presentación falla cardiáca (resumen guias aha 2013)

Falla Cardiaca

Falla Cardiaca Lina Mara Botero Mora Medicina - Semestre VIIIUniversidad de AntioquiaRotacin Medicina Interna 2015-1

DefinicinSndrome clnico que ocurre en pacientes en los que, por una anomala hereditaria o adquirida en la estructura o funcin cardiaca, desarrollan una constelacin de sntomas (disnea y fatiga) y signos (edema y crpitos) que llevan a hospitalizaciones frecuentes, pobre calidad de vida y disminucin de la expectativa de vidaLongo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.HF is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and/ or splanchnic congestion and/or peripheral edema.Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Epidemiologa> 20 millones de pacientes en el mundo.Prevalencia adultos: 2% pases desarrollados.Edad: 6 10% >65 aos. > Hombres, (~50% mujeres)~50% FC con FE conservada.

Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.Problema en ascenso, que aumenta con los aos. Although the relative incidence of HF is lower in women than in men, women constitute at least one-half the cases of HF because of their longer life expectancyThe overall prevalenceof HF is thought to be increasing, in part because currenttherapies for cardiac disorders, such as myocardialinfarction (MI), valvular heart disease, and arrhythmias,are allowing patients to survive longer.

Although HFonce was thought to arise primarily in the setting of adepressed left ventricular (LV) ejection fraction (EF),epidemiologic studies have shown that approximatelyone-half of patients who develop HF have a normal orpreserved EF (EF 4050%). Accordingly, HF patientsare now broadly categorized into one of two groups:

Although survival has improved, the absolute mortality ratesfor HF remain approximately 50% within 5 years of diagnosis.3Etiologa

Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.Any condition that leads to an alteration in LV structure or function can predispose a patient to developing HF. Although the etiology of HF in patients with a preserved EF differs from that of patients with depressed EF, there is considerable overlap between the etiologies of these two conditions. In industrialized countries, coronary artery disease (CAD) has become the predominant cause in men and women and is responsible for 6075% of cases of HF. Hypertension contributes to the development of HF in 75% of patients, including most patients with CAD. Both CAD and hypertension interact to augment the risk of HF, as does diabetes mellitus.

In 2030% of the cases of HF with a depressed EF, the exact etiologic basis is not known. These patients are referred to as having nonischemic, dilated, or idiopathic cardiomyopathy if the cause is unknown ( Chap. 21 ).

Prior viral infection or toxin exposure (e.g., alcoholic or chemotherapeutic) also may lead to a dilated cardiomyopathy.

Moreover, it is becoming increasingly clear that a large number of cases of dilated cardiomyopathy are secondary to specific genetic defects, most notablythose in the cytoskeleton. Most forms of familial dilated cardiomyopathy are inherited in an autosomal dominant fashion. Mutations of genes that encode cytoskeletal proteins (desmin, cardiac myosin, vinculin) and nuclear membrane proteins (laminin) have been identified thus far. Dilated cardiomyopathy also is associated with Duchennes, Beckers, and limb-girdle muscular dystrophies.

Conditions that lead to a high cardiac output (e.g., arteriovenous fistula, anemia) are seldom responsible for the development of HF in a normal heart;4

Yelle D, Chaudhry S.McMasters Pathophysiology: Heart Failure. http://www.pathophys.org/heartfailure/ (accessed 15 February 2015).In contrast to the left ventricle, the right ventricle is thin-walled and highly compliant, and therefore adapts well to a wide range of filling volumes when working against a low pulmonary vascular resistance. However, it is quite susceptible to failure when there is a sudden increase in afterload, such as in left-sided heart failure (retrograde pressure transmission to the pulmonary circulation). Consequently, the most common cause of right-sided heart failure is left-sided heart failure. Although less common, isolated right heart failure does arise as a result of primary lung pathology and in such cases is referred to as cor pulmonale.5Fisiopatologa

Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.6

Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.

Mecanismos compensadores: la activacion (RAA) y del sistema nervioso adrenergico: Mantienen gasto cardiaco a traves del incrementoen la retencion de sal y agua incremento de la contractilidad miocardica. Activacion de la familia de vasodilatadores, lo que incluye a los peptidos auricular y encefalico natriureticos PNA y PNB, prostaglandinas (PGE2 y PGI2) y oxido nitrico (NO, nitric oxide), que evitan la vasoconstriccion periferica excesiva.

La disminucion del gasto cardiaco en pacientes con insuficiencia cardiaca produce disminucion de la carga de los barorreceptores de alta presion(circulos) en el ventriculo izquierdo, seno carotideo y arco aortico. Esta descarga de los barorreceptores perifericos conduce a la perdida del tono parasimpatico en el sistema nervioso central (SNC), con el resultado de un aumento generalizado en el tono simpatico eferente y liberacion no osmotica de arginina vasopresina (AVP) de la hipofisis (VC que aumenta permeabilidad de tubulo colector al agua, reabsorcin)

Estas senales aferentes al SNC tambien activan las vias eferentes del sistema nervioso simpatico que inerva en el corazon, rinones, vasos perifericos y musculo estriado. Riones: liberacion de renina, activa sistema RAA, su activacion aumenta reabs sodio y agua, genera VC vasos perifricos, hipertrofia miocrdica, muerte celular de miocitos y fibrosis miocrdica.Mecanismos neurohormonales facilitan la adaptacion a corto plazo al mantener la presion arterial y por tanto la irrigacion a organos vitales, pero se cree que estos mecanismos neurohormonales contribuyen a los cambios en organos terminales en el corazon y la circulacion y a la retencion excesiva de sal y agua en la insuficiencia cardiaca avanzada

Transicion a HF sintomatica se acompana de incremento en la activacion de los sistemas neurohormonales, adrenergicos y de citocinas que conducen a una serie de cambios adaptativos en el miocardio, que en conjunto se conocen como remodelacin del ventrculo izquierdo

El estimulo biologico para estos cambios profundos incluye tension mecanica del miocito, neurohormonas circulantes (p. ej., noradrenalina, angiotensina II), citocinas infl amatorias [p. ej., factor de necrosis tumoral (TNF, tumor necrosis factor)],7Fisiopatologa

Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.Disfuncin sistlicaDisfuncin diastlicaActivacion neurohormonal sostenida y la sobrecarga mecanica producen cambios transcripcionales que regulan la excitacion-contraccion y la interaccionen los puentes transversales de actina y mioscina.

Calcio disminucin en ATPasa de Calcio del reticulo sarcoplasmico, disminuye la captacin de calcio en el RE, permite la fuga de Calcio del reticulo.Actina: disminucin en expresin de ciertas cadenas de la actina lo que afecta la biologa del proceso de contraccin muscular, en conjunto menos contractilidad.

Disfuncin diastlica:Relajacin depende de ATP (se capta calcio en el sarcoplasma y necesitamos que salga tambien por el sarcolema), que disminye en la isquemia, lo que interfiere con la relajacin miocrdica.Fibrosis o hipertrofia tambien pueden disminuir la distensibilidad del ventrciloIncremento en la FC disminuye el volumen diastlico.Aumento de la rigidez cardiaca por aumento del colgeno..

8Remodelacin ventricular

Jessup M, Brozena S. Heart Failure.N Engl J Med 2003; 348:2007-2018Cambios en masa, forma y composicin del VI Lesin cardiaca agudaCargas hemodinmicas anormales.Desequilibrio funcional de la poscarga: Adelgazamiento pared + aumento poscarga = Vol sistlicoAumento tensin oxidativa+ ROSTensin msculos papilares, insuficiencia mitral.Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J.Harrison's Cardiovascular Medicine, 2nd ed. New York: McGraw Hill; 2013.Ademas de incrementar elvolumen telediastolico del LV, tambien ocurre adelgazamiento de la paredventricular izquierda conforme inicia la dilatacion del LV. El incrementoen el adelgazamiento parietal junto con el incremento en laposcarga creada por la dilatacion del ventriculo izquierdo conduce a undesequilibrio funcional de la poscarga9

Yelle D, Chaudhry S.McMasters Pathophysiology: Heart Failure. http://www.pathophys.org/heartfailure/ (accessed 15 February 2015).



Yelle D, Chaudhry S.McMasters Pathophysiology: Heart Failure. http://www.pathophys.org/heartfailure/ (accessed 15 February 2015).http://circ.ahajournals.org/content/128/16/e240.extract

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.HFpEF: Sntomas de HF. FE normal o preservada, disfuncin diastlica del LV documentada por ecocardiografa o cateterismo. Diagnstico ms dificil. more challenging than the diagnosis of HFrEF because it islargely one of excluding other potential noncardiac causes ofsymptoms suggestive of HF.

16Cmo ms clasificamos?

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Therapeutic interventions in each stageaimed at modifying risk factors (stage A), treating structuralheart disease (stage B), and reducing morbidity and mortality(stages C and D) (covered in detail in Section 7) are reviewedin this document. The17Factores de riesgoHipertensin (> mujeres hipertensas, HTA de larga data, cifras tensionales ms altas. Tto antiHTA 50%)Diabetes mellitus (Asociado adems a peor pronstico)Sndrome metablico (HiperTAG, obesidad abdominal, HDLc , HTA, hiperglucemia en ayunas)Pacientes con enfermedad ateroesclertica (coronaria, cerebral, priferica)

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.18Evaluacin inicialHC completa en todos los pacientes con sntomas de HF (desordenes cardiacos vs no cardiacos, presencia de factores que causen o precipiten) (I)Historia familiar de 3 generaciones en pacientes con DCM idioptica. (I)Tomar signos vitales SIEMPRE y tratar de determinar estado de balance hdrico (peso, PVJ, edema perifrico, ortopnea) (I)

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.19

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Evaluacin inicialRealizar clasificacin de riesgo de mortalidad del paciente segn el contexto IIa.Ambulatorio: Seattle Heart Failure Model (App en internet) Descompensacin: ADHERERiesgo de mortalidad pero NO de readmisin hospitalaria (PNA como marcador)


One well-validated risk score, the Seattle Heart FailureModel, is available in an interactive application on theInternet210 and provides robust information about risk of mortalityin ambulatory patients with HF. For patients hospitalizedwith acutely decompensated HF, the model developedby ADHERE

22Exmenes diagnsticosLaboratorios iniciales: Hemograma, uroanlisis, ionograma, BUN, creatinina, glucosa, perfil de lpidos en ayunas, funcin heptica y TSH (I)Monitoreo seriado de electrolitos sricos y funcin renal (I)EKG en la admisin del paciente. Hemocromatosis, HIV en pacientes seleccionados (IIa)Estudios para enf reumatolgicas, amiloidosis o feocromocitoma en pacientes con sospecha clnica (IIa)Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Initial laboratory evaluation of patients presentingwith HF should include complete blood count,

urinalysis, serum electrolytes (including calcium andmagnesium), blood urea nitrogen, serum creatinine,glucose, fasting lipid profile, liver function tests, andthyroid-stimulating hormone. (Level of Evidence: C)2. Serial monitoring, when indicated, should includeserum electrolytes and renal function. (Level ofEvidence: C)3. A 12-lead ECG should be performed initially on allpatients presenting with HFScreening for hemochromatosis or HIV is reasonablein selected patients who present with HF.216 (Level ofEvidence: C)2. Diagnostic tests for rheumatologic diseases, amyloidosis,or pheochromocytoma are reasonable inpatients presenting with HF in whom there is a clinicalsuspicion of these diseases. (Level of Evidence: C)23Biomarcadores

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.BNP or its amino-terminal cleavage equivalent (NT-proBNP) is derived from a common 108-amino acid precursor peptide (proBNP108) that is generated by cardiomyocytes in the context of numerous triggers, most notably myocardial stretch. Following several steps of processing, BNP and NT-proBNPare released from the cardiomyocyte, along with variable amounts of proBNP108, the latter of which is detected by all assays that measure either BNP or NT-proBNP.

Los peptidos natriureticos sirven para apoyar la el jucio clnico ante el diagnstico o la exclusin de la falla cardiaca, especialmente cuando la disnea no es de clara etiologa.

Although lower values of BNP or NT-proBNP exclude the presence of HF and higher values have reasonably high positive predictive value to diagnose HF, clinicians should be aware that elevated plasma levels for both natriuretic peptides have been associated with a wide variety of cardiac and noncardiacCauses

BNP and NT-proBNP levels improve with treatment of chronic HF,225,272274 with lowering of levels over time in general, correlating with improved clinical outcomes. Se ha estudiado guiar la terapia como por metas a traves de estos marcadores, pero los ensayos clinicos han demostrado resultados inconsistentes.

Biomarcadores de injuria miocardica: troponinas, por su alta correlacion con IAMFalla aguda24Imgenes no invasivas

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.RX 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.Eco: HF to assess ventricular function, size, wall thickness, wall motion, and valve function25Evaluacin invasiva

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Tratamiento

Etapa A ACCF/AHAControlar HTA y desordenes lipdicos segn las guas actuales (JNC8, ATP IV) (I)Otras comorbilidades que puedan llegar o contribuir a HF como obesidad, DM, uso de tabaco, consumo o exposicin a sustancias cardiotxicas deben ser controladas o evitadas. (I)Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Diureticbasedantihypertensive therapy has repeatedly been shown toprevent HF in a wide range of patients; ACE inhibitors, ARBs,and beta blockers are also effective. calcium antagonists and alpha blockers in reducing the riskfor incident HF.28Etapa B ACCF/AHA

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Todos: IECAS (o ARAs)Betabloqueadores Control de PA ojo con bloq Ca++ (ojo con Verapamilo y Diltiazem)

1. In all patients with a recent or remote history of MIor ACS and reduced EF, ACE inhibitors should beused to prevent symptomatic HF and reduce mortality.342344 In patients intolerant of ACE inhibitors,ARBs are appropriate unless contraindicated.314,345(Level of Evidence: A)2. In all patients with a recent or remote history of MIor ACS and reduced EF, evidence-based beta blockersshould be used to reduce mortality.346348 (Level ofEvidence: B)3. In all patients with a recent or remote history of MIor ACS, statins should be used to prevent symptomaticHF and cardiovascular events.104,349354 (Level ofEvidence: A)29Etapa C ACCF/AHATratamiento no farmacolgicoEducacin Consumo de lquidosEstimular ejercicio fsicoToma adecuada de medicamentos.Restriccin de la ingesta de sodio: para pacientes con HF sintomtica. 1500 mg/d Estadio A y B< 3g Estadio C y DManejo de SAHOS: Presin positiva continua nocturnaEjercicio (mejorar clase funcional) - Programas de rehabilitacin cardiaca



Diureticos de asa, preferidos. Diuretics: Selection of Patients. Diuretics shouldbe prescribed to all patients who have evidence of, and tomost patients with a prior history of, fluid retention. Diureticsshould generally be combined with an ACE inhibitor, betablocker, and aldosterone antagonist. Few patients with HF willbe able to maintain target weight without the use of diuretics.Generalmente se empieza en dosis bajas y se va subiendo (asegurando diuresis y perdida de peso 0,5-1 kg/d)

The combination of hydralazine and isosorbidedinitrate is recommended to reduce morbidity andmortality for patients self-described as AfricanAmericans with NYHA class IIIIV HFrEF receivingoptimal therapy with ACE inhibitors and betablockers, unless contraindicated.423,424 (Level ofEvidence: A)Class IIa1. A combination of hydralazine and isosorbide dinitratecan be useful to reduce morbidity or mortalityin patients with current or prior symptomaticHFrEF who cannot be given an ACE inhibitor orARB because of drug intolerance, hypotension, orrenal insufficiency, unless contraindicated.449 (Levelof Evidence: B)

Iecas reducen riesgo de muerte y hospitalizacion FX renal a los 15 diasOjo con PAS 3 potasio >5

Bisoprolol B1, carvedilol y metoprolol succinato alfa1 b1 y b2 de liberacion sostenida B1 ojo con signos vitales, cuadrar dosis despacioRetencion de liquidos y empeoramiento,, fatiga, bradicardia, bloqueo e hipotension

Aldosterone receptor antagonists (or mineralocorticoidreceptor antagonists) are recommended inpatients with NYHA class IIIV HF and who haveLVEF of 35% or less, unless contraindicated, toreduce morbidity and mortality. Patients with NYHAclass II HF should have a history of prior cardiovascularhospitalization or elevated plasma natriureticpeptide levels to be considered for aldosterone receptorantagonists. Creatinine should be 2.5 mg/dL or lessin men or 2.0 mg/dL or less in women (or estimatedglomerular filtration rate >30 mL/min/1.73 m2), andpotassium should be less than 5.0 mEq/L. Carefulmonitoring of potassium, renal function, and diureticdosing should be performed at initiation and closelyfollowed thereafter to minimize risk of hyperkalemiaand renal insufficiency.425,426,478 (Level ofEvidence: A)31

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.7.3.2.7.1. Digoxin: Selection of Patients. Clinicians may consideradding digoxin in patients with persistent symptoms ofHFrEF during GDMT Digoxin may also be added to the initialregimen in patients with severe symptoms who have notyet responded symptomatically during GDMT.Patients should not be given digoxin if they have significantsinus or atrioventricular block unless the block has beenaddressed with a permanent pacemaker. The drug should beused cautiously in patients taking other drugs that can depresssinus or atrioventricular nodal function or affect digoxin levels(eg, amiodarone or a beta blocker), even though such patientsusually tolerate digoxin without difficulty32

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.1. Calcium channelblocking drugs are not recommendedas routine treatment for patients withHFrEF.551,574,575 (Level of Evidence: A)By reducing peripheral vasoconstriction and LV afterload, calciumchannel blockers were thought to have a potential rolein the management of chronic HF. However, first-generationdihydropyridine and nondihydropyridine calcium channelblockers also have myocardial depressant activity.

Despite their greater selectivity for calciumchannels in vascular smooth muscle cells, second-generationcalcium channel blockers, dihydropyridine derivatives suchas amlodipine and felodipine, have failed to demonstrateany functional or survival benefit in patients with HF.533

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.HF con FE preservada estado C



Estado D ACCF/AHA


Paciente hospitalizadoFalla cardiaca descompensada.

Perfil del pacienteIgual proporcin de sexosHistoria de HTAOtras comorbolidades (ERC, hiponatremia, anomalas hematolgicas, EPOC)Igual proporcin de pacientes con HFpEF y HFrEF

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.such patients are elderly or near elderly, equally male or female,and typically have a history of hypertension, as well as othermedical comorbidities, including chronic kidney disease, hyponatremia,hematologic abnormalities, and chronic obstructivepulmonary disease.107,706,70871342

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Congestin/perfusin perifrica

RX trax, pptidos?43Cul fue la causa?SCA: EKG, troponinasOtrosFalta de adherencia al tratamiento o a la restriccin de sodio y lquidosHTA fuera de metasFA, otras arritmiasMedicamentos con efecto inotrpico negativo (verapamilo, diltiazem, nifedipino, betabloqueadores)TEPMedicamentos que aumentan la retencin de sodio: Esteroides, TZD, AINESInfeccionesOtras enfermedades cardiacas agudas

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Common Factors That Precipitate AcuteDecompensated HF Nonadherence with medication regimen, sodium and/orfluid restriction Acute myocardial ischemia Uncorrected high blood pressure AF and other arrhythmias Recent addition of negative inotropic drugs (eg, verapamil,nifedipine, diltiazem, beta blockers) Pulmonary embolus Initiation of drugs that increase salt retention (eg, steroids,thiazolidinediones, NSAIDs) Excessive alcohol or illicit drug use Endocrine abnormalities (eg, diabetes mellitus, hyperthyroidism,hypothyroidism) Concurrent infections (eg, pneumonia, viral illnesses) Additional acute cardiovascular disorders (eg, valve diseaseendocarditis, myopericarditis, aortic dissection)44Manejo del paciente descompensadoContinuar tratamiento crnico si el paciente est hemodinmicamente estable y no hay contraindicaciones.Si se van a iniciar betabloqueadores, solo hacerlo en el paciente estable, luego de haber mejorado la sobrecarga hdrica y haber descontinuado vasopresores e inotrpicos.

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Patients with HF admitted with evidence of significantfluid overload should be promptly treated withintravenous loop diuretics to reduce morbidity.737,738(Level of Evidence: B)2. If patients are already receiving loop diuretic therapy,the initial intravenous dose should equal or exceed theirchronic oral daily dose and should be given as eitherintermittent boluses or continuous infusion. Urine outputand signs and symptoms of congestion should be seriallyassessed, and the diuretic dose should be adjustedaccordingly to relieve symptoms, reduce volume excess,and avoid hypotension.739 (Level of Evidence: B)3. The effect of HF treatment should be monitored withcareful measurement of fluid intake and output, vitalsigns, body weight that is determined at the same timeeach day, and clinical signs and symptoms of systemicperfusion and congestion. Daily serum electrolytes,urea nitrogen, and creatinine concentrations shouldbe measured during the use of intravenous diuretics oractive titration of HF medications. (Level of Evidence: C)Class IIa1. When diuresis is inadequate to relieve symptoms, itis reasonable to intensify the diuretic regimen usingeither:a. higher doses of intravenous loop diuretics38,739(Level of Evidence: B); orb. addition of a second (eg, thiazide) diuretic.740743(Level of Evidence: B).

Intravenous loop diureticshave the potential to reduce glomerular filtration rate, furtherworsen neurohumoral activation, and produce electrolytedisturbances. Thus, although the use of diuretics may relievesymptoms, their impact on mortality has not been well studied.Diuretics should be administered at doses sufficient to achieveoptimal volume status and relieve congestion without inducingan excessively rapid reduction in intravascular volume,which could result in hypotension, renal dysfunction, or both.46

Yancy CW, et al. (2013). 2013 ACCF/AHA Guideline for the management ofheartfailure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 62(16): e147e239.Gracias!

presentación falla cardiáca (resumen guias aha 2013)

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