Diagnostic Tests for Bradycardia
Bradycardia Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Bradycardia:
- High Blood Pressure: Home Testing
- Heart Health: Home Testing:
Bradycardia Diagnosis: Book Excerpts
Diagnostic Tests for Bradycardia: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the diagnostic tests for Bradycardia.
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.
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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.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
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
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
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.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Pulsus paradoxus:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient doesn’t have cardiac tamponade, find out if he has a history of chronic cardiac or pulmonary disease. Ask about the development of associated signs and symptoms, such as a cough or chest pain. Then auscultate for abnormal breath sounds.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
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
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
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
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
Pulsus paradoxus:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient doesn’t have cardiac tamponade, find out if he has a history of chronic cardiac or pulmonary disease. Ask about the development of associated signs and symptoms, such as a cough or chest pain. Auscultate for abnormal breath sounds.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth 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
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.
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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.
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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.
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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.
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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.
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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.
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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.
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Source: Field Guide to Bedside Diagnosis, 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
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
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
Pulsus paradoxus:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Auscultate for abnormal breath sounds. Next, complete your cardiac and pulmonary assessments.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 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.
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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.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
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.)
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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?
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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.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Pulsus paradoxus:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient doesn't have signs of cardiac tamponade, find out if he has a history of chronic cardiac or pulmonary disease. Ask about the development of associated signs and symptoms, such as a cough or chest pain. Then auscultate for abnormal breath sounds.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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