Clinical factors affecting serum potassium concentration in cardio-renal decompensation syndrome.
ABSTRACT Renin-angiotensin-aldosterone system (RAAS) inhibitors are currently indispensable for the treatment of heart failure. It is well known that hyperkalemia is likely to occur in renal failure; however, it has not yet been clarified how the serum potassium concentration changes as heart failure progresses. Currently, the cardio-renal decompensation syndrome holds that the serum potassium concentration is altered similarly by both heart failure and renal failure; however, there are no definitive reports on this. In order to use RAAS inhibitors more safely and effectively in heart failure, it is necessary to understand the factors affecting serum potassium concentration in the clinical setting.
We examined the clinical factors affecting serum potassium concentration in 1035 consecutive patients with cardiovascular disease who were hospitalized in our institution. Multiple regression analysis showed that the independent factors associated with an elevated serum potassium concentration were renal insufficiency evaluated by estimated glomerular filtration rate (eGFR) (P<0.0001), diabetes mellitus evaluated by HbA(1c) (P=0.0005) and the use of RAAS inhibitors (P=0.0010). The independent factors associated with a decreased serum potassium concentration were mean blood pressure (P<0.0001), heart failure evaluated by log BNP (P=0.0164) and the use of diuretics (P=0.0232).
The serum potassium concentration decreases with the severity of heart failure if renal function is preserved. From the perspective of potassium homeostasis, we could use the RAAS inhibitors more aggressively in patients with heart failure who do not have renal failure.
- SourceAvailable from: Paul Palevsky[show abstract] [hide abstract]
ABSTRACT: Hyperkalemia is a common, potentially life-threatening disorder. Electrocardiograms are considered to be sensitive indicators of the presence of hyperkalemia. Since the treatment of hyperkalemia involves relatively few maneuvers and because its success can be objectively scored, we investigated how physicians manage this disorder and how successful their prescribed therapy is. We also sought to determine whether treatment could be improved by providing the treating physicians with therapy guidelines on a real-time basis. Consecutive patients with hyperkalemia were identified by review of laboratory records. During the observation-only phase of the study, demographic data, contributing causes, electrocardiogram findings, treatments used, compliance with prescribing guidelines, and patient outcome were recorded. During the subsequent notification phase of the study, treatment recommendations were sent to the patient's ward when the elevated potassium value was noted. The same outcome data were collected. There were 127 episodes of hyperkalemia during the observation-only phase and 115 during the notification phase. No patients died or had life-threatening cardiac arrhythmias. Electrocardiographic abnormalities consistent with hyperkalemia were observed in only 14% of episodes. Renal failure (77%), drugs (63%), and hyperglycemia (49%) contributed to most episodes. Treatments used were exchange resin (51%), insulin (46%), calcium (36%), bicarbonate (34%), and albuterol (4%). The agents were equally efficacious. The time to first treatment was shorter in patients with potassium levels of 6.5 mmol/L or more than in patients with lower values (2.1 +/- 2.2 vs 2.8 +/- 2.4 hours; P<.05). Treatment was better in the intensive care unit than on regular wards. Only 39% of episodes during the observation-only period met the predetermined criteria for monitoring and diagnosis, initial treatment, and follow-up. During the notification period, physician performance was no better; only 42% of episodes met all criteria. The laboratory transmitted a copy of the guidelines to the patient's ward only 38% of the time. In a separate analysis of these episodes, there was no improvement in treatment. Physicians who did not receive the notification fulfilled all treatment criteria more often than physicians who did (50% vs 30%; P<.05). Although treatment of hyperkalemia was frequently suboptimal, no serious arrhythmias and no deaths complicated management of 242 episodes of severe hyperkalemia. A narrowly targeted effort to improve physician management of a disorder with discrete treatment options did not improve therapy.Archives of Internal Medicine 05/1998; 158(8):917-24. · 11.46 Impact Factor
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ABSTRACT: Because of inappropriate signals from the volume-regulation system and a reduction in renal blood flow, the kidney is not able to prevent sodium and water retention in chronic congestive heart failure (CHF). A brief summary of normal renal function and renal involvement in CHF is given and a study of renal function in patients with moderate or severe chronic CHF is presented. To evaluate the impact of cardiac output reduction on the regulation of the glomerular filtration rate (GFR) in heart failure, GFR (inulin clearance), renal plasma flow [p-aminohippurate (PAH) clearance], invasive haemodynamics, blood volume, plasma renin and plasma catecholamines were measured in 34 patients with chronic CHF. The patients were divided into 3 groups according to their cardiac index (CI): CI greater than 2.0 L/min/m2 (group A), CI 1.5 to 2.0 L/min/m2 (group B), and CI less than 1.5 L/min/m2 (group C). Differences in the relationship between GFR, renal plasma flow and filtration fraction for the 3 groups emerged. Despite an intergroup reduction in the renal fraction of cardiac output and renal blood flow, GFR was similar in groups A and B (62 and 67 ml/min/1.73 m2, respectively), and was accompanied by a compensatory increase in filtration fraction, from 24% in group A to 35% in group B. Group C had a much lower GFR (38 ml/min/1.73 m2), however, the filtration fraction (28%) was intermediate in value between those of groups A and B. The differences in GFR were reflected by blood urea nitrogen levels but not by serum creatinine levels. The occurrence of a non-compensatory filtration fraction response in the patients with the greatest impairment of CI and renal blood flow suggests that GFR becomes dependent on afferent arteriolar flow in the most severe heart failure, despite stimulation of haemodynamic and hormonal pathways, which would normally increase efferent arteriolar tone. It is thus suggested that GFR becomes flow dependent in patients in the most severe stage of chronic CHF.Drugs 02/1990; 39 Suppl 4:10-21; discussion 22-4. · 4.63 Impact Factor
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ABSTRACT: Plasma concentrations of A type or atrial natriuretic peptide (ANP) and B type or brain natriuretic peptide (BNP) are increased in patients with congestive heart failure (CHF). To examine the haemodynamic and hormonal responses, especially of ANP and BNP, to oral administration of an angiotensin-converting enzyme (ACE) inhibitor in patients with CHF and in controls. 12 patients with CHF and 11 controls. Haemodynamic variables and plasma concentrations of ANP, BNP, and other hormones were serially measured for 24 hours after alacepril (37.5 mg) was given by mouth. Pulmonary capillary wedge pressure and systemic vascular resistance decreased significantly in both groups. The cardiac index increased only in the CHF group. In patients with CHF pulmonary capillary wedge pressure, systemic vascular resistance, and cardiac index were significantly changed from 1 to 12 hours after alacepril administration. Plasma ANP and BNP decreased significantly after alacepril was given to the CHF group: neither concentration changed in the control group. In the CHF group plasma ANP was significantly lower between 1 and 6 hours and was highly significantly correlated with pulmonary capillary wedge pressure. Plasma BNP, however, was significantly lower between 6 and 24 hours after alacepril and was not correlated with pulmonary capillary wedge pressure. The response of plasma BNP after alacepril administration occurred later and lasted longer than the plasma ANP response. This may indicate that the mechanisms of synthesis, secretion, or degradation of the two peptides are different.Heart 01/1995; 72(6):528-33.