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 central circulation and do not shed any light on the status of specific organ blood flow or microcirculation. As discussed in Chapter 7, Doppler assessment of large arteries supplying major organs can provide useful information about the status of specific organ blood flow. As for the assessment of microcirculation, other methodologies such as near-infrared or visible light spectroscopy, laser Doppler, or orthogonal polarization spectral imaging can be used.1 Description of these techniques is beyond the scope of this book.
Cardiac output is the product of stroke volume and heart rate. Stroke volume is in turn determined by the preload, contractility and afterload. Assessment of determinants of cardiac output can further assist the clinician in evaluation of the underlying cause of cardiovascular compromise (Figure 10-1). Below we will discuss echocardiographic assessment of the preload, contractility and afterload. It is important to point out that little is known about the effect of each of these factors on cardiac output in the neonatal period.
FIGURE 10-1.
Blood pressure is the product of the interaction between cardiac output and systemic vascular resistance. Assessment of each component of this interaction is important and useful in identifying the underlying cause of cardiovascular compromise. Cardiac output is determined by the heart rate and stroke volume. Changes in preload, contractility, and afterload affect the stroke volume.
Preload is the amount of stretch of the myocardial sarcomere just prior to contraction. Therefore, preload can be described in terms of ventricular pressure or volume. For the purpose of assessment by echocardiography, preload can be defined as the volume of blood in the ventricle at the end of diastole. Using this definition, one can appreciate that preload is affected by a host of factors such as circulating blood volume and systolic and diastolic cardiac function, as well as extracardiac factors such as intrathoracic pressure. For assessment of systolic and diastolic function, refer to Chapter 8. Several indices have been used as a measure of preload. These include quantitative measures such as left atrium to aortic root ratio (see Chapter 11), left ventricular internal diameter at the end of diastolic (LVIDD), diameter of inferior vena cava (IVC), and IVC collapsibility index, as well as qualitative measures such as visual assessment of collapsibility of IVC during inspiration or appearance of an “underfilled” ventricle.
LVIDD is perhaps the most commonly used index of preload. LVIDD can be measured by M-mode or 2D echocardiography from the parasternal short- or long-axis view, as described for the measurement of the shortening fraction (Chapter 8). Normal LVIDD for a 3.5-kg infant is 18.8±1.7 mm.2 The reported LVIDD in preterm infants varies significantly.3–5 The variation is most likely due to differences in the population studied and possibly due to the method used. In hemodynamically stable preterm infants ≤30 weeks’ gestation, average LVIDD was 11.9±1.3 mm (range 8.8–15.6) in the first 3 postnatal days and 11.3±1.3 mm (range 9.3–15.6) from 4–14 days after birth.5
Given that LVIDD depends on the size of the patient, for comparison to other patients, adjustment for body weight is necessary. From this perspective, LVIDD adjusted for weight (aLVIDD) is a better index than unadjusted LVIDD. Dividing LVID by weight in kilogram yields aLVIDD. In hemodynamically stable preterm infants ≤30 weeks’ gestation, aLVIDD was 15.2±2.5 mm/kg in the first 3 postnatal days and 15.6 ± 2.3 mm/kg from 4–14 days after birth.5 However, as discussed in Chapter 11, the size of heart structures and weight do not have a perfect positive linear relationship (ie, the size of heart structure does not increase by 2-fold if the weight is doubled). Therefore, adjusting for a fixed heart structure (eg, aortic root diameter) might be a better option. On the other hand, incorporating another measured diameter into the index will certainly introduce another potential error.
The fluid status affects the IVC diameter (Figures and Videos 10-2 to 10-3). In hypovolemia, the IVC diameter is small and the IVC may collapse during inspiration in hypovolemic spontaneously breathing patients. IVC diameter is usually measured just below the diaphragm after the connection with the hepatic veins, using the subcostal longitudinal (sagittal) view. For the IVC diameter to be meaningful, it needs to be indexed to other cardiac structures. In older children and adults, IVC diameter is divided by aortic (Ao) diameter (measured in the same view as IVC). This IVC to Ao ratio has been found to be a useful tool in the assessment of fluid status in children with dehydration and in adults with septic shock.6,7 Another measure of fluid status using IVC diameter is the collapsibility index: diameter in expiration–diameter in inspiration divided by diameter in expiration. This is based on the principle that the IVC is prone to collapse during inspiration and even more so when circulating blood volume is decreased. In adults, even a visual estimate of changes in IVC diameter with respiration has been found to be helpful in the assessment of fluid status.8 However, none of these measurements or indices has been validated in the neonatal population, and therefore their utility is unknown.9 Apart from changes in intravascular volume, many other factors can affect the IVC diameter and collapsibility index, including cardiac function, pericardial and pleural pressure, and positive pressure ventilation.
One can describe contractility in terms of myocardial fiber shortening without any regards to the preload and afterload. Such load-dependent measures of contractility include shortening fraction and heart rate-corrected velocity of circumferential fiber shortening (VCFC). Alternatively, and perhaps more appropriately, contractility can be defined as the ability of myocardium to contract when adjustment for variability in preload and afterload are made. This is considered true or load-independent contractility. Stress-velocity index, the relationship between VCFC and wall stress, is thought to be relatively load-independent. Both load-dependent and -independent measures of contractility provide us with important clinically relevant information. Using a load-dependent index, the clinician gains insight on how the myocardium fares under current loading conditions; assessment by a load-independent index might help the clinician in ascertaining if an inherent contractility problem is the cause of cardiovascular compromise (irrespective of any abnormalities in preload or afterload). The pros and cons of each method, as well as measurement techniques, have been discussed in detail in Chapter 8.
In Chapter 8 we discussed that left ventricular wall stress (WS) is a measure of afterload and that WS is directly related to left ventricular diameter and pressure and inversely related to ventricular wall thickness (by the law of Laplace). WS changes during the cardiac cycle, and end-systolic WS is considered the best indicator of afterload. Figure 10-4 illustrates the effect of left ventricular diameter and thickness on WS. In patients with a dilated ventricle secondary to heart failure or dilated cardiomyopathy, for the same blood pressure, the afterload is much greater than in a patient with a normally sized ventricle. On the other hand, a thick myocardium or a ventricle with a small cavity would have lower afterload for a given blood pressure. Finally, the higher the blood pressure, the higher the afterload for a given ventricular size and thickness. It is important to distinguish SVR from afterload; while related (primarily via SVR’s effect on blood pressure), they are not the same and should not be used interchangeably (for further discussions see “Wall Stress” in Chapter 8).
FIGURE 10-4.
End-systolic wall stress is considered a good measure of the afterload. Left ventricular (LV) wall stress is directly related to LV diameter and LV pressure (which in turn is related to systemic blood pressure) and inversely proportional to LV wall thickness. In hypertrophic cardiomyopathy, the afterload is very low promoting a hyperdynamic state, while in the case of dilated cardiomyopathy, the afterload is very high, further compromising systolic function.
Normal vascular tone is maintained by a myriad of cellular signals, which can be hormonal, neuronal, or local. These mediators modulate vascular tone by inducing changes in the amount of intracellular calcium via second messengers or by direct activation of enzymes. Most of the mediators involved in regulation of vascular tone such as nitric oxide also play a role in pathogenesis of vasodilatory shock. Under physiologic conditions, there is a balance between the vasodilator and vasoconstrictor forces. In a pathologic condition, the balance might favor excessive vasoconstriction over vasodilation.
The conditions that can lead to vasodilatory shock in the neonatal period include sepsis, respiratory distress syndrome, necrotizing enterocolitis, and absolute/relative adrenal hypoplasia. In addition, severe peripheral vasodilatation causing vasodilatory shock can ensue after prolonged and severe shock from other causes.
Clinically, vasodilatory shock is characterized by hypotension, warm and pink extremities, bounding pulses, and a relatively rapid capillary refill time.
The echocardiographic findings of vasodilatory shock depend upon the adequacy of compensatory function. Without compensation, the findings are mainly secondary to a decreased return of venous blood to the heart and a relatively inadequate volume status due to maldistribution (ie, decreased preload). However, in the neonatal population one often encounters some degree of compensation with a hyperdynamic myocardium and high cardiac output. The calculated SVR is low and blood pressure is low despite the high cardiac output (incomplete compensation) (Figure and Video 10-5). Depending on the cause of vasodilatory shock and the stage of shock, myocardial contractility might also be affected. For example, in the late stage of septic shock, echocardiography can show an abnormally low shortening fraction and/or stress-velocity index.
FIGURE and VIDEO 10-5.
Parasternal short-axis view showing hyperdynamic myocardium in a hypotensive extremely preterm infant with necrotizing enterocolitis receiving high-dose dopamine. Despite cardiac output being in the high normal range (250 ml/kg/min), the patient was severely hypotensive. This suggests that despite some degree of compensatory increase in cardiac output, the pathological peripheral vasodilation was severe enough to result in hypotension.
Timely recognition of septic shock can reduced mortality.10 There are limited data on cardiac function in neonates with shock.11,12 In one study, preterm infants with sepsis were found to have high cardiac output and low vascular resistance.12 While as a group, the survivors maintained their cardiac output and mildly raised their SVR, there was significant hemodynamic variability among individual patients. On the other hand, the non-survivors had a drop in cardiac output and abrupt rise in SVR. It is unclear if the drop in cardiac output was the result of excessive increase in SVR or the rise in SVR was a last-ditch effort by the body to maintain perfusion pressure in the setting of low cardiac output.
