Shock

Shock
Shock
Shock is the physiologic state characterized by
significant reduction of systemic tissue
perfusion, resulting in decreased tissue
oxygen delivery.
This creates an imbalance between oxygen
delivery and oxygen consumption.
Prolonged oxygen deprivation leads to cellular
hypoxia and derangement of critical biochemical
processes at the cellular level, which can
progress to the systemic level
Effect of Shock
Cellular effects include cell membrane ion pump
dysfunction, intracellular edema, leakage of
intracellular contents into the extracellular space,
and inadequate regulation of intracellular pH
Systemic effects include alterations in the serum
pH, endothelial dysfunction, and further stimulation
of inflammatory and antiinflammatory cascades
Types of Shock
Hypovolemic
Cardiogenic
Distributive
Combined
Hypovolemic Shock
Hypovolemic shock is a consequence of
decreased preload due to intravascular volume
loss.
The decreased preload diminishes stroke
volume, resulting in decreased cardiac output
(CO). The systemic vascular resistance (SVR) is
typically increased in an effort to compensate for
the diminished CO and maintain perfusion to
vital organs.
Cardiogenic Shock
Cardiogenic shock is a consequence of cardiac
pump failure, resulting in decreased CO.
The SVR is typically increased in an effort to
compensate for the diminished CO.
Distributive Shock
Distributive (vasodilatory) shock is a
consequence of severely decreased SVR. The CO
is typically increased in an effort to compensate
for the diminished SVR.
Combined
Different types of shock can coexist.
As an example, patients with septic shock have
a hypovolemic component due to decreased oral
intake, insensible losses, vomiting, or diarrhea;
a cardiogenic component due to sepsis-related
myocardial dysfunction;
a distributive component due to activation of
inflammatory and antiinflammatory cascades and
their effects on vascular permeability and
vasodilation
Stages of Shock
Regardless of the type of shock, there exists a
physiologic continuum.
Shock begins with an inciting event, such as a focus
of infection (eg, abscess) or an injury (eg, gunshot
wound).
This produces a systemic circulatory abnormality,
which may progress through several complex and
intertwined stages preshock, shock, and endorgan dysfunction.
This progression can culminate in irreversible endorgan damage and death
Stages of Shock
Preshock
Shock
End-organ dysfunction
Preshock
Preshock is also referred to as warm shock or
compensated shock.
It is characterized by rapid compensation for
diminished tissue perfusion by various homeostatic
mechanisms.
As an example, compensatory mechanisms during
preshock may allow an otherwise healthy adult to be
asymptomatic despite a 10 percent reduction in total
effective blood volume.
Tachycardia, peripheral vasoconstriction, and either
a modest increase or decrease in systemic blood
pressure may be the only clinical signs of shock.
Shock
During shock, the compensatory mechanisms become overwhelmed
and signs and symptoms of organ dysfunction appear.
These include tachycardia, dyspnea, restlessness, diaphoresis,
metabolic acidosis, oliguria, and cool clammy skin.
The signs and symptoms of organ dysfunction typically correspond
to a significant physiologic perturbation.
Examples include a 20 to 25 percent reduction in effective blood
volume in hypovolemic shock, a fall in the cardiac index to less than
2.5 L/min/M2 in cardiogenic shock, or activation of innumerable
mediators of the systemic inflammatory response syndrome (SIRS)
in distributive shock.
End-organ dysfunction
Progressive end-organ dysfunction leads to
irreversible organ damage and patient death.
During this stage, urine output may decline
further (culminating in anuria and acute renal
failure), acidemia decreases the cardiac output
and alters cellular metabolic processes, and
restlessness evolves into agitation, obtundation,
and coma.
Hypovolemic Shock
Hemorrhage-induced
Causes include blunt or penetrating trauma, upper or lower

gastrointestinal bleeding, ruptured hematoma, hemorrhagic
pancreatitis, fractures, or a ruptured aortic, abdominal, or
left ventricular free wall aneurysm.
Fluid loss-induced
Causes include diarrhea, vomiting, heat stroke, inadequate

repletion of insensible losses, burns, and "third spacing".
Third-space losses are common postoperatively and in
patients who have intestinal obstruction, pancreatitis, or
cirrhosis.
Cardiomyopathies
Cardiogenic
Shock 1
Cardiomyopathic causes of shock include myocardial

infarction involving greater than 40 percent of the left
ventricular myocardium, right ventricular infarction, dilated
cardiomyopathies, stunned myocardium following prolonged
ischemia or cardiopulmonary bypass, and myocardial
depression due to advanced septic shock .
Arrhythmias
Both atrial and ventricular arrhythmias can produce

cardiogenic shock. Atrial fibrillation and atrial flutter reduce
CO by interrupting coordinated atrial filling of the ventricles.
Ventricular tachycardia, bradyarrhythmias, and complete
heart block reduce CO, while ventricular fibrillation abolishes
CO.
Cardiogenic Shock 2
Mechanical abnormalities
Mechanical causes of cardiogenic shock include valvular defects,

ventricular septal defects, atrial myxomas, and a ruptured ventricular free
wall aneurysm. Valvular defects include rupture of a papillary muscle or
chordae tendineae, acute aortic insufficiency caused by retrograde
dissection of the ascending aorta into the aortic valve ring, and critical
aortic stenosis. An atrial myxoma can reduce ventricular filling, while a
ruptured left ventricular free wall aneurysm can produce pump failure,
hypovolemia, and sudden death if is not contained by the pericardial sac.
Extracardiac abnormalities
Extracardiac (obstructive) causes of cardiogenic shock include massive

pulmonary embolism, tension pneumothorax, severe constrictive
pericarditis, pericardial tamponade, and severe pulmonary hypertension
producing Eisenmenger's physiology. These conditions can also present
clinically as hypovolemic shock when their primary physiologic
disturbance is decreased preload, rather than pump failure.
Distributive Shock
Septic Shock
Systemic Inflammatory Response Syndrome
Anaphylaxis and anaphylactoid reactions
Drug or toxin reactions, including insect bites,
tranfusion reactions, heavy metal poisoning
Addisonian crisis
Myxedema coma
Neurogenic shock
Systemic Inflammation Response

Syndrome
Temperature >38.5C or <35C
Heart rate >90 beats/min
Respiratory rate >20 breaths/min or PaCO2
<32 mmHg
WBC >12,000 cells/mm3, <4000 cells/mm3, or
>10 percent immature (band) forms
SIRS can result from a variety of conditions,

such as autoimmune disorders, pancreatitis,
vasculitis, thromboembolism, burns, or surgery.
Sepsis In sepsis, the clinical signs that define

SIRS are present and are due to either a cultureproven infection or an infection identified by
visual inspection.
The severity of sepsis is graded according to the
associated organ dysfunction and hemodynamic
compromise.
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Shock

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Shock

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Shock

Causes include blunt or penetrating trauma, upper or lower

Causes include diarrhea, vomiting, heat stroke, inadequate

Cardiomyopathic causes of shock include myocardial

Both atrial and ventricular arrhythmias can produce

Mechanical causes of cardiogenic shock include valvular defects,

Extracardiac (obstructive) causes of cardiogenic shock include massive

Systemic Inflammation Response

SIRS can result from a variety of conditions,

Sepsis In sepsis, the clinical signs that define

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