Shock

Circulatory shock
• Circulatory shock means generalized inadequate
blood flow through the body, to the extent that the
body tissues are damaged because of too little flow,
• especially because of too little oxygen and other
nutrients delivered to the tissue cells.
• Even the CVS itself—the heart musculature, walls
of the blood vessels, vasomotor system, and
other circulatory parts
• —begins to deteriorate, so that the shock, once
begun, is prone to become progressively worse.

Causes of Shock
• Circulatory Shock Caused by Decreased Cardiac Output
• 1. Cardiac abnormalities that decrease the ability of the
heart to pump blood.
• MI, severe heart valve dysfunction, heart arrhythmias
• The circulatory shock that results from diminished cardiac
pumping ability is called cardiogenic shock.
• as many as 85 per cent of people who develop cardiogenic
shock do not survive.

Causes of Shock
• Circulatory Shock Caused by Decreased Cardiac
Output
• 2. Factors that decrease venous return also decrease
cardiac output because the heart cannot pump blood
that does not flow into it.
• diminished blood volume, decreased vascular tone,
obstruction to blood flow at some point in the
circulation,
• especially in the venous return pathway to the heart.

Causes of Shock
• Circulatory Shock That Occurs Without
Diminished Cardiac Output
• (1) excessive metabolism of the body, so that
even a normal cardiac output is inadequate
• (2) abnormal tissue perfusion patterns,
• so that most of the cardiac output is passing
through blood vessels above and beyond those
that supply the local tissues with nutrition.

What Happens to the Arterial
Pressure
• arterial pressure can often be seriously misleading.
• A person may be in severe shock and still have an almost
normal arterial pressure because of powerful nervous
reflexes that keep the pressure from falling.
• Arterial pressure can fall to half of normal, but the
person still has normal tissue perfusion and is not in shock.
• In most types of shock, especially shock caused by severe
blood loss, the arterial blood pressure decreases at the
same time as the cardiac output decreases

Tissue Deterioration Is the End
Result
• Once circulatory shock reaches a critical state of severity,
regardless of its initiating cause, the shock itself raises more
shock.
The inadequate blood flow causes the body tissues to begin
deteriorating, including the heart and circulatory system itself
even greater decrease in cardiac output vicious circle results
with progressively increasing circulatory shock less
adequate tissue perfusion more shock death.
• appropriate physiologic treatment can often reverse the rapid
slip to death.

Stages of Shock
• 1. A nonprogressive stage (sometimes called the
compensated stage), in which the normal circulatory
compensatory mechanisms eventually cause full
recovery without help from outside therapy.
• 2. A progressive stage, in which, without therapy, the
shock becomes steadily worse until death.
• 3. An irreversible stage, in which the shock has
progressed to such an extent that all forms of known
therapy are inadequate to save the person’s life, even
though, for the moment, the person is still alive.

Hypovolemic — Hemorrhagic
Shock
• Hypovolemia means diminished blood volume.
• Hemorrhage is the most common cause of
hypovolemic shock.
• Hemorrhage decreases the filling pressure of the
circulation and, as a consequence, decreases
venous return.
• As a result, the cardiac output falls below normal,
and shock may follow.

Sympathetic Reflex
• (1) The arterioles constrict in most parts of the
systemic circulation, thereby increasing the total
peripheral resistance.
• (2) The veins and venous reservoirs constrict,
thereby helping to maintain adequate venous
return despite diminished blood volume.
• (3) Heart activity increases markedly, sometimes
increasing the heart rate from the normal value of
72 beats/min to as high as 160 to 180 beats/min.

Sympathetic Reflex
• The sympathetic reflexes are more helpful for
maintaining arterial pressure than for maintaining
output.
• They increase the arterial pressure mainly by
increasing the total peripheral resistance, which has
no beneficial effect on cardiac output;
• however, the sympathetic constriction of the veins is
important to keep venous return and cardiac output
from falling too much, in addition to their role in
maintaining arterial pressure.

Sympathetic Reflex
• The sympathetic stimulation does not cause significant
constriction of either the cerebral or the cardiac vessels.
• In addition, local blood flow autoregulation is excellent in
brain and heart, which prevents decreasing their blood flows.
• blood flow through the heart and brain is maintained
essentially at normal levels as long as the arterial pressure
does not fall below about 70 mm Hg,
• blood flow in some other areas of the body might be
decreased very much by this time because of
vasoconstriction.

Nonprogressive Shock — Compensated
Shock
• 1. Baroreceptor reflexes, which elicit powerful
sympathetic stimulation of the circulation.
• 2. CNS ischemic response, which elicits even more
powerful sympathetic stimulation throughout the body
but is not activated significantly until the arterial
pressure falls below 50 mm Hg.
• 3. Reverse stress-relaxation of the circulatory system,
which causes the blood vessels to contract around the
diminished blood volume, so that the available blood
volume fills the circulation adequately.

Shock
• 4. Formation of angiotensin by the kidneys,
• which constricts the peripheral arteries and
• also causes decreased output of water and salt by
the kidneys,
• both of which help prevent progression of shock.
• 5. Formation of vasopressin (antidiuretic
hormone) by the posterior pituitary gland,
• which constricts the peripheral arteries and veins
• and greatly increases water retention by the
kidneys.

Shock
• 6. Compensatory mechanisms that return the blood
volume back toward normal,
• including absorption of large quantities of fluid from
the intestinal tract,
• absorption of fluid into the blood capillaries from the
interstitial spaces of the body,
• conservation of water and salt by the kidneys, and
• increased thirst and increased appetite for salt,
• which make the person drink water and eat salty foods
if able.

Shock
• The sympathetic reflexes provide immediate help toward
bringing about recovery because they become maximally
activated within 30 seconds to a minute after hemorrhage.
• The angiotensin and vasopressin mechanisms, as well as the
reverse stress-relaxation that causes contraction of the
blood vessels and venous reservoirs, all require 10 minutes to
1 hour to respond completely,
• Finally, readjustment of blood volume by absorption of fluid
from the interstitial spaces and intestinal tract,
• as well as oral ingestion and absorption of additional
quantities of water and salt, may require from 1 to 48 hours,

Progressive Shock
• Cardiac Depression.
• When the arterial pressure falls low enough, coronary
blood flow decreases below that required for
adequate nutrition of the myocardium.
• This weakens the heart muscle and thereby decreases
the cardiac output more.
• Thus, a positive feedback cycle has developed,
whereby the shock becomes more and more severe.

Progressive Shock
• Vasomotor Failure.
• In the early stages of shock, various circulatory reflexes cause intense
activity of the sympathetic nervous system - helps delay depression of
the cardiac output and helps prevent decreased arterial pressure.
• However, there comes a point when diminished blood flow to the
brain’s vasomotor center depresses the center so much that it, too,
becomes progressively less active and finally totally inactive.
• complete circulatory arrest to the brain causes, during the first 4 to 8
minutes, the most intense of all sympathetic discharges, but by the
end of 10 to 15 minutes, the vasomotor center becomes so depressed that
no further sympathetic discharge can be seen
• Fortunately, the vasomotor center usually does not fail in the early
stages of shock if the arterial pressure remains above 30 mm Hg.

Progressive Shock
• Blockage of Very Small Vessels—“Sludged Blood.”
• In time, blockage occurs in many of the very small blood vessels in the
circulatory system, and this also causes the shock to progress.
• The initiating cause of this blockage is sluggish blood flow in the micro
vessels.
• Because tissue metabolism continues despite the low flow, large
amounts of acid, both carbonic acid and lactic acid, continue to empty into
the local blood vessels and greatly increase the local acidity of the blood.
• This acid, plus other deterioration products from the ischemic tissues,
causes local blood agglutination, resulting in minute blood clots, leading
to very small plugs in the small vessels.
• an increased tendency for the blood cells to stick to one another makes
it more difficult for blood to flow through the microvasculature - Sludged
blood.

Progressive Shock
• Increased Capillary Permeability.
• After many hours of capillary hypoxia and lack of other
nutrients, the permeability of the capillaries gradually
increases, and large quantities of fluid begin to transude
into the tissues.
• This decreases the blood volume even more, with a
resultant further decrease in cardiac output, making the
shock still more severe.
• Capillary hypoxia does not cause increased capillary
permeability until the late stages of prolonged shock.

Progressive Shock
• Release of Toxins by Ischemic Tissue.
• shock causes tissues to release toxic substances, such as
histamine, serotonin, and tissue enzymes,
• that cause further deterioration of the circulatory system.
• Cardiac Depression Caused by Endotoxin.
• Endotoxin is released from the bodies of dead gram-negative
bacteria in the intestines.
• Diminished blood flow to the intestines often causes enhanced
formation and absorption of this toxic substance.
• The circulating toxin then causes increased cellular
metabolism despite inadequate nutrition of the cells;
• this has a specific effect on the heart muscle, causing cardiac
depression.

Generalized Cellular
Deterioration• Liver - because of lack of enough nutrients to support the
normally high rate of metabolism in liver cells,
• also because of the extreme exposure of the liver cells to any
vascular toxin or other abnormal metabolic factor occurring in
shock.
• 1. Active transport of sodium and potassium through the cell
membrane is greatly diminished.
• As a result, sodium and chloride accumulate in the cells, and
potassium is lost from the cells.
• In addition, the cells begin to swell.

Deterioration• 2. Mitochondrial activity in the liver cells, as well as in many
other tissues of the body, becomes severely depressed.
• 3. Lysosomes in the cells in widespread tissue areas begin to
break open, with intracellular release of hydrolases that
cause further intracellular deterioration.
• 4. Cellular metabolism of nutrients, such as glucose,
eventually becomes greatly depressed in the last stages of
shock.
• The actions of some hormones are depressed as well,
including almost 100 per cent depression of the action of
insulin.

Deterioration
• (1) the liver, with depression of its many
metabolic and detoxification functions;
• (2) the lungs, with eventual development
of pulmonary edema and poor ability to
oxygenate the blood; and
• (3) the heart, further depressing its
contractility.

Tissue Necrosis in Severe
Shock• necrosis in the center of a liver lobule
• the cardiac lesions play an important role in leading to the
final irreversible stage of shock.
• Deteriorative lesions also occur in the kidneys, especially in
the epithelium of the kidney tubules, leading to kidney
failure and occasionally uremic death several days later.
• Deterioration of the lungs also often leads to respiratory
distress and death several days later — called the shock
lung syndrome.

Acidosis in Shock
• poor delivery of oxygen to the tissues, which greatly diminishes
oxidative metabolism of the foodstuffs.
• anaerobic process of glycolysis, which leads to tremendous
quantities of excess lactic acid in the blood.
• Poor blood flow through tissues prevents normal removal of
carbon dioxide.
• The carbon dioxide reacts locally in the cells with water to form
high concentrations of intracellular carbonic acid; this, in turn,
reacts with various tissue chemicals to form still other
intracellular acidic substances.
• both generalized and local tissue acidosis, leading to further
progression of the shock itself.

Vicious Circle of Progressive
Shock• In mild degrees of shock, the negative feedback
mechanisms of the circulation
• —sympathetic reflexes, reverse stress-relaxation mechanism
of the blood reservoirs, absorption of fluid into the blood from
the interstitial spaces, and others—
• can easily overcome the positive feedback influences and,
therefore, cause recovery.
• But in severe degrees of shock, the deteriorative feedback
mechanisms become more and more powerful,
• leading to such rapid deterioration of the circulation that all
the normal negative feedback systems of circulatory
control acting together cannot return the cardiac output to
normal.

Irreversible Shock
• After shock has progressed to a certain stage, transfusion or
any other type of therapy becomes incapable of saving the
person’s life.
• The person is then said to be in the irreversible stage of
shock.
• even in this irreversible stage, therapy can, on rare
occasions, return the arterial pressure and even the cardiac
output to normal or near normal for short periods,
• But the circulatory system yet continues to deteriorate, and
death follows in another few minutes to few hours.

Irreversible Shock
• Multiple deteriorative changes have occurred in the muscle
cells of the heart that may not necessarily affect the heart’s
immediate ability to pump blood but,
• over a long period, depress heart pumping enough to cause
death.
• Beyond a certain point, so much tissue damage has occurred,
so many destructive enzymes have been released into the
body fluids, so much acidosis has developed, and so many
other destructive factors are now in progress that
• even a normal cardiac output for a few minutes cannot reverse
the continuing deterioration.
• in severe shock, a stage is eventually reached at which the
person will die even though vigorous therapy might still
return the cardiac output to normal for short periods.

Irreversible Shock
• The high-energy phosphate reserves in the tissues of the body,
especially in the liver and the heart, are greatly diminished in
severe degrees of shock.
• Essentially all the creatine phosphate has been degraded, and
almost all the ATPs has downgraded to ADPs, AMPs, and,
eventually, adenosine.
• much of this adenosine diffuses out of the cells into the
circulating blood and is converted into uric acid, a substance that
cannot re-enter the cells to reconstitute the adenosine phosphate
system.
• once the high-energy phosphate stores of the cells are depleted,
they are difficult to replenish.

Shock Caused by Plasma
Loss• 1. Intestinal obstruction is often a cause of severely reduced plasma
volume. Distention of the intestine in intestinal obstruction partly
blocks venous blood flow in the intestinal walls, which increases
intestinal capillary pressure.
• This in turn causes fluid to leak from the capillaries into the intestinal
walls and also into the intestinal lumen.
• Because the lost fluid has a high protein content, the result is
reduced total blood plasma protein as well as reduced plasma volume.
• 2. In almost all patients who have severe burns or other shedding
conditions of the skin, so much plasma is lost through the shed skin
areas that the plasma volume becomes markedly reduced.
• the blood viscosity increases greatly as a result of increased RBC
concentration in the remaining blood, and this worsens the
sluggishness of blood flow.

Shock Caused by Dehydration
• Loss of fluid from all fluid compartments of the body
is called dehydration - can reduce the blood volume
and cause hypovolemic shock
• (1) excessive sweating,
• (2) fluid loss in severe diarrhea or vomiting,
• (3) excess loss of fluid by nephrotic kidneys,
• (4) inadequate intake of fluid and electrolytes, or
• (5) destruction of the adrenal cortices, with loss of
aldosterone secretion and consequent failure of the
kidneys to reabsorb sodium, chloride, and water

Shock Caused by Trauma
• Often the shock results simply from hemorrhage caused by
the trauma,
• but it can also occur even without hemorrhage, because
extensive contusion of the body can damage the
capillaries sufficiently to allow excessive loss of plasma into
the tissues.
• there might be role of Toxic factors released by the
traumatized tissues as one of the causes of shock after
trauma
• there might also be a moderate degree of associated
neurogenic shock caused by loss of vasomotor tone

Neurogenic Shock
• the vascular capacity increases so much that even the
normal amount of blood becomes incapable of filling the
circulatory system adequately.
• sudden loss of vasomotor tone throughout the body, resulting
especially in massive dilation of the veins - neurogenic shock.
• either an increase in vascular capacity or a decrease in
blood volume reduces the mean systemic filling pressure,
which reduces venous return to the heart.
• Diminished venous return caused by vascular dilation is
called venous pooling of blood.

Neurogenic Shock
• 1. Deep general anesthesia often depresses the vasomotor center
enough to cause vasomotor paralysis, with resulting neurogenic shock.
• 2. Spinal anesthesia, when blocks the sympathetic nervous outflow
from the nervous system and can be a potent cause of neurogenic
shock.
• 3. Brain damage is often a cause of vasomotor paralysis.
• Many patients who have had brain injury in the basal regions of the
brain develop profound neurogenic shock.
• Also, even though brain ischemia for a few minutes almost always
causes extreme vasomotor stimulation,
• prolonged ischemia (lasting longer than 5 to 10 minutes) can cause
total inactivation of the vasomotor neurons in the brain stem

Anaphylactic & Histamine
Shock• Anaphylaxis is an allergic condition in which the cardiac output and
arterial pressure often decrease severely – results from an antigen-
antibody reaction after an antigen to which the person is sensitive enters
the circulation.
• One of the principal effects is to cause the basophils in the blood and mast
cells to release histamine or a histamine-like substance. The histamine causes
• (1) an increase in vascular capacity because of venous dilation, thus
causing a marked decrease in venous return;
• (2) dilation of the arterioles, resulting in greatly reduced arterial
pressure;
• (3) greatly increased capillary permeability, with rapid loss of fluid and
protein into the tissue spaces.
• The net effect is a great reduction in venous return and sometimes such
serious shock that the person dies within minutes.
• I.V. injection of large amounts of histamine causes “histamine shock,”

Septic Shock
• A condition that was formerly known by the popular name
“blood poisoning” is now called septic shock
• This refers to a bacterial infection widely spread to many
areas of the body, with the infection being spread through
the blood from one tissue to another and causing extensive
damage.
• There are many varieties of septic shock because of the
many types of bacterial infections that can cause it and
because infection in different parts of the body produces
different effects.
• septic shock is the 2nd most frequent cause of shock-
related death in the modern hospital – 1st cardiogenic shock

Causes of Septic Shock
• 1. Peritonitis caused by spread of infection from the uterus and
fallopian tubes, sometimes resulting from instrumental
abortion performed under unsterile conditions.
• 2. Peritonitis resulting from rupture of the gastrointestinal
system, sometimes caused by intestinal disease and sometimes
by wounds.
• 3. Generalized bodily infection resulting from spread of a skin
infection such as streptococcal or staphylococcal infection.
• 4. Generalized gangrenous infection resulting specifically from
gas gangrene bacilli, spreading first through peripheral tissues
and finally by way of the blood to the internal organs, especially
the liver.
• 5. Infection spreading into the blood from the kidney or urinary
tract, often caused by colon bacilli.

Features of Septic Shock
• 1. High fever.
• 2. Often marked vasodilation throughout the body, especially in the infected
tissues.
• 3. High cardiac output caused by arteriolar dilation in the infected tissues
and by high metabolic rate and vasodilation elsewhere in the body,
• resulting from bacterial toxin stimulation of cellular metabolism and from
high body temperature.
• 4. Sludging of the blood, caused by red cell agglutination in response to
degenerating tissues.
• 5. Development of micro–blood clots in widespread areas of the body, a
condition called disseminated intravascular coagulation.
• Also, this causes the blood clotting factors to be used up, so that
hemorrhaging occurs in many tissues, especially in the gut wall of the
intestinal tract.

Features of Septic Shock
• In early stages of septic shock, the patient usually does not
have signs of circulatory collapse but only signs of the bacterial
infection.
• As the infection becomes more severe, the circulatory system
usually becomes involved either because of direct extension of
the infection or secondarily as a result of toxins from the
bacteria,
• with subsequent loss of plasma into the infected tissues
through weakening blood capillary walls.
• There finally comes a point at which weakening of the
circulation becomes progressive in the same way that
progression occurs in all other types of shock.

Physiology of Treatment
• Replacement Therapy
• Blood and Plasma Transfusion
• If a person is in shock caused by hemorrhage, the best
possible therapy is usually transfusion of whole blood.
• If the shock is caused by plasma loss, the best therapy is
administration of plasma;
• when dehydration is the cause, administration of an
appropriate electrolyte solution can correct the shock.
• Whole blood is not always available, such as under
battlefield conditions - Plasma can usually substitute
adequately for whole blood because it increases the blood
volume and restores normal hemodynamics.

Physiology of Treatment
• Replacement Therapy
• Blood and Plasma Transfusion
• Plasma cannot restore a normal hematocrit, but the human
body can usually stand a decrease in hematocrit to about half
of normal before serious consequences result, if cardiac
output is adequate.
• So, in emergency conditions, it is reasonable to use plasma in
place of whole blood for treatment of hemorrhagic or most
other types of hypovolemic shock.
• Sometimes plasma is unavailable - various plasma
substitutes have been developed that perform almost exactly
the same functions as plasma - dextran solution.

Dextran Solution
• The principal requirement of a truly effective plasma
substitute is that it remain in the circulatory system — that is,
not filter through the capillary pores into the tissue spaces.
• the solution must be nontoxic and must contain appropriate
electrolytes to prevent imbalance of the body’s ECF
electrolytes on administration.
• To remain in the circulation, the plasma substitute must
contain some substance with large enough molecular size
to exert colloid osmotic pressure.
• One of the most satisfactory substances developed for this
purpose is dextran, a large polysaccharide polymer of
glucose.

Dextran Solution
• Certain bacteria secrete dextran as a byproduct
of their growth, and commercial dextran can be
manufactured using a bacterial culture procedure.
• By varying the growth conditions of the bacteria,
the molecular weight of the dextran can be
controlled to the desired value.
• Dextrans of appropriate molecular size do not
pass through the capillary pores and, therefore,
can replace plasma proteins as colloid osmotic
agents.

Sympathomimetic Drugs
• A sympathomimetic drug is a drug that mimics
sympathetic stimulation.
• These drugs include norepinephrine, epinephrine,
and a large number of other long-acting drugs
• In two types of shock, sympathomimetic drugs have
proved to be especially beneficial.
• The first of these is neurogenic shock, in which the
sympathetic nervous system is severely depressed.
• Administering a sympathomimetic drug takes the
place of the diminished sympathetic actions and can
often restore full circulatory function.

Sympathomimetic Drugs
• The second type of shock in which sympathomimetic drugs are
valuable is anaphylactic shock, in which excess histamine plays
a prominent role.
• The sympathomimetic drugs have a vasoconstrictor effect
that opposes the vasodilating effect of histamine.
• Therefore, sympathomimetic drug is often lifesaving.
• Sympathomimetic drugs have not proved to be very valuable
in hemorrhagic shock.
• The sympathetic nervous system is almost always maximally
activated by the circulatory reflexes already;
• so much norepinephrine and epinephrine are already
circulating in the blood that sympathomimetic drugs have
essentially no additional beneficial effect.

Head-Down Position
• When the pressure falls too low in most types of
shock, especially in hemorrhagic and neurogenic
shock,
• placing the patient with the head at least 12 inches
lower than the feet helps greatly in promoting venous
return,
• thereby also increasing cardiac output.
• This head down position is the first essential step in
the treatment of many types of shock.

Oxygen Therapy
• Because the major deleterious effect of most
types of shock is too little delivery of oxygen to
the tissues, giving the patient oxygen to breathe
can be of benefit in many instances.
• However, this frequently is far less beneficial
because the problem in most types of shock is
not inadequate oxygenation of the blood by
the lungs but inadequate transport of the blood
after it is oxygenated

Glucocorticoids
• (1) experiments have shown that glucocorticoids
frequently increase the strength of the heart in
the late stages of shock;
• (2) glucocorticoids stabilize lysosomes in tissue
cells and thereby prevent release of lysosomal
enzymes into the cytoplasm of the cells, thus
preventing worsening from this source;
• (3) glucocorticoids help in the metabolism of
glucose by the severely damaged cells.

Circulatory Arrest
• A condition closely similar to circulatory shock is circulatory arrest, in
which all blood flow stops.
• This occurs frequently on the surgical operating table as a result of
cardiac arrest or ventricular fibrillation.
• Ventricular fibrillation can usually be stopped by strong electroshock of
the heart
• Cardiac arrest often results from too little oxygen in the anesthetic
gaseous mixture or from a depressant effect of the anesthesia itself.
• A normal cardiac rhythm can usually be restored by removing the
anesthetic and immediately applying cardiopulmonary resuscitation
procedures, while at the same time supplying the patient’s lungs with
adequate quantities of ventilatory oxygen.

Effect of Circulatory Arrest
• In general, more than 5 to 8 minutes of total circulatory
arrest can cause at least some degree of permanent brain
damage in more than half of patients.
• Circulatory arrest for as long as 10 to 15 minutes almost
always permanently destroys significant amounts of mental
power.
• severe brain damage that occurs from circulatory arrest is
caused mainly by permanent blockage of many small
blood vessels by blood clots,
• thus leading to prolonged ischemia and eventual death of
the neurons.

Hypovolemic shock (decreased blood volume)
Hemorrhage
Trauma
Surgery
Burns
Fluid loss due to vomiting and/or diarrhea
Distributive shock (marked vasodilation; also called vasogenic or low-resistance shock)
Fainting (neurogenic shock)
Anaphylaxis
Sepsis (also causes Hypovolemia due to increased capillary permeability with loss of fluid
into tissues)
Cardiogenic shock (inadequate output by a diseased heart)
Myocardial infarction
Congestive heart failure
Arrhythmias
Obstructive shock (obstruction of blood flow)
Tension pneumothorax
Pulmonary embolism
Cardiac tumor
Cardiac tamponade

Shock

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