Pathophysiology and compensatory mechanisms in Hypovolemic Shock

In response to large-volume fluid loss, the body initiates physiological responses that act to
maintain an adequate blood supply to essential organs. These compensatory mechanisms aim to
prevent damage through the redirection and preservation of blood supply, ensuring adequate
levels of oxygen, nutrients and tissue perfusion are maintained.

Catecholamine response

Baroreceptors in the major blood vessels, including the carotid and aortic bodies, identify a drop
in arterial pressure and initiate compensatory pathways. The baroreceptors activate an ischaemic
response that results in the release of catecholamines such as norepinephrine to restore adequate
tissue perfusion and oxygen supply ( Kelley 2005 ). Norepinephrine acts on the cardiac
pacemaker cells of the myocardium, resulting in increased cardiac contractility and subsequently
an increased heart rate and cardiac output. Catecholamines also increase myocardial contraction,
venous return and arterial pressure through the mechanism of vasoconstriction ( Gutierrez et al
2004 ). Vasoconstriction acts to redirect the blood supply from peripheral vessels to those
essential organs that have a high oxygen and metabolic demand, to maintain adequate perfusion
and visceral function. Therefore, blood is redistributed from the skin, muscle and gastrointestinal
tract, resulting in the presenting symptoms of pallor, weakness, delayed capillary refill and
decreased radial pulse pressure ( Udeani 2015 ). The patient may experience tremors and anxiety
as a result of the catecholamine response.

Anaerobic response

In response to a reduced oxygen supply and poor tissue perfusion, the cells convert from aerobic
metabolism to anaerobic metabolism. Aerobic metabolism refers to the process by which the
cells convert glucose into pyruvic acid, releasing units of cellular energy called adenosine
triphosphate (ATP). This process can only take place in the presence of an adequate oxygen
supply and results in the by-products of carbon dioxide and water. In contrast, in anaerobic
metabolism, the cells release energy in the form of ATP in the absence of oxygen and produce
lactic acid as a by-product.

Lactic acidosis

Impaired electrolyte balance and cell metabolism lead to impaired muscle contraction, increased
risk of cardiac arrhythmias, fatigue and weakness. The build-up of lactic acid in the blood causes
a drop in pH that results in metabolic acidosis, which along with an electrolyte imbalance causes
depressed myocardial contractility, dysrhythmias and increased resistance by peripheral blood
vessels to catecholamines ( Gunnerson 2015 ). Increased production of hydrogen ions as a result
of lactic acidosis causes increased activity in the carbon dioxide/bicarbonate buffer system, and
production of carbon dioxide increases in an effort to prevent pH change. This carbon dioxide is
excreted through the lungs, as evidenced by increasing respiratory rate and depth. However, this
activity continues only as long as the kidneys can regenerate bicarbonate. This mechanism acts
to stabilise the metabolic acidosis and prevent further deterioration ( Galvagno 2013 ). An
increased respiratory rate is an indicator of impending clinical deterioration, since the
compensatory mechanisms are beginning to fail as the severity of shock increases ( Spahn et al
2013 ).

Coagulopathy

It is essential to identify and stop the source of the uncontrolled bleeding in the case of
haemorrhagic shock, to prevent further haemodynamic instability, cardiovascular collapse and
organ damage. The activation of coagulation factors secondary to severe blood loss results in the
constriction of blood vessels at the source of the haemorrhage and initiation of the clotting
process through platelet response. Coagulopathy in the trauma patient presenting with
haemorrhagic shock is associated with a high mortality rate. Therefore, early recognition of this
condition and early implementation of clinical interventions are essential to promote successful
resuscitation ( Spahn et al 2013 ).

Coagulopathy is defined as a clotting disorder whereby the blood's ability to clot has been
impaired. This may develop secondary to a deficit in circulating clotting factors.
Thrombocytopenia, an abnormally low platelet count, may lead to the development of
coagulopathy; this can be caused by a number of different clinical factors. The effects of large-
volume fluid administration of intravenous fluids or blood products can lead to complications by
depleting the body of platelets. The lack of circulating blood volume can result in insufficient
levels of clotting factors ( Cherkas 2011 ). Hypothermia in the trauma patient is likely to result in
the impairment of platelet and coagulation factors and fibrinolysis ( Spahn et al 2013 ).

Renal response

The renal system responds to an inadequate blood supply by initiating a compensatory pathway
to counteract the physiological effects of large-volume blood loss and impending cardiovascular
collapse. Renin is an enzyme that mediates extracellular fluid volume and regulates blood
pressure through the renin-angiotensin-aldosterone system. Renin is secreted in response to a
drop in circulating blood volume, resulting in elevated angiotensin II plasma levels. The main
physiological actions of angiotensin II are to control arterial blood pressure through
vasoconstriction, release aldosterone, reabsorb sodium and water, and secrete vasopressin, an
antidiuretic hormone that prevents further loss of fluid ( Corrêa et al 2015 ). Aldosterone is a
steroid hormone that responds to a decrease in blood flow to the kidneys and acts to maintain and
restore fluid volume through sodium reabsorption ( Kolecki 2014 ). The effect of this can reduce
potentially the severity of haemorrhagic shock through the redistribution and/or replenishment of
fluid volume, and angiotensin II can help to correct or restore blood pressure through the action
of vasoconstriction ( Corrêa et al 2015 ).

Electrolyte imbalance

Several electrolyte imbalances occur in haemorrhagic shock: hyperkalaemia is one such

imbalance that may have detrimental effects on prognosis and has been associated directly with
cardiovascular collapse. When anaerobic metabolism starts to fail and all channels of deriving
energy have been exhausted, the ischaemic cells are unable to function properly or maintain
control of fluid shifts, thereby allowing potassium to escape into the extracellular fluid. The
onset of hyperkalaemia can lead to significant cardiac arrhythmias ( Uyehara and Sarkar 2013 ).
Aldosterone also acts to promote the excretion of potassium from the body in an attempt to re-
establish and correct electrolyte balance ( Kolecki 2014 ).

The neuroendocrine system also acts to increase water and salt reabsorption through the
mechanisms of the antidiuretic hormone. This hormone is released by the pituitary gland,
secondary to a drop in blood pressure identified by the baroreceptors in the blood vessels and can
aid in the restoration of fluid volume and haemodynamic stability ( Kolecki 2014 ). Both of these
coping mechanisms result in a reduction in urine output because they try actively to conserve
water to replenish blood volume, and oliguria may be noted as the physiological response
progresses.

Failure of compensatory mechanisms

Compensatory mechanisms maintain haemodynamic stability in the early stages of haemorrhagic

shock. However, unless the underlying pathological cause of the bleeding is rectified and
resuscitation techniques are implemented, these mechanisms fail. Signs of anxiety, confusion,
agitation and loss of consciousness are associated with cerebral hypoxia. Insufficient blood
supply and oxygenation to the heart results in poor contraction, reduced or inadequate cardiac
output and tissue necrosis, leading to myocardial ischaemia and cardiac arrest, unless prompt and
appropriate treatment is initiated ( Kolecki 2014 ).