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Chapter 30 Coordinating Care for Patients With Cardiac Disorders
blood flow to the kidneys. The kidneys interpret this as decreased volume and release an enzyme, renin. Renin converts angiotensinogen, an inactive peptide released by the liver, to angiotensin I. Angiotensin I is enzymatically converted to angiotensin II by angiotensin-converting enzyme released by the lungs. Angiotensin II produces peripheral vasoconstriction, which helps increase blood pressure and venous return to the heart. Angiotensin II also stimulates the release of aldosterone from the adre- nal cortex, which results in sodium and water retention. As with the sympathetic nervous system, these changes are effective in the short term, but in the long term, they overtax an already weak heart with increased volume and workload. Another neurohormonal compensatory response is the release of natriuretic peptides. Brain natriuretic peptide, or B-type natriuretic peptide (BNP), is a hormone pro- duced by the ventricular cardiac muscle. It is released in reaction to “overstretching” of the ventricle in response to increased pressure and volume. The result is a natural diuresis as well as arterial and venous dilation. This action decreases both preload and afterload, which decreases the workload on the heart. Heart failure is classified based on ejection fraction (EF), which is the percentage of blood that is ejected from the ventricle with each contraction. Normal values range from 55% to 70% of the total volume. Patients with low EF are diagnosed with heart failure with reduced ejection fraction (HFrEF). Patients with HFrEF have a weakened contraction, with an EF of 40% or less. Those patients with clinical manifestations of heart failure but an EF of greater than 50% are diagnosed with heart failure with preserved ejection fraction (HFpEF). HFpEF is characterized by the inability of the ventricles to fill. These patients tend to be older and female. Traditionally, HF treatment focused on HFrEF, but there is a growing body of evidence to support HFpEF treatment. It is esti- mated that about half of HF patients have HFpEF, and half have HFrEF. Heart failure is also described according to anatomical dysfunction, disease progression, and severity of symp- toms. Heart failure can affect one or both sides of the heart. When both sides of the heart are affected, this is known as biventricular failure . Left-sided HF refers to the dysfunction of the left ventricle. Right-sided HF refers to the inability of the right side of the heart to effectively pump blood to the pulmonary vasculature. Clinical Manifestations Clinical manifestations of HF vary depending on the type, onset, and severity of the failure. The timing of onset and severity of symptoms can be used to determine if HF is acute or chronic. Acute HF has a sudden onset of symp- toms and requires immediate intervention. Chronic HF describes the baseline set of symptoms and limitations that are relatively stable with treatment and self-management.
Clinical congestion is an important sign of HF to recog- nize. Findings of congestion include orthopnea, bendopnea, edema, and jugular vein distention. Other common signs include fatigue, weight gain, faster heart rates, and hypoten- sion or hypertension. Heart murmurs may be present if the cause of HF is valve dysfunction. When auscultating heart tones, a third heart sound, S3, may be a warning sign of worsening HF. An S4 is common in chronic HF. The point of maximal intensity may be enlarged or displaced when ventricles enlarge. The clinical presentation of HF can depend on the side of the heart most affected (Table 30.5). In left-sided HF, the weakened contraction results in poor peripheral perfusion and backflow of blood that causes fluid accumulation in the lungs. This produces classic symptoms such as SOB (dyspnea), orthopnea, bendopnea (increased ventricular filling pressure when bending forward), fatigue, and crackles heard on aus- cultation. Other symptoms of left-sided failure include fatigue, poor color, delayed capillary refill, weak pulses, and cool temperature in the extremities. The weakened contraction of the right ventricle, right-sided HF, results in a backflow of blood into the right atrium and venous circulation and is characterized by JVD, generalized dependent edema, hepatomegaly, and ascites. Left-sided HF can eventually cause right-sided HF, or the entire heart may be initially affected. If that happens, the symp- tom classification becomes less clear. In severe HF exac- erbations, the patient may present with hypotension, cool extremities, decreased or no urine output, and poor or decreasing mentation. In such cases, both S3 and S4 may be heard. There are several classifications of HF. The AHA and American College of Cardiology (ACC) classify the stages of HF development from A through D. The New York Heart Association (NYHA) classifies functional status as I through IV according to the clinical manifes- tations of HF (Table 30.6). It is important to note that a patient can fluctuate between NYHA classes I and IV with interventions such as diuresis; however, patients do not regress back to a previous stage in the AHA/ACC classification.
Table 30.5 Clinical Manifestations of Right- and Left-Sided Heart Failure
Right-Sided Heart Failure z Jugular vein distention z Dependent edema z Hepatomegaly z Ascites
Left-Sided Heart Failure
z Shortness of breath or dyspnea or orthopnea z Crackles on auscultation z Pale color, weak pulses, cool tempera- ture in extremities, delayed capillary refill z Fatigue, weakness
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