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lipoprotein cholesterol. The estimated glomerular filtration rate (GFR) or creatinine
clearance should be calculated using available formulas (see Table 7.9.4). If a second-
ary cause of HTN is suspected, the appropriate specific laboratory workup should be
included.
2. An electrocardiogram may assist with recognizing a previously damaged myocardium,
rhythm disturbances, or changes consistent with left ventricular hypertrophy (LVH).
3. Imaging studies may be useful. A chest x-ray may be useful when attempting to evalu-
ate the patient for cardiomegaly, but a limited echocardiogram will give more detailed
information about cardiac function and LVH.
D. Genetics. To date, genetic studies have not identified any single gene or combination of
genes that appreciably accounts for HTN in the general population.
III. DIAGNOSIS
A. Differential diagnosis
1. Essential HTN
2. Secondary HTN
a. Renovascular HTN
i. Stenosis of main renal arteries and/or major branches is responsible for 2–5% of
patients with HTN.
ii. Initial workup involves Doppler ultrasonography with measurement of the intra-
renal resistance index.
iii. This diagnosis includes the subgroups preeclampsia and eclampsia.
b. Renal parenchymal HTN. Diseases that injure renal parenchymal tissue result
in inflammatory and fibrotic changes of small intrarenal vessels, thereby causing
decreased profusion and resultant HTN.
c. Primary aldosteronism. A tumor or bilateral adrenal hyperplasia should be
sought.
d. Cushing’s syndrome
i. Truncal obesity, fatigability, purplish abdominal striae, amenorrhea, hirsutism,
edema, glucosuria, moon facies, and buffalo hump
ii. Most common in the third or fourth decade of life
iii. Failure to suppress cortisol level with dexamethasone challenge
e. Pheochromocytoma
i. Most common in young to mid adult life
TABLE 7.9.4 Equations for Estimation of GFR from Plasma Creatinine
Concentration (P
cr
)
1. Equation from the Modication of Diet in Renal Disease Study
a
Estimated GFR (mL/min/1.73 m
2
) 1.86 (P
cr
)
–1.154
(age)
–0.203
Multiply by 0.742 for women
Multiply by 1.21 for African Americans
2. Cockcroft-Gault equation
Estimated creatinine clearance (mL/min)
(140 – age) body weight (kg)
72 (P
cr
)(mg/dL)
Multiply by 0.85 for women
GFR, glomerular filtration rate.
a
Kasper DL, Braunwald E, Fauci AS, et al. Harrison’s principles of internal medicine, 16th ed.
Part8; Chapter 230. McGraw-Hill Companies, 2005.
138
Taylor’s DifferenTial Diagnosis Manual
ii. Headaches, palpitations, excessive sweating, impaired glucose tolerance, hypercal-
cemia, weight loss, and anxiety
iii. Twenty-four hour urine collection assayed for vanillylmandelic acid, metaneph-
rine, and “free” catecholamines
f. Coarctation of the aorta
i. Cardiac murmur, possibly heard in the back, over spinous processes, and lateral
thorax
ii. Decreased, delayed, or absent femoral pulses
iii. Chest x-ray reveals “the three sign” at coarctation sight and notched ribs
g. Hyperparathyroidism
i. Hypercalcemia
ii. Renal parenchymal damage due to nephrocalcinosis and renal stones
h. Oral contraceptive medications
i. Malignant HTN (3)
i. Diastolic blood pressure usually greater than 130 mmHg
ii. Papilledema, retinal hemorrhages, and exudates
iii. Possibly vomiting, severe headache, transient visual changes or loss, stupor, coma,
oliguria, and cardiac decompensation
j. Obstructive sleep apnea
B. Clinical manifestations. Individuals may have high blood pressure for years and not
know it. Sometimes HTN may have subtle symptoms such as epistaxis, hematuria, episodic
weakness, dizziness, palpitations, easy fatigability, and impotence. If HTN is part of a dis-
ease process, such as secondary HTN, it may be joined by other symptoms of the influenc-
ing disease process.
REFERENCES
1. American Heart Association Inc. Accessed at www.americanheart.org, on April 11, 2006.
2. Department of Health and Human Service, National Institutes of Health. The Seventh Report of
the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure. Accessed at www.nhlbi.nih.gov/guidelines/hypertension, on April 11, 2006.
3. Kasper DL, Braunwald E, Fauci AS, et al. Harrison’s principles of internal medicine, 16th ed. Part 8;
Chapter 230. New York, NY: McGraw-Hill, 2005.
4. Bickley LS, Szilagyi PG. Beginning the physical examination: general survey and vital signs. In: Guide
to physical examination and history taking, 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins,
2003:75–78.
5. U.S. Preventive Services Task Force. Screening for high blood pressure: reaffirmation recommendation
statement. Am Fam Physician 2009; 79(12) 1087–1088.
7.10
Palpitations
Naureen Raq
I. BACKGROUND. Palpitations are an unpleasant abnormal awareness of the heartbeat. They are
usually described as a pounding or racing of the heart.
II. PATHOPHYSIOLOGY
A. Etiology.
Palpitations are a common presenting complaint encountered by the primary
care physicians and cardiologists. The list of underlying causes of palpitations is extensive
(see Table 7.10.1).
Chapter 7 • Cardiovascular Problems
139
B. Epidemiology. One prospective cohort study of 190 patients showed that 43% had
palpitations due to cardiac causes, 31% due to anxiety or panic disorder, and 16% due to
an undetermined etiology (1). Remembering that the heart is electrically paced, a good
mnemonic to assist in recalling causes of palpitations is E-PACED (Electrolytes, Psychiatric,
Anemia, Cardiac, Endocrine, and Drugs) (2).
C. Symptoms. The symptoms can range from just awareness of heart rhythm to chest tight-
ness, shortness of breath, dizziness, light-headedness, or syncope. They can last from a few
seconds to prolonged periods of time.
III. EVALUATION. Because patients rarely experience an episode while in the physician’s office, the
history and physical examination are the most crucial elements of the investigation. Moreover,
only occasionally does physical examination provide clues or supporting evidence to affirm a
diagnosis, thereby making a thorough and descriptive history assume even greater importance.
A. History. The history should focus on the age of the patient, detailed description of symp-
toms, and information such as the circumstances during occurrence, intermittency, dura-
tion, and precipitating and resolving factors.
1. The circumstances during which palpitations occur may indicate an association with
anxiety or panic attacks, although one should also keep in mind excess catecholamine
during times of stress. Validated screening tools are readily available to assist in identi-
fying patients with such psychiatric illness (3). Occurrence at night while lying down
could result from atrial or ventricular premature contractions. Positional changes might
indicate atrioventricular nodal tachycardia.
TABLE 7.10.1 Some Causes of Palpitations
Cardiac Medications
Arrhythmias Alcohol
Atrial brillation/atrial utter Anticholinergics
Multifocal atrial tachycardia Caffeine
Premature ventricular contractions Illicit drugs like cocaine
Sick sinus syndrome Nicotine
Sinus node dysfunction Sympathomimetics
Sinus tachycardia Amphetamines
Supraventricular tachycardia Endocrine/metabolic
Ventricular tachycardia Hyperthyroidism
Wolff-Parkinson-White syndrome Hypoglycemia
Other cardiac causes Pheochromocytoma
Cardiac shunts Psychiatric
Cardiomyopathy Anxiety disorder
Pacemaker Panic attacks
Valvular heart disease like mitral stenosis Somatization disorder
Stress
Others
Anemia
Fever
Strenuous physical activity
140
Taylor’s DifferenTial Diagnosis Manual
2. Isolated or skipped beats could be premature contractions or benign ectopy.
3. Palpitations precipitated by exercise may be associated with supraventricular arrhythmias
or atrial fibrillation. Palpitations terminated by vagal maneuvers point to paroxysmal
supraventricular tachycardia.
4. Palpitations described as rapid and regular may indicate paroxysmal supraventricular
tachycardia and ventricular tachycardias. Palpitations described as rapid and irregular
could imply atrial fibrillation, multifocal atrial tachycardia, and atrial flutter with variable
block. Flip-flopping or stopping–starting sensations may be caused by supraventricular
or ventricular premature contractions. Palpitations may be sensed as a pounding in the
neck. Notably, atrioventricular nodal reentrant tachycardia is associated with a rapid
regular pounding in the neck, whereas such a sensation that is less regular and more
intermittent may be premature ventricular contractions.
5. The physician should keep in mind that dizziness, presyncope, or syncope accompanying
palpitations are factors that help identify patients at risk for fatal results. These symptoms
should prompt an investigation for ventricular tachycardias.
6. Age at onset in childhood may suggest supraventricular tachycardia. Symptoms of hyper-
thyroidism such as heat intolerance should be elicited. Illicit drugs, caffeine, and nicotine
habits as well as anemia and metabolic disorders are all important possible associations
that should be considered.
B. Physical Examination. The findings of the physical examination may give clues such as
a heart murmur, indicating the possibility of valvular disease or cardiomyopathies or the
midsystolic click of mitral valve prolapse. A brisk walk down a corridor might reveal a poorly
controlled ventricular response and resultant palpitations in a patient with atrial fibrillation
and palpitations (1). It is necessary to search for signs of congestive heart failure.
C. Workup
1. Twelve-lead electrocardiography
It is indicated and should be analyzed for short PR interval and delta waves (ventricular
pre-excitation), Q waves indicating left ventricular hypertrophy or prior infarction, premature
contractions, long QT intervals, heart blocks, or any other abnormality.
2: Laboratory testing
It can usually be limited to investigation of anemia, thyroid function, and electrolyte distur-
bances (potassium and magnesium). Ambulatory electrocardiography (ECG) can be used
for further investigation.
3: Holter monitoring
It should suffice for patients with daily symptoms.
4: Continuous-loop event recorder
It provides a better diagnostic yield (4, 5).
5: Echocardiogram
It can be done to detect any structural abnormality of the heart like valvular heart disease.
IV. DIAGNOSIS. The list of causes of palpitations is extensive (Table 7.10.1). In most cases, the
cause is benign. Life-threatening causes are suggested by associated symptoms such as dizziness
or syncope. The history is the most important diagnostic tool, and a thorough and descriptive
inquiry should be made. The physical examination may provide further clues or supporting
evidence. Testing involves 12-lead ECG and a limited laboratory investigation.
REFERENCES
1. Abbott AV. Diagnostic approach to palpitations. Am Fam Physician 2005;71:743–750.
2.
Weber BE, Kapoor WN. Evaluation and outcomes of patients with palpitations. Am J Med
1996;100:138–148.
3. Taylor RB, ed. The 10-minute diagnosis manual, 1st ed. Philadelphia, PA: JB Lippincott, 1994.
4. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl J Med 1998;338:
1369–1373.
5. Zimetbaum P, Josephson ME. The evolving role of ambulatory monitoring in general clinical practice.
Ann Intern Med 1999;130:848–856.
Chapter 7 • Cardiovascular Problems
141
7.11
Pericardial Friction Rub
Stephen L. George
I. BACKGROUND. The pericardium is a sac-like structure consisting of an outer parietal layer and
an inner visceral layer that envelops the heart and root of the great vessels. There is approximately
5–50 mL of ultrafiltrate of plasma between the two layers. It is innervated by the phrenic nerve.
It primarily drains into the right pleural space via the thoracic duct. A friction rub is present in
85% of cases of pericarditis and is essentially diagnostic of pericarditis. Patients typically present
with acute chest pain and characteristic serial electrocardiographic changes (1–4).
II. PATHOPHYSIOLOGY
A. Etiology of Acute Pericarditis.
Acute pericarditis (AP) is generally a benign, self-limited,
and readily treatable condition. Inflammation between the two layers can produce a serous,
fibrinous, or purulent reaction. A pericardial effusion is not necessarily present. Together,
idiopathic and viral (coxsackie virus, echovirus, Epstein-Barr virus, influenza virus, human
immunodeficiency virus, hepatitis viruses, varicella, measles, and mumps) etiologies account
for 80–90% of cases. Malignancies are the third leading cause at 5%. A specific cause is
identified in only about 7% of cases (6, 7). Other etiologies include bacterial (tuberculosis,
Staphylococcus, Haemophilus, Pneumococcus, Salmonella, Meningococcus, and syphilis), fungal
(histoplasmosis, blastomycosis, coccidioidomycosis, and aspergillosis), parasitic (echino-
coccosis, amebiasis, Rickettsia, and Toxoplasma), rheumatoid arthritis, systemic lupus
erythematosus, gout, scleroderma (up to 85%), rheumatic fever, sarcoidosis, other inflam-
matory conditions (Sjögren syndrome, mixed connective tissue disease, Reiter’s syndrome,
Whipple’s disease, familial Mediterranean fever, and serum sickness), uremia, dialysis,
hypothyroidism, cholesterol pericarditis, 1–4 days after myocardial infarction, 1–3 days
postpericardiotomy, metastatic (breast, lung, lymphoma, melanoma, and leukemia), irradia-
tion, drugs (penicillin, cromolyn sodium, doxorubicin, cyclophosphamide, procainamide,
phenytoin, and minoxidil), aortic dissection, cardiac trauma, after cardiac catheterization or
pacemaker placement, and hemorrhagic. Infarction-associated pericarditis has diminished
significantly with the advent of reperfusion interventions. Dressler’s syndrome occurs weeks
to months post-acute myocardial infarction (AMI) (1–7).
B. Epidemiology of AP. AP occurs in approximately 0.1% of hospitalized patients and 5%
of noncardiac chest pain patients in the emergency department (1, 2, 4) and is more com-
mon in males and adults 20–50 years old. Up to 15% of patients may experience recurrence
of symptoms within a few months and 25% will eventually have a recurrence (2, 5–7).
III. EVALUATION
A. History
1. Most patients have acute sharp, sternal or left precordial pain. However, they may have
a dull, aching, burning, or pressure-type pain. Pain is characteristically referred to the
trapezius ridge, worse with inspiration, lying down, swallowing, or body motion and
relieved by sitting upright or leaning forward. It may also radiate to the neck, jaw, or
arms and is usually not relieved with nitroglycerine (1, 3, 4, 6, 7).
2. There is often a prodrome of fever, malaise, and myalgias. Associated symptoms may
include dyspnea (pariticularly with tamponade), weight loss (malignancy), produc-
tive cough (with pneumonia and purulent pericarditis) or hemoptysis (tuberculosis).
Nonspecific symptoms include hiccups, cough, hoarseness (phrenic nerve), palpitations,
nausea, and vomiting (1, 4, 6).
3. Past medical and surgical history may be suggestive of a causal illness or procedure.
Examples are recent pericardiotomy, renal failure, rheumatologic diseases, trauma,
malignancy, or the use of suspect medications (1–7).
142
Taylor’s DifferenTial Diagnosis Manual
B. Physical Examination. Pericardial friction rub is a creaking leather or scratching
high-pitched sound best heard with the diaphragm along the left lower sternal border
with the patient leaning forward at end expiration. Most often triphasic (atrial systole,
ventricular systole, and early ventricular diastole), but it can be biphasic or monophasic.
It can be intermittent and therefore overlooked without serial exams. Beck’s triad (muf-
fled heart sounds, JVD, and hypotension) pulsus paradoxus or Kussmaul sign suggest
tamponade. With rapid accumulation, tamponade can occur with as little as 200 mL of
fluid (1–5).
C. Testing
1. Laboratory tests. Clinical circumstances will dictate specifics of testing. The minimum
workup should include a complete blood count, erythrocyte sedimentation rate,
C-reactive protein, blood urea nitrogen, creatinine, and cardiac enzymes. Elevated
cardiac enzymes occur 35–55% of the time due to myopericarditis. Specific rheuma-
tologic testing such as a rheumatoid factor or antinuclear antibody panel may be indi-
cated. For tuberculosis, skin testing and an adenosine deaminase test of pericardial
fluid are indicated. Thyroid function tests, streptococcal antigen testing, cytology of
pericardial fluid, antibody titers, or pericardial biopsy may be warranted (1, 2, 5, 6).
2. Electrocardiogram (ECG). The ECG is indispensable in the diagnosis and manage-
ment of AP. At first, current injury changes of upwardly concave ST elevation and PR
depression is seen in the precordial and limb leads with reciprocal changes in leads V1
and aVR. T waves gradually flatten and then invert. Persistent T wave inversion beyond
3 weeks indicates a chronic fluid accumulation and the need for further testing. Distinct
from AMI, there are no Q waves or reciprocal changes. Electrical alternans may be seen
with an effusion or tamponade. Electrical alternans with tachycardia is relatively specific
for tamponade (1, 2, 4, 6, 8).
3. Imaging studies. Echocardiography should be performed to assist with the diagnosis,
management, and guidance of interventions such as pericardiocentesis. Flask-shaped
cardiomegaly on chest radiography requires at least a 200 mL effusion (1, 2, 4, 5).
IV. DIAGNOSIS. The differential diagnosis is extensive, similar to that for chest pain, and is guided
by the clinical situation. Salient conditions to consider include acute coronary syndromes,
aortic dissection, esophageal rupture, pulmonary embolism, pulmonary infarct, pneumothorax,
esophagitis, esophageal spasm, acute gastritis, pneumonia, cholecystitis, and costochondritis
(1, 2, 6, 7).
REFERENCES
1. Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial disease: diagnosis and management.
Mayo Clin Proc 2010;85(6):572–593.
2. Tingle LE, Moina D, Calvert CW. Acute pericarditis. Am Fam Physician 2007;76:1509–1514.
3. Leal ME. Pericarditis and pericardial effusions. In: Bope ET, Kellerman RD. Bope and Kellerman:
Conn’s current therapy 2012, 1st ed. St. Louis: W.B. Saunders, 2012:458–460.
4. Stehlik J, Benjamin IJ. Pericardial and myocardial disease. In: Andreoli TE, Ivor BJ, Griggs RC, Wing
EJ. Andreoli and Carpenter’s Cecil essentials of medicine, 8th ed. Philadelphia, PA: Saunders Elsevier,
2010:145–148.
5. Delgado GA, Ferri FF, Forunato DJ. Ferri’s clinical advisor 2012, 1st ed. Philadelphia, PA: Mosby,
2012:768–769.
6. Wu K. Pericarditis. 2011. Accessed at https://www.online.epocrates.com/noFrame/Showpage.do?
method=disease&MonographId=243 on May 19, 2012.
7. Massimo I, LeWinter MM. Clinical presentation and diagnostic evaluation of acute pericarditis. 2011.
Accessed at http://www.uptodate.com/contents/clinical-presentation-and-diagnostic-evaluation-of-
acutepericarditis?source=searchresult&search=pericarditis&selectedTitle=1%7E150 on May 19,
2012.
8. Goldberger A. Goldberger: clinical electrocardiography: a simplified approach, 7th ed. Philadelphia, PA:
Mosby Elsevier, 2006:139–140.
Chapter 7 • Cardiovascular Problems
143
7.12
Raynaud’s Disease
Sandra B. Baumberger
I. BACKGROUND
A. Definition.
Raynaud’s disease is a vasospastic disorder causing episodic ischemia of the
digits of the hands, lasting a varying amount of time. It was named after Maurice Raynaud,
who first noted the disorder in 1862. Although the disorder mainly affects the finger
and toes, it can also affect the tongue, the nose, the ears, and the nipples (1). Raynaud’s
disease not associated with any underlying disease is also known as primary Raynaud’s
disease (PRD). This type of Raynaud’s disease tends to be less severe and is more common.
Secondary Raynaud’s disease (SRD) or Raynaud’s phenomenon is often associated with an
underlying illness (2).
II. PATHOPHYSIOLOGY.
A. Etiology.
Emotional stress and cold seem to be the biggest triggers for attacks. The attacks
may last minutes to hours. Classically, the attacks have a three-stage color change. Stage one
consists of pallor of the skin, which is sometimes associated with coldness, numbness, and/or
paresthesias. The second stage, if present, consists of cyanosis and may include some of the
symptoms associated with stage one. Finally, the third stage consists of erythema, which may
be associated with throbbing of the digits (3). PRD carries a low risk of progression to an
autoimmune disorder, if after 2 years of attacks no other signs or symptoms of autoimmune
processes are present. Conversely, Raynaud’s can be the presenting sign for scleroderma. It
has been proven that those who suffer from PRD or SRD have abnormal blood flow to the
digits and abnormal recovery from cold stimulus. In patients with scleroderma, the blood
vessels are already narrowed from proliferation of the intimal area. This exacerbates the
ischemia caused by the cold stimulus (3).
B. Epidemiology. The prevalence of Raynaud’s disease in women ranges from 3% to 20%
and in men from 3% to 14%. The prevalence of PRD in the United States is around 5%,
while in France it may be as high as 17% (4). PRD usually begins in the second or third
decade of life. SRD may begin with the underlying disorder and/or be the presenting sign
of an autoimmune disorder. Raynaud’s disease is more common in cold climates. It is some-
times associated with certain occupations such as those that require exposure to mechanical
vibration on an ongoing basis (5). Other disorders associated with SRD include systemic
lupus erythematosus (SLE), rheumatoid arthritis, dermatomyositis, polymyositis, hypervis-
cosity syndromes, antineoplastic medications, and beta blockers. Vasospastic processes such
as vascular headaches, atypical angina, and primary pulmonary hypertension may also be
associated with SRD (6).
III. EVALUATION.
A. History and Physical.
When interviewing the patient, it is important to determine
when the symptoms appear. Patients note that symptoms appear during relative shifts from
warm to cold temperatures. Emotional stress is also reported to cause symptoms via the
activation of the sympathetic nervous system. Medications used and history of smoking are
also important questions to cover during the history (4). Also, questions about the use of
machines or tools that produce vibration or other repetitive activities done with the fingers
may help determine if the patient has a variant of Raynaud’s disease known as hand–arm
vibration syndrome (1). The physical exam should focus on a thorough examination of the
digits. Inspect the digits carefully for sclerodactyly or digital ulcers and examine the nail fold
capillaries for abnormally large capillary loops, alternating with areas without any capillaries.
This pattern is suggestive of scleroderma (4). Also inspect for Malar rash, persistent cyanosis,
and/or necrotic tissue of the digits.
144
Taylor’s DifferenTial Diagnosis Manual
B. Genetics. Although the exact pathophysiology of PRD and SRD remain unclear, there do
seem to be strong genetic influences. Familial analysis and twin studies have confirmed the
role of hereditary factors. Pedigree analysis indicates the possibility of an autosomal domi-
nant transmission influenced by sex in some families. At this time, sequencing of candidate
genes for genetic mutations remains negative (7).
IV. DIAGNOSIS.
A. Differential Diagnosis.
PRD is the most likely diagnosis in a young woman with less
severe symptoms and no underlying disease. SRD should be considered in anyone with a
known autoimmune disorder such as scleroderma or SLE. Other diagnoses to be considered
include thromboangiitis obliterans in a man who smokes, thoracic outlet syndrome, carpal
tunnel syndrome related to repetitive use of the hands, acrocyanosis, and cryoglobulinemia,
especially associated with hepatitis B or C. Drugs that may induce SRD include but are not
limited to beta blockers, oral contraceptives, antineoplastic drugs, ergot alkaloids, cyclospo-
rine, and alfa-interferon (8).
B. Clinical Manifestations. Color changes of the digits when exposed to the cold is the
classic presentation. Patients may not undergo all three color changes. Some literature states
that pallor followed by cyanosis is the most common pattern, while other sources note that
patients who have episodes with cyanosis have more severe disease (1). The most important
thing to keep in mind when diagnosing patients with Raynaud’s disease is that patients with
SRD will almost always have other symptoms of connective tissue disease in addition to the
symptoms of Raynaud’s disease.
REFERENCES
1. Block, JA. Raynaud’s phenomenon. Lancet 2001;357:2042–2048.
2. National Heart Lung and Blood Institute. Accessed at www.nhlbi.nih.gov/health/health-topics/topics/
raynaud/ on February 23, 2012.
3. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Accessed at www.niams.nih.gov
on April 1, 2012.
4. Clinical manifestations and diagnosis of the Raynaud phenomenon. Accessed at www.uptodate.com on
April 9, 2012.
5. Canada’s National Occupational Health and Safety Resource. Accessed at www.ccohs.ca/oshanswers/
diseases/raynaud/html on April 11, 2006.
6. Raynaud’s phenomenon, 2004. Accessed at www.firstconsult.com.
7. Pistorius MA, Planchon B, Schott JJ, Lemarec H. Hereditary and genetic aspects of Raynaud’s disease.
J Mal Vasc 2006;31(1):10–15.
8. Raynaud’s phenomenon, 2004. Accessed at www.imedicine.com.
7.13
Tachycardia
Hannah M. Heckart
I. BACKGROUND. Tachycardia is defined as a condition in which the heart rate is greater than
100 beats/minute for three or more beats. It can be categorized into two main types, supra-
ventricular or ventricular, with the former being further categorized into either wide complex
tachycardia or narrow complex tachycardia (1).
II. PATHOPHYSIOLOGY. In the evaluation of the patient with tachycardia, one needs to discover
the etiology of the tachycardia and then identify the specific arrhythmia. Symptoms of tachy-
cardia include chest discomfort, dyspnea, fatigue, light-headedness, presyncope, syncope, and
palpitations (2). Conditions to look for in the past medical history may include myocardial
Chapter 7 • Cardiovascular Problems
145
infarction, ventricular hypertrophy, heart failure, valvular heart disease, or congenital abnormali-
ties. Caffeine use, alcohol use, stress, and hypothyroidism can also precipitate tachycardia (1).
III. EVALUATION
A. History.
Determine if the patient is hemodynamically stable and if he or she is symptom-
atic (distressed or unconscious) or asymptomatic (awake and not distressed).
B. Physical Examination. Auscultate the heart, listening for murmurs, rubs, or gallops.
Look for jugular venous distention and lower extremity edema, which would indicate heart
failure. Listen to the lung fields for crackles. Feel the thyroid for enlargement.
C. Testing
1. Electrocardiogram (ECG). Obtain a 12-lead ECG and determine the rate, rhythm, and
QRS duration on the rhythm strip (commonly lead II).
2. Laboratory tests. Look for hypomagnesemia, hypokalemia, anemia, hyperthyroidism,
hypoxemia, illicit drugs, β-type natriuretic peptide, and digitalis toxicity.
IV. DIAGNOSIS
A. Narrow complex tachycardia (QRS < 120 ms)
1. Sinus tachycardia. There are numerous reasons for sinus tachycardia in adults: patho-
logic (anemia, thyrotoxicosis, hypoxemia, hypotension, hypovolemia) or physiologic
(anemia, fever). Normal P wave and QRS complexes are seen on the ECG. Therapy
consists in treating the underlying cause.
2. Atrial fibrillation. Atrial fibrillation is an irregularly irregular rhythm with a variable
ventricular rate and no discernable P waves on the ECG. If there is an aberrant conduc-
tion from the atria to ventricles or prior bundle branch block, it may be difficult to
distinguish atrial fibrillation from atrial flutter as it commonly shifts between fibrillation
and flutter.
3. Atrial flutter. In atrial flutter, cardiac monitoring shows the classic P wave “sawtooth”
appearance with a rate between 180 and 350 beats/minute. The ventricles have a slower
rate, demonstrating either 2:1 or 4:1 block with a corresponding ventricular rate of 150
to 75 beats/minute. Atrial flutter is associated with a risk of atrial thromboembolism.
4. Paroxysmal supraventricular tachycardia (SVT). Paroxysmal SVT is a rhythm that is
most commonly caused by the reentry of the atrial impulse at the atrioventricular (AV)
node. Morphology of the rhythm shows a sudden onset with a regular QRS complex and
a rate from 140 to 250 beats/minute. P wave may not be apparent because of retrograde
atrial depolarization that typically occurs simultaneously with ventricular depolarization.
Wolff-Parkinson-White syndrome occurs when there is antegrade conduction via an
accessory pathway, producing delta waves (upsloping prior to the QRS complex) and
shortened PR intervals.
5. Multifocal atrial tachycardia (MAT). MAT is an arrhythmia that may occur in cases of
heart failure or chronic obstructive pulmonary disease. MAT exists when there are three
different P-wave morphologies unrelated to each other.
B. Wide complex tachycardia (QRS >120 ms)
1. Ventricular Tachycardia (VT). There can be much difficulty in distinguishing SVT
with an aberrant conduction from VT. If there is any doubt about the origin of a
wide-complex tachycardia, the patient should be treated as if the rhythm is VT. These
electrocardiogram (EKG) clues can help differentiate between SVT and VT (3).
a. If an RS complex cannot be identified in any precordial leads, it is VT.
b. If an RS complex is identified, then an RS interval (the R wave onset to the S wave
nadir) of greater than 100 ms strongly suggests a VT.
c. If the RS interval is less than 100 ms, then there is either a ventricular or a supraven-
tricular origin site of the tachycardia and AV dissociation must be evaluated. However,
if AV dissociation is present, it is VT.
d. If the RS interval is <100 ms and there is no demonstrable AV dissociation, then look
for concordance of the precordial QRS complexes (leads V1–V6 all have a similar
negative appearance), which would also indicate VT.
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2. Torsade de Pointes (TdP). A form of polymorphic VT with varying amplitudes of the
QRS complex. Particularly seen in patients with a prolonged QT interval. May present
in patients with hypokalemia and hypomagnesemia. Medications like erythromycin,
phenothiazines, haloperidol, or methadone may cause TdP.
3. Ventricular fibrillation (VF). VF is a life-threatening arrhythmia resulting from abnor-
mal ventricular depolarizations that prevent an unified contraction of cardiac muscle.
On EKG, VF is characterized by a chaotic irregular appearance without discrete QRS
waveforms.
REFERENCES
1. Lilly, L. Pathophysiology of heart disease, 4th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2007.
2. Colucci R, Silver M, Shubrook J. Common types of supraventricular tachycardia: diagnosis and man-
agement. Am Fam Physician 2010;82(8):942–952.
3. Eckardt L, Breithardt G, Kirchhof P. Approach to wide complex tachycardias in patients without
structural heart disease. Heart 2006;92(5):704–711.
Chapter 7 • Cardiovascular Problems
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