eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Shock and Hypotension in the Newborn

Author: Samir Gupta, MD, MRCP, FRCPCH, Consulting Neonatologist, University Hospital of North Tees
Coauthor(s): Sunil K Sinha, MBBS, MD, MRCP, PhD, FRCP, FRCPCH, Director of Neonatal Services, South Cleveland Hospital, UK; Steven M Donn, MD, Professor of Pediatrics, Director, Neonatal-Perinatal Medicine, Department of Pediatrics, University of Michigan Health System
Contributor Information and Disclosures

Updated: Jun 25, 2008

Introduction

Background

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.

Pathophysiology

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.

Cardiac output is the product of heart rate and stroke volume. Neonatal cardiac output depends more on heart rate than stroke volume; therefore, both 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 3 factors: preload, afterload, and myocardial contractility.

• 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 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 is a semiquantitative measure of ventricular function. 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 1.36 mL 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 also 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.

Inadequate tissue perfusion may result from defects of the pump (cardiogenic), inadequate blood volume (hypovolemic), abnormalities within the vascular beds (distributive), flow restriction (obstructive), or inadequate oxygen-releasing capacity (dissociative). These are summarized in History.

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 5^th (or 10th) and 95th (or 90th) percentiles.

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 30 mm 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.¹

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.

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.

Frequency

United States

The true frequency of neonatal shock is unknown because it is primarily a clinical syndrome.

International

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.²

Mortality/Morbidity

Shock remains a major cause of neonatal morbidity and mortality. Because shock accompanies other primary conditions, specific figures are unavailable. Morbidity as a consequence of end-organ injury and organ dysfunction is similar.

Race

No predilection based on race has been reported.

Sex

No predilection based on sex has been reported.

Clinical

History

• Causes of neonatal shock include the following:
  • Hypovolemic shock is caused by acute blood loss or fluid and electrolyte losses.
  • Distributive shock is caused by sepsis, vasodilators, myocardial depression, or endothelial injury.
  • Cardiogenic shock is caused by cardiomyopathy, heart failure, arrhythmias, or myocardial ischemia.
  • Obstructive shock is caused by tension pneumothorax or cardiac tamponade.
  • Dissociative shock is caused by profound anemia or methemoglobinemia.
• Risk factors for neonatal shock include the following:
  • Umbilical cord accident
  • Placental abnormalities
  • Fetal or neonatal hemolysis
  • Fetal or neonatal hemorrhage
  • Maternal infection
  • Maternal anesthesia, hypotension
  • Intrauterine asphyxia, intrapartum asphyxia
  • Neonatal sepsis
  • Pulmonary air leak syndromes
  • Lung overdistension during positive pressure ventilation
  • Cardiac arrhythmias

Physical

Clinical manifestations of hypotension include prolonged capillary refill time, tachycardia, mottling of the skin, cool extremities, and decreased urine output. Carefully observe heart sounds, peripheral pulses, and breath sounds.

The physical examination should also carefully assess these factors, as well as accurately assess blood pressure. Measurement of neonatal blood pressure can be completed directly through invasive techniques or indirectly through noninvasive techniques. Invasive methods include direct manometry using an arterial catheter or use of an in-line pressure transducer and continuous monitor. Noninvasive methods include manual oscillometric techniques and automated Doppler techniques. A good correlation between the systolic blood pressure measured by Doppler and by direct manometry using an intra-arterial catheter is observed.

Causes

Shock is a progressive disorder but can generally be divided into 3 phases: compensated, uncompensated, and irreversible. Each phase has characteristic clinicopathologic manifestations and outcomes; however, in the neonatal setting, distinguishing them may be impossible. Initiate aggressive treatment in all cases where shock is suspected.

• Compensated shock
  • 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.
• Uncompensated shock
  • 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.
• Irreversible shock: 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.

• Search for CME/CE on This Topic »

• Shock Center
• Public Health Center
• Shock Causes
• Cardiopulmonary Resuscitation (CPR)
• Shock Overview
• Shock Symptoms
• Shock Treatment