SEMINAR ON SHOCK AND

HEMORRHAGE

SUBMITTED TO: MRS SHINY T SAM

ASSOCIATE PROFESSOR
TMM COLLEGE OF NURSING

SUBMITTED BY: ELSY MAYJO

1ST YEAR MSC NURSING
TMM COLLEGE OF NURSING
 HEMORRHAGE
INTRODUCTION
Hemorrhaging or hemorrhaging (American and British spelling differences) or bleeding is the loss of blood from
the circulatory system. Bleeding can occur internally, where blood leaks from blood vessels inside the body or
externally, either through a natural opening such as mouth, nose, vagina, ear, or anus, or through a break in the
skin. The complete loss of blood is referred to as exsanguination, and desanguination is a massive blood loss.
Typically, a healthy person can endure, a loss of 10-15% of the total blood volume without serious medical
difficulties, and blood donation typically takes 8-10% of the donor’s blood volume.

MEANING
It is derived from Greek word ‘haima’, which means ‘blood’ and ‘rhegnynai’ which means ‘burst forth’ or ‘gush’.

DEFINITION
• Hemorrhage is defined as abnormal severe (internal or external) discharge of blood from body.
• It is the loss of blood from the blood vessels, it is caused due to any injury or any accident which result
in rupturing of blood vessel.
• If the hemorrhage is severe that may lead to patient in shock.

NATURAL ARREST OF HEMORRAGE

Hemostasis is your body's natural reaction to an injury that stops bleeding and repairs the damage. This capability
is usually for your benefit, conserving blood and preventing infections. In rare cases, the process doesn't work as
it should, and this can cause problems with too much or too little clotting.
Adequate amount of calcium is required and all the clotting factors are essential for the natural arrest of
hemorrage.the blood in the circulation is kept fluid by a fine balance between clotting and fibrinolysis.when a
tissue is damaged the prothrombin is converted in to its active form of thrombin( in to presence of
calcium).soluble fibrinogen in plasma then transformed by thrombin to fibrin. Then the mesh is formed by
platelets and other blood to form clot.

FACTORS AFFECTING CLOTTING

• Calcium: it helps in clotting of blood.it can displaced from the blood by 3.8% of solution of sodium citrate,
acid citrate dextrose solution, EDTA. Acid citrate dextrose and acid citrate phosphate solutions are used
to prevent clotting of stored blood.
• Prothrombin: it is formed from Vitamin K, fat soluble vitamin absorbed from small intestine, a patient
suffering from obstructive jaundice will not absorb vitamin K and therefore they may bleed if operated
upon. For this reason, vitamin K injection is given so as to restore the pro –thrombin level of blood.
• Fibrinogen: it is the precursor of fibrin. It is the substance which dissolves fibrin by a phenomenon known
as fibrinolysis. In its absence severe bleeding may occur.
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The fibrinolytic activity of blood may be increased in the following situations
- In complicated obstetric cases associated with hemorrhage
- After strenuous activity
- In presence of some malignant growth.

ETIOLOGY
• Loss of total blood: the commonest cause of hypovolemic shock is hemorrhage and called hemorrhagic
shock
• Loss of plasma: as in burns and peritonitis
• Loss of body fluid: as in severe vomiting, diarrhea & intestinal obstruction.

CLASSIFICATION
❖ ETIOLOGY:
a- Traumatic: wounds, fractures, operations, abrasion, excoriation, hematoma, laceration, incision,
contusion, crushing injuries, gunshot wounds.
b- Pathological –erosion of a vessel by an ulcer, a malignancy, or infection.
c- Spontaneous: hemorrhagic disease, e.g., hemophilia, leukemia, thrombocytopenic purpura, or
liver insuffiency.
d- Others: platelets; NSAIDS; cause bleeding by inhibiting activating platelets
E.g., Aspirin, ibuprofen, and related drugs.

❖ RELATION TO TRAUMA: hemorrhage may be

a) PRIMARY HEMORRHAGE: at the time of trauma or immediately after it. i.e.: cut on a finger or
operative incision.
b) REACTIONARY / INTERMEDIATE HEMORRHAGE: occur during the first 24 hours after trauma ,
it may be due to :
- Slipped ligature
- Raising of b p (due to correction of shock or post-operative pain) bleeding starts from an injured vessel
which was not bleed because of hypotension.
c) SECONDARY HEMORRHAGE: occur 1-2 weeks after trauma, it is due to infection which dissolves
the clot, erodes the vessel wall or granulation tissue.

❖ SOURCES OF HEMORRHAGE
a) Arterial: occurring in jets, bright red and spurts with the heartbeat and more from the proximal end. Blood
loss is more rapid from a vessel of corresponding size.
b) Venous: occur as a continuous flow, dark red & more from the distal end.
c) Capillary: The blood oozes over the surface of the capillary. occur as a diffuse ooze of bright red blood.

❖ SITE (According to The Clinical Classification of Hemorrhage)

a) External hemorrhage/ Revealed hemorrhage: is visible as it occurs through skin (wound or ulcer) or
from a natural orifice e.g., hematemesis, hematuria, etc.

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 b) Internal hemorrhage / concealed hemorrhage: is invisible because it collects in a body cavity as in
intracranial hemorrhage, hemo –thorax, hemo-pericardium and hemo-peritoneum... Etc.
c) Interstitial hemorrhage: the blood collect in the tissue planes as fracture hematoma.
❖ ACUTE OR CHRONIC HEMORRHAGE
HEMORRHAGE CLASSIFICATION

Hemorrhage

Blood loss by origin

-Class 1 - class 3 -mouth -lungs

-Class 2 - class 4 -upper head -gynecological

• BY BLOOD LOSS
CLASS 1 CLASS 2 CLASS 3 CLASS 4
HEMORRHAGE HEMORRHAGE HEMORRHAGE HEMORRHAGE
❖ 15% blood loss ❖ 15-30% total blood ❖ 30-40% loss of ❖ Loss of more than
volume circulatory blood 40% of circulatory
volume blood volume
❖ No change in ❖ Tachycardia, skin may ❖ Blood pressure ❖ Limit of body’s
vital signs start to look pale and drops, the heart compensation
be cool in touch rate increases, reached
capillary refill
worsens.
❖ Fluid ❖ Volume resuscitation ❖ Fluid resuscitation ❖ Aggressive
resuscitation is with crystalloids with crystalloids resuscitation is
not usually (saline solution or and blood required to prevent
necessary lactated ringers’ transfusion are death
solution) usually necessary
❖ Blood transfusion is
not typically required
• BY ORIGIN
MOUTH:
1. HEMATEMESIS – vomiting fresh blood
2. HEMOPTYSIS – coughing up blood from lungs
3. HEMATOCHEZIA – rectal blood
4. HEMATURIA – blood in the urine from urinary bleeding
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UPPER HEAD
1. Intracranial hemorrhage – bleeding in skull
2. Cerebral hemorrhage – bleeding with in the brain tissue
3. Intracranial hemorrhage – bleeding in the brain due to rupture of the blood vessels within the
head
4. Subarachnoid hemorrhage – presence of blood with in the subarachnoid space from some
pathologic process.
LUNGS
Pulmonary hemorrhage
GYNAECOLOGICAL
Vaginal bleeding, PPH and APH, first trimester bleeding, ovarian bleeding.
UPPER GI BLEEDING
WORLD HEALTH ORGANIZATION
The WHO made standardized grading scale to scale to measure the severity of hemorrhage
Grade 0 No bleeding
Grade 1 Petechial bleeding
Grade 2 Mild blood loss ( clinically significant)
Grade 3 Gross blood loss , require transfusion ( severe)
Grade 4 Debilitating blood loss, retinal or cerebral associated
with family.

PATHOPHYSIOLOGY
The severity of hemorrhage is divided into a class system organized by the percent of blood volume loss. Up to
15% of blood volume loss classifies as a Class I hemorrhage. The patient is generally asymptomatic, and vital
signs are within normal limits. Class II hemorrhage is a loss of 15 to 30% of total blood volume. Common
manifestations include complaints of nausea and fatigue.
Class III hemorrhage is 30 to 40% of total blood volume loss. Common manifestations include delayed capillary
refill, and changes in mental status. Drastic blood pressure deviations are generally not seen until 30% of the
blood volume is lost. Vital signs may reflect a systolic less than 90 mmHg or 20 to 30% of original measurement;
HR is greater than 120; changes in mental status; and narrow pulse pressure (less than 25 mm Hg).
Class IV hemorrhage is defined as greater than 40% of total blood volume loss. There is commonly a lack of urine
output, absent peripheral pulses, and further deviations in vital signs. Severe hemorrhaging can lead to shock,
which occurs when the blood loss becomes significant enough that it is unable to meet the oxygen demands of
the tissue. Cellular aerobic metabolism shuts down, and anaerobic metabolism begins, leading to the production
of lactic acid and, ultimately, metabolic acidosis. The risk is very high for organ failure, coma, and death, absent
the timely implementation of life-saving interventions.

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 Hemorrhage from small venules and veins

Decreased filling of right heart

Decreased filling of pulmonary vasculature

Decreased filling of left atrium and ventricle

Left ventricular stroke volume decreases (frank starling)

Drop in arterial blood pressure to pulmonary arteries

Cardiac depression and pump failure

Hypovolemic shock Decreased effective circulating blood volume

Decreased venous return to heart

Septic shock Decreased cardiac output

Decreased blood flow

Cardiogenic shock Decreased supply of oxygen

Anoxia

SHOCK

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SIGNS AND SYMPTOMS
Early signs and symptoms
❖ Restlessness and anxiety
❖ Feeling faint
❖ Coldness (temperature slightly subnormal)
❖ Pallor
❖ Patient feels thirsty
Signs and symptoms after severe hemorrhage
❖ Extreme pallor
❖ Child sensation
❖ Air hunger
❖ Rapid thready pulse
❖ Extremely low blood pressure
❖ Extreme thirst
❖ Diminished urine volume (acute renal failure)
❖ Blindness, tinnitus and coma occur prior to death.
Others
❖ Pain
❖ Hypoxia
❖ Cyanosis
❖ Delayed capillary refill
❖ Increased heart rate
❖ Difference between systolic and diastolic
❖ Stupor
❖ Disability
❖ Confused mental state
❖ Moist skin
Signs and symptoms of internal bleeding
❖ Discolored, tender, swollen, or hard skin, rigid abdomen
❖ Absence of distal pulse
❖ Increased respiratory and pulse rates
❖ Pale, cool, moist skin
❖ Nausea and vomiting
❖ Thirst
❖ Mental status changes
❖ Bleeding from body orifices

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DIAGNOSTIC TESTS
HISTORY COLLECTION:
1. Site of hemorrhage
2. Duration of hemorrhage
3. Precipitating causes
4. Surgical history
5. Family history
6. Systemic illness
7. Drugs
8. WHO bleeding scale

▪ SITE OF HEMORRHAGE
- Muscle and joint bleeds indicate coagulatory defect
- Prolonged hemorrhage from nose epistasis, GI hemorrhage indicate failure of preventive hemostasis due
to platelets decreases
- Recurrent bleeds at a single site suggest a local structural abnormality
▪ DURATON OF HISTORY
- It may be possible to assess whether the patient has a congenital or acquired disorder.
▪ PRECIPATING CAUSES
- Hemorrhage arising spontaneously indicates a more severe deficit than hemorrhage arises only after
trauma.
▪ SURGICAL HISTORY
- Enquiry about cell operation is useful in particular dental extraction, tonsillectomy and circumcision, as
these are all stressful of the hematic system.
- Hemorrhage starts immediately after surgery indicates defective platelets plug formation
- Bleeding comes after several hours is more indicate of failure of platelets plug stabilization by fibrin due
to coagulation defect.
▪ FAMILY HISTORY
- Help in the identification of all type of genetically and hereditary caused bleeding disorder. Example:
hemophilia
▪ SYSTEMIC ILLNESS
- Many diseases of hemorrhage is and its treatment is associated with the significant bleeding.
- But it is particularly important to consider the possibility of hepatitis, or renal failure, paraprotemanemia
or connective tissue diseases.
▪ DRUGS
- Almost any medicine can potentially produce bleeding, either by depressing bone marrow function with
consequent to thrombocytopenia or by interacting with warfarin.
- NSAID inhibits platelet’s function effect of aspirin may last up to 10 days of single tablets

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PHYSICAL EXAMINATION:
OBSERVATION:
- This examination is to identify and diagnosis the type, duration and characterize of hemorrhage, and its
site.
- Helps to assess the type of hemorrhage, massive hemorrhage etc. Complete physical examination is to
mark and to find the hemorrhage.

WHO BLEEDING SCALE:

COAGULATION SCREENING TEST
SL INVESTIGATION NORMAL RANGE SITUATION IN WHICH TEST MAY
NO BE ABNORMAL
1 Platelet count 150-400*10/1 thrombocytopenia
2 Bleeding time < 8 min Thrombocytopenia
Abnormal platelets function
Deficiency of von will brand factor
vascular abnormality
3. Prothrombin time 12-15 sec Deficiencies of factors II, V , VII , X
(PT)
4 Activated platelet 30-40sec Deficiencies of factors II, V, VII, X.
thromboplastic time Antibiotic against clotting factor
(APTT) Lumpus antigen
5 fibrinogen 1.5 -4.0g/I Hypofibrinogenous
COMPLICATION
- Hypovolemic shock
- Infection
- Thrombocytopenia
- Shock/ coma
- Death

TREATMENT AND MANAGEMENT

METHODS OF ACHIVING HEMOSTASIS:
• MECHANICAL METHODS
• CHEMICAL METHODS
• THERMAL AGENTS

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MECHANICAL METHODS:
1. pressure
2. hemostat
3. Sutures and ligation

CHEMICAL METHODS:
1. Local agents:
• Adrenaline
• Thrombin
• Surgicel
• Oxycel
• Surgical fibrillar
• Gelatin sponge
• Microfibrillar collagen
• Fibrous glue
• Styptics and astringents
• Alginic acid
• Natural collagen sponge
• Bone wax
• Ostene
2. Systemic agents
• Whole blood
• Platelet rich plasma
• Fresh frozen plasma
• Cryoprecipitate

THERMAL AGENTS
1. Cautery
2. Electrocautery
3. Cryosurgery
4. Lasers

MECHANICAL METHODS:

1. PRESSURE:
- Immediate measure for capillary or venous bleeding
- Firm pressure should be applied over the bleeding site using either fingers or gauze for at least 5
minutes.
- This would control most hemorrhages by counteracting the hydrostatic pressure of the bleeding
vessel.
2. HEMOSTAT:
- application of hemostat at the bleeding point helps in direct occlusion of the bleeding vessel
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3. SUTURES AND LIGATION:
- Severed blood vessel may be tied with ligatures. a ligature replaces the hemostat as a permanent
method of effective hemostasis.
- For large pulsatile artery, a trans – fixation suture to prevent slipping is indicated.
- Non- resorbable sutures such as silk and polyethylene are used as they evoke less tissue reaction.
CHEMICAL METHODS
❖ LOCAL AGENTS:
1. Adrenaline
o Topical application of adrenaline brings about vasoconstriction of bleeding capillaries
o Available in ampoule, which is applied with the help of gauze
o Concentration of 1 in 1000 is used for hemostasis over the oozing site.
2. Thrombin
o Helps in converting fibrinogen into fibrous clot
3. Surgical
o oxidized cellulose polymer obtained by dissolving pure alpha cellulose in an alkaline solution
o Acts by forming acid products from partial dissolution that coagulates the plasma proteins to form a
black or brown sticky gelatinous clot.
o Applied surgical resorbs from the site in 4- 8 weeks.
o Disadvantages is that the surgical clot is not formed by normal physiological mechanism.
4. Surgical fibrillar
o Modified surgical or oxidized regenerated cellulose in layers that can be adapted to irregular
surfaces and in accessible areas
o Complete resorption occurs in 2 weeks.
5. Gelatin sponge or gel foam or surgifoam
o Formed from purified pork skin gelatin
o Completely absorbable material
o Has the capacity to absorb 45 times its weight in blood
o Resorbs completely in 4-6 weeks.
6. Oxycel
o Oxidized cellulose polymer product
o This absorbable hemostatic material is manufactured by controlled oxidation of cellulose using
nitrous dioxide.
o Cellulosic acid present in it has affinity for hemoglobin which leads to the formation of artificial
clot.
o Should be applied on the dry surface as the acid formed during the wetting process inactivates the
thrombin.
o The platelets plug into its meshwork like surface and helps in clot formation.
7. Microfibrillar collagen (AVITENE)
o Collagen derived from bovine skin cause contact activation in addition to direct platelet
aggregation.
o Absorption time is 3 months.
8. Fibrin glue
o Biological adhesive which contains thrombin, fibrinogen, factor XIII, aprotinin.

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 o Thrombin converts fibrinogen to unstable fibrin clot; factor XIII stabilizes the clot and aprotinin
prevents its degradation.
9. Styptics and astringents
o Precipitates protein and arrests bleeding
o Commonly used styptics and astringents are monsel’s solution containing ferric subsulfate and
tannic acid.
o Thrombin and gelatin sponge are now widely used.
10. Alginic acid
o Placed over the bleeding sites, a protective film is formed over the bleeding site, this film
compresses the capillaries and stabilizes the blood clot.
11. Natural collagen sponge
o White sponge material, fully absorbable. it stimulates the platelet aggregation there by enhancing
hemostasis.
o Activates coagulation factors XI and XIII.
o Preferred in patients who are susceptible for hemorrhage after dental surgical procedures.
12. Fibrin sponge
o Obtained from bovine material
o Chemically treated to avoid allergic reactions
o Applied o the bleeding site especially in post extraction socket.
o Fully absorbed by the tissues within -6 weeks.
13. Ostene (a new water-soluble bone hemostatic agent)
o New bone hemostatic agent, made of water soluble alkylene oxide copolymers.
o Showed no incidence of adverse response in the cortical defect site, medullary cavity or the
surrounding tissue.
14. Bon wax
o Sterilized, non-absorbable mix of waxes
o Consists of seven parts by weight of wax (white bees wax, paraffin wax and an isopropyl ester of
palmitic acid), two parts of olive oil and one part of phenol.
o Indicated in cases of bleeding from the bone or from chipped edges of bone.
o Bone wax is softened with the fingers to desired consistency and then applied over the bleeding
site.
o Its hemostatic mechanism is through mechanical obstruction of the osseous cavity containing the
bleeding vessels.

❖ SYSTEMIC AGENTS:

1. WHOLE BLOOD:
o Fresh whole blood refers to blood that is administered within 24 hours of its donation.
o Whole blood transfusion indicated when there is excessive blood loss.
o Contains all factors for coagulation.
o Must be checked for HIV, hepatitis B, C viruses.
2. PLATELET RICH PLASMA:
o Platelets can be collected from donated whole blood
o Platelet concentrates are viable for 3 days hen stored at room temperature.

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 o Must be infused quickly via short iv transfusion set.
o One unit raises platelet count by approx. 7,000 to 10,000 cells per cu mm.
3. FRESH FROZEN PLASMA
o Unit of fresh frozen plasma is collected from one donor and contains all coagulation factors.
o Stored at 30degree Celsius, should be infused within 2 hours once defrosted.
4. CRYOPRECIPITATE
o Stored at 30 degrees Celsius
o Each bag is derived from single donor and is not treated to inactivate viruses.
o Associated with a substantial risk of viral transmission.

THERMAL AGENTS
Heat achieves hemostasis by denaturation of proteins
1. CAUTERY:
• Heat is transmitted from instrument by conduction directly to the tissues.
• Electro- cautery has replaced direct heat application.
• Dental burnisher like instrument can be directly heated over flame and applied directly to the
bleeding point.
2. ELECTROCAUTERY:
• Most widely used
• Electrocautery can be applied directly to bleeding point.
• Cautery point is touched to the hemostat, causing sealing of vessel through action of heat.
• Causes tissue destruction producing burning smell and smoke during application.
• Effective and convenient way of controlling hemorrhage.
3. CRYOSURGERY:
• Extreme cooling has been used for hemostasis
• Temperature ranging from -20degree C – 180degree C are used.
• Tissues, capillaries, smart arterioles and venules undergo cryogenic necrosis.
• Caused by dehydration and denaturation of lipid molecules.
• Specially used to treat superficial hemangiomas.
4. LASERS:
• Lasers usually results in bloodless surgery
• Effectively coagulate the small blood vessel during cutting of tissues.

FIRST AID: (initial management)

- MINOR BLEEDING / HEMORRHAGE
- EMERGENCY BLEEDING CONTROL
- BLEEDING FROM BODY CAVITIES (EXTERNAL BLEEDING)
- INTERNAL BLEEDING
- RISK OF BLOOD CONTAMINATION.
All people who have been injured should receive a thorough assessment. It should be divided into a primary and
secondary survey and performed in a stepwise fashion, following the “ABCs”.
- PRIMARY ASSESSMENT:
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 a) Examines and verifies that the patients Airway is intact, and patient is breathing and that circulation is
working. A similar scheme and mnemonic is used as in CPR.
b) During the pulse check of C, attempts should also be made to control bleeding and to assess perfusion,
usually by checking capillary refill.
c) Additionally, a person mental status should be assessed (disability) or either an AVPU scale or via a formal
Glasgow coma scale
- SECONDARY ASSESSMENT:
a) Is performed by removing of the cloth on case of minor cases. Examining the patient from head to toe for
other injuries.
b) Important aspect is that the survey or assessment should not delay treatment and transportation if non
correctable problem is identified.
• MINOR BLEEDING OR HAEMORRHAGE
- Minor bleeding is bleeding that falls under a class I hemorrhage and the bleeding is easily stopped with
pressure.
- The largest danger in a minor wound is infection.
- Hemorrhage can be stopped with direct pressure and elevation, and the wound should be washed well with
soap and water.
- A dressing typically made of gauze, should be applies. Peroxide or iodine solutions (such as betadine) can
injure the cells that promote healing and may actually impair proper wound healing and delay closure.
• EMERGENCY BLEEDING CONTROL
- Severe bleeding poses a very real risk of death to the causality if not treated quickly. Therefore,
preventing major bleeding should take priority over the conditions.
- Save failure of the heart or lungs. Most protocols advise the use of direct pressure, rest and elevation of
the wound above the heart to control bleeding.
- The use of a tourniquet is not advised in most cases, as it can lead to unnecessary necrosis or even loss
of a limb.
- Tourniquets should rarely be used as it is usually possible to stop bleeding by the application of manual
pressure.
Note: (immediate management for hemorrhage)
1. Rest
2. Elevation
3. Direct pressure
• BLEEDING FROM BODY CAVITIES:( external bleeding )
Recognition:
-recognizing external bleeding is usually easy, as the presence of blood should alert you to it. It should however
be remembered that blood may be underneath or behind a victim.
-it may be difficult to find the source of bleeding, especially with large wounds or even quite small wounds with
large amounts of bleeding. If there is more than 5 cups of bleeding, then the situation is life threatening.
Treatment:
- In all first aid situations, the priority is to protect yourself, so put on protective gloves before
approaching the victim.
- All external bleeding is treated using three key techniques, which allow the body’s natural repair process
to start. These can be remembered using the acronym mnemonic RED, which stands for
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 • Rest
• Elevation
• Direct pressure
Rest:
In all cases, of hemorrhage resting client in one place is very important because frequent movement will
increase the bleeding or hemorrhage.
Elevation:
- In case of larger bleeds, it may be necessary to elevate the wound above the level of the heart (whilst
maintaining direct pressure the whole time)
- This decreases the blood flow to the affected area, slowing the blood flow, and assisting clotting
- Elevation only works on the peripheries of the body (limbs and head) and is not appropriate for body
wounds. You should ask the victim to hold their wound as high as possible.
- You should assist them to do this if necessary, and use furniture or surrounding items to help support them
in this position. If it is the legs affected, you should lie them on their back (supine) and raise their legs.

Direct pressure:

- This is simply placing pressure on the wound in order to stem the flow of blood. this is best done using a
dressing, such as sterile gauze pad (although in an emergency, any material is suitable)
- If the blood starts to come through the dressing you are using, add additional dressing to the top, to a
maximum of three. If you reach three dressings, you should remove all but the one in contact with the
wound itself (as this may cause it to reopen) and continue to add pads on top.

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 - Repeat this again when you reach three dressings. The reason for not simply adding more dressings is that
it becomes harder to apply the direct pressure which is clearly needed if this much blood is produced.
- When the articulate area of the body is wounded (such as arms or hands), it is important to consider the
position of the area in keeping pressure of the wound.
- In most cases, during the initial treatment of the bleed, you will apply pressure by hand in order to stem
the flow of blood. In some cases, a dressing may help you do this as it can keep pressure consistently on
the wound. If you stop the flow by hand, you should then consider dressing the wound properly.

Dressing
- Once the bleeding is slowed or stopped, or in some cases, to assist the slowing of the blood flow you
should consider dressing the wound properly.
- To dress a wound, use a sterile low – adherent pad, which will not stick to the wound, but will absorb the
blood coming from it. Once this is in place, wrap a crepe or conforming bandage around firmly.
- It should be tight enough to apply some direct pressure, but should not be so tight as to cut blood flow
below the bandage. A simple check for the bandage being too tight on a limb wound is a capillary refill
check.
- If the blood starts to come through the dressing you have applied, add another on top, to a maximum of
three. If these are all saturated, remove the top two, leaving the closest dressing to the wound in place.
This ensures that any blood clots that have formed are not disturbed; otherwise, the wound would be
opened a new.
• SPECIAL CASES
❖ Nosebleeds (Epistaxis)
- If a person has nosebleed, have them “pinch the soft part” of the nose firmly between thumb and forefinger,
just below the end of the bone. If necessary, do this yourself, but it is preferable to have them do it
themselves if they are able to do it effectively.
- The victim should lean their head slightly forward and breathe through their mouth. You can also leave
the head in a neutral position, but never tilt the head back. Tilting the head forward ensures that blood
isn’t ingested (as it can cause vomiting) or inhaled (choking hazard).
- If you are unsuccessful at stopping the bleeding after 10 minutes of direct pressure, you should assess the
blood flow. If the blood flow is minor, you could consider using an Ice pack on the Bridge of the nose to
help stem the flow.
- If the nose continuous to bleed with a fast flow, you should seek medical assistance, probably from the
ambulance.
❖ Embedded objects
- If there is something embedded in the wound, do not remove it. Instead apply pressure.
- Around the object using sterile described above. Rolled bandages are perfect for this.be careful not to
disturb the object, as moving it may exacerbate the bleeding. this doesn’t apply to superficial splinters and
such.
❖ Stab, puncture or gunshot wounds to the body
- These wounds are life threatening
- And after assessing the ABCs of the victim, you should immediately call an ambulance.

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 - As always, you should check that you are not in danger when approaching these victims (from someone
with a knife or gun, for instance). As with all embedded objects, ensure you do not remove the item from
the body.
- If possible, you should sit the victim up (as blood in the body will go to the lowest point, allowing the
heart and lungs to work as efficiently as possible). You should also lean them to the injured side, keeping
the healthy side free from incursion by blood.
- Assess the victim for open chest wounds or abdominal injuries, and treat accordingly.
❖ Amputations
- If a body part has been amputated summon ambulance assistance, and treat the bleeding as above. Cover
the amputated part with a moist dressing and get it into a clean plastic bag.
- And place this bag into a bag of ice and water, sending it with the victim to the hospital. (Label date and
time, mention the name of body part).
- You should avoid putting the part indirect with ice, as this can cause irreparable damage, meaning that
surgeons are unable to reattach it.
• INTERNAL BLEEDING
Internal bleeding is bleeding which occurs inside the body. Sometimes the blood will leak from inside
the body through natural openings. Other times the blood stays inside the body, causing pain and shock.
Even though you cannot see the blood loss.
Recognition:
A person may be bleeding internally if one of these things happens.
- Blood comes out of the nose / mouth (occurs from severe head trauma)
- Blood or clear fluid comes out of the ear (CSF leakage due to severe head trauma)
- Blood is the stool / urine (hematochezia / hematuria)
- Bright red color or blood like coffee –grounds, is in the vomit
- Vaginal bleeding after an injury or during pregnancy
- Bruising over the abdominal or chest area.
- Pain over the vital organs
- Fractured femur
Check the skin color changes. In case of internal bleeding the skin become pale and cold and cyanosis may be
present.
First aid treatment:
o Check the victims ABCs
o If the victim has ABC complications, treat those first.
o Call an ambulance
o Treat for shock
o Assist the victim into the most comfortable position
o Monitoring vitals until medical attention.
• RISK OF CONTAMIATION
- Skin is watertight, there is no immediate risk of infection to the aide from contact with blood, provided
the exposed area has not been previously wounded or diseased.
- Before any further activity (especially eating, drinking, touching the eyes / mouth, nose), the skin should
be thoroughly cleaned in order to avoid cross contamination.

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 - To avoid any risk, the hands can be prevented from contact with a glove. Or an improvised method such
as plastic bag or a cloth. This is taught as important part of protecting the rescuer in most first aid protocols.

MANAGEMENT IN EMERGENCY
1. Immediate measures
2. Fluid replacement
3. Measure for internal bleeding
4. Measure for oxygen and cardiac function
Immediate measures:
- Cut the patient clothing away and carry out a rapid physical examination
- Apply firm pressure over the bleeding area
- Apply firm pressure dressing over the bleeding site
- Elevate the injured part to stop venous capillary bleeding above the heart level.
- Immobilize the injured part that may be extremity to control blood loss.
Fluid Replacement:
- Insert intravenous cannula to provide means of blood replacement
- Withdraw blood sample for analysis, typing and cross matching.
- Give fluid replacement including balanced electrolyte solution (RL) and blood, depending on chemical
estimation of blood loos to correct intravascular deficit and interstitial fluid space deficit.
- Fresh whole blood is infused in case of massive hemorrhage
- Platelets and coagulation factors are given in large amount of blood are needed since replacement blood
is deficit in clotting factors.
- Warm the blood because the massive blood replacement has a cooling effectiveness causing cardiac arrest.
- Rate of infusion depends on severity of blood loss and chemical evidence of hypoxia.

Measures for Internal Hemorrhage:

- Suspect internal bleeding in patient with hypovolemic shock with no external signs of bleeding
- Apply pneumatic anti shock garment I available to control internal bleeding and to facilitate blood flow
to vital areas. (Primary use is for hypovolemic shock secondary to bleeding into lower part of the body)
- Monitor the patient’s hemodynamic response. Obtain blood gas determination, establish venous return
monitoring as an index of the amount of replacement fluid to the patient.
- Maintain patient in supine position with hemodynamic / circulatory parameter begin to improve.

Measures for Oxygenation and Cardiac Function:

- Administer humidified oxygen
- Watch for cardiac arrest, patient who have hemorrhage are candidates for cardiac arrest caused by
hypovolemic with secondary anoxia.
- Assess with ECG monitoring for dysrhythmias

18
POST OPERATIVE MANAGEMENT
- In case of shock, patient shall be shock position (lying flat on back with legs elevated at 20 degree angle
while knees are kept straight).
- Sedatives or analgesics is administered as by prescription order. Wound should be inspected for any
bleeding and apply a sterile dressing should be done.
- In case of hemorrhage elevated the affected part above the heart level , and start a transfusion of blood
and products and determining the cause of hemorrhage as the initial therapeutic as the initial therapeutic
measure.

NURSING MANAGEMENT
➢ Fluid volume related to bleeding
➢ Ineffective tissue perfusion related to bleeding
➢ Risk for infection related to bleeding
➢ Risk for hypovolemic shock related to bleeding
➢ Fear and anxiety related to changes in circumference or the threat of death

IMPROVE OXYGENATION:
❖ Reassure the patient and make the patient comfortable
❖ Calm down the patient as anxiety may increase heart rate further causes complications
❖ If patient is restless, irritable never give him opioids as it may further cause hypoxia
❖ Clear the air way if it obstructed with blood clots, blood, or some dust particles.
❖ Turn the head to one side
❖ Administer oxygen by nasal cannula at the rate of 4 liter per minute
❖ During hypoxia patient is confused hence explain him the need of oxygenation and purpose of nasal
cannula.

RESTORE AND MAINTAIN ADEQUATE PERFUSION

❖ Assess the patient for the manifestations of hypoxia
❖ Avoid hot application to treat hypothermia as it dilates the peripheral blood vessels and pull away blood
from vital organs.
❖ Use modified Trendelenburg position for the patient to increase the cardiac output.
❖ Provide blanket to the patient to prevent hypothermia
❖ Check vital signs in every 5 minutes specially pulse and blood pressure

TEMPERATURE MONITORING
❖ Temperature monitoring is very important inpatient with shock
❖ check temperature rectally by using rectal thermometer

CARDIAC MONITORING
❖ Monitor blood pressure of the patient in every 5 minutes till patient systolic blood pressure comes to
100mmof hg

19
 ❖ check the pulse for rate and rhythm
❖ Monitor patients closely on cardiac monitors as patients with hemorrhagic shock tend to have
arrhythmias due to severe electrolyte imbalance.
❖ Measurement of CVP is important in hypovolemic shock as it helps us to prevent fluid overload.

BLEEDIND CONTROL
❖ Assess the wound for the bleeding
❖ Apply direct and firm pressure on the bleeding site
❖ Inform the doctor immediately regarding bleeding
❖ Prepare the patient for the surgery if required
❖ Assist the doctor in ligation and closure of wound.
❖ Assure aseptic technique throughout the procedure, assess that wound is cleaned properly no foreign
particles are left behind in the wound.

FLUID OVERLAOD
❖ While treating hypovolemia often rigorous fluid is given in which may cause complication such as
pulmonary edema if not done carefully.
❖ Be alert the signs and symptoms of pulmonary edema
❖ During fluid therapy, assess the cardiac as well as respiratory signs and symptoms which indicate
pulmonary edema, inform unfavorable changes immediately.

RELIEVING ANXIETY
❖ assure the patient and his family
❖ As anxiety increase oxygen demand by increasing the heart rate hence calm down the patient.
❖ Keep family members informing about recent updates of patient condition and his progress.
❖ Explain the use of various equipment’s to the client.
❖ Explain regarding the procedure and equipment’s.

NUTRITION
❖ When patient is in hypovolemia, the patient BMR is increased hence there is more need of energy.
❖ Nutrition supplement is initiated as soon as possible.

CONCLUSION
In conclusion, the hemorrhage seminar emphasized the importance of early recognition, effective
intervention, and comprehensive management strategies to address various causes of excessive bleeding.
Gained insights into the latest advancements in hemorrhage control, emphasizing the significance of a
multidisciplinary approach in ensuring optimal patient outcomes.

20
REFERENCES
❖ Judith Wilkinson, “Text book of fundamentals of nursing, volume -1, jaypee publication, p.p
no 346, 146.
❖ Erb Bermans Burke, “Text book of Fundamentals of Nursing”, 1st edition 2003, Pearson
publication, p.p.no.35-37.
❖ Potter & Perry, “Textbook of fundamentals of nursing,” 7th edition 2009, Elsevier publication,
p.p.no.49-50.
❖ Luckmann and Sorensen, “Medical Surgical Nursing”, 2nd edition (1980), W.D.Saunders Co,
Philadelphia, page no: 670, 1221-1225, 1604, 1791-1795.
❖ Potter A.Partricia and Anne Griffin Perry, (2005), “Fundamentals of Nursing”6th edition,
J.B.Lippincott Co, Philadelphia, Page no: 301-332.
❖ William S.Linda and Hopper D. Palua, “Understanding Medical Nursing”,2nd edition,
F.A.Davis Co,Philadelphia, page no:70-79
❖ Neelima anil malik, “text book of oral and maxillofacial surgery”, 3 rd. edition, page no:
1162-1164
❖ Brunner and suddarata’s, 2004, “medical and surgical nursing”, 7 th edition, J.B Lippincott
Co, Philadelphia, Page no: 301-332.
❖ Lewis. Medical Surgical Nursing: Assessment and Management of Clinical Problems. 8 th
Edition. USA: Elsevier Publications; 2011. Page no: 1722-1744

WEB REFERENCES:
❖ https://www.slideshare.net/UthamalingamMurali/haemorrhage
❖ En.Wikipedia.Org/Wiki/Bleeding
❖ Http://Nursing care plansblogspot.In/2012

21
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 major determinate in the perfusion 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 and stroke volume. 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.

DEFINITION
❖ 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
❖ shock is defined on a complex life-threatening condition characterized by inadequate blood supplied to
the tissues and cells of body
Brunner and Siddharth

22
 ❖ In medicine critical condition that is brought on by a sudden drop in blood flow through the body. The
circulatory system fails to maintain adequate blood flow, sharply curtailing the delivery of oxygen and
nutrients to vital organs.
❖ It is defined on a clinical syndrome resulting from gross impairment of tissues perfusion and wide
spread cellular dysfunctions caused by diminished O2 delivery.
K.V Krishnardan.

SHOCK AND 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 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 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 heath 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
o Coronary artery occlusion with acute myocardial ischemia.
o trauma with structural damage to heart
o toxemia - viral or bacterial
o Effects of drugs.
2. deficient oxygenation of blood in lungs
Amongst any causes the following are the most important
o post-operative atelectasis
o thoracic injuries particularly of chest that is pneumothorax, crushing and laceration of lung
o obstruction of pulmonary artery by an embolus
o Disturbances of lung function following surgery and anesthesia.
3. Reduction in blood volume (oligemia and hypervolemia)
This may occur from loss of
o whole blood – hemorrhage (internal or external)
23
 o plasma – this is particularly significant in burns
o Water and electrolyte which occurs from peritonitis, intestinal obstruction, paralytic ileus, acute
dilation of the stomach, severe diarrhea 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 improved towards heart.
• Contraction of skin vessel: contraction of arterioles and venules of the skin is usual so as to converse the blood
supply to the more vital organ. The application of heat dilates the ski vessels there by aggravating the condition
and should not be used.
• Insensitivity: A much collapsed patient usually have little pain. Large quantities of pain-relieving drugs are
necessary and are ineffective because they cannot be absorbed unless given by intravenous route.
• Urinary secretions: these are diminished to converse 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 hock.
All these compensatory mechanisms are temporary in their beneficial effects and if the condition of circulation
is restored to normal.

24
 PATHOPHYSIOLOGY
Initial physiological insult leading to shock state

Decrease in cardiac output and tissue perfusion

Sympathetic nervous system activation

Endocrine response renin angiotensin

Activation

Increased vasoconstriction and activation

Of antidiuretic hormone which increase preload

Renal system converse sodium

And water to increase preload

Increased blood pressure,

Heart rate & myocardial contractility

Restoration of tissue perfusion

25
 METABOLIC CHANGES AND EFFCETS IN
SHOCK
Carbohydrate metabolism:
➢ Compensated shock: hyperglycemia due to increased hepatic glycogenolysis.
➢ Decompensated shock: hypoglycemia due to hepatic glycogen depletion and increased consumption of
glucose by tissue.
➢ Anerobic glycolysis occurs as assessed by high blood levels of lactate and pyruvate.

Protein metabolism
➢ Increased intracellular protein catabolism
➢ Conversion of amino acids to urea.
➢ Increased blood non- nitrogen protein.

Fat metabolism
➢ Increased endogenous fat metabolism
➢ Rise of fatty acid level in blood.

Water and electrolyte disturbances

➢ Failure of sodium pump – potassium leaves the cell (hyponatremia) – causes cellular swelling.
➢ Shock due to loss of plasma only (in burns)- hemoconcentration.
Metabolic acidosis
➢ Hypoxia of kidney, renal function is impaired blood vessels of acids like lactate, pyruvate, phosphate
and sulfate rise causing metabolic acidosis.

Morphologic complications
➢ Morphologic changes in shock are due to hypoxia. Resulting in degeneration and necrosis in various
organ.
➢ Organs affected are: brain, heart, lungs, kidneys, adrenals, and GIT.

Hypoxic encephalopathy
➢ Compensated shock results in cerebral ischemia which produce altered state of consciousness. however,
if blood pressure falls below 50 mm of hg as in systemic hypotension in prolonged shock and cardiac
arrest, brain suffers serious ischemic damage with loss of cortical functions , coma and vegetative state.

Heart in shock
➢ 2 types of morphologic changes in heart
- Hemorrhages and necrosis: located in subepicardial and subendocardial region.
- Zonal lesion: opaque transverse contraction bands in a myocyte near an intercalated disc.
26
shock lung
➢ Lungs have dual blood supply and generally not affected by hypovolemic shock
➢ But in septic shock. Shock lung seen as symptoms of ARDS including congestion, interstitial and
alveolar edema, interstitial lymphocytic infiltrate, alveolar hyaline membrane.
➢ Thickening and fibrosis of alveolar septa, fibrin and platelet thrombi in pulmonary microvasculature.

Shock kidney
➢ Irreversible renal injury- important complication of shock
➢ Renal ischemia following systemic hypotension is considered responsible for renal changes in shock –
end result is generally anuria and death.

Adrenals in shock
➢ Adrenals show stress response in shock, it includes
1. Release of aldosterone in response to hypoxic kidney.
2. Release of glucocorticoids from adrenal cortex and catecholamine like adrenaline from adrenal
medulla.
“SEVERE SHOCK RESULTS IN ADRENAL HAEMORRHAGES”

GIT
➢ Hypo perfusion f alimentary tract- mucosal and mural infarction called “hemorrhage gastroenteropathy”
➢ In shock include focal necrosis, fatty change, impaired liver function.

27
Cardiovascular effects
➢ Decrease of preload and afterload
➢ Baroreceptor response
➢ Elease of catecholamines
➢ Tachycardia and vasoconstriction
Respiratory
➢ Metabolic acidosis
➢ Increase respiratory rate and excretion of carbon dioxide
➢ Results in compensatory respiratory alkalosis.

Renal and endocrine

➢ Decreased urine output
➢ Stimulation of renin angiotensin and aldosterone axis
➢ Release of vasopressin from hypothalamus
➢ Resulting vasoconstriction and increase Na+ and water reabsorption.

Microvascular
➢ Cells switch from aerobic to anaerobic metabolism- decreased ATP production- lactic acidosis-glucose
exhausts and aerobic respiration ceases- Na+/ K+ pump impaired- lysosomes release autodigestive
enzymes – mitochondria damage – cell death.

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 responses and subsequent clinical signs and symptoms is to
divide the continuum in to separate stages.

STAGE 1: INITIAL STAGE

STAGE 2: COMPENSATORY STAGE
STAGE 3: PROGRESSIVE STAGE (DECOMPENSATE)
STAGE 4: IRREVERSIBLE STAGE (REFRACTORY)

28
 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

Buildup of lactic acid and pyruvic acid

Systemic metabolic acidosis

The process removing the components in the cells by the liver requires oxygen.
STAGE 2: COMPENSATORY STAGE
In the compensatory stages of shock, the BP remains within the normal limit. 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 catecholamine’s (Epinephrine and nor
epinephrine). Patients display 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 skin is cool and clammy, bowel sounds are hypoactive and urine output decreases in
response to the release of aldosterone and ADH
CLINICAL MANIFESTATIONS:
❖ Inadequate organ perfusion
❖ Metabolic acidosis
29
 ❖ Tachycardia
❖ Compensatory respiratory alkalosis
❖ Confusion
❖ Combativeness
❖ Flat neck veins
❖ Dry warm skin
❖ Irritability
❖ Deep rapid respiration
❖ Dilated reactive pupil
❖ Bounding pulse
MEDICAL AND 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 defined as a systolic BP of less than 90 mm
hg or a decrease in systolic BP of 40 mm of hg
PATHOPHYSIOLOGY:

Although all organ system suffer from the hypo perfusion 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
permeability, with are as a released by the cells, resulting in increased capillary permeability, with are as an
arteriolar and venous constriction further 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
edema and 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 and a vicious circle ensures.

CLINICAL MENIFESTSTIONS:
▪ Respiratory effects
- Thirst
- Rapid shallow breathing
- ARDS
30
 - Hypoxemia
▪ Cardiovascular 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 diarrhea
▪ Hematologic effects
- Hypotension
- Disseminated intravascular coagulation
MEDICAL MANAGEMENT
To restore the perfusion by:
❖ optimizing 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 and the shock can no longer be reversed. Brain damage and cell death will
occur. Death of the person will occur immediately.
CLINICAL MANIFESTATION:
1. Unconsciousness
2. Absence of reflexes
3. ARDS
4. DIC
5. Bradycardia
6. Cyanosis
7. Absence of bowel sounds
8. Immune system collapse
9. Anuria
MEDICAL AND NURSING MANAGEMENT:
- Fluid replacement
- Monitoring the patient
- Vasoactive medications
- Nutritional therapy

31
 CLASSIFICATION OF SHOCK AND
MANAGEMENT
Conventionally, the primary underlying pathophysiologic process and underlying disorders are used to classify
the shock state. Shock can be classified according to the etiology and can be describes.
1. Hypovolemic shock
2. Cardiogenic shock
3. Circulatory shock or distributive shock
• Septic shock
• Obstructive shock
• Neurogenic shock
• Anaphylactic shock
Regardless of the initial cause of shock, researches have gradually concluded that certain physiologic responses
are common to all type of shock. These physiologic responses are hypo perfusion of the tissues, hyper metabolism,
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
VASCULAR RESPONSES
Oxygen attaches to the hemoglobin 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 flow to a specific area and on blood oxygen concentration.
Blood is continuously recycling through the lungs to be re oxygenated and to eliminate and 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 and dynamic vasculature
consisting of arteries, arterioles, capillaries, venules, and veins. The vasculature can dilate or constrict based on
the central and 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 and nutrients. A biochemical mediator is a substance
released by a cell or immune cells such as monocytes and 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 and vasculature – must respond
effectively to complex neural, chemical and hormonal feedback system effecting both cardiac output and
peripheral vascular resistance. This relationship is expressed in the following term of equation:
MEAN ARTERIAL BP = CARDIAC OUTPUT x PERIPHERAL RESISTANCE
1. HYPOVOLEMIC SHOCK
It’s the most common type of shock, is characterized by a decreased intravascular volume. Body fluid is contained
in the intracellular and extra cellular compartments. Intracellular fluid accounts for about two third of the total

32
body water. The extra cellular body fluids are found in one of two compartments: intravascular or interstitial. 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 750 ml to 1300 ml of blood
in a 70 kg person.
RISK FACTORS:

External: fluid loss Internal: fluid shift

o trauma o hemorrhage
o surgery o burns
o vomiting o ascites
o diarrhea o peritonitis
o diuresis o dehydration
o diabetic insipidus

PATHOPHYSIOLOGY:

Relative hypovolemia absolute hypovolemia

Decreased circulatory volume

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Ineffective tissue perfusion

33
 Impaired cellular metabolism
MEDICAL MANGEMENT
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 and blood replacement
5. Pharmacologic therapy e.g.: desmopressin, anti- diarrheal agents, anti- emetic agents.
NURSING MANGEMENT:
- 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 and documenting their administration and effects.
- Monitor signs of complication and side effects of treatment and reporting these signs early in treatment
- Oxygen administration.

2. CARDIOGENIC SHOCK
Cardiogenic shock occurs when the hearts’ ability to contract and to pump blood is impaired and supply of oxygen
is inadequate for the heart and tissue. the cause of cardiogenic shock is known as either coronary or no coronary.
Coronary cardiogenic shock is more common than non-coronary cardiogenic shock and is seen most often in
patient with myocardial infraction. Coronary cardiogenic shock occurs when a significant amount of the left
ventricular myocardium has been damaged. patient who experiences 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 anterior descending coronary artery. no coronary artery causes of cardiogenic shock are
related to conditions that stress the myocardium (e.g.: severe hypoxemia, acidosis, hypoglycemia, hypocalcemia,
tension pneumothorax) as well as conditions that results in ineffective myocardial function (e.g.:
cardiomyopathies, valvular damage, cardiac tamponade)
PATHOPHYSIOLOGY

Decreased cardiac contractility

Decreased stroke volume & cardiac

Output

pulmonary congestion Decreased systemic tissue decreased coronary

Perfusion perfusion

34
CLINICAL MANIFESTATION
o Pain
o Dysrhythmias
o 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
- 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 – glycerin
- Dopamine
- Antiarrhythmic medication
- Vasoactive agents (epinephrine, nor epinephrine)
- Diuretics (furosemide)
- 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 MANGEMENT
- Preventing cardiogenic shock
1. Identifying the risk patients
2. Administer supplemental oxygen
3. Conserves patient energy
- Monitoring hemodynamic status
1. Arterial lines and ECG monitoring
2. Maintain IV fluids
3. Monitoring lab values

35
 4. Physical assessment of patient
5. Monitor ABG values.
- Administering medications
- Maintaining intra-aortic balloon counter pulsation
- Enhancing safety and comfort
1. Proper medications
2. Preventing infections
3. Monitoring respiratory and renal function
4. Proper positioning of the patient
5. 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 and by local regulatory mechanisms, as in tissue demands for oxygen and
nutrients. Therefore, 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.
1. septic shock
2. obstructive shock
3. neurogenic shock
4. 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 in critical ill
patients that may progress to septic shock. Most frequently originate the blood stream; lungs and urinary tract.
Other infections include abdominal infection, wound infection, bacteremia associated with intra vascular catheters.
Additional risk factors that contribute to the growing incidence of septic shock are increased awareness and
identification of the condition; the increased number of immunocompromised patients; the increased number of
resistant microorganisms, and the increasingly older population. A significant body of research the morbidity and
mortality caused by septic shock. It can cause multiple organ dysfunction syndrome and death.
PATHOPHYSIOLOGY
Infectious toxins

UNREGULATED IMMUNE VESSELS ENDOTHELIAL AND

36
SYSTEM ACTIVATION PLATELET DAMAGE

Profound cardiovascular, release of kinin, serotonin &

Pulmonary & hemostatic histamine
Changes

Capillary permeability & vaso

Vasodilation. Absolute
And 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 bacteremia
in high-risk patients.
▪ Fluid replacement must be instituted to correct the hypovolemia.
PHARMACOLOGIC MANAGEMENT
o broad spectrum antibiotics
o 3rd generation cephalosporin + aminoglycoside
o 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 and venous puncture sites, surgical incisions, traumatic wounds, urinary catheters, and
pressure ulcers must be monitored for signs of infections in all patients.

37
▪ 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 and 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 and interrupting venous return by compressing the inferior or superior Ven
cava. Tension pneumothorax – herniation of abdominal contents in to the thorax, and positive pressure
ventilation are processes that result in decreased cardiac compliance and destruction of the Ven cava,
decreased preload and decreased cardiac output.
MANAGEMENT
o prompt relief of obstruction e.g.: pericardiocentesis for tamponade, chest drain for tension
pneumothorax
o fluid and inotrope for temporary support

➢ Neurogenic shock
This is a very uncommon type of shock. It’s most often seen in patient who have had an extensive spinal
cord injury. In neurogenic shock, vasodilation occurs as a result of a loss of balance between
parasympathetic and sympathetic stimulation. Sympathetic stimulation causes the 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 overriding parasympathetic
stimulation causes vasodilation lasting for an extended period, leading to a relative hypovolemic state
and also cause drastic change in the patient’s systemic vascular resistance and bradycardia. Neurogenic
shock may have prolonged course.

PATHOPHYSIOLOGY

Disruption of sympathetic nervous system

Loss of sympathetic tone

Venous and arterial vasodilation

Decreased venous return

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 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 stabilization of a spinal
cord injury or in the instances of spinal anesthesia, by positioning the patient properly. Specific treatment depends
on cause of the shock. If hypoglycemia is the cause, glucose is rapidly administered.
NURSING MANGEMENT:
❖ Elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when a patient
receives spinal receives spinal or epidural anesthesia.
❖ careful immobilization of patient in case of spinal injury
❖ Apply elastic compression stockings and elevate the foot end of bed may minimize the pooling of blood
in legs.
❖ Pooling cause 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 and 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

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 Release of histamine

Vasodilation

Increased capillary permeability

Severe Broncho dilation

Decreased oxygen supply and utilization

Inadequate tissue perfusion

MEDICAL MANAGEMENT
➢ Removing the causative antigen
➢ Administration of epinephrine, histamines if needed
➢ Fluid therapy
➢ Oxygen administration
DIAGNOSIS OF SHOCK
It’s essential for proper treatment and management
▪ Conducts head to toe examination for signs of shock
▪ Assess 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.
▪ Assess for renal status. Anuria and renal failure can occur.
▪ Assess for integumentary status, check the skin color, cold and clammy skin, and cyanosis.
▪ Assess gastro intestinal status. Hypo active bowel sounds.
▪ Assess for the metabolic status. Metabolism acidosis will be there.
NURSING MANAGEMENT
❖ Nurse management assess all patients for allergies or previous reactions to antigens and communicate the
existence of these allergies or reactions to others.
❖ The nurse must be knowledge about the clinical signs of anaphylaxis
❖ Monitoring the patient’s 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:

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 o Remove the cause of accident from near the causality. if possible, remove the causality from danger such
as burning house, room with poisonous gases.
o Handling the patient with due care and attention to reduce pain and to prevent worsening of the condition.
o Constant observation should be provided to the causality to identify failure of breasting, bleeding and then
to take appropriate measures to treat problems.
o Using material available at hand
o Clear the crowd around the causality
o Transport the casualty to the doctor as early as possible.
FIRST AID IN SHOCK:
1. Reassure the causality
2. Lay him down on his back comfortably with head low and turned to one side except in case of head injury.
3. Loosen the clothing around the neck, chest and waist.
4. Keep the causality warm.
5. Give him sips of water if he is thirsty. Never give any alcoholic drinks.
6. never use hot water bag or mange the limbs
7. Arrest hemorrhage by adequate measures.
8. Check pulse, respiration and level of consciences.
9. Transport the causality to the hospital immediately.

NURSING DIAGNOSIS
❖ FLUID VOLUME DEFICIT RELATED TO HAEMORRHAGE
• Monitor the signs and symptoms of internal bleeding
• check for blood pressure
• give comfortable position
• keep the patient warm and monitor temperature in hourly
• administer oxygen as ordered

❖ RISK FOR INFECTION RELATED TO INTERRUPTION OF SKIN INTEGRITY FROM

INVASIVE PROCEDURES
• Take precaution 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

❖ ALTERED NUTRITION LESS THAN BODY REQUIREMENT RELATED TO DECREASE

ORAL INTAKE
• Monitor daily weight and identify weight loss
• Consult nutritionist for recommendations about diet
• Check your gastric residuals every 4 hourly, notify the physician if it is greater than 100ml.
• Monitor for hematocrit, hemoglobin to assess adequacy of nutritional replacement.
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 ❖ ALTERED PERPHERAL TISSUE PERFUSION RELATED TO EDEMA FROM STASIS OF
BLOOD IN THE CAPILLARIES AND VASOCONSTRICTION
• Monitor daily weight and identify weight loss
• Monitor the extent of fluid retention
• Monitor / determine the severity of edema
• Monitor / determine the severity of edema
• Watch for elevation in central venous pressure
• Check signs and symptoms of fluid over load

❖ DECREASED CARDIAC OUT PUT RELATED TO INEFFECTIVE CARDIAC FUNCTION

• Administer IV fluids
• Monitor urine output
• Monitor blood pressure and pulse rate
• Administer inotropic agents.

PREVENTION OF SHOCK
PREOPERATIVE 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 the ward to theatre.
PREOPERATIVE MEASURES
➢ 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
1. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
It’s previously called adult respiratory distress syndrome. It is a severe form of acute lung injury. The clinical
syndrome is characterized by a hidden and preventive pulmonary edema, increasing bilateral infiltrates of
chest x-ray, hypoxemia refractory to oxygen supplementations, and reduced lung compliance. These signs
occur in the absence of left sided heart failure. Patients with ARDS usually require mechanical ventilation
with a higher – than normal air way pressure. The major cause of death in ARDS is no pulmonary multiple
system organ failure, often with sepsis.

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 2. MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)
MODS is altered organ function in actually ill patients that require medical intervention to support continued
organ function. It’s 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. It’s otherwise called
multiple organ failure.

PROMOTING HOME AND COMMUNITY –

BASED CARE
TEACHING PATEINTS SELF CARE
Patients whose experience and survive shock may be 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 may occur after patient is
discharged from the hospital. Depending on the type of shock and its management. The patient or family may
enquire instruction about treatment modalities such as emergency administration of medication, IV therapy,
parenteral 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.

CONTINIUNG 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 and 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 patient’s chances of surviving this life-
threatening condition. Shock is a catastrophic and result of circulating collapse and in adequate cardiac output,
characterized by end organ hypoxemia, ischemia and failure, while the pathophysiologic mechanism of
distributive, obstructive, hypovolemic and cardiogenic shock are distinct, they may result in similar initial
presentation with end organ damage and cardio circulatory insuffiency. Hypotension is common, but not
obligatory, for the diagnostic of shock. Over all it’s a threatening clinical condition

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REFERENCES
- Suzanne C Smelter, Brenda. G Bare; Brunner and Suddarths Text book of Medical Surgical Nursing 11 th
edition; Volume – 1 ; Published by Wolters Kluwer (India) pvt .Ltd ; New Delhi ; Page No: 355- 379 ; 655-
658

- Shebeer P Basheer, S Yaseen Khan; A Concise Text Book of Nursing Practice; 2nd Edition; EMMESS
Medical Publishers; Page no :239-246.

- Sandra M nettine , the Lippincott manuals nursing practice, 78 th edition, jaypee brothers medical publisher
Pvt .Ltd page no: 1076-1078

- Sharma Asha, Lewis medical surgical nursing, Elsevier publication, page no:1722-1750

- Joycee M black, medical and surgical nursing, 6th edition, volume 2, page no:2231 -2258

- Sharon mantik lewis medical surgical nursing, Mosbys year book publication,3rdedition, page no:740-757

WEB REFERENCES
- www.scribd.com
- https:emtprep.com
- https://www.slideshare.net/aby1992/shock-244914155
- https://www.ncbi.nlm.nih.gov/books/NBK531492/
- https://www.researchgate.net/publication/264395155_Fluid_Management_of_Shock_in_Severe_Malnutriti
on_What_is_the_Evidence_for_Current_Guidelines_and_What_Lessons_Have_Been_Learned_from_Clini
cal_Studies_and_Trials_in_other_Pediatric_Populations
- https://www.slideshare.net/DrShilpaShiv/shock-42363315

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