Chapter 4
Shock
REQUIRMENTS
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To master the definitions of shock, shock lung and multiple organ
dysfunction syndrome
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To master the pathogenesis of shock including the changes of
microcirculation in different stages and the actions of relative
factors
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To master the functional and metabolic changes in shock
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To be familiar with the etiology and classification of shock
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To be familiar with the characteristics of different kinds of shock
and treatment principle
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To apprehend the pathological changes of shock lung
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To understand the pathogenesis of multiple organ dysfunction
syndrome
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COURSE CONTENT
I. The generality and clinical
feature of shock
Shock
is not a disease but rather a clinical syndrome leading to reduced perfusion of
tissues and organs and, eventually, organ dysfunction and failure.
The classical signs and symptoms of shock include changes of blood
pressure (hypotension or decrease of pulse pressure ), overbreathing
(hyperventilation), a weak rapid pulse, cold clammy grayish-bluish (cyanotic)
skin, decreased urine flow (oliguria), and mental changes (a sense of great
anxiety and foreboding, confusion and, sometimes, combativeness). Even
with treatment, shock has a high mortality rate once the body's compensatory
mechanisms fail.
Ⅱ. Shock
Classification
⑴
Based on the etiology, shock can be classified into seven major categories: ①
hemorrhagic shock; ② traumatic shock; ③ infectious shock; ④ burn shock; ⑤
cardiogenic shock; ⑥ anaphylactic shock;
⑦ neurogenic shock
⑵
Shock can be
classified into three major categories according to
starting segment that influences the
perfusion of tissue: ① hypovolemic shock; ② vasogenic shock; ③ cardiogenic shock
⑶
Shock can be
classified into two major categories based on the
changes of blood dynamics: ① hypodynamic
shock; ② hyperdynamic shock
Ⅲ. Pathophysiology of shock
There
are three basic stages common to hemorrhagic shock: the compensatory,
progressive, and irreversible or refractory stages.
1. Compensatory stage (Ischemic
hypoxia stage)
In the stage, the manifestation of microcirculation is the velocity of capillary
blood flow decreased gradually due to local arteriolar and precapillary
sphincter constriction.
When arterial pressure and tissue perfusion are reduced, compensatory mechanisms
are activated to maintain perfusion to the heart and brain. As the baroreceptors
in the carotid sinus and aortic arch sense a drop in blood pressure, epinephrine
and norepinephrine are secreted to increase peripheral resistance, blood
pressure, and myocardial contractility. Reduced blood flow to the kidney
activates the renin-angiotensin-aldosterone system, causing vasoconstriction and
sodium and water retention, leading to increased blood volume and venous return.
As a result of these compensatory mechanisms, cardiac output and tissue
perfusion of important organ, such as heart and brain, are maintained.
The effects on body-compensatory are maintain of BP and redistribution of blood
flow. Clinical signs in this stage: blood pressure is maintained even though
cardiac output has fallen.
2. Progressive stage (Stagnant
hypoxic stage)
The manifestation of microcirculation in this stage: blockade of the
micro-vessels.
This
stage of shock begins as compensatory mechanisms fail to maintain cardiac
output. Tissues become hypoxic because of poor perfusion. As cells switch to
anaerobic metabolism, lactic acid builds up, producing metabolic acidosis. This
acidotic state depresses myocardial function and blunts the vasomotor response
to catecholamines. Tissue hypoxia also promotes the release of endothelial
mediators, which produce vasodilation and endothelial abnormalities, leading to
venous pooling and increased capillary permeability. Sluggish blood flow
increases the risk of disseminated intravascular coagulation.
The effects on body: decompensation causes decreased blood flow return and
constantly decreasing BP. Clinical signs of this stage: blood pressure is
decreased.
3. Microcirculatory failure stage (irreversible stage, refractory stage or DIC
stage)
The manifestations of microcirculation at this stage
include congestion of microcirculation, no reaction of micro-vessel,
formation of micro-thrombus, no-reflow
of capillary, hemorrhage and DIC, obstinate low blood pressure, severity damage
of important tissues and organs, severity anoxia and acidosis.
As the shock syndrome progresses, permanent organ damage occur as compensatory
mechanisms can no longer maintain cardiac output. Reduced perfusion damages cell
membranes, lysosomal enzymes are released, and energy stores are depleted,
possibly leading to cell death including necrosis and apoptosis. As cells use
anaerobic metabolism, lactic acid accumulates, increasing capillary permeability
and the movement of fluid out of the vascular space. This loss of intravascular
fluid further contributes to hypotension. Perfusion to the coronary arteries is
reduced, causing myocardial depression and a further reduction in cardiac
output. Eventually, circulatory and respiratory failure occurs. Death is
inevitable.
Effect on body: ①multiple organ failure (MOF); ② DIC
Ⅳ. Functional and metabolic changes
Organ failures includes shock lung, shock kidney,
functional changes of heart, brain, digestive system and
multiple organ failure syndrome.
Possible complications of shock include: ①acute respiratory distress syndrome;
②acute tubular necrosis; ③disseminated intravascular coagulation (DIC);
④cerebral hypoxia
Disturbance of cellular metabolism of nutrients such as glucose and the
activities of some hormones are depressed as well include a depression in the
action of insulin.
Ⅴ. Types of shock
Ⅵ. Treatment
Correction of shock typically involves the following measures:
1. Identifying and
treating the underlying cause, if possible
2. Maintaining a patent airway; preparing for intubation and mechanical
ventilation if the patient develops respiratory distress
3. Supplemental
oxygen to increase oxygenation
4. Continuous cardiac monitoring to detect changes in heart rate and rhythm;
administration of antiarrhythmics, as necessary
5. Initiating and maintaining at least two intravenous lines with large-gauge
needles for fluid and drug administration
6. Intravenous fluids, crystalloids, colloids, or blood products, as necessary,
to maintain intravascular volume. Fluids such as normal saline or lactated
Ringer's solution, initially, to restore filling pressures
EXERCISES
Ⅰ. True or false questions
(mark √ for true question, mark
´ for false
question. If it is false, correct it. )
1. Change of blood pressure is the important sign and symptom for
diagnosis of shock.
2. At early stage, shock can develop acute functional renal failure, but
at late stage always develops parenchymal.
3.
Shock is not a disease but rather a clinical syndrome with high mortality rate.
4. MDF only has the role of inhibiting cardiac
muscle.
5. At
progressive stage of shock, no-reflow can be seen.
Ⅱ. Fill in blanks
1.
There are three basic stages in the process of hemorrhagic shock, they are
,
, and
.
2. The
immature immune system of
, and the
weakened immune system of
, often accompanied by chronic illness, make these populations more
susceptible to septic shock.
3. The
classification of shock according to the cause of shock is
, ,
,
,
,
and
.
4. Based on major
determinants that influence the tissue perfusion, shock is divided into three
types, they are
, and
.
5.
Based on peripheral vascular resistance and cardiac output shock is divided into
two types, they are and
.
6. Reduced blood flow to the kidney activates the
system, causing vasoconstriction and sodium and water retention,
leading to increased blood volume and venous return.
7. The
principle of supplying fluid for treating shock is according to the
, not according to the
.
Ⅲ.
Multiple choice questions of type A
1. The most common cause of cardiogenic shock is
A. Arrhythmias
B. Obstruction
C. Heart failure
D. Myocardial infarction
E. Pulmonary embolism
2. The most common cause of hypovolemic shock is:
A. Blood loss
B. Burns
C. Fluid shifts
D. Peritonitis
E. Ascites
3. Most common cause of septic shock is
A. gram-positive bacteria
B. gram-negative bacteria
C. Protozoa
D. ABO-incompatible blood
E. Viruses.
4. Which factor of the following keeps balance with TXA2?
A .NO
B. SOD
C. ADH
D. MDF
5. What is the major clinical signs in irreversible stage of shock?
A. Cold clammy grayish-bluish
B. Oliguria
C.
Overbreathing
D. Hypotension
E. Hyperventilation
6. Anaphylactic shock
is triggered by an allergic reaction, anaphylactic shock occurs when a person is
exposed to an antigen to which he has already been sensitized. Which kind of
cells play important role in this kind of shock?
A. White blood cells
B. Red blood cells
C. Mast cells
D. Acidocyte
E. Myocyte
7.Which factor directly trigger the septic shock?
A. Tumor necrosis factor (TNF)
B. Endotoxin
C. Thromboxane A2
D. Leukotrienes
E. Platelet-activating factor (PAF)
8. What is the manifestation of microcirculation at
early stage of shock?
A. Precapillary sphincter constriction
B. Blockade of the micro-vessels
C. No-reflow
D. Formation of micro-thrombus
E. Blood flow stop
9. For drug administration of early hypovolemic shock, the better choice is:
A. Avidin
B.
Medicine of dilatating vessel
C. Medicine of constricting vessel
D. Antibiotics
E. Anticoagulant
10.
For septic
shock, which kind of medicine is absolutely necessary?
A. Antibiotics
B. Diuretic
C. Histamine
D. Manitol
E. Heparin
Ⅳ. Multiple choice questions of type X
1. Causes of neurogenic shock may include
A. Spinal cord injury
B.
Spinal anesthesia
C. Vasomotor center depression
D. Hypoglycemia
E. Medications
2. Causes of septic shock may include
A. Gram-negative bacteria
B. Gram-positive bacteria
C. Protozoa
D. ABO-incompatible blood
E. Viruses
3.
What factors can cause hypovolemic shock?
A. Blood loss
B. Burns
C. Fluid shifts
D. Gastrointestinal fluid loss
E. Dehydration caused by excessive perspiration
4. Causes of anaphylactic shock may include
A. Vaccines
B. Spinal anesthesia
C. ABO-incompatible blood
D. Hypoglycemia
E. Venom
5.
What can cause cardiogenic shock?
A. Myocardial
infarction
B. Cardiomyopathy
C. Heart
failure
D. Pericardial tamponade
E. Tension
pneumothorax.
6. In ischemic hypoxia stage of shock, besides hyperactivity of
sympathetic- adrenal medulla system, some other vasoconstrictors also
have effects on
microcirculation. These vasoconstrictors
include
A. AngiotensinⅡ
B.
Antidiuretic,hormone (ADH)
C. Myocardial depressant factor (MDF)
D. Thromboxane A2 (TXA2)
E. Endothelin (ET)
7. Which factors are relative to
septic shock?
A. Tumor necrosis factor (TNF)
B. Endotoxins
C. Thromboxane A2
D. Leukotrienes
E. Platelet-activating factor (PAF)
8. What are the manifestations of microcirculation at
DIC stage of shock?
A. Congestion of microcirculation
B. Microvessel contraction
C. No-reflow of capillary
D. Formation of micro-thrombus
E. Blood flow became slow
9.
In the compensatory stage of shock, which signs and symptoms can be observed?
A. Tachycardia and bounding pulse due to sympathetic stimulation
B. Restlessness and irritability related to cerebral hypoxia
C. Tachypnea to compensate for hypoxia
D. Reduced urinary output secondary to vasoconstriction
E. Cool, pale skin associated with vasoconstriction, warm, dry skin in septic
shock due to vasodilation.
Ⅴ. Term explanations
1. shock
2. shock lung
3. hypodynamic
shock
4. hypovolemic shock
5. MDF
Ⅵ. Questions to be answered briefly
1. In compensatory stage of shock, what are the
compensatory significances?
2. Why does the body can maintain the BP in normal level in the ischemic
hypoxia stage of shock?
3. What factors are released into blood during
progressive stage of shock?
4. What are the manifestations of microcirculation at
DIC stage of shock?
5. What are the principles of treatment for shock?
6. What are the complications of shock?
Ⅶ. Questions to be answered in detail
1. What changes of microcirculation can occur in the
ischemic hypoxia stage of shock? Please describe the mechanisms of these changes
and significances of these changes.
2.
What are pathophysiology changes of progressive stage?
3.
Try to explain the clinical signs and
microcirculatory changes in DIC stage of shock.