Review Article

Hypovolemic shock - A review

J. A.Shagana1, M. Dhanraj1, Ashish R. Jain1*, T. Nir osa2

ABSTRACT

Shock is described traditionally as tissue hypoxia due to inadequate perfusion which is classified as hypovolemic, cardiogenic,
obstructive, and distributive. Hypovolemic shock is an important life-threatening emergency. In hypovolemic shock, there is
decreased circulating blood volume due to the loss of intravascular fluid. Hemorrhagic shock is the most common form of
hypovolemic shock and must be recognized early which prevent progression, morbidity, and mortality. Hence, this article will
discuss about the causes, clinical features, diagnosis, and treatment of hypovolemic shock.

KEY WORDS: Blood pressure, Cardiac output, Circulating blood volume, Hypovolemic shock and organ dysfunction

INTRODUCTION The systemic vascular resistance (SVR) is typically

Shock is defined as the state in which profound and
widespread reduction of effective tissue perfusion
leads first to reversible, and then if prolonged,
to irreversible cellular injury. It is classified as
hypovolemic/hemorrhagic shock, cardiogenic
shock, obstructive shock, and distributive shock.[1].
Hypovolemic shock is defined as the rapid fluid loss or
blood loss which results in multiple organ dysfunction
due to inadequate circulating blood volume and
perfusion. It is caused by a loss of intravascular
fluid which is usually whole blood or plasma. Whole
blood loss from an open wound is an obvious cause
for hypovolemic shock. An intravascular volume
depletion may occur with any condition which leads to
excessive extracellular fluid loss with or without loss
of plasma protein.[2] Hypovolemic shock is secondary
to hemorrhagic shock (rapid blood loss) which is
rare but cause serious complications and mostly
occurs in obstetrical situations. Hypovolemic shock
is associated with disorders that cause an underlying
hemodynamic defect of a low intravascular volume
and a reduction in myocardial contractility.[3] It is a
consequence of decreased preload due to intravascular
volume loss. The decreased preload diminishes stroke
volume, resulting in decreased cardiac output (CO).
increased in an effort to compensate for the diminished
CO and maintain perfusion to vital organs. The early
stage of recognition and intervention will help to
prevent death.[4]
ETIOLOGY
Hypovolemic shock is caused by sudden blood or fluid
losses within your body. The most common clinical
causes of hypovolemic shock are hemorrhage, vomiting,
diarrhea, severe burns, and excessive sweating.[5] Since
arterial blood pressure (BP) is dependent on the CO
and SVR, marked reduction in either of these variables
without a compensatory elevation results in systemic
hypotension. In hypovolemic shock, the volume
loss is exogenous or endogenous. Restoration blood
volume is both simple and effective if applied before
irreversible tissue damage occurs.[6] The external fluid
losses and the internal sequestration will cause reduced
venous return and decreased CO. This leads to set of
reflex responses designed to maintain the oxygen
to critical organs such as brain and heart. However,
these responses may limit perfusion of other organs
such as gut as to produce necrosis. The consequences
of reduced tissue perfusion are similar in all forms of
shock.[7]

SYMPTOMS
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The symptoms can vary with the previous level of
organ function, compensatory mechanisms, severity of

1
Department of Prosthodontics, Saveetha Dental College and Hospital, Saveetha University, Chennai, Tamil Nadu, India,
2
Department of Public Health Dentistry, Saveetha Dental College and Hospital, Saveetha, University, Chennai, Tamil Nadu,
India

*Corresponding author: Dr. Ashish R. Jain, Department of Prosthodontics, Saveetha Dental College and Hospital, Saveetha
University, Poonamalle High Road, Chennai - 600 127, Phone: +91-9884233423. E-mail: dr.ashishjain_r@yahoo.com

Received on: 09-02-2018; Revised on: 06-04-2018; Accepted on: 17-05-2018

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 J. A. Shagana, et al.
organ dysfunctions, and the cause of shock syndrome.
The symptoms of hypovolemic shock include pallor,
tachycardia, hypotension, dyspnea, diaphoresis,
tachypnea, cyanosis, faint heart sounds, agitation,
mental status changes, pinpoint pupils, cool and clammy
skin, lactic acidosis, and poor urine output.[8] Right-heart
catheterization will usually reveal a low central venous
pressure (CVP), pulmonary artery occlusion pressure
(PAOP), CO, and mixed venous oxygen content.
During spontaneous ventilation, pulsus paradoxus
may occur, whereas during mechanical ventilation,
the systolic BP only transiently increases during the
inspiratory phase followed by a rapid decrease (with
a systolic pressure variation of >10  mmHg) being
suggested as a method to diagnose hypovolemia in a
mechanically ventilated patient with normal pulmonary
compliance.[9] The presence of cardiovascular disease,
autonomic neuropathy or anemia, or prior treatment
with β-adrenergic blockers or calcium channel blockers
may worsen the cardiovascular response to blood loss.[10]
EFFECTS ON CEREBRAL
AND OTHER REGIONAL
CIRCULATIONS
Cerebral Circulation
Although central nervous system neurons are extremely
sensitive to ischemia, the vascular supply is highly
resistant to extrinsic regulatory mechanisms. Patients
without a primary cerebrovascular impairment support
their cerebral function well until the mean arterial
pressure falls below approximately 50–60  mmHg.
At this point, irreversible ischemic injury may occur
to the most sensitive areas of the brain, i.e.  cerebral
cortex and watershed areas of the spinal cord. 58, 59
Before such injury, an altered level of consciousness
varying from confusion to unconsciousness may be
seen depending on the degree of perfusion deficit.
Electroencephalographic recordings demonstrate non-
specific changes compatible with encephalopathy.[11]
Cardiovascular System
Initially, the cardiovascular system responds to
hypovolemic shock by increasing the heart rate,
constricting peripheral blood vessels, and increasing
myocardial contractility. This occurs secondary to an
increased release of norepinephrine and decreased
baseline vagal tone regulated by the baroreceptors
in the carotid arch, aortic arch, left atrium, and
pulmonary vessels. Further redistribution of the blood
to the brain, heart, kidneys and the skin, muscle,
and gastrointestinal tract, the cardiovascular system
responses to shock.[11]
Respiratory System
Increased respiratory drive resulting from peripheral
stimulation of pulmonary receptors and carotid body
Drug Invention Today | Vol 10 • Issue 7 • 2018
chemoreceptors as well as hypoperfusion of the
medullary respiratory center results in increased minute
volume (tachypnea and hyperpnea), hypocapnia, and
primary respiratory alkalosis. With increased minute
volume and decreased CO, the V/Q ratio is increased.
Coupled with an increased workload, respiratory,
and diaphragmatic muscle impairment caused by
hypoperfusion may lead to early respiratory failure.
If shock is not promptly reversed and the initiating
condition controlled, adult respiratory distress
syndrome may develop.[11]
Renal System
It responds to hemorrhagic shock by stimulating an
increase in renin secretion from the juxtaglomerular
apparatus. Renin converts angiotensinogen to
angiotensin I, which subsequently is converted to
angiotensin II by the lungs and liver. Angiotensin II
has two main effects, both of which help to reverse
hemorrhagic shock, vasoconstriction of arteriolar
smooth muscle, and stimulation of aldosterone
secretion by the adrenal cortex. Aldosterone is
responsible for active sodium reabsorption and
subsequent water conservation.[11]
Neuroendocrine System
In neuroendocrine system, an increase in circulating
antidiuretic hormone is responds to shock which is
released from the posterior pituitary gland in response
to a decrease in BP (as detected by baroreceptors) and
a decrease in the sodium concentration (as detected by
osmoreceptors). It leads to an increased reabsorption
of water and salt (NaCl) by the distal tubule, the
collecting ducts, and the loop of Henle.[11]
INVESTIGATIONS
The diagnostic evaluation should occur as same
as resuscitation if patient is suspected of having
shock. Laboratory tests may help identify the cause
of shock and early organ failure.[12] They should be
performed early in the evaluation of undifferentiated
shock which include complete blood count with
differential, basic chemistry tests (sodium, potassium,
chloride, and serum bicarbonate), blood urea
nitrogen, creatinine, liver function tests, amylase,
lipase, prothrombin time or international normalized
ratio, partial thromboplastin time, fibrinogen, fibrin
split products or dimer, cardiac enzymes (troponin
or creatine phosphokinase isoenzymes), urinalysis
with a detailed sediment analysis, arterial blood gas
(ABG), toxicology screen, and lactate level.[13] A
chest radiograph, abdominal radiograph for intestinal
obstruction, abdominal computed tomography (CT),
head CT scan, electrocardiogram, echocardiogram,
or urinalysis may also be helpful.[14] Gram stain of
material from sites of possible infection (sputum,
urine, and wounds) may give early clues to the etiology
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 J. A. Shagana, et al.
of infection while cultures are incubating. Blood
should be taken from two distinct venipuncture sites
and inoculated into standard blood culture media.[15]
Arterial pressure catheter is a must for all patients
suspected of having circulatory shock. Marked
peripheral vasoconstriction may make the
assessment of BP by manual sphygmomanometry
or automated non-invasive oscillometric technique
inaccurate. Furthermore, continuous monitoring of
the rapidly changing hemodynamic status of unstable
patients and access for ABG samples is available
with arterial catheter in place.[16] Pulmonary artery
catheterization is a hemodynamic measurements
obtained by pulmonary catheterization which can be
helpful in determining the type of shock that exists,
particularly the CO, PAOP, and systemic vascular
pressure.[17] CVP monitoring is not an accurate means
of monitoring volume resuscitation and should be
used only as a rough guide. An initially low CVP
(i.e.  <5  mmHg) may indicate hypovolemia, and it
is inadequate for the hemodynamic assessment of
critically ill patients.[18]
The other non-invasive monitoring devices include
pulse oximetry which has a limited use in the
acute management of circulatory shock and more
helpful in the post-resuscitation monitoring. Near-
infrared spectroscopy to detect oxygen availability
and utilization at tissue level for continuous CO
measurements.[19]
TREATMENT
The basic goal of circulatory shock therapy is the
restoration of effective perfusion to vital organs and
tissues before the onset of cellular injury. There are
three goals in emergency with hypovolemic shock
including maximizing oxygen delivery, control further
blood loss, and fluid resuscitation.[20] The patient
should be treated in a properly equipped intensive
care unit where continuous intra-arterial monitoring,
pulmonary artery wedge, and central venous is
possible, and determination of ABG, pH, and serum
electrolyte is also necessary. The most effective means
of restoring adequate circulation are by rapid infusion
of volume expanding fluids.[21] Shock is secondary
to or accompanied by cardiac failure. So here
attention must be directed toward restoring cardiac
function with cardiotonic drugs such as digitalis
glycosides and isoproterenol to support arterial
pressure.[22] Intra-aortic balloon counterpulsation with
a sympathomimetic amine may be used to treat this
state. A  Swan-Ganz balloon-tipped catheter is best
means for continuously monitoring ventricular filling
pressure.[23] Medicines such as dopamine, dobutamine,
epinephrine, and norepinephrine may be needed to do
increase BP and CO.[24]
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CONCLUSION
In general, people with milder degrees of shock tend
to do better than those with more severe shock. Even
with immediate medical attention, severe hypovolemic
shock may lead to death. Older adults are more likely
to have poor outcomes from shock. Mortality due to
hypovolemic shock is more variable. It depends on the
cause and the duration until recognition and treatment.
Successful treatment of patients with shock requires
prompt recognition of the shock state and a thorough
understanding of various types of shock to reduce the
mortality.
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Source of support: Nil; Conflict of interest: None Declared
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