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HEART FAILURE DR ZIAD NOFAL CARDIOLOGIST DAMASCUS HOSPITAL heart failure outlines – Definition – Causes and pathophysiology – Clinical manifestations – Classification of heart failure – Diagnostic evaluation – Medical management Heart Failure Definition • A complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. • Cardinal manifestations are dyspnea and fatigue (which may limit exercise tolerance), and fluid retention (which may lead to pulmonary congestion and peripheral edema). Hunt SA et al. J Am Coll Cardiol. 2005; 46: e1-e86. Prevalence • Framingham Heart Study found a prevalence of HF in men of 8 per 1000 at age 50 to 59 years, increasing to 66 per 1000 at ages 80 to 89 years. similar values (8 and 79 per 1000) were noted in women . • The prevalence in African-Americans is reported to be 25 percent higher than in whites. Cardiovascular Deaths 300,000 death/yr Mode of Death by NYHA Class NYHA II Other 24% HF 12% NYHA III Other 15% SD 64% HF 26% MERIT-HF Study Group. Lancet. 1999; 353: 2001-2007. NYHA IV Other 11% SD 59% SD 33% HF 56% heart failure outlines – Definition – Causes and pathophysiology – Clinical manifestations – Classification of heart failure – Diagnostic evaluation – Medical management Italian registry of over 6200 unselected outpatients with HF • • • • • Ischemic heart disease — 40 percent Dilated cardiomyopathy — 32 percent Primary valvular heart disease — 12 percent Hypertensive heart disease — 11 percent Other — 5 percent Causes of systolic heart failure • Coronary artery disease • High blood pressure • Heart valves disorders • Inflammation of Heart muscle (myocarditis, cardiomyopathy) Causes of diastolic heart failure Coronary artery disease. High blood pressure. Hypertrophic obstructive cardiomyopathy . Restrictive cardiomyopathy. Diastolic dysfunction • The most common conditions associated with diastolic dysfunction are aging , hypertension, diabetes mellitus, left ventricular hypertrophy, coronary disease, and infiltrative cardiomyopathies. Left ventricular hypertrophy • Whether due to hypertension, coronary disease, valve disease, or diabetes, left ventricular hypertrophy (LVH) is a prominent feature of evolving HF. • Among patients with HF in the general population, antecedent evidence of LVH is present in approximately 20 percent by ECG and 60 to 70 by echocardiogram. Stage B (cont.) I IIaIIbIII I IIaIIbIII In patients with structural cardiac abnormalities, including LV hypertrophy, in the absence of a history of MI or ACS, blood pressure should be controlled in accordance with clinical practice guidelines for hypertension to prevent symptomatic HF. ACE inhibitors should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not have a history of MI. I IIaIIbIII Beta blockers should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not have a history of MI. NHANES I • • • • • • Coronary heart disease — relative risk 8.1 Cigarette smoking — relative risk 1.6 Hypertension — relative risk 1.4 Overweight — relative risk 1.3 Diabetes — relative risk 1.9 Valvular heart disease — relative risk 1.5 however, valve disease is an increasingly common cause of HF at older ages, with calcific aortic stenosis being the most common disorder requiring surgery New Classification of Heart Failure Stage Patient Description A High risk for developing heart Hypertension • CAD • failure (HF) B Asymptomatic HF C Symptomatic HF D Refractory end-stage HF Hunt SA et al. J Am Coll Cardiol. 2005; 46: e1-e86. Diabetes mellitus • Family history of cardiomyopathy • Previous MI • LV systolic dysfunction • Asymptomatic valvular disease • Known structural heart disease • Shortness of breath and fatigue • Reduced exercise tolerance • Marked symptoms at rest despite maximal • medical therapy (eg, those who are recurrently hospitalized or cannot be safely discharged from the hospital without specialized interventions) Role of Inflammation in HF - One belief is that the progression of HF is heavily influenced by inflammation. -Proinflammatory cytokines ( CRP, TNF, interleukin 6) produce toxins that directly affect the heart and peripheral vasculature. - In response to cardiac stress such as a myocardial infarction (MI), increased pressure or volume overload, myocardial cells produce cytokines especially TNF Secretes more cytokines Tissue Release of Attract monocytes -> mature Releases damage, cytokines into macrophages toxins infection (TNF, IL 6) Decreased CO HF Remodeling (hypertrophy, dilation) Increased workload on heart to meet body needs Kills cardiomyocytes Role of genetics in HF -Researchers are beginning to trace the etiology of HF partly to genetics -The fundamental basis for heart cells are -1) the generation of a contractile force, - 2) transmission of this force throughout. -Mutations in the sarcomere proteins of muscle cells have been linked to HF. These mutations - cause uncoordinated heart contractions increased energy consumption - cause changes in calcium homeostasis apoptosis and fiber formation inflammation األسباب (1 (2 (3 (4 (5 (6 (7 (8 أمراض الشرايين االكليلية أمراض الصمامات اعتالالت العضلة القلبية ارتفاع التوتر الدموي الشرياني األمراض الغدية(السكري,فرط أو قصور الدرق,تناذر كوشينغ,ورم القواتم.)..... أمراض ارتشاحية(الساركوئيد,داء الصباغ الدموي,الداء النشواني.).... طبيعة الحياة(التدخين,الكحول,البدانة,نقص الفيتامينات وخاصة)...B1 األدوية(مضادات األورام,حاصرات قنوات الكالسيوم,حاصرات بيتا.)... Essential functions of the heart are secured by integration of electrical and mechanical functions of the heart Cardiac output (CO) = heart rate (HR) x stroke vol.(SV) - changes of the heart rate - changes of stroke volume • Control of HR: - autonomic nervous system - hormonal(humoral) control • Control of SV : - preload - contractility - afterload Adaptive mechanisms of the heart to increased load • Frank - Starling mechanism • Ventricular hypertrophy – increased mass of contractile elements strength of contraction • Increased sympathetic adrenergic activity – increased HR, increased contractility • Incresed activity of R–A–A system General pathomechanisms involved in heart failure development Cardiac mechanical dysfunction can develop as a consequence in preload, contractility and afterload disorders Disorders of preload preload length of sarcomere is more than optimal strength of contraction preload length of sarcomere is well below the optimal strength of contraction Causes of heart pump failure A. MECHANICAL ABNORMALITIES 1. Increased pressure load – central (aortic stenosis, aortic coarctation...) – peripheral (systemic hypertension) 2. Increased volume load – valvular regurgitation – hypervolemia 3. Obstruction to ventricular filling – valvular stenosis – pericardial restriction 2. Changes of neurohumoral control of the heart function • Physiology: • SNS contractility HR activity of physiologic pacemakers Mechanism: sympathetic activity cAMP Ca ++i contractility sympathetic activity influence of parasympathetic system on the heart • Pathophysiology: normal neurohumoral control is changed and creation of pathologic neurohumoral mechanisms are present Chronic heart failure (CHF) is characterized by an imbalance of neurohumoral adaptive mechanisms with a net results of excessive vasoconstriction and salt and water retention Catecholamines : - concentration in blood : - norepinephrin – 2-3x higher at the rest than in healthy subjects - circulating norepinephrin is increased much more during equal load in patients suffering from CHF than in healthy subject - number of beta 1 – adrenergic receptors sensitivity of cardiomyocytes to catecholamines contractility System rennin – angiotensin – aldosteron heart failure CO kidney perfusion stim. Of RAA system Important: Catecholamines and system RAA = compensatory mechanisms heart function and arterial BP The role of angiotensin II in development of heart failure vasoconstriction ( in resistant vesels) retention of Na blood volume releasing of arginin – vasopresin peptide (AVP ) from neurohypophysis Main causes and pathomechanisms of diastolic heart failure 1. structural disorders passive chamber stiffness a) intramyocardial – e.g. myocardial fibrosis, amyloidosis, hypertrophy, myocardial ischemia... b) extramyocardial – e.g. constrictive pericarditis 2. functional disorders relaxation of chambers e. g. myocardial ischemia, advanced hypertrophy of ventricles, failing myocardium, asynchrony in heart functions Result of Compensatory Mechanisms > Heart Failure Heart Failure Explained Hypertension • Hypertension — Data from the Framingham Heart Study found that, after age 40, the lifetime risk of developing HF was twice as high in subjects with a blood pressure ≥160/100 mmHg compared to <140/90 mmHg . • Another analysis from the Framingham study suggests that baseline systolic pressure and pulse pressure have a greater impact on the risk of subsequent HF than the diastolic pressure. heart failure outlines – Definition – Causes and pathophysiology – Clinical manifestations – Classification of heart failure – Diagnostic evaluation – Medical management Definition of Heart Failure Classification I. Heart Failure with Reduced Ejection Fraction (HFrEF) Ejection Fraction ≤40% Description Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients that efficacious therapies have been demonstrated to date. ≥50% Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified. a. HFpEF, Borderline 41% to 49% These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF. b. HFpEF, Improved >40% It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients. II. Heart Failure with Preserved Ejection Fraction (HFpEF) قصور القلب االنقباضي /االنبساطي في القصور االنقباضي يكون االضطراب األساسي هو عدم القدرة على ضخ دم كاف بسبب اضطراب القلوصية (التالي مثالً العتالل عضلة القلب التوسعي أو االحتشاء) وهنا يتوسع البطين ويتمدد أثناء االنبساط , وبالتالي يزداد حجم نهاية االنبساط ,ولكن دون ازدياد مو في حجم النفضة . أما في القصور االنبساطي فتضطرب قدرة البطين على االرتخاء جيدا ً أثناء االنبساط ,لذا يضطرب الملء االنبساطي ويكون ضغط نهاية االنبساط مرتفعا ً مهما كان حجم نهاية االنبساط ,وبمعنى آخر تكون العالقة بين حجم النفضة وحجم نهاية االنبساط سوية (فالقلب يقذف جيدا ً ما يحتوي من دم ولكن مشكلته هي في قلة ما يحتويه من هذا الدم ,عكس القصور االنقباضي حيث يحتوي دما ً كثيرا ً ولكنه يعجز عن قذفه ) . ونرى القصور االنبساطي في اعتالل العضلة القلبية الضخامي مثالً . قصور القلب الحاد /المزمن يظهر القصور الحاد مثالً في سياق أحتشاء واسع أو تمزق صمامي مفاجئ ,فيقل النتاج القلبي ويهبط ضغط الدم الشرياني دون حدوث وذمات محيطية. القلب المزمن يكون ضغط الدم سويا ً ( بسبب نشاط آليات المعاوضة كضخامة عضلة القلب ونشاط الجهاز الودي وازدياد الكاتيوكول آمينات ) ,لكن تحدث الوذمات المحيطة نتيجة تراكم السوائل في األنسجة الخاللية. قصور أيسر القلب /أيمن القلب في قصور أيسر القلب التالي لضعف في عضلة القلب كاالحتشاء أو كالتضيق األبهري ,تتراكم السوائل ويرتفع الضغط خلف البطين األيسر نتيجة ضعف الضخ ,فيرتفع الضغط في األوردة الرئوية وفي األوعية الشعرية الرئوية وتظهر أعراض االحتقان الرئوي . أما في قصور القلب األيمن فتتراكم السوائل خلف البطين األيمن , فتظهر الوذمات المحيطة وضخامة الكبد االحتقانية والتوسع الوريدي الجهازي . مالحظة :تكون الحدود بين هذين الشكلين أقل وضوحا ً في الحاالت المزمنة . قصور القلب عالي النتاج /منخفض النتاج يحدث القصور عالي النتاج مشاركا ً لفرط الدرقية وفقر الدم الشديد و النواسير الشريانية الوريدية وداء باجت ...ألنه على القلب أن يضخ كميات كبيرة من الدم لكي يوصل األوكسجين بكميات كافية الحتياجات النسج التي لديها زيادة في االستقالب .لذا تكون األطراف دافئة وضغط النبض واسعا ً ( أو على األقل سويا ً ). على عكس القصور منخفض النتاج حيث يحدث تقبض وعائي محيطي ,وتكون األطراف باردة شاحبة وأحيانا ً مزرقة ,وفي الحاالت المتقدمة يصبح ضغط النبض صغيرا ً بسبب حجم النفضة . قصور القلب اإلقبالي Forward - اإلدباري Backward و هذا التفريق لتمييز اآلليات المحدثة الحتباس السوائل و الوذمات .حيث يقول مؤيدو نظرية القصور اإلدباري إنه عند حدوث القصور يفشل البطين في ضخ محتوياته و لذا ترتفع الضغوط خلفه و يحدث احتباس للماء و الصوديوم كنتيجة الرتفاع الضغوط الشعرية و الوريدية و ارتشاح السوائل إلى المسافات الخاللية . أما أصحاب نظرية القصور اإلقبالي فيدعون أن قصور القلب في ضخ الدم إلى الشرايين الجهازية يؤدي إلى إقفار كلوي و ازدياد عودة امتصاص الصوديوم في النبيبات القريبة كنتيجة لتحريض جهاز الرينين – ألدسترون و بذلك يحدث احتباس الماء و الملح . تصنيف قصور القلب وفقا لمراحل الزلة التنفسية NYHAتبعا للجمعية األمريكية ألمراض القلب class I II III IV الزلة التنفسية تحدث عند الجهد الشديد تحدث عند الجهود المتوسطة كاألعمال المنزلية تحدث عند الجهود الخفيفة تحدث على الراحة Ischemic cardiomyopathy • Ischemic cardiomyopathy is diagnosed in patients with HF who have had a myocardial infarction or have evidence of hibernating myocardium or, on angiography, severe coronary disease. • In contrast, patients with single vessel disease who have no evidence of myocardial infarction or revascularization have a similar prognosis as those with nonischemic cardiomyopathy . A STAGE تشمل المرضى الذين لديهم عوامل خطورة لتطور قصور القلب(المسنين,السكري,ارتفع الضغط الشرياني,ارتفاع الكوليسترول,التدخين,)......وهؤالء المرضى ليس لديهم أي أعراض أو عالمات أو اضطراب في بنية العضلة القلبية. جميع هؤالء المرضى يجب أن يخضعوا للعالج الدوائي لمنع التطور للمرحلة التالية B STAGE هم المرضى الذين تطور لديهم خلل في بنية العضلة القلبة لكنهم ما زالوا ال يعانون من أي أعراض أو عالمات لقصور القلب. STAGE C هم المرضى الذين تطور لديهم أعراض قصور القلب باالضافة لوجود الخلل في بنية العضلة القلبية. D STAGE هي مرحلة متطورة من قصور القلب حتى أن معظم العالجات المستخدمة لم تعد تفيد. %50من هؤالء المرضى يموتون خالل 6أشهر وهم يقابلون المرحلة IVمن تصنيف .NYHA Sensitivity, Specificity, and Predictive Accuracy of Symptoms and Signs for Diagnosing Heart Failure Modified Framingham clinical criteria for the diagnosis of heart failure Major • Paroxysmal nocturnal dyspnea • Orthopnea • Elevated jugular venous pressure • Pulmonary rales • Third heart sound • Cardiomegaly on chest x-ray • Pulmonary edema on chest x-ray • Weight loss ≥4.5 kg in five days in response to treatment of presumed heart failure Framingham criteria - c • • • • • • • • Minor Bilateral leg edema Nocturnal cough Dyspnea on ordinary exertion Hepatomegaly Pleural effusion Tachycardia (heart rate ≥120 beats/min) Weight loss ≥4.5 kg in five days question • 1. A 75 year-old male presents to you with a gradual onset of symptoms suggestive of heart failure and sinus rhythm and examination confirms the presence of biventricular failure. Following confirmation of the diagnosis by chest x-ray and electrocardiography you should take the following steps: a. Treat the heart failure with diuretics and ACE inhibitors . b. Treat the heart failure with digoxin and diuretics. c. Treat he patient with diuretics, ACE inhibitors and anticoagulants . d. Try to establish the cause of the heart failure with echocardiography, cardiac catheterisation and whatever other investigations are appropriate . e. Use ACE inhibitor, vasodilator therapy and diuretic . CLINICAL Evaluation • The approach to the patient with suspected HF includes the FOLLOWING : • history • physical examination • diagnostic tests to help establish the diagnosis • assess acuity and severity • initiate assessment of etiology. History and Physical Examination I IIaIIbIII I IIaIIbIII I IIaIIbIII A thorough history and physical examination should be obtained/performed in patients presenting with HF to identify cardiac and noncardiac disorders or behaviors that might cause or accelerate the development or progression of HF. In patients with idiopathic DCM, a 3-generational family history should be obtained to aid in establishing the diagnosis of familial DCM. Volume status and vital signs should be assessed at each patient encounter. This includes serial assessment of weight, as well as estimates of jugular venous pressure and the presence of peripheral edema or orthopnea. History • Classic exertional angina usually indicates ischemic heart disease. • Acute HF after an antecedent flu-like illness suggests viral myocarditis. . • Long-standing hypertension or alcohol use suggests hypertensive or alcoholic cardiomyopathy. • Primary valvular dysfunction should be considered in a patient with a history of murmurs. HISTORY -C • a family history of unexplained cardiomyopathy, low voltage on EKG, left ventricular hypertrophy (especially without hypertension),and a history of heavy proteinuria. • A diagnosis of amyloidosis should be strongly considered • HF may be provoked or worsened by drugs, including antiarrhythmic agents such as disopyramide and flecainide ; calcium channel blockers, particularly verapamil ; beta blockers; and nonsteroidal antiinflammatory drugs (NSAIDs) . • (Acute pulmonary edema occurring during, or shortly after, infusion of blood products suggests transfusional volume overload. Vital signs and appearance • Four major findings suggest severity of the cardiac dysfunction: • resting sinus tachycardia, narrow pulse pressure, diaphoresis, and peripheral vasoconstriction. • A decrease in cardiac output should be suspected when the pulse pressure is reduced below 25 mmHg. • Pulsus alternans, if present, is virtually pathognomonic of severe left ventricular failure. Volume assessment • There are three major manifestations of volume overload in patients with HF: • pulmonary congestion, • peripheral edema, • and elevated jugular venous pressure. Diagnostic Tests I IIaIIbIII A 12-lead ECG should be performed initially on all patients presenting with HF. I IIaIIbIII I IIaIIbIII Screening for hemochromatosis or HIV is reasonable in selected patients who present with HF. Diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma are reasonable in patients presenting with HF in whom there is a clinical suspicion of these diseases. Electrocardiogram • prior or acute myocardial infarction or ischemia. • Left ventricular hypertrophy due to hypertension. • Low limb lead voltage on the surface ECG with a pseudo-infarction pattern (loss of precordial R wave progression in leads V1-V6) can suggest an infiltrative process such as amyloidosis. • Low limb lead voltage with precordial criteria for left ventricular hypertrophy is most suggestive of idiopathic dilated cardiomyopathy. A widened QRS complex and/or a left bundle branch block pattern is also consistent with this diagnosis. • Heart block, that may be complete, and various types of intraventricular conduction defects are observed in patients with cardiac sarcoidosis. • The presence of a persistent tachycardia such as atrial fibrillation with a rapid ventricular response may result from or lead to HF, since this arrhythmia can cause cardiomyopathy (tachycardia-mediated cardiomyopathy). Noninvasive Cardiac Imaging I IIaIIbIII Patients with suspected or new-onset HF, or those presenting with acute decompensated HF, should undergo a chest x-ray to assess heart size and pulmonary congestion, and to detect alternative cardiac, pulmonary, and other diseases that may cause or contribute to the patients’ symptoms. I IIaIIbIII A 2-dimensional echocardiogram with Doppler should be performed during initial evaluation of patients presenting with HF to assess ventricular function, size, wall thickness, wall motion, and valve function. I IIaIIbIII Repeat measurement of EF and measurement of the severity of structural remodeling are useful to provide information in patients with HF who have had a significant change in clinical status; who have experienced or recovered from a clinical event; or who have received treatment, including GDMT, that might have had a significant effect on cardiac function; or who may be candidates for device therapy. Chest x-ray • cardiomegaly (cardiac-to-thoracic width ratio above 50 percent) • cephalization of the pulmonary vessels • Kerley B-lines, and pleural effusions . • The cardiac size and silhouette may also reveal signs of congenital anomalies (ventricular or atrial septal defect) or valvular disease (mitral stenosis or aortic stenosis). الموجودات على صورة الصدر الشعاعية CX-RAY زيادة المشعر القلبي الصدري. زيادة االحتقان الرئوي على شكل وذمة خاللية(خطوط كيرلي)أو وذمة سنخية(منظر جناحي الخفاش). اعادة توزع األوعية لألعلى. انصباب جنب. This plain frontal radiograph of the chest in a 51year-old male demonstrates marked enlargement of the cardiac silhouette compatible with a dilated cardiomyopathy. Cardiomegaly is nonspecific and can be seen with any etiology of cardiomyopathy. ECHOCARDIOGRAPHY • Atrial and ventricular sizes, • Global left and right ventricular systolic function (left and right ventricular ejection fraction, LVEF and RVEF). • Diastolic left ventricular function. • Regional wall motion abnormalities in a coronary distribution are suggestive of coronary heart disease but segmental abnormalities also occur commonly in patients with dilated cardiomyopathy • Pericardial disease includes thickening suggestive of constrictive pericarditis or effusion which may or may not be associated with tamponade. • Valvular heart disease Diagnostic Tests I IIaIIbIII I IIaIIbIII Initial laboratory evaluation of patients presenting with HF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone. Serial monitoring, when indicated, should include serum electrolytes and renal function. Initial blood tests • A complete blood count which may suggest concurrent or alternate conditions. Anemia or infection can exacerbate preexisting HF. • Serum electrolytes, blood urea nitrogen and creatinine may indicate associated conditions. • Hyponatremia generally indicates severe HF, though it may occasionally result from excessive diuresis . • Renal impairment may be caused by and/or contribute to HF exacerbation. Baseline evaluation of electrolytes and creatine is also necessary when initiating therapy with diuretics and/or angiotensin converting enzyme inhibitors. • Liver function tests, which may be affected by hepatic congestion. • Fasting blood glucose to detect underlying diabetes mellitus. Additional tests • Thyroid function tests, particularly in patients over the age of 65 or in patients with atrial fibrillation. Thyrotoxicosis is associated with atrial fibrillation and hypothyroidism may present as HF. • Iron studies (ferritin and TIBC) to screen for hereditary hemochromatosis (HH). In the past, prior to increased screening, cardiac disease was the presenting manifestation in up to 15 percent of patients with HH. Thus, the absence of other characteristic findings of HH does not preclude the diagnosis. BNPالببتيد المدر للصوديوم • يفرز من قبل البطين كاستجابة للشد على جدره ,بسبب ارتفاع الضغط داخل أجواف القلب ,في مرضى استرخاء القلب االحتقاني . • يتناسب مستوى ارتفاع , plasma BNP levelsتبعا للضغط في نهاية االنبساط. Ambulatory/Outpatient I IIaIIbIII I IIaIIbIII In ambulatory patients with dyspnea, measurement of BNP or N-terminal pro-B-type natriuretic peptide (NT-proBNP) is useful to support clinical decision making regarding the diagnosis of HF, especially in the setting of clinical uncertainty. Measurement of BNP or NT-proBNP is useful for establishing prognosis or disease severity in chronic HF. Ambulatory/Outpatient (cont.) I IIaIIbIII BNP- or NT-proBNP guided HF therapy can be useful to achieve optimal dosing of GDMT in select clinically euvolemic patients followed in a well-structured HF disease management program. I IIaIIbIII The usefulness of serial measurement of BNP or NT-proBNP to reduce hospitalization or mortality in patients with HF is not well established. I IIaIIbIII Measurement of other clinically available tests such as biomarkers of myocardial injury or fibrosis may be considered for additive risk stratification in patients with chronic HF. Hospitalized/Acute I IIaIIbIII Measurement of BNP or NT-proBNP is useful to support clinical judgment for the diagnosis of acutely decompensated HF, especially in the setting of uncertainty for the diagnosis. I IIaIIbIII Measurement of BNP or NT-proBNP and/or cardiac troponin is useful for establishing prognosis or disease severity in acutely decompensated HF. Hospitalized/Acute (cont.) I IIaIIbIII The usefulness of BNP- or NT-proBNP guided therapy for acutely decompensated HF is not well-established. I IIaIIbIII Measurement of other clinically available tests such as biomarkers of myocardial injury or fibrosis may be considered for additive risk stratification in patients with acutely decompensated HF. الموجودات المخبرية قد تكون طبيعية أو تدل على وجود مرض معين (فقر الدم,فرط الدرق,ارتفاع أو هبوط الكالسيوم أو البوتاسيوم)..... الببتيد الطارح للصوديوم BNPمستواه من 400-100فاذا كان : 100<BNP تشخيص السبب القلبي غير محتمل 400-100=BNPالتشخيص غير أكيد 400>BNP يوجد اضطراب بنيوي في عضلة القلب . القيم التشخيصية • BNP level below 100 pg per milliliter indicates that heart failure is unlikely • BNP level greater than 500 pg per milliliter indicates heart failure • BNP levels between 100 and 500 pg per milliliter provide inadequate diagnostic discrimination. Causes for Elevated Natriuretic Peptide Levels Cardiac Heart failure, including RV syndromes Acute coronary syndrome Heart muscle disease, including LVH Valvular heart disease Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Cardioversion Noncardiac Advancing age Anemia Renal failure Pulmonary causes: obstructive sleep apnea, severe pneumonia, pulmonary hypertension Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults, including cancer chemotherapy and envenomation Noninvasive Cardiac Imaging (cont.) I IIaIIbIII Magnetic resonance imaging is reasonable when assessing myocardial infiltrative processes or scar burden. I IIaIIbIII No Benefit Routine repeat measurement of LV function assessment in the absence of clinical status change or treatment interventions should not be performed. Invasive Evaluation (cont.) I IIaIIbIII When ischemia may be contributing to HF, coronary arteriography is reasonable for patients eligible for revascularization. I IIaIIbIII Endomyocardial biopsy can be useful in patients presenting with HF when a specific diagnosis is suspected that would influence therapy. EXERCISE TESTING • Exercise testing should be part of the initial evaluation of any patient with HF. In addition to detection of ischemic heart disease, assessment of exercise capacity can be used for risk stratification and determining prognosis; serial measurements also can assess the efficacy of therapy and clinical stability of patients over time. • A simple alternative that provides an estimate of exercise function is the six minute walk test. مؤشرات الموت في مرضى استرخاء القلب • • • • • نقص Naالدم عرض QRS ارتفاع مستوى النورابينفرين نقص LV EF % ارتفاع BNP SUMMARY AND RECOMMENDATIONS • Initial evaluation of patients with symptoms or signs suggestive of heart failure (HF) includes clinical assessment (history and physical exam), electrocardiogram, blood tests, and chest x-ray. • Early measurement of plasma BNP or NT proBNP levels is suggested in patients with suspected HF in whom the diagnosis is uncertain. • In patients with symptoms and signs of HF, echocardiography is useful for evaluating hemodynamics and identifying potential causes of HF.