Shock and Hypotension in the Newborn

Updated: Nov 27, 2021
  • Author: Samir Gupta, MD, DM, FRCPCH, FRCPI; Chief Editor: Muhammad Aslam, MD  more...
  • Print


Shock is a complex clinical syndrome caused by an acute failure of circulatory function. It is characterized by an imbalance between tissue demand and the supply of substrates. [1] 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. Shock is an independent predictor of mortality, and survivors have a greater risk for neurologic impairment. [2, 3] 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.) Preterm infants are particularly prone to injury related to hypoperfusion and hypoxemia owing to their immature cardiovascular system and impaired compensatory/autoregulatory mechanisms. [4] In addition, preterm infants also often have relative renal insufficiency. [3] In a study of the variation in the prevalence of hypotension among low–birth-weight infants, 16-52% received volume expansion and 4-39% received vasopressors. [5]

Patient education

Parents should be informed of the risk of mortality and morbidity in the form of neurodevelopmental problems 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).



Maintenance of adequate tissue perfusion depends on a combination of three 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 Medication.)

Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV) (CO = HR × SV). 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 raise 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 is required to generate 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 semi-quantitative 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. 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. [6]

Blood pressure measurement is limited to assessing systemic blood flow. In the presence of physiologic shunts in newborns, the estimation of superior vena cava (SVC) flow is observed to correlate with low flow states rather than left ventricular output (LVO).

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.

Mean blood pressure, rather than systolic pressure, is usually used to judge the normality of data obtained from indwelling arterial lines. Mean blood pressure is thought to be free of artifacts caused by resonance, thrombi, and air bubbles, but this may not always be true. Based on published 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 mmHg 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 the normal long-term outcome have systolic blood pressures below the reference range for the gestational age. [7]

A low upper body blood flow is common in the first day of life in preterm infants younger than 30 weeks' gestation; this has a strong correlation with periventricular or intraventricular hemorrhage. The presence of fetal shunts in premature babies, 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 predominantly systemic pulmonary shunts, there may be volume overloading of the left side of the heart, which 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. Furthermore, it has been observed that estimations of blood pressure (mean and systolic) have poor correlation with cardiac output in babies with a PDA. [8]

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; 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 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.

Hemoglobin content

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 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. Oxygen delivery to 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 image below.

Shock and Hypotension in the Newborn. Determinants Shock and Hypotension in the Newborn. 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.




Shock is a progressive disorder, but it can generally be divided into three phases: compensated, uncompensated, and irreversible.

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, may be absent or minimal.

Increased secretion of angiotensin and vasopressin allows the kidneys to conserve water and salt. The release of catecholamines enhances myocardial contractility, whereas 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 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 increases significantly, resulting in 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.

Anaerobic metabolism further results in failure of the energy-dependent sodium-potassium pump, which maintains a normal homeostatic environment for cell 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

In the setting of irreversible shock, 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 in preventing progression to this stage.



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

  • Mixed shock: Can occur in various disease conditions like sepsis, where there may be distributive shock to begin with and then cardiogenic shock develops later 

Risk factors

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, maternal hypotension

  • Intrauterine asphyxia, intrapartum asphyxia

  • Neonatal sepsis

  • Pulmonary air leak syndromes

  • Lung overdistention during positive pressure ventilation

  • Cardiac arrhythmias



Shock remains a major cause of neonatal morbidity and mortality, although—because it accompanies other primary conditions—specific figures for the frequency of shock in this population 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.


During and following restoration of circulation, varying degrees of organ damage may remain and should be actively sought out 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 the most anxiously monitored following shock, because the brain is so sensitive to hypoxic-ischemic injury once compensation fails. (See Pathophysiology.)