Management of shocks, types, stages, mechanisms, hypovolemic shock, cardiogenic shock, septic shock, neurogenic shock, anaphylactic shock, hypogeneric shock, traumatic shock, compensated shock, decompensated shock, progressive shock, stages of shock, clinical complications, manifestations, pharmacology

1. Types of Shocks
Mr. Jaineel R Dharod
Dept. of Pharmacology
Pathophysiology of

2. Introduction
 Shock is a life-threatening clinical syndrome of cardiovascular
collapse characterised by:
 an acute reduction of effective circulating blood volume
(hypotension);
 and an inadequate perfusion of cells and tissues
(hypoperfusion).
 If uncompensated, these mechanisms may lead to impaired
cellular metabolism and death.

3. Definition
 Thus, by definition “true shock” is a circulatory imbalance
between oxygen supply and oxygen requirements at the
cellular level, and is also called as circulatory shock.

4.  The term “initial (or primary) shock” is used for transient
and usually a benign vasovagal attack resulting from sudden
reduction of venous return to the heart caused by neurogenic
vasodilatation and consequent peripheral pooling of blood e.g.
immediately following trauma, severe pain or emotional
overreaction such as due to fear, sorrow or surprise.
Characteristics

5. Clinical signs
 Clinically, patients of primary shock suffer from the attack
lasting for a few seconds or minutes and develop brief
unconsciousness, weakness, sinking sensation, pale and
clammy limbs, weak and rapid pulse, and low blood pressure.
 Another type of shock which is not due to circulatory
derangement is anaphylactic shock from type 1 immunologic
reaction

7. Classification
of
Shocks

8. Classification of Shock
1. HYPOVOLAEMIC SHOCK
2. CARDIOGENIC SHOCK
3. SEPTIC SHOCK
4. OTHER TYPES:
a) Traumatic shock
b) Neurogenic shock
c) Hypoadrenal shock

9. General
Pathophysiology

10. General Pathophysiology
In general, all forms of shock involve following 3 derangements:
A. Reduced effective circulating blood volume.
B. Reduced supply of oxygen to the cells and tissues with
resultant anoxia.
C. Inflammatory mediators and toxins released from shock
induced cellular injury.

11. As a Result
 These derangements initially set in compensatory mechanisms
(discussed below) but eventually a vicious cycle of cell injury
and severe cellular dysfunction lead to breakdown of organ
function

12. 1 Reduced effective circulating blood volume.
It may result by either of the following mechanisms:
i. by actual loss of blood volume as occurs in hypovolemic
shock; or
ii. by decreased cardiac output without actual loss of blood
(normovolaemia) as occurs in cardiogenic shock and septic
shock.

13. 2 Impaired tissue oxygenation
 Following reduction in the effective circulating blood volume
from either of the above two mechanisms and from any of the
etiologic agents, there is decreased venous return to the
heart resulting in decreased cardiac output.
 This consequently causes reduced supply of oxygen to the
organs and tissues and hence tissue anoxia, which sets in
cellular injury.

14. 3 Release of inflammatory mediators
 In response to cellular injury, innate immunity of the body gets
activated as a body defence mechanism and release
inflammatory mediators but eventually these agents themselves
become the cause of cell injury.
 Several pro-inflammatory inflammatory mediators are released
from monocytes-macrophages, other leucocytes and other body
cells, the most important being the tumour necrosis factor-
(TNF)-α and interleukin-1 (IL-1) cytokines

16. Stages
of
Shock

19. COMPENSATED SHOCK
(NON-PROGRESSIVE, INITIAL, REVERSIBLE)
 In the early stage of shock, an attempt is made to maintain
adequate cerebral and coronary blood supply by redistribution
of blood so that the vital organs (brain and heart) are
adequately perfused and oxygenated.
 This is achieved by activation of various neurohormonal
mechanisms causing
1. Widespread vasoconstriction
2. Fluid conservation by the kidney
3. Stimulation of Adrenal Medulla

20. 1. Widespread Vasoconstriction
 In response to reduced blood flow the neural and humoral
factors (e.g. baroreceptors, chemoreceptors, Catecholamines,
renin, and angiotensin-II) are activated.
 However, in septic shock, there is initial vasodilatation
followed by vasoconstriction. Besides, in severe septic shock
there is elevated level of thromboxane A2 which is a potent
vasoconstrictor and may augment the cardiac output along
with other sympathetic mechanisms.

21. 2. Fluid Conservation by Kidney
The following factors may assist in restoring the blood volume and
improve venous return to the heart:
 Release of aldosterone from hypoxic kidney by activation of renin-
angiotensin-aldosterone mechanism.
 Release of ADH due to decreased effective circulating blood
volume.
 Reduced glomerular filtration rate (GFR) due to arteriolar
constriction.

22. 3. Stimulation of adrenal medulla
 In response to low cardiac output, adrenal medulla is
stimulated to release excess of catecholamines (epinephrine
and non-epinephrine) which increase heart rate and try to
increase cardiac output.

23. PROGRESSIVE DECOMPENSATED SHOCK
 This is a stage when the patient suffers from some other stress or
risk factors (e.g. pre-existing cardiovascular and lung disease)
besides persistence of the shock so that there is progressive
deterioration.
 The effects of progressive decompensated shock due to tissue
hypoperfusion are as under:
i. Pulmonary hypoperfusion
ii. Tissue ischaemia

24.  i) Pulmonary hypoperfusion. Decompensated shock worsens
pulmonary perfusion and increases vascular permeability
resulting in tachypnoea and adult respiratory distress syndrome
(ARDS).
 ii) Tissue ischaemia. Impaired tissue perfusion causes switch
from aerobic to anaerobic glycolysis resulting in metabolic lactic
acidosis. Lactic acidosis lowers the tissue pH which in turn
makes the vasomotor response ineffective. This results in
vasodilatation and peripheral pooling of blood.
Clinically at this stage the patient develops confusion and worsening
of renal function.

25. IRREVERSIBLE DECOMPENSATED SHOCK
 When the shock is so severe that in spite of compensatory
mechanisms and despite therapy and control of etiologic agent
which caused the shock, no recovery takes place, it is called
decompensated or irreversible shock.

26. Its effects due to widespread cell injury include the following:
i. Progressive vasodilatation
ii. Increased vascular permeability
iii. Myocardial depressant factor
iv. Worsening pulmonary hypoperfusion
v. Anoxic damage to heart, kidney, brain
vi. Hypercoagulability of blood

27. i) Progressive vasodilatation. During later stages of shock, anoxia
damages the capillary and venular wall and arteioles become
unresponsive to vasoconstrictors listed above and begin to dilate.
Vasodilatation results in peripheral pooling of blood which further
deteriorate the effective circulating blood volume.
ii) Increased vascular permeability. Anoxic damage to tissues
releases inflammatory mediators which cause increased vascular
permeability. This results in escape of fluid from circulation into the
interstitial tissues thus deteriorating effective circulating blood
volume.

28. iii) Myocardial depressant factor (MDF). Progressive fall in the
blood pressure and persistently reduced blood flow to
myocardium causes coronary insufficiency and myocardial
ischaemia due to release of myocardial depressant factor (MDF).
This results in further depression of cardiac function, reduced
cardiac output and decreased blood flow.
iv) Worsening pulmonary hypoperfusion. Further pulmonary
hypoperfusion causes respiratory distress due to pulmonary
oedema, tachypnoea and adult respiratory distress syndrome
(ARDS).

29. v) Anoxic damage to heart, kidney, brain. Progressive tissue
anoxia causes severe metabolic acidosis due to anaerobic
glycolysis. There is release of inflammatory cytokines and other
inflammatory mediators and generation of free radicals. Since
highly specialised cells of myocardium, proximal tubular cells of
the kidney, and neurons of the CNS are dependent solely on
aerobic respiration for ATP generation, there is ischaemic cell
death in these tissues.

30. vi) Hypercoagulability of blood. Tissue damage in shock
activates coagulation cascade with release of clot promoting
factor, thromboplastin and release of platelet aggregator,
ADP, which contributes to slowing of blood-stream and
vascular thrombosis. In this way, hypercoagulability of blood
with consequent micro thrombi impair the blood flow and
cause further tissue necrosis.

31. As a result
 Clinically, at this stage the patient has features of
coma, worsened heart function and progressive renal
failure due to acute tubular necrosis.

32. Clinical Features and
Complications

33. The classical features of decompensated shock are characterised
by depression of 4 vital processes:
 Very low blood pressure
 Subnormal temperature
 Feeble and irregular pulse
 Shallow and sighing respiration
In addition, the patients in shock have pale face, sunken eyes,
weakness, cold and clammy skin.

34. Life-threatening complications in shock are due to hypoxic cell injury
resulting in immuno-inflammatory responses and activation of various
cascades (clotting, complement, kinin). These include the following*:
 Acute respiratory distress syndrome (ARDS)
 Disseminated intravascular coagulation (DIC)
 Acute renal failure (ARF)
 Multiple organ dysfunction syndrome (MODS)
With progression of the condition, the patient may develop stupor,
coma and death.

35. Types of shocks
(Mechanism & Management)

36. Hypovolemic
Shock

37. Case:
 John was involved in a car accident. He was rushed to the
nearest emergency department as he is bleeding profusely.
Upon arrival, his blood pressure has dropped, his heart rate
and respirations are rapid, and his skin is cold and clammy.
His output is decreased and he is disoriented. John is
suffering from hypovolemic shock due to active fluid loss

38.  Hypovolemic shock is one of the most common cardiac
complications.
 In hypovolemic shock, reduced intravascular blood volume
causes circulatory dysfunction and inadequate tissue
perfusion.
 Vascular fluid volume loss causes extreme tissue
hypoperfusion.

39. Pathophysiology
 Fluid loss. Fluid loss can either be internal or external fluid
loss.
 Compensatory mechanism: The resulting drop in the arterial
blood pressure activates the body’s compensatory mechanisms
in an attempt to increase the body’s intravascular volume.
 Venous return. Diminished venous return occurs as a result
of the decrease in arterial blood pressure.
 Preload. The preload or the filling pressure becomes reduced.

40. Pathophysiology
 Stroke volume. The stroke volume is decreased.
 Cardiac output. Cardiac output is decreased because of the
decrease in stroke volume.
 Arterial pressure. Reduced mean arterial pressure follows as
the cardiac output gradually decreases.
 Compromised cell nutrients. As the tissue perfusion
decreases, the delivery of nutrients and oxygen to the cells
are decreased, which could ultimately lead to multiple organ
dysfunction syndrome.

41. Causes
Hypovolemic shock usually results from acute blood loss- about one-fifth
of the total volume.
 Internal fluid loss. Internal fluid losses can result from haemorrhage or
third-space fluid shifting.
 External fluid loss. External fluid loss can result from severe bleeding
or from severe diarrhea, diuresis, or vomiting.
 Inadequate vascular volume. Inadequate vascular volume leads to
decreased venous return and cardiac output.

42. Clinical Manifestations
 Hypotension. Hypovolemic shock produces hypotension with narrowed pulse
pressure.
 Cognitive. The patient experiences decreased sensorium.
 Tachycardia. The body compensates for the decreased cardiac output by
pumping faster than normal, resulting in tachycardia.
 Rapid, shallow respirations. Due to the decrease in oxygen delivery around the
body systems, the respiratory system compensates by rapid, shallow
respirations.
 Oliguria. There is oliguria or decreased urine output of less than 25ml/hour.
 Clammy skin. The patient develops cool, clammy, and pale skin.

43. Prevention
For prevention of hypovolemic shock, the following must be
implemented:
 Early detection. Recognize patients with conditions that
reduce blood volume as at-risk patients.
 Accurate I&O. Estimate fluid loss and replace, as necessary,
to prevent hypovolemic shock.

44. Complications
Hypovolemic shock, if left untreated, would result to the following complications:
 Acute respiratory distress syndrome occurs when fluid builds up in the tiny,
elastic air sacs in the lungs.
 Acute tubular necrosis is a kidney disorder involving damage to the tubule cells
of the kidneys, which can lead to acute kidney failure.
 Disseminated intravascular coagulation is a pathological process characterized
by a widespread activation of the clotting cascades that results in the formation
of blood clots in the small blood vessels.
 Multiple organ dysfunction syndrome is the end result of hypovolemic shock.

45. Assessment and Diagnostic Findings
No single symptom or diagnostic test establishes the diagnosis or severity
of shock.
 Laboratory findings. There is elevated potassium, serum lactate, and
blood urea nitrogen levels.
 Urine characteristics. The urine specific gravity and urine osmolality
are increased.
 Blood considerations. Decreased blood pH, partial pressure of oxygen,
and increased partial pressure of carbon dioxide.

46. Medical Management
Emergency treatment measures must include prompt and adequate fluid and blood
replacement to restore intravascular volume and raise blood pressure.
 Volume expansion. Saline solution or lactated Ringer’s solution, then possibly plasma
proteins or other plasma expanders, may produce adequate volume expansion until whole
blood can be matched.
 Pneumatic antishock garment. A pneumatic antishock garment counteracts bleeding and
hypovolemia by slowing or stopping arterial bleeding; by forcing any available blood from
the lower body to the brain, heart, and other vital organs; and by preventing return of
the available circulating blood volume to the legs.
 Treat underlying cause. If the patient is haemorrhaging, efforts are made to stop the
bleeding or if the cause is diarrhea or vomiting, medications to treat diarrhea and
vomiting are administered.
 Redistribution of fluid. Positioning the patient properly assists fluid redistribution,
wherein a modified Trendelenburg position is recommended in hypovolemic shock.

47. Pharmacologic Therapy
 Vasoactive drugs. Vasoactive drugs that prevent cardiac failure are
given.
 Insulin is administered if dehydration is secondary to hyperglycemia.
 Desmopressin (DDAVP). Desmopressin is administered
for diabetes insipidus.
 Antidiarrheal drugs. If dehydration is due to diarrhea, antidiarrheal
medications are administered.
 Antiemetics. If the cause of diarrhea is vomiting, antiemetics are given.

48. Cardiogenic
Shock

49. Case
 Mr. Patton was admitted due to myocardial infarction. Two
hours after the admission, his skin became cool and clammy.
Latest BP shows a decrease in the systolic blood pressure.
His heart rate and respirations are gradually increasing, and
his urine output is decreasing.
 Mr. Patton is experiencing cardiogenic shock due to
myocardial infarction.

50. Introduction
 Cardiogenic shock is also sometimes called “pump failure”.
 Cardiogenic shock is a condition of diminished cardiac output
that severely impairs cardiac perfusion.
 It reflects severe left-sided heart failure.

51. Pathophysiology
 Inability to contract. When the myocardium can’t contract
sufficiently to maintain adequate cardiac output, stroke volume
decreases and the heart can’t eject an adequate volume of blood
with each contraction.
 Pulmonary congestion. The blood backs up behind the weakened left
ventricle, increasing preload and causing pulmonary congestion.
 Compensation. In addition, to compensate for the drop
in stroke volume, the heart rate increases in an attempt to maintain
cardiac output.

52. Pathophysiology
 Diminished stroke volume. As a result of the diminished
stroke volume, coronary artery perfusion and collateral blood
flow is decreased.
 Increased workload. All of these mechanisms increase the
heart’s workload and enhance left-sided heart failure.
 End result. The result is myocardial hypoxia,
further decreased cardiac output, and a triggering of
compensatory mechanisms to prevent decompensation and
death.

53. Classification
 Coronary. Coronary cardiogenic shock is more common than
noncoronary cardiogenic shock and is seen most often in
patients with acute myocardial infarction.
 Noncoronary. Noncoronary cardiogenic shock is related to
conditions that stress the myocardium as well as conditions
that result in an ineffective myocardial function.

54. Causes
 Myocardial infarction (MI). Regardless of the underlying cause, left
ventricular dysfunction sets in motion a series of compensatory
mechanisms that attempt to increase cardiac output, but later on
leads to deterioration.
 Myocardial ischemia. Compensatory mechanisms may initially
stabilize the patient but later on would cause deterioration with the
rising demands of oxygen of the already compromised myocardium.
 End-stage cardiomyopathy. The inability of the heart to pump
enough blood for the systems causes cardiogenic shock.

55. Clinical Manifestations
Cardiogenic shock produces symptoms of poor tissue perfusion.
 Clammy skin. The patient experiences cool, clammy skin as the
blood could not circulate properly to the peripheries.
 Decreased systolic blood pressure. The systolic blood pressure
decreases to 30 mmHg below baseline.
 Tachycardia. Tachycardia occurs because the heart pumps faster
than normal to compensate for the decreased output all over the
body.

56. Clinical Manifestations
 Rapid respirations. The patient experiences rapid, shallow
respirations because there is not enough oxygen circulating in the
body.
 Oliguria. An output of less than 20ml/hour is indicative of oliguria.
 Mental confusion. Insufficient oxygenated blood in the brain could
gradually cause mental confusion.
 Cyanosis. Cyanosis occurs because there is insufficient oxygenated
blood that is being distributed to all body systems.

57. Assessment and Diagnostic Findings
 Auscultation. Auscultation may detect gallop rhythm, faint heart
sounds and, possibly, if the shock results from rupture of the
ventricular septum or papillary muscles, a holosystolic murmur.
 Pulmonary artery pressure (PAP). PAP monitoring may show
increase in PAP, reflecting a rise in left ventricular end-diastolic
pressure and increased resistance to the afterload.
 Arterial pressure monitoring. Invasive arterial pressure monitoring
may indicate hypotension due to impaired ventricular ejection.

58. Assessment and Diagnostic Findings
 Electrocardiography. Electrocardiography may show possible
evidence of acute MI, ischemia, or ventricular aneurysm.
 Echocardiography. Echocardiography can determine left ventricular
function and reveal valvular abnormalities.
 Enzyme levels. Enzyme levels such as lactic dehydrogenase,
creatine kinase. Aspartate aminotransferase and alanine
aminotransferase may confirm MI.

59. Medical Management
The aim of treatment is to enhance cardiovascular status by:
 Oxygen. Oxygen is prescribed to minimize damage to muscles and
organs.
 Angioplasty and stenting. A catheter is inserted into the blocked
artery to open it up.
 Balloon pump. A balloon pump is inserted into the aorta to help
blood flow and reduce workload of the heart.

60. Medical Management
 Pain control. In a patient that experiences chest pain,
IV morphine is administered for pain relief.
 Hemodynamic monitoring. An arterial line is inserted to enable
accurate and continuous monitoring of BP and provides a port
from which to obtain frequent arterial blood samples.
 Fluid therapy. Administration of fluids must be monitored
closely to detect signs of fluid overload.

61. Pharmacologic Therapy
 IV dopamine. Dopamine, a vasopressor, increases cardiac output, blood
pressure, and renal blood flow.
 IV Dobutamine. Dobutamine is an inotropic agent that increase
myocardial contractility.
 Norepinephrine. Norepinephrine is a more potent vasoconstrictor that
is taken when necessary.
 IV nitroprusside. Nitroprusside is a vasodilator that may be used with a
vasopressor to further improve cardiac output by decreasing peripheral
vascular resistance and reducing preload.

62. Surgical Management
When the drug therapy and medical procedures don’t work, then
the last option is for surgical procedure.
 Intra-aortic balloon pump (IABP). The IABP is a mechanical-
assist device that attempts to improve the coronary artery
perfusion and decrease cardiac workload through an inflatable
balloon pump which is percutaneously or surgically inserted
through the femoral artery into the descending thoracic aorta.

63. Septic
Shock

64. CASE
 Pamela, a 22-year old, has just undergone an appendectomy.
She is currently in the recovery room when
the nurse assigned to her noticed that her vital signs are not
going well. Her heart rate is increasing, but
her blood pressure is decreasing. Her breathing is rapid and
her urine output for the past hour is only 15 mL.
 She was diagnosed by the physician of septic shock.

65. Description
 One of the most common types of circulatory shock and the
incidences of this disease continue to rise despite the technology.
 Sepsis is a systemic response to infection. It is manifested by two
or more of the SIRS (Systemic Inflammatory Response Syndrome)
criteria as a consequence of documented or presumed infection.
 Septic shock is associated with sepsis. It is characterized by
symptoms of sepsis plus hypotension and hypoperfusion despite
adequate fluid volume replacement.

66. Pathophysiology
 Microorganisms invade the body tissues and in turn, patients exhibit an
immune response.
 The immune response provokes the activation of biochemical cytokines and
mediators associated with an inflammatory response.
 Increased capillary permeability and vasodilation interrupt the body’s ability
to provide adequate perfusion, oxygen, and nutrients to the tissues and cells.
 Proinflammatory and anti-inflammatory cytokines released during the
inflammatory response and activates the coagulation system that forms clots
whether or not there is bleeding.
 The imbalance of the inflammatory response and the clotting and fibrinolysis
cascades are critical elements of the physiologic progression of sepsis in
affected patients.

67. Causes
 Patients with immunosuppression have greater chances of acquiring septic shock
because they have decreased immune system, making it easier for microorganisms to
invade the body tissues.
 Extremes of age. Elderly people and infants are more prone to septic shock because
of their weak immune system.
 Malnourishment. Malnourishment can lower the body’s defences, making it
susceptible to the invasion of pathogens.
 Chronic illness. Patients with a longstanding illness are put at risk for sepsis because
the body’s immune system is already weakened by the existing pathogens.
 Invasive procedures. Invasive procedures can introduce microorganisms inside the
body that could lead to sepsis.

68. Clinical Manifestations
 Since the ability of the body to provide oxygen and nutrients is
interrupted, the heart compensates by pumping faster.
 Hypotension occurs because of vasodilation.
 To compensate for the decreased oxygen concentration, the
patient tends to breathe faster, and also to eliminate more
carbon dioxide from the body.
 The inflammatory response is activated because of the invasion
of pathogens.

69. Clinical Manifestations
 Decreased urine output. The body conserves water to avoid
undergoing dehydration because of the inflammatory
process.
 Changes in mentation. As the body slowly becomes acidotic,
the patient’s mental status also deteriorates.
 Elevated lactate level. The lactate level is elevated because
there is maldistribution of blood.

70. Prevention
 Strict infection control practices. To prevent the invasion of microorganisms
inside the body, infection must be put at bay through effective aseptic
techniques and interventions.
 Prevent central line infections. Hospitals must implement efficient programs
to prevent central line infections, which is the most dangerous route that can
be involved in sepsis.
 Early debriding of wounds. Wounds should be debrided early so that necrotic
tissue would be removed.
 Equipment cleanliness. Equipment used for the patient, especially the ones
involved in invasive procedures, must be properly cleaned and maintained to
avoid harboring harmful microorganisms that can enter the body.

71. Complications
Complications could happen in a patient with sepsis if it is not properly
treated or not treated at all.
 Severe sepsis. Sepsis could progress to severe sepsis with symptoms
of organ dysfunction, hypotension or hypoperfusion, lactic acidosis,
oliguria, altered level of consciousness, coagulation disorders, and
altered hepatic functions.
 Multiple organ dysfunction syndrome. This refers to the presence of
altered function of one or more organs in an acutely ill patient
requiring intervention and support of organs to achieve physiologic
functioning required for homeostasis.

72. Assessment and Diagnostic Findings
 Blood culture. To identify the microorganism responsible for the
disease, a blood culture must be performed.
 Liver function test. This should be performed to detect any
alteration in the function of the liver.
 Blood studies. Hematologic test must also be performed to check
on the perfusion of the blood.

73. Medical Management
 Fluid replacement therapy. The therapy is done to correct the
tissue hypoperfusion, so aggressive fluid resuscitation must be
implemented.
 Pharmacologic therapy. Drotrecogin alfa is used to act as
antithrombotic, anti-inflammatory, and profibrinolytic agent.
 Nutritional therapy. Aggressive nutritional supplementation is
critical in the management of septic shock because malnutrition
further impairs the patient’s resistance to infection.

74. Anaphylactic
Shock

75. Case
 Kaye went on a picnic with her friends at the beach. Everyone
brought food and shared them for lunch. Moments after biting
off a chunk of sandwich, Kaye went dizzy and complained of
severe shortness of breath. IT turned out that the sandwich
is a peanut butter and jelly ensemble, and Kaye is allergic to
peanuts.
 She was immediately rushed to the emergency department
and was diagnosed with anaphylactic shock.

76. Introduction
 Anaphylactic shock occurs rapidly and is life-threatening.
 Anaphylactic shock is a systemic, type I hypersensitivity
reaction that often has fatal consequences.
 Anaphylaxis causes the immune system to release a flood of
chemicals that can cause a person to go into shock.

77. Pathophysiology
Anaphylaxis occurs in an individual after reexposure to an antigen to which that
person has produced a specific IgE antibody.
 Reexposure. Upon reexposure to the sensitized allergen, the allergen may
cross-link the mast cell or basophil surface-bound allergen-specific IgE
resulting in cellular degranulation as well as de novo synthesis of mediators.
 Binding. Immunoglobulin E (IgE) binds to the antigen (the foreign material
that provokes the allergic reaction).
 Activation. Antigen-bound IgE then activates FcεRI receptors on mast cells
and basophils.

78. Pathophysiology
 Inflammatory mediators release. This leads to the release of inflammatory
mediators such as histamine.
 Histamine release. Many of the signs and symptoms of anaphylaxis are
attributable to binding of histamine to its receptors; binding to H1 receptors
mediates pruritus, rhinorrhoea, tachycardia, and bronchospasm.
 Prostaglandin D2. Prostaglandin D2 mediates bronchospasm and vascular
dilatation, principle manifestations of anaphylaxis.
 Leukotriene C4. Leukotriene C4 is converted into LTD4 and LTE4,
mediators of hypotension, bronchospasm, and mucous secretion during
anaphylaxis in addition to acting as chemotactic signals for eosinophils and
neutrophils.

79. Causes
 Food allergies. The most common anaphylaxis triggers in children are
food allergies, such as to peanuts, and tree nuts, fish, shellfish and
milk.
 Medication allergies. Certain medications, including antibiotics, aspirin
and other over-the-counter pain relievers, and the intravenous (IV)
contrast used in some imaging tests.
 Insect allergies. Stings from bees, yellow jackets, wasps, hornets and
fire ants.
 Latex allergy. Latex allergy develops after many previous exposures to
latex.

80. Clinical Manifestations
 Anxiety.
 Skin reactions.
 Shortness of breath.
 Hypotension.
 Tachycardia.
 Dizziness.

81. Complications
 Respiratory obstruction. The trachea may close up due to
severe inflammation which could result to respiratory
obstruction.
 Systemic vascular collapse. Sudden loss of blood flow to the
brain and other organs could cause systemic vascular collapse.

82. Assessment and Diagnostic Findings
Because anaphylaxis is primarily a clinical diagnosis, laboratory
studies are not usually required and are rarely helpful.
 Histamine and tryptase assessment.
 5-hydroxyindoleacetic acid levels.
 Testing for food allergy.
 Testing for medication allergy.
 Testing for suspected insect bites or sting.

83. Medical Management
 Remove antigen. Removing the causative antigen such as discontinuing an antibiotic
agent could stop the progression of shock.
 Administer medications. Administer medications that restore vascular tone and
provide emergency support of basic life functions.
 Cardiopulmonary resuscitation. If cardiac arrest and respiratory arrest are
imminent or have occurred, cardiopulmonary resuscitation is performed.
 Endotracheal intubation. Endotracheal intubation or tracheostomy may be necessary
to establish an airway.
 Intravenous therapy. IV lines are inserted to provide access for administering fluids
and medications.

84. Pharmacologic Therapy
Medications used for a patient at risk or under anaphylactic shock are:
 Epinephrine. Epinephrine is given for its vasoconstrictive reaction; for
emergency situations, an immediate injection of 1:1, 000 aqueous
solution, 0.1 to 0.5 ml, repeated every 5 to 20 minutes is given.
 Diphenhydramine. Diphenhydramine (Benadryl) is administered to reverse
the effects of histamine, thereby reducing capillary permeability.
 Albuterol. Albuterol (Proventil) may be given to reverse histamine-
induced bronchospasm.

85. Neurogenic
Shock

86. Case
 Mila and her friends went partying on a Friday night. Her friend,
who was drunk, drove them home. As they were crossing an
intersection, their car was hit by a ten-wheeler truck. Mila
sustained a spinal cord injury. Upon arrival at the emergency
department, her BP was 80/40, she had warm, dry skin, and her
pulse is 44 beats per minute.
 Mila is progressing towards neurogenic shock due to spinal cord
injury.

87. Introduction
Neurogenic shock is a distributive type of shock.
 In neurogenic shock, vasodilation occurs as a result of a loss of
balance between parasympathetic and sympathetic stimulation.
 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.

88. Pathophysiology
 Stimulation. Sympathetic stimulation causes vascular smooth muscle to constrict, and
parasympathetic stimulation causes vascular smooth muscle to relax or dilate.
 Vasodilation. The patient experiences a predominant parasympathetic stimulation that
causes vasodilation lasting for an extended period of time, leading to a relative
hypovolemic state.
 Hypotension. Blood volume is adequate, because the vasculature is dilated; the blood
volume is displaced, producing a hypotensive (low BP) state.
 Cardiovascular changes. The overriding parasympathetic stimulation that occurs with
neurogenic shock causes a drastic decrease in the patient’s systemic vascular
resistance and bradycardia.
 Insufficient perfusion. Inadequate BP results in the insufficient perfusion of tissues
and cells that is common to all shock states.

89. Causes
 Spinal cord injury. Spinal cord injury (SCI) is recognised to cause
hypotension and bradycardia (neurogenic shock).
 Spinal anaesthesia. Spinal anaesthesia injection of an anaesthetic into
the space surrounding the spinal cord or severance of the spinal cord
results in a fall in blood pressure because of dilation of the blood
vessels in the lower portion of the body and a resultant diminution of
venous return to the heart.
 Depressant action of medications. Depressant action of medications
and lack of glucose could also cause neurogenic shock.

90. Clinical Manifestations
The clinical manifestations of neurogenic shock are signs of parasympathetic stimulation.
 Dry, warm skin. Instead of cool, moist skin, the patient experiences dry, warm skin
due to vasodilation and inability to vasoconstrict.
 Hypotension. Hypotension occurs due to sudden, massive dilation.
 Bradycardia. Instead of getting tachycardia, the patient experience bradycardia.
 Diaphragmatic breathing. If the injury is below the 5th cervical vertebra, the patient
will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal
muscles (which are required for thoracic breathing).
 Respiratory arrest. If the injury is above the 3rd cervical vertebra, the patient will
go into respiratory arrest immediately following the injury, due to loss of nervous
control of the diaphragm.

91. Assessment and Diagnostic Findings
 Computerized tomography (CT) scan. A CT scan may provide a
better look at abnormalities seen on an X-ray.
 X-rays. Medical personnel typically order these tests on people
who are suspected of having a spinal cord injury after trauma.
 Magnetic resonance imaging (MRI). MRI uses a strong magnetic
field and radio waves to produce computer-generated images.

92. Medical Management
 Restoring sympathetic tone. It would be either through the
stabilization of a spinal cord injury or, in the instance of spinal
anesthesia, by positioning the patient appropriately.
 Immobilization. If the patient has a suspected case of spinal cord
injury, a traction may be needed to stabilize the spine to bring it to
proper alignment.
 IV fluids. Administration of IV fluids is done to stabilize the
patient’s blood pressure.

93. Pharmacologic Therapy
 Inotropic agents. Inotropic agents such as dopamine may be infused for
fluid resuscitation.
 Atropine. Atropine is given intravenously to manage severe
bradycardia.
 Steroids. Patient with obvious neurological deficit can be given I.V.
steroids, such as methylprednisolone in high dose, within 8 hours of
commencement of neurogenic shock.
 Heparin. Administration of heparin or low molecular-weight heparin as
prescribed may prevent thrombus formation.

94. Other
Shocks

95. Traumatic shock.
 Shock resulting from trauma is initially due to hypovolaemia,
but even after haemorrhage has been controlled, these
patients continue to suffer loss of plasma volume into the
interstitium of injured tissue and hence is considered
separately in some descriptions.

96. Hypoadrenal shock
 Hypoadrenal shock occurs from unknown adrenal insufficiency
in which the patient fails to respond normally to the stress of
trauma, surgery or illness.