Retribuciones del profesorado y los directores

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Thyrotoxicosis

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Pregnancy

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Nutritional deficiencies: beriberi, thiamine deficiency

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Anaemia

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Paget’s disease

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Systemic arteriovenous fistulae

Causes of a raised JVP

Aside from the aetiology of congestive heart failure, the differential diagnoses of key clinical signs need consideration, such as a raised JVP or peripheral oedema:

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Congestive cardiac failure versus isolated right-sided heart failure. Isolated acute right heart failure in the context of RV infarction or pulmonary embolism presents with a raised JVP but clear lung fields. In this setting, identification of isolated right heart failure is key, as treatment is aimed at fluid administration to support the right heart circulation rather than diuresis in the example of RV failure due to infarction

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Pulmonary hypertension

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Significant tricuspid regurgitation: giant ‘v’ waves

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Superior vena cava obstruction: non- pulsatile, distended JVP

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Cardiac tamponade and pericardial constriction: look for Kussmaul’s sign, which is an increase in the level of the JVP on inspiration. The JVP usually falls on inspiration through increased venous return to the right heart, but in constriction and tamponade the right ventricle is unable to accommodate the increased inspiratory filling which is thus transmitted to the JVP Be careful not to confuse Corrigan’s sign (an arterial pulsation) in severe AR with a raised JVP. If congestive cardiac failure has resulted from severe AR, both signs may be present.

Peripheral oedema

The differential diagnosis of peripheral oedema includes:

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Cardiac failure

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Hypoalbuminaemia which can be due to impaired hepatic synthesis, malnutrition, gastrointestinal or renal losses

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Renal impairment

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Nephrotic syndrome

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Chronic venous insufficiency

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A pelvic mass with impaired lymphatic drainage

Demonstrate the importance

of clinical context – suggest

relevant questions that would be

taken in a patient history

Important questions in a history regarding cardiac failure include:

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Dyspnoea: ask to quantify exercise tolerance and categorise according to NYHA class

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Orthopnoea and paroxysmal nocturnal dyspnoea

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Peripheral oedema: are shoes or trousers more difficult to fit?

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Palpitations or syncope suggestive of arrhythmia

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Angina

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Cardiovascular risk factors

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History of previous cardiovascular, renal or liver disease

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Medication history

Demonstrate an understanding

of the value of further

investigation

Important investigations in the assessment of cardiac failure include:

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Laboratory blood tests:

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Full blood count for anaemia

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Natriuretic peptides (BNP or NT-proBNP) as markers of myocardial stretch and thus volume overload

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Urea, creatinine and electrolytes: deranged renal function has implications on prognosis and may be the result of cardiorenal syndrome or the deleterious impact of heart failure treatment. Renal impairment is an independent marker of poor prognosis in patients with heart failure, impacting upon both survival and the scope for certain medical therapies with known survival benefit. This is an important consideration in managing cardiac failure

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A 12-lead electrocardiogram may some or all of the following:

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Evidence of previous ischaemia, arrhythmia, left ventricular hypertrophy

Chapter 1 Cardiovascular system (station 3)

32

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Left bundle branch block, the duration of the QRS complex being a criteria for cardiac resynchronisation therapy

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A normal ECG renders systolic heart failure unlikely (<10%) as the cause of the patient’s symptoms

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A plain chest radiograph may show a variable combination of cardiomegaly, pleural effusions, alveolar pulmonary oedema , Kerley B lines, fluid in the fissure, and upper lobe blood diversion

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Echocardiography is the investigation of choice. It allows assessment of biventricular size, systolic and diastolic function, and can demonstrate evidence of a previous infarction. It also allows assessment of valvular aetiologies or consequences of cardiac failure and the impact of left heart failure on estimated pulmonary artery pressure

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Cardiac MRI allows additional assessment of myocardial (especially infiltrative) disease and viability when revascularisation is being considered

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Cardiac catheterisation is used to investigate coronary lesions responsible for impaired systolic function. It also allows assessment of haemodynamic parameters, such as left ventricular end-diastolic pressure, pulmonary capillary wedge and pulmonary arterial pressures. Endomyocardial biopsy is rarely required but can be considered in certain cases.

Always offer a management plan

General principles that should be applied include:

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Treat the underlying cause, such as targeted therapy for hypertensive heart disease or intervention on symptomatic valvular heart disease

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Fluid and salt restriction

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Immunisations (influenza, pneumococcal) Symptomatic treatment includes diuresis with either oral or intravenous preparations. In cases of congested gut mucosa, bumetanide has superior oral bioavailability compared with furosemide. Metolazone can be combined with intravenous diuresis in severe cases of fluid retention, but warrants careful monitoring of renal function and electrolytes. Ultrafiltration can be used in cases of fluid overload refractory to diuretics. There is some evidence that this treatment modality may also ‘reset’ the sensitivity of the kidneys to diuretic therapy. While diuretics only provide symptomatic benefit, several medications have evidence of mortality benefit. These include:

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ACE inhibitors, or angiotensin receptor blockers if intolerant of ACE inhibtors, in patients with systolic dysfunction (ejection fraction ≤ 40%)

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Beta-blockers in patients with systolic dysfunction (ejection fraction ≤ 40%)

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Mineralocorticoid receptor antagonists (potassium-sparing diuretics) in patients with systolic dysfunction (ejection fraction ≤ 35%) and NYHA class II–IV symptoms

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Adding ivabradine, an inhibitor of the I_f ion channel highly expressed in the sinoatrial node, is indicated in patients in sinus rhythm over 70 beats per minute who remain in NYHA classes II–IV with an EF ≤ 35% and on optimal therapy.

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The combination of hydralazine and isosorbide dinitrate (ISDN) may be considered to reduce the risk of heart failure or hospitalisation in patients intolerant of ACE inhibitors or angiotensin receptor blockers. One study (A-HeFT) showed a mortality benefit of this combination specifically in African-Americans. These medications must be prescribed initially at an introductory dose and then up-titrated to the maximum tolerated dose, bearing in mind side effects (especially renal dysfunction and hypotension). Trial data for mortality benefit is derived from up-titration of medication to optimal doses rather than remaining on the introductory dose. This is where an MDT approach, with input from a community heart failure nurse specialist, is key.

Other ongoing treatment considerations which should be recognised include:

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Anticoagulation in the presence of AF or apical thrombus

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Devices: cardiac resynchronisation therapy (CRT, also known as biventricular pacing), implantable cardiac defibrillators (ICDs, with or without CRT) (see Infraclavicular mass, p. 33)

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Referral to a specialist centre for

transplantation assessment and bridges to transplantation (ventricular assist devices)

Further reading

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; 29:2388–2442.

Instruction to the candidate

In document Panorama de la educación Indicadores de la OCDE 2021 (página 121-149)