 Effects of drugs.
2. Deficient oxygenation of blood in lungs
Amongst any causes the following are the most important.
 Post-operative atelectasis.
 Thoracic injuries particularly of chest that is pneumothorax,
crushing and laceration of lung.
 Obstruction of pulmonary artery by an embolus.
 Disturbances of lung function following surgery and anaesthesia.
3. Reduction in blood volume [ Oligaemia & Hypervolemia ]
This may occur from loss of

5
  Whole blood- haemorrhage [ internal or external ]
 Plasma-this is particularly significant in burns.
 Water and electrolyte which occurs from peritonitis, intestinal
obstruction, paralytic ileus, acute dilation of the stomach, severe
diarrhoea and vomiting.
4. Miscellaneous
There are number of other conditions that may lead to shock state
with low blood pressure
 Faintness
 Acute anaphylaxis
 Acute adrenal deficiency [ Addison’s diseases ]
 Over dosage of drugs e.g. Analgesics like pethidine.
 Following therapy with beta blocking agents.
 Noxian stimuli such as pain, if severe will cause vaso dilatation
particularly of splenetic vessels with cooling of blood in the area.
This is the mechanism of primary shock.

COMPENSATORY MECHANISM

Whatever is the cause of sudden collapse; there are certain

compensatory physiological mechanisms 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 vessel: contraction of arterioles & venules of
the skin is usual so as to conserve the blood supply to the more vital
organ. The application of heat dilates the ski vessels there by
aggravating the condition & should not be used.

6
  Intensitivity : A much collapsed patient usually have little pain
.Large quantities of pain relieving drugs are unnecessary & 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 acceleration :It occurs in most forms of circulatory failure
with the important exception of faint . It is an attempt to ensure that
remaining fluids is circulated as rapidly as possible there by providing
sufficient oxygen to tissues.
Subnormal temperature: this reduces the requirement 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 there beneficial effects &
if the condition of circulation is restored to normal.

7
 PATHOPHYSIOLOGY

Initial physiological insult

leading to shock state

Decrease in cardiac output &

tissue perfusion

Sympathetic nervous system

activation

Endocrine response Renin- angiotensin

activation

Increased vasoconstriction &activation of

antidiuretic hormone which increase preload

Renal system conserves

sodium & water to increase
preload
Increased blood pressure ,
heart rate , & myocardial
contractility
Restoration of tissue
perfusion

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CONDITIONS PRECIPITATING SHOCK

Classification of shock

Conventionally , the primary underlying pathophysiologic process & underlying

disorders are used to classify the shock state .Shock can be classified according
to the etiology & can be describes

1 Hypovolemic shock

2 Cardiogenic shock

3 Circulatory shock or Distributive shock

a. Septic shock
b. Obstructive shock
c. Neurogenic shock
d. Anaphylatic shock

Regardless of the initial cause of shock, researchers have gradually concluded

that certain physiologic responses are common to all type of shock. These
physiologic responses are hypoperfusion of the tissues, hypermetabolism, and
activation of the inflammatory process. A de arrangement in the compensatory
mechanism to effectively restore physiologic balance is the final pathway of
all shock states. Once shock develops in particular patient survival may have
more to do with the body’s response rather than initial cause of shock
(Klienpell).

VASCULAR RESPONSES

Oxygen attaches to the haemoglobin molecule in red blood cells, and the
blood carries it to body cells. The amount of oxygen that is delivered into the
cells depends both on blood flow to a specific area & on blood oxygen

9
concentration. Blood is continuously recycles through the lungs to be re
oxygenated & to eliminate & products of cellular metabolism, such as carbon
dioxide. The heart muscle is the pump that propels the freshly oxygenated
blood out to the body tissues. This process of circulation is facilitated through
an elaborate & dynamic vasculature consisting of arteries, arterioles,
capillaries , venules & veins. The vasculature can dilate or constrict based on
the central & local regulatory mechanism. Central regulatory mechanism
stimulates dilation or constriction of the vasculature to maintain an adequate
blood pressure. Local regulatory mechanisms , referred to as autoregulation,
stimulate vasodilation or vasoconstriction in response to biochemical
mediators(cytokines) released by the cell, communicating its need for oxygen
&nutrients . A biochemical mediator is a substance released by a cell or
immune cells such as monocytes & macrophages ; the substance triggers an
action at a cell site or travels in the blood stream to a distant site, where it
triggers action.

BLOOD PRESSURE REGULATION

Three major component of the circulatory system – blood volume , cardiac

pump & the vasculature – must respond effectively to complex neural ,
chemical & hormonal feed back systems to maintain an adequate BP &
ultimately perfuse body tissues. BP is regulated through a complex interaction
of neural , chemical & hormonal feed back system effecting both cardiac
output & peripheral vascular resistance. This relation ship is expressed in the
following term of equation:

Mean arterial BP = Cardiac output * Peripheral resistance

STAGES OF SHOCK

Shock is believed to progress along a continuum of stages through which a

patient struggles to survive . A convenient way to understand the physiologic

10
 responses & subsequent clinical signs & symptoms is to divide the continuum
into separate stages.

Stage 1: Initial stage

Stage 2: Compensatory stage

Stage 3: Progressive stage (Decompensate)

Stage 4: Irreversible stage (Refractory)

Stage 1: Initial stage

During this stage

Inadequate perfusion

Cellular hypoxia

Mitochondria become unable to produce ATP

Due to lack of oxygen cell membrane become damaged

Leakage to the extra cellular fluid

Cell performs anaerobic respiration

Build up of lactic acid & pyruvic acid

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Systemic metabolic acidosis

The process removing the components in the cells by the liver requires oxygen.
(Which is absent)

Stage 2: Compensatory stage

In the compensatory stage of shock , the BP remains with in the normal limit.
Vasoconstriction , increased heart rate & increased contractility of the heart
contribute to maintaining adequate cardiac output . This results from stimulation
of the sympathetic nervous system & subsequent release of catecholamines
(Epinephrine & Nor epinephrine).Patients display the often described “fight or
flight “response. The body shunts blood from organs such as the skin , kidneys
& gastrointestinal tract to the brain & heart to ensure adequate blood supply to
these vital organs . As a result , the skin is cool & clammy , bowel sounds are
hypoactive & urine output decreases in response to the release of aldosterone &
ADH.

Clinical manifestations:

 Inadequate organ perfusion

 Metabolic acidosis
 Tachycardia
 Compensatory respiratory alkalosis
 Confusion
 Combativeness
 Flat neck veins
 Dry warm skin
 Irritability
 Deep rapid respiration
 Dilated reactive pupil
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  Bounding pulse

Medical & Nursing management:

 Identify the cause

 Monitor vital signs
 IV fluid therapy
 Beta blocking agents /Calcium channel blockers etc
 Assess the patient for risk factor of shock
 Special consideration in geriatric patients
 Monitoring tissue perfusion
 Reducing anxiety
 Promoting safety

Stage 3: Progressive stage(De- compensating)

In the progressive stage of shock , the mechanisms that regulate the BP can no
longer compensate, and the MAP falls below normal limit of patients are
clinically hypotensive ; this is defined as a systolic BP of less than 90 mm hg or
a decrease in systolic BP of 40 mm hg (Klienpell).

PATHOPHYSIOLOGY

Although all organ system suffer from the hypoperfusion at this stage, two
events perpetuate the shock syndrome. First the over worked 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 shock
is not of cardiac origin.

Second ,the auto regulatory function of the micro circulation fails in response to
numerous bio chemical mediators released by the cells, resulting in increased
capillary permeability, with are as a of arteriolar & venous constriction further

13
compromising cellular perfusion. At this stage the patient prognosis is worsen,
The relaxation of pre capillary sphincters causes fluid to leak from the
capillaries , creating interstitial oedema & return 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 & a vicious circle ensures.

Clinical manifestations:

 Respiratory effects
-Thirst
-Rapid shallow breathing
-ARDS
-Hypoxemia
 Cardio vascular effects
-Chest pain
-Tachycardia
 Neurologic effects
-Confusion
-Lethargy
-Loss of consciousness
-Dilated sluggish pupil
 Renal effects
-Acute renal failure
 Hepatic effects
-Jaundice
 Gastro intestinal effects
-GI bleeding
-Bloody diarrhoea
 Hemotologic effects
-Hypotension

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 -Disseminated intravascular coagulation
Medical management:
To restore the perfusion by;
 Optimising the intra vascular volume
 Supporting the pumping action of the heart
 Improving the competence of the vascular system
 Supporting the respiratory system
Stage 4: Irreversible stage
At this stage vital organs have failed & the shock can no longer be
reversed. Brain damage & cell death will occur. Death of the person will
occur immediately.
Clinical manifestation:
 Unconsciousness
 Absence of reflexes
 ARDS
 DIC
 Bradycardia
 Cyanosis
 Absence of bowel sounds
 Immune system collapse
 Anuria
Medical & Nursing management:
 Fluid replacement
 Monitoring the patient
 Vasoactive medications
 Nutritional therapy

CLASSIFICATION OF SHOCK

15
Shock can be classified according to the aetiology & can be described as:

1 Hypovolemic shock

2 Cardiogenic shock

3 Circulatory shock (Distributive shock)

 Septic shock
 Obstructive shock
 Neurogenic shock
 Anaphylactic shock

1 Hypovolemic shock

It’s the most common type of shock, is characterised by a decreased

intravascular volume. Body fluid is contained in the intracellular & extra
cellular compartments. Intracellular fluid accounts for about two third of the
total body water. The extra cellular body fluids is found in one of two
compartments : intravascular(inside blood vessel) or interstitial (surrounding
tissue). The volume of interstitial fluid is about three to four times that of
intravascular fluid. Hypovolemic shock occurs when there is a reduction in
intravascular volume by 15% to 25% which represents a loss of 750ml to
1300ml of blood in a 70 kg person.

Pathophysiology
Absolute hypovolemia
Relative hypovolemia

Decreased circulatory volume

Decreased venous return

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 Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Ineffective tissue perfusion

Impaired cellular metabolism

Risk factors

 External : fluid loss

 Trauma
 Surgery
 Vomiting
 Diarrhoea
 Diuresis
 Diabetic Insipidus
 Internal : fluid shift
 Haemorrhage
 Burns
 Ascites
 Peritonitis
 Dehydration

Medical management

17
Major goals in the treatment of hypovolemic shock are

1. To restore intravascular volume to reverse the sequence of events leading

to inadequate tissue perfusion
2. To redistribute fluid volume
3. To correct the underlying cause of the fluid loss as quickly as possible
4. Fluid & blood replacement
5. Pharmacologic therapy eg: Desmopressin , Anti- diarrheal agents ,
Anti- emetic agents

Nursing management

 Closely monitor the patient who are at risk for fluid volume deficit
 Assisting with fluid replacement before intravascular volume is depleted
ensuring safe administration of prescribed fluids & medication &
documenting their administration & effects
 Monitor signs of complication & side effects of treatment & reporting
these signs early in treatment
 Oxygen administration

2 Cardiogenic shock

Cardiogenic shock occurs when the hearts ability to contract & to pump blood is
impaired & the supply of oxygen is inadequate for the heart & tissue . The
cause of cardiogenic shock are known as either coronary or non -coronary.
Coronary cardiogenic shock is more common than noncoronary cardiogenic
shock & is seen most often in patient with myocardial infarction. Coronary
cardiogenic shock occurs when a significant amount of the left ventricular
myocardium has been damaged . Patient who experience an anterior wall
myocardial infection are at greatest risk for cardiogenic shock because of the
potentially extensive damage to the left ventricle caused by occlusion of the left

18
anterior descending coronary artery . Noncoronary artery causes of cardiogenic
shock are related to conditions that stress the myocardium (eg: severe
hypoxemia , acidosis , hypoglycaemia ,hypocalcemia , tension pneumothorax)
as well as conditions that results in ineffective myocardial function (eg :
cardiomyopathies , valvular damage , cardiac tamponade).

Pathophysiology

Decreased cardiac
contractility

Decreased stroke volume &

cardiac output

Pulmonary Decreased Decreased

congestion systemic coronary
tissue perfusion
perfusion

Clinical manifestation:

 Pain (Anginal pain)

 Dysrhythmias
 Hemodynamic irritability

Medical management:

Goals include

 To limit further myocardial damage

 Improving cardiac function by increasing cardiac contractility
 Correction of underlying causes
 Initiation of first line treatment

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 -Supplying supplemental oxygen
-Controlling chest pain
-Providing selected fluid support
-Administering vasoactive medications
-Implementing mechanical cardiac support
-Hemodynamic monitoring
-Laboratory marker monitoring (Markers of ventricular function level ,
cardiac enzyme level )
-Obtain 12 lead ECG
 Pharmacologic therapy
-Dobutamine
-Nitro-glycerine
-Dopamine
-Antiarrhythmic medication
-Vasoactive agents(Epinephrine , Nor epinephrine etc)
-Diuretics(Frusemide)
-Fluid therapy
 Mechanical assistive devices which;
-Increased stroke volume
-Improved coronary artery perfusion
-Decreased pre load
-Decreased cardiac work load
-Decreased myocardial oxygen demand

Nursing management

 Preventing cardiogenic shock

-Identifying the risk patients
-Administer supplemental oxygen
-Conserves patient energy

20
  Monitoring hemodynamic status
-Arterial lines & ECG monitoring
-Maintain IV fluids
-Monitoring lab values
-Physical assessment of patient
-Monitor ABG values
 Administering medications
 Maintaining intra aortic balloon counter pulsation
 Enhancing safety & comfort
-Proper medications
-Preventing infections
-Protecting skin
-Monitoring respiratory & renal function
-Proper positioning of the patient
-Monitor vitals

3 Circulatory shock

Circulatory shock occurs when blood volume is abnormally displaced in the

vasculature. The displacement of blood returns to the heart ; which leads to
subsequent in adequate tissue perfusion. The ability of the blood vessels to
constrict helps return the blood to the heart. The vascular tone is determined
both by central regulatory mechanisms , as in BP regulation & by local
regulatory mechanisms , as in tissue demands for oxygen & nutrients. There
fore circulatory shock can be caused either by a loss of sympathetic or by
release of biochemical mediators from cells.

The varying mechanisms leading to the initial vasodilation in circulatory shock

further classified into four types:

 Septic shock

21
 Obstructive shock
 Neurogenic shock
 Anaphylactic shock

 Septic shock

Septic shock the most common type of circulatory shock ,is caused by
wide spread infection . Despite the increased sophistication of antibiotic
therapy the incidence of septic shock has continued to use during the past
year . Nosocomial infection in critically ill patients that may progress to
septic shock . most frequently originate in the blood stream ; lungs &
urinary tract . Other infections include abdominal infection ,wound
infection , bacteraemia associated with intra vascular catheters .
Additional risk factors that contribute to the growing incidence of septic
shock are increased awareness & identification of the condition ; the
increased number of immunocompromised patients ; the increased use of
invasive procedures & indwelling medical devices ; the increased
number of resistant micro organisms , and the increasingly older
population . A significant body of research has been conducted in the past
decade in an effort aimed at reducing the morbidity & mortality caused
by septic shock . It can cause multiple organ dysfunction syndrome &
death.

Pathophysiology

Infectious toxins

Unregulated Vessels endothelial &

immune 22 platelet damage
system activation
Profound Release of kinin
cardiovascular , ,serotonin & histamine
pulmonary &
haemostatic Capillary permeability
changes & vasodilation.
Absolute & relative
hypovolemia

Decreased BP

tissue perfusion

Medical management:

 Specimens of blood , sputum , urine ,wound drainage ; and tips of

invasive catheters are collected for culture using aseptic technique
 Potential root of infection may be eliminated
 Antibiotic coated IV central lines may be inserted to decrease the risk of
invasive line -related bacteraemia in high risk patients
 Fluid replacement must be instituted to correct the hypovolemia

Pharmacologic management:

 Broad spectrum antibiotics

 3rd generation cephalosporin + Aminoglycoside

23
  Studies recently demonstrated that recombinant human activated protein
(rh APC ) reduces mortality in patients with severe sepsis

Nursing management:

 All invasive procedures must be carried out with aseptic technique after
careful hand hygiene
 IV lines , arterial & venous puncture sites , surgical incisions ,traumatic
wounds , urinary catheters , and pressure ulcers must be monitored for
signs of infections in all patients
 Identify the risk groups
 Monitor patients vitals slowly
 Administration of prescribed medications properly
 Monitor the lab values
 When caring the patient with septic shock , the nurse collaborates with
other health team members to identify the site & source of sepsis and
specific organism involved in it

 Obstructive shock
Obstructive shock results from either a critical disease in pre load or an
increase in left ventricle out flow obstruction . Extra cardiac process that
increase intra thoracic pressure can result in obstructive shock by
decreasing cardiac compliance & interrupting venous return by
compressing the inferior or superior venacava . Tension pneumothorax
-herniation of abdominal contents into the thorax , and positive pressure
ventilation are processes that result in decreased cardiac compliance &
destruction of the venacava , decreased pre load & decreased cardiac
output .

24
 Management:
 Prompt relief of obstruction eg : Pericardiocentesis for
tamponade ,Chest drain for tension pneumothorax
 Fluid & inotrope for temporary support

 Neurogenic shock
This is a very uncommon type of shock . Its most often seen in patient
who have had an extensive spinal cord injuries . In neurogenic shock ,
vasodilation occurs as a result of a loss of balance between
parasympathetic & sympathetic stimulation . Sympathetic stimulation
causes vascular smooth muscles to constrict , and parasympathetic
stimulation causes the vascular smooth muscles to relax or dilate . The
patient experiences a predominant parasympathetic stimulation that
causes vasodilation lasting for an extended period , leading to a relative
hypovolemic state . The over riding parasympathetic stimulation causes
vasodilation lasting for an extended period , leading to a relative
hypovolemic state & also cause drastic change in the patients systemic
vascular resistance & bradycardia .Neurogenic shock may having
prolonged course .

Pathophysiology

Disruption of sympathetic
nervous system

Loss of sympathetic tone

25
 Venous and arterial
vasodilation

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen

supply

Impaired tissue perfusion

Impaired cellular metabolism

Medical management:

Treatment of neurogenic shock involves restoring sympathetic tone , either

through the stabilisation of a spinal cord injury or in the instances of spinal
anaesthesia , by positioning the patient properly . Specific treatment depends on
cause of the shock . If hypoglycaemia is the cause , glucose is rapidly
administered.

26
Nursing management :

 Elevate & maintain the head of the bed at least 300 to prevent neurogenic
shock when a patient receives spinal or epidural anaesthesia
 Careful immobilisation of patient in case of spinal injury
 Apply elastic compression stockings & elevate the foot end of bed may
minimise the pooling of blood in legs
 Pooling causes thrombus formation , so the nurse must not it
 Administration of heparin or low molecular weight heparin as prescribed
 Closely monitor the patient for any signs of internal bleeding

 Anaphylactic shock

Anaphylactic shock occurs rapidly & is life-threatening .Because

anaphylactic shock occurs in patients already exposed to an antigen and who
have developed antibodies to it , it can often be prevented. Patient with known
allergy should understand the consequences of subsequent exposure to the
antigen and should wear medical identification that list their sensitivities . This
could prevent in advertent administration of a medication that would lead to
anaphylactic shock.

Pathophysiology

Due to antibody response

Release of histamine

Vasodilation

27
 Increased capillary
permeability

Severe bronchodilation

Decreased oxygen
supply &utilization

Inadequate tissue
perfusion

Medical management:

 Removing the causative antigen

 Administration of Epinephrine, Histamines if needed
 Fluid therapy
 Oxygen administration

Diagnosis of shock :

Its essential for proper treatment and management

 Conducts head to toe examination for signs of shock

 Asses neurological status of the person by assessing the level of the
person by assessing the level of consciousness
 Assess the cardiovascular status. Blood pressure varies with the stages of
shock

28
  Assess for renal status .Anuria & Renal failure can occur
 Assess for integumentary status .Check for skin color , cold & clammy
skin , cyanosis
 Assess gastro intestinal status .Hypo active bowel sounds
 Assess for the metabolic status. Metabolism acidosis will be there

Nursing management:

 Nurse must assess all patients for allergies or previous reactions to

antigens & communicate the existence of these allergies or reactions to
others
 The nurse must be knowledge about the clinical signs of anaphylaxis
 Monitoring the patients response according to treatment
 Continuous monitoring of vital signs should be done
 Check for the urine output of client
 Provision of supplemental oxygen therapy to the patient
 Proper documentation about the particular medication that we should
administered to the patient

First Aid in Case of Shock

Principles Involved in First aid:

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

• Handling the patient with due care & attention to reduce pain & to
prevent worsening of the condition.

29
• Constant observation should be provided to the causality to identify
failure of breasting, bleeding & then to take appropriate measures to treat
problems.

• Using material available at hand.

• Clear the crowd around the causality

• 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 & turned to one

side except in case of head injury.

• Loosen the clothing around the neck, chest & 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 manage the limbs.

• Arrest haemorrhage by adequate measures.

• Check pulse, respiration & level of conciseness.

• Transport the causality to the hospital immediately.

Nursing Diagnosis in case of shock.

1. FLUID VOLUME DEFICIT RELATED TO HAEMORRHAGE.

Nursing Intervention:

• Monitor the signs & symptoms of internal bleeding.

• Check for blood pressure.

30
• Give comfortable position.

• Keep the patient warm & monitor temperature in hourly.

• Administer intravenous fluids as ordered.

• Monitor urine output.

• Administer oxygen as ordered.

2. RISK FOR INFECTION RELATED TO INTERRUPTION OF SKIN

INTEGRITY FROM INVASIVE PROCEDURES

Nursing Intervention:

• Take pre-caution to prevent nosocomial reactions

- Wash hands frequently

- The aseptic techniques

- Monitor sites of insertion for night of injection

- Change the intravenous catheter every three days

- Provide indwelling catheter were frequently

- Monitor for white blood cell count for elevation greater than 10,000 cell

per mm3

3. ALTERED NUTRITION LESS THAN BODY REQUIREMENT

RELATED TO DECREASE ORAL INTAKE

Nursing interventions

• Monitor daily weight and identify weight loss.

• Consult nutritionist for recommendation about diet.

• Check your gastric residuals every 4 hrly, notify the physician if it is

greater than 100ml.

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• Monitor for haematocrit ,haemoglobin to asses adequacy of nutritional

replacement.

4 ALTERED PERIPHERAL TISSUE PERFUSION RELATED TO EDEMA

FROM SATSIS OF BLOOD IN THE CAPILLARIES AND

VASOCONSTRICTION

Nursing Intervention

• Monitor daily weight and identify weight loss.

• Monitor the extent of fluid retention

• Monitor/determine the severity of oedema

• Watch for elevation in central venous pressure

• Check signs and symptoms of fluid over load.

5 DECREASED CARDIAC OUT PUT RELATED TO INEFFECTIVE

CARDIAC FUNCTION

Nursing interventions

 Administer IV fluids
 Monitor urine output
 Monitor blood pressure & pulse rate
 Administer ionotropic agents

PREVENTION OF SHOCK

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Pre-operative measures:

Circulatory collapse should be assessed by strenuous measures if at all

possible. Pre-operatively 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 this journey from ward to theatre

Post Operatively:

• Fluid and electrolyte replacement should be done with normal saline, 5%

Dextrose , 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 persist can be given.

Dopamine can be given to improve blood pressure.

COMPLICATIONS

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Its previously called adult respiratory distress syndrome. It’s a severe

from of acute lung injury. The clinical syndrome in characterized by a hidden
and preventive pulmonary oedema ,increasing bilateral infiltrates of chest x-
ray ,hypoxemia refractory to oxygen supplementations, and reduced lung

33
compliance. These signs occur in the absence of left sided heart failure.
Patients with ARD usually require mechanical ventilation with a higher – than-
normal air way pressure. The major cause of death in ARD is no pulmonary
multiple system organ failure, often with sepsis .

MULTIPLE ORGAN DYSFUNCTION SYNDROME(MODS)

MODS is altered organ function in actually ill patients that require

medical intervention to support continued organ function .Its another phase in
the progression of shock states. The actual incidence is difficult to determine,
because it develops with acute illness that compromise tissue perfusion. Its
other wise called multiple organ failure.

PROMOTING HOME & COMMUNITY – BASED CARE

TEACHING PATIENTS SELF CARE

Patients whose experience and survive shock may have been unable to
get out of bed for an extended period of time and are likely to have a slow
prolonged recovery. The patient and family are instructed about strategies to
prevent further episodes of shock by identifying the factors implicated in the
initial episode. In addition , the patient and family require instruction about
amendments needed to identify the complication that many occur after patient is
discharged from the hospital. Depending on the type of shock & its
management., the patient or family may enquire instruction about treatment
modalities such as emergency administration of medication ,IV therapy,
parental nutrition, skin care ,exercise and ambulation .The patient and family
are the instructed about the need for gradual increase in ambulation and other
activity. The need for adequate nutrition and another crucial aspect of reaching.

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CONTINUING CARE:

Because of the physical toll associated with recovery from shock patients
may be cared for in an extended care facility or rehabilitation setting after
hospital discharge. Alternatively ,a referral may be made for the home care.
The home care nurse assess the adequacy of treatments that are continued at
home and the abilities the patients and family to cope with these treatments .
The patient is likely to require close medical supervision until complete
recovery occur. The home care nurse reinforces the importance of continuing
medical care and helps the patient and family identify the mobilize community
resources

CONCLUSION

Shock is a state of acute circulatory failure leading to decreased organ

perfusion, with inadequate delivery of oxygenated blood to nurses and resultant
and organ .function. The mechanisms that can result in shock are divided in four
categories; hypovolemic, distributive, cardiogenic & obstructive while much is
known regarding treatment of patients in shock. Several controversies continue
in the literature studies about this also. Adherence to evidence based care of the
specific causes of shock can optimize a patients chances of surviving this life
threatening condition. Shock is a catastrophic & result of circulating collapse &
in adequate cardiac output, characterised by end organ hypoxemia, ischemia &
failure , While the path physiologic mechanism of distributive, obstructive,
hypovolemic & cardiogenic shock are distinct, they may result in similar initial
presentation with end-organ damage & cardio circulatory insufficiency.
Hypotension is common, but not obligatory, for the diagnostic of shock. Overall
it’s a life threatening clinical condition.

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