Chapter 158 Congestive Heart Failure
Chronic CHF is most often due to the long-term effects of high blood pressure, previous myocardial infarction, disorder of a heart valve, cardiomyopathy, or chronic lung disease. These conditions produce CHF by affecting one or more of the primary determinants of myocardial contractile function. (Precipitating or exacerbating factors in CHF are presented in Box 158-1.)
One of the most serious consequences of reduced cardiac output is a reduction in renal blood flow and glomerular filtration rate, which in turn lead to sodium and fluid retention. Adding more stress is activation of the renin-angiotensin-aldosterone system, leading to an increase in peripheral vascular resistance; increased ventricular afterload, and increased levels of circulating vasopressin, which also serves as a vasoconstrictor and antidiuretic.
In an attempt to compensate for the reduced cardiac output, several compensatory mechanisms occur: tachycardia, increased activation of the sympathetic nervous system, ventricular dilation, and hypertrophy. These mechanisms are a bit of a mixed blessing. For example, while the increase in sympathetic activity increases cardiac output by increasing heart rate and force of contraction, it also leads to increased vascular resistance.
The signs and symptoms of CHF depend on which ventricle has failed. The clinical symptoms of left ventricular failure are dominated by symptoms of pulmonary congestion and edema, whereas right ventricular failure is characterized by signs of systemic venous congestion and peripheral edema. Weakness, fatigue, and shortness of breath are common to both right and left ventricular failure as well as biventricular failure.
CHF is most effectively treated via natural measures in the early stages. Hence early diagnosis and prevention by addressing causative factors are imperative. The first symptom of CHF is usually shortness of breath. A chronic nonproductive cough may also be the first manifesting symptom. Patients suspected of having CHF should have an extensive cardiovascular evaluation including a complete physical examination to look for the characteristic signs of CHF (e.g., peripheral signs of heart failure, enlarged and sustained left ventricular impulse, diminished first heart sound, gallop rhythm), electrocardiography, and echocardiography.
In the initial stages of CHF, natural measures designed to address the underlying cause (e.g., hypertension) or improve the metabolic functions of the myocardium (described later, as well as measures described in Chapter 145) are often effective. In later stages, however, medical treatment involving the use of diuretics and angiotensin-converting enzyme (ACE) inhibitors, digitalis glycosides, or both, is indicated in most cases. The measures described here can be used as adjunctive therapy in these more severe cases. The New York Heart Association (NYHA) staging system for CHF can be used in an effort to better identify likely respondents to natural therapy alone (Table 158-1). In general, excellent clinical results can be expected in stages I and II with the use of the natural measures described below.
|Stage I||Patient is symptom-free at rest and with treatment.|
|Stage II||Patient experiences impaired heart function with moderate physical effort. Shortness of breath with exertion is common. There are no symptoms at rest.|
|Stage III||Even minor physical exertion results in shortness of breath and fatigue. There are no symptoms at rest.|
|Stage IV||Symptoms such as shortness of breath and signs such as lower extremity edema are present when the patient is at rest.|
The natural approach focuses on improving myocardial energy production, as CHF is always characterized by a state of energy depletion. This impaired energy production is often the result of nutrient or coenzyme deficiency (e.g., magnesium, thiamine, coenzyme Q10 [CoQ10], carnitine). The dietary recommendations given in Chapter 174 are appropriate for most patients with CHF, especially if the CHF is due to long-term hypertension. Of particular importance is a diet low in sodium and high in potassium. A high intake of sodium greatly exacerbates the hemodynamic aspects of CHF. Sodium intake should be restricted to below 1.8 g daily. Furthermore, the dietary intake of several nutrients is usually well below recommended levels in patients with CHF.1 Most notably low are magnesium, calcium, zinc, copper, manganese, thiamine, riboflavin, and folic acid. A high-potency multivitamin/multimineral formula is critical in these patients, especially if they are taking a diuretic.
Low magnesium levels (particularly white blood cell magnesium) are commonly found in patients with CHF. This association is extremely significant, since magnesium levels have been shown to correlate directly with survival rates. In one study, CHF patients with normal levels of magnesium had 1- and 2-year survival rates of 71% and 61%, respectively, compared with rates of 45% and 42%, respectively, in patients with lower magnesium levels.2 These results are not surprising considering that magnesium deficiency is associated with cardiac arrhythmias, reduced cardiovascular prognosis, worsened ischemia, and increased mortality in acute myocardial infarction.
The magnesium deficiency probably stems from a combination of inadequate intake and increased wasting due to overactivation of the renin-angiotensin-aldosterone system, as is commonly seen in patients with heart failure. It can also be the effect of diuretics like furosemide.
In addition to providing benefits of its own in CHF, magnesium supplementation prevents the magnesium depletion caused by the conventional drug therapy for CHF (i.e., digitalis, diuretics, and vasodilators such as beta blockers and calcium channel blockers). Magnesium supplementation has even been shown to produce positive effects in CHF patients receiving conventional drug therapy even if serum magnesium levels are normal.3 However, magnesium supplementation is not indicated in patients with renal failure, as this condition predisposes them to hypermagnesemia—a significant risk factor for mortality.4 ACE inhibitors appear to produce a magnesium-sparing effect in patients on furosemide.5 Typical dosages are 200 to 300 mg one to three times per day of magnesium in the citrate form. Oral magnesium can be effective in raising white blood cell magnesium and potassium levels.6 It is highly important to monitor serum magnesium levels so as to prevent hypermagnesemia in patients with renal impairment as well as those on digoxin. Magnesium significantly reduces the frequency and complexity of ventricular arrhythmias in digoxin-treated patients with CHF even without the presence of digoxin toxicity, but too much magnesium may interfere with digoxin.7