LESS CAPABLE OF DEVELOPING CONTRACTILE FORCE

The immature myocardium has more loose connective tissue than the adult, but fewer sarcomeres per gram of tissue. The arrangement of myofibrils in the myocyte, and of myocytes in the myocardium, is less parallel than in the adult. Intracellular desmin fibrils which link the contractile elements are more randomly arranged in the infant heart. Less efficient calcium uptake, storage and release from sarcoplasmic reticulum (SR) and a higher density of cell membrane Na/Ca exchangers mean that excitation–contraction coupling is more dependent on trans-sarcolemmal Ca⁺⁺ flux, and on ECF Ca⁺⁺ concentration than the adult.

LESS DIASTOLIC COMPLIANCE THAN THE ADULT HEART

MORE TOLERANT OF HYPOXAEMIA

Although the infant heart has fewer mitochondria per gram of tissue, and a lower oxidative capacity, it has a lower oxygen demand per gram, larger glycogen reserves and a higher capacity for anaerobic glycolysis.⁷ Glucose is the major myocardial energy source (rather than long chain fatty acids as in older children) and hypoglycaemia causes severe myocardial depression.

IMMATURE AUTONOMIC INNERVATION

Parasympathetic innervation of the heart is more complete than sympathetic in infants, and the infant response to severe stress (e.g. hypoxia) tends to be bradycardia rather than tachycardia.

The infant myocardium has fewer β-receptors, more α-receptors, and is more sensitive to noradrenaline (norepinephrine) than the adult. Stimulation of myocardial α-receptors in the infant is more likely to cause tachycardia than bradycardia.⁸

HIGH PULMONARY VASCULAR RESISTANCE⁸

In the fetus, the small pulmonary arteries are narrow, the pulmonary vascular resistance is high, and pulmonary blood flow is less than one-tenth of systemic flow. A thick layer of smooth muscle, which extends further out into the vascular tree than in the adult, is highly sensitive to hypoxia, hypercarbia, acidaemia, sepsis and central neural stimuli such as pain.

At birth, after the first breaths are taken, the smooth muscle cells gradually relax and become more fusiform in shape. Pulmonary vascular resistance falls immediately, then gradually declines to adult levels by 6–8 weeks of age, and smooth muscle bulk falls to adult levels by 3–4 months.⁹ In the presence of lung disease, high pulmonary venous pressures (e.g. due to aortic stenosis or stenosis of the pulmonary veins) or large left-to-right shunts (e.g. ventricular septal defect (VSD) or truncus arteriosus), the high pulmonary vascular resistance and the extensive and bulky vascular smooth muscle fail to decline normally. The infant is then vulnerable to episodes of acute right heart failure whenever the pulmonary vascular resistance increases abruptly.

HYPOVOLAEMIC SHOCK (SEE Table 101.1)

The child may have a history of fluid or blood loss, reduced fluid intake or bowel-related illness. Signs of dehydration (see Chapter 99), external bleeding or haematoma may be present. The presence of hypovolaemic shock implies a blood volume deficit greater than 30 ml/kg.

Signs of homeostatic compensation, such as tachycardia (Table 101.3), narrow pulse pressure, cool mottled limbs and slow capillary refill usually precede the onset of hypotension, which tends to occur late (after loss of 15–20% of blood volume) and precipitously in young children. In severe shock of any cause, signs of multiple organ hypoperfusion (e.g. oliguria of less than 0.5 ml/kg per hour, lethargy or coma, hypothermia, tachypnoea and increasing lactic or other metabolic acidosis) are found. Bleeding due to disseminated intravascular coagulation and liver dysfunction may occur in the first 6 hours.

Table 101.3 Normal blood pressure, heart rate and respiratory rate in childhood¹⁰

In early shock, these changes are reversible by plasma volume expansion with boluses of 20 ml/kg 0.9% saline or blood, repeated as necessary. Failure to respond to two such boluses with a decrease in heart rate and capillary refill time (normal < 2 seconds after 5 seconds’ pressure over the sternum) indicates refractory shock requiring more aggressive treatment (see below).

Investigations (see Table 101.4) include:

Table 101.4 Investigation of shock in children

CARDIOGENIC SHOCK

Tachycardia, hypotension, low volume pulses and signs of homeostatic compensation and poor organ perfusion (see above) are usually present. Cardiomegaly, muffled heart sounds and a gallop rhythm may be found. New murmurs may appear (e.g. mitral systolic murmur due to left ventricular dilatation with consequent mitral regurgitation, or aortic diastolic murmur due to endocarditis). Chest rales, tachypnoea and wheezing indicate left heart failure, while in right heart failure, oedema appears first in the eyelids and dorsum of hands and feet. Hepatomegaly develops rapidly in children, and is a more reliable sign of right heart failure than a raised jugular venous pressure (JVP) which may be hard to detect in infants.

Combinations of signs specific to individual congenital heart lesions are described below. Such signs when present (e.g. absent femoral pulses in aortic coarctation, or skull, liver or renal bruits of arteriovenous fistulae) may indicate the cause of the shock (Table 101.5), while diagnostically useful murmurs are not always present.

Table 101.5 Causes of cardiogenic shock in childhood

Investigations (see Table 101.4) should include:

SEPTIC SHOCK

Septic infants usually present with a hypodynamic circulation, low cardiac output and cool extremities. Early septic shock in older children may be hypodynamic, or may be similar to that in adults, in which tachycardia, tachypnoea and hypotension are accompanied by warm extremities, wide pulse pressure and increased cardiac output. Lethargy or stupor, oliguria and Kussmaul breathing characteristic of metabolic acidosis indicate inadequate tissue oxygenation.

Severely septic children are often hypothermic rather than febrile.

As shock progresses, myocardial depression by endotoxin, tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) (see Chapter 11) decreases the cardiac output earlier than is the case in adults, as the less compliant infant ventricle cannot dilate to sustain the stroke volume in the face of a reduced ejection fraction.^11,12 Furthermore, the rapid and severe capillary leak that is characteristic of paediatric sepsis leads to hypovolaemia in the underresuscitated child, further reducing preload and cardiac output. For this reason, septic children often respond well to aggressive fluid resuscitation (> 60 ml/kg in the first hour). Peripheral oedema caused by leakage of proteinaceous fluid from injured capillary endothelia exacerbates cellular hypoxia by increasing the diffusion distance for oxygen between capillaries and cells.

DISTRIBUTIVE SHOCK

The main features are hypotension, vasodilatation and hypovolaemia due to plasma leakage from capillaries. The child’s extremities are warm and pink, the blood pressure is low and the pulse pressure is wide. There is tachycardia, oliguria and stupor. Other evidence of anaphylaxis (wheezing, urticaria, swollen face or tongue), spinal cord injury (bradycardia, quadriparesis, lax anal sphincter) or drug intoxication (history, tablets, coma out of proportion to shock) may be present (Table 101.6).

Table 101.6 Causes of distributive shock in childhood

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