SHOCK Discussion

7/29/2019 SHOCK Discussion

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MEDICAL SURGICAL NURSING

DISCUSSION

ON

SHOCK

SUBMITTED TO SUBMITTEDBYMISS LIYA JOHN NAVPREETKAURLECTURER M.Sc.NURSING 2ND YEAR


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MEDICAL SURGICAL NURSINGDATE: 13-02-2013

SHOCKINTRODUTION:

Shockis a serious, life-threatening medical emergency and one of the most common causes of death forcritically ill people.

The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly

this is called a hypoperfusional.

DEFINITION:

Shock is a clinical syndrome characterized by a systematic imbalance between oxygen supply and

demand. This imbalance results in a state of inadequate blood flow to body organs and tissue, causing

life-threatening cellular dysfunctions.

Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism. Thisresults in as imbalance between the supply of and demand for oxygen and nutrients. The exchange of

oxygen and nutrients at the cellular level is associated to life.

INCIDENCE:

Both sexes are common

Children and old age group more prone for shock

80% of mortality rate is caused by shock

CLASSIFICATION OF SHOCK:

In 1972 Hinshaw and Cox suggested the following classification which is still used today. It uses Four Types

of Shock,

1. HYPOVOLEMIC SHOCK

2. CARDIOGENIC SHOCK

3. DISTRIBUTIVE SHOCK

a. Septic Shock

b. Anaphylactic Shock

c. Neurogenic Shock

4. OBSTRUCTIVE SHOCK5. ENDOCRINE SHOCK, (Recently a 5th form of shock has been introduced)

1. HYPOVOLEMIC SHOCK:

This is the most common type of shock and based on insufficient circulating volume.

Its primary cause is loss of fluid from thecirculation from either an internal or external source.

An internal source may behaemorrhage. External causes may include extensive Bleeding, High

Output Fistulae or Severe burns.

2. CARDIOGENIC SHOCK:

This type of shock is caused by the failure of the heart to pump effectively.

This can be due to damage to the heart muscle, most often from a large Myocardial infarction.
http://en.wikipedia.org/wiki/Perfusionhttp://en.wikipedia.org/wiki/Circulatory_systemhttp://en.wikipedia.org/wiki/Circulatory_systemhttp://en.wikipedia.org/wiki/Hemorrhagehttp://en.wikipedia.org/wiki/Stoma_(medicine)http://en.wikipedia.org/wiki/Burn_(injury)http://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Perfusionhttp://en.wikipedia.org/wiki/Circulatory_systemhttp://en.wikipedia.org/wiki/Hemorrhagehttp://en.wikipedia.org/wiki/Stoma_(medicine)http://en.wikipedia.org/wiki/Burn_(injury)http://en.wikipedia.org/wiki/Myocardial_infarction


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Other causes of cardiogenic shock includeArrhythmias, Cardiomyopathy, Congestive heart failure

(CHF), Contusio cordis orcardiac valve problems.

3. DISTRIBUTIVE SHOCK:

As in hypovolaemic shock there is an insufficient intravascular volume of blood.

This form of"relative" hypovolaemia is the result of dilation of blood vessels which diminishes

Systemic vascular resistance.

a) Septic shock:

- This is caused by an overwhelming infection leading to vasodilation, such as by Gram negative

bacteria i.e.Escherichia coli, Proteus species,Klebsiella pneumoniae which release an endotoxin which

produces adverse biochemical, immunological and occasionally neurological effects which are harmful

to the body.

- Gram-positive cocci, such aspneumococci and streptococci, and certain fungi as well as Gram-

positive bacterial toxins produce a similar syndrome.

-

b) Anaphylactic shock:

Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the

release of histamine which causes widespread vasodilation, leading to hypotension and increased

capillary permeability.

c) Neurogenic shock:

- Neurogenic shock is the rarest form of shock. It is caused by trauma to the spinal cord resulting

in the sudden loss of autonomic and motor reflexes below the injury level.

- Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled,

resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilation and hypotension.

-4. OBSTRUCTIVE SHOCK:

In this situation the flow of blood is obstructed which impedes circulation and can result in

circulatory arrest. Several conditions result in this form of shock.

o Cardiac tamponade in which blood in the pericardium prevents inflow of blood into the

heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens,

is similar in presentation.

o Tension Pneumothorax. Through increased intrathoracic pressure, blood flow to the heart is

prevented (venous return).

o Massive pulmonary embolism is the result of a thromboembolic incident in the blood

vessels of the lungs and hinders the return of blood to the heart.

o Aortic stenosis hinders circulation by obstructing the ventricular outflow tract.o

5. ENDOCRINE SHOCK: Based on endocrine disturbances.

o Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension

and respiratory insufficiency.

o Thyrotoxicosis may induce a reversible cardiomyopathy.

o Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment

without tapering the dosage. However, surgery and intercurrent disease in patients on

corticosteroid therapy without adjusting the dosage to accommodate for increased

requirements may also result in this condition.

ETIOLOGY: Haemorrhage

Burns

Dehydration

Myocardial Infraction
http://en.wikipedia.org/wiki/Cardiac_arrhythmiahttp://en.wikipedia.org/wiki/Cardiac_arrhythmiahttp://en.wikipedia.org/wiki/Cardiomyopathyhttp://en.wikipedia.org/wiki/Congestive_heart_failurehttp://en.wikipedia.org/wiki/Myocardial_contusionhttp://en.wikipedia.org/wiki/Cardiac_valvehttp://en.wikipedia.org/wiki/Vasodilationhttp://en.wikipedia.org/wiki/Gram_negativehttp://en.wikipedia.org/wiki/Escherichia_colihttp://en.wikipedia.org/wiki/Klebsiella_pneumoniaehttp://en.wikipedia.org/wiki/Endotoxinhttp://en.wikipedia.org/wiki/Gram-positivehttp://en.wikipedia.org/wiki/Pneumococcihttp://en.wikipedia.org/wiki/Streptococcihttp://en.wikipedia.org/wiki/Cardiac_arrhythmiahttp://en.wikipedia.org/wiki/Cardiomyopathyhttp://en.wikipedia.org/wiki/Congestive_heart_failurehttp://en.wikipedia.org/wiki/Myocardial_contusionhttp://en.wikipedia.org/wiki/Cardiac_valvehttp://en.wikipedia.org/wiki/Vasodilationhttp://en.wikipedia.org/wiki/Gram_negativehttp://en.wikipedia.org/wiki/Escherichia_colihttp://en.wikipedia.org/wiki/Klebsiella_pneumoniaehttp://en.wikipedia.org/wiki/Endotoxinhttp://en.wikipedia.org/wiki/Gram-positivehttp://en.wikipedia.org/wiki/Pneumococcihttp://en.wikipedia.org/wiki/Streptococci


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Anaphylactic Shock

Neurogenic Shock

Septic Shock

Vascular Insufficiency and Cardiac dysfunction

Obstructive Condition

Diarrhoea and Dysentery

RISK FACTORS:

Major Trauma History of previous myocardial damage

Immosuppersive therapy

STAGE OF SHOCK:

1. Early reversible and compensatory shock Mean arterial pressure (MAP) drops 10 -15 mm Hg

Decrease in circulating blood volume (25-35%) 1000ml

Sympathetic nervous system stimulated; release of catecholamine Stages of Shock cont.

To maintain blood pressure: increase in heart rate and contractility; increase in peripheral vasoconstriction Circulation maintained, but can only be sustained short time without harm to tissues

Underlying cause of shock must be addressed and corrected or will progress to next stage.

2. Intermediate or progressive shock Further drop in MAP (20%)

Increase in fluid loss (1800 25400 ml)

Vasoconstriction continues and leads to oxygen deficiency

Body switches to anaerobic metabolism forming lactic acid as a waste product.

Body increases heart rate and vasoconstriction.

Heart and brain become hypoxic

More severe effects on other tissues which become: ischemic and anoxic

State of acidosis with hyperkalemia develops Needs rapid treatment

3. Refractory or irreversible shock Tissues are anoxic, cellular death widespread

Even with restoration of blood pressure and fluid volume there is too much damage to restore homeostasis

of tissues

Cellular death leads to tissue death; vital organs fail and death occurs

PATHOPHYSIOLOGY:

Whatever may be the initial cause of shock the patho physiological response is the same.

Cell throught the body are deprived of oxygen, resulting in cell membrane damage. Histamine and kinins are released in response to the damage and cause released in response to

the damage and cause vasodilation and increased capillary permeability.

WBC leaks out of the capillaries and protein pars into extra cellular fluid. Edema results with

in the cell and interstinal fluids volume increased the fluid breaks done.

This results in decreased in the circulatory blood volume and consequent reduction in venous

return in the amount, of the blood available for oxygenation and in cardiac output (Co).

Metabolism continuous within the cell despite the lack of oxygen and lactic acid, produced as

a result of cellular metabolism.

The result is Metabolic Acidosis


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HYPOVOLEMIC SHOCK:

Hemorrhage or other fluid loss decreased intra vascular volume

Decreased Cardiac Output

Decreased Tissue Perfusion

Compensatory Mechanism are Activated

Epinephrine and Nor Epinephrine Renin-Angiotensin Aldosterone System Stimulation

relaxed

ADH released

Increased Heart rate and Systemic

Vascular Resistance Intracellular fluid shift to Intravascular

Space

Increased Blood Volume

Increased Cardiac Output

Compensatory Mechanism Fails

Decreased Cardiac Output

Decreased Blood Pressure

Decreased Perfusion of Vital Organ

Multi System Organ Failure result

Sign and Symptoms:

- Increased Heart Rate

- Hypotension

- Cold and Clammy Skin- Thirst

Emergency Care:

- Fluid Replacement


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CARDIOGENIC SHOCK;

Due to Myocardial Infarction, Cardiac Insufficiency

Increased Hearts Pumping Ability

Decreased Venous Return

Increased carbon-dioxide

Decreased Circulation / Circulated Blood Volume

Decreased Inadequate Tissue Perfusion

Sign and Symptoms:


- Hypotension

- Cyanosis

- Cold and Clammy Skin Emergency Management:

- Initial drug therapy for Myocardial Infraction,

- Replace Fluids,

- Consider possible emergency coronary bypass surgery


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ANAPHYLATIC SHOCK:

Antigen re-Exposure

Hypersensitive Antibody response

Vasoactive mediator release

Massive Vasodilation Increased Capillary Permeability

Profound Hypovolaemia Vascular Collapse

Angio Edema

Uriticaria

Pulmonary Congestion

Airway Obstruction

Respiratory Arrest

Cardiac Arrest

Sign and Symptoms:

- Throat Edema

- In congestion with Increasing breathing difficulty

- Hypotension


Emergency Care:

- Manage ABC,

- Administer (Adrenaline) Epinephrine,- Administer Diphenlydramine hydrochloride (Benadry)


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SEPTIC SHOCK:

Severe Localized Infection of Gram Negative Bacilli

Bacterial Invasion of Blood stream (Septicaemia)

Inflammatory Response

Endotoxins are released into Circulation

Immune system releases Histamine and many other Chemical Mediators

Massive Vasodilation Increased Capillary

Permeability

Inadequate tissue Perfusion

Compensatory mechanism are activated

Decreased perfusion of Vital Organs

Multiple Organ Failure

Sign and Symptoms:

- Hot, Dry, Flushed skin,

- Hypotension,

- Increased Heart Rate,

Emergency Care:

- Locate the source of infection and trust with broad spectrum antibiotic,

- Replace fluids,


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NEUROGENIC SHOCK:

Spinal Cord Injury, Spinal Anaesthesia centre Depression

Increased Sympathetic Tone

Arterial and Venous dilation

Arterial/ Venous Blood pooling

Hypotension

Bradycardia Warm, Dry, Flushed skin

Decreased Perfusion of vital organs

Multisystem Organ Failure

Sign and Symptoms:

- Slowed heart rate,

- Hypotension,

Emergency Care:

- Replace fluids,

- Administer drugs to increase blood pressure and heart rate.

SIGN AND SYMPTOMS:

HYPOVOLEMIC SHOCK:

Anxiety, restlessness, altered mental state due to decreased cerebral perfusion

and subsequent hypoxia.

Hypotension due to decrease in circulatory volume.

A rapid, weak, thready pulse due to decreased blood flow combined withtachycardia.

Cool, clammy skin due to vasoconstriction and stimulation of

vasoconstriction.


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Rapid and shallow respirations due to sympathetic nervous system stimulation

and acidosis.

Hypothermia due to decreased perfusion and evaporation of sweat.

Thirst and dry mouth, due to fluid depletion.

Fatigue due to inadequate oxygenation.

Cold and mottled skin (cutis marmorata), especially extremities, due to

insufficient perfusion of the skin.

Distracted look in the eyes or staring into space, often with pupils dilated. CARDIOGENIC SHOCK:

o Distended jugular veins due to increased jugular venous pressure.

o Absent pulse due to tachyarrhythmia.

o OBSTRUCTIVE SHOCK:

o Distended jugular veins due to increased jugular venous pressure.

o Pulsus paradoxus in case of tamponade,

SEPTIC SHOCK:

o Pyrexia and fever, or hyperthermia, due to overwhelming bacterial infection.

o Vasodilation and increased cardiac output,

NEUROGENIC SHOCK:

o Skin is warm and dry.

ANAPHYLACTIC SHOCK:

o Skin eruptions and large welts.

o Localised edema, especially around the face.

o Weak and rapid pulse.

o Breathlessness and cough due to narrowing of airways and swelling of the throat

DIAGNOSTIC STUDIES: History Collection,

Physical Examination,

Blood haemoglobin and hematocrit: change in haemoglobin and hematocrit

concentration usually occur in hypovolemic shock.

Arterial blood gas (ABG): to determine oxygen and carbon-dioxide levels and

pH. The effects of shock and of the bodys compensatory mechanisms causes a

decrease in pH (indication acidosis), a decrease in partial pressure of the oxygen

(PaO2) and in total oxygen saturation, and an increase in the partial pressure of

carbon-dioxide (PaCO2).

HISTORY COLLECTION:

- Obtaining the patients medical and surgical history of recent, (Upper respiratory tract

infection, Surgery, Chest pain,)

PHYSICAL EXAMINATION:

- OBSERVATION:

- Is done to identify the colour, type, of the skin to detect presence of cyanosis, cold

and clammy skin,

- PALPATION:

- This is done to identify the flat neck veins etc.


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DIAGNOSTIC STUDIES:

o Laboratory Abnormalities in shock:

S.No: Laboratory Studies Findings Significance Of Finding1) Blood:

A) Red blood cell

count, Hematocrit,

Hemoglobin,

B) DIC Screen

- Fibrin split

Products(FSP)

- Fibrinogen Level

- Platelet Count

-Thrombin Time

- D-Dimer

- Creatine Kinase

- Troponin

- Normal

- Decreased

- Increased

- Increased

- Decreased

- Decreased

- Prolonged

- Increased

- Increased

- Increased

- Remains within normal limits in shock because

of relative hypovolemia and pump failure and in

haemorrhagic shock before fluid restoration,

- Decreased in hemorrhagic shock after fluid

resuscitation which when fluids other than blood

are used,

- Increased in non haemorrhagic shock due toactual hypovolemic because of fluid lost does

not contain erthocytes,

- Acute DIC can develop within hours to develop

within hours to days after an initial assault on the

body.(Eg: Shock)

-Increase in trauma, MI in response to cellular

changes ans / or hypoxia.

- Increases in MI,

- Indicates impaired kidney function due to

hypoperfusion as a result severs

vasoconstritionan occurs secondary to


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- BUN

-Creatinine

- Glucose

- Serum Electrolyte

Sodium

- Potassium

- Increased

- Increased

- Increased

- Increased

- Decreased

- Increased

-Decreased

- Increased

catabolism of cell(Eg: Trauma,Infecton)

- Indicates impaired kidney function due to

hypoperfusion a result of sever vasoconstriction

is more sustitive indicator or renal function than

BUN,

- Found in early shock because of release of live

glycogen stores in response to symptoms

nervous system stimulation and control, insulin

will be developed.

- Occurs because of depleted glycogen stores

with hepatocellular dysfunction possible asshock progress,

- Found in early shock because of increased

secretion of aldosterone causing renal retention

of Sodium,

- May occur iatrogenic ally when excess

hypotonic fluids is administered after fluid loss,

- Results when cellular duration liberates

intracellular potassium, also occurs in acute renal

failure and the pressure of acidosis,

- Found in early shock secondary to

hypoventilation,

- Occurs late in shock when organic acid such as

blood from anaerobic metabolism,


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- Arterial Blood gases

- Base Deficit

-Blood Cultures

- Liver Enzymes

(AZT, AST, GST)

-Urine Specific Gravity

- Decreased

- Respiratory

alkalosis

- Metabolic acidosis

> - 6

- Increased

- Increased

- Increased fixed at

1.010

- Indicates acid production secondary to hypoxia,

- May organism grows in patient who are in

septic Shock,

- Usually increases once significant

hypoperfusion and improvement at the cellular

level have occurred by product of anaerobic

metabolism,

- Elevation indicates liver cell destruction in

progressive stage of shock,

- Occurs secondary to the action of ADH,

- Occurs in renal failure,


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TREATMENT:

o DRUG THERAPY

o FLUID THERAPY IN SHOCK

DRUG THERAPY:

o Dobutamine (Dobutrex)

o Nitroglycerin (Tridic)

o Sodium Nitroprusside (Nipride)

o Dopamine (Itropin)

o Epinephrine (Adrenalin)

o Non-Epinephrine (Levophed)

o Phenylephrine (Neo-Synephrine)


15/22

FLUID THERAPY IN SHOCK:

S.No: Fluid type Mechanism of Action Type of Shock Nursing Implication

1)

2)

3)

CRYSTALLOIDS

ISOTONIC:

- 0.9% Nacl

- Lactate Ringers

BLOOD/BLOOD

PRODUCTS:

-Whole blood /

packed red blood

cells

COLLOIDS:

- Hetastarat

(Hespan)

- Fluid primarily remains in the

intravascular space, Increasing

intravascular Volume,

-Replace blood loss, increase oxygen

caring Capacity,

- Made from starch and act as volumeexpander is at as effective as albumin

can exert osmotic effect for up to 36hours,

- Used for initial volume

replacement in most types of

shock,

- All types of shock if haemoglobin

is


16/22

- Human serum

albumin protein

fraction (5%

albumin is 500 mlNSS)

- DEXTRAN

- DEXTRAN 40

- DEXTRAN 70

- Can increase plasma colloid osmotic

pressure, Rapid volume expansion,

- Hyperosmotic glucose polymer has

similar degree of volume expansion

with dextran 40 and dextran 70, and

longer duration of action with

dextran70,

- All types of shock expect

cardiogenic

- Limited use because of side effect

including platelets, dilution

clotting factor,

- Monitor for circulatory

overload ,

- Mild side effect of chills, fever,and urticaria may develop

- Increases risk bleeding

important to monitor patient for

aller


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NURSING DIAGNOSIS:

Fluid volume deficit related to loss of circulatory volume,

Decreased cardiac output related to decreased central venous pressure,

Ineffective breathing pattern related to inadequate Oxygenation,

-Impaired systemic tissue perfusion related to hypovolemic shock,

Impaired skin integrity related to Oedema,

Fear and anxiety related to severity of the disease Condition,

Nutritional pattern less than body requirement related to anorexia nervosa.

Sleep pattern disturbance related to hospitalization,

Impaired sensory and Perceptual activities related to dilated pupils,


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NURSING PROCESS:

S.No: ASSESSMENTNURSING

DIAGNOSIGOAL INTERVENTION RATIONAL

EXPECTED

OUTCOME

1) Subjective Data:

-

Objective Data:

- The client is

suffering from sever

haemorrhage

-Fluid volume

deficit related to

loss of circulatory

Volume

- To improve

and maintain

fluid loss,

- Assess the current fluid

volume status,

- To plan for necessary

informations,

- The client fluid

volume will be

Improved and

Maintained.

- Identify the causes of

shock and stop the

haemorrhage,

- To avoid further loss

of health fluid

continuously,

- Start immediately the IV

infusion,

- To maintain fliud

volume,

- Administer blood

transfusion, plasma to the

client,

- To maintain and

improve circulatoryvolume,


19/22



EXPECTED

OUTCOME

2) Subjective Data:

-

Objective Data:

- The patient is

suffering from

decreased blood

volume in systemic

circulation

- Decreased cardiac

output related to

decreased central

venous pressure

(CVP)

- To

Improve

And

Maintain

cardiac out

put,

- Monitor vital, CVP,

Pulmonary artery every 15

min to 1 hour,

- To monitor patient

status and detect or

excess,- The client

Cardiac output will

be improved and

mentioned..

- Administer crystalloids

colloids and/ or blood ,

- To restore blood and

fluid volume to maintain

perfusion of vitalOrgans,

- Examine laboratory and

X-Ray findings,

- To evaluate patient

response to treatment,

- Keep patient at normal

body temperature,

- To prevent an increase

in metabolism need for

oxygen and Co2 isincreased Production,

- Record accurately Input

and Output Chart daily ,- To monitor fluid

balance status,


20/22



EXPECTED

OUTCOME

2) Subjective Data:

-

Objective Data:

- The patient is

suffering from

hypoxia, Cyanosis.

- Ineffective

breathing pattern

related to

Inadequate O2.

- To

Improve

And

Maintain

Breathing

Pattern.

- Assess the currentbreathing sounds, and

other respiratory

parameters,

(Respiratory Rate)

- To monitor trends and

effectiveness of

intervention, - The client

Breathing pattern

will be improved.- Monitor the clients

ABC and go for a

investigation,

- To check arterial

oxygen saturation levelin the blood,

- Administer comfortable

position and device to

client (Folwer Position)

- To improve lung

expansion to for good

breathing,

- Provide humidified

oxygen to the client,- To increase oxygenlevel in the blood,

- Monitor patient

respiratory distress and

place patient back on

Ventilator,

- To ensure adequate

ventilation,


21/22

HEALTH EDUCATION:

o Given printed notes to the client and family members regarding shock

its causes, stage and it types and sign and symptoms,

o Taught all initial treatment measures to family members to avoid

shock,

o Asked the client not to worry about the disease condition, Because it

may lead to stress that may still worsen the condition,

o Advised the client to take good nutritious food to improve nutritious

status,

o Encouraged the client to take medication regulatory and come for

regular checkups,

CONCLUSION:

o Shock is a serious,life threating medical condition where insufficient

blood carries oxygen and nutrients around the body is reduced flowhinders the delivery of these components to tissue, Which stops

functioning. Which results in coma and brain Death, If not treated at

correct time.


22/22

BIBLIOGRAPHY

BOOK REFERENCE:

LEWIS HEITKEMPER, Medical and Surgical Nursing, 6 th Edition 2000,

Published by Mosby, Page No: 1760,

JOYCE AND BLACK, Medical and Surgical Nursing,7th Edition 2001,

Published by Lippincott, Page No:2444-443

BRUNNER AND SUDDARTHS, Medical and Surgical Nursing,9th Edition,

Published by Lippincott, Page No:274-276,

MANDHAN NEIGHBOURS, Medical and Surgical Nursing,2nd Edition

1998,Published by Saderson Company,

BRIAN DOLAN AND LYNDA HOLT, Accident and Emergency, 4 th

edition, Published by Bailliere Tindal, Page No:303, TORTORA.G.J, Principles of Anatomy and Physiology New Jerrsy willy

Publication,

Pricilla lemone & Karen burke Medical surgical nursing critical thinkinh in

client care 4th edition. Published by Dorling Kindersely (India).

Journal reference:

o LEDINGHAM AND RAMSEY, Shock, British Journal of

Anaesthesia Vol:58, Page No: 169-189,

o IRWIN,R.S.RIPPE, Procedure and Techniques in Intensive care

medicine, Lippincott publication,o KARL JASPER, Nursing Times , Subdural Haemorrhage, Mosby

Publication,

NET ABSTRACT:

o http://en.wikipedia.org/wiki/Bleeding,

o http://en.wikipedia.org/wiki/Shock
http://en.wikipedia.org/wiki/Bleedinghttp://en.wikipedia.org/wiki/Shockhttp://en.wikipedia.org/wiki/Bleedinghttp://en.wikipedia.org/wiki/Shock

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