Ace844

In my experience in both life and EMS, you leave little to nothing to chance/assumption as far as most things are concerned. As far as experience here, it like everything else is varied... We have all sorts of posters here.. out here, Ace844

Such as??? please quantify/clarify your question..??? out here, Ace844

You're joking right???? :roll: :idea::!: Do they have the same training as well??!!!

You fail to mention if you yourself have any experience operating Emergency vehicles, its alot different than "regular" driving. Also, You think you have "experience" I'll tell ya, for a real thrill and to test your skills, sometime, try "driving' on the "outer ring road" in Moscow, that'll really cause you to evaluate your skills sometime!! Those Russians will hand you your cajones in a hurry...Better yet, try to cross the street and see what happens..!! out here, Ace884

"Dust," That's easy. 1.) There's no shortage of undereducated morons in the US 2.) You don't have to pay them a whole lot, so your profit margin soars! 3.) They are endlessly replaceable 4.) You can just teach them things like: If your patient says this...these are always the actions you take. Don't think, just do.... 4.) Writng is ancillary to sriving and making sure those dialysis and Nh pt's get to where they need to be...its only a transfer after all...:roll: :idea:.. out here, Ace844

"ER Doc," I'm curious as to what you think of this issue. Would you support it's use in your system, if not then why? What are your thoughts on this.. out here, Ace844

Hi All, In my state there are some communities where responses are like were described in the aforementioned posts. For example: This takes place In a Major city in Mass: 1 Fire engine, 1-2 PD/LEO cars, Depending on the call-1 BLS, 1-ALS ambulance responding.....So here's in my experience how it brakes down. Fire: because they want the call #'s to justify having a job(they mostly hang out and do little to nothing for the patient), Police (our safety, mostly they watch as well..:roll:), BLS/ALS: depends on the call and "dispatched percieved acuity of the call"... Out here, Ace844

I'm trying to make you crazy and blind...Is it working..!?!?!?

"Rid," As far as a true "EMS" journal, the closest i have found is "Pre-hospital Emergency Care", which "AZCEP," mentioned as well. out here, Ace844

Hi All, I was just wondering as a group how many of us read "professional medical journals" (not including JEMS, EMS, Fire Rescue, which are more magazines..). If you do which ones and why? Do you concentrate on EM/EMS related journals or read whatever you have access to..? Do you think this is important to our profession..? out here, Ace844

Hi All, In relation to my other post and some others that have been posted on this board recently, I got to wondering how common is research in EMS in general. It seems that most of the studies come from a few select areas....So lets hear from everyone, and what they think about the renewed push towards evidenced based medicine in EMS!! Out here, Ace844

Hi All, I'd like to hear what some of the docs who post/frequent here think of these issues....Any takers?!?!?!? :idea: :!:

What no takers....comments, or anything relating to this....topic?!!?!?!? :roll: :idea:

So which are you a proponent of...?

As far as the dispatch accuracy issue...I believe that one of the links I posted at the top of my original post covers this issue as well....

Part 2 Diastolic Dysfunction Diastolic dysfunction is diagnosed in those patients with HF symptoms that are found to have preserved systolic dysfunction and an EF greater than 40%. Some of the disorders associated with diastolic dysfunction include: restrictive cardiomyopathy, obstructive and non-obstructive cardiomyopathy, and infiltrative cardiomyopathies1. With diastolic dysfunction, filling of the ventricles is impeded due to fibrosis and the lack of relaxation. HF is predominately found in elderly women with hypertension 10 . Making the diagnosis of diastolic dysfunction is often difficult. The diagnosis is generally made by findings on an echocardiogram. These patients that are found to have signs or symptoms of HF with a normal ejection fraction are diagnosed with diastolic dysfunction1. There have been few clinical trials to evaluate the treatments for diastolic dysfunction. Treatment is generally based on physiologic factors such as blood pressure, heart rate, uncontrolled blood volume and ischemia. Hypertension can cause both functional and structural changes in the heart. Both systolic and diastolic blood pressure should be controlled using published guidelines to prevent the development of diastolic dysfunction1. Tachycardia shortens both the ventricular filling time and perfusion of the coronary arteries. Those medications that slow the heart rate can improve symptoms in diastolic dysfunction. Diuretics may also decrease blood volume, thus improving shortness of breath in these patients. If patients are ischemic they should be considered for revascularization to alleviate ischemia and ultimately improve their symptoms. Improving outcomes in diastolic heart failure Techniques to evaluate underlying causes and target therapy Mikhail Torosoff, MD, PhD; Edward F. Philbin, MD VOL 113 / NO 3 / MARCH 2003 / POSTGRADUATE MEDICINE This is the second of three articles on heart failure. Preview: Abnormal diastolic function is a common cause of clinical heart failure, particularly among elderly patients. Through early diagnosis and careful management of diastolic dysfunction, these patients can expect improved functional capacity and, in some cases, a favorable long-term outcome. In this article, Drs Torosoff and Philbin discuss how to confirm the diagnosis of diastolic heart failure through objective testing. Current approaches to the treatment of symptoms, including reduction of intravascular volume, heart rate control, and elimination of precipitating factors, are also presented. Torosoff M, Philbin EF. Improving outcomes in diastolic heart failure. Postgrad Med 2003;113(3):51-58 -------------------------------------------------------------------------------- The possible causes of diastolic dysfunction include hypertensive heart disease, left ventricular hypertrophy, acute and chronic coronary artery disease (CAD), aging, and infiltrative cardiomyopathies (eg, amyloidosis, hemochromatosis), thyroid disease, myocardial ischemia, and pericardial disease. In this condition, diminished myocardial relaxation raises filling pressures, lowers cardiac output, and causes pulmonary congestion. Exercise, tachycardia, anemia, fever, and other systemic stressors may provoke or worsen symptoms in patients with diastolic dysfunction. Although clinical heart failure may be diagnosed at a patient's bedside, diastolic dysfunction is confirmed by objective testing. Two-dimensional and Doppler echocardiographic techniques often are used to evaluate left ventricular structure and patterns of blood flow. Treatment of diastolic dysfunction includes preventive measures, management of symptoms and, when possible, treatment of underlying causes. In treating symptoms, reduction of intravascular volume, control of heart rate, and elimination of precipitating factors are essential. Patients with diastolic heart failure can anticipate improved functional capacity and perhaps an improved long-term outcome with careful clinical management. Diastolic properties and dysfunction Broadly defined, diastolic dysfunction is a change in cardiac properties that impairs the ability of the ventricular cavity to accommodate normal end-diastolic volume at normal filling pressures--either at rest or during exercise (1,2). A slower rate of filling causes elevated diastolic pressure and, in the extreme, diminished cardiac output. The lessened output leads to such symptoms as dyspnea, effort intolerance, and edema. Many factors that interfere with the normal active and passive phases of filling can cause clinically apparent diastolic dysfunction. Normal diastolic characteristics Diastole is an active, energy-requiring process in which the heart relaxes immediately after contraction, vigorously filling the ventricular cavity with blood (1,2). Diastole can be divided into four phases: isovolumic relaxation, early passive filling, diastasis, and filling during atrial contraction. In isovolumic relaxation, intracellular calcium is sequestered in the sarcoplasmic reticulum, deactivating actin-myosin crossbridges. During this phase, vigorous relaxation produces a suction effect that facilitates active early ventricular filling. Ischemia (which reduces the energy supply) or other processes that slow calcium sequestration within the myocyte can prolong the isovolumic relaxation time and impair ventricular filling. With the opening of the mitral valve, isovolumic relaxation ends and early passive ventricular filling commences. Filling is dependent on the pressure gradient between the left atrium and left ventricle, as well as the viscoelastic properties of the myocardium. Early in the course of diastolic dysfunction, when left ventricular relaxation is slowed but atrial pressure has not yet risen, the gradient is diminished, reducing ventricular filling. During diastasis, pressures in the left atrium and ventricle equilibrate, which results in slowed blood flow across the mitral valve. Finally, with atrial contraction, an active pressure gradient between the left atrium and ventricle is again produced and facilitates late diastolic filling. Properties of diastolic dysfunction When diastolic dysfunction is present, late filling must increase in a compensatory fashion to bring ventricular end-diastolic volume to its normal level, and proportionately more ventricular filling is shifted to the later moments of diastole. In severe cases of diastolic dysfunction, the ventricle becomes so stiff that even the atrial muscle fails and normal end-diastolic volume is not achieved, despite elevated filling pressure. This process leads to reduced stroke volume and the clinical manifestations of low cardiac output. Many experts call this final stage restrictive physiology. Because normal cardiac relaxation requires a rich supply of high-energy compounds, myocardial relaxation is impaired early and significantly in the presence of acute cardiac ischemia. This usually occurs before any systolic dysfunction is apparent (1,2). Therefore, during ordinary angina episodes or in the context of acute coronary syndromes, transient periods of diastolic dysfunction typically are present. On the other end of the spectrum, left ventricular hypertrophy and fibrosis affect the viscoelastic properties of myocardium in a more chronic way, making the myocardium less compliant and predisposing to chronic heart failure. Considering the prevalence of CAD, hypertension, and left ventricular hypertrophy in the US population, the public health implications of diastolic dysfunction are apparent (3-5). Diastolic dysfunction occurs early in the course of many cardiac diseases and increases in frequency with age. Whereas it is the underlying cause of heart failure in 35% to 45% of cases, diastolic dysfunction accounts for at least 70% of heart failure in patients aged 80 years and older. Diastolic heart failure Many patients with clinical heart failure have normal systolic function of the left ventricle when its contractile properties are measured with such laboratory tests as echocardiography or angiography. When this occurs, physicians often suspect abnormal cardiac filling as the cause of a patient's heart failure and call this syndrome diastolic heart failure. However, more precise and accurate use of the term also requires laboratory evidence of abnormal diastolic function (6-8). Diastolic function can be assessed by various commonly available tests, including echocardiography, nuclear left ventriculography, and cardiac catheterization. Some patients with acute systolic heart failure may experience improvement in ejection fraction either spontaneously or in response to initial treatment. Thus, patients who display normal ejection fraction during testing performed at a time distant from a clinical episode of heart failure may have had transient systolic dysfunction and not diastolic failure. Moreover, patients with acute respiratory insufficiency and normal ejection fraction may have had an acute noncardiac event, such as asthma or pneumonia, and not cardiac failure. Diastolic dysfunction may be discovered in a previously symptom-free patient during a laboratory test performed for other indications. In fact, some degree of diastolic dysfunction is part of normal aging. Although such patients usually have a truly pathologic ventricular filling pattern, the clinical significance of isolated and asymptomatic diastolic dysfunction is unclear. By definition, some degree of diastolic dysfunction is usually present when heart failure is caused by systolic dysfunction (low ejection fraction). In such cases, however, the thrust of treatment is on the systolic components of the heart failure syndrome. When severe diastolic failure (restrictive physiology) and severe systolic failure coexist, the patient's prognosis is particularly poor. With these details in mind, a reasonable definition of diastolic heart failure requires the following: Presence of symptoms, physical findings, and results of basic laboratory tests (eg, chest radiograph) that are compatible with heart failure Exclusion of other medical conditions that can masquerade as heart failure, such as asthma and pneumonia Results of tests of cardiac function performed in close proximity to the clinical episode that show normal left ventricular systolic function but abnormal diastolic function Evaluation of left ventricular diastolic function A carefully taken history and physical examination are the first steps to discovering evidence of underlying diastolic dysfunction. Older age, hypertension, and CAD are common clinical risk states (4,5). Rarely, infiltrative diseases that involve the heart, such as amyloidosis or hemochromatosis, are the cause. Both hypothyroidism and hyperthyroidism can cause or precipitate diastolic dysfunction. Orthopnea, dyspnea, exercise intolerance, chest discomfort, palpitations, weight gain, and peripheral edema are common presenting symptoms. In the early stages of diastolic dysfunction, some symptoms may occur only with exertion or physical stress. In its extreme form, diastolic dysfunction may cause such problems as impaired cognitive function and renal dysfunction as manifestations of low cardiac output. Findings on physical examination are similar in systolic and diastolic heart failure. In fact, neither the physical examination (9) nor the chest radiograph reliably distinguishes between these entities (10). Electrocardiography may show left ventricular hypertrophy due to hypertensive heart disease or other causes. Arrhythmias, particularly atrial fibrillation, may be present and may contribute to the clinical presentation but are not thought to directly cause diastolic dysfunction. Laboratory tests can greatly aid in confirming the presence and elucidating the cause of diastolic dysfunction. Echocardiography is very useful in the noninvasive evaluation of suspected diastolic dysfunction (6,7). It allows determination of ventricular size, wall thickness, isovolumic relaxation time, and quantitative and qualitative assessment of early and late diastolic filling. Information can also be obtained about pericardial properties and pericardial effusion. Left ventricular wall thickness that exceeds 11 mm in the presence of a normal left ventricular end-diastolic dimension (<55 mm) confirms ventricular hypertrophy. Atrial enlargement is usually found with long-standing diastolic dysfunction. Discrete regional abnormalities of ventricular contraction suggest acute or chronic ischemic injury as a consequence of CAD. Infiltrative cardiomyopathies can cause changes in tissue characteristics of the myocardium, which are detectable by ultrasound. Thickening of the valve leaflets is typically present with amyloidosis but is rare with other infiltrative cardiomyopathies. Significant information can be gained from interrogation of blood flow between the left atrium and left ventricle at the level of the mitral valve. Because intracardiac blood flow is a function of the pressure gradient between contiguous cardiac chambers and the size of the orifice between them, blood flow velocities can be used to estimate pressure gradients and the changes in these gradients over time and under various conditions. Early ventricular filling correlates with the E wave of the transmitral Doppler flow pattern; late active filling correlates with the A wave (figure 1). The normal transmitral filling pattern is characterized by a predominant E wave that has a duration (deceleration time) of more than 200 milliseconds. When relaxation is impaired, ventricular pressure falls more slowly than normal, and the early diastolic left atrium-left ventricle pressure gradient decreases. Accordingly, the velocity (height) of the E wave diminishes and typically becomes less than the velocity of the A wave. This pattern reflects the fact that late diastolic filling is more significant under abnormal conditions than it is normally (figure 2). As diastolic dysfunction progresses over time, absolute left atrial pressure rises and restores the left atrium-left ventricle pressure gradient to its "normal" range. Even though the gradient is normal, absolute pressures in both the ventricle and atrium are supranormal, giving rise to the term pseudonormalization. The Doppler pattern of pseudonormalization is characterized by a tall but abnormally narrow E wave and a deceleration time of less than 140 milliseconds (figure 3). In end-stage diastolic dysfunction, the atrium fails and is unable to generate pressure. Accordingly, the Doppler pattern of late and advanced diastolic dysfunction (restricted) is abnormally low-velocity A waves. Computed tomography and magnetic resonance imaging can aid in the evaluation of pericardial disease by showing thickening, calcification, and effusion. Nuclear imaging can provide information about ejection fraction, chamber volume, and rate of ventricular filling. This technique is especially useful with large patients or others with difficult acoustic windows that preclude precise echocardiographic imaging. Cardiac catheterization is usually not required to document the physiology of diastolic dysfunction. However, the hemodynamic patterns of diastolic dysfunction are present when such patients undergo catheterization for other reasons, such as the evaluation of coronary disease. Myocardial biopsy can be used to evaluate infiltrative diseases of the heart. Precipitating causes of heart failure Most patients with isolated diastolic dysfunction are free of symptoms when at rest or when not faced with such physical stressors as ischemia, exercise, cardiac arrhythmias, infection or inflammation, anemia, thyrotoxicosis, or fever (table 1). Table 1. Common precipitating factors in diastolic heart failure Volume overload Tachycardia Hypertension Ischemia Exercise Conduction disturbances and arrhythmias Atrial fibrillation Atrioventricular nodal block Intraventricular conduction delays Systemic stressors Anemia Fever Infection Inflammation Thyrotoxicosis Emotional stress Pericardial effusion Withdrawal of effective cardiac medications -------------------------------------------------------------------------------- By directly or indirectly impairing ventricular filling or by augmenting venous return, these stressors can exacerbate the physiologic factors of diastolic dysfunction. Regardless of cause, tachycardia often provokes clinical symptoms in patients with underlying diastolic dysfunction. By definition, it reduces the time available for cardiac filling as it trims the last milliseconds from diastole. Normally, most filling occurs in early diastole. Tachycardia does not compromise cardiac filling in healthy persons. However, among patients with delayed cardiac relaxation, tachycardia can profoundly affect diastolic filling, elevate left atrial pressure, and produce symptoms of heart failure. In patients with tachycardia and loss of atrioventricular synchrony (as occurs with rapid atrial fibrillation), both tachycardia and the loss of synchronized atrioventricular contraction contribute independently to diastolic dysfunction. Under such circumstances, loss of atrioventricular synchrony in and of itself may cause a 20% to 25% decrease in cardiac output. Exercise presents a physiologic challenge for patients with diastolic dysfunction. During exercise, a healthy person augments cardiac output severalfold by increasing venous return, raising end-diastolic volume, and increasing heart rate. The compliance of the healthy heart allows tachycardia and increased venous return during exercise without a significant rise in ventricular end-diastolic pressure. In contrast, in a patient with diastolic dysfunction, exercise-related tachycardia and increased venous return produce a sharp rise in filling ventricular pressures and place the patient at risk for symptomatic decline (2). Ischemia causes diastolic dysfunction because depletion of energy-rich compounds impedes the relaxation process. Thus, both acute and chronic ischemic heart disease can cause or exacerbate diastolic dysfunction. The presence of a new third heart sound in a patient with other manifestations of acute ischemic heart disease is often due to diastolic dysfunction. Treatment Although there is no specific short-term therapy for the cellular or subcellular abnormalities that cause diastolic dysfunction, a variety of effective treatment measures can be used to ameliorate symptoms of acute and chronic heart failure and prevent exacerbations. Management of diastolic dysfunction also includes prevention of the onset and progression of predisposing conditions. Successful treatment of diastolic dysfunction involves the definition and management of its origin and underlying mechanism or mechanisms. Primary and secondary prevention of CAD can avert cases of diastolic dysfunction associated with myocardial ischemia. Likewise, aggressive treatment of hypertension with the goal of preventing or reversing left ventricular hypertrophy is beneficial. Treatment of hypertension in elderly patients can reduce the incidence of heart failure significantly (11,12). The goals of medical treatment of diastolic dysfunction involve optimization of hemodynamic conditions, including cardiac preload and afterload, as well as treatment of symptoms (table 2). Angiotensin-converting enzyme (ACE) inhibitors reduce blood pressure, prevent or reverse left ventricular hypertrophy, reduce preload, and favorably affect vascular and cardiac remodeling. Accordingly, there is a strong rationale for their use in diastolic heart failure. Although preliminary studies suggest that ACE inhibitors benefit patients with diastolic heart failure (5,13), confirmation awaits the completion of large, placebo-controlled randomized mortality trials. Until then, it is reasonable for physicians to prescribe ACE inhibitors when hypertension is linked to diastolic heart failure and perhaps in other cases of diastolic dysfunction as well. Table 2. Treatment approach to diastolic heart failure Primary and secondary prevention of diastolic dysfunction Prevention and treatment of hypertension and other causes of left ventricular hypertrophy Prevention and treatment of ischemic heart disease Surgical removal of diseased pericardium for pericardial constraint Chemotherapy for infiltrative cardiomyopathies Optimization of circulating volume Salt and water restriction Diuresis, dialysis, or plasmapheresis Use of angiotensin-converting enzyme (ACE) inhibitors Use of aldosterone antagonists (theoretical benefit) Management of tachycardia and tachyarrhythmia Use of beta-adrenergic blockers (preferred) Use of calcium channel blockers (as second-line agents) Use of digoxin (Digitek, Lanoxicaps, Lanoxin) (controversial; has produced inconsistent results) Atrioventricular node ablation when necessary in rare cases Maintenance of normal sinus rhythm for atrial fibrillation and other arrhythmias Dual-chamber pacemaker for significant bradycardia Optimization of neurohormonal milieu ACE inhibitors Beta-adrenergic blockers Aldosterone antagonists -------------------------------------------------------------------------------- The hormone aldosterone promotes fibrosis in the heart and thus contributes to diastolic stiffness. The aldosterone antagonist spironolactone has been shown in a preliminary study (14) to reduce myocardial fibrosis and may prove to have a role in the treatment of diastolic heart failure. Maintenance of optimum intravascular volume is important to minimize dyspnea and avoid episodes of acute heart failure. Volume overload can be prevented or minimized by a low-salt diet, judicious use of diuretics and, if necessary, renal dialysis. Control of heart rate and prevention of tachycardia are important in patients with diastolic dysfunction. In theory, heart rate control optimizes cardiac filling by maximizing the diastolic filling period. Beta-blockers are particularly useful for this purpose. They prevent tachycardia, lower blood pressure, reverse left ventricular hypertrophy, and antagonize the excessive adrenergic stimulation common in heart failure. Calcium channel blockers also are useful for controlling heart rate and lowering blood pressure. They can be used if beta-blockers are contraindicated (eg, in patients with severe asthma) or when a full-dose beta-blockade inadequately controls heart rate. However, calcium channel blockers have not been proved in large, prospective, randomized controlled trials to reduce mortality in patients with normal ejection fraction and heart failure due to isolated diastolic dysfunction. Because digoxin (Digitek, Lanoxicaps, Lanoxin) raises intracellular calcium levels, it might be ineffective in the treatment of diastolic heart failure. In fact, a specific subset of patients with diastolic failure--elderly patients with ventricular hypertrophy--appear to do worse with digoxin than without it. However, the Digitalis Investigation Group trial showed clinical benefit of digoxin use in patients with chronic heart failure, normal sinus rhythm, and an ejection fraction of more than 45% (15). Because laboratory confirmation of diastolic dysfunction was not required for enrollment in this trial, it is unknown which patients truly had the condition. Accordingly, the exact role of digoxin in the treatment of diastolic heart failure remains unclear. Maintenance of synchrony of atrial and ventricular contractions is required for preservation of normal filling patterns. Whenever possible, atrial fibrillation should be converted to sinus rhythm. If maintenance of sinus rhythm is not possible, the ventricular rate should be well controlled through use of drugs or ablation of the atrioventricular node, if necessary. Prognosis Diastolic dysfunction often is discovered in a previously symptom-free patient during a laboratory test performed for other indications, such as hypertension, valve disease, or CAD. The survival of patients without heart failure or other symptoms of diastolic dysfunction has not been thoroughly examined in well-done community-based studies (16). It is reasonable to assume that coexistent conditions that cause diastolic dysfunction, such as hypertension or CAD, are more powerful determinants of a person's longevity than the presence of diastolic dysfunction itself. It is also reasonable to postulate that diastolic dysfunction is a potent risk factor for clinical heart failure, although the exact incidence of this event in previously asymptomatic persons with diastolic dysfunction also is unknown. Short-term survival among patients with a normal ejection fraction who are hospitalized for heart failure is better than survival among those with a low ejection fraction but worse than that of age-matched control subjects without heart failure. Diastolic heart failure is a major cause of cardiovascular morbidity, especially in the elderly population (4,5,16). Clinical disability, lifestyle impairment, and rehospitalization rates are similar among heart failure patients with low versus normal ejection fraction. Conclusion Diastolic dysfunction is a common condition that is highly prevalent among elderly persons. A host of cardiac disorders predispose to diastolic dysfunction, including hypertension, ischemic heart disease, myocardial hypertrophy, and infiltrative cardiomyopathies. Exercise, tachycardia, anemia, fever, and many systemic illnesses may provoke symptomatic decline in patients with this condition. Diagnosis of diastolic dysfunction relies on careful clinical bedside evaluation supplemented with a laboratory workup. Of diagnostic procedures, two-dimensional and Doppler echocardiographic techniques are uniquely suited to evaluate the changes in left ventricular structure and physiology that are typical in diastolic dysfunction. Successful treatment of diastolic dysfunction includes preventive measures focused on hypertension, left ventricular hypertrophy, and atherosclerotic heart disease. When acute exacerbations occur, intravascular volume reduction, heart rate control, and elimination of precipitating factors are essential. Diuretics, beta-blockers, and ACE inhibitors are particularly useful in prevention and treatment. Patients with diastolic dysfunction can anticipate improved functional capacity and perhaps improved long-term outcomes with careful clinical management. References Bonow RO, Udelson JE. Left ventricular diastolic dysfunction as a cause of congestive heart failure: mechanisms and management. Ann Intern Med 1992;117(6):502-10 Grossman W. Diastolic dysfunction in congestive heart failure. N Engl J Med 1991;325(22):1557-64 Senni M, Tribouilloy CM, Rodeheffer RJ, et al. Congestive heart failure in the community: a study of all incident cases in Olmsted County, Minnesota, in 1991. Circulation 1998;98(21):2282-9 Vasan RS, Benjamin EJ, Levy D. Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol 1995;26(7):1565-74 Philbin EF, Rocco TA Jr, Lindenmuth NW, et al. Systolic versus diastolic heart failure in community practice: clinical features, outcomes, and the use of angiotensin-converting enzyme inhibitors. Am J Med 2000;109(8):605-13 Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 1988;12(2):426-40 Little WC, Downes TR. Clinical evaluation of left ventricular diastolic performance. Prog Cardiovasc Dis 1990;32(4):273-90 Vasan RS, Levy D. Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation 2000;101(17):2118-21 Philbin EF, Hunsberger S, Garg R, et al. Usefulness of clinical information to distinguish patients with normal from those with low ejection fractions in heart failure. Am J Cardiol 2002;89(10):1218-21 Philbin EF, Garg R, Danisa K, et al. The relationship between cardiothoracic ratio and left ventricular ejection fraction in congestive heart failure. Digitalis Investigation Group. Arch Intern Med 1998;158(5):501-6 Gueyffier F, Bulpitt C, Boissel J-P, et al. Antihypertensive drugs in very old people: a subgroup meta-analysis of randomised controlled trials. INDANA Group. Lancet 1999;353(9155):793-6 Levy D, Larson MG, Vasan RS, et al. The progression from hypertension to congestive heart failure. JAMA 1996;275(20):1557-62 Philbin EF, Rocco TA Jr. Use of angiotensin-converting enzyme inhibitors in heart failure with preserved left ventricular systolic function. Am Heart J 1997;134(2 Pt 1):188-95 Brilla CG, Matsubara LS, Weber KT. Antifibrotic effects of spironolactone in preventing myocardial fibrosis in systemic arterial hypertension. Am J Cardiol 1993;71(3):12A-16A The effect of digoxin on mortality and morbidity in patients with heart failure. Digitalis Investigation Group. N Engl J Med 1997;336(8):525-33 Senni M, Redfield MM. Heart failure with preserved systolic function: a different natural history? J Am Coll Cardiol 2001;38(5):1277-82 Dr Torosoff is assistant professor of medicine and Dr Philbin is George E. Pataki Chair in Cardiology, division of cardiology, department of medicine, Albany Medical College, Albany, New York. Correspondence: Edward F. Philbin, MD, George E. Pataki Chair in Cardiology, Albany Medical College, Mail Code 44, 47 New Scotland Ave, Albany, NY 12208. E-mail: philbie@mail.amc.edu.

Hi All, I got very little response from my first post, but I decided to follow it up with another and see if that helps some...So here's the next teaching post in the "Heart Failure" realm... There's also a link here to some great powerpoint slides... Hope this helps, Ace844 ACC/AHA 2005 Guideline Update for the Diagnosis andManagement of Chronic Heart Failure in theAdult—Summary Article. Heart Failure Powerpoint @ info... Evidence based treatment guidelines... CHF Diagnosis and Treatment of Diastolic Heart Failure HOWARD D. WEINBERGER University of Colorado Up to 40% of patients with heart failure have isolated diastolic dysfunction. With proper management, the prognosis is generally more favorable than in systolic dysfunction. Distinguishing diastolic from systolic dysfuntion is essential since the optimal therapy for one condition may aggravate the other. New echocardiographic methods enable accurate diagnoses. For patients older than 65, heart failure is the leading reason for hospitalization in the United States. It is also the most expensive condition to treat. In 1991, for example, hospitalization costs were greater for heart failure than for myocardial infarction and all forms of cancer combined. The total cost of treatment, including inpatient, outpatient, and pharmacy costs, is now estimated to exceed $52 billion a year. Classically, heart failure has been almost synonymous with left ventricular systolic failure (pump failure). In the last 10 to 20 years, however, it has become apparent that in nearly 40% of cases, systole is normal and diastole abnormal. In 31 studies of heart failure published between 1970 and 1995, the prevalence of isolated diastolic dysfunction ranged from 13% to 74%. Two of the studies suggest that the condition is age-related. The average incidence was 8% for subjects younger than 65 and 32% for those older than 65. As the population of the United States continues to age, the proportion of heart failure cases due to isolated diastolic dysfunction seems destined to increase. Physiology of Diastole The cycle of myocardial contraction and relaxation is directly related to cytosolic calcium concentration. With electrical depolarization, calcium enters the myocyte via slow (L-type) calcium channels. This triggers the release of massive amounts of additional calcium stored in the sarcoplasmic reticulum. The calcium diffuses into the sarcomere, causing a conformational change in the troponin-tropomyosin complex that permits myosin to interact with actin and the myocyte to contract. For the myocyte to relax, the process must be quickly reversed. Up to 90% of the calcium is actively removed by the calcium-ATPase pump in the sarcoplasmic reticulum and the rest by sodium-calcium exchange and other mechanisms (Figure 1). Working against a 10,000-fold concentration gradient requires a high expenditure of energy--one molecule of ATP is consumed for every two molecules of calcium removed by the calcium-ATPase pump. The relaxation part of the cardiac cycle is subdivided into four phases: 1) isovolumic relaxation, 2) rapid filling, 3) slow filling (diastasis), and 4) atrial contraction (Figure 2). In the first phase, between the time of aortic valve closing and mitral valve opening, calcium is rapidly removed from the cytoplasm and resequestered in the sarcoplasmic reticulum. The next phase begins when pressure in the left ventricle falls below that in the left atrium, causing the mitral valve to open and the left ventricle to begin filling; it ends when pressure in the two chambers is equalized. Although this rapid-filling phase comprises only about 30% of diastole, it accounts for up to 80% of left ventricular volume. The third phase is the slow-filling phase. What little filling there is comes from pulmonary vein flow. With increased heart rate, this phase shortens more than the other three. The fourth phase, atrial contraction, contributes 15% to 25% of the left ventricular volume under normal conditions but can contribute as much as 40% if left ventricular relaxation is diminished. D.L. Brutsaert and colleagues consider the first two phases to be the end of systole. By their definition, diastole would consist of phases 3 and 4. It would thus comprise about 50% of the cardiac cycle but at normal heart rates would contribute only the last 5% to 15% of the ventricular volume. Etiology of Diastolic Dysfunction In 1991, Kitzman and colleagues demonstrated that pulmonary venous pressure, and hence left ventricular filling pressure, is elevated at rest in patients with isolated diastolic dysfunction. With exercise, the filling pressure further increases, but the left ventricular volume decreases (Figure 3). Even higher filling pressures would be required to fill the left ventricle and maintain normal cardiac output. Diastolic heart failure is an insidious disease. Insults to the myocardium are followed by a series of compensatory changes that are beneficial in the short run but have long-term deleterious effects. Structural remodeling and other factors, including myocardial ischemia, left ventricular hypertrophy, increased heart rate, and abnormal calcium flux, can impair diastolic function and cause an increase in left ventricular filling pressures (Table 1). Table 1. Factors Increasing Diastolic Pressure Impaired Ventricular Relaxation -------------------------------------------------------------------------------- Hypertrophy Myocardial ischemia Hypertension Collagen deposition and fibrosis Regional asynchrony Increased preload, afterload Abnormal calcium flux Tachycardia Decreased Ventricular Compliance -------------------------------------------------------------------------------- Hypertrophy Hypertension Collagen deposition and fibrosis Cellular disarray Myocardial infiltration Pericardial constriction or restriction Right ventricle-left ventricle interactions Both ischemia and hypertrophy impair relaxation in early diastole--ischemia by restricting the supply of high-energy phosphates required for rapid removal of calcium from the cytoplasm and hypertrophy by slowing the rate of myosin-actin dissociation. Hypertrophy also decreases left ventricular compliance in all phases of diastole. The probability of ischemia or left ventricular hypertrophy increases with age. Additional correlates of aging, such as hypertension and increased interstitial collagen deposition, result in decreased left ventricular compliance. It is thus not surprising that old age is among the most frequently cited risk factors for isolated diastolic dysfunction. Other leading causes of the condition are coronary artery disease, hypertension, diabetes, obesity, and aortic stenosis (Table 2). Up to 90% of patients with coronary artery disease have abnormal diastolic function, and approximately 60% of patients with heart failure and normal systolic function have hypertension. Obese patients, with or without hypertension also have an increased risk of heart failure due to diastolic dysfunction. Table 2. Causes of Isolated Diastolic Dysfunction Common -------------------------------------------------------------------------------- Coronary artery disease Hypertension Aging Diabetes mellitus Obesity Aortic stenosis Less Common -------------------------------------------------------------------------------- Hypertrophic cardiomyopathy Infiltrative cardiomyopathies Endocardial fibroelastosis Pericardial disease Diagnosis It is important to distinguish between systolic and isolated diastolic dysfunction since the treatment for one condition may aggravate or worsen the other. Unfortunately, the classic manifestations of heart failure are not helpful in this regard. Studies conducted by H. H. Echeverria and colleagues demonstrated that eight of the most common signs and symptoms of heart failure are present with nearly equal frequency in systolic and diastolic dysfunction (Figure 4). The diagnostic workup must not only confirm signs and symptoms of heart failure but include an assessment of systolic as well as diastolic function. Valvular, pericardial, and pulmonary function must also be evaluated. The methods used most frequently are two-dimensional echocardiography, Doppler echocardiography, and radionuclide ventriculography. Two-dimensional echocardiography provides the necessary structural and functional information on chamber size, wall thickness and motion, systolic function, intracardiac valves, and the pericardium. Additional information on blood flow, valvular stenosis, regurgitation, and intracardiac pressures is obtained by Doppler echocardiography. Doppler measurements also allow estimates of right atrial pressure, right ventricular systolic pressure, and pulmonary artery systolic pressure. The relative velocities of blood flow into the left ventricle in the rapid-filling and atrial contraction phases of diastole allow an assessment of left ventricular relaxation and compliance. Similarly, the pattern of pulmonary vein flow allows an estimation of left ventricular end-diastolic pressure and left atrial pressure. A quantitative left ventricular ejection fraction can be obtained by radionuclide ventriculography (gated blood-pool scanning). With the proper equipment, the peak filling rate and time to peak filling can also be obtained. The left ventricular volume, and perhaps the thickness of the chamber wall, can be estimated, but the methodology does not permit direct visualization of cardiac chambers, walls, valves, or pericardium. Nor does it allow evaluation of intracardiac pressures. For these reasons, echocardiography is the best noninvasive means of evaluating left ventricular diastolic function. Tissue Doppler echocardiography of the mitral annulus and color M-mode echocardiography have been recently validated in clinical trials. The assessments obtained by these techniques were in excellent agreement with invasive measurements. Those obtained by tissue Doppler echocardiography appeared to be relatively preload-independent and thus particularly useful for evaluating isolated diastolic dysfunction. Treatment Numerous agents have been shown to be beneficial for treatment of systolic heart failure, but the efficacy of these or other agents for treatment of isolated diastolic failure has not been adequately tested. The underlying or aggravating causes of isolated diastolic failure, as well as the abnormalities produced, may require drugs with different mechanisms of action. As in any disease, the treatment should be as specifically directed as possible (Table 3). Table 3. Goals in Treating Isolated Diastolic Heart Failure Resolve causative or aggravating factors Enhance left ventricular relaxation if necessary Decrease left ventricular filling pressure without decreasing cardiac output Slow heart rate if too rapid Control ventricular rate if atrial fibrillation is present Maintain atrial-ventricular synchrony Maintain sinus rhythm Prevent excess contractility Isolated diastolic heart failure is currently treated with calcium channel blockers (mainly verapamil and diltiazem), beta-adrenergic receptor blockers, or angio-tensin-converting enzyme (ACE) inhibitors. In cases of pulmonary congestion or ischemia, patients may also receive diuretics or nitrates, respectively. Calcium channel antagonists can improve diastolic function directly, by attenuating calcium homeostasis, or indirectly, by reducing blood pressure, reducing or preventing myocardial ischemia, promoting regression of left ventricular hypertrophy, slowing heart rate (verapamil, diltiazem), and improving left ventricular filling parameters. Thus far, verapamil is the only drug shown by objective criteria to improve diastolic function, ameliorate symptoms, and increase exercise tolerance. In a five-week, double-blind cross-over trial conducted in 1990 by J.F. Setaro and colleagues, 20 elderly men with isolated diastolic dysfunction were treated with verapamil or placebo. In those receiving the drug, symptoms improved, exercise time increased 33%, peak left ventricular filling rate increased 30%, and heart rate decreased 10% (p<.05 for all). Table 4. Therapies for Isolated Diastolic Dysfunction Calcium channel blocker Beta-adrenergic receptor ACE inhibitor Diuretic Nitrate Enhances myocardial relaxation + ­ ? ­ ­ Reduces blood pressure + + + + ­ Reduces or prevents ischemia + + ­ ­ + Promotes regression of left ventricular hypertrophy ++ + ++ + ­ Slows heart rate + + ­ ­ ­ Reduces collagen deposition and fibrosis ­ ­ + ­ ­ Improves left ventricular filling parameters + ? + ? ? Improves symptoms + ? + +* ? ? = no studies, * = pulmonary congestion Beta-adrenergic receptor blockers have no direct effect on myocardial relaxation but have proven benefits in reducing blood pressure, reducing or preventing myocardial ischemia, promoting regression of left ventricular hypertrophy, and slowing heart rate. ACE inhibitors, on the other hand, may directly affect myocardial relaxation and compliance by inhibiting production of angiotensin II, which is known to be involved in interstitial collagen deposition and fibrosis. The indirect benefits of ACE inhibitors include reducing blood pressure, improving left ventricular filling parameters, and promoting regression of left ventricular hypertrophy. Positive inotropic or chronotropic agents (e.g., digoxin or dobutamine), potent arterial vasodilators (hydralazine), and alpha-adrenergic receptor blockers (prazosin) should be avoided. In the absence of systolic dysfunction, they are likely to worsen diastolic function by increasing contractile force or heart rate. Diuretics and nitrates may be used in certain cases, but it is important to realize that if abnormally high pressure is required to fill the left ventricle, decreasing the preload can worsen cardiac output. Prognosis The annual mortality of patients with isolated diastolic heart failure appears to be three- to fourfold lower on average than that of patients with systolic heart failure. The figures reported for isolated diastolic failure (1.3%-17.5%), however, are more variable than for systolic failure (15%-20%). This may relate to differences in the age of the subjects, the prevalence of coronary artery disease or left ventricular hypertrophy in the study cohort, or the treatment received. In the Vasodilator in Heart Failure Trial I (V-HeFT I), for example, the annual mortality for patients with a normal left ventricular ejection fraction was less than half that of patients with a reduced left ventricular ejection fraction (8% vs. 19%, p=.0001; Figure 5). The difference might have been even greater had not all of the patients been treated with preload or afterload reducing agents (nitrates; hydralazine, prazosin) that could have worsened diastolic function. Coronary artery disease, hypertension, and a number of other conditions may cause systolic as well as diastolic heart failure. In such cases, diastolic dysfunction precedes systolic dysfunction. Unless the underlying cause of heart failure is identified and adequately controlled, the patient's condition will progressively worsen. Summary Congestive heart failure is a major contributor to morbidity, mortality, hospitalization, and medical costs in the United States. Up to 40% of cases are due to isolated diastolic dysfunction, most of which result from coronary artery disease, hypertension, aging, diabetes mellitus, obesity, or aortic stenosis. Isolated diastolic heart failure cannot be reliably diagnosed by history and physical examination alone. It is imperative to make an accurate diagnosis since treatments for systolic and diastolic dysfunction differ; what is optimal for one may aggravate or exacerbate the other. Echocardiography is the best means of diagnosing the condition noninvasively. Treatment for isolated diastolic dysfunction may include the use of calcium channel antagonists, beta-adrenergic receptor blockers, ACE inhibitors, and the careful use of diuretics for pulmonary congestion and nitrates for myocardial ischemia. Positive inotropic or chronotropic agents, potent vasodilators, and alpha-adrenergic receptor blockers should be avoided, since they can worsen diastolic function when systolic function is normal. HOWARD D. WEINBERGER University of Colorado::http://www.hosppract.com/issues/1999/03/weinb.htm Diastolic Dysfunction Ventricular function is highly dependent upon preload as demonstrated by the Frank-Starling relationship. Therefore, if ventricular filling (preload) is impaired, this will lead to a decrease in stroke volume. The term "diastolic dysfunction" refers to changes in ventricular diastolic properties that have an adverse effect on stroke volume. Ventricular filling (i.e., end-diastolic volume and hence sarcomere length) depends upon the venous return and the compliance of the ventricle during diastole. A reduction in ventricular compliance, as occurs in ventricular hypertrophy, will result in less ventricular filling (decreased end-diastolic volume) and a greater end-diastolic pressure (and pulmonary capillary wedge pressures) as shown to the right by changes in the ventricular pressure-volume loop. Stroke volume, therefore, will decrease. Depending on the relative change in stroke volume and end-diastolic volume, there may or may not be a small decrease in ejection fraction. Because stroke volume is decreased, there will also be a decrease in ventricular stroke work. A second mechanism can also contribute to diastolic dysfunction: impaired ventricular relaxation (reduced lusitropy). Near the end of the cycle of excitation-contraction coupling in the myocyte, the sarcoplasmic reticulum actively sequesters Ca++ so that the concentration of Ca++ in the vicinity of troponin-C is reduced allowing the Ca++ to leave its binding sites on the troponin-C and thereby permit disengagement of actin from myosin. This is a necessary step to achieve rapid and complete relaxation of the myocyte. If this mechanism is impaired (e.g., by reduced rate of Ca++ uptake by the sarcoplasmic reticulum), or by other mechanisms that contribute to myocyte relaxation, then the rate and perhaps the extent of relaxation are decreased. This will reduce the rate of ventricular filling, particularly during the phase of rapid filling. An important and deleterious consequence of diastolic dysfunction is the rise in end-diastolic pressure. If the left ventricle is involved, then left atrial and pulmonary venous pressures will also rise. This can lead to pulmonary congestion and edema. If the right ventricle is in diastolic failure, the increase in end-diastolic pressure will be reflected back into the right atrium and systemic venous vasculature. This can lead to peripheral edema and ascites. Pulmonary edema Pulmonary edema is a condition associated with increased loss of fluid from the pulmonary capillaries into the pulmonary interstitium and alveoli. Pulmonary edema of cardiac origin usually results from an increase in pulmonary capillary pressure caused by an elevation of left atrial pressure associated with left ventricular failure or valve disease (e.g., mitral or aortic regurgitation, mitral or aortic stenosis). Pulmonary hypertension can also lead to elevated capillary pressures and pulmonary edema. The physical factors and dynamics of edema formation. Tissue Edema and General Principles of Transcapillary Fluid Exchange · General Principles · Factors Precipitating Edema · Prevention and Treatment of Edema Edema refers to the swelling of tissues that result from excessive accumulation of fluid within the tissue. Edema can be highly localized, for example, a small region of the skin subjected to a bee sting. Edema, however, can also comprise an entire limb, specific organs such as the lungs (e.g., pulmonary edema) or the whole body. General principles To understand how edema occurs, it is first necessary to explain the concept of tissue compartments. There are two primary fluid compartments in the body between which fluid is exchanged - the intravascular and extravascular compartments. The intravascular compartment contains fluid (i.e., blood) within the cardiac chambers and vascular system of the body. The extravascular system is everything outside of the intravascular compartment. Fluid and electrolytes readily move between these two compartments. The extravascular compartment is made up of many subcompartments such as the cellular, interstitial, and lymphatic subcompartments, and a specialized system containing cerebrospinal fluid. The movement of fluid and accompanying solutes between compartments (mostly water, electrolytes, and smaller molecular weight solutes) is governed by physical factors such as hydrostatic and oncotic forces. These forces are normally balanced in such a manner the fluid volume remains relatively constant between the compartments. If the physical forces or barriers to fluid movement are altered, the volume of fluid may increase in one compartment and decrease in another. In some cases, total fluid volume increases in the body so that both intravascular and extravascular compartments increase in volume. This can occur, for example, when the kidneys fail to excrete sufficient amounts of sodium and water. When the fluid volume within the interstitial compartment increases, this compartment will increase in size leading to tissue swelling (i.e., edema). When excess fluid accumulates within the peritoneal space, this is termed "ascites." Pulmonary congestion, which can occur in heart failure as the left atrial pressure increases and blood backs up in the pulmonary circuit, causes pulmonary edema. A model that helps us to understand what causes edema is shown to the right. In most capillary systems of the body, there is a net filtration of fluid from the intravascular to the extravascular compartment. In other words, capillary fluid filtration exceeds reabsorption. This would cause fluid to accumulate within the interstitium if it were not for the lymphatic system that removes excess fluid from the interstitium and returns it back to the intravascular compartment. Circumstances, however, can arise where net capillary filtration exceeds the capacity of the lymphatics to carry away the fluid (i.e., net filtration > lymph flow). When this occurs, the interstitium will swell with fluid, thereby become edematous. Factors Precipitating Edema · Increased capillary hydrostatic pressure (as occurs when venous pressures become elevated by gravitational forces, in heart failure or with venous obstruction) · Decreased plasma oncotic pressure (as occurs with hypoproteinemia) · Increased capillary permeability caused by proinflammatory mediators (e.g., histamine, bradykinin) or by damage to the structural integrity of capillaries so that they become more "leaky" (as occurs in tissue trauma, burns, and severe inflammation) · Lymphatic obstruction (as occurs in filariasis) Prevention and Treatment of Edema The treatment for edema involves altering one or more of the physical factors that regulate fluid movement. For example, in edema (pulmonary or systemic) secondary to heart failure, diuretics are given to reduce blood volume and venous pressure. If a patient suffers from ankle edema, that person will be instructed to keep their feet elevated whenever possible (to diminish the effects of gravity on capillary pressure), use tight fitting elastic hose (to increase tissue hydrostatic pressure), and possibly be prescribed a diuretic drug to enhance fluid removal by the kidneys.

That's it for responses...!?!?!!? Does anyone think that it's just as efficacious as needle thoracostomy???....

"Ruff," I'll submit one more to your list off the top of my and that is "Foreign body airway obstruction". The difference of a minute or 2 is truely the difference between life and death..... out here, Ace844

I wonder if your potentially critically ill and sick patients and their families feel the same way...If that was you..how would you feel about this policy?!!?!?

The data speaks for itself again..!! Seizures in Hyperglycemia James C. Kolb, Robert Cox, Loretta Jackson-Williams and Samuel Nicholson University of Mississippi Medical Center: Jackson, MS, Scott and White Hospital: Temple, TX ABSTRACT Background: Seizures are sometimes attributed to hyperglycemia. Objectives: To evaluate the frequency and type of seizure, and glucose (glu) level of patients with hyperglycemia. Methods: This study is part of a study that focused on focal deficits but prospectively asked about seizures in patients with hyperglycemia. This IRB-approved study looked at consecutive patients > 15 years with glu level over 400 mg/dL. Physicians using a computerized chart were required to answer four questions before they could close the chart: "Does the patient have a glucose > 400 mg/dl?", "Does the patient have a focal neurologic deficit?", "Does the patient have a history of prior neurologic deficit?", and "Has the patient had any seizure activity with current episode?" "Focal deficit" was not defined to encourage all deficit inclusion. Level of alertness was determined by a modification of the Ramsey scale. Results: 10 of 813 hyperglycemic episodes had entries for apparent seizure. Of these, one had a questionable seizure the day before, a normal neurologic examination, and presented for axillary abscess, and another had spasms of right thumb that were felt to not be seizure. Only eight of 813 (1%) of patients with glu >400 had a seizure. Six were new-onset and, of these, two had generalized status epilepticus (one had glu 447 and residual brain scar from brain abscess, and the other, glu 539 with no brain abnormality), three had focal seizures (glu of 859, 1,833, 1,013), and one a generalized seizure (glu 1,227). Two had known seizure disorder, one was therapeutic on carbamazepine (glu 450), the other subtherapeutic on phenytoin (glu 564). Two patients had preceding known structural brain abnormality and one had new-onset stroke with seizure. Only three of 44 patients with glucose >1,000 (7%) had a seizure activity. Conclusions: Seizures induced by hyperglycemia are rare even at high levels of glucose but can occur in the absence of other precipitants and can be focal or generalized. hope this helps..., Ace844

I've always enjoyed going to calls similar to those, especially when the dispatcher give us the following info:: "Ambulance 1, respond to XYZ Rehad for the patient 'not breathing, and not doing well', facility staff state that the pt is in no distress and no ALS will be required or wanted..."!! out here, Ace844

"Buddy@Everyone," Here's another study which you may find useful FYI...and which is quite relevant to our discussion here... Utility of NT-proBNP for the Diagnosis of Congestive Heart Failure in Patients with Pulmonary Disease Carlos A. Camargo, Jr., Roderick H. Tung, Daniel G. Krauser, Saif Anwaruddin, Aaron L. Baggish, Annabel A. Chen and James L. Januzzi, Jr. Massachusetts General Hospital: Boston, MA ABSTRACT Background: The diagnosis of acute congestive heart failure (CHF) in patients (pts) with pulmonary disease can be challenging. Objective: We hypothesized that N-terminal proBNP (NT-proBNP) testing would prove useful for the diagnosis of acute CHF in pts with prior chronic obstructive pulmonary disease or asthma (COPD/asthma). Methods: We enrolled consecutive emergency department (ED) pts with COPD/asthma who presented with dyspnea to a large urban ED. Pts were analyzed according to their final diagnosis of acute CHF versus COPD/asthma exacerbation, as adjudicated by study physicians based on clinical data from ED presentation through 60 days. At enrollment, ED physicians gave a probability (0–100%) of acute CHF as the cause of dyspnea. NT-proBNP measurements were compared to clinician estimates using area under the receiver-operating characteristic curve (AUC) tests. Results: Among 216 pts with COPD/asthma, 164 (76%) did not have a prior history of CHF, while 52 (24%) did. In pts without prior CHF, median NT-proBNP levels were significantly higher in pts with (new-onset) CHF compared to those with COPD/asthma exacerbation (1,561 vs. 168 pg/mL, p < 0.001). High clinical suspicion for CHF (probability 80%) detected only 23% of pts with new-onset CHF. In pts with histories of both prior CHF and COPD/asthma, median NT-proBNP levels were significantly higher in those with acute CHF than in those with COPD/asthma exacerbation (4,435 vs. 536 pg/mL, p < 0.001). Using previously established cutoffs (>450 pg/mL for age < 50 years, >900 pg/mL for age 50 years), the overall sensitivity and specificity of NT-proBNP for acute CHF were both 83%. NT-proBNP outperformed clinical estimation (AUC 0.90 vs. 0.83; p = 0.02). The combination was best (AUC 0.94, with p = 0.05 for combo vs. NT-proBNP alone, and p = 0.01 for combo vs. clinical estimation alone). Conclusions: NT-proBNP testing in dyspneic pts with prior COPD/asthma helps clinicians to detect new-onset CHF in pts without prior CHF history and to better differentiate the cause of dyspnea in pts with histories of both CHF and COPD/asthma.

Hi All, I thought that I'd post a little something on CHf here for ya...I hope this helps and that we can continue to discuss CHF, management, etc... here in this thread...I remember awhile back "Ridryder," et.al., did a few of these but most likely got too busy to continue to do so. If you all like the idea of "teaching posts" speak up and let us all know!!!! ( credit goes to New Insights into Decompensated Heart Failure; Emerg Med 37(6)18-25:, 2005) In the past decade a more refined understanding of the pathogenesis of heart failure has emerged to guide therapy. The authors review the science, point out the clinical pitfalls, and discuss the diagnostic use of natriuretic peptides as well as various therapeutic agents. By Mark Sutter, MD, and Deborah B. Diercks, MD, FACEP Heart failure is a disease that has reached epidemic proportions in the United States. There are approximately 550,000 new cases diagnosed every year in this country, bringing the prevalence of the disease to more than 4.5 million patients. The epidemiology of heart failure demonstrates a correlation with age; the incidence in persons over the age of 65 is 10 per 1000. These numbers are staggering, and they are expected to increase as the population ages. The complexity of heart failure is challenging. Poorly controlled diabetes, hypertension, and dyslipidemias are often found in patients with heart failure. In addition, the number of patients with a previous myocardial infarction and renal disease is increasing. All of these conditions are risk factors for impaired systolic function and predispose patients to heart failure. As the prevalence of heart failure increases, so does the financial burden associated with the treatment of patients with this disease. It should be our goal to initiate appropriate aggressive therapy for these patients and avoid unnecessary hospitalization. To improve our ability to best utilize our resources, it is necessary to better understand the pathogenesis and treatment of heart failure. INCREASED UNDERSTANDING Over the last 10 years, our understanding of heart failure at the molecular and hormonal level has greatly increased. Everyone will agree that the final outcome is the heart's inability to adequately pump blood, but our new understanding of the neurohormonal cascade will help guide therapy. Traditionally, heart failure has been classified as systolic dysfunction (decreased contractility) and diastolic dysfunction (increased resistance to diastolic filling). The foundation to the pathophysiology of heart failure is based on numerous studies demonstrating ventricular remodeling as a result of the activation of neurohormonal pathways. These pathways include the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS). The neurohormonal model of heart failure is based on a precipitating event, which puts increased stress on the heart, activating many inflammatory cytokines and neurohormones. These mediators cause a structural change in the ventricular wall that decreases left ventricular function, leading to the clinical syndrome of heart failure (see table). The Development of Heart Failure Precipitating event Structural change Syndrome of failure cardiac causes -acute coronary syndrome -valvular disease -arrhythmias acute inflammation hypertension extracardiac illness medication noncompliance dietary noncompliance endothelial dysfunction myocyte hypertrophy ventricular fibrosis cell necrosis sodium retention leg edema pulmonary congestion Heart failure leads to a drop in cardiac output, which results in decreased renal perfusion. In response, the body activates the RAAS. The kidneys release the hormone renin and trigger a downstream cascade. Renin will act on circulating angiotensinogen and convert it to angiotensin I. The vascular endothelium responds by releasing angiotensin-converting enzyme (ACE), which converts angiotensin I to angiotensin II. This protein acts as a potent vasoconstrictor, thus increasing renal blood flow. Angiotensin II also has a direct pathologic effect in the vessel wall, inducing oxidative stress that causes injury to the vessel. These oxidative stressors and vessel injury trigger further immunologic damage. This contributes to the vascular remodeling that leads to heart failure. In addition, angiotensin II stimulates the adrenal glands to release aldosterone. This promotes increased absorption of sodium in exchange for potassium in the renal tubules, which increases total body fluid volume. Aldosterone also reduces nitric oxide release and promotes endothelial dysfunction; it has also been implicated in increasing myocardial hypertrophy, fibrosis, and necrosis. These effects all lead to stiffness of the ventricles and vasculature, worsening left ventricular function. This pathologic sequence illustrates how activation of the RAAS as a result of decreased renal blood flow actually exacerbates heart failure by promoting salt retention and ventricular remodeling. AUGMENTED EFFECTS The effects of the RAAS are augmented by the SNS. As the heart is stressed, the SNS is activated, releasing norepinephrine and other hormones. These work in a variety of ways to exacerbate heart failure. They include direct myocardial toxicity, heightened myocardial demand, increased salt and water retention, peripheral vasoconstriction, and apoptosis. This combination of effects not only can worsen heart failure but can also lead to life-threatening arrhythmias. The RAAS and SNS are not the only compensatory mechanisms activated when stress is placed on the heart. The ventricles will release B-type natriuretic peptides (BNPs) that cause the efferent renal arteries to constrict and the afferent arteries to dilate. This promotes diuresis and sodium excretion, which will decrease total body fluid volume and help off-load the work placed on the heart. In addition to their effects on the renal vasculature, the natriuretic peptides have other beneficial properties. They are known to decrease circulating endothelin, a potent vasoconstrictor, and the production of renin and aldosterone. These complex biochemical chains of events that occur when the heart is stressed seemingly counteract one another. However, the natriuretic system is not as powerful as the RAAS and SNS combined. The balance is tipped toward sodium retention, volume preservation, and increased vascular tone. This neurohormonal pathway contributes to the development of heart failure in patients with both systolic and diastolic dysfunction. In patients with diastolic dysfunction, neurohormonal activation contributes to the progression of the disease by increasing blood pressure and impairing relaxation through myocardial fibrosis and worsening left ventricular hypertrophy. PATIENT EVALUATION A definitive diagnosis of heart failure is normally made using modalities not readily available in an emergency department, such as right heart catheterization and echocardiography. This has led to the diagnosis and treatment of heart failure as a uniform entity without regard to etiology or systolic function in the emergency department. Nevertheless, the emergency physician should use the available resources to diagnose heart failure. This usually includes a history, physical examination, ECG, chest radiograph, and laboratory evaluation. Patients often give a history of nonspecific symptoms, but most do complain of some degree of shortness of breath. Dyspnea, in fact, is the most common symptom in patients presenting with heart failure, but it is also a predominant symptom in other diseases (see box). It is important to take a thorough history to not only evaluate for other causes of heart failure, but also to evaluate for arrhythmias and acute coronary syndrome. These can often be present with heart failure and can be immediately life-threatening. Classic historical complaints such as paroxysmal nocturnal dyspnea and orthopnea are specific for heart failure but not sensitive. Differential Diagnosis of Dyspnea • acute coronary syndrome • aortic dissection • pulmonary embolism • valvular dysfunction • esophageal perforation • chronic obstructive pulmonary disease • pneumonia • bronchitis • anemia • sepsis • obesity • trauma • pneumothorax • vasculitis • autoimmune disorders Other symptoms such as fatigue, weakness, and leg swelling often indicate elevated filling pressures, but they can also be due to other causes such as venous insufficiency, right heart failure, or pelvic vein obstruction. Despite the nonspecific constellation of symptoms, perhaps the most indicative historical finding is a prior history of heart failure. Electrocardiograms are routine in the evaluation of patients with dyspnea and a suspected diagnosis of heart failure. While an ECG may be of limited use in diagnosing heart failure, it can help to identify a precipitating event such as ischemia, infarct, or arrhythmias. Chest radiography can be an important source of information in the evaluation of a patient for heart failure. The major findings on chest x-ray include cardiomegaly, vascular redistribution (cephalization), and interstitial edema. While these are common, they have not been shown to be sensitive. About 20% of cardiomegaly confirmed by echocardiography is missed on chest radiographs. Studies have also shown that agreement among clinicians in chest x-ray interpretation is "moderate to almost perfect" for interstitial edema, but only "moderate" for cardiomegaly and vascular redistribution. Patients with chronic heart failure are also known to have increased lymphatic drainage; in such cases, radiographs might underestimate the degree of heart failure present. TOOL OF THE FUTURE The diagnostic tool of the future for heart failure seems to be the evaluation of natriuretic peptides. Two peptides have moved into the forefront in the diagnosis of heart failure in patients presenting to the emergency department: the BNPs and the N-terminal pro-BNP (NBNP). In response to ventricular wall stretch, both of these peptides are released. B-type natriuretic peptides have been evaluated in several studies demonstrating their usefulness in diagnosing heart failure in patients with undifferentiated dyspnea. The Breathing Not Properly study showed that BNP levels greater than 100 pg/ml were more accurate than clinical judgment and Framingham criteria in differentiating heart failure from other causes of dyspnea. The odds ratio for BNP of 29.6 was the strongest predictor of heart failure, far superior to any of the physical exam findings. Jugular venous distension had an odds ratio of 1.87; for lower extremity edema, it was 2.88. It is important to recognize that there are confounders that can cause an elevated BNP level. These occur in conditions that are known to cause elevated right ventricular pressures. Examples of such conditions include pulmonary embolism, fluid overload states such as dialysis and cirrhosis, primary pulmonary hypertension, and possibly even hormone replacement therapy. These conditions can cause BNP levels to rise to the 100 to 500 pg/ml range. Also, in obese patients, the BNP level has been shown to be lower than in nonobese patients, which may decrease its diagnostic utility in those patients. Recent studies suggest that BNP levels can also be used for risk stratification. One study suggests that a BNP level above 350 pg/dl at the time of hospital discharge is an independent marker of death or readmission, and it is considered more relevant than clinical or echocardiographic parameters and the percentage change in BNP levels during the patient's hospitalization. N-terminal Pro-BNP is a biologic inert product of BNP synthesis that is believed to be a future marker in the diagnosis of heart failure. Its utility has been evaluated and shown to be useful in the dyspneic patient. Although this marker has not been as extensively evaluated as BNP, it has some useful properties. Unlike with BNP, NBNP values can be used clinically when the patient is being treated with natriuretic peptides. In patients with decompensated heart failure, NBNP levels will be more elevated than BNP and will have a longer half-life. This may alter their utility in the acute setting. Although there are many clinical studies evaluating the use of NBNP, there are no studies that compare NBNP levels with the clinical diagnosis. MANAGEMENT OF HEART FAILURE The management goal for all patients with heart failure is to decrease afterload and ventricular wall stretch in an attempt to limit the neurohormonal cascade. To meet this goal, physicians can use nonpharmacologic options such as bilevel positive airway pressure (BiPAP) and mechanical ventilation for critically ill patients in combination with pharmacologic agents. These include inotropic drugs, arterial and venous vasodilators, diuretics, morphine, and natriuretics. Inotropic drugs. The most commonly used inotropes in heart failure are dobutamine, dopamine, and milrinone. Dobutamine is a catecholamine that acts directly on the beta-1 receptor, causing both a chronotropic and an inotropic response from the heart. Dopamine is also a catecholamine that increases both the chronotropic and inotropic responses of the heart. In addition to its beta-1 actions, dopamine also works on both alpha and dopaminergic receptors. Milrinone is a phosphodiesterase inhibitor that allows for more cyclic adenosine monophosphate to remain in the cell. This results in increased calcium levels and increased contractility. Inotropes, while effective in increasing contractility in the short term, have been found to have their negative side effects. All of the inotropes can induce arrhythmias, tachycardias, and activate the RAAS; they are also associated with increased mortality. Dobutamine is associated with peripheral vasodilation and tachyphylaxis. Dopamine will induce alpha effects as the dose is increased, thus placing more strain on the heart. Milrinone has been shown to have increased adverse effects and is associated with prolonged hospitalizations. Arterial and venous dilators. These drugs work to decrease the afterload and preload placed on the heart. Commonly used medications in this category for heart failure are nitroglycerin, nitroprusside, and the ACE inhibitors. Nitroglycerin works to relax smooth muscle by increasing cyclic guanosine monophosphate, which dephosphorylates myosin, leading to vascular relaxation. It has almost no effects on cardiac and skeletal muscle; it works primarily on the venous system. Nitroglycerin will cause venous dilation, resulting in increased venous capacitance and decreased preload. Nitroglycerin is associated with tachycardia, tachyphylaxis, and neurohormonal activation. Nitroprusside has basically the same mechanism of action as nitroglycerin, but it has dramatic effects on both the arterial and venous systems. Nitroprusside can significantly decrease blood pressure by reducing afterload, but it can be effective in lowering preload as well. Prolonged use of nitroprusside can lead to an accumulation of cyanide. Data from a multicenter heart failure registry reported in the ADHERE trial suggested that patients treated with any intravenous (IV) vasodilator in the emergency department, versus later in their hospital stay or not at all, had lower mortality and shorter hospital stays. The ACE inhibitors have also been used in the treatment of acute heart failure. They work by blocking the formation of angiotensin II, thereby stopping the effects of its vasoconstrictive properties and thus decreasing afterload. A randomized, double-blind study using IV enalapril in acute pulmonary edema found it to be both effective and well tolerated. Enalapril decreased not only systemic blood pressure but also pulmonary capillary wedge pressure. Hamilton and colleagues demonstrated in a randomized, prospective, placebo-controlled study that sublingual captopril decreased respiratory distress and produced more rapid clinical improvement when added to standard therapy with nitrates, morphine, oxygen, and furosemide compared to standard therapy alone. Diuretics. The purpose behind using diuretics in heart failure is to decrease pulmonary congestion and leg edema. Diuretics decrease plasma volume and sodium retention, which subsequently decreases venous return to the heart. This occurs through the induction of diuresis in the kidneys, resulting in a redistribution of fluid and further reduction in fluid overload and a decrease in vascular resistance. It is the vasodilatory effect of the loop diuretics that has the greatest initial impact in symptom reduction in acute decompensation. In heart failure, loop diuretics such as furosemide are commonly used. The starting dose for furosemide is usually 40 mg or the patient's prehospitalization daily dose, given intravenously. Peak diuretic effects occur 30 to 60 minutes after IV administration. If the patient fails to respond, the common practice is to double the initial dose. Doses higher than 160 to 320 mg should be avoided because side effects, such as electrolyte abnormalities, volume depletion, and activation of the RAAS, are more likely. If the patient is diuretic-resistant, an alternative approach would be to use a more potent loop diuretic. Torasemide and bumetanide, for example, are reasonable options when furosemide is ineffective. Bumetanide is reportedly 40 to 50 times more potent than furosemide on a milligram-for-milligram basis. If one is still unable to achieve the desired diuresis with these more potent loop diuretics, metolazone can be added. Metolazone is a thiazide-type diuretic that is often administered in conjunction with loop diuretics. Thiazide diuretics must be used cautiously to avoid electrolyte abnormalities and overdiuresis. There are various options for delivering loop diuretics. The most commonly used routes are oral and IV bolus doses, but continuous infusion of loop diuretics is also effective. It has been shown that a continuous infusion of a diuretic is more effective and less toxic than bolus dosing in the treatment of heart failure in patients with renal insufficiency. Morphine. Morphine has been used for decades in the treatment of heart failure. It appears to improve symptoms by reducing anxiety and venodilation. Unfortunately, there is little clinical evidence on the effect of morphine on mortality and morbidity in patients with acute heart failure exacerbation. A pre-hospital trial of morphine in patients with acute pulmonary edema found no benefit in the use of morphine in these patients. Another trial reported that the use of morphine was associated with an increased risk of ICU admission. Natriuretics. The newest pharmacologic agents in the treatment of heart failure are the natriuretics. In 2001, the Food and Drug Administration approved the use of nesiritide for the treatment of acutely decompensated heart failure. Nesiritide is a BNP that acts as an endogenous natriuretic, causing renal vascular changes that promote diuresis. This medication has the potential to tip the balance of power away from the RAAS and SNS and push it toward natriuresis. Nesiritide has been shown to produce early symptomatic relief and a reduction in pulmonary capillary wedge pressures within 15 minutes. Its effects peak at 30 to 60 minutes. Another advantage is that because it has no effect on heart rate, it does not increase myocardial oxygen consumption. This can be an important advantage with a patient who is acutely decompensated. Nesiritide does require adjustments in the use of other drugs. Loop diuretics can be used, but the dose must be decreased because nesiritide itself produces a mild to moderate diuresis. Also, ACE inhibitors and other antihypertensives should be withheld for the first hour, until nesiritide's effects have been observed. It is not recommended at this time to combine IV nitroglycerin and nesiritide because of the lack of data on this combination. In the PROACTION study, 237 patients in an emergency department observation unit who had decompensated heart failure were randomized to standard therapy or at least 12 hours of IV nesiritide. The study results showed that in the nesiritide group there was an 11% decrease in the need for hospital admission from the observation unit, a 21% decrease in heart failure readmission, and a 29% decrease in readmission for patients with New York Heart class III and IV disease. Of note, these differences did not reach statistical significance due to the low number of patients in the study. The two major disadvantages with nesiritide are the cost and the lack of large clinical trials. Head-to-head comparison trials are not complete, and there are questions regarding the renal impact of nesiritide. As further research is conducted, we will learn if the efficacy of nesiritide will compensate for its cost. APPLYING THE THERAPEUTIC OPTIONS Having discussed the therapeutic options, we will now review their application to individual patients. If the patient is in obvious respiratory distress or imminent respiratory failure, the patient should be mechanically ventilated, either via Bi-PAP or endotracheally, along with aggressive blood pressure management. If the blood pressure is elevated, nitroglycerin or nitroprusside is an option, with hemodynamic monitoring and ICU admission. If there is cardiogenic shock or symptomatic hypotension, the use of an inotrope such as dobutamine, dopamine, or milrinone is appropriate, with hemodynamic monitoring and ICU admission. This group of patients needs immediate attention, often before the underlying cause of their symptoms is known. Once additional data are gathered from the history and laboratory results, more targeted therapy can be initiated. If the patient does not fall into the critically ill category, a thorough workup and appropriate diagnostic tests should be performed. Once the diagnosis of heart failure is clear, an attempt should be made to classify the patient as being in high-, medium-, or low- severity heart failure. Studies indicate that approximately 10% of heart failure patients will be in the high-severity group, another 10% in the low-severity group, and the remaining 80% in the medium-severity group. High-severity patients are usually the ones that will end up in the ICU or at least a telemetry unit. Recommendations for this group include oxygen, a loop diuretic, and nitroglycerin or nitroprusside. Nesiritide can also be used in this group. Patients in the moderate-severity group often require a floor or telemetry bed, but an observation unit, if available, is a viable option. Treatment usually includes oxygen, a loop diuretic, and nitrates. Aggressive therapy with nesiritide may help limit hospitalizations and keep more patients on observation status. As more studies become available, this option might turn out to be more financially advantageous if lengths of stay can be shortened. Low-severity patients should receive oxygen, nitrates, and a trial of loop diuretics. A period of observation in the emergency department will usually demonstrate diuresis and symptomatic relief. The physician should use this time for patient education; in many cases, the precipitating event will be something as simple as medication noncompliance or dietary indiscretion. These patients are usually discharged. NEW REGIMENS Improved understanding of the pathophysiology in heart failure may lead to the development of new therapeutic regimens. Currently, tezosentan, an endothelin-1 antagonist, is being investigated in the treatment of decompensated heart failure. Initial trials of this drug, however, have not been encouraging. Tolvaptan, a vasopressin antagonist, has also been evaluated in the treatment of decompensated heart failure. Initial studies have shown it to provide added value to diuretics. Another group of medications used in the management of heart failure is the aldosterone antagonists. While they are not commonly used in the management of an acutely decompensated heart failure patient, they are often included in the outpatient regimen. Spironolactone is in this class of medications. It works by preventing sodium reabsorption, leading to retention of potassium. These drugs also have a very mild diuretic effect. Eplerenone is the newest aldosterone antagonist; it has more selectivity than spironolactone and causes less gynecomastia and progesterone stimulation. Its effects on electrolyte balance appear to be the same as spironolactone's in early studies. A major risk with patients on aldosterone antagonists is hyperkalemia. A potential problem with spironolactone, which is recommended in severe heart failure, is that patients in that category are usually also on an ACE inhibitor. If the patient has a episode of decompensation, the combination of an ACE inhibitor and an aldosterone antagonist can lead to the deadly complications of hyperkalemia. A recent study in the New England Journal of Medicine showed that since the RALES trial demonstrated a benefit to adding spironolactone to an ACE inhibitor in patients with severe heart failure, the rates of both hospitalization and mortality due to hyperkalemia have increased significantly. DISPOSITION OF PATIENTS Depending on institutional policies, new-onset heart failure patients and patients diagnosed with heart failure for the first time usually are admitted to the hospital or undergo echocardiographic evaluation prior to discharge. Echocardiography can not only confirm the diagnosis of heart failure, but it can also help identify systolic or diastolic dysfunction and aid in future treatment plans. Depending on the suspected etiology of new-onset heart failure, additional diagnostic tests to evaluate for underlying coronary artery disease may be performed. Risk Findings in Heart Failure High risk new-onset heart failure ischemic changes on ECG low serum sodium increased respiratory rate low systolic blood pressure age >70 chest pain elevated creatinine poor diuresis after four hours pulmonary edema on chest x-ray severe comorbidities electrolyte abnormalities syncope valvular disease hemoglobin <10 mg/dl Low risk Absence of high-risk features Normal vital signs and symptomatic improvement after treatment Good support system and outpatient follow-up Normal laboratory parameters (electrolytes, cardiac markers) Possible risk-related considerations in the disposition of patients with heart failure are summarized in the table above. Appropriate discharge from the emergency department must be combined with adequate follow-up. Instruction on diet recommendations, medication schedules, and the importance of tracking body weight are important in preventing readmission. Suggested Reading Badgett RG, et al.: Can the clinical examination diagnose left-sided heart failure in adults? JAMA 277(21):1712, 1997. Bussmann WD and Schupp D: Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema. Am J Cardiol 41(5):931, 1978. DiDomenico RJ, et al.: Guidelines for acute decompensated heart failure treatment. Ann Pharmacother 38(4):649, 2004. Krum H and Gilbert RE: Demographics and concomitant disorders in heart failure. Lancet 362(9378):147, 2003. Lee DS, et al.: Predicting mortality among patients hospitalized for heart failure: derivation and validation of a clinical model. JAMA 290(19):2581, 2003. evy D, et al.: Long-term trends in the incidence of and survival with heart failure. N Engl J Med 347(18):1397, 2002. Maisel AS, et al.: Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 347(3):161, 2002. Peacock WF and Emerman CE: Safety and efficacy of nesiritide in the treatment of decompensated heart failure in observation patients. J Am Coll Cardiol 41(suppl A):336A, 2003. Publication Committee for the VMAC Investigators: Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA 287(12):1531, 2002. Schrier RW and Abraham WT: Hormones and hemodynamics in heart failure. N Engl J Med 341(8):577, 1999 Hope this helps, Ace844

Morphine at 0.1 Mg/kg Does Not Control Severe Pain NEW YORK (Reuters Health) Nov 02 - Intravenous morphine at 0.1 mg/kg does not effectively control severe acute pain in most patients, according to researchers at the Albert Einstein College of Medicine in the Bronx. Lead author Dr. Polly E. Bijur and colleagues prospectively evaluated the analgesic effect of 0.1 mg/kg intravenous morphine in 119 patients, between 21 and 65 years old, who presented to the emergency department with acute, severe pain. The subjects rated the intensity of their pain on a validated 11-point verbal numeric scale that ranged from 0 (no pain) to 10 (worst possible pain) immediately before they received the morphine and 30 minutes later. The median baseline pain score was 10. The main outcome measure was the proportion of patients whose pain decreased by less than 50% during the 30-minute interval, according to the report in the October issue of the Annals of Emergency Medicine. Eighty patients (67%) who received intravenous morphine at 0.1 mg/kg reported a less than 50% decrease in pain from baseline. Overall, 19 patients (16%) had no change in pain or an increase in pain in the 30-minute interval. None of the patients required an opioid antagonist at any time during or after the study period. "Acute pain might be better controlled in the ER by increasing the dose of morphine or using alternative opioid analgesics if patient safety can be assured," Dr. Bijur said in an interview with Reuters Health. "Administering multiple small doses of morphine until pain is controlled is an optimal strategy, though difficult to achieve in a busy ER setting." The investigator noted that they are currently comparing a 50% higher dose of morphine, 0.15 mg/kg, with the standard dose. In addition, the team is conducting studies of hydromorphone (Dilaudid), another potent opioid analgesic. "Pain is seriously under-treated in the ER and we feel it is an ethical obligation for physicians to adequately manage pain and alleviate suffering of our patients," Dr. Bijur explained. Ann Emerg Med 2005;46:362-367. Eleven Common Myths About Pain Control According to the most recent studies, widely prevalent assumptions with little, if any, basis in fact are leading clinicians to use analgesic drugs ineffectively. By Robert Dachs, MD Dr. Dachs is chairman, department of emergency medicine, Westerly Hospital, Westerly, Rhode Island. The message is loud and clear: timely and compassionate pain management is expected for all patients with acutely painful conditions. Professional organizations, most notably the American Pain Society, as well as our anesthesiology and nursing colleagues, hospital administrators, regulators, and the public at large have championed this issue and raised it to its current prominence. In an attempt to meet these expectations, a critical look at common myths associated with acute pain care can be enlightening. MYTH 1 Physicians, nurses, and prehospital care providers do a good job of providing adequate analgesia to patients in pain. The data are unequivocal: on average, health care providers do a terrible job of managing acute pain. Physicians order inadequate doses of analgesics or no analgesia at all for patients in pain. Nurses, when given a dose range for analgesics, tend to give lower doses or withhold analgesia in PRN cases. Even prehospital care providers with access to analgesics rarely give these drugs to patients with painful conditions such as suspected extremity fractures. This widespread practice of not providing adequate analgesia has been termed oligoanalgesia, and it has been documented in emergency departments, intensive care units, and medical and surgical wards here in the United States and abroad. Further, certain groups of patients are particularly likely to be on the receiving end of this practice. Both the very young and very old, for example, often receive inadequate analgesia. Dr. Knox Todd and colleagues have demonstrated that Hispanic and African American patients with extremity fractures receive less analgesia than white patients with these same conditions. A good working knowledge of how to provide appropriate analgesia, together with an honest self-appraisal by all health care providers, is necessary to combat this disservice to our patients. MYTH 2 Codeine is an effective analgesic and antitussive. Codeine is a very weak analgesic. In standard doses, codeine produces no more pain relief than NSAIDs or acetaminophen alone. When acetaminophen plus codeine was compared with the NSAID du jour in multiple studies involving postsurgical pain or acute musculoskeletal injuries, the combination was noted to have equivalent analgesic efficacy. Further, when deCrean reviewed 24 trials comparing acetaminophen with codeine to acetaminophen alone, he found only a 5% difference in pain intensity between the agents, as rated by subjects on a 1 to 10 scale (British Medical Journal, vol. 313, p. 321, 1996). This difference is statistically significant, but it has no clinical significance. Codeine's adverse effects, on the other hand, are legendary. Nausea, vomiting, and constipation are common. Geriatricians often note that codeine produces the "terrible C's"–confusion and constipation–in their patient population. As for controlling a cough, codeine in standard doses has no more antitussive effect than placebo. The bottom line with this drug is that in the absence of any clear benefit and considering its troublesome side effects, it is difficult to recommend codeine as an analgesic or as an antitussive. MYTH 3 Propoxyphene is an effective and safe analgesic. Propoxyphene possesses negligible analgesic effects. When researchers at Texas A&M compared propoxyphene with ibuprofen 400 mg and placebo in patients with acute musculoskeletal trauma, no clinical difference in pain relief was noted between propoxyphene and placebo. Further, a review of 26 trials of propoxyphene with acetaminophen versus acetaminophen alone concluded that there was no evidence to support the use of the combination product. Propoxyphene and its metabolites have been associated with cardiotoxicity, neurologic sequelae, and death. The major metabolite, norpropoxyphene, has a half life of 30 to 36 hours and produces local anesthetic and antiarrhythmic effects similar to those of lidocaine and quinidine. When it accumulates, either from chronic administration or acute overdose, norpropoxyphene can produce arrhythmias, cardiogenic shock, mental status changes, seizures, coma, and death. Consensus committees have clearly indicated that propoxyphene should not be given to geriatric patients. In fact, the argument can be made that this drug should not be given to any patient, regardless of age. Fortunately, there are better choices than codeine and propoxyphene for pain management. Hydrocodone and oxycodone, with and without acetaminophen, are effective analgesics. Oxycodone is available in a long-acting preparation. Transnasal butorphanol is also effective, but it is expensive. MYTH 4 Morphine 2 mg IV provides adequate analgesia in healthy adults. The American College of Critical Care Medicine has recognized morphine as the drug of choice in critically ill patients who require analgesia. The dose is a 0.05 to 0.1 mg/kg bolus; it can then be rapidly increased to achieve the desired effect. In many emergency departments, morphine doses of 10, 20, or 30 mg in the first hour are not unusual. Unfortunately, the all-too-common order of 2 mg of morphine will often leave patients in pain. MYTH 5 "Meperidine 50 mg with hydroxyzine 25 mg IM q4hrs prn" is an appropriate order for hospitalized patients. This order is so common many physicians can recite it by rote. But how appropriate is it? Meperidine's clinical effect is very short-lived, often lasting only two or three hours. The need for subsequent repetitive doses can result in deleterious central nervous system side effects. This is because meperidine's inactive metabolite, normeperidine, has a long half-life, and when it accumulates it produces central nervous system excitation and the risk of seizures. That is why many experts recommend avoiding or minimizing meperidine use in hospitalized patients. If meperidine is necessary, the addition of an antiemetic (traditionally, hydroxyzine) will not potentiate the effect of the narcotic, as is widely believed. While an antiemetic may make the patient drowsy and decrease nausea, the clinician should not lower the dose of the analgesic if an antiemetic is added. And hydroxyzine should never be chosen as the antiemetic. The drug can only be given intramuscularly and is extraordinarily painful and irritating to soft tissue. Again, better choices exist. Adequate doses of morphine would be the first-line choice. Fentanyl is an excellent alternative in hemodynamically unstable patients or those with exaggerated histamine response to morphine. Hydromorphone is another excellent alternative. MYTH 6 Use of narcotic analgesic agents will result in chronic opioid dependence. Avoiding the use of appropriate narcotic analgesia out of fear of inducing chronic opioid dependence and drug-seeking behavior is completely unfounded. Researchers at Boston University reviewed the records of 11,882 patients given narcotics during a hospital stay and found only four patients who later developed an opioid dependence. When a clinician subscribes to this myth and avoids using these drugs, he or she may actually help perpetuate a course of chronic pain and unwittingly create a reliance on analgesics in patients. With undertreatment of acute pain, recruitment of increasing numbers of nerve fibers occurs. The ensuing windup of the sensory nervous system can result in long-standing modification in pain sensation. Consequently, early and aggressive use of analgesics followed by a rapid tapering of the dose is encouraged in patients with acute pain. MYTH 7 Injectable ketorolac is more effective and has less gastrointestinal toxicity than oral NSAIDs. Many clinicians mistakenly believe that ketorolac possesses some magical analgesic property because it can be administered intramuscularly or intravenously. Study after study, however, has refuted this theory. Also, regardless of the route of administration, ketorolac's ability to inhibit prostaglandin synthesis can disrupt the stomach's mucosal barrier. Therefore, even though the drug is not taken orally, gastrointestinal toxicity is still possible. MYTH 8 NSAIDs have more analgesic effect than acetaminophen. In a landmark study, Bradley and colleagues randomly assigned patients with osteoarthritis of the knee to receive either 4000 mg acetaminophen, 1200 mg ibuprofen, or 2400 mg ibuprofen per day. The result: acetaminophen was just as effective as either dose of ibuprofen (New England Journal of Medicine, vol. 325, p. 87, 1991). It seems reasonable that 4000 mg acetaminophen and 1200 mg ibuprofen per day would produce similar results. But why doesn't the 2400-mg/day dose of ibuprofen produce additional analgesic effect? Because increased doses of NSAIDs further inhibit prostaglandin synthesis. This is useful in managing patients with prostaglandin-mediated diseases such as rheumatoid arthritis. However, when it comes to analgesia, NSAIDs have a ceiling effect–that is, no further analgesic effect will occur with increased doses. Therefore, 2400 mg/day of ibuprofen in non-prostaglandin-mediated diseases such as osteoarthritis and soft tissue injury will produce no additional analgesia. MYTH 9 NSAIDs should be first-line agents in soft-tissue injuries such as ankle sprains. NSAIDs do have a role in the care of patients with acutely painful conditions that involve a prostaglandin-mediated process. Examples of such conditions include renal colic, biliary colic, dysmenorrhea, and gout. Soft-tissue injuries, however, are not primarily prostaglandin-mediated events, and there are no data to support NSAID use for such injuries. In addition, when treating patients with non-life-threatening conditions such as sprains and strains, the clinician must seriously consider the dangers associated with NSAIDs. Wolfe and colleagues documented that the mortality rate associated with NSAID use in 1997 was equivalent to the mortality rate from AIDS in the United States that same year (New England Journal of Medicine, vol. 340, p.1888, 1999). Cautious use of these agents is clearly warranted. MYTH 10 COX-2 inhibitors are more effective than traditional NSAIDs in controlling pain. When it comes to analgesic efficacy, the newer COX-2 inhibitors, celecoxib and rofecoxib, are no more potent than their traditional counterparts. Even the question of whether these newer agents produce fewer gastrointestinal complications than NSAIDs is up for debate. Two recent high-profile studies found a 50% decrease in the rate of gastrointestinal complications with COX-2 inhibitors. However, both studies were manufacturer-supported trials with design flaws that may invalidate the findings. Further, the CLASS trial noted that no decrease in the rate of gastrointestinal complications was associated with celecoxib use in patients taking just one aspirin a day. MYTH 11 Tramadol is an effective analgesic. In separate studies, pain relief with tramadol has been shown to be inferior to hydrocodone with acetaminophen and codeine with acetaminophen and no more effective than placebo. This lack of analgesic effect was noted with both the 50- and 100-mg doses. Tramadol is simply not an effective analgesic. ELIMINATING OLIGOANALGESIA The goal of eliminating the practice of oligoanalgesia should be at the top of every primary care provider's agenda. Being aware of common myths associated with pain management is a key step in moving toward this goal.