Critical Care Nurse Student | Assistant Clinical Researcher | Chairperson National Nurses of Kenya-Siaya Branch | Mentor | SRHR & Boys Advocate. Young and energetic healthcare professional with a strong belief in the basic tenets of human development and quality of life. My key qualities include integrity, hardworking, team player and keenness to achieve results.

1. SHOCK
Otieno Leonard, CCN Student

2. Objectives
At the end of the session, we should be able to: -
1. Define shock
2. Differentiate (classify) categories of shock
3. Describe the stages of shock
4. Outline management principles
5. Discuss goals of fluid resuscitation

3. Definitions
Shock is a syndrome characterized
by decreased tissue perfusion and
impaired cellular metabolism
•Imbalance in supply/demand for O₂ and
nutrients

4. Definitions
Shock can be defined as a clinical syndrome of decreased
blood flow to body tissues resulting in cellular dysfunction &
eventual organ failure
• Inadequate perfusion=poor perfusion
• Inadequate tissue perfusion can result in:
• Inadequate supply of O₂ & nutrients to cells.
• widespread impairment of cellular metabolism
• tissue damage organ failure
• death

5. Classification of Shock
Classified into 3 major
Classes: -
•Blood VOLUME. problem
Hypovolemic shock
•Blood PUMP problem
Cardiogenic shock
•Blood VESSEL problem
Distributive shock

6. 1. Hypovolemic Shock
• Absolute hypovolemia: Is due to inadequate circulating blood
volume resulting from: -
 Hemorrhage with blood loss: Trauma, surgery, GI bleeding
 GI loss with of fluid volume (e.g. vomiting & diarrhea leading to dehydration)
 Excessive diuresis, Diabetes insipidus etc..
• Most common
• Develops when the intravascular volume decreases to the point
where compensatory mechanisms are unable to maintain organ and
tissue perfusion

7. Hypovolemic Shock
• Relative hypovolemia: Results when fluid volume moves out of
vascular space into extravascular space (e.g. interstitial or
intracavitary space): -
• Fluid shifts as in burns with loss of plasma proteins, Ascites
• Internal bleeding: Ruptured spleen, Hemothorax
• Massive vasodilation as in sepsis
Termed third spacing

8. Etiology/Risk factors
• d/t loss of plasma or blood
• Conditions causing critical loss of circulating blood vol. incl.
• Haemorrhage
Hypovolemic shock begins to appear with blood loss of 15-25%
(500-1500 mls)
Note: Shock fully develops when abt ⅓ of the normal circulating
blood vol. of 5l is lost

9. • Etiology/Risk factors….
• Burns
Shock occurs most often with large partial-thickness burns d/t shift
of plasma from the vascualar space into the interstitial space
• Dehydration
d/t reduced fluid intake or significant loses of fluid

10. Classification of Hemorrhagic shock

11. Hypovolemic
Clinical Manifestation
• Anxiety
• Tachypnoea d/t metabolic acidosis, pt. hyperventilates
• CO & HR
• Initially: ↑CO, ↑ HR (tachycardia with a weak thready pulse)
• Late stages: ↓CO ↓CVP
• Skin – cool, pale, clammy skin d/t peripheral vasoconstriction.
• Mental status changes

12. Cl. Manifestation Cont’d….
• Hypotension. ↓BP leads to:
• Myocardial depression d/t myocardial ischaemia which becomes
severe leading to cardiac depression resulting to ↓HR and ↓BP
• Vasomotor center depression
• Thrombosis of minute vessels d/t pooling of blood
• Acidosis as a by product of anaerobic respiration

13. Cl. Manifestation Cont’d….
• Cyanosis
• Extreme thirst d/t reduction in interstitial fluid
• Decreased urine output: dark & concentrated
*Oliguria & most probably anuria d/t poor renal perfusion)

14. Cardiogenic Shock
Is due to the inadequate pumping action of the heart
There is: -
• Systolic or diastolic dysfunction
• Systolic dysfunction: inability of the heart to pump blood forward: MI, Blunt cardiac
injury, Severe systemic or pul. Hypertension
• Diastolic dysfunction: inability of the heart to fill during diastole: pericardial
tamponade, ventricular hypertrophy
• Compromised cardiac output (CO)
Has 50-85% mortality

15. Etiology/Risk factors
Myocardial infarction
• Cardiomyopathy
• Blunt cardiac injury
• Severe systemic or pulmonary hypertension
• Obstructive Conditions
• Pericardiac tamponade, large pulmonary embolism, tension pneumothorax
• Myocardial depression from metabolic problems

16. Clinical Manifestation
• Early manifestations
• Tachycardia; Hypotension
• Narrowed pulse pressure
• ↑ myocardial O₂ consumption
• Physical examination
• Tachypnea, pulmonary congestion
• Pallor; cool, clammy skin
• Dec capillary refill time
• Anxiety, confusion, agitation
• ↑CVP
• Dec renal perfusion and UOP

17. Distributive Shock
• Decreased Systemic Vascular Resistance: Is due to changes in the
blood vessels tone that increases the size of the vascular space
without an increase in circulating blood vol. This results in a relative
hypovolemia (total fluid vol. remains same but is redistributed)
• Divided in 3 types: -
1.Anaphylactic Shock
2.Neurogenic Shock
3.Septic Shock

18. Distributive Shock
1.Anaphylactic Shock
 Mechanism: severe allergic reaction
 Defn: Is a severe hypersensitivity reaction resulting in massive systemic
vasodilatation
2.Neurogenic Shock
 Mechanism: Massive vasodilation 2◦ to loss of sympathetic tone.
 Interference with the NS control of the blood vessels, as in spinal cord
injury (esp. Cervical spine injury); Spinal anesthesia or severe vasovagal
reaction d/t pain or psychic trauma

19. Distributive Shock
3.Septic Shock
 Mechanism: overwhelming infection
 At one end of the continuum is infection.
 Presence of microorganisms stimulate the body to activate the
inflammatory response
 As inflammatory response becomes more widespread, systemic
inflammatory response develops = release of vasoactive substances
 Sepsis then progress to severe sepsis, in which the inflammatory
response, initiated to help the body, begins to have harmful effects.
 Imbalance btwn coagulation & fibrinolysis

20. Distributive Shock
Etiology/Risk factors
• Etiologies
• Sepsis (Most common)
• Sever anaphylactic reactions
• Neurogenic shock
• Mechanism
• Results from inadequate vascular tone but blood vol. remains
normal.
• Size of the vascular space increases d/t massive vasodilation resulting
to maldist.

21. Distributive Shock
Pathophysiology of anaphylactic shock.
Acute and life threatening hypersensitivity reaction resulting from:-
antigen exposure. The body is stimulated to produce immunoglobuline
E antibodies specific to antigen such drugs, bites, contrast, blood, food
and vaccines.
Reexposure to antigen, IgE binds to mast cells and basophils.

22. Patho…..

23. Cl. Manifestation of Anaphylactic Shock...
 Almost immediate response to inciting antigen.
Anxiety, confusion, dizziness
 Cutaneous manifestations.
urticaria, erythema, pruritis, swelling of the lips and tongue, angioedema
 Respiratory compromise.
stridor, wheezing, resp. distress
Sense of impending doom, Chest pain
 Circulatory collapse
tachycardia, vasodilation, hypotension.

24. Cl. Manifestation of Neurogenic Shock.
*Hypotension
*Bradycardia
• Temperature dysregulation (resulting in heat loss)
• Dry skin
• Poikilothermia (taking on the temp. of the environment).

25. Pathophysiology of Septic Shock
• Sepsis: systemic inflammatory response to confirmed or suspected
infection
• Severe sepsis = Sepsis + Organ dysfunction -Presence of sepsis, organ
dysfunction, hypoperfusion begins
-Hypotension despite adequate fluid resuscitation
-Presence of tissue perfusion abnormalities
-Lactic acidosis
-MODS
-Most common cause of ICU death.

26. Clinical Manifestation of Septic Shock
2 phases: -
“Warm” shock - early phase
•hyperdynamic response, Vasodilation
“Cold” shock - late phase
•hypodynamic response
•Decompensated State

27. Distributive shock
Cl. Manifestation of Septic Shock….
Early: Hyperdynamic State-compensation
• Massive vasodilation
• Pink, warm, flushed skin
• Increased HR; full bounding
pulse
• Tachypnea; hyperventilation
• ↑ Coagulation and
inflammation; ↓ fibrinolysi
• Formation of microthrombi:
obstruction of
microvasculature
• Decreased SVR*
• ↑ CO (because pt has ↑HR d/t
fever & ↑metabolism
• SVO₂ will be abnormally high
• Temperature dysregulation;
chills
• ↓ urine output
• Crackles
• Nausea and vomitting

28. Cl. Manifestation of Septic Shock….
.
• Vasoconstriction
• Skin is pale & cool
• Significant tachycardia
• ↓ BP
• Altered neurologic status
(change in LOC)
• Increase SVR
• ↓ CO
• ↓ UOP
• GI dysfunction
• Respiratory failure common.
• Metabolic & respiratory
acidosis with hypoxemia
• Leucocytosis in septic shock,
abnormal bleeding time
Late: Hypodynamic State-Decompensation

29. Stages of Shock
Note: -
• A mean arterial pressure (MAP) of 80-120 mmHg is needed for cells to
receive the oxygen and nutrients needed to metabolize energy in amnts
sufficient to sustain life.
• The body has compensatory mechanisms to assist in maintaining this MAP
in response to changes in volume, pumping ability of the heart and
changes in the vascular system.
• As long as these mechanisms are effective, the body can survive the
changes. When these mechanisms fail, tissues are inadequately perfused &
shock begins

30. Stages of shock
• Shock is a continuum that progresses from reversible to irreversible
• The events are grouped into 4 stages
I – Initial Stage
II – Compensation Stage (“Pre-shock”)
III – Decompensation/Progressive Stage (“Shock”)
IV– Refactory/Irreversible Stage (“End-organ failure”)

31. Stages of shock
I – Initial Stage
Body is able to compensate for ↓perfusion
• Usually not clinically apparent; No visible changes
• Tissues are under perfused
• CO is decreased d/t loss of actual or relative blood vol. and tissue
perfusion is impaired.
• MAP decreased less than 10mm Hg. Compensation is effective.

32. Stages of shock
Initial Stage Cont’d…..
• As the blood supply to the cells decreases, metabolism changes from
aerobic to anaerobic.
• Lactic acid accumulates - must be removed by blood and broken down by
liver.
• Process requires supplemental O₂.

33. Stages of shock
II – Compensation Stage
• Once the BP goes low, the body will start the compensatory
mechanism so as to maintain BP within a normal range or low
normal range so as to maintain tissue perfusion to the vital organs
• Body’s primary goal is to maintain blood flow to heart & brain
through vasoconstriction (epinephrine ) & shunting to vital
organs. Anaerobic metabolism occurs

34. Stages of shock
Compensation Stage….
• Clinically apparent – Neural, hormonal & biochemical compensatory
mechanisms as the body employs these mechanisms in an attempt to
reverse the condition
* Attempts aimed to overcome consequences of anaerobic
metabolism & maintaining homeostasis

35. Stages of shock
Compensation Stage……
The mechanism consists of: -
1. Hyperventilation to neutralize lactic acidosis:
 As a result of 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

36. Stages of shock
Compensation Stage…..
2.Release of catecholamines causing vasodilation of coronary arteries
and vasoconstriction of periphery.
• Vasodilation of coronary arteries aims in improving O₂ supply to the
heart muscles
• Vasoconstriction of periphery aims at improving the BP

37. Stages of shock
Compensation Stage…..
3.Baroreceptors reflexes
Baroreceptors in carotid and aortic bodies activate SNS in response to
↓ BP.
SNS stimulation: -
 ↑HR
 increases myocardial O₂ demands
 Vasoconstriction (d/t epinephrine & norepinephrine release) while blood
shunted to vital organs

38. Stages of shock
Compensation Stage…..
Baroreceptors reflexes Cont’d….
 Shunting blood from lungs increases physiologic dead space.
• ↓ arterial O₂ levels
• Increase in rate/depth of respirations
• V/Q mismatch

39. Stages of shock
Compensation Stage…..
4.Renin-Angiotensin-Aldosterone mechanism
• ↓ bld to kidneys > activates renin– angiotensin system – ↑
venous return to heart, CO, BP
Vasoconstriction of the afferent and efferent vessels of the kidney –
aims at ↓ amt H₂O of being lost in urine d/t little blood being subjected
to kidneys

40. Stages of shock
Compensation Stage…..
5.CNS Ischaemic Response:
This is where the MAP go below 50mmHg. It stimulates the
vasomotor centre and as a result of the stimulation, there is
generalized vasoconstriction. This is also aided by PCO₂ values of 50-
60mmHg

41. Stages of shock
Compensation Stage…….
6.Antidiuretic Hormone (ADH)
• Osmoreceptors in hypothalamus stimulated
• ADH released by Posterior pituitary gland. Its function is to prevent
excretion of H₂O
 Acts on renal tubules to retain H₂O: It causes re-absorption of H₂O in
the DCT
 Has vasopressor effect: causes vasoconstriction and an increase BP

42. Stages of shock
Compensation Stage…….
7.Stimulation of anterior pituitary release Adrenocorticotropic
hormone (ACTH).
• ACTH stimulates prodn. of glucorticoids, which raises glucose
levels
• Blood glucose increases to meet increased metabolic needs

43. Stages of shock
Compensation Stage
8.Fluid shift =Capillary fluid shift.
↓CO – ↓Blood flow to capillaries – ↓Hydrostatic pressure – in an
attempt to equalize pressure, fluid shift from interstitial space into
the vascular compartment – ↑blood vol.

44. Stages of shock
III – Decompensation/Progressive Stage
• Compensatory mechanisms overwhelmed
• The body's compensatory responses are no longer sufficient to maintain
systolic and diastolic pressure at normal level (body begins to lose its
ability to compensate)
• Begins when compensatory mechanisms fail
 Inadequate perfusion begins---cont’d vasoconstriction --- ↓ O₂ supply to
tissues --- Anaerobic metabolism ---Lactic Acidosis ---Acidosis and ↑ PCO₂
cause vessels to dilate --- ↓venous return and ↓ circulation of O₂.

45. Stages of shock
Decompensation/Progressive Stage…..
• Note:
There is need for aggressive interventions to prevent multiple organ
dysfunction syndrome (MODS)
• Hallmarks -↓ cellular perfusion & altered capillary
permeability
• Leakage of protein into interstitial space
• ↑ systemic interstitial edema

46. Stages of shock
Decompensation/Progressive Stage…….
• Mov’nt of fluid from pulmonary vasculature to interstitium
 Pulmonary edema
 Bronchoconstriction
 ↓ Residual capacity
• Fluid moves into alveoli
 Edema-Dec surfactant
 Worsening V/Q mismatch
 Tachypnea, Crackles
 Inc work of breathing

47. Stages of shock
Decompensation/Progressive Stage….
• CO begins to fall
 Dec peripheral perfusion
 Hypotension
 Weak peripheral pulses
 Ischemia of distal extremities
• Myocardial dysfunction results in
 Dysrhythmias
 Ischemia: Myocardial infarction
 End result: complete deterioration of CVS

48. Stages of shock
Decompensation/Progressive Stage…..
• Liver fails to metabolize drugs and waste.
 Jaundice; Elevated enzymes
 Loss of immune function
 Risk for DIC and significant bleeding
• Mucosal barrier of GI system becomes ischemic
 Ulcers
 Bleeding
 Risk of translocation of bacteria
 Dec ability to absorb nutrients

49. Stages of shock
IV – Refractory/Irreversible Stage
• End-organ dysfunction
• Tissue perfusion is negligible= anaerobic metabolism.
• Shock becomes severe (Profound hypotension & hypoxaemia)
• Acidosis is prevalent (acc. of lactic acid)
• Cellular ischaemia & necrosis occur d/t lack of O₂
• Irreversible cell and tissue damage
• ↑ capillary permeability
• Massive DIC
• Multi-system organ failure death

50. Diagnostic Studies
• Thorough Hx and P/E
• Blood studies
• Hemodynamic monitoring

51. Collaborative Management
General Management
• General management strategies
• Ensure patent airway.
• Maximize oxygen delivery
• 100% O₂ via a non re-breather mask
• Assist ventilations if necessary
• Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock =
Volume expansion
• Gain IV access
• Isotonic crystalloids (e.g., NS or LR) for initial resuscitation of shock
• Fluid replacement is calculated using a 3:1 rule

52. mgt
General Management Cont’d…
• Volume expansion: If patient does not respond to 2 to 3ltrs of crystalloids, blood
administration & central venous monitoring may be instituted.
• Perform focused assessment
• Position patient to assist perfusion
• Keep patient warm
• Monitor and adjust O₂, cardiac monitor, pulse oximetry

53. Mgt…….
General Management Cont’d…
• Drug therapy = Primary goal is correct decreased tissue perfusion
• Vasopressor drugs
• Achieve/maintain MAP > 60mm Hg.
• Reserved for pts unresponsive to fluid resuscitation
• Vasodilator therapy (e.g. nitroglycerin, nitroprusside)
• Achieve/maintain MAP > 65 mm Hg.

54. Mgt……..
Specific Medical Management
I) Hypovolemic shock
• Management focuses on stopping loss of fluid and restoring
circulating volume
• Fluid replacement is calculated using a 3:1 rule (3 mL of isotonic
crystalloid for every 1 mL of estimated blood loss)
• IVFs: Excessive use of fluids avoided to prevent
haemodilution
• Give plasma expanders: Blood, albumin

55. Mgt
Hypovolemic shock Cont’d…
– Respiratory Support: Maintain adequate ventilation and
where need be, then pt put on mechanical ventilation
– Position: Elevate the legs, leave the trunk flat, and elevate
head and shoulders slightly
– Critical monitoring:
• IVFs and Electrolytes -Urine out r/o impaired
• Acid base balance –do BGAs renal function

56. mgt
II) Cardiogenic shock
• Treatment requires an aggressive approach
• The major goals of therapy is to: -
• Treat the underlying cause
• Enhance the effectiveness on the pump
• Improve tissue perfusion
• Identify the etiologic factors of pump failure.

57. mgt
Cardiogenic shock Cont’d….
• Administer pharmacologic agents to enhance CO
 Give inotropics to increase contractility and vasoconstrictors (vasoactive
agents): Dopamine, Dobutamine, Isopreteronol, Digoxin
 Give Calcium chloride/gluconate
 Give Sodium Nitroprosside (Nipride) if peripheral resistance is high,
↓arterial pressure
 Give adrenaline and atropine incase of bradycardia

58. mgt
Cardiogenic shock Cont’d….
• Valve replacement
• Hemodynamic monitoring
• Diuretics
• Circulatory assist devices (e.g., intra-aortic balloon pump)

59. mgt
Anaphylactic shock
• Maintaining patent airway:
• Nebulized bronchodilators
• Endotracheal intubation
• Give Epinephrine
• Aggressive fluid replacement
• IVF resuscitation with N/saline
• Steroids I.V to reduce oedema
• IV Aminophylline for broncospasms
• Vasopressors to constrict blood vessels and raise BP e.g.. Dopamine

60. mgt
Septic shock
• C/S: Blood, wound exudates, urine etc
• Fluid replacement to restore perfusion
• IVF resuscitation with N/saline
• Hemodynamic monitoring
• Medications and other treatment
 Antibiotics (after cultures are obtained)
• Penicillin, Vancomycin, Cephalosporin
 Inotropics & Vasopressors
 IV Corticosteroids
 Low dose heparin (for DVT prophylaxis)
 Blood Transfusion

61. mgt
Neurogenic shock
• Specific Tx depend on the cause
• Positioning
• IVF resuscitation with N/saline
*Fluids used cautiously as hypotension generally is not related to fluid loss
• Medications
 Atropine for bradycardia
 Vasopressors to raise BP
 Analgesics for pain

62. Nursing Management
Assessment
• ABCs: airway, breathing, and circulation
• Perform focused assessment of tissue perfusion
• Vital signs
• Peripheral pulses
• Level of consciousness
• Capillary refill
• Skin (e.g., temperature, color, moisture)
• UO
• Brief Hx: Events leading to shock, onset & duration of s/sx
• Details of care given prior to admission

63. Nursing Management
Diagnosis
•Ineffective Tissue Perfusion: renal, cerebral,
cardiopulmonary, GI, hepatic, and peripheral
•Decreased Cardiac Output r/t alterations in contractility and
heart rate; sympathetic blockade
•Fluid Volume Deficit r/t relative loss
•Anxiety r/t biologic, psychologic or social integrity
•Fear

64. Nursing Management
Diagnosis Cont’d…
• Imbalanced nutrition: less than body requirements r/t increased
metabolism.
• Risk for Injury
• Risk for Infection
•Potential complication: organ ischemia/ dysfunction
• Compromised family coping related to critically ill family member

65. Nursing Management
Planning
• Goals
• Assurance of adequate tissue perfusion
• Restoration of normal or baseline BP
• Return/recovery of organ function
• Avoidance of complications from prolonged states of hypoperfusion

66. Nursing Management
Planning Cont’d…
• Interventions
* Plan and implement nursing interventions & therapy
• Assess the neurologic status: orientation & level of consciousness
• Maintain a patent airway
• Assess cardiac status: -
• Continuous ECG, VS, capillary refill, haemodynamic parameters-CVP e.t.c, Heart
sounds

67. Nursing Management
Planning Cont’d…
• Interventions Cont’d…
• Assess the respiratory status: -
• RR & rhythm, Breath sounds, continuous pulse oximetry,
ABGs.
• Note: Most patients will be intubated and mechanically
ventilated.
• Gain IV access: Large bore vascular access
• Maximize O₂ delivery: Supplemental O₂ therapy
• Fluid replacement – Crystalloid infusions

68. Nursing Management
Interventions
• Vasopressors
• Prevent heat loss ( warmed IV fluids) , Keep pt warm
• Nutritional Support
• Comfort & Emotional support

69. Complications
• Adult respiratory Syndrome: Shocked lung – there is an increase in
resistance to blood flow with hypoxia with interstitial lung oedema
• Renal Failure d/t poor perfusion leading to ischaemia – Acute tubular
necrosis
• Cardiac Failure – Myocardial injury and infarction leading to reduced
contractility

70. Complications
• Liver dysfunction
• DIC (Disseminated Intravascular Coagulopathy) where clotting &
bleeding factors are destroyed
• Cerebral infarction d/t poor supply with O₂

71. References
• Linda D. Urden, Kathleen M. Stacy, Mary E lough: Thelan’s Critical
Care Nursing, 8th Edition 2013 (437-446)
• Medical Surgical Nursing, Brunners and Suddarth text 12th edition.
• Critical Care Critical Care Notes Clinical Pocket Guide 2nd Edition

72. end
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