Spring 2014 Adult Acute Care Bulletin

Spring 2014 Adult Acute Care Bulletin

Chair
Keith Lamb, RRT-ACCS
Adult Critical Care Supervisor
UnityPoint Health System
Des Moines, IA
keith.lamb@unitypoint.org

Editor
Joe Hylton, RRT-NPS, CPFT

Co-Editor
Brady Scott, MS, RRT-ACCS
Clinical Education Coordinator and Assistant Professor
Department of Respiratory Care
Rush University Medical Center
Chicago, IL
Jonathan_B_Scott@rush.edu


Laboratory Analysis of Electrolyte Disturbances

Joe Hylton, BSRT, RRT-ACCS, RRT-NPS, NREMT-P, FAARC, FCCM

Electrolyte disturbances may occur in our patients and it is essential that we understand them. This article will review lab profiles for common electrolyte disturbances —

Sodium (Na+)

Sodium exists primarily as an extracellular cation. It is an easy marker of general fluid status and a key component of serum osmolarity. Chemistry profiles measure extracellular sodium; the generally accepted normal levels are 135-145 mEq/L. Abnormalities in sodium levels will primarily affect the neuronal/neuromuscular function, usually in the form of altered mental status, confusion, lethargy, seizures, coma, and muscle weakness/twitching.

Increased levels of glucose, proteins or lipids, and mannitol can promote hyponatremia. Increased levels of anti-diuretic hormone (ADH) can also promote hyponatremia. Hypovolemia (vomiting/diarrhea/diuretic use/aldosterone deficiency/renal tubule dysfunction) or hypervolemia (CHF/cirrhosis/renal failure) can precipitate/worsen hyponatremia. Hyponatremia can also been seen in a euvolemic state (polydipsia/SIADH/hypothyroidism/adrenal insufficiency). Hyponatremia is usually corrected slowly, attempting to achieve a 0.5 mEq/L per hour increase until sodium reaches a normal level.

Hypernatremia can result from increased water loss (diarrhea/vomiting/diuresis/excessive diaphoresis/diabetes insipidus), reduced water intake (altered thirst/impaired access to water), or excessive sodium intake (salt tablets/hypertonic saline/sodium bicarbonate). Treatment for hypernatremia focuses on correcting the underlying issue and almost always involves replacing free-water.

Potassium (K+)

Potassium exists primarily as an intracellular cation. Only 2% of total body potassium exists extracellularly. Potassium is a vital part of the cell electrical membrane potential. Chemistry profiles measure extracellular potassium; the generally accepted normal levels are 3.5-5.0 mEq/L. Abnormalities in potassium levels will primarily affect cardiovascular (arrhythmias, ECG abnormalities), neuromuscular (weakness/paralysis/parasthesias), and gastrointestinal function (ileus, abdominal cramps, nausea/vomiting).

Hypokalemia can result from renal loss (diuresis/DKA/renal tubular defects/vomiting/Cushings syndrome) or extrarenal loss (diarrhea/profuse diaphoresis/NG suction), transcellular shifts (alkalosis/insulin/hyperventilation/beta adrenergic agonists), or decreased intake (malnutrition/alcoholism/anorexia). Treatment of hypokalemia is focused on treating the underlying cause and administering potassium.

Hyperkalemia can be caused by renal dysfunction, acidemia, hypoaldosteronism, drugs (NSAIDS/ACE inhibitors/succinylcholine/diuretics), cell death (rhabdomyolysis /tumor lysis/burns/hemolysis), and excessive potassium intake. Treatment targets the recognition and treatment of underlying diseases/causes and potential reduction of potassium. Calcium chloride or calcium gluconate can be administered to promote myocardial cell stabilization and decrease arrhythmia potential. Insulin, sodium bicarbonate, and inhaled beta-agonists can shift potassium back into the cells. Glucose will be administered when insulin is given to avoid hypoglycemia. Loop diuretics can be utilized to increase urine output. Sodium polystyrene (Kayexolate) can be administered enterally or by enema to promote potassium loss. Dialysis can also be utilized to decrease potassium levels.

Chloride (Cl-)

Chloride exists as the predominant extracellular anion. Its negative charge offsets the positive charge of sodium and potassium, allowing electrical neutrality within the human body. The kidneys utilize chloride to concentrate urine. Chemistry profiles measure extracellular chloride; the generally accepted normal levels are 96-106 mEq/L. Chloride will generally trend the same way as sodium. Abnormalities in chloride levels will primarily affect neurological and renal function (circumoral numbness/tingling, muscle hypertonicity, decreased RR/Vt, renal dysfunction).

Carbon dioxide (CO2)

The venous bicarbonate level is a rudimentary indication of the acid-base status of a patient. Carbon dioxide, as it is expressed on the chemistry panel, isn’t really a true CO2 level. Carbon dioxide exists as a gas and must be expressed as a partial pressure, usually in mmHg. Bicarbonate is an ion and as such must be expressed as a concentration. As such, the total CO2 level isn’t a CO2 level at all, but an indication of the amount of bicarbonate present in the venous sample. This phenomenon occurs via the carbonic acid-bicarbonate buffer system (CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3). The generally accepted normal levels in a chemistry profile for CO2 are 21-28 mEq/L; HCO3 acceptable normal levels are generally 22-28 mEq/L.

Blood urea nitrogen (BUN)

Urea is a product of protein metabolism. It is related to the amount of protein intake, metabolism, and excretion. Urea is a close marker of renal function, as the urea level in kidney filtrate is usually the same as in serum. The normal range for BUN is 8-23 mEq/dL. BUN can increase with age, as renal function normally declines. BUN can elevate in the face of decreased renal function, in a high protein diet, and in the presence of a high protein catabolic state such as burns or crush injuries.

Creatinine

Creatinine is a waste product of creatine, a phosphate found intramuscularly. Creatinine is filtered by the kidneys and excreted in the urine. The normal range for creatinine is 0.6-1.2 mg/dL. Because of its steady-state metabolism, creatinine is a good marker to assess renal function. Specifically, creatinine is the most accurate measure of glomerular filtration in the kidney. However, an abnormal creatinine level will not necessarily indicate what is causing impaired function. Muscle damage from trauma (rhabdomyolysis) can elevate creatinine levels, but renal function isn’t necessarily impaired. Elevated creatinine levels require rapid assessment to identify the cause because renal failure can occur, requiring dialysis and/or renal transplantation.

Glucose

Glucose is by far the most important carbohydrate. Maintaining glucose levels within normal levels is pertinent for homeostasis. The normal range for glucose is 70-110 mg/dL. Hyperglycemia can result in coma and death if not recognized and corrected. Hypoglycemia can present with blurred vision, dizziness, nausea/vomiting, shakiness, confusion, altered mental status, and unresponsiveness/death. Insulin can be used to treat hyperglycemia. Glucagon and/or glucose can be used to treat hypoglycemia. (Clinical states involving glucose were reviewed in the Fall and Winter editions of the Bulletin.)

Calcium

Calcium is an essential element responsible for multiple functions such as intracellular signal transduction, hormone secretion, blood clotting, cell division, cell motility, wound healing, and muscle contraction. It exists in three states in the body: free, chelated, and bound. Free calcium is the largest portion at around 47%. Roughly 43% exists as bound calcium, existing mostly as albumin. Chelated calcium makes up roughly 10% of existing calcium, in the form of citrate, bicarbonate, lactate, and sulfate. The normal range for calcium is 8.2-10.2 mg/dL. Hyperparathyroidism and parathyroid secreting tumors can elevate calcium levels. Renal insufficiency decreases parathyroid states; hypomagnesaemia, hyperphosphatemia, and massive blood transfusions can decrease calcium levels as well.

Ionized Calcium

Free calcium is the only state that is physiologically active. Altered fractions of bound or chelated calcium warrant an assessment of free calcium levels. Renal failure, hypoalbuminemia, acid-base derangements, or changes (increases or decreases) in chelating compounds (albumin, bicarbonate, lactate, phosphate, and sulfate) can affect free calcium levels. Ionized calcium levels provide that assessment. The normal range for ionized calcium is 4.6-5.08 mg/dL. Decreased levels of ionized calcium can cause cardiac arrhythmias.

Magnesium

Magnesium is an important electrolyte for energy transfer and electrical stability. Magnesium levels are usually altered by the GI and endocrine systems, although others can also impact levels. The normal levels for magnesium are 1.3-2.1 mEq/L. Hypomagnesemia is usually caused by renal loss (diuresis, hypokalemia, renal tubular dysfunction, drugs), GI loss (malabsorption, diarrhea, NG suction), transcellular shift (refeeding, hypothermia recovery), and decreased intake (malnutrition, alcoholism, parenteral nutrition). Clinically, hypomagnesemia usually coincides with hypokalemia and hypocalcemia. Cardiovascular/ECG abnormalities (prolonged QT interval, arrhythmias, vasospasm, myocardial ischemia) and neuromuscular abnormalities (tremors, weakness, seizures, tetany, coma) can manifest from hypomagnesemia. Although rare, hypermagnesemia can be seen in the face of renal defects, severe dehydration, magnesium overdose, and aspiration of sea water.

Phosphate

Phosphate is an important electrolyte in body energy stores; specifically, cellular energy metabolism. It also acts as a buffer in the intracellular space, much like bicarbonate. The normal range for phosphate is 1.8-2.6 mEq/L. Hyperphosphatemia can result from hypoparathyroidism, renal failure, increased levels of growth hormone, and vitamin D intoxication. This will usually result in muscle weakness, rhabdomyolysis, paresthesias, lethargy, seizures, and coma. Hypophosphatemia can result from hyperparathyroidism, diuresis, malnutrition/malabsorption, carbohydrate loading, and antacid abuse.

Resources

  • Fundamental critical care support, 4th edition. Mount Prospect, IL: Society of Critical Care Medicine; 2007.
  • Critical care transport, 1st edition. Sudbury, MA: Jones and Bartlett Publishers; 2010.
  • Critical care medicine, 3rd edition. Philadelphia, PA: Lippincott, Williams and Wilkins Publishers; 2006.
  • The ICU book, 3rd edition. Philadelphia, PA: Lippincott, Williams and Wilkins Publishers; 2007.
  • Critical care paramedic, 1st edition. Upper Saddle River, NJ: Pearson Education, Inc.; 2006.

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Pulmonary Vasculature and the Respiratory Therapist

April Gochberg, PhD, RRT-ACCS, Director, Respiratory Care
The Christ Hospital Health Network, Cincinnati, OH

When it comes to the health of the pulmonary vasculature, the respiratory therapist is uniquely poised to be a principle player. Our understanding of smooth muscle relaxation in the airways translates easily to the understanding of smooth muscle relaxation in the endothelium.

The lungs are the only organ to receive the entire cardiac output.1 There is about 180 ml of blood volume in the arterial side of the pulmonary vasculature and approximately 80 ml in the venous.1The walls of the pulmonary vasculature are more thin-walled than systemic arteries due to less need to withstand high pressures.

Another unique feature of the pulmonary arteries is the presence of smooth muscle within the walls of smaller pulmonary arteries. This smooth muscle layer is responsible for vasoconstrictive responses to different stimuli, including hypoxia. This responsive vasoconstriction allows down regulation of perfusion to poorly ventilated alveoli. The response can be localized or generalized depending on the amount of alveolar involvement.

The response to acute hypoxia (PO2 < 60 torr) is production of endothelin1, a potent vasoconstrictor. The response to chronic hypoxia is remodeling of pulmonary vascular architecture and is most likely due to the release of endothelin. This is a process that may lead to pulmonary hypertension. Other influencers on the smooth muscle of the pulmonary endothelium are the humoral immune system, endogenous nitric oxide (a vasodilator), endogenous endothelin, and circulating bioactive agents.

Respiratory therapists are taught about the primary functions of the lung, oxygenation and ventilation, but spend little time on the secondary functions of the lung1, including filtration, defense against inhaled substances, and metabolism of endogenous compounds. A basic understanding of these additional roles of the pulmonary system will give the therapist a broader view when dealing with the critically ill patient.

Non-respiratory functions of the lung1

First, let’s look at filtration. As you are sitting reading this article, your pulmonary vasculature is breaking down hundreds of small clots. The lungs are rich in heparin; in fact the drug heparin is made from bovine lung tissue. This filtration through the pulmonary vasculature is protective of the circulatory system as a whole. Thrombi are cleared more rapidly from the lungs than any other organ. The particulate matter is either removed or biotransformed through the coagulation cascade.

The defense of inhaled substances, through the protease transport system, is probably more familiar to the therapist. Activation of neutrophils causes the neutrophils to travel to the site of infection. This leads to the release of two proteases, elastase and trypsin. These proteases allow neutrophils to physically get through the elastic fibers of the tissue and target the invader.

Both elastase and trypsin have the potential to destroy invaders, but if left unchecked also have the ability to destroy the lung tissue. This system is inactivated by alpha-1-antitrypsin. As a side note, those individuals who do not have the antitrypsin compound frequently develop a COPD-like disease. Over the last few years more and more information has emerged about the biochemical and biophysical injury caused by circulating chemokines and cytokines, but this is not the topic of this article.

The production and metabolism of endogenous compounds is probably a book in and of itself, but the endogenous compounds most pertinent to this article are nitric oxide (NO), prostaglandins, and endothelin-1. What are the tools respiratory therapists have in their tool box to help care for the critically ill exhibiting pulmonary hypertension and right ventricular dysfunction? There are both pharmacologic and non-pharmacologic strategies to help the patient maintain homeostasis, or more accurately, vascular tone and hemostasis.

Pulmonary vasculature non-pharmacologic management2

Two principal methods to help manage the vasculature are prevention of hypercapnia/hypoxemia and prevention of high plateau pressures. The former lead to vasoconstriction and the latter has the potential to reduce pulmonary blood flow by compressing the pulmonary capillaries.2 This topic is very thoroughly covered in articles about lung protective strategies. Mechanical interventions to support the heart (right and left ventricular assist devices and intra-aortic balloon pumps) also fall into this category.

Pulmonary vasodilator pharmacologic management2

It should go without saying that prior to use of pulmonary vasodilators there should be good fluid management of cardiac output and right ventricular perfusion. One should also remember that oxygen alone is a potent dilator of the pulmonary vasculature.

Inhaled nitric oxide

Inhaled nitric oxide (iNO) has been used very successfully in the presence of right ventricular dysfunction and pulmonary hypertension. There are many benefits to iNO, including a decrease in pulmonary vascular resistance, improvement in cardiac output and oxygenation, and attenuating lung inflammation by reducing leucocyte adhesion and activation. Inhaled nitric oxide is a potent pulmonary vasodilator and does not cause systemic vasodilation due to rapid inactivation by binding with the heme of iron.3 It rarely ever exits the pulmonary vasculature.

Nitric oxide and O2 compete for the heme of iron, so there is a potential risk for methemoglobinemia for which methylene blue, an inhibitor of guanylate cyclase4, is an antidote. Other risks include the very short half-life of less than 5 seconds; the potential risk for nitrogen dioxide toxicity, especially in the presence of high FiO2; and the increased risk of renal dysfunction.3,5 Inhaled nitric oxide should be weaned slowly due to the risk of rebound pulmonary hypertension and right ventricular dysfunction. Weaning slowly allows reestablishment of endogenously created NO.

Inhaled prostacyclins

Inhaled prostacyclins can be used alone or in combination with iNO. When used together, there is a synergistic effect. Prostacyclins (prostaglandins) are endogenously produced in the lung vasculature and are not broken down during passage through the lungs. Prostacyclins can also be given exogenously and used as an inhaled substance. When prostacyclins are inhaled they are potent pulmonary vasodilators and have antiplatelet and antiproliferative effects.2

Although there is a risk of bleeding, a study by Haraldsson et al. in 2000 found it was not a factor in post cardiac surgery and cardiopulmonary bypass. It should, however, be remembered as a potential risk, especially if other anticoagulant therapy is in use. Prostacyclins reduce PVR and improve both RV function and oxygenation. An added benefit is that prostacyclins do not produce toxic metabolites1, yet care should be taken when discontinuing therapy because as with iNO, there may be rebound pulmonary hypertension and cardiovascular collapse.6

Epoprostenol (Flolan)

Epoprostenol (Flolan) can be used as an inhaled drug; it should be used with a dedicated pump, so there is no opportunity for the drug to be delivered intravenously. This form of the drug is unstable at room temperatures and has a short half-life of approximately six minutes.

Iloprost

A more chemically stable option is inhaled Iloprost, which is stable at room temperature and has a half-life of approximately 20-25 minutes. The drug can be delivered by regular aerosol (i.e., Aeroneb) and is recommended every three hours but can be used as often as every hour.

Phosphodiesterase inhibitors

Phosphodiesterase is an enzyme that hydrolyzes cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) and is strongly expressed in the lung.3Phosphodiesterase inhibitors work by increasing cGMP signaling, and they potentiate the effects of iNO. Phosphodiesterase inhibitors prevent the breakdown of both cAMP and cGMP, both of which are instrumental in smooth muscle relaxation. Nasogastric sildenafil (Revatio) may facilitate weaning from iNO.2 Phosphodiesterase inhibitors can be used to augment the pulmonary vascular response to iNO and help prevent rebound.

Endothelin inhibitors

Endothelin inhibitors may also be considered at times. The endogenous method of vasoconstriction is the release of endothelin-1. Endothelin-1 has been implicated in tissue remodeling, which may lead to pulmonary hypertension, as mentioned earlier. Endothelin levels are increased in all forms of shock, and especially in septic shock.3 Bosentan is a dual endothelin-1 receptor blocker and abrisentan is a selective endothelin-A receptor antagonist. There is no real evidence to support the use of Bosentan in critical care and it has only been mentioned as a rescue drug in some instances. Bosentan is primarily used in the treatment of chronic pulmonary hypertension.3

Deserving of attention

The primary goal of these treatments is to increase intracellular concentrations of cGMP; this causes a decrease in intracellular calcium, leading to smooth muscle relaxation. Inhaled nitric oxide does this through binding with guanylate cyclase. Prostacyclins activate adenylyl cyclase to produce cAMP, which also causes smooth muscle relaxation leading to vasodilation. Phosphodiesterase inhibitors prevent the breakdown of the newly formed cGMP and cAMP, allowing them to remain in the system longer, which in turn allows a more lasting vasodilation.

By using these drugs alone or, at times, in combination, the respiratory therapist can assist the physician in maintaining endothelial health and vascular tone in times of crisis. The pulmonary endothelium is part of the barrier between the capillaries and the alveoli and there are a plethora of biochemical and molecular changes happening continuously. It is an area of complex physiology and one that deserves our special attention. The endothelium is very sensitive to the effects of reactive oxygen species and has built in antioxidant systems that provide protection from injury. Stresses created by oxygen-based free radicals are a topic all on their own and are intimately tied to lung injury and vascular response. Vascular injury and repair are areas for future investigation, as there is a need for deeper understanding for the therapist.

References

  1. Lumb AB. Nunn’s applied respiratory physiology. Philadelphia: Elsevier, Butterworth Heinemann; 2005.
  2. Price LC, Wort SJ, Finney SJ, Marino PS, Brett SJ. Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review. Crit Care Med 2010;14(5):169-191.
  3. Sidebothan D, McKee A, Gillhan M, Levy JH. Cardiothoracic critical care. Philadelphia: Elsevier, Butterworth Heinemann; 2007.
  4. Quinn AC, Petros AJ, Vallance P. Nitric oxide: an endogenous gas. Brit Jour Anesthesia 1995;74:443-451.
  5. Adhikari NK, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H, et al. Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: systematic review and meta-analysis. Crit Care Med 2014;42(2):404-412.
  6. Vincent JL, Abraham E, Moore FA, Kochanek PM, Fink MP. Textbook of critical care. Philadelphia: Elsevier, Saunders; 2011.

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Why Does My Patient Keep Failing Weaning Trials after an Excellent Weaning Assessment? Consider the B-type Natriuritec Peptide (BNP)

Mary Ann Couture, MS, RRT-ACCS
Hartford Hospital, Hartford, CT

One of the more frustrating reasons for mechanical ventilation weaning failure may be due to a cardiac origin. The patient passes short-term weaning criteria, but over a period of time may become dyspneic and/or hypoxemic with increased work of breathing.

If the patient is already extubated, there are additional problems associated with reintubation. Most ventilated patients do not have a pulmonary artery catheter or other invasive hemodynamic sensing device to gather information that indicates whether the patient is in fluid overload. The B-type natriuritec peptide (BNP) obtained by blood sample is a cardiac biomarker that is secreted by cardiomyocytes when the cardiac muscle wall is stretched and stressed. The “B” stands for “Brain,” which can be misleading because it was first discovered in pig brains. High levels cause arteries to dilate as a mechanism to reduce stress on the heart.

While primarily used in the diagnosis of heart failure, there are other reasons for increased levels of BNP: age, hypertension, infections such as pneumonia and sepsis, asthma exacerbation, recent MI, certain medications that aid the body in retaining sodium, and obstructive sleep apnea.

Landmark trial

A landmark trial published in 2002, the “Breathing Not Properly” multinational study, was a seven-center, prospective study of 1586 patients who came to the emergency department with acute dyspnea. They were assessed for the BNP marker.1 The researchers found that BNP was more accurate in identifying congestive heart failure as the cause of dyspnea than any other lab value measured in the past. The diagnostic accuracy of BNP for heart failure was 83.4%. This has since created a gold standard for congestive heart failure.

Twelve years later, numerous studies have contributed to enhanced capabilities in diagnostic decision-making prognosis and cost effectiveness of certain treatments for heart failure. Since that landmark study, BNP is now established in the evaluation of acute dyspnea from uncertain causes. High levels of BNP can also predict mortality due to cardiovascular events.

Guidelines for levels are listed below:

  • 100 µg/mL indicates no heart failure (some facilities list a normal range up to 150 µg/mL)
  • 100-300 µg/mL suggests heart failure is present
  • 300 µg/mL indicates mild heart failure (and dyspnea may be a symptom)
  • 600 µg/mL indicates moderate heart failure
  • 900 µg/mL indicates severe heart failure

Useful tool

BNP measurement can be a useful tool when obtained prior to mechanical ventilator weaning and after the initial cause of illness is resolved or stabilized. Levels will rapidly increase as the heart is stressed by reducing ventilator load and increasing spontaneous workload, which in turn leads back to respiratory failure. Even though the patient may pass his weaning assessment during a short trial, it may not reflect long-term weaning. In patients with heart failure, the BNP level will increase during the trial. If levels do not change during weaning, then the failure may be of pulmonary origin such as COPD.2 An elevated level prior to a weaning trial may also suggest that the patient is volume overloaded and should not wean until adequately diuresed.

A recent randomized trial looked at 306 mechanically ventilated patients with elevated BNP of >200 µg/ml placed into two groups. Treatment was guided either by usual care or by aggressive use of diuretics. The investigators looked at extubation rates and continued ventilator liberation of greater than 72 hours as the end points. The group that was treated aggressively had a significant reduction in ventilator days; however this did not alter length of stay or mortality.3

Data to aid in determining BNP levels for successful ventilator liberation are scarce. One small study looked at 30 patients to assess the BNP levels associated with weaning failure; the cut-off to discriminate patients with heart failure during MV was 286 µg/mL.4 In another study, 102 patients were assessed for ventilator liberation of greater than 48 hours in correlation to BNP levels. Thirty-seven patients failed either a t-piece trial or pressure support trial, and five failed extubation. After aggressive diuresis, BNP levels were reduced from an average of 517 to 226 µg/mL in nine of the patients, and all nine were successfully liberated from the ventilator.5

Much promise

BNP measurement shows much promise as a diagnostic marker for congestive heart failure, which is a multi-system disease. It should not be considered a stand-alone test in interpreting why patients cannot wean. Chest x-ray and a longer spontaneous breathing trial with or without PEEP may aid in the decision for successful ventilator liberation. However, measuring BNP levels in conjunction with clinical judgment increases the ability to distinguish between congestive heart failure and non-cardiac causes such as COPD. When BNP levels are greater than 200 µg/mL, successful ventilator liberation may become more difficult.

Consideration of BNP levels may aid in ventilator weaning decision-making when other hemodynamic measurements are not readily available. When differentiation of the causes of weaning failure needs to be assessed, it may be prudent to obtain pre and post BNP levels during the weaning trial to determine direction of care in terms of heart failure or failure from chronic pulmonary disease.

References

  1. Maisel AS, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:161-167.
  2. Grasso S,Description: http://scopus.com/static/images/s.gifet al. Use of N-terminal pro-brain natriuretic peptide to detect acute cardiac dysfunction during weaning failure in difficult-to-wean patients with chronic obstructive pulmonary disease. Crit Care Med 2007;35:96-105.
  3. Dessap AM, et al. Natriuritec peptide-driven fluid management during ventilator weaning. Am J Respir Crit Care Med 2012;186:1256-1263.
  4. Principi T, et al. Behavior of B-type natriuretic peptide during mechanical ventilation and spontaneous breathing after extubation. Minerva Anestesiol 2009;75:179-183.
  5. Mekontso-Dessap A, et al. B-type natriuretic peptide and weaning from mechanical ventilation. Intensive Care Med 2006;10:1529-1536.

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Section Connection

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Bulletin Deadlines: Winter Issue: December 1; Spring Issue: March 1; Summer Issue: June 1; Fall Issue: September 1.

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