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• is a serious medical condition
where the tissue perfusion is
insufficient to meet demand for
oxygen and nutrients.
Pathophysiology Adequate blood volume, an
effective cardiac pump, and an
Precipitating cause of shock effective vasculature are
necessary to maintain blood
pressure and tissue perfusion.
↓ Circulating blood volume
When one of the three
components of this system
↓ Cardiac output begins to fail, the body is able to
compensate to increased work by
Hypotension and ↓ tissue perfusion the other two. When
compensatory mechanism can no
longer compensate for the failed
Baroreceptors stimulated system, body tissues are
inadequate perfused and shock
↑ Sympathetic stimulation occurs. Without prompt
and cardiovascular system intervention, shock progresses,
resulting in organ dysfunction,
↑ Heart rate; ↑ contractility Arteriolar constriction organ failure, and death.

↑ Cardiac output ↑ Blood pressure

Venous constriction

↑ Venous return
Four Stages of
In this stage, the hypoperfusional state causes hypoxia,
leading to the mitochondria being unable to produce
adenosine triphosphate. Due to this lack of oxygen, the
cell membranes become damaged and the cells perform
anaerobic respiration. This causes a build-up of lactic and
pyruvic acid which results in systemic metabolic acidosis.
The process of removing these compounds from the cells
by the liver requires oxygen, which is absent.
• This stage is characterised by the body employing physiological
mechanisms, including neural, hormonal and bio-chemical mechanisms in
an attempt to reverse the condition. As a result of the acidosis, the person
will begin to hyperventilate in order to rid the body of carbon dioxide
(CO2). CO2 indirectly acts to acidify the blood and by removing it the
body is attempting to raise the pH of the blood. The baroreceptors in the
arteries detect the resulting hypotension, and cause the release of
adrenaline and noradrenaline. Noradrenaline causes predominately
vasoconstriction with a mild increase in heart rate, whereas adrenaline
predominately causes an increase in heart rate with a small effect on the
vascular tone; the combined effect results in an increase in blood
pressure. Renin-angiotensin axis is activated and arginine vasopressin is
released to conserve fluid via the kidneys. Also, these hormones cause the
vasoconstriction of the kidneys, gastrointestinal tract, and other organs to
divert blood to the heart, lungs and brain. The lack of blood to the renal
system causes the characteristic low urine production. However the
effects of the Renin-angiotensin axis take time and are of little
importance to the immediate homeostatic mediation of shock.
• Should the cause of the crisis not be successfully treated, the
shock will proceed to the progressive stage and the
compensatory mechanisms begin to fail. Due to the decreased
perfusion of the cells, sodium ions build up within while
potassium ions leak out. As anaerobic metabolism continues,
increasing the body's metabolic acidosis, the arteriolar and
precapillary sphincters constrict such that blood remains in the
capillaries. Due to this, the hydrostatic pressure will increase
and, combined with histamine release, this will lead to leakage
of fluid and protein into the surrounding tissues. As this fluid is
lost, the blood concentration and viscosity increase, causing
sludging of the micro-circulation. The prolonged
vasoconstriction will also cause the vital organs to be
compromised due to reduced perfusion.
• At this stage, the vital organs have
failed and the shock can no longer be
reversed. Brain damage and cell death
have occurred. Death will occur
Types of Shock
  A.  Hypovolemic shock
• This is the most common type of shock and
based on insufficient circulating volume.
Its primary cause is loss of fluid from the
circulation from either an internal or
external source. An internal source may be
hemorrhage. External causes may include
extensive bleeding, high output fistulae or
severe burns.
B. Cardiogenic shock
• This type of shock is caused by the failure
o fthe heart to pump effectively. This can
be due to damage to the heart muscle, most
often from a large myocardial infarction.
Other causes of cardiogenic shock include
arrhythmias, cardiomyopathy, congestive
heart failure (CHF), contusio cordis or
cardiac valve problems.
C. Distributive shock
• As in hypovolaemic shock there is an
insufficient intravascular volume of blood.
This form of "relative" hypovolaemia is the
result of dilation of blood vessels which
diminishes systemic vascular resistance.
Examples of Distributive
o Septic  shock  -  This is caused by an overwhelming
infection leading to vasodilation, such as by Gram
negative bacteria i.e. Escherichia coli, Proteus
species, Klebsiella pneumoniae which release an
endotoxin which produces adverse biochemical,
immunological and occasionally neurological effects
which are harmful to the body. Gram-positive cocci,
such as pneumococci and streptococci, and certain
fungi as well as Gram-positive bacterial toxins
produce a similar syndrome.
o Anaphylactic  shock  -  Caused by a severe
anaphylactic reaction to an allergen, antigen,
drug or foreign protein causing the release of
histamine which causes widespread
vasodilation, leading to hypotension and
increased capillary permeability.
o Neurogenic  shock  -  is the rarest form of
shock. It is caused by trauma to the spinal cord
resulting in the sudden loss of autonomic and
motor reflexes below the injury level. Without
stimulation by sympathetic nervous system the
vessel walls relax uncontrolled, resulting in a
sudden decrease in peripheral vascular
resistance, leading to vasodilation and
D. Obstructive shock
• In this situation the flow of blood is
obstructed which impedes circulation and
can result in circulatory arrest.
Several conditions result of 
Obstructive shock
– Cardiac tamponade in which blood in the pericardium prevents
inflow of blood into the heart (venous return). Constrictive
pericarditis, in which the pericardium shrinks and hardens, is
similar in presentation.
– Tension pneumothorax. Through increased intrathoracic
pressure, bloodflow to the heart is prevented (venous return).
– Massive pulmonary embolism is the result of a
thromboembolic incident in the bloodvessels of the lungs and
hinders the return of blood to the heart.
– Aortic stenosis hinders circulation by obstructing the
ventricular outflow tract.
Fifth form of shock 
• Endocrine shock based on endocrine disturbances. 
– Hypothyroidism,  in  critically  ill  patients,  reduces  cardiac 
output  and  can  lead  to  hypotension  and  respiratory 
– Thyrotoxycosis may induce a reversible cardiomyopathy.
– Acute  adrenal  insufficiency  is  frequently  the  result  of 
discontinuing  corticosteroid  treatment  without  tapering  the 
dosage. However, surgery and intercurrent disease in patients 
on  corticosteroid  therapy  without  adjusting  the  dosage  to 
accommodate  for  increased  requirements  may  also  result  in 
this condition.
– Relative  adrenal  insufficiency  in  critically  ill  patients  where 
present  hormone  levels  are  insufficient  to  meet  the  higher 
- Restlessness, confusion
- ↑ PR, RR
- Diaphoresis
- Cool, clammy skin (warm, flushed skin in septic shock)
- Normal/ ↓ BP
- ↓ pulse pressure
- ↓ urine output
- Thirst, dry mucus membrane
- Respiratory alkalosis
- Hypokalemia
– shallow respiration - DIC

– ↓ BP - Lethargy

– ↑ PR - ↓ bowel sounds
– Oliguria/ Anuria - Cyanosis (nailbeds)
– Hypokalemia - Dilated pupils
– Metabolic Acidosis/Respiratory Acidosis
– Edema
– Cool, clammy skin(hypovolemic, cardiogenic, septic shock)
– Cool mottled skin(neurogenic and vasogenic shock)
– Hypothermia
• Ineffective tissue perfusion may be
related to changes in circulating volume
and/or vascular tone, possibly evidenced by
changes in color/temperature and pulse
pressure, reduced blood pressure, changes
in mentation, and decreased urinary output.
• Anxiety may be related to change in health status
and threat of death, possibly evidenced by
increased tension, apprehension, sympathetic
stimulation, restlessness, and expressions of
• Decreased cardiac output may be related to
structural damage, decreased myocardial
contractility, and presence of dysrhythmias,
possibly evidenced by ECG changes, variations in
hemodynamic reading, jugular vein distention,
cold/clammy skin, diminished peripheral pulses,
and decreased urinary output.
• Risk for impaired gas exchange: risk factors may
include ventilation perfusion imbalance, alveolar-
capillary membrane changes.
• Fluid volume deficit may be related to excessive
vascular loss, inadequate intake/replacement,
possibly evidenced by hypotension, tachycardia,
decreased pulse volume and pressure, change in
mentation, and decreased, concentrated urine.
• Restore intravascular volume to reverse 
the sequence of events leading to 
inadequate tissue perfusion.
• Redistribute fluid volume.
• Correct the underlying cause of the fluid 
loss as quickly as possible.
• Teaching plan about the condition.
• Fluid replacement to restore intravascular volume
◦ Whole blood and blood products
◦ Colloid solutions (e.g albumin, plasma protein factor)
◦ Plasma expanders (e.g dextran, hetastarch, mannitol)
◦ Crystalliod solutions (hypotonic); 45% NSS, 5%
dextrose in water (D5W)
◦ Crystalliod solution (isotonic); (e.g NSS, Lactated
Ringer’s solution, Ringer’s solution).
• Vasoactive medication to restore vasomotor tone and 
improve cardiac function.

Amrinone (Inocor) Epinephrine(Adrenalin)
Milrinone (Primacor) Dobutamine (Dobutrex)
Nitroglycerine (Tridil)
Nitroprusside (Nipride)
Norepinephrine (Levophed)
Phenylephrine (Neo-Synephrine)
Vasopressin (Pitressin)
• Nutritional  support  to  address  the  metabolic 
requirements  that  are  often  dramatically 
increased in shock
• Promoting safety
◦Soft restraints if restless and attempts to remove
life-saving equipment.
◦Practice strict asepsis.
◦Prevent complication of immobility.
◦Protect from chills which causes sludging of
blood in microcirculation.
• Maintain fluid volume at a functional 
level as evidence by individually 
adequate urinary output with normal 
specific gravity, stable vital signs, and 
moist mucous membrane.
• Verbalized understanding of condition 
and when to contact healthcare provider.
• Chapter 56 in Smeltzer and Bare: Brunner &
Suddarth’s Textbook of Medical-Surgical
Nursing, 10th edition. Philadelphia: Lippincott
William & Wilkins, 2004
• Udan J.Q Medical-Surgical Nursing: Concepts
and Clinical Application, 1st edition. Ermita,
Manila, Philippines, 2002