sodium-bicarbonate and Heart-Failure

Topics: Animals; Antidepressive Agents, Tricyclic; Antidotes; Aspirin; Heart Failure; Humans; Hypokalemia; Injections, Intravenous; Sodium Bicarbonate; Tachycardia, Ventricular

The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) has updated its 1999 guidelines on contrast medium-induced nephropathy (CIN).. Topics reviewed include the definition of CIN, the choice of contrast medium, the prophylactic measures used to reduce the incidence of CIN, and the management of patients receiving metformin. Key Points • Definition, risk factors and prevention of contrast medium induced nephropathy are reviewed. • CIN risk is lower with intravenous than intra-arterial iodinated contrast medium. • eGFR of 45 ml/min/1.73 m (2) is CIN risk threshold for intravenous contrast medium. • Hydration with either saline or sodium bicarbonate reduces CIN incidence. • Patients with eGFR ≥ 60 ml/min/1.73 m (2) receiving contrast medium can continue metformin normally.

Topics: Contrast Media; Coronary Angiography; Europe; Female; Fluid Therapy; Gadolinium; Glomerular Filtration Rate; Heart Failure; Humans; Injections, Intra-Arterial; Injections, Intravenous; Iodine; Male; Practice Guidelines as Topic; Renal Insufficiency; Risk Factors; Sodium Bicarbonate; Sodium Chloride

Intravenous sodium bicarbonate has been proposed to reduce the risk for contrast-induced nephropathy (CIN).. To determine the effect of sodium bicarbonate on the risk for CIN.. MEDLINE, PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials from 1950 to December 2008; conference proceedings; and ClinicalTrials.gov, without language restriction.. Randomized, controlled trials of intravenous sodium bicarbonate that prespecified the outcome of CIN as a 25% increase in baseline serum creatinine level or an absolute increase of 44 micromol/L (0.5 mg/dL) after radiocontrast administration.. Using standardized protocols, 2 reviewers serially abstracted data for each study.. 23 published and unpublished trials with information on 3563 patients and 396 CIN events were included. The pooled relative risk was 0.62 (95% CI, 0.45 to 0.86), with evidence of significant heterogeneity across studies (I(2) = 49.1%; P = 0.004). Some heterogeneity was due to the difference in the estimates between published and unpublished studies: relative risk, 0.43 (CI, 0.25 to 0.75) versus 0.78 (CI, 0.52 to 1.17), respectively. Meta-regression showed that small, poor-quality studies that assessed outcomes soon after radiocontrast administration were more likely to suggest benefit (P < 0.05 for all). No clear effects of treatment on the risk for dialysis, heart failure, and total mortality were identified.. Power to assess clinical end points was limited.. The effectiveness of sodium bicarbonate treatment to prevent CIN in high-risk patients remains uncertain. Earlier reports probably overestimated the magnitude of any benefit, whereas larger, more recent trials have had neutral results. Large multicenter trials are required to clarify whether sodium bicarbonate has value for prevention of CIN before routine use can be recommended.. None.

Topics: Acetylcysteine; Contrast Media; Heart Failure; Humans; Injections, Intravenous; Kidney Diseases; Mortality; Renal Dialysis; Risk; Sodium Bicarbonate

We randomized patients with chronic kidney disease (serum creatinine ≥ 1.5 mg/dl or glomerular filtration rate (GFR) <60 ml/min/1.73 m²) in a double-blind fashion to receive saline or sodium bicarbonate prior to and after cardiac or vascular angiography. The primary endpoint was contrast-induced nephropathy (CIN), defined as an increase in serum creatinine by 25% or by 0.5 mg/dl from baseline. Patients with congestive heart failure (CHF), cardiac ejection fraction (EF) <30%, or GFR < 20 ml/min/1.73 m² were excluded. The study was discontinued (after 142 patients were randomized) due to a low incidence of CIN (1.5%). We retrospectively identified all cases of CIN (n = 30) at our institution during the same time period to see if these patients differed from our trial sample. There was no difference in serum creatinine (1.7 ± 0.4 vs. 1.7 ± 0.6 mg/dL), GFR (42.7 ± 9.7 vs. 45.3 ± 3.2 ml/min), incidence of diabetes (51.8% vs. 63.3%), contrast volume (121.7 ± 63.8 vs. 122.7 ± 68.3 ml), ACE inhibitor or angiotensin receptor blocker use (54.0% vs 63.3%), and periprocedure diuretic use (33.1% vs 26.7%). On multivariate analysis, only a cardiac ejection fraction (EF) of less than 40% was significantly associated with CIN (odds ratio, 4.52; 95% confidence interval, 1.30-15.71; P = 0.02). In all, 22/30 patients (73.3%) who developed CIN had at least one or more characteristics that would have excluded their enrollment in our randomized trial including evidence of congestive heart failure (17/30 patients), EF less than 30% (9 patients), age greater than 85 years (2 patients), or advanced renal failure with a baseline GFR of less than 20 cc/min (1 patient). In summary, patients with CKD without evidence of CHF who receive adequate hydration appear to have a very low risk of CIN associated with angiography. A low EF (less than 40%) appeared to be the most significant risk factor for CIN in our population.

Topics: Aged; Chronic Disease; Contrast Media; Double-Blind Method; Heart Failure; Humans; Incidence; Kidney Diseases; Retrospective Studies; Sodium Bicarbonate

An important role of the increased stimulation of skeletal muscle ergoreceptors (intramuscular afferents sensitive to products of muscle work) in the genesis of symptoms of exertion intolerance in chronic heart failure (CHF) has been proposed. With the use of selective infusions and dietary manipulation methods, we sought to identify the role of H+, K+, lactate, and peripheral hemodynamics on ergoreflex overactivation.. Ten stable CHF patients (aged 67.9+/-2.5 years, peak oxygen uptake 16.3+/-1.2 mL x kg(-1) x min(-1)) and 10 age-matched and sex-matched healthy subjects were studied. The ergoreflex contribution to ventilation was assessed by post-handgrip regional circulatory occlusion (PH-RCO) and computed as the difference in ventilation between PH-RCO and a control run without PH-RCO. This test was performed on 6 separate occasions. On each occasion a different chemical was infused (insulin, sodium nitroprusside, sodium bicarbonate, dopamine, or saline) or a 36-hour glucose-free diet was undertaken before the test. During all stages of the protocol, the local muscular blood effluent concentrations of H+, K+, glucose, and lactate were assessed. An ergoreflex effect on the ventilatory response was seen in patients (versus control subjects) during the saline infusions (6.7+/-2.3 L/min versus -0.1+/-0.5 L/min, P<0.01). The only intervention to significantly lower the ergoreflex was sodium bicarbonate (0.4+/-0.3 L/min versus -0.2+/-0.4 L/min in control subjects, P=NS; versus saline P<0.05), which also reduced H(+) concentration during exercise (47.4+/-1.3 versus 50.0+/-1.4 nmol/L on saline, P<0.05).. A reduction of the H+ concentration by infusion of sodium bicarbonate abolishes the increased ergoreceptor activity in CHF, suggesting a role of H+ in ergoreflex activation, either directly or indirectly.

Topics: Aged; Chemoreceptor Cells; Dopamine; Exercise Test; Female; Food, Formulated; Hand Strength; Heart Failure; Hemodynamics; Humans; Hydrogen-Ion Concentration; Infusions, Intravenous; Insulin; Lactic Acid; Male; Middle Aged; Muscle, Skeletal; Nitroprusside; Potassium; Protons; Reference Values; Reflex; Sodium Bicarbonate; Sodium Chloride; Ventilation

Patients with chronic kidney disease often experience metabolic acidosis. Whether oral sodium bicarbonate can reduce mortality in patients with metabolic acidosis has been debated for years. Hence, this study was conducted to evaluate the utility of sodium bicarbonate in patients who will undergo dialysis therapy. In this study, we investigated the effect of oral sodium bicarbonate therapy on mortality in patients with end-stage kidney disease (ESKD) initiated on dialysis therapy.. We conducted an observational study of patients when they started dialysis therapy. There were 17 centres participating in the Aichi Cohort Study of Prognosis in Patients Newly Initiated into Dialysis. Data were available on patients' sex, age, use of sodium bicarbonate, drug history, medical history, vital data, and laboratory data. We investigated whether patients on oral sodium bicarbonate for more than three months before dialysis initiation had a better prognosis than those without sodium bicarbonate therapy. The primary outcome was defined as all-cause mortality.. The study included 1524 patients with chronic kidney disease who initiated dialysis between October 2011 and September 2013. Among them, 1030 were men and 492 women, with a mean age of 67.5 ± 13.1 years. Of these, 677 used sodium bicarbonate and 845 did not; 13.6% of the patients in the former group and 21.2% of those in the latter group died by March 2015 (p <  0.001). Even after adjusting for various factors, the use of sodium bicarbonate independently reduced mortality (p <  0.001).. The use of oral sodium bicarbonate at the time of dialysis initiation significantly reduced all-cause mortality in patients undergoing dialysis therapy.

Topics: Acidosis; Administration, Oral; Aged; Female; Heart Failure; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prognosis; Propensity Score; Prospective Studies; Renal Dialysis; Renal Insufficiency, Chronic; Sodium Bicarbonate

Contrast-Associated Acute Kidney Injury (CA-AKI) is a serious complication associated with percutaneous coronary intervention (PCI). Patients with chronic kidney disease (CKD) have an elevated risk for developing this complication. Although CA-AKI prophylactic measures are available, the supporting literature is variable and inconsistent for periprocedural hydration and N-acetylcysteine (NAC), but is stronger for contrast minimization.. We assessed the prevalence and variability of CA-AKI prophylaxis among CKD patients undergoing PCI between October 2007 and September 2015 in any cardiac catheterization laboratory in the VA Healthcare System. Prophylaxis included periprocedural hydration with normal saline or sodium bicarbonate, NAC, and contrast minimization (contrast volume to glomerular filtration rate ratio ≤ 3). Multivariable hierarchical logistic regression models quantified site-specific prophylaxis variability. As secondary analyses, we also assessed CA-AKI prophylaxis measures in all PCI patients regardless of kidney function, periprocedural hydration in patients with comorbid CHF, and temporal trends in CA-AKI prophylaxis.. From 2007 to 2015, 15,729 patients with CKD underwent PCI. 6928 (44.0%) received periprocedural hydration (practice-level median rate 45.3%, interquartile range (IQR) 35.5-56.7), 5107 (32.5%) received NAC (practice-level median rate 28.3%, IQR 22.8-36.9), and 4656 (36.0%) received contrast minimization (practice-level median rate 34.5, IQR 22.6-53.9). After adjustment for patient characteristics, there was significant site variability with a median odds ratio (MOR) of 1.80 (CI 1.56-2.08) for periprocedural hydration, 1.95 (CI 1.66-2.29) for periprocedural hydration or NAC, and 2.68 (CI 2.23-3.15) for contrast minimization. These trends were similar among all patients (with and without CKD) undergoing PCI. Among patients with comorbid CHF (n = 5893), 2629 (44.6%) received periprocedural hydration, and overall had less variability in hydration (MOR of 1.56 (CI 1.38-1.76)) compared to patients without comorbid CHF (1.89 (CI 1.65-2.18)). Temporal trend analysis showed a significant and clinically relevant decrease in NAC use (64.1% of cases in 2008 (N = 1059), 6.2% of cases in 2015 (N = 128, p = < 0.0001)) and no significant change in contrast-minimization (p = 0.3907).. Among patients with CKD undergoing PCI, there was low utilization and significant site-level variability for periprocedural hydration and NAC independent of patient-specific risk. This low utilization and high variability, however, was also present for contrast minimization, a well-established measure. These findings suggest that a standardized approach to CA-AKI prophylaxis, along with continued development of the evidence base, is needed.

Topics: Acetylcysteine; Acute Kidney Injury; Aged; Contrast Media; Coronary Angiography; Female; Fluid Therapy; Free Radical Scavengers; Glomerular Filtration Rate; Heart Failure; Humans; Male; Middle Aged; Percutaneous Coronary Intervention; Perioperative Care; Postoperative Complications; Practice Guidelines as Topic; Renal Insufficiency, Chronic; Saline Solution; Sodium Bicarbonate; United States; Veterans Health Services

Topics: Acidosis, Lactic; Acute Kidney Injury; Aged; Alanine; Continuous Renal Replacement Therapy; Diabetes Mellitus, Type 2; Female; Heart Failure; HIV Infections; Humans; Oliguria; Reverse Transcriptase Inhibitors; Sodium Bicarbonate; Tenofovir

An 82-year-old man presented with 6 months of difficulties of falling asleep. He described a feeling of fading breath culminating in breathing arrest when he becomes drowsy. These recurrent events prevented him from falling asleep. Symptoms would only appear when he went to sleep but not during wakefulness. Medical history comprised several episodes of acute decompensated heart failure due to supraventricular tachyarrhythmia with need for hospitalization during the last 2 years. He additionally had two-vessel coronary artery disease with myocardial infarction, pulmonary hypertension, chronic atrial fibrillation, peripheral arterial disease, and chronic kidney disease (stage 3). Medication included diuretics, sodium bicarbonate, angiotensin II receptor antagonist, beta-blocker, statin, clopidogrel, and phenprocoumon without sedatives or analgesics.

Topics: Aged, 80 and over; Alkalosis, Respiratory; Heart Failure; Humans; Male; Sleep Apnea, Central; Sleep Initiation and Maintenance Disorders; Sodium Bicarbonate

A 59-year-old man was referred to the hospital for psychiatric reasons. To control hypertension and chronic heart failure he had been treated with 5 mg ramipril and 12.5 mg hydrochlorothiazide. In addition, he received 25 mg spironolactone. A prostate disease was diagnosed two months ago.. Laboratory analysis revealed a severe hyperkalemia (9.3 mmol/l) as well as an increase in creatinine (24.3 mg/dl) and urea nitrogen (349.0 mg/dl). The ECG showed a bradycardia with increased T-wave amplitudes. Abdominal sonography revealed a full urinary bladder.. Administration of terbutaline, sodium bicarbonate, and glucoseinfusion lowered potassium level to 6.3 mmol/l before hemodialysis was started. Hyperplasia of the prostate gland was found to be the reason for acute renal failure. Dialysis treatment was only temporarily necessary; afterwards, the patient was transferred to the urology department for subsequent therapy.. Hyperkalemia is a life-threatening emergency that requires immediate therapy. Conservative treatment allows to partially correct water-electrolyte imbalance until hemodialysis can be performed. Hyperkalemia often results from the administration of combination therapy with ACE-inhibitors/AT (1)-antaganonists and antikaliuretic diuretics (spironolactone) in renal failure.

Topics: Acute Kidney Injury; Adrenergic beta-Agonists; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Bradycardia; Diuretics; Drug Therapy, Combination; Electrocardiography; Emergencies; Glucose; Heart Failure; Humans; Hydrochlorothiazide; Hyperkalemia; Hypertension; Male; Mental Disorders; Middle Aged; Prostatic Hyperplasia; Ramipril; Renal Dialysis; Sodium Bicarbonate; Terbutaline

Severe coagulation defects often develop in neonates undergoing cardiac surgery, both as a result of the surgical intervention, and as pre-existing defects in the hemostatic mechanisms. The following case report describes a newborn patient with complex congenital heart disease and respiratory failure whose pre-operative coagulopathy was aggressively managed prior to surgical correction. A 5-day-old, 2.5 kg child presented with interrupted aortic arch, ventricular septal defect, atrial septal defect, and patent ductus arteriosus. On admission, he was in respiratory arrest suffering from profound acidemia. In addition, the child was hypothermic (30.1 degrees C), septic (Streptococcus viridans), and coagulopathic (disseminated intravascular coagulation-DIC). The patient was immediately intubated and initial coagulation assessment revealed the following: prothrombin time (PT) 48.9 s (international normalized ratio (INR) 15.7), activated partial thromboplastin time (aPTT) >106 s, platelet count 30,000 mm(3), fibrinogen 15 mg dL(-1) and antithrombin III (AT-III) 10%. Before cardiac surgery could be performed, the patient's DIC was corrected with the administration of cryoprecipitate (15 ml), fresh frozen plasma (300 ml), and platelets (195 ml). In spite of the large transfusion of fresh frozen plasma, the AT-III activity, measured as a percentage, remained depressed at 33. Initial thromboelastographic (TEG) determination revealed an index of +2.02, and following 100 IU administration of an AT-III concentrate, declined to -2.32. Sequential TEG profiles were performed over several days, with the results used to guide both transfusion and medical therapy. The congenital heart defect correction was subsequently performed with satisfactory initial results, but the patient developed a fungal infection and expired on the 16th post-operative day. The present case describes techniques of coagulation management for a newborn with both a severe hemostatic defect and congenital heart disease.

Topics: Acidosis, Respiratory; Anti-Bacterial Agents; Antithrombin III; Antithrombin III Deficiency; Blood Coagulation Tests; Colloids; Combined Modality Therapy; Disseminated Intravascular Coagulation; Dobutamine; Dopamine; Drug Therapy, Combination; Endocarditis, Bacterial; Fatal Outcome; Fungemia; Heart Defects, Congenital; Heart Diseases; Heart Failure; Humans; Infant, Newborn; Male; Nitric Oxide; Plasma; Platelet Transfusion; Postoperative Complications; Preoperative Care; Sodium Bicarbonate; Streptococcal Infections; Thrombosis

We experienced two Duchenne muscular dystrophy patients with advanced congestive heart failure, who showed abrupt severe hyponatremia, hyperkalemia and metabolic acidosis. Two patients received respiratory management, parenteral nutrition, and drugs including angiotensin converting enzyme inhibitors (ACEI). The patient 1 who was 19 years old showed abdominal pain, hematuria, diarrhea and disorientation. Laboratory findings were as follows; Na 120 mEq/L, K 7.3 mEq/L, BUN > 140 mg/dl (scale over), ACTH 20.2 pg/ml, cortisol 25 micrograms/dl, renin 40.7 ng/ml/hr and aldosterone 203 ng/dl. Arterial blood gas analysis (ABG) showed metabolic acidosis (pH 7.232). Combination therapy with hydrocortisone, glucose-insulin therapy (GIT) and NaHCO3 successfully rescued this patient. The patient 2 (28 years of age) was admitted to our hospital because of congestive heart failure. Laboratory findings were as follows; Na 129 mEq/L, K 5.5 mEq/L, BUN 60 mg/dl, cortisol 21 micrograms/dl, renin 36 ng/ml/hr and aldosterone 47 ng/dl. He complained abdominal discomforts from the next day of admission. Ten days after the admission Na, K and BUN were 111 mEq/L, 6.2 mEq/L and 154 mg/dl, respectively. ABG showed compensated metabolic acidosis. He fell into shock during GIT therapy. Laboratory findings at that time were as follows; Na 108 mEq/L, K 3.2 mEq/L, ACTH 77.6 pg/ml, cortisol 24 micrograms/dl, renin 58 ng/ml/hr and aldosterone 24 ng/dl. Although hydrocortisone was introduced, he could not recover and died. There are some reports about life-threatening electrolyte abnormalities and metabolic acidosis in the patients receiving ACEI. These phenomena were more frequent in patients with renal dysfunction and/or congestive heart failure. Hyponatremia, hypovolemia, combination therapy with nonsteroidal anti-inflammatory drugs (NSAID) and/or potassium sparing diuretics were reported as risk factors. We could not prove the correlation between the acute changes in our cases and ACEI. However ACEI is suspicious, because many of these risk factors were observed in our cases. Aldosterone was extremely elevated in the patient 1 when potassium was severely elevated. On the other hand, the patient 2 showed lower aldosterone level after correction of potassium than that on admission. Potassium is regarded as a major secretion factor of aldosterone for patients receiving ACEI. The fact the patient 2 fell into shock during GIT, tells us that we should use steroid simultaneously when we try to

Topics: Acidosis; Adult; Angiotensin-Converting Enzyme Inhibitors; Anti-Inflammatory Agents, Non-Steroidal; Diuretics; Glucose; Heart Failure; Humans; Hydrocortisone; Hyponatremia; Insulin; Male; Muscular Dystrophy, Duchenne; Risk Factors; Sodium Bicarbonate; Treatment Outcome; Water-Electrolyte Imbalance

Topics: Bicarbonates; Carbon Dioxide; Cardiac Output; Heart Failure; Humans; Oxygen Consumption; Sodium; Sodium Bicarbonate

In a patient with viral pneumonia, acute respiratory and renal failure and metabolic acidosis, a reduction in left ventricular stroke work was observed on the three occasions that 100 ml of 8.4% sodium bicarbonate was infused. Blood pressure and cardiac output decreased on two of the occasions. Since intravenous sodium bicarbonate may produce adverse cardiovascular effects, a right heart catheter should be inserted to monitor these effects when alkali therapy is administered to an acutely ill patient with metabolic acidosis.

Topics: Acidosis; Acute Kidney Injury; Aged; Bicarbonates; Heart Failure; Hemodynamics; Humans; Male; Pneumonia, Viral; Sodium; Sodium Bicarbonate

A case of self-poisoning with ethylene glycol is presented. The metabolic upset induced by ingestion of this substance is discussed and the principles underlying treatment with ethyl alcohol, sodium bicarbonate and renal dialysis are outlined. The practical problems experienced with this therapy are detailed. The need for immediate instigation of treatment and for intensive care are emphasised.

Topics: Aged; Bicarbonates; Critical Care; Ethanol; Ethylene Glycols; Heart Failure; Humans; Kidney Failure, Chronic; Male; Peritoneal Dialysis; Sodium Bicarbonate