hemorrhage and shock

1. HEMORRHAGE AND SHOCK
Submitted by:
Nikita Sharma
MSc(N) 1st year
Roll no- 9
Submitted to:
Mrs. Prabhjot saini
Prof. & H.O.D Med. Surg. Nsg.

2. HEMORRHAGE………
DEFINITION:
 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.

3. Natural arrest of hemorrhage
Tear in blood vessels
Collagen comes into Damaged cell membranes release phospholipids
contact with blood
Platelets form plug over tear
Plasma proteins are activated
Prothrombin
Thrombin
Soluble fibrinogen in plasma Insoluble fibrin
Forms network of fibres to cover the tear

4. 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 vit- K and therefore they may bleed if operated upon. For this
reason, Vit-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.

5. FIBRINOYTIC ACTIVITY OF BLOOD
MAY BE INCREASED :
 In complicated obstetric cases associated with hemorrhage.
 After strenuous activity.
 In presence of some malignant growth.

6. TYPES
Hemorrhage
According to
vessels involved
According to the
time of the wound
According to the
clinical classification
of the hemorrhage

7. ACCORDING TO VESSELS INVOLVED
• The blood is bright red and spurts with the heartbeat.
• Escapes from both ends of vessels
• Blood loss is more rapid from a vessel of corresponding size.
ARTERIAL
• The blood oozes over the surface of the capillary.
• Darkish in colorCAPILLARY
• Dark red in color
• No spurting, rate of loss is less severe.
• When there is injury to large vessels is to be a serious matter.
• If air is sucked to damaged vein, fatal air embolism may
occur.
VENOUS

8. ACCORDING TO THE TIME OF WOUND
Primary
• Immediate hemorrhage
• e.g.- cut on a finger or operative incision
Intermediat
e or
reactionary
• Occurs in 1st 24 hours after operation.
secondary
• Due to sloughing off the wall of blood vessels.
• Cause bacteria and enzyme (acid pepsin on peptic
ulcer)

9. ACCORDING TO CLINICAL
CLASSIFICATION OF HEMORRHAGE
REVEALED/
EXTERNAL
It is a type when bleeding
can be seen externally.
CONCEALED/
INTERNAL
Bleeding cannot be seen
externally
It occur one of the body cavity
e.g- abdomen,
intestines, tissues.

10. TERMINOLOGY
Mean arterial pressure (MAP)- It is an average blood
pressure in an individual during a single cardiac cycle.
MAP= Systolic B.P + 2( diastolic pressure)
3

11. CLASSIFICATION
Hemorrhage
By Blood loss
-Class 1
- Class 2
-Class 3
-Class 4
By Origin
- Mouth
-upper head
-Lungs
-Gynaecological

12. BY BLOOD LOSS
Class 1 hemorrhage Class 2 hemorrhage Class 3 hemorrhage Class 4 hemorrhage
 15 % blood loss  15-30% total
blood volume
 30-40% loss of
circulatory blood
volume
 Loss of more than
40% of circulatory
blood volume
 No change in vital
signs
 Tachycardia, Skin
may start to look
pale and be cool
in touch
 Blood pressure
drops, the heart
rate increases,
capillary refill
worsens
 Limit of body’s
compensation
reached
 Fluid
resuscitation is
not usually
necessary
 Volume
resuscitation with
crystalloids
(Saline solution
or lactated
Ringer’s solution)
 Blood transfusion
is not typically
 Fluid
resuscitation with
Crystalloids and
blood Transfusion
are usually
necessary
 Aggressive
resuscitation is
required to
prevent death

13. BY ORIGIN
Mouth
 Hematemesis- Vomiting fresh blood
 Hemoptysis- coughing up blood from lungs
 Hematochezia- Rectal blood
 Hematuria – Blood in the urine from urinary bleeding

14. UPPER HEAD
o Intracranial Hemorrhage : bleeding in skull
o Cerebral Hemorrhage : bleeding with in the brain
tissue
o Intracerebral Hemorrhage : bleeding in the brain due
to rupture of the blood vessels within the head
o Subarachnoid Hemorrhage : presence of blood with in
the subarachnoid space from some pathologic process.

15. CONTINUE……..

16. Lungs- Pulmonary hemorrhage
Gynaecological- Vaginal bleeding , PPH and APH, First
trimester bleeding, ovarian bleeding.
Upper GI Bleeding.
CONTINUE…..

17. 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.

18. CAUSES
Traumat
ic injury
• Abrasion, Excoriation, Hematoma, Laceration, incision,
• Puncture Wound, Contusion.
Medical
condition
s
• Intravascular changes ( Increased B.P, decreased clotting)
• Intramural changes (aneurysm, dissections)
• Extravascular changes ( H.Pylori infection, Brain abscess)
Others
• Platelets ;NSAIDS; cause bleeding by inhibiting activating
platelets.
• E.G: Aspirin, Ibuprofen, and related drugs

19. PATHOPHYSIOLOGY

21. SIGN & SYMPTOMS

22. CONTINUE…..
 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

24. DIAGNOSTIC TESTS
 History collection
 Medical conditions
 Use of medicines
 Family history
 Present medical and surgical history
 Physical examination
 Systematically examination
 WHO bleeding scale

25. DIAGNOSTIC TESTS
 Evaluation of patient with co – ordinated history and physical
examination provides valuable clues.
 History should include following questions:
1. Is there any personal or family history of bleeding tendency?
2. Has the patient undergone surgery or extractions previously?
3. Any history of hematuria, GIT hemorrhage, epistaxis?
4. What medication is the patient taking or has taken recently?

26. CONTINUE….
 Note for any splenomegaly, hepatomegaly.
 Hepatic insufficiency should be assessed.
 Assessment of skin and mucosal surfaces

27. DIAGNOSTIC TESTS
 LABORATORY TESTS:
1. Bleeding Time (BT): Patients with BT more than 10
minutes have increased risk of bleeding.
 Various methods for measuring BT, e.g. Ivy, Duke and
template.
 BT is prolonged in thrombocytopenia, Von –
Willebrand’s disease and platelet dysfunction.

28. CONTINUE…..
2. Platelet count: Normal count: 1.5 – 4.5 lakhs per cu mm of
blood.
 When count becomes 50,000 – 1 lakh per cu mm, there is mild
prolongation of BT.
 Patients with count less than 50,000 per cu mm have easy
bruising.
 Minor oral surgical procedures can be done if count is above
80,000 – 1 lakh per cu mm

29. CONTINUE…..
3. Prothrombin Time (PT):
 Normal PT is usually 12 – 14 seconds.
 Prolonged in patients on warfarin anticoagulant therapy, vitamin K
deficiency or deficiency of factor V, VII, X, prothrombin or fibrinogen.
4. Partial Thromboplastic Time (PTT):
 Prolonged in hemophiliacs.
 Normal PTT is less than 45 seconds.
 PTT is relatively insensitive to changes in intrinsic coagulation
system.
 Small changes in PTT may be of great significance

30. TREATMENT
 ARREST OF HEMORRHAGE:
• External hemorrhage: pressure will control all forms of external
bleeding. According to its severity there is a choice of methods.
• Pad or Bandage: this simple method is applying direct pressure to
a bleeding wound. It is effective and causing no damage.
• Digital pressure: it is applied over the pressure point of artery
supplying the area of wound will control hemorrhage temporarily. It
is particularly valuable in the neck where other methods are
inapplicable.

31. CONT…….
• Elevation of limb: it will control venous hemorrhage this
is the classical method of dealing with the sudden
hemorrhage from a ruptured varicose vein of the leg.
• Applicable of tourniquet: this is rarely required except
for the control of the torrential hemorrhage from the
limb.
• Blood transfusion: blood component therapy:
- Packed RBCs, clotting factors transfusion
- platelets etc.

32. Cont……
 Various modalities :
• Emergency treatment:
 The main objective is to stop bleeding
 Give first aid management
 Do firm pressure dressing over artery Proximal to area
 Give direct pressure
First aid:- Check the victims ABC
 Call the ambulance
 Treat the shock
 Assist the victim in most comfortable position.
 Monitor ABC and vitals till the ambulance arrives.

33. IMMEDIATE MEASURES
 Cut the patient clothing away and carry out rapid
physical examination
 Apply firm pressure over the bleeding area
 Elevate the injured part
 Immobilize the injured part.

34. FOR EXTERNAL BLEEDING
 “RED”
 R- Rest
 E- Elevation
 D- Direct pressure/ Dressing

35. Medical management of hemorrhage
Drug therapy:
• Aminocaproic acid used to treat excessive
bleeding with fibrinolysis
• Anti-Inhibitor coagulation therapy
- Autoplax-T
- Feiba VH
- I/V Morphine for internal bleeding

36. Fluid replacement/ I/V infusion: I/V fluid
replacement
 Isotonic electrolyte solution
 E.G :- RL, NS, Colloids.
Supplemental therapy:
- Vitamin B12
- Folic acid
- Ferrous sulphate

37. Measures for oxygenation and cardiac function
 Administer humidified oxygen
 Watch for cardiac arrest caused by hypovolemic shock
secondary to anoxia.
 Assess with ECG monitoring for dysrhythmias.

38. SPECIAL MEASURES
 ANTI- SHOCK GARNMENTS:
1. Non- Pneumatic anti- shock garments (NASG)
2. Pneumatic anti shock garments

39. NON-PNEUMATIC ANTI SHOCK GARNMENT

40. PNEUMATIC ANTI SHOCK GARMENTS

41. Nursing Management
AssessmentHistory
Taking
Origin
Previous
drug
history
Surgical
history
Type of
hemorrhage
Severity of
hemorrhage
Causes/
Diagnostic
test

42. Nursing Diagnosis:
1.Deficit fluid volume related to blood loss
Goal: To maintain the adequate fluid volume
 Interventions:
• To maintain the hydration level of the patient.
• To check for the diagnostic test for Hb, hematocrit level etc.
• To assess the electrolyte level of the patient.
• To check the weight of the patient.
• To maintain intake output chart of the patient.
• To administer the IV fluids.
• To encourage the patient to take fluid orally.

43. Other Diagnosis:
 Ineffective tissue perfusion related to low
hemoglobin level secondary to hemorrhage.
 Risk of infection related to low immune level
secondary to hemorrhage
 Risk of bleeding related to decreased platelet
count secondary to excessive blood loss.

44. SHOCK

45. SHOCK
 Introduction:
Shock is the state of not enough blood flow to the
tissues of the body as a result of problems with the
circulatory system. Initial symptoms may include
weakness, fast heart rate, fast breathing, sweating,
anxiety, and increased thirst. This may be followed
by confusion, unconsciousness, or cardiac arrest as
complications worsen .

46. Definition
 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 buildup of waste
products. Shock can result in serious damage or even
death.
(OR)
According to Merriam Webster: a state of profound
depression of the vital processes associated with reduced
blood volume and pressure and caused usually by severe
especially crushing injuries, hemorrhage, or burns.

47. CAUSES OF CIRCULATION FAILURE
 Circulation may fail from:
Sudden Deficient oxygenation Reduction
Miscellaneous
-Malfunction -of blood in lungs -in blood volume
-Of Heart
-Coronary -COPD -Hypovolemia -Infection
Artery disease -Emphysema -Severe anemia -Allergy
- High B.P -Bronchitis -Dehydration

48. C
A
U
S
E
Hemorrhage
Burns
Dehydration
MI
Anaphylaxis
Neurogenic condition
Sepsis
Cardiac dysfunction
Obstructive condition
Diarrhea and dysentery

49. PATHOPHYSIOLOGY OF SHOCK

50. STAGES OF SHOCK

51. CONTINUE…..

52. INITIAL STAGE
 During this stage, the state of hypoperfusion causes
hypoxia.
 Due to the lack of oxygen, the cells perform lactic acid
fermentation.
 Since oxygen, the terminal electron acceptor in the
electron transport chain, is not abundant, this slows
down entry of pyruvate into the Krebs cycle, resulting in
its accumulation.
 Accumulating pyruvate is converted to lactate by lactate
dehydrogenase and hence lactate accumulates (causing
lactic acidosis).

54. COMPENSATORY STAGE
 This stage is characterized by the body employing
physiological mechanisms, including neural, hormonal
and bio-chemical mechanisms in an attempt to reverse
the condition.
 As a result of the acidosis, the person will begin to
hyperventilate in order to rid the body of carbon dioxide
(CO2). CO2 indirectly acts to acidify the blood and by
removing it the body is attempting to raise the pH of the
blood.
 The baroreceptors in the arteries detect the resulting
hypotension, and cause the release of epinephrine and
norepinephrine.

55. Norepinephrine causes predominately vasoconstriction with a
mild increase in heart rate, whereas epinephrine predominately
causes an increase in heart rate with a small effect on the vascular
tone; the combined effect results in an increase in blood pressure.
The renin–angiotensin axis is activated, and arginine vasopressin
(Anti-diuretic hormone; ADH) is released to conserve fluid via the
kidneys.
These hormones cause the vasoconstriction of the kidneys,
gastrointestinal tract, and other organs to divert blood to the heart,
lungs and brain. The lack of blood to the renal system causes the
characteristic low urine production. However the effects of the
renin–angiotensin axis take time and are of little importance to the

56. PROGRESSIVE STAGE
 Should the cause of the crisis not be successfully
treated, the shock will proceed to the progressive stage
and the compensatory mechanisms begin to fail.
 Due to the decreased perfusion of the cells, sodium ions
build up within while potassium ions leak out.
 As anaerobic metabolism continues, increasing the
body's metabolic acidosis, the arteriolar smooth muscle
and precapillary sphincters relax such that blood
remains in the capillaries.

57. CONT.…..
 Due to this, the hydrostatic pressure will increase and,
combined with histamine release, this will lead to
leakage of fluid and protein into the surrounding tissues.
 As this fluid is lost, the blood concentration and
viscosity increase, causing sludging of the micro-
circulation.
 The prolonged vasoconstriction will also cause the vital
organs to be compromised due to reduced perfusion.
 If the bowel becomes sufficiently ischemic, bacteria
may enter the blood stream, resulting in the increased
complication of endotoxin shock.

58. REFRACTORY STAGE
 At this stage, the vital organs have failed and the shock
can no longer be reversed.
 Brain damage and cell death are occurring, and death
will occur imminently.
 One of the primary reasons that shock is irreversible at
this point is that much cellular ATP has been degraded
into adenosine in the absence of oxygen as an electron
receptor in the mitochondrial matrix.

59. CONT.….
 Adenosine easily perfuses out of cellular
membranes into extracellular fluid, furthering
capillary vasodilation, and then is transformed
into uric acid. Because cells can only produce
adenosine at a rate of about 2% of the cell's total
need per hour, even restoring oxygen is futile at
this point because there is no adenosine to
phosphorylate into ATP.

60. CLASSIFIATION
HINSHAW & COX categorizes shock into 4
Types:
HYPOVOLEMIC
SHOCK
CARDIOGENIC
SHOCK
DISTRIBUTIVE
SHOCK
OBSTRUCTIVE
SHOCK
SHOCK

61. 5TH TYPE OF SHOCK
Endocrine shock……

62. HYPOVOLEMIC SHOCK
• Most common type of shock.
• It is due to inadequate circulating blood volume
resulting from;
-Hemorrhage ( blood loss)
-Burns (loss of plasma protein & fluid shift)
- Dehydration ( Loss of fluid Volume)

67. CARDIOGENIC SHOCK

68. CARDIOGENIC SHOCK
 Cardiogenic shock occurs when there is failure of the pump action of
the heart, resulting in a decrease in cardiac output causing reduced
end-organ perfusion. This leads to acute hypoperfusion and hypoxia
of the tissues and organs, despite the presence of an adequate
intravascular volume.
 Cardiogenic shock can be defined as the presence of the following
(despite adequate left ventricular filling pressure):
• Sustained hypotension (systolic blood pressure (BP) <90 mm Hg for
more than 30 minutes).
• Tissue hypoperfusion (cold peripheries, or oliguria <30 ml/hour, or
both).

69. CARDIOGENIC SHOCK
 Cardiogenic shock most commonly occurs as a
complication of acute myocardial infarction
(MI). It occurs in 7% of patients with ST-
segment elevation MI and 3% with non ST-
segment elevation MI. It is a medical emergency
requiring immediate resuscitation

70. CAUSES
Ventricular
Ischemia
• Myocardial
infarction
• Open Heart
Surgery
• Cardiac Arrest
Structural
Problem
• Valvular
dysfunction
• Septal rupture
• Cardiomyopath
ies
Dysrhythmias
• Brady
dysrhythmias
• Tachy
Dysrhythmias

71. PATHOPHYSIOLOGY

72. CLINICAL MANIFESTATION
 When the shock is due to left-sided failure, blood backs
up into the pulmonary circulation resulting in,
• Pulmonary edema
• Crackles in Lungs
• Increased Pulmonary capillary wedge pressure (PCWP)
- Low blood pressure and diminished urine output
- Dilated Pupils
- Cyanosis

73. CONT….
Pallor, cold and clammy skin
Restlessness, anxiety, Irritability,
weakness
Rapid Shallow breathing

74. SIGN AND SYMPTOMS
 Distended jugular veins due to increased jugular
venous pressure
 Absent pulse due to tachyarrythmia

75. EMERGENCY MANAGEMENT
 Initial drug therapy for myocardial infarction
 Replace fluids
 Special measures:
Aim:
• To restore blood flow

76. SPECIAL MEASURES
 Thrombolytic therapy
 Angioplasty with stenting
 Emergency revascularization
 Valve replacement
 Cardiac catheterization
 Drugs:
• Nitrates- To decrease the workload of heart
• Diuretics- to reduce preload
• Vasodilators- to reduce afterload
• Beta- adrenergic blockers- to reduce heart rate and contractility
• IABP and VAD

78. DISTRIBUTIVE SHOCK
 Distributive shock is a medical condition in which abnormal
distribution of blood flow in the smallest blood vessels results in
inadequate supply of blood to the body's tissues and organs. It is
one of four categories of shock, a condition where there is not
enough oxygen-carrying blood to meet the metabolic needs of the
cells which make up the body's tissues and organs. Distributive
shock is different from the other three categories of shock in that
it occurs even though the output of the heart is at or above a
normal level. The most common cause is sepsis leading to type of
distributive shock called septic shock, a condition that can be
fatal.
 Distributive shock results from excessive vasodilation and the
impaired distribution of blood flow.

79. DISTRIBUTIVE SHOCK
 Distributive shock results from excessive
vasodilation and the impaired distribution of
blood flow

80. Types of Distributive shock

82. ANAPHYLACTIC SHOCK
 Anaphylaxis is a serious allergic reaction that is rapid in
onset and may cause death. It typically causes more than
one of the following: an itchy rash, throat or tongue
swelling, shortness of breath, vomiting, lightheadedness,
and low blood pressure. These symptoms typically come
on over minutes to hours.
(OR)
 It is defined as the hypersensitivity reaction to the
ingestion or injection of a substance (a protein or drug)
resulting from prior contact with a substance

83. PATHOPHYSIOLOGY
Antigen re-exposure
Hypersensitivity antibody response
Vasoactive mediator release
Massive Vasodilation Capillary permeability
Profound hypovolemia Vascular collapse
Angioedema
Urticaria
Pulmonary congestion
Airway obstruction Respiratory arrest
Cardiac arrest

84. SIGN AND SYMPTOMS
 Throat edema
 In congestion with increasing breathing difficulty
 Hypotension
 Increased heart rate
 Skin eruptions and large welts
 Localized edema especially around the face
 Weak and rapid pulse
 Breathlessness and cough due to narrowing of airways
and swelling of throat

85. MANAGEMET
 Manage ABC
 Administer epinephrine
 Administer diphenlyhydramine
hydrochloride(Benadryl)

87. NEUROGENIC SHOCK
 It is a type of shock (a life-threatening medical
condition in which there is insufficient blood flow
throughout the body) that is caused by the sudden loss
of signals from the sympathetic nervous system that
maintain the normal muscle tone in blood vessel walls.
The blood vessels relax and become dilated, resulting in
pooling of the blood in the venous system and an overall
decrease in blood pressure. Neurogenic shock can be a
complication of injury to the brain or spinal cord.

88. PATHPHYSIOLOGY
Spinal cord injury, spinal anesthesia centre depression
increased sympathetic tone
Arterial and venous dilation
Arterial and venous blood pooling
Hypotension
Bradycardia warm, dry, flushed skin
Decreased perfusion of vital organs
Multisystem organ failure

89. SIGN AND SYMPTOMS
Slowed heart rate
Hypotension
Skin is warm and dry

90. EMERGENCY CARE
Replace fluids
Administer drugs to increase B.P and Heart rate

92. SEPTIC SHOCK
 Sepsis is the result of an infection, and causes
drastic changes in the body. It can be very
dangerous and potentially life-threatening.
 It occurs when chemicals that fight infection by
triggering inflammatory reactions are released
into the bloodstream.
 There are three stages of sepsis:

93. SEPTIC SHOCK
 Sepsis is when the infection reaches the bloodstream
and causes inflammation in the body.
 Severe sepsis is when the infection is severe enough to
affect the function of organs, such as the heart, brain,
and kidneys.
 Septic shock is when there is experience of a significant
drop in blood pressure that can lead to respiratory or
heart failure, stroke, failure of other organs, and death.

94. Causes of Septic Shock

95. TYPES OF SEPTIC SHOCKS
 Early (Warm)
• Decreased peripheral vascular resistance
• Increased cardiac output
 Late (cold)
• Increased peripheral vascular resistance
• Decreased cardiac output

96. PATHOPHYSIOLOGY
Severe localized infection of gram negative bacilli
Bacterial invasion of blood stream (septicemia)
Inflammatory response
Endotoxins are released into circulation
Immune system release histamines and many other chemical mediators
Massive vasodilation Capillary permeability Time-spacing
fluids
Inadequate tissue perfusion
Compensatory mechanism is activated
perfusion of vital organs
Multiple organ failure

97. SIGN AND SYMPTOMS
 Hot , dry, flushed skin
 Hypotension
 Increased heart rate
 Hyperthermia due to overwhelming bacterial infection,
 Vasodilation and increased cardiac output

98. EMERGENCY CARE
 Locate the source of infection and treat with
broad spectrum antibiotic
 Replace fluids

99. OBSTRUCTIVE SHOCK
The blood flow is obstructed , which impedes circulation and can results in
circulatory arrest. Several conditions result in this form of shock:
 Cardiac tamponade: blood in the pericardium prevents the inflow of
blood into the heart(venous return). Constrictive pericarditis, in which the
pericardium shrinks and hardens, is similar in presentation.
 Tension pneumothorax: through increased intrathoracic pressure, blood
flow to the heart is prevented (venous return)
 Massive pulmonary embolism: it is the result of a thromboembolic
incident in the blood vessels of the lungs and hinders the return of blood
to the heart.
 Aortic stenosis: hinders circulation by obstructing the ventricular outflow
tract.

100. SIGN AND SYMPTOMS
 Distended jugular veins due to increased jugular
venous pressure
 Pulsus paradoxus in case of tamponade.

101. ENDOCRINE SHOCK BASED ON
ENDOCRINE DISTURBANCES
 Hypothyroidism, in critically ill patients, reduces
cardiac output and can lead to hypotension and
respiratory insufficiency
 Thyrotoxicosis may induce a reversible cardiomyopathy
 Acute adrenal insufficiency is frequently the results of
discontinuing corticosteroid treatment without tapering
the dosage.
 However, surgery and intercurrent disease in patients on
corticosteroid therapy without adjusting the dosage to
accommodate for increased requirements may also
results in this condition.

102. DIAGNOSTIC TESTS
 History collection- medical, surgical history of recent
ailment (URTI, surgery, chest pain)
 Physical examination- to identify flat neck veins
 ECG 12 leads
 Continuous cardiac monitoring
 X-ray chart
 Hemodynamic monitoring
 Continuous pulse oximetry

103. LABOARTORYABNORMALITIES IN SHOCK
TESTS FINDINGS POSSIBLE
ETIOLOGY
..
CBC Hb/ Hematocrit
WBC /
Platelets
Hemorrhage, fluid
resuscitation,
hemolysis, sepsis,
DID
100% O2, control
bleeding, titrate
fluids, cultures,
antibiotics, transfuse
platelets
Glucose / Stress, sepsis,
decrease in
production
Glucose infusion
(hypoglycemia)
Potassium / Renal dysfunction,
acidosis
Treat acidosis
Calcium Sepsis , BT Give calcium
Lactate Tissue hypoxia Correct acidosis
ABG pH Hypoperfusion, renal
failure, poisoning,
diarrhea, DKA
Five fluids,
ventilation and
buffer
Venous O2 Variable Low O2 delivery or Attempts O2

104. COMPLICATION OF SHOCK
MULTIPLE ORGAN
DYSFUNCTION
SYNDROME (MODS)

105. MANAGEMENT
OF
SHOCK

106. AIM OF MANAGEMENT
• To prevent anaerobic metabolism in the
tissue.
• To correct the underlying cause
• To augment perfusion and oxygen delivery
and minimize organ damage until the body’s
homeostatic mechanism return.

107. GENERAL MANAGEMENT OF SHOCK
 Reassure the patient if the patient is conscious.
 Place the patient comfortably on his back. Except in
cases of injury to the head, chest or abdomen, lower the
head slightly and turn to one side. In case of vomiting,
place in three-quarter back up position.
 Loosen tight clothing but do not remove clothing.
 Wrap in light bed sheet or a thin rug.
 Never use hot water bottles or very warm rugs. Do not
rub any part of the body with anything.

108. CONT…….
 Do not administer anything by mouth especially in cases
of injuries to the chest or abdomen, as an operation may
be required soon.
 If the patient is conscious and there is no injury to the
chest or abdomen, give a little water, hot coffee or tea.
Never give any alcoholic drinks.
 Transport the patient quickly to the hospital.
 Remember that in shock a delay of even a few minutes
may mean death. So attend to the patient as quickly as
possible.

109. CORRECTION OF CAUSATIVE FACTOR:
 Assessment and an accurate differential medical
diagnosis, which establish the specific cause of shock
state, form the basis for treatment.
 Some forms of the shock more easily recognized are
hypovolemic shock that is due to extensive burns or
trauma and cardiogenic shock with severe chest pain
and acute MI.

110. Improve oxygenation:
 Maintaining the client’s airway is vital to the
treatment of shock.
 In all types of shock, supplemental oxygen is
administered to protect against hypoxemia.
 Oxygen can be delivered via nasal cannula , a
mask, a high flow non breathing mask, an
endotracheal tube, or a tracheostomy.

111. Assist circulation:
 Mechanical devices that assist circulation or
decrease the workload of the heart may be used
temporary measures in managing clients in shock.
 Examples of these include the military or medical
antishock trousers (MAST), IABP, and external
counterpulsation device.

112. MAST garments:
• Also called Pneumatic antishock garment, encases the lower part
of the body in a one- piece , three chambered ( 1 abdominal and
2 leg chambered ) suit from the lower costal margin to the
ankles.
• The external pressure provided by the MAST garment causes
increased vascular resistance and reduces the diameter of blood
vessels in the abdomen and legs.
• This results in impendence of blood flow and may decrease
leakage into the tissue, resulting in increased perfusion of vital
organs.
• Cardiac output and arterial BP increases.

113. • It is used primarily in clients with cardiogenic shock
and after open heart surgery.
• The ability of the heart to adequately pump blood is
augmented by a balloon- tipped catheter placed In the
descending thoracic aorta.
• The catheter is attached to a unit that inflates during
diastolic and deflates just before systole.
• This counterpulsation displaces blood back into the
aorta and improves coronary artery circulation.
INTRAAORTIC BALOON PUMP

115. EXTERNAL COUNTER PULSATION DEVICE
• This device uses the same general principles as an
IABP but is applied externally to the legs.
• The legs are encased in air-or-water filled tubular
bags connected to a pumping unit.
• Pressure is applied to the legs during diastolic and
is released in systole.
• A form of external counterpulsation is also being
used in the cardiac setting with clients
experiencing chronic angina, because it has been
shown in some client groups to decrease their
episodes of angina.

117. Modified Trendelenburg Position
• A client in shock is usually placed in a modified
trendelenburg position with the lower extremities elevated
30-40 degrees, the knee straight, the trunk horizontal or very
slightly raised, and the neck comfortably positioned with the
head level with chest or slightly higher.
• This position promotes increased venous return from the
lower extremities without compressing the abdominal organs
against the diaphragm.
• Elevating the legs mobilizes blood that has pooled in the
lower extremities. As a result of gravity, the additional
circulating blood increases venous return to the heart, thus
improving cardiac output.

119. PHARMACOLOGICAL MANAGEMENT
• Replace Fluid Volume: the mainstay of
hypovolemic shock therapy is expansion of
circulating blood volume by IV administered
of blood or other appropriate fluids.
• Crystalloids or balanced salt solutions
• Colloid solutions
• Blood

120. CRYSTALLOID SOLUTIONS:
 ISOTONIC :
• Normal saline: - It increases plasma volume and replaces body
fluid.
• Lactated Ringer’s solution: Increases body fluid and buffers
acidosis.
• Ringer's solution: Replaces body fluid, provides additional
potassium and calcium.
- HYPOTONIC:
• ½ Normal Saline: Raises total body volume
• 5% dextrose in water (D5W): Raises total fluid volume,
Provides 0.2 Kcal/ml.

121. COLLOID SOLUTIONS:
 PLASMA PROTEIN FRACTION: Expands
plasma volume, increases serum colloid osmotic
pressure.
 5% or 25% (salt poor) albumin: Increases plasma
colloid osmotic pressure, expands plasma volume,
25% albumin is used in patients with pulmonary
edema, peripheral edema, and hyperproteinemia.
• PLASMA EXPANDERS:
- Hetastarch (hespan): Expands plasma volume.

122. BLOOD AND BLOOD PRODUCTS:
 WHOLE BLOOD: Replaces blood volume,
provides intravascular volume
 PACKED RBCs: Increases hematocrit,
Improves oxygen- carrying capacity of blood.
 HUMAN PLASMA: Increase osmotic
pressure to improve circulating volume,
Restores plasma volume, Restore clotting
factors.

123. COMMON MEDICATIONS FOR SHOCK:
 Positive Ionotropic Drugs: Increases contractile force of
Heart.
• e.g:- Dopamine
- Dobutamine
- Amrinone
- Norepinephrine
- Drugs that affect preload: Causes vasoconstriction,
increases and decrearses venous return to heart.
• Increases preload: - Epinephrine
- norepinephrine

124. CONT…..
• Decreasing preload: - Nitroprusside
- Drugs that affect afterload: Increases vascular tone,
venous return, cardiac output
• Increasing afterload: -Dopamine
- Norepinephrine
- Phenylephrine
• Decreasing Afterload: -Nitroprusside
- Nitroglycerine

125. CONTINUE…..
Positive chronotropic agents: Increases
heart rate and force of contraction
• Atropine
• Isoproterenol

126. NURSING MANAGEMENT
 ASSESSMENT:
• The first step in assessing a person in shock is a general
overview, giving attention to airway, breathing and
circulation (ABC).
• Improve oxygenation- to determine the patency of
airway.
• Restore and maintain adequate perfusion- assess the
client’s pulse, state of hydration and skin perfusion(E.g
capillary refill time is less than 3 sec)
• Temperature monitoring

127. CONT…….
• Cardiac monitoring: the electrical activity of
the heart needs to be continuously
monitored in all clients in shock, regardless
of age.
• Hemodynamic monitoring- measurement of
CVP is one necessary.

128. NURSING DIAGNOSIS
-Ineffective tissue perfusion related to actual or
relative hypovolemia secondary to shock
Expected outcome: - adequate blood flow and cellular
oxygenation are achieved to maintain the integrity of the
tissue or organ.
- The metabolic needs of the tissue or organ are reduced.
INTERVENTIONS:
• To assess the condition of the client continuously.
• To assess the cardiovascular and respiratory changes
promptly.
• To assess the oxygenation level by placing the pulse
oximetry.

129. CONT……
• To promote rest by decreasing the total body work,
pain, anxiety and temperature to decrease the tissue
oxygen demand
• To keep the equipment and supplies (e.g. suction,
emergency drugs) available in working condition.
• To take measures for the pain reduction, because pain
intensifies shock.

130. Other Nursing Diagnosis:
 Decreased cardiac output related to decreased venous
return.
 Deficient fluid volume related to shifting of plasma
from tissue to extracellular space.
 Activity intolerance related to decreased tissue
perfusion secondary to disease condition.