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===Heart catheterization=== | ===Heart catheterization=== | ||
Heart catheterization is not always part of the routine diagnosis and work-up of patients with HF. It should be considered however to exclude coronary heart disease (Class of recommendation IIa, level of evidence C, see Table 4). Coronary angiography is recommended in patients at high risk of coronary artery disease (Class of recommendation I, level of evidence C) and in HF patients with significant valvular disease (Class of recommendation IIa, level of evidence C). | Heart catheterization is not always part of the routine diagnosis and work-up of patients with HF. It should be considered however to exclude coronary heart disease (Class of recommendation IIa, level of evidence C, see [[Heart_Failure_Table_4|Table 4]]). Coronary angiography is recommended in patients at high risk of coronary artery disease (Class of recommendation I, level of evidence C) and in HF patients with significant valvular disease (Class of recommendation IIa, level of evidence C). | ||
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==Etiology of heart failure== | ==Etiology of heart failure== | ||
===Coronary heart disease=== | ===Coronary heart disease=== | ||
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Deficiency of thiamine, selenium, or camitine, in states of severe cachexia. | Deficiency of thiamine, selenium, or camitine, in states of severe cachexia. | ||
Infiltrative and storage disorders | ===Infiltrative and storage disorders=== | ||
*Sarcoidosis | *[[Sarcoidosis]] | ||
*Amyloidosis | *[[Amyloidosis]] | ||
*Haemochromatosis | *[[Haemochromatosis]] | ||
*Connective tissue disease | *Connective tissue disease | ||
===Infectious disease=== | ===Infectious disease=== | ||
*Chagas’ disease | *[[Chagas’ disease]] | ||
*HIV infection | *[[HIV infection]] | ||
*Viral, bacterial or protozoal diseases causing myocarditis. | *Viral, bacterial or protozoal diseases causing myocarditis. | ||
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|bgcolor="99FFCC" align="center"|'''Aldosteron antagonist''' | |bgcolor="99FFCC" align="center"|'''Aldosteron antagonist''' | ||
|bgcolor="99FFCC"| | |bgcolor="99FFCC"| | ||
|bgcolor="9ACD32" align="center"|'''EF | |bgcolor="9ACD32" align="center"|'''EF < 35%''' | ||
|bgcolor="9ACD32" align="center"|'''EF | |bgcolor="9ACD32" align="center"|'''EF < 35%''' | ||
|bgcolor="9ACD32" align="center"|'''EF | |bgcolor="9ACD32" align="center"|'''EF < 35%''' | ||
|- | |- | ||
|bgcolor="99FFCC" align="center"|'''Nitrate / Hydralazine''' | |bgcolor="99FFCC" align="center"|'''Nitrate / Hydralazine''' | ||
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|bgcolor="9ACD32" align="center"|'''Afro-American''' | |bgcolor="9ACD32" align="center"|'''Afro-American''' | ||
|bgcolor="9ACD32" align="center"|'''Afro-American''' | |bgcolor="9ACD32" align="center"|'''Afro-American''' | ||
|- | |||
|bgcolor="99FFCC" align="center"|'''Ivabradine''' | |||
|bgcolor="99FFCC"| | |||
|bgcolor="9ACD32" align="center"|'''SR>75/min & EF<35%''' | |||
|bgcolor="9ACD32" align="center"|'''SR>75/min & EF<35%''' | |||
|bgcolor="9ACD32" align="center"|'''SR>75/min & EF<35%''' | |||
|- | |- | ||
|bgcolor="99FFCC" align="center"|'''Digoxin''' | |bgcolor="99FFCC" align="center"|'''Digoxin''' | ||
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===Angiotensin-converting enzyme (ACE) inhibitors=== | ===Angiotensin-converting enzyme (ACE) inhibitors=== | ||
An ACE inhibitor | An ACE inhibitor is indicated for every patient with symptomatic systolic HF and an EF ≤40 % (NYHA class II-IV). (Class I recommendation, level of evidence A) Contraindications for the use of ACE inhibitors are: | ||
*History of angioedema | *History of angioedema | ||
*Bilateral renal artery stenosis | *Bilateral renal artery stenosis | ||
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===Diuretics (Loop of Henle diuretics, Thiazides, Aldosterone antagonists)=== | ===Diuretics (Loop of Henle diuretics, Thiazides, Aldosterone antagonists)=== | ||
[[Image:Henle_loop.svg|thumb|400px|'''Figure 6.''' Diuretics and site of action in the nephron.]] | |||
Diuretics reduce preload by venous vasodilatation and by increasing diuresis. As a result, filling pressures of the heart and the lung vasculature decrease. Although the effects of diuretics on mortality and morbidity have not been studied in patients with HF (irrespective of EF), it is recommended in patients with signs and symptoms of congestion as diuretics relieve dyspnea and edema. Figure 6 depicts the nephron and the sites where different diuretics work. | Diuretics reduce preload by venous vasodilatation and by increasing diuresis. As a result, filling pressures of the heart and the lung vasculature decrease. Although the effects of diuretics on mortality and morbidity have not been studied in patients with HF (irrespective of EF), it is recommended in patients with signs and symptoms of congestion as diuretics relieve dyspnea and edema. Figure 6 depicts the nephron and the sites where different diuretics work. | ||
===Loop of Henle diuretics=== | ====Loop of Henle diuretics==== | ||
Loop of Henle diuretics act on the ascending loop of Henle in the kidney tubules to inhibit sodium and chloride (and indirectly calcium and magnesium) reabsorption. This will ultimately result in increased urine production of sodium and water. Compared to thiazides, loop diuretics produce a more intense and shorter diuresis. | Loop of Henle diuretics act on the ascending loop of Henle in the kidney tubules to inhibit sodium and chloride (and indirectly calcium and magnesium) reabsorption. This will ultimately result in increased urine production of sodium and water. Compared to thiazides, loop diuretics produce a more intense and shorter diuresis. | ||
===Thiazides=== | ====Thiazides==== | ||
Thiazide increases urine production by decreasing reabsorption of sodium in the distal tubule. This type of diuretic is often used in combination with loop diuretics to enhance their effects, but may be less effective in patients with a severely reduced kidney function. | Thiazide increases urine production by decreasing reabsorption of sodium in the distal tubule. This type of diuretic is often used in combination with loop diuretics to enhance their effects, but may be less effective in patients with a severely reduced kidney function. | ||
===Aldosterone antagonists=== | ====Aldosterone antagonists==== | ||
Adding this drug is suggested for patients with moderate to severe symptomatic HF (NYHA class II to IV, refer to Table 2) and an LVEF < 35%. (Class I recommendation, level of evidence A) Contraindications: | Adding this drug is suggested for patients with moderate to severe symptomatic HF (NYHA class II to IV, refer to Table 2) and an LVEF < 35%. (Class I recommendation, level of evidence A) Contraindications: | ||
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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> | ||
====Choice and combination of diuretics==== | |||
===Choice and combination of diuretics=== | |||
Patients with heart failure may be treated with a thiazide diuretic, which should be switched to a loop diuretic if a suboptimal response occurs. In patients with a decreased renal function, a loop diuretic is the mainstay of treatment. Addition of a thiazide diuretic to a loop diuretic can be considered in case of a suboptimal response of loop diuretic alone, when given in sufficient doses (furosemide 250 mg twice daily), suggesting that diuretic resistance is due to distal tubular increased activity of retaining sodium. In all patients with NYHA II or more, except in those with a creatinine clearance < 20 ml/min (creatinine > 220 micromol/L), addition of an aldosterone antagonist should be considered. In special cases in which hypercapnia plays a role, metabolic alkalosis can result from diuretics, and acetazolamide, a reversible carbonic anhydrase inhibitor, is then prescribed as an alternative diuretic. | Patients with heart failure may be treated with a thiazide diuretic, which should be switched to a loop diuretic if a suboptimal response occurs. In patients with a decreased renal function, a loop diuretic is the mainstay of treatment. Addition of a thiazide diuretic to a loop diuretic can be considered in case of a suboptimal response of loop diuretic alone, when given in sufficient doses (furosemide 250 mg twice daily), suggesting that diuretic resistance is due to distal tubular increased activity of retaining sodium. In all patients with NYHA II or more, except in those with a creatinine clearance < 20 ml/min (creatinine > 220 micromol/L), addition of an aldosterone antagonist should be considered. In special cases in which hypercapnia plays a role, metabolic alkalosis can result from diuretics, and acetazolamide, a reversible carbonic anhydrase inhibitor, is then prescribed as an alternative diuretic. | ||
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==Therapy of acute heart failure== | ==Therapy of acute heart failure== | ||
[[Image:acute_hf_flowchart.svg|400px|thumb|'''Figure 7.''' Flowchart acute HF.]] | |||
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. | ||
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|- | |- | ||
|'''Diuretics''' | |'''Diuretics''' | ||
|Adequate blood pressure and signs of overfilling | |colspan="2"|Adequate blood pressure and signs of overfilling | ||
|- | |- | ||
| | | | ||
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Renal failure | Renal failure | ||
|40 mg | |40 mg | ||
125 mg – max 1000 mg | |||
|- | |- | ||
| | | | ||
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Renal failure | Renal failure | ||
|1 mg | |1 mg | ||
3 mg – max 25 mg | |||
|- | |- | ||
|'''Vasodilators''' | |'''Vasodilators''' | ||
|Adequate blood pressure and signs of severe overfilling | |colspan="2"|Adequate blood pressure and signs of severe overfilling | ||
|- | |||
| | | | ||
*Nitroglycerine i.v. | *Nitroglycerine i.v. | ||
| | | | ||
|20 µg/min – max 200 µg/min (guided by blood pressure) | |20 µg/min – max 200 µg/min (guided by blood pressure) | ||
|- | |||
| | | | ||
*Nitroprusside i.v. | *Nitroprusside i.v. | ||
| | ||Hypertensive crisis or in combination with inotropic in case of a cardiogenic shock | ||
|Hypertensive crisis or in combination with inotropic in case of a cardiogenic shock | |||
|0.3 µg/kg/min – max 5 µg/kg/min (guided by blood pressure) | |0.3 µg/kg/min – max 5 µg/kg/min (guided by blood pressure) | ||
|- | |- | ||
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|- | |- | ||
|valign="top"| | |valign="top"| | ||
*Lisinopril | *Lisinopril | ||
| | | | ||
|Start 2.5-5mg | |Start 2.5-5mg | ||
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*Valsartan | *Valsartan | ||
| | | | ||
|Start | |Start 40mg twice daily | ||
3-5 weeks | 3-5 weeks 80mg twice daily. | ||
>7 weeks | >7 weeks 160mg twice daily. | ||
|- | |- | ||
|colspan="3" bgcolor="#F0F0F0 "|'''Hydralazine and isosorbide dinitrate (H-ISDN)''' | |colspan="3" bgcolor="#F0F0F0 "|'''Hydralazine and isosorbide dinitrate (H-ISDN)''' | ||
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===Prognosis=== | ===Prognosis=== | ||
The life expectancy of a patient with heart failure is determined by age, NYHA class, LVEF, normal level of sodium, systolic blood pressure, use of medication and use of ICD or CRT-D (Seattle Heart failure score). The mean yearly annual mortality is approximately 10%, varying from <6% per year when a normal LVEF is identified, to > 14% per year with an EF of <15%. | The life expectancy of a patient with heart failure is determined by age, NYHA class, LVEF, normal level of sodium, systolic blood pressure, use of medication and use of ICD or CRT-D ([http://depts.washington.edu/shfm/app.php Seattle Heart failure score]). The mean yearly annual mortality is approximately 10%, varying from <6% per year when a normal LVEF is identified, to > 14% per year with an EF of <15%. | ||
Trials with medication illustrate that the (short term) benefit of medication is highest when the NYHA class is higher (Figure 9).<cite>11</cite> | Trials with medication illustrate that the (short term) benefit of medication is highest when the NYHA class is higher (Figure 9).<cite>11</cite> | ||