Pharmacotherapy in Congestive Heart Failure: Drug Absorption
Pharmacotherapy in Congestive Heart Failure: Drug Absorption
Congestive heart failure is a disease state distinguished by the regular presence of both renal and hepatic abnormalities in drug handling. One such abnormality involves flaws in the process of drug absorption. In most instances, congestive heart failure-related abnormalities in drug absorption are of inconsequential significance. However, this is not the case with loop diuretics. Loop diuretic action ordinarily tracks the rate and extent of absorption if a sufficient amount of diuretic has been given to exceed the threshold for diuretic effect. In congestive heart failure, both the rate and absolute amount of loop diuretic absorbed can be reduced as a function of the heart failure state itself. In this setting, drug dissolution characteristics can assume added significance. Furosemide is the loop diuretic with the widest intra-and interpatient variability of absorption. Alternatively, the loop diuretic torsemide is rapidly and fairly completely absorbed independent of the heart failure state. This pattern of absorption establishes it as the preferred loop diuretic in the otherwise diuretic-resistant heart failure patient. However, the exact role of torsemide in the outpatient management of congestive heart failure remains to be determined.
The effects of congestive heart failure (CHF) on drug disposition are multifaceted, with distinct influences on pharmacokinetic parameters such as rate and extent of drug absorption and systemic drug elimination. Reduced gastric emptying leads to a lag in drug absorption and decreased peak plasma concentrations of a number of medications. Moreover, drugs with a high hepatic extraction ratio achieve higher-than-expected plasma concentrations in patients with CHF. Alternatively, drugs requiring biotransformation to active forms– like angiotensin-converting enzyme (ACE) inhibitors–generally are marked by a delay in the conversion process. Nonetheless, the pharmacotherapy of CHF is such that ACE inhibitors and angiotensin-receptor blockers are often administered. These drugs often reduce the glomerular filtration rate, which slows drug elimination and offsets circumstances of reduced absorption.
Congestive heart failure is a disease state distinguished by the regular presence of both renal and hepatic abnormalities in drug handling. One such abnormality involves flaws in the process of drug absorption. In most instances, congestive heart failure-related abnormalities in drug absorption are of inconsequential significance. However, this is not the case with loop diuretics. Loop diuretic action ordinarily tracks the rate and extent of absorption if a sufficient amount of diuretic has been given to exceed the threshold for diuretic effect. In congestive heart failure, both the rate and absolute amount of loop diuretic absorbed can be reduced as a function of the heart failure state itself. In this setting, drug dissolution characteristics can assume added significance. Furosemide is the loop diuretic with the widest intra-and interpatient variability of absorption. Alternatively, the loop diuretic torsemide is rapidly and fairly completely absorbed independent of the heart failure state. This pattern of absorption establishes it as the preferred loop diuretic in the otherwise diuretic-resistant heart failure patient. However, the exact role of torsemide in the outpatient management of congestive heart failure remains to be determined.
The effects of congestive heart failure (CHF) on drug disposition are multifaceted, with distinct influences on pharmacokinetic parameters such as rate and extent of drug absorption and systemic drug elimination. Reduced gastric emptying leads to a lag in drug absorption and decreased peak plasma concentrations of a number of medications. Moreover, drugs with a high hepatic extraction ratio achieve higher-than-expected plasma concentrations in patients with CHF. Alternatively, drugs requiring biotransformation to active forms– like angiotensin-converting enzyme (ACE) inhibitors–generally are marked by a delay in the conversion process. Nonetheless, the pharmacotherapy of CHF is such that ACE inhibitors and angiotensin-receptor blockers are often administered. These drugs often reduce the glomerular filtration rate, which slows drug elimination and offsets circumstances of reduced absorption.
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