II
Chapter
29
Shock States
Lincoln S. Smith and Lynn J. Hernan
PEARLS
• S hock is recognized by the features of tachycardia,
tachypnea, and abnormalities of perfusion, as evidenced
by skin perfusion, quality of pulses, mental status, and
dysfunction of other organ systems.
• P ediatric patients with shock most often present with
myocardial dysfunction (“cold” shock), although older
children and adolescents may present with the adult picture
of vascular dysfunction (“warm” shock).
• N eonates in shock must be treated for both septic shock and
cardiogenic shock resulting from ductal-dependent congenital
heart disease until an echocardiogram can confirm the cardiac
anatomy. These conditions cannot be ruled out by physical
examination. Therefore, all neonates with shock should be
given prostaglandin infusion as part of their resuscitation.
Pulmonary hypertension, hypocalcemia, and hypoglycemia
frequently complicate shock in neonates.
• P ediatric patients in shock generally have absolute or relative
hypovolemia, and the first line of resuscitation should be a
fluid bolus of 20 mL/kg. Administration of more fluid should
be based on rapid assessment of hemodynamic status.
• E arly endotracheal intubations allow advantageous
redistribution of the compromised cardiac output, and
afterload reduces the left ventricle.
• T imely recognition and early aggressive goal-directed therapy
reduces mortality in septic shock.
The clinical syndrome of shock is one of the most dramatic,
dynamic, life-threatening problems faced by the physician
in the critical care setting. Although untreated shock is uni-
versally lethal, mortality may be considerably reduced with
proper recognition, diagnosis, monitoring, and treatment.
Definition and Physiology
Shock is an acute, complex state of circulatory dysfunction
that results in failure to deliver sufficient amounts of oxygen
and other nutrients to meet tissue metabolic demands. If pro-
longed, it leads to multiple organ failure and death. There-
fore shock states can be viewed as a state of acute cellular
oxygen deficiency. Shock can be caused by any serious dis-
ease or injury, but whatever the causative factors, it is always a
364
problem of inadequate cellular sustenance. It is the final com-
mon pathway to death.
Delivery of oxygen is a direct function of cardiac output
(CO) and arterial oxygen content (CaO2):
Delivery of oxygen:
DO2 = CO × CaO2
CO = Heart rate (HR) × Stroke volume (SV)
CaO2 = (Hgb × 1.34 × SaO2 ) + (0.003 × PaO2 )
Stroke volume is a function of preload, afterload, contrac-
tility, and diastolic relaxation. Therefore optimizing heart
rate, contractility and diastolic relaxation, and preload and
afterload improves cardiac output. Oxygen-carrying capac-
ity can be increased by raising hemoglobin and optimizing its
saturation with oxygen. Oxygen delivery can be improved by
manipulation of all these factors.
Calculation of oxygen delivery provides a measure of global
oxygen delivery and may not reflect regional hypoperfu-
sion and localized ischemia. Inadequate oxygen delivery can
result from either limitation or maldistribution of blood flow.
Reduced oxygen content (anemia, poor arterial oxygen satu-
ration) necessitates higher cardiac output to maintain oxygen
delivery. In certain situations (fever, sepsis, trauma), meta-
bolic demands may exceed normal oxygen delivery. Impair-
ment of the extraction or utilization of oxygen by cells and
mitochondria creates a functional arteriovenous shunt and
may be the harbinger of multiorgan dysfunction syndrome.1-3
When oxygen delivery fails to meet cellular oxygen demands,
various compensatory mechanisms are activated. Therefore
shock is a dynamic process. The exact cardiorespiratory pat-
tern detected clinically depends on the complex interaction of
patient, illness, time elapsed, and treatment provided.
Because of its progressive nature, shock can be divided into
phases: compensated, uncompensated, and irreversible. In
compensated shock, vital organ function is maintained pri-
marily by intrinsic regulatory mechanisms. Previously healthy
children can compensate and maintain normal blood pres-
sure during hypoperfusion states. Therefore identification of
the early compensated stage of shock is crucial. Diagnosing a
patient as having early compensated shock, rather than mere
dehydration, may be the difference between a patient who is
appropriately resuscitated and one for whom resuscitative
efforts are delayed. As shock progresses, the cardiovascular
system’s ability to compensate is exceeded, and microvascular