Shock is defined as inadequate tissue perfusion resulting in decreased oxygen delivery and buildup of waste, and can progress from early compensated stages to intermediate stages involving organ damage and late irreversible stages involving multiple organ failure. The document outlines the pathophysiology and stages of shock including effects on body systems, clinical markers, causes, and treatment focusing on restoring tissue perfusion through fluid resuscitation and management of the underlying cause.

1. SHOCK

2. Definition
Shock is a state of inadequate perfusion, which does not
sustain the physiologic needs of organ tissues.
A physiological state characterized by a significant,
systemic reduction in tissue perfusion, resulting in decreased
tissue oxygen delivery and insufficient removal of cellular metabolic
products, resulting in tissue injury.

3. SRUP
• Inadequate tissue perfusion
• Decreased oxygen supply
• Anaerobic metabolism
• Accumulation metabolic waste

4. Pathophysiology
Alteration in hemodynamic results in a drop in arterial blood
pressure by one of these mechanisms:
• Decrease in cardiac output (ability of heart to supply adequate
circulation)
• Decrease in circulating blood volume
• Increase in size of vascular bed

6. Vicious cycle of shock

7. Stage of shock

8. Early reversible and compensatory shock
• Mean arterial pressure drops 10 -15 mmHg
• Decrease in circulating blood volume (25-35%) 1000ml
• Sympathetic nervous system stimulated; release of
catecholamine

9. Early reversible and compensatory shock
Findings
• Increase in heart rate and contractility
• Increase in peripheral vasoconstriction
• Circulation maintained, but can only be sustained short time
without harm to tissues
• Underlying cause of shock must be addressed and corrected or
will progress to next stage

10. Intermediate or progressive shock
• Further drop in MAP (20%)
• Increase in fluid loss (1800 – 25400 ml)
• Vasoconstriction continues and leads to oxygen deficiency
• Body switches to anaerobic metabolism forming lactic acid as a
waste product

11. Intermediate or progressive shock
Findings
• Body increases heart rate and vasoconstriction
• Heart and brain become hypoxic
• More severe effects on other tissues which become: ischemic
and anoxic
• State of acidosis with hyperkalemia develops
Needs rapid treatment

12. Refractory or irreversible shock
• Tissues are anoxic, cellular death widespread
• Even with restoration of blood pressure and fluid volume there is
too much damage to restore homeostasis of tissues
• Cellular death leads to tissue death; vital organs fail and death
occurs

13. Effects of Shock on
Body Systems

14. Cardiovascular system
• Initially: slight tachycardia, normal blood pressure
• Progresses to weak, rapid pulse with dysrhythmias
• Progressive decrease in systolic and diastolic blood pressures
with narrowing of pulse pressure; blood pressure becomes
inaudible

15. Respiratory system
• Initially: Increased respiratory rate, but gas exchange is
impaired; leads to anaerobic metabolism and development of
acidosis
• Acute Respiratory Distress Syndrome (ARDS): complication of
decreased lung perfusion

16. Gastrointestinal and Hepatic
• GI organs become ischemic, with blood circulation shunted to
heart and brain
Complications :
• Stress Ulcers
• Paralytic Ileus
• Altered liver metabolism: hypoglycemia, fat breakdown leads to
ketones and metabolic acidosis

17. • Neurologic system
Develops cerebral hypoxia
Restlessness initially, then altered level of consciousness,
lethargy, coma ,Thirsty from dehydration
• Renal
Decreased kidney perfusion leads to oliguria (urine output
< 0.5 ml/kg/hr)
• Skin
Skin: cool, pale, hypothermic

18. Causes of Shock [-]
• Severe or sudden blood loss
• Large drop in body fluids
• Myocardial infarction
• Major infections
• High spinal injuries
• Anaphylaxis
• Extreme heat or cold

19. Clinical Markers of Shock
• Brachial systolic blood pressure: < 110mmHg
• Sinus tachycardia: > 90 beats/min
• Respiratory rate: < 7 or > 29 breaths/min
• Urine Output: < 0.5 cc/kg/hr
• Metabolic acidemia: [HCO3] < 31mEq/L or base deficit >
3mEq/L
• Hypoxemia: 0-50yr: < 90 mmHg; 51-70 yr: < 80mmHg; > 71yo <
70mmHg
• Cutaneous vasoconstriction vs. vasodilatation.
• Mental Changes: anxiousness, agitation, indifference, lethargy,
obtundation

20. Classification of Shock
• Hypovolemic shock
• Septic/Inflammatory shock
• Cardiogenic shock
• Neurogenic shock
• Anaphylactic shock
• Obstructive shock
• Traumatic shock

21. Hypovolemic Shock
A medical or surgical condition in which rapid fluid loss
results in multiple organ failure due to inadequate circulating
volume and subsequent inadequate perfusion. Most often,
hypovolemic shock is secondary to rapid blood loss
(hemorrhagic shock).

22. SRUP
• Hemorrhage: Overt or occult
• Reduction in circulating volume
• Reduction in venous return and CO
• O2 supply-demand imbalance
• Lactic acidosis
• Reduction in venous oxygen saturation
• Non hemorrhagic hypovolemic
– Severe burns, vomiting and diarrhea

23. • Decreased preload->small ventricular end-diastolic volumes ->
inadequate cardiac generation of pressure and flow
• Causes:
-- bleeding: trauma, GI bleeding, ruptured aneurysms,
hemorrhagic pancreatitis
-- protracted vomiting or diarrhea
-- adrenal insufficiency; diabetes insipidus
-- dehydration
-- third spacing: intestinal obstruction, pancreatitis, cirrhosis

26. Cause
• Acute external blood loss secondary to penetrating trauma and severe GI
bleeding disorders are 2 common causes of hemorrhagic shock.
• Hemorrhagic shock can also result from significant acute internal blood
loss into the thoracic and abdominal cavities
• Two common causes of rapid internal blood loss are solid organ injury
and rupture of an abdominal aortic aneurysm.
• Hypovolemic shock can result from significant fluid (other than blood)
loss. Two examples of hypovolemic shock secondary to fluid loss include
refractory gastroenteritis and extensive burns

27. Pathophysiology:
• The human body responds to acute hemorrhage by activating
the following major physiologic systems:
• The hematologic
• Cardiovascular
• Renal
• Neuroendocrine systems.

28. The hematologic
• The hematologic system responds to an acute severe blood loss
by activating the coagulation cascade and contracting the
bleeding vessels (by means of local thromboxane A2 release).
• In addition, platelets are activated (also by means of local
thromboxane A2 release) and form an immature clot on the
bleeding source.
• The damaged vessel exposes collagen, which subsequently
causes fibrin deposition and stabilization of the clot.
• Approximately 24 hours are needed for complete clot fibrination
and mature formation.

29. Cardiovascular
• The cardiovascular system initially responds to hypovolemic
shock by increasing the heart rate, increasing myocardial
contractility, and constricting peripheral blood vessels.
• This response occurs secondary to an increased release of
norepinephrine and decreased baseline vagal tone (regulated
by the baroreceptors in the carotid arch, aortic arch, left atrium,
and pulmonary vessels).
• The cardiovascular system also responds by redistributing
blood to the brain, heart, and kidneys and away from skin,
muscle, and GI tract.

30. Renal
• The renal system responds to hemorrhagic shock by stimulating an
increase in renin secretion from the juxtaglomerular apparatus.
• Renin converts angiotensinogen to angiotensin I, which subsequently is
converted to angiotensin II by the lungs and liver
• Angiotensin II has 2 main effects, both of which help to reverse
hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and
stimulation of aldosterone secretion by the adrenal cortex.
• Aldosterone is responsible for active sodium reabsorption and
subsequent water conservation.

31. Neuroendocrine systems
• The neuroendocrine system responds to hemorrhagic shock by
causing an increase in circulating antidiuretic hormone (ADH).
• ADH is released from the posterior pituitary gland in response to
a decrease in BP (as detected by baroreceptors) and a
decrease in the sodium concentration (as detected by
osmoreceptors).
• ADH indirectly leads to an increased reabsorption of water and
salt (NaCl) by the distal tubule, the collecting ducts, and the
loop of Henle.

32. Clinical Signs of Acute Hemorrhagic
Shock
Parameter Class I Class II Class III Class IV
Blood loss (%) <15 15-30 30-40 >40
Blood loss (ml) <750 750-1500 1500-2000 >2000
Heart rate (bpm) <100 >100 >120 >140
Blood pressure Normal Orthostatic Hypotension Severe hypotension
CNS symptom Normal Anxious Confused Obtunded

33. Signs of Shock
• Cold, clammy and pale skin
• Rapid, weak pulse
• Shallow, rapid breathing
• Oliguria
• Reduction in MAP
• Cyanosis
• Loss of consciousness

34. The 4 areas in which life-threatening
hemorrhage can occur are as follows: chest,
abdomen, thighs, and outside the body.

35. • The chest should be auscultated for decreased breath
sounds, because life-threatening hemorrhage can occur
from myocardial, vessel, or lung laceration
• The abdomen should be examined for tenderness or
distension, which may indicate intraabdominal injury

36. • The thighs should be checked for deformities or
enlargement (signs of femoral fracture and bleeding into
the thigh).
• The patient's entire body should then be checked for
other external bleeding

37. • Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lactic acid
and PCWP
• Treatment: ABCs, IVF (crystalloid), Transfusion Stem ongoing
Blood Loss

38. Treatment of Shock
**Increase tissue perfusion and oxygenation status
• Maintain airway
• Control bleeding
• Baseline vital signs
• Level of consciousness

39. Treatment of Shock
• Positioning
• ABCD approach
• Fluid therapy
• Drug therapy
• Keep patient at normal temperature
– Prevent hypothermia
– Minimize effect of shock
• On-going assessment - every 10-15 minutes

40. • Crystalloid solutions for intravascular volume replenishment are
typically isotonic (e.g. 0.9% saline or Ringer's lactate [RL]).
• Both 0.9% saline and RL are equally effective; RL may be
preferred in hemorrhagic shock because it somewhat minimizes
acidosis.

41. • Colloid solutions (e.g. hydroxyethyl starch, albumin, dextrans)
are also effective for volume replacement during major
hemorrhage.
• Despite theoretical benefits over crystalloid, no differences in
survival have been proven.
• Both dextrans and hydroxyethyl starch adversely affect
coagulation when > 1.5 L is given.

42. • Blood typically is administered as packed RBCs, which should
be cross-matched, but in an urgent situation, 1 to 2 units of type
O Rh-negative blood is an acceptable alternative.
• When > 1 to 2 units are transfused (e.g. in major trauma), blood
is warmed to 37° C.
• Patients receiving > 8 to 10 units may require replacement of
clotting factors with infusion of fresh frozen plasma or
cryoprecipitate and platelet transfusion

43. Route and Rate of Administration
• Standard, large (eg, 14- to 16-gauge) peripheral IV catheters are
adequate for most fluid resuscitation.
• With infusion pump they typically allow infusion of 1 L of
crystalloid in 10 to 15 min and 1 unit of packed RBCs in 20 min.

44. • For patients at risk of exsanguination, a large (eg, 8.5 French)
central venous catheter provides more rapid infusion rates; a
pressure infusion device can infuse 1 unit packed RBCs in < 5
min.

45. • Patients in shock typically require and tolerate infusion at the
maximum rate. Adults are given 1 L of crystalloid (20 mL/kg in
children) or, in hemorrhagic shock, 5 to 10 mL/kg of colloid or
packed RBCs, and the patient is reassessed.
• An exception is a patient with cardiogenic shock who typically
does not require large volume infusion.

46. Specific measures
• Hypovolaemia: Blood transfusion
• Electrolyte/acid base imbalance
• Sepsis: Antibiotics, ?steroids
• Neurogenic: Steroids
• Anaphylactic: Adrenalin

47. Invasive monitoring
• Essential in the definitive treatment
• Direct arterial pressure
• Central venous pressure
• Cardiac output

48. • The actual endpoint of fluid administration in shock is
normalization of DO2.
• However, this parameter is not often measured directly.
Surrogate endpoints include clinical indicators of end organ
perfusion and measurements of preload.
• Adequate end organ perfusion is best indicated by urine output
of > 0.5 to 1 mL/kg/h

49. • Heart rate, mental status, and capillary refill may be affected by
the underlying disease process and are less reliable markers.
• Because of compensatory vasoconstriction, mean arterial
pressure (MAP) is only a rough guideline; organ hypoperfusion
may be present despite apparently normal values

50. • Because urine output does not provide a minute-to-minute
indication, measures of preload may be helpful in guiding fluid
resuscitation for critically ill patients
• Central venous pressure (CVP) is the mean pressure in the
superior vena cava, reflecting right ventricular end-diastolic
pressure or preload.

51. • Normal CVP ranges from 2 to 7 mm Hg (3 to 9 cm H20). A sick
or injured patient with a CVP < 3 mm Hg is presumed to be
volume depleted and may be given fluids with relative safety.

52. Septic shock

53. Criteria for Four Categories of the Systemic
Inflammatory Response Syndrome
1. Systemic Inflammatory Response Syndrome (SIRS)
Two or more of the following:
– Temperature (core) >38°C or <36°C
– Heart rate >90 beats/min
– Respiratory rate of >20 breaths/min for patients spontaneously ventilating or a
PaCO2 <32 mm Hg
– White blood cell count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature
(band) cells in the peripheral blood smear

54. Criteria for Four Categories of the Systemic
Inflammatory Response Syndrome
2. Sepsis
Same criteria as for SIRS but with a clearly established focus of infection
3. Severe Sepsis
Sepsis associated with organ dysfunction and hypoperfusion
Indicators of hypoperfusion:
- Systolic blood pressure <90 mmHg
- > 40 mmHg fall from normal systolic blood pressure
- Lactic acidemia
- Oliguria
- Acute mental status changes

55. Phases of Septic Shock
• Warm Phase (early): skin flushed, warm due to vasodilatation
• Cold Phase (late): skin cool due to fluid deficit with shock

56. Sign & symptom
• Lactic acidosis • Oliguria
• Renal failure • Hypotension
• Altered mentation • Decrease cardiac output
• DIC • Hypoxia
• Respiratory failure
• Bleeding

57. Risk factors
– Diabetes
– Diseases of the genitourinary system, biliary system, or intestinal system
– Immunocompromised host such as AIDS , Leukemia , steroid medications
– Indwelling catheters
– Recent surgery or medical procedure

58. Septic Shock in trauma patients
• Develops 2 - 5 days after injury occurs
• Carries a poor prognosis
• Assess for:
– Penetrating abdominal injuries
– Signs of infection
– Warm pink skin and dry elevated body temperature
– Tachycardia
– Wide pulse pressures

59. Septic shock management

61. Anaphylactic shock

62. Anaphylactic shock
• DEFINITION
– Anaphylaxis is a sudden-onset, life-threatening type I hypersensitivity
• Anaphylaxis results from sudden release into the systemic circulation of histamine,
tryptase, and other inflammatory mediators from basophiles and mast cells.

63. Diagnosis
• Anaphylaxis remains a clinical diagnosis
• directly challenging the patient with the suspected agent

64. CLINICAL PRESENTATION

65. Management of anaphylaxis
• Assessment of airway, breathing, circulation
• Epinephrine is the drug of choice
– IM every 5 to 15 minutes to control symptoms and blood pressure
• Oxygen administration
• Fluid replacement
– Normal saline is preferred, because lactated Ringers may contribute to metabolic
acidosis

66. • Vasopressors
– should be administered if epinephrine injections fail to alleviate hypotension
– Dopamine increases the force and rate of myocardial contractions while
maintaining or enhancing renal and mesenteric blood flow
• Antihistamines
• Inhaled B2 agonists
• Corticosteroids

67. References
• Schwartz’s .Principle of surgery.8th edition
• Sabiston.Textbook of surgery.18th edition
• ตาราศัลยศาสตร์ .คณะแพทยศาสตร์ จฬาลงกรณ์มหาวิทยาลัย พิมพ์ครังที่ 11
ุ ้
• สรี รวิทยา 2.คณะแพทยศาสตร์ ศิริราชพยาบาล

68. Anaphylactic Shock
• Rapid onset
• Primary systems:
– Cardiovascular, Respiratory
– Skin, Gastrointestinal, coagulation
• Face, pharynx and laryngeal oedema
• Adrenaline is life saving

69. Anaphylactic Shock
• Diffuse vasodilatation
• Increase size of vascular bed
• Blood is trapped in small vessels and viscera
• Temporary loss in total circulatory volume
• Sudden severe allergic reaction to:
– Drugs, Toxins, Foods, Plants

70. Symptoms
• Apprehension and flushing
• Wheezing or shortness of breath & cough
• Rapid, weak pulse
• Cyanosis
• Generalized itching or burning
• Watering and itching of the eyes
• Hypotension
• Coma

71. Evaluation of Shock
• Internal or external hemorrhage
• Underlying cardiac problems
• Sepsis
• Trauma to spine cord
• Contact with known allergic substance
• Determine amount of blood loss
• How long has casualty been bleeding?

72. Obstructive Shock

73. Obstructive Shock
•Tension pneumothorax
•Air trapped in pleural space with 1 way valve, air/pressure builds up
•Mediastinum shifted impeding venous return
•Chest pain, decreased breath sounds
•Rx: Needle decompression, chest tube

74. Obstructive Shock
•Cardiac tamponade
•Blood in pericardial sac prevents venous return to and contraction of
heart
•Related to trauma, pericarditis, MI
•Beck’s triad: hypotension, muffled heart sounds, JVD
•Diagnosis: large heart CXR, echo
•Rx: Pericardiocentisis

75. Treatment
• airway and ventilation
• fluid resuscitation and restoration of
intravascular volume
• vasoconstrictors will improve peripheral
vascular tone, decrease vascular
capacitance, and increase venous return
• dopamine
• phenylephrine

76. • Management of acute spinal cord injury
-blood pressure
-oxygenation
-hemodynamics

77. Obstructive Shock
•Pulmonary embolism
•Virscow triad: hypercoaguable, venous injury, venostasis
•Signs: Tachypnea, tachycardia, hypoxia
•Rx: Heparin, thrombolytics

78. Obstructive Shock
•Aortic stenosis
•Resistance to systolic ejection causes decreased cardiac function
•Chest pain with syncope
•Systolic ejection murmur
•Diagnosed with echo
•Rx: Valve surgery

79. Etiology & Hemodynamic Changes in Shock
Etiology of shock example CVP CO SVR VO2 sat
preload hypovolemic low low high low
contractility cardiogenic high low high low
afterload Hyperdynamic Low/Hi High Low High
Septic gh
Hypodynamic Low/Hi Low High Low/High
Septic gh
Neurogenic Low Low Low Low
Anaphylactic Low Low Low Low