1. CIRCULATORY SHOCK
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2. Circulatory shock Circulatory shock means
Generalized inadequacy of blood flow
throughout the body
including Heart, brain, liver, kidneys, GIT
to the extend that the body tissues are damaged.
Tissue damage occur because of too little flow,
especially because of too little delivery of oxygen and other nutrients to the tissue cells.
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3. Circulatory Shock Symptoms Initially are agitation and restlessness
which later progress to lethargy, confusion and coma.
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4. Stages of shock. Non progressive stage Progressive stage
Irreversible stage
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5. Non progressive stage Also known as compensated stage
Normal circulatory compensatory mechanisms
eventually cause full recovery
without help form outside therapy.
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6. Progressive stage Shock become steadily worse until death
If no therapy
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7. Irreversible stage The shock has progressed to such an extent
that all forms of known therapy are inadequate to save life
Even though the moment, the person is still alive.
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8. Irreversible shock Even in this stage, therapy can on rare occasions,
still return the arterial pressure
and even the CO to normal or near normal for short period
But the circulatory system nevertheless
continue to deteriorate
and death ensues in another few minutes to few hours.
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9. Irreversible shock Hemorrhage 100 – -- CO (% of normal)
25 --
Progressive stage
CO (% of normal)
Transfusion
Irreversible shock
minutes
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10. Irreversible shock There is depletion
of cellular high Energy Phosphate reserves
Creatine Phosphate, ATP
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11. Pathophysiology of shock
Shock usually results from inadequate CO.
Therefore any condition that reduces CO
will probably lead to circulatory shock.
These include
diminished cardiac pumping ability
Factors decreasing venous return
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12. Diminished cardiac pumping ability
Cardiac abnormalities
that decrease the pumping ability of the heart.
include:
Myocardial infarction
Severe heart valve dysfunction
Cardiac arrhythmias
Other cardiac diseases
Circulatory shock resulting
from diminished cardiac pumping ability
cardiogenic shock.
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13. Cardiogenic shock Results from markedly decreased CO
Inadequate cardiac function
eg from MI,mechanical disorders
Abnormally slow or fast ventricular rate.
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14. Factors that decrease the venous return
Decreased vascular tone
esp. of the venous reservoirs
Low resistance shock
Diminished blood volume
Hypovolemic shock
The most common type.
Obstruction to blood flow
at some point in the circulation
esp. in the venous return pathway to the heart.
obstructive shock
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15. Low resistance shock Occurs when neural reflexes or toxic substances
cause excessive vasodilatation
Leading to
Reduced venous return
Low CO
Diminished venous return
caused by vascular dilatation
venous pooling of blood.
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16. Low resistance shock This includes Primary shock/neurogenic shock
Anaphylactic shock
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17. Primary /neurogenic shock
Also called syncope, fainting
Leads to loss of consciousness
Due to increased vascular capacity
Caused by a reflex
that produce arteriolar and venous dilatation
causing peripheral pooling of blood.
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18. Primary /neurogenic shock
Increased vascular capacity
reduces the mean systemic filling pressure
Which in turn reduces venous return
Without an adequate venous return
the cardiac output declines,
arterial blood pressure decreases,
and blood flow to the brain decreases.
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19. Primary /neurogenic shock
One of the major causes,
is sudden loss of vasomotor tone throughout the body
Causing esp. massive dilatation of the veins
Some of the factors that can cause loss of vasomotor tone include
Deep general anesthesia
often depresses the vasomotor center
Spinal anesthesia,
can block the sympathetic nervous system.
Brain damage
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20. Primary/neurogenic shock
provoked by pain, stress, fright or heat.
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21. Vasovagal Syncope Emotional fainting Not caused by vasomotor failure
Results from strong emotional activation
of parasympathetic signals to slow the heart
and also activation of inverse sympathetic signals
to dilate the peripheral vasculature
thereby reducing CO and arterial pressure
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22. Vasovagal Syncope Called Vasovagal Syncope
to differentiate it from other fainting
that result from other neurogenic causes of reducing CO
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23. Anaphylactic shock Antigen antibody reaction Histamine causes:
cause the basophils and mast cells to release histamine or a histamine like substance
Histamine causes:
An increased vascular capacity because of venous dilatation
Dilatation of the arterioles
reduce TPR
Increased capillary permeability
The net effect is a great reduction in venous return
and often such serious shock that the person dies within minutes.
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24. Other causes of low resistance shock
Severe hypoxia, drugs overdose, trauma to the nervous system.
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25. Hypovolemic shock. Caused by low blood volume Includes
Hemorrhagic shock
Plasma loss
Dehydration shock
Septic shock
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26. Hemorrhagic shock Hemorrhage is the most common cause
of hypovolemic shock
Occurs as a result of internal or external blood loss
caused by rupture of vessels.
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27. Hemorrhagic shock Hemorrhage As a consequence decreases venous return
decreases the filling pressure of the circulation
As a consequence decreases venous return
As a result the CO falls bellow normal and shock ensues.
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28. Hypovolemic shock caused by Plasma loss
Plasma loss can be severe enough
to reduce the total Blood volume markedly
leading to hypovolemic shock similar to that caused by hemorrhage
Severe plasma loss occurs in
Intestinal obstruction
Severe burn
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29. Intestinal obstruction
Distention of intestines
partly blocks venous blood flow in the intestinal circulation
Increasing intestinal capillary pressure
Fluid leakage into the intestinal walls and into the intestinal lumen.
Severe burn
Also causes plasma loss
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30. Dehydration Dehydration can reduce the blood volume
and cause hypovolemic shock
similar to that resulting from hemorrhage.
Some of the causes of dehydration are:
Fluid loss from
GIT
diarrhea, vomiting
Skin
burns ,Excessive sweating
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31. Dehydration Kidneys Inadequate intake of fluid and electrolytes
Diabetes mellitus/insipidius,
excessive use of diuretics
Nephrotic syndrome
Destruction of the adrenal cortex
absence of aldosterone
Inadequate intake of fluid and electrolytes
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32. Septic shock Infections in the blood stream Gram –negative sepsis
esp. Gram –negative bacteria
or bacterial toxins released from an infected site
cause hypotension
Gram –negative sepsis
increase the permeability of the microvasculature,
facilitating the movement of fluid into the tissues
and intensifying the hypotension.
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33. Obstructive shock CO is reduced as a result of
a mechanical impediment
to Lt or Rt ventricular filling
Massive pulmonary emboli, tension pneumothorax, cardiac tamponade
can all lead to obstructive shock.
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34. More Causes of shock
Occasionally the CO is normal or even greater than normal
and yet a person is in circulatory shock.
This can result from
Excessive metabolism of the body
Abnormal tissue perfusion patterns
Note:
Arterial pressure may be almost normal in severe shock
powerful nervous reflexes
Arterial pressure can fall to one – half normal
but the person still has normal tissue perfusion
and is not in shock.
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35. Trauma . Trauma is one of the most common cause of circulatory shock
Hemorrhage
Contusion of the body can damage the capillaries sufficiently to allow
Excessive loss of plasma into the tissues
Pain of trauma can cause neurogenic shock
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36. Circulatory shock Tissue deterioration
is the end stage of circulatory shock.
Inadequate blood flow causes the tissues
to begin deteriorating
including the heart and circulatory system itself.
This causes even more decrease in CO,
And vicious circle ensues with progressive increasing circulatory shock,
less adequate tissue perfusion
more shock and so forth until death.
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37. Compensatory mechanisms
The factors that cause a person to recover
from moderate degrees of shock
are all the negative feedback control mechanisms of the circulation
that attempt to return Cardiac output
and arterial pressure back to normal levels.
They compensate enough
to prevent further deterioration of the circulation.
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38. Compensatory mechanisms
They include
Sympathetic reflexes
and factors that return blood volume
back towards normal
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39. Sympathetic reflexes These include Baroreceptor reflexes
CNS ischaemic response
Chemoreceptor response
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40. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
About 10% of total blood volume
can be removed
with almost no effect on either arterial pressure or CO
Greater blood loss usually diminishes
the CO first and later the pressure
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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41. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
Both of these falling to zero
when about 35 – 45% total blood volume has been removed.
Sympathetic reflexes
maintain BP.
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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42. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
Powerful sympathetic reflexes initiated
mainly by the baroreceptors
and by low pressure vascular stretch receptors
These reflexes stimulate SNS
Vasoconstriction
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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43. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
constriction of arterioles
increases the TPR
Constriction of veins
helps to maintain adequate venous return
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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44. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
Sympathetic stimulation
increases heart activity
increasing HR to as high as 160 – 180 beats/min
Also force of contraction
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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45. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
Without sympathetic reflexes
only 15 – 20% of blood can be removed over a period of 30min before a person dies.
Cf. 30 – 40% blood volume loss that a person can sustain when the reflexes are intact.
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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46. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
Sympathetic reflexes
are geared more for maintaining arterial pressure
than for maintaining cardiac output.
TPR.
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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47. CO&Arterial pressure (% of normal)
Relationship of bleeding volume to CO and BP
Second plateau at about 50mmHg
in the arterial pressure curve is due to activation of CNS ischaemic response.
Which causes extreme stimulation of SNS
due to brain hypoxia
100 BP
CO&Arterial pressure (% of normal) 50 CO
% of total blood removed
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48. Note Sympathetic stimulation does not cause significant constriction
of either the cerebral
or the cardiac vessels
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49. Factors that restore blood volume
Rennin Angiotensin system
Release of ADH (vasopressin)
Compensatory mechanisms
that return the blood volume back toward normal
may require 1 – 48hrs
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50. Decompensatory mechanisms
Progressive shock
Is caused by a vicious circle of cardiovascular deterioration
Caused by decompensatory mechanisms
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51. Decompensatory mechanisms
These include:
Cardiac depression
Vasomotor failure
Blockage of minute vessels
Increased capillary permeability
Release of toxins by ischaemic tissues
Generalized cellular deterioration
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52. Cardiac depression When arterial pressure falls low enough
Coronary blood flow decreases below that required
for adequate nutrition of myocardium.
This weakens the heart muscle
and thereby decreases the CO still more.
Thus a positive feedback cycle has developed
whereby the shock becomes more and more severe.
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53. Vasomotor failure. There comes a point in which diminished blood flow
to the brain’s vasomotor center
so depresses the center
that it becomes progressively less active
And finally totally inactive
Vasomotor center fails only in the late stage of shock
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54. Blockage of minute vessels
Initiated by sluggish blood flow in the microvessels
Metabolic activities lead to accumulation of acids
Acidity plus other products from ischaemic tissues
cause local blood agglutination,
resulting in minute blood clots
and leading to minute plugs in the small vessels
This causes shock to progress.
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55. Increased capillary permeability
Occur after many hours of capillary hypoxia
and lack of other nutrients
Large quantities of fluid transude into the tissues
decreasing the blood volume even more
with resultant further decrease in CO
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56. Release of toxins by Ischaemic tissues
Toxic substances such as histamine, serotonin and tissue enzymes
cause further deterioration of the circulatory system.
Endotoxin causes greatly increased cellular metabolism,
despite the inadequate nutrition of the cells
It affects cardiac muscle to cause cardiac depression.
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57. Generalized cellular deterioration
As shock becomes severe,
many signs of generalized cellular deterioration
occur throughout the body.
Among the damaging cellular effects are:
diminished active transport of Na+ and K+(greatly)
Depressed mitochondria activity (severely)
Intracellular release of hydrolases from lysosomes
causing further intracellular deterioration
Depressed cellular metabolism of nutrients such as glucose.
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58. Decompensatory mechanisms
Decreased CO
Arterial pressure
Systemic blood flow
Cardiac nutrition
Nutrition of tissues
Vascular system
nutrition
Intravascular clotting
Brain nutrition
Vasomotor activity
Tissue ischemia
Capillary
permeability
Release of toxins
Vascular dilatation
Blood volume
Venous pooling of blood
Cardiac depression
Venous return
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59. Treatment of shock Replacement therapy Sympathomimetic drugs
Blood and plasma transfusion
Plasma substitute
Sympathomimetic drugs
eg. Epinephrine, norepinephrine
Sometimes useful, sometimes not
Useful in neurogenic and anaphylactic shock
Not proved to be very valuable in hemorrhage shock
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60. Treatment of shock Other therapy Glucocorticoids Head down position
Oxygen therapy
glucocorticoids
Glucocorticoids
Increases the strength of the heart
in the late stage of shock
Stabilize the lysosomal membrane
Might aid in the metabolism of glucose
by the severely damaged cells.
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