Advances in Diagnosis and Management of Hemodynamic Instability in Neonatal Shock

Abstract

Shock in newborn infants has unique etiopathologic origins that require careful assessment to direct specific interventions. Early diagnosis is key to successful management. Unlike adults and pediatric patients, shock in newborn infants is often recognized in the uncompensated phase by the presence of hypotension, which may be too late. The routine methods of evaluation used in the adult and pediatric population are often invasive and less feasible. We aim to discuss the pathophysiology in shock in newborn infants, including the transitional changes at birth and unique features that contribute to the challenges in early identification. Special emphasis has been placed on bedside focused echocardiography/focused cardiac ultrasound, which can be used as an additional tool for early, neonatologist driven, ongoing evaluation and management. An approach to goal oriented management of shock has been described and how bed side functional echocardiography can help in making a logical choice of intervention (fluid therapy, inotropic therapy or vasopressor therapy) in infants with shock.

Keywords: cardiac output; functional echocardiography; hemodynamic; neonatal shock; tissue perfusion.

Figure 1

Relationship between heart rate (HR), cardiac filling, and cardiac output (CO). Excessive tachycardia may decrease CO by decreasing preload and hence stroke volume. It may also impair cardiac function from decreased coronary perfusion in shortened diastole.

Figure 2

Goal oriented targeted management and role of echocardiography in instituting specific intervention.

Figure 3

Assessment on cardiac filling on visual inspection “eyeballing.” Images (A,B) show under-filled heart in apical 4 chamber (A4C) and parasternal long axis (PLAX) views. Images (C,D) show volume overloading of left atrium (LA) and left ventricle (LV) in A4C and PLAX views.

Figure 4

Physiological variation in inferior vena cava (IVC) diameter. Normal collapsibility of (A) IVC during inspiration (D_min) and (B) expansion during expiration (D_max). In hypovolemia, IVC may be collapsed while in hypervolemia there is minimal or no collapsibility.

Figure 5

Pericardial effusion in (A) subcostal and (B) apical 4 chamber views. In large pericardial effusion and cardiac tamponade, there may be collapse of cardiac chambers—first seen collapse of right atrium followed by right ventricle.

Figure 6

Interventricular septum (IVS) and left ventricle (LV) shape in pulmonary hypertension on visual inspection. Image (A) shows normal circular LV and IVS shapes. Image (B) shows right ventricular dilatation and hypertrophy of right ventricle, flattening of IVS and “D” shaped LV in pulmonary hypertension.

Figure 7

Quantitative assessment of pulmonary artery systolic pressure (PAP) by measuring tricuspid valve regurgitation velocity [tricuspid regurgitation (TR) jet]. PAP = right atrial (RA) pressure + pressure gradient between RA and RV (estimated by TR jet). (A) TR jet on A4C. (B) TR Doppler.