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KEY WORDS
Heart Failure
Patient Evaluation
Common Symptoms
Diagnostic Testing
Clinical Evaluation of the
Heart Failure Patient
by
Sara Paul, RN, MSN, FNP
Hickory Cardiology Associates, Hickory, NCJana Glotzer RN, MSN, CCRN, ACNP
University of North Carolina Heart Failure Program, Chapel Hill, NC The clinical presentation of heart failure (HF) isdynamic and changes continually. The same patient may have different symptoms each time they present to their health care provider, or even no symptoms. Signs and symptoms vary widely among patients; a HF finding that is commonly found in one patient may be absent in another. Patients presenting with HF may have vague symptoms such as shortness of breath or fatigue, or they may have overt signs such as peripheral edema. The patient’s symptoms may be immediately obvious or may be subtle, requiring careful evaluation in order to distinguish their presence. In any case, it is important for the health care provider to use a consistent systematic approach with each patient to look for obvious, as well as subtle, indications of worsening heart failure. The purpose of this article is to review the clinical evaluation of the heart failure patient, focusing on obtaining a pertinent history, performing a detailed physical exam, and interpreting key diagnostic tests. Henry Marriott once said, “A healthcare provider who cannot take a good history and a patient who cannot give one are in danger of giving and receiving bad treatment”.
That is certainly true for HF patients. Many of the symptoms that are associated with this disease are non-specific and could easily apply to conditions other than HF. For that reason, it is important to ask the correct questions that focus on differentiating the cause of the patient’s symptoms and to avoid questions that are not pertinent to the patient’s situation. It is best to ask one question at a time, rather than a series of questions, which may confuse the patient and prevent clear answers.
There are a number of major symptoms of heart disease, but those that relate specifically to HF include shortness of breath, orthopnea, paroxysmal nocturnal dyspnea (PND) and chest pain or discomfort. Other less specific symptoms include fatigue, cough, dizziness, palpitations and syncope. Infrequently, patients may complain of
right upper quadrant pain, nausea or early satiety in the presence of liver congestion from volume overload. Their spouse may complain of the patient’s snoring or apneic episodes during sleep. If a patient answers with a positive for any of the above symptoms, the nurse should query the patient with a symptom analysis, consisting of the following questions:
• When did the symptom begin? • Has it happened before?
• How did it begin (gradual onset versus sudden onset)?
• Was the symptom brought on with activity or did it occur at rest?
• How long does it last when it occurs? • How often does it occur?
• What relieves the symptom?
• Are there any other symptoms associated with it? • If the symptom is pain, where is the pain located and does it radiate to another area?
• On a scale from 1 to 10 (1 being the least amount of pain and 10 being the worst possible pain), where is the patient’s pain on that scale?
It is important to let the patient use their own words to describe their symptoms and it may be helpful to have the patient’s spouse or a family member present to offer a different perspective on the patient’s symptoms. Quite often, a patient may not even realize that they are experiencing symptoms such as shortness of breath, but they decrease their activity level to accommodate their breathing. Observations from others who live with the patient may be helpful in obtaining more objective data regarding the patient’s symptoms and functional status.
Introduction
Taking a Pertinent History
The patient’s cardiac history is an important aspect of their disease. Coronary artery disease accounts for the etiology of most HF cases. Obviously, it is important to know about the patient’s history of coronary artery disease and any surgery or coronary interventions the patient has undergone in the past. The nurse should ask about any procedures the patient may have undergone, such as pacemaker or defibrillator implant, ablation or congenital heart defect repair. Other cardiovascular (CV) illnesses such as arrhythmias, myocardial infarction, hypertension, stroke and peripheral vascular disease should be
evaluated. It is also important to determine any pertinent family history of premature coronary heart disease, sudden death or cardiomyopathy.
Pertinent non-cardiac illnesses include diabetes, hypercholesterolemia and lung disease. Other disease states may have an impact on the CV system or may mimic symptoms of CV disease, such as gastroesophageal reflux, anemia or thyroid disorders, and it is vital to question the patient about the presence of these and any other conditions. Childhood illnesses, especially streptococcal infections, should also be noted.
The patient should be asked about allergies to medications, food or anything else. Women should be questioned about their menstrual status. The patient’s social history should include information about education level, job situation, marital status, living situation, children, and support people who may help the patient at home. Is the patient living in a house that requires stair-climbing? Personal habits such as exercise, cigarette smoking, alcohol consumption and illicit or over-the-counter drug use should be ascertained. A detailed diet history is
important, focusing especially on fluid and sodium intake. It is crucial to make an accurate list of medications the
patient is taking, either prescription or over-the-counter. Many “natural” or over-the-counter drugs interact with prescription medications, so it is important to obtain the names of all pills that the patient is taking. This also offers a good opportunity to assess the patient’s
knowledge of their medicines. The best evaluation of the patient’s medicines can be performed when the patient brings all their pill bottles with them to the appointment. Opening the bottles and looking at the pills can be very informative if pills are broken in half or if the number of pills in the bottle does not correspond accurately with the date the prescription was filled. It is very important to ask the patient about how they pay for their medications, as this may play a role in determining which medications are prescribed in the future. It is also helpful to ascertain how patients remember to take their medications—a pill box, a list, help from spouse, etc.
There are two major classes of symptoms in HF: those due to excess fluid accumulation (dyspnea, edema, hepatic congestion, and ascites) and those due to a reduction in cardiac output (fatigue and weakness). The two most
Common Presenting Symptoms
common complaints among heart failure patients are dyspnea and fatigue.
Dyspnea is one of the cardinal symptoms of heart failure, and may be described as an uncomfortable awareness of breathing that occurs at rest or at a level of physical activity where it is not expected. It is a symptom that is associated with many other diagnoses such as lung disease, cancer, anemia and anxiety. The patient’s degree of dyspnea may vary along a continuum, from dyspnea at rest to dyspnea only with extreme exertion. Patients may note that their dyspnea had a gradual onset over days or weeks, or they may have had an acute onset of shortness of breath, that occurred within minutes, from pulmonary edema. It is important to determine the level of activity required to cause the patient to become dyspneic. A patient who becomes dyspneic walking across the room is considerably worse than a patient who only becomes dyspneic when climbing stairs.
The physiologic mechanism of dyspnea is not well understood. Unless frank pulmonary edema is present, there is little correlation between pulmonary capillary wedge pressure and exertional dyspnea in HF patients. More than likely, dyspnea is related to multiple complex mechanisms involving a build-up of lactic acid in the working muscles that causes an increased ventilatory response to exercise.
Traditionally, the origin of fatigue in HF was thought to be related to poor cardiac output, but more recent information suggests that it is due to abnormalities of skeletal muscles and other comorbidities such as anemia. There are major alterations in the skeletal muscle of patients with HF, including skeletal muscle atrophy. Fatigue promotes inactivity and leads to deconditioning and further fatigue. Heart failure patients who remain physically active can decrease skeletal muscle alterations and improve exercise tolerance.
Patients with HF often have some degree of cough. They may complain of an occasional cough, which is no different than many non-HF people experience, or they may have a persistent troublesome cough. It is important to question the patient carefully about their cough, since there are many possible etiologies. If the cough is of recent onset following a period of non-compliance with sodium, worse when supine, wakes the patient from sleep or is associated with rales, the source may be due to pulmonary congestion. If the patient complains of a persistent and dry cough, it is possible that they are coughing due to the effect of an angiotensin converting
Other Symptoms of Heart Failure
Cough 2 3 2 4, 5 6 7 Fatigue Dyspnea
enzyme inhibitor (ACEI) drug. The key word is
persistent. Many patients have a dry or productive cough in the morning when they first rise from bed, but it clears up quickly and they aren’t bothered with coughing for the remainder of the day. Patients with an ACEI cough are plagued by persistent coughing, both day and night, which is disruptive and bothersome to their day-to-day living. Before discontinuing an ACE inhibitor due to cough, it is very important to make sure the patient is not coughing from some other cause such as obstructive lung disease, pulmonary congestion or a common cold.
Orthopnea refers to increased shortness of breath when the patient is supine. This occurs due to increased venous return to the heart when elevating the legs, which increases blood flow into the lungs and promotes lung stiffness. Orthopnea may be worse when the patient has volume overload. PND occurs when fluid is reabsorbed from the extravascular space of dependent extremities (usually the legs) while the patient is sleeping in a supine position. The slow expansion of blood volume increases ventricular filling pressure, leading to increased diastolic and pulmonary capillary pressure. Eventually, the patient awakens with dyspnea. Usually, sitting on the edge of the bed or standing up will relieve the patient’s symptoms as venous return is decreased by this change in position.
Patients with volume overload or right heart failure may experience early satiety or poor appetite due to passive liver congestion. Other symptoms of liver congestion include nausea, abdominal fullness or right upper quadrant pain. Patients who accumulate fluid in the abdominal area may complain of feeling bloated. Patients may suffer diarrhea due to chronic bowel edema, with concomitant poor absorption of oral medications. Rarely, patients may experience dysgeusia as a side effect of ACEI therapy. They usually describe this as “a bad taste” in their mouth when eating, which makes the food taste unpleasant and unappetizing, and they are unable to eat despite feeling hungry.
Chest pain may be associated with ischemic heart disease, but may also occur in non-ischemic HF patients in the presence of increased intravascular volume. The stretch of the ventricular myocardium due to increased preload may cause chest pain by compressing the microvasculature within the ventricles. Ischemic coronary heart disease may be worsened by neurohormonal activation if the
renin-angiotensin-aldosterone system and the sympathetic nervous system are not adequately blocked with
medication.
The purpose of a physical exam in HF patients is twofold: to determine the cause of heart failure if it is a new
diagnosis; and to assess the severity of the patient’s disease (Table 1). The physical exam begins the moment the patient is in sight. Observation of the patient’s respiratory status begins as the patient speaks. Shortness of breath or labored breathing simply after answering questions, or even before they converse, are important keys to their clinical status. Overt peripheral edema or ascites may often be seen from across the room. Discoloration of extremities or cyanosis due to circulatory abnormalities is also quite obvious.
Occasionally, a precordial lift may be noted without even touching the patient’s chest. All of these overt signs of heart disease emphasize the importance of removing the patient’s clothing from the waist up, as well as their shoes and socks.
Physical Examination and Findings
Table 1. Possible Findings in Heart Failure Patients
Vital Signs
Resting tachycardia Increased respiratory rate
Decreased strength of peripheral pulses
Orthostatic changes in pulse and blood pressur e
Neck examination
Carotid bruits
Jugular venous distention
Abdominojugular (also known as hepatojugular) reflux
Pulmonary
Rales Wheezes
Decreased breath sounds (pleural effusion)
Cardiac
Increased heart rate
Irregular rhythm (ectopic beats or atrial fibrillation) Displaced point of maximum impulse
Parasternal lift or thrill S3 extra cardiac sound
Murmurs of mitral regurgitation or tricuspid insufficiency
Abdominal Exam
Ascites
Right upper quadrant pain/tenderness to palpation Enlarged liver span > 17cm
Liver palpated below costal margin, spongy or pulsatile
Extremities
Reduced strength of arterial pulses Cyanosis Peripheral edema Muscle wasting 8 8 9 2
Orthopnea/Paroxysmal Nocturnal Dyspnea
Gastrointestinal Symptoms
Patients should be examined first while sitting up, then while lying supine with their head raised at 45 degrees (Table 2). Examination should always be performed from the patient’s right side and the practitioner should develop the habit of using the same systematic procedure for every patient.
Each patient’s exam begins by obtaining their blood pressure, heart rate and respiratory rate. Orthostatic blood pressure and pulse readings with the patient supine, sitting and standing may be helpful to determine if the patient is dehydrated or over-diuresed. Initial assessment of the patient’s vital signs may seem like a trivial item, but can lead to an inappropriate treatment plan if not carefully obtained. The blood pressure is a measure of the heart’s ability to pump and also an indicator of the degree of antihypertensive effect from an ACEI or beta blocker. The size of the inflatable bladder inside of the blood pressure cuff must be appropriate for the patient’s size in order to obtain an accurate blood pressure. Using a bladder that is too large will result in a falsely low reading, while a bladder that is too small will result in a falsely high blood pressure reading. The width of the inflatable bladder should be 40% of the circumference of the arm (12 to 14 centimeters in an average adult), and the length of the bladder should be 80% of the arm circumference, nearly long enough to encircle the arm. Since titration of ACEIs or beta blockers may depend upon the blood pressure measurement, it is critical to have a correct reading. Non-invasive blood pressure devices are often used to measure heart rate and blood pressure. It is important to note that these devices do not provide accurate
measurements when the patient has an irregular heart beat (such as premature ventricular complexes or atrial
fibrillation).
Likewise, examination of the heart rate and rhythm is important. The heart rate should be obtained through auscultation of the chest or with an electrocardiogram, since premature beats may not be palpated at the radial pulse. Regularity of the pulse can be informative. An irregularly irregular pulse may indicate atrial fibrillation, while frequent premature beats may indicate atrial or ventricular ectopic beats. A resting tachycardic pulse rate indicates that the patient is not adequately beta blocked, and may be an indicator of poor prognosis. Conversely, a bradycardic heart rate may be indicative of heart block, sinus bradycardia or may be a result of aggressive beta blockade. In some situations, bradycardia may be an indication for pacemaker insertion. Although it is rare, a strong pulse alternating with a weak pulse, known as pulsus alternans, is virtually diagnostic of severe advanced heart failure.
The HF-focused cardiac exam should be performed from the head down to the toes. The patient’s neurological status is obtained by assessing their responses to questions and their ability to recall past events in their medical history. It may be helpful to have the patient’s spouse or family member in the room to corroborate the patient’s
memory of facts while gathering the history. With the patient sitting up, the carotid pulses should be palpated one side at a time. Diminished carotid pulsations may be caused by heart failure, hypovolemia, severe aortic stenosis or atherosclerotic narrowing of the carotid artery. Bounding carotid pulses may be caused by fever, anemia, hyperthyroidism aortic regurgitation or
bradycardia. The bell of the stethoscope is used to auscultate over the carotid arteries. The patient should hold their breath while the nurse carefully listens for a low pitched flow murmur in the carotids, called a bruit, which would indicate obstruction to blood flow.
While the patient remains sitting up, the lungs should be auscultated over the anterior, posterior and lateral chest, bilaterally from the top downward, alternating listening over the right and left sides. Respiratory rate and pattern should also be noted. Tachypnea with minimal exertion, such as climbing onto the exam table, may indicate decompensated or end stage heart failure. Breath sounds should be assessed for rales, rhonchi or wheezing, which may indicate pulmonary congestion, pulmonary
infection, or chronic lung disease. The absence of rales does not exclude the possibility of pulmonary edema. Patients with chronic HF often have vigorous pulmonary interstitial lymphatic drainage, leading to the absence of rales, even though cardiac filling pressures are elevated. Decreased breath sounds may be indicative of a pleural effusion.
Table 2. Head-to-Toe Cardiac Exam of the Heart Failure Patient
Sitting up on exam table: General inspection Mental status Respiratory effort Skin color
Obvious abdominal or peripheral edema Carotid pulses/carotid bruits
Lung sounds (posterior and anterior)
Supine with exam table head at 45 degrees : Inspect jugular veins
Inspect chest
Palpate chest with finger pads and heel of han d Locate point of maximum impulse
Auscultate heart sounds Percuss and palpate abdomen Percuss and palpate liver Inspect skin color
Palpate arterial pulses bilaterally Assess for peripheral edema 10
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The patient can then be placed in a supine position for the remainder of the exam. As the patient assumes this position, the nurse should observe for any change in breathing status. Patients with volume overload may become dyspneic and/or tachypneic when reclining. If a patient’s dyspnea improves with reclining, HF is not likely the source of the patient’s symptom.
The neck is examined for jugular venous distention with the patient supine at 45 degrees. Jugular venous pressure is a reflection of right heart filling pressures and an indirect reflection of the patient’s volume status. The internal jugular vein is assessed from the patient’s right side, shining a light tangentially across the right side of the patient’s neck. With normal intracardiac filling pressures, the neck veins should not be distended. In patients with mild heart failure, the jugular vein may not be distended when the patient is at 45 degrees, but rises when compressing the patient’s abdomen. This is referred to as the abdominojugular reflux. The presence of
abdominojugular reflux is a sign that intracardiac filling pressures are elevated above normal, and the right ventricle is unable to accommodate augmented venous return. Constrictive pericarditis, right ventricular infarction, restrictive cardiomyopathy and volume overload are common causes of a positive finding. Left ventricular failure may also induce the sign, but only when the pulmonary capillary wedge pressure is greater than 15. Examination of the chest may reveal a normal,
hyperdynamic or sustained precordial pulsation. The point of maximum impulse (PMI) is normally located in the 5th intercostal space on the left anterior chest, but may be displaced laterally in the presence of cardiomegaly. The PMI should be the size of a quarter and tapping in quality when palpated with the fingertips, but in left ventricular hypertrophy or dilated cardiomyopathy, the PMI may be more forceful. The PMI is not palpable in some patients. An anterior systolic movement along the left parasternal border is known as a lift or heave, and may be felt with the finger pads. It may be caused by right ventricular pressure overload or volume overload. A thrill is a vibratory sensation that corresponds to a loud, harsh murmur. It is palpated with the heel of the hand and feels similar to the vibration of a purring cat. Each area of cardiac
auscultation (as described below) should be palpated with the finger pads and the heel of the hand to assess for a lift or thrill.
In HF, the heart sounds can reflect changes in volume status, pulmonary artery pressures, and valvular and ventricular function. Therefore, a skillful assessment of heart sounds can be a vital tool in evaluating the patient with chronic HF. A quality stethoscope, a methodical auscultory routine, and a knowledge of which chest piece of the stethoscope at what location will enable detection of common abnormal sounds in heart failure are vital to a thorough clinical evaluation. Proper patient positioning can also amplify soft heart sounds. It is also important to explain to patients that you will listen to their heart sounds
in many different places and with both chest pieces so that they do not fear that something is wrong.
The auscultory sequence should be performed in the same order every time. Adhering to a strict routine minimizes the risk of being distracted and overlooking other adventitious heart sounds after finding the first abnormal heart sound. If the nurse already has a routine, ingrained sequence that is followed for every patient exam, this should continue to be the method used. However, if just now developing a routine, the following sequence is suggested. Use the diaphragm first as it best captures the high pitched sounds of S1 and S2. At each auscultory point one should listen for S1, systole, S2, and diastole. S1-4 are often attributed to valve closure, but are actually generated by the sudden cessation of blood flow that occurs as a consequence of valve closure.
Start at the apex of the heart where S1 is most
pronounced. In the normal patient, the apex is typically at the 5th intercostal space (ICS) mid-clavicular line. However, in the patient with chronic HF, the apex can often be laterally displaced. Again listen for S1, systole, S2, and diastole. The systolic murmur most commonly auscultated at this position is mitral regurgitation (MR). A mitral regurgitation murmur is most often
characterized as holosystolic, radiates to the axilla and is augmented by placing the patient in the left lateral decubitus position.
Next, place the diaphragm of the stethoscope over the left lower sternal border at the 4th -5th ICS. This is known as the tricuspid region. Here, a pathological splitting of S1 can often be auscultated in HF when there is a right bundle branch block (BBB). Another finding in this region that is common in HF is a systolic murmur due to tricuspid regurgitation.
The base of the heart should be auscultated next, by placing the diaphragm at the pulmonic region--the 2nd ICS at the left sternal border. Here S2 will be far more prominent than S1. A paradoxical splitting of S2 may be indicative of a left BBB, right ventricular pacing, or premature ventricular complexes, all of which can be common findings in HF. Pulmonic stenosis can be auscultated here but is not a usual finding in HF. The final auscultory location with the diaphragm of the
stethoscope is the right sternal border at the 2nd ICS. This is known as the aortic region which also assesses the base of the heart. The murmur of aortic stenosis may be heard here. This murmur is not a common sign in HF; rather, it indicates probable valve pathology. Next, the chest piece should be changed to the bell and
the sequence should be reversed. The bell will allow the examiner to hear low-pitched heart sounds that occur in diastole. In particular, the bell is best for auscultating S3, S4 and diastolic murmurs due to mitral and
tricuspid stenosis. With the bell at the base in the aortic and pulmonic regions, no specific sounds related to HF
are auscultated, as the diastolic murmurs due to semilunar valve incompetence are high pitched and best heard with the diaphragm.
Moving down to the lower left sternal border with the bell of the stethoscope, the diastolic sounds of a right
ventricular S3 and S4 can be auscultated. Then, listening at the apex with the bell, a left ventricular S3 and S4 can be auscultated. An S3 is associated with decreased ventricular compliance and it can be more easily heard if the patient is placed in the left lateral decubitus position. A left ventricular S3 is heard just at the beginning of the rapid ventricular filling phase of the cardiac cycle. It has been said to sound like “Kentucky” and “lub-dub-da”, as it occurs immediately after S2. A left ventricular S3 is one of the first clinical signs of left ventricular failure, and is indicative of high left ventricular filling pressures and decreased left ventricular compliance.
The S4 occurs in the final phase of diastole, which is when the atria give one final push to fill the ventricles. Therefore, this sound occurs just prior to the S1 and is absent in atrial fibrillation.. It has been said to sound like “Tennessee”, or “da-lub-dub”. An S4 is caused by atrial systole ejecting blood into a non-compliant ventricle. It is common in hypertension, the elderly, cardiomyopathy and aortic stenosis. A right ventricular S3 and right ventricular S4 are indicative of high pulmonary artery pressures, decreased ventricular compliance and right-sided failure. Examination of the abdomen is an important element in the assessment of a HF patient to determine the presence of ascites, hepatomegaly, or a pulsatile or tender liver. An abdomen that is distended in appearance and firm to palpation may be a sign of fluid accumulation. Some patients with HF never develop peripheral edema, but rather, retain fluid only in the abdomen. Occasionally, some patients will have swelling in both the abdomen and the periphery. Overt ascites may be noted during
observation of the abdomen, however, the nurse may need to assess for a fluid wave to determine if fluid has
accumulated in the abdominal area. Percussion of the abdomen may also offer clues as to the presence of ascites. Tympanic sounds usually indicate gas in the gastrointestinal tract, but dullness on percussion may indicate the presence of fluid. Percussion of the liver is helpful to assess the vertical span of the liver. Palpation of the liver should be done slowly and carefully to determine if the liver edge is noted below the costal margin. An enlarged, spongy, tender or pulsatile liver may indicate passive liver congestion from right heart failure or acute decompensation of HF.
Peripheral pulses need to be palpated bilaterally and compared for symmetrical equality at the radial, brachial, femoral, popliteal, dorsalis pedis and posterior tibial sites. Pulses of unequal strength on both sides may be indicative of reduced arterial blood flow on the side with the weaker pulse. Each of these sites should be auscultated for bruits using the bell of the stethoscope placed lightly over the artery. If a bruit is present, it represents about 50%
obstruction of the arterial blood flow and may be significant for peripheral vascular disease. The greater the arterial obstruction to flow, the louder and higher pitched the bruit.
When checking for peripheral edema, the nurse should press a thumb firmly but gently into the extremity for at least 3 seconds. The depth of the indentation that remains after the thumb is removed is indicative of the degree of edema, which is graded on a 4-point scale. Slight edema is 1+, while very marked edema is 4+. It is important to note if the edema is unilateral or bilateral. Causes of peripheral edema include fluid volume excess, deep venous thrombosis, chronic venous insufficiency or medication effect (most notably from some calcium channel blocking agents). Some patients will note the presence of pedal edema during the day while they are upright but that the swelling is gone when they awaken after sleeping supine for several hours. The higher up the leg that edema is noted, the greater the fluid volume excess. Edema that encompasses the legs, thighs and possibly extends up to the waist is termed “anasarca”. Cachexia refers to a state of ill health, malnutrition and wasting. Cardiac cachexia is seen in some patients with end stage heart failure and portends a poor prognosis. It is defined as a weight loss of more than 7.5% within six months without dieting, without edema and without change in activity. These patients have a very reduced appetite. The exact mechanism of cardiac cachexia is not known, but it is believed to be related to cytokines that are increased in patients with severe HF. It is
challenging to perform a physical exam on cachectic patients, as their lean body mass may be masked by marked fluid retention, highlighting the chronicity of their heart failure. The nurse should be alert for subtle changes in body habitus such as the loss of upper extremity or peripheral muscle loss in these patients.
Assessment of Functional Capacity
The New York Heart Association (NYHA) classification for stratifying HF patients based on functional ability is a system that has withstood the test of time. Although this system is subjective in measurement, it continues to be widely applied to HF patients in the ongoing review of clinical status and it serves as a helpful reference to the patient’s baseline compensated state when initiating interventions such as medication titration. Other
classification systems have been developed, but none are as widely applied in HF patients as the NYHA. In NYHA class I, patients have no perceived HF symptoms or limitations to activity. In NYHA class II, patients experience symptoms such as dyspnea and fatigue, but only with moderate exertion. NYHA class III patients have no resting symptoms, but develop symptoms easily with minimal exertion, such as activities of daily living. Many HF providers divide this class into IIIA and IIIB, reflecting early versus late symptom manifestation within
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the stage. Class IV patients experience HF symptoms at rest and have a significantly worse prognosis than HF patients in NYHA classes I and II. Typical activities of normal age and gender-matched non-HF individuals should be used as a reference for determining a HF patient’s NYHA classification. Interestingly, NYHA symptom class does not correspond to left ventricular ejection fraction.
Diagnostic Testing
The goals of diagnostic testing beyond the physical exam
are to 1) establish the diagnosis of HF, 2) identify the underlying pathology (systolic versus diastolic heart failure) and 3) identify abnormalities amenable to
treatment. Routine blood tests may help to establish other conditions such as severe anemia, renal dysfunction, thyroid disorders, liver disease and hemochromatosis that either mimic HF, contribute to the development of HF or worsen HF. Whether the HF is of new onset or a chronic condition, a battery of routine lab tests are helpful in making a diagnosis and planning therapeutic strategies (Table 3). Minimum lab testing should include complete Table 3. Diagnostic Tests in Heart Failure
TEST FINDING SUSPECTED DIAGNOSIS
Electrocardiogram Acute ST-T wave changes
Atrial fibrillation; other tachyarrhythmia
Bradyarrhythmia
Previous myocardial infarct (ie Q waves) Low voltage
LV hypertrophy
Myocardial ischemia
Thyroid disease or heart failure due to rapid ventricular rate
Heart failure due to low rate or medication effect Heart failure due to reduced LV performance Pericardial effusion
Cardiomegaly Chest x-ray Cardiomegaly
Increased pulmonary venous congestion (interstitial, alveolar edema)
Pleural effusion
Dilated cardiomyopathy
RV failure & pulmonary edema (LV failure) Fluid volume overload
CBC Anemia Heart failure due to or aggravated by decreased oxygen-carrying capacity
Urinalysis Proteinuria
Red blood cells or cellular casts
Nephrotic syndrome Glomerular nephritis Serum BUN &
creatinine Elevated Volume overload due to renal failure Electrolytes Low sodium (<135 mEq/L)
Low potassium
Activated renin-angiotensin system Increased risk of arrhythmia
Liver function Altered liver enzymes May indicate passive liver congestion or medication effects (statin, amiodarone) Serum albumin Decreased Increased extravascular volume due to
hypoalbuminemia
Lipids Elevated Promote atherosclerosis
T4 & TSH Abnormal T4 or TSH Heart failure due to or aggravated by hypo/hyperthyroidism
Serum iron, ferritin Decreased Hemochromatosis
BNP Elevated in HF May help differentiate HF from pulmonary causes of symptoms
Doppler echo Normal ejection fraction Decreased ejection fraction Abnormal wall motion Abnormal valve function
Possibly diastolic failure Systolic heart failure Possible ischemia/infarct Mechanical cause of heart failure Cardiac catheterization
or thallium scan Coronary occlusion or myocardial ischemia Coronary artery disease Key: LV= left ventricular; RV=right ventricular; BUN= blood urea nitrogen; BNP=B-type natriuretic peptide
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blood count, complete metabolic profile, magnesium, liver function tests, thyroid panel, B-type natriuretic peptide (BNP) and a urinalysis. Additionally, a drug screen may be necessary if illicit drug use is suspected, and arterial blood gas measurement may be assessed if pulmonary embolism or CO2 retention is a concern. A chest x-ray (CXR) establishes a baseline if the patient’s status changes and may be helpful to assess cardiac size and shape, pulmonary vascularity and congestion, or pleural effusion. It is important to remember that many patients with acute decompensated HF present with normal CXR findings. An electrocardiogram may reveal atrial fibrillation or other arrhythmias, conduction abnormalities, ventricular hypertrophy or previous myocardial infarction. It is important to note the QRS duration for future consideration of cardiac
resynchronization therapy. The measurement of QRS voltage is also important because it is reduced with loss of functional myocardium.
Echocardiography is the standard tool for determining the presence of HF. It provides assessment of the size, shape and systolic and diastolic function of both ventricles, as well as the extent of hypertrophy. The degree of pulmonary hypertension, presence of shunt lesions and abnormal diastolic filling patterns can be determined by using Doppler techniques. Valve stenosis, insufficiency and function can be assessed. Also, the presence of pericardial effusion is best detected by echocardiogram. Heart failure is caused by coronary artery disease in about
two-thirds of patients with systolic dysfunction. Most patients with HF should undergo diagnostic coronary angiography to determine the presence or absence of coronary artery disease, especially those patients in whom revascularization is an option. Coronary disease is not always readily established through the patient’s history, physical exam, labs and echocardiogram. If the patient has angina and HF, they should undergo catheterization, particularly if there is a chance that ventricular
dysfunction could be reversed by restoring coronary blood flow.
Assessment of myocardial viability may be performed in patients with HF of ischemic origin to determine if they have a sizeable amount of viable myocardium and coronary vessels amenable to percutaneous coronary intervention or bypass surgery. Risks and benefits of revascularization procedures can then be determined. The presence of viable myocardium may be evaluated with dobutamine stress echocardiography, single photon emission computed tomography (SPECT) using thallium or technetium sestamibi, positron emission tomography or magnetic resonance imaging. Which of these tests is used depends largely on the evaluating physician’s experience and expertise.
Other possible diagnostic tests that may be performed include right heart catheterization to evaluate filling pressures, endomyocardial biopsy to evaluate for the
presence of a viral myocarditis, and cardiopulmonary stress testing for risk stratification and to rule out other causes of symptoms.
Assessment data obtained from the patient’s history, physical exam and diagnostic tests are used to formulate a diagnosis, establish goals for patient care, and evaluate outcomes of therapy. The patient’s history reveals information that may lead to a diagnosis, while the physical exam and diagnostic tests add objective
information. Over the course of multiple visits, the nurse may better understand the patient’s response to HF and their manifestation of the disease, and can tailor the patient’s therapy to meet their needs. By using careful assessment skills and paying attention to details, the nurse may optimize the HF patient’s care and improve
outcomes. References
1. Paul S. History taking for the cardiovascular patient. In: Davis L, ed. Cardiovascular Nursing Secrets. St. Louis: Elsevier Mosby; 2004:3-10.
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