Hemorrhage & Shock

2. Presented By,
Baishakhi Das
M.Sc Nursing 1st Year Student
Apollo Gleneagles Nursing College

3. DEFINITION
 The term hemorrhage refers to excess loss of blood due to rupture of blood
vessel.
Or
 Lose blood from the body as a result of injury or illness
Or
 Hemorrhage means the loss of blood from the vascular
system associated with an absolute reduction in the
circulating blood volume

4. NATURAL ARREST OF HEMORRHAGE
Adequate amount of calcium is required & all the clotting factors are essential for the natural
arrest of hemorrhage. The blood in the circulation is kept fluid by a fine balance between clotting
& fibrinolysis.
When a tissue is damaged
Prothrombin is converted in to its active form thrombin(into presence of calcium)
Fibrinogen then transformed by thrombin to fibrin
Mesh is formed by platelets & other blood to form clot

5. CAUSES
 Wounds: A break in the continuity of skin, is termed as wound
 Fracture of large bones
 Intra-operative period
 Road traffic accident
 Blunt traumatic injury
 Invasive diagnostic procedures
 Anatomical defects
 Varicose bleeding

6. CLASSIFICATION OF HEMORRHAGE
 World health organization:
 Grade0-no bleeding
 Grade1-petechial bleeding
 Grade2-mild blood loss(clinically significant)
 Grade3-gross blood loss, requires transfusion
 Grade4-debilitating blood loss, retinal or cerebral associated with fatality.
 American College of Surgeons' advanced trauma life support (ATLS):
 Class I: Haemorrhage involves up to 15% of blood volume.
 Class II: Haemorrhage involves 15-30% of total blood volume.
 Class III: Haemorrhage involves loss of 30-40% of circulating blood volume.
 Class IV: Haemorrhage involves loss of >40% of circulating blood volume.

7. CONT…
 According to situation:
 Arterial haemorrhage
 Capillary haemorrhage
 Venous haemorrhage
 According to the time of wound:
 Primary haemorrhage
 Reactionary or intermediate haemorrhage
 Secondary haemorrhage
 According to source of bleeding:
 External Hemorrhage
 Internal Hemorrhage

8. SIGN & SYMPTOMS OF HEMORRHAGE
 Early signs & symptoms:
 Restlessness & anxiety
 Feeling faint
 Coldness( temperature slightly subnormal)
 Pallor
 Patient feels thirsty
 Signs & symptoms after severe haemorrhage:
 Extreme pallor
 Air hunger
 Extremely low blood pressure
 Extreme thirst
 Diminished urine output
 Coma occur prior death

9. STAGES OF HEMORRHAGE
Stage 1:
 15% loss of circulating blood volume
Stage 2:
 15–25% loss of circulating blood volume
Stage 3:
 25–35% loss of circulating blood volume
Stage 4:
 >35% circulating blood volume loss

10. First Aid Treatment for External Bleeding
 Brings the sides of wound together & press firmly.
Press on the pressure point for 10-15min.
Place the causality in comfortable position & raise the injured part & reassure.
Apply clean pad larger than the wound & press it firmly with the palm until bleeding
becomes less.
If bleeding continues do not take off original dressing but add more pads.
First Aid Treatment for Severe Internal Bleeding
 Lay the causality down with head low; rise patient’s legs by use of pillow.
Keep the patient clam & relaxed and do not allow to move.
Keep up the body heat with thin blankets or coat.
Do not give anything to eat or drink; aspiration occur.
Take the patient to the hospital as early as possible.

11. Control of External Haemorrhage
 Pad & Bandage:
 This is the simple method of applying direct pressure to a bleeding wound &
is applicable to vast majority of cases.
 It is effective & causes no damage.
 Digital pressure:
 It is the pressure applied on the point of artery supplying blood to the area of
wound.
 This will control haemorrhage temporally & is called indirect pressure.
 Elevation of the limb:
 It will control venous haemorrhage.
 This is a classical method of dealing with a sudden haemorrhage from a
ruptured varicose vein of leg

12. CONT…
 Application of tourniquet:
 A temporary tourniquet may have to be devised in sudden emergency.
 It should be 3-4 inches wide.
 The great danger of tourniquet is that if it is self on for more than 30 min then gangrene of
the limb may occur.
 Surgical ligation:
 It is necessary if the bleeding is persistent.
 Coagulation:
 It can be used to coagulate the blood from small blood vessels.
 Pack:
 It will temporarily control severe haemorrhage.
 This method is used in operation theatre to control temporary or sudden haemorrhage.
 Styptics:
 These are also used to control bleeding & they act as astringents. Astringents such as snake
venom or adrenaline may be used locally in certain cases.

13. Control of Internal haemorrhage
 The organ is emptied of blood clots if possible in case of severe bleeding
from bladder, a catheter is passed & bladder is emptied.
 The vessels are encouraged to contact a lots of saline or sodium
bicarbonate to which a few drops of adrenaline solution have been added,
is of great value in washing the organ. This can be repeated every two
hourly.
 The use of Ergometrine after the birth of placenta is an example of
stimulating the vessel. Pitocin IV may effective in control of bleeding.
 Packing can be done with gauze soaked in adrenaline is effective.
 Surgical ligature can be done in case of ruptured spleen.

14. NURSING MANAGEMENT
ASSESSMENT:
Frequent nursing assessment is very important.
Document the progress and response of the patient
Assess blood chemistries, blood gas, oxygen saturation and
electrolytes.
Assess for the air way breathing and the circulation.
Identify the bleeding site, amount of blood loss and nature of injury.
Assess respiratory tract for the clearance , rate of respiration and
auscultation the respiratory sounds for any abnormality

15. NURSING DIAGNOSIS
 Fluid volume deficit related to bleeding.
 Ineffective tissue perfusion related to bleeding.
 Anxiety / fear related to changes in circumstances or the
threat of death.
 Risk for infection related to bleeding.
 Risk for shock (hypovolemic) related to bleeding

16. SHOCK
 Shock is defined as a condition where the tissues in the body don't receive
enough oxygen and nutrients to allow the cells to function.
Or,
 Shock is a medical emergency in which the organs and tissues of the body are
not receiving an adequate flow of blood. This deprives the organs and tissues
of oxygen (carried in the blood) and allows the build-up of waste products.
Shock can result in serious damage or even death.

17. CLASSIFICATION OF SHOCK
 Low blood flow
 Cardiogenic Shock
 Hypovolemic Shock
 Maldistribution of blood flow
 Septic Shock
 Anaphylactic Shock
 Neurogenic Shock

18. CARDIOGENIC SHOCK
 Cardiogenic shock occurs when either systolic or diastolic dysfunction of the
heart’s pumping action results in reduced cardiac output (CO), stroke volume
(SV), and BP.
 These changes compromise myocardial perfusion, further depress myocardial
function, and decrease CO and perfusion.
 Mortality rates for patients with cardiogenic shock are around 50%. It is the
leading cause of death from acute myocardial infarction (MI).

19. Causes:
 Acute MI
 Pump failure
 Mechanical complications
 Right ventricular infarction
 Other conditions
 End-stage cardiomyopathy
 Myocarditis (fulminant myocarditis)
 Myocardial contusion
 Prolonged cardiopulmonary bypass
 Septic shock with myocardial depression
 Valvular disease

20. Pathophysiology:

21. Clinical Manifestations:
 Angina Pectoris, squeezing pain in centre of chest.
 Dysrhythmias
 Diminished heart sounds
 Acute drop in blood pressure > 30 mm Hg
 Decreased cardiac output
 Tachypnea, shortness of breath
 Weak, thready pulse
 Sweating, cold hand & feet
 Urine output < 30 mL/hr

22. Management:
 Physical examination: Any signs of tachypnea, pulmonary congestion, pallor; cool, clammy
skin, decreased capillary refill time, anxiety, confusion, agitation
 Increase in pulmonary artery wedge pressure
 Decreased renal perfusion
 Correct dysrhythmias
 Drug Therapy:
 Nitrates
 Inotropes
 Diuretics
 Beta blockers

23. HYPOVOLEMIC SHOCK
 Hypovolemic shock occurs from inadequate fluid volume in the intravascular
space to support adequate perfusion.
 The volume loss may be either an absolute or a relative volume loss.
 Absolute hypovolemia results when fluid is lost through haemorrhage,
gastrointestinal (GI) loss (e.g., vomiting, diarrhoea), fistula drainage, diabetes
insipidus, or diuresis.
 In relative hypovolemia, fluid volume moves out of the vascular space into
the extravascular space (e.g., intracavitary space). We call this type of fluid
shift third spacing.

24. Causes:
 Absolute hypovolemia
 Hemorrhage
 GI loss (e.g., vomiting, diarrhea)
 Fistula drainage
 Diabetes insipidus
 Hyperglycemia
 Diuresis
 Relative hypovolemia

25. Pathophysiology:

26. Clinical Manifestations:
 Tachypnea
 Tachycardia – weak, thready pulse
 Orthostatic Hypotension
 Delayed Capillary refill
 Cool clammy skin
 Oliguria
 Anxiety

27. Management:
 Correcting the underlying cause
 Administer warm fluids
 May need supportive therapy with vasopressors
 Ensure a patent airway
 Administer oxygen
 Place client in Modified Trendelenburg
 If overt bleeding, apply pressure to the site
 Monitor vital signs every 5 minutes
 Administer medicines as ordered
 Increase the rate of fluid delivered

28. NEUROGENIC SHOCK
 Neurogenic shock is a hemodynamic phenomenon that can occur within 30
minutes of a spinal cord injury and last up to 6 weeks.
 Neurogenic shock related to spinal cord injuries is generally associated with a
cervical or high thoracic injury.
 The injury results in a massive vasodilation without compensation because of
the loss of SNS vasoconstrictor tone.
 This massive vasodilation leads to a pooling of blood in the blood vessels,
tissue hypo perfusion, and impaired cellular metabolism.

29. Causes:
 Motor vehicle accidents
 Falls
 Acts of violence
 Sports and injuries
 Spinal cord injury
 Uses of opioids, benzodiazepines

30. Pathophysiology:

31. Clinical Manifestations:
 Extreme back pain
 Weakness, incoordination or paralysis in any part of your body
 Numbness, tingling or loss of sensation in your hands, fingers, feet or toes
 Loss of bladder or bowel control
 Difficulty with balance and walking
 Impaired breathing after injury
 Weakness from irregular blood circulation
 Bradycardia, or a slower heart rhythm
 Cyanosis, or discoloured lips and fingers
 Hypothermia, or decreased body temperature

32. Management:
 High dose steroids: to help decrease inflammation surrounding spinal cord
 Treat the symptoms
 Elevate and maintain head of bed 30 degrees
 Support cardiovascular and neurologic function
 Prevent blood pooling in lower extremities
 Apply TED stockings
 Prevent DVTs

33. ANAPHYLACTIC SHOCK
 Anaphylactic shock is an acute, life-threatening hypersensitivity (allergic) reaction to a
sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom).
 The reaction quickly causes massive vasodilation, release of vasoactive mediators, and an
increase in capillary permeability.
 As capillary permeability increases, fluid leaks from the vascular space into the interstitial
space.
 Anaphylactic shock can lead to respiratory distress due to laryngeal edema or severe
bronchospasm and circulatory failure from the massive vasodilation.

34. Causes:
 A patient can have a severe allergic reaction, possibly leading to anaphylactic shock, after
contact, inhalation, ingestion, or injection with an antigen (allergen) to which the person
has previously been sensitized.
 IV administration of the antigen (allergen) is the route most likely to cause anaphylaxis.
 However, oral, topical, and inhalation routes can cause anaphylactic reactions.

35. Pathophysiology:

36. Clinical Manifestations:
 Swelling of the lips and tongue, angioedema
 Peri-orbital edema
 Wheezing
 Stridor
 Flushing, pruritus, urticarial
 Respiratory distress and circulatory failure

37. Management:
 Assess for allergies
 Communication
 Assess for sign and symptoms
 Airway management
 Epinephrine 0.3mg SQ or IM
 BLS/ACLS

38. SEPTIC SHOCK
 Sepsis is a life-threatening syndrome in response to an infection.
 It is characterized by a dysregulated patient response along with new organ dysfunction
related to the infection.
 In as many as 30% of patients with sepsis, the causative organism is not identified.
 Sepsis and septic shock have a high incidence worldwide, with a mortality rate of 25%
or higher.
 Septic shock is a subset of sepsis. It has an increased mortality risk due to profound
circulatory, cellular, and metabolic abnormalities.

39. Causes:
 The main organisms that cause sepsis are gram-negative and gram-positive bacteria.
Parasites, fungi, and viruses can also cause sepsis and septic shock.
 Predisposing factors are:
 Extended hospitalization
 Advanced age
 Immunodeficiency disorder
 Pneumonia
 Skin and soft tissue infections
 GI infections
 Hematoma

40. Pathophysiology:

41. Clinical Manifestations:
 Early stage (compensated/warm shock):
 Febrile (38.2-41°C )
 Shivering and malaise
 Warm dry and flushed skin.
 Hyperventilation
 Rapid bounding pulse
 Late stage (decompensated/ cold shock):
 Hypovolemia with superimposed sepsis
 Altered sensorium
 Cold clammy skin
 Weak pulse
 Oliguria

42. Management:
 Asepsis and maintain hygiene
 Parenteral therapy and medication
 CABs: circulation Airway, breathing, and Focused assessment of tissue perfusion
 Monitor vital signs
 Assess peripheral pulses
 Level of consciousness assessment
 Fluid administration
 Antibiotics: broad spectrum until source is identified

43. STAGES OF SHOCK
 Initial stage
 Compensatory stage
 Progressive stage
 Refractory stage

44. Initial stage
 The continuum begins with the initial stage of shock that occurs at a
cellular level.
 This stage is usually not clinically apparent.
 Metabolism changes at the cellular level from aerobic to anaerobic,
causing lactic acid build-up.
 Lactic acid is a waste product that is removed by the liver.
 However, this process requires O2, which is unavailable because of the
decrease in tissue perfusion.

45. Compensatory stage
Reversible stage during which compensatory mechanisms are effective and homeostasis
is maintained.
Clinical presentation begins to reflect the body’s response to the imbalance of oxygen
supply and demand
Metabolism changes at the cellular level from aerobic to anaerobic, causing the lactic
acid build up which is removed by the liver, but needs oxygen.
At first, blood pressure will decrease, which happens because of the decrease in cardiac
output (CO) and a narrowing of the pulse pressure.
Blood flow to the vital organs, such as the heart and brain, are maintained, while blood
flow to non-vital organs, the kidneys, liver, skin, GI tract and the lungs, is shunted.
At this stage, the body is able to compensate for the changes in tissue perfusion. If the
underlying cause is corrected, the patient will recover with little to no residual effects. If
the body is unable to compensate the body will enter the progressive stage of shock.

46. Progressive stage
 This stage of shock begins when the body’s compensatory mechanisms fail
 Immediate interventions are need to prevent the development of multiple organ dysfunction
syndrome (MODS)
 Continued decreased cellular perfusion and resulting alerted capillary permeability are the
distinguishing features of this stage
 Altered capillary permeability allows leakage of fluid and protein out of the vascular space
into the surrounding interstitial space causing a decrease in circulating volume and an
increase in systemic interstitial edema.
 This fluid leak from the vascular space also affects the solid organs, liver, spleen, GI tract,
lungs, and peripheral tissues by further decreasing oxygen perfusion

47. Refractory stage
 Final stage of shock
 Decreased perfusion from peripheral vasoconstriction and decreased cardiac output
exacerbate anaerobic metabolism
 Lactic acid accumulates and contributes to an increased capillary permeability and dilation
of the capillaries
 Increased capillary permeability allows for fluid and plasma to leave the vascular space and
move to the interstitial space
 Blood pools in the capillary beds secondary to constricted veins and dilated arteries
 Loss of intravascular volume leads to worsening of hypotension and tachycardia resulting in
a decrease in coronary blood flow
 Decreased coronary blood flow results in decreased cardiac output
 Cerebral blood flow cannot be maintained and cerebral ischemia results

48. MANAGEMENT
Fluid Management:
 Crystalloids: increase intravascular volume through actual volume administered
 Colloids: pull fluid into the vascular space through osmosis
 Isotonic: similar in composition to body fluid. Provides greater intravascular in the
vascular space
 Hypotonic fluid: shift fluid into intracellular spaces. Useful in preventing cellular
dehydration. They deplete circulatory volume
 Hypertonic: move fluid from cells to extravascular space, may be used to replace
electrolytes and promote diuresis
 Drug Therapy:
 Sympathomimetic
 Vasodilators

49. Nursing Assessment:
 CABs: circulation Airway, breathing, and Focused assessment of tissue perfusion
 Vital signs
 Peripheral pulses
 Level of consciousness
 Capillary refill
 Skin (e.g., temperature, colour, moisture)
 Urine output
 Brief history (Events leading to shock, Onset and duration of symptoms)
 Details of care received before hospitalization
 Allergies

50. Nursing Diagnosis:
 Deficient fluid volume related to active fluid loss
 Ineffective tissue perfusion related to severe blood loss
 Decreased cardiac output may be related to cardiac muscle disease, dysrhythmias,
increased or decreased preload or afterload, impaired left ventricular (LV) contractility
possibly evidenced by changes in the level of consciousness, crackles, dyspnoea and
pulmonary congestion, cyanosis and mottling of the extremities, metabolic acidosis.
 Impaired gas exchange related to ventilation- perfusion imbalance possibly evidence by
bronchospasm, dyspnoea, hypotension, shock, shortness of breath, tachycardia
 Risk For Infection related to compromised immune system

51. SUMMARIZATION
&
CONCLUSION