SHOCK INTERNAL EVENTS

7. PATH PHYSIOLOGY OF SHOCK

Hypo-perfusion, and O2 lack, are common to all types of shock
syndromes.
Shock syndromes, may vary in severity, from silent tissue hypoxia,
to multiple organ failure.
In cases of septic shock, hyper-dynamic circulatory state, is
accompanied by a high O2 debt, due to excessive O2 demand in the presence of infection resulting in hypoxia.

Any Impaired tissue perfusion, leads to low delivery of oxygen in
relation to tissue needs,this is the basic cause of shock state.
The precise role of hypoxia, in pathogenesis of shock, is not clear as yet.
With improved techniques, it is hoped this role will be better
understood. However the events that follow shock states are;

7.1 Acidosis

As the oxygen delivery is deficient to meet O2 demand of tissues,
anaerobic glycolysis (breakdown) starts.
In the absence of O2 pyruvate is converted to lactate, and two molecules of adenosine troposphere (ATP) are made available.
In cases of adequate O2 3 molecules of ATP are released per one molecule of glucose utilized.

As the O2 diminishes, lactate increases and pyruvate diminishes.
This high Lactate level has been correlated with survival in
studies where lactate concentration increase beyond O-2m mol per
liter.

The effects of metabolic acidosis are;
-bradycardia,
-vasodilatation,
-decreased cardiac output and
-ventricular fibrillation.

7.2 Circulatory Redistribution

As a result of hypoxia, the homeostatic response is to preserve
oxygen delivery, to heart and the brain.
This is achieved by diverting blood flow, from other organs (skin, GI tract).
This is achieved through vasoconstriction of skin and visceral
circulation.
The agents responsible for this vasoconstriction
are :

* Catecholamine
* Angiotensin-II
* Vasopressin
* Endothelin
* Thromboxane A2

The changes in microcirculation in redistribution of blood flow
leads to slowing of flow, high viscosity of blood and sludging,
leading to intravascular coagulation and occlusion of capillary
channels.

As a consequence, intestinal mucosal injury occurs, gut
permeabilty may increase, and enteric bacteria and toxins move
across the gut wall, and invade the circulation via lymphatics and
portal venous system.
This is known as bacterial translocation.
Thus, the end effect of vasoconstriction in gut circulation can
lead to ischaemia and irreveresable shock, SIRS and MODS.
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SHOCK COMPENSATORY CASCADE

6. COMPENSATORY MECHANISM
6.1 The baroreceptors in the aortic arch and carotid sinus receive the signal of falling BP and send less afferent stimuli to the vasomotor centre in the medulla.
This results in enhanced sympathetic tone ending in arteriorlar and venous constriction.
There is increase in the after load and increase in venous
return to the heart (increase pre-load).
The vascular constriction is least in cardiac and cerebral circulation.
The enhanced adrenal medullary output of catacholamines results in
increased heart rate and mycardial contractility.
All these mechanisms improve cardiac output.

6.2 Antidiuretic hormone (ADH) is also released from the
posterior pituitary in response to the hypovolemia.
This ADH produces vaso-constriction in the visceral circulation and
increased re-absorbtion of water from the distal tubules of the
kidney.

6.3 Renin secretion is also stimulated by the hypo-perfusion of
juxta-glomerular apparatus in the kidney.
This leads to formation of angiotensin-I in the liver and later to angiotensin-II in the lungs.
This angiotensin-II is a powerful vasoconstrictor. This
is also a signal for release of aldersterone from the adrenal
cortex.

6.4 The aldersterone is a valuable restorer of circulating volume
by re-absorbtion of sodium from the renal tubules.
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SHOCK TO RECOGNISE AND MANAGE

5. MANAGEMENT
HYPOVOLEMIC SHOCK is the common form in practice, we use this form as working model.

The signs and symptoms appear only when the loss from
the circulatory system is above a certain volume usually (750 cc)
The compensatory mechanism fail and tissue perfusion suffers as
a result.
A summary of these volume losses and manifestations
in a seventy kilogram man are given below:


-Thus the first sign may be a rise in pulse rate because of increase in catecholamine.
-As the loss of blood or fluid continues the pulse rises and the systolic BP falls.
-The urine production per hour drops.
-The mental state passes through stages of apprehension, anxiety and lethargy to coma

A clinical staging system of hemorrhagic shock based on the percentage of acute blood volume loss has been described

Typically
-Classes I(Loss of 750cc of blood) and II(loss of 750-1500) are referred to as compensated shock states in which the adrenergic response maintains a normal blood pressure.
-Passing from a compensated state of shock to class IV (uncompensated) shock may occur rapidly in children and young adults.
-De-compensation of homeostatic mechanisms and inability to maintain systolic blood pressure above 90 mmHg after trauma induced hypovolemia are associated with a mortality of more than 50%.
However, rapid and adequate restoration of circulating blood volume simultaneous with control of bleeding can reverse even severe hemorrhagic shock.
It is thus crucial to recognize compensated shock early and intervene with speed for good results.
Laboratory evaluation may provide some diagnostic information.
- Non hemorrhagic forms of hypovolemic shock cause hemoconcentration.
- If there is loss of free water, then hemoconcentration will occur with hyponatremia.
- Following acute hemorrhage there may be no alteration in the hemoglobin or hematocrit values when compensatory fluid shifts occur fluids are administered hemoglobin and hematocrit will drop.
In clinical situations in which the cause of underlying shock state is not clear, the most critical decision is to ensure that cardiogenic shock is not cause.
The findings of jugular venous distension, rates, and the presence of an S3 gallop in cardiogenic shock may assist in diagnosis.
Both forms of shock, however, are associated with a reduction in cardiac output and a compensatory sympathetic mediated response.
Further, both types of shock may be treated with, and respond to, volume resuscitation.
If the diagnosis is in doubt or the clinical situation suggests both as a possibility, then invasive monitoring with a pulmonary artery catheter may required to assess effect of therapy.
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SHADES OF SHOCK 5

4.5 Decreased respiratory ventilation and SHOCK LUNG
There is a decrease in available O2 in these in all cases as OF:
i) Pneumothorax
ii) Pulmonary embolus
iii) Shock lung or adult respiratory distress syndrome (ARDS).
This is met with in trauma, sepsis, aspiration of
gastric contents, and pneumonia

All these conditions lead to injury to the lung
tissue resulting in damage to the alveolar epithelium/
Capillary bed interface producing leakage of protein
Rich fluid into the interstitial space and later into
The alveolar space leading to respiratory distress.
This impairs gas exchange capacity of the lung The clinical features of ARDS of hypoxia, low lung
compliance and all these conditions interfere with
tissue perfusion with O2 because of impaired gas
exchange.
A diffuse interstitial pattern on X-ray is
visible.

4.1.1+ 2 and 4.3 are due to Pre-load and after-load effects
while 4.4 is due to cardiac muscle fuction impairment (infarct
/compression). All have low available O2 in the
blood.
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