Generic Tiazac er (Diltiazem hcl 120mg)
DILTIAZEM HCI
Tablets: 30, 60, 90 and 120 mg (Rx) Various, Cardizem (Marion Merrell Dow)
Capsules, sustained-release: 60, 90, 120, Various, Cardizem SR (Marion Merrell Dow)
180, 240, 300 and 360 mg (Rx) Cardizem CD (Marion Merrell Dow),
Dilacor XR (Rhone-Poulenc Rorer), Tiazac (Forest)
Injections: 25 mg (5 mg/50 mL),
50 mg (5 mg/mL) (Rx) Cardizem (Marion Merrell Dow)
Oral-
Tablets: Start with 30 mg 4 times/day before meals and at bedtime; gradually increase dosage to 180 to 360 mg (given in divided doses 3 or 4 times/day) at 1-to 2-day intervals until optimum response is obtained.
Sustained release:
Cardizem SR -Start with 60 to 120 mg twice daily. Adjust dosage when maximum antihypertensive effect is achieved (usually by 14 days chronic therapy). Optimum dosage range is 240 to 360 mg/day, but some patients may respond to lower doses.
Cardizem CD -
Hypertension: 180 to 240 mg once daily; some patients may respond to lower doses. Maximum antihypertensive effect is usually achieved by 14 days chronic therapy; therefore, adjust dosage accordingly. Usual range is 240 to 360 mg once daily; experience with doses > 360 mg is limited.
Angina: Start with 120 or 180 mg once daily. Some patients may respond to higher doses of up to 480 mg once daily. When necessary, titration may be carried out over a 7- to 14-day period.
Cardizem CD may be opened and administered, but do not crush.
Dilacor XR -
Hypertension: 180 to 240 mg once daily; adjust dose as needed. Individual patients, particularly those > 60 years of age, may respond to a lower dose of 120 mg. Usual range is 180 to 480 mg once daily. Although current clinical experience with the 540 mg dose is limited, the dose may be increased to 540 mg with little or no increased risk of adverse reactions. Do not exceed 540 mg once daily. Angina: Adjust dosage to each patient's needs, starting with a dose of 120 mg once daily, which may be titrated to doses of up to 480 mg once daily, when necessary, titration may be carried out over a 7- to 14-day period.
Hypertensive or anginal patients treated with other formulations of diltiazem can safely be switched to Dilacor XR at the nearest equivalent total daily dose. However, subsequent titration to higher or lower doses may be necessary and should be initiated as clinically indicated.
Administration in the morning on an empty stomach is recommended.
Parenteral -
Direct IV single injections (bolus): The initial dose is 0.25 mg/kg as a bolus administered over 2 minutes (20 mg is a reasonable dose for the average patient). If response is inadequate, a second dose may be administered after 15 minutes. The second bolus dose should be 0.35 mg/kg administered over 2 minutes (25 mg is a reasonable dose for the average patient). Individualize subsequent IV bolus doses. Dose patients with low body weights on a mg/kg basis. Some patients may respond to an initial dose of 0.15 mg/kg, although duration of action may be shorter.
Continuous IV infusion: For continued reduction of the heart rate (up to 24 hours) in patients with atrial fibrillation or atrial flutter, an IV infusion may be administered. Immediately following bolus administration of 20 mg (0.25 mg/kg) or 25 mg (0.35 mg/kg) and reduction of heart rate, begin an IV infusion. The recommended initial infusion rate is 10 mg/hr. Some patients may maintain response to an initial rate of 5 mg/hr. The infusion rate may be increased in 5 mg/hr increments up to 15 mg/hr as needed, if further reduction in heart rate is required. The infusion may be maintained for up to 24 hours. Therefore, infusion duration > 24 hours and infusion rates > 15 mg/hr arc not recommended.
Concomitant therapy: Concomitant therapy with p-blockers or digitalis is usually well tolerated, but the effects of co-administration cannot be predicted, especially in patients with left ventricular dysfunction or cardiac conduction abnormalities. Use caution in titrating dosages for impaired renal or hepatic function patients, since dosage requirements are not available.
CARDIO & BLOOD – CHOLESTEROL
CONGESTIVE HEART FAILURE AND PHYSICAL ACTIVITY
Epidemiology
The incidence of congestive heart failure (CHF) has been steadily increasing over the last 10 years. Today, 4.6 million individuals in the U.S. have CHF; 400,000 new cases are added annually; and 43,000 individuals die of CHF. Hospitalizations for CHF increased from 377,000 to 870,000 between the years 1979 and 1996. CHF is a multifactorial condition, and some of its precipitating causes are: coronary artery disease (60%), hypertension (10%), physical inactivity (9%), obesity (8%), and diabetes (3%). Lack of physical activity is considered an independent risk factor for the development of CHF. In fact, bed rest and exercise restriction lead to deconditioning and increased morbidity in patients with symptomatic heart failure. Therefore, physical inactivity can exacerbate conditions associated with previously diagnosed CHF.
Tertiary Prevention
Patients diagnosed with CHF benefit greatly from participating in exercise training programs. For example, exercise training of patients with moderate to severe CHF lowered all-cause mortality by 63% and reduced hospital readmission for heart failure by 71 %! While the primary defective organ in CHF is the heart, the peripheral musculature becomes a secondary defective organ of major clinical significance, in that skeletal muscle, rather than the congestive heart, appears to limit exercise tolerance. In the heart failure syndrome, two of the main symptoms are fatigue and limitation in exercise capacity. In many heart failure patients, an inherent defect in skeletal muscle function is operative, rather than a hemodynamic limitation.
The evidence is quite clear that exercise training improves the overall function and exercise capacity of people inflicted with CHF. Exercise capacity correlates well with measures of peripheral muscular strength and endurance (r = 0.90), which suggests that alterations in the periphery greatly contribute to exercise intolerance in CHF patients. Exercise training does not improve function of the primary defective organ, i.e., the heart. Only moderate improvements are noted in left ventricular performance or central hemodynamics after exercise training in CHF patients. Therefore, reductions in exercise capacity observed in CHF patients are nor due solely to alterations in myocardial function. For example, various indicators of cardiac function (e.g., ejection fraction) do not correlate well (r = - 0.06) with overall exercise capacity. The fact remains, however, these same patients do exhibit significant improvements in overall exercise capacity, as skeletal muscle dysfunction in CHF does improve with exercise training. Physically active skeletal muscles generally mean improved quality of life for these patients. Exercise training often improves their condition, while physical inactivity may actually increase their risk of mortality.
Biochemical Mechanisms
We have just described the physiological mechanisms by which physical inactivity affects patients with CHF. Now let us turn our attention to how physical activity can improve function in this disease. Simply put, increased blood flow improves mitochondrial function, which raises functional capacity and reduces skeletal muscle fatigue.
As for biochemical mechanisms: Oxidative stress in the congestive heart produces endothelial dysfunction. Usage of an endothelial cell inhibitor of xanthine oxidase, allopurinol, in CHF patients improved endothelium-dependent vasodilation and exercise capacity. The congestive failing heart produces NO (nitric oxide) from inducible NOS, whose blockage enhances myocardial contractility, but inhibition of NOS does not affect contractility in the normal heart.
*6/282/5*
CARDIO & BLOOD
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