Heart failure compensated

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... 

Heart failure/hypotension - May cause or aggravate CFIF or produce severe hypotension, especially in patients with depressed systolic function. Do not use in patients with uncompensated or marginally compensated CFIF or hypotension unless secondary to cardiac arrhythmia. Treat patients with a... 

Cardiac failure Avoid use in overt CHF may be used with caution in patients with a history of heart failure who are well compensated. CHF has been observed in patients receiving labetalol. 

Geriatric Considerations - Summary Fluid retention may lead to mild CHF in patients with CAD and unrecognized or compensated heart failure. Discontinue drug with any sign of decline in cardiac function. Avoid in older adults with NYHA Class 111 or IV cardiac status. Demonstrated effectiveness in patients 65 years of age and older. 

The primary signs and symptoms of all types of heart failure include tachycardia, decreased exercise tolerance, shortness of breath, peripheral and pulmonary edema, and cardiomegaly. Decreased exercise tolerance with rapid muscular fatigue is the major direct consequence of diminished cardiac output. The other manifestations result from the attempts by the body to compensate for the intrinsic cardiac defect. 

Neurohumoral (extrinsic) compensation involves two major mechanisms (previously presented in Figure 6-7)—the sympathetic nervous system and the renin-angiotensin-aldosterone hormonal response—plus several others. Some of the pathologic as well as beneficial features of these compensatory responses are illustrated in Figure 13-2. The baroreceptor reflex appears to be reset, with a lower sensitivity to arterial pressure, in patients with heart failure. As a result, baroreceptor sensory input to the vasomotor center is reduced even at normal pressures sympathetic outflow is increased, and parasympathetic outflow is decreased. Increased sympathetic outflow causes tachycardia, increased cardiac contractility, and increased vascular tone. Vascular tone is further increased by angiotensin II and endothelin, a potent vasoconstrictor released by vascular endothelial cells. The result is a vicious cycle that is characteristic of heart failure (Figure 13-3). Vasoconstriction increases afterload, which further reduces ejection fraction and cardiac output. Neurohumoral antagonists and vasodilators... 

Chen LA, Vatner DE, Vatner SF, Hiffinger L, Homey CJ. 1991. Decreased Gs alpha mRNA levels accompany the fall in Gs and adenylyl cyclase activities in compensated left ventricular hypertrophy. In heart failure, only the impairment in adenylyl cyclase activation progresses. J Clin Invest 87 293-298. 

Trx and Grx being the key redox sensors, their functions are modulated by ROS. While at a lower dose, ROS can induce their expression, thereby eliciting an adaptive response massive generation of ROS inactivates these proteins by posttranslational modifications (Kondo et al. 2006). In heart failure patients, a significant correlation between the serum concentration of Trx-1 and the severity of the disease has also been documented (Jekell et al. 2004). The increased Trx-1 activity is likely to be due to the adaptive response during the failure to compensate for the increased ROS activities. 

If the mechanisms listed above adequately restore cardiac output, then the heart failure is said to be compensated. However, these compensations increase the work of the heart and contribute to further decline in cardiac performance. If the adaptive mechanisms fail to maintain cardiac output, the heart failure is termed decompensated. 

Q7 Yes. The renal and respiratory compensations can normally rectify the changes in pH and blood gases, unless there are also problems within the lung or heart which limit normal gas exchange and cardiac output. Many stroke patients unfortunately also have concomitant conditions such as heart failure, atherosclerosis or diabetes, since strokes are more common in the elderly population. 

Ofran Y, Bursztyn M, Ackerman Z. Rofecoxib-induced renal dysfunction in a patient with compensated cirrhosis and heart failure. Am J Gastroenterol 2001 96(6) 1941. 

Materials and Methods. Subjects ranging in age between 21-89 years were randomly selected from the Domiciliary Care Veterans Facility at the Central State Hospital. Determination of copper and ceruloplasmin was made on venous blood drawn from 180 males and 44 females. We have made no attempt to exclude from this study patients with chronic illnesses since it would be highly unlikely that such aged populations would be completely free of these conditions. However, patients with acute intercurrent illnesses and hepatic renal or symptomatic cardiovascular diseases were eliminated from this study. Individuals with acute illnesses as well as pregnant females or females on oral contraceptive agents also have been excluded. Some of the older patients did have evidence of atherosclerosis, mild diabetes mellitus, or compensated heart failure. 

Similar studies with the two nonsynonymous polymorphisms of the PrAR have revealed additional phenotypes. The majority of studies have been with the PrAR position 389 variants. Alone, neither allelic variant appears to be associated with heart failure. Of note, the combination of prArg389 and 02C-Del322-325 appears to impart heart failure risk in African Americans (37). In patients with compensated... 

Pulmonary edema may result from the failure of any of a number of homeostatic mechanisms. The most common cause of pulmonary edema is an increase in capillary hydrostatic pressure because of left ventricular failure. Excessive fluid administration in compensated and decompensated heart failure patients is the most frequent cause of iatrogenic pulmonary edema. Besides hydrostatic forces, other homeostatic mechanisms that may be disrupted include the osmotic and oncotic pressures in the vasculature, the integrity of the alveolar epithelium, interstitial pulmonary pressure, and the interstitial lymph flow. The edema fluid in cardiogenic pulmonary edema contains a low amount of protein, whereas noncardiogenic pulmonary edema fluid has a high protein concentration. This indicates that noncardiogenic pulmonary edema results primarily from disruption of the alveolar epithehum. The reader is referred to Chap. 28 for a detailed discussion of this topic. 

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