Anatomy clinical correlates: Heart

Have you ever wondered what the secret to someone’s heart is? That's right, a chest x-ray! All right, so, here at Osmosis we don't actually have the secret to one’s heart, but we do know how to identify the different medical conditions that can affect the heart.

Let's start off by identifying the heart borders on a chest x-ray. The heart silhouette is between the lungs, and the right border, made up by the right atrium, as well as the left border, made up by the left ventricle and part of the left auricle, can be clearly seen. Above the left auricle, we can identify the pulmonary artery and the aortic arch. And in some clinical circumstances, the silhouette sign can be present, which is when the normal heart silhouette of the heart compared to the lungs is lost. More appropriately, you might want to think about it as a “loss of the heart silhouette”. The loss of the heart silhouette only occurs when the pathological process is in direct anatomical contact with the heart. Usually, the middle lobe is seen close to the right border of the heart. So, consolidation in the right middle lobe can also obscure the x-ray silhouette of the right heart border.

All right, now, even though the heart is protected by the sternum and thoracic cage, it’s still susceptible to injury. During penetrating trauma, like, for example, a stab wound, the right ventricle is the most commonly injured structure because of its anterior position in the chest and the fact that it forms the majority of the anterior surface of the heart, followed by the left ventricle which forms the apex of the heart and may be injured as far laterally as the left midclavicular line at the 5th intercostal space. The atria are less commonly injured than the ventricles. It’s also worth noting that the lungs overlap most of the anterior surface of the heart, so many penetrating injuries to the heart will also result in concurrent lung injury particularly to the parietal pleura.

Are you ready to listen to your heart? We’re now going to talk about heart auscultation! The gist of it is to listen to the areas that best project the sound coming from each heart valve. Blood tends to carry the sounds in the direction of its flow so each area is situated superficial to the chamber or vessel into which the blood has passed and in a direct line with the valve orifice.

Let’s start with the aortic valve, which is located posterior to the left of the sternum at the level of the third intercostal space. To auscultate the aortic valve, you need to move your stethoscope at the second intercostal space, right of the sternal angle. Moving on to the pulmonary valve, it’s located at level of the left third costal cartilage and is auscultated at the second intercostal space, left to the sternal angle. The tricuspid valve is posterior to the body of the sternum to the right side at the level of the fourth and fifth intercostal space, and it’s auscultated at the 4th or 5th intercostal area, left to the sternal edge. The mitral valve is located posterior to the sternum at the level of the fourth costal cartilage to the left and is auscultated at the left 5th intercostal space on the midclavicular line

And now let’s talk about conditions that may affect the heart. First, there’s dextrocardia, which is a rare embryological folding defect where the heart is reversed so the apex is misplaced to the right instead of the left. Dextrocardia is associated with mirror image positioning of the great vessels and arch of the aorta. Basically, everything that normally is on the left is on the right and vice-versa. This condition might be part of something called situs inversus, which is a general transposition of the thoracic and abdominal viscera, or it occurs as isolated dextrocardia, where the transposition only affects the heart. When dextrocardia is associated with situs inversus, the incidence of other cardiac defects is low and the heart usually performs normally. However, in isolated dextrocardia, the congenital anomaly is complicated by severe cardiac anomalies, such as transposition of the great arteries.

Clinically, dextrocardia can be determined by palpating the apex beat over the right chest. Typically the apex beat, which is the most lateral inferior palpable portion of the heart on the chest wall typically found in the 4th or 5th intercostal space at the mid clavicular line, is on the right side. An x-ray can then be done to confirm dextrocardia.

And while dextrocardia is rare, a myocardial infarction, unfortunately, is not uncommon. That’s when an artery of the heart is blocked by an embolus, and the myocardium supplied by the occluded vessel no longer receives blood. If that area can undergo necrosis, resulting in a myocardial infarction. Symptoms of a myocardial infarction include severe crushing chest pain that can often radiate to the back, jaw, left arm, right arm, shoulder, or atypical chest pain that is felt in the abdomen. Associated symptoms include dyspnea, diaphoresis, which means profuse sweating, as well as nausea and vomiting. The three most common sites of coronary artery occlusion are: the anterior interventricular branch of the left coronary artery approximately 40-50% of the time, the right coronary artery approximately 30-40% of the time, and the circumflex branch of the left coronary artery approximately 15-20% of the time.

Now, dominance of the coronary arterial system also affects what areas of the heart are affected during a myocardial infarction, as dominance determines whether the right or left coronary artery gives off the posterior interventricular branch. Therefore, during an occlusion to the right or left coronary artery, dominance will determine if the area supplied by the posterior interventricular branch will be affected.

In 67-85% of people, the right coronary artery gives rise to the posterior interventricular branch. In about 8-15% of cases, the left coronary artery is dominant and the posterior interventricular branch comes from the circumflex artery.

In 7-18% of people, there is codominance and both right and left coronary arteries give rise to branches that run in or near the posterior interventricular groove. So, if the right coronary artery is occluded, then the right atrium, parts of both ventricles and the sino-atrial and atrioventricular nodes are affected along with the area supplied by the posterior interventricular branch which is the inferior adjacent area of ventricles and the posterior third of the interventricular septum. If the left coronary artery is occluded, then the left atrium, along with parts of both ventricles, the AV bundle, the anterior 2 thirds of the interventricular septum, along with the area supplied by the posterior interventricular artery if it is dominant. Also remember, the right coronary artery supplies the SA node via the SA nodal branch 60% of the time, and the AV node via the AV nodal branch when it has dominance, so the loss of blood supply to these two nodes also varies during a myocardial infarction.

Following a myocardial infarction, the conducting system of the heart might be damaged. The left coronary artery gives off the anterior interventricular branch which gives rise to the septal branches that supply the AV bundle in most people. Additionally, the branches of the right coronary artery mainly supply both the sinoatrial and atrioventricular nodes as we have said before. The occlusion of one of these arteries can lead to a heart block. In this case, the ventricles will begin to contract independently at their own rate which is approximately 25 to 30 per minute as they do not receive a signal from the SA or AV node, which is slower than their slowest normal rate of 40 to 45 per minute.

If the sinoatrial node has been spared, the atria continue to contract at the normal rate, but the impulse generated by the sinoatrial node doesn’t reach the ventricles. Damage to either the left or right AV bundle branches leads to a bundle branch block, where excitation passes along the unaffected branch and causes a normal systole of that ventricle only, and the affected ventricle receives conduction via muscle propagation to produce a late asynchronous contraction.