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Diseases » Heart disease » Tests
 

Diagnostic Tests for Heart disease

Contents
  1. Heart disease: Introduction
  2. Tests for Heart disease
  3. Symptoms of Heart disease
  4. Diagnosis
  5. Home Diagnostic Testing
  6. Failure to Diagnose
  7. Alternative Diagnoses
  8. Misdiagnosis
  9. Complications

Heart disease: Diagnostic Tests

The list of diagnostic tests mentioned in various sources as used in the diagnosis of Heart disease includes:

Heart disease Tests: Book Excerpts

Home Diagnostic Testing

These home medical tests may be relevant to Heart disease:

Heart disease Diagnosis: Book Excerpts

Tests and diagnosis discussion for Heart disease:

Keep your heart and blood vessels healthy: NIDDK (Excerpt)

Which medical tests will help me keep track of any heart or blood vessel problems?

  • Have your blood pressure checked every time you see your doctor. Ask your doctor what your blood pressure is and what it should be.

  • Your doctor may order an exercise stress test to see if you have any problems. The doctor will see how your heart performs during exercise.

  • Have your blood fats checked once each year. This checkup includes four tests:

    • Blood cholesterol. Your number should be 200 or lower. 
    • LDL (bad cholesterol). Your number should be 100 or lower. 
    • HDL (good cholesterol). Your number should be 45 or higher. 
    • Triglycerides (try-GLISS-er-ides) (the form in which energy is stored in your fat cells). Your number should be 200 or lower.

If your numbers are not normal, ask your doctor if you should take medicine to make them normal. (Source: excerpt from Keep your heart and blood vessels healthy: NIDDK)

NHLBI Heart Disease & Women Are You At Risk: NHLBI (Excerpt)


BLOOD PRESSURE CATEGORIES IN WOMEN
(18 YEARS AND OLDER)*

Blood pressure is shown as two numbers--the systolic pressure as the heart is beating and the diastolic pressure between heartbeats. Both numbers are important.

Blood Pressure Level in mmHg

Category

Systolic

  

Diastolic

Optimal**

<120

and

<80

Normal

<130

and

<85

High-normal

130-139

or

85-89

Hypertension      

Stage 1

140-159

or

90-99

Stage 2

160-179

or

100-109

Stage 3

>=180

or

>=110

(Source: excerpt from NHLBI Heart Disease & Women Are You At Risk: NHLBI)

Diagnosis of Heart disease: medical news summaries:

The following medical news items are relevant to diagnosis of Heart disease:

Diagnostic Tests for Heart disease: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the diagnostic tests for Heart disease.

CARDIOMEGALY: DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)

A CBC, sedimentation rate, ANA, chemistry panel, VDRL test, thyroid profile, EKG, and chest x-ray should be done on all patients. An echocardiogram will be helpful in diagnosing valvular disease, myocardiopathies, congestive heart failure, and pericardial effusion. If congestive heart failure is suspected, venous pressure and circulation time can be measured, and one should do pulmonary function studies. If there is fever, then one would want to do a streptozyme test, ASO titer, and serial blood cultures. If there is hypertension, a hypertensive workup may be indicated . Patients with cyanosis need a workup for congenital heart disease, which will probably include cardiac catheterization and angiocardiography.

Most prudent physicians will refer the patient with cardiomegaly to a cardiologist before pursuing this extensive diagnostic workup.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

CARDIAC ARRHYTHMIA: DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)

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

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

CARDIAC MURMURS: DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)

If the murmur is believed to be organic, the most cost-effective approach would be to consult a cardiologist at the outset. If the astute clinician wishes to pursue the diagnostic workup on his own, it is suggested that a CBC, sedimentation rate, chemistry panel, VDRL test, and thyroid profile should be done for the initial blood work. In addition, a chest x-ray including obliques, congestive heart failure, phonocardiograms, and EKG should be performed. These findings may provide a diagnosis. If there is fever, a streptozyme test, antistreptolysin-O (ASO) titer, and serial blood culture should be performed. If congestive heart failure is suspected, venous pressure and circulation time should be determined. Pulmonary function studies are also helpful. Echocardiography will be extremely helpful in diagnosing the various forms of valvular disease and will also help in identifying a pericardial effusion, congestive heart failure, or the various cardiomyopathies. Cardiac catheterization and angiography and angiocardiography will identify the various congenital heart lesions and valvular disease. These studies, however, are most important when surgery is being considered.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Cardiomegaly: Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

The typical signs of CHF are usually noted on examination. A decreased arterial pulse with narrowed pulse pressure is common. Cyanosis is rare. Significant cardiac enlargement should be evident on physical examination. Examples of these finding include the following:

A. Lung sounds. Rales or pleural effusion with dullness to percussion and decreased breath sounds may be indicative of left ventricular failure.

 B. Heart sounds. Gallops, soft heart sounds, and regurgitant heart murmurs are nonspecific findings of advanced CHF. Alterations in S1 or S2, specific murmurs, (e.g., a Valsalva-enhanced systolic murmur in hypertrophic obstructive cardiomyopathy), and muffled sounds with pericardial effusion, all indicate specific underlying pathology.

 C. Cardiac pulsations or point of maximal impulse (PMI). Visible pulsations seen lateral to the midclavicular line signify cardiac enlargement unless is found a thoracic deformity or congenital absence of the pericardium.

 D. Apical beat or PMI. The apical beat, or PMI, which is typically palpable in only 40% of cases, is highly dependent on body habitus. Use the flat of the hand to palpate the PMI. Time the pulsations using the carotid pulse or auscultated heart sounds. The left lateral decubitus position increases the palpability of both normal and pathologic apical beats.

A PMI within or superior to the fifth intercostal space is normal. Left ventricular enlargement displaces the PMI laterally and downward. A PMI lateral to the midclavicular line or more than 10 cm lateral to the midsternal line is a sensitive but nonspecific indicator of left ventricular enlargement. An apical impulse of more than 3 cm diameter is an accurate sign of left ventricular enlargement.

With moderate or severe left ventricular hypertrophy, the outward systolic thrust persists throughout ejection, often lasting up to the second heart sound. In patients with volume overload or sympathetic stimulation, the left ventricular impulse is brisker and larger than normal but is hypokinetic in patients with reduced stroke volume (e.g., acute myocardial infarction or dilated cardiomyopathy). Large left ventricular aneurysms are palpable above and medial to the apex beat. Thoracic deformities—particularly scoliosis and pectus excavatum—can laterally displace a normal heart.

 E. Percussion. In the absence of an apical beat, as in patients with pericardial effusion or with dilated cardiomyopathy and a markedly displaced, hypokinetic apical beat, the left border of the heart can be outlined by means of percussion. Percussed dullness in the left fifth intercostal space more than 10.5 cm from the midsternal line is sensitive and specific for cardiomegaly (3).

Testing

 A. Radiographs. The cardiothoracic ratio is quick to measure and relatively reliable as an indicator of cardiomegaly on an adequate, upright, posterior–anterior chest film. Watch for rotation and adequate inspiration: the diaphragm should be lowered to at least the posterior portion of the ninth rib. Calculate the ratio by first measuring the transverse cardiac diameter horizontally through the widest part of the cardiac silhouette. Divide this by the chest diameter measured at the widest part between the inner surface of the ribs. A ratio of 0.5 to 0.55 or less can be considered within the limits of normal for an adult. Ratios of up to 0.6 are normal in children and infants. Fluid accumulation in the pericardium causes distention, enlarging the cardiac silhouette and overlapping and obscuring the hilar vessels. In CHF, the vessels become congested and appear more prominent than normal. Also, the epicardial fat line (radiolucent stripe) on the lateral chest film between the anterior surface of the heart and the retrosternal mediastinal fat should be no more than 1 to 2 mm. Widening beyond this is a reliable indicator of pericardial effusion.

B. Sonography. An echocardiogram is generally considered the standard in assessing cardiac dimensions. With evidence of cardiomegaly on physical examination, an echocardiogram is appropriate if clinically useful in the patient’s care.

 C. ECG. The ECG is almost invariably abnormal in true cardiomegaly. Common findings are premature ventricular contractions, atrial fibrillation, atrioventricular and intraventricular conduction abnormalities, and nonspecific ST segment and T-wave changes. Left ventricular hypertrophy and atrial enlargement can be diagnosed by morphology and voltage, but the ECG is rarely diagnostic of a specific underlying cause. Pericarditis causes ST elevation with flat or concave ST segments. Pseudoinfarction patterns are seen in hypertrophic obstructive cardiomyopathy (4).

Diagnostic assessment

The significance of cardiomegaly is determined by the underlying pathology. The most common presenting conditions to consider are listed in Table 7.1.


References

1. Frishman WH. Cardiomegaly on chest x-ray: prognostic implications from a ten-year cohort study of elderly subjects: a report from the Bronx Longitudinal Aging Study. Am Heart J 1992;124:1026–1030.

2. Craddock LD. Cardiac enlargement and the cardiomyopathies. In: Friedman HH, ed. Problem oriented medical diagnosis, 5th ed. Boston: Little, Brown and Company, 1991:67–71.

3. Heckerling PS. Accuracy of precordial percussion in detecting cardiomegaly. Am J Med 1991;91:328–334.

4. Kamiyama N. Electrocardiographic features differentiating dilated cardiomyopathy from hypertrophic cardiomyopathy. J Cardiol 1997;30:301–306.

» READ BOOK EXCERPT ONLINE »

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

Congestive Heart Failure: Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Focused physical examination. In general, the physical examination is more sensitive in detecting acute CHF than it is in detecting chronic CHF. Evaluate the following:

1. Vital signs. Note the blood pressure; hypertension with acute CHF suggests diastolic dysfunction (4). Obtain pulse, respiratory rate, and pulse oximetry to detect hypoxia.

2. Neck. Look for jugular venous distension, one of the more reliable physical examination indicators of CHF (4).

3. Lungs. Rales are commonly heard, but wheezing (“cardiac asthma”) can also appear.

4. Heart. Palpate the apical impulse. If laterally displaced, diffuse, and especially of sustained duration, CHF caused by reduced left ventricular (LV) systolic function is likely (4). Listen for murmurs, gallops, and rubs. An S3 gallop is generally suggestive of CHF (4), whereas an S4 gallop may be a nonpathologic, age-related finding in elderly patients (3).

5. Abdomen. Assess for hepatosplenomegaly and try to elicit abdominojugular reflux.

 6. Extremities. Look for leg edema (pitting in acute CHF, brawny in chronic CHF).

 B. Additional physical examination. Further examination is appropriate if the history suggests specific causes for CHF: funduscopic examination to search for hypertensive retinopathy; thyroid palpation and auscultation; palpation of peripheral pulses; and carotid palpation and auscultation for evidence of stenosis, a marker of coronary atherosclerosis.

Testing

 A. Preliminary evaluation. Obtain the following when acute CHF is suspected to assess for confirmatory signs, triggers, and associated conditions: electrocardiogram (MI) or ischemia, dysrhythmia; chest radiograph (cardiomegaly, pulmonary vascular redistribution, alveolar edema); serum electrolytes, albumin, blood urea nitrogen, creatinine (hypokalemia, hypoalbuminemia, acute renal failure); complete blood count (anemia); and urinalysis (nephrosis).

 1. In the setting of suggestive symptoms, anterior Q waves and left bundle branch block on electrocardiography are each nearly 90% specific for LV systolic dysfunction (4).

 B. Confirmatory evaluation. Echocardiography (ECHO) should be expeditiously obtained in all patients when new-onset CHF is suspected clinically. An LV ejection fraction (EF) ≤ 40% indicates systolic dysfunction, whereas a normal EF accompanied by findings suggestive of increased LV end-diastolic pressure suggests diastolic dysfunction. ECHO is technically inadequate in up to 18% of patients (2). Radionuclide ventriculography can be used in such cases, but it is less able to detect valvular disease and LV hypertrophy.

 C. Additional testing. Because of frequent comorbid lung disease, pulmonary function testing should be considered in older patients before dyspnea is attributed to CHF. The need for other tests (e.g., thyroid-stimulating hormone) is determined by findings on the history and physical examination.

Diagnostic assessment

 The two keys to the diagnosis of CHF are:

A. A high index of suspicion in patients with potential causes and suggestive symptoms. However, findings on history and physical examination are neither sensitive nor specific. Half of all CHF diagnoses made in the primary care setting using clinical indicators alone are inaccurate (5).

 B. ECHO. This critical diagnostic study may also indicate which type of CHF is present which, in turn, facilitates the selection of an appropriate therapeutic regimen. Nevertheless, ECHO has some limitations. Current techniques cannot provide definitive proof of diastolic dysfunction, so a thorough search for other causes of CHF with preserved systolic function should be conducted before accepting this diagnosis. Furthermore, LV systolic dysfunction can be a transient phenomenon in patients with acute myocardial ischemia. Therefore, a repeat ECHO should be obtained after stabilization of such patients.


References

1. Croft JB, Giles WH, Pollard RA, Keenan NL, Casper ML, Anda RF. Heart failure survival among older adults in the United States. Arch Intern Med 1999;159:505–510.

2. Agency for Health Care Policy and Research. Clinical practice guideline. Heart failure: evaluation and care of patients with left-ventricular systolic dysfunction. Silver Spring, MD: Agency for Health Care and Research, 1994.

3. Tresch DD. The clinical diagnosis of heart failure in older patients. J Am Geriatr Soc 1997;45:1128–1133.

4. Badgett RG, Lucey CR, Mulrow CD. Can the clinical examination diagnose left-sided heart failure in adults? JAMA 1997;227:1712–1719.

5. Vasan RS, Benjamin EJ, Levy D. Congestive heart failure with normal left ventricular systolic function. Arch Intern Med 1996;156:146–157.

» READ BOOK EXCERPT ONLINE »

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

Heart Murmur, Diastolic: Physical examination (PE)
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Table 7.3 lists characteristic PE findings of diastolic murmurs.

B. Fine points of the physical examination

1. Is the murmur of AR louder at the right sternal border? If so, consider aortic root dilation. Remember, whereas the duration of the chronic AR murmur is directly proportional to the severity of the regurgitation, the duration of the acute AR murmur may not predict its severity (3).

2. Is the murmur of MS shorter, or does it extend closer to S2? The length of this murmur, not its intensity, is directly proportional to the severity of the stenosis (3). In addition, the murmur may not be audible with increased heart rates because of shortening of diastole.

 3. Does the murmur of MS vary from examination to examination? If so, and especially if it is introduced by a “plop” sound, consider atrial myxoma.

Testing

Echocardiogram is the essential test for confirming the anatomic location of the murmur and its severity. Transthoracic echocardiography (ECHO) is generally sufficient, unless endocarditis is suspected, in which case a transesophageal ECHO is preferred to evaluate for vegetations. If aortic root dilatation is present on ECHO, a computed tomography or magnetic resonance imaging scan may help to delineate the anatomy further. Additional laboratory testing may be warranted to further evaluate the underlying cause (e.g., serologic studies for collagen vascular disease, serologic test for syphilis, and so on).

Diagnostic assessment

With a careful examination and thorough history, the valve causing the murmur and the probable cause of the valvular lesion can be identified prior to ordering the definitive test (ECHO). The most common cause of all diastolic murmurs is still rheumatic heart disease, even though the incidence of acute rheumatic fever has decreased. Mitral stenosis is almost invariably caused by rheumatic heart disease (98% in one study of excised valves) (3,4), with the remainder caused by vegetations (from endocarditis) or congenital factors (4). Tricuspid stenosis is also predominantly rheumatic in origin and is rarely an isolated lesion. Other causes of TS include carcinoid and congenital malformations. Rheumatic heart disease is the leading cause of chronic AR, followed by congenital bicuspid valves and aortic root dilatation (Marfan’s syndrome, Ehlers-Danlos syndrome, ankylosing spondylitis, and syphilitic aortitis). If chronic, AR can result in LV dilation and compensation; if acute, it can be associated with severe LV overload and significant symptoms. Acute AR is most often related to endocarditis, aortic dissection, and trauma. Pulmonary regurgitation without hypertension has multiple causes, including pulmonary trunk dilation, endocarditis, carcinoid, trauma (from balloon-tipped catheters), and rheumatic fever. The nonstenotic physiologic murmurs are related to high-flow states across an otherwise normal mitral
or tricuspid valve. For a mitral flow murmur, the primary lesions are usually mitral regurgitation, ventricular septal defects, or patent ductus arteriosus. For a tricuspid flow murmur, an atrial septal defect or severe tricuspid regurgitation is the most common cause. The Austin–Flint murmur, caused by increasing left ventricular pressure pushing the anterior mitral leaflet into the flow of blood coming from the atrium, is the result of significant aortic regurgitation.


References

1. Chizner MA, ed. Classical teachings in clinical cardiology. Chatham, New Jersey: Laennec Publishing, 1996.

2. Coblyn JS, Weinblatt ME. Rheumatic disease and the heart. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine, 5th ed. Philadelphia: WB Saunders, 1997:1776–1785.

3. Abrams J, ed. Synopsis of cardiac physical diagnosis. Philadelphia: Lea & Febiger, 1989.

4. Olson LJ, Subramanian MB, Ackermann DM, Orszulak TA, Edwards WM. Surgical pathology of the mitral valve: a study of 712 cases spanning 21 years. Mayo Clin Proc 1987;62:22–34.

» READ BOOK EXCERPT ONLINE »

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

Heart Murmur, Systolic: Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Technique. Auscultate the heart with the bell to best detect lower frequencies and the heart sounds (S1-S4). The quality of the murmur is best heard with the diaphragm. Inspiration increases the audibility of right ventricular sounds.

 B. Murmur characteristics. Table 7.4 presents a summary of the characteristics of different causes of systolic murmurs (2,3). Etchell et al. (3) have prepared a comprehensive review on the usefulness of specific physical examination findings in the diagnosis of systolic murmurs.

Testing

Testing of an undiagnosed cardiac murmur can include an electrocardiogram (ECG), a chest x-ray study (CXR), and an echocardiogram. Echocardiograms, although useful for quantification of stenotic valvular disease, can overestimate the degree of regurgitation.

A. Aortic stenosis. Specific ECG findings in aortic stenosis can include left ventricular hypertrophy (LVH), left axis deviation, conduction disturbances, and atrial hypertrophy. On CXR, cardiac size remains normal until stenosis is severe, then signs of CHF may be present. The echocardiogram may reveal thickened or calcified aortic leaflets, bicuspid valve, and LVH. The size of
the valve can be estimated and the pressure gradient across the valve can
be assessed. Cardiac catheterization can also be used to assess the size of the valve and the gradient. Even though echocardiography is accurate in measuring valve area and gradient, catheterization is usually indicated because 50% of patients above age 40 years have coronary artery disease.

 B. Mitral regurgitation. In mitral regurgitation, the ECG may reveal LVH with left atrial enlargement and later in the course, atrial fibrillation. In severe disease, CXR usually reveals cardiomegaly without pulmonary venous congestion. The echocardiogram reveals valvular anatomy, but can overestimate the severity of the regurgitation. Exercise testing can be used to determine clinical deterioration in mitral regurgitation. Catheterization is used to assess the contractile state of the ventricle as well as the regurgitant and forward stroke volume.

 C. Other disease processes. The ECG with tricuspid insufficiency often reveals atrial fibrillation. The CXR may show right atrial hypertrophy, and the echocardiogram shows valvular anatomy. Pulmonic stenosis will lead to ECG findings consistent with right ventricular hypertrophy. Hypertrophic cardiomyopathy is best diagnosed by echocardiography. ECG may reveal LVH and occasionally a shortened PR interval is seen. Cardiac catheterization can be used to quantify the gradient caused by the hypertrophic lesion.

Diagnostic assessment

 The history and physical examination with special emphasis on auscultation are the keys to the diagnosis of systolic murmurs. Those with symptomatic murmurs or in whom valvular disease is suspected should have an ECG, CXR, and echocardiogram. Murmurs of unknown duration or new murmurs should be worked up promptly with consideration of acute infarction in mind. If aortic stenosis is suspected, the workup should be expedited because sudden death can be the first clinical presentation. Valvular disease must always be considered with new onset congestive heart failure. Table 7.5 lists some of the online resources available to assist in the evaluation of heart murmurs.


References

1. Rackley C. Valvular heart disease. In: Bennett JC, Plum F, eds. Cecil textbook of medicine, 20th ed. Philadelphia: WB Saunders, 1996.

2. O’Connor D. The art of auscultation. Patient Care 1998;38:56–60.

3. Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA 1997;277:564–571.

» READ BOOK EXCERPT ONLINE »

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

Cardiomegaly/Congestive Heart Failure: Diagnostic Approach
(Field Guide to Bedside Diagnosis)

The Framingham criteria for congestive heart failure are a good reference point. Major criteria include paroxysmal nocturnal dyspnea, rales, cardiomegaly, acute pulmonary edema, third heart sound, jugular pressure greater than 16 cm, and positive abdominojugular reflex. Minor criteria include edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, and pulse rate slower than 120. Functional limitation is most often classified using the New York Heart Association (NYHA) system: Class I—symptoms of heart failure only at levels of exertion that would limit normal individuals; Class II—symptoms of heart failure with ordinary exertion; Class III—symptoms of heart failure with less than ordinary exertion; Class IV—symptoms of heart failure at rest.

History is key in CHF. Findings due to excess fluid accumulation include dyspnea, edema, hepatic congestion, and ascites. Findings due to reduced cardiac output include weakness and fatigue, more pronounced with exertion. Acute and subacute CHF produce primarily shortness of breath with exertion or at rest. Other common symptoms include orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant discomfort due to hepatic congestion in right heart failure.

Decreased cardiac output is counterbalanced by increased sympathetic activity, manifest as sinus tachycardia, diaphoresis, and peripheral vasoconstriction (cool and cyanotic extremities due to decreased perfusion and increased oxygen extraction). A prominent dicrotic notch may be felt in severe left ventricular dysfunction, as the compensitory increase in total peripheral resistence and corresponding reduced aortic compliance accentuate the aortic valve closure. Pulsus alternans (alternating strong and weak pulse beats) is uncommon but pathognomonic of advanced heart failure. Volume overload is manifest as pulmonary congestion (rales), peripheral edema, and elevated jugular venous pressure. The medulla controls the respiratory rate based on pCO 2. The length of the Cheyne-Stokes cycle is proportional to the circulatory delay from the alveoli to the arterioles (r = 0.80).

Systolic heart failure is marked by decreased cardiac output, with manifestations such as weakness, fatigue, and decreased exercise tolerance. Mitral regurgitation, especially when acute, augments early diastolic inflow and may produce an S3 with normal systolic function. Diastolic heart failure is associated with reduced ventricular compliance and increased filling pressures with manifestations of dyspnea and rales.

Findings suggesting left ventricular hypertrophy include a sustained forceful apical thrust, a double apical impulse, an apical impulse larger than 3 cm, and a fourth heart sound on auscultation. Left ventricular enlargement will cause the apical impulse (PMI) to be displaced downward and to the left. Right ventricular hypertrophy will cause a sustained right parasternal lift. It is seen with pulmonary hypertension, pulmonic stenosis, and volume overload with tricuspid regurgitation or atrial septal defect. Right ventricular failure is recognized by edema, jugular venous distension, and abdominojugular reflex.

Key findings on physical examination:

Rales  Increased interstitial fluid/pressure causes alveoli to pop open. Pulmonary venous capacitance increases in chronic heart failure, and rales may be absent.

Third heart sound (S3)  Ventricular vibration occurs during rapid inflow of blood in early diastole when the long-axis expansion limit is reached, due to reduced LV compliance or increased filling pressure. S3 is a low-pitched sound over the apex, and yield is doubled in the 45 degree left lateral decubitus position. JVD and S3 are independent on multivariate analysis.

JVD  The IJ is a right atrial manometer. High JVD (present .45 deg) has a LR 4.1 that CVP is .10 cm. Low JVD (present ,30 deg) has a LR 3.4 that CVP is ,5 cm.

Abdominojugular reflux  Apply abdominal pressure for 10 sec. A positive AJR is a 4 cm or greater drop in JVP after release, due to decreased RV compliance or increased LVEDP.

Edema  With renin-angiotensin-aldosterone activation, pulmonary and peripheral fluid accumulates. After the extracellular fluid is in excess of about five liters, symmetric, dependent, and pitting peripheral edema develops.

Valsava response  The normal response is for BP to rise .15 mm Hg during valsalva, but to fall before 10 seconds passes. When valsalva is released, the BP rises again .15 mm over the resting threshold. In CHF, an abnormal response can consist of absent phase 4 overshoot or a square wave in phase 2.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Discrete Heart Sounds: Diagnostic Approach
(Field Guide to Bedside Diagnosis)

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.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

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

  • To distinguisha normal from a pathologic murmur, physicians must rely on theirskill in physical exam of cardiovascular system; on their interpretationof chest radiograph, ECG, and 2-D echocardiogram; and on their knowledgeof the diagnostic possibilities that each murmur suggests.
  • In most cases, cardiovascular examat bedside can distinguish a normal from a pathologic murmur.

  • With a normalmurmur, no tests are needed. Physicians can reassure parents andexplain that the murmur is a normal phenomenon due to normal turbulenceof blood flow. They can also emphasize that the murmur is not indicativeof mild heart disease, nor is it of any importance whether it disappears.
  • With a pathologic murmur, precise diagnosismust be made because subsequent management depends on it. Diagnosisof pathologic murmurs is based on cardiovascular exam in conjunctionwith chest radiograph and ECG and sometimes 2-D echocardiogram.
  • Only rarely are cardiac catheterizationand angiography needed to clarify etiology of murmurs in asymptomaticchildren.

    • » READ BOOK EXCERPT ONLINE »

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

    Cardiac Failure: Diagnostic Approach
    (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

    Diagnosis of Cardiac Failure

  • Diagnosisof cardiac failure is clinical and is based on history and physicalexam findings.
  • Most cardiac disease produces LV orbiventricular failure. Pure right heart failure is uncommon.
  • Manifestations of cardiac failure ininfants are increased work of breathing, tiring with feedings, andpoor weight gain.
  • Tachycardia, sweating, gallop rhythm,and cardiac enlargement indicate impaired myocardial performance.
  • Tachypnea, dyspnea, wheezing, cough,crackles, and cyanosis are manifestations of pulmonary venous congestion.
  • Signs of systemic venous congestionare hepatomegaly, neck vein distension, peripheral edema, splenomegaly,and ascites.
  • Diminished peripheral pulses and hypotensionreflect decreased cardiac output.
  • In infancy, crackles may not be heard,neck vein distension is difficult to evaluate, and peripheral edemais uncommon.
  • Once diagnosis is made, next task isto determine specific cause.

    • Age of Onset of Cardiac Failure

  • Often providesclue to specific cause of cardiac failure.
  • Birth–1 wk: Causes of cardiacfailure include perinatal asphyxia, severe anemia, complete heartblock, supraventricular tachycardia, hypoplastic left heart syndrome,critical aortic stenosis, critical pulmonary stenosis, complex coarctationof aorta, VSD with absent pulmonary valve, aortic incompetence (aorta–LVtunnel syndrome), isolated tricuspid incompetence, and Ebstein anomaly.
  • 1–6 wks: Common causes ofcardiac failure include patent ductus arteriosus, VSD, complete AVcanal, double-outlet RV, truncus arteriosus, transposition of greatarteries with large VSD or patent ductus arteriosus, univentricularAV connections, simple or complex coarctation of aorta, total anomalous pulmonaryvenous connection with obstruction, severe aortic stenosis, anycause of pulmonary venous obstruction, myocarditis, anomalous leftcoronary artery, and any cause of severe anemia.
  • Common acquired causes of cardiac failureare myocarditis, cardiomyopathy, pericarditis, acute rheumatic fever,endocarditis, postcardiac surgery for complex lesions, and arrhythmias.

    • Diagnostic Categories

  • Many cardiaclesions can be grouped together in diagnostic categories based onpresence or absence of cyanosis, physical exam findings, and chestradiographic findings (Table 7.1 ).
  • Other tests (e.g., ECG, 2-D echocardiographywith Doppler methods and cardiac catheterization with angiography)can be used to make definitive diagnosis.

    • » READ BOOK EXCERPT ONLINE »

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


     » Next page: Diagnosis of Heart disease

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