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Straight to the Heart
As EMS providers, we are inundated with information, guidelines and protocols regarding cardiac emergencies and conditions. Even in the absence of a cardiac emergency, patients commonly give a history of a "heart murmur," "a hole in my heart," "mitral valve prolapse" and other cardiac-related conditions. This article provides a review of cardiac anatomy as it relates to conditions you may encounter in the field.
THE BASICS
In its normal position, the heart occupies the inferior part of the mediastinum (chest cavity) with two-thirds of its bulk to the left of midline. The terms "right" and "left" as they refer to the heart are slightly misleading. The heart lies in such a position within the chest cavity that the right atrium and ventricle are, in fact, mostly anterior structures, while the left atrium and ventricle are mostly posterior structures.
The heart is a four-chambered pump that beats approximately 100,800 times per day. The top two chambers are the right atrium and left atrium; the bottom chambers are the right and left ventricles. Blood returns to the heart's right atrium chiefly from three vessels: the superior vena cava, the inferior vena cava and the coronary sinus. The superior vena cava is a large vein that drains blood from the head, arms and chest. The inferior vena cava is a large vein that returns blood from the legs, pelvis and abdomen. The coronary sinus is the vessel into which the cardiac veins drain. These vessels all drain into the right atrium.
Flow of blood through the cardiac circulation starts in the right atrium, with low-oxygenated blood returning from the body, and ends in the left ventricle, with highly oxygenated blood leaving the heart to nourish the body's tissues. Blood flows through the heart's chambers and valves, which act as gates to prevent blood from going backwards.
Blood passes from the right atrium through the tricuspid valve and into the right ventricle. The right ventricle contracts, and the pressure inside the ventricle increases. The pressure surpasses the pressure in the right atrium, closing the tricuspid valve and preventing regurgitation of blood from the right ventricle back into the right atrium. The pressure in the right ventricle rises until it is greater than the pressure in the next stop, a large vessel called the pulmonary trunk. This causes the pulmonic valve to open, allowing blood to eject into the pulmonary trunk. The pulmonary trunk divides into a pair of left pulmonary arteries and a pair of right pulmonary arteries. You may think of arteries as bearing bright red oxygen-rich blood. The pulmonary arteries are unique, as they carry blood that is not highly oxygenated because it has not yet reached the lungs.
So pulmonary arteries bring blood into the lungs, where it is oxygenated and returned to the left atrium by pulmonary veins. The valve between the left atrium and left ventricle is the bicuspid or mitral valve, so named because, to early anatomists, it resembled a bishop's two-pointed hat--the miter. Pressure in the left ventricle soon eclipses that in the left atrium and closes the bicuspid (mitral) valve, preventing regurgitation of blood from the left ventricle back into the left atrium. Soon pressure in the left ventricle rises until it is greater than the pressure in the aorta. This causes the aortic valve to open, allowing oxygenated blood to eject into the aorta and go on to perfuse the body organs.
From the left ventricle, oxygenated blood is pushed up past the aortic valve into the ascending aorta. Note that blood is pumped "up" from the left ventricle into the aorta, not down. The left ventricle is thicker than the right ventricle, as it needs to generate more force to pump blood up into the aorta than the right ventricle does to pump blood "next door" to the lungs.
Attack Facts
According to the American Heart Association, in 2003, there were approximately 1.2 million new and recurrent coronary attacks. About 40% of people who experience a coronary attack in a given year die from it; more than 13 million persons with angina, heart attack and other forms of coronary heart disease are still living. It is estimated that 6.5 million people in the United States suffer from angina. An estimated 400,000 new cases of stable angina occur each year.
CARDIAC VALVES
As noted in the above general anatomy section, four valves within the heart act as gates to prevent backward flow of blood. Proper opening and closing of these valves provide one-directional blood flow through the heart. It is closure of the valves that creates the two basic heart sounds: S1 and S2, or "lub" and "dub." There are certain, specific places where the heart is auscultated to detect murmurs (see Figure 1).
The opening of normal cardiac valves creates no audible sounds. Murmurs are the sounds heard due to improper opening or closing of a valve. A murmur may have no pathological significance, or it may be an important clue to the presence of valvular, congenital or other structural heart abnormalities.
Closing of the mitral and tricuspid valves at the beginning of ventricular systole cause the first part of the "lub-dub" sound made by the heart as it beats. Formally, this first sound is known as "S1." The second part of the "lub-dub" (the second heart sound, or "S2") is caused by closure of the aortic and pulmonic valves at the end of ventricular systole.
Valvular problems are due to stenosis, regurgitation or prolapse. Stenosis is the narrowing of a valve, usually due to a buildup of calcium on the valve. Think of stepping on a flowing garden hose and narrowing that opening. There is increased pressure behind the obstruction and low pressure after it. The bicuspid and tricuspid valves are shaped somewhat like a parachute and are attached to papillary muscle in the underlying ventricle by string-like structures called chordae tendinae (pronounced core-day tendon eye). These tendinae play a role in preventing the cusps or leaflets from billowing up or "prolapsing" into the atrium. Regurgitation is the leakage of blood from one chamber to another due to an incompetent or poorly closing valve. Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to 5% of the mortality after acute MI.1
The most common issue with heart valves is mitral valve prolapse. In the United States, MVP can be identified by echocardiography in 3%-4% of the general population; it is identified in 7% of autopsies.
Acute mitral regurgitation after acute MI predicts poor prognosis. Nevertheless, MR of mild to moderate severity is found in 13%-45% of patients after acute MI.2,3
HOLE IN MY HEART
The left and right sides of the heart are separated by the cardiac septum, similar to how the left and right aspects of the nose are separated by the nasal septum. Essentially, blood in the right-sided chambers of the heart is not as oxygenated as blood in the left-sided chambers because blood in the right side has not yet reached the lungs. A hole, or defect, in the septum causes highly oxygenated blood from the left to mix with poorly oxygenated blood on the right. There can be either an atrial septal defect or ventricular septal defect.
Ventricular septal defects are among the most common congenital heart defects, occurring in between 0.1%-0.4% of all live births, and make up about 20%-30% of congenital heart lesions. Ventricular septal defects are probably one of the most common reasons for referring an infant to a cardiologist. Small ventricular septal defects rarely cause problems.
Fetuses have a normal opening between the left and right atria of the heart--the foramen ovale--which allows blood to bypass the lungs, as oxygenated blood is supplied from the mother. If this opening fails to close naturally soon after birth, an openable flap of tissue, the patent foramen ovale, remains. A patent foramen ovale is detected in 10%-15% of the normal population using echocardiography. The literature is unclear about the importance of a PFO. There appears to be an increased association between PFO and embolic events, such as TIA and stroke. (A patent foramen ovale was found in Israeli Prime Minister Ariel Sharon's heart and blamed for his embolic stroke. It was closed by catheterization.)
Fetuses also have a connection between their pulmonary trunk and the aorta, the ductus arteriosus. Similar to the PFO, this opening normally closes shortly after birth, but in some cases may remain open, where it is termed a patent ductus arteriosus (PDA). Blood flows from the aorta back to the pulmonary trunk, which can overload the lungs.
ELECTRICAL ANATOMY
The heart pumps in response to electrical impulses. We know that when these impulses are disorganized and random, ventricular fibrillation, for example, the heart quivers instead of forcefully contracting.
The impulses start in a tiny area in the right atrium called the sinoatrial (SA) node, which stimulates the atria to contract. The impulse is carried to a second node located in the bottom of the left atrium, the atrioventricular (AV) node. The AV node slows down conduction of the impulse so the ventricles contract after the atria for better cardiac output. This impulse is further transmitted to the bundle of His and down the septum through the right and left bundle branches. You may be familiar with the terms RBBB or LBBB for right or left bundle branch block, respectively. These are two types of electrical conduction disturbances. The impulse is then distributed from the bottom to the top of the right and left ventricles by Purkinje fibers, resulting in one heartbeat (see Figure 2).
Dysrhythmia is the most common complication after acute MI. It is related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium. Premature ventricular contractions occur in approximately 90% of acute MI patients.
CORONARY CIRCULATION
Blood leaves the left ventricle through the aortic valve and enters the ascending aorta, which is the body's main artery. At the very beginning of the ascending aorta are the right and left coronary arteries, which nourish the heart muscle. Occlusion or spasm of these arteries causes angina or myocardial infarction.
The initial segment of the left coronary artery is the left main coronary artery. This blood vessel is approximately the width of a soda straw and is less than an inch long. It branches into two slightly smaller arteries: the left anterior descending (LAD) coronary artery and the left circumflex coronary artery. The left anterior descending coronary artery is embedded in the surface of the front side of the heart. The left circumflex coronary artery circles around the left side of the heart and is embedded in the surface of the back of the heart. The left coronary artery supplies oxygenated blood to the left side of the heart, including the anterior wall of the left ventricle, interventricular septum, right bundle branch and papillary muscles to the mitral valve.
The main portion of the right coronary artery provides blood to the right side of the heart. The rest of the right coronary artery and its main branch, the posterior descending artery, together with the branches of the circumflex artery, run across the surface of the bottom of both ventricles. The right coronary artery supplies the sinoatrial node of the heart in 55% of the population. In 90% of people, the right coronary artery also supplies the atrioventricular (AV) node.
MYOCARDIAL INFARCTION
Myocardial infarction literally means death of heart muscle. Most commonly, infarction occurs when the oxygenated blood supply from the coronary arteries is interrupted. The left ventricle is by far most commonly affected by a myocardial infarction. A right ventricular infarct is rare, and an atrial infarct is so rare it is not even discussed.
Currently, MIs are divided into two categories: STEMI (ST elevation MI) and NSTEMI (non-ST elevation MI). "ST" represents the ST segment of an ECG tracing, which is beyond the scope of the article. NSTEMIs are "heart attacks," but they do not give off the typical electrocardiographic changes associated with MI. NSTEMIs have the hallmark elevations of cardiac enzymes, which are diagnostic of infarction. Clinically, the classification is important, because NSTEMIs do not respond to "clotbuster" thrombolytic therapies.
The inferior wall is located on the surface of the myocardium above the diaphragm. The culprit vessel in inferior myocardial infarction may be either the right coronary artery (in 80% of cases) or the left circumflex artery. Inferior wall MIs are the most common type of infarct. Remember that the right coronary artery is also supplying the atrioventricular node in 90% of the population and the sinoatrial node in 55% of the population, as well as the bundle of His. Therefore, conduction defects, especially AV blocks, are common. A recent review reported a 19% incidence of second- or third-degree heart block in patients with inferior MI.4 Patients who develop this complication are at higher risk of death from their MI. In addition, papillary muscle rupture is most common with an inferior MI, leading to acute mitral valve regurgitation and possibly sudden severe heart failure. Approximately one-third of all inferior-wall MI patients also have damage to the right ventricle.
Infarction involving only the right ventricle is unusual, and the diagnosis is rarely made early in presentation. Right ventricular infarction usually results from occlusion of the right coronary artery proximal to the right ventricular marginal branches, hence its association with inferior-wall infarction. Because the right ventricle is thin-walled and has a low oxygen demand, there is coronary perfusion during the entire cardiac cycle. Therefore, widespread irreversible infarction is rare.5
Anterior wall MIs involve the anterior wall of the left ventricle, which is typically supplied by the left anterior descending artery. The anterior wall MI can be serious due to actual death of left ventricle muscle. Conduction disturbances with wide complex ventricular escape rhythms occur most frequently in large anterior MIs and imply a very poor prognosis. Anterior-wall MI is associated with more myocardial damage than inferior infarcts. An infarction of more than 40% of the left ventricular myocardium is generally associated with cardiogenic shock.6
A posterior-wall MI refers to the dorsal area of the heart, nearer to the back, involving either the left circumflex coronary artery or dominant right coronary artery. Current literature associates approximately 40% of inferior-wall MIs with some posterior wall involvement. Interestingly, standard 12-lead ECGs have demonstrated little usefulness in assessing and diagnosing posterior MIs. As a result, 15- or 18-lead ECGs are being discussed as standard of care for evaluating suspected MI patients (see Figure 3).
Lateral wall MIs involve the wall of the left ventricle, which faces up toward the shoulder. It is supplied by the left circumflex artery. Lateral wall infarcts usually present with little or no symptomatology, and are quite often the "silent" MIs detected on routine ECGs or later on. However, myocardial rupture occurs in 3% of MI patients and accounts for approximately 10% of mortality after MI, with the lateral wall being the most commonly involved.
CONCLUSION
Hopefully, this article has taken some of the mystery out of terms that are commonly heard but not usually explained. By understanding the heart's anatomy, which is relatively straightforward, you can understand cardiac disorders and terminology.
References
- Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction etiologies, management and outcome: A report from the SHOCK Trial Registry. J Am Coll Cardiol 36(3 Suppl A):1063-1070, 2000.
- Barzilai B, Gessler C Jr, Perez JE, et al. Significance of Doppler-detected mitral regurgitation in acute myocardial infarction. Am J Cardiol 61:220-223, 1988.
- Lehmann KG, Francis CK, Dodge HT. Mitral regurgitation in early myocardial infarction. Incidence, clinical detection, and prognostic implications. TIMI Study Group. Ann Intern Med 117:10-17, 1992.
- Clemmensen P, Bates ER, Califf ER, et al. Is complete heart block in inferior infarction a benign phenomenon following reperfusion therapy? (Abstract) J Am Coll Cardiol 13(suppl II):26, 1989.
- Dell'Italia LJ, Lembo NJ, Starling MR, et al. Hemodynamically important right ventricular infarction: Follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange. Circulation 75:996-1003, 1987.
- Page DL, et al. Myocardial changes associated with cardiogenic shock. N Engl J Med 285(3):133-137, 1971.
Rob Curran, DC, EMT, has been an EMT in New York City for over 13 years and is an instructor of pathophysiology at the State University of New York--Downstate Medical Center. He can be reached at rpbda@yahoo.com.
