● Introduction 211 ● Pathophysiology and implications for treatment 211 ● Therapeutic objectives and general measures for chronic heart failure 213 INTRODUCTION Heart failure occurs when the heart fails to deliver adequate amounts of oxygenated blood to the tissues during exercise or, in severe cases, at rest. Such failure of the pump function may be chronic, in which case symptoms of fatigue, ankle swelling, effort dyspnoea and orthopnoea predominate, or it may be acute, with sudden onset of shortness of breath due to pulmonary oedema (Figure 31.1). Both acute and chronic heart failure severely reduce life expectancy (Figure 31.2). The most severe form of heart failure (low cardiac output circulatory failure, ‘cardiogenic shock’) is managed with pressor drugs (e.g. adrenaline) or with mechanical support (e.g. intra-aortic balloon pump), in an intensive care unit. Such treatment is highly individualized (and specialized) and mortality even with the best treatment is very high. In this chapter, we cover the more common syndrome of chronic congestive heart failure and discuss the treatment of acute pulmonary oedema, since this is a common emergency. CHAPTER 31 HEART FAILURE (a) (b) ● Drugs for heart failure 213 PATHOPHYSIOLOGY AND IMPLICATIONS FOR TREATMENT Heart failure is an end result of many diseases (not only of the myocardium, pericardium and valves, but also of extracardiac disorders, including systemic or pulmonary hypertension, fluid overload, vascular shunts, anaemia and thyrotoxicosis). The most common of these are ischaemic heart disease (Chapter 29), idiopathic congestive cardiomyopathy and cor pulmonale (Chapter 33). Specific measures are needed in each case and these are covered in other chapters. Here, Figure 31.1: Peripheral oedema with evidence of pitting (left) and pulmonary oedema on chest x-ray (right), both important consequences of uncontrolled and inadequately treated heart failure.
212 HEART FAILURE we focus on aspects common to heart failure irrespective of aetiology. Heart failure triggers ‘counter-regulatory’ responses (Figure 31.3), which make the situation worse, not better. Our ancestors encountered low cardiac output during haemorrhage rather than as a result of heart failure. Mechanisms to conserve blood volume and maintain blood pressure would have provided selective advantage. However, reflex and endocrine changes that are protective in the setting of haemorrhage (volume depletion ‘shock’) negatively impact patients with low cardiac output due to pump failure. Proportion surviving 1.00 0.75 0.50 No CHF CHS only 0.25 Framingham only Concordant 0.00 0 2 4 6 Time since index date (years) Figure 31.2: Kaplan–Meier survival curves for subjects in the Cardiovascular Health Study (CHS), United States, 1989–2000. Subjects either had no congestive heart failure (CHF) or had CHF diagnosed by different criteria (Framingham only, CHS only or both, i.e. concordant). (Redrawn with permission from Schellenbaum GD et al. American Journal of Epidemiology 2004; 160: 628–35.) ↓ Cardiac output ↓ Renal perfusion Activation of renin–angiotensin– aldosterone system ↓ Firing of arterial baroreceptors (Carotid sinus, Aortic arch) Endothelial dysfunction Activation of sympathetic nervous system ↑ Endothelin ↓ Nitric oxide Figure 31.3: Compensatory counter-regulatory responses in heart failure and their consequences. Treatment of heart failure is aimed at reversing these counterregulatory changes, which include: • activation of the renin–angiotensin–aldosterone system; • activation of the sympathetic nervous system; • release of vasopressin (an antidiuretic hormone, see Chapter 42). Cardiac performance is determined by preload, afterload, myocardial contractility and heart rate. Treatment targets these aspects, often by blocking one or other of the counterregulatory mechanisms. PRELOAD Cardiac preload, the cardiac filling pressure, is determined by blood volume – increased by salt and water retention – and capacitance vessel tone, increased by sympathetic nervous system activation. Drugs can reduce blood volume (diuretics) and reduce capacitance vessel tone (venodilators). AFTERLOAD Afterload is determined by the systemic vascular resistance and by aortic stiffness. Drugs that relax arterial smooth muscle reduce cardiac afterload. MYOCARDIAL CONTRACTILITY Positive inotropes (i.e. drugs that increase the force of contraction of the heart) can improve cardiac performance temporarily by increasing contractility, but at the expense of increased oxygen consumption and risk of dysrhythmia. HEART RATE Cardiac function deteriorates as heart rate increases beyond an optimum, due to insufficient time for filling during diastole. Heart rate can usefully be slowed by negative chronotropes (i.e. drugs that slow the heart). Vasoconstriction Salt and water retention Short-term Maintenance of blood pressure Longer-term Worsening of tissue perfusion Worsening of fluid retention Progressive cardiomyocyte death and fibrosis Death
Soliman s Auricular Therapy Textbook: New Localizations and Evidence Based Therapeutic Approaches was created ( M.D. Nader Soliman )
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Soliman s Auricular Therapy Textbook This textbook is considered the finest ever written in the field of auricular therapy. The auricular acupuncture microsystem is one of the most widely used special acupuncture techniques. This textbook is dedicated to teaching the sound foundations of this unique approach as introduced by its founder Dr. Paul Nogier of France. The scientific bases of the acupuncture microsystem with its three dime... Full description
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