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Diseases » Tachycardia » Diagnosis
 

Diagnosis of Tachycardia

Tachycardia Diagnosis: Book Excerpts

Diagnostic Tests for Tachycardia: Online Medical Books

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


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.

 

» READ BOOK EXCERPT ONLINE »

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.

 

» READ BOOK EXCERPT ONLINE »

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.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

» READ BOOK EXCERPT ONLINE »

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
    >

    » READ BOOK EXCERPT ONLINE »

    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

    » READ BOOK EXCERPT ONLINE »

    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

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    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
      >>>>

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

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

    A chest x-ray with anterior oblique films during a barium swallow along with an ECG, sedimentation rate, a blood serology thyroid profile, and CBC are basic in the workup of a murmur. If there is a fever or if there is recent onset of the murmur, blood cultures, an ASO titer and C-reactive protein (CRP) should be done. An ANA test, echocardiogram, and phonocardiogram are frequently done. Referral to a cardiologist is wise if the cause is obscure or if one is unable to spend the time for a careful workup. Angiocardiography and cardiac catheterization are the only sure ways to determine the location of the valvular disease, and, in many cases, the exact cause.

    » 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 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.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

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

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

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

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

    » READ BOOK EXCERPT ONLINE »

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

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

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

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

    » READ BOOK EXCERPT ONLINE »

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

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

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

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

    » READ BOOK EXCERPT ONLINE »

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

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

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

    » READ BOOK EXCERPT ONLINE »

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

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

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

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

    » READ BOOK EXCERPT ONLINE »

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

    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

    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

    Respirations, grunting: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    After addressing the child’s respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.

    Begin the physical examination by auscultating the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Characterize the color, amount, and consistency of any discharge or sputum. Note the characteristics of the cough, if any.

    » READ BOOK EXCERPT ONLINE »

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

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

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

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

    » READ BOOK EXCERPT ONLINE »

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

    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).

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

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

    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.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    Source: Field Guide to Bedside Diagnosis, 2007

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

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

    Physical examination

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

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

    » READ BOOK EXCERPT ONLINE »

    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.)

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Respirations, grunting: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    After addressing the child’s respiratory status, ask his parents when the grunting respirations began. Is he usually healthy with normal growth and development? If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.

    Physical examination

    Begin the physical examination by inspecting the rate, depth, and ease of respirations and any signs of respiratory distress. Auscultate the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Also, characterize the color, amount, and consistency of discharge or sputum. Note the characteristics of the cough, if any. Observe for abrupt behavior changes and lowered level of consciousness.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

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

    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.

    » READ BOOK EXCERPT ONLINE »

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

    Respirations, grunting: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    After addressing the child’s respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.

    » READ BOOK EXCERPT ONLINE »

    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.

    » READ BOOK EXCERPT ONLINE »

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

    Heart Murmurs (Asymptomatic): Clinical Features and Diagnosis
    (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

    Normal Murmurs

    Systolic Ejection Murmurs

  • Normal systolicejection murmurs are grade III or less.
  • They begin after S1 following the isovolumiccontraction period and end before S2.
  • They vary from cycle to cycle withrespiration or change in position.
  • Intensity increases with fever, anxiety,or exercise.
  • Although heard with maximum intensityat specific locations on the chest wall, they are louder in supineposition.

    • Vibratory Systolic Murmur

  • Commonlyheard in childhood and less often in infancy.
  • Usually grade II/VI but canrange from grade I to III.
  • Heard with maximum intensity at lowerleft sternal border or between this area and apex.
  • Has distinctive vibratory quality.

    • Pulmonary Systolic Murmur

  • Frequentlyheard in childhood and adolescence.
  • Maximum intensity is in second intercostalspace at upper left sternal border.
  • Usual intensity is grade II/VIwith range from grade I to III.
  • Higher in pitch than vibratory systolicejection murmur.
  • Also heard in straight back syndrome,which is characterized by absence of normal thoracic kyphosis andnarrow anterior-posterior diameter of chest. RV and pulmonary arterylie against sternum, and murmur is easily heard. Straight back syndromealso may be associated with mitral valve prolapse.

    • Physiologic Peripheral Pulmonary Systolic Murmur

  • May be heardin neonates, especially in preterm infants.
  • Intensity is usually grade I–II/VI.
  • Heard equally well in right and leftanterior chest, axillae, and back.
  • Usually disappears by 3–6mos of age.

    • Supraclavicular or Brachiocephalic Murmur

  • May be heardin childhood or adolescence.
  • Usually grade II or III/VI.
  • Maximum intensity is always above medialaspect of clavicles in supraclavicular fossa but may be heard belowclavicles.
  • Usually louder on right side.
  • Shoulder maneuvers are useful in distinguishingit from other murmurs. When physician is listening for murmur, childshould sit with shoulders relaxed and arms in front of chest. Murmurdiminishes or disappears when shoulders are hyperextended with elbowsbrought behind back.

    • Continuous Murmurs

    Venous Hum

  • Commonlyheard in sitting position.
  • Grade II–IV/VI continuousmurmur with maximal intensity in supraclavicular fossa, just lateralto sternocleidomastoid muscle with transmission below clavicles.
  • Usually more prominent on right side.
  • Diminishes or disappears with compressionof ipsilateral jugular vein, head/neck turning or positioning,or with lying down.

    • Pathologic Murmurs

  • Can be systolic,diastolic, or continuous.
  • Intensity is usually grade III or more,but can be grade I or II if lesion is mild.
  • Duration is usually longer than thatof normal murmur.
  • Heard with maximum intensity at specificlocations on chest wall.

    • Systolic Murmurs

    Maximal Intensity at Upper Right Sternal Border

    Valvar Aortic Stenosis

  • Most commontype of LV outflow tract obstruction.
  • Produces grade II–IV/VIharsh systolic ejection murmur that is heard with maximum intensityat upper right sternal border.
  • Aortic ejection click also can be heardalong left sternal border and at apex.
  • Prominent apical impulse is palpable.
  • Chest radiography shows normal to mildlyenlarged heart, normal pulmonary vascular markings, and mild dilatationof ascending aorta.
  • ECG is normal or shows LV hypertrophy.
  • 2-D echocardiography shows abnormalvalve. Doppler methods demonstrate abnormal flow pattern.

    • Maximal Intensity at Upper Left Sternal Border

    Valvar Pulmonic Stenosis

  • Associatedwith prominent RV impulse over lower sternum, normal S2, and systolic ejectionclick (louder on expiration) along left sternal border.
  • Grade II–IV/VI harshsystolic ejection murmur transmits to neck and back.
  • In infants, click may be absent withmild stenosis.
  • Chest radiograph shows normal heartsize, normal pulmonary vascular markings, and dilated main pulmonaryartery segment.
  • ECG is normal or shows RV hypertrophy.
  • 2-D echocardiography shows abnormalvalve. Doppler methods demonstrate abnormal flow pattern.

    • Atrial Septal Defects

  • Includeostium secundum, ostium primum, and sinus venosus defects.
  • Physical exam is similar with all defects.
  • Prominent RV impulse, grade II–III/VIsystolic ejection murmur with maximum intensity at upper left sternalborder, usually wide fixed splitting of S2, and grade II–III/VImid-diastolic rumbling murmur with maximum intensity at lower leftsternal border.
  • In infants, splitting of S2 may benormal or wide and not fixed.
  • Systolic murmur signifies increasedblood flow across pulmonic valve, and diastolic murmur reflectsincreased flow across tricuspid valve.
  • Chest radiography shows mild cardiomegaly,increase in pulmonary vascular markings, and enlarged pulmonaryartery segment.
  • ECG shows RV hypertrophy. In ostiumprimum defect, frontal plane QRS axis often shows left axis deviation,which signifies conduction system displacement. P wave on ECG ismore horizontal with sinus venosus defect.
  • 2-D echocardiography visualizes defectsand can distinguish between them.

    • Mild-to-Moderate Coarctation of Aorta

  • BP in rightarm is significantly higher than that in legs with coarctation ofaorta.
  • Femoral pulses are diminished comparedwith brachial or radial pulses.
  • Prominent apical impulse.
  • Grade II–III/VI harshsystolic ejection murmur is commonly heard at upper left sternalborder and left back.
  • Grade II–III/VI high-pitchedcontinuous murmur may be heard over left side of spine along scapularedge.
  • Presence of aortic ejection click andsystolic ejection murmur at upper right sternal border usually signifiesbicuspid aortic valve, which is commonly associated with coarctationof aorta.
  • Chest radiograph shows normal or mildlyenlarged heart and normal pulmonary vasculature. Ascending aortamay be dilated. In older infants and children, indentation of descendingaorta just distal to aortic arch produces "3" sign.Erosion of bone by large intercostal arteries can produce notchingof lower margins of posterior ends of ribs 3–9.
  • In early infancy, ECG usually showsRV hypertrophy, whereas in children it may be normal or show mildLV hypertrophy.
  • 2-D echocardiography can often demonstratecoarctation. In older children, if coarctation is not well demonstratedby echocardiography, it may be visualized by MRI.

    • Small Patent Ductus Arteriosus

  • Common interm infants and very common in preterm infants, especially in thosewith birth weight <1,500 g.
  • Murmur is usually grade II–III/VIand is systolic or continuous. Systolic ejection sounds are occasionallyheard along left sternal border.
  • Chest radiography shows normal sizeor mildly enlarged heart with increased pulmonary vascular markings.
  • ECG is either normal or shows mildLV hypertrophy.

    • Maximal Intensity at Lower Left Sternal Border

    Normal vibratory ejection murmur must bedistinguished from 2 pathologic systolic murmurs that are heardwith maximum intensity at lower left sternal border: murmurs ofventricular septal defect and tricuspid incompetence.

    Ventricular Septal Defect

  • Murmur ofsmall VSD may be heard as early as 1–3 days of age as pulmonaryvascular resistance decreases and left-to-right shunt develops.
  • Palpation reveals normal-sized or mildlyenlarged heart.
  • Intensity and splitting of S2 are normal.
  • Murmur is grade II–IV/VIand is heard throughout systole. It is harsh in quality with maximalintensity at lower left sternal border.
  • If defect begins to close with time,duration of murmur is less.
  • No diastolic murmur is heard at apexunless pulmonary:systemic flow ratio is ≥2:1.
  • Chest radiograph shows normal or mildlyenlarged heart, and increased pulmonary vascular markings.
  • ECG is normal or shows mild LV hypertrophy.
  • 2-D echocardiography may not visualizesmall defects.

    • Tricuspid Incompetence

  • Murmur ishigh pitched, usually grade II–III/VI, and heardthroughout systole with maximal intensity at lower left sternalborder.
  • May be heard in asymptomatic lesions(isolated mild congenital tricuspid incompetence, atrioventricularcanal defects, Ebstein anomaly) or in symptomatic ones (atrioventricularcanal defects, Ebstein anomaly, pulmonary atresia with intact septum,endocarditis, perinatal asphyxia).

    • Maximal Intensity at Apex

    Mitral Incompetence

  • Murmur ishigh pitched, usually grade II–IV/VI, and heardthroughout systole at apex with transmission to left axilla andback.
  • Heart is normal sized or mildly enlarged.
  • Chest radiograph and ECG are usuallynormal.
  • Causes include congenital defects ofmitral valve, atrioventricular canal defects, anomalous left coronaryartery from pulmonary artery, hypertrophic cardiomyopathy, Marfansyndrome, and Hurler syndrome.
  • Symptomatic causes include these lesionsas well as acute rheumatic fever, myocarditis, endocarditis, endocardialfibroelastosis, and perinatal asphyxia.

    • Mitral Valve Prolapse

  • Can occuras isolated defect or in association with ostium secundum atrialseptum defect, endocarditis, Hurler syndrome, Marfan syndrome, orEhlers-Danlos syndrome.
  • Usual finding is midsystolic nonejectionclick followed by late systolic murmur of mitral incompetence.
  • Murmur is heard best at apex, especiallyin standing position after squatting.
  • Chest radiograph is normal.
  • ECG may show inverted T waves in leadsII, III, and aVF as well as ST depression in left precordial leads.
  • Clinical diagnosis can be confirmedby M-mode or 2-D echocardiography.

    • Diastolic Murmurs

  • There havebeen some reports of normal diastolic murmurs occurring in infantsand children, but this is rare.
  • For this discussion, all diastolicmurmurs are considered pathologic. These murmurs usually 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

    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

    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

    Respirations, grunting: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    After addressing the child's respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child's activity level or feeding pattern to determine if the child is lethargic or less alert than usual.

    Begin the physical examination by auscultating the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Characterize the color, amount, and consistency of any discharge or sputum. Note the characteristics of the cough, if any. Note the respiratory rate. Assess accessory muscle use for breathing and cyanosis.

    » 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

    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
    VIND
    VascularInflammatoryNeoplasmDegenerative
        
    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
     
     

    TACHYCARDIA
    ICATE
    IntoxicationCongenitalAllergic andTraumaEndocrine
      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

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007


     » Next page: Signs of Tachycardia

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