Diagnosis \200\224immediate questions Does this patient has HF? The diagnosis of AHF is bas ed on the symptoms and clini- cal \201 ndings, supported by appropriate investigations su ch as ECG, CXR, biomarkers and Doppler echocardiography. Up to 75% of AHF patients will hav e at presentation a pre- vious diagnosis of HF, and the available information may help the clinician. Dyspnoea is a common presenting symp- tom in patients with AHF syndromes. Normotensive AHF The other common type of AHF is characterized by a nor- mal SBP, usually w ith a history of progressive or chronic HF. In these patients, symptoms and signs develop g radually, over days or weeks, and pulmonary and systemic conges- tion (jugular venous diste nsion, pulmonary rales and peripheral oedema) are usually present. They usually have a redu ced EF. Despite high LV \201 lling pressures they may present several degrees of pulmonar y congestion (clinical 302 M TAVARES, A EL GHORCH, & A MEBAZAA Dyspnoea is the primary reason that patients present for medical care with AHF. In the ADHE RE (n = 163 447) and OPTIMIZE-HF (n = 48 612) registries, 89 and 90% of patientsm respectiv ely, initially presented with a complaint of dyspnoea. Dyspnoea on exertion is the most sen sitive symptom (neg- ative likelihood ratio 0.45, 95% CI 0.35 \200\2230.67), whereas par- o xysmal nocturnal dyspnoea is the most speci \201 c (positive likelihood ratio 2.6, 95% CI 1.5 \200\2234.5). Elevated JVP is the best indicator for identifying acute decompensated he art failure (positive likelihood ratio 5.1, 95% CI 3.2 \200\2237.9, nega- tive likelihood r atio 0.66, 95% CI 0.57 \200\2230.77), although measurement of JVP by clinicians is notoriou sly inaccurate. A murmur may point to a new valvular disease or a compli- cation of a previ ously known heart disease. An auscultated S3 gallop is not only diagnostic for AHF but pred icts an increased risk of subsequent adverse events. Both ven- tricular gallops and jugular venous distension are limited by interobserver variation and low sensitivity. In the emerg ency department, rapid measurement of brain natriuretic peptide (BNP) used in conjunction w ith other clinical information is useful in establishing or excluding the diagnosis of cong estive HF in patients with acute dyspnoea, and improves the evaluation and treatment of pat ients with acute dyspnoea, thereby reducing the time to dis- charge and the total cost of t reatment. In patients with acute shortness of breath, HF patients have higher mean levels o f both BNP or NT-proBNP blood levels (see car- diac peptides below). Although the pulmonary artery catheter may provide a good measure of \201 lling pressures and an estimate of ca rdiac output in the patient in shock, therapy to reduce volume overload during hospitalizat ion for heart failure led to marked improve- ment in signs and symptoms of elevated \201 lling pressures with or without the PAC. Addition of the PAC to careful clinical assessment increased anticipated adverse events, but did not affect overall mortality and hospitaliza tion. Are there other conditions/co-morbidities that may contribute to the picture? Patients with AHF also have signi \201 cant cardiac and non- cardiac underlying conditions that may not be the main etiology but may contribute to the pathogenesis of AHF, including CAD (ischaem ia, hibernating myocardium and endothelial dysfunction), hypertension, AF and type II dia- betes mellitus. Many patients have other complications of atherosclerosis, hypertension or diabetes, while other con- ditions share a common etiology such as smoking-related chronic pulmonary disease or renal vascular disease. Some co-morbidities are complications of HF or the combination of HF, its underlying etiology and advanced age, such as renal impairment, stroke, and atrial and ventricular arrhyth- mias. Patients with renal failure are less lik ely to be pre- scribed ef \201 cacious therapies, but have better outcomes if they receive these medications. The importance of certain co-morbidities as independent predictors of p oor outcome showed the importance of considering them as potential therapeutic targets, suc h as anemia or obstructive sleep apnoea. Troponin, worsening renal function, hyponatraemia, lung con- gestion persistence after initial treatment and low SBP have all been described as the main prognostic factors in AHF. Hypertensive, normotensive or hypotensive? Most patients with AHF present with either norma l SBP or elevated blood pressure. Patients who present with ele- vated SBP usually have pul monary congestion and a rela- tively preserved LVEF, and have symptoms that typically devel op abruptly, with severe lung congestion and minimal weight gain often being seen in elderl y women. Their response to therapy is usually rapid. Patients with normal SBP presenting wi th systemic congestion and reduced LVEF are usually younger, with a history of chronic HF, and have symptoms that develop gradually over days or weeks. Usually they present signi \201 cant weight gain with oedema, liver and renal dysfunction, and hyponatraemia. Their lu ng congestion may not be so evident and, although they may improve with initial therapy, th ey will continue to have sys- temic congestion during the next days. What is the etiology? The HF etiology is the next question to answer as it may imply speci \201 c management. Systolic dysfunction or preserved EF? The patient should be classi \201 ed as soon as poss ible accord- ing to previously described criteria for systolic and/or pre- served dysfuncti on, and by the characteristics of left or right HF. Are there any precipitating factors? The presence of any precipitating factors should be so ught as its correction may be of most importance to stabilize the patient, such as a hypert ensive emergency, anemia, dysrhythmia or infection (Table 18.7.3). Investigations ECG Besides signs of heart disease, the ECG may provide important aetiologic al information such as ACS or rhythm disturbances. Table 18.7.3 AHF precipitating factors Lack of compliance with medical treatment Acute arrhythmia Hypertensive crisis Volume overl oad Infection, particularly sepsis Severe brain insult Major surgery Reduction in renal fun ction Asthma New medications (excess B-blockade) Alcohol abuse Drug abuse Phaeochromocytoma Chest X-ray Although chest radiography is routine in the evaluation of patients with shortn ess of breath and a quick and inexpen- sive examination, 1 of every 5 patients admitted fr om the emergency department with AHF have no signs of conges- tion on chest radiography, an d patients lacking signs of con- gestion on emergency department chest radiography were mor e likely to have an emergency department non-HF diagnosis than patients with signs of conge stion in the ADHERE registry. Cardiac peptides When the heart muscle cell is stretched, as in HF, the car- diac peptide, NT-proBNP, is released into the bloodstream. 303 CHAPTER 18.7 Acute heart failure: assessment the heart, echocardiography, is widely accepted as an objective diagnostic tool in characte rizing cardiac dysfunc- tion. Besides ventricular function, evaluation echocardiog- raphy m ay provide early aetiological information, such as ischaemic regional motion abnormalities that could not yet be seen in the ECG, signs of muscular, valvular or pericar- dial disease . It should be done in every patient as soon as possible. Limited emergency echocardiograph y to evaluate wall motion and EF performed by emergency physicians has been shown to correl ate well with de \201 nitive testing. Patients with HF have increased blood levels of NT-proBNP, and the worse the disease, the h igher the NT-proBNP level. Taken together with clinical information, BNP is a quantita- tiv e marker of HF that summarizes systolic and diastolic LV dysfunction, as well as valvular h eart disease and RV dys- function. In all patients presenting with dyspnoea to emergency se rvices, a history, physical examination, CXR and ECG should be undertaken, together with la boratory measure- ments that include BNP. The knowledge of a patient \200\231s base- line B NP level may further improve emergency department physician diagnostic accuracy. BNP levels should be interpreted as a continuous variable. However, for reasons of simplicity, the us e of cut-off values makes sense. When using cut-off values in patients with acute dyspnoea, one should apply two: one to \200\231rule out \200\231 (<100) and one to \200\230rule in \200\231 HF (>400). The gray zone area needs extra physician attention and ancillary testi ng. This gray zone (100 \200\223400pg/ml) represents 25% of dyspnoeic patients, 75% of whom will have HF as the ultimate diagno- sis. This HF tends to be mild. The overall prognosis for dys- pnoeic patients with BNP levels in the gray zone is good and may help risk-stratif y patients for admission or dis- charge. There seems to be a linear relationship between BM I and BNP. Patients who are obese or very obese should have their BNP multiplied by 2.0 to obtain a BNP level of similar severity to those of normal weight. BNP levels in the dysp- n oeic patient do not have to be adjusted for age or gender. However, to optimize diagnostic accuracy, adjustments should be made for renal dysfunction and obesity. One should not forg et that both BNP and NT-proBNP blood levels are markers of heart muscle cell stretch, and t here may be causes other than HF to justify their increased levels, either of cardiac origi n as in ACS, hypertension, LV hypertrophy or valvular heart disease, or of non-cardiac orig in, such as pulmonary embolism, pulmonary hyperten- sion or sepsis. Other investigations As appropriate, depending on the HF type and severity. Patients with A CS or serious mechanical cardiac disorders should proceed rapidly to angiography and cathet erization for evaluation and therapeutic measures, including surgery or PCI. Further reading Adams KF, Jr, Fonarow GC, Emerman CL, et al. Characteristics and outcomes o f patients hospitalized for heart failure in the United States: rationale, design, and prel iminary observations from the \201 rst 100,000 cases in the Acute Decompensated Heart Fai lure National Registry (ADHERE). Am Heart J 2005; 149: 209 \200\22316. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of conges- tive heart failure a nd pulmonary artery catheterization effective- ness: the ESCAPE trial. JAMA 2005; 294: 1625 \200\22333. Cleland JG, Swedberg K, Follath F, et al. The EuroHeart Failure sur- vey program a survey on the quality of care among patients with heart failure in Europe. Part 1: patient charac teristics and diagnosis. Eur Heart J 2003; 24: 442 \200\22363. Dries DL, Exner DV, Domanski MJ, et al. The prognostic implica- tions of renal insuf \201 ciency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J Am Coll Cardiol 2000; 35: 681 \200\2239. Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associate d with hypertension. N Engl J Med 2001; 344: 17 \200\22322. Gheorghiade M, Abraham WT, Albert NM, et al. Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. JAMA 2006 ; 296: 2217 \200\22326. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002; 347: 161 \200\2237. Blood gas analysis, lytes, renal function, routine hematology Pulse oximetry is a valuable option for immediate evalua- tion of oxygenation, but if the patient presents with signs of compromised peripheral perfusion or fatigue, blood gas analysis is useful in order to eval uate acid \200\223base and lactate status, and to follow the response to treatment. Electro lyte abnormal values are often associated with rhythm distur- bances, may be the result of abnormal renal function or drug administration and are often administrated to com- pensate the use of some drugs. Anemia is a common pre- cipitating cause, and AHF may just be the sy mptom translation of anemia that may bene \201 t from treatment. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evalu ation and management of acute dyspnea. N Engl J Med 2004; 350: 647 \200\22354. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J 2005; 26: 384 \200\223416. Nieminen MS, Brutsaert D, Dickstein K, et al. EuroHeart Failure Survey II (EHFS II): a surv ey on hospitalized acute heart failure patients: description of population. Eur Heart J 200 6; 27: 2725 \200\22336. Echocardiography When it comes to HF, clinical examination alone may be an inaccurate diagn ostic approach. Ultrasound examination of 304 M TAVARES, A EL GHORCH, & A MEBAZAA Acute heart failure: management Introduction AHF is de \201 ned as gradual or rapid change in HF signs and symptoms, resul ting in a need for urgent therapy. The vast majority of patients present with dyspnoea, due to increased LV \201 lling pressures, with or without low cardiac output, with reduced o r preserved EF. Until recently, the clinical characteristics, management pat- terns and out comes of patients admitted with AHF have been poorly de \201 ned, due to lack of speci \201 c data. AHF syn- dromes have traditionally been viewed as part of the chronic HF natur al evolution, and lung congestion is often regarded as aconsequence of volume overload and/ or low cardiac output, usually precipitated by dietary indiscretion and/or medication non-a dherence, but several large AHF registries shed new light on the way we see and manage AHF. Yet, admission SBP has been show to be an independent predictor of morbidity and mortality in patients with AHF with either reduced or relatively preserved systolic func- tion. High SBP patients were more likely to have preserved systolic function, while patients with low SBP at admission had 3 \200\2234 times higher in-hospital and post-discharge mor- tality r ates. Low SBP (<120mm Hg) at hospital admission identi \201 es patients who have a poor pr ognosis despite med- ical therapy. This is a marker of advanced HF in a patent that usually has a history of cardiac disease, shows periph- eral oedema, enlarged liver, decreased ren al and liver func- tion and hyponatraemia. HF where low cardiac output is more prevalent, low BP adds a critical component, especially in patients with CAD, aggravating myocardial perfusion. In each episode, the big- ger the oxygenation compromise, the bigger the hypoten- sion, the greater myocardial damage will ha ppen. New arrhythmia during an exacerbation of HF identi \201 es a high risk group with hi gher in-hospital and 60-day mor- bidity and mortality. Thus, each episode of AHF contribute s more myocardial damage and worsens long-term progno- sis. AHF initial management Goals for AHF patient management \200 Immediate \200\224improve sy mptoms Restore oxygenation and improve organ perfusion \200 Avoid or limit cardiac, renal and other organ damage \200 Intermediate \200\224stabilize patient and optimize treatmen t Initiate life-saving therapies \200 Long-term \200\224disease management Prevent early readmission \200 Improve symptoms and survival \200 As in other medical emergencies, AHF needs a rapid, initial integrative approach where asse ssment and management are provided in the shortest time, in a parallel way, in order to sto p an episode that continues damaging the heart after presentation, and, like thrombolysis o r aspirin in patients with AMI, short-term intervention can lead to long-term bene \201 t. The immediate priority in AHF patients should be the sta- bilization of the respiratory fa ilure to restore oxygenation and prevent further deterioration. The initial therapy for pat ients with AHF should improve symptoms and haemo- dynamics without causing myocardial injur y that may adversely affect post-discharge morbidity and mortality. Several common therapie s such as loop diuretics, mor- phine, inotropes or inodilators have long been used as \201 rst-line therapy without sound evidence from randomized studies on their bene \201 t on morbidity or survival. However, all patients are not created equal, and in euvolaemic or hypovolaemic patients, loop diuretics may induce marked decreases in SV and cardiac output , hypotension or wors- ening renal function, while inodilators used in patients with preser ved systolic function may increase mortality and hospital stay. Several therapies in AHF ma nagement have an unaccepta- bly high incidence of hypotension that may per se increase card iac, renal and other organ damage. Their use should require frequent, or preferably, contin uous BP monitoring and pre-emptive measures to avoid it. If arrhythmia is likely to be the cause of pulmonary oedema or ACS, one should consider emergency cardioversion. Bradycardia should be addressed if it is the cause of symp- tomatic low cardiac output. Patients with A CS or serious mechanical cardiac disorders should proceed rapidly to angiography and cathet erization for therapeutic measures, including PCI or surgery. NIV should be given early to every patient admitted with AHF, as it is the only tool with proven improvement in morbidit y and mortality. If the respiratory acidosis is asso- ciated with mental status changes, en dotracheal intubation The problem: increased intracardiac diastolic pressure and oxygen disrupted balance The hea rt pumping function maintains low intracardiac diastolic pressures allowing systemic and pu lmonary venous return. Increased LV diastolic pressures lead to pul- monary congestion and poorer oxygenation. Increased RV diastolic pressures lead to peripheral oedema, liver, kidn ey and mesenteric vein increased pressures, with decreased function in these organs. Becaus e they share a common septum, increased pressures in one side of the heart push the septum, increasing pressure and decreasing telediasto- lic volume in the other side, further compr omising stroke volume and cardiac output. This is particularly important with hypoxia, cons equent to lung congestion, which may markedly increase PVR, causing an increase in RV end- diastolic pressure that will further contribute to increased LV end-diastolic pressure and decreased LV diastolic vol- ume. If there is deterioration in ventricular \201 lling, as in HF with preserved EF, pressure is increased from the beginning of diastole. If the systo lic function is compromised, the heart will try to maintain its output at the cost of incre ased diastolic ventricular volume, and the pressure goes up. Increased intracardiac diastol ic pressure increases wall ten- sion, decreasing at the same time coronary blood \202 ow when the oxygen consumption is greater. In the AHF patient with lung congestion, this becom es more noticea- ble due to poorer blood oxygenation, and, in each episode, the heart oxyge n balance is further compromised by decreased myocardial perfusion due to increased diastol ic pressures, increased heart rate or arrhythmia, with further impairment of cardiac contra ctility, enhancing the process of pulmonary congestion, thus contributing to ongoing irrevo cable myocardial damage. In the later stage of chronic 305 CHAPTER 18.8 Acute heart failure: management and mechanical ventilation should be considered, as NIV needs patient cooperation. Signs of poor organ perfusion should be addressed immediately as in any acute circula- tory failure . MI. The initial management of hypertensive AHF patients should include: \200 \200 \200 NIV Immediate sublingual or inhaled nitrates Cautious diuretic use as they are euvolaemic o r often mildly hypovolaemic due to their usual medication If BP persists >160/100 start IV vasodilator If BP persists <160/100 estimate severity of illness: \200 Hypertensive AHF \200\224congestive form with preserved SBP and likely preserved LVEF Most patients admitted to hospital with AHF have a nor- mal-to-high SBP. In the recently publish ed Italian survey on AHF, up to 43% of patients had an SBP >140mm Hg. The elevated BP usual ly develops rapidly and is possibly related to increased sympathetic tone. It results in ne urohormonal activation and increased LV afterload with impairment of cardiac function. Beca use symptoms develop abruptly, these patients tend to be euvolaemic or sometimes mildly hyp ovolaemic, due to their usual therapy, and present with pulmonary rather than systemic cong estion, often with severe pulmonary oedema. Most patients are older, more likely to be wome n, to have a higher incidence of hypertension, LV hypertrophy, diabetes and to show AF in t heir \201 rst ECG than patients admitted with AHF and systolic dysfunction. In a landmark paper, Gandhi et al. found that in patients with pulmonary oedema presenting to the emerge ncy room with high blood pressure, the echocardiographic EF was almost within the normal ra nge (EF = 0.5 0.15). In these patients, capable of maintaining high SBP, who present wit h pulmonary oedema, hypertensive crisis or exacerbated HF with high blood pressure, pulmona ry oedema is not caused by \202 uid accumulation but rather by \202 uid redistribution that is directed into the lungs because of HF caused by a combination of progressive excess ive vasoconstriction superimposed on reduced LV functional reserve. Recent data suggest tha t this combination of events in which an inappropriate increase in SVR is met with insuf \201 - cient systolic and diastolic myocardial functional reserve leads to an acute afterlo ad mismatch. A vicious cycle is established by which impaired function is met with inap- pr opriately high resistance, causing additional impairment in contractility. This increased S VR leads to increased LV diastolic pressures, which are transferred backwards to the pulmon ary veins leading to pulmonary oedema. Reduced systemic oxygen saturation leads to further impairment of cardiac contractility, enhancing the process of pulmonary oedema. The combina tion of increased pul- monary venous pressure, decreased oxygen saturation and sympathetic activity induces a marked increase in PVR, causing an increase in RV end-diastolic pressure that will further contribute to increased LV end-diastolic pressure and decreased LV diast olic volume. Therefore, the immediate treatment of these AHF patients should favor the admi nistration of strong, fast-acting IV vasodilators such as nitrates or nitroprusside instead of diuretics. This is not the usual practice. In the ADHERE reg- istry, 88% of AHF patient s received IV loop diuretics, with 64% receiving it as monotherapy. The results of a prospe ctive study comparing predominant IV isosorbide dinitrate with predominant frusemide in the treatment of patients presenting with pulmonary oedema showed that in all primary and seco ndary end-point meas- ures, patients treated by high-dose frusemide faired signi \201 - ca ntly worse than patients treated with lower doses of frusemide and high-dose nitrates with fewer numbers of deaths, adverse events, need for mechanical ventilation or \200 Low risk: good response to treatment, adequate urine output, SBP >90, SBP <210, troponin ne gative. Admit to intermediate care with close surveillance High risk: poor response to trea tment, inadequate urine output, SBP <90, SBP >210, troponin elevated, tachycardia, high res piratory rate, persistent hypoxia, increased Uurea or creatinine. Admit to ICU According to their evolution patients may go from inter- mediate care to ICU or from ICU to intermediate care. After initial stabilization, baseline therapy should be directed at red ucing recurrent episodes of AHF, by preven- tion of repeated episodes of excessive vasocons triction along with efforts to optimize cardiac function. Normotensive AHF \200\224systolic dysfunction This other common type of AHF is characterize d by a nor- mal SBP, usually with a history of progressive or chronic HF and often with mul tiple AHF events. In these patients, symp- toms and signs develop gradually, over days or w eeks, and pulmonary and systemic congestion (jugular venous disten- sion, hepatomegaly, pul monary rales and peripheral oedema) are usually present. They usually have a weight above t heir normal dry weight and they often know that they have a reduced EF. Despite high LV \201 lling pressures, they may present several degrees of pulmonary congestion (clinical an d/or radiographic) but some may have minimal pulmo- nary congestion with signs of RV failur e. These patients often present with hyponatremia, increased urea and creati- nine, and som etimes discrete signs of liver dysfunction. In these patients, volume overload is central t o the patho- physiology of most episodes of acute decompensated HF. Loop diuretics should b e the mainstay of their therapy because they produce signi \201 cantly more natriuresis th an other diuretics, particularly in the setting of decreased GFRs. IV loop diuretics may sh ow a substantial difference, because increased mesenteric venous pressure may decrease the absorption of oral diuretic administration. The initial management of these patients should include: \200 \200 \200 NIV IV loop diuretics Estimate severity of illness: \200 High risk: poor response to treatment, renal dys- function, diuretic resistance, elevated S BP, troponin elevated, low urine output. Admit to ICU. Non-high risk: good response to trea tment, normal renal function, normal SBP, troponin negative, ade- quate urine output. Admit to intermediate care with close surveillance. Hypotensive AHF: see below Start IV vasodilator If worsening or lack of improvement admit to ICU and consider addition al monitoring and therapy. \200 These patients need time progressively to increase neurohu- moral antagonism with some nega tive \202 uid balance for symp- tom improvement. Excessive negative \202 uid balance ma y induce hypotension with vasodilatation or B-blocker use. 306 M TAVARES, A EL GHORCH, & A MEBAZAA lactatem start IV vasodilator. Consider more invasive monitoring. If severe hypervolaemia, consider diu- retic or ultra \201 ltration Hypotensive AHF Patients admitted to hospital with AHF and low BP repre- sent a subgroup wi th high in-hospital and post-discharge mortality rates. These patients present with evidenc e of low cardiac output, decreased perfusion, cool extremities, altered mental status and h ypotension. The reduction in cardiac function is not met by an adequate increase in PVR, le ading to signi \201 cant decrease in blood pressure and end- organ perfusion. The treatmen t of cardiogenic shock should be directed at improving cardiac performance (by optimizing \201 lling pressure, intra-aortic balloon pump and immediate revascularization) and admini stration of periph- eral vasoconstrictors. Most of these patients require IV inotropic ther apy. However, the use of current IV inotropes has been associ- ated with risk for hypotensi on, atrial and ventricular arrhythmias and possibly increased post-discharge mortal- ity, p articularly in those with CAD. The initial management of hypotensive AHF patients should in clude: \200 NIV \200 Consider \202 uid challenge \200 Start IV inotrope/inodilator \200 Admit to ICU \200 Consider vasopressor for maintaining coronary per- fusion Assess response to therapy: \200 Further reading Atherton JJ, Moore TD, Lele SS, et al. Diastolic ventricular interac- tion in chronic heart failure. Lancet 1997; 349: 1720 \200\2234. Benza RL, Tallaj JA, Felker GM, et al. The impact of arrhythmias in acute heart failure. J Card Fail 2004; 10: 279 \200\22384. Fonarow GC. The Acute Decompensated Heart Failure National Registry (ADHERE): opportunities to improve care of patients hospitalized with acute decompensated heart failure. Rev Cardi ovasc Med 2003; 4 (Suppl. 7): S21 \200\22330. Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associate d with hypertension. N Engl J Med 2001; 344: 17 \200\22322. Gheorghiade M, Abraham WT, Albert NM, et al. Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. JAMA 2006 ; 296: 2217 \200\22326. Gheorghiade M, Filippatos G. Reassessing treatment of acute heart failure syndromes: the AD HERE Registry. Eur Heart J 2005; 7 (Suppl B): B13 \200\2239. Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure syn- dromes: current state and framework for future research. Circulation 2005; 112: 3958 \200\22368. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J 2005; 26: 384 \200\223416. Tavazzi L, Maggioni AP, Lucci D, et al. Nationwide survey on acute heart failure in cardiol ogy ward services in Italy. Eur Heart J 2006; 27: 1207 \200\22315. If adequate response with improvement of peripheral perfusion, increasing urine output, dec reasing acido- sis or lactatem consider transfer to intermediate care with close surveillan ce If pulmonary congestion, persistence of decreased perfusion, low urine output, persisten t acidosis or Zannad F, Mebazaa A, Juilliere Y, et al. Clinical pro \201 le, contempo- rary management a nd one-year mortality in patients with severe acute heart failure syndromes: The EFICA stud y. Eur J Heart Fail 2006; 8: 697 \200\223705. This page intentionally left blank 308 A SMITH Bacterial endocarditis Introduction The reported incidence of infective endocarditis (IE) in the Western world is 1.8 \200\2236.2 per 100 000, population with men more commonly affected than women and a ri sing incidence with age to >10 per 100 000 for people aged >50yrs. IE predominantly affects those individuals with structural cardiac lesions who develop a bacteraemia with organisms likely to cause endocarditis. Further risk factors include any conditions likely to result in bacteraemia (immunosuppression, diabetes, poor dental hygiene, chronic haemodialysis, c hronic alcoholism). Endocarditis may be caused by bacterial organisms or fungi, or may be c ulture negative (5 \200\22310%). Culture-negative endocarditis may be due to concomitant an tibiotic therapy, fungal organ- isms or slower growing organisms. Endocarditis may result f rom non-infective causes, e.g. SLE, or in malignant disease. criteria \200\224these are described in the Duke classi \201 cation (Table 18.9.2). Two ma jor criteria, one major and three minor criteria, or \201 ve minor criteria con \201 rm the diagnosis. Possible IE may be diagnosed where there are \201 ndings that fall short o f the de \201 nite criteria but the diagnosis is not rejected. IE diagnosis is \200\230re jected \200\231 when there is a sound alternative diagnosis, or the manifestations have res olved with antimicrobial treatment for <4 days, or there is no pathological evidence of IE at surgery or autopsy. Table 18.9.1 Investigations Blood cultures (90% yield positive culture; 10% are sterile) FBC, differential, ESR and CRP CXR and ECG Echo TTE (transthoracic) and/or TOE (transoesophageal) Pathogenesis Endocarditis can affect native valves and prosthetic valves, and usually norma l cardiac tissue is resistant to infection. Transient bacteraemia is very common, and the i mmune system plays an effective role in preventing endocarditis. Endothelial damage results in platelet and \201 brin deposition forming a non-bacterial thrombotic lesion (vegetati on). When a bacteraemia occurs from any potential source, e.g. intravascular catheter, post -dental work, wound infections, urinary and respiratory tract infections, these vegetations can be colonized. Renal function (including urinalysis) Infection-related antiphospholipid antibodies Special cultures for Coxiella, Bartonella and mycoplasma if initial cultures are negative Pre-operative MRSA screen Common sites of infection \200 \200 Prosthetic valves Left-sided structures (>85%) Aortic lesions (55 \200\22360%) \200 Mitra l lesions (25 \200\22330%) \200 Mitral + aortic lesions (15%) \200 Right-sided structur es (10 \200\22315%) Clinical features The clinical features of bacterial endocarditis will depend on a number o f factors including the nature of the underly- ing lesion and the virulence of the infectin g organism. Acute bacterial endocarditis presents as a sudden illness charac- terized by hi gh temperatures, rigors, exhaustion, weakness and collapse. Patients are frequently very un well. Subacute endocarditis tends to present in a more insidious non-spe- ci \201 c manner with symptoms of anorexia, weight loss, fever, myalgia, arthralgia or fatigue. The clinica l features of IE are due to: \200 Treatment IE causes signi \201 cant morbidity and mortality. Prevention is a priority, alt hough early diagnosis and appropriate therapy are essential. Once the diagnosis is establis hed, treatment should be commenced according to local guidance or directed by microbiologic al advice. Treatment should be initiated once blood cultures have been taken, and subsequen tly adjusted once the results are known. Early involvement of cardiolo- gists, microbiologi sts and cardiac surgeons is advisable. The majority of endocarditis is caused by streptococ cal organisms (50 \200\22370%) with S. viridans accounting for half of these; staphylococca l organisms account for 25%, although in IV drug abusers this increases to 60%, with assoc iated increases in fungal and anaerobic organisms, and entero- cocci (10%). Empirical treat ment depends on the likely organism. \200 Bacteraemia/septicaemia \200\224fever, rigors, chills, malaise, anorexia, confusion, arthra lgia. Tissue destruction \200\224valvular incompetence, root and myocardial abscess (20 \200\22340%), prosthetic valve dehis- cence, heart block, cardiac failure. Embolic phenomen a \200\224occur in 50% cases of infective endocarditis resulting in: cerebrovascular accide nt (CVA), acute peripheral limb ischaemia, MI, TIAs, spleen and kidney infarction, PE and m ycotic aneurysms (2 \200\223 15%). Immunological phenomena \200\224splinter hemorrhages (5 \200\223 15%), Osler \200\231s nodes (5 \200\22310%) (tender nodes in pulp of \201 ngerti ps), Janeway lesions (10 \200\22320%) (macules on palms or wrists), vasculitis rash, Roth s pots ( \202 ame-shaped hemorrhages in the retina), arthralgia, nephritis, splenomegaly (30 \200\22350%). Acute onset (often staphylococcal organisms) \200\224flu- cloxacillin (8 \200\22312g IV dai ly in 4 \200\2236 divided doses) plus gen- tamicin (1mg/kg body weight IV 8 hourly, modifie d according to renal function). Gradual presentation (often A-haemolytic streptococcal orga nisms) \200\224penicillin (7.2g IV daily in six divided doses) or ampicillin/amoxicillin (2 g IV 6 hourly) plus gentamicin (1mg/kg body weight 8 hourly IV, modi \201 ed according to renal function). Patients with penicillin allergy, intracardiac prosthesis or suspected MRS A \200\224vancomycin (1g 12 hourly IV, modi \201 ed according to renal function) plus rifa mpicin Table 18.9.1 outlines commonly useful investigations. The diagnosis of IE is based on the c ombination of clinical, microbiological and echocardiographic \201 ndings. De \201 nite IE is diagnosed on (1) pathological criteria where microorganisms are found by culture or h istology in an embolized vegetation, an intracardiac abscess or (2) clinical 309 CHAPTER 18.9 Bacterial endocarditis shock due to valvular heart disease, or those with pros- thetic valve endocarditis. Early i ntervention may be associ- ated with improved outcome. Antibiotic therapy should be continu ed for 4 \200\2236 weeks. Response to treatment should be carefully monitored with repeated evaluation of clinical state and laboratory investi- gations. Table 18.9.2 The Duke classi \201 cation. Major criteria Positive blood culture of organisms known to cause IE from 2 separate blood cultures. Persistently positive blood cultures In 2 blood cultures drawn >12h apart Mortality Overall mortality remains at 20%. Prosthetic valve endo- carditis carries an eve n higher mortality rate (26 \200\22370%). Right-sided endocarditis is usually related to IV drug abuse and carries a more favorable mortality risk at 4 \200\2235%. IE with staphyloco ccal organisms or with fungi have a high associated mortality (50%) when compared with ente ro- cocci (25%) or streptococci (15%). In all of 3 or majority of 4 separate blood cultures with the \201 rst and last drawn ove r 1h apart Evidence of endocardial involvement Positive echocardiographic \201 ndings Mobile intracardiac mass on valve or supporting structures or in the path of a regurgitant jet, or on implanted material. Prophylaxis People with predisposing factors for bacterial endocarditis include those with prosthetic heart valves, previous bacte- rial endocarditis, acquired valvular heart disease with ste- nosis or regurgitation, structural congitential heart disease (excluding fully r epaired atrial and venticular septal defects and patent ductus arteriosous), and hypertroph ic cardio- myopathy. At present antibiotic prophylaxis against infec- tive endocarditis is not recommended for people undergoing dental procedures and other invasive clincial procedu res involving the respiratory, genitourinary (includ- ing urological, gynecological, obstet ric procedures, and childbirth), and the upper and lower gastrointestinal tracts. Recommend ations may change, and it is wise to consult a national formulary. Episodes of infection in those at risk of infective endocardi- tis should be investigated and treated promptly to r educe the risk of endocarditis developing. If a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a procedure at a site where th ere is a suspected infection, the person should receive an antibiotic that covers organisms that cause infective endo- carditis. Abscess New dehiscence of prosthetic valve or new valve regurgitation Clinical evidence of new valvular regurgitation Positive serology e.g. Q fever, Bartonella spp, Chlamydia Spp Positive identi \201 cation of a microorganism Using molecular biology methods Minor criteria Predisposition Predisposing heart lesion or IV drug abuse Fever Temperature >38.0 C Vascular phenomena Arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conj unctival hemorrhage, Janeway lesions, new \201 nger clubbing, splinter hemorrhages, splen omegaly Immunological phenomena Glomerulonephritis, Osler \200\231s nodes, Roth spots, +ve rheumatoid factor, raised ESR (> 1.5 \227 normal) raised CRP (>100mg/dl) Further reading NICE clinical guideline 64. Prophylaxis against infective endocardi- tis: a ntimicrobial prophylaxis against infective endocarditis in adults and children undergoing i nterventional procedures. March 2008. Microbiological evidence Positive blood cultures but not meeting major criteria (300 \200\223600mg 12 hourly by mouth) plus gentamicin (1mg/ kg body weight 8 hourly IV, mo di \201 ed according to renal function). Surgery is indicated in up to 25 \200\22330% of infections. These tend to be in those with life-threatening congestive HFor This page intentionally left blank 311 Chapter 19 Renal disorders Chapter contents Prevention of acute renal failure 312 Diagnosis of acute renal failure 314 312 M JOANNIDIS Prevention of acute renal failure