Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the CNS is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. Cardiac cach-exia can be defined as a nonedematous weight loss greater than 6% of the previous normal weight over a period of at least 6 months. HF prognosis worsens considerably once cardiac cachexia has been diagnosed, regardless of HF severity. This results from several factors including loss of appetite, malabsorption due to GI edema, elevated metabolic rate, and elevated levels of norepinephrine and pro-inflammatory cytokines.
Absorption of fats is especially affected, leading to deficiencies of fat soluble vitamins.
Patients can experience a variety of symptoms related to buildup of fluid in the lungs. Dyspnea, or shortness of breath (SOB), can result from pulmonary congestion or systemic hypoperfusion due to LVF. Exertional dyspnea occurs when patients describe breathlessness induced by physical activity or a lower level of activity than previously known to cause breathlessness. Patients often state that activities such as stair climbing, carrying groceries, or walking a particular distance cause SOB. Severity of HF is inversely proportional to the amount of activity required to produce dyspnea. In severe HF, dyspnea will be present even at rest.
Orthopnea is dyspnea that is positional. Orthopnea is present if a patient is unable to breathe while lying flat on a bed (i.e., in the recumbent position). It manifests within minutes of a patient lying down and is relieved immediately when the patient sits upright. Patients can relieve orthopnea by elevating their head and shoulders with pillows. The practitioner should inquire as to the number of pillows needed to prevent dyspnea as a marker of worsening HF. PND occurs when patients awaken suddenly with a feeling of breathlessness and suffocation. PND is caused by increased venous return and mobilization of interstitial fluid from the extremities leading to alveolar edema, and usually occurs within 1 to 4 hours of sleep. In contrast to orthopnea, PND is not relieved immediately by sitting upright and often takes up to 30 minutes for symptoms to subside.
Pulmonary congestion may also cause a nonproductive cough that occurs at night or with exertion. Cheyne-Stokes respiration, or periodic breathing, is also common in advanced HF. It is usually associated with low-output states and may be perceived by the patient as either severe dyspnea or transient cessation of breathing. In cases of pulmonary edema, the most severe form of pulmonary congestion, patients may produce a pink, frothy sputum and experience extreme breathlessness and anxiety due to feelings of suffocation and drowning. If not treated aggressively, patients can become cyanotic and acidotic. Severe pulmonary edema can progress to respiratory failure, necessitating mechanical ventilation.
Systemic venous congestion results mainly from RVF. A clinically validated assessment of the jugular venous pressure (JVP) is performed by examining the right internal jugular vein for distention or elevation of the pulsation while reclining at a 45-degree angle. A JVP of more than 4 cm above the sternal angle is indicative of elevated right atrial pressure. JVP may be normal at rest, but if application of pres sure to the abdomen can elicit a sustained elevation of JVP, this is defined as hepatojugular reflux (HJR). A positive finding of HJR indicates hepatic congestion and results from displacement of volume from the abdomen into the jugular vein because the right atrium is unable to accept this additional blood. Hepatic congestion can cause abnormalities in liver function, which can be evident in liver function tests and/or clotting times. Development of hepatomegaly occurs infrequently and is caused by long-term systemic venous congestion. Intestinal or abdominal congestion can also be present, but usually doesn't lead to characteristic signs unless overt ascites is evident. In advanced RVF, evidence of pulmonary hypertension may be present (e.g., right ventricular heave).
The most recognized finding of systemic congestion is peripheral edema. It usually occurs in dependent areas of the body, such as the ankles (pedal edema) for ambulatory patients, or the sacral region for bedridden patients. Weight gain often precedes signs of overt peripheral edema. Therefore, it is crucial for patients to weigh themselves daily even in the absence of symptoms to assess fluid status.
Patients may complain of swelling of their feet and ankles, which can extend up to their calves or thighs. Abdominal congestion may cause a bloated feeling, abdominal pain, early satiety, nausea, anorexia, and constipation. Often patients may have difficulty fitting into their shoes or pants due to edema.
A thorough history is crucial to identify cardiac and noncardiac disorders or behaviors that may lead to or accelerate the development of HF. Past medical history, family history, and social history are important for identifying comorbid illnesses that are risk factors for the development of HF or underlying etiologic factors. A complete medication history (including prescription and nonprescription drugs, herbal therapy, and vitamin supplements) should be obtained each time a patient is seen to evaluate adherence, to assess appropriateness of therapy, to eliminate drugs that may be harmful in HF (Table 6-4), and to determine additional monitoring requirements. For newly diagnosed HF, previous use of chemotherapeutic agents as well as current or past use of alcohol and illicit drugs should be assessed. In addition, for patients with a known history of HF, questions related to symptomatology and exercise tolerance are essential for assessing any changes in clinical status that may warrant further evaluation or adjustment of the medication regimen.
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