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Heart Failure: Difference between revisions
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==Introduction== | ==Introduction== | ||
[[File:Foxglove_(digitalis).png|thumb|150px|right| | [[File:Foxglove_(digitalis).png|thumb|150px|right|Foxglove (digitalis), used as a medicine for heart failure.]] | ||
===History=== | ===History=== | ||
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|'''''And''''' | |'''''And''''' | ||
*'''Signs typical of heart failure''' | *'''Signs typical of heart failure''' | ||
**Elevated jugular venous pressure **Hepatomegaly | **Elevated jugular venous pressure **Hepatomegaly | ||
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|'''''And''''' | |'''''And''''' | ||
*'''Objective evidence of a structural or functional abnormality of the heart at rest''' | *'''Objective evidence of a structural or functional abnormality of the heart at rest''' | ||
**Abnormal echocardiogram | **Abnormal echocardiogram | ||
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===Pathophysiology of heart failure=== | ===Pathophysiology of heart failure=== | ||
[[Image:frank_starling.svg|thumb|right|400px|Figure 1. Frank-Starling curve]] | [[Image:frank_starling.svg|thumb|right|400px|'''Figure 1.''' Frank-Starling curve]] | ||
[[Image:pressure_volume_curve.svg|thumb|400px|''Figure 2. Effects of decreased afterload. Red arrows indicate aortic valve opening, which occurs later and at higher LV systolic pressure when the diastolic aortic pressure is higher. Blue arrows indicate closing of the aortic valve. Bidirectional arrows represent stroke volume. When aortic pressure is decreased, stroke volume increases as a result of a lower aortic pressure during closure of the aortic valve.]] | [[Image:pressure_volume_curve.svg|thumb|400px|'''Figure 2.''' Effects of decreased afterload. Red arrows indicate aortic valve opening, which occurs later and at higher LV systolic pressure when the diastolic aortic pressure is higher. Blue arrows indicate closing of the aortic valve. Bidirectional arrows represent stroke volume. When aortic pressure is decreased, stroke volume increases as a result of a lower aortic pressure during closure of the aortic valve.]] | ||
[[Image:management_outline.svg|thumb|400px|Figure 3 | [[Image:management_outline.svg|thumb|400px|'''Figure 3.''' Management in heart failure.]] | ||
HF is caused by a loss of cardiac pump function, which can be due to a structural abnormality of the heart muscle (e.g. myocardial infarction) or a change in the heart function (and often structure) in response to an abnormal load (e.g. aortic valve stenosis). The relationship between loading the ventricle (by filling it) and its output was described by Frank and Starling in 1918 and has become the cornerstone in understanding heart failure and how to treat it. The relationship states that as a result of loading the heart (increasing its filling or its pressure), the output increases (Figure 1). A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens (LV dilatation and increased filling pressure) when the heart does not pump out enough volume, and, in the first phase of disease, compensates for the loss of contractility. It takes more energy from the heart to work at an increased loading, but the heart has a reasonable energy reserve. In a chronic situation, remodeling of the heart progresses (by hypertrophy of the myocytes and dilatation by increasing myocyte length and matrix changes), which, in the long term, leads to a further loss in function. The result of this dysfunction is further increased loading pressures in the heart and, by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded and leak water into the lungs. This is the practical restriction of further filling the heart as a tool to improve its function; even poor left ventricles may be filled more to increase their output <cite>6</cite> but the patients’ pulmonary capillaries cannot tolerate these hydrostatic pressures and start to leak water. | HF is caused by a loss of cardiac pump function, which can be due to a structural abnormality of the heart muscle (e.g. myocardial infarction) or a change in the heart function (and often structure) in response to an abnormal load (e.g. aortic valve stenosis). The relationship between loading the ventricle (by filling it) and its output was described by Frank and Starling in 1918 and has become the cornerstone in understanding heart failure and how to treat it. The relationship states that as a result of loading the heart (increasing its filling or its pressure), the output increases (Figure 1). A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens (LV dilatation and increased filling pressure) when the heart does not pump out enough volume, and, in the first phase of disease, compensates for the loss of contractility. It takes more energy from the heart to work at an increased loading, but the heart has a reasonable energy reserve. In a chronic situation, remodeling of the heart progresses (by hypertrophy of the myocytes and dilatation by increasing myocyte length and matrix changes), which, in the long term, leads to a further loss in function. The result of this dysfunction is further increased loading pressures in the heart and, by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded and leak water into the lungs. This is the practical restriction of further filling the heart as a tool to improve its function; even poor left ventricles may be filled more to increase their output <cite>6</cite> but the patients’ pulmonary capillaries cannot tolerate these hydrostatic pressures and start to leak water. | ||
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A standard blood assessment includes a complete blood count, electrolytes, renal function, glucose and liver function. Furthermore, urinalysis and other tests, depending on the clinical condition of the patient, complete the laboratory assessment. For example, cardiac troponins must be sampled if an ACS is in the differential diagnosis. In patients suspected of HF, values of natriuretic peptides (such as B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)) can provide important information regarding the diagnosis, management and prognosis of HF. Natriuretic peptides are enzymes, secreted by the atria or ventricles in response to myocardial wall stress. The most commonly used tests are BNP and NT-proBNP measurements, which despite their different half-lives in the plasma, do not differ substantially in terms of diagnostic ability. Cut-off values are different in acute settings with acute dyspnea compared to chronic settings. Normal values are almost 100% specific, and exclude heart failure in patients >18 year old. Abnormal values do not have a 100% predictive value, and objective evidence for heart failure is still needed. The values for BNP and NTproBNP are also used to evaluate the prognosis in patients with known HF, in whom higher values carry a worse prognosis. | A standard blood assessment includes a complete blood count, electrolytes, renal function, glucose and liver function. Furthermore, urinalysis and other tests, depending on the clinical condition of the patient, complete the laboratory assessment. For example, cardiac troponins must be sampled if an ACS is in the differential diagnosis. In patients suspected of HF, values of natriuretic peptides (such as B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)) can provide important information regarding the diagnosis, management and prognosis of HF. Natriuretic peptides are enzymes, secreted by the atria or ventricles in response to myocardial wall stress. The most commonly used tests are BNP and NT-proBNP measurements, which despite their different half-lives in the plasma, do not differ substantially in terms of diagnostic ability. Cut-off values are different in acute settings with acute dyspnea compared to chronic settings. Normal values are almost 100% specific, and exclude heart failure in patients >18 year old. Abnormal values do not have a 100% predictive value, and objective evidence for heart failure is still needed. The values for BNP and NTproBNP are also used to evaluate the prognosis in patients with known HF, in whom higher values carry a worse prognosis. | ||
[[Image:suspected_heart_failure.svg|thumb|400px|Figure 4 | [[Image:suspected_heart_failure.svg|thumb|400px|'''Figure 4.''' Flowchart suspected heart failure <cite>3</cite>]] | ||
===Exercise test=== | ===Exercise test=== | ||
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*Recommendation in favor of treatment or procedure being useful/effective | *Recommendation in favor of treatment or procedure being useful/effective | ||
*Some conflicting evidence from single randomized trial or non-randomized studies | | *Some conflicting evidence from single randomized trial or non-randomized studies | ||
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*Recommendation’s usefulness/efficacy less well established | *Recommendation’s usefulness/efficacy less well established | ||
*Greater conflicting evidence from single randomized trial or non-randomized studies | | *Greater conflicting evidence from single randomized trial or non-randomized studies | ||
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*Recommendation that procedure or treatment not useful/effective and may be harmful | *Recommendation that procedure or treatment not useful/effective and may be harmful | ||
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A flowchart for the treatment of patients presenting with systolic HF is depicted in Figure 5. Medications with a class I indication in patients with systolic heart failure are summarized in Table 5. Indications, mode of action, contraindications of the medication, and possible side effects of drugs included in this algorithm are discussed below. | A flowchart for the treatment of patients presenting with systolic HF is depicted in Figure 5. Medications with a class I indication in patients with systolic heart failure are summarized in Table 5. Indications, mode of action, contraindications of the medication, and possible side effects of drugs included in this algorithm are discussed below. | ||
[[Image:management_chronic_systolic_hf.svg|thumb|400px|Figure 5. Treatment options for patients with chronic systolic HF]] | [[Image:management_chronic_systolic_hf.svg|thumb|400px|'''Figure 5.''' Treatment options for patients with chronic systolic HF]] | ||
{| class="wikitable" border="1" cellpadding="1" cellspacing="1" width="600px" | {| class="wikitable" border="1" cellpadding="1" cellspacing="1" width="600px" | ||
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Possible side effects include hyperkalemia, hyponatremia, worsening renal function, and breast tenderness and/or enlargement. Eplerenon has less mastopathy side effects and is an alternative to spironolacton. In patients with severe heart failure, spironolactone in addition to standard therapy, reduces morbidity and mortality. <cite>20</cite> | Possible side effects include hyperkalemia, hyponatremia, worsening renal function, and breast tenderness and/or enlargement. Eplerenon has less mastopathy side effects and is an alternative to spironolacton. In patients with severe heart failure, spironolactone in addition to standard therapy, reduces morbidity and mortality. <cite>20</cite> | ||
[[Image:Henle_loop.svg|thumb|400px|Figure 6. Diuretics and site of action in the nephron.]] | [[Image:Henle_loop.svg|thumb|400px|'''Figure 6.''' Diuretics and site of action in the nephron.]] | ||
===Choice and combination of diuretics=== | ===Choice and combination of diuretics=== | ||
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The H-ISDN combination acts by decreasing peripheral vascular resistance. | The H-ISDN combination acts by decreasing peripheral vascular resistance. | ||
Possible side effects include symptomatic hypotension or drug-induced lupus-like syndrome. | Possible side effects include symptomatic hypotension or drug-induced lupus-like syndrome. | ||
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When severe symptoms of heart failure quickly develop over time, it is termed acute heart failure. In Table 6, common acute HF medications and their recommended doses are summarized. In Figure 7, a flowchart for the treatment of acute HF is depicted. The mainstay of acute heart failure therapy includes diuretics, vasodilators, inotropics and vasopressors. Moreover, oxygen and morphine can be added. | When severe symptoms of heart failure quickly develop over time, it is termed acute heart failure. In Table 6, common acute HF medications and their recommended doses are summarized. In Figure 7, a flowchart for the treatment of acute HF is depicted. The mainstay of acute heart failure therapy includes diuretics, vasodilators, inotropics and vasopressors. Moreover, oxygen and morphine can be added. | ||
[[Image:acute_hf_flowchart.svg|400px|thumb|Figure 7. Flowchart acute HF.]] | [[Image:acute_hf_flowchart.svg|400px|thumb|'''Figure 7.''' Flowchart acute HF.]] | ||
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==Management of HF beyond medication== | ==Management of HF beyond medication== | ||
[[Image:CRT_flowchart.svg|thumb|400px|Figure 8. flowchart CRT | [[Image:CRT_flowchart.svg|thumb|400px|'''Figure 8.''' flowchart CRT]] | ||
===Device treatment=== | ===Device treatment=== | ||
Prevention of sudden death is an important goal in HF because approximately half of the deaths occur suddenly, and many of these are related to ventricular arrhythmias. Implantable cardioverter-defibrillator (ICD) therapy is recommended in survivors of cardiac arrest , irrespective of EF, when life expectancy is >1 year. (Class I recommendation, level of evidence A). | Prevention of sudden death is an important goal in HF because approximately half of the deaths occur suddenly, and many of these are related to ventricular arrhythmias. Implantable cardioverter-defibrillator (ICD) therapy is recommended in survivors of cardiac arrest , irrespective of EF, when life expectancy is >1 year. (Class I recommendation, level of evidence A). | ||
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===Heart transplantation and Left Ventricular Assist Devices=== | ===Heart transplantation and Left Ventricular Assist Devices=== | ||
When a patient has severe and progressive HF, his or her prognosis is grim. Considering the paucity of donor hearts, the waiting list for heart transplantation may be long and early consideration of heart transplantation is part of the treatment strategy in HF. Average 2-year survival rates after cardiac transplantation are approximately 80%. A patient in NYHA class III should be evaluated with an exercise test for maximal oxygen uptake, in order to consider further steps. Indication for heart transplantation includes a VO<sub>2max</sub> < 14 ml/min/kg.<cite>17</cite> Exclusion criteria are pulmonary hypertension (risk of immediate RV donor failure), severe comorbidity, and diabetes mellitus with organ damage. Left Ventricular Assist Devices are more commonly used as a bridge to transplantation, when the patient in on a waiting list. They have evolved from pulsatile to continuous flow pumps, with less complications and a longer durability. Often Left Ventricular Assist Devices become destination therapy. | When a patient has severe and progressive HF, his or her prognosis is grim. Considering the paucity of donor hearts, the waiting list for heart transplantation may be long and early consideration of heart transplantation is part of the treatment strategy in HF. Average 2-year survival rates after cardiac transplantation are approximately 80%. A patient in NYHA class III should be evaluated with an exercise test for maximal oxygen uptake, in order to consider further steps. Indication for heart transplantation includes a VO<sub>2max</sub> < 14 ml/min/kg.<cite>17</cite> | ||
[[Image:HF_prognosis_trials.svg|thumb|right|400px|'''Figure 9.''' Two-year mortality in landmark contemporary clinical heart failure trials (from Cleland et al)]] | |||
Exclusion criteria are pulmonary hypertension (risk of immediate RV donor failure), severe comorbidity, and diabetes mellitus with organ damage. Left Ventricular Assist Devices are more commonly used as a bridge to transplantation, when the patient in on a waiting list. They have evolved from pulsatile to continuous flow pumps, with less complications and a longer durability. Often Left Ventricular Assist Devices become destination therapy. | |||
===Management of HF patients with preserved LVEF (HFPEF)=== | ===Management of HF patients with preserved LVEF (HFPEF)=== | ||