I found this question tricky. The separate findings are: normal pH but with alkalosis tendency, acute respiratory failure, hypocapnia and normal bicarbonate. The most appropriate answer seems to me to be 1, since the patient does not present a metabolic alkalosis (bicarbonate would be higher), much less an acidosis (bicarbonate would be low). The alkalosis is not mixed either, but is mainly respiratory. The patient is probably hyperventilating because of her respiratory failure, and the kidney which always compensates later is starting to retain HCO3 to compensate and maintain pH. Therefore I believe the correct answer is 1.

I found this question tricky. The separate findings are: normal pH but with alkalosis tendency, acute respiratory failure, hypocapnia and normal bicarbonate. The most appropriate answer seems to me to be [HIDDEN], since the patient does not present a metabolic alkalosis (bicarbonate would be higher), much less an acidosis (bicarbonate would be low). The alkalosis is not mixed either, but is mainly respiratory. The patient is probably hyperventilating because of her respiratory failure, and the kidney which always compensates later is starting to retain HCO3 to compensate and maintain pH. Therefore I believe [HIDDEN].

A 67-year-old woman with a history of congestive heart failure (treated with ramipril and furosemide) and type 2 diabetes (treated with insulin) comes to the emergency room for dyspnea. Blood gas analysis performed while breathing room air shows pH 7.45, paO2 56, PaCO2 30 mm Hg, HCO3 26 mm Hg. What gasometric alteration does the patient present?

Hypoxemic respiratory failure with compensated respiratory alkalosis.

Acute metabolic alkalosis with hypoxemic and hypocapnic respiratory failure.

Chronic normocapnic respiratory insufficiency, without alteration of acid-base balance.

Chronic hypoxemic respiratory failure with compensated metabolic acidosis.

Hypoxemic respiratory failure with compensated mixed alkalosis.

ANESTHESIOLOGY, CRITICAL CARE AND EMERGENCIES

Mixed acid-base disorders, hydroelectrolyte imbalance and lactate production in hypercapnic respiratory failure: the role of noninvasive ventilation.

Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO(2) and PaCO(2) and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis-metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.1 ± 9.8, 36.2 ± 8.9 and 53.3 ± 4.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (p<0.001), lower pH (p = 0.016), lower serum sodium (p = 0.014) and lower chloride (p = 0.038). Hyponatremia without hypervolemic hypochloremia occurred in 11 respiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis-metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated.

Acid–base homeostasis

Acidemia and alkalemia unambiguously refer to the actual change in the pH of the extracellular fluid (ECF). Two other similar sounding terms are acidosis and alkalosis. They refer to the customary effect of a component, respiratory or metabolic. Acidosis would cause an acidemia on its own (i.e. if left "uncompensated" by an alkalosis). Similarly, an alkalosis would cause an alkalemia on its own. In medical terminology, the terms acidosis and alkalosis should always be qualified by an adjective to indicate the etiology of the disturbance: respiratory (indicating a change in the partial pressure of carbon dioxide), or metabolic (indicating a change in the Base Excess of the ECF). There are therefore four different acid-base problems: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. One or a combination of these conditions may occur simultaneously. For instance, a metabolic acidosis (as in uncontrolled diabetes mellitus) is almost always partially

Intravenous hydrochloric acid in patients with metabolic alkalosis and hypercapnia.

During a seven-year period, 15 patients admitted to an intensive care unit with a metabolic alkalosis resistant to saline and potassium chloride infusions and with an arterial pH of greater than 7.44 and arterial carbon dioxide pressure (PaCO2) of greater than 50 mm Hg, while breathing spontaneously, were given hydrochloric acid at 200 mmol/24 h through a central venous line until the arterial pH had decreased to less than 7.36 or PaCO2 had decreased to less than 40 mm Hg. Five patients without respiratory failure had a significant decrease in PaCO2, pH, bicarbonate Ion (HCO3-), and base excess (BE). Four patients with acute respiratory failure had a significant decrease in PaCO2, HCO3-, and BE and an increase in arterial oxygen pressure, indicating that in both of these patient groups alveolar ventilation had improved. Six patients with chronic respiratory failure had a significant decrease in pH, HCO3-, and BE, although there was no significant change in PaCO2, indicating that in this patient group alveolar ventilation could not be consistently increased in response to a reduction in arterial pH.

Acid-base patterns in acute severe asthma.

Acid-base status in acute severe asthma (ASA) remains undefined; some studies report complete absence of metabolic acidosis, whereas others describe it as present in one fourth of patients or more. Conclusion discrepancies would therefore appear to derive from differences in assessment methodology. Only a systematic approach centering on patient clinical findings can correctly establish true acid-base disorder prevalence levels. This study examines acid-base patterns in ASA (314 patients), taking into account both natural history of disease and treatment, in patients free of other diseases altering acid-base status. Data were collected from patients admitted for ASA without prior history of chronic bronchitis, emphysema, kidney or liver disease, heart failure, uncontrolled diabetes mellitus or gastrointestinal illness. Informed consent was obtained for all patients, after study protocol approval by the Institutional Review Board. Arterial blood gases, plasma electrolytes, lactate levels, and FEV(1) were measured on arrival. Severe airway obstruction was found with FEV(1) values of 25.6 ± 10.0%, substantial hypoxemia (PaO(2) 66.1 ± 11.9 mmHg) and increased A-a O(2) gradient (39.3 ± 12.3 mmHg) breathing room air. While respiratory alkalosis occurred in patients with better preservation of FEV1, respiratory acidosis was observed with more severe airway obstruction, as was increased lactate in the majority of patients, independent of PaO(2) and PaCO(2) levels. Predominant acid-base patterns observed in ASA in this patient population included primary hypocapnia, or less frequently, primary hypercapnia. Lactic acidosis occurred in 11% of patients and presented consistently as a mixed acid-base disorder. These findings suggest lactic acidosis results from the combined effects of both ASA and medication-related sympathetic effects.

Base excess

A high base excess, thus metabolic alkalosis, usually involves an excess of bicarbonate. It can be caused by Compensation for primary respiratory acidosis Excessive loss of HCl in gastric acid by vomiting Renal overproduction of bicarbonate, in either contraction alkalosis or Cushing's disease A base deficit (a below-normal base excess), thus metabolic acidosis, usually involves either excretion of bicarbonate or neutralization of bicarbonate by excess organic acids. Common causes include Compensation for primary respiratory alkalosis Diabetic ketoacidosis, in which high levels of acidic ketone bodies are produced Lactic acidosis, due to anaerobic metabolism during heavy exercise or hypoxia Chronic kidney failure, preventing excretion of acid and resorption and production of bicarbonate Diarrhea, in which large amounts of bicarbonate are excreted Ingestion of poisons such as methanol, ethylene glycol, or excessive aspirin

Acid–base homeostasis

and respiratory alkalosis. One or a combination of these conditions may occur simultaneously. For instance, a metabolic acidosis (as in uncontrolled diabetes mellitus) is almost always partially compensated by a respiratory alkalosis (hyperventilation). Similarly, a respiratory acidosis can be completely or partially corrected by a metabolic alkalosis.

Respiratory acidosis

Types Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mEq/L). Causes Acute Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Respiratory acidosis

Diagnosis Diagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH <7.35 and a PaCO2 >45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH. Terminology Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36. See also Acidosis Alkalosis Arterial blood gas Chemical equilibrium pCO2 pH pKa Metabolic acidosis Metabolic alkalosis Respiratory alkalosis References External links Acid–base disturbances

Respiratory alkalosis

Diagnosis The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual. The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentrations (and blood pH) after a respiratory or metabolic acid-base disturbance Classification There are two types of respiratory alkalosis: chronic and acute as a result of the 3–5 day delay in kidney compensation of the abnormality. Acute respiratory alkalosis occurs rapidly, have a high pH because the response of the kidneys is slow. Chronic respiratory alkalosis is a more long-standing condition, here one finds the kidneys have time to decrease the bicarbonate level. pH Alkalosis refers to the process due to which there is elevation of blood pH. Alkalemia refers to an arterial blood pH of greater than 7.45.

[Respiratory regulation system].

In 1874, Kussmaul described "featiful terminal dyspnea" in a case of severe diabetic coma. Probably, this was the first sign of respiratory regulation for metabolic acidosis. After this first case, about 40 years has been needed to establish the theory of acid-base equiribration, namely Henderson-Hasselbalch's equation. pH = 6.1 + log [HCO3-]/[H2CO3] This equation indicates that plasma pH is determined by the ratio of HCO3 concentration and H2CO3 concentration. Because of linear relationship between H2CO3 and PaCO2, pH depend on the ratio of HCO3- and PaCO2. In the state of metabolic acidosis, increase of [H+] stimulates ventilation and decreases the PaCO2. Inversely, in the state of metabolic alkalosis, increase of PaCO2 occurs. These reactions are called "respiratory compensation" or "respiratory regulation". The respiratory regulation system will not retern pH to normal (7.4), but compensation has some limitation which is shown as "SIGNIFICANCE BAND". In this paper, physiological and clinical importance of respiratory regulation and significance band is discussed.

Arterial Blood Gas -- Clinical Significance

Acid-base balance can be affected by the aforementioned respiratory system abnormalities. For instance, acute respiratory acidosis and alkalemia result in acidemia and alkalemia, respectively. Additionally, hypoxemic hypoxia leads to anaerobic metabolism, which causes metabolic acidosis that results in acidemia. Metabolic system abnormalities also affect acid balance, as acute metabolic acidosis and alkalosis result in acidemia and alkalemia. [25] Patients with diabetic ketoacidosis, septic shock, renal failure, drug or toxin ingestion, and gastrointestinal or renal HCO 3 loss exhibit metabolic acidosis. [28] Conditions such as kidney disease, electrolyte imbalances, prolonged vomiting, hypovolemia, diuretic use, and hypokalemia cause metabolic alkalosis. [36]

Arterial Blood Gas -- Results, Reporting, and Critical Findings

Example 1 [28] : ABG: pH = 7.39, PaCO 2 = 51 mm Hg, PaO 2 = 59 mm Hg, HCO 3 = 30 mEq/L and SaO 2 = 90%, on room air. pH is in the normal range, so use 7.40 as a cutoff point, in which case it is < 7.40, and acidosis is present. The elevated PaCO 2 indicates respiratory acidosis, and the elevated HCO 3 indicates a metabolic alkalosis. The value consistent with the pH is PaCO 2 . Therefore, this is a primary respiratory acidosis. The acid-base that is inconsistent with the pH is the elevated HCO3, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective. Last, the decreased PaO 2 indicates an abnormality with oxygenation. However, a history and physical will help delineate the severity and urgency of required interventions, if any. Example 2 [28] : ABG: pH = 7.45, PaCO 2 = 32 mm Hg, PaO 2 = 138 mm Hg, HCO 3 = 23 mEq/L, the base deficit = 1 mEq/L, and SaO 2 is 92%, on room air.

A case of Cushing's syndrome associated with chronic respiratory failure due to metabolic alkalosis.

A case of Cushing's syndrome associated with chronic respiratory failure is presented. Although arterial blood gas analysis showed severe metabolic alkalosis, hypoxemia and mild hypercapnia, the patient had no evidence of pulmonary disease or neuromuscular disorder. Voluntary hyperventilation and inhalation of 100% oxygen (O2) revealed normalized arterial oxygen tension (PaO2). Following the recovery from metabolic alkalosis by the treatment with potassium chloride, PaO2 was elevated and arterial carbon dioxide tension (PaCO2) was lowered. Therefore, it was strongly suggested that the main cause of chronic respiratory failure was compensatory alveolar hypoventilation as a response to metabolic alkalosis.

Respiratory alkalosis

pH Alkalosis refers to the process due to which there is elevation of blood pH. Alkalemia refers to an arterial blood pH of greater than 7.45. Treatment Respiratory alkalosis is very rarely life-threatening, though pH level should not be 7.5 or greater. The aim in treatment is to detect the underlying cause. When PaCO2 is adjusted rapidly in individuals with chronic respiratory alkalosis, metabolic acidosis may occur. If the individual is on a mechanical ventilator then preventing hyperventilation is done via monitoring ABG levels. In popular culture In The Andromeda Strain, one of the characters is exposed to contamination, but saves himself by increasing his respiratory rate to induce alkalosis. See also References Further reading External links Acid–base disturbances

Respiratory compensation

In metabolic alkalosis, chemoreceptors sense a deranged acid-base balance with a plasma pH of greater than normal (>7.4). The chemoreceptors send afferent fibers to the brainstem respiratory centers. The brainstem respiratory centers decrease alveolar ventilation (hypoventilation) to create a rise in arterial carbon dioxide () tension, resulting in a decrease of plasma pH. The respiratory brainstem centers can only compensate for metabolic acid-base disturbances (metabolic acidosis and metabolic alkalosis). Renal compensation is needed to balance respiratory acid-base syndromes (respiratory acidosis and respiratory alkalosis). The kidneys can compensate for both, respiratory and metabolic acid-base imbalances. References Acid–base disturbances

Multiple organ dysfunction syndrome

Four clinical phases have been suggested: Stage 1: the patient has increased volume requirements and mild respiratory alkalosis which is accompanied by oliguria, hyperglycemia and increased insulin requirements. Stage 2: the patient is tachypneic, hypocapnic and hypoxemic; develops moderate liver dysfunction and possible hematologic abnormalities. Stage 3: the patient develops shock with azotemia and acid-base disturbances; has significant coagulation abnormalities. Stage 4: the patient is vasopressor dependent and oliguric or anuric; subsequently develops ischemic colitis and lactic acidosis. Definition Multiple dysfunction syndrome is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. It usually involves two or more organ systems. It calls for an immediate intervention.

Base excess

Interpretation Base excess beyond the reference range indicates metabolic alkalosis if too high (more than +2 mEq/L) metabolic acidosis if too low (less than −2 mEq/L) Blood pH is determined by both a metabolic component, measured by base excess, and a respiratory component, measured by PaCO2 (partial pressure of carbon dioxide). Often a disturbance in one triggers a partial compensation in the other. A secondary (compensatory) process can be readily identified because it opposes the observed deviation in blood pH. For example, inadequate ventilation, a respiratory problem, causes a buildup of CO2, hence respiratory acidosis; the kidneys then attempt to compensate for the low pH by raising blood bicarbonate. The kidneys only partially compensate, so the patient may still have a low blood pH, i.e. acidosis. In summary, the kidneys partially compensate for respiratory acidosis by raising blood bicarbonate.

InternalMed_Harrison

pneumonia) leading to respiratory acidosis or alkalosis. Patients with underlying pulmonary disease (e.g., chronic obstructive pulmonary disease) may not respond to metabolic acidosis with an appropriate ventilatory response because of insufficient respiratory reserve. Such imposition of respiratory acidosis on metabolic acidosis can lead to severe acidemia. When metabolic acidosis and metabolic alkalosis coexist in the same patient, the pH may be normal or near normal. When the pH is normal, an elevated anion gap (AG; see below) reliably denotes the presence of an AG metabolic acidosis at a normal serum albumin of 4.5 g/dL. Assuming a normal AG of 10 mmol/L, a discrepancy in the ∆AG (prevailing minus normal AG) and the ∆HCO3 (normal value of 25 mmol/L minus abnormal HCO3 in the patient) indicates the presence of a mixed high-gap acidosis— metabolic alkalosis (see example below). A diabetic patient with ketoacidosis may have renal dysfunction resulting in simultaneous metabolic

Respiratory acidosis

Acute respiratory acidosis: HCO3− increases 1 mEq/L for each 10 mm Hg rise in PaCO2. Chronic respiratory acidosis: HCO3− rises 3.5 mEq/L for each 10 mm Hg rise in PaCO2. The expected change in pH with respiratory acidosis can be estimated with the following equations: Acute respiratory acidosis: Change in pH = 0.08 X ((40 − PaCO2)/10) Chronic respiratory acidosis: Change in pH = 0.03 X ((40 − PaCO2)/10) Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia. Diagnosis

Respiratory acidosis

Physiological response Mechanism Metabolism rapidly generates a large quantity of volatile acid (H2CO3) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2. The CO2 combines with H2O to form carbonic acid (H2CO3). The lungs normally excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO2 can cause a respiratory acid-base disorder. The PaCO2 is maintained within a range of 35–45 mm Hg in normal states. Alveolar ventilation is under the control of the respiratory center, which is located in the pons and the medulla. Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem, and in the aortic and carotid bodies as well as by neural impulses from lung stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO2.

Winters' formula

Winters' formula, named for Dr. R.W. Winters, is a formula used to evaluate respiratory compensation when analyzing acid–base disorders and a metabolic acidosis is present. It can be given as , where HCO3− is given in units of mEq/L and pCO2 will be in units of mmHg. Winters' formula gives an expected value for the patient's PCO2; the patient's actual (measured) PCO2 is then compared to this: If the two values correspond, respiratory compensation is considered to be adequate. If the measured PCO2 is higher than the calculated value, there is also a secondary respiratory acidosis or mixed acid base disorder. If the measured PCO2 is lower than the calculated value, there is also a secondary respiratory alkalosis or mixed acid base disorder. References Respiratory therapy Mathematics in medicine

Metabolic alkalosis

To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used: pCO2 = 0.7 [HCO3] + 20 mmHg ± 5 pCO2 = 0.7 [HCO3] + 21 mmHg Treatment To effectively treat metabolic alkalosis, the underlying cause(s) must be corrected. A trial of intravenous chloride-rich fluid is warranted if there is a high index of suspicion for chloride-responsive metabolic alkalosis caused by loss of gastrointestinal fluid (e.g., due to vomiting). Terminology Alkalosis refers to a process by which the pH is increased. Alkalemia refers to a pH which is higher than normal, specifically in the blood. See also Hypokalemia Metabolic acidosis Respiratory acidosis Respiratory alkalosis References External links Acid–base disturbances

Alkalosis

Metabolic alkalosis can be caused by repeated vomiting, resulting in a loss of hydrochloric acid in the stomach contents. Severe dehydration, and the consumption of alkali, are other causes. It can also be caused by administration of diuretics and endocrine disorders such as Cushing's syndrome. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increase serum carbon dioxide, a condition leaning toward respiratory acidosis. As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and vice versa, a delicate balance is created between these two conditions. See also References External links Acid–base disturbances

First_Aid_Step1

Features of renal disorders Key: • = compensatory response. [HCO3 −]Henderson-Hasselbalch equation: pH = 6.1 + log 0.03 P2 Predicted respiratory compensation for a simple metabolic acidosis can be calculated using the Winters formula. If measured Pco2 > predicted Pco2  concomitant respiratory acidosis; if measured Pco2 < predicted Pco2 • concomitant respiratory alkalosis: Pco2 = 1.5 [HCO3–] + 8 ± 2 Acidosis and alkalosis Check arterial pH pH < 7.35 Pco2 > 44 mm Hg HCO3 – < 20 mEq/L Acidemia Respiratory acidosis Metabolic acidosis Hypoventilation Airway obstruction Acute lung disease Chronic lung disease Opioids, sedatives Weakening of respiratory muscles •Anion gap MUDPILES: Normal anion gap Check anion gap Methanol (formic acid) Uremia Diabetic ketoacidosis Propylene glycol Iron tablets or INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late) HARDASS:= Na+ – (CI + HCO3 )– _

Case Study: 60-Year-Old Female Presenting With Shortness of Breath -- Diagnosis

Myxedema coma or severe hypothyroidism Pericardial effusion secondary to myxedema coma COPD exacerbation Acute on chronic hypoxic respiratory failure Acute respiratory alkalosis Bilateral community-acquired pneumonia Small bilateral pleural effusions Acute mild rhabdomyolysis Acute chronic, stage IV, renal failure Elevated troponin I levels, likely secondary to Renal failure Diabetes mellitus type 2, non-insulin-dependent Extreme obesity Hepatic dysfunction

Acid-base balance in heart failure.

In end-stage heart failure, various acid-base disorders can be discovered due to the renal loss of hydrogen ions and hydrogen ion movements into cells, the reduction of the effective circulating volume, hypoxemia and renal failure. This justifies the occurrence of metabolic alkalosis, metabolic acidosis, respiratory alkalosis, as well as respiratory acidosis alone or in combination. Several studies have been published on the acid-base state in heart failure. In a 1951 study, Squires et al analyzed the distribution of body fluid in congestive heart failure by taking into consideration the abnormalities in serum electrolyte concentration and in acid-base equilibrium. A recent study by Milionis et al, analyzed 86 patients with congestive heart failure receiving conventional treatment; the majority of these patients exhibited hypokalemia, hyponatremia, hypocalcemia and hypophosphatemia. Disorders in acid-base balance were noted in 37.2% of patients. In a recent study, 70 patients with severe congestive heart failure before heart transplantation showed high-normal pH, slightly reduced pCO 2 and a slight loss of hydrogen ions. After heart transplantation, stability of blood pH and hydrogen ion concentrations was found. In contrast, bicarbonate and pCO 2 increased significantly. The data led us to formulate the diagnosis of a mixed acid-base disorder that includes respiratory alkalosis and metabolic alkalosis before heart transplantation. In heart failure, the presence of acid-base imbalance associated with the activation of mechanisms that lead to salt and water retention reveals evidence concerning the pivotal role of the kidney in determining the outcome of these patients.

Metabolic acidosis

Signs and symptoms Acute metabolic acidosis Symptoms are not specific, and diagnosis can be difficult unless patients present with clear indications for arterial blood gas sampling. Symptoms may include palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. People with acute metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia can also lead to neurological and cardiac complications:

Acidosis

Acid consumption from poisoning such as methanol ingestion, elevated levels of iron in the blood, and chronically decreased production of bicarbonate may also produce metabolic acidosis. Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid. This is a result of stimulation to chemoreceptors, which increases alveolar ventilation, leading to respiratory compensation, otherwise known as Kussmaul breathing (a specific type of hyperventilation). Should this situation persist, the patient is at risk for exhaustion leading to respiratory failure. Mutations to the V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural deafness.

Impairment of ventilatory response to metabolic acidosis in insulin-dependent diabetic patients with advanced nephropathy.

Sudden cardiopulmonary arrest due to a defective respiratory reflex is observed in diabetic patients. Impaired ventilatory response in diabetic patients to acute hypoxia or hypercapnia induced by the inhalation of an artificial gas has been reported. Little is known regarding the respiratory compensatory ability for mild to moderate metabolic acidosis due to renal failure in insulin-dependent diabetic subjects. Arterial blood pH, HCO3-, PaCO2 and PaO2 were measured in 13 insulin-dependent diabetic subjects with advanced nephropathy and in 33 non-diabetic subjects with end-stage renal failure. The diabetic group consisted of six predialysis patients and seven on regular hemodialysis (HD) and the non-diabetic group, ten predialysis patients and 23 on HD. Differences between measured partial arterial pressure of carbon dioxide (PaCO2) and predicted PaCO2 determined from HCO3- were examined. PaCO2 was significantly higher in the diabetic than in non-diabetic group (40.0 +/- 7.4 versus 31.1 +/- 5.1 mmHg, p < 0.05 in predialysis, 42.0 +/- 6.4 versus 36.0 +/- 2.6 mmHg, p < 0.05 in HD), though plasma pH was essentially the same for either. Differences in measured PaCO2 and predicted PaCO2 were significantly larger in the diabetic group than in non-diabetic group. Ventilatory response to uremic acidosis may thus be considered impaired in subjects with advanced diabetic nephropathy.

Respiratory failure

Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases (hypoxemia, hypercapnia, or both), and evidence of increased work of breathing. Respiratory failure causes an altered mental status due to ischemia in the brain. The typical partial pressure reference values are oxygen Pa O2 more than 80 mmHg (11 kPa) and carbon dioxide Pa CO2 less than 45 mmHg (6.0 kPa). Cause

Davenport diagram

Respiratory and metabolic acid-base disturbances One of the most important features of the Davenport diagram is its usefulness in depicting movement from one point on the equilibrium surface to another following changes in respiration and/or metabolism. Four fundamental changes may occur that affect acid-base balance in the body: respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis. Additionally, a respiratory and a metabolic disturbance may occur simultaneously, such as respiratory acidosis followed by a compensatory shift towards metabolic alkalosis. Respiratory disturbances

Hypophosphatemia and acute respiratory failure in a diabetic patient.

A previously healthy 48-year-old male developed diabetic ketoacidosis and severe hypophosphatemia. Within a few hours, acute respiratory insufficiency developed with a marked discrepancy between the pulmonary pathology and the very poor oxygenation seen. We argue that this was due to the effect of hypophosphatemia on respiratory muscle- and heart function and P50, leading to impaired oxygen delivery.


Since it is the first episode of atrial fibrillation, it is the ideal candidate for catheter ablation.

A 76-year-old patient with hypertension and diabetes mellitus comes to the emergency department because he has been experiencing palpitations and decreased capacity to exert himself for 72 hours. On arrival, atrial fibrillation with ventricular response of around 120 bpm was documented. Which of the following options is FALSE?

This patient should be orally anticoagulated for life, unless contraindicated.

If we decide to perform cardioversion on arrival at the ED, it would be necessary to perform transesophageal echocardiography beforehand.

Being the first episode of atrial fibrillation, it is the ideal candidate for catheter ablation.

Beta-blockers may be used to slow the heart rate.

Management of the older person with atrial fibrillation.

Atrial fibrillation (AF) is associated with a higher incidence of mortality, stroke, and coronary events than is sinus rhythm. AF with a rapid ventricular rate may cause a tachycardia-related cardiomyopathy. Immediate direct-current (DC) cardioversion should be performed in patients with AF and acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta blockers, verapamil, or diltiazem may be given to slow immediately a very rapid ventricular rate in AF. An oral beta blocker, verapamil, or diltiazem should be used in persons with AF if a fast ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected patients with symptomatic life-threatening AF refractory to other drugs. Nondrug therapies should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drugs. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in patients with AF and with symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds that are not drug-induced. Elective DC cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than does medical cardioversion in converting AF to sinus rhythm. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective DC or drug cardioversion of AF and should be continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer, especially in older persons, ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiarrhythmic drugs. Digoxin should not be used to treat patients with paroxysmal AF. Patients with chronic or paroxysmal AF at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Patients with AF at low risk for stroke or with contraindications to warfarin should receive 325 mg of aspirin daily.

Atrial fibrillation in the elderly: facts and management.

Although atrial fibrillation is not widely known by the general public, in developed countries it is the most common arrhythmia. The incidence increases markedly with advancing age. Thus, with the growing proportion of elderly individuals, atrial fibrillation will come to represent a significant medical and socioeconomic problem. The consequences of atrial fibrillation have the greatest impact. The risk of thromboembolism is well known; other outcomes of atrial fibrillation are less well recognised, such as its relationship with dementia, depression and death. Such consequences are responsible for diminished quality of life and considerable economic cost. Atrial fibrillation is characterised by rapid and disorganised atrial activity, with a frequency between 300 and 600 beats/minute. The ventricles react irregularly, and may contract rapidly or slowly depending on the health of the conduction system. Clinical symptoms are varied, including palpitations, syncope, dizziness or embolic events. Atrial fibrillation may be paroxysmal, persistent or chronic, and a number of attacks are asymptomatic. Suspicion or confirmation of atrial fibrillation necessitates investigation and, as far as possible, appropriate treatment of underlying causes such as hypertension, diabetes mellitus, hypoxia, hyperthyroidism and congestive heart failure. In the evaluation of atrial fibrillation, cardiac exploration is invaluable, including electrocardiogram (ECG) and echocardiography, with the aim of detecting cardiac abnormalities and directing management. In elderly patients (arbitrarily defined as aged >75 years), the management of atrial fibrillation varies; it requires an individual approach, which largely depends on comorbid conditions, underlying cardiac disease, and patient and physician preferences. This management is essentially based on pharmacological treatment, but there are also nonpharmacological options. Two alternatives are possible: restoration and maintenance of sinus rhythm, or control of ventricular rate, leaving the atria in arrhythmia. Pharmacological options include antiarrhythmic drugs, such as class III agents, beta-blockers and class IC agents. These drugs have some adverse effects, and careful monitoring is necessary. The nonpharmacological approach to atrial fibrillation includes external or internal direct-current cardioversion and new methods, such as catheter ablation of specific foci, an evolving science that has been shown to be successful in a very select group of atrial fibrillation patients. Another serious challenge in the management of chronic atrial fibrillation in older individuals is the prevention of stroke, its primary outcome, by choosing an appropriate antithrombotic treatment (aspirin or warfarin). Several risk-stratification schemes have been validated and may be helpful to determine the best antithrombotic choice in individual patients.

Emergency medicine considerations in atrial fibrillation.

Atrial fibrillation (AF) is an abnormal heart rhythm which may lead to stroke, heart failure, and death. Emergency physicians play a role in diagnosing AF, managing symptoms, and lessening complications from this dysrhythmia. This review evaluates recent literature and addresses ED considerations in the management of AF. Emergency physicians should first assess patient clinical stability and evaluate and treat reversible causes. Immediate cardioversion is indicated in the hemodynamically unstable patient. The American Heart Association/American College of Cardiology, the European Society of Cardiology, and the Canadian Cardiovascular Society provide recommendations for management of AF. If hemodynamically stable, rate or rhythm control are options for management of AF. Physicians may opt for rate control with medications, with beta blockers and calcium channel blockers the predominant medications utilized in the ED. Patients with intact left ventricular function should be rate controlled to <110 beats per minute. Rhythm control is an option for patients who possess longer life expectancy and those with AF onset <48 h before presentation, anticoagulated for 3-4 weeks, or with transesophageal echocardiography demonstrating no intracardiac thrombus. Direct oral anticoagulants are a safe and reliable option for anticoagulation. Clinical judgment regarding disposition is recommended, but literature supports discharging stable patients who do not have certain comorbidities. Proper diagnosis and treatment of AF is essential to reduce complications. Treatment and overall management of AF include rate or rhythm control, cardioversion, anticoagulation, and admission versus discharge. This review discusses ED considerations regarding AF management.

Management of atrial fibrillation in the elderly.

Atrial fibrillation (AF) is associated with a higher incidence of mortality, stroke, and coronary events than is sinus rhythm. AF with a rapid ventricular rate may cause a tachycardia-related cardiomyopathy. Immediate direct-current (DC) cardioversion should be performed in patients with AF and acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta blockers, diltiazem, or verapamil may be administered to slow immediately a very rapid ventricular rate in AF. An oral beta blocker, verapamil, or diltiazem should be used in persons with AF if a fast ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected patients with symptomatic life-threatening AF refractory to other drugs. Digoxin should not be used to treat patients with paroxysmal AF. Nondrug therapies should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drugs. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in patients with AF and symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds which are not drug-induced. Elective DC cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than does medical cardioversion in converting AF to sinus rhythm. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective DC or drug cardioversion of AF and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer, especially in older patients, ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiar-rhythmic drugs. Patients with chronic or paroxysmal AF at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Patients with AF at low risk for stroke or with contraindications to warfarin should be treated with aspirin 325 mg daily.

Atrial fibrillation.

The prevalence and incidence of atrial fibrillation increase with age. Atrial fibrillation is associated with a higher incidence of coronary events, stroke, and mortality than sinus rhythm. A fast ventricular rate associated with atrial fibrillation may cause tachycardia-related cardiomyopathy. Management of atrial fibrillation includes treatment of underlying causes and precipitating factors. Immediate direct-current cardioversion should be performed in persons with atrial fibrillation associated with acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta-blockers, verapamil, or diltiazem may be used to immediately slow a fast ventricular rate associated with atrial fibrillation. An oral beta-blocker, verapamil, or diltiazem should be given to persons with atrial fibrillation if a rapid ventricular rate occurs a rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening atrial fibrillation refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic atrial fibrillation in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal atrial fibrillation associated with the tachycardia-bradycardia syndrome should be managed with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with atrial fibrillation in whom symptoms such as dizziness or syncope associated with non-drug-induced ventricular pauses longer than 3 seconds develop. Elective direct-current cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than medical cardioversion in converting atrial fibrillation to sinus rhythm. Unless transesophageal echocardiography shows no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of atrial fibrillation and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy of ventricular rate control plus warfarin rather than to maintain sinus rhythm with antiarrhythmic drugs, especially in older patients. Digoxin should not be used in persons with paroxysmal atrial fibrillation. Patients with chronic or paroxysmal atrial fibrillation who are at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio (INR) of 2.0 to 3.0. Persons with atrial fibrillation who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg aspirin daily.

To review the management of the older person with atrial fibrillation (AF). A computer-assisted search of the English language literature (MEDLINE) database followed by a manual search of the bibliographies of pertinent articles. Studies on the management of persons with AF were screened for review. Studies of persons older than age 60 and recent studies were emphasized. Pertinent data were extracted from the reviewed articles. Emphasis was placed on studies involving older persons. Relevant articles were reviewed in depth. Available data about the management of persons with paroxysmal or chronic AF were summarized Management of AF includes treatment of the underlying disease and precipitating factors. Immediate direct-current cardioversion should be performed in persons with AF associated with an acute myocardial infarction, chest pain caused by myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous verapamil, diltiazem, or beta-blockers should be used to slow a very rapid ventricular rate associated with AF immediately. Oral verapamil, diltiazem, or a beta-blocker should be given if a rapid ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected persons with symptomatic life-threatening AF refractory to other drug therapy. Nondrug therapies should be performed in persons with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drug therapy. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in persons with AF who develop cerebral symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds that are not drug-induced. Elective cardioversion of AF should not be performed in asymptomatic older persons with chronic AF. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective direct-current or drug cardioversion of AF and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer the treatment strategy, especially in older persons, of ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiarrhythmic drugs. Digoxin should be avoided in persons with sinus rhythm who have a history of paroxysmal AF. Older persons with chronic or paroxysmal AF who are at high risk for stroke or who have a history of hypertension and no contraindications to warfarin should receive long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Older persons with AF who are at low risk for stroke or who have contraindications to warfarin should receive 325 mg of aspirin daily.

Treatment strategies for atrial fibrillation.

Atrial fibrillation is the most common arrhythmia observed in clinical practice, occurring in 0.4% of the general population and in up to 4% of people greater than 60 years old. It is often associated with other cardiovascular disorders, such as hypertension, coronary artery disease, or cardiomyopathy. Critical evaluation and management of patients with atrial fibrillation requires knowledge of etiology, prognosis, and treatment options of this arrhythmia. On initial presentation, emergency electrical cardioversion should be performed if the patient is hemodynamically unstable. If the patient is stable, initial rate control is recommended, using atrioventricular nodal blocking agents. Further treatment mainly depends upon the duration of the episode. Patients who are in atrial fibrillation <48 hours can be safely cardioverted. Patients who are in atrial fibrillation for >48 hours are commonly anticoagulated for 3 to 4 weeks before and after cardioversion because of the risk of thromboembolism formation in the left atrial appendage. An alternate strategy, which is especially attractive when immediate cardioversion is desired, is transesophageal echocardiography to exclude left atrial thrombus followed by prompt cardioversion. After cardioversion, sinus rhythm can be maintained with class I and III drugs, such as flecainide and propafenone or amiodarone and sotalol. New treatment options, such as atrial defibrillation, atrioventricular junctional ablation, or modification of atrial pacing to prevent atrial fibrillation, are currently under investigation. Although atrial fibrillation is so common in clinical practice, it still remains difficult to treat. Conversion and maintenance to sinus rhythm with antiarrhythmic drug therapy has not shown any improvement in mortality, and some patients may benefit more from ventricular rate control. This review article discusses different treatment strategies for patients with atrial fibrillation.

Optimal management of older patients with atrial fibrillation.

Long term oral warfarin should be administered to elderly patients with atrial fibrillation who are at high risk for developing thromboembolic stroke and who have no contraindications to anticoagulant therapy. Oral aspirin (acetylsalicylic acid) 325mg daily may be given to elderly patients with chronic atrial fibrillation who have contraindications to anticoagulant therapy or who are not at high risk for developing thromboembolic stroke. Management of atrial fibrillation includes treatment of the underlying disease and precipitating factors. If patients have paroxysmal atrial fibrillation with a very rapid ventricular rate associated with hypotension, severe left ventricular failure or chest pain due to myocardial ischaemia, immediate direct-current cardioversion should be performed. Intravenous verapamil, diltiazem or a beta-blocker should be used for immediate slowing of a very rapid ventricular rate associated with atrial fibrillation. If a rapid ventricular rate associated with atrial fibrillation persists at rest or during exercise despite digoxin, then oral verapamil, diltiazem or a beta-blocker should be added. Low dosages of oral amiodarone (200 to 400 mg/day) may be used in selected patients with symptomatic life-threatening atrial fibrillation refractory to other therapy. No medication which depresses atrioventricular conduction should be given to patients with atrial fibrillation and a slow ventricular rate. Cardioversion should not be performed in asymptomatic elderly patients with chronic atrial fibrillation. This author would use a beta-blocker for control of ventricular arrhythmias and following conversion of atrial fibrillation to sinus rhythm. Should atrial fibrillation recur, beta-blockers have the additional advantage of slowing the ventricular rate.

Atrial Fibrillation: The New Epidemic of the Ageing World.

The prevalence of atrial fibrillation (AF) increases with age. As the population ages, the burden of AF increases. AF is associated with an increased incidence of mortality, stroke, and coronary events compared to sinus rhythm. AF with a rapid ventricular rate may cause a tachycardia-related cardiomyopathy. Immediate direct-current (DC) cardioversion should be performed in patients with AF and acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta blockers, diltiazem, or verapamil may be administered to reduce immediately a very rapid ventricular rate in AF. An oral beta blocker, verapamil, or diltiazem should be used in persons with AF if a fast ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected patients with symptomatic life-threatening AF refractory to other drugs. Digoxin should not be used to treat patients with paroxysmal AF. Nondrug therapies should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drugs. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in patients with AF and symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds which are not drug-induced. Elective DC cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than does medical cardioversion in converting AF to sinus rhythm. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective DC or drug cardioversion of AF and continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer, especially in elderly patients , ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiarrhythmic drugs. Patients with chronic or paroxysmal AF at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Patients with AF at low risk for stroke or with contraindications to warfarin should be treated with aspirin 325 mg daily.

Management of atrial fibrillation: out-of-hospital approach.

Atrial fibrillation is increasingly common with advancing age and is responsible for 10% of the half-million strokes that occur annually in the United States. When a patient presents with atrial fibrillation, the physician's first task is to use the history, physical examination, and electrocardiogram to determine whether hospitalization is necessary. Factors indicating a need for hospital care include evidence of infarction or ischemia, congestive heart failure, hypotension or hypoperfusion, excessive rate, or pre-excitation. In addition, if the episode began within 48 hours, consider early cardioversion, which also requires hospitalization. Next, the need for control of the ventricular rate should be assessed. A heart rate under 90 beats/min at rest and under 120 beats/min after 1 minute of step exercise is a reasonable goal. Dixogin usually controls the resting rate, but sometimes beta-blockers or calcium channel blockers are needed to control the exercise rate. The need for anticoagulation is determined by the presence of clinical risk factors such as valvular heart disease, previous thromboembolism, hypertension, age over 65 years, congestive heart failure, and left atrial enlargement. An echocardiogram is necessary to complete this assessment. Patients having one or more of these risk factors are most effectively treated with warfarin, as evident from several clinical trials. Although patients over age 65 demonstrate reduced thromboembolism with warfarin therapy, they also are more prone to cerebral hemorrhage, thus, their international normalization ratio (INR) should be kept at the lower end of the therapeutic range [2,3]. Other patients can be treated with aspirin, although stroke reduction in these patients may be more related to reduction of arterial thrombosis than thromboembolism. Patients under age 65 with no risk factors have a very low annual risk of stroke without therapy (approximately 1%). If symptoms persist or if this is a first episode in someone without left atrial enlargement, cardioversion can be considered after 3 weeks of warfarin therapy with INR in the therapeutic range. Otherwise, warfarin should be continued indefinitely. Prevention of recurrence with antiarrhythmic drugs is somewhat problematic because of incomplete efficacy (30% recurrence at 1 year) and the potential for inducing other, life-threatening arrhythmias.

Management of newly detected atrial fibrillation: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians.

The Joint Panel of the American Academy of Family Physicians and the American College of Physicians, in collaboration with the Johns Hopkins Evidence-based Practice Center, systematically reviewed the available evidence on the management of newly detected atrial fibrillation and developed recommendations for adult patients with first-detected atrial fibrillation. The recommendations do not apply to patients with postoperative or post-myocardial infarction atrial fibrillation, patients with class IV heart failure, patients already taking antiarrhythmic drugs, or patients with valvular disease. The target physician audience is internists and family physicians dedicated to primary care. The recommendations are as follows: RECOMMENDATION 1: Rate control with chronic anticoagulation is the recommended strategy for the majority of patients with atrial fibrillation. Rhythm control has not been shown to be superior to rate control (with chronic anticoagulation) in reducing morbidity and mortality and may be inferior in some patient subgroups to rate control. Rhythm control is appropriate when based on other special considerations, such as patient symptoms, exercise tolerance, and patient preference. Grade: 2A. RECOMMENDATION 2: Patients with atrial fibrillation should receive chronic anticoagulation with adjusted-dose warfarin, unless they are at low risk of stroke or have a specific contraindication to the use of warfarin (thrombocytopenia, recent trauma or surgery, alcoholism). Grade: 1A. RECOMMENDATION 3: For patients with atrial fibrillation, the following drugs are recommended for their demonstrated efficacy in rate control during exercise and while at rest: atenolol, metoprolol, diltiazem, and verapamil (drugs listed alphabetically by class). Digoxin is only effective for rate control at rest and therefore should only be used as a second-line agent for rate control in atrial fibrillation. Grade: 1B. RECOMMENDATION 4: For those patients who elect to undergo acute cardioversion to achieve sinus rhythm in atrial fibrillation, both direct-current cardioversion (Grade: 1C+) and pharmacological conversion (Grade: 2A) are appropriate options. RECOMMENDATION 5: Both transesophageal echocardiography with short-term prior anticoagulation followed by early acute cardioversion (in the absence of intracardiac thrombus) with postcardioversion anticoagulation versus delayed cardioversion with pre- and postanticoagulation are appropriate management strategies for those patients who elect to undergo cardioversion. Grade: 2A. RECOMMENDATION 6: Most patients converted to sinus rhythm from atrial fibrillation should not be placed on rhythm maintenance therapy since the risks outweigh the benefits. In a selected group of patients whose quality of life is compromised by atrial fibrillation, the recommended pharmacologic agents for rhythm maintenance are amiodarone, disopyramide, propafenone, and sotalol (drugs listed in alphabetical order). The choice of agent predominantly depends on specific risk of side effects based on patient characteristics. Grade: 2A.

Management of atrial fibrillation

The main risk of cardioversion is systemic embolization of a thrombus (blood clot) from the previously fibrillating left atrium. Cardioversion should not be performed without adequate anticoagulation in patients with more than 48 hours or unknown duration of AF. Anticoagulation is adequate if warfarin is given with target INR between 2 and 3 for three to four weeks prior to cardioversion, and continued for at least four weeks after cardioversion. Cardioversion may be performed in instances of AF lasting more than 48 hours if a transesophogeal echocardiogram (TEE) demonstrates no evidence of clot within the heart. Whichever method of cardioversion is used, approximately 50% of patients relapse within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and old age.

Acute Tachycardia-Induced Cardiomyopathy: A Case Report.

BACKGROUND Tachycardia from atrial fibrillation or flutter can lead to left ventricular systolic dysfunction. Some patients deteriorate quickly, and there is an acute drop in their left ventricular systolic function; however, they tend to normalize rapidly after treatment of the underlying arrhythmia. The aim of publishing the present case is to maintain awareness that tachycardia is one of the etiologies of acute systolic heart failure, which is potentially reversible by treatment when recognized. CASE REPORT An 88-year-old woman with a history of hypertension and diabetes presented to the emergency department with shortness of breath and new-onset atrial fibrillation. The physical examination revealed jugular vein distention, an irregular heart rate of approximately 140 beats/min, bilateral basal lung crackles, and no murmurs. One week before this presentation, she underwent electrocardiography, which showed she was in sinus rhythm, and transthoracic echocardiography, which indicated an ejection fraction of 65%. After hospital admission, she was started on beta-blockers for heart rate control and diuretics for heart failure management. As her symptoms persisted, she underwent a transesophageal echocardiography-guided cardioversion, where her ejection fraction was 30%. A repeat transthoracic echocardiography 3 days after the cardioversion indicated the ejection fraction had normalized to 60%. She was followed up every month in the Outpatient Cardiology Clinic and has remained asymptomatic for 1 year to date. CONCLUSIONS Although most literature describes tachycardia-induced cardiomyopathy as a chronic process, it can be acute. Patients benefit from rhythm control, and with early diagnosis and appropriate management, the prognosis is good.

Treatment of Atrial Fibrillation.

Atrial fibrillation is a common arrhythmia that affects more than 2.5 million people in the United States and causes substantial morbidity and mortality, especially regarding the increased risk of stroke. To summarize atrial fibrillation treatment exclusive of stroke prevention. An Ovid MEDLINE comprehensive literature search was performed on atrial fibrillation therapy excluding anticoagulation and emphasizing studies published within the last 5 years through April 2015 (N = 5044 references). The 2014 atrial fibrillation guideline from the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society also was reviewed. Reversible causes of atrial fibrillation should be identified. Risk factor modification, including weight loss and treatment of hypertension, diabetes, and obstructive sleep apnea can reduce atrial fibrillation episodes. Appropriate anticoagulation is necessary for patients at substantial stroke risk regardless of rate or rhythm treatment strategy. Sinus rhythm is often needed to control symptoms; however, an alternative strategy for atrial fibrillation is appropriate rate control. Rate control is safe in older patients (those who are about age ≥65 years) followed up for a few years, but no such safety data exist for patients younger than 60 years or for those followed up for longer periods. Thus, selection of therapy is individualized, taking into account present and future medical problems for the patient. Choice of an antiarrhythmic drug is based on safety first vs efficacy. Catheter ablation is an effective nonpharmacological alternative that is often, but not always, the second-line treatment. Reduction of the frequency and duration of atrial fibrillation episodes that result in a significant improvement in quality of life is a good marker of drug treatment success and complete elimination of atrial fibrillation is not required in many patients. Rate control is usually achieved with a β-blocker or non-dihydropyridine calcium channel blockers. It is important to assess adequate rate control during both rest and activity. If the ventricular rate goes uncontrolled for a prolonged period, tachycardia-mediated cardiomyopathy can occur. Therapy for atrial fibrillation includes prevention and modification of inciting causes and appropriate anticoagulation. Rate control is necessary for all patients. Maintenance of sinus rhythm with drugs or catheter ablation should be considered based on the individual needs of each patient.

[Combined Approach for Management of the Chronic Heart Failure with Preserved Left Ventricular Ejection Fraction and Permanent Atrial Fibrillation: a Case Report].

The article described a clinical case of a patient with chronic heart failure (CHF) with preserved ejection fraction (CHF-PEF) and permanent normosystolic atrial fibrillation (AF). A 73 year-old man (body mass index, 26.4 kg /m2) with permanent normosystolic AF (duration, 10 years) was hospitalized for augmenting of CHF symptoms. The patient had NYHA II-III functional class CHF and a history of long-standing arterial hypertension. The patient received chronic therapy according to the effective guidelines (angiotensin receptor blockers, diuretics, beta-blockers, and new oral anticoagulants). Transthoracic echocardiography showed a normal ejection fraction (EF) (57 %), a moderate enlargement of the left atrium (48 mm), and moderate left ventricular (LV) hypertrophy. Radiofrequency catheter ablation (RFCA) of left atrial AF was performed. For preparation to the RFCA, the patient was administered propanorm two weeks prior to the procedure. Following external electrical cardioversion (ECV) after RFCA, sinus rhythm did not recover. The patient was prescribed amiodarone, and repeat ECV was performed in a month, which resulted in successful recovery of sinus rhythm. However, due to an increase in serum thyrotropic hormone, amiodaron was replaced with the sotalol therapy (240 mg/day). This resulted in development of symptomatic sinus bradycardia and AF relapse at 3 days after ECV. A dual-chamber cardioverter defibrillator was implanted to the patient; in another three months, repeat AF RFCA was performed with successful recovery of sinus rhythm. During the cardioverter testing for one year, the patient had one more AF episode, which was stopped by external ECV. Also, a 6-hour AF episode occurred at three months after the repeat RFCA. Symptoms of CHF disappeared by the 12th month. The combination therapy administered to the patient with normosystolic permanent AF and preserved EF, which included a pathogenetic therapy for CHF, antiarrhythmic drugs, implantation of a dual-chamber ECV, two sessions of AF RFCA, and repeat external ECVs, provided considerable improvement of CHF symptoms and stable sinus rhythm during a one-year follow-up. The return to sinus rhythm after 10 years of permanent AF necessitated changing the arrhythmia diagnosis to long-standing, persistent AF.

Cardioversion in Acute Atrial Fibrillation Without Anticoagulation.

A major concern in cardioversion of newly detected atrial fibrillation is the risk of thromboembolic events. The vast majority of these events occur in the first week following cardioversion. Transesophageal echocardiography has demonstrated that thrombus and dense spontaneous echo contrast may occur in the left atrium and left atrial appendage in patients with acute atrial fibrillation (<48 hours) scheduled for cardioversion. Moreover, atrial function may become impaired immediately following successful cardioversion. The risk of thromboembolic events increases with the presence of stroke risk factors, such as heart failure, hypertension, diabetes, prior stroke, female sex and age above 65-75 years. Thus, the current guidelines of the ESC and ACC/AHA/Heart Rhythm Society recommend that patients with acute atrial fibrillation should undergo cardioversion under cover of unfractionated or low-molecular weight heparin followed by oral anticoagulation for at least 4 weeks in patients in patients at moderate-to-high risk for stroke. In line with the guidelines, new evidence from a large patient population suggests that after successful cardioversion of acute atrial fibrillation, patients have a low overall risk of thromboembolic events without any anticoagulation when they have no risk factors for thromboembolism. In contrast, the risk is in the range of 10% in patients with multiple classic risk factors for thromboembolism.

Management of atrial fibrillation

The management of atrial fibrillation (AF) is focused on preventing temporary circulatory instability, stroke and other ischemic events. Control of heart rate and rhythm are principally used to achieve the former, while anticoagulation may be employed to decrease the risk of stroke. Within the context of stroke, the discipline may be referred to as stroke prevention in atrial fibrillation (SPAF). In emergencies, when circulatory collapse is imminent due to uncontrolled rapid heart rate, immediate cardioversion may be indicated. The primary factors determining AF treatment are duration and evidence of circulatory instability. Cardioversion is indicated with new onset AF (for less than 48 hours) and with circulatory instability. If rate and rhythm control cannot be maintained by medication or cardioversion, it may be necessary to perform electrophysiological studies with ablation of abnormal electrical pathways.

[Anticoagulation and electrical cardioversion of chronic atrial fibrillation: proposal for an abbreviated protocol].

Several weeks of prophylactic anticoagulation are routinely prescribed before and after electrical cardioversion of atrial fibrillation. Recent studies have supported the use of transesophageal echocardiography to guide early cardioversion: patients in whom no thrombus is observed are treated with heparin followed by one month of warfarin therapy after the procedure. This kind of treatment requires hospital admission during heparin infusion, because of the need for monitoring partial thromboplastin time. To evaluate if a short at-home treatment (three days) with warfarin is sufficient to reach a good level of anticoagulation, in order to permit safe electrical cardioversion in day-hospital for patients who show no thrombi on transesophageal echocardiography. One hundred twenty-four patients with atrial fibrillation, who were candidates for cardioversion, were treated with warfarin: 10 mg the first and second day, 5 mg the third day in group A patients (n = 79); 15 mg the first day, 10 mg the second and third day in group B patients (n = 45). On the fourth day, INR value was measured and if it was < 2, warfarin therapy was prolonged until patients reached a good level of anticoagulation. Transesophageal echocardiography was performed when the INR was > or = 2, and patients were cardioverted with DC shock if there were no thrombi. The patients were discharged on the same day of the procedure, and warfarin therapy was continued for 4 weeks there-after. If a thrombus was detected, patients repeated transesophageal echocardiography after 6 weeks of warfarin therapy, and were cardioverted if the thrombus disappeared. Otherwise, cardioversion was deferred and they received prolonged warfarin treatment. If there was poor visualization of the left atrial appendage, patients received conventional warfarin therapy for 3 weeks before and 4 weeks after electrical cardioversion. Mean INR value after three days of warfarin treatment was 2.41 in group A patients and 3.02 in group B patients. Twenty-one patients from group A and 3 patients from group B required anticoagulant therapy for a mean of 3.3 and 5.1 days, respectively, before reaching a good level of anticoagulation (INR value > or = 2). Eight patients reverted spontaneously to sinus rhythm before transesophageal echocardiography. Eighteen thrombi (15.5%) were identified on the transesophageal echocardiography, all of which were in the left atrial appendage. In 11 cases, thrombus disappeared after 6 weeks of warfarin therapy. In 7 patients (6%), the atrial appendage was not sufficiently visualized. Electrical cardioversion was performed on 109 patients and was successful in 88 (80.7%). None of them experienced a clinical thromboembolic event. In the majority of patients in atrial fibrillation, a short at-home warfarin treatment is sufficient to reach a good level of anticoagulation in order to permit safe electrical cardioversion in a day-hospital situation. Larger initial doses can achieve even better results. This treatment algorithm minimizes the anticoagulation period, hospital stay, overall duration of atrial fibrillation and the time required for the mechanical function of the left atrium to return.

Antithrombotic therapy in atrial fibrillation: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.

This chapter about antithrombotic therapy in atrial fibrillation (AF) is part of the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs. Grade 2 suggests that individual patients' values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004; 126:179S-187S). Among the key recommendations in this chapter are the following (all vitamin K antagonist [VKA] recommendations have a target international normalized ratio [INR] of 2.5; range, 2.0 to 3.0): In patients with persistent or paroxysmal AF (PAF) [intermittent AF] at high risk of stroke (ie, having any of the following features: prior ischemic stroke, transient ischemic attack, or systemic embolism, age > 75 years, moderately or severely impaired left ventricular systolic function and/or congestive heart failure, history of hypertension, or diabetes mellitus), we recommend anticoagulation with an oral VKA, such as warfarin (Grade 1A). In patients with persistent AF or PAF, age 65 to 75 years, in the absence of other risk factors, we recommend antithrombotic therapy with either an oral VKA or aspirin, 325 mg/d, in this group of patients who are at intermediate risk of stroke (Grade 1A). In patients with persistent AF or PAF < 65 years old and with no other risk factors, we recommend aspirin, 325 mg/d (Grade 1B). For patients with AF and mitral stenosis, we recommend anticoagulation with an oral VKA (Grade 1C+). For patients with AF and prosthetic heart valves, we recommend anticoagulation with an oral VKA (Grade 1C+); the target INR may be increased and aspirin added depending on valve type and position, and on patient factors. For patients with AF of > or = 48 h or of unknown duration for whom pharmacologic or electrical cardioversion is planned, we recommend anticoagulation with an oral VKA for 3 weeks before and for at least 4 weeks after successful cardioversion (Grade 1C+). For patients with AF of > or = 48 h or of unknown duration undergoing pharmacologic or electrical cardioversion, an alternative strategy is anticoagulation and screening multiplane transesophageal echocardiography (Grade 1B). If no thrombus is seen and cardioversion is successful, we recommend anticoagulation for at least 4 weeks (Grade 1B). For patients with AF of known duration < 48 h, we suggest cardioversion without anticoagulation (Grade 2C). However, in patients without contraindications to anticoagulation, we suggest beginning IV heparin or low molecular weight heparin at presentation (Grade 2C).

Atrial fibrillation

If a blood clot is seen on TEE, then cardioversion is contraindicated due to the risk of stroke, and anticoagulation is recommended. Ambulatory Holter monitoring A Holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations regularly, a Holter monitor may be of benefit to determine whether rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.

Beta blocker

Hyperthyroidism Abrupt withdrawal can result in a thyroid storm. Bradycardia or AV block Unless a pacemaker is present, beta blockers can severely depress conduction in the AV node, resulting in a reduction of heart rate and cardiac output. One should be very cautious with the use of beta blockers in tachycardic patients with Wolff-Parkinson-White Syndrome, as it can result in life-threatening arrhythmia in certain patients. By slowing the conduction through the AV node, preferential conduction through the accessory pathway is favored. If the patient happens to develop atrial flutter, this could lead to a 1:1 conduction with very fast ventricular rate, or worse, ventricular fibrillation in the case of atrial fibrillation.

Rate control versus rhythm control in atrial fibrillation: lessons learned from clinical trials of atrial fibrillation.

Ample evidence supports the statement that in patients with atrial fibrillation in whom treatment is warranted, either rhythm control or rate control are acceptable primary therapeutic options. If a rhythm control strategy is chosen, it is important to consider that recurrence of atrial fibrillation is not treatment failure per se. Occasional recurrence, with cardioversion if necessary, may be quite acceptable. The latter will depend on the frequency, duration and symptoms associated with recurrence, and may require a change in the rhythm control therapy, e.g., change the antiarrhythmic drug, or initiate or redo atrial fibrillation ablation. And a rhythm control strategy should include careful attention to and treatment of comorbidities (hypertension, heart failure, diabetes, etc.). If a rate control strategy is chosen, treatment with a beta blocker or nondihydropyridine calcium channel blocker is almost always required to achieve adequate rate control. Digoxin is often useful to obtain satisfactory rate control in combination with a beta blocker or nondihydropyridine calcium channel blocker. Digoxin may be useful as primary therapy in the presence of hypotension or heart failure. Satisfactory ventricular rate control is usually a resting rate less than 110 beats per minute, although resting rates below 90 beats per minute are probably wiser. Finally, when pursuing a rhythm control strategy, because recurrence of atrial fibrillation is common, rate control therapy should be a part of the treatment regimen.

Systematic review of the management of atrial fibrillation in patients with heart failure.

To systematically review the management of atrial fibrillation (AF) in patients with heart failure. Studies investigating the management of AF in patients with heart failure published between 1967 to 1998 were identified using MEDLINE, the Cochrane register and Embase databases. Reference lists from relevant papers and reviews were hand searched for further papers. Eight studies pertaining to acute and twenty-four pertaining to chronic AF were identified. For patients with acute AF ventricular rate control, anticoagulation and treatment of heart failure should be pursued simultaneously before cardioversion is attempted. Digoxin is relatively ineffective at controlling ventricular response and for cardioversion. Intravenous diltiazem is rapidly effective in controlling ventricular rate and limited evidence suggests it is safe. Amiodarone controls ventricular rate rapidly and increases the rate of cardioversion. There are insufficient data to conclude that immediate anti-coagulation, trans-oesophageal echocardiography to exclude atrial thrombi followed by immediate cardioversion is an appropriate strategy. Patients with chronic AF should be anti-coagulated unless contra-indications exist. It is not clear whether the preferred strategy should be cardioversion and maintenance of sinus rhythm with amiodarone or ventricular rate control of AF combined with anticoagulation to improve outcome including symptoms, morbidity and survival. Electrical cardioversion has a high initial success rate but there is also a high risk of early relapse. Amiodarone currently appears the most effective and safest therapy for maintaining sinus rhythm post-cardioversion. Digoxin is fairly ineffective at controlling ventricular rate during exercise. Addition of a beta-blocker reduces ventricular rate and improves symptoms. Whether digoxin is required in addition to beta-blockade for the control of AF in this setting is currently under investigation. If pharmacological therapy is ineffective or not tolerated then atrio-ventricular node ablation and permanent pacemaker implantation should be considered. There is a paucity of controlled clinical trial data for the management of AF among patients with heart failure. The interaction between AF and heart failure means that neither can be treated optimally without treating both. Presently treatment should be on a case by case basis.

Atrial fibrillation and heart failure comorbidity.

Atrial fibrillation and heart failure have in common that they mainly occur in older patients and the patients have similar underlying heart diseases. The prevalence of atrial fibrillation in heart failure patients varies from 10% to 30%. There are conflicting data whether the presence of atrial fibrillation is an independent predictor for an increased mortality in heart failure. Optimal medical heart failure therapy can improve outcome and may influence the relationship between atrial fibrillation and survival. Keystones for the management of atrial fibrillation in heart failure patients are the optimal treatment of heart failure, the use of oral anticoagulation, the case-adjusted decision of rhythm or rate control, and the primary prevention of sudden cardiac death. Heart failure patients with atrial fibrillation should receive long-term oral anticoagulation. The two options to treat atrial fibrillation are rhythm control and rate control. Given the findings of randomised trials, rhythm control of atrial fibrillation with the aim to improve survival is not justified in heart failure patients because of uncertainty about the role of atrial fibrillation as a predictor of worse outcomes and the safety of antiarrhythmic drugs. Rhythm control can be attempted, if rate control is chosen and symptoms persist. The indications for rhythm control are to control symptoms, including a deterioration of heart failure related to a loss of atrial contraction. Amiodarone seems to be the drug of choice to maintain sinus rhythm in patients with paroxysmal atrial fibrillation as well as in patients who returned to sinus rhythm after cardioversion. New non pharmacologic approaches for rhythm control such as catheter-based techniques seem to be highly effective. Rate control to prevent rapid atrial fibrillation is an acceptable approach in otherwise asymptomatic heart failure patients. Slowing of the ventricular rate often leads to a moderate improvement in left ventricular function in many patients. Standard therapy for rate control in heart failure patients consists of partial atrioventricular (AV) node blockade with digoxin and a beta-blocker. Amiodarone is also highly effective to reduce ventricular rate in patients with atrial fibrillation. When rate control remains refractory to medical therapy, rate control is achieved with AV node ablation and subsequent pacemaker implantation. Non pharmacological treatments for the primary prevention of sudden cardiac death are the implantation of a defibrillator.

Atrial fibrillation.

In 2000, some 2.3 million Americans were affected by atrial fibrillation, and that number is expected to rise as our population ages. Atrial fibrillation is both a reflection of active physiologic stressors on the body and a marker of future cardiac disease progression. The disorganized atrial activity that characterizes atrial fibrillation affects cardiac function, metabolic demand, and quality of life. However, our understanding of the etiology and treatment of this condition continues to advance with the result of recent large-scale clinical trials. Diabetes, hypertension, congestive heart failure, valvular disease, and myocardial infarction are all risk factors in the development of atrial fibrillation. And the diagnosis confers a five-fold increase in the incidence of stroke. (Patients at increased risk for stroke include those with congestive heart failure, hypertension, age greater than 75, diabetes, and previous stroke.) Anticoagulation is a critical action in most cases of atrial fibrillation, as data show a 68% relative risk reduction of stroke when patients are treated with warfarin. Prior to recent trials, achieving sinus rhythm was thought to invariably improve symptoms, cardiac function, and mortality. The adverse effects of antiarrhythmic medications are now being recognized, and treatment strategies emphasizing ventricular rate control have been recommended in recent clinical practice guidelines. This shift in thinking is influencing both outpatient and emergency department management. Controlling the ventricular rate in atrial fibrillation increases cardiac output, decreases the metabolic demand of the heart, and avoids the potentially dangerous side effects of rhythm-control drugs. Rate-control agents should be selected based on the clinical profile of individual patients. A well-chosen subset of patients may benefit from either chemical or electrical cardioversion; this appears to be a reasonably safe procedure and can be accomplished on an outpatient basis. Understanding causal etiologies, managing risk for stroke (and need for anticoagulation), addressing rate, and assessing the risks of cardioversion are key elements in a comprehensive approach to atrial fibrillation.

Atrial Fibrillation -- Treatment / Management

The management of atrial fibrillation in the acute setting depends on hemodynamic stability and risk stratification. In cases where the patient is hemodynamically unstable, it is recommended to carry out immediate cardioversion with anticoagulant therapy. Although TEE is recommended before any cardioversion; however, if the patient is hemodynamically unstable due to a rapid ventricular response, cardioversion may be indicated without prior TEE. If there is evidence of rapid ventricular response, a beta-blocker or calcium-channel blocker should be commenced for rate control. These options can be used in the intravenous (IV) form for rapid response. Usually, a bolus is administered to the patient and then started on a drip if symptoms do not resolve. Digoxin can be considered for rate control but is not advised as a first-line agent pertaining to its adverse effects and tolerance. Amiodarone can also be given as a rhythm control agent but is also not a first-line option in the acute setting. In any case, if the decision to start amiodarone is made, cardiology should be consulted before its administration.

Presentation and management of patients admitted with atrial fibrillation: a review of 291 cases in a regional hospital.

Two hundred and ninety one patients admitted with atrial fibrillation through the emergency room of a regional hospital in the year 1993 were reviewed to evaluate the presenting features and in-hospital treatment of patients with symptomatic atrial fibrillation. The incidence of atrial fibrillation increased with age (mean age was 73 +/- 12 years) and the ratio of female to male was 1.8:1. The commonest presenting features were palpitation (42.3%), dyspnoea (38.1%) and heart failure (16.4%). The most frequently associated cardiac conditions were hypertension (28.9%), atherosclerotic cardiovascular disease (24.7%) and rheumatic heart disease (17.5%). Pulmonary diseases (18.6%), diabetes mellitus (12.7%) and thyrotoxicosis (6.2%) were the principal associated non-cardiac conditions. Thromboembolic complications were found in 15 patients at presentation (5.2%). Cardiac enzyme assessment was investigated in two thirds of the patients (68.1%), while thyroid function test (59.5%) and echocardiography (29.6%) were less commonly investigated. Digoxin was still the most popular drug used for ventricular rate control, and cardioversion was performed in only 6.9% of patients. Antithrombotic therapy was used in 5.8% of patients only although it was clinically indicated in more than half of the patients (52%). Contraindications of anticoagulation were found in 23 patients (7.9%), including a history of gastrointestinal or cerebrovascular bleeding, active bleeding, chronic renal failure and poor drug compliance. The mean hospital stay was 5 +/- 4 days, compared to a mean stay of 2.7 days for other medical patients. Fourteen patients (4.8%) died during hospitalisation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial fibrillation

In those with chronic AF either beta blockers or calcium channel blockers are recommended. In addition to these agents, amiodarone has some AV node blocking effects (in particular when administered intravenously) and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension). Cardioversion Cardioversion is the attempt to switch an irregular heartbeat to a normal heartbeat using electrical or chemical means. Electrical cardioversion involves the restoration of normal heart rhythm through the application of a DC electrical shock. The exact placement of the pads does not appear to be important. Chemical cardioversion is performed with medications, such as amiodarone, dronedarone, procainamide (especially in pre-excited atrial fibrillation), dofetilide, ibutilide, propafenone, or flecainide.

Management of atrial fibrillation

Catheter ablation In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart – the atrioventricular node – which regulates heart rate, and to implant a pacemaker instead. This "ablate and pace" technique has an important place in the treatment of AF< as it is the only reliably effective method for relieving the symptoms of the arrhythmia and can be used when other methods have failed (as they do in up to 50% of cases of persistent AF). Although this procedure results in a regular (paced) heart rhythm it does not prevent the atria from fibrillating and therefore long-term warfarin anticoagulation may still be required.

Atrial fibrillation.

The incidence and prevalence of atrial fibrillation are increasing because of both population ageing and an age-adjusted increase in incidence of atrial fibrillation. Deciding between a rate control or rhythm control approach depends on patient age and comorbidities, symptoms and haemodynamic consequences of the arrhythmia, but either approach is acceptable. Digoxin is no longer a first-line drug for rate control: beta-blockers and verapamil and diltiazem control heart rate better during exercise. Anti-arrhythmic drugs have only a 40%-60% success rate of maintaining sinus rhythm at 1 year, and have significant side effects. The selection of optimal antithrombotic prophylaxis depends on the patient's risk of ischaemic stroke and the benefits and risks of long-term warfarin versus aspirin, but is independent of rate or rhythm control strategy. Ischaemic stroke risk is best estimated with the CHADS2 score (Congestive heart failure, Hypertension, Age > or = 75 years, Diabetes, 1 point each; prior Stroke or transient ischaemic attack, 2 points). For patients with valvular atrial fibrillation or a CHADS(2) score > or = 2, anticoagulation with warfarin is recommended (INR 2-3, higher for mechanical valves) unless contraindicated or annual major bleeding risk > 3%. Aspirin or warfarin may be used when the CHADS(2) score = 1. Aspirin, 81-325 mg daily, is recommended in patients with a CHADS(2) score of 0 or if warfarin is contraindicated. Stroke rate is similar for paroxysmal, persistent, and permanent atrial fibrillation, and probably for atrial flutter.

Management of atrial fibrillation

Rate control Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, effectively decreasing the number of impulses that conduct down into the ventricles. This can be done with: Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, bisoprolol, atenolol) Calcium channel blockers (i.e. diltiazem or verapamil) Cardiac glycosides (i.e. digoxin) – have limited use, apart from in the sedentary elderly patient In addition to these agents, amiodarone has some AV node blocking effects (particularly when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension). Diltiazem has been shown to be more effective than either digoxin or amiodarone. Drugs used to control the rate of AF may cause side effects, especially fatigue and dyspnea. These are avoided by the more radical "ablate and pace" treatment (see below).

Canadian Cardiovascular Society atrial fibrillation guidelines 2010: management of recent-onset atrial fibrillation and flutter in the emergency department.

Atrial fibrillation (AF) is the most common arrhythmia managed by emergency physicians. There is increasing evidence that most patients with recent-onset AF or atrial flutter (AFL) can be safely managed in the emergency department (ED) without the need for hospital admission. The priorities for ED management of recent-onset AF/AFL include rapid assessment of potential hemodynamic instability and identification and treatment of the underlying or precipitating cause. A careful evaluation of the patient's history should be performed to determine the time of onset of the arrhythmia. All patients should be stratified using a predictive index for the risk of stroke (eg, CHADS(2)). For stable patients with recent-onset AF/AFL, a strategy of either rate control or rhythm control could be selected based on multiple factors including the duration of AF and the severity of symptoms. If a strategy of rhythm control has been selected, either electrical or pharmacologic cardioversion may be used. Before proceeding to cardioversion in the absence of systemic anticoagulation, physicians must be confident that the duration of AF/AFL is clearly <48 hours and that the patient is not at a particularly high risk of stroke. When the duration of AF/AFL is >48 hours or uncertain, rate control should be optimized first and the patients should receive therapeutic anticoagulation for 3 weeks before and 4 weeks after planned cardioversion. Adequate follow-up of patients with recent-onset AF/AFL is recommended to identify structural heart disease and evaluate the need for long-term antithrombotic or antiarrhythmic therapy.