vasogenic shock also known as vasodilatory shock causes drastic effects in animals. vasogenic shock is due to increased vascular capacitance,while the blood volume is normal. Based on the causes,it can be grouped into septic,neurogenic and anaphylactic shock

1. Class work, unpublished.
shareefngunguni@gmail.com
VASOGENIC
SHOCK
Authored By:
LUANAR 2018
Shareef Ngunguni, BVM
Precious mastala, BVM
Enock kanyika, BVM

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VASOGENIC SHOCK
1. INTRODUCTION
Shock is a failure of the cardiovascular
system to deliver enough O2 and nutrients to
meet cellular metabolic needs (Tortora and
Derrickson, 2009). The causes of shock are
many and varied, but all are characterized by
inadequate blood flow to body tissues. With
inadequate oxygen delivery, cells switch from
aerobic to anaerobic production of ATP, and
lactic acid accumulates in body fluids. If
shock persists, cells and organs become
damaged, and cells may die unless proper
treatment begins quickly. Shock can be of
four different types: (1) hypovolemic shock
due to decreased blood volume, (2)
cardiogenic shock due to poor heart
function, (3) obstructive shock due to
obstruction of blood flow and (4) vascular/
vasogenic shock (Perry et al, 1983).
Vasogenic shock is caused by widespread
vasodilation from decreased vasomotor
tone. Blood volume remain within normal
limits but the capacity of the vessels is
increased. This increased capacity of vessels
without corresponding increase in blood
volume leads to decrease venous return that
results in diminished cardiac output.
Vasogenic is divided into three forms
namely, septic shock, anaphylactic shock
and neurogenic shock (Perry et al, 1983).
2. CAUSES
Vascular shock can be caused by factors
like; systemic response to infection;
noninfectious systemic inflammation like
pancreatitis and burns; anaphylaxis; acute
adrenal insufficiency; prolonged, severe
hypotension; hemorrhagic shock;
cardiogenic shock; cardiopulmonary bypass;
and metabolic effects like hypoxic lactic
acidosis and carbon monoxide poisoning.
Vasogenic/Vasodilatory shock can be
manifested in three forms namely Septic
shock, Anaphylactic shock, and Neurogenic
shock.
i. Septic Shock
During sepsis there is an increase in
inducible form Nitric oxide which is triggered
by proinflammatory agents like endotoxins
and cytokines. Nitric oxide reduces
intracellular calcium causing relaxation of
vascular smooth muscle and vasodilation
(Barret et al, 2010). Most common causes

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VASOGENIC SHOCK
include [1] systemic response to endotoxin,
viruses, fungi and yeast, [2] noninfectious
systemic inflammation like pancreatitis and
burns
ii. Anaphylactic shock
In anaphylactic shock, a severe allergic
reaction which results from the reaction of
allergen with IgE antibodies bound strongly
on the surface of mast cell which
degranulate releasing mediators like
histamine, heparin, neutral protease,
interleukins eosinophil and neutrophil
chemotactic factors and platelet activating
factor. These promote the synthesis of
Prostaglandin D2 and thromboxanes (John,
2009). Under normal circumstances, these
mediators help to orchestrate the
development of a defensive acute
inflammatory reaction; but when there is a
massive release of these mediators under
abnormal conditions, as in atopic disease,
there are bronchoconstrictive and
vasodilatory effects which result in
vasodilatory shock (Perry et al, 1983).Most
common causes include allergen such as [1]
drugs for example antibiotics-penicillin,
analgesia, anesthetics e.g. lidocaine [2]Food
such as milk, soybean, milk and [3] bites
from venomous snakes and stings from
bees, wasps,
iii. Neurogenic shock
Neurogenic shock refers to diminished
tissue perfusion as a result of loss of
vasomotor tone to peripheral arterial beds
(Kumar et al, 2005). Loss of vasoconstrictor
impulses results in increased vascular
capacitance, decreased venous return, and
decreased cardiac output. The causes of
neurogenic shock include: Spinal cord
trauma, Spinal cord neoplasm or Spinal/
e p i d u r a l a n e s t h e t i c .
Acute spinal cord injury may result in
bradycardia, hypotension, cardiac
dysrhythmias, reduced cardiac output, and
decreased peripheral vascular resistance.
Neurogenic shock is usually secondary to
spinal cord injuries from vertebral body
fractures of the cervical or high thoracic
region that disrupt sympathetic regulation of
peripheral vascular tone (Kumar et al,
2005).
3. DIAGNOSIS
i. Septic Shock

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VASOGENIC SHOCK
Diagnosis is based on manifestations of the
host-response to infection in addition to
identification of an offending organism (Perry
et al, 1983). Patients with sepsis have
evidence of an infection, as well as systemic
signs of inflammation like fever,
leukocy t osis, and t ac hyc ardia.
Hypoperfusion with signs of organ
dysfunction is termed severe sepsis
associated with more significant evidence of
tissue hypoperfusion and systemic
hypotension.
ii. Neurogenic Shock
Acute spinal cord injury may result in
bradycardia, hypotension, cardiac
dysrhythmias, reduced cardiac output, and
decreased peripheral vascular resistance
and so diagnosis can be based on detection
of these parameters. The other method of
diagnosis is imaging or radiography which
works in cases of vertebral fractures and
neural tumors (Kumar et al, 2005).
iii. Anaphylactic Shock
Defined by airway compromise, hypotension,
or involvement of cutaneous, respiratory, or
GI systems and also looking for exposure to
drug, food, or insect. Laboratories do not
usually play a role in diagnosis of
anaphylactic shock, however the presence of
proteins secreted from mast cells or
eosinophils in the serum or urine could
provide important alternative markers of
disease and might predict exacerbations
(Perry et al, 1983)
4. MANAGEMENT
i. Septic Shock
Assessment of the adequacy of their airway
and ventilation. Severely obtunded patients
and patients whose work of breathing is
excessive require intubation and ventilation
to prevent respiratory collapse. Because
vasodilation and decrease in total peripheral
resistance may produce hypotension, fluid
resuscitation and restoration of circulatory
volume with balanced salt solutions is
essential.
Treatment can further be through surgical
intervention in cases of abscess or retained
fetal parts being the source and requires
that the abscess is drained. This may be
coupled with antibiotic therapy like

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VASOGENIC SHOCK
aminoglycocides e.g. Gentamycin; penicillin
and cephalosporins (Aiello and Moses,
2016).
ii. Neurogenic Shock
After the airway is secured and ventilation is
adequate, fluid resuscitation and restoration
of intravascular volume often will improve
perfusion in neurogenic shock. Most patients
with neurogenic shock will respond to
restoration of intravascular volume alone,
with satisfactory improvement in perfusion
and resolution of hypotension.
Administration of vasoconstrictors improves
peripheral vascular tone, decrease vascular
capacitance, and increase venous return,
but is only considered once hypovolemia is
excluded as the cause of the hypotension
and the diagnosis of neurogenic shock is
established (Aiello and Moses, 2016). If the
patient’s blood pressure has not responded
to what is felt to be adequate volume
resuscitation, dopamine may be used first. A
pure α agonist, such as phenylephrine, is
used primarily or in patients unresponsive to
dopamine (Aiello and Moses, 2016).
iii. Anaphylactic Shock
Firstly, provide ventilation, and restore
adequate circulation. The following drugs
may be used; epinephrine, corticosteroids
like Prednisone, and anti-histamine drugs
(H1 antagonists like Cetirizine and H2
antagonists like Ranitidine) (Aiello and
Moses, 2016).
5. CONCLUSION
All in All, vasogenic shock is associated with
widespread vasodilation and has three forms
namely septic shock, anaphylaxis shock and
neurogenic shock. The report has further
discussed the causes, diagnosis and
management of each form
6. REFERENCES
Aiello. E.S and Moses.A.M (2016).The Merk
Veterinary Manual. 11th Edition.Merk and
Co,Inc. Kenilworth.
Barret K.,Brooks H.,BoitanoS.,and Barman S.
(2010).Ganongs Review of Medical
physiology.23rd Edition.McGraw Hill
companies,inc.NewYork.
John.A.Z.(2009).Essentials Clinical
Immunology.Cambridge University
Press.New York

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VASOGENIC SHOCK
K u ma r ,V .,A b b a s, K . ,F a u st o , N .
(2005).Robbins and Cotran Pathologic Basis
o f D i s e a s e s . 7 t h E d i t i o n .
Elsevier,Inc.Philadelphia
Perry,G.A.,Potter,P.A.,Niedrighaus,L.,Smith-
Collins,A.,and Myers,J.L.
(1983).Shock:Comprehensive Nursing
Management.The C.V. Mosby Company.St
Louis.
T o r t o r a , G . J a n d D e r r i c k s o n , B .
(2009).Principles of Anatomy and
Physiology.12th Edition.John Wiley and
Sons,Inc.New York