Heart failure_ac1913ae315a48271b58f2feb9e01f98.pdf

Heart failure (HF) ILOs At the end of this session, the student will be able to:  Define HF and its etiology and pathophysiology.  Identify types of HF.  Identify signs and symptoms of HF.  Identify the management plan of HF. Definition HF is a clinical syndrom...

Heart failure (HF) ILOs At the end of this session, the student will be able to:  Define HF and its etiology and pathophysiology.  Identify types of HF.  Identify signs and symptoms of HF.  Identify the management plan of HF. Definition HF is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles, and peripheral oedema) caused by a structural and/or functional cardiac abnormality. Terminology A. Terminology related to the left ventricular ejection fraction (LVEF): Traditionally, HF has been divided into distinct phenotypes based on the measurement of left ventricular ejection fraction (LVEF) 1. HF with reduced EF (HFrEF): Reduced LVEF is defined as _50%, have HFpEF. B. Right ventricular dysfunction: Heart failure can also be a result of right ventricular (RV) dysfunction. RV mechanics and function are altered in the setting of either pressure or volume overload. Although the main etiology of chronic RV failure is LV dysfunction- induced pulmonary hypertension, there are a number of other causes of RV dysfunction (e.g. myocardial infarction, arrhythmogenic right ventricular cardiomyopathy (ARVC), or valve disease). 1 C. Terminology related to the time course of HF: 1. "Acute HF" The term is used to mean rapid and sudden onset. 2. "Chronic HF" CHF describes those who have had an established diagnosis of HF or who have a more gradual onset of symptoms. 3. " Decompensated HF" If CHF deteriorates, either suddenly or slowly, the episode may be described as ‘decompensated’ HF. 4. "Stable HF" A treated patient with symptoms and signs that have remained generally unchanged for at least 1 month is said to be stable HF. 5. "Congestive HF" is a term that is sometimes used and may describe acute or chronic HF with evidence of volume overload. Epidemiology and prognosis The prevalence of HF is approximately 1–2% of the adult population in developed countries, the prevalence increases with age: from around 1% for those aged 10% in those aged 70 years or over. Patients with heart failure have a poor prognosis, with high rates of hospital admission and mortality, with a mortality rate ranges from 6–7% per year in patients with stable heart failure to 25% or more per year in patients admitted to hospital with acute heart failure. Etiology of heart failure: In Western-type and developed countries, coronary artery disease (CAD) and hypertension are predominant factors. The most common causes of heart failure are: A. Diseased myocardium B. Abnormal loading conditions C. Arrhythmias A. Diseased myocardium: 1. Coronary artery disease 2. Cardiomyopathy: (Dilated, hypertrophic, restrictive, ARVC, peripartum, Takotsubo syndrome, toxins {e.g. Alcohol, cocaine, iron, copper}) 3. Endomyocardial disease (Endomyocardial fibrosis/eosinophilia, radiotherapy, carcinoid) 4. Drug induced: Anthracyclines, Trastuzumab, vascular endothelial growth factor inhibitors, Proteasome inhibitors, antidepressant drugs, antiarrhythmics, non- steroidal anti-inflammatory drugs, and anesthetics. 2  5. Infectious: Viral myocarditis, bacteria, spirochaetes, fungi, protozoa, parasites (Chagas disease), rickettsiae. 6. Noninfectious: giant cell myocarditis, autoimmune diseases (e.g. Graves’ disease, rheumatoid arthritis, connective tissue disorders, mainly systemic lupus erythematosus), hypersensitivity and eosinophilic myocarditis 7. Infiltration (malignancy, amyloidosis, sarcoidosis) 8. Storage diseases (glycogen storage diseases, hemochromatosis, Fabry disease) 9. Endocrinal disorders (thyroid disease, parathyroid disease, acromegaly hypercalcemia, Addison disease, diabetes, metabolic syndrome, phaeochromocytoma) 10. Nutritional disease (thiamine, vitamin B1 and selenium deficiencies) 11. Neuromuscular disease (Friedreich’s ataxia, muscular dystrophy). B. Abnormal loading conditions: 1. Hypertension 2. Valvular diseases (Primary valve disease, secondary valve disease, congenital valve disease) 3. Congenital defects (shunt defects, congenitally corrected/repaired transposition of great arteries, repaired tetralogy of Fallot, Ebstein’s anomaly) 4. Pericardial disease (pericardial effusion, and constrictive pericarditis, infiltrative). C. Arrhythmias 1. Atrial tachyarrhythmia 2. Ventricular tachyarrhythmia Pathophysiology of Heart Failure There are several compensatory mechanisms that occur as the failing heart attempts to maintain adequate function, most important among the adaptations are the followings as shown in figure 1. 3  Figure 1: Neurohormonal derangement in heart failure Chronic heart failure Key steps in the diagnosis of chronic heart failure A. presence of symptoms and/or signs of HF B. Essential initial investigations C. Investigations to determine the underlying aetiology of chronic heart failure. A. Symptoms and signs A detailed history should always be obtained. HF is unusual in an individual with no relevant medical history, the symptoms and signs of heart failure are necessary but not sufficient for its diagnosis. B. Essential initial investigations 1. Laboratory tests:  Basic investigations such as serum urea and electrolytes, creatinine, full blood count, liver, thyroid function tests, transferrin saturation, and ferritin levels.  Natriuretic peptides (NPs): The plasma concentration of natriuretic peptides; brain natriuretic peptide (BNP) or the N-terminal prohormone of BNP (NT- proBNP) can be used as an initial diagnostic test, especially in the non-acute setting when echocardiography is not immediately available. 4 2. 12-lead ECG is recommended in all patients with HF in order to determine heart rhythm, heart rate, QRS morphology, and QRS duration, and to detect other relevant abnormalities. 3. Chest radiography (X-ray) is recommended in patients with HF to detect/exclude alternative pulmonary or other diseases, which may contribute to dyspnea. It may also identify pulmonary congestion/oedema and is more useful in patients with suspected HF in the acute setting. 4. Echocardiography is recommended for the assessment of myocardial structure and function in subjects with suspected HF in order to establish a diagnosis of either HFrEF, HFmrEF or HFpEF. C. Investigations to determine the underlying aetiology of chronic heart failure Which can include cardiac magnetic resonance (CMR), Invasive coronary angiography, Computed tomography coronary angiography (CTCA), cardiopulmonary exercise testing, right heart catheterization and endomyocardial biopsy. Treatment of HF. A. Treatment of patients with HFpEF B. Treatment of patients with HFmrEF C. Treatment of patients with HFrEF A. Treatment of patients with HFpEF 1. Screening for, and treatment of, aetiologies, and cardiovascular and non- cardiovascular comorbidities is recommended. 2. Diuretics are recommended in congested patients. B. Treatment of patients with HFmrEF 1. It is recommended to screen patients for both cardiovascular and non- cardiovascular comorbidities, which if present, should be treated. 2. Diuretics are recommended in congested patients in order to alleviate symptoms and signs. (class I) 3. An ACE-I, an ARB , a beta-blocker, an MRA , and Sacubitril/valsartan may be considered for patients with HFmrEF to reduce the risk of HF hospitalization and death.(class IIb) 5  C. Treatment of patients with HFrEF i. Pharmacological treatments ii. Device treatment iii. Surgical treatment i. Pharmacological treatment of patients with HFrEF Pharmacotherapy is the cornerstone of treatment for HFrEF and should be implemented before considering device therapy, and alongside non- pharmacological interventions. A. Drugs recommended in all patients with heart failure with HFrEF: 1. Angiotensin-converting enzyme inhibitors (ACEIs)  ACE-Is were the first class of drugs shown to reduce mortality and morbidity in patients with HFrEF.  They are recommended unless contraindicated or not tolerated in all symptomatic patients.  ACEIs should be up-titrated to the maximum tolerated dose in order to achieve adequate inhibition of the renin–angiotensin–aldosterone system. 2. Beta-blockers  Betablockers is recommended, in addition ACEIs, for patients with stable symptomatic HFrEF to reduce mortality and morbidity.  Betablockers should be initiated in clinically stable, euvolemic patients at a low dose and gradually up titrated to the maximum tolerated dose.  Bisoprolol, carvedilol, metoprolol succinate, and nebivolol are the beta-blockers recommended in HF patient. 3. Mineralocorticoid receptor antagonists (MRA)  MRAs (spironolactone or eplerenone) are recommended, in addition to an ACE-I and a beta-blocker, in all patients with HFrEF to reduce mortality and the risk of HF hospitalization.  Caution should be exercised when MRAs are used in patients with impaired renal function and in those with serum potassium levels ˃5.0 mmol/L. 6  4. Angiotensin receptor neprilysin inhibitor (ARNI)  Sacubitril/valsartan in fixed dose combination is recommended as a replacement for an ACE-I to further reduce the risk of HF hospitalization and death in ambulatory patients with HFrEF who remain symptomatic despite optimal treatment with an ACEIs or ARB, a beta-blocker and an MRA  Sacubitril (neprilysin inhibitor) by inhibiting neprilysin, the degradation of NPs, bradykinin and other peptides is slowed. High circulating A-type natriuretic peptide (ANP) and BNP exert physiologic effects through binding to NP receptors, thereby enhancing diuresis, natriuresis and myocardial relaxation. 5. Sodium-glucose co-transporter 2 inhibitors (SGLT2 inhibitor) – Dapagliflozin or empagliflozin are recommended for patients with HFrEF to reduce the risk of HF hospitalization and death. – SGLT2 inhibitors enhance the natriuresis and stimulate the osmotic diuresis by inhibiting SGLT2 in the proximal tubule of the kidney. – The diuretic/ natriuretic properties of SGLT2 inhibitors may offer additional benefits in reducing congestion and may allow a reduction in loop diuretic requirement. B. Other treatments recommended in selected symptomatic patients with HFrEF 1. Diuretics  The aim of diuretic therapy is to achieve and maintain euvolaemia with the lowest achievable dose.  Loop diuretics produce a more intense and shorter dieresis than thiazides, although they act synergistically, and the combination may be used to treat resistant oedema. 2. Angiotensin II type 1 receptor blockers(ARBs) The place of ARBs in the management of HFrEF has changed over the last few years. They are now recommended for patients who cannot tolerate ACE-I or ARNI because of serious side effects. 3. If-channel inhibitor  Ivabradine should be considered to reduce the risk of HF hospitalization and cardiovascular death in symptomatic patients with LVEF ≤35%, in sinus rhythm and a resting heart rate 70 bpm despite treatment with an evidence-based dose 7  of beta blocker (or maximum tolerated dose below that) , or who are unable to tolerate or have contra-indications for a beta-blocker. To reduce the risk of HF hospitalization and CV death. Patients should also receive an ACE-I (orARNI) and an MRA.  Ivabradine slows the heart rate through inhibition of the If channel in the sinus node and therefore should only be used for patients in sinus rhythm. 4. Combination of hydralazine and isosorbide dinitrate In a fixed dose combination should be given in self-identified black patients with HFrEF and in NYHA Class III–IV despite treatment with an ACEIs a beta- blocker and an MRA to reduce the risk of HF hospitalization and death. 5. Digoxin  Digoxin may be considered in symptomatic patients in sinus rhythm despite treatment with an ACE-I (or ARB), a beta-blocker and an MRA, to reduce the risk of hospitalization.  In patients with symptomatic HF and AF, digoxin may be useful for the treatment of patients. C. Treatments not recommended in symptomatic patients with HFrEF  Thiazolidinediones (glitazones), NSAIDs or COX-2 inhibitors, non- Dihydropyridines calcium channel blockers (e.g., Diltiazem or verapamil), the addition of an ARB to the combination of an ACE-I and an MRA. ii. Device treatment in patients with HFrEF  Implantable cardioverter-defibrillator (ICD): An ICD is recommended to reduce the risk of sudden death in patients who have recovered from a ventricular arrhythmia causing haemodynamic instability.  Cardiac resynchronization therapy (CRT): CRT is recommended for symptomatic patients with HF in sinus rhythm with a QRS duration of 130 msec and LBBB QRS morphology and with LVEF ≤35% despite OMT in order to improve symptoms and reduce morbidity and mortality.  Short-term Mechanical circulatory support (MCS): Short-term MCS devices are indicated to reverse critical end organ hypoperfusion and hypoxia in the setting of cardiogenic shock. Short-term MCS should be used as a bridge to decision (BTD), bridge to recovery (BTR), bridge to bridge (BTB) for either long-term MCS or urgent heart transplantation. 8   Long-term Mechanical circulatory support(MCS): is recommended for patients with advanced HF despite optimal medical/ device therapy, Patients being considered for long-term MCS must have good compliance, appropriate capacity for device handling and psychosocial support. iii. Surgical treatment – Aortic valve replacement whether surgical (SAVR) or transcatheter (TAVI) for aortic stenosis, TEE mitral valve repair for mitral regurgitation, or coronary artery bypass graft(CABG) for coronary artery disease – Cardiac transplantation is recommended for patients with advanced HF, refractory to medical/ device therapy and who do not have absolute contraindications. Acute heart failure (AHF) Definition AHF refers to rapid or gradual onset of symptoms and/or signs of HF, severe enough for the patient to seek urgent medical attention, leading to an unplanned hospital admission or an emergency department visit. Causes and factors triggering acute heart failure.  Acute coronary syndrome.  Excessive rise in blood pressure.  Infection (e.g. pneumonia, infective endocarditis, sepsis).  Tachyarrhythmias (atrial fibrillation, ventricular tachycardia)  Non-adherence to diet/drug therapy  Toxic substances (alcohol, recreational drugs).  Drugs (e.g. NSAIDs, corticosteroids, negative inotropic substances, cardiotoxic chemotherapeutics).  Exacerbation of chronic obstructive pulmonary disease.  Pulmonary embolism.  Surgery and perioperative complications.  Increased sympathetic drive, stress-related cardiomyopathy.  Metabolic/hormonal derangements (e.g. thyroid dysfunction, diabetic ketosis, adrenal dysfunction, pregnancy and peripartum related abnormalities).  Cerebrovascular insult. 9   Acute mechanical cause: myocardial rupture complicating acute coronary syndrome (free wall rupture, ventricular septal defect, acute mitral regurgitation), chest trauma or cardiac intervention, acute native or prosthetic valve incompetence secondary to endocarditis, aortic dissection or thrombosis. Diagnosis and approach to patient with AHF Symptoms and signs: It is recommended that initial diagnosis of AHF should be based on a thorough history assessing symptoms, prior cardiovascular history and potential cardiac and non-cardiac precipitants, as well as on the assessment of signs/symptoms of congestion and/or hypoperfusion by physical examination and further confirmed by appropriate additional investigations.  Symptoms/signs of congestion Orthopnoea, paroxysmal nocturnal dyspnoea, pulmonary rales (bilateral), peripheral oedema  Symptoms/signs of hypoperfusion: Clinical: cold sweated extremities, oliguria, mental confusion, dizziness, narrow pulse pressure. Laboratory measures: metabolic acidosis, elevated serum lactate, elevated serum creatinine. Hypoperfusion is not synonymous with hypotension, but often hypoperfusion is accompanied by hypotension. Careful clinical evaluation needs to be followed by these additional investigations:  Chest X-ray can be a useful test for the diagnosis of AHF. Pulmonary venous congestion, pleural effusion, interstitial or alveolar oedema and cardiomegaly are the most specific findings for AHF, although in up to 20% of patients with AHF, chest X-ray is nearly normal. Chest X-ray is also useful to identify alternative non-cardiac diseases that may cause or contribute to the patient’s symptoms (i.e. pneumonia, non- consolidative pulmonary infections).  ECG is rarely normal in AHF, it is also helpful in identifying underlying cardiac disease and potential precipitants (rapid AF, acute myocardial ischaemia).  Immediate echocardiography is mandatory only in patients with haemodynamic instability (particularly in cardiogenic shock) and in patients suspected of acute life- threatening structural or functional cardiac abnormalities (mechanical complications, acute valvular regurgitation, and aortic dissection). 10  Natriuretic peptides. should be measured in all patients with acute dyspnoea and suspected AHF to help in the differentiation of AHF from non-cardiac causes of acute dyspnoea.( thresholds: BNP ,100 pg/mL, NT-proBNP ,300 pg/mL).  Laboratory assessments in the blood: cardiac troponins, urea, creatinine, electrolytes (sodium, potassium), glucose, complete blood count, liver function tests and TSH. Treatment of AHF 1. Identification of precipitants/causes leading to decompensation that needs urgent management. 2. Criteria for hospitalization in ward vs. intensive care/coronary care unit. The criteria for ICU/CCU admission include any of the following: – Need for intubation (or already intubated) – Signs/symptoms of hypoperfusion – Oxygen saturation (SPO2) ≤90% (despite supplemental oxygen) – Use of accessory muscles for breathing, respiratory rate 25/min – Heart rate≤40 or130 bpm, SBP≤90 mmHg. 3. Standard non-invasive monitoring of heart rate, rhythm, respiratory rate, oxygen saturation and blood pressure is recommended in all patients with AHF. 4. Management of the early phase Oxygen therapy and/or ventilatory support  Oxygen therapy is recommended in patients with AHF and SpO2