Diagnostic Tests for Heart conditions
Heart conditions Tests: Book Excerpts
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Heart conditions Diagnosis: Book Excerpts
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Diagnostic Tests for Heart conditions: Online Medical Books
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Review excerpts from medical books online, free, without registration,
for more information about the diagnostic tests for Heart conditions.
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.
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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.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Murmurs:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 406.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.
Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient’s medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.
Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Pulse rhythm abnormality:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient’s compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.
Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Murmurs:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 517.) Use the bell of your stethoscope for low-pitched murmurs; the diaphragm for high-pitched murmurs.
Next, obtain a patient history. Ask if the murmur is a new discovery, or if it has been known since birth or childhood. Find out if the patient has experienced any associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. (See Differential diagnosis: Murmurs, pages 518 and 519.) Explore the patient’s medical history, noting especially any incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.
Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient’s liver tender or palpable? Does he have peripheral edema?
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Pulse rhythm abnormality:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient’s condition permits, ask if he’s experiencing pain. If so, find out about onset and location. Does the pain radiate? Ask about a history of heart disease and treatments for arrhythmias. Obtain a drug history and check compliance. Also, ask about any caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.
Next, check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Report your findings to the physician.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
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.
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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.
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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.
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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.
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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.
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Source: Field Guide to Bedside Diagnosis, 2007
Diastolic Murmur:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
A diastolic murmur is always abnormal. An early diastolic murmur, caused by aortic or pulmonic regurgitation, is high-pitched and decrescendo. The duration of the murmur is an index of severity. A mid-diastolic murmur suggests mitral or tricuspid stenosis.
The murmur of mitral stenosis decreases or does not change with inspiration whereas the murmur of tricuspid stenosis increases.
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Source: Field Guide to Bedside Diagnosis, 2007
Systolic Murmur:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The intensity of the murmur is proportional to the degree of stenosis until flow decreases markedly. Intensity can be expressed semiquantitatively, from grade 1/6, heard only with concentration, to grade 4/6, a loud murmur associated with a palpable thrill, to grade 6/6 with a thrill and murmur heard with the stethoscope off the chest. The duration of the murmur is proportional to the pressure differential between the two chambers.
An early systolic murmur, decrescendo at the apex, occurs in acute, severe mitral regurgitation (MR) with papillary muscle rupture, endocarditis, ruptured chordae tendineae, or blunt chest trauma. A midsystolic murmur is typical of aortic stenosis (AS). It can also be found with hypertrophic obstructive cardiomyopathy (HOC) and with hyperdynamic states. A late systolic murmur is usually heard with mitral valve prolapse (MVP) in association with a midsystolic click. A holosystolic murmur can be produced by severe MR or tricuspid regurgitation (TR), or by a ventricular septal defect (VSD), when the pressure differential between chambers persists throughout systole. Holosystolic murmurs are almost never innocent.
Handgrip decreases AS and HOC murmurs but increases MR, aortic regurgitation (AR), VSD, and mitral stenosis (MS). Transient arterial occlusion by a blood pressure cuff 20 mm above systolic increases left-sided murmurs. Valsalva decreases most murmurs (decreased right and left ventricular filling), except HOC and MVP, which increase.
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Source: Field Guide to Bedside Diagnosis, 2007
Continuous Murmur:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
Continuous murmurs begin in systole and extend into diastole without interruption. The murmur results from blood flow from a higher pressure chamber or vessel to a lower pressure system, with the gradient maintained during both systole and diastole, for example with aortopulmonary and arteriovenous connections.
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Source: Field Guide to Bedside Diagnosis, 2007
Murmurs:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Perform a systematic physical assessment. 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: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulse rhythm abnormality:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Check the patient’s apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats — possibly indicating premature atrial contractions — or other variations in heart rate or rhythm. Take the patient’s apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 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.
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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.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Murmurs:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If you discover a murmur, try to determine its type through careful auscultation. (See Identifying common murmurs, page 398.) Use the bell of your stethoscope for low-pitched murmurs and the diaphragm for high-pitched murmurs.
Next, obtain a patient history. Ask if the murmur is a new discovery or if it has been known since birth or childhood. Find out if the patient has experienced associated symptoms, particularly palpitations, dizziness, syncope, chest pain, dyspnea, and fatigue. Explore the patient's medical history, noting especially an incidence of rheumatic fever, recent dental work, heart disease, or heart surgery, particularly prosthetic valve replacement.
Perform a systematic physical examination. Note especially the presence of cardiac arrhythmias, jugular vein distention, and such pulmonary signs and symptoms as dyspnea, orthopnea, and crackles. Is the patient's liver tender or palpable? Does he have peripheral edema?
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Pulse rhythm abnormality:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient's condition permits, ask if he's experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient's compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias.
Next, check the patient's apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beats—possibly indicating premature atrial contractions—or other variations in heart rate or rhythm. Take the patient's apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Place the patient on a cardiac monitor and obtain an ECG to evaluate the cardiac rhythm. Report your findings to the practitioner.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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