Approach to The Cardiovascular Patient Part 3

Diagnostic tests

The ECG is the first step in the diagnostic evaluation of a patient with palpitations [see Figure 3]. A short PR interval and delta wave (Wolff-Parkinson-White syndrome), prolonged QT interval (long QT syndrome), and left bundle branch block (structural heart disease) are notable findings. Certain medications [see Table 7] may result in prolongation of the QT interval (i.e., acquired prolonged QT) and increase the risk of arrhythmias. Extreme voltage amplitudes and Q waves in leads I, aVL, and V4 through V6 are seen with hypertrophic cardiomyopa-thy. Pathologic Q waves indicate prior myocardial infarction and therefore a substrate for ventricular arrhythmias. Left ventricular hypertrophy or atrial abnormalities are nonspecific findings but suggest underlying structural heart disease. Many pertinent findings for various causes of palpitations can be obtained from the history, physical examination, and ECG [see Table 8].

If the cause of palpitations is not apparent after the initial evaluation (history, physical examination, and ECG), additional diagnostic testing is indicated for certain patients [see Figure 3].27 Such patients include those with presumed arrhythmias that remain undiagnosed and those with prior myocardial infarction, dilated cardiomyopathy, hypertrophic cardiomyopathy, or significant valvular or congenital heart disease. In addition, patients who desire a specific diagnosis should be considered for additional testing.

Table 8 Diagnosis of the Underlying Etiology of Palpitations

Condition	History	Physical Examination	ECG	Underlying Etiology of Palpitations
Congenital long QT syndrome	Symptom onset in adolescence; episodes may be triggered by emotional stress and strenuous exercise	Normal	Prolonged QT interval	Ventricular arrhythmias
Atrioventricular bypass tract (e.g., Wolf-Parkinson-White syndrome)	Childhood episodes of palpitations	Normal	Short PR interval, delta wave	Supraventricular arrhythmias
Inherited dilated cardiomyopathy	Family history of cardiomyopathy, syncope, or sudden cardiac death	Abnormal cardiac impulse, systolic murmur (MR), third heart sound	Atrial enlargement, IVCD, LBBB, ventricular ectopic beats, or Q waves	Supraventricular or ventricular arrhythmias
Hypertrophic cardiomyopathy	Family history of cardiomyopathy, syncope, or sudden cardiac death	Systolic murmur	Increased voltage amplitude (LVH), Q waves in V4-V6, I, aVL	Supraventricular or ventricular arrhythmias
Anxiety, panic, or somatization disorder	Sense of doom, panic, or anxiety associated with episodes; coexisting psychiatric illness	Normal	Normal	Psychiatric
Mitral valve prolapse	Associated fatigue, dyspnea	Midsystolic click, systolic murmur (MR)	Normal or left atrial enlargement	Supraventricular arrhythmias

IVCD—interventricular conduction defect

LBBB—left bundle branch block

LVH—left ventricular hypertrophy

MR—mitral regurgitation

Ambulatory ECG devices include Holter monitoring and continuous-loop event recorders. Holter monitors continuously record the heart rhythm for 24 or 48 hours. Patients are asked to maintain a diary documenting the time and describing the symptoms during the monitoring period. The key is to correlate patient symptoms with documented rhythm abnormalities. Patients with significant complaints of palpitations that correlate with periods of normal sinus rhythm should be further evaluated for underlying psychiatric disorders. Event monitors also continuously record the heart rhythm but require the patient to trigger the device to save the information. These devices can be kept by patients for several weeks and are especially useful when symptoms are infrequent. Event monitors are more cost-effective than Holter monitors for evaluating palpitations.31,32 For patients with underlying structural heart disease and documented ventricular arrhythmias on ambulatory ECG monitoring, additional evaluation is warranted, including determination of left ventricular function and, occasionally, electrophysiologic testing.

Syncope

Background

Syncope refers to a transient loss of consciousness accompanied by loss of postural tone. Roughly one third of all persons have an episode of syncope during their lifetime. It is a particularly common problem encountered in emergency departments and accounts for approximately 6% of all hospital admissions.33 Determining which patients require hospital admission is difficult, given the large number of potential causes of syncope. Although many conditions that result in syncope are life threatening, other common etiologies, such as medication side effects, orthostatic hypotension, and psychiatric disorders, are benign.

Syncope is classified on the basis of the underlying etiology [see Table 9]. In elderly patients, the etiology may be multifactor-ial and related to medication side effects (particularly antihyper-tensives and antidepressants),34 orthostatic hypotension, and bradyarrhythmias. Various medications are associated with prolongation of the QT interval and the development of ventricular arrhythmias and resulting syncope [see Table 7]. Vasovagal syncope is particularly common in otherwise healthy patients and has a benign prognosis. Episodes often occur in response to injury and are characterized by a sudden decline in blood pressure with or without associated bradycardia.

Establishing the presence of structural heart disease in the evaluation of patients with syncope is essential because such patients may have a 1-year mortality as high as 30%.35,36 Structural heart disease is usually apparent on the basis of history, physical examination, and information from the baseline ECG. Occasionally, additional diagnostic testing with echocardiography, tilt-table testing, or electrophysiologic testing may be required.

History and physical examination

The first step in establishing the presence of structural heart disease is to obtain an accurate description of the episode of syn-cope.

Table 9 Classification of Syncope Based on Etiology

Cardiac

Blood flow obstruction

Aortic stenosis

Pulmonic stenosis

Left atrial myxoma

Hypertrophic cardiomyopathy

Massive pulmonary embolism

Reduction in forward cardiac output

Pericardial tamponade

Severe pump failure

Arrhythmia

Tachyarrhythmias

Ventricular tachycardia

Supraventricular tachycardia

Bradyarrhythmias

Sinus bradycardia

Sick sinus syndrome

Atrioventricular block

Carotid sinus hypersensitivity (can also be considered

neurologic cause)

Neurologic

Vasovagal

Situational (micturition)

Seizures

Cerebrovascular accident

Cerebrovascular insufficiency

Orthostatic hypotension—autonomic dysfunction

Other

Volume depletion

Drugs

Hypoglycemia

Anxiety attack

Psychogenic

Key elements of the history include the presence of postural or exertional symptoms; associated chest pain, shortness of breath, or palpitations; and the situation in which the episode occurred (e.g., during micturition). Neurologic symptoms such as focal motor weakness, arm or leg movement, tongue biting, or a postictal state suggest a neurologic rather than cardiac event. However, seizures can occur from cardiac causes if a patient is kept upright during an episode (usually the result of a well-meaning bystander) because of cerebral hypoperfusion. A witness to the episode of syncope may provide a clear description of the event and should be questioned if possible. Medications associated with QT prolongation [see Table 7], blood pressure lowering (antihypertensives), and volume depletion (diuretics) should be reviewed. A family history of sudden cardiac death, syncope, or heart failure suggests hypertrophic car-diomyopathy, an inherited dilated cardiomyopathy, or long QT syndrome. A history of myocardial infarction or congestive heart failure raises the possibility of ventricular arrhythmias.

The physical examination focuses on determining whether structural heart disease is present and excluding common causes of syncope. Orthostatic vital signs should be obtained in all patients. Focal neurologic findings such as a motor deficit or a visual-field defect may indicate a neurologic cause for syncope. Pertinent findings on cardiovascular examination include a delayed carotid upstroke (aortic stenosis), an abnormal point of maximal cardiac impulse (cardiomyopathy), an irregular or bradycardiac rhythm (arrhythmias), a third heart sound (car-diomyopathy), a midsystolic murmur (aortic stenosis, hyper-trophic cardiomyopathy), and a holosystolic murmur (mitral re-gurgitation secondary to left ventricular dilatation).

Figure 4 Evaluation of patients with syncope.37-39 (ECG— electrocardiogram; OHD—organic heart disease)

Less common findings include an early diastolic sound (so-called tumor plop, indicating a left atrial myxoma), asymmetrical peripheral pulses (aortic dissection), and a loud second heart sound (pulmonary hypertension secondary to pulmonary embolism). Information from the history and physical examination yields a cause for syncope in approximately 45% of patients.37

Diagnostic tests

An ECG is the initial diagnostic test for all patients with syncope. Although the yield of the baseline ECG is low (approximately 5%), a number of potential findings are useful,37 including bundle branch block, Q waves indicating prior myocardial infarction, left ventricular hypertrophy, prolonged QT interval, or evidence of atrioventricular block. The presence of sinus bradycardia, first-degree atrioventricular block, and bundle branch block suggests bradyarrhythmias as the cause of syncope. Extreme voltage amplitudes and Q waves in leads I, aVL, and V4 through V6 suggest hypertrophic cardiomyopathy and therefore the possibility of ventricular arrhythmias. An uncommon but unique ECG abnormality is the combination of a right bundle branch block, T wave inversions in leads V1 through V3, and an epsilon wave (a positive wave on the terminal portion of the QRS complex)—findings that indicate right ventricular dys-plasia, which is associated with ventricular arrhythmias. Ventricular arrhythmias are also seen in the Brugada syndrome, which can be identified on the ECG by an incomplete right bundle branch block and ST segment elevation in leads V1 through V3.38 A short PR interval and slurring of the initial portion of the

Table 10 Differential Diagnosis of Claudication

Condition	History	Physical Examination	Diagnostic Tests	Comments
Peripheral vascular disease	Symptoms occur with exercise and are relieved by rest	Diminished or absent peripheral pulses	ABI, arterial duplex ultrasound	Angiography reserved for those with severe disease who are considering surgical or percutaneous revas-cularization
Lumbar spinal stenosis	Paresthesias occur with standing and walking Symptoms are relieved by sitting and/or leaning forward History may include chronic low back pain and prior lumbar surgery	Normal peripheral pulses	Computed tomography or magnetic resonance imaging of the lumbar spine	Referred to as pseudo-claudication
Arthritis	Pain localized to the joint area as opposed to adjacent muscles	Normal peripheral pulses	Radiograph of affected joint
Myalgia	Pain within a muscle group at rest and with exertion No relief with rest	Tenderness to palpation of the affected muscle group; reduced muscle strength	Laboratory evaluation of muscle inflammation with CPK, aldolase	Associated with hypothy-roidism and end-stage renal disease; may be related to drug side effect (e.g., HMG-CoA reductase inhibitors)

ABI—ankle-brachial index

CPK—creatinine phosphokinase

QRS complex (the delta wave) suggests preexcitation (i.e., Wolff-Parkinson-White syndrome), with the possibility of rapid antegrade conduction via the accessory pathway.

If the etiology of syncope remains unclear after reviewing the history, physical examination, and ECG, additional diagnostic testing should be pursued. For patients with findings suggestive of an underlying cardiac cause, echocardiography and coronary angiography can be performed; for those with a possible neurologic cause, brain imaging (computed tomography or magnetic resonance imaging), neurovascular studies (carotid and trans-cranial Doppler ultrasound studies), and electroencephalogra-phy can be performed; and for those with a presumed pulmonary cause, lung scanning can be considered [see Figure 4]. If the diagnosis remains uncertain despite these tests, one of three pathways can be followed.39

The first pathway is for patients with structural heart disease or an abnormal ECG, who therefore have an increased likelihood for underlying arrhythmias or valve disease as a cause for syncope. Echocardiography, noninvasive stress testing, and ambulatory ECG monitoring using either a Holter monitor or continuous-loop event recorder should be considered for these patients. Event recorders have been found to be more accurate than Holter monitors in the diagnosis of syncope and presyn-cope; however, some patients find event recorders difficult to operate correctly.40 If ambulatory ECG monitoring documents normal sinus rhythm in the setting of reported syncope, psychiatric evaluation and possibly tilt-table testing are warranted.

The second pathway is for patients older than 60 years, who are more likely to have valve disease (aortic stenosis), ischemic heart disease, carotid sinus syncope, cerebrovascular disease (transient ischemic attacks), and situational events (micturition, defecation, postural) as a basis for syncope. Carotid sinus massage (in the absence of carotid bruits, recent myocardial infarction, or stroke) should be the initial diagnostic test for these patients.41,42 A positive test is defined as asystolic arrest lasting 3 seconds or longer and may identify those with cardioinhibitory hypersensitivity of the carotid sinus who will benefit from pacemaker placement. For those with a negative test result, echocardiography, noninvasive stress testing, and ambulatory ECG monitoring can be performed.

The third pathway is for patients with unexplained syncope and no suspected structural heart disease. For those who have had a single episode, additional evaluation can be deferred until a second episode occurs. In patients with more than one episode, ambulatory ECG monitoring or tilt-table testing and, possibly, psychiatric evaluation should be considered.

Tilt-table testing was initially developed in the 1980s to evaluate patients with presumed vasovagal syncope. The passive portion of the test involves quickly raising a patient from the supine position to an angle of 60° (the tilt angle) for approximately 45 minutes, which causes pooling of venous blood in the lower extremities, a decrease in venous return, compensatory tachycardia, and enhanced ventricular contraction. For individuals with vasovagal syncope, augmented ventricular contraction causes activation of vasodepressor reflexes that result in hypotension, bradycardia, or both. Approximately 49% of patients referred for evaluation of vasovagal syncope have positive responses, compared with 9% of control patients.43 The active portion of tilt-table testing uses an iso-proterenol infusion to enhance the vasodepressor reflex.

Table 11 Ankle-Brachial Index (ABI) Values and Accompanying Findings in Peripheral Vascular Disease (PVD)

Condition	Symptoms	Physical Findings	ABI
Normal	None	None	> 1.0
Mild PVD	Mild claudication on exertion	Diminished pulses	0.8-0.9
Moderate PVD	Moderate or severe claudica-tion on exertion	Diminished or absent pulses; nonhealing ulcers or skin wounds	0.5-0.8
Severe PVD	Severe claudica-tion; symptoms may occur at rest	Absent pulses; nonhealing ulcers or skin wounds	< 0.5