Diagnosis of Bradycardia
Bradycardia Diagnosis: Book Excerpts
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BRADYCARDIA:
Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- Is there fever? If there is fever, one should look for yellow fever, diphtheria, cerebral abscess, or meningitis. Perhaps the fever is related to increased intracranial pressure from apoplexy.
- Are there episodes of syncope? The addition of syncope should make one think of a sick sinus syndrome, complete heart block, vasovagal syncope, or carotid sinus syncope.
- Is there a heart murmur present? Heart murmurs are found in complete heart block, but they are also a sign of aortic stenosis, which can cause bradycardia.
- Is there a history of drug ingestion? Several drugs can induce bradycardia, the most notable being digitalis; propranolol, quinidine, and various cholinergic drugs also may induce bradycardia. Opium poisoning may cause bradycardia.
- Is there nonpitting edema? Obviously, this is a sign of myxedema and should be looked for in any patient presenting with bradycardia.
- Is there chest pain? An acute myocardial infarction may present with bradycardia, although it is more typical for tachycardia to be associated with this condition. Heart disease can cause a second- and third-degree block, which may result in bradycardia, but also various other types of arrhythmia that cause the slowing of the pulse.
DIAGNOSTIC WORKUP
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:
Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- Could the murmur be extracardiac in origin? Extracardiac murmurs include the pericardial friction rub and cardiorespiratory murmurs.
- Is the murmur continuous? A continuous murmur is most often due to a patent ductus arteriosus or combined valvular stenosis and insufficiency. However, arteriovenous aneurysms and ruptured aneurysm of the sinus of Valsalva must also be considered.
- Is the murmur systolic or diastolic? Diastolic murmurs include aortic regurgitation and mitral stenosis and are always organic. Many systolic murmurs are functional in nature.
- Is there associated cardiomegaly? An enlarged heart associated with the murmur makes it more likely that it is pathologic. One would consider mitral regurgitation, aortic regurgitation, and aortic stenosis and various forms of congenital heart disease.
- Is there hepatomegaly? Hepatomegaly associated with the murmur would make one think of congestive heart failure or tricuspid regurgitation and tricuspid stenosis.
- Is there associated fever? Cardiac murmurs occurring with fever suggest acute rheumatic fever and subacute bacterial endocarditis.
- Is there dyspnea? Dyspnea associated with a cardiac murmur suggests congestive heart failure.
- Is there chest pain? If there is chest pain associated with a cardiac murmur, one must consider pericarditis and myocardial infarction.
- Is there an enlarged thyroid or intention tremor? These findings suggest hyperthyroidism.
- Is there cyanosis or clubbing? These findings suggest congenital heart disease.
DIAGNOSTIC WORKUP
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
Bradycardia:
Differential Diagnosis
(In a Page: Signs and Symptoms)
- Sinus bradycardia
–Heart rate <60 bpm with normal-appearing P waves before each QRS wave (narrow complex)
–Most often due to increased vagal tone or medications (e.g., β-blockers)
–Normally seen in healthy young adults and well-trained athletes
–May occur with hypothermia, advanced liver disease, hypothyroidism, sinoatrial node disease, anorexia nervosa, sleep disorders, and increased intracranial pressure
- Medications (e.g., β-blockers)
- Sinus node dysfunction
–May occur as result of sinus node fibrosis (e.g., aging) or infiltrative diseases (e.g., amyloidosis)
–SSS: Symptomatic bradycardia with sinus node dysfunction
–Tachycardia-bradycardia syndrome: SSS manifested by tachyarrhthymias alternating with bradyarrhthymias
- Heart block
–First-degree AV block: Fixed prolongation of PR interval (PR ≥200 msec); results from slowed conduction through AV node
–Second-degree AV block, Mobitz I (Wenckebach): Results from delayed conduction through AV node; progressive prolongation of PR interval occurs until a QRS is dropped (typically benign)
–Second-degree AV block, Mobitz II: Results from disease in the bundle of His; PR is constant, but sporadic P waves are not conducted (may be life threatening because of risk of complete heart block or ventricular asystole)
–Complete heart block: Atrial impulses are not conducted to the ventricles; thus, atrial activity occurs independent of ventricular activity (AV dissociation, with atrial rate faster than ventricular rate)
-
Congenital heart block
-
Aortic stenosis
-
Myocardial infarction
–More common with inferior wall MI
-
Atrial fibrillation/flutter with high-degree block
-
Infections (e.g., Lyme disease)
Workup and Diagnosis
- History and physical exam
–Associated symptoms may include lightheadedness,
palpitations, dyspnea, chest pain, and syncope
–Medication history
–Thorough review of symptoms to identify precipitants of
increased vagal tone (e.g., nausea, pain, headache)
–Assess for hemodynamic instability (blood pressure, level of consciousness), jugular venous pressure (cannon A waves are highly suggestive of AV dissociation), and soft S1 (suggests PR prolongation)
-
ECG is diagnostic
-
Further diagnostic tests may include echocardiogram, electrophysiologic testing, and cardiac catheterization
>
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Source: In a Page: Signs and Symptoms, 2004
Murmurs - Diastolic:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Aortic insufficiency
–Decrescendo murmur heard best at the right second intercostal space -
Austin Flint murmur
–Late diastolic rumble of severe aortic regurgitation
–A result of aortic regurgitation so severe that it causes diastolic mitral regurgitation -
Mitral stenosis
–Opening snap with mid-diastolic rumble, especially in the left lateral decubitus position -
Pulmonary insufficiency
–Accentuated P2 and decrescendo murmur at the left second/third intercostal spaces -
Tricuspid stenosis
–Mid-diastolic rumble at the left sternal
border
–Increases with inspiration
-
Cervical venous hum (disappears upon pressure to the jugular vein)
-
Hepatic venous hum (disappears with epigastric pressure)
-
Mammary souffle (in pregnancy; disappears on compressing breast)
-
PDA (continuous machinery sound)
-
Coronary or pulmonary arteriovenous fistula
-
Coarctation of the aorta
-
ASD with left-to-right shunt
-
Atrial myxoma (“tumor plop”)
-
Pericardial knock (constrictive pericarditis)
-
Bronchial collaterals (congenital heart disease)
-
Anomalous pulmonary venous drainage with left-to-right shunt
-
Pulmonary artery branch stenosis
-
Carey-Coombs murmur (mid-diastolic murmur that occurs in acute rheumatic fever)
Workup and Diagnosis
-
Complete history and physical examination, including cardiac maneuvers
-
ECG
-
Echocardiogram
-
Consider chest X-ray
-
Laboratory studies may include CBC, electrolytes, glucose, BUN/creatinine, TSH, liver function tests, pulse oximetry, and/or arterial blood gas
-
Consider cardiology consult
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Source: In a Page: Signs and Symptoms, 2004
Murmurs - Systolic:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Innocent systolic murmur
–Heard at left sternal border
–Increased when supine
–May be caused by increased flow states
(e.g., anemia, hypovolemia, fever)
-
Still's murmur
-
Mitral valve prolapse
–Midsystolic click with late systolic murmur that shifts with maneuvers
-
Aortic stenosis
–Right side at second intercostal space
–Radiates to carotid arteries
-
Aortic sclerosis
–Right side at second intercostal space
–Midsystole
-
Hyperthyroidism
-
Cervical venous hum
–Disappears with jugular vein pressure
-
Hepatic venous hum
–Disappears with epigastric pressure
-
Mammary souffle
–Occurs in pregnancy
–Disappears upon compression of breast -
Bicuspid aortic valve
–Right side at second intercostal space
–Little radiation
–Possible early diastolic aortic murmur
–Opening sound of aortic valve heard in early systole (systolic ejection click) -
Mitral insufficiency
–Holosystolic murmur heard best in the left lateral decubitus position
–S1 is usually diminished in intensity
-
Tricuspid insufficiency
–Holosystolic murmur at second/third intercostal spaces
-
Endocarditis
–Abrupt onset of new murmur
-
Peripheral pulmonary artery stenosis
-
Atrial or ventricular septal defect
-
Ventricular septal defect
-
Patent ductus arteriosus (continuous machinery sound, second left intercostal space)
-
Coarctation of the aorta
-
Left ventricular outflow tract obstruction
-
Pulmonary artery stenosis
-
Prosthetic valve noises
-
Pericardial friction rubs
-
Papillary muscle dysfunction
-
Pulmonic outflow obstruction
-
Coronary/pulmonary arteriovenous fistula
Workup and Diagnosis
- History and physical examination
–Family history of sudden cardiac death
–Past medical history of heart disease, murmurs, or
rheumatic fever
–Evaluation for jugular venous distention, carotid upstroke,
and/or bruits
–Heart, lung, and abdominal examinations
–Peripheral pulses and evaluation for peripheral edema
-
ECG
-
Chest X-ray
-
Echocardiogram
-
Laboratory studies may include CBC, electrolytes, BUN/creatinine, glucose, and TSH
-
Consider cardiac enzymes
-
Consider blood cultures
-
Consider cardiology referral
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Source: In a Page: Signs and Symptoms, 2004
Bradycardia:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Vasovagal response
–Defecation, yawning, rectal stimulation, placement of nasogastric tube, sight of blood, etc.
-
Drug reaction
–β-blockers, calcium channel blockers (diltiazem, verapamil), carbamates, clonidine, digoxin, opiates, organophosphates, gamma-hydroxybutyrate (“date rape” drug), and plants (lily of the valley, foxglove, oleander)
-
Healthy athlete
–Sinus bradycardia
-
Hypothermia
-
GER (in infants, especially premature)
-
Low birth weight infants: Sinus bradycardia (great variations in sinus rate, can have junctional escape beats)
-
Congenital complete heart block: Associated with maternal SLE
-
Congenital heart disease
-
Sepsis
- Obstructive sleep apnea
–Seen in children with obesity, tonsillar or adenoid hypertrophy, craniofacial anomalies, neuromuscular diseases
–Hypoxia and hypercapnia lead to pulmonary hypertension and arrhythmia
-
Electrolyte abnormalities can lead to dysrhythmias
-
Anorexia nervosa
–Prolonged QT syndrome and junctional arrhythmia
–Associated hypokalemia may also cause ECG changes and life-threatening dysrhythmias
-
AV node blocks (second- and third-degree)
-
Idioventricular rhythm
-
Hypothyroidism (myxedema)
-
Allergic reaction/anaphylaxis
-
Increased intracranial pressure (IVH, extradural hemorrhage, trauma, etc.)
-
Sick sinus syndrome (tachy-brady syndrome)
-
Psittacosis, typhoid fever, Lassa fever
-
Myocardial infarction
Workup and Diagnosis
- History
–For acute patients, history of present illness, associated
symptoms
–Birth history, PMH, and review of systems
–Medications, medications around the house, alternative
medicines/herbs
- Physical exam
–Vital signs, growth parameters, nutritional status,
physical fitness
–Craniofacial and ENT exam
–Complete cardiac exam: Evaluate cardiovascular
stability, BP, pulse, perfusion, mental status, tachypnea, as well as heart sounds, murmurs, distal pulses
-
Labs
–ECG: Look for block, prolonged QTc, abnormal P
-
wave, or QRS complex
–Electrolytes (include potassium, calcium, magnesium)
–CBC: Look for infection
–Consider drug screen: Look for toxic ingestion
-
Studies
–Consider upper GI series, pH probe, or pneumogram (if suspect apnea as well) to look for GER
–Consider 24-hour Holter monitor if episodic bradycardia
–Consider echocardiogram to rule out congenital heart disease
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Source: In A Page: Pediatric Signs and Symptoms, 2007
MURMURS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
A chest x-ray with anterior oblique films during a barium swallow along with an ECG, sedimentation rate, a blood serology thyroid profile, and CBC are basic in the workup of a murmur. If there is a fever or if there is recent onset of the murmur, blood cultures, an ASO titer and C-reactive protein (CRP) should be done. An ANA test, echocardiogram, and phonocardiogram are frequently done. Referral to a cardiologist is wise if the cause is obscure or if one is unable to spend the time for a careful workup. Angiocardiography and cardiac catheterization are the only sure ways to determine the location of the valvular disease, and, in many cases, the exact cause.
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Source: Differential Diagnosis in Primary Care, 2007
BRADYCARDIA:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The finding of bradycardia in an otherwise healthy adult is probably normal. Nevertheless, other symptoms and signs should be looked for. Fever suggests meningitis, yellow fever, or a cerebral abscess. A history of syncope requires that sinus arrest or complete heart block be ruled out. If a heart murmur is present, aortic stenosis must be considered. If there is nonpitting edema and brittle hair and nails, myxedema should be ruled out. If there is a history of chest pain, perhaps the patient has had a recent myocardial infarction. It is important to find out what medications the patient is taking. ϐ-Blockers, digitalis, quinidine, and various cholinergic drugs may induce bradycardia.
The initial workup should include a CBC, urinalysis, thyroid profile, sedimentation rate, chemistry panel, ECG, and chest x-ray. If there is fever, febrile agglutinins and a survey for other infections should be made. If there is nuchal rigidity, a spinal tap should be done, preferably after a CT scan. If a myocardial infarction is suspected, serial cardiac enzymes and ECGs should be done. If valvular heart disease is suspected, echocardiography should be done. If there is a history of syncope, the patient needs 24- to 48-hour Holter monitoring. When this is unrevealing, a continuous-loop event recording may be conducted over a 1- to 2-week period.
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Source: Differential Diagnosis in Primary Care, 2007
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?
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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
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:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Symptoms. Bradyarrhythmias may or may not cause symptoms. When symptoms do occur, they are caused by either an awareness of the irregular rhythm (palpitations) or a reduced cardiac output (lightheadedness, syncope, fatigue, shortness of breath, or chest pain) (3) (Chapter 7.9).
B. Exercise tolerance. Ask patients about their level of physical fitness. In the well-conditioned patient, impulse generation in the sinus node is often slowed.
C. Underlying conditions. It is important to determine any underlying medical conditions that can cause bradycardia [e.g., ischemic heart disease (IHD), cardiomyopathies, previous arrhythmias, rheumatic heart disease, or thyroid disease].
D. Medications. Typical medications associated with bradycardia include digoxin, phenothiazines, quinidine, procainamide, beta-blockers, calcium channel blockers, clonidine, reserpine, methyldopa, flecainide, encainide, propafenone, and lithium.
E. Cardiac risk factors. Elicit risk factors for coronary heart disease (family history, tobacco use, hypercholesterolemia, diabetes, or hypertension).
Physical examination
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.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Heart Murmur, Diastolic:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Symptoms. Many patients with diastolic murmurs will not present with specific complaints; rather, the murmurs will be found in the course of a routine medical examination. With symptomatic lesions, the patient may experience dyspnea, chest pain, or palpitations. Pulmonary regurgitation (PR) is usually asymptomatic except in its most severe forms. More specific symptoms include chest or neck pounding in aortic regurgitation (AR); hemoptysis, embolism, or hoarseness (left recurrent laryngeal nerve compression from the left atrium) in mitral stenosis (MS); failure to thrive or frequent respiratory infections with congenital MS; edema in tricuspid stenosis (TS); and fever, anemia, weight loss, embolism, digital clubbing, arthralgias, syncope, rash, and Raynaud’s phenomenon with an atrial myxoma (1).
B. Past medical history. Does the patient have a history of rheumatic fever (RF)? RF is the most common cause of all diastolic murmurs (mitral → aortic → tricuspid → pulmonic) (2). Of patients with mitral stenosis, 50% will have a history of rheumatic fever (3).
1. Endocarditis. Vegetations can lead to either AR/PR or MS/TS.
2. Pulmonary hypertension with PR is classically associated with the Graham Steell murmur, heard in the left third interspace near the sternum and propagated down the sternum.
3. Connective tissue and collagen vascular diseases predispose to aortic root dilatation and AR.
4. Congenital heart malformations can be associated with multiple valvular lesions, left ventricular (LV) outflow tract abnormalities, or shunts (with resultant volume overload).
5. Atrial myxoma is a rare cause of variable AV valve obstruction.
6. Syphilis can cause aortitis and AR.
Physical examination (PE)
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.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Heart Murmur, Systolic:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General issues in the history. The history can provide important clues as to whether the murmur is clinically significant. Any history of rheumatic fever, previously known valvular disease, congenital heart disease, or intravenous drug abuse would be important to ascertain.
Murmurs of early adulthood suggest congenital or rheumatic disease, whereas murmurs with onset later in life are consistent with degenerative valvular changes.
B. Patient symptoms. Patients should be asked about shortness of breath, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Patients with these symptoms warrant an expedited evaluation because these symptoms suggest cardiac decompensation. Advanced aortic stenosis specifically is associated with chest pain, syncope, and heart failure, although a gradient across the valve can exist for years prior to symptom onset. Chest discomfort is often present in advanced disease, but sudden death occurs in 15% of patients with no previous symptoms (1).
C. Association of a murmur with a specific disease. Recent myocardial infarction endocarditis could cause papillary muscle dysfunction resulting in mitral or tricuspid regurgitation. Mitral regurgitation can be seen in connective tissue disease, coronary artery disease, and congenital disease, but is commonly associated with conditions leading to left ventricular dilatation such as congestive heart failure (CHF) (Chapter 7.5). Endocarditis, myocardial infarction, trauma, prolapse, or congenital heart disease usually precede tricuspid regurgitation. Mitral valve prolapse, which is clinically characterized by palpitations, fatigue, and chest pain, is often associated with anxiety. Hypertrophic cardiomyopathy can be seen in patients with a family history and usually presents between the ages of 20 and 40 years. Presenting symptoms include dyspnea on exertion, chest pain, palpitations, or syncope. It is an important cause of sudden death in athletes. A history of anemia, thyroid disease, or fever should also be elicited from patients being evaluated for
a systolic murmur as each of these conditions can cause a murmur from increased flow.
Physical examination
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.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Bradycardia:
Differential Overview
(Field Guide to Bedside Diagnosis)
Sinus Bradycardia
❑ Hypothyroidism
❑ Hypervagotonia
❑ Hypersensitive carotid sinus
❑ Hypothermia
❑ Acute increased intracranial pressure
Complete Heart Block
❑ Inferior myocardial infarction
❑ Drugs
❑ Sick sinus syndrome
❑ Viral myocarditis
❑ Lyme disease
❑ Sarcoidosis
❑ Acute rheumatic fever
Diagnostic Approach
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:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Aortic regurgitation
❑ Pulmonic regurgitation
❑ Mitral stenosis
❑ Tricuspid stenosis
❑ Atrial septal defect
❑ Left anterior descending artery stenosis
❑ Atrial myxoma
Diagnostic Approach
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:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Systolic ejection murmur
❑ Mitral regurgitation
❑ Mitral valve prolapse
❑ Aortic stenosis
❑ Aortic valve sclerosis
❑ Hypertrophic obstructive cardiomyopathy
❑ Atrial septal defect
❑ Pulmonic stenosis
❑ Tricuspid regurgitation
❑ Ventricular septal defect
❑ Aortic coarctation
Diagnostic Approach
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:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Aortic stenosis/aortic insufficiency
❑ Pericardial friction rub
❑ Pulmonary arteriovenous fistula
❑ Venous hum
❑ Mammary souffle
❑ Aortic coarctation
❑ Mediastinal air dissection
❑ Patent ductus arteriosis
❑ Ruptured sinus of Valsalva
❑ Coronary artery fistula
Diagnostic Approach
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
Murmurs:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
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. 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.
Physical examination
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.
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: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Pulse rhythm abnormality:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
If the patient’s condition permits, ask if he’s experiencing pain. If so, ask about its 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 caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of a sympathomimetic (such as epinephrine), quinidine, caffeine, cocaine, methamphetamine, or alcohol may cause arrhythmias.
Physical examination
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: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Bradycardia:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
After detecting bradycardia, check for related signs of life-threatening disorders before proceeding with a history. (See Managing severe bradycardia, page 62.) Determine if the patient or a family member has a history of a slow pulse rate. Check for underlying metabolic disorders, such as hypothyroidism, which can precipitate bradycardia. Obtain a medication history and make sure that the prescribed schedule and dosage is followed.
Physical examination
Monitor the patient’s vital signs, temperature, pulse, respirations, blood pressure, and oxygen saturation. If he’s on a cardiac monitor, frequently assess cardiac rhythm and note changes.
Assess for changes in the patient’s level of consciousness (LOC) or respiratory status.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Pulsus paradoxus [Paradoxical pulse]:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
If you’ve ruled out cardiac tamponade, obtain the patient’s history. Does he have a history of chronic cardiac or pulmonary disease? Ask about the development of associated signs and symptoms, such as cough or chest pain.
Physical examination
Auscultate for abnormal breath sounds and assess the patient’s respiratory status, oxygenation, and effort. Assess the patient’s vital signs and cardiovascular system, and monitor his cardiac rhythm.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Pulse, absent or weak:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
After you detect an absent or weak pulse, review the patient’s history of heart disease. Ask him what medications he’s taking and whether he has any other illnesses. Also, question him about associated signs and symptoms, such as chest pain or dyspnea.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Murmurs:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs.) 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. 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.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulse rhythm abnormality:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
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.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulsus paradoxus:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
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.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Bradycardia:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
After detecting bradycardia, check for related signs of life-threatening disorders. If the patient’s bradycardia isn’t accompanied by unfavorable 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.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Heart Murmurs (Asymptomatic):
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Normal Murmurs
Systolic Ejection Murmurs
Normal systolicejection murmurs are grade III or less.They begin after S1 following the isovolumiccontraction period and end before S2.They vary from cycle to cycle withrespiration or change in position.Intensity increases with fever, anxiety,or exercise.Although heard with maximum intensityat specific locations on the chest wall, they are louder in supineposition. Vibratory Systolic Murmur
Commonlyheard in childhood and less often in infancy.Usually grade II/VI but canrange from grade I to III.Heard with maximum intensity at lowerleft sternal border or between this area and apex.Has distinctive vibratory quality. Pulmonary Systolic Murmur
Frequentlyheard in childhood and adolescence.Maximum intensity is in second intercostalspace at upper left sternal border.Usual intensity is grade II/VIwith range from grade I to III.Higher in pitch than vibratory systolicejection murmur.Also heard in straight back syndrome,which is characterized by absence of normal thoracic kyphosis andnarrow anterior-posterior diameter of chest. RV and pulmonary arterylie against sternum, and murmur is easily heard. Straight back syndromealso may be associated with mitral valve prolapse. Physiologic Peripheral Pulmonary Systolic Murmur
May be heardin neonates, especially in preterm infants.Intensity is usually grade I–II/VI.Heard equally well in right and leftanterior chest, axillae, and back.Usually disappears by 3–6mos of age. Supraclavicular or Brachiocephalic Murmur
May be heardin childhood or adolescence.Usually grade II or III/VI.Maximum intensity is always above medialaspect of clavicles in supraclavicular fossa but may be heard belowclavicles.Usually louder on right side.Shoulder maneuvers are useful in distinguishingit from other murmurs. When physician is listening for murmur, childshould sit with shoulders relaxed and arms in front of chest. Murmurdiminishes or disappears when shoulders are hyperextended with elbowsbrought behind back. Continuous Murmurs
Venous Hum
Commonlyheard in sitting position.Grade II–IV/VI continuousmurmur with maximal intensity in supraclavicular fossa, just lateralto sternocleidomastoid muscle with transmission below clavicles.Usually more prominent on right side.Diminishes or disappears with compressionof ipsilateral jugular vein, head/neck turning or positioning,or with lying down. Pathologic Murmurs
Can be systolic,diastolic, or continuous.Intensity is usually grade III or more,but can be grade I or II if lesion is mild.Duration is usually longer than thatof normal murmur.Heard with maximum intensity at specificlocations on chest wall. Systolic Murmurs
Maximal Intensity at Upper Right Sternal Border
Valvar Aortic Stenosis
Most commontype of LV outflow tract obstruction.Produces grade II–IV/VIharsh systolic ejection murmur that is heard with maximum intensityat upper right sternal border.Aortic ejection click also can be heardalong left sternal border and at apex.Prominent apical impulse is palpable.Chest radiography shows normal to mildlyenlarged heart, normal pulmonary vascular markings, and mild dilatationof ascending aorta.ECG is normal or shows LV hypertrophy.2-D echocardiography shows abnormalvalve. Doppler methods demonstrate abnormal flow pattern. Maximal Intensity at Upper Left Sternal Border
Valvar Pulmonic Stenosis
Associatedwith prominent RV impulse over lower sternum, normal S2, and systolic ejectionclick (louder on expiration) along left sternal border.Grade II–IV/VI harshsystolic ejection murmur transmits to neck and back.In infants, click may be absent withmild stenosis.Chest radiograph shows normal heartsize, normal pulmonary vascular markings, and dilated main pulmonaryartery segment.ECG is normal or shows RV hypertrophy.2-D echocardiography shows abnormalvalve. Doppler methods demonstrate abnormal flow pattern. Atrial Septal Defects
Includeostium secundum, ostium primum, and sinus venosus defects.Physical exam is similar with all defects.Prominent RV impulse, grade II–III/VIsystolic ejection murmur with maximum intensity at upper left sternalborder, usually wide fixed splitting of S2, and grade II–III/VImid-diastolic rumbling murmur with maximum intensity at lower leftsternal border.In infants, splitting of S2 may benormal or wide and not fixed.Systolic murmur signifies increasedblood flow across pulmonic valve, and diastolic murmur reflectsincreased flow across tricuspid valve.Chest radiography shows mild cardiomegaly,increase in pulmonary vascular markings, and enlarged pulmonaryartery segment.ECG shows RV hypertrophy. In ostiumprimum defect, frontal plane QRS axis often shows left axis deviation,which signifies conduction system displacement. P wave on ECG ismore horizontal with sinus venosus defect.2-D echocardiography visualizes defectsand can distinguish between them. Mild-to-Moderate Coarctation of Aorta
BP in rightarm is significantly higher than that in legs with coarctation ofaorta.Femoral pulses are diminished comparedwith brachial or radial pulses.Prominent apical impulse.Grade II–III/VI harshsystolic ejection murmur is commonly heard at upper left sternalborder and left back.Grade II–III/VI high-pitchedcontinuous murmur may be heard over left side of spine along scapularedge.Presence of aortic ejection click andsystolic ejection murmur at upper right sternal border usually signifiesbicuspid aortic valve, which is commonly associated with coarctationof aorta.Chest radiograph shows normal or mildlyenlarged heart and normal pulmonary vasculature. Ascending aortamay be dilated. In older infants and children, indentation of descendingaorta just distal to aortic arch produces "3" sign.Erosion of bone by large intercostal arteries can produce notchingof lower margins of posterior ends of ribs 3–9.In early infancy, ECG usually showsRV hypertrophy, whereas in children it may be normal or show mildLV hypertrophy.2-D echocardiography can often demonstratecoarctation. In older children, if coarctation is not well demonstratedby echocardiography, it may be visualized by MRI. Small Patent Ductus Arteriosus
Common interm infants and very common in preterm infants, especially in thosewith birth weight <1,500 g.Murmur is usually grade II–III/VIand is systolic or continuous. Systolic ejection sounds are occasionallyheard along left sternal border.Chest radiography shows normal sizeor mildly enlarged heart with increased pulmonary vascular markings.ECG is either normal or shows mildLV hypertrophy. Maximal Intensity at Lower Left Sternal Border
Normal vibratory ejection murmur must bedistinguished from 2 pathologic systolic murmurs that are heardwith maximum intensity at lower left sternal border: murmurs ofventricular septal defect and tricuspid incompetence.
Ventricular Septal Defect
Murmur ofsmall VSD may be heard as early as 1–3 days of age as pulmonaryvascular resistance decreases and left-to-right shunt develops.Palpation reveals normal-sized or mildlyenlarged heart.Intensity and splitting of S2 are normal.Murmur is grade II–IV/VIand is heard throughout systole. It is harsh in quality with maximalintensity at lower left sternal border.If defect begins to close with time,duration of murmur is less.No diastolic murmur is heard at apexunless pulmonary:systemic flow ratio is ≥2:1.Chest radiograph shows normal or mildlyenlarged heart, and increased pulmonary vascular markings.ECG is normal or shows mild LV hypertrophy.2-D echocardiography may not visualizesmall defects. Tricuspid Incompetence
Murmur ishigh pitched, usually grade II–III/VI, and heardthroughout systole with maximal intensity at lower left sternalborder.May be heard in asymptomatic lesions(isolated mild congenital tricuspid incompetence, atrioventricularcanal defects, Ebstein anomaly) or in symptomatic ones (atrioventricularcanal defects, Ebstein anomaly, pulmonary atresia with intact septum,endocarditis, perinatal asphyxia). Maximal Intensity at Apex
Mitral Incompetence
Murmur ishigh pitched, usually grade II–IV/VI, and heardthroughout systole at apex with transmission to left axilla andback.Heart is normal sized or mildly enlarged.Chest radiograph and ECG are usuallynormal.Causes include congenital defects ofmitral valve, atrioventricular canal defects, anomalous left coronaryartery from pulmonary artery, hypertrophic cardiomyopathy, Marfansyndrome, and Hurler syndrome.Symptomatic causes include these lesionsas well as acute rheumatic fever, myocarditis, endocarditis, endocardialfibroelastosis, and perinatal asphyxia. Mitral Valve Prolapse
Can occuras isolated defect or in association with ostium secundum atrialseptum defect, endocarditis, Hurler syndrome, Marfan syndrome, orEhlers-Danlos syndrome.Usual finding is midsystolic nonejectionclick followed by late systolic murmur of mitral incompetence.Murmur is heard best at apex, especiallyin standing position after squatting.Chest radiograph is normal.ECG may show inverted T waves in leadsII, III, and aVF as well as ST depression in left precordial leads.Clinical diagnosis can be confirmedby M-mode or 2-D echocardiography. Diastolic Murmurs
There havebeen some reports of normal diastolic murmurs occurring in infantsand children, but this is rare.For this discussion, all diastolicmurmurs are considered pathologic. These murmurs usually indicateSemilunarvalve incompetence (aortic or pulmonic valve)Atrioventricular valve stenosis (mitralor tricuspid valve)Severe mitral or tricuspid valve incompetenceIncreased blood flow across the tricuspidvalve (atrial septal defect) or mitral valve (large ventricularseptal defect or patent ductus arteriosus) Maximal Intensity at Upper Right Sternal Border
Aortic Valve Incompetence
Can occuras isolated congenital lesion or in association with valvar aorticstenosis, discrete subaortic stenosis, ventricular septal defect,acute rheumatic fever, or endocarditis.Diastolic murmur of aortic valve incompetenceis grade I–IV/VI and is characterized by its highpitched decrescendo sound. Heard with maximum intensity at upperright sternal border but is also heard along left midsternal border.Murmur begins with aortic closure, and the more severe the incompetence,the longer the murmur and the wider the pulse pressure. Usuallyis louder when patient is sitting up and leaning forward.Apical impulse may be prominent, dependingon degree of incompetence.Chest radiography shows normal or mildlyenlarged heart.ECG is normal or shows LV hypertrophy. Maximal Intensity at Upper Left Sternal Border
Pulmonic Valve Incompetence
Producesmedium-pitched, grade I–IV/VI, diastolic decrescendomurmur, which begins with pulmonary closure and varies in durationdepending on severity of lesion.Longer murmur signifies more severeincompetence.Causes include congenital pulmonicvalve incompetence, idiopathic dilatation of pulmonary artery, valvarpulmonic stenosis, postsurgical repair (valvar pulmonary stenosis,tetralogy of Fallot), and endocarditis. Maximal Intensity at Lower Left Sternal Border
Atrial Septal Defects
Diastolic flow rumble, usually grade I–III/VI,can be heard with maximal intensity at lower left sternal borderwith any type of ASD.
Tricuspid Stenosis
Rare lesionthat can occur as isolated congenital lesion or in association withsevere valvar pulmonic stenosis, hypoplasia of right ventricle withpulmonary atresia, or chronic rheumatic heart disease.Murmur is grade I–III/VIdiastolic rumble with presystolic accentuation, which may increasein intensity with inspiration. Opening snap also may be heard. Moderate-to-Severe Tricuspid Incompetence
Grade I–III/VIdiastolic flow rumble of tricuspid incompetence reflects increasein blood flow across tricuspid valve during diastole.Systolic murmur of tricuspid incompetencealso is heard at lower left sternal border.Affected children are usually symptomatic.See section Tricuspid Incompetence. Maximal Intensity at Apex
Mitral Stenosis
Murmur isgrade I–II/VI, diastolic, low-rumbling murmurwith presystolic accentuation and opening snap.Heard with maximum intensity at apex.May occur as isolated congenital defect,as part of Shone syndrome, or secondary to rheumatic fever. Moderate-to-Severe Mitral Incompetence
Diastoliclow-pitched murmur heard with mitral incompetence reflects increasedantegrade blood flow across mitral valve.Murmur varies in intensity and durationwith severity of incompetence and is heard with maximal intensityat apex.Systolic murmur of mitral incompetenceis also heard at apex. Moderate Left-to-Right Shunt Lesions
Lesions(e.g., VSD and patent ductus arteriosus) may produce moderate orlarge left-to-right shunts.Grade I–III/VI low-pitcheddiastolic flow murmur can be heard at apex because of increased bloodflow across mitral valve in diastole.Children with large left-to-right shuntsare in cardiac failure. Continuous Murmurs
Maximal Intensity at Upper Left Sternal Border
Moderate Patent Ductus Arteriosus
Typicalmurmur of moderate-sized patent ductus arteriosus is continuousmachinery-like murmur, usually at least grade III/VI, withmaximum intensity at upper left sternal border, and transmissionalong left sternal border and in lung fields.There is often increased LV impulse,wide but variable split of S2, and increased pulse pressure.Chest radiograph shows mild cardiomegalyand increased pulmonary vascular markings.ECG shows LV hypertrophy and occasionallyleft atrial enlargement.2-D echocardiography with Doppler methodsis confirmatory. Maximal Intensity at Left Midsternal Border
Aortic Pulmonary Window
There iscommunication between ascending aorta and main pulmonary artery.Defect is usually large, which resultsin large amount of pulmonary blood flow.Murmur is heard with maximum intensityat left midsternal border.Primarily systolic with diastolic component.However, continuous murmur may be heard with rare small aortic pulmonarywindow.Chest radiographic and ECG findingsare similar to those of patent ductus arteriosus.2-D echocardiography with Doppler methodsis diagnostic. Maximal Intensity with Variable Location
Coronary Arteriovenous Fistula
Communicationbetween coronary artery and heart, usually right atrium or pulmonaryartery.Continuous murmur is usually heardover lower precordium, away from area where ductus is heard.Cardiac catheterization and angiographyare usually necessary for definitive diagnosis. Systemic Arteriovenous Fistula
This typeof connection within thorax can occur with communications betweensubclavian artery and innominate vein, between internal mammaryartery and vein, between bronchial arteries and branches of systemicazygous system, and between other chest wall vessels.Continuous murmur is heard over areaof abnormal communication.Cardiac catheterization and angiographyare necessary for definitive diagnosis. Diagnostic Approach
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.)
» 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
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
MURMURS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
A chest x-ray with anterior oblique films during a barium swallow along
with an electrocardiogram (ECG), sedimentation rate, blood serology thyroid
profile, and CBC are basic in the workup of a murmur. If there is a fever or
if there is recent onset of the murmur, blood cultures, an
antistreptolysin-O (ASO) titer, and a C-reactive protein (CRP) test should
be done. An antinuclear antibody (ANA) test, ECG, and phonocardiogram are
frequently done. Referral to a cardiologist is wise if the cause is obscure
or if one is unable to spend the time for a careful workup.
Angiocardiography and cardiac catheterization are the only sure ways to
determine the location of the valvular disease, and, in many cases, the
exact cause.
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Source: Differential Diagnosis in Primary Care, 2007
Bradycardia:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The finding of bradycardia in an otherwise healthy adult is probably
normal. Nevertheless, other symptoms and signs should be looked
for. Fever suggests meningitis, yellow
fever, or a cerebral abscess. A history of syncope requires that sinus
arrest or complete heart block be ruled out. If a heart murmur is present,
aortic stenosis must be considered. If there is nonpitting edema and brittle
hair and nails, myxedema should be ruled out. If there is a history of chest
pain, perhaps the patient has had a recent myocardial infarction. It is
important to find out what medications the patient is taking. β -Blockers,
digitalis, quinidine, and various cholinergic drugs may induce bradycardia.
The initial workup should include a CBC, urinalysis, thyroid profile,
sedimentation rate, chemistry panel, electrocardiogram (ECG), and chest
x-ray. If there is fever, febrile agglutinins and a laboratory survey for other
infections should be made. If there is nuchal
rigidity, a spinal tap should be done, preferably after a CT scan. If a
myocardial infarction is suspected, serial cardiac enzymes and ECGs should
be done. If valvular heart disease is suspected, echocardiography should be
done. If there is a history of syncope, the patient needs 24 to 48-hour
Holter monitoring. When this is unrevealing, a continuous-loop event
recording may be conducted over a 1 to 2-week period.
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Source: Differential Diagnosis in Primary Care, 2007
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