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Hypovolemic shock - A review

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 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

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

1102 Drug Invention Today | Vol 10 • Issue 7 • 2018

 J. A. Shagana, et al.

organ dysfunctions, and the cause of shock syndrome. chemoreceptors as well as hypoperfusion of the
The symptoms of hypovolemic shock include pallor, medullary respiratory center results in increased minute
tachycardia, hypotension, dyspnea, diaphoresis, volume (tachypnea and hyperpnea), hypocapnia, and
tachypnea, cyanosis, faint heart sounds, agitation, primary respiratory alkalosis. With increased minute
mental status changes, pinpoint pupils, cool and clammy volume and decreased CO, the V/Q ratio is increased.
skin, lactic acidosis, and poor urine output.[8] Right-heart Coupled with an increased workload, respiratory,
catheterization will usually reveal a low central venous and diaphragmatic muscle impairment caused by
pressure (CVP), pulmonary artery occlusion pressure hypoperfusion may lead to early respiratory failure.
(PAOP), CO, and mixed venous oxygen content. If shock is not promptly reversed and the initiating
During spontaneous ventilation, pulsus paradoxus condition controlled, adult respiratory distress
may occur, whereas during mechanical ventilation, syndrome may develop.[11]
the systolic BP only transiently increases during the
inspiratory phase followed by a rapid decrease (with Renal System
a systolic pressure variation of >10  mmHg) being It responds to hemorrhagic shock by stimulating an
suggested as a method to diagnose hypovolemia in a increase in renin secretion from the juxtaglomerular
mechanically ventilated patient with normal pulmonary apparatus. Renin converts angiotensinogen to
compliance.[9] The presence of cardiovascular disease, angiotensin I, which subsequently is converted to
autonomic neuropathy or anemia, or prior treatment angiotensin II by the lungs and liver. Angiotensin II
with β-adrenergic blockers or calcium channel blockers has two main effects, both of which help to reverse
may worsen the cardiovascular response to blood loss.[10] hemorrhagic shock, vasoconstriction of arteriolar
smooth muscle, and stimulation of aldosterone
EFFECTS ON CEREBRAL secretion by the adrenal cortex. Aldosterone is
AND OTHER REGIONAL responsible for active sodium reabsorption and
subsequent water conservation.[11]
CIRCULATIONS
Neuroendocrine System
Cerebral Circulation
In neuroendocrine system, an increase in circulating
Although central nervous system neurons are extremely antidiuretic hormone is responds to shock which is
sensitive to ischemia, the vascular supply is highly released from the posterior pituitary gland in response
resistant to extrinsic regulatory mechanisms. Patients to a decrease in BP (as detected by baroreceptors) and
without a primary cerebrovascular impairment support a decrease in the sodium concentration (as detected by
their cerebral function well until the mean arterial osmoreceptors). It leads to an increased reabsorption
pressure falls below approximately 50–60  mmHg. of water and salt (NaCl) by the distal tubule, the
At this point, irreversible ischemic injury may occur collecting ducts, and the loop of Henle.[11]
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
INVESTIGATIONS
varying from confusion to unconsciousness may be The diagnostic evaluation should occur as same
seen depending on the degree of perfusion deficit. as resuscitation if patient is suspected of having
Electroencephalographic recordings demonstrate non- shock. Laboratory tests may help identify the cause
specific changes compatible with encephalopathy.[11] of shock and early organ failure.[12] They should be
performed early in the evaluation of undifferentiated
Cardiovascular System shock which include complete blood count with
Initially, the cardiovascular system responds to differential, basic chemistry tests (sodium, potassium,
hypovolemic shock by increasing the heart rate, chloride, and serum bicarbonate), blood urea
constricting peripheral blood vessels, and increasing nitrogen, creatinine, liver function tests, amylase,
myocardial contractility. This occurs secondary to an lipase, prothrombin time or international normalized
increased release of norepinephrine and decreased ratio, partial thromboplastin time, fibrinogen, fibrin
baseline vagal tone regulated by the baroreceptors split products or dimer, cardiac enzymes (troponin
in the carotid arch, aortic arch, left atrium, and or creatine phosphokinase isoenzymes), urinalysis
pulmonary vessels. Further redistribution of the blood with a detailed sediment analysis, arterial blood gas
to the brain, heart, kidneys and the skin, muscle, (ABG), toxicology screen, and lactate level.[13] A
and gastrointestinal tract, the cardiovascular system chest radiograph, abdominal radiograph for intestinal
responses to shock.[11] obstruction, abdominal computed tomography (CT),
head CT scan, electrocardiogram, echocardiogram,
Respiratory System or urinalysis may also be helpful.[14] Gram stain of
Increased respiratory drive resulting from peripheral material from sites of possible infection (sputum,
stimulation of pulmonary receptors and carotid body urine, and wounds) may give early clues to the etiology

Drug Invention Today | Vol 10 • Issue 7 • 2018 1103

 J. A. Shagana, et al.

of infection while cultures are incubating. Blood CONCLUSION

should be taken from two distinct venipuncture sites
and inoculated into standard blood culture media.[15] In general, people with milder degrees of shock tend
to do better than those with more severe shock. Even
Arterial pressure catheter is a must for all patients with immediate medical attention, severe hypovolemic
suspected of having circulatory shock. Marked shock may lead to death. Older adults are more likely
peripheral vasoconstriction may make the to have poor outcomes from shock. Mortality due to
assessment of BP by manual sphygmomanometry hypovolemic shock is more variable. It depends on the
or automated non-invasive oscillometric technique cause and the duration until recognition and treatment.
inaccurate. Furthermore, continuous monitoring of Successful treatment of patients with shock requires
the rapidly changing hemodynamic status of unstable prompt recognition of the shock state and a thorough
patients and access for ABG samples is available understanding of various types of shock to reduce the
with arterial catheter in place.[16] Pulmonary artery mortality.
catheterization is a hemodynamic measurements
obtained by pulmonary catheterization which can be REFERENCES
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Source of support: Nil; Conflict of interest: None Declared
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