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Pericarditis must be distinguished from myocardial infarction because the treatment and prognosis are quite different. As in patients with myocardial infarction, patients with pericarditis complain of continuous central chest pain that may radiate to one or both arms. Unlike myocardial infarction, however, the pain from pericarditis may be relieved by sitting forward. An electrocardiogram (ECG) is used to help differentiate between the two conditions. It usually shows diffuse ST elevation. Echocardiography can also be performed if there is clinical or radiographic suspicion of pericardial effusion. |
In the clinicNormally, only a tiny amount of fluid is present between the visceral and parietal layers of the serous pericardium. In certain situations, this space can be filled with excess fluid (pericardial effusion) (Fig. 3.62). |
Because the fibrous pericardium is a “relatively fixed” structure that cannot expand easily, a rapid accumulation of excess fluid within the pericardial sac compresses the heart (cardiac tamponade), resulting in biventricular failure. Removing the fluid with a needle inserted into the pericardial sac can relieve the symptoms. |
In the clinicAbnormal thickening of the pericardial sac (constrictive pericarditis), which usually involves only the parietal pericardium, but can also less frequently involve the visceral layer, can compress the heart, impairing heart function and resulting in heart failure. It can present acutely but often results in a chronic condition when thickened pericardium with fibrin deposits causes pericardial inflammation, leading to chronic scarring and pericardial calcification. As a result, normal filling during the diastolic phase of the cardiac cycle is severely restricted. The diagnosis is made by inspecting the jugular venous pulse in the neck. In normal individuals, the jugular venous pulse drops on inspiration. In patients with constrictive pericarditis, the reverse happens and this is called Kussmaul’s sign. Treatment often involves surgical opening of the pericardial sac. |
In the clinicValve problems consist of two basic types: incompetence (insufficiency), which results from poorly functioning valves; and stenosis, a narrowing of the orifice, caused by the valve’s inability to open fully. |
Mitral valve disease is usually a mixed pattern of stenosis and incompetence, one of which usually predominates. Both stenosis and incompetence lead to a poorly functioning valve and subsequent heart changes, which include: left ventricular hypertrophy (this is appreciably less marked in patients with mitral stenosis); increased pulmonary venous pressure; pulmonary edema; and enlargement (dilation) and hypertrophy of the left atrium. |
Mitral valve stenosis can be congenital or acquired; in the latter, the most common cause is rheumatic fever. Stenosis usually occurs decades after an acute episode of rheumatic endocarditis. |
Aortic valve disease, both aortic stenosis and aortic regurgitation (backflow), can produce marked heart failure. Aortic valve stenosis is the most common type of cardiac valve disease and results from atherosclerosis causing calcification of the valve leaflets. It can also be caused by postinflammatory or postrheumatic conditions. These may lead to aortic regurgitation such as infective endocarditis, degenerative valve disease, rheumatic fever, or trauma. |
Valve disease in the right side of the heart (affecting the tricuspid or pulmonary valve) is most likely caused by infection. Intravenous drug use, alcoholism, indwelling catheters, and extensive burns predispose to infection of the valves, particularly the tricuspid valve. The resulting valve dysfunction produces abnormal pressure changes in the right atrium and right ventricle, and these can induce cardiac failure. |
In the clinicIn practice, physicians use alternative names for the coronary vessels. The short left coronary artery is referred to as the left main stem vessel. One of its primary branches, the anterior interventricular artery, is termed the left anterior descending artery (LAD). Similarly, the terminal branch of the right coronary artery, the posterior interventricular artery, is termed the posterior descending artery (PDA). |
In the clinicA heart attack occurs when the perfusion to the myocardium is insufficient to meet the metabolic needs of the tissue, leading to irreversible tissue damage. The most common cause is a total occlusion of a major coronary artery. |
Occlusion of a major coronary artery, usually due to atherosclerosis, leads to inadequate oxygenation of an area of myocardium and cell death (Fig. 3.80). The severity of the problem will be related to the size and location of the artery involved, whether or not the blockage is complete, and whether there are collateral vessels to provide perfusion to the territory from other vessels. Depending on the severity, patients can develop pain (angina) or a myocardial infarction (MI). |
This is a technique in which a long fine tube (a catheter) is inserted into the femoral artery in the thigh and passed through the external and common iliac arteries and into the abdominal aorta. It continues to be moved upward through the thoracic aorta to the origins of the coronary arteries. The coronaries may also be approached via the radial or brachial arteries. A fine wire is then passed into the coronary artery and is used to cross the stenosis. A fine balloon is then passed over the wire and may be inflated at the level of the obstruction, thus widening it; this is termed angioplasty. More commonly, this is augmented by placement of a fine wire mesh (a stent) inside the obstruction to hold it open. Other percutaneous interventions are suction extraction of a coronary thrombus and rotary ablation of a plaque. |
If coronary artery disease is too extensive to be treated by percutaneous intervention, surgical coronary artery bypass grafting may be necessary. The great saphenous vein, in the lower limb, is harvested and used as a graft. |
It is divided into several pieces, each of which is used to bypass blocked sections of the coronary arteries. The internal thoracic and radial arteries can also be used. |
In the clinicThe most common abnormalities that occur during development are those produced by a defect in the atrial and ventricular septa. |
A defect in the interatrial septum allows blood to pass from one side of the heart to the other from the chamber with the higher pressure to the chamber with the lower pressure; this is clinically referred to as a shunt. An atrial septal defect (ASD) allows oxygenated blood to flow from the left atrium (higher pressure) across the ASD into the right atrium (lower pressure), resulting in a left to right shunt and volume overload in the right-sided circulation. Many patients with ASD are asymptomatic, but in some cases the ASD may cause symptoms and needs to be closed surgically or by endovascular devices. Occasionally, increased blood flow into the right atrium over many years leads to right atrial and right ventricular hypertrophy and enlargement of the pulmonary trunk, resulting in pulmonary arterial hypertension. In such cases, the patients can present with shortness of breath, increasing tiredness, palpitations, fainting episodes and heart failure. In ASD, the left ventricle is not enlarged as it is not affected by increased returning blood volume. |
The most common of all congenital heart defects are those that occur in the ventricular septum—ventriculoseptal defect (VSD). These lesions are most frequent in the membranous portion of the septum and they allow blood to flow from the left ventricle (higher pressure) to the right ventricle (lower pressure), leading to an abnormal communication between the systemic and pulmonary circulation. This leads to right ventricular hypertrophy, increased pulmonary blood flow, elevated arterial pulmonary pressure, and increased blood volume returning to the left ventricle, causing its dilation. Increased pulmonary pressure in most severe cases may cause pulmonary edema. If large enough and left untreated, VSDs can produce marked clinical problems that might require surgery. VSD may be an isolated abnormality or part of a syndromic constellation, such as the tetralogy of Fallot. |
The tetralogy of Fallot, the most common cyanotic congenital heart disorder diagnosed soon after birth, classically consists of four abnormalities: pulmonary stenosis, VSD, overriding aorta (originating to a varying degree from the right ventricle), and right ventricular hypertrophy. The underdevelopment of the right ventricle and pulmonary stenosis reduce blood flow to the lungs, leading to reduced volume of oxygenated blood returning to the heart. The defect in the interventricular septum causes mixing of oxygenated and nonoxygenated blood. The mixed blood is then delivered by the aorta to the major organs, resulting in poor oxygenation and cyanosis. Infants can present with cyanosis at birth or develop episodes of cyanosis while feeding or crying (tet spells). Most affected infants require surgical intervention. The advent of cardiopulmonary bypass was crucial in delivering highly satisfactory surgical results. |
Occasionally, the ductus arteriosus, which connects the left branch of the pulmonary artery to the inferior aspect of the aortic arch, fails to close at birth. This is termed a patent or persistent ductus arteriosus (PDA). When this occurs, the oxygenated blood in the aortic arch (higher pressure) passes into the left branch of the pulmonary artery (lower pressure) and produces pulmonary hypertension and left atrial and ventricular enlargement. The prognosis in patients with isolated PDA is extremely good, as most do not have any major sequelae after surgical closure. |
All of these defects produce a left-to-right shunt, indicating that oxygenated blood from the left side of the heart is being mixed with deoxygenated blood from the right side of the heart before being recirculated into the pulmonary circulation. These shunts are normally compatible with life, but surgery or endovascular treatment may be necessary. |
Rarely, a shunt is right-to-left. In isolation, this is fatal; however, this type of shunt is often associated with other anomalies, so some deoxygenated blood is returned to the lungs and the systemic circulation. |
In the clinicAuscultation of the heart reveals the normal audible cardiac cycle, which allows the clinician to assess heart rate, rhythm, and regularity. Furthermore, cardiac murmurs that have characteristic sounds within the phases of the cardiac cycle can be demonstrated (Fig. 3.81). |
In the clinicClassic symptoms of heart attackThe typical symptoms are chest heaviness or pressure, which can be severe, lasting more than 20 minutes, and often associated with sweating. The pain in the chest (which may be described as an “elephant sitting on my chest” or by using a clenched fist to describe the pain [Levine sign]) often radiates to the arms (left more common than the right), and can be associated with nausea. The severity of ischemia and infarction depends on the rate at which the occlusion or stenosis has occurred and whether or not collateral channels have had a chance to develop. |
In the clinicAre heart attack symptoms the same in men and women? |
Although men and women can experience the typical symptoms of severe chest pain, cold sweats, and pain in the left arm, women are more likely than men to have subtler, less recognizable symptoms. These may include abdominal pain, achiness in the jaw or back, nausea, shortness of breath, or simply fatigue. The mechanism of this difference is not understood, but it is important to consider cardiac ischemia for a wide range of symptoms. |
In the clinicThe cardiac conduction system can be affected by coronary artery disease. The normal rhythm may be disturbed if the blood supply to the coronary conduction system is disrupted. If a dysrhythmia affects the heart rate or the order in which the chambers contract, heart failure and death may ensue. |
In the clinicEctopic parathyroid glands in the thymusThe parathyroid glands develop from the third pharyngeal pouch, which also forms the thymus. The thymus is therefore a common site for ectopic parathyroid glands and, potentially, ectopic parathyroid hormone production. |
In the clinicLarge systemic veins are used to establish central venous access for administering large amounts of fluid, drugs, and blood. Most of these lines (small-bore tubes) are introduced through venous puncture into the axillary, subclavian, or internal jugular veins. The lines are then passed through the main veins of the superior mediastinum, with the tips of the lines usually residing in the distal portion of the superior vena cava or in the right atrium. |
Similar devices, such as dialysis lines, are inserted into patients who have renal failure, so that a large volume of blood can be aspirated through one channel and reinfused through a second channel. |
In the clinicUsing the superior vena cava to access the inferior vena cava |
Because the superior and inferior venae cavae are oriented along the same vertical axis, a guidewire, catheter, or line can be passed from the superior vena cava through the right atrium and into the inferior vena cava. This is a common route of access for such procedures as: transjugular liver biopsy, transjugular intrahepatic portosystemic shunts (TIPS), and insertion of an inferior vena cava filter to catch emboli dislodged from veins in the lower limb and pelvis (i.e., patients with deep vein thrombosis [DVT]). |
In the clinicCoarctation of the aortaCoarctation of the aorta is a congenital abnormality in which the aortic lumen is constricted just distal to the origin of the left subclavian artery. At this point, the aorta becomes significantly narrowed and the blood supply to the lower limbs and abdomen is diminished. Over time, collateral vessels develop around the chest wall and abdomen to supply the lower body. Dilated and tortuous intercostal vessels, which form a bypass to supply the descending thoracic aorta, may lead to erosions of the inferior margins of the ribs. This can be appreciated on chest radiographs as inferior rib notching and is usually seen in long standing cases. The coarctation also affects the heart, which has to pump the blood at higher pressure to maintain peripheral perfusion. This in turn may produce cardiac failure. |
In the clinicDiffuse atherosclerosis of the thoracic aorta may occur in patients with vascular disease, but this rarely produces symptoms. There are, however, two clinical situations in which aortic pathology can produce life-threatening situations. |
The aorta has three fixed points of attachment: the aortic valve, the ligamentum arteriosum, and the point of passing behind the median arcuate ligament of the diaphragm to enter the abdomen. |
The rest of the aorta is relatively free from attachment to other structures of the mediastinum. A serious deceleration injury (e.g., in a road traffic accident) is most likely to cause aortic trauma at these fixed points. |
In certain conditions, such as in severe arteriovascular disease, the wall of the aorta can split longitudinally, creating a false channel, which may or may not rejoin into the true lumen distally (Fig. 3.91). This aortic dissection occurs between the intima and media anywhere along its length. If it occurs in the ascending aorta or arch of the aorta, blood flow in the coronary and cerebral arteries may be disrupted, resulting in myocardial infarction or stroke. In the abdomen the visceral vessels may be disrupted, producing ischemia to the gut or kidneys. |
In the clinicThe normal aortic arch courses to the left of the trachea and passes over the left main bronchus. A right-sided aortic arch occurs when the vessel courses to the right of the trachea and passes over the right main bronchus. A right-sided arch of aorta is rare and may be asymptomatic. It can be associated with dextrocardia (right-sided heart) and, in some instances, with complete situs inversus (left-to-right inversion of the body’s organs). It can also be associated with abnormal branching of the great vessels, particularly with an aberrant left subclavian artery. |
In the clinicAbnormal origin of great vesselsGreat vessels occasionally have an abnormal origin, including: a common origin of the brachiocephalic trunk and the left common carotid artery, the left vertebral artery originating from the aortic arch, and the right subclavian artery originating from the distal portion of the aortic arch and passing behind the esophagus to supply the right arm—as a result, the great vessels form a vascular ring around the trachea and the esophagus, which can potentially produce difficulty swallowing. This configuration is one of the most common aortic arch abnormalities. |
In the clinicThe vagus nerves, recurrent laryngeal nerves,The left recurrent laryngeal nerve is a branch of the left vagus nerve. It passes between the pulmonary artery and the aorta, a region known clinically as the aortopulmonary window, and may be compressed in any patient with a pathological mass in this region. This compression results in left vocal cord paralysis and hoarseness of the voice. Lymph node enlargement, often associated with the spread of lung cancer, is a common condition that may produce compression. Chest radiography is therefore usually carried out for all patients whose symptoms include a hoarse voice. |
More superiorly, in the root of the neck, the right vagus nerve gives off the right recurrent laryngeal nerve, which “hooks” around the right subclavian artery as it passes over the cervical pleura. If a patient has a hoarse voice and a right vocal cord palsy is demonstrated at laryngoscopy, chest radiography with an apical lordotic view should be obtained to assess for cancer in the right lung apex (Pancoast’s tumor). |
In the clinicWhen patients present with esophageal cancer, it is important to note which portion of the esophagus contains the tumor because tumor location determines the sites to which the disease will spread (Fig. 3.100). |
Esophageal cancer spreads quickly to lymphatics, draining to lymph nodes in the neck and around the celiac artery. Endoscopy or barium swallow is used to assess the site. CT and MRI may be necessary to stage the disease. |
Once the extent of the disease has been assessed, treatment can be planned. |
In the clinicThe first case of esophageal rupture was described by Herman Boerhaave in 1724. This case was fatal, but early diagnosis has increased the survival rate up to 65%. If the disease is left untreated, mortality is 100%. |
Typically, the rupture occurs in the lower third of the esophagus with a sudden rise in intraluminal esophageal pressure produced by vomiting secondary to an uncoordination and failure of the cricopharyngeus muscle to relax. Because the tears typically occur on the left, they are often associated with a large left pleural effusion that contains the gastric contents. In some patients, subcutaneous emphysema may be demonstrated. |
Treatment is optimal with urgent surgical repair.A 65-year-old man was admitted to the emergency room with severe central chest pain that radiated to the neck and predominantly to the left arm. He was overweight and a known heavy smoker. |
On examination he appeared gray and sweaty. His blood pressure was 74/40 mm Hg (normal range 120/80 mm Hg). An electrocardiogram (ECG) was performed and demonstrated anterior myocardial infarction. An urgent echocardiograph demonstrated poor left ventricular function. The cardiac angiogram revealed an occluded vessel (Fig. 3.114A,B). Another approach to evaluating coronary arteries in patients is to perform maximum intensity projection (MIP) CT studies (Fig. 3.115A,B). |
This patient underwent an emergency coronary artery bypass graft and made an excellent recovery. He has now lost weight, stopped smoking, and exercises regularly. |
When cardiac cells die during a myocardial infarction, pain fibers (visceral afferents) are stimulated. These visceral sensory fibers follow the course of sympathetic fibers that innervate the heart and enter the spinal cord between the TI and TIV levels. At this level, somatic afferent nerves from spinal nerves T1 to T4 also enter the spinal cord via the posterior roots. Both types of afferents (visceral and somatic) synapse with interneurons, which then synapse with second neurons whose fibers pass across the cord and then ascend to the somatosensory areas of the brain that represent the T1 to T4 levels. The brain is unable to distinguish clearly between the visceral sensory distribution and the somatic sensory distribution and therefore the pain is interpreted as arising from the somatic regions rather than the visceral organ (i.e., the heart; Fig. 3.114C). |
The patient was breathless because his left ventricular function was poor. |
When the left ventricle fails, it produces two effects.First, the contractile force is reduced. This reduces the pressure of the ejected blood and lowers the blood pressure. |
The left atrium has to work harder to fill the failing left ventricle. This extra work increases left atrial pressure, which is reflected in an increased pressure in the pulmonary veins, and this subsequently creates a higher pulmonary venular pressure. This rise in pressure will cause fluid to leak from the capillaries into the pulmonary interstitium and then into the alveoli. Such fluid is called pulmonary edema and it markedly restricts gas exchange. This results in shortness of breath. |
This man had a blocked left coronary artery, as shown in Fig. 3.114B. |
It is important to know which coronary artery is blocked. |
The left coronary artery supplies the majority of the left side of the heart. The left main stem vessel is approximately 2 cm long and divides into the circumflex artery, which lies between the atrium and the ventricle in the coronary sulcus, and the anterior interventricular artery, which is often referred to as the left anterior descending artery (LAD). |
When the right coronary artery is involved with arterial disease and occludes, associated disorders of cardiac rhythm often result because the sinu-atrial and the atrioventricular nodes derive their blood supplies predominantly from the right coronary artery. |
When this patient sought medical care, his myocardial function was assessed using ECG, echocardiography, and angiography. |
During a patient’s initial examination, the physician will usually assess myocardial function. |
After obtaining a clinical history and carrying out a physical examination, a differential diagnosis for the cause of the malfunctioning heart is made. Objective assessment of myocardial and valve function is obtained in the following ways: |
ECG/EKG (electrocardiography)—a series of electrical traces taken around the long and short axes of the heart that reveal heart rate and rhythm and conduction defects. In addition, it demonstrates the overall function of the right and left sides of the heart and points of dysfunction. Specific changes in the ECG relate to the areas of the heart that have been involved in a myocardial infarction. For example, a right coronary artery occlusion produces infarction in the area of myocardium it supplies, which is predominantly the inferior aspect; the infarct is therefore called an inferior myocardial infarction. The ECG changes are demonstrated in the leads that visualize the inferior aspect of the myocardium (namely, leads II, III, and aVF). |
Chest radiography—reveals the size of the heart and chamber enlargement. Careful observation of the lungs will demonstrate excess fluid (pulmonary edema), which builds up when the left ventricle fails and can produce marked respiratory compromise and death unless promptly treated. |
Blood tests—the heart releases enzymes during myocardial infarction, namely lactate dehydrogenase (LDH), creatine kinase (CK), and aspartate transaminase (AST). These plasma enzymes are easily measured in the hospital laboratory and used to determine the diagnosis at an early stage. Further specific enzymes termed isoenzymes can also be determined (creatine kinase MB isoenzyme [CKMB]). Newer tests include an assessment for troponin (a specific component of the myocardium), which is released when cardiac cells die during myocardial infarction. |
Exercise testing—patients are connected to an ECG monitor and exercised on a treadmill. Areas of ischemia, or poor blood flow, can be demonstrated, so localizing the vascular abnormality. |
Nuclear medicine—thallium (a radioactive X-ray emitter) and its derivatives are potassium analogs. They are used to determine areas of coronary ischemia. If no areas of myocardial uptake are demonstrated when these substances are administered to a patient the myocardium is dead. |
Coronary angiography—small arterial catheters are maneuvered from a femoral artery puncture site through the femoral artery and aorta and up to the origins of the coronary vessels. X-ray contrast medium is then injected to demonstrate the coronary vessels and their important branches. If there is any narrowing (stenosis), angioplasty may be carried out. In angioplasty tiny balloons are passed across the narrowed areas and inflated to refashion the vessel and so prevent further coronary ischemia and myocardial infarction. |
A 53-year-old man presented to the emergency department with a 5-hour history of sharp pleuritic chest pain and shortness of breath. The day before he was on a long haul flight, returning from his holidays. He was usually fit and well and was a keen mountain climber. He had no previous significant medical history. |
On physical examination his lungs were clear, he was tachypneic at 24/min, and his saturation was reduced to 92% on room air. Pulmonary embolism was suspected and the patient was referred for a CT pulmonary angiogram. The study demonstrated clots within the right and left main pulmonary arteries. There was no pleural effusion, lung collapse, or consolidation. |
He was immediately started on subcutaneous enoxaparin and converted to oral anticoagulation over the course of a couple of days. The whole treatment lasted 6 months as no other risk factors (except immobilization during a long haul flight) were identified. There were no permanent sequelae. |
The embolic material usually originates in the peripheral deep veins of the lower limbs and less commonly in the pelvic, renal, or upper limb deep veins. The material gets detached from the main thrombus in the deep veins and travels into the pulmonary circulation, where it can lodge either in the pulmonary trunk and main pulmonary arteries, giving rise to central pulmonary embolism or in the lobar, segmental, or subsegmental branches, giving rise to peripheral embolism. |
The gravity of symptoms is partly dependent on the thrombus load and on which part of the pulmonary arterial tree is affected. Large pulmonary embolisms can lead to severe hemodynamic and respiratory compromise and death (e.g., a saddle thrombus lodged in the pulmonary trunk and in both main pulmonary arteries). |
Common risk factors include immobilization, surgery, trauma, malignancy, pregnancy, oral contraceptives, and hereditary factors. |
A young man has black areas of skin on the tips of his fingers of his left hand. A clinical diagnosis of platelet emboli was made and a source of the emboli sought. |
Emboli can arise from many sources. They are clots and plugs of tissue, usually platelets, that are carried from a source to eventually reside in small vessels which they may occlude. Arterial emboli may arise in the heart or in the arteries that supply the region affected. In cases of infected emboli, bacteria grow on the valve and are showered off into the peripheral circulation. |
A neck radiograph and coronal CT image of the neck demonstrates a cervical rib (eFig. 3.116). |
Cervical ribs may produce three distinct disease entities:Arterial compression and embolization—the cervical rib (or band) on the undersurface of the distal portion of the subclavian artery reduces the diameter of the vessel and allows eddy currents to form. Platelets aggregate and atheroma may develop in this region. This debris can be dislodged and flow distally within the upper limb vessels to block off blood flow to the fingers and the hand, a condition called distal embolization. |
Tension on the T1 nerve—the T1 nerve, which normally passes over rib I, is also elevated by the presence of a cervical rib; thus the patient may experience a sensory disturbance over the medial aspect of the forearm, and develop wasting of the intrinsic muscles of the hand. |
Compression of the subclavian vein—this may induce axillary vein thrombosis. |
A Doppler ultrasound scan revealed marked stenosis of the subclavian artery at the outer border of the rib with abnormal flow distal to the narrowing. Within this region of abnormal flow there was evidence of thrombus adherent to the vessel wall. |
This patient underwent surgical excision of the cervical rib and had no further symptoms. |
A 52-year-old man presented with headaches and shortness of breath. He also complained of coughing up small volumes of blood. Clinical examination revealed multiple dilated veins around the neck. A chest radiograph demonstrated an elevated diaphragm on the right and a tumor mass, which was believed to be a primary bronchogenic carcinoma. |
By observing the clinical findings and applying anatomical knowledge, the site of the tumor can be inferred. |
The multiple dilated veins around the neck are indicative of venous obstruction. The veins are dilated on both sides of the neck, implying that the obstruction must be within a common vessel, the superior vena cava. Anterior to the superior vena cava in the right side of the chest is the phrenic nerve, which supplies the diaphragm. Because the diaphragm is elevated, suggesting paralysis, it is clear that the phrenic nerve has been involved with the tumor. |
A 35-year-old man was shot during an armed robbery. The bullet entry wound was in the right fourth intercostal space, above the nipple. A chest radiograph obtained on admission to the emergency room demonstrated complete collapse of the lung. |
A further chest radiograph performed 20 minutes later demonstrated an air/fluid level in the pleural cavity (eFig. 3.117). |
Three common pathological processes may occur in the pleural cavity. |
If air is introduced into the pleural cavity, a pneumothorax develops and the lung collapses because of its own elastic recoil. The pleural space fills with air, which may further compress the lung. Most patients with a collapsed lung are unlikely to have respiratory impairment. Under certain conditions, air may enter the pleural cavity at such a rate that it shifts and pushes the mediastinum to the opposite side of the chest. This is called tension pneumothorax and is potentially lethal, requiring urgent treatment by insertion of an intercostal tube to remove the air. The commonest causes of pneumothorax are rib fractures and positive pressure ventilation lung damage. |
The pleural cavity may fill with fluid (a pleural effusion) and this can be associated with many diseases (e.g., lung infection, cancer, abdominal sepsis). It is important to aspirate fluid from these patients to relieve any respiratory impairment and to carry out laboratory tests on the fluid to determine its nature. |
Severe chest trauma can lead to development of hemopneumothorax. A tube must be inserted to remove the blood and air that has entered the pleural space and prevent respiratory impairment. |
This man needs treatment to drain either the air or fluid or both. |
The pleural space can be accessed by passing a needle between the ribs into the pleural cavity. In a normal healthy adult, the pleural space is virtually nonexistent; therefore, any attempt to introduce a needle into this space is unlikely to succeed and the procedure may damage the underlying lung. |
Before any form of chest tube is inserted, the rib must be well anesthetized by infiltration because its periosteum is extremely sensitive. The intercostal drain should pass directly on top of the rib. Insertion adjacent to the lower part of the rib may damage the artery, vein, and nerve, which lie within the neurovascular bundle. |
Appropriate sites for insertion of a chest drain are either in the fourth or fifth intercostal space between the anterior axillary and midaxillary anatomical lines. |
This position is determined by palpating the sternal angle, which is the point of articulation of rib II. Counting inferiorly will determine the rib number and simple observation will determine the positions of the anterior axillary and midaxillary lines. Insertion of any tube or needle below the fifth interspace runs an appreciable risk of crossing the pleural recesses and placing the needle or the drain into either the liver or the spleen, depending upon which side the needle is inserted. |
An elderly woman was admitted to the emergency room with severe cardiac failure. She had a left-sided pacemaker box, which had been inserted for a cardiac rhythm disorder (fast atrial fibrillation) many years previously. An ECG demonstrated fast atrial fibrillation. A chest radiograph showed that the wire from the pacemaker had broken under the clavicle. |
Anatomical knowledge of this region of the chest explains why the wire broke. |
Many patients have cardiac pacemakers. A wire arises from the pacemaker, which lies within the subcutaneous tissue over the pectoralis major muscle and travels from the pacemaker under the skin to pierce the axillary vein just beneath the clavicle, lateral to the subclavius muscle. The wire then passes through the subclavian vein, the brachiocephalic vein, the superior vena cava, and the right atrium, and lies on the wall of the right ventricle (where it can stimulate the heart to contract) (eFig. 3.118). If the wire pierces the axillary vein directly adjacent to the subclavius muscle, it is possible that after many years of shoulder movement the subclavius muscle stresses and breaks the wire, causing the pacemaker to fail. Every effort is made to place the insertion point of the wire as far laterally as feasible within the first part of the axillary vein. |
A 20-year-old man visited his family doctor because he had a cough. A chest radiograph demonstrated translucent notches along the inferior border of ribs III to VI (eFig. 3.119). He was referred to a cardiologist and a diagnosis of coarctation of the aorta was made. The rib notching was caused by dilated collateral intercostal arteries. |
Coarctation of the aorta is a narrowing of the aorta distal to the left subclavian artery. This narrowing can markedly reduce blood flow to the lower body. Many of the vessels above the narrowing therefore enlarge due to the increased pressure so that blood can reach the aorta below the level of the narrowing. Commonly, the internal thoracic, superior epigastric, and musculophrenic arteries enlarge anteriorly. These arteries supply the anterior intercostal arteries, which anastomose with the posterior intercostal arteries that allow blood to flow retrogradely into the aorta. Enlargement of the intertcostal vessels results in notching of the ribs. |
The first and second posterior intercostal vessels are supplied from the costocervical trunk, which arises from the subclavian artery proximal to the coarctation, so do not enlarge and do not induce rib notching. |