Introduction Blood pressure, pulse rate and respiratory rate are the routine vital signs measured in medicine.

These vital signs remain relatively constant throughout our adult life. However, as infants and children grow and age, the normal range changes. Two tables of normal vital signs for the pediatric population are presented below. Age (yr) <1 1-2 2-5 6-12 >12 Lower limits of systolic pressure 0-28 days: 60 mmHg 1-12 months: 70 mm Hg 1-10 years: 70 mm Hg + (2 age in years) Reference: Rosen's Emergency Medicine: Concepts and Clinical Practice 5th Edition Vital Signs at Various Ages Age Premature 0-3 mo 3-6 mo 6-12 mo 1-3 yr 3-6 yr 6-12 yr Heart Rate (beats/min) 120-170 * 100-150 * 90-120 80-120 70-110 65-110 60-95 Blood Pressure (mm Hg) 55-75/35-45 65-85/45-55 70-90/50-65 80-100/55-65 90-105/55-70 95-110/60-75 100-120/60/75 Respiratory Rate (breaths/min) 40-70 35-55 30-45 25-40 20-30 20-25 14/22 Respiratory Rate (breaths/min) 30-60 24-40 22-34 18-30 12-16 Heart Rate (beats/min) 100-160 90-150 80-140 70-120 60-100

12 * yr 55-85 110-135/65/85 12-18 References: Behrman, Nelson Textbook of Pediatrics: 17th edition. * From Dieckmann R, Brownstein D, Gausche-Hill M (eds): Pediatric Education for Prehospital Professionals. Sudbury, Mass, Jones & Bartlett, American Academy of Pediatrics, 2000, pp 43-45.

Background
Shock is a leading cause of morbidity and mortality in the pediatric population.Shock is a clinically diagnosed condition that results from many varied etiologies. It can damage any and all tissues and organ systems in the body. Delay in recognizing and quickly treating a state of shock results in a progression from compensated reversible shock to widespread multiple system organ failure to death. (See Pathophysiology and Etiology.) Morbidity from shock may be widespread and can include renal failure, brain damage, gut ischemia, hepatic failure, metabolic derangements, disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS), cardiac failure, and death. (See the image below.)

Chest radiograph of patient with cardiomegaly, which may accompany cardiogenic shock.

This article reviews the common physiologic foundations of shock that underpin all patients with this condition. The different pathophysiologic classifications of shock are defined along with their etiologies. The defining clinical findings of shock are described, and current diagnostic and therapeutic strategies are presented to help guide the most effective and appropriate treatment for resuscitating the child in shock. (See Pathophysiology, Presentation, Workup, Treatment, and Medication.)

Pathophysiology
Shock is defined physiologically as inadequate delivery of substrates and oxygen to meet the metabolic needs of the tissues. As cells are starved of oxygen and substrate, they can no longer sustain efficient aerobic energy production. Aerobic metabolism generates 36 adenosine triphosphate (ATP) molecules per glucose molecule. As oxygen delivery (DO 2) is impaired, the cell must switch to the much less efficient anaerobic metabolic pathway, which generates only 2 ATP molecules per molecule of glucose, with resulting production and accumulation of lactic acid. Eventually, cellular metabolism is no longer able to generate enough energy to power the components of cellular homeostasis, leading to the disruption of cell membrane ionic pumps, accumulation of intracellular sodium with an efflux of potassium, and accumulation of cytosolic calcium. The cell swells, the cell membrane breaks down, and cell death ensues. Widespread cellular death results in multiple system organ failure and, if irreversible, death. This metabolic disruption may occur from either an absolute deficiency of DO 2, defined as hypoxic shock, or a combination of hypoxia and deficient substrate delivery, predominantly of glucose, defined as ischemic shock. Most often they develop in combination, which results clinically in hypoxic-ischemic injury. Because DO2 is critical in either hypoxic or ischemic shock, considering DO 2when defining shock physiologically is useful.

Oxygen delivery
DO2 is defined as the amount of oxygen delivered to the tissues of the body per minute. DO 2 depends on the amount of blood pumped per minute, or cardiac output (CO), and the arterial oxygen content of that blood (CaO2). Thus, DO2 may be defined by the following equation: DO2 (mL O2/min) = CaO2 (mL O2/100mL blood) CO (L/min) 10 The CaO2 depends on how much oxygen-carrying capacity is available, which is a function of the hemoglobin (Hb) level and the Hb oxygen content, defined as the arterial oxygen saturation (SaO 2). A small, but clinically irrelevant, amount of oxygen is directly dissolved in the blood rather than bound to Hb. Therefore, CaO2may be defined by the following formula: CaO2 (mL/100mL) = Hb (g/100mL) SaO2 1.34mL O2/g + (0.003 X PaO2) A state of clinical shock may occur when CaO 2 is impaired either by hypoxia, which decreases SaO 2, or by anemia, which reduces the amount of Hb and, hence, reduces the body's total oxygen-carrying capacity. CO depends on the amount of blood pumped with each heartbeat, known as stroke volume (SV), and the heart rate (HR). SV depends on the ventricular end-diastolic filling volume (commonly referred to as ventricular preload), the state of myocardial contractility, and the afterload on the heart. Each of these variables, which affect CO, can be impaired in clinical shock states. Thus, the following relationship is observed: CO = HR (beats/min) SV (mL/beat) The recognition and treatment of pediatric shock depends on an understanding of these physiologic principles and definitions. Once understood, the different clinical presentations and causes of shock, as well as their most appropriate treatment strategies, are easily appreciated. (See the image below.)

Determinants of cardiac function and oxygen delivery to tissues. Adapted from Strange GR. APLS: The Pediatric Emergency Medicine Course. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1998:34.

Etiology
Several etiologic classifications of shock are recognized. In each of these classifications, 1 or more of the physiologic principles that govern oxygen delivery are disturbed. The major categories are as follows: Hypovolemic Distributive Cardiogenic Septic Obstructive Miscellaneous The frequency of the different causes of shock varies around the world. [1]Hypovolemia resulting from gastroenteritis is the major cause of shock in developing regions. In developed regions, a study by Fisher et al of pediatric patients who presented to a pediatric emergency department over an 8-year period identified sepsis as the leading cause of shock, occurring in 57% of patients. This was followed by hypovolemic shock (24%), distributive shock (14%), and cardiogenic shock (5%).[1]

Hypovolemic shock
Hypovolemic shock results from an absolute deficiency of intravascular blood volume. It is a leading cause of pediatric mortality in the United States and worldwide, although the specific causative agents may be different around the world. Causes of hypovolemic shock include the following: Intravascular volume loss - Eg, from gastroenteritis, burns, diabetes insipidus, heat stroke Hemorrhage - Eg, from trauma, surgery, gastrointestinal (GI) bleeding (see the image below) Interstitial loss - Eg, from burns, sepsis, nephrotic syndrome, intestinal obstruction, ascites

Hemodynamic response to hemorrhage model for cardiovascular response to hypovolemia from hemorrhage (based on normal data). Adapted from Schwaitzberg SD, Bergman KS, Harris BH. A pediatric trauma model of continuous hemorrhage. J Pediatr Surg. Jul 1988;23(7):605-9.

Gastroenteritis Gastroenteritis results in 6-20 million deaths in infants and children annually worldwide. Children with gastroenteritis may lose 10-20% of their circulating volume within 1-2 hours.[2] Rehydration is often impeded by concurrent vomiting, and deterioration may be rapid. Common infectious causes of gastroenteritis include bacteria such as Salmonella, Shigella,Campylobacter species, Escherichia coli, and Vibrio cholerae and viruses such as rotaviruses, adenoviruses, norovirus, and enteroviruses. Worldwide, amebiasis and cholera are also important causes. Physiologically, rapid loss of intravascular volume reduces ventricular preload, resulting in decreased stroke volume and CO and, thus, decreased DO2. In addition, a hemorrhagic component (ie, dysentery) may reduce Hb content, resulting in decreased CaO2. Trauma In the United States, the leading cause of death in children older than 1 year is trauma. Trauma kills more children than all other causes of death combined.[3] A major component of traumatic death is hemorrhage. Hemorrhagic shock reduces CaO2 and preload, resulting in decreased DO2 to the tissues. Third spacing Other causes of hypovolemia include capillary leak and tissue third spacing, which results in leakage of fluid out of the intravascular space into the interstitial tissues. Etiologies include burns, sepsis, and other systemic inflammatory diseases. Patients with such etiologies may appear "puffy" and overloaded with total-body fluid; however, they may be significantly intravascularly depleted, with inadequate preload, and in significant shock. Through understanding of the physiologic disturbance affecting intravascular volume and preload, it becomes clear that such patients need additional fluid administration despite their overall edematous appearance, in order to improve DO2 and prevent or correct a state of shock.