Diseases » Heart failure » Diagnosis

Diagnosis of Heart failure

Diagnostic Test list for Heart failure:

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

• Physical examination
• Stethoscope
• Electrocardiogram
• Echocardiography
• Chest x ray

Heart failure Diagnosis: Book Excerpts

• Ask the following questions - CARDIOMEGALY
• Differential Diagnosis - Cardiomegaly
• Differential Diagnosis - Paroxysmal Nocturnal Dyspnea
• Differential Diagnosis - Heart Failure
• Approach to the Diagnosis - CARDIOMEGALY
• History and physical examination - Paroxysmal nocturnal dyspnea
• History and physical examination - Pulse pressure, narrowed
• History and physical examination - Paroxysmal nocturnal dyspnea
• History and physical examination - Pulse pressure, narrowed
• History - Cardiomegaly
• History - Congestive Heart Failure
• Differential Overview - Cardiomegaly/Congestive Heart Failure
• Diagnosis - Heart failure
• History - Pulse pressure, narrowed
• Clinical Features and Diagnosis - Cardiac Failure
• History and physical examination - Paroxysmal nocturnal dyspnea
• History and physical examination - Pulse pressure, narrowed
• Approach to the Diagnosis - CARDIOMEGALY

Tests and diagnosis discussion for Heart failure:

In many cases, physicians diagnose heart failure during a physical examination. Readily identifiable signs are shortness of breath, fatigue, and swollen ankles and feet. The physician also will check for the presence of risk factors, such as hypertension, obesity, and a history of heart problems. Using a stethoscope, the physician can listen to a patient breathe and identify the sounds of lung congestion. The stethoscope also picks up the abnormal heart sounds indicative of heart failure.

If neither the symptoms nor the patient's history point to a clear-cut diagnosis, the physician may recommend any of a variety of laboratory tests, including, initially, an electrocardiogram , which uses recording devices placed on the chest to evaluate the electrical activity of a patient's heartbeat.

Echocardiography is another means of evaluating heart function from outside the body. Sound waves bounced off the heart are recorded and translated into images. The pictures can reveal abnormal heart size, shape, and movement. Echocardiography also can be used to calculate a patient's ejection fraction, a measure of the amount of blood pumped out when the heart contracts.

Another possible test is the chest x ray, which also determines the heart's size and shape, as well as the presence of congestion in the lungs. (Source: excerpt from NHLBI, Heart Failure: NHLBI)

Diagnosis of Heart failure: medical news summaries:

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

• Diabetes and risk reduction
• FDA approves new pulmonary arterial hypertension drug
• Increasing incidence of chronic disease, not just for the elderly
• More news »

Diagnostic Tests for Heart failure: Online Medical Books

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

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

1. Is there a murmur? Cardiomegaly with cardiac murmurs suggests valvular disease, but it also suggests congestive heart failure and advanced myocardiopathies. One should also be sure that the murmur is not a pericardial friction rub.
2. Is there fever? Fever with cardiomegaly should suggest rheumatic heart disease and bacterial endocarditis. However, it may also suggest an acute myocarditis or acute pericarditis.
3. Is there chest pain? Cardiomegaly with chest pain would certainly suggest a myocardial infarction, but it also may suggest an acute pericarditis.
4. Is there hepatomegaly? Cardiomegaly and hepatomegaly suggest congestive heart failure. Hepatomegaly also may suggest one of the systemic diseases that causes a myocardiopathy such as amyloidosis.
5. Is there edema? The presence of peripheral edema would suggest congestive heart failure, and if it is nonpitting, it would suggest myxedema.
6. Is there hypertension? Cardiomegaly with hypertension would suggest that the cardiomegaly is due to left ventricular enlargement from the chronic hypertension.
7. Is there cyanosis? Cardiomegaly with cyanosis, particularly if there is an associated murmur, suggests congenital heart disease of the cyanotic type.

DIAGNOSTIC WORKUP

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.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

• Congestive heart failure
• Ischemic heart disease
• Hypertension (with left ventricular hypertrophy)
• Valvular disease (primarily MR, AS, AR)
• Hypertrophic cardiomyopathy
• Congenital heart disorders (e.g., ASD, VSD, PDA, coarctation of the aorta, Ebstein's anomaly, tetralogy of Fallot)
• Idiopathic cardiomyopathy
• Alcoholic cardiomyopathy
• Lung disease (leading to right-sided enlargement)
  –Pulmonary embolus
  –COPD
  –Cor pulmonale
  –Primary pulmonary hypertension
• Subacute bacterial endocarditis
• Myocarditis
• Renal failure (risk of pericardial effusion)
• Anemia
• Scleroderma
• Systemic lupus erythematosus
• Sickle cell disease
• Marfan's syndrome
• Pregnancy
• Drugs (numerous drugs are cardiotoxic)
• Postradiation
• Normal, “athletic” heart
• Mediastinal mass
• Kyphoscoliosis
• Rheumatoid arthritis
• Less common etiologies include infiltrative diseases (e.g., amyloidosis, hemochromatosis, atrial myxoma, endocardial fibroelastosis, Fabry's disease, Hurler's syndrome, Pompe's disease), epicardial fat pad, carcinoid, acromegaly, hyper- or hypoparathyroidism, and severe cases of hypocalcemia, hypomagnesemia, and/or hypophosphatemia

Workup and Diagnosis

• Complete history and physical exam
  –Associated symptoms may include fatigue, dyspnea at rest and/or on exertion, palpitations, dizziness, or syncope
  –Note use of alcohol or recreational drugs
  –Family history of heart disease or sudden death
• Chest X-ray and ECG
• Echocardiogram is indicated in all patients to evaluate for valvular disease, chamber size, wall motion abnormalities, and ventricular function
  
• Stress testing if coronary artery disease is suspected
• Cardiac catheterization may be indicated to evaluate for coronary artery disease and valvular disease
• Laboratory studies may include CBC, ESR, electrolytes, BUN/creatinine, glucose, TSH, calcium, magnesium, and phosphorus
  
• Blood cultures are indicated in some cases
• Consider ANA, rheumatoid factor, and screening for pheochromocytoma (i.e., urinary metanephrines and VMA) and hemochromatosis (i.e., iron studies) in selected patients

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Source: In a Page: Signs and Symptoms, 2004

Paroxysmal Nocturnal Dyspnea: Differential Diagnosis
(In a Page: Signs and Symptoms)

• CHF is the most common cause
  –Etiologies include uncontrolled HTN, pulmonary embolus, endocarditis, hyperthyroidism, pericardial disease, endocardial disease (e.g., valvular stenosis, insufficiency, rupture, endocarditis), and myocardial disease (e.g., MI, ischemia, arrhythmias)
• Mitral stenosis
  –Almost always secondary to rheumatic heart disease (after 15–40 years)
  –Advanced cases result in pulmonary hypertension and right heart failure
  –Dyspnea is the most significant symptom
  –Classic triad: Diastolic rumble, opening snap, and loud first heart sound
• Aortic regurgitation
  –Most commonly due to rheumatic fever
• Cardiomyopathies
  –Abnormal myocardium, resulting in impaired cardiac output and CHF
• Aortic stenosis
  –Due to senile valve degeneration, rheumatic disease, or congenital
  –Associated with angina, syncope, and CHF
• Congenital heart disease
  –May see failure to thrive, progressive CHF symptoms, cyanosis, and/or murmur
  • “Cardiac asthma”
    –Bronchospasm secondary to pulmonary congestion and interstitial edema that compresses small airways
    –Standing decreases lung congestion
  • Anxiety
  • Severe COPD and emphysema
  • Asthma
  • Obstructive sleep apnea
  • Obesity/hypoventilation
  • Tropical pulmonary eosinophilia (filariasis)

  Workup and Diagnosis

  • Complete history and physical exam with special attention to cardiac and respiratory systems
  • Initial laboratory studies may include CBC, pulse oximetry, electrolytes, BUN/creatinine, glucose, and calcium
  • Chest X-ray to evaluate for effusion and heart size
  • Echocardiogram may be used to evaluate valves, chamber size, and ventricular function
  • ECG
  • Consider cardiology consult
  • Cardiac catheterization may be indicated for valvular disease, cardiomyopathies, and congenital heart disease

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Source: In a Page: Signs and Symptoms, 2004

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

Increased afterload

• Most common in the neonate due to left-sided obstructive lesions, which present acutely
• Aortic coarctation is most common
  –Increased pulse/BP in right arm
  –Decreased pulse/BP in lower extremities
• Critical aortic stenosis
  –Poor pulses, loud murmur
• Hypoplastic left heart syndrome, aortic arch interruption

Left-to-right shunt lesions
• Normal cardiac muscle funtion but overcirculation of lungs due to a congenital connection between the right and left side of the heart and low PVR
• Usually presents at 1–2 months of age
  –PVR drops and systemic resistance becomes higher than PV
  –Blood shunts from left to right (systemic circulation to pulmonary circulation)
  –Pulmonary overcirculation and poor systemic output (poor peripheral perfusion, low urine output)
• Ventricular septal defect (most common)
• Atrioventricular septal defect (AV canal, endocardial cushion defect), associated with Down syndrome
• Patent ductus arteriosus
• Atrial septal defect (usually asymptomatic)

Intrinsic myocardial disease
• More common cause of heart failure in older children and adolescents
• Myocarditis
  –Acute inflammation and dysfunction of cardiac muscle, usually postviral
  –1/3 remain stable, 1/3 return to normal cardiac function, and 1/3 deteriorate
• Cardiomyopathy
  –Dilated most common, but also hypertrophic and restrictive
  –Multiple genetic and metabolic causes, often positive family history, some represent old, “burned-out” myocarditis
• Myocardial infarction (rare)
  –Kawasaki disease
  –Congenital coronary abnormalities (anomalous left coronary artery)

Workup and Diagnosis

• Neonate
  –Consider left-sided obstructive lesions in any neonate with poor or differential pulses/perfusion
  –Often have respiratory distress, hepatomegaly, and metabolic acidosis
  –Critically ill requiring supplemental O2 and ventilatory support; transfer to tertiary care ICU

• Infants/children
  –History: Activity tolerance, poor feeding, diaphoresis, respiratory symptoms (wheezing or frequent infections due to pulmonary overcirculation), weight gain (poor due to increased metabolic demands or excess due to activity intolerance and edema), dyspnea on exertion for older patients
  –Physical exam: Vital signs (tachypnea, tachycardia), perfusion/pulses, edema (especially of face/eyes for infants), increased work of breathing/retractions, hepatomegaly, increased jugular venous distension

• Chest X-ray often reveals nonspecific cardiomegaly and pulmonary venous congestion
• ECG: Evaluate for ventricular hypertrophy (left-to-right shunt lesions, hypertrophic cardiomyopathy); low QRS voltage (myocarditis, dilated cardiomyopathy)
• Echocardiography and/or cardiac catheterization to further define anatomy and function
• Serum electrolytes, BUN/creatinine, and LFTs (including total protein and albumin) to further define current metabolic state before therapy

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

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

The diagnosis of cardiomegaly can be further developed be a good history and the association of other symptoms and signs. Is there a history of hypertension, alcoholism, rheumatic fever or other systemic disease? Has the patient experienced shortness of breath, angina, fever, joint pains, and so forth? Are there findings of pedal edema, hepatomegaly, or jugular venous distention (CHF)? Are there hypertension and proteinuria (renal disease or essential hypertension)? Is there a significant heart murmur (congenital heart disease, rheumatic heart disease)?

The diagnostic workup will include a CBC, urinalysis, chemistry panel, sedimentation rate, a chest x-ray, and ECG. At this point, it is wise to consult a cardiologist. Echocardiography will be helpful in diagnosing valvular heart disease, myocardiopathy, and pericardial effusion. If CHF is suspected, a venous pressure and circulation time as will as spirometry will support the diagnosis. Echocardiography can diagnose congestive heart failure by determining the left ventricular ejection fraction (LVEF). If there is unexplained fever, an ASO titer or streptozyme test should be ordered to rule out rheumatic fever and perhaps serial blood cultures need to be done to exclude subacute bacterial endocarditis. If there is hypertension the patient may need a hypertensive workup (see page 299).

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Source: Differential Diagnosis in Primary Care, 2007

Paroxysmal nocturnal dyspnea: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Begin by exploring the patient’s complaint of dyspnea. Does he have dyspneic attacks only at night or at other times as well, such as after exertion or while sitting down? If so, what type of activity triggers the attack? Does he experience coughing, wheezing, fatigue, or weakness during an attack? Find out if he has a history of lower extremity edema or jugular vein distention. Ask if he sleeps with his head elevated and, if so, on how many pillows or if he sleeps in a reclining chair. Obtain a cardiopulmonary history. Does the patient or a family member have a history of a myocardial infarction, coronary artery disease, or hypertension or of chronic bronchitis, emphysema, or asthma? Has the patient had cardiac surgery?

Next perform a physical examination. Begin by taking the patient’s vital signs and forming an overall impression of his appearance. Is he noticeably cyanotic or edematous? Auscultate the lungs for crackles and wheezing and the heart for gallops and arrhythmias.

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

Pulse pressure, narrowed: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

After you detect a narrowed pulse pressure, check for other signs of heart failure, such as hypotension, tachycardia, dyspnea, jugular vein distention, pulmonary crackles, and decreased urine output. Also check for changes in skin temperature or color, the strength of peripheral pulses, and the patient’s level of consciousness (LOC). Auscultate the heart for murmurs. Ask about a history of chest pain, dizziness, or syncope.

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

Paroxysmal nocturnal dyspnea: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Begin by exploring the patient’s complaint of dyspnea. Does he have dyspneic attacks only at night or at other times as well, such as after exertion or while sitting down? If so, what type of activity triggers the attack? Does he experience coughing, wheezing, fatigue, or weakness during an attack? Find out if he has a history of lower extremity edema or jugular vein distention. Ask if he sleeps with his head elevated and, if so, on how many pillows or if he sleeps in a reclining chair. Obtain a cardiopulmonary history. Does the patient or a family member have a history of a myocardial infarction, coronary artery disease, or hypertension, or of chronic bronchitis, emphysema, or asthma? Has the patient had cardiac surgery?

Next perform a physical examination. Begin by taking the patient’s vital signs and forming an overall impression of his appearance. Is he noticeably cyanotic or edematous? Auscultate the lungs for crackles and wheezing and the heart for gallops and arrhythmias.

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

Pulse pressure, narrowed: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

After you detect a narrowed pulse pressure, check for other signs of heart failure, such as hypotension, tachycardia, dyspnea, jugular vein distention, pulmonary crackles, and decreased urine output. Check for changes in skin temperature or color, strength of peripheral pulses, and level of consciousness (LOC). Auscultate the heart for murmurs. Ask about a history of chest pain, dizziness, or syncope.

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

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

 A. Presenting symptoms. As congestive heart failure (CHF) and cardiomegaly represent the final common path for many patients with these common conditions, the typical symptoms are exertional dyspnea, syncope, fatigue, and angina. Many patients are asymptomatic at the time of diagnosis and sudden death can be the presenting event (2) (Chapter 7.5).

 B. Etiology. The most common conditions that result in cardiomegaly include hypertension, coronary artery disease, rheumatic and degenerative valvular heart disease, anemia, alcoholism, endocrinopathies, and infectious and inflammatory conditions.

C. Family history. Premature atherosclerosis and ischemic cardiomyopathy can be caused by familial dyslipidemia. A family history of early CHF may indicate familial dilated cardiomyopathy and premature sudden death may indicate familial hypertrophic obstructive cardiomyopathy.

Physical examination

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).

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

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

A. Common presenting symptoms. Does the patient have orthopnea, paroxysmal nocturnal dyspnea, or dyspnea on exertion? How much exertion triggers dyspnea? These are relatively specific symptoms for CHF. Less specific symptoms include swelling of the legs, increasing weight, and generalized fatigue. Older patients with CHF may not have dyspnea on exertion because of a sedentary baseline status; they often present with atypical symptoms such as dry cough, daytime oliguria with nocturia, and confusion (3).

B. Past medical history. Are conditions present that can cause CHF (Table 7.2)? If so, are they well-controlled with lifestyle changes, medications, or both? Uncontrolled hypertension, myocardial ischemia, and medication noncompliance frequently trigger CHF.

 C. Psychosocial history. Is there current or previous heavy alcohol use, tobacco use, or stimulant drug use? Is the patient consuming too much dietary sodium (> 2 g/d)? Are symptoms hindering the patient’s ability to perform daily activities? Is the patient depressed? How is the family coping? Poor understanding of lifestyle factors, depression, and limited family resources can lead to noncompliance and frequent CHF exacerbations.

Physical examination

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.

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

Cardiomegaly/Congestive Heart Failure: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Congestive heart failure

❑ Hypertensive left ventricular hypertrophy

❑ Anterior myocardial ischemia

❑ Athlete’s heart

❑ Mitral regurgitation

❑ Aortic stenosis

❑ High output

❑ Hypertrophic obstructive cardiomyopathy

❑ Pulmonary hypertension

❑ Cor pulmonale

❑ Dilated cardiomyopathy

❑ Endocarditis

❑ Pericardial effusion

❑ Left ventricular aneurysm

❑ Mitral stenosis

❑ Amyloidosis

Diagnostic Approach

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

Heart failure: Diagnosis
(Handbook of Diseases)

The following tests are used to diagnose heart failure:

❑ Electrocardiography reflects heart strain, enlargement, and ischemia. It may also reveal atrial enlargement, tachycardia, and extrasystole.

❑ Chest X-ray shows increased pulmonary vascular markings, interstitial edema, pleural effusion, and cardiomegaly.

❑ Pulmonary artery monitoring typically demonstrates elevated pulmonary artery and pulmonary artery wedge pressures, elevated left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial pressure or central venous pressure in right-sided heart failure.

❑ Echocardiography demonstrates left ventricular dysfunction with a reduced ejection fraction.

❑ Brain natriuretic peptide (BNP) assay detects abnormal hormone levels produced by failing ventricles.

❑ Cardiopulmonary exercise testing determines oxygen consumption and severity of heart failure.

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Source: Handbook of Diseases, 2003

Pulse pressure, narrowed: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Ask the patient about specific cardiac symptoms, such as chest pain, dizziness, or syncope. Obtain his past medical history, and assess his risk factors for heart disease.

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

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

Excessive Volume Load

Left-to-Right Shunt Lesions

Patent Ductus Arteriosus

Fetal ductusarteriosus is open communication between upper descending aortaand junction of main and left pulmonary arteries.

Usually closes within 1–2days after birth but can remain open, especially in preterm infants whoweigh <1,500 g.

Development of cardiac failure, whichusually occurs in neonatal period, depends on size of communicationand relationship between pulmonary and systemic resistances.

Usual physical findings include enlargedheart with prominent LV and RV impulses, narrowly split S2, gradeII–IV/VI continuous or long systolic murmur withmaximum intensity at upper left sternal border, S3 at apex, hepatomegaly,and wide pulse pressure. Systolic ejection sounds may occasionallybe heard along left sternal border.

Chest radiography shows marked cardiomegaly,enlarged left atrium, prominent main pulmonary segment, increasedpulmonary vascular markings, and occasionally Kerley b lines.

ECG shows RV or biventricular hypertrophy.

Ductus can often be visualized with2-D echocardiographic techniques and Doppler methods.

Clinical diagnosis can be difficultin preterm infants with respiratory distress syndrome who requiremechanical ventilation. Murmur may not be heard, and heart may notbe enlarged on chest radiograph. Cardiac failure should be suspectedif arterial blood gas status deteriorates or need for mechanical ventilationis prolonged.

Most children do not need invasivestudies before surgical ligation unless other defects are suspected.Cardiac catheterization and angiography may be necessary with atypicalmurmur or if findings suggest increase in pulmonary artery pressure.

Ventricular Septal Defect

Definedas opening of variable size in ventricular septum, and >1defect can exist.

Cardiac failure occurs between 1 and2 mos of age in infants with medium to large defects.

Clinical manifestations include tachypnea,tiring with feeding, and poor weight gain. Hepatomegaly and sometimessplenomegaly occur. Lung crackles and pedal edema are unusual ininfants.

Cardiac exam reveals cardiac enlargementwith prominent RV and LV impulses. Usually S2 is narrowly splitand pulmonic component is louder than normal. S3 or S4 gallop orboth may be heard. Grade III–V/VI harsh, holosystolicmurmur is heard with maximum intensity at lower left sternal border withtransmission to apex, axilla, and back. Grade I–II/VIapical mid-diastolic rumble signifies increased blood flow acrossmitral valve.

Chest radiography shows marked cardiomegaly,large left atrium, prominent main pulmonary artery segment, increasedpulmonary vascular markings, and occasionally Kerley b lines.

ECG usually shows biventricular hypertrophy.

2-D echocardiography shows VSD.

Atrial Septal Defect (Ostium Secundum)

AlthoughASD does not usually lead to cardiac failure during infancy andchildhood, cardiac failure may occur if large left-to-right shuntexists. Cardiac failure also may occur with combination of moderatesize ASD and VSD.

Tachypnea, tachycardia, cardiomegaly,and usually hepatomegaly occur.

Physical exam, radiographic, and ECGfindings are similar to those with ostium primum defect (see nextsection). Although frontal plane ECG axis of <–30degrees suggests AV canal defect, this pattern occurs in about 10% ofchildren with ostium secundum defects.

2-D echocardiography confirms diagnosis.

Atrioventricular Canal Defects

2 basictypes of AV canal defects are ostium primum and complete AV canaldefects.

In hearts with 2 ventricles, absenceor decrease in septal tissue immediately above and below normallevel of AV valves characterizes these defects.

Ostium Primum Defect

Clinicalpresentation is similar to that of ostium secundum defect, exceptthat mitral incompetence can occur with ostium primum defect becauseof cleft in mitral valve.

With presence of severe mitral incompetence,cardiac failure is more likely to occur.

Usual physical findings are enlargedheart, prominent RV impulse, normal or wide split of S2, grade II–III/VIsystolic ejection murmur with maximum intensity along upper leftsternal border, grade I–II/VI diastolic rumbleat lower left sternal border, and hepatomegaly. With significantmitral incompetence, murmur of mitral incompetence may be heardat apex.

Chest radiography shows cardiomegaly,prominent main pulmonary artery segment, and increased pulmonaryvascular markings.

ECG shows RV hypertrophy and QRS frontalplane axis that is more superior, especially in infants.

2-D echocardiography demonstrates defect.

Complete Atrioventricular Canal

Clinicalmanifestations are more diverse than those of other defects becauseof different hemodynamic situations that can exist. Lesion consistingof small VSD, large ostium primum defect, and normal mitral valvefunction presents like ostium primum defect. Lesion consisting oflarge VSD and normal mitral valve function presents like isolatedVSD. In either of these circumstances, if significant AV valve dysfunctionwith mitral or tricuspid incompetence exists, cardiac failure usuallyoccurs during first month of life.

Chest radiography shows marked cardiomegaly,enlarged main pulmonary artery segment, and increased pulmonaryvascular markings.

ECG shows RV or biventricular hypertrophyand frontal plane QRS axis of –40 to –150 degrees.

Defect may be seen with 2-D echocardiography.

Aortic Pulmonary Window

Due to failureof formation of base of spiral septum, which generally producescommunication between aorta and pulmonary artery just above semilunarvalves.

Cardiac failure occurs in early infancy.

Usual physical findings are markedcardiomegaly, accentuated pulmonary closure sound, long systolicmurmur of variable intensity along left sternal border in thirdand fourth intercostal spaces, hepatomegaly, and wide pulse pressure.

Radiographic and ECG findings are similarto those of large VSD or patent ductus arteriosus.

Usual method of diagnosis is 2-D echocardiography.

Total Anomalous Pulmonary Venous Connection without Obstruction

Severaltypes may occur. Most common is connection between pulmonary veinsand confluence behind left atrium. From this confluence, blood flowsvia anomalous vertical vein to left innominate vein and then toright superior vena cava and right atrium. Pulmonary veins alsomay connect at level of coronary sinus or posterior right atrium.

Clinical presentation and findingsare similar to those of large ASD, and cardiac failure may occurin infancy.

Chest radiography shows moderate cardiomegalywith increase in pulmonary vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography may show echo-freespace posterior to left atrium.

Cardiac catheterization and angiographyare frequently not needed.

Systemic Arteriovenous Fistulas

Usuallycongenital and can occur in cranium, liver, thorax, or extremity.

Clinical course is determined by amountof blood flow through fistula. If flow is large enough, increasein venous return produces increased volume load on heart.

Usual physical findings are markedcardiomegaly; normally split S2 with accentuated pulmonary component;continuous murmur over cranium, liver, or extremity; hepatomegaly;and wide pulse pressure. With intracranial fistula, neck veins aredistended and carotid pulses are bounding.

Chest radiography shows enlarged heartand increase in pulmonary vascular markings.

ECG shows RV or biventricular hypertrophy.

Head CT or MRI can help visualize anyintracranial pathology. Definitive diagnosis of intracranial orperipheral fistulas can be made by angiography.

Valvular Incompetence

Aortic Incompetence

Can be associatedwith unicuspid or bicuspid aortic valve, acute rheumatic fever,endocarditis, supracristal VSD, and Marfan syndrome.

Clinical course depends on acutenessof onset and severity of incompetence.

Mild aortic incompetence is asymptomatic,whereas acute severe aortic incompetence results in low cardiacoutput and hypotension. Chronic moderate-to-severe incompetenceproduces cardiac failure. Diastolic pressure of <50 mmHg and pulse pressure >50 mm Hg indicate significant incompetence.

When severe, LV impulse is increasedand displaced toward axilla. Pulse pressure is wide with boundingpulses. Murmur of aortic incompetence is diastolic decrescendo murmurthat begins with aortic closure. Its maximum intensity is at upperright sternal and left midsternal borders. The longer the murmur,the more severe the incompetence. Fluttering of anterior mitralvalve leaflet also can produce mid-diastolic apical murmur (AustinFlint murmur).

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG shows LV hypertrophy. Severe lesionmay produce subendocardial ischemia with ST depression and T-waveinversion.

2-D echocardiography with Doppler methodsis usually diagnostic.

Mitral Incompetence

Congenitalmitral incompetence is rare but may be due to underdevelopment ofvalve leaflets or short, thick chordae tendinae (parachute mitralvalve). Also may occur with AV canal defects and idiopathic hypertrophicsubaortic stenosis.

Acquired mitral incompetence is morecommon and can be seen with acute rheumatic fever or any cause ofLV failure, when there is dilatation of mitral valve annulus. Closedchest trauma, anomalous left coronary artery, Kawasaki disease,severe aortic stenosis, or coronary arterial disease may cause papillarymuscle infarction or rupture. Endocarditis may perforate valve orrupture chordae tendinae. Mitral valve also may undergo degenerationwith Marfan or Hurler disease. Another cause is prolapsing mitralleaflet syndrome, but severe incompetence is unusual with this lesion.

Clinical course depends on how severethe lesion is. Mild incompetence is asymptomatic, and moderate incompetencemay be tolerated for many years before cardiac failure occurs. Classicmurmur of mitral incompetence is grade III–IV/VIhigh pitched holosystolic murmur with maximum intensity at apexand transmission to left axilla and back. In severe mitral incompetence,prominent LV impulse, S3, and diastolic rumble at apex are commonfindings.

Chest radiography shows marked cardiomegalywith enlarged left atrium and pulmonary venous congestion.

ECG shows left atrial enlargement andmay show LV hypertrophy.

2-D echocardiography can assess anatomyof valve and its attachments as well as any associated abnormalities.Doppler methods can assess severity of incompetence.

Pulmonary Incompetence

Most commoncause is surgical valvotomy. Other causes include isolated congenital incompetenceof pulmonic valve, bicuspid pulmonic valve, and idiopathic dilatationof main pulmonary artery. Absence of pulmonic valve, which is usuallyassociated with VSD and infundibular pulmonic stenosis, causes severeincompetence.

Usual physical findings with moderate-to-severeincompetence include prominent RV impulse, delayed or absent pulmoniccomponent of S2, and characteristic grade II–IV/VImedium-pitched diastolic decrescendo murmur heard with maximum intensityat upper and middle left sternal border.

Chest radiography shows marked cardiomegaly.

ECG shows RV hypertrophy.

2-D echocardiography and Doppler methodsare usually diagnostic.

Tricuspid Incompetence

Congenitaland acquired cardiac lesions may produce tricuspid incompetence.Occasionally, valve leaflets do not form and cardiac failure mayoccur in utero. Isolated tricuspid incompetence may be due to dysmorphicvalve, cleft in valve, or abnormal chordae tendinae. Incompetenceof tricuspid valve also may occur with AV canal defects and Ebsteinanomaly. Acquired causes include severe perinatal asphyxia, acuterheumatic fever, and endocarditis.

Physical exam can establish diagnosisof significant tricuspid incompetence. Typical murmur is grade III/VIhigh-pitched holosystolic murmur that is louder on inspiration andheard with maximum intensity at lower left sternal border. Livermay be enlarged and show systolic pulsations. Jugular venous pulseshows prominent v wave followed by deep y descent. Mid-diastolicrumble that reflects increased blood flow across tricuspid valvealso may be heard at lower left sternal border. Other findings can includecyanosis, peripheral edema, and ascites.

Chest radiography shows cardiomegaly,which is due to large right atrium.

ECG findings depend on associated lesions,but large P waves indicate right atrial enlargement.

2-D echocardiography can assess anatomy,whereas Doppler methods can be helpful in estimating severity ofincompetence.

Excessive Pressure Load

Left Ventricular Outflow Tract Obstruction

Hypertrophic Cardiomyopathy

Genetictransmission is usually autosomal-dominant.

Some individuals have obstructive form,with massive hypertrophy of ventricular musculature, especiallyventricular septum. Abnormal systolic anterior motion of anteriormitral leaflet also produces dynamic subaortic obstruction. Besidescardiac failure, angina and syncope also may occur.

Usual physical findings include sustainedthrusting single or bifid apical pulse, variable splitting of S2depending on how severe obstruction is, grade II–III/VIsystolic ejection murmur with maximum intensity along left midsternalborder, jerky pulse with rapid upstroke, and hepatomegaly. Occasionally,murmur of mitral incompetence is heard at apex.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG shows LV or biventricular hypertrophy.

2-D echocardiography can effectivelydelineate extent of hypertrophy.

Congenital Valvar Aortic Stenosis

Due to imperfectcusp development and leaflet thickening.

Severe stenosis can cause cardiac failurein early infancy.

Usualphysical findings include ejection click and systolic ejection murmur,which may be heard with maximum intensity at upper right and middleleft sternal borders. If cardiac output is reduced, murmur may besoft or absent.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG often shows RV forces in infants <1mo of age. In infants with critical aortic stenosis, ST depressionand T-wave inversion may be seen in left precordial leads.

2-D echocardiography usually showsabnormal aortic valve and poorly contractile LV.

Other manifestations in older childrenare angina, dyspnea on exertion, and syncope.

There is usually prominent LV impulseat apex, narrowly or paradoxically split S2, grade II–IV/VIharsh systolic ejection murmur with maximum intensity at upper rightsternal border, aortic ejection click, sometimes S3 and S4 at apex,and pulse with slow upstroke and narrow pulse pressure.

Chest radiography shows enlarged heartwith prominent ascending aorta and pulmonary venous congestion.

ECG usually shows LV hypertrophy withor without ST depression and T-wave inversion.

2-D echocardiography shows abnormalaortic valve, and Doppler methods can estimate pressure differenceacross valve.

Discrete Subvalvar Aortic Stenosis

Obstructionbelow aortic valve may be due to thin membrane diaphragm or thickfibromuscular tissue. Diaphragm also may be associated with aorticinsufficiency.

Clinical findings are similar to thosewith valvar aortic stenosis, except that aortic ejection click isless common and aortic dilatation is less prominent.

2-D echocardiography usually demonstratestype and location of obstruction. Otherwise, cardiac catheterizationand angiography are diagnostic.

Supravalvar Aortic Stenosis

Definedas localized or diffuse narrowing of ascending aorta just abovelevel of coronary arteries.

Can occur as familial or sporadic isolatedlesion but is often associated with Williams syndrome, whose featuresinclude elfin facies and mental retardation. Many individuals, especiallyif they have Williams syndrome, usually have RV outflow tract obstruction,which can occur at valvar, supravalvar, and peripheral pulmonaryartery levels.

Clinical findings are similar to thoseof congenital valvar aortic stenosis, except that murmur is heardhigher on chest wall and ejection click is unusual. Suprasternalnotch thrill is common.

BP in right arm may be 20 mm Hg higherthan that in left arm because of stenosis at origin of left subclavianartery or jet effect of blood with ejection from LV into ascendingaorta.

Chest radiography shows enlarged heartwithout poststenotic dilatation of ascending aorta.

ECG shows LV hypertrophy and, if stenosisis severe, T-wave inversion in left chest leads.

2-D echocardiography demonstrates narrowing,and Doppler methods can assess pressure gradient across ascendingaorta.

Cardiac catheterization and angiographyare usually performed because of high incidence of associated abnormalities,which include patent ductus arteriosus, coarctation of aorta, pulmonarystenosis, and mitral insufficiency.

Aortic Arch Hypoplasia or Interruption

Most commonlyoccurs in aortic isthmus but may occur anywhere in aortic arch.Most extreme form is interruption of arch, which can occur proximalto left carotid artery, distal to left subclavian artery, or betweenleft subclavian and left carotid arteries.

In almost all cases, patent ductusarteriosus provides blood flow to lower part of body.

With rare exceptions, there are associateddefects (e.g., VSD, double outlet RV, AV canal defect, and tricuspidatresia with aortopulmonary transposition).

Clinical findings depend on severityof intracardiac defects, pulmonary vascular resistance, and sizeof ductus arteriosus. Almost all infants develop severe cardiacfailure during first week of life.

Differential cyanosis of extremitiesdepends on degree of ventricular shunting and is variable finding.

Femoral pulses are diminished or absent.No murmur is specific.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG may show RV or biventricular hypertrophy.

Although 2-D echocardiography may bediagnostic, cardiac catheterization and angiography are definitive.

Localized Juxtaductal Coarctation of Aorta

Definedas congenital narrowing of upper descending aorta that is usuallylocated near ductus arteriosus.

Primary coarctation of aorta occurswith or without patent ductus arteriosus but without other majorcardiac defects.

Complex coarctation is associationof other cardiac defects with coarctation [e.g., VSD, aorticvalvar stenosis, or mitral stenosis (Shone syndrome)].

Severe primary coarctation of aortausually presents with cardiac failure during first month of life.Delay in onset is possibly related to ductal closure at aortic end.With complex coarctation, cardiac failure usually appears duringfirst week of life.

Usual physical findings in child withprimary coarctation of aorta are arm BP that is ≥20 mm Hg higherthan pressure in legs, diminished or absent femoral pulses, andgrade II–III/VI systolic ejection murmur withmaximum intensity along left sternal border or over scapula in leftback. Arm BPs may be unequal if anomalous right subclavian arteryis present below coarctation or left subclavian artery is narrowedat origin of coarctation. Clinical findings with complex coarctationdepend on presence of associated lesions. Murmurs of VSD, valvaraortic stenosis, or mitral incompetence usually can be heard ifthese defects are present.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

In early infancy, ECG usually showsRV hypertrophy. In later infancy and childhood, it usually showsLV or biventricular hypertrophy, which is usual finding with complexcoarctation.

In neonates 2-D echocardiography canoften visualize coarctation, and Doppler methods can estimate itsseverity.

MRI can help define anatomy in somecases. If precise diagnosis of coarctation and associated lesionscan be accurately made, cardiac catheterization may not be necessary.

Right Ventricular Outflow Tract Obstruction

Can occurat level of pulmonary valve or above or below valve leaflets.

Valvar pulmonic stenosis is most commonform.

Congenital Valvar Pulmonic Stenosis

Neonateswith critical pulmonary valvar stenosis develop cardiac failurein immediate postnatal period.

Often infundibular hypertrophy occurswith valvar stenosis and tends to be progressive. Asymptomatic infantsand children may develop progressive severe pulmonary stenosis withonset of cardiac failure in adulthood.

Usual physical findings are prominentRV impulse; normal or diminished pulmonary component of S2; gradeII–IV/VI systolic ejection murmur with maximumintensity at upper left sternal border; and hepatomegaly. Severestenosis produces delay in peak intensity of murmur and delay in pulmonaryvalve closure. Occasionally, continuous murmur of patent ductusarteriosus or pansystolic murmur of tricuspid incompetence is heard.

Chest radiography shows cardiomegalyand decreased pulmonary vascular markings.

ECG usually shows RV hypertrophy, unlessRV is hypoplastic. T-wave inversion is sometimes seen in right precordialleads.

2-D echocardiography can visualizethickened, stenotic valve and narrowed infundibulum. Doppler methodsindicate severity of obstruction.

Left Ventricular Inflow Tract Obstruction

Pulmonary Vein Stenosis

Obstructionof normally connected pulmonary veins may be due to intrinsic narrowing(diffuse hypoplasia, localized diaphragm, narrowing on entry toleft atrium) or occasionally by external compression by posteriormediastinal mass.

Presentation is similar to that oftotal anomalous pulmonary venous connection with obstruction. Usualphysical findings are prominent RV impulse and accentuated pulmonaryclosure sound. No specific murmurs are heard.

Chest radiography shows near-normalheart size with increase in pulmonary venous vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography can sometimesview stenoses directly.

Cardiac catheterization and angiographyare definitive.

Total Anomalous Pulmonary Venous Connection with Obstruction

Pulmonaryvenous drainage below diaphragm to ductus venosus with venous return viainferior vena cava produces pulmonary venous obstruction.

Supracardiac or cardiac connectionsof pulmonary veins can cause pulmonary venous obstruction, but thisis uncommon.

Severe obstruction produces severecyanosis and respiratory distress in neonatal period.

Usual physical findings are prominentRV impulse, narrowly split S2, and hepatomegaly. These murmurs aresometimes heard: murmur of tricuspid incompetence; continuous murmuralong left sternal border, which reflects blood flow through anomalouschannel; and systolic ejection murmur along upper left sternal border,which reflects blood flow across pulmonary valve.

Chest radiography usually shows mildcardiomegaly and intense increase in pulmonary vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography shows enlargedRV, and no pulmonary veins are seen entering left atrium. If pulmonaryveins empty into coronary sinus or into large channel behind atria,these structures can be seen.

Cardiac catheterization and angiographyare definitive.

Cor Triatriatum

Failureof resorption of common pulmonary vein results in cor triatriatumwith division of left atrium into upper and lower chambers usuallyconnected by restrictive opening.

Clinical presentation is same as pulmonaryvenous obstruction. Usual physical findings are prominent RV impulseand accentuated pulmonary closure sound. No specific murmurs are heard.

Chest radiography shows mild cardiomegalyand increase in pulmonary venous vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography or MRI can bediagnostic.

Supravalvular Stenosing Ring of Left Atrium

Fibrousring located on atrial side of mitral annulus sometimes protrudesinto mitral orifice, causing inflow obstruction of LV. Occurs asisolated lesion or in association with parachute mitral valve, subaorticstenosis, and coarctation of aorta (Shone syndrome).

Clinical presentation and findingsare similar to those for cor triatriatum.

Although this lesion can be visualizedby 2-D echocardiography, cardiac catheterization and angiographyare definitive.

Tumor

Tumor withinleft atrium, usually myxoma, can produce findings similar to mitral stenosis,but if tumor is on pedicle that sometimes protrudes into mitralvalve orifice, findings may be intermittent.

2-D echocardiography and MRI revealtumor mass.

Mitral Valve Obstruction (Atresia, Stenosis, Parachute Mitral Valve)

Most severeform is mitral atresia, which is discussed later in section Hypoplastic Left Heart Complex.

Mitral stenosis is prototype lesionof LV inflow tract obstruction. Congenital mitral stenosis occursas isolated lesion or in association with other lesions (e.g., aorticstenosis, VSD, ASD, coarctation of aorta, or endocardial fibroelastosis).Cusps may be abnormal, commissures may fuse, or chordae tendinaemay join below valve ring. Parachute valve with chordae tendinaeattached to single papillary muscle also may cause obstruction toblood flow at mitral valve level.

Congenital forms of mitral stenosisare usually severe, and infants present with cardiac failure. Usualphysical findings are prominent RV impulse, loud S1, and accentuatedpulmonic component of S2. Apical mid-diastolic murmur with presystolicaccentuation may not be heard with severe cardiac failure but maybe heard once failure is controlled. Opening snap of mitral valvemay not be heard because of thickness and immobility of valve. Variousdegrees of mitral incompetence may occur, and typical apical murmurof mitral insufficiency may be heard. With severe pulmonary arteryhypertension and RV dilatation, murmur of tricuspid insufficiencyalso may be heard.

Chest radiography shows left atrialenlargement out of proportion to cardiac enlargement, large pulmonaryartery segment, and pulmonary edema in severe cases.

ECG shows hypertrophy of RV and bothatria.

2-D echocardiography shows anatomyand function of valve and presence of any other abnormalities. Dopplermethods can also estimate flow and pressure difference across valve.

Diagnosis rarely needs confirmationby cardiac catheterization and angiography.

Right Ventricular Inflow Tract Obstruction

Systemic Venous Obstruction

May be dueto obstruction of venous return in superior or inferior vena cavaby thrombus, mediastinal mass, or secondary to atrial baffle procedurefor aortopulmonary transposition.

Venous distension and edema of thatportion of body drained by obstructed vessel usually occurs.

Right Atrium Obstruction

Thrombusformation may produce obstruction and can be complication of indwelling cathetersin vena cava or right atrium.

Right atrial myxoma and extension ofWilms tumor or hepatic tumor also may produce obstruction.

Tricuspid Valve Obstruction

Tricuspidatresia is most severe form of tricuspid valve obstruction. See Chap. 12, Cyanosis.

Isolated tricuspid stenosis is rare,and if atrial septum is intact, findings are those of venous obstruction.If stenosis is severe, there is mid-diastolic rumbling murmur atlower left sternal border, and prominent S3 and S4.

ECG shows tall peaked P waves indicativeof right atrial enlargement. Right atrium is also enlarged on chestradiograph.

2-D echocardiography is diagnostic.

Ebstein Anomaly

Septal andinferior leaflets of tricuspid valve are displaced into RV withanomalous attachments to wall of RV.

Depending on specific anatomy, widespectrum of clinical presentations occurs. With severe RV dysfunctionand increased pulmonary vascular resistance, intense cyanosis andcardiac failure can occur in neonatal period. Usual physical findingsare wide splitting of S2, prominent S3 and S4, murmur of tricuspidincompetence, and hepatomegaly.

Chest radiography shows marked cardiomegalywith enlargement of right atrium (heart shape is globular) and usuallydecreased pulmonary vascular markings.

ECG commonly shows right atrial hypertrophy,prolonged PR interval, right bundle branch block, and sometimesWolff-Parkinson-White syndrome.

2-D echocardiography is diagnostic.

When specific anatomic details needto be evaluated, cardiac catheterization and angiography are necessary.

Cor Pulmonale

Definedas pulmonary hypertension complicating lung disease.

Most common causes in pediatric populationare bronchopulmonary dysplasia, cystic fibrosis, and chronic upperairway obstruction.

Patients may experience dyspnea, fatigue,exercise intolerance, chest pain, syncope, and cyanosis. Physicalfindings include RV heave, increase in intensity of S2 with narrowor fixed splitting, jugular venous distension, hepatomegaly, andperipheral edema.

Chest radiographic findings may showevidence of chronic lung disease with RV enlargement and dilatedcentral pulmonary arteries.

ECG usually shows RV hypertrophy.

Systemic Hypertension

Althoughcommon cause of cardiac failure in adults, children with hypertensiondo not usually develop failure unless onset is acute or hypertensionis extremely severe.

Most common cause of acute severe hypertensionin childhood is acute glomerulonephritis.

BP should always be measured in anyonewith cardiac failure.

See Chap.32, Hypertension.

Disturbance in Myocardial Function

Acute Rheumatic Fever and Rheumatic Heart Disease

Acute andchronic cardiac failure can result from rheumatic heart disease.Most common valve lesions are mitral and aortic incompetence.

See Chap.37, Limp.

Kawasaki Disease

Most seriouscomplications are coronary artery aneurysm, coronary thrombosis,myocarditis, mitral valve incompetence, pericardial effusion, andarrhythmias.

Indications of cardiac involvementare murmur of mitral incompetence, pericardial friction rub, chestradiographic findings of cardiomegaly and pulmonary venous congestion,ST and T-wave changes on ECG, and coronary aneurysms as shown by2-D echocardiography.

See Chap.21, Fever.

Myocarditis

Usual causeis enteroviral infection. Isolation of pathogen from myocardiumis most reliable way to determine etiology; however, this is notalways possible. Isolation from other tissues or body fluids orserologic tests can be used.

Clinical manifestations include fatigue,dyspnea, chest pain, and tachypnea. Cardiac failure with pulmonaryedema and shock also may occur.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG findings suggestive of myocarditisare generalized low-voltage QRS complexes, T-wave inversion, andarrhythmias (e.g., ventricular extrasystoles and atrial tachycardia).

2-D echocardiography shows dilatationof chambers and poor contractility.

Pericarditis

Acute pericarditisis inflammation of parietal pericardium, which can be associated withinfectious or noninfectious disorder.

Infectious causes include viruses (enterovirusesmost commonly), pyogenic bacteria (S. aureus, S. pneumoniae, N.meningitidis, and H. influenzae type b most commonly), M. tuberculosis, andfungi (Candida and Aspergillus species).

Noninfectious causes include acuterheumatic fever, juvenile rheumatoid arthritis, Kawasaki disease,and postpericardiotomy syndrome.

Can occur in asymptomatic individualwith mild pericardial effusion or as life-threatening process inwhich large effusion may compromise cardiac function (cardiac tamponade).Chest pain is most common symptom of pericarditis, but exerciseintolerance and fever also may occur. Cardiac exam reveals muffledheart sounds, tachycardia, and friction rub if effusion is smallvolume. Rub is grating to and fro sound heard best in inspirationwith patient leaning forward. Manifestations of tamponade includetachycardia, reduced BP, and pulsus paradoxus with >10mm Hg decrease in systolic BP during inspiration as result of decreasedcardiac filling.

Chest radiography shows increase insize of cardiac shadow.

ECG shows low-voltage QRS complexesand generalized ST segment elevation.

2-D echocardiography can demonstrateeffusion.

Specific etiology of infectious pericarditisis best determined by evaluation of pericardial fluid obtained bypericardiocentesis. Appropriate viral, bacterial, mycobacteria,and fungal cultures should be performed. Serologic tests may benecessary for diagnosis of viral disease.

Endocarditis

Infectionof cardiac endothelial surface signifies endocarditis.

In pediatric population, usually occursas complication of congenital or rheumatic heart disease, valvehomografts, or artificial heart valves. Most frequent pathogensin childhood are viridans streptococci and S. aureus.

Common findings include fever, malaise,anorexia, and weight loss. New or changed murmur, splenomegaly,petechiae, and embolic phenomena are often found, but Osler nodes,Roth spots, Janeway lesions, and splinter hemorrhages are uncommon.

Although clinical findings suggestdiagnosis, positive blood culture confirms specific pathogen involved.2-D echocardiography can show characteristic vegetations.

Cardiomyopathy

Chronicmyocardial diseases can be classified as dilated, hypertrophic,or restrictive cardiomyopathies.

Dilated cardiomyopathy is thought to be primaryor result from viral myocarditis.

Hypertrophic cardiomyopathy is oftengenetic and may be associated with neuromuscular disorders.

Restrictive cardiomyopathy may be associatedwith infiltrative disorders.

Chest radiography usually shows enlargedheart.

ECG often shows LV hypertrophy, STsegment flattening, and T-wave inversion.

Echocardiography shows marked ventricularenlargement and poor contractile function with dilated cardiomyopathy,massive septal hypertrophy with hypertrophic cardiomyopathy, andlarge dilated atria with reduced ventricular filling with restrictivecardiomyopathy.

Cardiac biopsy is only occasionallyuseful in making specific diagnosis.

Myocardial Infarction

Anomalous Left Coronary Artery from Pulmonary Artery

May presentwith acute myocardial infarction and cardiac failure in infancy.Murmur of mitral incompetence may be heard.

Chest radiography shows cardiomegalyand pulmonary venous congestion.

ECG shows anterior or anteroseptalmyocardial infarction with deep Q waves and T-wave inversion inleads 1, aVL, and left precordial leads.

2-D echocardiography with Doppler methodsis almost always diagnostic.

Cardiac catheterization and angiographyare definitive.

Older children are usually asymptomaticand may only present with murmur of mitral incompetence or continuousmurmur at upper left or mid-sternal border. Presence of deep Q wavesin leads 1, aVL, and V4–V6 suggests diagnosis.

Atherosclerosis

Familialhypercholesterolemia (familial hyperlipoproteinemia type II) cancause atherosclerosis and myocardial infarction in childhood.

Genetic transmission is autosomal-dominant.

Tendon and tuberous xanthomas are common.

Plasma cholesterol is high (600–1,000mg/dL), plasma triglycerides are normal, and low-densitylipoproteins are elevated.

Cardiac Tumor

Mass withinchamber can cause inflow or outflow tract obstruction. Involvementof myocardium can cause cardiac failure.

Benign tumors include rhabdomyoma,fibroma, myxoma, and teratoma, whereas malignant tumors includerhabdomyosarcoma and teratoma. Leukemia and lymphoma can involvepericardium and cause pericardial compression.

Clinical manifestations vary dependingon location and histologic type.

2-D echocardiography and MRI locateand define extent of mass lesion.

Histologic diagnosis is definitive.

Metabolic Heart Disease

Severalcommon metabolic problems that affect myocardial function are discussedin this section.

See Garson et al. (1998) for detaileddiscussion of metabolic disorders affecting heart.

Perinatal Asphyxia

Can producetransient ischemia of myocardium and cardiac failure.

Gallop rhythm and murmurs of mitralor tricuspid incompetence may be heard.

Chest radiography shows cardiomegalywith pulmonary venous congestion.

ECG shows RV hypertrophy, ST depression,and T-wave flattening. Abnormal Q waves in limb and chest leadssuggest anterior or inferior myocardial infarction.

2-D echocardiography sometimes showsdecreased myocardial contractility.

Hypocalcemia

Can causedilated cardiomyopathy in neonates and older children.

Cardiac failure usually resolves withrepletion of calcium.

Hypoglycemia

In neonateshypoglycemia may cause cardiomegaly and cardiac failure.

Risk factors include maternal diabetesmellitus, low birth weight, and septicemia.

Severe Anemia

Any severe chronic anemia with hemoglobinconcentration <5 g/dL may produce cardiac failure.

Drugs

Anthracyclineantibiotics doxorubicin and daunomycin are cancer chemotherapeutic agentsthat can damage myocardium. Development of cardiac failure is relatedto cumulative dose.

Echocardiographic ejection fractionmeasurements are useful for monitoring individuals who are takingthese drugs.

Complex Anatomic Lesions

5 lesionsin this section involve intracardiac or ductal right-to-left shunts.

Cardiac failure is most obvious manifestation,and cyanosis is not often clinically visible.

Hypoplastic Left Heart Complex

2 basic types of hypoplastic left heart complexare (a) aortic and mitral atresia with absent or slitlike LV, and(b) aortic and mitral stenosis with small LV.

Aortic and Mitral Atresia

Usuallypresent within 48 hrs of birth with cardiac failure and mild cyanosis.Usual physical findings are prominent RV impulse, single loud S2,grade II/VI systolic ejection murmur along left sternalborder, hepatomegaly, and diminished peripheral pulses.

Chest radiography shows moderate cardiomegalyand pulmonary venous congestion.

ECG shows RV hypertrophy.

2-D echocardiography shows large RV,small or absent LV, mitral and aortic atresia, and hypoplastic ascendingaorta.

Aortic and Mitral Stenosis

Usuallypresent with cardiac failure in first or second week after birth.Usual physical findings are prominent RV impulse or LV impulse dependingon size of LV, single or narrow split of S2, murmur of aortic stenosis,hepatomegaly, and diminished pulses.

Chest radiography shows enlarged heartand pulmonary venous congestion.

ECG usually shows LV hypertrophy withoccasional ST depression and T-wave flattening or inversion in leftprecordial leads.

2-D echocardiography is usually diagnostic.

Transposition of Great Arteries with Large Ventricular SeptalDefect

The aortarises from RV, while pulmonary artery arises from LV. Large communicationexists at ventricular level and also may occur at ductal level.

Cardiac failure and mild cyanosis occurat 2–4 wks of age. Murmur of VSD can be heard. S2 is narrowwith accentuated pulmonary component.

Chest radiography shows cardiomegaly,increase in pulmonary vascular markings, an absent pulmonary arterysegment.

ECG shows RV or biventricular hypertrophy.

2-D echocardiography is diagnostic.

Double-Outlet Right Ventricle

Both aortaand pulmonary artery arise entirely or in large part from RV. VSDis part of this lesion and can be subaortic, subpulmonic, doublycommitted, or noncommitted. Subaortic and subpulmonic defects aremost common.

Clinical presentation of subaorticdefect is similar to that of isolated large VSD, whereas clinicalpresentation of subpulmonic defect is similar to that of transpositionof great arteries with intact ventricular septum.

2-D echocardiography is usually diagnostic.

Cardiac catheterization and angiographyare important in planning of surgery.

Truncus Arteriosus

1 greatartery with single semilunar valve arises from base of heart. Systemic,coronary, and 1 or 2 pulmonary arteries arise from this artery.Beneath valve is VSD. Usually presents during neonatal period withcardiac failure and mild cyanosis.

Usual physical findings are diffuseprominent impulse at lower left sternal border, occasional ejectionclick, grade II–IV/VI systolic ejection murmuralong left sternal border, wide pulse pressure, and hepatomegaly.Other possible findings are early diastolic murmur along left sternalborder, which signifies truncal incompetence, or continuous murmurat 1 or both upper sternal borders, which reflects stenosis of originof 1 or both pulmonary arteries. Stenosis of truncal valve may produceharsh systolic ejection murmur at upper right sternal border.

Chest radiography shows cardiomegaly,increase in pulmonary vascular markings, deficient main pulmonaryartery segment, and frequently right aortic arch.

ECG shows RV hypertrophy and frequentlybiventricular hypertrophy.

2-D echocardiography is diagnostic.

Cardiac catheterization and angiographycan define anatomy of pulmonary arteries, aortic arch, truncal valve,and hemodynamic state.

Univentricular Atrioventricular Connections

Definedas malformations in which both AV valves or common AV valve openinto same ventricle.

In absence of pulmonary stenosis oratresia, clinical presentation of this lesion is similar to thatof large VSD.

Chest radiography shows cardiomegalywith increase in pulmonary vascular markings.

ECG may show increased voltage in eitherright or left precordial leads.

2-D echocardiography and cardiac catheterizationand angiography are diagnostic.

Abnormal Cardiac Rhythms

Supraventricular Tachycardia

Most childrenhave structurally normal heart; however, some may have Wolff-Parkinson-Whitesyndrome.

Mechanisms include reentry using accessorypathway, reentry without accessory pathway, and automatic tachycardia.

In infants <1 yr of age, ventricularrate varies from 220 to 280 bpm, whereas in older children it variesfrom 180 to 240 bpm. RR interval is regular, and onset and terminationof rhythm are usually sudden. P waves may or may not be visible.They follow or precede each QRS or are unrelated (AV dissociation).

In infants left bundle branch blockpattern with aberrant conduction is common. Neonates may developcardiac failure if arrhythmia lasts only few hours. Infants whohave this abnormal rhythm for >24 hrs are at risk for developmentof cardiac failure.

ECG confirms diagnosis. Fetal echocardiographymay confirm diagnosis in utero.

Atrial Flutter

Can occurin individuals with normal heart, in those with structural defects,and after surgery for congenital heart defects.

Can cause cardiac failure, especiallyin young infant.

Atrial rate varies from 250 to 500bpm. With 1:1 conduction, ventricular rate is too fast for ventriclesto fill in diastole, and low cardiac output occurs. With some degreeof AV block such that conduction is 2:1, assuming atrial rate of300 bpm and ventricular rate of 150 bpm, cardiac failure is unlikely. RRinterval is usually regular, but it can be irregular in presenceof AV block.

Sawtooth flutter waves are diagnostic.

Complete Heart Block

Congenitalcomplete heart block can occur in infants with otherwise normalheart, in some neonates whose mothers have systemic lupus erythematosus,and in infants with ventricular inversion and transposition of greatarteries.

May occur following surgical correctionof congenital heart defects.

Cardiac failure occurs only if ventricularrate is too slow to maintain normal cardiac output. In neonates,ventricular rate of <40 bpm usually results in cardiacfailure, whereas infants with ventricular rate of >50 bpmare usually asymptomatic.

ECG shows lack of conduction of atrialimpulses to ventricles with faster atrial rate and slower ventricularrate.

Diagnostic Approach

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.

Table 7.1. Diagnostic Classification of Common Causes of CardiacFailure

Group	Findings	Possible Causes
I	Acyanotic	Left-to-right shunt lesions
	Cardiomegaly
	Increased pulmonary vascular markings
II	Acyanotic	Left-sided obstructive lesions
	Cardiomegaly
	Pulmonary venous congestion
III	Acyanotic usually	Myocarditis
	Cardiomegaly	Cardiomyopathy
	Pulmonary venous congestion	Anomalous coronary artery
	No heart murmur frequently
IV	Mild cyanosis	Transposition with large VSD
	Cardiomegaly	Hypoplastic left heart syndrome
	Increased pulmonary vascular markings	Double-outlet RV
		Truncus arteriosus
		Univentricular AV connections
V	Marked cyanosis	Pulmonary venous obstruction
	Normal-sized heart or mild cardiomegaly
	Pulmonary venous congestion
VI	Cyanosis	Critical pulmonic stenosis
	Cardiomegaly	Ebstein anomaly
	Decreased pulmonary vascular markings

Evaluation

These testsshould generally be performed in any infant or child with cardiacfailure: chest radiography; ECG; CBC with differential; analysisof serum electrolytes, glucose, creatinine; blood urea nitrogen;pulse oximetry; and 2-D echocardiography.

Chest radiography shows presence ofcardiomegaly and whether pulmonary vascular markings are normal,increased, or decreased.

ECG indicates presence of hypertrophyof chambers and permits diagnosis of arrhythmias.

Hyponatremia is common and reflectsincrease in water retention in excess of sodium.

2-D echocardiography with Doppler methodsis often diagnostic or at very least provides useful informationin many cases of cardiac failure. Cardiac catheterization with angiographyprovides definitive diagnosis for selected heart lesions.

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

Paroxysmal nocturnal dyspnea: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Begin by exploring the patient's complaint of dyspnea. Does he have dyspneic attacks only at night or at other times as well, such as after exertion or while sitting down? If so, what type of activity triggers the attack? Does he experience coughing, wheezing, fatigue, or weakness during an attack? Find out if he has a history of lower extremity edema or jugular vein distention. Ask if he sleeps with his head elevated and, if so, on how many pillows or if he sleeps in a reclining chair. Obtain a cardiopulmonary history. Does the patient or a family member have a history of a myocardial infarction, coronary artery disease, or hypertension or of chronic bronchitis, emphysema, or asthma? Has the patient had cardiac surgery?

Next perform a physical examination. Begin by taking the patient's vital signs and forming an overall impression of his appearance. Is he noticeably cyanotic or edematous? Auscultate the lungs for crackles and wheezing and the heart for gallops and arrhythmias.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Pulse pressure, narrowed: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

After you detect a narrowed pulse pressure, check for other signs of heart failure, such as hypotension, tachycardia, dyspnea, jugular vein distention, pulmonary crackles, and decreased urine output. Also check for changes in skin temperature or color, the strength of peripheral pulses, and the patient's level of consciousness (LOC). Auscultate the heart for murmurs. Ask about a history of chest pain, dizziness, or syncope. Obtain a complete drug history.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

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

The diagnosis of cardiomegaly can be further developed by a good history and the association of other symptoms and signs. Is there a history of hypertension, alcoholism, rheumatic fever, or other systemic disease? Has the patient experienced shortness of breath, angina, fever, joint pains, and so forth? Are there findings of pedal edema, hepatomegaly, or jugular venous distention (CHF)? Are there hypertension and proteinuria (renal disease or essential hypertension)? Is there a significant heart murmur (congenital heart disease, rheumatic heart disease)? The diagnostic workup will include a CBC, urinalysis, chemistry panel, sedimentation rate, chest x-ray, and ECG. At this point, it is wise to consult a cardiologist. Echocardiography will be helpful in diagnosing valvular heart disease, myocardiopathy, and pericardial effusion. If CHF is suspected, a venous pressure and circulation time as well as spirometry will support the diagnosis. Echocardiography can diagnose CHF by determining the left ventricular ejection fraction (LVEF). If there is unexplained fever, an antistreptolysin O (ASO) titer or streptozyme test should be ordered to rule out rheumatic fever, and perhaps serial blood cultures should be done to exclude subacute bacterial endocarditis. If there is hypertension, the patient may need a hypertensive workup .

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

 » Next page: Signs of Heart failure

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