Decompensation

E Partial agonist Full agonist Acute cardiac decompensation... 

In theory, one could utilise GC-A ligands to lower blood pressure and to reduce blood volume as they increase the excretion of water and salt. Nesiritide, human recombinant BNP, is the first member of this new class of drugs approved for the initial intravenous treatment of acutely decompensated congestive heart failure. Whether nesiritide can be a valuable addition to the standard therapy of decompensated heart failure remains to be demonstrated. 

Both carvedilol and labetalol are contraindicated in patients with hypersensitivity to the drag, bronchial asthma, decompensated heart failure, and severe bradycardia The drugs are used cautiously in patients with drag-controlled congestive heart failure, chronic bronchitis, impaired hepatic or cardiac function, in those with diabetes, and during pregnancy (Category C) and lactation. 

The thiazide diuretics are contraindicated in patients with known hypersensitivity to the thiazides or related diuretics, electrolyte imbalances, renal decompensation, hepatic coma, or anuria. A cross-sensitivity reaction may occur with the thiazides and sulfonamides. Some of the thiazide diuretics contain tartrazine, which may cause allergic-type reactions or bronchial asthma in individuals sensitive to tartrazine. 

Psychoses, when they occur, appear to be due to drug effect interacting with a vulnerable personality organization (Luisada 1978). Our experience has been that some adolescents with borderline personality disorders, as well as adolescents at risk of schizophrenic decompensation, may have this vulnerability. Although we do not have hard data to support the hypothesis that patients with PCP psychoses that are most resistant to treatment have the poorest long-term prognosis (Erard et al. 1980), our observations have been that persistence of symptoms of psychosis after the first 2 to 3 weeks of treatment often correlates with extended periods of impai rment. 

Surgical embolectomy may be an alternative to IV thrombolysis in patients with decompensated shock (no prospective clinical trials)... 

Catheter-based embolectomy—limited experience in shock (not appropriate for patients with decompensated shock [personal opinion])... 

The phrase acute heart failure (AHF) is used to signify either an acute decompensation of a patient with a history of chronic heart failure or to refer to a patient presenting with new-onset HF symptoms. Terms commonly associated with HF, such as cardiomyopathy and LV dysfunction, are not equivalent to HF but describe possible structural or functional reasons for the development of HF. 

There is growing evidence of a link between renal disease and HF.8 Renal insufficiency is present in one-third of HF patients and is associated with a worse prognosis. In hospitalized HF patients, the presence of renal insufficiency is associated with longer lengths of stay, increased in-hospital morbidity and mortality, and detrimental neurohormonal alterations. Conversely, renal dysfunction is a common complication of HF or results from its treatment. Renal failure is also a common cause for HF decompensation. 

Heart failure patients exist in one of two clinical states. When a patient s volume status and symptoms are stable, their HF condition is said to be compensated. In situations of volume overload or other worsening symptoms, the patient is considered decompensated. Acute decompensation can be precipitated by numerous etiologies that can be grouped into cardiac, metabolic, or patient-related causes (Table 3-3).5... 

HF medications deserves special attention, as it is the most common cause of acute decompensation and can be prevented. As such, an accurate history regarding diet, food choices, and the patient s knowledge regarding sodium and fluid intake (including alcohol) is valuable in assessing dietary indiscretion. Nonadherence with medical recommendations such as laboratory and other appointment follow-up can also be indicative of non-adherence with diet or medications. 

It is important for the clinician to identify the cause(s) of AHF in order to maximize treatment efficacy and reduce future disease exacerbations. Cardiovascular, metabolic, and lifestyle factors can all precipitate AHF. The most common precipitating factors for acute decompensation and how they contribute pathophysiologically are listed in Table 3-3. 

DiDomenico RJ, Park HY, Southworth MR, et al. Guidelines for acute decompensated heart failure treatment. Ann Pharmacother 2004 38 649-660. 

The most serious side effects of P-blocker administration early in ACS are hypotension, bradycardia, and heart block. While initial, acute administration of P-blockers is not appropriate for patients who present with decompensated heart failure, initiation of P-blockers maybe attempted before hospital discharge in the majority of patients following treatment of acute heart failure. P-Blockers are continued indefinitely. 

Adverse effects and contraindications of calcium channel blockers are described in Table 5-2. Verapamil, diltiazem, and first-generation dihydropyridines should also be avoided in patients with acute decompensated heart failure or left... 

Although P-blockers should be avoided in patients with decompensated heart failure from left ventricular systolic dysfunction complicating an MI, clinical trial data suggest that it is safe to initiate P-blockers prior to hospital discharge in these patients once heart failure symptoms have resolved.64 These patients may actually benefit more than those without left ventricular dysfunction.65 In patients who cannot tolerate or have a contraindication to a P-blocker, a calcium channel blocker can be used to prevent anginal symptoms, but should not be used routinely in the absence of such symptoms.2,3,62... 

Intravenous diltiazem can be used cautiously for up to 24 hours in patients with non-decompensated heart failure, bpm, beats per minute CCB, calcium channel blocker (diltiazem or verapamil) HF, heart failure LV, left ventricular LVEF, left ventricular ejection fraction. 

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

Ascites is the accumulation of fluid in the peritoneal space and is often one of the first signs of decompensated liver disease. Ascites is the most common complication of cirrhosis and portends a dire prognosis.14... 

In some cases, cirrhosis is diagnosed incidentally before the patient develops symptoms or acute complications. Other patients may have decompensated cirrhosis at initial presentation they may present with variceal bleeding, ascites, SBP, or HE. Patients may also have some of the laboratory abnormalities and/or signs and symptoms listed above that are associated with cirrhosis.28... 

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