PEDIATRICS 2

II. HYPOVOLEMIA-HEMMORHAGIC SHOCK

F.15 CIRCULATORY SHOCK AND PHYSIOLOGY OF ITS
TREATMENT  HYPOVOLEMIA - diminished blood volume.
Dr. Balanag | May 09, 2019  HEMORRHAGE - most common cause of hypovolemic shock.
 decreases the filling pressure
 decreases venous return
OUTLINE:  CO falls below normal, and shock may ensue
I. CIRCULATORY SHOCK
II. HYPOVOLEMIA-HEMMORHAGIC SHOCK
III. PROGRESSIVE VS. NON-PROGRESSIVE HEMORRHAGIC SHOCK
IV. IRREVERSIBLE SHOCK
V. HYPOVOLEMIC SHOCK
VI. NEUROGENIC SHOCK
VII. ANAPHYLACTIC SHOCK
VIII. SEPTIC SHOCK
IX. TREATMENT

I. CIRCULATORY SHOCK

 State of acute circulatory dysfunction → failure of delivery of sufficient

oxygen and other nutrients to meet the metabolic demands of the
tissues. Since there is no more blood flow, acidosis happens. It
contributes to the vicious cycle. The more acidotic, the more it will
proliferate decrease in musculature, decrease in pumping of the
blood, decrease in the usage of nutrients. Acidosis begets further
acidosis. Eventually leading to shock. SYMPATHETIC REFLEX

 Heart musculature, blood vessels, vasomotor system begins to 3 important effects:

deteriorate → once begun, is prone to become progressively worse 1. The arterioles CONSTRICT → increasing the TPR
2. The veins and venous reservoirs CONSTRICT → maintain adequate
CAUSES OF SHOCK venous return despite diminished blood volume
3. Heart activity INCREASES, to as high as 160 to 180 beats/min
1. DECREASED CARDIAC OUTPUT
 In the absence of the sympathetic reflexes, only 15-20% of the BV
 2 factors that can reduce cardiac output: can be removed over a period of 30 min before a person dies
CARDIAC ‒ myocardial infarction  Sympathetic reflexes delays death by 2x
ABNORMALITIES ‒ toxic states of the heart ‒ geared more for maintaining arterial pressure than for
(just think of 3 ‒ severe heart valve dysfunction maintaining output
things: cardiac ‒ heart arrhythmias  Second plateau at about 50 mm Hg
itself, preload & ‒ cardiogenic shock: 85% of people do not  “last-ditch stand” - activation of the CNS ischemic response
after load) survive ‒ extreme stimulation of the sympathetic nervous system when the
DECREASE ‒ diminished blood volume brain begins to suffer from lack of oxygen or from excess build-
VENOUS RETURN ‒ decreased vascular tone up of carbon dioxide
‒ obstruction to blood flow
PROTECTION OF CORONARY/CEREBRAL BLOOD FLOW
2. WITHOUT DIMINISHED CARDIAC OUTPUT
AUTOREGULATION
a) excessive metabolism of the body  Moderate decreases in arterial pressure from significantly
b) abnormal tissue perfusion patterns decreasing their blood flows.
 Inadequate delivery of nutrients to critical tissues and critical organs ‒ blood flow through the heart and brain is maintained essentially
→ inadequate removal of cellular waste products from the tissues. at normal levels as long as the arterial pressure does not fall below
 Vicious circle: Progressive circulatory shock → less adequate tissue about 70 mm Hg
perfusion → more shock → death
III. PROGRESSIVE VS.
STAGES OF SHOCK NONPROGRESSIVE HEMORRHAGIC SHOCK

1. NON-PROGRESSIVE STAGE (COMPENSATED STAGE): normal

circulatory compensatory mechanisms (neurohormonal) cause full
recovery without help from outside therapy

2. PROGRESSIVE STAGE: without therapy, the shock becomes steadily

worse until death.

3. IRREVERSIBLE STAGE: all forms of known therapy are inadequate to

save the person's life, even though, for the moment, the person is still
alive

Transcribers: DATUD, ALCANTARA, TOLIONGCO Page 1 of 4

 PEDIATRICS 2
NON-PROGRESSIVE SHOCK
 Negative feedback control mechanisms
‒ Baroreceptor
‒ Central nervous system ischemic response
‒ Reverse stress-relaxation of the circulatory system
‒ Formation of angiotensin by the kidneys
‒ Formation of vasopressin (antidiuretic hormone) by the
posterior pituitary gland
‒ Compensatory mechanisms that return the blood volume back
toward normal
PROGRESSIVE SHOCK
“POSITIVE FEEDBACK” can lead to progression of shock
 Positive feedback control mechanisms
‒ Cardiac Depression
‒ Vasomotor Failure
‒ Blockage of Very Small Vessels - "Sludged Blood”
‒ Increased Capillary Permeability
‒ Release of Toxins by Ischemic Tissue
‒ Cardiac Depression Caused by Endotoxin
‒ Generalized Cellular Deterioration
PROGRESSIVE DETERIORATION OF THE HEART AT DIFFERENT
TIMES AFTER THE ONSET OF SHOCK
Transcribers: DATUD, ALCANTARA, TOLIONGCO
 In the early stages of shock:
‒ plays very little role in the condition of the person
‒ deterioration of the heart is not severe during the first hour
‒ Heart has tremendous reserve capability (300 to 400%)
 Deterioration of the heart is the most important factor in the final
lethal progression of the shock.
 GENERALIZED CELLULAR DETERIORATION
‒ Diminished active transport of sodium and potassium
‒ Mitochondrial activity depression
‒ Lysosomes break open
‒ Cellular metabolism depression
 FURTHER DETERIORATION OF ORGANS
Liver - depression of its many metabolic and detoxification functions
Lungs - eventual development of pulmonary edema and poor ability
to oxygenate the blood
Heart - further depressing its contractility
 TISSUE NECROSIS IN SEVERE SHOCK-PATCHY AREAS OF
NECROSIS DUE TO PATCHY BLOOD FLOWS IN DIFFERENT
ORGANS
‒ Not all cells are equally damaged
‒ Cells adjacent to the arterial ends of capillaries receive better
nutrition than cells adjacent to the venous ends of the same
capillaries
‒ Similar punctate lesions occur in heart muscle, kidney tubules,
lungs (shock lung syndrome)
 ACIDOSIS IN SHOCK
‒ anaerobic process of glycolysis → excess lactic acid
‒ Decreased removal of carbon dioxide
 CO2 reacts locally in the cells with water to form carbonic
acid → local tissue acidosis → further progression of the
shock
IRREVERSIBLE SHOCK
 Transfusion during the irreversible stage can sometimes cause the
cardiac output (as well as the arterial pressure) to return to normal
 Beyond a certain point
‒ tissue damage
‒ destructive enzymes
‒ acidosis
 Many other destructive factors have caused the continuing
deterioration
 Depletion of Cellular High-Energy Phosphate Reserves in
Irreversible Shock
‒ Creatine phosphate → adenosine triphosphate → adenosine
diphosphate → adenosine monophosphate → adenosine →
diffuses out of the cells into the circulating blood → Converted
into uric acid → cannot re-enter the cells to reconstitute the
adenosine phosphate system
 New adenosine can be synthesized at a rate of 2% of
the normal cellular amount an hour
‒ Cellular depletion of high-energy compounds
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 PEDIATRICS 2
 Hypovolemic Shock Caused by Plasma Loss
‒ Intestinal obstruction
‒ Severe burns
‒ Blood viscosity increases greatly → increased RBC
concentration → exacerbates the sluggishness of blood flow
HYPOVOLEMIC SHOCK
DEHYDRATION - loss of fluid from all fluid compartments of the body
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
5. Destruction of the adrenal cortices, with loss of aldosterone
secretion and consequent failure of the kidneys to reabsorb
sodium, chloride, and water, which occurs in the absence of the
adrenocortical hormone aldosterone
NEUROGENIC SHOCK
 Results without any loss of blood volume
 Vascular capacity increases so much
 Sudden loss of vasomotor tone
 Causes of Neurogenic Shock:
‒ Deep general anesthesia
‒ Spinal anesthesia
‒ Brain damage
ANAPHYLACTIC SHOCK
ANAPHYLAXIS - an allergic condition in which the cardiac output and
arterial pressure often decrease drastically
‒ Results from an antigen-antibody formation
‒ Basophils in the blood and mast cells in the pericapillary
tissues to release histamine or a histamine-like substance
1. venous dilation
2. dilation of the arterioles
3. greatly increased capillary permeability
‒ Intravenous injection of large amounts of histamine causes
"histamine shock," which has characteristics almost identical
to those of anaphylactic shock
SEPTIC SHOCK
 Bacterial infection widely disseminated to many areas of the body,
with the infection being borne through the blood from one tissue to
another and causing extensive damage.
 Most frequent cause of shock-related death in the modern hospital
‒ Peritonitis e.g. instrumental abortion, ruptured viscus
‒ Skin infection e.g. Streptococcal or Staphylococcal infection
‒ Gangrenous infection
‒ Urosepsis
 Special Features of Septic Shock
‒ High fever
‒ Marked vasodilation
‒ High cardiac output
‒ High metabolic rate
‒ Sludging of the blood
‒ Disseminated intravascular coagulation
Transcribers: DATUD, ALCANTARA, TOLIONGCO
PHYSIOLOGY OF TREATMENT IN SHOCK
1. REPLACEMENT THERAPY
a. 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. 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. Therefore, 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. In these instances, various plasma
substitutes have been developed that perform almost exactly the same
hemodynamic functions as plasma. One of these is dextran solution.
b. Dextran Solution as a Plasma Substitute
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. In addition, the solution must be nontoxic
and must contain appropriate electrolytes to prevent derangement of
the body's extracellular fluid electrolytes on administration.
2. SYMPATHOMIMETIC DRUG
A sympathomimetic drug is a drug that mimics sympathetic
stimulation. These drugs include norepinephrine, epinephrine, and a
large number of long-acting drugs that have the same effect as
epinephrine and norepinephrine.
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.
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,
either norepinephrine or another sympathomimetic drug is often
lifesaving.
Sympathomimetic drugs have not proved to be very valuable in
hemorrhagic shock. The reason is that in this type of 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.
3. HEAD-DOWN POSITION
4. OXYGEN THERAPY
5. GLUCOCORTICOIDS (ADRENAL CORTEX HORMONES THAT
CONTROL GLUCOSE METABOLISM)
 experiments have shown empirically that glucocorticoids
frequently increase the strength of the heart in the late stages of
shock
 stabilize lysosomes in tissue cells
 Aid in the metabolism of glucose by the severely damaged cells.
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 PEDIATRICS 2
CIRCULATORY ARREST

 >5 - 8 min of total circulatory arrest → some degree of permanent

brain damage in more than half of patients
 10 - 15 min almost always permanently destroys significant amounts
of mental power
 Acute cerebral hypoxia that occurs during circulatory arrest
 If blood clots are prevented from occurring in the brain → prevents
most of the early deterioration of the brain during circulatory arrest
 All the blood was removed from the animal's blood vessels at
the beginning of circulatory arrest → replaced at the end of
circulatory arrest so that no intravascular blood clotting could
occur

Transcribers: DATUD, ALCANTARA, TOLIONGCO Page 4 of 4