Many conditions and pathophysiologic disturbances are associated with shock and hypotension in the newborn, ranging from acute blood loss (hypovolemic shock) to heart failure (cardiogenic shock). (See Etiology.)
Shock is a complex clinical syndrome caused by an acute failure of circulatory function and is characterized by inadequate tissue and organ perfusion.  When this occurs, inadequate amounts of oxygen and nutrient substrate are delivered to body tissues, and removal of metabolic waste products is inadequate. This results in cellular dysfunction, which may eventually lead to cell death. Failure of perfusion may involve isolated organs or the entire organism. Hypotension (ie, lower-than-expected blood pressure) frequently, but not always, accompanies shock. (See Pathophysiology and Etiology.)
In one study of the variation in prevalence of hypotension, authors noted that, among low–birth-weight infants, 16-52% received volume expansion and 4-39% received vasopressors. 
Maintenance of adequate tissue perfusion depends on a combination of 3 major factors: (1) cardiac output; (2) integrity and maintenance of vasomotor tone of local vascular beds, including arterial, venous, and capillary; and (3) the ability of the blood to perform its necessary delivery of metabolic substrates and removal of metabolic wastes. (See Treatment and Medications.)
Cardiac output is the product of heart rate and stroke volume. Neonatal cardiac output depends more on heart rate than stroke volume; therefore, very high (>180 beats per minute [bpm]) and very low (< 80 bpm) heart rates are likely to compromise cardiac output if prolonged. However, not all infants with subnormal heart rates have impaired perfusion. At higher rates, ventricular filling time and end-diastolic volume are diminished, and myocardial oxygen consumption is increased. Because myocardial perfusion occurs during diastole, further increases in heart rate may produce undesirable cardiac ischemia, leading to ventricular dysfunction.
Stroke volume, the other major determinant of cardiac output, is influenced by preload, afterload, and myocardial contractility, as follows:
Preload - Preload corresponds to the myocardial end-diastolic fiber length and is determined by the amount of blood filling the ventricles during diastole; increases in preload increase stroke volume up to a maximum value, beyond which stroke volume falls according to the Starling law
Afterload - Afterload is the force that the myocardium generates during ejection against systemic and pulmonary vascular resistances (for the left and right ventricles, respectively); reductions in afterload increase stroke volume if other variables remain constant
Contractility - Contractility is a semiquantitative measure of ventricular function, and an increase in contractility produces an increase in stroke volume if preload and afterload are unchanged; this is determined by the percentage of fractional shortening, which depends on the ventricular end diastolic and end systolic diameter
Clinically significant alterations in preload, afterload, and contractility may be achieved by the use of vasoactive pharmacologic agents, administration of inotropic agents, changes in blood volume, or a combination of these methods.
Blood flow to tissues and organs is influenced by their vascular beds, which are under the control of central and local vasoregulation, also referred to as autoregulation. This provides different organs with the ability to maintain internal blood flow over a wide range of arterial blood pressure fluctuations. When autoregulation is lost, blood flow becomes pressure passive, and this may lead to ischemic or hemorrhagic consequences. The biochemical mediators of vasomotor tone for each vascular bed are different, and their complex interactions are not yet fully understood.
The ability of the blood to impart delivery of oxygen and nutrients and to remove metabolic excretory products is largely determined by adequate lung ventilation and perfusion, oxygen-carrying capacity, and oxygen extraction by the tissues.
Although each gram of hemoglobin can bind 1.36mL of oxygen, fetal hemoglobin binds oxygen more tightly than adult hemoglobin and, thus, has a relatively reduced oxygen-unloading capacity at the tissue level. This results in a leftward shift of the oxygen-hemoglobin dissociation curve. Other factors that may cause a significant leftward shift of this curve frequently accompany shock and include hypothermia and hypocarbia. Under these circumstances, oxygen extraction by tissues may be decreased despite adequate oxygen delivery.
Usually, mean blood pressure, rather than systolic pressure, is used to judge the normality of data obtained from the indwelling arterial line. Mean blood pressure is thought to be free of the artifact caused by resonance, thrombi, and air bubbles, but this may not always be true. Based on these data, the statistically defined lower limits of mean blood pressure during the first day of life are approximately numerically similar to the gestational age reference range of the infant.
However, most preterm infants, even at 24-26 weeks' gestation, have a mean blood pressure of 30mm Hg or greater by the third day of life. The systolic blood pressure correlates with the gestational age reference range 4-24 hours after birth; only 3% of babies with normal long-term outcome have systolic blood pressures below the reference range for the gestational age. 
A low upper body blood flow is common in first day of life in preterm infants younger than 30 weeks' gestation; this has strong correlation with periventricular or intraventricular hemorrhage. Blood pressure measurement is limited to assessing the systemic flow, particularly in the presence of physiologic shunts; thus, the estimation of superior vena cava (SVC) flow is observed to correlate with the low flow states rather than the left ventricular output (LVO). The low flow states are also associated with hyperkalemia in premature infants.
In premature babies, the presence of fetal shunts such as patent ductus arteriosus (PDA) and patent foramen ovale (PFO) further affects the systemic and pulmonary blood flow. Depending on the size of these shunts, blood may be shunted to lower downstream pressure bed, which, in turn, can cause volume overloading of the left side of the heart (PDA) and could lead to cardiac failure and other complications, including low blood pressure. Shock unresponsive to inotropes in the first few days of life in preterm babies can be caused by a large PDA. Further, it has been observed that estimations of blood pressure (mean and systolic) have poor correlation with cardiac output in babies with a PDA. 
A linear relationship between blood pressure and both gestational age or birthweight and postnatal age is recognized; however, only preliminary data are available on the gestational age–dependent and postnatal age–dependent organ blood flow autoregulatory range and on the relation among blood pressure and systemic blood flow, cardiac output, and neonatal mortality and morbidity.
Oxygen delivery to the tissues is influenced by cardiac output and blood flow more so than blood pressure; hence, values of blood pressure that are statistically abnormal are not necessarily pathologic. This is true for systolic, diastolic, and mean arterial blood pressures. Similarly, hypotension is not synonymous with shock but may be associated with the later stages of shock. Determinants of cardiac function and oxygen delivery to tissues are shown in the illustration below.
During and following restoration of circulation, varying degrees of organ damage may remain and should be actively sought and managed. For example, acute tubular necrosis may be a sequela of uncompensated shock. (See Pathophysiology.)
The liver and bowel may be damaged by shock, leading to GI bleeding and increasing the risk for necrotizing enterocolitis, particularly in the premature infant.
The extent of irreversible brain damage is probably most anxiously monitored following shock, because the brain is so sensitive to hypoxic-ischemic injury once compensation fails. (See Pathophysiology.)
Parents should be informed of the risk for neurodevelopmental handicaps as well as the need for intensive follow-up care for medical and neurologic problems. For patient education information, see Shock and Cardiopulmonary Resuscitation (CPR).
Shock is a progressive disorder but can generally be divided into 3 phases: compensated, uncompensated, and irreversible.
In compensated shock, perfusion to vital organs, such as the brain, heart, and adrenal glands, is preserved by sympathetic reflexes, which increase systemic arterial resistance. Derangement of vital signs, such as heart rate, respiratory rate, blood pressure, and temperature, is absent or minimal.
Increased secretion of angiotensin and vasopressin allows the kidneys to conserve water and salt. The release of catecholamines enhances myocardial contractility, and decreased spontaneous activity reduces oxygen consumption.
Clinical signs at this time include pallor, tachycardia, cool peripheral skin, and prolonged capillary refill time. As these homeostatic mechanisms are exhausted or become inadequate to meet the metabolic demands of the tissues, the uncompensated stage ensues.
During uncompensated shock, delivery of oxygen and nutrients to tissues becomes marginal or insufficient to meet demands. Anaerobic metabolism becomes the major source of energy production, and lactic acid production is excessive, which leads to systemic metabolic acidosis. Acidosis reduces myocardial contractility and impairs its response to catecholamines.
Numerous chemical mediators, enzymes, and other substances are released, including histamine, cytokines (especially tumor necrosis factor and interleukin-1), xanthine oxidase (which generates oxygen free radicals), platelet-aggregating factor, and bacterial toxins (in the case of septic shock). This cascade of metabolic changes further reduces tissue perfusion and oxidative phosphorylation.
A further result of anaerobic metabolism is the failure of the energy-dependent sodium-potassium pump, which maintains the normal homeostatic environment in which cells function. The integrity of the capillary endothelium is disrupted, and plasma proteins leak, with the resultant loss of oncotic pressure and extravasation of intravascular fluids into the extravascular space.
Sluggish flow of blood and chemical changes in small blood vessels lead to platelet adhesion and activation of the coagulation cascade, which may eventually produce a bleeding tendency and further deplete blood volume.
Clinically, patients with uncompensated shock present with falling blood pressure, very prolonged capillary refill time, tachycardia, cold skin, rapid breathing (to compensate for the metabolic acidosis), and reduced or absent urine output. If effective intervention is not promptly instituted, progression to irreversible shock follows.
A diagnosis of irreversible shock is actually retrospective. Major vital organs, such as the heart and brain, are so extensively damaged that death occurs despite adequate restoration of the circulation. Early recognition and effective treatment of shock are crucial to prevent inevitable progression to this stage.
Inadequate tissue perfusion may result from the following:
Defects of the pump (cardiogenic)
Inadequate blood volume (hypovolemic)
Abnormalities within the vascular beds (distributive)
Flow restriction (obstructive)
Inadequate oxygen-releasing capacity (dissociative)
A hemodynamically significant patent ductus arteriosus (PDA) in the first postnatal week can account for inadequate tissue perfusion in babies with birth weights below 1000g. This may be due to failure of a compensatory increase in the cardiac output secondary to myocardial immaturity and the ductal steal phenomenon, which accounts for uniform reduction in systolic and diastolic blood pressure.
A significant decrease in systolic blood pressure occurs only when the PDA shunt is moderate or large, yet a decrease in diastolic and mean blood pressure can occur when the shunt is small.
Hypotension refers to a blood pressure lower than the expected reference range. Although the normal physiologic range for blood pressure (defined by the presence of normal organ blood flow) is not well studied in the newborn population, in clinical practice the reference range blood pressure limits are defined as the gestational age–dependent and postnatal age–dependent blood pressure values between the 5th (or 10th) and 95th (or 90th) percentiles. 
Types of shock
Many conditions and pathophysiologic disturbances are associated with shock and hypotension. Causes of neonatal shock include the following:
Hypovolemic shock - Caused by acute blood loss or fluid and electrolyte losses
Distributive shock - Caused by sepsis, vasodilators, myocardial depression, or endothelial injury
Cardiogenic shock - Caused by cardiomyopathy, heart failure, arrhythmias, or myocardial ischemia
Obstructive shock - Caused by tension pneumothorax or cardiac tamponade
Dissociative shock - Caused by profound anemia or methemoglobinemia
Risk factors for neonatal shock include the following:
Umbilical cord accident
Fetal or neonatal hemolysis
Fetal or neonatal hemorrhage
Maternal anesthesia, hypotension
Intrauterine asphyxia, intrapartum asphyxia
Pulmonary air leak syndromes
Lung overdistension during positive pressure ventilation
Shock remains a major cause of neonatal morbidity and mortality, although because it accompanies other primary conditions, specific figures for the frequency of shock are unavailable. Prognosis following neonatal shock is related to the underlying cause (eg, sepsis, heart disease) and the injuries sustained during the period of inadequate perfusion. Early recognition and treatment is essential to maximizing outcome in neonatal shock. Morbidity as a consequence of end-organ injury and organ dysfunction is similar. Frequent sequelae include pulmonary, renal, endocrine, gastrointestinal (GI), and neurologic dysfunction. Delayed diagnosis and treatment can lead to permanent neurologic sequelae such as cerebral palsy, epilepsy, and mental retardation.
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