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TEXTBOOK PRESENTATION

Typically, patients with HF complain of shortness of breath, dyspnea on exertion, fatigue, and orthopnea. (See Chapter 15, Dyspnea for a complete discussion of HF.)

DISEASE HIGHLIGHTS

  1. Hyponatremia is observed in patients with severe HF and is associated with an increased risk of death.

  2. Patients with HF and hyponatremia have marked increases in total body sodium causing volume overload and edema.

  3. In addition, free water clearance is also impaired. Water retention exceeds sodium retention, causing the hyponatremia.

    1. Free water clearance is impaired in large part secondary to elevated ADH levels. This develops when the low cardiac output triggers carotid baroreceptors that stimulate ADH release increasing water reabsorption in the collecting tubules and thereby hyponatremia.

    2. Other factors that contribute to the hyponatremia include a decrease in the GFR (due to decreased renal perfusion) and an increase in proximal sodium reabsorption. (In order to excrete free water, sodium must be delivered more distally, where it can be pumped out of the impermeable parts of the tubule, leaving solute free water behind which can be excreted.)

    3. If used, thiazides diuretics (but not usually loop diuretics) can worsen the hyponatremia.

EVIDENCE-BASED DIAGNOSIS

See HF discussion in Chapter 15, Dyspnea.

TREATMENT

  1. Treatment of underlying HF

    1. Similar to other patients with HF (see Chapter 15, Dyspnea).

    2. Angiotensin-converting enzyme (ACE) inhibitors

      1. Can help restore sodium levels to normal. ACE inhibitors (and angiotensin receptor blockers) improve cardiac output, decrease ADH secretion, and facilitate free water excretion. ACE inhibitors also directly antagonize the effect of ADH on the collecting tubules.

      2. Hyponatremic HF patients usually have activation of the renin angiotensin system and are susceptible to ACE inhibitor–induced hypotension. Therefore, therapy with ACE inhibitors should be initiated at low doses.

    3. Loop diuretics can treat both the hypervolemia and hyponatremia.

    4. Avoid NSAID use, which can decrease prostaglandin-dependent renal blood flow and worsen kidney function.

  2. Treatment of hyponatremia

    1. Patients with severe symptomatic hyponatremia (comas, seizures) should receive 3% normal saline (see Table 24-2). Furosemide should be given concurrently to prevent volume overload.

    2. Loop diuretics as above

    3. Asymptomatic or mildly symptomatic patients

      1. Restrict water intake < 1000 mL/day and add furosemide to volume overloaded patients to facilitate natriuresis and augment free water loss.

      2. ADH receptor antagonists (vaptans) may be an option if free water restriction and furosemide are inadequate (Table 24-6). However, hospitalization and careful monitoring are required to ensure that the correction of serum sodium is not too rapid. Therapy should be limited to < 30 days and avoided in patients with liver disease.

      3. The rate of rise of serum sodium should be carefully monitored. Recent recommendations guide the goal and maximal rate of rise for the serum sodium (Table 24-2). Correction that exceeds these limits should be countered with therapy to reduce the serum sodium (Table 24-3).

      4. Discontinue thiazide diuretics.

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