Assessment of systemic perfusion in children

INTRODUCTION — A rapid assessment of the adequacy of systemic perfusion is an essential part of pediatric care. The pathophysiology and assessment of perfusion in children are reviewed here.

Additional information on the initial assessment and stabilization of children with circulatory compromise and the pathophysiology and classification of shock in children are discussed separately:

●(See "Pathophysiology and classification of shock in children".)

●(See "Initial evaluation of shock in children".)

●(See "Shock in children in resource-abundant settings: Initial management".)

●(See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management".)

●(See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)

DEFINITIONS — Systemic perfusion involves the delivery of blood through the circulatory system to organs and tissues to provide substrate (eg, oxygen and glucose) and to remove products of metabolic processes (eg, lactic acid). Adequate perfusion depends upon the interplay of cardiac output and systemic vascular resistance. (See "Pathophysiology and classification of shock in children", section on 'Physiology'.)

Shock is a state of severe substrate deficiency due to hypoperfusion leading to cellular injury and dysfunction at the level of capillaries in the tissues. In its most severe form, hypoperfusion will lead to tissue ischemia and necrosis. In more moderate states, the body will compensate through a variety of mechanisms, including the redistribution of perfusion from the skin and periphery to vital organs including the brain, heart, and adrenals. The goal of resuscitation is to recognize and reverse deficits in perfusion. (See "Pathophysiology and classification of shock in children", section on 'Definition'.)

In states of hyperperfusion, such as inflammation, there may be findings of hyperemia; additionally, after periods of low perfusion, reperfusion can be associated with hyperperfusion and lead to clinical sequelae or reperfusion injury affecting multiple organs (including the brain, heart, and kidneys), followed by multisystem organ failure. (See "Pathophysiology and classification of shock in children", section on 'Physiology'.)

PATHOPHYSIOLOGY — Poor perfusion can be attributed to low arterial pressure caused by three factors, either alone or in combination:

●Cardiac dysfunction (eg, decreased contractility, arrhythmia, or outflow obstruction [tamponade])

●Low circulating intravascular volume due to blood or fluid losses

●Low vascular tone caused by conditions such as sepsis, anaphylaxis, central nervous system injury, or toxins

Arterial blood pressure largely determines systemic perfusion and is the product of cardiac output and systemic vascular resistance (figure 1). Cardiac output is the volume of blood ejected by the heart each minute; it is the product of heart rate and stroke volume. The stroke volume is the volume of blood ejected by the ventricles with each contraction; it may be reduced by inadequate intravascular volume, myocardial dysfunction, or excessive systemic or pulmonary vascular resistance [1]. Cardiac output declines if either heart rate or stroke volume decrease without a commensurate increase in the other component.

Heart rate and blood pressure are the only variables affecting cardiac output that can be directly and noninvasively measured. Stroke volume may be indirectly assessed by examining the volume and strength of the pulses. During childhood, the heart rate is faster and the stroke volume is smaller than during adulthood. In children, particularly in infants, cardiac output is increased primarily by increasing the heart rate [1,2].

Systemic vascular resistance may be estimated by evaluating skin perfusion and/or capillary refill. Examination of the jugular veins to estimate venous pressure also may be useful in assessing the volume status in older children and adolescents. However, because low values may be normal, this technique is most useful in distinguishing among the causes of generalized edema. (See "Examination of the jugular venous pulse".)

Tachycardia and prolonged capillary refill are clinical manifestations of compensatory mechanisms designed to maintain a normal arterial perfusion pressure in the face of cardiopulmonary compromise. However, these compensatory mechanisms can be maintained only until cardiac reserve is depleted. Systemic vasoconstriction increases left ventricular afterload and myocardial oxygen consumption. Tachycardia, which also increases myocardial oxygen consumption, can be marked in an ill child. Hypotension is a late and often sudden sign of cardiovascular decompensation in children (figure 2) [2].

BEDSIDE ASSESSMENT — The bedside assessment of systemic perfusion is accomplished through the holistic interpretation of qualitative and quantitative information. Mental status and skin appearance give rapid qualitative information about the degree of systemic perfusion. (See 'Qualitative assessments' below.)

The quantitative assessment of perfusion includes noninvasive measures of the pulse rate, blood pressure, temperature, capillary refill time, and urine output, all of which can be followed over time to document response to interventions. (See 'Quantitative assessments' below.)

Inadequate perfusion will also result in hypoxemia and lactic acidosis with characteristic changes on measurement of blood gases, blood lactate, and electrolytes. (See "Arterial blood gases" and "Venous blood gases and other alternatives to arterial blood gases", section on 'Correlation with arterial blood gases'.)

Qualitative assessments — Qualitative signs of decreased systemic perfusion are important components of the pediatric assessment triangle, a rapid method of global assessment for circulatory or respiratory compromise in children. (See "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Pediatric assessment triangle'.)

Altered mental status — Decreased levels of consciousness (ie, lethargy or coma) accompany decreased systemic perfusion because of diminished cerebral perfusion and oxygenation. The initial signs of altered mental status may be subtle, particularly in young infants. Parents/caregivers may be the first to recognize these signs but may be unable to describe them other than to say something is wrong. Failure of a child to recognize or respond to their caregiver or to respond to a painful stimulus is an ominous sign.

The mnemonic TICLS provides a way to categorize findings that indicate significant compromise of mental status in the pediatric patient (see "Initial assessment and stabilization of children with respiratory or circulatory compromise", section on 'Appearance'):

●T: Tone – Decreased tone (eg, lack of normal flexed posture in a young infant ["floppy baby"], head lag in an older infant, or older child who is unable to stand or walk)

●I: Interactiveness – Lack of appropriate interaction with the patient's environment (eg, decreased age-appropriate responsiveness to the parent/caregiver or examiner in infants or confusion in older children)

●C: Consolability – Inability to console an infant or agitation in the older child

●L: Look/gaze – Faraway stare rather than fixed gaze on parent/caregiver or provider

●S: Speech/cry – Weak or diminished cry in the infant

Skin appearance — A child with hypoperfusion to the skin can present with cool, pale, mottled, or ashen skin. The skin is a reliable organ for assessment of systemic perfusion because it is an indicator of systemic vascular resistance and the degree of shunting that is necessary to maintain blood pressure [3]. The nail beds, mucous membranes, palms of the hands, and soles of the feet are pink and warm in a child with normal cardiorespiratory function.

Temperature at the periphery will decrease in states of hypoperfusion as the circulation is shunted away from the skin to the vital organs. This can be assessed by a feeling of coolness to touch. Cooling of the skin begins peripherally and extends proximally when cardiac output decreases [4].

Quantitative assessments

Capillary refill time — Capillary refill time is a valuable initial physiologic parameter that can be evaluated without the need for technology or equipment. To measure capillary refill, the extremity should be lifted slightly above the level of the heart to ensure assessment of arteriolar capillary refill and not venous stasis. Light pressure is applied to blanch the fingernail bed. The pressure is released, and the number of seconds required for color return is measured.

Normal capillary refill in children is less than two seconds. Volume depletion or hypotension can delay capillary refill for more than three seconds [5]. Arterial vasodilation in patients with warm shock can cause "flash" capillary refill (<1 second). (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

The usefulness of capillary refill is limited by interobserver variability and by the effect of environmental temperature [6]. Prolongation of capillary can be induced in children with normal circulatory status by placing them in a cool environment such as an air-conditioned room [6]. Thus, capillary refill should not be used as the sole indicator of compromised systemic perfusion.

Pulses — The rate, strength (or volume), and regularity of the central and peripheral pulses provide rapid clues to perfusion status:

●Rate – The pulse rates in infants and children vary depending on age; familiarity with normal rates for age is needed to determine if a child requires a resuscitative intervention (table 1) [7]. A rapid pulse is a nonspecific clinical sign of distress and may result from stress (anxiety, pain, or fear), fever, infection, medications, hypoxia, hypercapnia, hypovolemia, or cardiac impairment [1,2]. The development of bradycardia in a child with cardiorespiratory distress is a late sign, usually indicating that arrest is imminent [2].

●Strength (volume) – The strength or volume of a pulse is related to pulse pressure, defined as the difference between systolic and diastolic blood pressure. The pulse pressure narrows when cardiac output decreases, rendering the pulse thready and difficult to feel. An exception may occur in early septic shock which may be characterized by warm shock. Warm shock is a high cardiac output state characterized by a wide pulse pressure and bounding pulses caused by rapid runoff associated with systemic vasodilatation. (See "Sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

When compromised systemic perfusion is suspected, the pulse strength should be assessed peripherally (radial, dorsalis pedis, posterior tibial) and centrally (carotid, axillary, brachial, femoral). A (table 1) discrepancy of pulse strength between central and peripheral pulses may be caused by vasoconstriction associated with a cold ambient temperature [6], or it may be an early sign of decreased cardiac output and diminished peripheral perfusion. Absence of appreciable peripheral pulses does not always equate with cardiac arrest. Absence of central pulses indicates ineffective or absent cardiac contractions and signifies the need for immediate cardiopulmonary resuscitation.

●Regularity – An irregular pulse (other than normal respiratory variation) usually is a warning of cardiac dysrhythmia. It is somewhat uncommon in previously healthy infants and children.

Pulses should be readily palpable in most healthy infants and children. The carotid artery, on the side of the neck, is the most accessible artery to palpate in children older than one year of age. The short, chubby necks of children younger than one year of age render rapid location of the carotid artery difficult. Thus, palpation of the brachial artery or femoral artery is recommended in the rapid cardiopulmonary assessment of infants [2].

The apical precordial impulse is not considered to be a "pulse." Heart sounds that are heard over the apex of the heart represent electrical activity that may not be adequate to produce a perfusing pulse. Alternatively, the child's precordium may be quiet, and a precordial impulse may not be palpated despite the presence of satisfactory cardiac function and a strong central pulse [8].

Blood pressure — The blood pressure of the child with compensated shock may be normal; signs of inadequate perfusion such as decreased level of consciousness, prolonged capillary refill, and tachycardia are typically observed before hypotension is seen. (See "Pathophysiology and classification of shock in children".)

Hypotension is a late and ominous finding of inadequate systemic perfusion. For children, hypotension is defined as a systolic blood pressure that is less than the fifth percentile of normal for age [2]:

•<60 mmHg in term neonates (0 to 28 days)

•<70 mmHg in infants (1 to 12 months)

•<70 mmHg + (2 x age in years) in children 1 to 10 years

•<90 mmHg in children 10 years of age or older

Below this limit, the child would be considered hypotensive. Hypotension is a late finding in children with cardiopulmonary compromise and heralds the onset of hypotensive shock; even mild hypotension must be treated aggressively because cardiopulmonary arrest may be imminent (in contrast to an adult with hypotension) [2].

The proper measurement of blood pressure in children is discussed in detail separately. (See "Definition and diagnosis of hypertension in children and adolescents", section on 'Measurement of blood pressure'.)

Urine output — Urine output is a noninvasive method to measure fluid balance once intravascular volume has been restored. Normal urine output is defined as 1.5 to 2 mL/kg per hour in infants and young children and 1 mL/kg per hour in older children and adolescents [2]. When urine output decreases below these thresholds, it is a marker of reduced kidney perfusion and is associated with acute kidney injury and mortality [9,10]. Urine output provides important information to guide fluid and electrolyte management. Critically ill children warrant ongoing measurement of urine output with an indwelling bladder catheter and collection system. The initial volume of urine during catheterization is not an accurate assessment of kidney function because it may have been produced prior to the onset of decreased systemic perfusion. (See "Acute kidney injury in children: Clinical features, etiology, evaluation, and diagnosis", section on 'Classifications'.)

In diapered infants who are not critically ill, urine output can be estimated by weighing a wet diaper and subtracting the dry weight of the diaper with 1 gram of difference equal to 1 mL of urine volume.

Bedside ultrasound — When available, point-of-care ultrasonography performed by well-trained, experienced acute care providers can rapidly identify myocardial sources of poor systemic perfusion, such as diminished cardiac contractility or tamponade, and may provide a general assessment of central venous pressure based upon the collapsibility of the inferior vena cava (IVC) and ratio of IVC to aorta diameter [11]. (See "Initial evaluation of shock in children", section on 'Ancillary studies'.)

Noninvasive monitors — Compromised perfusion may impact noninvasive monitoring in important ways:

●Pulse oximetry – With significant hypoperfusion, the oxygenation of tissues may be compromised, leading to a reduction in the value of cutaneous pulse oximetry (falsely low oxygen saturation) compared with arterial blood gases. (See "Respiratory support, oxygen delivery, and oxygen monitoring in the newborn", section on 'Pulse oximetry' and "Pulse oximetry", section on 'Troubleshooting sources of error'.)

●End-tidal carbon dioxide (ETCO₂) – ETCO₂, either in spontaneously breathing or endotracheally intubated patients, can be low (when there is decreased or no perfusion to the lungs) or high (when there is limited respiratory drive due to cerebral underperfusion, causing carbon dioxide accumulation in the lungs). (See "Carbon dioxide monitoring (capnography)".)

SUMMARY

●Bedside assessment – Patients with decreased systemic perfusion present with one or more of the following findings:

•Qualitative findings:

-Decreased level of consciousness (ie, lethargy or coma) (see 'Altered mental status' above)

-Cool, pale, mottled, or ashen skin (see 'Skin appearance' above)

•Quantitative findings:

-Tachycardia (table 1), which may be accompanied by a thready pulse or peripheral pulses that are weaker than central pulses (see 'Pulses' above)

-Prolonged capillary refill time (>2 seconds) (see 'Capillary refill time' above)

-Hypotension (see 'Blood pressure' above)

-Decreased urine output (see 'Urine output' above)

Hypotension is a late finding in children with cardiopulmonary compromise; even mild hypotension must be treated aggressively because cardiopulmonary arrest may be imminent. (See 'Blood pressure' above and "Shock in children in resource-abundant settings: Initial management".)

Pulse rate, blood pressure, skin temperature, capillary refill time, and urine output can be followed over time to document response to interventions. (See 'Quantitative assessments' above.)

●Bedside ultrasound – When available, point-of-care ultrasonography performed by well-trained, experienced acute care providers can rapidly identify myocardial sources of poor systemic perfusion and may provide a general assessment of central venous pressure. (See 'Bedside ultrasound' above.)

●Noninvasive monitors – Compromised systemic perfusion may cause falsely low pulse oximetry readings and low or elevated end-tidal carbon dioxide (ETCO₂) readings. (See 'Noninvasive monitors' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Pamela Bailey, MD, who contributed to earlier versions of this topic review.