Shock is a pathophysiologic state characterized by poor tissue perfusion, resulting in a decrease in oxygen delivery that leads to tissue hypoxemia. If circulatory compromise is prolonged, it can lead to disrupted membrane pump function, energy failure, anaerobic metabolite accumulation, cell death, and eventually organ failure.
In the neonate, shock can be described by etiology (vasodilatory, cardiogenic, and hypovolemic shock), timing (immediate postnatal or out of transitional period), and progression of severity (compensated, uncompensated, and irreversible shock). This chapter focuses on the description of shock based upon pathogenesis, and the concomitant echocardiography findings. Understanding the developmental cardiovascular physiology along with the etiology of shock allows the clinician to arrive at a timely and appropriate therapy for this disease state.
It is important to point out that limited data are available on echocardiographic assessment of patients with shock in the neonatal period and early infancy. Nevertheless, systematic assessment of the cardiac function, preload, afterload, and systemic vascular resistance (SVR) can often direct the clinician to the underlying cause of cardiovascular compromise and help with formulating a treatment strategy based upon the pathophysiology. For patients in shock, it is prudent that echocardiographic evaluation be considered as an adjunct to clinical assessment rather than a replacement for it.
Understanding the interaction between blood pressure and flow is important in the assessment of the cause of cardiovascular compromise. Poiseuille's law states that flow is directly related to the pressure gradient and the diameter of the tube, and inversely related to the viscosity of the fluid and the length of the tube. While Poiseuille's law is important in understanding the interaction between various factors that affect the flow, it cannot be used clinically. Instead, in clinical practice, Ohm's law is used to describe the interaction between flow and pressure. Accordingly:
In this formula, SVR is a calculated factor. Therefore, by measuring the blood pressure and estimating cardiac output, one can calculate SVR. As atrial pressure is not routinely measured, the formula can be rewritten as:
Given that blood pressure is routinely measured in the neonatal intensive care setting, the ability to assess cardiac output and, as a result, to estimate SVR would significantly enhance our understanding of the hemodynamic status. Unfortunately, estimation of cardiac output has its own limitation, especially during the transitional period when the fetal channels are open (see Chapter 7). Furthermore, the above measurements only describe ...