CIRCULATORY FAILURE (SHOCK)

Dr. Bernardo Dámaso Mata

 CIRCULATORY FAILURE (SHOCK)
• Circulatory shock can be described as an acute failure of the
circulatory system to supply the peripheral tissues and organs of
the body with an adequate blood supply, resulting in cellular
hypoxia.
• Most often hypotension and hypoperfusion are present, but shock
may occur in the presence of normal vital signs.
 CIRCULATORY FAILURE (SHOCK)
• Shock is not a specific disease but a syndrome that can occur in the
course of many life-threatening traumatic conditions or disease
states.
• It can be caused by an alteration in cardiac function (cardiogenic
shock), a decrease in blood volume (hypovolemic shock), excessive
vasodilation with maldistribution of blood flow (distributive shock),
or obstruction of blood flow through the circulatory system
(obstructive shock).
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• Circulatory failure results in hypoperfusion of organs and tissues,
which in turn results in insufficient supply of oxygen and nutrients
for cellular function.
• There are compensatory physiologic responses that eventually
decompensate into various shock states if the condition is not
properly treated in a timely manner.
– The most immediate of the compensatory mechanisms are the
sympathetic and renin systems, which are designed to maintain
cardiac output and blood pressure.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• There are two types of adrenergic receptors for the sympathetic
nervous system: α and β.
– The β receptors are further subdivided into β1 and β2 receptors.
– Stimulation of the α receptors causes vasoconstriction;
stimulation of β1 receptors, an increase in heart rate and force
of myocardial contraction; and of β2 receptors, vasodilation of
the skeletal muscle beds and relaxation of the bronchioles.
• In shock, there is an increase in sympathetic outflow that results in
increased epinephrine and norepinephrine release, and activation
of both α and β receptors.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• Thus, increases in heart rate and vasoconstriction occur in most
types of shock.
• There also is an increase in renin release, leading to an increase in
angiotensin II, which augments vasoconstriction and leads to an
aldosterone-mediated increase in sodium and water retention by
the kidneys.
– In addition, there is local release of vasoconstrictors, including
norepinephrine, angiotensin II, vasopressin, and endothelin,
which contribute to arterial and venous vasoconstriction.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• The compensatory mechanisms that the body recruits are not
effective over the long term and become detrimental when the
shock state is prolonged.
• The intense vasoconstriction causes a decrease in tissue perfusion
and insufficient supply of oxygen.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• Cellular metabolism is impaired, vasoactive inflammatory mediators
such as histamine are released, production of oxygen free radicals is
increased, and excessive lactic acid and hydrogen ions result in
intracellular acidity.
• Each of these factors promotes cellular dysfunction or death. If
circulatory function is reestablished, whether the shock is
irreversible or the patient will survive is determined largely at the
cellular level.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• Shock ultimately exerts its effect at the cellular level, with failure of
the circulation to supply the cell with the oxygen and nutrients
needed for production of ATP. The cell uses ATP for a number of
purposes, including operation of the sodium potassium membrane
pump that moves sodium out of the cell and potassium back into
the cell.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• The cell uses two pathways to convert nutrients to energy.
– The first is the anaerobic (non–oxygen-dependent) glycolytic
pathway, which is located in the cytoplasm. Glycolysis converts
glucose to ATP and pyruvate.
– The second pathway is the aerobic (oxygen-dependent)
pathway, called the citric acid cycle, which is located in the
mitochondria. When oxygen is available, pyruvate from the
glycolytic pathway moves into the mitochondria and enters the
citric acid cycle, where it is transformed into ATP and the
metabolic byproducts carbon dioxide and water.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• When oxygen is lacking, pyruvate does not enter the citric acid
cycle; instead, it is converted to lactic acid. The anaerobic pathway,
although allowing energy production to continue in the absence of
oxygen, is relatively inefficient and produces significantly less ATP
than the aerobic pathway.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• In severe shock, cellular metabolic processes are essentially
anaerobic owing to the decreased availability of oxygen.
• Excess amounts of lactic acid accumulate in the cellular and the
extracellular compartments, and limited amounts of ATP are
produced. Without sufficient energy production, normal cell
function cannot be maintained. The sodium potassium membrane
pump is impaired, resulting in excess sodium inside the cells and
potassium loss from cells.
CIRCULATORY FAILURE (SHOCK)
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• The increase in intracellular sodium results in cellular edema and
increased cell membrane permeability. Mitochondrial activity
becomes severely depressed and lysosomal membranes may
rupture, resulting in the release of enzymes that cause further
intracellular destruction.
• This is followed by cell death and the release of intracellular
contents into the extracellular space. The destruction of the cell
membrane activates the arachidonic acid cascade, release of
inflammatory mediators, and production of oxygen free radicals
that extend cellular damage.
 CIRCULATORY FAILURE (SHOCK)
Pathophysiology of Circulatory Shock
• The extent of the microvascular injury and organ dysfunction is
primarily determined by the extent of the shock state and whether
it is prolonged.
• Interventions are targeted at both prevention and early
intervention, when possible.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
• Cardiogenic shock occurs when the heart fails to pump blood
sufficiently to meet the body’s demands. Clinically, it is defined as
decreased cardiac output, hypotension, hypoperfusion, and
indications of tissue hypoxia, despite adequate intravascular
volume.
• Cardiogenic shock may occur suddenly from a number of causes,
including myocardial infarction, myocardial contusion, sustained
arrhythmias, and cardiac surgery. Cardiogenic shock also may ensue
as an end-stage condition of coronary artery disease or
cardiomyopathy.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• The most common cause of cardiogenic shock is myocardial
infarction. Most patients who die of cardiogenic shock have had
extensive damage to the contracting muscle of the left ventricle
because of a recent infarct or a combination of recent and old
infarctions.
• Cardiogenic shock can occur with other types of shock because of
inadequate coronary blood flow, or it can develop because
substances released from ischemic tissues impair cardiac function.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• One unidentified substance, called myocardial depressant factor, is
thought to be released into the circulation during septic shock.
There are conflicting data on the identity of myocardial depressant
factor; however, inflammatory mediators such as TNF have been
suggested as possible agents.
• It has been hypothesized that the myocardial depressant factor
produces severe but potentially reversible myocardial depression,
ventricular dilation, and decreased left ventricular ejection fraction
and diastolic pressure.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• Regardless of cause, persons with cardiogenic shock have a
decrease in stroke volume and cardiac output, which results in
insufficient perfusion to meet cellular demands for oxygen.
• The poor cardiac output is due to decreased myocardial
contractility, increased afterload, and excessive preload. Mediators
and neurotransmitters, including norepinephrine, produce an
increase in systemic vascular resistance, which increases afterload
and contributes to the deterioration of cardiac function.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• Preload, or the filling pressure of the heart, is increased as blood
returning to the heart is added to blood that previously was not
pumped forward, resulting in an increase in left ventricular end-
systolic volume. Activation of the renin-angiotensin aldosterone
mechanism worsens both preload and afterload by producing an
aldosterone-mediated increase in fluid retention and an
angiotensin-II–mediated increase in vasoconstriction.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• The increased resistance (i.e., afterload) to ejection of blood from
the left ventricle, in combination with a decrease in myocardial
contractility, results in an increase in end-systolic ventricular volume
and preload, which further impairs the heart’s ability to pump
effectively.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• Eventually, coronary artery perfusion is impaired because of the
increased preload and afterload, and cardiac function decreases
because of poor myocardial oxygen supply. There is an increase in
intracardiac pressures due to volume overload and ventricular wall
tension in both diastole and systole.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
Pathophysiology
• Excessive pressures decrease coronary artery perfusion during
diastole, and increased wall tension decreases coronary artery
perfusion during systole. If treatment is unsuccessful, cardiogenic
shock may result in a systemic inflammatory response syndrome,
evidenced by increased white blood cell count, increased
temperature, and release of inflammatory markers such as CRP.
 CIRCULATORY FAILURE (SHOCK)
Cardiogenic Shock
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
• Hypovolemic shock is characterized by diminished blood volume
such that there is inadequate filling of the vascular compartment.
• It occurs when there is an acute loss of 15% to 20% of the
circulating blood volume.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
• The decrease may be caused by an external loss of whole blood
(e.g., hemorrhage), plasma (e.g., severe burns), or extracellular fluid
(e.g., severe dehydration or loss of gastrointestinal fluids with
vomiting or diarrhea).
• Hypovolemic shock also can result from an internal hemorrhage or
from third-space losses, when extracellular fluid is shifted from the
vascular compartment to the interstitial space or compartment.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Pathophysiology
• Hypovolemic shock, which has been the most widely studied type
of shock, is often used as a prototype in discussions of the
manifestations of shock. Figure shows the effect of removing blood
from the circulatory system during approximately 30 minutes.
CIRCULATORY FAILURE (SHOCK)
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Pathophysiology
• Approximately 10% of the total blood volume can be removed
without changing cardiac output or arterial pressure. The average
blood donor loses approximately 500 mL or 10% of their blood
without experiencing adverse effects.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Pathophysiology
• As increasing amounts of blood (10% to 25%) are removed, the
stroke volume falls but arterial pressure is maintained because of
sympathetic-mediated increases in heart rate and vasoconstriction.
Vasoconstriction results in an increased diastolic pressure and
narrow pulse pressure.
• Blood pressure is the product of cardiac output and systemic
vascular resistance (blood pressure = cardiac output × systemic
vascular resistance).
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Pathophysiology
• An increase in systemic vascular resistance maintains mean arterial
pressure for a short time despite decreased cardiac output.
• Cardiac output and tissue perfusion decrease before signs of
hypotension appear. Cardiac output and arterial pressure fall to
zero when approximately 35% to 45% of the total blood volume has
been removed.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• Without compensatory mechanisms to maintain cardiac output and
blood pressure, the loss of vascular volume would result in a rapid
progression from the initial to the progressive and irreversible
stages of shock.
• The most immediate of the compensatory mechanisms are the
sympathetic-mediated responses designed to maintain cardiac
output and blood pressure .
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• Within seconds after the onset of hemorrhage or the loss of blood
volume, tachycardia, increased cardiac contractility,
vasoconstriction, and other signs of sympathetic and adrenal
medullary activity appear.
• The sympathetic vasoconstrictor response also mobilizes blood that
has been stored in the venous side of the circulation as a means of
increasing venous return to the heart.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• There is considerable capacity for blood storage in the large veins of
the abdomen, and approximately 350 mL of blood that can be
mobilized in shock is stored in the liver.
• Sympathetic stimulation does not initially cause constriction of the
cerebral and coronary vessels, and blood flow to the heart and
brain is maintained at essentially normal levels as long as the mean
arterial pressure remains above 70 mm Hg.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• Compensatory mechanisms designed to restore blood volume
include absorption of fluid from the interstitial spaces, conservation
of sodium and water by the kidneys, and thirst.
• Extracellular fluid is distributed between the interstitial spaces and
the vascular compartment. When there is a loss of vascular volume,
capillary pressures decrease and water is drawn into the vascular
compartment from the interstitial spaces. The maintenance of
vascular volume is further enhanced by renal mechanisms that
conserve fluid.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• A decrease in renal blood flow and glomerular filtration rate results
in activation of the renin angiotensin-aldosterone mechanism,
which produces an increase in sodium reabsorption by the kidneys.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• The decrease in blood volume also stimulates centers in the
hypothalamus that regulate ADH release and thirst. ADH, also
known as vasopressin, constricts the peripheral arteries and veins
and greatly increases water retention by the kidneys.
• Although the mechanism of ADH is more sensitive to changes in
serum osmolality, a decrease of 10% to 15% in blood volume serves
as a strong stimulus for thirst.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• During the early stages of hypovolemic shock, vasoconstriction
decreases the size of the vascular compartment and increases
systemic vascular resistance. This response usually is all that is
needed when the injury is slight and blood loss is minimal.
 CIRCULATORY FAILURE (SHOCK)
Hypovolemic Shock
Compensatory Mechanisms.
• As hypovolemic shock progresses, vasoconstriction of the blood
vessels that supply the skin, skeletal muscles, kidneys, and
abdominal organs becomes more severe, with a further decrease in
blood flow and conversion to anaerobic metabolism resulting in
cellular injury.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
• Distributive or vasodilatory shock is characterized by loss of blood
vessel tone, enlargement of the vascular compartment, and
displacement of the vascular volume away from the heart and
central circulation.
• In distributive shock, the capacity of the vascular compartment
expands to the extent that a normal volume of blood does not fill
the circulatory system. Therefore, this type of shock is also referred
to as normovolemic shock.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
• Two main causes result in the loss of vascular tone:
– a decrease in the sympathetic control of vasomotor tone or
– the release of excessive vasodilator substances.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
• It can also occur as a complication of vessel damage resulting from
prolonged and severe hypotension due to hemorrhage, known as
irreversible or late-phase hemorrhagic shock.
• There are three shock states that share the basic circulatory pattern
of distributive shock:
– neurogenic shock,
– anaphylactic shock, and
– septic shock.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Neurogenic Shock
• Neurogenic shock is caused by decreased sympathetic control of
blood vessel tone due to a defect in the vasomotor center in the
brain stem or the sympathetic outflow to the blood vessels. The
term spinal shock describes the neurogenic shock that occurs in
persons with spinal cord injury.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Neurogenic Shock
• Output from the vasomotor center can be interrupted by brain
injury, the depressant action of drugs, general anesthesia, hypoxia,
or lack of glucose (e.g., insulin reaction).
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Neurogenic Shock
• Fainting due to emotional causes is a transient form of impaired
sympathetic outflow. Many general anesthetic agents can cause a
neurogenic shock–like reaction, especially during induction,
because of interference with sympathetic nervous system function.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Neurogenic Shock
• Spinal anesthesia or spinal cord injury above the mid-thoracic
region can interrupt the transmission of outflow from the
vasomotor center.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Neurogenic Shock
• In contrast to other shock states due to the loss of blood volume or
impaired cardiac function, the heart rate in neurogenic shock often
is slower than normal, and the skin is dry and warm. This type of
distributive shock is rare and usually transitory.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• Anaphylaxis is a clinical syndrome that represents the most severe
systemic allergic reaction.
• Anaphylactic shock results from an immunologically mediated
reaction in which vasodilator substances such as histamine are
released into the blood. These substances cause vasodilation of
arterioles and venules along with a marked increase in capillary
permeability. The vascular response in anaphylaxis is often
accompanied by life-threatening laryngeal edema and
bronchospasm, circulatory collapse, contraction of gastrointestinal
and uterine smooth muscle, and urticaria (hives) or angioedema.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• Among the most frequent causes of anaphylactic shock are
reactions to medications, such as penicillin; foods, such as nuts and
shellfish; and insect venoms.
• The most common cause is stings from insects of the order
Hymenoptera (i.e., bees, wasps, and fire ants). Latex allergy causes
life-threatening anaphylaxis in a growing segment of the
population.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• Health care workers and others who are exposed to latex are
developing latex sensitivities that range from mild urticaria, contact
dermatitis, and mild respiratory distress to anaphylactic shock.
• Children with spina bifida also are at extreme risk for this serious
and increasingly common allergy.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• The onset and severity of anaphylaxis depend on the sensitivity of
the person and the rate and quantity of antigen exposure.
• Signs and symptoms associated with impending anaphylactic shock
include abdominal cramps; apprehension; warm or burning
sensation of the skin, itching, and urticaria (i.e., hives); and
coughing, choking, wheezing, chest tightness, and difficulty in
breathing.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• After blood begins to pool peripherally, there is a precipitous drop
in blood pressure and the pulse becomes so weak that it is difficult
to detect.
• Life-threatening airway obstruction may ensue as a result of
laryngeal angioedema or bronchial spasm. Anaphylactic shock often
develops suddenly; death can occur within minutes unless
appropriate medical intervention is promptly instituted.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• Treatment includes immediate discontinuation of the inciting agent
or institution of measures to decrease its absorption (e.g.,
application of ice to the site of an insect bite); close monitoring of
cardiovascular and respiratory function; and maintenance of
respiratory gas exchange, cardiac output, and tissue perfusion.
Epinephrine is given in an anaphylactic reaction because it
constricts blood vessels and relaxes the smooth muscle in the
bronchioles, thus restoring cardiac and respiratory function.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• Other treatment measures include the administration of oxygen,
antihistamine drugs, and corticosteroids. The person should be
placed in a supine position. This is extremely important because
venous return can be severely compromised in the sitting position.
This in turn produces a pulseless mechanical contraction of the
heart and predisposes to arrhythmias. In several cases, death has
occurred immediately after assuming the sitting position.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• The prevention of anaphylactic shock is preferable to treatment.
Once a person has been sensitized to an antigen, the risk of
repeated anaphylactic reactions with subsequent exposure is high.
All health care providers should question patients regarding
previous drug reactions and inform patients as to the name of the
medication they are to receive before it is administered or
prescribed.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Anaphylactic Shock
• Persons with known hypersensitivities should wear Medic Alert
jewelry and carry an identification card to alert medical personnel if
they become unconscious or unable to relate this information.
Persons who are at risk for anaphylaxis should be provided with
emergency medications (e.g., epinephrine autoinjector) and
instructed in procedures to follow in case they are inadvertently
exposed to the offending antigen.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Septic shock, which is the most common type of vasodilatory shock, is
associated with severe infection and the systemic response to
infection.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
The nomenclature related to sepsis and septic shock has been
evolving.
– Sepsis is currently defined as suspected or proven infection, plus
a systemic inflammatory response (e.g., fever, tachycardia,
tachypnea, and elevated white blood cell count, altered mental
state, and hyperglycemia in the absence of diabetes).
– Severe sepsis is defined as sepsis with organ dysfunction (e.g.,
hypotension, hypoxemia, oliguria, metabolic acidosis,
thrombocytopenia, or obtundation).
– Septic shock is defined as severe sepsis with hypotension,
despite fluid resuscitation.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
• It is estimated that more than 750,000 cases of sepsis occur each
year in the United States, leading to approximately 225,000 deaths.
The growing incidence has been attributed to enhanced awareness
of the diagnosis, increased number of resistant organisms, growing
number of immunocompromised and elderly persons, and greater
use of invasive procedures.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
• With early intervention and advances in treatment methods, the
mortality rate has decreased; however, the number of deaths has
increased because of the increased prevalence.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Mechanisms.
• The pathogenesis of sepsis involves a complex process of cellular
activation resulting in the release of proinflammatory mediators
such as cytokines; recruitment of neutrophils and monocytes;
involvement of neuroendocrine reflexes; and activation of
complement, coagulation, and fibrinolytic systems.
• Initiation of the response begins with activation of the innate
immune system by pattern-recognition receptors (e.g., Toll-like
receptors [TLRs]) that interact with specific molecules present on
microorganisms.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Mechanisms.
• Binding of TLRs to epitopes on microorganisms stimulates
transcription and release of a number of proinflammatory and anti-
inflammatory mediators. Two of these mediators, TNF-α and
interleukin-1, are involved in leukocyte adhesion, local
inflammation, neutrophil activation, suppression of erythropoiesis,
generation of fever, tachycardia, lactic acidosis, ventilation-
perfusion abnormalities, and other signs of sepsis.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Mechanisms.
• Although activated neutrophils kill microorganisms, they also injure
the endothelium by releasing mediators that increase vascular
permeability. In addition, activated endothelial cells release nitric
oxide, a potent vasodilator that acts as a key mediator of septic
shock.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Mechanisms.
• Another important aspect of sepsis is an alteration of the
procoagulation–anticoagulation balance with an increase in
procoagulation factors and a decrease in anticoagulation factors.
Lipopolysaccharide on the surface of microorganisms stimulates
endothelial cells lining blood vessels to increase their production of
tissue factor, thus activating coagulation.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Mechanisms.
• Fibrinogen is then converted to fibrin, leading to the formation of
microvascular thrombi that further amplify tissue injury.
• In addition, sepsis lowers levels of protein C, protein S,
antithrombin III, and tissue factor pathway inhibitor, substances
that modulate and inhibit coagulation.
 CIRCULATORY FAILURE (SHOCK)
Distributive Shock
Sepsis and Septic Shock
Mechanisms.
• Lipopolysaccharide and TNF-α also decrease the synthesis of
thrombomodulin and endothelial protein C receptor, impairing
activation of protein C, and they increase the synthesis of
plasminogen activator inhibitor-1, impairing fibrinolysis.
 CIRCULATORY FAILURE (SHOCK)
Obstructive Shock
• The term obstructive shock describes circulatory shock that results
from mechanical obstruction of the flow of blood through the
central circulation.
 CIRCULATORY FAILURE (SHOCK)
Obstructive Shock
• Obstructive shock may be caused by a number of conditions,
including dissecting aortic aneurysm, cardiac tamponade,
pneumothorax, atrial myxoma, and evisceration of abdominal
contents into the thoracic cavity because of a ruptured
hemidiaphragm.
• The most frequent cause of obstructive shock is pulmonary
embolism.
 CIRCULATORY FAILURE (SHOCK)
Obstructive Shock
• The primary physiologic result of obstructive shock is elevated right
heart pressure due to impaired right ventricular function.
• Pressures are increased despite impaired venous return to the
heart. Signs of right heart failure occur, including elevation of CVP
and jugular venous distention.
 CIRCULATORY FAILURE (SHOCK)
Obstructive Shock
• Treatment modalities focus on correcting the cause of the disorder,
frequently with surgical interventions such as pulmonary
embolectomy, pericardiocentesis (i.e., removal of fluid from the
pericardial sac) for cardiac tamponade, or the insertion of a chest
tube for correction of a tension pneumothorax or hemothorax.
• In severe or massive pulmonary embolus, fibrinolytic drugs may be
used to break down the clots causing the obstruction.
 CIRCULATORY FAILURE (SHOCK)
Complications of Shock
• Carl Wiggers, a noted circulatory physiologist, stated, “Shock not
only stops the machine, but it wrecks the machinery.”
• Many body systems are wrecked by severe shock.
 CIRCULATORY FAILURE (SHOCK)
Complications of Shock
• Five major complications of severe shock are pulmonary injury,
acute renal failure, gastrointestinal ulceration, disseminated
intravascular coagulation, and multiple organ dysfunction
syndrome.
• These complications of shock are serious and often fatal.
 CIRCULATORY FAILURE (SHOCK)
Complications of Shock
– Acute Lung Injury/Acute Respiratory Distress Syndrome
– Acute Renal Failure
– Gastrointestinal Complications
– Disseminated Intravascular Coagulation
– Multiple Organ Dysfunction Syndrome