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Any condition that results in inadequate tissue oxygen delivery triggers an autonomic response in human body to maintain homeostasis. A cellular response to decreased oxygen delivery activates cascades of physiologic compensatory mechanisms to maintain normal functions. Therefore, in a state of shock, inadequate oxygen delivery fails to meet cellular metabolic demands and results in global tissue hypoperfusion and metabolic acidosis. Cellular response to decreased oxygen delivery causes adenosine triphosophate (ATP) depletion, energy-dependent ion pump dysfunction, and loss of cell membrane integrity. These events lead to systemic lactic acidosis with overpowering of various compensatory mechanisms that progress to multiple organ failure and ultimately death.

Clinically, shock is a complex syndrome associated with acute disruption of macro-and microcirculation resulting from disruption of blood flow. Hypotension may present in shock, but shock may not be diagnosed by virtue of hypotension alone. In the pediatric patient, presence of hypotension is regarded as a sign of decompensated shock.



Blood (fluid) is pumped from the heart (pump), carried in the vessels (pipe), and delivered to the tissues. Therefore, inadequate perfusion may result from malfunction of the pump; that is, decreased cardiac output (CO) from inadequate preload, poor contractility, and excessive afterload. These result in decreased stroke volume (SV). Because CO is a function of SV and heart rate (HR), diminished HR may also cause decrease in tissue perfusion. Stroke volume is the difference between end-diastolic volume (EDV) and end systolic volume (ESV), as expressed in the following equation.

Cardiac output (CO) = stroke volume (SV) × heart rate (HR)


Stroke volume = end-diastolic volume (EDV) - end-systolic volume (ESV);


CO = EDV - ESV × HR.

End-diastolic volume is largely dependent on preload, whereas ESV reflects afterload. The parameter that best relates to SV and can be measured is ejection fraction (EF), the fraction of blood that is ejected by the left ventricle during the contraction or ejection phase of the cardiac cycle (systole). Normal range of EF is 55-70%. Increasing EDV with volume resuscitation and decreasing ESV by increasing myocardial contractility or decreasing afterload, will increase SV and hence the cardiac output.

Inadequate fluid volume causes a state of hypovolemia, decreased EDV, and decreased tissue perfusion. Increased HR (tachycardia) and increased vasodilatation with a decrease in systemic vascular resistance (SVR) may be an initial compensatory mechanism during early stages of shock to restore cardiac output, as expressed in the following equation.

Blood pressure (BP) = cardiac output (CO) × systemicvascular resistance (SVR);



However, cardiac output decreases eventually and hypotension ensues because of decrease in preload. Changes that occur in a state of shock are loss of preload ...

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