• Hypovolaemic 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 haemorrhage. External causes may include extensive
bleeding, high output fistulae or severe burns.
• Cardiogenic shock - This type of shock is caused by the failure of the 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.
• 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 this form of shock are:
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 - 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 hypotension.
• Obstructive shock - In this situation the flow of blood is obstructed which impedes circulation
and can result in circulatory arrest. Several conditions result in this form of shock.
o 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.
o Tension pneumothorax. Through increased intrathoracic pressure, bloodflow to the heart
is prevented (venous return).
o 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.
o Aortic stenosis hinders circulation by obstructing the ventricular outflow tract

Recently a fifth form of shock has been introduced:[1]

• Endocrine shock based on endocrine disturbances.

o Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to
hypotension and respiratory insufficiency.
o Thyrotoxycosis may induce a reversible cardiomyopathy.
o 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.
o Relative adrenal insufficiency in critically ill patients where present hormone levels are
insufficient to meet the higher demands

Signs and symptoms

• Hypovolaemic shock
 o Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and
subsequent hypoxia.
o Hypotension due to decrease in circulatory volume.
o A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia.
o Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction.
o Rapid and deep respirations due to sympathetic nervous system stimulation and acidosis.
o Hypothermia due to decreased perfusion and evaporation of sweat.
o Thirst and dry mouth, due to fluid depletion.
o Fatigue due to inadequate oxygenation.
o Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient
perfusion of the skin.
• Cardiogenic shock, similar to hypovolaemic shock but in addition:
o Distended jugular veins due to increased jugular venous pressure.
o Absent pulse due to tachyarrhythmia.
• Obstructive shock, similar to hypovolaemic shock but in addition:
o Distended jugular veins due to increased jugular venous pressure.
o Pulsus paradoxus in case of tamponade
• Septic shock, similar to hypovolaemic shock except in the first stages:
o Pyrexia and fever, or hyperthermia, due to overwhelming bacterial infection.
o Vasodilation and increased cardiac output due to sepsis.
• Neurogenic shock, similar to hypovolaemic shock except in the skin's characteristics. In
neurogenic shock, the skin is warm and dry.
• Anaphylactic shock
o Skin eruptions and large welts.
o Localised edema, especially around the face.
o Weak and rapid pulse.
o Breathlessness and cough due to narrowing of airways and swelling of the throat.

Management of Compressive Shock

In many cases, extracardiac compressive and extracardiac obstructive shock, being conditions
that can kill quickly, will already have been treated by this point in management. It is wise,
however, to keep these two causes of shock in mind as workup proceeds: they often develop
secondarily. Examples of problems that can arise as treatment progresses are a tension pneumo-
thorax that develops in a mechanically ventilated patient who is being worked up or treated for
some nonpulmonary problem and an abdominal compartment syndrome that develops in a
patient who is being resuscitated after a major injury or burn. In patients with more complicated
problems (e.g., possible abdominal compartment syndrome), a Swan-Ganz catheter should be
inserted. When dealing with the conflicting demands made on the cardiovascular system in
compressive shock, one needs all the information one can get.

Management of Intravascular Obstructive Shock

The immediately life-threatening problems caused by intravascular obstruction should already

have been treated by this point. The pharmacologically treatable problems (e.g., systemic
hypertension) should be treated with diuresis, beta blockade, ACE inhibition, and nitroglycerin, as
described (see above). If hypertension persists and inadequate ventricular production of power is
a possibility, a Swan-Ganz catheter should be inserted. The goal is to adjust the afterload for
each ventricle so that it is approximately 50% of the contractility.

This goal can be particularly difficult to achieve for the right ventricle and the pulmonary
vasculature. In patients with severe ARDS, there is some evidence to suggest that administration
of prostacyclin or inhaled nitrous oxide may help reduce excessive right ventricular afterload,59
though these interventions have not been particularly successful in our own experience. In any
case, one should always attempt to address the underlying problem causing the ARDS. One can
try to adjust the ventilator in an effort to relieve the potentially confounding problem of
extravascular obstruction of the vasculature.

To achieve the desired goal in the systemic vasculature, it may be necessary to employ aortic
balloon counterpulsation to deal with the reflected waves generated by the transmission of energy
into these vessels. This measure can be extremely effective; however, it puts the perfusion of the
limb with the cannulated artery at risk. Furthermore, it is only a short-term solution: the underlying
problem will have to be dealt with eventually [seeManagement of Cardiogenic Shock -- omitted,
below].

Management of Neurogenic Shock

The initial management of neurogenic shock is much the same as that of hypovolemic and
inflammatory shock, with two exceptions: the use of the Trendelenburg position and the use of
vasoconstrictors.

Trendelenburg Position

Patients in neurogenic shock often benefit from being placed in the Trendelenburg position.
Autonomic denervation of the systemic venules and small veins leads to pooling of blood in these
capacitance vessels. The Trendelenburg position causes this blood to be translocated to the
vascular structures in the chest, including the heart, thereby helping to restore ventricular end-
diastolic volumes.

Patients with other forms of shock, however, derive no benefit from the Trendelenburg position.60
In hypovolemic shock, for example, the systemic venules and small veins are already depleted of
blood as a consequence of both volume loss and adrenergic constriction of the vessel walls. In
cardiogenic shock, the end-diastolic volumes are already too large, and there is no point in trying
to increase them.

Administration of Vasoconstrictors

As noted (see above), vasoconstrictors should play almost no role in the initial management of
hypovolemic or inflammatory shock. For these forms of shock, fluid replenishment is the crucial
initial measure, and these agents can shut off residual flow to organs already rendered ischemic
by the shock state. For the initial management of neurogenic shock, however, vasoconstrictors
are often beneficial. In neurogenic shock, the denervated arterioles are fully dilated, leading to
substantial (and sometimes profound) drops in the central arterial pressure. Cerebral or
myocardial infarction may occur. Constriction of the arterioles increases the pressure and offers
protection. In addition, constriction of the denervated systemic venules and small veins causes
translocation of blood back into the chest and helps restore depleted ventricular end-diastolic
volumes.

If the heart rate is slow, as it may be if denervation extends high enough to block the sympathetic
nerves going to the heart, dopamine may be given. If the heart rate is rapid, norepinephrine or
phenylephrine (in an initial dosage of 100 to 180 µg/min, which is then decreased to 40 to 60
µg/min) may be used.

The danger in giving a vasoconstrictor to a patient in neurogenic shock is that the underlying
condition that caused the shock state may also have caused occult bleeding. Thus, the
vasoconstrictor may maintain the blood pressure, reassuring the physician while the patient
bleeds to death. Vasoconstrictors should be employed to treat neurogenic shock only after it has
been established that the shock state has no hypovolemic component. If there is a possibility that
hypovolemia or another abnormality (e.g., cardiac compression) may be contributing to the shock
state, a Swan-Ganz catheter should be inserted. Treatment should then be governed by the
information gathered by means of the catheter.

Management of Cardiogenic Shock

If the priority is the heart and there is comparatively little reason for concern about noncardiac
tissues, treatment is usually straightforward, though the results may be less than might be hoped
for. The approach to treatment of a patient in cardiogenic shock should be patterned on the
approach to treatment of a patient in hypovolemic or inflammatory shock in whom there are
grounds for concern about myocardial viability or formation of edema (see above).

If the ventricular end-diastolic volumes seem excessively large, either diuresis should be initiated
or morphine sulfate, 1 to 4 mg/hr, should be given, both to relieve pain and stress and to allow
pooling of blood in the systemic capacitance vessels.

If the heart rate is excessively rapid, beta blockade is indicated, accompanied, if necessary, by
calcium channel blockade. If myocardial ischemia is a possibility, the heart rate should not be
allowed to exceed 75 beats/min. If myocardial damage is unlikely, as in a patient with
uncomplicated valvular problems, the heart rate should not be allowed to reach or exceed 90
beats/min.

If the ventricular end-systolic pressure seems excessively high, more aggressive attempts should
be made to reduce arterial stiffness with diuresis and beta blockade. An ACE inhibitor and
nitroglycerin should be added as needed. As a rule, hydralazine should not be used. Because its
principal effects are on the arterioles, not the arteries, it lowers the MAP without reducing the
stiffness of the arteries (which is more important for decreasing the ventricular oxygen
requirements). Hydralazine can also increase the heart rate and thereby markedly increase
myocardial oxygen requirements, thus defeating the very purpose for which it was originally
given. The use of clonidine should also be avoided if possible. It, too, works mainly on the
arterioles instead of the arteries, and it can cause nightmares and disorientation, side effects that
can be a major problem in critically ill patients.

The goal of treatment is to achieve an acceptable LVESP, an adequate MAP, adequate peripheral
perfusion, and an acceptable heart rate, with no sign of myocardial ischemia. If this goal cannot
be achieved, the next step is to insert a Swan-Ganz catheter and manage the patient so that the
left ventricular afterload is 50% of the attainable contractility. Some degree of compromise may
prove necessary, but every effort should be made to keep the afterload from exceeding this value.
A high afterload will indeed produce a higher blood pressure, but only at the cost of increased
myocardial oxygen requirements, which are rarely desirable in a patient with a compromised
myocardium.

In some patients with acute myocardial ischemia and shock, all of the aforementioned treatments
will fail. Such patients should undergo emergency coronary angiography, as should any patient
with an acute coronary syndrome that becomes unstable or that is associated with ST-T segment
elevation. The purpose of the angiography is to find a correctable lesion that can be treated with
coronary angioplasty, stenting, or surgical revascularization. If necessary, an intra-aortic balloon
pump may be placed before or at the time of angiography, angioplasty, or stenting. This pump can
be left in place while the underlying problem awaits possible surgical correction (if indicated).

Treatment of primary right-side cardiogenic shock is the same as that of primary left-side
cardiogenic shock, except that in right-side failure, it may be possible to adjust the ventilator so as
to reduce the right ventricular afterload.
The hemoglobin concentration should probably be maintained at a generous level (i.e., 10
to 11 g/dl) in patients with cardiogenic shock, especially if the higher levels obliterate
symptoms of ischemia.