Diseases » Arrhythmias » Diagnosis

Diagnosis of Arrhythmias

Diagnostic Test list for Arrhythmias:

The list of medical tests mentioned in various sources as used in the diagnosis of Arrhythmias includes:

• Physical exam
• Stethoscope
• Electrocardiogram (ECG)
  • Resting ECG
  • Exercise ECG (stress test)
  • 24-hour ECG (Holter) monitoring
  • Transtelephonic monitoring
• Electrophysiologic study (EPS)

Arrhythmias Diagnosis: Book Excerpts

• Ask the following questions - BRADYCARDIA
• Ask the Following Questions - PALPITATIONS
• Ask the Following Questions - TACHYCARDIA
• Ask the following questions - CARDIAC ARRHYTHMIA
• Ask the following questions - CARDIAC MURMURS
• Differential Diagnosis - Bradycardia
• Differential Diagnosis - Palpitations
• Differential Diagnosis - Tachycardia
• Differential Diagnosis - Irregular Heart Rhythms
• Differential Diagnosis - Murmurs - Diastolic
• Differential Diagnosis - Murmurs - Systolic
• Differential Diagnosis - Bradycardia
• Differential Diagnosis - Tachycardia/Palpitations
• Approach to the Diagnosis - BRADYCARDIA
• Approach to the Diagnosis - MURMURS
• Approach to the Diagnosis - TACHYCARDIA
• Approach to the Diagnosis - CARDIAC ARRHYTHMIAS
• Approach to the Diagnosis - PALPITATION
• History and physical examination - Bradycardia
• History and physical examination - Murmurs
• History and physical examination - Palpitations
• History and physical examination - Pulse rhythm abnormality
• History and physical examination - Pulse, absent or weak
• History and physical examination - Pulsus bisferiens
• History and physical examination - Tachycardia
• Diagnosis - Cardiac arrhythmias
• History and physical examination - Bradycardia
• History and physical examination - Murmurs
• History and physical examination - Palpitations
• History and physical examination - Pulse rhythm abnormality
• History and physical examination - Pulse, absent or weak
• History and physical examination - Pulsus bisferiens
• History and physical examination - Tachycardia
• History - Bradycardia
• History - Palpitations
• History - Tachycardia
• History - Heart Murmur, Diastolic
• History - Heart Murmur, Systolic
• Differential Overview - Bradycardia
• Differential Overview - Palpitations/Tachycardia
• Differential Overview - Diastolic Murmur
• Differential Overview - Systolic Murmur
• Differential Overview - Continuous Murmur
• History - Bradycardia
• History - Murmurs
• History - Palpitations
• History - Pulse rhythm abnormality
• History - Tachycardia
• History - Bradycardia
• History - Murmurs
• History - Palpitations
• History - Pulse rhythm abnormality
• History - Pulse, absent or weak
• History - Pulsus bisferiens
• History - Tachycardia
• Clinical Features and Diagnosis - Heart Murmurs (Asymptomatic)
• History and physical examination - Bradycardia
• History and physical examination - Murmurs
• History and physical examination - Palpitations
• History and physical examination - Pulse rhythm abnormality
• History and physical examination - Pulse, absent or weak
• History and physical examination - Pulsus bisferiens
• History and physical examination - Tachycardia
• Approach to the Diagnosis - Bradycardia
• Approach to the Diagnosis - MURMURS
• Approach to the Diagnosis - TACHYCARDIA
• Approach to the Diagnosis - CARDIAC ARRHYTHMIAS
• Approach to the Diagnosis - PULSE RHYTHM ABNORMALITIES

Tests and diagnosis discussion for Arrhythmias:

NHLBI, Arrhythmia: NHLBI (Excerpt)

Sometimes an arrhythmia can be detected by listening to the heart with a stethoscope. However, the electrocardiogram is the most precise method for diagnosing the arrhythmia.

An arrhythmia may not occur at the time of the exam even though symptoms are present at other times. In such cases, tests will be done if necessary to find out whether an arrhythmia is causing the symptoms. (Source: excerpt from NHLBI, Arrhythmia: NHLBI)

NHLBI, Arrhythmia: NHLBI (Excerpt)

First the doctor will take a medical history and do a thorough physical exam. Then one or more tests may be used to check for an arrhythmia and to decide whether it is caused by heart disease.

Tests for Detecting Arrhythmias Electrocardiogram (ECG or EKG). A record of the electrical activity of the heart. Disks are placed on the chest and connected by wires to a recording machine. The heart's electrical signals cause a pen to draw lines across a strip of graph paper in the ECG machine. The doctor studies the shapes of these lines to check for any changes in the normal rhythm. The types of ECGs are: Resting ECG. The patient lies down for a few minutes while a record is made. In this type of ECG, disks are attached to the patient's arms and legs as well as to the chest. Exercise ECG (stress test). The patient exercises either on a treadmill machine or bicycle while connected to the ECG machine. This test tells whether exercise causes arrhythmias or makes them worse or whether there is evidence of inadequate blood flow to the heart muscle ("ischemia"). 24-hour ECG (Holter) monitoring. The patient goes about his or her usual daily activities while wearing a small, portable tape recorder that connects to the disks on the patient's chest. Over time, this test shows changes in rhythm (or "ischemia") that may not be detected during a resting or exercise ECG. Transtelephonic monitoring. The patient wears the tape recorder and disks over a period of a few days to several weeks. When the patient feels an arrhythmia, he or she telephones a monitoring station where the record is made. If access to a telephone is not possible, the patient has the option of activating the monitor's memory function. Later, when a telephone is accessible, the patient can transmit the recorded information from the memory to the monitoring station. Transtelephonic monitoring can reveal arrhythmias that occur only once every few days or weeks. Electrophysiologic study (EPS). A test for arrhythmias that involves cardiac catheterization. Very thin, flexible tubes (catheters) are placed in a vein of an arm or leg and advanced to the right atrium and ventricle. This procedure allows doctors to find the site and type of arrhythmia and how it responds to treatment.

(Source: excerpt from NHLBI, Arrhythmia: NHLBI)

Diagnosis of Arrhythmias: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Arrhythmias:

• Reason for man's death misdiagnosed
• More news »

Diagnostic Tests for Arrhythmias: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Arrhythmias.

BRADYCARDIA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. 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.
2. 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.
3. 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.
4. 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.
5. Is there nonpitting edema? Obviously, this is a sign of myxedema and should be looked for in any patient presenting with bradycardia.
6. 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

PALPITATIONS: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Are the palpitations constant or intermittent? Constant palpitations may signify tachycardia, and that would suggest hyperthyroidism or overuse of caffeine and other drugs. Intermittent palpitations are more likely related to a cardiac arrhythmia, particularly extrasystoles. Also, constant palpitations may indicate a fever of unknown origin.
2. Are there associated symptoms? Palpitations with weight loss, increased appetite, and polyuria would suggest hyperthyroidism. Palpitations with shortness of breath and pitting edema would suggest congestive heart failure.
3. Are there positive physical findings? If there is cardiomegaly, one must think of the possibility of congestive heart failure or valvular heart disease. If one finds a cardiac murmur, it is more likely that there is valvular heart disease such as acute or chronic rheumatic fever. Cardiomegaly, murmur, and/or fever would suggest a bacterial endocarditis. Cardiomegaly without a murmur would suggest a myocardiopathy, congestive heart failure, and hypothyroidism. Palpitations with no cardiomegaly but with hypertension would suggest pheochromocytoma, particularly if it is systolic hypertension, but it also can be found in hyperthyroidism. Persistent or intermittent palpitations with a totally normal physical examination suggest sensitivity to caffeine or the use of other drugs.

DIAGNOSTIC WORKUP

Before initiating an expensive workup, the patient should eliminate use of all drugs, alcohol, caffeine, and nicotine, if possible, for several days. If this does not eliminate the palpitations, a careful inquiry into the dietary habits should be made, and a CBC should be done to eliminate anemia. In the presence of tachycardia, weight loss, and increased appetite, it is obvious that a thyroid profile should be drawn. If there are palpitations and fever, a workup for an infectious disease, particularly rheumatic fever and bacterial endocarditis, is in order. Blood cultures, ASO titers, sedimentation rate, and echocardiography are useful. If the palpitations are intermittent, a pheochromocytoma should be considered, and 24-hr urine collection for VMA or metanephrines should be ordered. A drug screen may be necessary to ensure patient cooperation in eliminating all drugs. Twenty-four-hr blood pressure monitoring is also useful. In addition, 24-hr or 48-hr Holter monitoring is very useful in the diagnosis of intermittent palpitations. Newer technology involving a continuous-loop event recorder allows monitoring for 2 weeks at a time. Arm-to-tongue circulation times as well as spirometry may diagnose early congestive heart failure.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

TACHYCARDIA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is there a positive alcohol or drug history? It is well known that alcohol can cause a myocardiopathy. Atropine, caffeine, and many other substances can cause a tachycardia.
2. Is the heart rate below 160 and/or reduced by carotid sinus massage? This finding would help confirm the diagnosis of sinus tachycardia and lead to a consideration of fever, thyrotoxicosis, shock, anemia, myocardial infarction, and other disorders as the cause of the tachycardia.
3. Is there fever? The presence of fever and tachycardia should make one suspect acute infectious diseases, rheumatic fever, and thyroid storm.
4. Is there a tremor, neck mass, or systolic hypertension? These findings suggest thyrotoxicosis.
5. Is there chest pain? The presence of chest pain should make one suspect myocardial infarction, pulmonary embolism, and acute pericarditis.
6. Is there pallor or sweating? The presence of pallor or sweating should make one think of anemia and shock.
7. Are there crepitant rales, an enlarged liver, or peripheral edema? These findings suggest congestive heart failure.
8. Is there hypotension? The presence of hypotension should make one think that there may be a pathologic tachycardia such as supraventricular tachycardia, auricular flutter, or auricular fibrillation. Auricular fibrillation is especially likely to be associated with significant hypotension.
9. Is the rate irregular? The presence of an irregular heart rate should make one suspect auricular fibrillation, or alternating flutter and fibrillation.

DIAGNOSTIC WORKUP

Routine diagnostic tests should include a CBC, sedimentation rate, urinalysis, chemistry panel, toxicology screen, thyroid profile, ANA titer, VDRL test, chest x-ray, and EKG. If there is fever, then an ASO titer and CRP, febrile agglutinins, and serial blood cultures should be done.

If a myocardial infarction is suspected, serial EKGs and cardiac enzymes need to be ordered. If a pulmonary embolism or infarction is suspected, arterial blood gases and lung scans need to be ordered, and, ultimately, pulmonary angiography may need to be done.

If congestive heart failure is suspected, a venous pressure and circulation time and possibly pulmonary function studies may be done. Echocardiography may be done to determine the LVEF.

If the tachycardia is paroxysmal, 24-hr Holter monitoring or admission to the hospital for ambulatory telemetry and observation may be necessary. A cardiologist should be consulted. Ultimately, a psychiatrist may need to be consulted also.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

CARDIAC ARRHYTHMIA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is it acute or chronic? An acute cardiac arrhythmia should make one consider a myocardial infarction first.
2. Is the heart rate slow, normal, or fast? A rapid cardiac arrhythmia may be associated with hyperthyroidism, congestive heart failure, or drug toxicity. A slow cardiac arrhythmia is more likely to be associated with heart block and syncope. A myocardial infarction may produce either the rapid or slow cardiac arrhythmia.
3. Is the rhythm regular or irregular? A tachycardia with a regular rhythm is more likely to be a supraventricular tachycardia or ventricular tachycardia. A tachycardia with an irregular rhythm is more likely to be atrial fibrillation, but atrial flutter can also cause a rapid irregular rhythm. Irregular premature contractions and ventricular premature contractions may be associated with rapid, slow, or normal cardiac rates. A slow, fairly regular heart rate is associated with complete heart block.
4. Is there chest pain associated with the cardiac arrhythmia? Chest pain should make one think of myocardial infarction, pericarditis, or coronary insufficiency.
5. Is there fever? If there is fever, one should consider rheumatic fever, subacute bacterial endocarditis, and thyroid storm.
6. Is there a heart murmur associated with the arrhythmia? A heart murmur associated with arrhythmia should make one think of rheumatic fever or subacute bacterial endocarditis, myocardiopathy, or acute congestive heart failure.
7. Are there signs of congestive heart failure? Hepatomegaly, jugular vein distention, and pitting edema of the extremities would make one think that congestive heart failure was the cause of the arrhythmia.
8. Is there a thyroid enlargement? An enlarged thyroid gland would certainly make one think of thyrotoxicosis.
9. Is there hypertension? Hypertension is another important cause of cardiac arrhythmias that should not be forgotten.

DIAGNOSTIC WORKUP

All patients should have an EKG, chest x-ray, and a CBC to rule out anemia. A thyroid profile should be done to look for both hyperthyroidism and hypothyroidism. In acute arrhythmias, serial EKGs and tests for cardiac enzymes need to be done to exclude an acute myocardial infarction. Venous pressure and circulation time should be determined to rule out congestive heart failure; pulmonary function tests may be helpful, as they may rule out both congestive heart failure and emphysema. Echocardiograms should be done to rule out valvular disease and cardiomyopathy. If there are paroxysmal arrhythmias, Holter monitoring needs to be done. An exercise tolerance test may allow the recording of an arrhythmia that is only induced on exercise. Signal-averaged EKG and electrophysiologic testing should also be considered. Patients on digitalis, quinidine, or other cardiac drugs should have blood levels of these drugs measured to determine if their levels are toxic. If there is a fever, blood culture should be done to rule out bacterial endocarditis. Referral to a cardiologist can be made at any point in the diagnostic workup.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

CARDIAC MURMURS: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Could the murmur be extracardiac in origin? Extracardiac murmurs include the pericardial friction rub and cardiorespiratory murmurs.
2. 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.
3. 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.
4. 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.
5. Is there hepatomegaly? Hepatomegaly associated with the murmur would make one think of congestive heart failure or tricuspid regurgitation and tricuspid stenosis.
6. Is there associated fever? Cardiac murmurs occurring with fever suggest acute rheumatic fever and subacute bacterial endocarditis.
7. Is there dyspnea? Dyspnea associated with a cardiac murmur suggests congestive heart failure.
8. Is there chest pain? If there is chest pain associated with a cardiac murmur, one must consider pericarditis and myocardial infarction.
9. Is there an enlarged thyroid or intention tremor? These findings suggest hyperthyroidism.
10. 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

Palpitations: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Premature atrial contractions
• Premature ventricular contractions
• Sinus tachycardia
  –Regular heart rhythm at 100–140 bpm
• Atrial fibrillation
  –Irregularly irregular heart rate
• Atrial flutter
  –Regular heart rhythm at about 150 bpm
• Drugs leading to tachyarrhythmias (e.g., aminophylline, amphetamines, alcohol, atropine, cocaine, coffee, epinephrine, ephedrine, MAO inhibitors, tea, thyroid extract, tobacco)
• Psychiatric disorders (anxiety, panic reactions)
• Anemia (with exertion)
• Heart failure (with exertion)
• Menopausal syndrome (with hot flashes)
• Paroxysmal atrial tachycardia
• Re-entry tachycardias, including Wolff-Parkinson-White syndrome
• Ventricular tachycardia
• Atrioventricular heart blocks
• Junctional tachycardia
• Mitral valve prolapse
• Myocardial ischemia
• Hyperthyroidism-associated arrhythmias
• Severe deconditioning (with exertion)
• Hypoglycemia
• Postural hypotension
• Atrial septal defect
• Adrenal tumor
• Pheochromocytoma

Workup and Diagnosis

• History and physical exam
  –Note duration, frequency, and precipitating factors
  –May be associated with chest pain, dyspnea, diaphoresis, or lightheadedness/syncope
  –Heart rhythm may be regular or irregular
  –May have family history of prolonged QT syndrome, hypertrophic cardiomyopathy, syncope, arrhythmias, or sudden death
• ECG
• 24-hour Holter monitor may be indicated
• Event monitor (if events are infrequent)
• Echocardiogram
• Exercise stress test if exercise-related
• Laboratory studies normally include CBC, electrolytes, glucose, TSH, calcium, magnesium
• Consider drug screen
• Consider cardiology consult
• Electrophysiologic studies may be necessary if symptoms suggest sustained arrhythmia

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Source: In a Page: Signs and Symptoms, 2004

Tachycardia: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Sinus tachycardia
  –Regular rhythm, narrow QRS complex
  –Originates at sinus node (normal P waves)
  –Occurs in response to physiologic stimuli (e.g., volume depletion, fever, pain, thyrotoxicosis)

Ectopic atrial tachycardia
–Regular rhythm, narrow QRS complex
–Atrial focus other than sinus node
–P waves are often inverted in inferior leads

• Atrial flutter
  –Narrow QRS complex
  –Usually regular, but may be irregular
  –Caused by a re-entrant circuit in atrium
  –Characteristic “sawtooth” pattern on ECG
  –Atrial rate typically 250–350 bpm
  –Ventricular rate usually 1/2 atrial rate (2:1 block), but may be 3:1, 4:1, etc.

Junctional tachycardia
–Regular rhythm, narrow QRS complex
–Originates in AV node
–P waves may be absent or retrograde

AVNRT
–Regular rhythm, narrow QRS complex
–Due to reentrant circuit in or near AV node
–Rate typically 170–220 bpm
–P waves may be absent or retrograde

Orthodromic AV reentrant tachycardia
–Regular rhythm, narrow QRS complex
–Caused by reentrant circuit at AV node
–Abrupt onset/offset
–WPW syndrome is most common example
–ECG reveals delta waves

Ventricular tachycardia
–Regular rhythm, wide QRS complex
–AV dissociation on ECG
–May cause sudden cardiac death
–Typically occurs in setting of acute coronary ischemia; other causes include cardiomyopathy, electrolyte disturbances (e.g., hypokalemia, hypomagnesemia), drug toxicity, or congenital abnormalities
–Torsade de pointes is a specific form of VT associated with electrolyte abnormalities and drug toxicity

Antidromic AVRT
–Wide QRS complex
–Conduction occurs down bypass tract and up AV node
–Less common than orthodromic AVRT

Workup and Diagnosis

• History and physical examination
  –Associated symptoms may include lightheadedness, palpitations, dyspnea, chest pain, and syncope
  –Assess for hemodynamic instability (blood pressure, level of consciousness) and jugular venous pulsations (cannon A waves are highly suggestive of AV dissociation)
• ECG is the key tool for establishing diagnosis
  –Determining supraventricular versus ventricular origin is the most critical distinction
  –Adenosine IV push may be used to transiently block the AV node to identify underlying rhythms
• Any wide-QRS complex tachycardia (QRS >0.12 seconds) is considered ventricular tachycardia until proven otherwise
  –Nonsustained VT lasts <30 seconds and is asymptomatic
  –Sustained VT lasts >30 seconds or results in hemodynamic compromise
  –Monomorphic VT is a single stable QRS complex
  –Polymorphic VT is a changing QRS morphology and axis—may have normal or prolonged QT interval (e.g., torsade de pointes) on baseline ECG

>

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Source: In a Page: Signs and Symptoms, 2004

Irregular Heart Rhythms: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Atrial fibrillation
  –One of the most common causes of irregular rhythm
  –Narrow QRS complex without organized atrial contraction (no P waves)
  –Etiologies include infection, thyrotoxicosis, alcohol, cocaine, amphetamines, myocarditis, pericarditis, hypertensive crisis, ischemia, MI, CHF, hypoxia, PE, hypertension, valvular heart disease
• Atrial flutter with variable block
  –Narrow QRS complex
  –ECG: “Sawtooth” flutter waves
  –Atrial rate is typically 250–350 bpm
  –Ventricular rate is usually 1/2 or 1/3 of atrial rate (2:1 or 3:1 block)
  –Irregular when variable block is present
  –Result of a macro-reentrant circuit in atrium

• Premature atrial contractions
• Paroxysmal atrial tachycardia
• Multifocal atrial tachycardia
  –Multiple areas of atrial impulses (more than three P wave morphologies) followed by a narrow QRS complex
  –HR ≥ 100 bpm
  –Most often seen in patients with lung disease
• Wandering atrial pacemaker
  –Multiple areas of atrial impulses (more than three P wave morphologies) followed by a narrow QRS complex
  –HR ≤ 100 bpm
  –Often occurs in athletes and the very young (increased vagal tone)

• Premature ventricular contractions
• Sinus arrhythmia

Workup and Diagnosis

• History and physical examination
  –Associated symptoms may include lightheadedness,
  palpitations, dyspnea, chest pain, or syncope
  –Assess for hemodynamic instability

ECG with rhythm strip is the key tool for establishing diagnosis

Initial laboratory evaluation may include CBC, electrolytes, BUN/creatinine, calcium, pulse oximetry, chest X-ray, and possibly an ABG

Consider cardiac enzymes, TSH, and toxicology screen

Echocardiogram may be necessary to evaluate for underlying disease or the presence of thrombi
–Transesophageal echocardiography is more sensitive than transthoracic echocardiography for detection of intracardiac thrombus (most commonly seen in left atrial appendage)

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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

Tachycardia/Palpitations: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Sinus tachycardia
  –Most common cause of a fast heart rate
  –Normal response to stress (fever, pain, anxiety, dehydration, exercise, anemia, caffeine, tobacco, albuterol)
  –<180 beats/min and variable; ECG shows an upright P wave in lead I and AVF

• Supraventricular tachycardia (SVT)
  –Most common pathologic cause of tachycardia/palpitations in children
  –Narrow QRS complex (<0.08 seconds)
  –Almost all hemodynamically stable
  –Often paroxysmal
  –Usually AV re-entry or AV node re-entry; both have HR >180 and intermittent sudden onset and resolution

• AV re-entry
  –Involves an accessory electrical bypass tract connecting the atrium and ventricle (thereby “bypassing” the AV node)
  –Often associated with Wolff-Parkinson-White (WPW) syndrome (short PR interval, widened QRS interval, “delta” wave)
  –Most common in <10 years of age

• AV node re-entry
  –Involves re-entry within the AV node
  –Most common in >10 yrs of age

• Atrial fibrillation/flutter
  –Occurs almost exclusively in patients with underlying congenital heart disease
  –Macro (flutter) or micro (fibrillation) re-entry circuits within the atrium, usually around an old surgical scar
  –Common in patients status post-Fontan or Mustard-Senning procedures

• Ectopic/multifocal atrial tachycardia
  –Involves one or more automatic electrical foci in the atrium causing irregular tachycardia with a heart rate <180
  –The tachycardia has a slow onset and resolution

• Wide-complex tachycardia
  –Assume ventricular tachycardia until proven otherwise
  –SVT with bundle branch block (either permanent or rate-related)
  –Antidromic WPW: Re-entry loop in which the ventricle is depolarized via the bypass tract, creating a wide-complex tachycardia

Workup and Diagnosis

• History
  –Onset (sudden vs slow acceleration), activity at time of onset, duration, regularity of rhythm, pulse rate, resolution (sudden vs slow; with vagal maneuvers)
  –Symptoms during tachycardia: Chest pain, pallor, diaphoresis, syncope
  –History of underlying congenital heart disease
  –Medication use: Caffeine, tobacco, albuterol
  –Underlying medical condition: Fever, pain, anxiety, dehydration, anemia, thyrotoxicosis
  • Physical exam
    –Evaluate cardiovascular stability (BP, perfusion, mental status, tachypnea)
    –All unstable patients with a fast heart rate require electrical cardioversion
    –Rarely, chronic incessant tachycardias can cause cardiomyopathy with congestive heart failure
  • 12-lead ECG
    –During tachycardia: Narrow vs. wide complex, regular vs. irregular rhythm, P wave axis, QRS wave
    –Baseline: Evaluate for WPW, prolonged QTc, bundle
  • branch block
    –During therapy: Record ECG while giving adenosine
  • 24-hour Holter monitor for daily symptoms
  • 30-day event monitor for intermittent symptoms (recording activated by patient when symptoms occur)
  • Exercise testing with ECG monitor for patients with symptoms only during exercise
  >>>>

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Source: In A Page: Pediatric Signs and Symptoms, 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

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

TACHYCARDIA: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The association of other clinical signs and symptoms will often help pinpoint the diagnosis. Tachycardia with tremor and an enlarged thyroid suggests hyperthyroidism. Tachycardia with respiratory wheezes suggests bronchial asthma. Tachycardia with a black stool suggests a bleeding peptic ulcer. If the blood pressure is low, the workup will proceed as that of shock (see page 317). On the other hand, tachycardia with a normal blood pressure should prompt thyroid function studies, pulmonary function studies, arterial blood gases, and a venous pressure and circulation time. Electrolyte determinations, a drug screen, and 24-hour urine for catecholamine determinations may be indicated if there is hypertension as well.

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Source: Differential Diagnosis in Primary Care, 2007

CARDIAC ARRHYTHMIAS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The diagnosis depends a lot on the type of arrhythmia. Atrial premature contractions are usually benign and an extensive workup is unnecessary unless other physical signs indicate the need for it. Infrequent ventricular premature contractions (VPCs) in otherwise healthy individuals probably can be handled the same way. When VPCs are frequent or multifocal, an exercise tolerance test, echocardiogram, and perhaps coronary angiography are indicated. Runs of ventricular tachycardia require an extensive workup, including coronary angiography, but usually there will be other signs to indicate the need for this.

Atrial tachycardia and fibrillation require a workup of hyperthyroidism and pulmonary disease, systemic hypertension, and congestive heart failure. Atrial obstruction and dilatation should be excluded by echocardiography.

Any arrhythmia warrants an ECG and possibly repeated ECGs. The Holter monitor should be used if there is doubt about the type of arrhythmia.

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Source: Differential Diagnosis in Primary Care, 2007

PALPITATION: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Valvular heart disease, anemia, and febrile disorders will usually be revealed on physical examination. It is important to inquire about drug, alcohol, and tobacco use. Caffeine is a frequent offender. It is helpful to eliminate any suspicious medications if possible. A drug screen may be useful in many cases. The initial diagnostic workup should include a CBC, chemistry profile, thyroid profile, sedimentation rate, ASO titer, ECG, and chest x-ray. If these have normal findings, 24-hour Holter monitoring or continuous loop event recording of the ECG should be undertaken.

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Source: Differential Diagnosis in Primary Care, 2007

Bradycardia: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

After detecting bradycardia, check for related signs of life-threatening disorders. (See Managing severe bradycardia.) If the patient's bradycardia isn't accompanied by untoward signs, ask the patient if he or a family member has a history of a slow pulse rate because this may be inherited. Also, find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he's taking and if he's complying with the prescribed schedule and dosage. Monitor his vital signs, temperature, pulse, respirations, blood pressure, and oxygen saturation.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Murmurs: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 406.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient’s medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Palpitations: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If the patient isn’t in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Make sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Also, ask about caffeine, tobacco, and alcohol consumption.

Then explore associated symptoms, such as weakness, fatigue, and angina. Finally, auscultate for gallops, murmurs, and abnormal breath sounds.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulse rhythm abnormality: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient’s compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulse, absent or weak: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If you detect an absent or a weak pulse, quickly palpate the remaining arterial
pulses to distinguish between localized or generalized loss or weakness. Then quickly check the patient’s other vital signs, evaluate his cardiopulmonary status, and obtain a brief history. Based on your findings, proceed with emergency interventions. (See Managing an absent or a weak pulse, pages 506 and 507.)

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Pulsus bisferiens: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

After you detect a biferious pulse, review the patient’s history for cardiac disorders. Next, find out what medication he’s taking, if any, and ask if he has other illnesses. Also, ask about the development of associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest. Then take his vital signs and auscultate for abnormal heart or breath sounds.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Tachycardia: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If the patient’s condition permits, take a focused history. Find out if he has had palpitations. If so, how were they treated? Explore associated symptoms. Is the 0patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.

Inspect the patient’s skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Cardiac arrhythmias: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis is made by tests that reveal the arrhythmia, such as 12-lead electrocardiography. Ambulatory cardiac monitoring (Holter monitoring), echocardiography, electrophysiology studies, and coronary angiography may also confirm or rule out suspected causes of arrhythmias and help determine treatment.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Bradycardia: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

After detecting bradycardia, check for related signs of life-threatening disorders. (See Managing severe bradycardia.) If bradycardia isn’t accompanied by untoward signs, ask the patient if he or a family member has a history of a slow pulse rate because this may be inherited. Also, find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he’s taking and if he’s complying with the prescribed schedule and dosage. Monitor vital signs, temperature, pulse rate, respirations, blood pressure, and oxygen saturation.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Murmurs: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 517.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery, or if it has been known since birth or childhood. Find out if the patient has experienced any associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. (See Differential diagnosis: Murmurs, pages 518 and 519.) Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Palpitations: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient isn’t in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Be sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Ask about caffeine, tobacco, and alcohol consumption.

Explore associated symptoms, such as weakness, fatigue, and angina. Auscultate for gallops, murmurs, and abnormal breath sounds.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulse rhythm abnormality: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about onset and location. Does the pain radiate? Ask about a history of heart disease and treatments for arrhythmias. Obtain a drug history and check compliance. Also, ask about any caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulse, absent or weak: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If you detect an absent or weak pulse, quickly palpate the remaining arterial pulses to distinguish between localized or generalized loss or weakness. Then quickly check other vital signs, evaluate cardiopulmonary status, and obtain a brief history. Based on your findings, proceed with emergency interventions. (See Managing an absent or weak pulse, pages 638 and 639.)

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Pulsus bisferiens: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

After you detect a bisferiens pulse, review the patient’s history for cardiac disorders. Next, find out what medication he’s taking, if any, and ask if he has any other illnesses. Ask about the development of any associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest. Take his vital signs and auscultate for abnormal heart or breath sounds.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Tachycardia: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient’s condition permits, take a focused history. Find out if he has had palpitations before. If so, how were they treated? Explore associated symptoms. Is the patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.

Inspect the patient’s skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.

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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

Palpitations: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 The history alone may suggest the underlying diagnosis.

A. Characteristics of the PPTs. Are the PPTs regular or irregular? Fast or slow? What descriptors does the patient use? Are the PPTs only in the chest? Ask patients to tap out the rhythm of their PPTs, and to check their pulse during an episode (3).

1. Rapid, irregular PPTs imply atrial fibrillation, multifocal atrial tachycardia, or atrial flutter with variable conduction.

2. Rapid, regular PPTs occur with supraventricular tachycardias (SVTs), including sinus tachycardia and ventricular tachycardia (VT).

3. A “stop-start,” “flip-flop,” or “turning over” sensation in the chest (postectopic pause and subsequent accentuated beat) is usually caused by premature ventricular contractions (PVCs) or premature atrial contractions (PACs).

 4. PPTs felt in the neck represent atria contracting against closed atrioventricular (AV) valves, with blood refluxing into the superior vena cava. The most common cause is AV nodal reentrant tachycardia (AVNRT), which generally causes rapid, regular, sustained pounding; it can also occur with PVCs (slower, less regular, less sustained) (3).

 B. Situations in which PPTs occur. PPTs can be associated with anxiety or somatization disorders. Although overlap is seen among patients with PPTs and those with psychiatric disorders, true arrhythmias do occur in such patients. Arrhythmias (SVT, VT, torsades de pointes) can occur with catecholamine release (exercise, emotional stress); PPTs occurring at rest may indicate benign conditions. PPTs associated with position may result from SVT or PVCs.

C. Onset and termination. Although abrupt onset and termination of PPTs suggests PSVT, this finding is neither sensitive nor specific. Anxiety can lead to sinus tachycardia following an arrhythmia, precluding the patient from sensing an abrupt cessation.

D. Associated symptoms. When syncope, presyncope, or dizziness occurs with PPTs, sustained or nonsustained VT must be ruled out (Chapters 2.2 and 2.12).

 E. Other information. Patients with structural heart disease are more likely to have arrhythmias. Age of onset in childhood or adolescence suggests SVT, especially preexcitation syndromes or long QT syndrome. Various substances can be associated with SVT (nicotine, caffeine, adrenergic or anticholinergic drugs, cocaine, amphetamines) or atrial fibrillation (alcohol). Findings consistent with hyperthyroidism or less common disorders causing PPTs (diabetes, Lyme disease, sarcoidosis, amyloidosis) should be pursued. Ask if the patient has found relief with beta-blockers (PVCs) or vagal maneuvers (SVT). Family history (arrhythmias, sudden death, other cardiovascular disease, syncope) can be helpful.

Physical examination (PE)

If the patient is not seen during an episode, aim the PE at detecting abnormalities that are associated with PPTs. Midsystolic click and murmur (mitral valve prolapse), harsh holosystolic murmur (hypertrophic cardiomyopathy), diastolic murmur (aortic regurgitation), or signs of congestive heart failure may aid in diagnosis. Look for stigmata of hyperthyroidism and other conditions noted above (II.E) (Chapter 14.8).

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Tachycardia: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Determining the cause. The clinical history is directed toward determining the underlying cardiac disease. Symptoms associated with tachycardia are palpitations, lightheadedness or presyncope, syncope, or congestive heart failure (CHF) (Chapters 2.12, 7.5, and 7.9). Some patients will also complain of irregular heartbeat, whereas others can be asymptomatic even with a profoundly abnormal rhythm. Prior history of myocardial infarction, cardiomyopathy (both ischemic and nonischemic heart disease), arrhythmias, pulmonary hypertension, cardiac surgery, rheumatic heart disease, valvular disease, and family history of cardiac arrythmias are all important. Medications such as any of the class IA or III antiarrythmic agents or over-the-counter cold preparations can cause tachyarrhythmias. Even a combination of medicines (e.g., certain antibiotics and newer nonsedating antihistamines) can contribute to tachyarrythmias.

Physical examination

The physical examination should include vital signs; pulse rate and blood pressure are the most important. Decreased blood pressure suggests a need for immediate treatment. A general assessment of mental status and skin perfusion also provides clues to the stability of the patient. A good cardiovascular and pulmonary examination is essential. Palpation of the heart (point of maximal impulse, PMI) can discern left ventricular enlargement. Auscultate systematically. The rhythm should be assessed to whether it is regular or irregular. Determine the specific heart rate. Next, determine if an associated murmur, rub, or gallop exists. Include in the examination an assessment for evidence of ventricular failure (e.g., pulmonary crackles, jugular venous distension, and lower extremity edema). In the respiratory assessment, include respiratory rate and evidence of labored breathing.

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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

Palpitations/Tachycardia: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Sinus tachycardia

❑ Paroxysmal supraventricular tachycardia

❑ Atrial fibrillation

❑ Atrial flutter

❑ AV nodal re-entrant tachycardia

❑ Ventricular premature beats

❑ Anxiety

❑ Drugs

❑ Anemia

❑ Multifocal atrial tachycardia

❑ Ventricular tachycardia

Diagnostic Approach

A disquieting awareness of the heartbeat described as pounding, skipping, racing, flopping, or fluttering is usually due to an arrhythmia, or a change in rhythm, rate, or contractility.

Arrhythmia should be approached both from the standpoint of determining the specific rhythm disturbance and recognizing it as a marker for other potentially serious disorders. Signs of underlying heart disease such as ischemia (exertional chest pain), cardiomyopathy (rales, S₃ gallop, diffuse PMI), or syncope must be searched for because they alter the prognostic implications of the rhythm disorder.

A sensation of pounding in the neck is associated with jugular cannon a waves. Presence of a cannon a wave implies atrial contraction and can rule out atrial fibrillation. Intermittent cannon a waves result from atrioventricular dissociation.

Carotid massage will suddenly halve the rate with atrial flutter, but there is a gradual slowing of the pulse with sinus tachycardia. Supraventricular tachycardia either continues or terminates abruptly with carotid massage.

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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

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

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

Palpitations: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

If the patient isn’t in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does he have a history of hypertension or hypoglycemia? Be sure to obtain a drug history. Has he recently started cardiac glycoside therapy? Also, ask about caffeine, tobacco, amphetamine, and alcohol consumption.

Physical examination

Perform a complete cardiac and pulmonary assessment. Then explore associated symptoms, such as weakness, fatigue, and angina. Finally, auscultate for gallops, murmurs, and abnormal breath sounds. Cardiac monitoring may be indicated when a cardiac arrhythmia is suspected. (See Palpitations: Causes and associated findings, pages 226 and 227.)

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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

Tachycardia: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

If the patient’s condition permits, obtain his medical history. Has he had palpitations before? If so, what treatment was he given? Explore associated symptoms: Is he dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Obtain a drug history, including prescription, over-the-counter, and illegal drugs, and ask whether the patient uses alcohol.

Physical examination

Inspect the patient’s skin for pallor, dehydration, or cyanosis. Assess pulses, noting peripheral edema. Assess the patient’s blood pressure. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 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.

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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

Palpitations: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If the patient isn’t in distress, take a complete cardiac history. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Be sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Also, ask about caffeine, tobacco, and alcohol consumption.

» 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

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.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Pulsus bisferiens: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

After you detect a bisferiens pulse, review the patient’s history for cardiac disorders. Next, find out what medication he’s taking, if any, and ask if he has any other illnesses. Also ask about the development of any associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Tachycardia: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If the patient’s condition permits, take a focused history. Find out if he has had palpitations before. If so, how were they treated? Explore associated symptoms. Is the patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.

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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 indicate

Semilunarvalve incompetence (aortic or pulmonic valve)

Atrioventricular valve stenosis (mitralor tricuspid valve)

Severe mitral or tricuspid valve incompetence

Increased 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.

>

» READ BOOK EXCERPT ONLINE »

Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Bradycardia: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

After detecting bradycardia, check for related signs of life-threatening disorders. (See Managing severe bradycardia, page 94.)

If the patient's bradycardia isn't accompanied by untoward signs, ask the patient if he or a family member has a history of a slow pulse rate because this may be inherited. Find out if he has an underlying metabolic disorder, such as hypothyroidism, which can precipitate bradycardia. Ask which medications he's taking and if he's complying with the prescribed schedule and dosage. Monitor his vital signs, temperature, pulse, respirations, blood pressure, and oxygen saturation.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Murmurs: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 398.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.

Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient's medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.

Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient's liver tender or palpable? Does he have peripheral edema?

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Palpitations: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient isn't in distress, perform a complete cardiac history and physical examination. Ask if he has a cardiovascular or pulmonary disorder, which may produce arrhythmias. Does the patient have a history of hypertension or hypoglycemia? Be sure to obtain a drug history. Has the patient recently started cardiac glycoside therapy? Also, ask about caffeine, tobacco, and alcohol consumption.

Then explore associated symptoms, such as weakness, fatigue, and angina. Finally, auscultate for gallops, murmurs, and abnormal breath sounds.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulse rhythm abnormality: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient's condition permits, ask if he's experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient's compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.

Next, check the patient's apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S₁ (lub) and S₂ (dub) may indicate a conduction defect. A faint or absent S₁ and an easily audible S₂ may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient's apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Place the patient on a cardiac monitor and obtain an ECG to evaluate the cardiac rhythm. Report your findings to the practitioner.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulse, absent or weak: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If you detect an absent or a weak pulse, quickly palpate the remaining arterial pulses to distinguish between localized or generalized loss or weakness. If localized, ask whether the patient has experienced or is presently experiencing pain in that area. Assess the limb for color and temperature. Then quickly check the patient's other vital signs, evaluate his cardiopulmonary status, and obtain a brief history. Based on your findings, proceed with emergency interventions. (See Managing an absent or a weak pulse, pages 498 and 499.)

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulsus bisferiens: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

After you detect a biferious pulse, review the patient's history for cardiac disorders. Next, find out what medication he's taking, if any, and ask if he has other illnesses. Also, ask about the development of associated signs and symptoms, such as dyspnea, chest pain, or fatigue. Find out how long he has had these symptoms and if they change with activity or rest. Then take his vital signs and auscultate for abnormal heart or breath sounds.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

Tachycardia: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient's condition permits, take a focused history. Find out if he has had palpitations in the past. If so, how were they treated? Explore associated symptoms. Is the patient dizzy or short of breath? Is he weak or fatigued? Is he experiencing episodes of syncope or chest pain? Next, ask about a history of trauma, diabetes, or cardiac, pulmonary, or thyroid disorders. Also, obtain an alcohol and drug history, including prescription, over-the-counter, and illicit drugs.

Inspect the patient's skin for pallor or cyanosis. Assess pulses, noting peripheral edema. Finally, auscultate the heart and lungs for abnormal sounds or rhythms.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 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.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

TACHYCARDIA: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The association of other clinical signs and symptoms will often help to pinpoint the diagnosis. Tachycardia with tremor and an enlarged thyroid suggests hyperthyroidism. Tachycardia with respiratory wheezes suggests bronchial asthma. Tachycardia with a black stool suggests a bleeding peptic ulcer. If the blood pressure is low, the workup will proceed as that of shock . In contrast, tachycardia with a normal blood pressure should prompt thyroid function studies, pulmonary function studies, arterial blood gases, and a venous pressure and circulation time. Electrolyte determinations, a drug screen, and 24-hour urine for catecholamine determinations may be indicated if there is hypertension as well.

---

TACHYCARDIA

	V	I	N	D
	Vascular	Inflammatory	Neoplasm	Degenerative
Decreased Intake of Oxygen	Aortic aneurysm with compression of bronchi	Laryngitis Bronchitis	Carcinoma of the lung	Pulmonary emphysema
Increased Oxygen Absorption	Pulmonary embolism	Pneumonia	Hemangioma Carcinoma of the lung	Pulmonary emphysema Fibrosis
Inadequate Oxygen Transport	Shock from myocardial infarction Congestive heart failure	Septicemic shock		Aplastic anemia
Peripheral Arteriovenous Shunts				Paget disease
Increased Tissue Demands for Oxygen		Septicemia Fever of any infection	Leukemia Hodgkin lymphoma Polycythemia vera
Disorders Affecting the Heart Directly	Myocardial infarction Essential hypertension	Myocarditis Tuberculosis Pericarditis	Rhabdomyosarcoma	Muscular dystrophy

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TACHYCARDIA

I	C	A	T	E
Intoxication	Congenital	Allergic and	Trauma	Endocrine
		Autoimmune
Pneumoconiosis	α 1-trypsin deficiency Cystic fibrosis	Bronchial asthma	Pneumothorax
Nitrofurantoin Pneumoconiosis Shock lung Lipoid pneumonia	Congenital cyst	Scleroderma Wegener granulomatosis	Shock lung	Fat emboli
Drug-induced shock Methemoglobinemia	Sickle cell anemia Cooley anemia	Hemolytic anemia (autoimmune)	Hemorrhagic shock
	Carotic–cavernous shunt		Popliteal aneurysm
				Hyperthyroidism
Caffeine Amphetamines Alcohol Hyperkalemia Digitalis	Wolff–Parkinson–White syndrome Glycogen storage disease	Lupus erythematosus	Traumatic aneurysm	Hyperthyroidism Pheochromocytomas

---

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Source: Differential Diagnosis in Primary Care, 2007

CARDIAC ARRHYTHMIAS: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

The diagnosis depends a lot on the type of arrhythmia. Atrial premature contractions are usually benign, and an extensive workup is unnecessary unless other physical signs indicate the need for it. Infrequent ventricular premature contractions (VPCs) in otherwise healthy individuals probably can be handled the same way. When VPCs are frequent or multifocal, an exercise tolerance test, echocardiogram, and perhaps coronary angiography are indicated. Runs of ventricular tachycardia require an extensive workup, including coronary angiography, but usually there will be other signs to indicate the need for this. Atrial tachycardia and fibrillation require a workup of hyperthyroidism and pulmonary disease, systemic hypertension, and congestive heart failure (CHF). Atrial obstruction and dilatation should be excluded by echocardiography.

Any arrhythmia warrants an electrocardiogram (ECG) and possibly repeated ECGs. The Holter monitor should be used if there is doubt about the type of arrhythmia.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

PULSE RHYTHM ABNORMALITIES: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

It is wise to get a cardiology consult at the outset. Routine workup includes a CBC, sedimentation rate, thyroid panel, chemistry panel, electrocardiogram (EKG), and chest x-rays. If rheumatic fever is suspected, an ASO titer or streptozyme test will be ordered. Echocardiography, Hiss bundle studies, and 24 hour Holter monitoring may be necessary. If a valvular lesion or coronary artery disease is suspected, cardiac catheterization and angiocardiography will be necessary.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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