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Shock is a syndrome with multiple etiologies characterized by an
impairment of tissue perfusion.
The impairment of tissue perfusion, regardless of cause, can lead to
cellular dysfunction, organ failure, and death.
The diagnosis of shock is made by the findings of impaired tissue
perfusion on physical examination, and hemodynamic and laboratory
changes consistent with impaired perfusion. Hypotension may or may
not be present. Hemodynamic monitoring is vital for the determination
of the type of shock and assessment of response to interventions.
Hypovolemic shock is caused by a reduction in intravascular volume,
which results in changes in the hemodynamic profile such as decreases
in blood pressure, central venous pressure, pulmonary capillary wedge
pressure, and cardiac output, and a compensatory increase in heart rate,
systemic vascular resistance, and myocardial contractility.
Resuscitation is required to treat hypovolemic shock to maintain
adequate tissue perfusion and oxygenation. This can be achieved by
administration of intravenous crystalloids, colloids, or blood.
The physiologic response to fluid loss or gain is described by the Frank–
Cardiogenic shock results from a decrease in the heart’s ability to
maintain cardiac output that is unrelated to hypovolemia.
Treatment of patients in cardiogenic shock involves optimization of
preload, increasing contractility, and reducing afterload if the blood
Septic shock is a type of distributive shock characterized by a profound
vasodilatory response and decrease in blood pressure.
Treatment of septic shock involves stabilization with fluids, vasopressors,
and inotropic agents and treatment of the underlying condition. Other
therapies involve modification of the body’s response to infection.
Patients with sepsis can experience disseminated intravascular
coagulation, which can lead to hemorrhagic and thrombotic
Shock is defined in simple terms as a syndrome of impaired tissue perfusion and
oxygenation usually, but not always, accompanied by hypotension. This impairment
of tissue perfusion eventually leads to cellular dysfunction, followed by organ
damage and death if untreated. The most common causes of shock are situations that
result in a reduction of intravascular volume (hypovolemic shock), myocardial pump
failure (cardiogenic shock), or increased vascular capacitance (distributive shock).
The type of treatment required depends on the etiology.
In recent years, medical support of patients with shock has improved because of
better technologies for hemodynamic monitoring, recognition of the value of vigorous
volume replacement, appropriate use of inotropic and vasoconstrictive agents, and
development of better ways to treat the underlying cause of the shock syndrome.
Understanding the principles of shock should further enhance the prompt recognition
of patients at risk, rapid initiation of corrective measures, and development of
innovative treatment regimens.
Shock is common among intensive care unit (ICU) patients and is present in up to
1 Table 17-1 outlines the classification of shock and
2 Recognition of the etiology and underlying pathology of the
various forms of shock is essential for managing this condition. The distinctions
among subtypes of shock only apply, however, in the relatively early stages. As the
syndrome evolves and compensatory mechanisms are overwhelmed, it becomes
increasingly difficult to determine the subtypes because the clinical and
pathophysiologic features of advanced shock are the same for all. Also, different
types of shock can occur at the same time (e.g., a patient with septic shock who is
also hypovolemic). The mortality rate for shock remains quite high—as high as 60%
to 80% in severe cases—despite recent improvements in its early recognition and
Tissue perfusion is a complex process of oxygen and nutrient delivery as well as
waste removal. When perfusion is impaired, it sets up a cascade of events that can
eventually end in death. Although the etiology of shock is varied, the eventual
progression (if untreated) to cell death and subsequent organ dysfunction results from
a common pathway of ischemia, endogenous inflammatory cytokine release, and the
generation of oxygen radicals. When cells are subjected to a prolonged period of
ischemia, anaerobic metabolism begins. This inefficient process results in a decrease
of adenosine triphosphate stores and causes the buildup of lactic acid and other toxic
substances that can alter mitochondrial function and eventually result in cell death. In
the advanced stages of shock, irreversible cellular damage leads to multiple organ
system failure, also known as multiple organ dysfunction syndrome.
Classification of Shock and Precipitating Events
Gastrointestinal bleeding (e.g., varices, peptic ulcer)
pancreatitis, postpartum hemorrhage
Gastrointestinal losses: vomiting, diarrhea, external drainage
Renal losses: diabetes mellitus, diabetes insipidus, overuse of diuretics
Sequestration: ascites, third-space accumulation
Cutaneous: burns, nonreplaced perspiration, and insensible water losses
Acute myocardial infarction (left or right ventricular infarction)
End-stage cardiomyopathy or severe acute exacerbation of heart failure
Bradyarrhythmia (Mobitz type II second-degree heart block, complete heart block)
Rupture of septum or free wall
Severe mitral or aortic valve insufficiency
Papillary muscle or chordae tendineae rupture or dysfunction
Septic (bacterial, fungal, viral, parasitic, mycobacterial)
Neurogenic (spinal cord injury, traumatic brain injury, cerebral damage, severe dysautonomia)
Inflammatory (burns, trauma, pancreatitis, air/fat embolism, post-cardiopulmonary bypass)
carbon monoxide, heavy metal, cyanide)
Endocrine (adrenal crisis, myxedema coma)
Adapted with permission from Gaieski D. Evaluation of and initial approach to the adult patient with
The body produces inflammatory cytokines in response to ischemia, injury, or
infection. The phrase systemic inflammatory response syndrome (SIRS) is the
recommended umbrella term to describe any acute, overwhelming inflammatory
response, independent of the cause.
3 This syndrome has best been described in the
sepsis literature; however, it can occur after a wide variety of insults, including
hemorrhagic shock, infection (septic shock), pancreatitis, ischemia, multi-trauma and
tissue injury, and immune-mediated organ injury. SIRS is usually a late manifestation
of hypovolemic forms of shock. It is uncommon in cardiogenic shock but is the
hallmark of septic shock. SIRS is clinically characterized by profound vasodilation,
which impairs perfusion, increases capillary permeability, and can reduce
CLINICAL PRESENTATION AND DIAGNOSIS
Independent of the pathophysiologic cause, the clinical syndrome of shock progresses
through several stages. During each step, the body uses and exhausts various
compensatory mechanisms to balance oxygen delivery (D.O2
) in an effort to maintain perfusion of vital organs. Oxygen
delivery is determined by the arterial concentration of oxygen multiplied by the blood
flow (cardiac output [CO]) (Fig. 17-1 and Table 17-2). Normally, consumption is
independent of supply, except at low rates of ḊO2
. In some critically ill patients,
perfusion is inadequate to meet metabolic demands and O2 becomes dependent on
the supply despite “normal” ḊO2
Although hypotension is often described as the hallmark of shock, it is not
necessarily present in all patients.
Figure 17-1 Determinants of blood pressure, cardiac output, and oxygen delivery.
Normal Hemodynamic Values and Derived Indices
Pressure in the central arterial bed,
determined by cardiac output and
Cardiac output (CO) Amount of blood ejected from the left
ventricle per minute; determined by
a Measures mean pressure in right
atrium and reflects right ventricular
filling pressure and volume status.
Primarily determined by venous return
to the heart. The goal in most critically
Heart rate (HR) (pulse) Number of myocardial contractions
Pulmonary artery pressure (PAP) Systolic (SPAP): Measures PAP
during systole; reflects pressure
generated by the contraction of the
Diastolic (DPAP): Measures PAP
during diastole; reflects diastolic filling
pressure in the left ventricle. May
approximate pulmonary capillary
gradient <5 mm Hg between DPAP
Mean (MPAP): Average measure of
PAP during the entire cardiac cycle;
mPAP ≥25 mm Hg at rest is defined
Pulmonary capillary wedge pressure
Measures pressure distal to the
pulmonary artery; reflects left
ventricular filling pressures (preload).
Usually lower than or within 5 mm
Hg of pulmonary artery diastolic
Central venous oxygen saturation
The oxygen saturation of blood
returning to the heart; a reflection of
oxygen extraction from the upper
Mixed venous oxygen saturation
The oxygen saturation of blood in the
pulmonary artery; a marker of the
relationship between cardiac output
and total body oxygen consumption.
Cardiac index (CI) Cardiac output per square meter of
Left ventricular stroke work index
Amount of work the left ventricle
exerts during systole; adjusted for
measure of contractility, the inotropic
Mean arterial pressure (MAP) MAP = [(2 × DBP) + SBP]/3 80–100 mm Hg
) The amount of oxygen delivered by
) The amount of oxygen consumed by
the body per unit time. The product of
cardiac output and the difference
between the arterial and venous
where CvO2 = Hgb × SvO2 × 13.9
Coronary artery perfusion pressure
The pressure gradient between the
coronary arteries and the pressure in
either the right atrium or the left
ventricle during diastole. A major
determinant of coronary blood flow
and oxygen supply to the heart.
Stroke volume (SV) Amount of blood ejected from the
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