• Home
  • Write for Us
  • Hire Us
  • Ask Us
  • Contact Us
  • Help Us
  • Advertise

Our Recent Posts

Monday, October 2, 2017

Heart Failure: Clinical Features (Symptoms & Signs) of Heart Failure

Today at The Health and Disease Blog we will discuss about the clinical features (symptoms and signs including physical examination findings) of heart failure. In our previous article regarding heart failure we discussed about the definition, causes, prognosis, epidemiology and the New York Heart Association Classification of Heart Failure.

Clinical Features (Symptoms & Signs) of Heart Failure

    The New York Heart Association (NYHA) classification of heart failure can be used to describe the symptoms of heart failure and limitation of exercise capacity, and is useful for assessing response to therapy. It does not include left ventricular ejection fraction as a means of determining severity of heart failure.

    Clinical features of heart failure |
    Symptoms Signs on physical examination
    • Exertional dyspnea
    • Orthopnea
    • Paroxysmal nocturnal dyspnea
    • Fatigue
    • Tachycardia
    • Elevated jugular venous pressure
    • Cardiomegaly
    • Third and fourth heart sounds
    • Bi-basal crackles (also called rales or crepitations)
    • Pleural effusion
    • Peripheral ankle edema
    • Ascites
    • Tender hepatomegaly

    Clinical Features of Heart Failure
    Clinical Features of Heart Failure

    Symptoms of Heart Failure 

    The cardinal symptoms of heart failure are fatigue and shortness of breath. Although fatigue traditionally has been ascribed to the low cardiac output in heart failure, it is likely that skeletal-muscle abnormalities and other noncardiac comorbidities (e.g., anemia) also contribute to this symptom.

    Exertional Dyspnoea 

    Exertional Dyspnea is a Symptom of Heart Failure
    Exertional Dyspnea is a Symptom of Heart Failure

    Exercise causes a sharp increase in left atrial pressure and this contributes to the pathogenesis of dyspnoea by causing pulmonary congestion with accumulation of interstitial or intra-alveolar fluid, which activates juxtacapillary J receptors, which in turn stimulate the rapid, shallow breathing characteristic of cardiac dyspnea.

    Other factors that contribute to dyspnea on exertion include reductions in pulmonary compliance, increased airway resistance, respiratory muscle and/or diaphragm fatigue, exertional acidosis and anemia. Dyspnea may become less frequent with the onset of right ventricular (RV) failure and tricuspid regurgitation.

    In the early stages of heart failure, dyspnea is observed only during exertion. However, as the disease progresses, dyspnea occurs with less strenuous activity, and it ultimately may occur even at rest. The origin of dyspnea in heart failure is probably multifactorial.


    Exertional Fatigue Is an Important Symptom of Heart Failure
    Exertional Fatigue Is an Important Symptom of Heart Failure

    Exertional fatigue is an important symptom of heart failure and is particularly troublesome towards the end of the day. It is caused partly by deconditioning and muscular atrophy but also by inadequate oxygen delivery to exercising muscle, reflecting impaired cardiac output.


    Orthopnea, which is defined as dyspnea occurring in the recumbent position, is usually a later manifestation of heart failure than is exertional dyspnea. It basically means shortness of breath that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair.

    It results from redistribution of fluid from the splanchnic circulation and lower extremities into the central circulation during recumbency, with a resultant increase in pulmonary capillary pressure.

    Nocturnal cough is a common manifestation of this process and a frequently overlooked symptom of heart failure.

    Orthopnea generally is relieved by sitting upright or sleeping with additional pillows (propped up position). Although orthopnea is a relatively specific symptom of heart failure, it may occur in patients with abdominal obesity or ascites and patients with pulmonary disease whose lung mechanics favor an upright posture.

    Paroxysmal Nocturnal Dyspnea

    Paroxysmal Nocturnal Dyspnea : Features and Mechanism
    Paroxysmal Nocturnal Dyspnea : Features and Mechanism

    This term refers to acute episodes of severe shortness of breath and coughing and fear of imminent death that generally occur at night and awaken the patient from sleep, usually 1–3 h after the patient retires.

    Paroxysmal nocturnal dyspnea may manifest as coughing or wheezing, possibly because of increased pressure in the bronchial arteries leading to airway compression, along with frank pulmonary edema on lying flat that leads to increased airway resistance. Whereas orthopnea may be relieved by sitting upright at the side of the bed with the legs in a dependent position, patients with paroxysmal nocturnal dyspnea often have persistent coughing and wheezing even after they have assumed the upright position. The symptoms my be corrected by standing upright, which allows gravitational pooling of blood to lower the left atrial and pulmonary capillary pressure. The patient often feels the need to obtain air at an open window.

    Cardiac asthma is closely related to paroxysmal nocturnal dyspnea, is characterized by wheezing secondary to bronchospasm, and must be differentiated from primary asthma and pulmonary causes of wheezing.

    Cheyne-Stokes respiration

    Hyperventilation with alternating episodes of apnea occurs in severe heart failure. This is also referred to as periodic respiration or cyclic respiration. Cheyne-Stokes respiration is present in 40% of patients with advanced heart failure and usually is associated with low cardiac output.

    Cheyne-Stokes respiration is caused by an increased sensitivity of the respiratory center to arterial carbon dioxide (PCO2).

    There is an apneic phase, during which arterial PO2 falls and arterial PCO2 rises. These changes in the arterial blood gas content stimulate the respiratory center, resulting in hyperventilation and hypocapnia, followed by recurrence of apnea. Cheyne-Stokes respirations may be perceived by the patient or the patient’s family as severe dyspnea or as a transient cessation of breathing.

    The condition can also occur in diffuse cerebral atherosclerosis, stroke or head injury, and may be exaggerated by sleep, barbiturates and opiates.

    Other Symptoms

    Patients with heart failure also may present with gastrointestinal symptoms.

    Anorexia, nausea, and early satiety associated with abdominal pain and fullness are common complaints and may be related to edema of the bowel wall and/or a congested liver.

    Congestion of the liver and stretching of its capsule may lead to right upper-quadrant pain.

    Cerebral symptoms such as confusion, disorientation, and sleep and mood disturbances may be observed in patients with severe heart failure, particularly elderly patients with cerebral arteriosclerosis and reduced cerebral perfusion.

    Nocturia is common in heart failure and may contribute to insomnia.

    Physical Examination (Signs) in Heart Failure

    A careful physical examination is always needed in the evaluation of patients with heart failure. The purpose of the examination is to help determine the cause of heart failure as well as to assess the severity of the syndrome.

    General Appearance and Vital Signs

    In mild or moderately severe heart failure, the patient appears to be in no distress at rest except for feeling uncomfortable when lying flat for more than a few minutes.

    In more severe heart failure, the patient must sit upright, may have labored breathing, and may not be able to finish a sentence because of shortness of breath.

    Systolic blood pressure may be normal or high in early heart failure, but it generally is reduced in advanced heart failure because of severe LV dysfunction. The pulse pressure may be diminished, reflecting a reduction in stroke volume.

    Sinus tachycardia is a nonspecific sign caused by increased adrenergic activity. Reduced cardiac output causes reflex peripheral vasoconstriction leading to cool peripheral extremities and cyanosis (blue discoloration of the skin and mucous membranes caused by increased concentration of reduced hemoglobin in the superficial blood vessels) of the lips and nail beds is also caused by excessive adrenergic activity.

    Anemia if present may exacerbate angina and heart failure.

    Jugular Veins

    Fluctuations in right atrial pressure during the cardiac cycle generate a pulse that is transmitted backwards into the jugular veins. Examination of the jugular veins provides an estimation of right atrial pressure.

    The jugular venous pressure is best examined in good light with the patient lying recumbent, with the head tilted at 45°. The jugular venous pressure should be quantified in centimeters of water (normal ≤8 cm) by estimating the height of the venous column of blood above the sternal angle in centimeters and then adding 5 cm.

    In the early stages of heart failure, the venous pressure may be normal at rest but may become abnormally elevated with sustained (~15 seconds) pressure on the upper right side of the abdomen (positive abdominojugular reflux). Giant v waves indicate the presence of tricuspid regurgitation.

    What are the causes of elevated jugular venous pressure

    • Congestive heart failure 
    • Cor pulmonale 
    • Pulmonary embolism 
    • Right ventricular infarction 
    • Tricuspid valve disease 
    • Tamponade 
    • Constrictive pericarditis 
    • Hypertrophic/restrictive cardiomyopathy 
    • Superior vena cava obstruction 
    • Iatrogenic fluid overload, particularly in surgical and renal patients

    Pulmonary Examination

    Pulmonary crackles (rales or crepitations) result from the transudation of fluid from the intravascular space into the alveoli.

    Crackles heard in the lungs of a person with heart failure

    In patients with pulmonary edema, rales may be heard widely over both lung fields and may be accompanied by expiratory wheezing (cardiac asthma).

    When present in patients without concomitant lung disease, rales are specific for heart failure.

    Importantly, rales are frequently absent in patients with chronic heart failure, even when LV filling pressures are elevated, because of increased lymphatic drainage of alveolar fluid.

    Pleural effusions result from the elevation of pleural capillary pressure and the resulting transudation of fluid into the pleural cavities. Since the pleural veins drain into both the systemic and the pulmonary veins, pleural effusions occur most commonly with biventricular failure. Although pleural effusions are often bilateral in heart failure, when they are unilateral, they occur more frequently in the right pleural space.

    Causes of Crackles |
    Phase of inspiration Cause
    Early Small airways disease, as in bronchiolitis
    Middle Pulmonary edema
    Late Pulmonary fibrosis (fine crepitations)
    Pulmonary oedema (medium crepitations)
    Bronchial secretions in COPD, pneumonia, lung abscess, tubercular lung cavities (coarse crepitations)
    Biphasic Bronchiectasis (coarse crepitations)

    Cardiac Examination

    Examination of the heart, although essential, frequently does not provide useful information about the severity of heart failure.

    Palpation of the Heart
    Palpation of the Heart

    If cardiomegaly is present, the point of maximal cardiac impulse, commonly called the apex beat, is usually displaced below the fifth intercostal space and/or lateral to the midclavicular line, and the impulse is palpable over two interspaces. Severe left ventricular hypertrophy leads to a sustained apex beat.

    Patients with enlarged or hypertrophied right ventricles may have a sustained and prolonged left parasternal impulse extending throughout systole.

    Auscultation of the heart in heart failure

    In some patients, a third heart sound (S3 or protodiastolic gallop) is audible and palpable at the apex. A third heart sound is most commonly present in patients with volume overload who have tachycardia and achypnea, and it often signifies severe hemodynamic compromise. In an adult with acute breathlessness a third heart sound is highly suggestive of heart failure with depressed left ventricular ejection fraction.

    The Third Heart Sound
    Third heart sound (S3) is a low-pitched early diastolic sound best heard with the bell at the apex. It coincides with rapid ventricular filling immediately after opening of the atrioventricular valves and is therefore heard after the second as ‘lub-dub-dum’. It is a normal finding in children, young adults and during pregnancy.

    Third heart sound is usually pathological after the age of 40 years. The most common causes are left ventricular failure, when it is an early sign, and mitral regurgitation, due to volume loading of the ventricle. In heart failure third heart sound occurs with a tachycardia, referred to as a ‘gallop’ rhythm, and first and second heart sounds are quiet (lub-da-dub).

    Causes of a Third Heart Sound |
    Physiological Pathological

    • Healthy young adults
    • Athletes
    • Pregnancy
    • Fever

    • Large, poorly contracting left ventricle
    • Mitral regurgitation

    A fourth heart sound (S4) is not a specific indicator of heart failure but is usually present in patients with diastolic dysfunction.

    The Fourth Heart Sound
    This is less common. It is soft and low-pitched, best heard with the stethoscope bell at the apex. It occurs just before the first heart sound (da-lub-dub).

    The fourth heart sound is always pathological and is caused by forceful atrial contraction against a non-compliant or stiff ventricle. It is most often heard with left ventricular hypertrophy (due to hypertension, aortic stenosis or hypertrophic cardiomyopathy). It cannot occur when there is atrial fibrillation.

    Both the third and fourth heart sound cause a ‘triple’ or ‘gallop’ rhythm

    The murmurs of mitral and tricuspid regurgitation are frequently present in patients with advanced heart failure.

    Abdomen and Extremities

    Hepatomegaly is an important sign in patients with heart failure. When it is present, the enlarged liver is frequently tender and may pulsate during systole if tricuspid regurgitation is present.

    Palpation of the Liver
    Palpation of the Liver

    Ascites, a late sign, occurs because of increased pressure in the hepatic veins and the veins draining the peritoneum.

    Ascites is a late sign in Heart Failure
    Ascites is a late sign in Heart Failure

    Jaundice, also a late finding in heart failure, results from impairment of hepatic function secondary to hepatic congestion and hepatocellular hypoxemia and is associated with elevations of both direct and indirect bilirubin.

    Yellow Sclera of Jaundice
    Yellow Sclera of Jaundice

    Peripheral subcutaneous edema is a cardinal manifestation of heart failure, but it is nonspecific and usually is absent in patients who have been treated adequately with diuretics. Peripheral edema is usually symmetric and dependent in heart failure and occurs predominantly in the ankles and the pretibial region in ambulatory patients. In bedridden patients, edema may be found in the sacral area (presacral edema) and the scrotum. Long-standing edema may be associated with indurated and pigmented skin.

    Edema in heart failure

    Excess fluid in the interstitial space causes edema (tissue swelling). The edema is peripheral and pitting in nature. It is usually gravity-dependent and so especially seen around the ankles, or over the sacrum in patients lying in bed. Pressure should be applied over a bony prominence (tibia, lateral malleoli of ankle, sacrum) to provide effective compression to see if pitting occurs. In general, if the jugular venous pressure is not elevated, then edema is not cardiogenic.

    Pitting Edema in Heart Failure
    Pitting Edema in Heart Failure

    Edema is caused by salt and water retention by the kidney. Two mechanisms are responsible:
    1. Reduced sodium delivery to the nephron. This is caused by reduced glomerular filtration due to constriction of the preglomerular arterioles in response to sympathetic activation and angiotensin II production. 
    2. Increased sodium reabsorption from the nephron. This is the more important mechanism. It occurs particularly in the proximal tubule early in heart failure but, as failure worsens, renin-angiotensin activation stimulates aldosterone release, which increases sodium reabsorption in the distal nephron.
    Salt and water retention expands plasma volume and increases the capillary hydrostatic pressure. Hydrostatic forces driving fluid out of the capillary exceed the osmotic forces reabsorbing it, so that edema fluid accumulates in the interstitial space. The effect of gravity on capillary hydrostatic pressure ensures that edema is most prominent around the ankles in the ambulant patient and over the sacrum and thighs in the bedridden patient. In advanced heart failure, edema may involve the legs, genitalia and trunk. Transudation into the peritoneal cavity (ascites), the pleural and pericardial spaces may also occur.

    Heart failure is not only cause of edema.

    What are the causes of peripheral edema?

    • Cardiac failure: right or combined left and right heart failure, pericardial constriction, cardiomyopathy
    • Chronic venous insufficiency: varicose veins
    • Hypoalbuminaemia: nephrotic syndrome, liver disease, protein-losing enteropathy; often widespread, can affect arms and face
    • Drugs:
      • Sodium retention: fludrocortisone, NSAIDs
      • Increasing capillary permeability: nifedipine, amlodipine
    • Idiopathic: women > men
    • Chronic lymphatic obstruction

    Cardiac Cachexia

    With severe chronic heart failure, there may be marked weight loss and cachexia. When present in heart failure, cachexia augurs a poor overall prognosis.

    Although the mechanism of cachexia is not entirely understood, it is probably multifactorial and includes:
    • Elevation of the resting metabolic rate
    • Anorexia, nausea, and vomiting due to congestive hepatomegaly and abdominal fullness
    • Elevation of circulating concentrations of cytokines such as TNF
    • Impairment of intestinal absorption due to congestion of the intestinal veins
    • Skeletal muscle atrophy due to immobility 

    Clinical Syndromes of Acute Heart Failure

    Clinical Syndromes of Acute Heart Failure |
    Type Clinical Features
    Acute decompensated heart failure Mild features of heart failure, e.g. dyspnoea
    Hypertensive acute heart failure High blood pressure, preserved left ventricular function, pulmonary edema on chest X-ray
    Acute pulmonary edema Tachypnea, orthopnea, pulmonary crackles, oxygen saturation <90% on air, pulmonary edema on chest X-ray
    Cardiogenic shock Systolic blood pressure <90mmHg, mean arterial pressure drop >30mmHg, urine output <0.5 mUkg per hour, heart rate >60b.p.m.
    High-output heart failure Warm peripheries, pulmonary congestion, blood pressure may be low, e.g. septic shock
    Right heart failure Low cardiac output, elevated jugular venous pressure, hepatomegaly, hypotension

    That's all for today!
    If you liked this article and found it helpful then please share it with your friends and family and please consider becoming our Patron or buying us a coffee through PayPal. Your support enables us to continue blogging and help people. Also make sure your subscribe to our Newsletter so that you don't miss out on our future posts! Thanks!

    No comments:

    Post a Comment

    Your comments are valuable to us. Please share your thoughts with us.

    Related Posts Plugin for WordPress, Blogger...