Idea Transcript
Damianus Journal of Medicine; Prompt diagnosis and management of acute heart failure syndrome Vol.10 No.2 Juni 2011: hal. 91–96
TINJAUAN PUSTAKA
PROMPT DIAGNOSIS AND MANAGEMENT OF ACUTE HEART FAILURE SYNDROME Leonardo P. Suciadi*, Bambang B. Siswanto**
ABSTRACT Gagal jantung akut merupakan kondisi dengan gejala dan tanda gagal jantung yang terjadi dalam onset cepat, dan disebabkan oleh gangguan fungsi jantung baik itu disfungsi sistolik atau diastolic, gangguan katup akut, aritmia maupun ketidaksesuaian antara preload dengan afterload. Penyebabnya bisa berasal dari beragam mekanisme, namun kondisi ini merupakan kegawatdaruratan sehingga penting untuk segera dideteksi dan diberikan terapi yang tepat untuk menekan angka mortalitas dan morbiditas. Terdapat 7 profil klinis dari sindrom gagal jantung akut; acute decompensated heart failure (ADHF), edema pulmoner akut, syok kardiogenik, gagal jantung akut pada sindrom koroner akut, gagal jantung kanan terisolir, gagal jantung high-output dan gagal jantung hipertensif. Pengenalan profil klinis tersebut akan sangat penting dalam menentukan terapi yang tepat. Diagnosa dibuat berdasarkan anamnesa yang cermat, pemeriksaan fisik serta disokong dengan berbagai pemeriksaan penunjang seperti foto rontgen dada, ekokardiografi dan tes biomarker di laboratorium. Tujuan utama terapi adalah mengatasi gejala yang ada dan menstabilkan hemodinamik, terutama menjamin oksigenisasi serta perfusi jaringan.
*
Emergency & Trauma Center, Siloam Hospitals Kebun Jeruk). **
Departemen Kardiologi dan Vaskular Pusat Jantung Nasional Harapan Kita/Fakultas Kedokteran Universitas Indonesia)
Kata kunci: gagal jantung akut, profil klinis, diagnosis, terapi
INTRODUCTION Acute Heart Failure Syndrome (AHFS) is one of the most common cause of hospital admission in patients >65 years of age in USA, accounting for more than 1 million hospital admissions annually, with more than 6 millions hospital days, and it has risen 175% from 1979 to 2004.1 Approximately 80% of these patients initially present to the Emergency Department.2 Between 1992 and 2001, there were 10.5 million Emergency Department visits for AHFS in USA, with an admission rate of 70-80%.3 These numbers are projected to increase along with increasing number of elderly population, increasing success of management of myocardial infarction patients, advanced in long term treatment of patients with chronic heart failure.2,3 AHFS is an emergency condition that need early diagnosis and prompts treatment to cut down the morbidity and mortality. From a large Indonesia ADHERE (Acute Decompensated Heart Failure Registry) study 2006, the in-hospital mortality in 5 hospitals in Indonesia ranges from 6 % to 12% and the 4 years mortality is 50 %, with re-hospitalization rate is 29%.4 Primary care physicians, especially they who work at emer-
gency department, could play an important role to manage these patients at the time of hospital admission. Many conditions could mimic symptoms and signs of AHFS in daily practice, and recognizing early signs of AHFS is challenging. Knowing pathophysiology and clinical features as well as proper treatment of AHFS are mandatory at this point because failure to early diagnosis and prompt treatment will results in mortality. The aim of this manuscript is to describe how to diagnose and make early management of this syndrome. Acute heart failure syndrome Acute heart failure (AHF) is defined as a rapid onset in the signs and symptoms of HF, secondary to cardiac dysfunction whether it is related to systolic or diastolic dysfunction, cardiac arrhythmias, valvular abnormalities or preload-afterload mismatch. These diverse aetiologies often interact resulting to a life threatening condition that requires urgent treatment.5 AHF is not a disease but rather it is a syndrome caused by different mechanism, and it may be either new HF or worsening of pre-existing chronic HF. A number of common causes and precipitating factors of AHF can be seen at Table
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1. Generally, AHF could be induced by one or a combination of hemodynamic mechanisms including increased afterload due to systemic or pulmonary hypertension or high output states (septicemia, anemia, thyrotoxicosis); increased preload due to volume overload; decreased cardiac contractility due to significant infarct or other myopathies; or diastolic dysfunction.5,6 Identifying the underlying factor is very crucial in strategy to manage patients with AHF. Table 1. Several precipitating factors of AHF
genic shock.5 Data from ESC-HF Pilot Survey8 showed that acute decompensated HF was most frequent presentation of AHF (75% of the cases) in clinical setting. The patients presenting with cardiogenic shock have the worst short-term prognosis with the highest in-hospital mortality rate so that patients presenting with this clinical profile should be aggressively treated. Whereas, the lowest mortality rate is in those with hypertensive HF. Furthermore, there are three major independent determinants of death in AHF, those are low systolic blood pressure, older age, and reduced renal function.8 Drugs induced: NSAID, COX inhibitors, thizolidinediones
Ischaemic heart disease † Acute coronary syndromes
Decompensation of pre-existing chronic HF † Mechanical complications of acute MI † Lack of adherence † Right ventricular infarction † Volume overload Circulation failure † Infections, especially pneumonia † Septicaemia † Cerebrovascular insult – severe brain injury † Thyrotoxicosis † Major surgery † Anaemia † Renal dysfunction † Shunts † Asthma, COPD † Cardiac tamponade † Drug abuse † Pulmonary embolism † Alcohol abuse Valvular Hypertensive crisis † Valve stenosis or regurgitation Acute arrhythmia † Endocarditis Myopathies † Aortic dissection † Postpartum cardiomyopathy † Acute myocarditis Look into its pathophysiology, there are three phases of AHF; Initiation, amplification and final vicious cycle.6 The disturbance in hemodynamic processes leads to the genesis of the initial phase of AHF which comprises both backward failure (increased LV filling pressure lading to pulmonary congestion) and forward failure (peripheral hypoperfusion). This phase is marked as acute diastolic dysfunction on echocardiography. Once initiated, AHF is amplified through several mechanisms; myocardial necrosis as measured by troponin release (PRESERVD-HF study), respiratory failure and leakage of the alveolar-capillary membrane, RV failure, renal failure, and arrhythmias especially atrial tachyarrhythmias which is a strong predictor of recurrent events and death.7 Finally the patients fall into
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vicious cycle leading into severe cardiovascular failure with low cardiac output, hypoxemia, activated neurohormonal and inflammatory modulators, vasoconstriction, decreased peripheral perfusion, respiratory failure, and if untreated, multi-organ failure and death. The clinical presentation of AHF reflects a spectrum of conditions. Some classifications have been applied in order to giving guide how to manage every distinct presentation of AHF and also to predict prognosis of the patients. The patients with AHF will usually present in one of 7 clinical categories; worsening or acute decompensated chronic HF, pulmonary oedema, hypertensive heart failure, high output failure, AHF in acute coronary syndrome, isolated RV failure, and cardio-
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Prompt diagnosis and management of acute heart failure syndrome
Acute Coronary Syndromes is the commonest cause of acute new-onset HF. Other useful clinical classification of AHF after acute MI is the Killip-Kimball Class. Specifically, Killip class I patients had no evidence of heart failure; Killip class II patients had mild heart failure with rales involving one third or less of the posterior lung fields and systolic blood pressure of 90 mmHg or higher; Killip class III patients had pulmonary oedema with rales involving more than one third of the posterior lung fields and systolic blood pressure of 90 mm Hg or more; and Killip class IV patients had cardiogenic shock with any rales and systolic blood pressure of less than 90 mm Hg. In a multivariate analysis of patients after acute MI, higher Killip class was associated with higher mortality at 30 days (2.8% in Killip class I vs 8.8% in class II vs 14.4% in class III/IV; P 90%), these signs are not sensitive in many cases (< 40%).12 Hepatomegaly, ascites and bilateral pretibial-pedal pitting oedema are easily found, accompanying elevated JVP in decompensated chronic HF patients. Cool clammy periphery along with low systolic blood pressure and rapid-weak pulse suggest low perfusion. Arrhythmias detected by cardiac auscultation or pulse palpation are not uncommon.6 Some confirmatory investigations are needed in making diagnosis of AHF. Chest X-ray should be performed as soon as possible at admission for all patients with AHF to assess the degree of pulmonary congestion and to differentiate from other pulmonary or cardiac pathologies. Arterial blood gas analysis usually shows hypoxemia with metabolic acidosis. Pulse oximetry can be used for practical reason, but it does not provide information about pCO2 or acid-base status.5 Natriuretic peptides (BNP and NT-proBNP) are very useful in determining diagnosis and prognosis of patients with AHF. Increased natriuretic peptides value has a negative predictive value for ruling out HF. Generally, BNP cutoff 100 pg/mL can be used to rule out HF and cutoff 400 pg/mL to rule in HF. The higher BNP value, the worse prognosis of patients, so that more aggressive therapy should be made for these patients.13 Echocardiography with Doppler is an essential tool for
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the evaluation of the functional and structural changes underlying or associated with AHF. All patients with AHF should be evaluated as soon as possible.5 MANAGING PATIENTS WITH ACUTE HEART FAILURE SYNDROME The immediate goals of treatment in AHF are to improve symptoms and to stabilize haemodynamic condition especially oxygenation and tissue perfusion.5 Planning follow up strategy is needed in hospitalized patients and also long-term management if the acute episode leads to chronic HF. Initial treatment in AHF can be seen at Figure 2. Oxygen therapy and relieving patients' distress are the initial treatment at admission. Non-invasive ventilation with positive pressure (NIPPV) is recommended as soon as possible in every patients with respiratory distress caused by acute pulmonary oedema, but this respiratory assist should be used with caution in cardiogenic shock as haemodynamic compromises would worsen. Intubation and mechanical ventilation should be restricted to patients who is failed with NIPPV or with increased respiratory failure or exhaustion as assessed by hypercapnia.5 A specific treatment strategy should be based on distinguishing the clinical conditions. In acute decompensated HF condition, vasodilators along with loop diuretics are recommended. Higher dose of diuretics is usually needed. Morphine is usually indicated in patients with pulmonary oedema, along with loop diuretics and vasodilators. Lowering blood pressure with titrated vasodilators simply improve symptoms of patients with hypertensive HF. Fluid resuscitation is suggested along with inotropic agents to support patients with right HF. Patients with cardiogenic shock need more aggressive therapy including fluid challenge in small amount (250 mL) followed by an inotrope. An Intra-Aortic Balloon Pump (IABP) and intubation should be considered.5,6 Selecting agents according to systolic blood pressure can be seen at Figure 3.
Dam J Med Volume 10, Nomor 2, 2011
Prompt diagnosis and management of acute heart failure syndrome
Figure 2. Initial treatment algorithm in AHF Immediate symptomatic treatment
Patient distressed or in pain
> Analgesia, sedation (morphine)
> YES
> Medical therapy; diuretic, vasodilator
> YES
> Increase Fi02; consider NIPPV; mechanical ventilation
> No
> Antiarrhythmics, pacing, cardioversion
> YES
Pulmonary congestion
SaO2 < 95%
Normal heart rate and rhythm
NIPPV = Non-Invasive Positive Pressure Ventilator (adapted from ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Figure 3. AHP treatment strategy according to systolic blood pressure. Initial assessment; ABC supports
SBP > 100 mmHg
SBP - 100 mmHg
SBP < 100 mmHg
Vasodilator (NTG, Nitroprusside, Nesititide
Vasodilator and/or inotrope (dobutamine), PDEI
Good response: Stabilize and initiate diuretics, ACEI/ARB, beta-blockers
Fluid resuscitation; unotrope (dopamine)
Poor response: Inotrope, vasopressor, mechanical support
ABD = Aorway-Breathing Circulation; SBP = Systolic blood pressure; NTC = Nytroglilcerin; PDEI = Phosphodiesterase Inhibitor (adapted from ESC Guidelines for diagnosis and treatment of acute and chronic heart failure 2002) Table 3. Common used agents in AHF therapy Agent
Indication
Dose and administering
Diuretics:
Symptoms secondary to congestion and fluid overload
Initial bolus 20-40 mg i.v continued with infusion of 5-40 mg/h. Higher dose is consider in severe overload as long as the total dose 90 mmHg
Drip; start 1 mg/h, increase up to 10 mg/h. Drip 0.3-5 mcg/kg/min. Bolus 2 mcg/kg + drip 0.015-0.03 mcg/kg/min.
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Inotropes: Dobutamine Dopamine Norepinephrine
SBP 90-100 mmHg without shock syndrome. SBP < 90 mmHg with shock syndrome.
Drip; 2-20 mcg/kg/min Drip; 2-20 mcg/kg/min Drip; 0.2-1.0 mcg/kg/min
SBP < 70 mmHg with shock syndrome; sepsis complicating AHF.
CONCLUSION
6.
O'Connor CM, editors. Managing Acute Decompensated Heart Failure. New York: Taylor & Francis; 2005.
AHF is an emergency situation in cardiovascular requiring prompt clinical evaluation, early diagnosis and immediate intervention to cut down the morbidity and mortality rates. Because this is a common case found at primary care, recognizing its symptoms and signs along with proper treatment is important. Diagnosis can be made by careful history taking and physical examination, confirmed by Chest-x ray, echocardiography, laboratory test, and ECG. Furthermore, clinical profile of patients with AHF should be performed in order to make suitable strategy to manage the patients. The goals of initial therapy are to improve symptoms and stabilize haemodynamic by maintaining oxygenation and tissue perfusion as early as possible. Proper oxygen therapy, pharmacological agents and devices should be used to reach these goals.
7.
Benza RL, Tallaj JA, Felker GM, et al. The impact of arrhythmias in acute heart failure. J Card Fail.2004;10:279-84.
8.
Maggioni AP, Dahlstrom U, Filippatos G, et al: Heart Failure Association of the ESC (HFA). EURObservational Research Programme: The Heart Failure Pilot Survey (ESC-HF Pilot).Euro J of Heart Failure.2010:10/1093.
9.
Khot UN, Jia G, Moliterno DJ, et al. Prognostic importance of physical examination for heart failure in NonST-Elevation Acute Coronary Syndromes. JAMA.2003;290:2174-81.
11. Chizner MA. Current Problems in Cardiology: The Diagnosis of Heart Disease by Clinical Assesment Alone. St.Louis: Mosby; 2001.
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American Heart Association. Heart Disease and Stroke Statistics-2007 Update. American Heart Association, Dallas, TX, 2006.
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Rowe BH, editors. Evidence-Based Emergency Medicine. West Sussex: Blackwell; 2009.
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Hugli O, Braun JE, Kim S, Pelletier AJ, Camargo CA, Jr. United States emergency department visits for acute decompensated heart failure, 1992 to 2001. Am J Cardiol. 2005;96(11):1537-42.
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Siswanto BB, Radi B, Kalim H, et.al. Acute Decompensated Heart Failure in 5 hospitals in Indonesia. CVD Prevention and Control. 2010;5:35-8.
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Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J. 2008;29:2388-442.
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10. Fonarow GC. The Acute Decompensated Heart Failure National Registry (ADHERE): Opportunities to improve care of patients hospitalized with acute decompensated heart failure. Rev Cardiovasc Med. 2003; 4:21-30.
12. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting. J Am Coll Cardiol. 2001;37:379-85. 13. Peacock WF, Mueller C, DiSomma S, et al. Emergency Department Perspectives on B-Type Natriuretic Peptide Utility. Congestive Heart Failure Jour. 2008;14(4):17-20 14. Opie LH, Gersh BJ. Drugs for the Heart. 6th ed. Philadelphia: Saunders; 2005.
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