Diuresis In Patients Research Articles

Abstract 14688: Relative Blood Volume Change After Single Doses of a Loop Diuretic to Assess Volume Status: A Patient Level Meta-analysis

Background: In patients with congestive heart failure administration of an intravenous diuretic results in increased urine production and, depending on the volume status, an immediate change in relative blood volume (RBV). Changes in RBV are already applied clinically to monitor fluid removal and better guide diuresis in patients who undergo peripheral ultrafiltration. Using individual level patient data, we explored whether it is possible to measure changes in RBV after a single intravenous dose of loop diuretic through the measurement of serial hematocrit values. Based on normally occurring variation in volume-stable patients, the smallest change in RBV that would be detectable by routine serial hematocrits ranges from 6.4% to 8.6%. Methods and Results: Electronic databases were queried for articles that contained predefined MeSH terms in order to identify all studies in which patients received intravenous diuretics. The 764 studies that met our entry criteria were systematically reviewed and manually screened. We then conducted a meta-analysis from 14 studies that provided individual, patient-level data from at least 2 time points: just before and within 3 hours of administration of an intravenous loop diuretic. We found that among a total of 240 patients, RBV decreased by 11% (95% CI 10 to 12%) at 2 hours after an intravenous loop diuretic was given (Figure); there was no significant difference in this finding based on whether or not patients had heart failure. Conclusion: We found that anticipated RBV change with single doses of intravenous loop diuretics exceeds the smallest detectable change in RBV that can be obtained by serial hematocrits. This implies that routine hematocrits can be used to track RBV change across serial doses of intravenous loop diuretics, potentially providing a target for a dry interstitium in acute heart failure.

Dialysis-associated hyperglycemia: manifestations and treatment.

Dialysis-associated hyperglycemia (DAH), is associated with a distinct fluid and electrolyte pathophysiology. The purpose of this report was to review the pathophysiology and provide treatment guidelines for DAH. Review of published reports on DAH. Synthesis of guidelines based on these reports. The following fluid and solute abnormalities have been identified in DAH: (a) hypoglycemia: this is a frequent complication of insulin treatment and its prevention requires special attention. (b) Elevated serum tonicity. The degree of hypertonicity in DAH is lower than in similar levels of hyperglycemia in patients with preserved renal function. Typically, correction of hyperglycemia with insulin corrects the hypertonicity of DAH. (c) Extracellular volume abnormalities ranging from pulmonary edema associated with osmotic fluid shift from the intracellular into the extracellular compartment as a consequence of gain in extracellular solute (glucose) to hypovolemia from osmotic diuresis in patients with residual renal function or from fluid losses through extrarenal routes. Correction of DAH by insulin infusion reverses the osmotic fluid transfer between the intracellular and extracellular compartments and corrects the pulmonary edema, but can worsen the manifestations of hypovolemia, which require saline infusion. (d) A variety of acid-base disorders including ketoacidosis correctable with insulin infusion and no other interventions. (e) Hyperkalemia, which is frequent in DAH and is more severe when ketoacidosis is also present. Insulin infusion corrects the hyperkalemia. Extreme hyperkalemia at presentation or hypokalemia developing during insulin infusion require additional measures. In DAH, insulin infusion is the primary management strategy and corrects the fluid and electrolyte abnormalities. Patients treated for DAH should be monitored for the development of hypoglycemia or fluid and electrolyte abnormalities that may require additional treatments.

Non-Invasive Venous Waveform Analysis but Not Thoracic Impedance Correlates with Diuresis in Hospitalized Heart Failure Patients

Background During hospitalization for acute decompensated heart failure (ADHF), diuresis is guided by weight change, net fluid output, exam and laboratory values with the goal of estimating hemodynamic decongestion. In this study, we compared the novel technology N on- I nvasive V enous waveform A nalysis (NIVA), which provides an estimate of PCWP, to thoracic impedance to determine correlation with diuresis in patients hospitalized for ADHF. Hypothesis Change in NIVA score correlates with changes in fluid balance and weight better than thoracic impedance ADHF patients. Methods Patients were recruited on admission for ADHF. Demographics, vital signs, fluid balance, physical exam and laboratory data were collected. NIVA and ZOE measurements were obtained on a daily basis. The clinical providers caring for the patients were blinded to the NIVA signal data and the ZOE® readings. Results NIVA value was captured in 30 patients with an average age of 64 years old, of which 57% were female, and 23% black. Fifteen patients had systolic heart failure, of which 12 patients had a left ventricular ejection fraction 35%. Two patients withdrew prior to discharge. Average fluid balance was negative 13,427mL (16,395) and average weight loss was 6.9kg (9.7). Change in NIVA score correlated with change in weight normalized to discharge weight (r= 0.29, p=0.02). Change in ZOE score did not correlate with change in discharge normalized weight (r=0.02, p=0.87) (Figure 1). NIVA score significantly decreased with diuresis (p Conclusions This observational study shows that change in NIVA value correlates with change in weight in patients admitted for ADHF with greater reliability than thoracic impedance measures. We also demonstrated that the use of NIVA technology is feasible in a hospital setting.

Non-invasive Assessment of Left Ventricular End Diastolic PressureChange with a Single Session of Outpatient Intravenous Diuresis in Patients with Heart Failure with Reduced Ejection Fraction

Background Admissions for acute decompensated heart failure (ADHF) may be prevented by early detection and treatment of elevated cardiac filling pressures before the onset of clinical symptoms. We have developed a noninvasive, handheld, point-of-care device to assess left ventricular end diastolic filling pressure (LVEDP). The device measures the change in pulse amplitude of a finger photoplethysmography signal (PPG) during a Valsalva maneuver (VM), which we previously showed reflects invasively measured LVEDP. Our objective in this study was to determine whether LVEDP changes in HF patients undergoing a session of outpatient intravenous (IV) diuresis. Methods Patients receiving IV diuresis at the Johns Hopkins Bayview Diuresis Clinic were recruited. Each enrolled participant performed a VM with expiratory effort of 20 mmHg into a pressure transducer for 10 seconds, before and after the diuresis session. Participants were guided by an automated graphical user interface. A continuous PPG signal was recorded during the testing. LVEDP was then calculated using an equation derived from a previous study we conducted of patients undergoing left heart catheterization. Urine output (UO) during the diuresis session was also measured. Statistical analysis was performed using t-test and regression testing. Results 37 participants (65 ± 15 years, 43% female, 51% white) underwent a total of 53 sessions of IV diuresis. The mean initial LVEDP was 19 ± 4 mmHg. The mean UO was 1.2 ± 0.6 liters. On average, the LVEDP did not change within the same diuresis session (mean LVEDP change -0.26 ± 3.4 mmHg). In participants with heart failure with reduced ejection fraction (HFrEF, EF ≤ 40%), the change in LVEDP was related to UO (r = 0.53, p = 0.028, n=17). Also in that subgroup, the change in LVEDP trended strongly towards being related to initial LVEDP (r = 0.52, p = 0.057, n=17). Conclusion In patients with HFrEF, the change in LVEDP during a session of outpatient IV diuresis was related to the volume of UO. However, despite the mean UO of all sessions among all patients being 1.2L, mean LVEDP did not change. Multiple outpatient IV diuresis sessions may be needed to obtain a measurable decrease in LVEDP. There was a strong trend toward greater LVEDP decrease with higher initial LVEDP in HFrEF patients. This may be related to the end-diastolic pressure-volume relation, in which a decrease in pressure per given decrease in volume is greater at higher end-diastolic volumes. More studies are warranted to determine if this noninvasive device can help guide outpatient IV diuresis in HF patients.

Efficacy of Intravenous Chlorothiazide for Refractory Acute Decompensated Heart Failure Unresponsive to Adjunct Metolazone.

To assess the efficacy of intravenous chlorothiazide in patients with acute decompensated heart failure (ADHF) who were determined to be loop diuretic resistant and refractory to metolazone. Retrospective cohort study with patients serving as their own controls. Large, academic, tertiary care hospital. Forty-five patients with ADHF who had an inadequate response to high-dose loop diuretics and then received at least one dose of oral metolazone 5 mg or greater (metolazone index dose) followed by at least one dose of intravenous chlorothiazide 500 mg (chlorothiazide index dose) if the response to metolazone was considered inadequate, according to the institutional protocol, between February 4, 2013, and February 28, 2015, were included. If multiple doses of metolazone were administered, the last dose given before the chlorothiazide index dose was considered the index dose; the metolazone index dose had to have been administered more than 2 hours before the chlorothiazide index dose. Data for a total of 90 diuretic doses (45 metolazone, 45 chlorothiazide) were included in the analysis. The median dose of loop diuretic in intravenous furosemide equivalents given over the 24-hour period before the metolazone index dose was 400 mg. The average length of stay was 34.7 days, and in-hospital mortality was 35.6% (16/45 patients). The primary end point of a net-negative urine output of 500 ml or greater during the 12 hours after the index dose occurred in 42.2% (19/45 patients) and 35.5% (16/45 patients) for the chlorothiazide and metolazone doses, respectively (p=0.581). The median 12-hour urine output following administration of metolazone was 810 ml (interquartile range [IQR] 866 ml) versus 1075 ml (IQR 940 ml) following administration of chlorothiazide (p=0.363). Compared with metolazone, the chlorothiazide doses did not result in an increase in urine output of at least 500 ml during the 12 hours following the dose relative to the 12 hours before the dose (31.1% vs 22.2%, p=0.754). No significant difference in achievement of net-negative urine output of 500 ml or greater during the 12 hours following the chlorothiazide or metolazone dose was noted (42.2% for chlorothiazide vs 35.5% for metolazone, p=0.581). The addition of intravenous chlorothiazide did not result in improved diuresis in patients with ADHF determined to be refractory to loop diuretics and adjunctive oral metolazone.

Safety and effectiveness of the combination acetazolamide and bicarbonates to induce alkaline diuresis in patients with rhabdomyolysis

ObjectivesThe therapeutic goal in rhabdomyolysis includes treatment of the causative factor and symptoms, and prevention of complications. Administration of intravenous fluids and forced alkaline diuresis are essential. Both intravenous bicarbonates...

Diagnostic value of 18F-FDG PET/CT delayed imaging after diuresis in patients with primary bladder tumor

Objective To explore the diagnostic value of 18F-FDG PET/CT delayed imaging after induced diuresis for primary bladder tumor. Methods Fourteen patients (12 males, 2 females; age range 35-88 years) with pathologically confirmed primary bladder tumor (clinical stage T1-3N0M0) were retrospectively analyzed. All patients underwent standard 18F-FDG PET/CT followed by a delayed (2.5-3.0 h later) pelvic imaging post intravenous injection of 20 mg furosemide and oral intake of 600 ml water. A positive lesion was defined as the uptake of 18F-FDG greater than the urine radioactivity and negative as equaled to or less than the urine radioactivity. Diagnostic efficacy of 18F-FDG PET/CT was calculated with pathology as the gold standard. Mann-Whitney u test was used to analyze data. Results There were 12 malignant (11 urothelium carcinomas and 1 squamous cell carcinoma) and 2 benign tumors (papillary epitheliomas). On standard PET/CT imaging, 3 of 12 malignant lesions showed increased metabolism of 18F-FDG and the other 9 were false negative; while the 2 benign tumors showed no abnormal 18F-FDG uptake. The sensitivity, specificity, and accuracy of 18F-FDG PET/CT were 3/12, 2/2 and 5/14, respectively. Sizes of the 3 18F-FDG-avid malignant lesions were greater than those of other 9 18F-FDG-negative lesions (26, 30, 35 mm vs (15.6±6.3) mm; Z=-2.315, P<0.05). The sensitivity, specificity, and accuracy of delayed pelvic imaging were 11/12, 2/2, 13/14, respectively. Conclusion 18F-FDG PET/CT delayed imaging after diuresis has a high diagnostic efficacy for primary bladder tumor. Key words: Bladder neoplasms; Tomography, emission-computed; Tomography, X-ray computed; Deoxyglucose

Should furosemide be avoided in acute right ventricular myocardial infarction?

BackgroundDiuretics are conventionally prohibited in acute right ventricular myocardial infarction. AimsTo assess the benefit of diuretics compared to fluid expansion in patients with inferior myocardial infarction extended to the right ventricule. MethodsOf 295 patients admitted for inferior or posterior acute myocardial infarction between November 2008 and November 2010, 77 had a right ventricular extension. Among these 77 patients, 19 presented with oligoanuria (<0.5mL/kg per hour) and no criteria for cardiogenic shock. Overall, 11 patients were treated by low dose of furosemide (40 to 80mg) and eight received fluid expansion using isotonic saline solution. ResultsBaseline right ventricular dilatation and dysfunction, systolic blood pressure and heart rate were similar between the groups. Twenty-four hours after treatment, urine output was similar between the two groups but only the patients in the diuretic group improved their blood pressure (103±16mmHg versus 127±20mmHg, P<0.001), heart rate (71±15 bpm versus 76±13 bpm, P=0.03), creatinin level and alanine aminotrasferase plasmatic level. Hospitalization duration and the need of inotropic support were similar in the two groups. ConclusionsDiuretics and fluid expansion provide similar efficiency for triggering diuresis in patients with right ventricular infarction and oligoanuria but only diuretics seem to be associated with improvement in hemodynamic status and venous congestion.

Dry Lungs Are Happy Lungs

In 2006, ARDSNet investigators demonstrated that aggressive diuresis of patients with acute respiratory distress syndrome (ARDS) resulted in earlier

Urinary output and fractional excretion of sodium and urea as indicators of transient versus intrinsic acute kidney injury during early sepsis

IntroductionThe pathophysiology of acute kidney injury (AKI) in sepsis is ill defined. We investigated parameters associated with low glomerular filtration, and their predictive value to discriminate transient from intrinsic septic AKI.MethodsIn 107 sepsis patients, AKI was defined by the Risk, Injury, Failure, Loss of Kidney Function, End-stage renal disease (RIFLE) urinary output or serum creatinine criterion, or both. Transient AKI (TAKI) versus intrinsic AKI was defined as RIFLE R, I, or F on the first day evolving to no AKI or not, respectively, over the following 5 days. Fractional excretion of sodium (FENa), urea (FEUrea), and NGAL (FENGAL) at admission (d0t0), 4 (d0t4), and 24 hours (d1) was determined.ResultsIncluding versus not including the urinary-output criterion of RIFLE increased AKI from 43% to 64.5%. Median uNGAL levels and FENGAL were lower in no AKI versus transient AKI when AKI was defined based on creatinine (P = 0.002 and P = 0.04, respectively), but not when based on urinary output (P = 0.9 and P = 0.49, respectively). FENa < 1% and FEUrea <35% was present in 77.3% and 63.2% of patients. Urinary NGAL was higher (P < 0.001) in those with high versus low fractional sodium excretion, but this was only in patients with transient or intrinsic AKI (P < 0.001 in subgroups), and not in patients without AKI. The negative predictive value for either intrinsic AKI or not restoring diuresis in patients with FENa > 0.36% and FEUrea > 31.5% was 92% and 94.5% respectively.ConclusionsA low FENa and FEUrea is highly prevalent in the first hours of sepsis. In sepsis, oliguria is an earlier sign of impending AKI than increase in serum creatinine. A combination of a high FENa and a low FEUrea is associated with intrinsic AKI, whereas a combined high FENa and FEUrea is strongly predictive of transient AKI.

Minimizing the Renal Toxicity of Iodinated Contrast

A substantial proportion of adults with coronary disease are at risk for contrast-induced acute kidney injury (CI-AKI), manifested primarily by underlying chronic kidney disease, defined as an estimated glomerular filtration rate <60 mL · min−1 · /1.73−2.1 Although patients commonly understand that they have heart disease, studies have shown that <10% of those with chronic kidney disease are actually aware of this problem; thus, if not emphasized by the cardiologist during the consent before angiography, CI-AKI may come as a surprise to patients and their families after the procedure.2–4 All forms of intravascular iodinated contrast are very water soluble, freely filtered by the glomerulus, and avidly taken up by renal tubular cells in the loop of Henle, and are retained in patients with chronic kidney disease within tubular cells and the peritubular space for ≈7 days where there is direct oxidative cellular damage, sloughing of renal tubular cells and brush border material, and acute tubular dysfunction.5 Thus, the interest in reducing CI-AKI and its translation, if …

Residual renal function and erectile dysfunction in patients on hemodialysis

Residual renal function and erectile dysfunction are important parameters of quality of life in dialysis patients. The purpose of our investigation was to determine correlations between erectile dysfunction and residual diuresis in patients on hemodialysis. The survey was organized as a cross-sectional study in men aged up to 65 years on hemodialysis. All respondents voluntarily completed the questionnaire of the International Index of Erectile Function (IIEF)-5. Demographic and anthropometric characteristics, the duration of dialysis, smoking, alcohol consumption, residual renal function, comorbidity, and routine biochemical parameters were determined for all patients. The adequacy of dialysis was calculated as Kt/V. Based on residual renal function, the patients were divided into a group without residual diuresis and a group with preserved residual renal function. Nearly two-thirds of our patients did not have preserved diuresis, while 82.8% of our respondents had erectile dysfunction. Patients with preserved residual renal function were heavier (P = 0.047) and had higher body mass index (P = 0.047), but the prevalence of cardiovascular disease (P < 0.0001) and erectile dysfunction (P < 0.0015) was lower, compared to patients without residual diuresis. The regression model also demonstrated a statistically significant relationship between the residual diuresis and the total IIEF score (b = 4.74; P < 0.001). Hemodialysis patients with preserved diuresis retain erectile function better.

Obesity and acute kidney injury: fact or artifact?

Dear Editor, We read with interest the article of Druml et al. [1] in which the authors argue that obesity is an independent risk factor for developing acute kidney injury (AKI) and that, in contrast to the usual bad prognosis for intensive care unit (ICU) patients with AKI, the riskadjusted hospital mortality rate in their study was lower in obese than in nonobese patients. In their study, AKI was established following the RIFLE F class criteria, in accordance with the recent International Consensus Conference recommending the RIFLE criteria for the diagnosis of AKI [2]. RIFLE criteria as well as the closely similar AKIN criteria are based on increased creatinine plasma levels and/or a state of persistent low diuresis in patients. When these definitions are applied, urinary output is expressed as milliliters (urinary output) per kilogram (body weight). However, the relation between urinary output and body weight is not easy to comprehend. Several factors in obese patients may interfere with renal function, such as abdominal compartment syndrome, especially in morbid obese patients [3] or hyperfiltration syndrome patients [4]. In addition, several mechanisms that are independent of body weight may influence urine production, such as osmotic balance and concentrating power of the kidneys. Thus, at the present time, there is no definitive evidence demonstrating that urinary output may be related to body weight. Druml et al. do not provide the creatinine plasma levels in their article [1]. Since RIFLE F can be assessed by a threefold increase in plasma creatinine or by a urinary output of\0.3/ml/kg/h persisting for 24 h, it is important to know, for each group in their study, the proportion of AKI diagnoses established only using the urinary output criteria. In a study involving 82 patients with body mass index (BMI) [35 compared to 102 patients with BMI\30, we did not find any difference in the occurrence of renal failure based on an assessment of plasma creatinine determination [5]. In another study in which the differences between RIFLE and AKIN scores were compared, urine output criteria was normalized, assuming an average patient weight of 70 kg [6]. Thus, it is important to know if the paradoxically better prognosis of AKI in obese patients in the study of Druml et al. [1] was not actually influenced by the power given to an overestimation of renal dysfunction in some of the obese patients.

Rubbing Salt into Wounds: Hypertonic Saline to Assist with Volume Removal in Heart Failure

Traditionally accepted management strategies for patients with heart failure include sodium and fluid restriction, neurohormonal blockade, and the use of loop diuretics to achieve and maintain euvolemia. Despite continued advances in medical and device therapy, fluid management remains a significant problem in patients with the cardiorenal syndrome (manifested as diuretic resistance and worsening renal function with more aggressive attempts at volume removal). This article examines the counterintuitive use of hypertonic saline as a potential therapy to facilitate diuresis in patients with decompensated heart failure and diuretic resistance. Low-volume hypertonic saline administration offsets counterproductive neurohormonal upregulation, transiently improves hemodynamics, and promotes renal sodium excretion with accompanied net water loss and preservation of renal function. This "new" therapeutic tool should be explored further as an adjunct to current medical therapies in the management of patients with refractory volume overload.

Effect of Right Ventricular Function and Venous Congestion on Cardiorenal Interactions During the Treatment of Decompensated Heart Failure

Recent reports have demonstrated the adverse effects of venous congestion on renal function (RF) and challenged the assumption that worsening RF is driven by decreased cardiac output (CO). We hypothesized that diuresis in patients with right ventricular (RV) dysfunction, despite decreased CO, would lead to a decrease in venous congestion and resultant improvement in RF. We reviewed consecutive admissions with a discharge diagnosis of heart failure. RV function was assessed by multiple echocardiographic methods and those with >or=2 measurements of RV dysfunction were considered to have significant RV dysfunction. Worsening RF was defined as an increase in creatinine of >or=0.3 mg/dl and improved RF as improvement in glomerular filtration rate >or=25%. A total of 141 admissions met eligibility criteria; 34% developed worsening RF. Venous congestion was more common in those with RV dysfunction (odds ratio [OR] 3.3, p = 0.009). All measurements of RV dysfunction excluding RV dilation correlated with CO (p <0.05). Significant RV dysfunction predicted a lower incidence of worsening RF (OR 0.21, p <0.001) and a higher incidence of improved RF (OR 6.4, p <0.001). CO emerged as a significant predictor of change in glomerular filtration rate during hospitalization in those without significant RV dysfunction (r = 0.38, p <0.001). In conclusion, RV dysfunction is a strong predictor of improved renal outcomes in patients with acute decompensated heart failure, an effect likely mediated by relief of venous congestion.

TORAFIC study protocol: torasemide prolonged release versus furosemide in patients with chronic heart failure

Loop diuretics, such as torasemide and furosemide, are important agents in the treatment of chronic heart failure. Beneficial effects of torasemide immediate-release formulation beyond diuresis have been documented as the ability of this compound to inhibit myocardial synthesis and deposition of collagen type I in patients with chronic heart failure. In addition, torasemide-treated patients, but not furosemide-treated patients, showed decreased serum concentrations of the C-terminal propeptide of procollagen type I, a biochemical marker of myocardial fibrosis. The aim of the TORAFIC study is to test the efficacy of torasemide prolonged-release formulation (PR) in reducing myocardial fibrosis in chronic heart failure in a large, randomized clinical trial. Methods: This prospective, Phase IV, randomized, blinded end point, active-controlled clinical trial will randomize 142 patients with chronic heart failure in New York Heart Association functional class II–IV to 8 months treatment with either torasemide-PR (10–40 mg daily) or furosemide (40–160 mg daily). The primary objective is to test the hypothesis that torasemide-PR is superior to furosemide in reducing myocardial fibrosis. The primary outcome measure is the difference in the change of serum propeptide of procollagen type I concentration from the initial to the final visit between both study groups. Secondary outcome measures include all efficacy variables related to heart failure (signs and symptoms, ECG, echocardiogram and serum levels of N-terminal brain natriuretic propeptide). Secondary safety variables are heart rate, blood pressure, laboratory data, adverse events, cardiovascular events (hospital admission, emergency department visits) and quality of life (Minnesota questionnaire). Discussion: This trial will test whether torasemide-PR possesses antifibrotic properties, which may provide an additional benefit beyond diuresis in patients with chronic heart failure.

Acute and chronic metabolic acidosis interferes with aquaporin-2 translocation in the rat kidney collecting ducts

Renal aquaporin-2 (AQP2) expression plays a key role in urine concentration. However, it is not known whether metabolic acidosis affects urine-concentrating ability through AQP2 expression in the kidney and urine. We examined urinary excretion and renal expression of AQP2 in control and acidosis rats, using RT-competitive PCR, immunoblot and immunocytochemistry. Urinary excretion of AQP2 is decreased by 92% even with the increase in AQP2 mRNA and protein expressions in the collecting ducts by metabolic acidosis in rats. Urine osmolality in control rats was 1670+/-198 mOsm per kg H(2)O, and immunocytochemistry revealed the presence of AQP2 in the apical plasma membrane of the principal cells in the collecting ducts. Urine osmolality in acidosis rats was lower than that in control (1397+/-243 mOsm per kg H(2)O), and immunocytochemistry showed the diffuse presence of AQP2 in the cytoplasm of the principal cells. Differential centrifugation-coupled immunoblot showed a significant decrease in the ratio of AQP2 in plasma membrane-enriched fraction to that in intracellular vesicle-enriched fraction by metabolic acidosis. In summary, AQP2 translocation is largely decreased by metabolic acidosis even with increased expression in the collecting ducts. A disorder of AQP2 translocation in the collecting ducts with acidosis may be responsible for the diuresis in patients with chronic renal failure.

ECG Leads I and II to Evaluate Diuresis of Patients with Congestive Heart Failure Admitted to the Hospital via the Emergency Department

Attenuation of electrocardiogram (ECG) QRS complexes is observed in patients with a variety of illnesses and peripheral edema (PERED), and augmentation with alleviation of PERED. Serial ECGs in stable individuals display variation in the amplitude of QRS complexes in leads V1-V6, stemming from careless placement of recording electrodes on the chestwall. Electrocardiographs record only leads I and II, and mathematically derive the other four limb leads in real time. This study evaluated the sum of the amplitudes of ECG leads I and II, along with other sets of ECG leads in the monitoring of diuresis in patients with congestive heart failure (CHF). Twenty patients with CHF had ECGs and weights recorded on admission and at discharge. The amplitude of the QRS complexes in all ECG leads were measured and sums of I and II, all limb leads, V1-V6, and all 12 leads were calculated. There was a good correlation between the weight loss and the increase in the sums of the amplitudes of the QRS complexes from leads I and II (r = 0.55, P = 0.012), and the six limb leads (r = 0.68, P = 0.001), but a poor correlation with the V1-V6 leads (r = 0.04, P = 0.85) and all 12 leads (r = 0.1, P = 0.40). Sums of the amplitudes of the ECG QRS complexes from leads I and II constitute a reliable, easily obtainable, ubiquitously available, bedside clinical index, which can be employed in the diagnosis, monitoring of management, and follow-up of patients with CHF.

ECG Changes and Voltage Attenuation in Congestive Heart Failure

The electrocardiogram (ECG) is invaluable in providing diagnosis, prognosis, and information for decision making in the management of patients with congestive heart failure (CHF). In addition to the traditional applications of the ECG, which are of importance in the management of patients with CHF, and include indeed the bulk of ECG derived information, a recently described association of peripheral edema with attenuated ECG voltage, provides an expanded dimension in diagnostics. These attenuations result in decreased amplitude of QRS complexes, P-waves, and shortened duration of QRS complexes and QT intervals, with significant diagnostic implications. Alleviation of peripheral edema in response to diuresis in patients with CHF reverses all above alterations.

Urodilatin: A better natriuretic peptide?

The kidney natriuretic peptide urodilatin (ie, ularitide) decreases pulmonary capillary wedge pressure (PCWP) but does not cause diuresis in persons with congestive heart failure (CHF). Thirty-three percent of patients with CHF treated with 30 ng/kg/min ularitide develop hypotension with systolic blood pressures below 90 mmHg. Nesiritide and atrial natriuretic peptide lower PCWP and cause hypotension. They do not produce diuresis or natriuresis in patients with CHF. The best natriuretic peptide for treating CHF is the cardiac hormone vessel dilator which decreases PCWP and decreases systemic and pulmonary vascular resistance while simultaneously increasing cardiac output and cardiac index. What makes the vessel dilator markedly better than atrial natriuretic peptide, nesiritide, and ularitide for treatment of CHF is that it enhances sodium excretion fivefold and causes a fivefold enhanced diuresis in patients with CHF with its biologic effects lasting over 6 hours compared with less than 30 minutes for the above peptides.