Types of Shock,Pathophysiology,Sign symptoms.First MBBS Lecture

1. Shock
Dr Raghuveer Choudhary

2. 2
The Physiology of Shock
R.E.B, 4MedStudents.com, 2003

3. Shock
• Shock is a syndrome in which there is
inadequate tissue perfusion associated with a
relative or absolute decrease in cardiac out
put.

7. • Shock occurs when
the rate of arterial blood flow is inadequate to meet
metabolic tissue needs and is the consequence of
cardio-vascular collapse
• Essentials of diagnosis are
– Hypotension (<60 mmHG)
– Tachycardia
– Oliguria
– Altered mental status
– Peripheral hypoperfusion and hypoxia

13. major types of shock
• Hypovolemic shock
– Decreased intravascular volume resulting form loss of
blood, plasma, or fluids and electrolytes
• Cardiogenic shock
– Pump failure due to myocardial damage or massive
obstruction of outflow tracts
• Distributive shock
– Reduction of vascular resistance form
• Sepsis
• Anaphylaxis
• Systemic inflammatory response syndrome (SIRS)

16. Hypovolemic shock
(most common type of shock)
• Loss of blood (hemorrhagic)
– External bleeding (wound to the outside or gastrointestinal)
– Internal bleeding (hematoma, hemothorax,
hemopertitoneum)
• Loss of plasma
– Burns
– Exfoliative dermatitis
• Loss of fluids and electrolytes
– External (vomiting, diarrhea, excessive sweating)
– Internal ( “third spacing” = pancreatitis, ascitis, bowl
obstruction
– Excessive sweating

23. Stages of hypovolemic shock
• Mild (loss of < 20% blood volume)
– Few external signs in supine young patients but
• Increased capillary refill time ( longer 3 sec. = 10% volume loss)
• Moderate (loss of 20-40% blood volume)
– Patient becomes increasingly anxious and tachycardic >100 beats/min
(sympathetic response)
– oliguria
– blood pressure may be maintained in supine patient
• Severe (loss of > 40% blood volume)
– Classic signs of shock appear with hemodynamic instability
(Cave: if mental confusion occurs is an ominous clinical sign)
Only very short time frame may separate mild and severe shock
symptoms that lead, when left untreated, to progressive and
irreversible cell injury and death

25. Signs and Symptoms
• Low Blood Pressure
– Systolic BP is usually below 90 mmHg
• Pulse is rapid and weak
• Respiration is rapid and shallow
• Skin is pale, cool, and clammy
• Drowsiness

26. Hypovolemic Shock
• Results from trauma in which there is blood
loss
• Decreased blood volume causes a decrease in
blood pressure
• Insufficient amounts of O2 is being
transported to body tissues and organs

29. Compensated Shock
• Early stages of shock where the body’s
compensatory mechanisms are able to
maintain normal perfusion

30. Decompensated Shock
• Advanced stage of shock that occurs when the
body’s compensatory mechanisms fail to
maintain normal perfusion

31. Irreversible Shock
• Stage of shock that has progressed to the point
that the body nor medical interventions correct
the problem

38. Compensated and Decompensated
shock
• Usually the body is able to compensate but
when these mechanisms fail shock develops
and may progress

39. Compensation Mechanisms
• Catecholamines may be secreted ( I.E.
Epinephrine and norepinephrine)
• The Renin-Angitensin system aids in
maintaining blood pressure
• Endocrine Response by pituitary gland results
in secretion of anti-diuretic hormone (ADH)

40. Catecholamine Release
• Epinephrine and Norepinephrine release
affects the cardiovascular system, causing
increase in HR, increase in Cardiac contractility
strength, arteriolar constriction which elevates
blood pressure

41. Renin-Angiotensin system
• Renin is released from the kidneys and acts on
specialized plasma protein called
Angiotensinogen & produces Angiotensin I.
• Angiotensin I is converted to Angiotensin II by
enzymes in the lungs called Angiotensin
Converting Enzyme (ACE)

42. Anti-Diuretic Hormone
• Causes the kidneys to reabsorb water creating
an additive to the aldostrone

43. Stages of Shock
• Initial non-progressive stage
– Baro-receptor reflexes
– Release of catecholamine
– Activation of renin-angiotensin-aldosteron system
– ADH release
results in tachycardia, peripheral vasoconstriction (cool skin) and renal fluid
conservation
• Progressive stage
– Widespread tissue hypoxia results in anaerobic glycolysis and
– Lactate acidosis (pH < 7.35)
– Vasodilation with blood pooling in microcirculation
– Declined cardiac output
– Oligouria
– Widespread tissue hypoxia
• Irreversible stage
– Widespread cell injury leading to
– Further decreased myocardial contractility
– Anuria with tubular necrosis
– Ischemic bowl may lead to leakage of bacterial flora
– Fluid in lung (ARDS)

48. S/S of Hypovolemic Shock
• Altered LOC
• Pale, cool, clammy skin
• Blood pressure may be normal then fall
• Pulse may be normal then become rapid, finally
slowing and disappearing
• Urination decreases
• Cardiac dysrhythmias may occur

49. Tx for Hypovolemic Shock
• Airway control
• Administer high flow oxygen
• Control severe bleeding
• Keep patient warm
• Elevate lower extremities
• Establish IV and administer bolus of crystalloid
solution for fluid replacement

53. Cardiogenic shock
• Pump failure
– Secondary to myocardial infarction (most common)
– Cardio-myophathy
– Acute valvular dysfunction (regurgitations)
– Rupture of the ventricular septum
• Arrhythmia
– Tachyarrhythmia
– Bradyarrhythmia
• Obstructions
– Tension pneumothorax
– Pericardial diseases (tamponade or constrictive pericarditis)
– Pulmonary hypertension (emboli or other vascular diseases)

55. Characteristics of Cardiogenic Shock
• Low cardiac output
• Peripheral vasoconstriction
• Left sided heart failure leads to pulmonary venous
congestion and pulmonary edema
• Right sided heart failure leads to systemic venous
congestion and peripheral edema

56. It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased
peripheral vascular resistance, however:
Cardiogenic shock:
jugular venous distention (high CVP)
Hypovolemic shock: collapsed
capacitance veins (low CVP)

57. Cardiogenic Shock
• The heart loses the ability to supply all body
parts with blood
• Usually the result of left ventricular failure
secondary to acute MI or CHF
• Many patients will have normal blood
pressures

58. S/S of Cardiogenic Shock
• Major difference between other types of shock
is presence of Pulmonary Edema
• Difficulty breathing
• Wheezes, Crackles, Rales are heard as fluid
levels increase
• Productive cough with white or pink-tinged
foamy sputum
• Cyanosis
• Altered mentation
• Oliguria ( decreased urination)

59. TX for Cardiogenic Shock
• Assure open airway
• Adminster oxygen
• Assist ventilations as needed
• Keep patient warm
• Place patient in position of comfort
• Establish Iv with minimal fluid administration
• Monitor Vitals
• May need to administer Dopamine or
Dobutamine

66. Distributive Shock
• Sepsis
– Due to gram negative or gram positive bacteria
• Anaphylaxis
– Due to previous sensitization to an allergen
• Neurogenic
– Due to traumatic spinal cord injury
– Effects of epidural or spinal anesthetics
– Reflex parasymapthetic stimulation

67. Types of Shock
Neurogenic Shock
• Results due to the overall dilation of the blood
vessels within the cardiovascular system
• Decreased blood pressure
• Insufficient amounts of O2 is being
transported to body tissues and organs

71. Neurogenic Shock
• Results from injury to brain or spinal cord
causing interruption of nerve impulses to
arteries
• Arteries lose tone and dilate causing
hypovolemia
• Sympathetic nerve impulses to the adrenal
glands are lost, which prevents the release of
catecholamines and their compensatory effects

72. Neurogenic Shock (con’t)
• High cervical injuries cause interruption of
impulse to peripheral nervous system causing
• Neurogenic shock is most commonly due to
severe injury to spinal cord or total transection
of cord (spinal shock)

73. S/S of Neurogenic Shock
• Warm, Dry, Red Skin
• Low Blood Pressure
• Slow Pulse

74. TX for Neurogenic Shock
• Airway control
• Maintain body temperature
• Immobilization if indicated
• Consider other causes of shock
• IV and medications that increase peripheral
vascular resistance (I.E. Norepinephrine,
Dopamine)

81. Anaphylatic Shock
• Severe immune response to foreign substance
• S/S most often occur within minutes but can
take up to hours to occur
• The faster the reaction develops the more
severe it is likely to be
• Death will occur if not treated promptly

83. S/S of Anaphylactic Shock
• Skin
- Flushing
- Itching
- Hives
-Swelling
-Cyanosis

84. S/S of Anaphylactic Shock
• Respiratory System
- Breathing difficulty
- Sneezing, Coughing
- Wheezing, Stridor
- Laryngeal edema
- Laryngospasm

85. S/S of Anaphylactic Shock
• Cardiovascular System
- Vasodilation
- Increased heart rate
- Decreased blood pressure

86. S/S of Anaphylactic Shock
• Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea

87. TX for Anaphylactic Shock
• Airway protection which may include
Endotracheal Intubation
• Establish IV with crystalloid solution
• Pharmacological interventions: Epinephrine,
Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)

90. Pathogenesis of Septic Shock
(vasodilatory shock)
• Sepsis is defined as a systemic inflammatory response
to a bacterial infection with bacteriemia (though
blood cultures can be negative)
• Severe sepsis is defined by additional end-organ
dysfunction (mortality rate: 25-30%)
• Septic shock is defined as sepsis with hypotension
despite fluid resuscitation and evidence of inadequate
tissue perfusion (40-70%)

92. NEJM 2004, Vol. 351;2 pp 159-169

93. Clinical Spectrum of Infection
Infection
Sepsis
Severe Sepsis
Septic Shock
Bacteremia

95. The syndrome of septic shock is characterized
by
• Systemic vasodilation (hypotension)
• Diminished myocardial contractility
• Widespread endothelial injury and activation leading
to fluid leakage (capillary leak) resulting in acute
respiratory distress syndrome (ARDS)
• Activation of the coagulation cascade (DIC)

97. Disseminated intravascular coagulation (DIC)
• is characterized by widespread activation of coagulation
resulting in the intravascular formation of fibrin and ultimately
thrombotic occlusion of small and midsize vessels
• leads to compromise of blood supply to organs and may
therefore contribute to multiple organ failure
• subsequent depletion of platelets and coagulation factors can
result in severe bleeding and may be the presenting symptom

98. Virtually all patients with sepsis have coagulation
abnormalities. The extreme form of it is called:
Acute disseminated intravascular coagulation (DIC)
Severe cutaneous bleeding as a result of fulminant Meningococcal
septicemia due to activation and consumption of all coagulation
factors (consumption coagulopathy)

100. Septic Shock
• An infection enters bloodstream and is carried
throughout body
• Toxins released overcome compensatory
mechanisms
• Can cause dysfunction of one organ system or
cause multiple organ dysfunction

101. S/S of Septic Shock
• Increased to low blood pressure
• High fever, no fever, hypothermic
• Skin flushed, Pale, Cyanotic
• Difficulty breathing and altered lung sounds
• Altered LOC

102. TX of Septic Shock
• Airway control
• Administer oxygen
• IV of crystalloid solution
• Dopamine for blood pressure support
• Monitor other vitals