of the pulmonary arteries: Reinhard Putz
Conservative treatment: Edda Spiekerkötter and Thomas Zeller
Endovascular treatment: Thomas Zeller
Surgical treatment: Matthias Thielmann
2.2.1.1 Anatomy of the pulmonary arteries
The right and left pulmonary arteries originate in a shallow bifurcation from the pulmonary trunk, which is approximately 5 cm long and 3 cm wide and lies in an oblique cranial position. The start of the trunk is marked by the pulmonary valve, which like the aortic valve is formed by three semilunar cusps. The three pockets formed in this way do not lead to any distension of the initial part of the trunk, however, since the systolic pressure in the pulmonary system is much lower than in the aorta. The walls of the large pulmonary arteries are accordingly slightly less robust comparatively and only contain a strong elastic fibrous lattice instead of an internal elastic membrane.
The trunk initially lies anterior to the ascending aorta and then ascends on the left side of it where it then divides under the aortic arch, which is then already located outside of the pericardium. The slightly longer and slightly wider right pulmonary artery passes behind the ascending aorta and superior vena cava, but in front of the right mainstem bronchus and esophagus, in an oblique dorsal course to the hilum of the right lung. The left pulmonary artery also crosses at a slightly oblique angle on the short path into the hilum of the left lung. Just after the division of the two pulmonary arteries, the ligamentum arteriosum connects the left pulmonary artery with the inner contour of the aortic arch. This “ligament,” which has highly variable alignments, is the rudimentary residue of the fetal ductus arteriosus (Fig. 2.2-1).
Fig. 2.2–1 Anterior view of the pulmonary arteries.
Before the division into the lobar branches, the trunk of the right pulmonary artery reaches its furthest cranial point in the hilum; on the left side, this occurs at the left mainstem bronchus. The primary branches of the two pulmonary arteries cross the bronchial tree ventrally and then enter the pulmonary lobes centrally along with the bronchi. Along with the bronchi, they divide further into the segmental arteries, which also lie centrally.
2.2.1.2 Clinical picture
The pathoanatomic correlate for pulmonary artery embolism is occlusion of the pulmonary arteries by thrombi (or rarely by fat, air, foreign bodies, tumor, or amniotic fluid) from another vascular region. The extent of the vascular obstruction and underlying cardiopulmonary function determine the severity and thus the mortality of pulmonary artery embolism.
Acute pulmonary embolism is the third most frequent cardiovascular disease; in the U.S. alone, it has an annual incidence of approximately 500,000 and is responsible for 200,000 deaths per year. In Germany, pulmonary embolism has a reported incidence of approximately 100,000 per year (one to three per 1000 inhabitants), with 20,000–30,000 of these cases having a fatal course, and it affects 0.1–0.4% of hospitalized patients, 12–14% of postoperative deaths and 45–90% of all deaths within 2 h.
Massive and fulminant acute pulmonary embolism (Grosser stages III and IV) as a sequela of deep venous thrombosis is life-threatening and has an overall mortality rate of more than 30%, with 50% of deaths occurring within the first 30 min, 70% within the first hour, and more than 85% within the first 6 h after the onset of symptoms. Particularly in patients requiring resuscitation, the prognosis without immediate revascularization treatment is unfavorable. Rapid diagnosis and appropriate therapy are therefore decisive for saving the patient’s life. Developments in fibrinolytic and percutaneous treatment have increasingly pushed surgical treatment for acute massive and fulminant pulmonary embolism into the background.
For chronic recurrent pulmonary embolism, see section A 2.2.2.
2.2.1.3 Diagnosis
Clinical findings
The clinical probability of pulmonary embolism and deep venous thrombosis is estimated as described above.
ECG
Laboratory findings
– Negative findings (< 500 μg/L) practically exclude pulmonary embolism; i.e., in 30% of patients with emergency admission, but fewer than 10% of inpatients, pulmonary embolism can be excluded using d-dimer assessment.
– Caution: d-dimers are also raised in infection, inflammation, carcinoma, status post surgery, cardiac insufficiency and renal insufficiency, acute coronary syndrome, pregnancy, and sickle-cell crisis.
– Troponin: evidence of hemodynamically significant pulmonary embolism, right ventricular enlargement, right cardiac ischemia
– Protein C
– Protein S
– Angiotensin III
– APC resistance
– Rheumatism serology, including anticardiolipin
Chest x-ray
Nonspecific changes include:
