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.