Shock pathophysiology

The pathophysiology of shock can be summarised as an acute state of energy failure, which prevents the metabolic demands of cells from being met. This primarily results from failure of the cardiovascular system to deliver adequate oxygen and/or glucose to the cells; however, mitochondrial dysfunction can also produce the same effect through failure of adenosine triphosphate (ATP) production.4 If shock is left untreated, it will progress through three stages:5

1. Compensatory stage: Neurohumoral mechanisms act to maintain blood pressure (BP), tissue perfusion and metabolic state.

2. Progressive stage: The compensatory mechanisms become overwhelmed and pathophysiological derangements worsen.

3. Refractory stage: Severe organ and tissue injury develops, which culminates in multiorgan failure and death.

The compensatory cardiovascular responses of the child differ from those of adults.6

In the paediatric patient, cardiac output (CO) is more dependent on heart rate (HR) than on stroke volume (SV) due to the lack of ventricular muscle mass and decreased ventricular elastance (ie, 1/Compliance).6 Consequently, tachycardia is the child’s principal means of compensating to maintain an adequate CO. As shock progresses, a further increase in HR may no longer be beneficial due to reduced ventricular diastolic filling time. Consequently, there is an increase in systemic vascular resistance through peripheral vasoconstriction mechanisms which are mediated by the sympathetic nervous system and the Renin-Angiotensin-Aldosterone system.7 CO has now been maintained by optimising preload, contractility and afterload, which are the determinants of SV (figure 1).8

• Download figure
• Open in new tab
• Download powerpoint

Figure 1

Determinants of stroke volume: preload, contractility and afterload.8 27

More specifically for septic shock, the progression of shock is often described in two phases, ‘warm shock’, which occurs early; and ‘cold shock’, which occurs late. Warm shock occurs as a result of compounds produced during the inflammatory response causing capillary leakage and vasodilation leading to a relatively warm and ‘flushed’ compensated patient. When these compensatory mechanisms start to fail, CO starts to fall and vasoconstriction dominates, leading the ominous later stage of cold shock.9 A key difference in paediatric shock (of any aetiology) is that left ventricular dysfunction occurs due to the vasoconstrictive mechanisms earlier and more commonly than in adult shock, making the distinguishing of cardiogenic shock due to a primary cardiac pathology versus a non-cardiac pathology sometimes difficult.10 11

In paediatric patients, BP can often be preserved, so BP is often a poor indicator of cardiovascular homeostasis. The evaluation of HR and end-organ perfusion, including the quality of the peripheral pulses, mental state, urine output, skin perfusion and acid-base status is much more valuable in determining a child’s circulatory status. The relationship between preload, contractility and afterload is of paramount importance, particularly when deciding whether to use volume resuscitation, vasopressors or an inotropic agent as the initial therapeutic approach to the patient in circulatory failure. Although there are an almost inexhaustible number of potential causes for circulatory shock in children, the choice narrows if the clinician uses a purely physiological classification.7

Aetiology of shock

The aetiology of shock can be broken down into five broad physiological categories (table 1).4 5

It should be noted that any one pathology may cause shock via a number of these mechanisms. For example, sepsis will initially cause a distributive shock but as increasing vascular permeability allows fluid to leave blood vessels, a hypovolaemic shock will ensue. Further progression leads to worsening acidosis and electrolyte imbalances, and eventually cardiogenic shock will ensue.12 13 As mentioned above, this happens earlier in the younger age groups.10 11

Paediatric shock POCUS protocol

Whatever protocol is used to assess the child in shock, POCUS is designed to help answer specific questions, as shown in box 1:

The adult RUSH protocol provides a framework for the attending clinician to perform a series of scans to obtain this information and help them determine the aetiology and subsequent management of the shock. Given that the majority of causes of shock are age independent, the adult RUSH protocol can be adapted for paediatric and neonatal practice. Figure 2 demonstrates a flow chart used by the authors at Southampton Children’s Hospital Paediatric Intensive Care Unit as a checklist for POCUS assessment of undifferentiated shock.

• Download figure
• Open in new tab
• Download powerpoint

Figure 2

Ultrasound examination approach to the child with undifferentiated shock. IVC, inferior vena cava; POCUS, point of care ultrasound.

At each stage of the POCUS examination, more information is gained, and the positive ultrasound features can then be used to determine which component of CO is contributing to the shocked state; is it preload, contractility or afterload?

Interpreting POCUS findings

The management of the patient can be tailored to more specifically address the underlying cause when the component of the CO leading to the shock is identified. For instance, in a shocked child with signs of pulmonary oedema (bilateral B lines on lung ultrasound with normal pleura) and a distended poorly contracting left ventricle, then impaired contractility is the likely cause. The Advanced Paediatric Life Support guidelines would initially suggest volume resuscitation for undifferentiated shock; however, now the management of this shocked child differs and earlier intervention with inotropes and ventilation may be indicated, with less or no fluid given. Following any intervention, the POCUS examination can be repeated, and this reassessment helps confirm the selected management strategy is correct. Table 2 provides a summary of how the POCUS findings can be used to identify the aetiology of shock.

Cardiorespiratory POCUS

A full detailed description of how to obtain the respiratory ultrasound views and interpret the findings relevant to shock has previously been discussed in this journal.18 The key respiratory pathologies to exclude in a shocked child include pulmonary oedema (suggestive cardiac impairment or overfilled circulation), tension pneumothorax or pleural effusions (both of which can cause a reduction in CO). Finding signs of consolidation may suggest a primary pneumonia as a source of sepsis.

Ultrasound assessment of cardiac function and ventricular filling for critical care purposes is best done by a global visual assessment of the heart. Descriptions of how to obtain key cardiac POCUS views are well documented.21 22 Assessment of cardiac filling/function should always be done in more than one view to ensure the findings are validated. For example, apical 4 chamber and parasternal long and short axis views are helpful together. Assessment of the LV should include a visual assessment of the size of the chamber, the wall movements and the interactions with the RV. Cardiac POCUS is very different to the detailed echocardiography assessment looking for congenital heart disease; cardiac POCUS is a brief functional assessment only to help guide immediate resuscitation.

Assessment of IVC

The use of the subcostal view to assess inferior vena cava (IVC) collapsibility and respiratory variation is thought to be a potential predictor of fluid responsiveness, if performed under the right conditions. To obtain the images, the probe should be placed to acquire the subcostal view of the heart, then the probe is moved progressively to the right to visualise the IVC/right atrium in the centre of the field. The probe is then rotated by 90° anticlockwise to obtain the IVC in its longitudinal plane.23 In a spontaneously breathing child, a variation in IVC diameter during respiration of >50% combined with an easily collapsible vessel suggests a low-volume state (figure 3A). Conversely, a variation of <50% with a distended or minimally collapsible IVC suggests a high-volume state or potential tamponade/obstructive physiology (figure 3B).22 The heterogeneity of studies performed in both adults and children have failed to fully support or refute the concept of IVC variability and fluid responsiveness.24 25 It is the view of the authors that the IVC POCUS assessment should not be used in isolation, and it must always be correlated with the patients history, examination and additional POCUS findings.

• Download figure
• Open in new tab
• Download powerpoint

Figure 3

Subcostal view of the IVC in Motion (M)-mode. The upper image shows the liver with a scan line, passing through the IVC. The lower image shows the movements of structures along that line and displays them against time. (A) shows significant variability in change of the IVC diameter and (B) shows no variability in IVC diameter. IVC, inferior vena cava.

Abdominal POCUS

Abdominal POCUS users should be trained to identify intra-abdominal and pelvic free fluid and major organ abnormalities (eg, large hepatic haemangioma causing high output cardiac failure); it is not intended to replace a formal departmental abdominal ultrasound. The ability to perform an abdominal POCUS provides us with a useful tool at the bedside to help determine the type of shock; however, it should be recognised that POCUS trained clinicians have a very limited diagnostic capability. If the clinician is not confident of the findings at any point in the POCUS assessment, then more specialised imaging may be indicated.

Cranial POCUS

Cranial ultrasound can be performed through any open fontanelle to obtain images of the brain. It remains a useful tool at identifying major intracranial pathology until these fontanelles start to close (perhaps up to 1 year of age).26 Many paediatric trainees are exposed to this during neonatal intensive care placements. Key pathologies to identify include hydrocephalus, extra/subdural/intraventricular blood or vein of Galen malformations.