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Diseases » Heart Murmur » Diagnosis
 

Diagnosis of Heart Murmur

Diagnostic Test list for Heart Murmur:

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

Heart Murmur Diagnosis: Book Excerpts

Diagnosis of Heart Murmur: medical news summaries:

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

Diagnostic Tests for Heart Murmur: Online Medical Books

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


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

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

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

Abdominal Bruit: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Abdominal aortic aneurysm
  • Hepatocellular carcinoma (hepatoma)
  • Cirrhosis
  • Liver hemangioma
  • Arteriovenous malformation
  • Renal artery stenosis
  • Celiac artery stenosis
  • Superior mesenteric artery stenosis
  • Tricuspid regurgitation
  • Turbulence of the splenic artery
    • Hepatic venous hum
      –High-pitched continuous murmur that decreases with forced held expiration
    • Cruveilhier-Baumgarten murmur
      –High-pitched venous hum of portal hypertension that becomes louder with forced expiration
    • Abdominal friction rub
      –Associated with hepatoma, cholangiocarcinoma, liver metastases, inflammatory processes
  • Takayasu's arteritis

Workup and Diagnosis

  • History and physical exam with focus on abdominal exam (may have palpable thrill), cardiac exam, four extremity pulses, and blood pressure
  • Ultrasound is often the initial test and is diagnostic for AAA, liver metastases, and liver and spleen sizes
  • Abdominal CT will demonstrate abdominal pathology and is useful to better delineate anatomy
  • Arterial Doppler ultrasound
  • Angiography is diagnostic for stenosis
  • Measuring renal vein renin levels following a captopril challenge is diagnostic for renal artery stenosis
  • Radionuclide nephrograms or IV urography will demonstrate differences in perfusion of kidneys with stenotic artery
  • Echocardiogram may be indicated to evaluate for valvular dysfunction
  • Laboratory studies may include a lipid panel to evaluate for arteriosclerosis; CBC and ESR if inflammatory processes are suspected; liver function tests to evaluate for liver dysfunction; and electrolytes and renal function tests if renal artery stenosis is suspected

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Carotid Bruits: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Internal carotid artery stenosis
  • External carotid artery stenosis
  • Normal (nonstenotic), yet tortuous, carotid arteries
  • Heart murmur with radiation to the neck (e.g., aortic stenosis)
  • Excessive compression of the stethoscope over the neck vessels, resulting in deformity of vessel wall and turbulence
    • Hyperthyroidism
      –Results in hyperdynamic circulation, tachycardia, and hypertension
    • Takayasu's arteritis
      –Decreased pulses and bruits may occur over the abdominal aorta, carotid arteries, brachial arteries, and subclavian arteries
    • Fisher's contralateral systolic bruit
      –Heard over the carotid bifurcation, eyeball, and/or skull on the “normal side” due to increased flow, as the “silent” side is completely occluded

    Workup and Diagnosis

    • Complete history and physical exam, with special attention to cardiac risk factors, TIA symptoms, cardiovascular exam, and neurologic exam
      –Bruit pitch increases as stenosis worsens, but may become silent when full occlusion occurs
      –Amaurosis fugax: Described as a “shade coming down over the eye” contralateral to the stenosis
  • Laboratory evaluation includes lipid panel, CBC, glucose, electrolytes, homocysteine level (an independent risk factor for stroke), vitamin B12 and folate levels, TSH, and ESR
  • Carotid duplex ultrasound will evaluate the degree of stenosis
  • MRA, CTA, or arteriography is indicated to better evaluate symptomatic stenosis that may require surgery

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Breath Sounds (Decreased): Differential Diagnosis
(In a Page: Signs and Symptoms)

Decreased airflow through respiratory tree

  • Airway obstruction
    –Aspirated foreign body
    –Asthma
    –Bronchitis
    –Bronchiolitis
    –Croup
    –Epiglottitis
    –Neoplasm
    –Goiter
  • Alveolar or interstitial processes
    –Pulmonary edema
    –Pneumonia
    –Pleurisy
    –Sarcoidosis
  • Decreased lung expansion
    –Atelectasis
    –COPD or emphysema
    –Bronchiectasis
    –Kyphosis or scoliosis
    –Increased abdominal girth (e.g., ascites, obesity, pregnancy)
    –Pulmonary fibrosis
    –Diaphragmatic paralysis
    –Abdominal, chest wall, or pleuritic pain
    Obstructed transmission of sound
    • Obesity
    • Pleural effusion
    • Pneumothorax, hemothorax, or chylothorax
    • Pleural thickening
    • Large pulmonary embolus
    • Less common etiologies (“zebras”) include cystic fibrosis, alveolar hemorrhage, BOOP, now called COP, pneumonectomy (postsurgical), systemic lupus erythematosus, vocal cord paralysis, vocal cord dyskinesia, and psychogenic

    Workup and Diagnosis

    • History and physical examination
      –History should include associated symptoms (e.g., fever, dyspnea, wheezing, chest pain) and a detailed past medical, surgical, and exposure history
      –Physical examination should include vital signs; examination of oral cavity and neck for evidence of mass, foreign body, or tracheal deviation; inspection and palpation of the chest wall to assess for symmetric movement; percussion and auscultation of all chest fields for related abnormalities (e.g., rhonchi, wheezes, rales, rubs, egophony)
    • Initial labs may include CBC, pulse oximetry, arterial blood gas, and TSH
    • Chest X-ray is the initial imaging test
      –Associate the area of decreased breath sounds to hyperlucency or increased opacity on chest X-ray
      –Tracheal shift to a side with a density and decreased breath sounds likely signifies atelectasis or endobronchial obstruction
      –Tracheal shift away from a side with hyperlucency and decreased breath sounds may indicate tension pneumothorax
    • Lateral neck X-ray may be indicated to rule out epiglottitis (“thumb sign”)
    • If there is evidence of external airway compression, chest and neck CT scans may be needed for further evaluation
    • Pulmonary function testing

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Abnormal Heart Sounds: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Abnormal S2 –Most important auscultatory finding; normally, S2 is single on inspiration and narrowly split on expiration, indicating normal pulmonary arterial pressures; difficult to learn, especially in babies with fast heart rates or a screaming child
    –Single and/or loud S2: Increased pulmonary artery pressure (large L to R shunt, pulmonary hypertension), also seen in patients with only single outlet from heart (i.e., pulmonary atresia)
    –Wide fixed-split S2: ASD, right bundle branch block, post-cardiac surgery
  • Systolic murmur
    –Up to 50% of children at some point in life
    –Mid-systolic/ejection type: S1 and S2 separate from the murmur (lub-shhh-dub), due to flow across semilunar valve, harsh indicates semilunar valve stenosis, whereas low-pitched, vibratory, musical indicates innocent murmur
    –Holosystolic/regurgitant murmur: Begins with S1 (which is not clearly heard); always pathologic (mitral valve regurgitation, VSD, subaortic stenosis)
  • Diastolic sounds
    –Always abnormal
    –Early and medium/high pitch murmur indicates semilunar valve insufficiency, low frequency rumbling indicates mitral/tricuspid stenosis
    –S3/S4/opening snap: Soft S3 can be normal in healthy children; any sound clearly heard is probably an abnormality of the mitral/tricuspid valve (opening snap) or ventricular filling (S3/S4)
  • Continuous murmur
    –Murmur in systole that continues into diastole (may not fill entire diastole)
    –Venous hum: Low pitched, continuous murmur at both upper sternal borders; disappears when supine; innocent
    –Patent ductus arteriosus: Harsh, machinery-like murmur at left upper sternal border (LUSB)
  • Systolic ejection click
    –High-pitched sound
    –Early: Bicuspid aortic valve, loudest at apex/LLSB, often confused with split S1
    –Mid/late: Mitral valve prolapse

Workup and Diagnosis

  • Majority of murmurs heard after the first year of life are systolic and innocent
  • Major innocent murmurs of childhood: All must have a normal S2 and no symptoms
    –Still (vibratory) murmur: Vibratory, musical, twangy midsystolic murmur loudest at the LLSB, louder when supine, heard in toddlers
    –Venous hum: Continuous low rumbling sound at upper sternal borders, disappears when supine
    –Peripheral pulmonary stenosis (PPS): Midsystolic murmur at LUSB, radiates to back and both axillae, normal up to 1 year of age (refer for evaluation if present afterwards)
    –Innocent pulmonary flow murmur: Midsystolic murmur, LUSB, loudest when supine, adolescent age range
  • Physical exam: Assess growth pattern, heart rate, organomegaly, and femoral pulses
  • Four-limb blood pressures very helpful in evaluating possible aortic coarctation (higher BP in arms, lower in legs)
  • Chest X-ray: Rarely useful in the routine evaluation of murmurs in children (unless pathology likely)
  • 12-lead electrocardiogram useful for assessment of atrial or ventricular enlargement/hypertrophy
  • Pulse-oximetry is very useful in the newborn to rule out mildly cyanotic lesions
  • Echocardiography

» READ BOOK EXCERPT ONLINE »

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
    >>>>

» 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

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

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

If you detect bruits over the abdominal aorta, check for a pulsating mass or a bluish discoloration around the umbilicus (Cullen's sign). Either of these signs — or severe, tearing pain in the abdomen, flank, or lower back — may signal life-threatening dissection of an aortic aneurysm. Also, check peripheral pulses, comparing intensity in the upper versus lower extremities.

If you suspect dissection, monitor the patient's vital signs constantly, and withhold food and fluids until a definitive diagnosis is made. Watch for signs and symptoms of hypovolemic shock, such as thirst; hypotension; tachycardia; a weak, thready pulse; tachypnea; an altered level of consciousness (LOC); mottled knees and elbows; and cool, clammy skin.

If you detect bruits over the thyroid gland, ask the patient if he has a history of hyperthyroidism or signs and symptoms of it, such as nervousness, tremors, weight loss, palpitations, heat intolerance, and (in females) amenorrhea. Watch for signs and symptoms of life-threatening thyroid storm, such as tremor, restlessness, diarrhea, abdominal pain, and hepatomegaly.

If you detect carotid artery bruits, be alert for signs and symptoms of a transient ischemic attack (TIA), including dizziness, diplopia, slurred speech, flashing lights, and syncope. These findings may indicate an impending stroke. Be sure to evaluate the patient frequently for changes in LOC and muscle function.

If you detect bruits over the femoral, popliteal, or subclavian artery, watch for signs and symptoms of decreased or absent peripheral circulation — edema, weakness, and paresthesia. Ask the patient if he has a history of intermittent claudication. Frequently check distal pulses and skin color and temperature. Also, watch for the sudden absence of pulse, pallor, or coolness, which may indicate a threat to the affected limb.

If you detect a bruit, make sure to check for further vascular damage and perform a thorough cardiac assessment.

» 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

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

If you detect bruits over the abdominal aorta, check for a pulsating mass or a bluish discoloration around the umbilicus (Cullen’s sign). Either of these signs—or severe, tearing pain in the abdomen, flank, or lower back—may signal life-threatening dissection of an aortic aneurysm. Also check peripheral pulses, comparing intensity in the upper and lower extremities.

If you suspect dissection, monitor the patient’s vital signs continuously, and withhold food and fluids until a definitive diagnosis is made. Watch for signs and symptoms of hypovolemic shock, such as thirst; hypotension; tachycardia; weak, thready pulse; tachypnea; altered level of consciousness (LOC); mottled knees and elbows; and cool, clammy skin.

If you detect bruits over the thyroid gland, ask the patient if he has a history of hyperthyroidism or signs and symptoms of it, such as nervousness, tremors, weight loss, palpitations, heat intolerance, and (in females) amenorrhea. Watch for signs and symptoms of life-threatening thyroid storm, such as tremor, restlessness, diarrhea, abdominal pain, and hepatomegaly.

If you detect carotid artery bruits, be alert for signs and symptoms of a transient ischemic attack (TIA), including dizziness, diplopia, slurred speech, flashing lights, and syncope. These findings may indicate an impending stroke. Be sure to evaluate the patient frequently for changes in LOC and muscle function.

If you detect bruits over the femoral, popliteal, or subclavian artery, watch for signs and symptoms of decreased or absent peripheral circulation—edema, weakness, and paresthesia. Ask the patient if he has a history of intermittent claudication. Frequently check distal pulses and skin color and temperature. Pallor, coolness, or the sudden absence of a pulse may indicate a threat to the affected limb.

If you detect a bruit, be sure to check for further vascular damage and perform a thorough cardiac assessment.

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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?

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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.

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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).

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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

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

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

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

Carotid Bruit: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Carotid artery stenosis

❑ Carotid artery ruptured plaque

❑ Transmitted valvular murmur

❑ Carotid tortuosity

❑ Carotid compression

❑ Jugular venous hum

❑ Thyrotoxicosis

Diagnostic Approach

Carotid bruits are imperfect markers of increased stroke risk because stroke is usually not due to progressive carotid stenosis, but rather to ruptured plaque, cardiac emboli from atrial fibrillation, emboli from aortic sources, or watershed ischemia due to decreased flow. A bruit is, however, an important marker of generalized atherosclerosis. The annual incidence of stroke in the territory of a carotid bruit is 1.7%/year and increases to 5.5%/year as stenosis exceeds 75%. The risk of death (usually cardiac) in a patient with a carotid bruit is 4%/yr. Bruits are clinically significant when associated with transient ipsilateral anterior circulation symptoms such as amaurosis fugax (transient monocular blindness), contralateral homonymous hemianopsia, hemiparesis, and hemisensory defect. Left hemispheric lesions are associated with aphasia, and right with visuospatial neglect and constructional apraxia.

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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

Discrete Heart Sounds: Differential Overview
(Field Guide to Bedside Diagnosis)

Phenomena

❑ S4 gallop

❑ Midsystolic click

❑ S3 gallop

❑ Loud S2

❑ Widely split S1

❑ Widely split S2

❑ Ejection click

❑ Variable S1

❑ Paradoxical splitting of S2

❑ Loud S1

❑ Fixed splitting of S2

❑ Opening snap

❑ Pericardial knock

❑ Tumor plop

❑ Sail sound

Diagnostic Approach

The A2-P2 interval normally increases with inspiration due to decreased intrathoracic pressure and increased venous return, which leads to increased stroke volume.

In my southern medical school I was taught that the cadence of the S3 gallop matches that of the spoken word Kentucky, and of S4, Tennessee.

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Source: Field Guide to Bedside Diagnosis, 2007

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

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

Physical examination

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

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

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

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

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

Obtain a medical history including past injuries, illnesses, surgeries, and family medical history. Ask about diet and alcohol intake. Take a drug history, including past and present prescriptions, over-the-counter drugs, and herbal remedies. Also obtain a social history.

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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.

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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

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

    If you detect bruits over the abdominal aorta, check for a pulsating mass or a bluish discoloration around the umbilicus (Cullen's sign). Either of these signs—or severe, tearing pain in the abdomen, flank, or lower back—may signal life-threatening dissection of an aortic aneurysm. Check peripheral pulses, comparing intensity in the upper versus lower extremities.

    If you suspect dissection, monitor the patient's vital signs constantly, and withhold food and fluids until a definitive diagnosis is made. Watch for signs and symptoms of hypovolemic shock, such as thirst; hypotension; tachycardia; a weak, thready pulse; tachypnea; an altered level of consciousness (LOC); mottled knees and elbows; and cool, clammy skin.

    If you detect bruits over the thyroid gland, ask the patient if he has a history of hyperthyroidism or signs and symptoms of it, such as nervousness, tremors, weight loss, palpitations, heat intolerance, and (in females) amenorrhea. Watch for signs and symptoms of life-threatening thyroid storm, such as tremor, restlessness, diarrhea, abdominal pain, and hepatomegaly.

    If you detect carotid artery bruits, be alert for signs and symptoms of a transient ischemic attack (TIA), including dizziness, diplopia, slurred speech, flashing lights, and syncope. These findings may indicate an impending stroke. Be sure to evaluate the patient frequently for changes in LOC and muscle function.

    If you detect bruits over the femoral, popliteal, or subclavian artery, watch for signs and symptoms of decreased or absent peripheral circulation, such as edema, weakness, and paresthesia. Ask the patient if he has a history of intermittent claudication. Frequently check distal pulses and skin color and temperature. Watch for the sudden absence of pulse, pallor, or coolness, which may indicate a threat to the affected limb.

    If you detect a bruit, make sure to check for further vascular damage and perform a thorough cardiac assessment.

    » 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

    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


     » Next page: Signs of Heart Murmur

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