Circulatory shock, commonly known simply as
shock, is a life-threatening medical condition that occurs due to inadequate substrate for
aerobic cellular respiration. In the early stages, this is generally an inadequate tissue
level of oxygen. The typical signs of shock are low blood pressure,
a rapid heartbeat and signs of poor end-organ perfusion or “decompensation/peripheral shut
down”. There are times that a person’s blood pressure may remain stable, but may still
be in circulatory shock, so it is not always a reliable sign. The shock index, defined
as heart rate divided by systolic blood pressure, is a more accurate measure of shock than hypotension
and tachycardia in isolation. Circulatory shock is not related to the emotional
state of shock. Circulatory shock is a life-threatening medical emergency and one of the most common
causes of death for critically ill people. Shock can have a variety of effects, all with
similar outcomes, but all relate to a problem with the body’s circulatory system. For example,
shock may lead to hypoxemia or cardiac arrest. One of the key dangers of shock is that it
progresses by a positive feedback mechanism. Once shock begins, it tends to make itself
worse, so immediate treatment of shock is critical to the survival of the sufferer. Signs and symptoms
The presentation of shock is variable with some people having only minimal symptoms such
as confusion and weakness. While the general signs for all types of shock are low blood
pressure, decreased urine output, and confusion, these may not always be present. While a fast
heart rate is common, those on β-blockers, those who are athletic and in 30% of cases
those with shock due to intra abdominal bleeding may have a normal or slow heart rate. Specific
subtypes of shock may have additional symptoms. Hypovolemic
Hypovolemia is a direct loss of effective circulating blood volume leading to:
A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia
Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction
Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis
Hypothermia due to decreased perfusion and evaporation of sweat
Thirst and dry mouth, due to fluid depletion Cold and mottled skin, especially extremities,
due to insufficient perfusion of the skin The severity of hemorrhagic shock can be graded
on a 1-4 scale on the physical signs. This approximates to the effective loss of blood
volume. The shock index is a stronger predictor of the impact of blood loss than heart rate
and blood pressure alone. This relationship has not been well established in pregnancy-related
Symptoms of cardiogenic shock include: Distended jugular veins due to increased jugular
venous pressure Weak or absent pulse
Arrhythmia, often tachycardia Pulsus paradoxus in case of tamponade
Distributive Distributive shock includes infectious, anaphylactic,
Endocrine and neurogenic causes. The SIRS features typically occur in early septic shock.
Septic shock Systemic leukocyte adhesion to endothelial
tissue Reduced contractility of the heart
Activation of the coagulation pathways, resulting in disseminated intravascular coagulation
Increased levels of neutrophils Main manifestations are produced due to massive
release of histamine which causes intense vasodilation.
Pathophysiology There are four stages of shock. As it is a
complex and continuous condition there is no sudden transition from one stage to the
next. At a cellular level shock is the process of oxygen demand becoming greater than oxygen
During this stage, the state of hypoperfusion causes hypoxia. Due to the lack of oxygen,
the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor
in the electron transport chain is not abundant, this slows down entry of pyruvate into the
Krebs cycle, resulting in its accumulation. Accumulating pyruvate is converted to lactate
by lactate dehydrogenase and hence lactate accumulates.
Compensatory 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 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 epinephrine and norepinephrine.
Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas
epinephrine 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. 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.
Progressive 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 smooth muscle and precapillary sphincters relax 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. If the bowel becomes sufficiently ischemic,
bacteria may enter the blood stream, resulting in the increased complication of endotoxic
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain
damage and cell death are occurring, and death will occur imminently. One of the primary
reasons that shock is irreversible at this point is that much cellular ATP has been degraded
into adenosine in the absence of oxygen as an electron receptor in the mitochondrial
matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering
capillary vasodilation, and then is transformed into uric acid. Because cells can only produce
adenosine at a rate of about 2% of the cell’s total need per hour, even restoring oxygen
is futile at this point because there is no adenosine to phosphorylate into ATP.
Diagnosis The first changes seen in shock is an increased
cardiac output followed by a decrease in mixed venous oxygen saturation as measured in the
pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation as measured
via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses
anaerobic metabolism will begin to occur with an increased blood lactic acid as the result.
While many laboratory tests are typically performed there is no test that either makes
or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful
to determine volume state. Differential diagnosis
Shock is a common end point of many medical conditions. It has been divided into four
main types based on the underlying cause: hypovolemic, distributive, cardiogenic and
obstructive. A few additional classifications are occasionally used including: endocrinologic
Hypovolemic shock is the most common type of shock and is caused by insufficient circulating
volume. Its primary cause is hemorrhage, or loss of fluid from the circulation. Vomiting
and diarrhea are the most common cause in children. With other causes including burns,
environmental exposure and excess urine loss due to diabetic ketoacidosis and diabetes
Cardiogenic 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 dysrhythmias, cardiomyopathy/myocarditis,
congestive heart failure, contusio cordis, or cardiac valve problems.
Obstructive Obstructive shock is due to obstruction of
blood flow outside of the heart. Several conditions can result in this form of shock.
Cardiac tamponade in which fluid in the pericardium prevents inflow of blood into the heart. 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.
Pulmonary embolism is the result of a thromboembolic incident in the blood vessels of the lungs
and hinders the return of blood to the heart. Aortic stenosis hinders circulation by obstructing
the ventricular outflow tract Distributive
Distributive shock is due to impaired utilization of oxygen and thus production of energy by
the cell. Examples of this form of shock are: Septic shock is the most common cause of distributive
shock. Caused by an overwhelming systemic infection resulting in vasodilation leading
to hypotension. Septic shock can be caused by Gram negative bacteria such as 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, and other Gram-positive cocci, such as pneumococci and streptococci, and certain
fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of
cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic
shock: “. . .sepsis-induced hypotension despite adequate fluid resuscitation along with the
presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis,
oliguria, or an acute alteration in mental status. Patients who are receiving inotropic
or vasopressor agents may have a normalized blood pressure at the time that perfusion
abnormalities are identified.” 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.
High spinal injuries may cause neurogenic shock. The classic symptoms include a slow
heartrate due to loss of cardiac sympathetic tone and warm skin due to dilation of the
peripheral blood vessels. Endocrine
Based on endocrine disturbances such as: Hypothyroidism in critically ill patients,
reduces cardiac output and can lead to hypotension and respiratory insufficiency.
Thyrotoxicosis 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 demands Management
The best evidence exists for the treatment of septic shock in adults and as the pathophysiology
appears similar in children and other types of shock treatment this has been extrapolated
to these areas. Management may include securing the airway via intubation to decrease the
work of breathing, oxygen supplementation, intravenous fluids and a passive leg raise,
and blood transfusions. It is important to keep the person warm as well as adequately
manage pain and anxiety as these can increase oxygen consumption.
Fluids Aggressive intravenous fluids are recommended
in most types of shock which is usually instituted as the person is being further evaluated.
Which intravenous fluid is superior, colloids or crystalloids, remains undetermined. Thus
as crystalloids are less expensive they are recommended. If the person remains in shock
after initial resuscitation packed red blood cells should be administered to keep the hemoglobin
greater than 100 gms/l. For those with hemorrhagic shock the current
evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries
allowing mild hypotension to persist. Targets include a mean arterial pressure of 60 mmHg,
a systolic blood pressure of 70-90 mmHg, or until their adequate mentation and peripheral
Vasopressors may be used if blood pressure does not improve with fluids. There is no
evidence of superiority of one vasopressor over another. Vasopressors have not been found
to improve outcomes when used for hemorrhagic shock from trauma but may be of use in neurogenic
shock. Activated protein C while once aggressively promoted for the management of septic shock
has been found not to improve survival and is associated with a number of complications.
The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.
If used at all it should only be considered if the pH is less than 7.0.
Treatment goals The goal of treatment is to achieve a urine
output of greater than 0.5 mlh, a central venous pressure of 8-12 mmHg and a mean arterial
pressure of 65-95 mmHg. In trauma the goal is to stop the bleeding which in many cases
requires surgical interventions. Epidemiology
Hemorrhagic shock occurs in about 1-2% of trauma cases.
Prognosis The prognosis of shock depends on the underlying
cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic
shock are readily treatable and respond well to medical therapy. Septic shock however,
is a grave condition with a mortality rate between 30% and 50%. The prognosis of cardiogenic
shock is even worse. History
In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today.