Bubbles almost certainly do not form from dissolved nitrogen in the arterial circulation because once the venous blood passes through the lungs, the dissolved PN2 in the blood and alveoli should have equilibrated, and the arterial blood leaving the lungs will no longer be supersaturated. Bubbles can be introduced into the arterial circulation by pulmonary barotrauma (see Chapter 6) and also by left-to-right (venous-to-arterial) transfer of VGE. This can occur via several recognized ‘shunt’ pathways.
The lesser known and least researched of these pathways are pulmonary ‘shunts’. The existence of such shunts has been known for some time. They can be detected in some subjects at rest and in many subjects during exercise. Indeed, their physiological role may be to unload the right side of the heart to some extent during heavy exercise. The increasing use of echocardiography in the observation of bubble behaviour after diving, and also in saline contrast tests for patent foramen ovale (PFO; see later), has revealed that VGE can sometimes be seen emerging from the pulmonary veins into the left side of the heart. Thus, these bubbles have crossed the pulmonary circulation rather than an intracardiac shunt. It is notable that one small study failed to detect pulmonary shunting of VGE in divers exercising after a dive. Nevertheless, pulmonary shunts may contribute to the development of the DCS syndromes known to be associated with right-to-left shunting of VGE (see later), especially where there is no PFO to explain the mechanism.
The better known and most widely researched pathway is an intracardiac shunt, usually a PFO. The foramen ovale is a communication through the atrial septum that during fetal life allows blood arriving at the right side of the heart in the inferior vena cava to be directed straight across the septum into the left atrium, thereby by-passing the right ventricle and pulmonary circulation. With the haemodynamic changes that occur at birth, the foramen ovale closes in a valve-like manner, with the higher left atrial pressures tending to keep it shut. In the majority of people, the tissue pads that close the foramen ovale become ‘healed’ in the shut position, but in a minority (some 25 to 30 per cent), the foramen ovale remains open, or at least able to open should pressures in the right atrium exceed those on the left for any reason. This is referred to as a ‘patent’ foramen ovale (PFO).
As implied earlier, a PFO can be found in 25 to 30 per cent of adults who are unaware they have one, and most go through life suffering no ill effects. However, there are now multiple case-control studies that collectively demonstrate associations between the presence of a PFO and DCS involving the brain, spinal cord, inner ear and skin. In the various relevant studies, these associations are established by a substantially higher prevalence of PFO among cases of DCS than found among control divers who have not suffered DCS. If we cautiously accept that causation can be inferred from this association, the clear implication is that VGE that become ‘arterialized’ across a PFO are important in the pathophysiology of these forms of DCS. The way these small arterial bubbles may cause harm is discussed in more detail later. Another unsurprising and consistent finding among the relevant studies is that the size, or more correctly the shunting behaviour, of the PFO seems important. Thus, a grade 1 (see later) or ‘small’ PFO is likely to represent little if any risk, whereas a grade 3 or spontaneously shunting PFO almost certainly imparts extra risk for the relevant forms of DCS.
Not surprisingly, divers may request testing for the presence of a PFO. The issues of which divers should be tested for a PFO and what should be done when a PFO is found are discussed later in Chapter 12; however, the testing process is described briefly here because some of the terminology that arises is relevant to discussion of the pathogenicity of arterial bubbles. The process involves performing echocardiography while introducing agitated saline (which somewhat paradoxically contains many small bubbles) into a peripheral vein. The arrival of the bubbles in the right side of the heart often causes its virtual opacification on echocardiography, and the left side of the heart is then monitored to see whether bubbles cross the interatrial septum. Release of a Valsalva manoeuvre causes a temporary rise in right atrial pressure and is used to unmask a PFO that remains closed most of the time but that can open if right atrial pressure rises. The results are often crudely graded as follows: 0 = no bubble shunting; 1 = few bubbles shunted even during a Valsalva manoeuvre; 2 = moderate numbers of bubbles shunted during a Valsalva manoeuvre; 3 = spontaneous shunting of bubbles without a Valsalva manoeuvre.
There has been debate about whether echocardiography should be transthoracic (less expensive and less invasive) or transoesophageal (better-quality imaging) for these tests. In general, it is agreed that in expert hands and provided good views can be obtained, transthoracic echocardiography is ideal for this purpose. In fact, it is more likely to result in accurate studies because patients are typically better able to cooperate with provocative manoeuvres such as Valsalva manoeuvres than during transoesophageal echocardiography, when patients may be uncomfortable or sedated. If transthoracic views are poor, then a transoesophageal investigation should be considered. Another variant of the ‘PFO test’ is the use of carotid or transcranial Doppler imaging to detect bubbles in the respective arteries after injection of saline contrast and a Valsalva manoeuvre. These tests detect a right-to-left shunt, but they do not definitively distinguish among the lesions that are potentially permitting it (e.g. PFO, pulmonary shunt, atrial septal defect).