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Bronchial circulation and its impact on the stroke volume -- a special circulation.

Some circulations differ from the normal series flow of blood across a tissue burden and a usual afterload. cerebral, coronary, hepatic and renal circulations are commonly called special circulations as they are broken down into a resistive capillary system before they reconstitute again and most of these have autoregulatory powers. The autoregulatory power allows them to intrinsically allow them to vary flow regionally inside these organs when there is a need, mainly metabolic and dependent upon neural and hormonal pathways.

The lung circulation is an example of an organ with two different circulatory systems --

  1. The pulmonary circulation. Though the blood is deoxygenated it forms the major bulk, accounts for 99% of the blood flow, and is mainly involved in gaseous exchange.

  2. The systemic bronchial circulation. Directly supplied by the aorta or one of its branches, the pressure is high though the amount of blood flow is small. This accounts for 1% of the cardiac output.

The bronchial arteries supply oxygenated blood with nutrients to the whole of the lung tissue along with the bronchioles, alveolar tissue, the lymph nodes, the visceral pleura and even the walls of the major pulmonary vessels. The wizard Leonardo da Vinci is said to have described this bronchial circulation first. The realization that the bronchial circulation was responsible for the transport of inflammatory mediators to the lung and that the bronchial arteries are responsible for 88% of massive or sub-massive hemoptysis occurred later. Commonly the bronchial arteries, two to the left lung and one to the right, arise directly from the descending aorta though there are many variations. The first two intercostal arteries were mostly implicated. The main bronchial arteries may arise from an intermediary intercosto-bronchial branch of the aorta and additional accessory bronchial arteries are not uncommon from the subclavian, brachiocephalic or internal thoracic arteries.

They supply the mediastinal part of the trachea and mainly ramify along the bronchus and their divisions. Despite massive differences, there are numerous intricate interconnecting channels between the two systems which help to explain flexibility of flow. Drainage of bronchial circulation can be extra-pulmonary, to azygos and hemi-azygos veins, and intra-pulmonary, directly to LA. This double mode of venous drainage also helps in flexibility depending upon the changing pressures.

There are distinct histological variations in the cut section of the bronchial and pulmonary arteries. The bronchial arteries are systemic in origin and exhibit a thick muscular and reactive medial coat with a well-defined internal elastic lamina, which is thinner and often deficient externally. The main pulmonary artery originates from the right ventricle. With its branches and ramifications up to the gas exchange units, these are conduits for low blood pressure in a large and compliant area. The media is thin but the elastic layers are well defined.

Considering all these, we have to appreciate that a pulmonary shunt happens when the alveoli or the gas exchange units are fluid-filled. Thus parts of the lung are not ventilated but perfused with blood and this unoxygenated venous blood usually returns by the bronchial venous system to the left side of the heart. Normally there is >= 5% of pulmonary shunt and this can be best demonstrated by a contrast trans-thoracic echocardiography.

Several conditions cause these shunts, viz, cyanotic heart disease, pneumonia, pulmonary oedema, ARDS, alveolar collapse due to any cause, pulmonary AV malformation, atelectasis, etc. Such shunting causes hypoxemia due to a ventilation-perfusion mismatch and the degree of desaturation depends upon the extent of the disease. The finding of an alveolar-arterial oxygen difference [P ( A-a)O2] with an increased FiO2 is suggestive.

The shunting causes a dead space in the lung and should never be equated with the dead space of anesthesia but may have an additive effect. The basic difference between a shunt and a dead space is that the alveoli are perfused but not ventilated in shunting. This a pathological condition. Dead space, on the other hand, consists of ventilation, often assisted, but perfusion is absent so that the aerated blood cannot flow back to the heart.

Ventilation-perfusion mismatch or the VQ mismatch, as it is known, is a confusing concept that is often generalized when referring to a shunt or a dead space defect. For knowledge, it is best remembered that with 4-litre ventilation in a normal person the perfusion is about 5 litres and so the ratio is 4/5 or 0.8 normally. V/Q mismatch is most often quoted as a regional defect in a lung.

As said earlier the normal circulation in the human circulating system is linear and best described in a series connection. Simply speaking, the venous blood is received by the atrial chambers from where the right ventricle gets it and propels it to the compliant

& voluminous pulmonary arterials system. Gaseous exchange occurs in the lung alveoli and the oxygenated blood is returned to the left atrium by the pulmonary veins. From there it enters the left ventricle which in turn pumps it into the hugely proliferated and resistant systemic arterial tree which is mainly there for perfusing the end organs. Normally we see a synchronous contraction of both the ventricles after a short & specific atrioventricular delay. The left ventricle is more muscular and stiffer than the right and it has been found that the left ventricle not only starts contracting 20 ms earlier than the right, it also empties an amount of diastolic volume equal to the right. By the time a lower pressure of 70-80 mm of Hg is reached, the aortic valve closes and the left ventricle enters the diastole. The right ventricle, on the other hand, is a compliant, low-pressure chamber and tries to accommodate the venous blood returning to the right atrium, including itself before the tricuspid valve closes. The phases of systolic contraction of the right ventricle start similarly and low pressure, voluminous pulmonary bed is perfused. The pulmonary component of the 2nd sound with its closure occurs only when an end-diastolic pressure of 10 mm of Hg is reached and only a short period from the aortic closure. An intricate scheme is at play to synchronize the whole system the details of which are not relevant in the present context. The Wigger's diagram is an attempt to describe and combine all the events during a cardiac cycle -----




Simply speaking the preload and the afterload, mainly governed by tissue perfusion and venous return, regulate cardiac performance and output. There still is a small mismatch between the right and left flow inputs and small intricate beat-to-beat adjustments happen to accommodate these and maintain a normal output. In the normal heart, we do not have to think about flow adjusters, alternate actuators or additional compliant chambers, as we have to do when we think about implantable artificial hearts. Certainly, the bronchial arterial flow to the lung circuit is extra and in addition to anastomoses with the pulmonary circulation, shunting between these two circuits happens at times of need so that a constant cardiac output is maintained.

1% of venous return approximately equates to 1 % of cardiac output. Autoregulation in the form of shunting happens only when adjustment in the cardiac output is required. The lung on each side thus has a dual blood supply and thus usually tissue death is a rarity with interruption of a circulatory supply to a region. There may be a ventilation-perfusion mismatch as a result. Even in a lung transplant, be it bilateral, single or lobar, the bronchial supply is interrupted and still, the graft survives. So, though the bronchial circulation though not essential, is important and should be understood.

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