• Part 1 Approach to the Patient (History and Physical)

• Part 2 Approach to the Electrocardiogram (ECG)

• Part 3 Providers and Procedures

Part 1. Cardiovascular History and Physical Examination

There are four main components of cardiovascular history and physical examination:

1. Taking a cardiovascular history

2. Performing the cardiovascular examination

3. Interpreting heart sounds

4. Evaluating cardiac murmurs

Despite the proliferation of medical technology over the past several decades, there remains no single imaging study or laboratory assay more valuable to patient care than a proper history and physical examination (H&P). A thoughtful H&P will provide you with the correct diagnosis for most patients presenting with cardiovascular disease complaints. The act of performing the H&P also affords the caregiver an opportunity to forge a therapeutic relationship with the patient. The attention paid to a frightened patient by a thoughtful practitioner during the H&P, however brief, can have both diagnostic and therapeutic benefits. Finally, in this current era of cost-conscious medical care, there are few tools as cost-effective as a good H&P.

A. TAKING A CARDIOVASCULAR HISTORY

Prior to entering into a discussion of the cardiovascular history, there are a few general rules of history taking that merit a review. The first is to establish a meaningful rapport with the patient. As the provider, you should be the adaptable member of this relationship as you will need to alter your history-taking approach from one patient to the next to account for differences in individual language comprehension, cultural background, and level of education. The use of medical or technical jargon during the history should be avoided. Similarly, common colloquial medical terms should be carefully scrutinized as they often mean different things to different patients. For example, a patient may tell you that she has had five heart attacks in the past 2 years, but a careful review of her records reveals no evidence of myocardial infarction but rather five emergency department visits for chest pain and severe hypertension in the setting of medication noncompliance.

Another important skill in history taking is the ability to adjust one’s interview style to best suit the patient and setting. It is generally advisable to begin the interview with open-ended questions (eg, "What brings you to the emergency department today, Mr. Smith?") to allow patients to guide you through their histories. However, there are certainly patients who do not provide much open-ended information (eg, "My wife made me come."), in which case direct initial questions may have a higher yield (eg, "Have you been having any chest pain, Mr. Smith?") . It is helpful to repeat the history back to the patient to ensure that the patient agrees with the history as you understand it. This approach tends to give patients a greater sense of involvement in the evaluation process and also an opportunity to edit the history before you proceed with the physical examination.

Finally, it is important to be consistent and thorough in your approach to each element of the cardiovascular history (Table I-1). Every symptom should be assessed for its subjective description and overall level of severity. The timeframe for each symptom, including time of onset, duration, frequency, and pattern of evolution should be ascertained. Whenever possible, one should quantify symptom severity (eg, "On a scale of 1 to 10 how severe was your chest pain?" or "How many yards can you walk before you develop calf pain?"). It is also important to know whether the symptom has any clear triggers or relieving factors. Understanding how symptoms impact the patient's quality of life is also instructive (eg, "We have discussed a number of symptoms, Mr. Jones; which one worries you the most?"). You will occasionally find that the presenting complaint is not the patient's major concern. For example, Mr. Jones may have visited the office today because his wife is worried about his newly swollen ankles, but the most concerning issue to Mr. Smith may be his worsening erectile dysfunction and the tension it is causing in his marriage.

Chest Pain

Chest pain is the most common complaint presented by patients to cardiologists. The differential diagnosis for chest pain is quite broad and includes both cardiac and noncardiac conditions. A full review of the approach to chest pain is beyond the scope of this introductory chapter, but the topic of chest pain is covered as a case file later in this book. In a patient complaining of chest pain, the principal concern is whether the patient is experiencing angina, or chest pain secondary to myocardial ischemia. Chest pain can be classified as typical for angina, atypical for angina, or noncardiac, on the basis of its description, triggers, and response to intervention (Table I-2).

Typical angina pectoris is relatively easy to recognize; unfortunately, many patients with myocardial ischemia lack typical symptoms of angina, especially women and patients with diabetes mellitus. Angina is typically described as diffuse and pressurelike and localizes to the retrosternal area. Dullness and burning are common descriptors of anginal chest pain, and the inability to adequately describe one’s chest pain is also suggestive of angina. The act of balling the fist and holding it against the chest while trying to describe chest pain, called Levine's sign, is actually fairly specific for angina. Pain radiating from the chest to the neck, jaw, or arms is suggestive of angina. Angina typically lasts between 5 and 30 minutes; chest pain lasting for mere seconds or for hours or days without resolution is practically never angina. Angina is usually triggered by physical activity or emotional distress and resolves with rest, relaxation, or sublingual nitroglycerin. Typical chest pain occurring 20–30 minutes after a meal is also consistent with postprandial angina, although this often is mislabeled as esophageal reflux or dyspepsia. Chest pain provoked or worsened by manual palpation is unlikely to be angina.

Angina severity is commonly graded using the Canadian Cardiovascular Society (CCS) classification system (Table I-3). Class 3 or 4 angina is considered to be severe. Recent-onset (within 2 weeks) severe angina is referred to as unstable angina and generally requires hospitalization and immediate medical attention. Angina present for more than 2 weeks that is clearly triggered by predictable physical activity is termed stable angina and is often managed in the outpatient setting.

Another common type of chest pain encountered in patients with heart disease is inflammatory chest pain, which can accompany conditions such as pericarditis, myocarditis, or acute pulmonary thromboembolism. Unlike angina, inflammatory chest pain is typically sharp and focal. It is commonly pleuritic, becoming more severe during inspiration or laying supine and improving with expiration or leaning forward. Pleuritic chest pain that can be reproduced by manual palpation of the chest wall is most likely related to costochondritis. Pulmonary infections such as pneumonia can also produce pleuritic chest pain, although there are often other symptoms that support the diagnosis such as fevers or productive cough. Pulmonary thromboembolic disease can also cause pleuritic plain and should be considered early in the differential diagnosis of any patient with pain and risk factors for venous thromboembolic disease. The combination of severe, tearing, or ripping chest and/ or back pain and hypertension raises the concern for an acute aortic syndrome such as aortic dissection. The evaluation and differential diagnosis of the patient presenting with chest pain is separately discussed later in this book.

Shortness of Breath

Shortness of breath (dyspnea) is another common symptom that can be the presenting complaint for many cardiac diagnoses, including heart failure, valvular heart disease, atrial fibrillation, and even myocardial ischemia. As with angina, we quantify shortness of breath using a four-point scale developed by the New York Heart Association (NYHA; Table I-3). Shortness of breath accompanied by difficulty breathing while supine (orthopnea) or paroxysmal nocturnal dyspnea (PND) is strongly suggestive of increased left atrial pressure, a common feature of heart failure or left-sided valvular heart disease. Associated symptoms such as exercise tolerance and fatigue are also suggestive of shortness of breath due to cardiovascular causes. Heart failure is also frequently accompanied by central volume overload; this may be heralded by symptoms such as leg swelling (edema), weight gain, or tighter-fitting clothes. Excessive somnolence, profound weakness, and a subjective decrease in urine output that accompanies shortness of breath may be features of advanced heart failure with low cardiac output. It should be noted that symptoms attributable to heart failure can be present in the setting of normal left ventricular systolic function. The differential diagnosis of dyspnea is enormous and includes a wide range of cardiac and noncardiac diagnoses. The evaluation and differential diagnosis of the patient presenting with shortness of breath is separately discussed later in this book.

Dizziness and Syncope

Loss of consciousness (syncope) and dizziness are also common cardiovascular complaints with a broad differential diagnosis. These complaints are common in patients presenting with rhythm disorders (both tachy- and bradyarrhythmias) and structural heart disease, particularly conditions that limit ventricular outflow such as aortic or mitral valve stenosis, or hypertrophic cardiomyopathy with dynamic obstruction of the left ventricular outflow tract. Syncope that occurs during or just after physical exertion suggests the presence of reduced outflow. Syncope that is accompanied by palpitations suggests the presence of a tachyarrhythmia. Syncope accompanied by lightheadedness and nausea and followed by diaphoresis suggests a neurocardiogenic cause such as vasovagal syncope. Ominous syncope features include abrupt onset without warning, prolonged unconsciousness, and injury as a result of syncope; these features suggest a high-risk cause for syncope such as a malignant arrhythmia.

Adjunctive History

A complete cardiac H&P should include a thorough noncardiac review of systems. This is important because cardiovascular diseases can have extracardiac manifestations and noncardiac illnesses can have cardiovascular implications. For example, erectile dysfunction in an otherwise asymptomatic patient might suggest the presence of occult vascular disease. Alternatively, a history of rash with swollen and painful joints can indicate the presence of rheumatoid arthritis, a diagnosis associated with an increased risk for many cardiovascular problems including coronary artery disease, pericarditis, and pulmonary arterial hypertension. Some noncardiac conditions are highly prevalent among patients with heart disease, particularly obstructive sleep apnea (OSA). Untreated severe OSA can have a major impact on a patient's general health and quality of life, and for this reason it is important to inquire about the signs and symptoms of OSA during the H&P, including daytime sleepiness, snoring, witnessed apneas, and cognitive impairment.

Another important and often overlooked feature of the H&P involves a thorough review of the patient's medication list for potential drug-drug or drug-food interactions and adverse drug reactions (ADRs). In some cases the patients' presenting complaints may be related to the adverse effects of their prescribed medications. Although some cardiovascular medications have well-described side effects or interaction potential (Table I-4), one must maintain a high index of suspicion for ADRs related to any agent, particularly when a patient has symptoms that are not readily explainable despite extensive evaluation or bear some temporal relationship to a recent hospital discharge, office visit, or other encounter where medications may have been introduced or changed. In keeping with this theme, it is also important to inquire about the use of over-the-counter and alternative medical agents.

B. PERFORMING THE CARDIOVASCULAR EXAMINATION

The physical examination of the cardiac patient, particularly cardiac auscultation, has intimidated medical students and residents alike since the invention of the stethoscope by Dr. René Laennec in 1816. The process of examination and cardiac auscultation can be challenging, but the experience need not be stressful if one has a solid understanding of cardiovascular physiology, a good stethoscope, a quiet examination area, patience, and a bit of curiosity. Like most things in life, good examination skills develop with practice over time. You should also appreciate the limitations of the physical examination; even the most experienced cardiologist will miss a soft diastolic murmur in a tachycardic, morbidly obese patient on mechanical ventilation in a noisy intensive care unit. Whenever possible, it is useful to compare your examination findings to the findings of dynamic cardiac studies such as echocardiograms and magnetic resonance images (MRIs). Did you miss the murmur of the severe, posteriorly directed mitral regurgitation that was seen by echocardiography? Go back and listen to the patient again, armed with the knowledge of the imaging study. You will probably hear the murmur and be able to recognize it when you admit your next patient with severe mitral regurgitation.

Nonauscultory Examination

The cardiovascular examination should begin with a general inspection of the patient and the patient's chest. You should note any obvious abnormalities, as these may provide you with diagnostic clues. Does the patient have any scars indicative of prior cardiac surgery? Is there an implanted cardiac device? Are there any chest wall deformities that might indicate a congenital disorder such as Marfan syndrome (pectus excavatum or carinatum) or Turner syndrome (shield-shaped chest)?

Blood pressure measurements should be obtained from both arms and compared; differences in systolic and diastolic blood pressures of greater than 10 or 5 mmHg, respectively, are considered abnormal and may warrant further investigation for disorders such as aortic dissection or subclavian stenosis. If one suspects the diagnosis of aortic coarctation, then bilateral lower extremity blood pressure measurements should also be obtained.

Jugular Veins Examination of the right internal jugular vein allows for estimation of a patient's central volume status and provides clues for the diagnosis of right-sided heart disease and pericardial disease. The right internal jugular vein is best examined with the patient seated at a 45° angle. It is noteworthy that, in patients with marked central volume overload, the top of the venous column of blood (meniscus) may not be visible until the patient is seated upright at 90°. Similarly, patients with low filling pressures may not exhibit a visible meniscus until they are nearly flat (180°).

To estimate the right atrial pressure, the examiner measures the distance between the sternal angle (angle of Louis) and the meniscus of the jugular pressure wave (Figure I-1). The jugular venous pulsation may be distinguished from the carotid pulse by applying gentle tension to the overlying skin with your finger; this should obliterate the venous pulse, whereas the arterial pulse should remain visible. The center of the right atrium is approximately 5 cm below the angle of Louis, so the measured distance (in centimeters) between the angle of Louis and the meniscus plus 5 cm approximates right atrial pressure. Normal jugular venous pressure is 8 cm or less. Recall that 1 cm H₂O is equivalent to 0.735 mmHg.

Increased jugular venous pressure is indicative of high right atrial pressure, and this finding can suggest several cardiac diagnoses, including left or right ventricular failure, tricuspid valve disease, and pericardial disease. During inspiration the normal right heart will dilate in response to negative intrathoracic pressure and accommodate more venous flow, resulting in a decrease of the jugular venous pulse (JVP). A paradoxical increase in the JVP during inspiration is called Kussmaul's sign, and this finding is indicative of abnormal right ventricular filling. Kussmaul's sign can be seen with pericardial disease (constriction and tamponade), restrictive cardiomyopathies, and advanced right ventricular systolic failure. The response of the jugular venous pulse to prolonged abdominal palpation, termed hepatojugular reflux or the abdominojugular test, can also be a useful examination tool. With this maneuver, the JVP is observed during and after at least 10 seconds of sustained firm palpation over the right upper quadrant or midepigastrium. This maneuver will increase venous return to the heart. A normal heart can quickly accommodate the extra preload, and the JVP will increase momentarily before returning to normal. Conversely, a patient with a sustained increase in JVP of >4 cm or an abrupt decrease in JVP of >4 cm on release of abdominal pressure is considered to have an abnormal response. Abnormal abdominojugular testing correlates with increased pulmonary capillary wedge pressure and is typically seen in patients with left ventricular failure.

The normal jugular vein has two visible waves, the A and V waves (Figure I-2). A third small c wave is measurable invasively but is practically never seen on physical examination. The c wave is essentially a ripple in the jugular waveform caused by the upward motion of the tricuspid valve during early right ventricular systole. The A and V waves are followed by negative pressure deflections, called the x and y descents, respectively. The A wave occurs just before the first heart sound (S1) and is caused by atrial contraction. If the patient has a fourth heart sound, the A wave will occur simultaneously with the S4. The x descent occurs during atrial relaxation after closure of the tricuspid valve. The V wave is the result of right atrial filling during ventricular systole and is normally smaller and broader than the A wave. The V wave is followed by the y descent, which is caused by emptying of the right atrium after opening of the tricuspid valve in early diastole.

Abnormalities of the right internal jugular venous waveforms are directly related to right-heart pathology. Consistently large A waves are present in disorders that result in right atrial pressure overload such as tricuspid stenosis or pulmonary hypertension. Intermittently large A waves, called "cannon A waves," can be seen during arrhythmias when the right atrium contracts while the tricuspid valve is closed. Complete absence of the A wave occurs when there is no atrial contraction such as in atrial fibrillation. Large V waves indicate volume overload of the right atrium during ventricular systole; this most commonly occurs with tricuspid regurgitation but can also be seen in patients with atrial septal defects. The x and y descents are often affected by pericardial diseases. In pericardial tamponade one typically sees a prominent x descent because the contracting right ventricle occupies less space within the fluid-engorged pericardial sac during systole, reducing the pericardial pressure around the adjacent right atrium and allowing it to expand in size. During diastole, pericardial pressure is highest as the ventricles expand and passive flow between the right atrium and ventricle practically stops, producing an absent or significantly blunted y descent. In pericardial constriction, hemodynamic changes occur more as the result of tethering of the cardiac chambers to the noncompliant pericardium. The x descent is steep because the right atrium is pulled toward the contracting right ventricle during systole, expanding its size. The y descent is also prominent because the resting early diastolic pressure in the right ventricle is typically much lower than the resting right atrial pressure, resulting in rapid early diastolic filling. The y descent abruptly ends by middiastole in constrictive pericarditis as the pressure hits a plateau ("square-root sign") because the thickened pericardium limits full expansion of the right ventricle. CLINICAL PEARL

• Examination of the internal jugular vein using oblique illumination by a penlight can often make the jugular venous pulse easier to see.

Arterial Pulse The normal arterial pulse has an initial brisk upstroke followed by a systolic peak that corresponds to early ventricular ejection (Figure I-3). This is followed by a decline in systolic pressure as the elastic aortic walls expand to accommodate the systolic pressure wave. Aortic valve closure produces the incisura, a small wave that appears at the end of the systolic pressure tracing in central aortic tracings but appears later in peripheral arterial tracings as the wave is transmitted down the arterial tree. Following systolic ejection, arterial runoff results in a decrease in atrial pressure during early diastole while pressure recovery due to the elastic recoil of the artery produces a plateau phase in the pressure tracing in late diastole.

Arterial pulses should be assessed for their contour, intensity, and timing relative to apical systolic ejection. Pulses with two palpable systolic peaks (bisferiens) can be due to dynamic left ventricular outflow obstruction or the combination of aortic valve stenosis and severe regurgitation; the latter is typically associated with a widened pulse pressure. In contrast, low-volume pulses with palpable peaks in systole and early diastole are common in low-cardiac-output states and are referred to as dicrotic pulses. A weak pulse (parvus) with a delayed peak (tardus) is the hallmark of severe aortic stenosis. A palpable low-frequency vibration over a peripheral artery (thrill) is indicative of peripheral arterial stenosis.

Peripheral pulses can also vary with the respiratory cycle. A small (<10 mmHg) decrease in systolic pressure during inspiration is considered normal, but variation greater than this (pulsus paradoxus) occurs in conditions such as pericardial tamponade, advanced systolic heart failure, or severe obstructive pulmonary disease. Interbeat variability of pulse intensity (pulsus alternans) can occur in advanced left ventricular systolic failure or as a consequence of frequent ectopic ventricular beats (ventricular bigeminy).

Precordial Palpation Palpation of the chest can provide useful diagnostic information. The patient should be examined in the supine and left lateral decubitus positions, and palpation should be performed over the LV apex and across the upper and lower portions of the sternum with the hand covering the left and right parasternal areas. Normal palpation is straightforward; the examiner will feel nothing other than the LV apical impulse, which should feel like a gentle tap against the finger in the 5th intercostal space near the midclavicular line during early systole. The apical impulse should be approximately 2 cm in diameter and brief. Abnormalities of apical palpation are described in Table I-5. Please note that the apical impulse and point of maximal impulse (PMI) are not synonyms, although the apical impulse is the PMI in normal patients.

Palpable impulses adjacent to the sternum are abnormal and should be noted. Impulses felt at the lower sternal border are usually caused by anterior motion of the right ventricle. A sustained lower apical impulse during systole can be seen with RV pressure overload in conditions such as pulmonic stenosis or pulmonary hypertension. Rarely, severe mitral regurgitation can produce a vigorous systolic pulse at the lower sternal border due to displacement of the right ventricle by an enlarged left atrium; posterior displacement of the left atrium is hindered by the spine. A dynamic, sometimes visible lower apical impulse during diastole can be seen with atrial septal defects or severe pulmonic regurgitation. Upper sternal border impulses are usually caused by enlargement of the great arteries. Pulmonary artery enlargement or increased pulmonary artery flow can produce a left upper sternal border pulsation, whereas palpable pulses at the right upper sternal border are usually due to aortic enlargement.

Cardiac Auscultation

To understand what you are hearing during cardiac auscultation, it is imperative that you understand what the valves and chambers are doing throughout the cardiac cycle and that you can readily identify systole and diastole (Figure I-4). Systole occurs between the first and second heart sounds and generally has a fixed duration. Systole includes an early period of isovolumic contraction of both ventricles followed by the opening of the semilunar valves (aortic and pulmonic valves) and ventricular ejection. The atria are filling during systole.

Diastole occurs between the second and first heart sounds, and its duration varies with heart rate; at normal heart rates [under 100 beats per minute (<100 bpm)], diastole is discernibly longer than systole, but in patients with tachycardia, systole and diastole can be of equal duration, which complicates differentiation of the cardiac cycle. Simultaneous palpation of the carotid pulse can help you identify systole in this case. Diastole includes an early period of isovolumic ventricular relaxation followed by opening of the atrioventricular (AV; mitral and tricuspid) valves and ventricular filling. The atria empty at this time with atrial contraction occurring in late diastole.

C. INTERPRETING HEART SOUNDS

The normal heart sounds are composite sounds meaning that they arise from events occurring on the right and left sides of the heart. The first heart sound (S1) is caused by closure of the mitral and tricuspid valves, while the second heart sound (S2) is caused by closure of the aortic and pulmonic valves. Splitting of S1 into its mitral and tricuspid components is normal but difficult to hear with a stethoscope. Pathologic splitting of S1 occurs in patients with right bundle branch block and Ebstein's anomaly. The left ventricle is the higher-pressure side of the heart, and the sounds originating from left-sided events such as mitral or aortic valve closure tend to dominate S1 and S2, respectively. The low-pressure right ventricle produces softer contributions to S1 and S2, and in a normal patient the sounds produced by closure of the tricuspid and pulmonic valves can be difficult to discern from their left-sided counterparts. However, the thin-walled right ventricle is influenced by fluctuations in intrathoracic pressure, and this can be appreciated during auscultation. With inspiration, S2 commonly splits into its aortic (A2) and pulmonic (P2) components with fusion of these components during expiration. S2 can best be appreciated in the 3rd intercostal space along the left sternal border (Erb's point; Figure I-5). Numerous pathologic states can affect the intensity and timing of S2 (see Table I-6). As before, the most important task in this chapter is to understand the physiology involved in these heart sounds and how pathophysiologic changes alter what you hear.

The relative intensities of S1 and S2 have diagnostic use. The intensity of S1 is reduced by reduced left ventricular systolic function, left bundle branch block, early mitral valve closure due to severe aortic regurgitation, and first-degree AV block. S2 is loud in mitral stenosis with a pliable valve, hyperdynamic left ventricular systolic function, and in patients with short PR intervals. A soft S2 is common in patients with reduced aortic or pulmonic valve mobility, whereas a loud S2 is often driven by the P2 component in patients with severe pulmonary hypertension.

The third heart sound (S3) is a low-pitched sound that occurs shortly (120–200 ms) after S2. S3 occurs as the result of rapid, turbulent flow into the ventricle in early diastole as a result of high atrial pressure (AV valve regurgitation, ventricular failure) or a ventricular septal defect. S3 is best heard with the bell of the stethoscope at the apex during expiration (for left ventricular S3) or the left lower sternal border during inspiration (for right ventricular S3).

The fourth heart sound (S4) occurs in late systole just before S1. It is also a low-pitched sound best heard with the bell of the stethoscope. S4 is caused by turbulent filling of the ventricle in late diastole during atrial contraction; patients in atrial fibrillation cannot have an S2. The presence of S4 correlates with increased left ventricular stiffness and is commonly seen in conditions such as systemic hypertension, severe aortic stenosis, hypertrophic cardiomyopathy, and myocardial ischemia.

Some abnormal heart sounds are fairly specific indicators of certain cardiac diagnoses. The "opening snap" (OS) is a brief, high-pitched sound heard in early diastole in patients with stenosis of the mitral or (less commonly) tricuspid valve. Patients with left atrial myxomas can present with a middiastolic tumor "plop" that can be distinguished from the opening snap by its very low pitch, best heard with the bell of the stethoscope. The OS associated with mitral stenosis is heard best at the lower left sternal border and radiates to the base of the heart. The presence of an OS implies that the mitral valve remains somewhat pliable; in advanced stenosis of a heavily calcified mitral valve, the OS typically disappears. The time interval between S2 and the OS, which represents the period of isovolumic relaxation, is inversely proportional to the severity of mitral stenosis, although any process that increases LA pressure can affect the S2-OS interval. The OS can be distinguished from a split S2 by having the patient stand during auscultation; the S2-OS should widen as preload decreases, but a split S2 should not change in duration. Clicks are also heard during cardiac auscultation. Early systolic or ejection clicks occur just after S1 and reflect abnormal semilunar valve opening or robust early systolic flow across a semilunar valve. Causes of ejection clicks include bicuspid aortic valve, congenital pulmonic valve disease, or dilatation of the aortic root or pulmonary artery. Midsystolic clicks are most commonly caused by mitral valve prolapse. Mitral valve clicks are affected by left ventricular loading conditions; decreasing preload by standing or performing the Valsalva maneuver will produce an earlier click, while increased preload from squatting or leg elevation will result in a later click.

Pericardial friction rubs can be heard in patients with active pericardial inflammation. The classic rub has three components heard in late diastole, systole, and early diastole. Friction rubs have a characteristically "squeaky" sound that is best heard with the patient leaning forward during inspiration. Friction rubs are notoriously transient accumulation of a pericardial effusion.

D. EVALUATING CARDIAC MURMURS

Blood flow within the heart is generally laminar and quiet. Murmurs are produced by turbulent flow between cardiac chambers or across cardiac valves and in most cases indicate some sort of pathology. Murmurs can be caused by valve stenosis, valve regurgitation, or abnormalities within the cardiac chambers due to some form of obstruction (hypertrophic cardiomyopathy) or shunt [atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA)].

Murmurs are classified principally by the phase of the cardiac cycle during which they occur (systolic, diastolic, or continuous) and can be further subcategorized by their timing within each phase (late systolic, holodiastolic, midpeaking systolic). The shape or contour of the murmur is commonly described and refers to the pattern of the murmur's intensity (crescendo, decrescendo, crescendo-decrescendo, or diamond-shaped or plateau). The subjective description a murmur's sound is also helpful (low-pitched/rumbling versus high-pitched/musical). The location of the murmur on the chest wall is also important in identifying the source of the murmur (Figure I-5). In certain circumstances it is helpful to have the patient perform maneuvers during auscultation in order to alter loading conditions. For example, right-sided murmurs typically vary much more in response to the respiratory cycle or Valsalva maneuver than left-sided murmurs. Although aortic stenosis and hypertrophic cardiomyopathy (HCM) both produce harsh systolic murmurs at the right upper sternal border, the murmur of HCM is dynamic and will soften with handgrip and become louder with the Valsalva maneuver.

Systolic murmur intensity is graded using a six-point scale (Table I-7). Grade 1 systolic murmurs are barely audible with a stethoscope and are most commonly due to increased transvalvular flow rather than actual valve pathology. Conversely, grade 6 murmurs are loud enough to be heard with the stethoscope off the chest wall, and in some cases they are audible without a stethoscope. A systolic murmur that is grade 4 or louder is associated with a palpable thrill. Diastolic murmurs are usually graded on a four-point scale (Table I-7). Diastolic murmurs are always abnormal and warrant investigation.

Systolic Murmurs

Most murmurs during systole arise from stenosis of the semilunar valves (aortic and pulmonic) or regurgitation of the atrioventricular valves (AV valves; mitral and tricuspid) (Figure I-6). Systolic murmurs also occur as the result of ventricular septal defects and dynamic obstruction of the left ventricular outflow tract in patients with HCM. The duration of the murmur in systole is important in the identification of systolic murmurs.

Holosystolic murmurs begin early in systole and tend to last for the duration of systole. AV valve regurgitation and ventricular septal defects are the main causes of holosystolic murmurs. Regurgitant AV valves tend to produce decrescendo, high-pitched murmurs, whereas murmurs due to VSD tend to be plateau-shaped. The pitch can vary greatly with the size of the defect and the systolic pressure gradient between the ventricles.

Midsystolic murmurs are most commonly caused by stenosis of the semilunar valves or dynamic left ventricular outflow tract (LVOT) obstruction. These murmurs are usually diamond-shaped and tend to have lower pitch than holosystolic murmurs. Soft midsystolic murmurs are often called "innocent" (innocuous) murmurs and are usually due to increased flow across a normal pulmonic valve. The murmur of aortic stenosis is harsh, and with severe stenosis, the murmur can obscure the second heart sound and radiate to the carotid arteries. The murmur of HCM with LVOT obstruction can be similar to that of aortic stenosis, but the diagnosis can nonetheless be made reliably by physical examination. HCM causes dynamic obstruction, so maneuvers that reduce left ventricular preload and/or afterload (Valsalva, use of amylnitrite) will increase murmur intensity, whereas maneuvers that increase ventricular preload and/or afterload (handgrip, squatting) soften the murmur. Aortic stenosis causes fixed obstruction, and thus the murmur remains unchanged during these same maneuvers. The murmur of HCM generally originates along the left lower sternal border and rarely radiates to the carotids, whereas aortic stenosis murmurs are loudest at the base of the heart and commonly project to the carotids.

Late systolic murmurs (murmurs that begin after midsystole) are uncommon and are best heard at the left ventricular apex. They can be due to mitral regurgitation caused by prolapse, and in this circumstance they may follow the midsystolic click. Late systolic murmurs can also be heard in patients with advanced ischemic heart disease, possibly as a result of mitral valve dysfunction caused by papillary muscle ischemia.

Pansystolic murmurs are typically caused by ventricular septal defects (VSDs). VSD murmurs often have a rectangular profile and an associated thrill, but their loudness and contour are heavily influenced by the pressure difference between the ventricles and the size of the defect.

Diastolic Murmurs

Diastolic murmurs are typically caused by stenosis of the atrioventricular (AV) valves or regurgitation of the semilunar valves (Figure I-7).

Early diastolic murmurs begin immediately after S2 and are caused by regurgitation of the semilunar valves. These murmurs are typically decrescendo in contour and high-pitched; they are best heard with the diaphragm of the stethoscope. The murmur of aortic regurgitation can be faint and difficult to hear. Maneuvers that increase afterload such as grip will increase the severity of aortic regurgitation and produce a louder murmur.

Middiastolic murmurs are most often caused by stenosis of the AV valves. These diastolic filling murmurs are low pitched or "rumbling" and typically loud. They tend to have a decrescendo-crescendo contour and are best heard with the bell of the stethoscope. The severity of AV valve stenosis is reflected more by the duration of the murmur than the murmur's loudness, which is proportional to transvalvular flow. A classic example of a middiastolic murmur is the murmur of mitral stenosis. The murmur of mitral stenosis begins with the opening snap (OS) and it is most clearly heard at the left ventricular apex. As the severity of mitral stenosis increases, the OS occurs earlier in diastole and the length of the murmur increases. At the same time there is a decrease in cardiac output that results in a decrease in murmur intensity.

Severe, acute aortic regurgitation can sometimes result in a middiastolic murmur due to diastolic mitral regurgitation. Diastolic mitral regurgitation occurs when left ventricular diastolic pressure exceeds left atrial pressure due to high-volume regurgitation, resulting in reversal of flow from the left ventricle to the left atrium. In chronic severe aortic regurgitation, this same phenomenon can occur in late systole as the left ventricle dilates in response to chronic volume overload. The late systolic murmur of diastolic mitral regurgitation caused by severe chronic aortic regurgitation is commonly referred to as the Austin-Flint murmur.

Late diastolic or presystolic murmurs begin just after atrial contraction and are caused by stenosis of the AV valves. These murmurs are low-pitched and rumbling but tend to have a crescendo contour and peak just before S1, which is usually increased in intensity. These murmurs cannot be heard in patients with atrial fibrillation.

Continuous Murmurs

Continuous murmurs are caused by abnormal flow throughout the cardiac cycle and are typically due to abnormal arteriovenous communications within the chest such as a patent ductus arteriosus, acquired or congenital arteriovenous fistulae, or anomalies of the coronary arteries. These murmurs tend to be loudest in systole, peaking in intensity with the second heart sound but with an audible component throughout diastole as well.

Part 2. Approach to the Electrocardiogram (ECG)

Three major topics are covered as follows:

1. ECG fundamentals

2. Approach to ECG interpretation

3. The ECG in cardiovascular disease

A. ECG FUNDAMENTALS

The 12-lead electrocardiogram (ECG) has endured throughout the years as the cardiologist's primary diagnostic tool. Although the ECG certainly has its limitations, the wide availability of bedside electrocardiography combined with its low cost and lack of risk has kept the ECG on the frontlines in the war against cardiovascular disease. Major management decisions in cardiology such as the late-night activation of the cardiac catheterization laboratory or the use of potent fibrinolytic therapy are made based on one’s interpretation of the ECG. For this reason it is essential that all physicians who care for patients with or at risk for cardiovascular disease have some basic understanding of electrocardiography and ECG interpretation.

ECG Setup

The ECG is a skin-surface recording of the extracellular electrical potentials produced by deeper cardiac tissues. The 12 individual leads on a standard surface ECG represent the same electrocardiographic events captured over the same period of time but from differing electrical "viewpoints" determined by the location of the lead and its polarity. The ECG itself can be regarded as a graph with voltage plotted on the Y axis (ordinate; vertical axis) and time plotted on the X axis (abscissa; horizontal axis). The appearance of ECG paper is standardized and consists of large 5×5-mm square boxes that each contain 25 1×1-mm boxes as shown in Figure I-8. At standard paper speed (25 mm/s) and standard voltage calibration (10 mm/mV), each large box represents 200 ms on the X axis and 0.5 mV on the Y axis, whereas the smaller boxes represent 40 ms and 0.1 mV on the X and Y axes, respectively.

The resting ECG is performed with the patient supine. Adhesive stickers or clips are placed on the patient's left arm, right arm, left leg, and right leg, and these are attached to their corresponding wires labeled LA, RA, LL, and RL, respectively. The right leg electrode is inert and can be considered a "ground." A second series of stickers are placed across the anterior chest wall starting at the right upper sternal border, and these are attached to their corresponding wires, labeled V1–V6. When all wires have been attached to their respective electrodes, the ECG is recorded with the patient remaining motionless and supine. Data acquisition takes approximately 12 seconds, and the machine prints the 12-lead tracing immediately after data acquisition. Most ECG tracings are printed with the six bipolar (limb) leads oriented to the left and the six unipolar (precordial) leads oriented to the right; the waveforms in each lead represent the same 3-second timespan (Figure I-9). Along the bottom of the tracing one may see three "rhythm strips," which are standard leads displayed continuously for the full 12 seconds. Leads V1, II, and V5 are typically shown as rhythm strips, but the operator can program the machine to display the ECG data in any number of ways. The voltage calibration and paper speed can be adjusted by the operator as needed; this information is printed along the bottom of the page and graphically displayed (a rectangle 10 mm high and 5 mm wide for standard settings) to the left of each row.

ECG Leads

There are 12 ECG leads: six limb leads and six precordial leads. The limb leads are so named because each lead has its positive pole on either arm or the left leg. The precordial leads are named for their location across the anterior chest wall.

The issue of lead polarity is important because it relates to perhaps the most important fundamental principle of electrocardiography; a positively charged wave-front moving toward a positive pole produces an upright deflection on the ECG. Similarly, a positively changed wavefront moving away from a positive pole produces a negative ECG deflection. In the normal heart the depolarization wave starts in the sinoatrial node and spreads via the atria to the atrioventricular node, then through the His bundle to the bundle branches and ventricles. The path of normal conduction is therefore from right to left and from base to apex. A lead with its positive pole at the apex (lead II) will have upright atrial and ventricular waveforms because the depolarization wave is moving toward the positive pole. A lead with its positive pole at the right arm (lead aVR) will have inverted waveforms because the wavefront is moving away from the positive pole.

The orientation and polarity of the limb leads are shown in Figure I-10a. The limb leads are oriented across the chest in the frontal plane like the spokes of a wheel. There are three bipolar limb leads, labeled I, II, and III. Lead I represents the potential difference between the left arm (positive pole) and right arm and its positive pole is located at 0°. Lead II represents the potential difference between the left leg (positive pole) and the right arm and is located at 60°. Lead III represents the potential difference between the left leg (positive pole) and left arm and is located at 120°. There are three additional limb leads referred to as augmented leads. The augmented leads represent the potential difference between electrodes on the right arm (aVR), left arm (aVL), and left foot (aVF), and a common reference electrode (Wilson's central terminal). Wilson's central terminal is created by connecting the remaining limb leads via resistors oriented in series. This results in a zero-potential reference electrode that acts as a negative pole; the positive pole for each of these leads is the named limb electrode. The use of a zero-potential reference electrode produces a smaller potential difference for these leads than their bipolar counterparts, so the signals are augmented for better detection.

The precordial leads are oriented in the horizontal plane from right to left across the chest (Figure I-10b) and represent the potential difference between the anterior chest wall and Wilson's central terminal. The surface electrodes are the positive poles for these leads, and because of their proximity to the heart, they do not require augmentation.

The Normal ECG

The ECG events that occur during a typical cardiac cycle are shown in Figure I-11. Another important concept in ECG interpretation is the understanding that QRS voltage is proportional to mass. The QRS is the largest complex on the ECG because it represents depolarization of the most massive cardiac structure, the left ventricle. Right ventricular depolarization is also represented by the QRS, but in the normal heart the right ventricle is only one-third the mass of the left ventricle so the size and contour of the QRS complex is dominated by the left ventricle. Other structures such as the His bundle are too small to produce a deflection on the surface ECG (although the His bundle can be visualized on an invasive intracardiac electrogram).

The P wave represents activation of the atria. It begins with firing of the sinoatrial node (SAN), which is located in the right atrium near the insertion of the superior vena cava. The depolarization wave spreads from the right atrium to the left atrium across the interatrial septum via organized tracts of tissue that allow both atria to depolarize nearly simultaneously. The P wave is normally 80–00 ms in duration and less than 2.5 mm (0.25 mV) in amplitude. Repolarization of the atria is not seen on the surface ECG because it occurs during ventricular activation and is hidden within the QRS.

The PR interval represents the time from the onset of the P wave to the onset of the QRS complex. This interval includes conduction through the atrioventricular node (AVN). The AVN is too small to produce a deflection on the surface ECG but the health of the AVN is assessed by the duration of the PR interval. The normal PR interval is 120–200 ms in duration.

The QRS complex represents ventricular depolarization. The positively changed depolarization wave spreads to the ventricles quickly via the left and right bundle branches before propagating cell to cell through specialized ventricular myocytes from the endocardium to the epicardium. The QRS duration is relatively short in a normal heart (60–100 ms). The QRS complex shown in Figure I-12 is a contrived one; the appearance of the QRS varies from lead to lead, and Q waves are not uniformly present. Small Q waves can be normal variants in most leads except leads V1–V3; the normal Q wave is felt to represent left-to-right depolarization of the interventricular septum.

The ST segment begins with the end of the QRS complex at the J point and ends with the onset of the T wave. The ST segment represents the period of time when the ventricles are fully depolarized, and in a normal heart this segment is isoelectric and level with the PR and TP segments. Myocardial ischemia and metabolic abnormalities can create electrical currents during this "quiet time" that can cause the ST segment to deviate.

The T wave represents repolarization of the ventricles. The normal T wave is oriented in the same direction as its preceding QRS complex because repolarization occurs in the opposite direction (negative wavefront moving epicardial to endocardial) as depolarization (positive wavefront moving endocardial to epicardial).

The QT interval begins with the onset of the QRS complex and ends with the end of the T wave. The QT interval represents the total time needed for depolarization and repolarization of the ventricles. The QT interval decreases as the heart rate increases and can be corrected (QTc) by the using the Bazett formula: QTc = QT/√RR, where RR is the interval between the two R waves on either side of the QT interval measured. A normal QTc is between 350 and 440 ms.

The U wave is a deflection that is sometimes seen on a normal ECG after the T wave. The U wave appearance is similar to that of the T wave, but the U wave is much smaller. The origin of the U wave is unclear but may represent repolarization of the mitral papillary muscles or the Purkinje fibers.

B. APPROACH TO ECG INTERPRETATION

There is no right or wrong way to read an ECG provided that the reader's approach is consistent and complete. Every ECG needs to be assessed for the features described in the paragraphs below; the order of that assessment is up to the individual reader. Clinical information is of major importance for correct ECG interpretation; whenever possible, one should know the patient's age, gender, and presenting complaint. A prior ECG for comparison is also extremely valuable, particularly in patients with chest pain and abnormal ST segments.

Rhythm

Assess each ECG to determine whether the rhythm is normal. Normal sinus rhythm is defined by the presence of sinus P waves (upright P waves in II, III, and aVF) that precede each QRS complex. The normal sinus rate is 60–100 bpm; bradycardia is defined as a heart rate < 60 bpm and tachycardia is defined as a heart rate > 100 bpm.

Heart Rate

The heart rate on the ECG can be calculated by noting the time interval between two R adjacent waves (provided that the rhythm is regular). Recall that if the paper speed is standard at 25 mm/s, then the time interval of one large square is 200 ms and the time interval of one small box is 40 ms (Figure I-8). The heart rate can then be determined by the following equation: HR = [1 beat / R-R interval (seconds)] × (60 sec / min). If there are three large boxes and two small boxes between two consecutive R waves, then the R-R interval is 680 ms or 0.68 second. The heart rate would then be 1/0.68 × 60/1 = 60/0.68 = 88 bpm. A common "quick and dirty" method for heart rate estimation is to simply count the number of large boxes between consecutive R waves. At standard paper speed the heart rate for R-R intervals of 1, 2, 3, 4, and 5 large boxes is 300, 150, 100, 75, and 60 bpm, respectively. If the rhythm is irregular or extremely slow, one can refer to the vertical hash marks situated at the bottom of most ECG tracings. These marks are spaced 3 seconds apart, so counting the number of complexes within a 6-second span and multiplying by 10 can give you an estimate of the heart rate. If the hash marks are not there, you can draw your own; 15 large boxes = 3 seconds.

Regularity

Each ECG should be assessed for rhythm regularity, and calipers are a useful tool for this purpose. One should assess the regularity of the atrial waveforms (P waves) and ventricular waveforms (QRS complexes) using the rhythm strips at the bottom of the ECG tracing. Are the P-P and R-R intervals regular? Are these intervals the same? With normal conduction the P-P and R-R intervals should match, but in disorders such as atrioventricular (AV) block or ventricular tachycardia, the intervals will differ. An atrial rate that is regular and greater than the ventricular rate is referred to as complete heart block. In complete heart block the atrial impulses are not activating the ventricles, forcing the QRS complexes to originate from a lower "secondary" pacemaker such as the AVN-His bundle junction. A ventricular rate that is regular and greater than the atrial rate is referred to as A-V dissociation. A-V dissociation is a hallmark finding in ventricular tachycardia where the ventricular complexes originate from an abnormal area of the ventricle that depolarizes independently.

QRS Axis

The QRS axis is a vector that represents the net direction of ventricular depolarization. Deviation of the QRS axis occurs in a number of cardiovascular disorders, and detection of QRS axis deviation is useful for generating a differential diagnosis. Axis deviation is also a criterion for some ECG diagnoses such as anterior and posterior fascicular blocks.

The limb leads form an axial array in the frontal plane that serves as the template for QRS axis derivation. Inspection of the limb leads will allow the reader to determine the QRS axis. In reality the QRS vector is three-dimensional (3D), but the bedside measurement of a 3D QRS vector using ECG data, although possible via a process called spatial vectorcardiography, is technically cumbersome and impractical in real-world cardiology practice.

The normal QRS vector lies between –30° and 90°in the frontal plane (Figure I-12). Deviation of the axis from –30° to –90° is termed left-axis deviation, and deviation of the axis between 90° and 180° is termed right-axis deviation. Left- or right-axis deviation can occur as the result of structural heart disease such as left or right ventricular hypertrophy or dilatation. Extreme axis deviation (180° to –90°) is typically seen with conduction from the ventricles such as during ventricular tachycardia.

There are numerous techniques available for determining the QRS axis. One commonly used method is to examine the orientation of the QRS complexes in leads I and aVF (see Figure I-12). A positive QRS deflection in lead I tells you that the QRS vector lies between 90° and –90°. A positive QRS deflection in lead aVF tells you that the QRS vector lies between 0° and 180°. Thus, if you have an upright QRS deflection in I and aVF, then the QRS vector must lie in the shared "right lower quadrant" between 0° and 90°, and therefore the axis must be normal. If you have a positive QRS in lead I but a negative QRS in lead aVF, the QRS axis might be normal (0° to –30°) or deviated to the left (–30° to –90°). In this case one should look at lead II. A positive deflection in lead II tells you that the QRS must lie between –30°and 150°. Thus, if you have an upright QRS in leads I and II, then the QRS axis must project to the shared area between 0° and –30°. If the QRS is negative in II, then left axis deviation is present.

Intervals

Assessment of the PR and QTc intervals should be performed on each ECG tracing using calipers. The best lead to use for this assessment is whichever lead gives you the best landmarks for caliper measurement. The PR interval can be shortened (< 140 ms) in conditions such as ventricular preexcitation or lengthened (> 200 ms) by AVN disease. The QTc can be lengthened by myocardial ischemia, hypokalemia, congenital ion channel disorders, and numerous medications (Table I-8). QTc prolongation is dangerous because it is associated with a form of ventricular tachycardia called torsades de pointes (TdP, commonly referred to simply as torsade). When the QTc is prolonged, there is a longer relative refractory period during which a premature beat may fall and cause early depolarization of myocardium that is not yet ready to be depolarized. These early "afterdepolarizations" (EADs) can reach a threshold potential and cause TdP (Figure I-13). Torsades de pointes has a characteristic undulating appearance from which its name (translated from French as "twisting of the points") is derived.

Segments

Part of the routine assessment of the ECG should include assessment of the segments between the individual waveforms on the ECG (Figure I-14). The segment between the T wave and the P wave of the next cardiac cycle is called the T-P segment. The T-P segment is an electrically silent period and serves as the baseline reference point for comparison with the other baseline segments for deviation. The PR segment is included within the PR interval. During the PR segment the depolarization wave-front is moving through the atrioventricular node, His bundle, and bundle branches. These structures have very little mass, and so their depolarization does not produce a deflection within the PR segment. Additionally the atria have already depolarized and have not yet repolarized (the wave of repolarization is normally buried within the QRS). For these reasons the normal PR segment is isoelectric. However, the PR segment can be elevated or depressed in the setting of atrial ischemia or injury, respectively. Atrial ischemia or infarction can sometimes occur in the setting of myocardial infarction. Pericarditis is also associated with PR segment depression.

The ST segment is the focus of extreme attention in patients presenting with chest pain or who are suspected of having an acute coronary syndrome. During the normal ST segment the ventricles have already depolarized but have not yet started to repolarize, and the atria have repolarized and are waiting to be depolarized again. Thus, like the PR segment, the normal ST segment is isoelectric. However, the ST segment can be elevated or depressed in the setting of ventricular injury or ischemia, respectively. ST segment deviation will be discussed more completely in the next section.

Waves and Complexes

Routine inspection of the ECG should also include assessment of each waveform for any diagnostic abnormalities. The normal P wave should be monophasic in every lead except for V1, and the P wave should be upright in the inferior limb leads (II, III, and aVF).

The normal QRS complex can vary in appearance from lead to lead. A small Q wave, which represents the normal left-to-right depolarization of the interventricular septum, is not seen in every lead and is most prominent in the lateral leads (I, aVL, V5, and V6). The R and S waves represent depolarization of the left and right ventricles together, but since the left ventricle is so massive, the appearance of the entire QRS complex is dominated by the left ventricle in a normal heart. The relative size and orientation of the R and S components of the QRS complex vary depending on which lead is being assessed. In general, as one progresses from right to left across the precordial leads, the R waves grow taller and the S waves grow shorter. Abnormalities in the amplitude and width of the QRS complex may indicate pathology such as ventricular hypertrophy or myocardial injury. The QRS complex is discussed in greater detail in the next section.

The normal T wave is monophasic and oriented in the same direction as the dominant vector of the QRS complex. This concordance between the QRS and the T wave occurs because the depolarization and repolarization waves of the left ventricle move in opposite directions (Figure I-15). The depolarization wave moves from the endocardium to the epicardium, converting the negative intracellular resting potential of the myocytes to the positive state along the way. Recall that ECG leads record extracellular potentials; the extracellular potential "seen" by a positive ECG electrode from an approaching depolarization wavefront is positive until the very end of depolarization, and so the QRS is recorded as an upright deflection. During repolarization the intracellular potential of the myocytes returns to the negative state with a positive extracellular charge. Since this process begins with the epicardial myocytes, the extracellular potential detected by the positive surface ECG pole is positive from the very beginning of repolarization and the recorded T wave appears upright as well.

C. THE ECG IN CARDIOVASCULAR DISEASE

The following section represents a cursory review of the ECG abnormalities associated with cardiovascular disease states; a complete review of this subject is beyond the scope of a single chapter. As previously mentioned proficient ECG interpretation comes from practice and correlation of ECG findings with clinical and cardiovascular imaging findings. Remember that a prior ECG tracing for comparison can be extremely helpful and should be sought whenever possible.

Ischemic Heart Disease

The management of ST segment elevation myocardial infarction (STEMI) by definition depends on the patient's presenting ECG. In a patient presenting with chest discomfort, regional ST segment elevation is usually caused by acute thrombotic occlusion of an epicardial coronary artery and is an indication for emergency coronary revascularization, either catheter-based or with fibrinolytic therapy. The location of the ST segment elevation often indicates the culprit epicardial vessel (Table I-9). One exception to this rule is myocardial infarction occurring in the setting of circumflex artery occlusion. The circumflex usually supplies the posterolateral aspect of the left ventricle, and the leads on a standard 12-lead ECG do not represent this area well. The diagnosis of a circumflex artery occlusion requires a high index of suspicion and can be aided by the use of unconventional ECG leads across the left scapular region (leads V7–V9). The ST segment elevation associated with myocardial infarction is typically horizontal or upwardly concave ("tombstone"); downwardly concave ST elevation can occur in the setting of myocardial infarction, but this is less specific (Figure I-16). Diffuse ST segment elevation that does not correspond to coronary anatomy may be due to diffuse processes such as acute pericarditis or myopericarditis. Diffuse precordial ST segment elevation within 80 ms of the J point in young subjects with no symptoms may represent normal variant early repolarization. In the clinical management of acute coronary syndromes, the discovery of a new left bundle branch block pattern in the setting of convincing chest pain and/or elevated cardiac biomarkers is treated as an anterior STEMI equivalent.

ST segment depression can be a manifestation of subendocardial ischemia. Unlike ST segment elevation, ST segment depression is less specific for ischemia and the location of the ST depression does not correlate well with the location of the culprit coronary vessel. Horizontal and downsloping ST segment depression is more consistent with ischemia than upsloping ST segment depression. The differential diagnosis of ST segment depression is long and includes left ventricular hypertrophy and digitalis effect.

T wave abnormalities can also occur in the setting of myocardial ischemia or infarction. T wave changes associated with myocardial ischemia are typically symmetric and often occur in the territory of the culprit coronary vessel. Deep, symmetric T wave inversions across the anterior precordial leads in a patient with chest pain are highly suggestive of proximal left anterior descending artery disease; this association is commonly referred to as Wellens' syndrome, after the physician who first described it (Figure I-17). As in ST segment depression, the causes of T wave abnormalities are numerous and asymmetric T wave abnormalities in otherwise asymptomatic patients are a common and nonspecific finding on many ECGs.

Prior myocardial infarction can be demonstrated by the presence of a pathologic Q wave on the ECG. Small Q waves are not uncommon in some ECG leads (particularly lateral leads) and represent normal depolarization of the interventricular septum. Any Q wave in leads V1–V3 should be considered abnormal. Q waves that are >30 ms in duration and >1 mm (0.1 mV) in depth should be considered abnormal and likely the consequence of an old myocardial infarction.

Chamber Enlargement

The relative size of the cardiac chambers can be ascertained from the surface ECG, and these findings provide valuable clues for making both cardiac and noncardiac diagnoses. As mentioned previously, the voltage amplitude of any waveform or complex on a surface ECG is proportional to mass. As such, enlargement or hypertrophy of the atria and ventricles can be detected on the basis of the voltage, duration, and appearance of P waves and QRS complexes, respectively.

Atrial enlargement can cause changes in the P wave. In most leads the P wave appears as a monophasic wave, but the exception to this rule is lead V1, which lies to the right of the upper sternum and is the lead nearest to the atria. In this lead the P wave is usually biphasic with the proximal half representing (roughly) right atrial depolarization and the terminal half representing left atrial depolarization. The first half of the P wave is positive in V1 because this lead is located directly above the right atrium and the wavefront (a 3D entity) moves toward it. The terminal portion of the P wave in V1 represents left atrial depolarization and produces a negative deflection. Since normal atria are similar in size, these deflections are practically mirror images of each other, but in the presence of right or left atrial enlargement one may see a disproportionally positive or negative P wave in V1, respectively (Table I-10). The inferior leads (particularly lead II) are also useful for assessment of the atria. Left atrial enlargement tends to prolong the duration of the P wave in lead II, and there is often a notched appearance to the P wave that resembles the letter M, called p mitrale, for the historic association between left atrial enlargement and severe mitral stenosis. Right atrial enlargement tends to affect the amplitude of the P wave in lead II; tall P waves with a sharp or peaked appearance are often called p pulmonale for the historic association between right atrial enlargement and severe pulmonic stenosis or pulmonary hypertension.

Left ventricular hypertrophy (LVH) causes a general increase in QRS voltage amplitude. There are several established criteria for the diagnosis of LVH. Of these, the Cornell criteria are considered the most sensitive and specific. With the Cornell criteria, one simply adds the height of the R wave in lead aVL to the depth of the S wave in lead V3; summed voltage > 28 mm for men and > 20 mm for women are indicative of LVH. Right ventricular hypertrophy is recognizable when there is a dominant R wave in the early precordial leads (R/S ratio in V1 > 1, R wave height in V1 > 7 mm, R in V1 + S in V5 or V6 > 10.5 mm) and rightward QRS axis deviation (≥100°).

Conduction Disease

Abnormal electrical conduction can occur at any level from the sinoatrial node to the bundle branches and Purkinje fibers. Disorders affecting the sinus node (sick sinus syndrome, sinus node arrest) may be difficult to distinguish from disorders affecting atrial activation by the sinus node (sinoatrial exit block) as both can result in intermittent or complete failure to generate atrial waveforms or propagate sinus impulses to the ventricles.

Disorders of the atrioventricular node (AVN) are not uncommon and are characterized by delayed or ineffective transmission of atrial impulses to the ventricles. First-degree AV block is characterized by fixed prolongation of the PR interval (>200 ms) and is a common finding with a long list of causes, including increased vagal tone and the effect of innumerable medications. There are two types of second-degree AV block. Mobitz type 1 AV block (often called Wenckebach AV block) is characterized by gradually lengthening of the PR interval until a point is reached when an atrial impulse arrives while the AVN is still refractory, resulting in failure to produce a QRS (Figure I-18a). This pause allows the AVN to repolarize and the cycle repeats itself. Wenckebach AV block is usually caused by dynamic inhibition of the AV node and is often the result of transient insults such as ischemia, vagal inhibition and drug effects. In Mobitz type 2 AV block the AV node can only handle a set number of consecutive atrial impulses before it fails to produce a QRS (Figure I-18b). The PR interval does not vary, but the ratio of conducted beats to blocked beats tends to follow an integral pattern such as 3:1 or 4:1. Mobitz type 2 AV block is more commonly the result of fixed injury to the AV node due to infarction, trauma, or age-related degeneration, and it carries a greater risk for progression to complete AV block than Wenckebach AV block. Occasionally patients will present with second-degree AV block with 2:1 conduction (Figure I-18c). The mechanism for this may be consistent with Mobitz type 1 or type 2 second-degree AV block; there are clinical and ECG features that can help you differentiate between the two (Table I-11).

The distinction has some clinical relevance as Mobitz type 2 AV block is associated with a higher risk for progression to complete AV block than Mobitz type 1. Third-degree AV block is characterized by complete electrical disconnection between the atria and ventricles. Also called complete heart block, this abnormality is characterized by the presence of an atrial rhythm with a regular P-P interval and fixed rate that is unrelated to the regular R-R interval and (usually) slower rate produced by a secondary "escape" rhythm, typically arising from the AVN-His junction.

Bundle branch blocks result from injury to the right and left bundle branches. This produces a wider, abnormal-appearing QRS complex as more of the ventricle is activated via cell-to-cell conduction (Figure I-19). In right bundle branch block the QRS complex begins normally as the usually left-to-right activation of the interventricular septum and left ventricle is unaffected. The latter portion of the QRS is wide and abnormal as the right ventricle slowly depolarizes, producing a characteristic second R wave or R′ in lead V1. With left bundle branch block the QRS is abnormal from the start as the interventricular septum actives from right to left via the intact right bundle. The entire left ventricle then depolarizes from the right, resulting in an extremely wide QRS with a characteristic slurred appearance.

Arrhythmias

Tachyarrhythmias and bradyarrhythmias are discussed in greater depth later in this book, so we will only review some general features here. One important question to ask during the interpretation of every ECG is whether the rhythm is in fact sinus. Sinus rhythm is defined by the presence of P waves with an axis between 0° and 70° (essentially upright in the inferior leads) that, provided the AV node is working properly, results in corresponding QRS complexes. If these criteria are not met, then the next question to ask is whether the rhythm is originating from above or below the AV node.

Supraventricular rhythms tend to produce narrow QRS complexes or QRS complexes that are identical to the patient's native QRS during sinus rhythm. If the rhythm appears to be supraventricular, then the presence of atrial waveforms will help distinguish automatic atrial arrhythmias (atrial tachycardia, atrial flutter) from reentrant supraventricular rhythms that produce no obvious antegrade atrial waves (AV nodal reentry or AV reentry). An irregular supraventricular rhythm with no obvious atrial waveforms is almost certain to be atrial fibrillation.

Wide complex tachycardias are often due to ventricular tachycardia, especially in adults with structural heart disease. If you can clearly demonstrate the presence of A-V dissociation on your ECG, then the rhythm is certain to be of ventricular origin. If you are uncertain as to whether a wide complex tachycardia has a ventricular origin (vs a supraventricular origin with aberrant ventricular conduction), it would be helpful to compare your ECG to a baseline tracing to see whether the QRS complexes have similar morphologies. If the wider QRS appears to have the same morphology as the baseline QRS, then the rhythm is more likely to be an aberrantly conducted supraventricular rhythm. However, in older adults with established cardiovascular disease or major risk factors for it, a wide complex tachycardia is usually ventricular tachycardia. Whenever there is doubt, it is safer to treat for presumed VT in these patients.

Part 3. Cardiovascular Providers and Procedures

Through my interactions with graduating medical students and newly minted interns over the years, I have come to realize that many young physicians have little idea about what a cardiologist actually is or does. To the outside observer, the management of patients with heart disease might seem utterly chaotic, and the specific roles of the patient's primary care physician, consulting cardiologist, consulting surgeon, and other providers may not be entirely clear. This part of Section I focuses on the types of physicians who specifically train to care for patients with cardiovascular disease and highlights some of the more common procedures these individuals perform to facilitate that care. Three major topics are discussed here:

A. CARDIOVASCULAR PROVIDERS

Medically Trained Providers

In the United States all postgraduate medical training programs are required to maintain accreditation by the Accreditation Council for Graduate Medical Education (ACGME). The ACGME routinely audits individual training programs for their clinical, educational, and procedural quality and to ensure compliance with various safety standards. Completion of an accredited training program then allows one to sit for a board certification examination provided by an academic society such as the American Board of Internal Medicine (ABIM) or the American Board of Thoracic Surgery (ABTS). These groups set quality standards for their diplomates and ongoing maintenance of certification by periodic reexamination, and the accumulation of continuing medical education (CME) credits is required over the course of one’s entire career.

Adult cardiovascular disease is a subspecialty of the ABIM. Training in adult cardiovascular medicine requires successful completion of training in general internal medicine. Most cardiovascular medicine fellowship programs are 3 years long, and on successful completion of an accredited training program, a cardiologist is eligible to sit for the ABIM certification examination in adult cardiovascular medicine. Cardiologists who begin practice after general fellowship training are typically referred to as general cardiologists or clinical cardiologists. Core general cardiology training focuses on the diagnosis and medical management of heart and vascular disease in its entirety, using fundamental cardiovascular procedures such as diagnostic coronary angiography, invasive hemodynamic assessment, cardiac imaging modalities, and inpatient and outpatient clinical care. Additionally, procedure-specific certification for some imaging procedures such as nuclear cardiology and echocardiography can be obtained from academic societies such as the American Society of Echocardiography (ASE).

After completion of training in adult cardiovascular disease, physicians may further advance their training in a specific area of cardiology by pursuit of a cardiology subspecialty fellowship. Subspecialty fellowship training programs are typically 1 or 2 years in length and often focus on acquisition of procedural expertise in a particular field. The ABIM offers subspecialty certification in interventional cardiology, clinical cardiac electrophysiology, advanced heart failure and transplantation, and adult congenital heart disease.

Interventional cardiologists perform percutaneous interventions to treat certain forms of heart disease such as coronary and peripheral arterial disease. Many programs also offer training in the catheter-based management of structural heart disease. Most accredited fellowship programs are 2 years long and include training in coronary artery, peripheral vascular, and structural cardiac interventions. Cardiac electrophysiologists specialize in the medical and catheter-based management of cardiac arrhythmias. These 2-year training programs provide instruction in catheter-based diagnostic and therapeutic procedures for the treatment and management of rhythm disorders and the implantation of cardiac devices such as pacemakers and automated cardiac defibrillators. Heart failure specialists focus on the medical treatment of patients with advanced ventricular failure. These clinical training programs also allow one to acquire expertise in the evaluation and management of patients before and after cardiac transplantation, including the proper management of patients with implanted ventricular assist devices, evaluation and listing of potential transplantation candidates, and the management of chronic immune suppression after transplantation. Adult congenital heart disease is a newly accredited 1-year training program that arose to address the needs of our constantly increasing population of patients with congenital heart disease who survive into adulthood. Training in this area focuses on gaining balanced expertise in the procedural, medical, and imaging aspects of care for adult patients with congenital heart disease. Physicians who have successfully completed training in an accredited adult Cardiovascular or pediatric disease fellowship program are eligible to apply.

In addition to the ABIM-accredited cardiovascular subspecialties mentioned above, there are other advanced cardiovascular medicine fellowships. Cardiac imaging fellowships allow one to focus on the diagnostic aspects of cardiology using modalities such as advanced echocardiography, computed tomography (CT), nuclear cardiology, and magnetic resonance imaging (MRI). Preventive cardiology focuses on the primary and secondary prevention of cardiovascular disease and the promotion of healthier lifestyles by integrating education with interventions such as supervised cardiac exercise. Vascular medicine fellowship can be pursued by physicians who have completed training in cardiology or internal medicine. These physicians focus on the medical and office-based procedural management of arterial and venous diseases. They also acquire experience in the diagnosis and treatment of hemostatic diseases.

The scope of practice among cardiologists is quite variable. Some subspecialty cardiologists maintain their general cardiology skills and maintain a diverse practice that can include percutaneous coronary interventions, device implantation, imaging expertise, and the clinical management of a broad range of cardiovascular diseases. This is more common with cardiologists in private practice, particularly in geographic areas where broad subspecialty care may be lacking. Conversely, other cardiologists, particularly those in larger academic centers, may focus the majority of their efforts on a solitary aspect of cardiovascular medicine such as percutaneous valve interventions or catheter-based ablation of cardiac arrhythmias. A cardiologist can have a career that is entirely office-based, entirely procedure-based, and everywhere in between.

Surgically Trained Providers

Surgeons also care for patients with cardiovascular disease and typically work in close partnership with cardiologists and other medicine-trained providers. The American Board of Thoracic Surgery certifies cardiothoracic surgeons after successful completion of an accredited general surgery residency (5 years) followed by a thoracic surgery residency (3 years), successful completion of an accredited joint general and thoracic surgery program (7 years total), or successful completion of a Thoracic surgery Directors Association (TSDA)–sponsored and ACGME-accredited integrated thoracic surgery residency (6 years). Cardiothoracic surgeons are trained to perform surgical interventions on the heart, lungs, thoracic vessels, and foregut (mediastinum, esophagus, and stomach). Thoracic surgery training programs provide training in all of these disciplines, but in practice many surgeons focus on particular aspects of that training such as cardiac surgery, lung surgery, and/or foregut surgery.

Vascular surgeons are trained to perform open surgical and percutaneous interventions on the aorta and peripheral blood vessels. The American Board of Surgery (ABS) offers certification to physicians who have completed training in an accredited general surgery program (5 years) and vascular surgery fellowship program (2 years) or in a combined general/vascular surgery residency program (5–6 years).

In recent years the boundaries between cardiologists and surgeons have become less well defined. This is due largely to the advancement of catheter-based therapies such as percutaneous revascularization, transcatheter aortic repair, and transcatheter valve replacement. These procedures may be performed by either interventional cardiologists or surgeons. In many centers this has increased the opportunity for collaboration between medical and surgical caregivers, allowing for hybrid, minimally invasive procedures for select patients. Collaborative opportunities such as these have influenced the organizational structure of many medical centers. With increasing frequency medical centers are moving away from a traditional departmental structure with separate departments of medicine and surgery in favor of an institute model that unites medical and surgical providers in the same administrative "home" that is centered around the management of organ system-based diseases. The institute model is designed to maximize collaboration between medical and surgical providers, promote clinical investigation, and eliminate waste or redundancy.

B. COMMON DIAGNOSTIC PROCEDURES

Cardiologists employ a broad array of diagnostic tests and procedures to accurately diagnose and treat patients with cardiovascular disease. The following text provides an overview of some of the more commonly used diagnostic studies. Each modality described below has its own strengths and limitations. However, a few "universal truths" apply to all cardiovascular tests (in fact, to all tests in general).

Prior to ordering any study, it is important to ask yourself "Will the results of this study change my management?" If the answer is "yes," then the study is likely worth doing. If the answer is "no," then one should question whether it needs to be done at all. For example, in a patient with pleuritic chest pain at low risk for venous thromboembolic disease, a normal D-dimer assay has a negative predictive value of nearly 100% for the diagnosis of pulmonary embolism. A contrast-enhanced CT of the chest to rule out pulmonary embolism is unlikely to influence your management and would expose the patient to needless risk from radiation and contrast.

Another important concept to appreciate is the influence of probability of disease on the outcome of your test. Simply interpreted, Bayes' theorem states that the probability that a patient with a positive test result actually has the disease being tested for is influenced by the prevalence of the disease in the study population. For example, an abnormal stress test in a 25-year-old healthy woman with no symptoms is most likely to be a false-positive finding, whereas the same abnormality in a 75-year-old male smoker with diabetes and classic angina symptoms is most likely a true positive. One must also weigh the risks involved in performing any test against the benefit provided by having the test result. Most cardiovascular tests carry little risk of physical harm; however, invasive studies, studies employing ionizing radiation, or those that require the use of potentially nephrotoxic contrast agents can pose risk to the patient.

Noninvasive Diagnostic Procedures

Echocardiography employs ultrasound waves to visualize the heart and surrounding structures by exploiting the fact that different tissues reflect sound waves to differing degrees, based on tissue characteristics. Reflected waves returning to the ultrasound transducer are processed by the machine to convert these differences into spectral waveforms and two- or three-dimensional (2D and 3D) anatomic images of the heart (Figure I-20). Echocardiograms provide both static and real-time dynamic information regarding cardiac chamber size, systolic and diastolic function, valvular integrity, and the integrity of the surrounding tissues. Transthoracic echocardiography (TTE) is performed with the ultrasound transducer placed on the surface of the chest. TTE provides accurate assessment of biventricular function, valve performance, and pericardial disease. Occasionally one needs to see posteriorly situated structures of the heart (mitral valve, left atrial appendage) with greater clarity than a transthoracic echocardiogram can provide. In these cases a transesophageal echocardiography (TEE) can be performed by having the patient swallow a long transducer probe with an ultrasound crystal at the tip. Echocardiography has several advantages, including its ubiquitous availability, general safety (although TEE does carry some small risk for esophageal and dental injury), and relatively low cost. Disadvantages include limited visualization of the heart in some patients due to technical issues such as obesity or advanced lung disease. Echocardiographic visualization can be enhanced in these cases with the use of echocardiographic contrast agents composed of noble gas–containing phospholipid "microbubbles" that are metabolized within the circulation to fatty acids within minutes of injection.

Computed tomography (CT) scanning is also a useful tool in the diagnosis of cardiovascular disease. CT involves the use of ionizing radiation to create detailed 2D and 3D anatomic images of the heart and surrounding chest structures using computerized processing of multiple images obtained from an external single axial source of radiation. CT is useful for the assessment of coronary and pulmonary artery anatomy, aortic anatomy, cardiac tumors, and the relationship between the heart and adjacent structures in the chest (Figure I-21). Advantages of CT imaging include its relatively wide availability and high speed of image acquisition. Disadvantages include the exposure risk related to moderate-to high-dose ionizing radiation and nephrotoxic iodinated contrast.

Magnetic resonance imaging (MRI) produces images of the heart by placing the patient within the field of a strong electromagnet. The magnetic field excites hydrogen ions, which then emit radiowaves that are collected and processed into viewable 2D and 3D anatomic images (Figure I-22). MRI images are occasionally enhanced via the use of intravenous chelated metal-containing contrast agents such as gadolinium. Cardiac MRI has a number of uses, including the precise assessment of ventricular function, quantification of valvular regurgitation, visualization of the aorta and other chest structures, and differentiation between healthy (normal, viable) and unhealthy (ischemic, scarred, or inflamed) myocardial tissue. Advantages of cardiac MRI include the relative objectivity of its findings (compared with echocardiography and CT) and general safety. Disadvantages include its higher cost, limited availability, and lack of safe use in subjects with implanted metallic devices or claustrophobia. In rare circumstances the contrast agents used in MRI may result in nephrotoxicity.

Nuclear medicine imaging is also used for the diagnosis and management of patients with heart disease, particularly ischemic heart disease. In cardiac nuclear imaging studies patients are given intravenous radiopharmaceutical agents that emit detectable energy waves that are subsequently detected, processed, and formatted as 2D or 3D anatomic images (Figure I-23). Single-photon emission computed tomography (SPECT) studies utilize gamma-emitting moieties such as technetium-99 or thallium-201, whereas positron emission tomography (PET) relies on positron-producing compounds such as fludeoxyglucose (fluorine-18) and rubidium-82. Unlike CT scans, where the radiation passes through the patient from an external source prior to detection, in nuclear cardiology studies the radiation source comes from within the patient. Nuclear studies are used predominantly for the assessment of myocardial health, including the presence of ischemia, scarring, viability, and inflammation. Advantages of nuclear scans include their relative safety (radiation dose is extremely low) and relatively wide availability (SPECT in particular). Disadvantages include the limited spatial resolution and long scan times for SPECT and the increased cost and limited availability of PET.

Stress Testing

Noninvasive assessment for the presence of myocardial ischemia can be achieved using a variety of studies, all of which are colloquially referred to as "stress tests." These studies are the most clinically useful in subjects with symptoms that may be consistent with angina pectoris who are at moderately increased risk for underlying coronary artery disease. Every noninvasive ischemic study has two principal components: a stimulus to provoke ischemia and a surrogate marker to measure for it. The two stimuli employed for the provocation of myocardial ischemia are exercise (treadmill or stationary bicycle) or a pharmacologic agent that can either increase heart rate and contractility (dobutamine infusion) or induce coronary vasodilatation (adenosine or dipyridamole). Exercise is superior to pharmacologic agents for both the provocation and electrocardiographic assessment of ischemia, and an exercise study should always be arranged unless the patient cannot safely exercise.

The presence of ischemia can be detected in several ways. All noninvasive ischemic evaluations employ continuous ECG monitoring as a means to assess for ischemia. ST segment depression is fairly sensitive for the detection of myocardial ischemia, but stress ECG alone lacks specificity for the detection of coronary disease, particularly in women. Still, a treadmill ECG is a reasonable study to perform in a low-to-moderate-risk patient with a normal resting ECG as the negative predictive value of a normal test is quite good. Pre- and postexercise echocardiographic imaging can be added to increase the specificity of the study, and this modality is commonly paired with dobutamine in patients who cannot exercise. Alternatively, one can perform nuclear imaging (SPECT or PET) to augment the specificity. Nuclear studies are commonly performed with vasodilator stimulation in patients who cannot exercise.

The literature comparing the accuracy of echocardiography versus nuclear imaging for the assessment of ischemia has yielded some inconsistent conclusions regarding which modality is better; in general, one can consider them to be comparably accurate. Regional expertise, cost, availability, and patient-specific factors should influence the decision about which type of study to order. For example, patients with wheezing or known reactive airway disease may not tolerate adenosine or dipyridamole, while patients with atrial fibrillation can become quite tachycardic on dobutamine. Morbidly obese patients might be better suited for a PET imaging study, whereas patients with undiagnosed murmurs would be better suited for echocardiography, as it would also provide visualization of the cardiac valves.

Invasive Diagnostic Procedures

Angiography is a procedure performed to diagnose intraluminal vascular disease, particularly arterial atherosclerosis and acute thromboembolic occlusion. During an angiogram the inner lumen of a blood vessel (typically an artery, but venous angiography is also performed) is opacified using an iodinated contrast agent that is directly injected into the vessel of choice via a hollow catheter. Images of the vessel lumen are obtained using a mobile radiographic image intensifier that is positioned by the operator via a mechanized gantry. Angiography can be performed in virtually any arterial bed. The most commonly studied arteries include the coronary arteries, carotid and cerebral arteries, distal lower extremity arteries, and pulmonary arteries (Figure I-24). Angiography is an invasive procedure that carries a small risk for hemorrhage, infection, vessel rupture, myocardial infarction, stroke, and even death. Other risks include those related to contrast exposure and the use of moderate sedation. For diagnostic coronary angiography, the combined risk for a major adverse event (death, nonfatal myocardial infarction, stroke, or vascular injury requiring emergency surgery) is approximately 0.1%.

Pulmonary artery catheterization (PAC), also referred to as right-heart catheterization or Swann-Ganz catheterization, can be useful for the diagnosis and management of such conditions as pulmonary hypertension, decompensated heart failure, and shock. During PAC a long, balloon-tipped hollow catheter is advanced from a central venous access point (typically the right internal jugular vein) through the right-heart chambers and into the branches of the pulmonary artery tree. The catheter has a pressure transducer distal to the balloon which is then "wedged" into a small pulmonary arteriole, allowing the catheter to read the pulmonary venous pressure that is reflected back to it through the capillary bed (Figure I-25). This pulmonary capillary wedge pressure (PCWP) serves as a surrogate for left atrial pressure and therefore left ventricular filling pressure. PAC can be performed as an isolated diagnostic procedure in the catheterization laboratory or as a bedside procedure in an intensive care setting. With the latter, the catheter typically remains in place so that management may be guided by the PAC data. Once the patient has been stabilized, the catheter is typically removed. PAC carries some risk for pulmonary arteriolar rupture, atrial and ventricular tachyarrhythmias, infection, and bleeding. Patients with an underlying left bundle branch block are also at risk for complete heart block because the catheter may irritate the right ventricular side of the interventricular septum and cause transient right bundle branch block.

Electrophysiology (EP) testing is performed to evaluate and treat a wide spectrum of cardiac arrhythmias. In this procedure arterial and venous access is obtained (typically from the femoral position) and electrode-tipped catheters are advanced toward key electrophysiologic structures within the heart. These electrodes can both record and stimulate electrical conduction, allowing the electrophysiologist to create a 3D electrical map of the heart using sophisticated medical software. In this way the origins and pathways of various rhythm abnormalities are identified and even treated via radiofrequency ablation. EP testing carries an obvious risk for arrhythmia but also cardiac perforation, pericardial tamponade, blood loss, infection, and thermal damage to the esophagus, which lies quite near the posterior aspect of the left atrium.

C. THERAPEUTIC PROCEDURES

Catheter-based procedures can be used for therapeutic interventions in addition to diagnosis. The advancement of catheter-based therapies in cardiovascular medicine since the early 1980s has been extensive, offering the option of endovascular treatment to an ever-growing list of cardiac disorders. The key feature of all percutaneous procedures is use of the modified Seldinger technique (named for Swedish radiologist Dr. Sven-Ivar Seldinger, 1921–1998). The Seldinger technique involves the use of a hollow-bore needle to introduce a flexible metal guidewire into an artery or vein. Over this guidewire one places a vascular sheath that consists of a relatively short, hollow catheter with a one-way diaphragm or valve that allows wires and catheters to be introduced into the vessel but prevents back bleeding. Through this sheath longer J-tipped guidewires wires can be negotiated through the vascular system to the point of interest using imaging (typically radiographic) guidance. Diagnostic and therapeutic catheters and equipment are then advanced over the wire like a monorail via a dedicated central lumen. The guidewire is removed and readvanced every time there is a catheter or equipment change. The Seldinger technique has made all percutaneous diagnostic and therapeutic interventions possible, from the simple placement of a central venous catheter to the percutaneous repair of the aorta.

Percutaneous Vascular Intervention

Percutaneous coronary intervention (PCI) can be performed to treat stenosis of the coronary arteries. During these procedures a small, steerable guidewire is advanced across the narrowed area (visualized via angiography), a balloon-tipped catheter is advanced into place, and the balloon is inflated to a set pressure with contrasted saline using a handheld inflation device. The expanding balloon crushes the plaque into the vessel wall. Most PCIs also involve deployment of an intracoronary stent. A stent is a balloon-expandable wire mesh tube that retains its size and cylindrical shape after balloon expansion (Figure I-26). Stents are composed of stainless steel or a metallic alloy such as cobalt chromium and stents may be bare metal stents (BMSs) or drug-luting stents (DESs). DESs are coated with a biodegradable polymer that contains an antineoplastic agent such as everolimus, paclitaxel, or zotarolimus. DES use is associated with a significant reduction in the risk for stent restenosis, but patients typically need a longer duration of dual antiplatelet therapy (eg, aspirin and a thienopyridine) to prevent stent thrombosis and allow endothelialization of the stent. Angioplasty and stenting may be performed in noncoronary arteries as well, including the carotid arteries, renal arteries, and the peripheral arteries of the lower extremities.

Since an angiogram only provides information regarding the relative size and contour of the vessel lumen, other intraarterial imaging modalities have been developed to aid in the diagnosis and management of arterial disease, coronary artery disease in particular. Intravascular ultrasound (IVUS) involves the use of a guidewire with an ultrasound crystal near the tip. The wire is introduced to the vessel of choice and gradually withdrawn, providing a 2D image of the vessel lumen and wall in real time that can be correlated with the patient's angiogram. IVUS is commonly used after PCI to assess the adequacy of stent deployment (Figure I-27). Fractional flow reserve (FFR) is another ultrasound-based intravascular modality that is commonly employed to assess the flow characteristics of a moderate angiographic stenosis. Using Doppler ultrasound the flow across the stenotic region is compared with flow in an angiographically normal segment of the same vessel after vasodilatation with adenosine. The FFR is a ratio of lesion flow to reference segment flow; an FFR of 0.8 or less is generally considered "flow-limiting." FFR is most commonly used to guide PCI in patients with angiographic stenoses of questionable severity.

Percutaneous technology is also used to replace the aortic valve during transcatheter aortic valve replacement (TAVR). During the TAVR procedure a large introducer sheath is placed within a large artery (femoral, ascending aorta) by the Seldinger technique or via the left ventricular apex via a partial thoracotomy incision. A guidewire is advanced across the aortic valve, and this is followed by balloon valvuloplasty and deployment of a bioprosthetic valve situated within a balloon-expandable stent. During valve deployment the heart is never stopped, but the patient is subjected to rapid right ventricular pacing via a temporary right ventricular pacing wire to transiently halt cardiac output. Similar percutaneous interventions have also been performed to replace the pulmonic and tricuspid valves. In addition to valve replacement, one can also attempt percutaneous repair of the regurgitation mitral valve by deployment of a clip to hold the tips of the mitral leaflets together.

Aortic aneurysms can also be repaired percutaneously via a procedure called endovascular aortic repair (EVAR). Employing the Seldinger technique, a surgeon or interventional cardiologist may introduce an expandable endovascular stent graft over a balloon in a manner analogous to percutaneous coronary intervention (Figure I-28). EVAR can be employed to treat abdominal or descending thoracic aortic disease, and its use has dramatically decreased the need for open aneurysm repair, a large and highly morbid surgery.

Electrophysiology Procedures

As described previously, patients with rhythm disorders can be diagnosed using an invasive EP study. During an EP study an electrophysiologist may be able to offer a therapeutic intervention such as catheter-based ablation of an abnormal focus of reentrant or automatic electrical activity. Catheter-based ablation is presently used to treat a number of rhythm disorders such as atrial flutter, atrial fibrillation, and ventricular tachycardia. In some patients with treatment-refractory atrial fibrillation with rapid ventricular heart rates, the atrioventricular node itself can be ablated and a pacemaker installed in order to control the heart rate.

Electrophysiologists can also implant devices such as pacemakers and defibrillations for the management of conditions such as symptomatic bradyarrhythmia and heart failure and for the prevention of sudden cardiac death in patients with reduced left ventricular systolic function or a prior history of ventricular tachyarrhythmia. Device implantation involves the placement of electrode wires within the right atrium and right ventricle or on the epicardial surface of the left ventricle via the retrograde placement of an electrode in a cardiac vein via the coronary sinus (Figure I-29). The wires are typically introduced via the left subclavian vein and connected to a device generator placed in a subcutaneous pocket created in the left pectoral area.

Surgical Procedures

Despite advancement of medical and percutaneous therapies for many forms of cardiovascular disease in recent years, a substantial number of patients require open cardiothoracic and vascular surgeries each year. These surgeries are invasive and carry considerable risk related not only to the cardiac issue being addressed but also to the technical aspects of surgery that are required to create a stable, blood-free operative field such as full circulatory arrest, cross-clamping of the aorta, and the use of a mechanical cardiopulmonary bypass circuit. Nonetheless, with the passage of time and with ongoing refinement of surgical techniques, these surgeries are becoming increasingly safer and less morbid.

Surgical coronary revascularization or coronary artery bypass grafting (CABG) is performed to treat advanced coronary artery disease. CABG is deemed superior to PCI in patients with severe multivessel disease that involves the left main coronary or proximal left anterior descending (LAD) coronary artery, particularly in patients with diabetes or left ventricular systolic dysfunction. CABG surgery is performed in most cases with a median sternotomy incision. Whenever possible, the left internal mammary artery is used as a bypass conduit because the use of the mammary conduit is associated with improved survival and better long-term bypass patency. The proximal end of the mammary artery remains in situ off the left subclavian artery, while the distal portion of the artery is removed from the interior chest wall and anastomosed to the LAD on a segment distal to the site of angiographic stenosis. In some patients the right internal mammary artery may also be used, although bilateral mammary use is generally avoided in diabetic patients because of risks for poor healing and mediastinal infection. Additional aortocoronary bypass grafts may be created using segments of harvested greater saphenous vein or radial artery; the proximal portion of the graft is anastomosed to the ascending aorta, and the distal segment of the graft is anastomosed to the target vessel distal to the site of stenosis.

Valve surgery is indicated in patients with symptomatic severe valvular regurgitation or stenosis or in asymptomatic patients with high-risk features such as left ventricular dilatation or dysfunction. Surgical valve repair is most commonly performed on regurgitant atrioventricular valves, the mitral valve in particular. Valve repair involves debridement of redundant or damaged valvular tissue and occasional repair or replacement of damaged chordae tendonae. This surgery typically involves the placement of a flexible semicircular annuloplasty band to improve leaflet apposition and maintain the integrity of the repair (Figure I-30). Mitral repair is preferred to replacement because repair is less disruptive to left ventricular filling and it preserves the complex geometric and functional relationship between the valve and the ventricle. Valvular repair can often be performed via a smaller lateral thoracotomy incision or with robotic assistance, making the surgery much less invasive. When repair is not feasible, cardiac valves may be replaced with a valvular prosthesis. Prosthetic valves can be mechanical or bioprosthetic; the latter are composed of animal tissue or in some cases donated human tissue. Mechanical prostheses have the advantage of durability but the disadvantage of necessitating lifelong anticoagulation to prevent valve thrombosis. Bioprosthetic valves do not require anticoagulation, but they may be less durable than mechanical valves; younger patients who receive bioprosthetic valves may require another valve replacement later in life.

Cardiac surgery may also help patients with advanced heart failure. Patients with progressive heart failure symptoms despite compliance with appropriate medical therapy may improve with support from a surgically implanted ventricular assist device (VAD). VADs involve the implantation of an inflow cannula at the ventricular apex attached to a continuous pump that directs flow through an outflow cannula placed in the ascending aorta. VAD therapy can be used to support the left or right ventricle, and a VAD may be used as a bridge to transplantation or as a permanent feature of therapy, termed "destination therapy." Highly motivated patients with advanced pump failure who fail medical and device therapy may be considered candidates for cardiac transplantation.