Diagnostic Tests for Arrhythmias
Arrhythmias: Diagnostic Tests
The list of diagnostic tests
mentioned in various sources as
used in the diagnosis of Arrhythmias
includes:
Arrhythmias Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Arrhythmias:
- High Blood Pressure: Home Testing
- Heart Health: Home Testing:
Arrhythmias Diagnosis: Book Excerpts
Tests and diagnosis discussion for Arrhythmias:
NHLBI, Arrhythmia: NHLBI (Excerpt)
Sometimes an arrhythmia can be detected by listening to the
heart with a stethoscope. However, the electrocardiogram is the most precise
method for diagnosing the arrhythmia.
An arrhythmia may not occur at the time of the exam even though symptoms are
present at other times. In such cases, tests will be done if necessary to find
out whether an arrhythmia is causing the symptoms.
(Source: excerpt from NHLBI, Arrhythmia: NHLBI)
NHLBI, Arrhythmia: NHLBI (Excerpt)
First the doctor will take a
medical history and do a thorough physical exam. Then one or more tests may be
used to check for an arrhythmia and to decide whether it is caused by heart
disease.
Tests for Detecting Arrhythmias
- Electrocardiogram (ECG or EKG). A record of the
electrical activity of the heart. Disks are placed on the chest and
connected by wires to a recording machine. The heart's electrical
signals cause a pen to draw lines across a strip of graph paper in the
ECG machine. The doctor studies the shapes of these lines to check for
any changes in the normal rhythm. The types of ECGs are:
- Resting ECG. The patient lies down for a few minutes while
a record is made. In this type of ECG, disks are attached to the
patient's arms and legs as well as to the chest.
- Exercise ECG (stress test). The patient exercises either on
a treadmill machine or bicycle while connected to the ECG machine.
This test tells whether exercise causes arrhythmias or makes them
worse or whether there is evidence of inadequate blood flow to the
heart muscle ("ischemia").
- 24-hour ECG (Holter) monitoring. The patient goes about his
or her usual daily activities while wearing a small, portable tape
recorder that connects to the disks on the patient's chest. Over time,
this test shows changes in rhythm (or "ischemia") that may not be
detected during a resting or exercise ECG.
- Transtelephonic monitoring. The patient wears the tape
recorder and disks over a period of a few days to several weeks. When
the patient feels an arrhythmia, he or she telephones a monitoring
station where the record is made. If access to a telephone is not
possible, the patient has the option of activating the monitor's
memory function. Later, when a telephone is accessible, the patient
can transmit the recorded information from the memory to the
monitoring station. Transtelephonic monitoring can reveal arrhythmias
that occur only once every few days or weeks.
- Electrophysiologic study (EPS). A test for
arrhythmias that involves cardiac catheterization. Very thin, flexible
tubes (catheters) are placed in a vein of an arm or leg and advanced to
the right atrium and ventricle. This procedure allows doctors to find
the site and type of arrhythmia and how it responds to treatment.
|
(Source: excerpt from
NHLBI, Arrhythmia: NHLBI)
Diagnosis of Arrhythmias: medical news summaries:
The following medical news items
are relevant to diagnosis of Arrhythmias:
Diagnostic Tests for Arrhythmias: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the diagnostic tests for Arrhythmias.
BRADYCARDIA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
If there is fever without any definite focal signs, a CBC, sedimentation rate, blood culture, chemistry panel, febrile agglutinins, and tests for other antibodies may be done. If there is fever with nuchal rigidity, a spinal tap should be done, preferably after a CT scan. An EKG will need to be done on all patients, and if this shows simple sinus bradycardia and there is no history of drug ingestion, a thyroid profile should be done. If there is chest pain, serial EKGs and cardiac enzymes should be done. If there is a heart murmur, echocardiography would be an important ancillary study. If the EKG shows various types of arrhythmia, a cardiologist should be consulted for further evaluation.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
PALPITATIONS:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
Before initiating an expensive workup, the patient should eliminate use of all drugs, alcohol, caffeine, and nicotine, if possible, for several days. If this does not eliminate the palpitations, a careful inquiry into the dietary habits should be made, and a CBC should be done to eliminate anemia. In the presence of tachycardia, weight loss, and increased appetite, it is obvious that a thyroid profile should be drawn. If there are palpitations and fever, a workup for an infectious disease, particularly rheumatic fever and bacterial endocarditis, is in order. Blood cultures, ASO titers, sedimentation rate, and echocardiography are useful. If the palpitations are intermittent, a pheochromocytoma should be considered, and 24-hr urine collection for VMA or metanephrines should be ordered. A drug screen may be necessary to ensure patient cooperation in eliminating all drugs. Twenty-four-hr blood pressure monitoring is also useful. In addition, 24-hr or 48-hr Holter monitoring is very useful in the diagnosis of intermittent palpitations. Newer technology involving a continuous-loop event recorder allows monitoring for 2 weeks at a time. Arm-to-tongue circulation times as well as spirometry may diagnose early congestive heart failure.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
TACHYCARDIA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
Routine diagnostic tests should include a CBC, sedimentation rate, urinalysis, chemistry panel, toxicology screen, thyroid profile, ANA titer, VDRL test, chest x-ray, and EKG. If there is fever, then an ASO titer and CRP, febrile agglutinins, and serial blood cultures should be done.
If a myocardial infarction is suspected, serial EKGs and cardiac enzymes need to be ordered. If a pulmonary embolism or infarction is suspected, arterial blood gases and lung scans need to be ordered, and, ultimately, pulmonary angiography may need to be done.
If congestive heart failure is suspected, a venous pressure and circulation time and possibly pulmonary function studies may be done. Echocardiography may be done to determine the LVEF.
If the tachycardia is paroxysmal, 24-hr Holter monitoring or admission to the hospital for ambulatory telemetry and observation may be necessary. A cardiologist should be consulted. Ultimately, a psychiatrist may need to be consulted also.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
CARDIAC ARRHYTHMIA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
All patients should have an EKG, chest x-ray, and a CBC to rule out anemia. A thyroid profile should be done to look for both hyperthyroidism and hypothyroidism. In acute arrhythmias, serial EKGs and tests for cardiac enzymes need to be done to exclude an acute myocardial infarction. Venous pressure and circulation time should be determined to rule out congestive heart failure; pulmonary function tests may be helpful, as they may rule out both congestive heart failure and emphysema. Echocardiograms should be done to rule out valvular disease and cardiomyopathy. If there are paroxysmal arrhythmias, Holter monitoring needs to be done. An exercise tolerance test may allow the recording of an arrhythmia that is only induced on exercise. Signal-averaged EKG and electrophysiologic testing should also be considered. Patients on digitalis, quinidine, or other cardiac drugs should have blood levels of these drugs measured to determine if their levels are toxic. If there is a fever, blood culture should be done to rule out bacterial endocarditis. Referral to a cardiologist can be made at any point in the diagnostic workup.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
CARDIAC MURMURS:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
If the murmur is believed to be organic, the most cost-effective approach would be to consult a cardiologist at the outset. If the astute clinician wishes to pursue the diagnostic workup on his own, it is suggested that a CBC, sedimentation rate, chemistry panel, VDRL test, and thyroid profile should be done for the initial blood work. In addition, a chest x-ray including obliques, congestive heart failure, phonocardiograms, and EKG should be performed. These findings may provide a diagnosis. If there is fever, a streptozyme test, antistreptolysin-O (ASO) titer, and serial blood culture should be performed. If congestive heart failure is suspected, venous pressure and circulation time should be determined. Pulmonary function studies are also helpful. Echocardiography will be extremely helpful in diagnosing the various forms of valvular disease and will also help in identifying a pericardial effusion, congestive heart failure, or the various cardiomyopathies. Cardiac catheterization and angiography and angiocardiography will identify the various congenital heart lesions and valvular disease. These studies, however, are most important when surgery is being considered.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Bradycardia:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
After detecting bradycardia, check for related signs of life-threatening disorders. (See Managing severe bradycardia.) If the patient's bradycardia isn't accompanied by untoward signs, ask the patient if he or a family member has a history of a slow pulse rate because this may be inherited. Also, find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he's taking and if he's complying with the prescribed schedule and dosage. Monitor his vital signs, temperature, pulse, respirations, blood pressure, and oxygen saturation.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Murmurs:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 406.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.
Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient’s medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.
Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Palpitations:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient isn’t in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Make sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Also, ask about caffeine, tobacco, and alcohol consumption.
Then explore associated symptoms, such as weakness, fatigue, and angina. Finally, auscultate for gallops, murmurs, and abnormal breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Pulse rhythm abnormality:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient’s compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.
Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Pulse, absent or weak:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If you detect an absent or a weak pulse, quickly palpate the remaining arterial
pulses to distinguish between localized or generalized loss or weakness. Then quickly check the patient’s other vital signs, evaluate his cardiopulmonary status, and obtain a brief history. Based on your findings, proceed with emergency interventions. (See Managing an absent or a weak pulse, pages 506 and 507.)
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Pulsus bisferiens:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
After you detect a biferious pulse, review the patient’s history for cardiac disorders. Next, find out what medication he’s taking, if any, and ask if he has other illnesses. Also, ask about the development of associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest. Then take his vital signs and auscultate for abnormal heart or breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Tachycardia:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient’s condition permits, take a focused history. Find out if he has had palpitations. If so, how were they treated? Explore associated symptoms. Is the 0patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.
Inspect the patient’s skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Bradycardia:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
After detecting bradycardia, check for related signs of life-threatening disorders. (See Managing severe bradycardia.) If bradycardia isn’t accompanied by untoward signs, ask the patient if he or a family member has a history of a slow pulse rate because this may be inherited. Also, find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he’s taking and if he’s complying with the prescribed schedule and dosage. Monitor vital signs, temperature, pulse rate, respirations, blood pressure, and oxygen saturation.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Murmurs:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 517.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.
Next, obtain a patient history. Ask if the murmur is a new discovery, or if it has been known since birth or childhood. Find out if the patient has experienced any associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. (See Differential diagnosis: Murmurs, pages 518 and 519.) Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.
Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Palpitations:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient isn’t in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Be sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Ask about caffeine, tobacco, and alcohol consumption.
Explore associated symptoms, such as weakness, fatigue, and angina. Auscultate for gallops, murmurs, and abnormal breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Pulse rhythm abnormality:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about onset and location. Does the pain radiate? Ask about a history of heart disease and treatments for arrhythmias. Obtain a drug history and check compliance. Also, ask about any caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.
Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Pulse, absent or weak:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If you detect an absent or weak pulse, quickly palpate the remaining arterial pulses to distinguish between localized or generalized loss or weakness. Then quickly check other vital signs, evaluate cardiopulmonary status, and obtain a brief history. Based on your findings, proceed with emergency interventions. (See Managing an absent or weak pulse, pages 638 and 639.)
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Pulsus bisferiens:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
After you detect a bisferiens pulse, review the patient’s history for cardiac disorders. Next, find out what medication he’s taking, if any, and ask if he has any other illnesses. Ask about the development of any associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest. Take his vital signs and auscultate for abnormal heart or breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Tachycardia:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient’s condition permits, take a focused history. Find out if he has had palpitations before. If so, how were they treated? Explore associated symptoms. Is the patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.
Inspect the patient’s skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Bradycardia:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Vital signs. Heart rate and blood pressure determine the immediacy of treatment.
B. Inspection, palpation, and auscultation. Bradycardia is best revealed on physical examination by inspection of the jugular pulses, palpation of the arterial pulse, and auscultation of the heart. Inspection of the jugular pulses is vital in the evaluation of bradycardia, and they often reveal atrial activity. For example, cannon waves are seen intermittently in complete heart block as the atrium contracts against a closed tricuspid valve. Palpation of the arterial pulse establishes the conducted ventricular rate. Auscultation establishes ventricular rate and rhythm. The intensity of S 1 is an important heart sound in the evaluation of bradycardia. A soft S1 suggests a first-degree AV block. A variation in S1 intensity suggests second- or third-degree AV block. In third-degree AV block, the intensity of heart sounds is augmented when an atrial systole immediately precedes ventricular contraction.
C. Associated conditions. The physical examination should include an assessment for evidence of cardiac decompensation (e.g., jugular venous distension, pulmonary crackles, lower extremity edema, gallops, murmurs), and thyroid disease.
Testing
A. Electrocardiogram (ECG). It is essential to obtain an ECG when evaluating a patient with bradycardia. Usually, a resting ECG is sufficient, but occasionally an ambulatory (Holter) monitor or exercise ECG is indicated. Atrial activity is best assessed in leads II, III, aVf, and V1. The presence of P waves, their configuration, and their relationship to QRS complexes must be established. Normally, the PR interval is between 0.12 and 0.20 seconds and each QRS complex is preceded by a P wave (5).
B. Laboratory. The following tests should be considered when appropriate:
1. Electrolytes: potassium, calcium, and magnesium
2. Drug levels: digoxin, quinidine, and procainamide
3. Thyroid function tests
Diagnostic assessment
The key to the diagnosis of bradycardia is a focused history, physical examination, and an ECG. No specific symptoms will separate the various causes of bradycardia.
A. Sinus bradycardia
1. Etiology. Normal (well-conditioned athletes), sleep, carotid sinus massage, glaucoma, increased intracranial pressure, and an acute inferior wall myocardial infarction.
2. ECG. Normal P-QRS-T sequence at a rate less than 60 beats/minute (5).
B. Sinus node exit block (sinoatrial node block, SA block).
1. Etiology. Medications (digitalis, quinidine, procainamide, salicylates), hyperkalemia, cardiomyopathy, IHD, and vagal stimulation or increased vagal tone.
2. ECG. A missing P wave is the hallmark of SA block. The prolonged PP interval must be a multiple of the baseline PP interval; otherwise it is called a sinus pause.
a. Incomplete SA block: occasional absence of P-QRS-T sequence.
b. Complete SA block: P waves absent, QRS-T sequence present but at a slow rate, QRS interval varies depending on the origin of the escape pacemaker (5).
C. Sick-sinus syndrome is a generalized abnormality of cardiac impulse formation and intraatrial and AV conduction abnormalities that can be manifested by various combinations of brady- and tachyarrhythmias (4).
1. Etiology. Idiopathic fibrosis or degeneration of sinoatrial and AV conduction system, IHD, amyloidosis, surgical injury, and hypertension. More prevalent in the geriatric population (4).
2. ECG. The hallmark is sinus nodal depression, including sinus bradycardia, sinus arrest, and sinoatrial exit block. Also seen are AV node dysfunction, and atrial fibrillation or atrial tachyarrhythmias with slow ventricular response (5).
D. First-degree AV block is defined as a prolonged PR interval. The block may be caused by a prolongation of conduction in any of the structures between the SA node and His bundle.
1. Etiology. Found in well-conditioned people (long distance runners, heavy laborers), elderly patients; other causes include increased vagal tone (pain, vomiting, vasovagal syncope), medications (digitalis, quinidine, procainamide, propranolol, verapamil), acute rheumatic fever, myocarditis, and congenital heart disease (4).
2. ECG. PR interval greater than 0.20 seconds. Each P wave followed by a QRS complex (5).
E. Second-degree AV Block, Mobitz I (Wenckebach), is characterized
by intermittent failure of conduction from atria to ventricles with progressive lengthening of the PR interval, eventually leading to a nonconducted P wave.
1. Etiology. Normal variant occurs in well-conditioned people; causes include medications (digitalis, beta-blockers, calcium blockers, clonidine, methyldopa, flecainide, encainide, propafenone, lithium), MI (especially inferior MI), acute rheumatic fever, and myocarditis (4).
2. ECG. PR interval progressively increases and the RR interval shortens until a nonconducted P wave occurs. Typically, small groups of beats occur, such as pairs and trios (5).
F. Second-degree AV Block, Mobitz II, is characterized by intermittent
failure of conduction from atria to ventricles where appropriately timed
P waves fail to conduct and no pattern is seen of progressive PR lengthening.
1. Etiology. Almost always secondary to organic heart disease (4).
2. ECG. PR interval is fixed with intermittent, nonconducted P waves. Conducted P waves with the same PR interval. Often it is associated with a bundle branch block (5).
G. Third degree block is defined as no atrial impulses reaching the ventricle through the AV conduction system.
1. Etiology. Causes include congenital heart block (maternal anti-Ro antibodies), cardiomyopathy, IHD, aortic valve disease, endocarditis, Lyme disease, infiltrative processes (amyloid, sarcoid), medications (digitalis, quinidine, procainamide), hyperkalemia, connective tissue disease, trauma, and acute rheumatic fever (4).
2. ECG. No AV conduction occurs. The atrial rate is faster than the ventricular rate. PP and RR intervals are constant: numerous P waves are seen, which occur at all phases of the ventricular cycle (5).
References
1. Emergency Cardiac Care Committee and Subcommittee, American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 1992;268:2171–2302.
2. Brady Jr WJ, Harrigan RA. Evaluation and management of bradyarrhythmias in the emergency department. Emerg Med Clin North Am 1998;16:361–388.
3. Alexander RW, Schlant RC, Fuster V. Bradydysrhythmias in the heart. New York: McGraw-Hill 1998:927–941.
4. DiMarco JP. Cardiac arrhythmias and conduction disorders. In: Freed M, Grimes C, ed. Essentials of cardiovascular medicine. New York: Physician’s Press 1994:137–138, 168, 181–185.
5. Marriott HJL. Practical electrocardiography, 8th ed. Baltimore: Williams & Wilkins, 1988:371, 353–376.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Palpitations:
Physical examination (PE)
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
If the patient is not seen during an episode, aim the PE at detecting abnormalities that are associated with PPTs. Midsystolic click and murmur (mitral valve prolapse), harsh holosystolic murmur (hypertrophic cardiomyopathy), diastolic murmur (aortic regurgitation), or signs of congestive heart failure may aid in diagnosis. Look for stigmata of hyperthyroidism and other conditions noted above (II.E) (Chapter 14.8).
Testing
A. 12-lead electrocardiogram (ECG). All patients with PPTs should have an ECG. The presence of an arrhythmia may be diagnostic. Findings between episodes can include short PR interval and delta waves (preexcitation),
Q waves (VT, PVCs), long QT interval (drugs, long QT syndrome), left ventricular hypertrophy with left atrial abnormality (AF), and complete heart block (PVCs, torsades de pointes) (3).
B. Laboratory testing. Initial laboratory testing consists of serum potassium, hemoglobin and hematocrit, and thyroid-stimulating hormone; serum glucose can be added with a suspicion of hypoglycemia.
C. Ambulatory ECG recording (AECG). For patients in whom a diagnosis has not been made with the initial evaluation, AECG monitoring is indicated. A Holter monitor (24- or 48-hour continuous ECG) should be the initial study for patients with daily symptoms. In those with less frequent episodes, a continuous-loop event recorder worn for a duration of 2 weeks is more cost-effective (4,5).
Diagnostic assessment
The history, PE, and ECG are important steps in the evaluation of PPTs, although many patients will require ambulatory ECG testing to reach a diagnosis. If symptoms correlate with arrhythmias on AECG monitoring, a diagnosis can be made and treatment begun, if appropriate. If no arrhythmia occurs and the patient has typical PPTs, a benign cause is likely. When no symptoms and no arrhythmias are found, the AECG is nondiagnostic and repeat testing or referral may be necessary, especially with underlying heart disease or poorly tolerated PPTs.
References
1. Weber BE, Kapoor WN. Evaluation and outcomes of patients with palpitations. Am J Med 1996;100:138–148.
2. Barsky AJ, Cleary PD, Coeytaux RR, Ruskin JN. The clinical course of palpitations in medical outpatients. Arch Intern Med 1995;155:1782–1788.
3. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl
J Med 1998;338:1369–1373.
4. Kinlay S, Leitch JW, Neil A, Chapman BL, Hardy DB, Fletcher PJ. Cardiac event recorders yield more diagnoses and are more cost-effective than 48-hour Holter monitoring in patients with palpitations. Ann Intern Med 1996;124:16–20.
5. Zimetbaum PJ, Kim KY, Josephson ME, Goldberger AL, Cohen DJ. Diagnostic yield and optimal duration of continuous-loop event monitoring for the diagnosis of palpitations. Ann Intern Med 1998;128:890–895.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Tachycardia:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
The physical examination should include vital signs; pulse rate and blood pressure are the most important. Decreased blood pressure suggests a need for immediate treatment. A general assessment of mental status and skin perfusion also provides clues to the stability of the patient. A good cardiovascular and pulmonary examination is essential. Palpation of the heart (point of maximal impulse, PMI) can discern left ventricular enlargement. Auscultate systematically. The rhythm should be assessed to whether it is regular or irregular. Determine the specific heart rate. Next, determine if an associated murmur, rub, or gallop exists. Include in the examination an assessment for evidence of ventricular failure (e.g., pulmonary crackles, jugular venous distension, and lower extremity edema). In the respiratory assessment, include respiratory rate and evidence of labored breathing.
Testing
A. Electrocardiogram (ECG). The main diagnostic test is the 12-lead ECG: a rhythm strip during a tachycardia event is ideal. The Holter or event monitor can also be used in diagnosis in an outpatient setting. Rhythm and the QRS width are important in distinguishing the major types of tachycardia.
B. Laboratory tests. Electrolyte abnormalities, especially hypomagnasemia and hypokalemia, can precipitate tachycardia. Digitalis toxicity can be another cause and, therefore, levels should be monitored. Also consider tests for common problems such as anemia, hyperthyroidism, and hypoxemia.
Diagnostic assessment
A. Narrow complex tachycardia (QRS < 120 msec)
1. Sinus tachycardia. Sinus tachycardia is normal in infants and children aged less than 2 years. In adults, it is often secondary to physiologic factors (anxiety, fever), pharmacologic factors (β-agonist therapy), and pathologic factors (anemia, thyrotoxicosis, hypoxemia, hypotension, pulmonary embolism). ECG findings reveal a normal P wave and PR interval. Management of sinus tachycardia is directed at correcting the underlying cause; specific therapy is rarely indicated.
2. Atrial fibrillation. Atrial fibrillation (AF) occurs in approximately 10% of patients aged more than 70 years. The hallmark on ECG is an irregularly irregular rhythm and rate with the absence of P waves. The rate in AF can vary from normal to fast (> 200 beats/min). The QRS morphology can vary a great deal as well. Usually, the impulse originates from the atrium and travels down the His or Purkinje system with depolarization of the ventricle. Occasionally, the impulse from the atrium travels down to the ventricle abnormally, resulting in aberrant conduction, and it can mimic ventricular tachycardia (VT). The key to distinguishing the two is recognizing a regular rhythm for VT and irregular rhythm for AF with aberrant conduction. In addition, patients with a prior bundle branch block who go into rapid AF can also mimic VT (see below). AF can result from cardiac [coronary artery disease, Wolff-Parkinson-White (WPW) syndrome, congestive heart failure, valvular abnormalities] or noncardiac (thyrotoxicosis, pulmonary embolism) sources. The underlying cause of the AF must be elucidated.
3. Atrial flutter. As with AF, atrial flutter can also be caused by both cardiac and noncardiac sources. The ECG is classically a “sawtooth” pattern in leads II, III, and aVF. The rate of the flutter waves is usually between 280 and 320 beats/minute. Ventricular conduction varies and usually demonstrates blocked conduction. The usual block is 2;1 or 4;1, with a ventricular rate of 150 to 75 beats/minute, respectively. Occasionally, the rate is too fast to discern any flutter waves. Carotid massage slows the ventricular rate, allowing for diagnosis. If carotid massage fails, pharmacologic treatment with adenosine or digitalis can slow the ventricular rate.
4. Paroxysmal supraventricular tachycardia (PSVT). PSVT is precipitated by reentry of the atrial impulse at the level of the atrioventricular (AV) node. This is the most common mechanism in the initiation of PSVT. PSVT is characterized by sudden onset of a narrow, regular QRS complex without discernible P waves. The rate varies from 160 to 190 beats/minute but can be as slow as 120 to 130 beats/minute. If the patient has a prior bundle branch block, a wide QRS complex will also be seen with PSVT. A specific subset of PSVT caused by reentry is the WPW syndrome. Conduction in WPW can occur via an accessory pathway. In the resting ECG, this is usually manifested by an upsloping tracing on the ECG prior to the QRS complex, known as the “delta wave.” PR interval is also shortened. The accessory tract can predispose to PSVT, atrial flutter, or AF.
5. Multifocal atrial tachycardia (MAT). This arrhythmia is usually seen in the setting of pulmonary disease, metabolic or electrolyte abnormalities, or, rarely, digitalis toxicity. ECG findings in MAT consists of an irregular rhythm combined with three different morphologies of P waves. The rate of this arrhythmia usually does not exceed 140 beats/minute. Removal of the inciting event can relieve the tachycardia, but patients may frequently have to tolerate a low-grade tachycardia (1,2).
B. Wide complex tachycardia (QRS > 120 msec)
1. Ventricular tachycardia versus SVT with aberrant conduction. This is probably the hardest to diagnose of the tachycardias. Brudaga (3) put forth a schema to diagnose VT from SVT with aberrant conduction. The criteria are as follows:
a. Initially rule out right or left bundle branch block.
b. Is there an absence of an RS complex in all precordial leads? If yes then VT, if no then proceed to c.
c. Is the RS interval more than 100 msec in any one precordial lead? If yes then VT, if no then proceed to d.
d. Is there AV dissociation? If yes then VT. If no is answered to all the above then the specificity or sensitivity that this is a SVT with aberrant conduction is 98% and 99%, respectively. Inexact features of VT are QRS more than 0.14 second, QRS concordance in all precordial leads, fusion or capture beats, and QRS negative in leads I and II.
2. Ventricular fibrillation (VF). VF is not really a tachycardia but represents abnormal ventricular depolarization. The ventricle has numerous areas of depolarization and, therefore, cannot have organized contraction. This type of unorganized contraction produces no cardiac output. On ECG, it often appears as a “bag of worms” with coarse or fine waves varying in amplitude and duration. Coarse VF indicates the recent onset of VF and is usually correctable with defibrillation, whereas fine VF is indicative of prolonged VF that approaches asystole.
References
1. Scheinman M. Tachyarrythmias in primary cardiology. In: Goldman L, Braunwald E, ed. Heart disease: a textbook of cardiovascular medcicine. Philadelphia: WB Saunders, 1998:330–352.
2. Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995; 332:162–173.
3. Brugada P. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649–1659. >>
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Heart Murmur, Diastolic:
Physical examination (PE)
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Table 7.3 lists characteristic PE findings of diastolic murmurs.
B. Fine points of the physical examination
1. Is the murmur of AR louder at the right sternal border? If so, consider aortic root dilation. Remember, whereas the duration of the chronic AR murmur is directly proportional to the severity of the regurgitation, the duration of the acute AR murmur may not predict its severity (3).
2. Is the murmur of MS shorter, or does it extend closer to S2? The length of this murmur, not its intensity, is directly proportional to the severity of the stenosis (3). In addition, the murmur may not be audible with increased heart rates because of shortening of diastole.
3. Does the murmur of MS vary from examination to examination? If so, and especially if it is introduced by a “plop” sound, consider atrial myxoma.
Testing
Echocardiogram is the essential test for confirming the anatomic location of the murmur and its severity. Transthoracic echocardiography (ECHO) is generally sufficient, unless endocarditis is suspected, in which case a transesophageal ECHO is preferred to evaluate for vegetations. If aortic root dilatation is present on ECHO, a computed tomography or magnetic resonance imaging scan may help to delineate the anatomy further. Additional laboratory testing may be warranted to further evaluate the underlying cause (e.g., serologic studies for collagen vascular disease, serologic test for syphilis, and so on).
Diagnostic assessment
With a careful examination and thorough history, the valve causing the murmur and the probable cause of the valvular lesion can be identified prior to ordering the definitive test (ECHO). The most common cause of all diastolic murmurs is still rheumatic heart disease, even though the incidence of acute rheumatic fever has decreased. Mitral stenosis is almost invariably caused by rheumatic heart disease (98% in one study of excised valves) (3,4), with the remainder caused by vegetations (from endocarditis) or congenital factors (4). Tricuspid stenosis is also predominantly rheumatic in origin and is rarely an isolated lesion. Other causes of TS include carcinoid and congenital malformations. Rheumatic heart disease is the leading cause of chronic AR, followed by congenital bicuspid valves and aortic root dilatation (Marfan’s syndrome, Ehlers-Danlos syndrome, ankylosing spondylitis, and syphilitic aortitis). If chronic, AR can result in LV dilation and compensation; if acute, it can be associated with severe LV overload and significant symptoms. Acute AR is most often related to endocarditis, aortic dissection, and trauma. Pulmonary regurgitation without hypertension has multiple causes, including pulmonary trunk dilation, endocarditis, carcinoid, trauma (from balloon-tipped catheters), and rheumatic fever. The nonstenotic physiologic murmurs are related to high-flow states across an otherwise normal mitral
or tricuspid valve. For a mitral flow murmur, the primary lesions are usually mitral regurgitation, ventricular septal defects, or patent ductus arteriosus. For a tricuspid flow murmur, an atrial septal defect or severe tricuspid regurgitation is the most common cause. The Austin–Flint murmur, caused by increasing left ventricular pressure pushing the anterior mitral leaflet into the flow of blood coming from the atrium, is the result of significant aortic regurgitation.
References
1. Chizner MA, ed. Classical teachings in clinical cardiology. Chatham, New Jersey: Laennec Publishing, 1996.
2. Coblyn JS, Weinblatt ME. Rheumatic disease and the heart. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine, 5th ed. Philadelphia: WB Saunders, 1997:1776–1785.
3. Abrams J, ed. Synopsis of cardiac physical diagnosis. Philadelphia: Lea & Febiger, 1989.
4. Olson LJ, Subramanian MB, Ackermann DM, Orszulak TA, Edwards WM. Surgical pathology of the mitral valve: a study of 712 cases spanning 21 years. Mayo Clin Proc 1987;62:22–34.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Heart Murmur, Systolic:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Technique. Auscultate the heart with the bell to best detect lower frequencies and the heart sounds (S1-S4). The quality of the murmur is best heard with the diaphragm. Inspiration increases the audibility of right ventricular sounds.
B. Murmur characteristics. Table 7.4 presents a summary of the characteristics of different causes of systolic murmurs (2,3). Etchell et al. (3) have prepared a comprehensive review on the usefulness of specific physical examination findings in the diagnosis of systolic murmurs.
Testing
Testing of an undiagnosed cardiac murmur can include an electrocardiogram (ECG), a chest x-ray study (CXR), and an echocardiogram. Echocardiograms, although useful for quantification of stenotic valvular disease, can overestimate the degree of regurgitation.
A. Aortic stenosis. Specific ECG findings in aortic stenosis can include left ventricular hypertrophy (LVH), left axis deviation, conduction disturbances, and atrial hypertrophy. On CXR, cardiac size remains normal until stenosis is severe, then signs of CHF may be present. The echocardiogram may reveal thickened or calcified aortic leaflets, bicuspid valve, and LVH. The size of
the valve can be estimated and the pressure gradient across the valve can
be assessed. Cardiac catheterization can also be used to assess the size of the valve and the gradient. Even though echocardiography is accurate in measuring valve area and gradient, catheterization is usually indicated because 50% of patients above age 40 years have coronary artery disease.
B. Mitral regurgitation. In mitral regurgitation, the ECG may reveal LVH with left atrial enlargement and later in the course, atrial fibrillation. In severe disease, CXR usually reveals cardiomegaly without pulmonary venous congestion. The echocardiogram reveals valvular anatomy, but can overestimate the severity of the regurgitation. Exercise testing can be used to determine clinical deterioration in mitral regurgitation. Catheterization is used to assess the contractile state of the ventricle as well as the regurgitant and forward stroke volume.
C. Other disease processes. The ECG with tricuspid insufficiency often reveals atrial fibrillation. The CXR may show right atrial hypertrophy, and the echocardiogram shows valvular anatomy. Pulmonic stenosis will lead to ECG findings consistent with right ventricular hypertrophy. Hypertrophic cardiomyopathy is best diagnosed by echocardiography. ECG may reveal LVH and occasionally a shortened PR interval is seen. Cardiac catheterization can be used to quantify the gradient caused by the hypertrophic lesion.
Diagnostic assessment
The history and physical examination with special emphasis on auscultation are the keys to the diagnosis of systolic murmurs. Those with symptomatic murmurs or in whom valvular disease is suspected should have an ECG, CXR, and echocardiogram. Murmurs of unknown duration or new murmurs should be worked up promptly with consideration of acute infarction in mind. If aortic stenosis is suspected, the workup should be expedited because sudden death can be the first clinical presentation. Valvular disease must always be considered with new onset congestive heart failure. Table 7.5 lists some of the online resources available to assist in the evaluation of heart murmurs.
References
1. Rackley C. Valvular heart disease. In: Bennett JC, Plum F, eds. Cecil textbook of medicine, 20th ed. Philadelphia: WB Saunders, 1996.
2. O’Connor D. The art of auscultation. Patient Care 1998;38:56–60.
3. Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA 1997;277:564–571.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Bradycardia:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The mean normal heart rate is 70 beats/minute, with 2 standard deviations below being 46 in men and 51 in women. Sinus bradycardia may occur in the absence of heart disease in young adults, well-conditioned athletes, and during sleep. Symptoms of bradycardia include paroxysmal dizziness, fatigue, presyncopal lightheadedness, and syncope. Sinus bradycardia is manifest as a regular slow rhythm. Complete heart block is usually accompanied by a very slow, usually irregular escape rhythm, and a symptomatic reduction in cardiac output producing lightheadedness and shortness of breath.
Relative bradycardia—that is, failure to respond to fever with tachycardia—suggests typhoid fever, mycoplasma pneumonia, factitious fever, or concomitant beta blockers.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Palpitations/Tachycardia:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
A disquieting awareness of the heartbeat described as pounding, skipping, racing, flopping, or fluttering is usually due to an arrhythmia, or a change in rhythm, rate, or contractility.
Arrhythmia should be approached both from the standpoint of determining the specific rhythm disturbance and recognizing it as a marker for other potentially serious disorders. Signs of underlying heart disease such as ischemia (exertional chest pain), cardiomyopathy (rales, S3 gallop, diffuse PMI), or syncope must be searched for because they alter the prognostic implications of the rhythm disorder.
A sensation of pounding in the neck is associated with jugular cannon a waves. Presence of a cannon a wave implies atrial contraction and can rule out atrial fibrillation. Intermittent cannon a waves result from atrioventricular dissociation.
Carotid massage will suddenly halve the rate with atrial flutter, but there is a gradual slowing of the pulse with sinus tachycardia. Supraventricular tachycardia either continues or terminates abruptly with carotid massage.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Diastolic Murmur:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
A diastolic murmur is always abnormal. An early diastolic murmur, caused by aortic or pulmonic regurgitation, is high-pitched and decrescendo. The duration of the murmur is an index of severity. A mid-diastolic murmur suggests mitral or tricuspid stenosis.
The murmur of mitral stenosis decreases or does not change with inspiration whereas the murmur of tricuspid stenosis increases.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Systolic Murmur:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The intensity of the murmur is proportional to the degree of stenosis until flow decreases markedly. Intensity can be expressed semiquantitatively, from grade 1/6, heard only with concentration, to grade 4/6, a loud murmur associated with a palpable thrill, to grade 6/6 with a thrill and murmur heard with the stethoscope off the chest. The duration of the murmur is proportional to the pressure differential between the two chambers.
An early systolic murmur, decrescendo at the apex, occurs in acute, severe mitral regurgitation (MR) with papillary muscle rupture, endocarditis, ruptured chordae tendineae, or blunt chest trauma. A midsystolic murmur is typical of aortic stenosis (AS). It can also be found with hypertrophic obstructive cardiomyopathy (HOC) and with hyperdynamic states. A late systolic murmur is usually heard with mitral valve prolapse (MVP) in association with a midsystolic click. A holosystolic murmur can be produced by severe MR or tricuspid regurgitation (TR), or by a ventricular septal defect (VSD), when the pressure differential between chambers persists throughout systole. Holosystolic murmurs are almost never innocent.
Handgrip decreases AS and HOC murmurs but increases MR, aortic regurgitation (AR), VSD, and mitral stenosis (MS). Transient arterial occlusion by a blood pressure cuff 20 mm above systolic increases left-sided murmurs. Valsalva decreases most murmurs (decreased right and left ventricular filling), except HOC and MVP, which increase.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Continuous Murmur:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Continuous murmurs begin in systole and extend into diastole without interruption. The murmur results from blood flow from a higher pressure chamber or vessel to a lower pressure system, with the gradient maintained during both systole and diastole, for example with aortopulmonary and arteriovenous connections.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Bradycardia:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Monitor vital signs, temperature, pulse, respirations, blood pressure, and oxygen saturation. Then perform a complete cardiac assessment.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Murmurs:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Perform a systematic physical assessment. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Palpitations:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Perform a complete cardiac and pulmonary assessment. Then explore associated symptoms, such as weakness, fatigue, and angina. Be sure to auscultate for gallops, murmurs, and abnormal breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulse rhythm abnormality:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulse, absent or weak:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If you detect an absent or weak pulse, palpate the remaining arterial pulses to distinguish between localized or generalized loss or weakness. (See Managing an absent or weak pulse, pages 532 and 533.) Then check other vital signs and evaluate cardiopulmonary status.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulsus bisferiens:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Take the patient’s vital signs, and auscultate for abnormal heart or breath sounds. Then complete the cardiopulmonary assessment.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Tachycardia:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Inspect the patient’s skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Heart Murmurs (Asymptomatic):
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
To distinguisha normal from a pathologic murmur, physicians must rely on theirskill in physical exam of cardiovascular system; on their interpretationof chest radiograph, ECG, and 2-D echocardiogram; and on their knowledgeof the diagnostic possibilities that each murmur suggests.In most cases, cardiovascular examat bedside can distinguish a normal from a pathologic murmur.With a normalmurmur, no tests are needed. Physicians can reassure parents andexplain that the murmur is a normal phenomenon due to normal turbulenceof blood flow. They can also emphasize that the murmur is not indicativeof mild heart disease, nor is it of any importance whether it disappears.With a pathologic murmur, precise diagnosismust be made because subsequent management depends on it. Diagnosisof pathologic murmurs is based on cardiovascular exam in conjunctionwith chest radiograph and ECG and sometimes 2-D echocardiogram. Only rarely are cardiac catheterizationand angiography needed to clarify etiology of murmurs in asymptomaticchildren.
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Bradycardia:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After detecting bradycardia, check for related signs of life-threatening disorders. (See Managing severe bradycardia, page 94.)
If the patient's bradycardia isn't accompanied by untoward signs, ask the patient if he or a family member has a history of a slow pulse rate because this may be inherited. Find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he's taking and if he's complying with the prescribed schedule and dosage. Monitor his vital signs, temperature, pulse, respirations, blood pressure, and oxygen saturation.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Murmurs:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 398.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.
Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient's medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.
Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient's liver tender or palpable? Does he have peripheral edema?
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Palpitations:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient isn't in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Be sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Also, ask about caffeine, tobacco, and alcohol consumption.
Then explore associated symptoms, such as weakness, fatigue, and angina. Finally, auscultate for gallops, murmurs, and abnormal breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Pulse rhythm abnormality:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient's condition permits, ask if he's experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient's compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.
Next, check the patient's apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient's apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Place the patient on a cardiac monitor and obtain an ECG to evaluate the cardiac rhythm. Report your findings to the practitioner.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Pulse, absent or weak:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If you detect an absent or a weak pulse, quickly palpate the remaining arterial pulses to distinguish between localized or generalized loss or weakness. If localized, ask whether the patient has experienced or is presently experiencing pain in that area. Assess the limb for color and temperature. Then quickly check the patient's other vital signs, evaluate his cardiopulmonary status, and obtain a brief history. Based on your findings, proceed with emergency interventions. (See Managing an absent or a weak pulse, pages 498 and 499.)
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Pulsus bisferiens:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After you detect a biferious pulse, review the patient's history for cardiac disorders. Next, find out what medication he's taking, if any, and ask if he has other illnesses. Also, ask about the development of associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest. Then take his vital signs and auscultate for abnormal heart or breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Tachycardia:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient's condition permits, take a focused history. Find out if he has had palpitations in the past. If so, how were they treated? Explore associated symptoms. Is the patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.
Inspect the patient's skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
A person with atrial fibrillation has two options; they can remain in atrial fibrillation or restore sinus rhythm. Learn the factors that may have an...
Learn about the treatment of atrial septal defect, ASD, a serious heart defect.
A pacemaker is an implanted device that helps the heart beat more regularly. Learn more about the different kinds of pacemakers and the heart...
A pacemaker is a battery-powered device that sends signals to the heart to help it beat properly. Tune in to find out more about these life-saving...
See full list of 9 related videos
» Next page: Diagnosis of Arrhythmias
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
