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In a dissection course, the opening of the thoracic cavity is one of the key processes which is met by teachers and students with a mixture of awe, suspense and interest. Exposing the heart and lungs as well as being allowed to grasp (literally and metaphorically) these vital organs of the body with one's own hands is considered a great privilege in these lessons.
The thoracic cavity (Cavitas thoracis) is enclosed by the thoracic cage (Cavea thoracis), consisting of ribs, thoracic spine and sternum. It is separated below by the diaphragm; above there is no clear boundary separating the neck. If the anterior thoracic wall, which is made up of important muscles to aid breathing, is removed, we can see the division of the Cavitas thoracis into two pleural cavities (Cavitates pleurales) containing the lungs, and the connective tissue space of the mediastinum lying in-between becomes visible.
Directly behind the sternum, the thymus is embedded in the mediastinum. The superior vena cava (V. cava superior) is shifted to the right. The curved main artery (aorta) dominates the upper mediastinum. Among the major vessels are the trachea, which divides into the right and left main bronchi (Bronchi principales), and, dorsally of the trachea, the oesophagus. In its pericardial sac (pericardium) within the inferior mediastinum, facing the diaphragm, the heart (Cor) which rests broadly on the diaphragm, dominates. The lungs (Pulmones) are located in both pleural cavities.
After working through this chapter, you should be able to:
describe the composition of the thoracic cavity with the mediastinum and pleural cavities, including their neurovascular pathways on a dissection;
describe the position and function of the thymus;
explain the development of the heart, including fetal circulation with any possible fundamental malformations;
illustrate the position, orientation and projection of the heart, clearly showing the margins, on a dissection and an X-ray;
describe the inner and outer structures of the heart chambers, as well as the wall layers, the pericardial sac and the cardiac skeleton on a dissection;
explain the structure, function and projection as well as the auscultation type of the various heart valves with their malfunctions on a dissection;
show the conduction system with accurate localisation of the sinoatrial and AV nodes on a dissection and understand the autonomic innervation of the heart;
indicate the Aa. coronariae with all the important branches on a dissection and describe their importance in the development, diagnosis and treatment of coronary heart disease (CHD); with the veins, only the main features will be necessary;
describe the structure of the lower respiratory tract and its development and describe the sections of the trachea;
indicate the projection of the lungs and their division into lobes and segments on a dissection, and also indicate the systematics of the bronchial tree;
describe the Vasa publica and privata of the lungs including origin, pathway and function, as well as the lymph vessel systems and the autonomic innervation;
indicate the sections and constrictions of the oesophagus with their positional relationships on a dissection;
describe the closing mechanisms of the proximal and distal oesophagus and their clinical significance;
explain the neurovascular pathways of the different sections of the oesophagus, including the relationship of the veins to the portal venous system.
In order not to lose touch with prospective everyday clinical life with so many anatomical details, the following describes a typical case that shows why the content of this chapter is so important.
A 22-year-old student is admitted to the emergency department in the morning. She reports having woken up in the morning with shortness of breath and coughing the day after she had returned from a flight to the USA. When getting up she noticed that her left lower leg was significantly thicker.
Cardiac (120/min) and respiratory rates (35/min) are significantly raised. The patient is conscious, awake and fully oriented. She has severe pain in the region of her left leg and is complaining of shortness of breath and chest pain. The lower left leg is reddened and shows expanded veins; the affected area has extended to the ankle and thigh.
The blood gas analysis shows a lowering of oxygen content in the blood. Due to a suspected pulmonary embolism, it is primarily coagulation values and D-dimers, formed by coagulated blood clots (thrombi), which are determined in blood sampling. The CT angiography of the Cavitas thoracis shows that several branches of the pulmonary arteries are displaced. The ultrasound examination of the heart (echocardiography) indicates stress on the right ventricle. A colour-coded duplex ultrasound confirms that the deep veins in the area of the femoral vein on the left-hand side of the leg are displaced by a blood clot (thrombus).
A pulmonary embolism from deep vein thrombosis ( Fig. a ). The clot from the V. femoralis seems to have detached in part and blocked the pulmonary arteries as an embolism. Before the exclusion of a clotting disorder, the transatlantic flight, the taking of oral contraceptives (‘the pill’), as well as smoking, are already present as risk factors.
Via venous access, a breakdown (thrombolysis) of the blood clots is initiated with a plasminogen activator. In addition, the patient is supplied with oxygen via a nasogastric tube. The thrombolysis is successful and the patient is largely symptom-free after a week.
To understand this clinical case, we need to look at two body regions: the veins of the leg and the organs of the Cavitas thoracis. Veins are generally a little neglected in anatomy lessons and are usually just considered to be the supporting structures of the arteries, in the way their pathways through the body and their designations correspond. In some regions there are, however, deviations from this rule or certain clinical references that require an explanation. At the extremities there is a superficial (epifascial) venous system which flows independently of the arteries, and a deep venous system (subfascial) in which two veins usually accompany the corresponding artery distally (in the forearm/lower leg) and proximally merge further on. However, superficial veins are connected to the deep venous system via perforating veins, which feature semilunar valves and allow blood flow only in the direction of the deep veins. Thus, the majority (approximately 75 %) of venous blood flows through this deep venous system back to the heart.
Blood clots in the veins are potentially life-threatening, as they can be dislodged into the blood stream. As embolisms they then move through the inferior vena cava (V. cava inferior) into the right atrium of the heart (Atrium dextrum) and through the right ventricle (Ventriculus dexter) into the pulmonary arteries (Aa. pulmonales), which channel deoxygenated blood into the lungs.
On the right-hand side the main bronchus is located above the artery, with the veins right at the front underneath. The black nodes on the surface of a removed lung are the hilum lymph nodes of the lung.
If one removes the parenchyma of the lung from the hilum onwards, one can see that the pulmonary arteries follow the branching of the bronchial tree, while the pulmonary veins (Vv. pulmonales) proceed independently. The yellow colour of the pulmonary arteries is characteristic because they, like all arteries proximal to the heart, are of the elastic type due to the many elastic fibres in their muscle layer. If, in the case of a pulmonary embolism, a considerable part of the vessel diameter is blocked, then a drastic diminution of the gas exchange surface results in acute laboured breathing. The life-threatening sign, however, is the rise in pressure in the pulmonary circulation, a condition the right ventricle can neither immediately nor permanently adapt to, and this can lead to right-sided heart failure (Cor pulmonale) and death. Therefore, when preparing the heart in the dissecting laboratory, one should always pay attention to the wall thickness of the right ventricle, which is normally 3–5 mm thick, approx. one third of the thickness of the left wall. A thicker wall diameter can be a sign of chronic damage to the right side of the heart.
The first time one holds a heart in one’s hands is a special feeling! In order to orientate oneself, one must always hold the heart in the same position in which it lies in the mediastinum. Then the right ventricle is at the front!
The treatment was changed to a six-month oral administration of Marcumar® for anticoagulation. Molecular biological investigation reveals a mutation of clotting factor V and thus an inherited genetic predisposition for the occurrence of thrombosis. The patient was therefore advised against ‘the pill' and smoking. For long trips and in the case of a planned pregnancy, a subcutaneous injection of low molecular weight heparin and the wearing of compression hosiery were recommended to the patient.
An increase in fluid in the Cavitas pleuralis (pleural effusion) may occur with pneumonia through inflammation of the pleura (pleurisy ), through vascular congestion in the case of (left-sided) heart failure, or with tumours of the lung and the pleura. Chylous pleural effusions may also occur, in which lymphs burst from the Ductus thoracicus into the Cavitas pleuralis. Pleural effusions cause dullness in percussion. Aspiration of pleural effusions is made from the costodiaphragmatic recess for diagnostic reasons and to improve respiratory excursion.
If lung excursion is impaired by an accumulation of blood in the pleural cavity (haemothorax) or by air congestion in the pleural cavity (tension pneumothorax ), or if the lung collapses in the case of a pneumothorax, a chest tube is applied in order to siphon off the blood and re-inflate the lung. For this there are two access routes, whereby the risk of damage to the surrounding organs is kept as low as possible:
MONALDI drainage: in the second ICS in the MCL. There should be no further medial insertion in order to avoid damage to the parasternal flowing thoracic artery and vein . The axillary neurovascular pathways and the intercostobrachial nerves lie laterally against them.
BÜLAU drainage: in the fifth ICS in the MAL. The liver, which is located below the right diaphragmatic dome, must not be punctured here. In maximum expiration, the latter may extend up into the fourth ICS.
In preclinical emergency care, both access routes are sensible; however, in a hospital situation, the MONALDI method is chosen in the case of a pneumothorax.
Structures of the Mediastinum superius | Structures of the Mediastinum inferius |
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The evolutionary pathway of the N . phrenicus has clinical significance in paraplegia . Caudal spinal cord lesions from C4 do not lead to any breathing dysfunction, while an injury to the C4 segment can lead to suffocation.
The innervation of liver and gallbladder via the phrenicoabdominal branches can lead to referred pain in the right shoulder (in the case of liver aspiration, a gallbladder inflammation). Splenic ruptures can cause a similar radiating pain in the left shoulder.
During surgical procedures involving the aortic arch , the cardiothoracic surgeon needs to consider the pathway of the thoracic nerves. Lesions of the left N. laryngeus recurrens may cause hoarseness of the voice and shortness of breath when exercising. Lesions of the left N. phrenicus may compromise respiratory function. The N. phrenicus runs laterally to the A. carotis communis sinistra and crosses the A. subclavis sinistra ventrally while remaining dorsal of the V. subclavia sinistra. It then crosses the Arcus aortae and the pulmonary vessels at the hilum of the lung ventrally ( Fig. 5.81 ). The N. vagus sinister descends dorsally of the V. brachiocephalica sinistra, laterally of the A. carotis communis sinistra and medially of the A. subclavia sinistra, and crosses the aortic arch ventrally before branching off the N. laryngeus recurrens. The N. vagus then runs dorsally and descends behind the hilum of the lung.
The scalene gap can be narrowed by an additional cervical rib at the seventh cervical vertebra. In this case, the Proc. transversus is elongated and comprises a rudimentary rib. Alternatively, an additional M. scalenus minimus may narrow the gap. Narrowing of the scalene gap causes the thoracic-outlet syndrome , a compression of the Plexus brachialis and the A. subclavia with elevation of the arm which may lead to a pulse deficit and numbness of the arm.
Branches | Individual arteries |
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Parietal branches on the thoracic wall |
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Visceral branches on the chest viscera |
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In cases of injury to the Ductus thoracicus during thoracic surgery involving the aortic arch or the oesophagus, or with oesophageal cancer or lymphoma in the posterior mediastinum, lymph leaks from the abdominal area into the pleural cavities, causing a chylothorax . The lymph from the Ductus thoracicus has a milky appearance as it contains the lipids resorped from the intestinal tract. Since 1–2 liters of lymph pass through the Ductus thoracicus daily, the milky effusions from a chylothorax usually have to be drained frequently. In addition, patients require total parenteral nutrition until the leak in the Ductus thoracicus is healed, and cannot receive any oral nutrition.
A surgical interruption (sympathicotomy ) or resection (sympathectomy ) of the thoracic sympathetic trunk is performed in rare cases when other therapies have failed, to reduce excessive sweating (hyperhidrosis) of the face, neck or arm or when excessive vasoconstriction in RAYNAUD syndrome causes pain in the fingers when cold. This is possible because the sudomotor neurons, which run via the sympathetic trunk to the sweat glands, arise from the T2–T7 segments to join the vasoconstrictive fibres. Visceral-afferent fibres also run along the sympathetic trunk.
The occlusion of an artery by a blood clot (embolus) or through atherosclerosis causes a reduction in blood flow (ischaemia ) to dependent organs (infarction ) or body parts. The occlusion of veins through localised formation of blood clots (thrombosis ) causes accumulation of blood in dependent body parts and increased venous pressure resulting in oedema. If venous thrombotic material dislodges from the vessel wall it travels as an embolus and may obstruct pulmonary blood vessels (pulmonary embolism) causing heart failure.
Pathologies of microvascular vessels may have similar consequences. Arteriosclerosis can cause high systemic blood pressure (arterial hypertension ). Thrombosis or changes in the corpuscular or plasma composition of blood can cause leakage of fluid into the interstitium (oedema). A swelling caused by inflammation results from extravasation of fluid from venules .
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