Arterial hypotension. Acute vascular insufficiency: faint, collapse, shock. Diagnostics. Emergency care. Tactics of a dentist in ambulatory terms
Acute and chronic heart failure. Definition. Ethioliogy. Pathogenesis. Classification. Clinical pattern. Diagnostics. Treatment. Emergency care
Arterial hypotension is characterised by clinical depression of arterial pressure below 100/60 mm hg For persons aged till 25 years and below 105/65 mm hg For persons is more senior 30 years.
Etiology and Pathogenesis
In modern clinical practice distinguish hypotensions physiological and pathological: though accurate border between them to spend it is not possible. The physiological arterial hypotension caused in basic constitutional and hereditary factors, meets quite often at absolutely healthy humans performing usual physical work, and is not accompanied by any complaints and pathological changes in an organism. The physiological hypotension of passing character at sportsmen is known.
Pathological hypotension is sectioned on primary and secondary (symptomatic), in each of which excrete acute and chronic forms. The neurocirculatory dystonia on a hypotonic type in essence is a hypotension synonym (or a primary arterial hypotension).
At the heart of a primary arterial hypotension rising of a tonus of parasympathetic part of vegetative excitatory system, disturbance of function of the higher vegetative centres of the vasculomotor regulation, conducting to nonperishable reduction of the general peripheric resistance to a blood flow lays. The compensatory augmentation of warm outlier in these cases appears insufficient for normalisation of arterial pressure. Rate of a blood flow at a primary chronic arterial hypotension usually it is not variated. The volume of circulating blood is in limens of norm or is a little lowered: sometimes there is a predilection to an euvolemic polycythemia.
Specified alterations are caused most likely by distinct reduction of cash and reserve glucocorticoid activity of a cortex of adrenals at not variated mineralocorticoid activity.
Egestion with adrenaline urine is authentically lowered, and Dofaminum – is raised. Electrolytic alterations (the tendency to a hyperpotassemia and a hyponatremia have certain value also at some enlarged egestion with urine of ions of sodium and reduced – potassium ions.
The major importance in hypotension occurrence, apparently, belongs to a long psychoemotional strain, on occasion – a mental trauma. On modern representations, the primary hypotension is the special form of a neurosis of the higher vasomotor centres with disturbance of regulation of a vascular tonus.
Clinical Picture
Complaints of patients are extraordinary various and numerous (slackness, apathy, sensation of sharp delicacy and fatigability in the mornings, the lowered working capacity).
Often the sensation of shortage of air in rest and the expressed dyspnea becomes perceptible at moderate physical work, edemas of anticnemions and autopodiums by the evening. At the majority of patients irritable emotional instability, disturbance of a sleep, a potency and a libido at men and a menstrual cycle at women become perceptible. Heavy feelings quite often join it in epigastric range and bitterness in a mouth, appetite depression, an eructation air, a heartburn, a meteorism, constipations.
On the basis of prevalence of pains in the field of heart or headaches distinguish mainly cardial or cerebral form of a primary arterial hypotension.
In difference from a stenocardia attack at a primary arterial hypotension stupid, pricking or aching (is much rarer pressing or compressing) the pain is localised basically in the field of a heart apex, does not irradiate, appears usually in rest or in the morning, after a sleep (occasionally at an excessive exercise stress). The pain proceeds some hours, is not stopped by antianginal agents (Nitroglycerinum application, on the contrary, worsens a condition of the patient) and taken out sometimes after easy physical exercises.
The habitual headache sometimes is the unique complaint of the patient, arises after a sleep ( especially diurnal ) or physical or mental work, ( up to sensation of exhaustion ). The stupid, pulling together, arching or pulsing headache grasps more often frontotemporal or parietofrontal range and proceeds from several o’clock till 2-3 days.
Periodic giddinesses with hypersensitivity to bright light, hum, loud speech and tactile stimuluses, a staggering are not less characteristic for a primary arterial hypotension at walking and syncopal conditions.
At a number of patients the position hypotension is observed. So, at transition from horizontal position in the erect the orthostatic or postural hypotension with sharp falling of mainly systolic arterial pressure and a loss of consciousness educes. In horizontal position the consciousness is quickly recovered.
In the first 8-12 weeks and in last trimester of pregnancy at the women, suffering the primary arterial hypotension, quite often observes an acute arterial hypotension in position on a back. Development of this syndrome is bound to a prelum the enlarged uterus of the inferior vena cava in position of the woman on a back.
At objective research at the majority of patients those or other vegetative disturbances are taped: a hyperhidrosis of anticnemions and autopodiums, a tremor of eyelids and dactyls of arms, pallor of a skin with an easy Crocq’s disease, a nonperishable red dermographism and disorders of a thermoregulation with the expressed daily fluctuations of a body temperature and its falling in the mornings more low 36.
At acute depression of arterial pressure development Meniere’s disease – epileptiform attacks and diencephalic paroxysms with a fever or abundant cold then, distinct paresthesias in extremities, imperative desires to an emiction and instability in a Romberg’s position is possible, at some patients largly wide nystagmus thus becomes perceptible.
Arterial pressure and sphygmus are very labile and conditions of the patient depend on position of a body, time of days. Practically at all patients stable depression of arterial pressure in a humeral artery takes place.
Heart borders usually are not variated, however probably small augmentation of the dimensions of its relative dullness basically for the account of dilating of a left ventricle. Over a heart apex the muting of 1st tint, sometimes easy systolic hum is defined.
Electrocardiographic data testify in some cases to a deflection of an electrical axis of heart to the left, a low voltage of a teeth and a sinus bradycardia.
Data of laboratory researches do not leave, as a rule, for norm limens. Only the small part of patients has a predilection to a moderate anaemia, a leukopenia with a lymphocytosis and ESR retardation. The tendency to a lipidemia, insignificant augmentation level of a filtrate nitrogen, a hypercholesteremia is possible also at the normal maintenance B – lipoproteins, to reduction of coagulabling ability of blood, depression of indicators of standard metabolism.
Differential diagnosis
Primary and secondary arterial hypotensions differentiate by an exception of the various pathological processes conducting to nonperishable depression of arterial pressure.
Treatment
Treatment of a chronic arterial hypotension assumes first of all performance of some hygienic actions. Them concern:
1. an accurate regimen of day (a night sleep not less than 8 hours, morning and industrial gymnastics, water tonic procedures)
2. correct organisation of work
3. high-grade and various four single food
The big diffusion to hypotension treatment have received vegetative and biological neurostimulator which the Eleuterococus extract, magnolia-vine tincture, Extractum Rhodiolae fluidum concern Pantocrinum, Tinctura Araliae, tinctura echinopanacis.
They are recommended to be prescribed a place with tincture from Valeriana root. Efficacyy of a combination of an Eleuterococus with Pantocrinum is noted. The positive effect gives application of Saparalum, caffeine (on 0,05 – 0,1gm. 2-3 times a day).
It is necessary to notice, that at headaches at sick of an arterial hypotension analgetics are ineffective, while at reception of caffeine and horizontal position of a pain decrease or disappear.
In refractory cases use Phethanolum on 1gm. 1 % of solution subcutaneously or inside on 0,005 gm 2-3 times a day; Securininum on 1gm 0,2 % of solution subcutaneously or inside on 0,002gm 2-3 times a day.
Heart failure
Despite advances in management of heart failure, the condition remains a major public-health issue, with high prevalence, poor clinical outcomes, and large health-care costs. Risk factors are well known and, thus, preventive strategies should have a positive effect on disease burden. Treatment of established systolic chronic heart failure includes use of agents that block the renin-angiotensin-aldosterone and sympathetic nervous systems to prevent adverse remodelling, to reduce symptoms and prolong survival. Diuretics are used to achieve and maintain euvolaemia. Devices have a key role in management of advanced heart failure and include cardiac resynchronisation in patients with evidence of cardiac dyssynchrony and implantation of a cardioverter defibrillator in individuals with low ejection fraction. Approaches for treatment of acute heart failure and heart failure with preserved ejection fraction are supported by little clinical evidence. Emerging strategies for heart failure management include individualisation of treatment, novel approaches to diagnosis and tracking of therapeutic response, pharmacological agents aimed at new targets, and cell-based and gene-based methods for cardiac regeneration.
Considerable advances have been made in management of heart failure over the past few decades. In outpatient-based clinical trials, mortality has more than halved in people with established systolic chronic heart failure; moreover, admissions have fallen and patients’ quality of life has risen. Nevertheless, heart failure remains a major public-health issue, with high prevalence and poor outcomes. Management of this condition includes appropriate non-pharmacological strategies, use of drugs (particularly those that inhibit key activated neurohormonal systems), and implantation of devices in appropriate patients. Surgery and transplantation are also options for selected individuals with highly advanced disease.
Despite the promise of new drugs, cell-based therapeutic approaches, and novel devices, a reduction of disease burden is likely to come from preventive strategies. The antecedents to heart failure are well known; enhanced diagnostic precision coupled with early intervention could lessen the burden of disease.
Heart failure is a clinical syndrome and, thus, definitions are imprecise. Most include references to typical symptoms and objective evidence of abnormal ventricular function. Estimates of heart failure prevalence and incidence vary greatly because of non-uniformity in the definition, absence of a gold-standard measure for the disorder, and paucity of adequate and true epidemiological surveys. Furthermore, such data are confined largely to developed countries, although heart failure seems to be growing in developing nations.
Prevalence of heart failure rises steeply with increasing decades of life, particularly from age 50 years; the condition is rare in individuals younger than this age. In a cross-sectional survey of residents of Olmsted County, MN, USA, older than 45 years, overall prevalence was 22%, falling to 0·7% in those aged 45—54 years and rising to 8·4% for those 75 years or older.4 Findings of previous studies in similar populations support these frequencies. Asymptomatic systolic left-ventricular dysfunction occurs in about half of patients with impaired left-ventricular systolic function.
Prevalence of heart failure with preserved ejection fraction is highly dependent on how this syndrome is defined, which in itself is a complex and controversial issue. Abnormalities of diastolic function rise more steeply with increasing decade of life than does left-ventricular systolic dysfunction, with prevalence up to 15·8% in people older than 65 years, on the basis of European echocardiographic criteria. In the Olmsted County study, researchers assessed echocardiographic variables for diastolic dysfunction and noted that 44% of people with heart failure had an ejection fraction higher than 50%.4 Furthermore, 7·3% of individuals older than 45 years had moderate or severe diastolic dysfunction, based on their meeting two or more predefined echocardiographic criteria for severity.
Assessments of incidence of heart failure are scarce. In the Hillingdon West London study, incidence in a population aged 45—55 years was 0·2 per 1000 person-years, rising to 12·4 per 1000 person-years in people older than 85 years. This rate was based oew admissions and clinical referrals for suspected heart failure, with diagnosis confirmed by a panel of cardiologists. In the Rotterdam study, incidence was slightly higher (44 per 1000 person-years in individuals 85 years or older) than in the Hillingdon study and was ascertained from symptoms, signs, and relevant drug use.
Age-adjusted incidence of heart failure has not declined substantially in the past 20—30 years, despite enhanced control of causal factors including myocardial infarction, coronary artery disease, and hypertension. Potential reasons for this absence of reduction in incidence include a rise in frequency of heart failure risk factors, such as diabetes and obesity. In view of the ageing of the population, non-age-adjusted incidence is likely to increase in the future. Indeed, lifetime risk of developing heart failure at the age of 40 years is close to 20% in both men and women.
Admissions for heart failure have risen greatly over the past few decades, but could have now peaked. The cause of the plateau in heart failure admissions might relate to improvements in pharmacological treatments and the advent of heart failure clinics and specific disease-management programmes. However, a growth in the proportion of patients admitted with heart failure with preserved ejection fraction has beeoted, again almost certainly on the basis of increasing prevalence of risk factors for this condition, such as hypertension, atrial fibrillation, and diabetes mellitus.
About two-thirds of the economic burden of heart failure is accounted for by admissions to hospital. In one study, 44% of patients admitted with a primary discharge diagnosis of heart failure were readmitted within 6 months, every admission costing in excess of US$7000 per patient. In Australia, with a population of just over 20 000 000, heart failure consumes AU$1000 million of the health-care budget every year.
Demographic characteristics of patients with chronic heart failure have been derived from data of community-based studies supplemented by information from randomised controlled trials of new therapeutic strategies. In general, findings of community-based assessments show that affected individuals are most likely to be old, female, and have associated comorbidity.
Comorbidities include either causal factors underlying heart failure or diseases that might affect prognosis or treatment. Systemic hypertension is the most frequent and well described comorbidity, relevant to both systolic heart failure and heart failure with preserved ejection fraction. Compared with data of epidemiological studies such as Framingham, findings of intervention studies in heart failure have underestimated the contribution of hypertension,19 perhaps because this diagnosis is usually embedded within ischaemic and other causes.
Coronary artery disease can lead to heart failure through various mechanisms. Extensive myocardial necrosis can result in pump failure. Infarction of small areas can cause regional contractile dysfunction and adverse remodelling with myocyte hypertrophy, apoptosis, and deposition of extracellular matrix. Furthermore, transient reversible ischaemia can arise with episodic dysfunction, even in the presence of typical resting left-ventricular function.
Diabetes mellitus is an important and sometimes overlooked comorbidity in patients with heart failure. People with diabetes are at strikingly higher risk of heart failure than are those without the disease, and they have higher mortality. The existence of a specific diabetic cardiomyopathy, independent of concomitant hypertension and large-vessel coronary artery disease, has been much debated. In support of this possibility, asymptomatic diastolic dysfunction is a frequent finding on echocardiographic investigation of individuals with diabetes. Furthermore, altered autonomic and endothelial function, advanced glycation end-product deposition, and disordered energy metabolism are shared traits of both diabetes and heart failure.
Both ventricular and atrial arrhythmias are typical associated disorders and can be implicated as causes of heart failure. Many factors contribute to the high rate of arrhythmias in chronic heart failure, including ischaemic heart disease, electrophysiological abnormalities, myocardial hypertrophy, and activation of several key neurohormonal systems. Moreover, patients might be taking proarrhythmic drugs. Furthermore, many heart failure agents cause electrolyte abnormalities that could exacerbate the underlying risk.
Other important comorbidities include respiratory disorders such as chronic airflow obstruction and sleep apnoea, cognitive dysfunction, depression, anaemia, chronic kidney disease, and arthritis. All comorbid disorders add considerable complexity to diagnosis and management.
Nearly 5 million Americans have heart failure today, with an incidence approaching 10 per 1000 population among persons older than 65 years of age. Heart failure is the reason for at least 20 percent of all hospital admissions among persons older than 65. Over the past decade, the rate of hospitalizations for heart failure has increased by 159 percent. In 1997, an estimated $5,501 was spent for every hospital-discharge diagnosis of heart failure, and another $1,742 per month was required to care for each patient after discharge. Accordingly, substantial efforts have been made to identify and treat the factors that predict recurrent hospitalization. End points of large randomized trials now include the effect of the studied intervention on the rate of hospital admissions. For example, angiotensin-converting–enzyme (ACE) inhibitors, angiotensin-receptor antagonists, beta-blockers, spironolactone, biventricular pacing, coronary bypass surgery, and the use of multidisciplinary teams to treat heart failure have all been shown to reduce the rate of hospitalizations substantially, as well as to reduce mortality or improve functional status. Considerable debate has focused on the mechanisms that reduce the rate of admissions and on the type of physician who should care for patients with heart failure. In the United States, more than two thirds of patients with heart failure are cared for exclusively by primary care practitioners.
Multiple clinical trials completed during the past 15 years have unequivocally shown a substantial reduction in mortality for patients with systolic heart failure. Simultaneously, however, large epidemiologic surveys, such as the ongoing Framingham Study, have not documented any meaningful change in overall death rates. (Death seems to have been delayed, however, and occurs a longer time after major cardiac events such as a myocardial infarction.) Symptomatic heart failure continues to confer a worse prognosis than the majority of cancers in this country, with one-year mortality of approximately 45 percent.
Why have the newer and successful therapies failed to result in a meaningful reduction in mortality due to heart failure? It is important to recognize that heart failure is a clinical syndrome arising from diverse causes. Not all patients with the condition have poorly contracting ventricles and a low ejection fraction. Many have uncorrected valvular disease, such as aortic stenosis or mitral regurgitation, or abnormal filling, resulting in diastolic heart failure. A large majority of patients with heart failure are elderly, and 75 percent of patients have a history of hypertension. Many patients have at least one serious coexisting condition, in addition to advanced age. Such patients have not usually been subjects in investigational trials. Moreover, until recently, the majority of patients entered into trials of investigational drugs were middle-aged white men with heart failure due to ischemic cardiomyopathy. Fewer women and members of racial minorities have taken part in trials, and very few trials have included persons older than 75 years of age. Thus, despite the acknowledged successes of the therapies outlined below, there is much to be done in the prevention and management of heart failure in the large subgroups of patients who are not well represented in trials. Certainly, successful treatments have not been systematically applied to the majority of patients with heart failure, and for the reasons stated above, those that have been applied may not be efficacious.
Although heart failure is a major public health problem, there are no national screening efforts to detect the disease at its earlier stages, as there are for breast and prostate cancer or even osteoporosis. Heart failure is largely preventable, primarily through the control of blood pressure and other vascular risk factors. Yet, until recently, the factors that render a patient at high risk for heart failure had not been clearly defined or publicized. The guidelines for the evaluation and management of chronic heart failure that were published recently by the American College of Cardiology and the American Heart Association have corrected this deficit. The writing committee developed a new approach to the classification of heart failure that emphasizes its evolution and progression and defined four stages of heart failure. Patients with stage A heart failure are at high risk for the development of heart failure but have no apparent structural abnormality of the heart. Patients with stage B heart failure have a structural abnormality of the heart but have never had symptoms of heart failure. Patients with stage C heart failure have a structural abnormality of the heart and current or previous symptoms of heart failure. Patients with stage D heart failure have end-stage symptoms of heart failure that are refractory to standard treatment.
This staged classification underscores the fact that established risk factors and structural abnormalities are necessary for the development of heart failure, recognizes its progressive nature, and superimposes treatment strategies on the fundamentals of preventive efforts. The classification is a departure from the traditional New York Heart Association (NYHA) classification, which has primarily been used as shorthand to describe functional limitations. Heart failure may progress from stage A to stage D in a given patient but cannot follow the path in reverse. In contrast, a patient with NYHA class IV symptoms might have quick improvement to class III with diuretic therapy alone. This staged heart–failure classification promotes a way of thinking about heart failure that is similar to our way of thinking about cancer — that is, the identification and screening of patients who are at risk, patients with in situ disease, and patients with established or widespread disease. The ensuing discussion about the treatment of heart failure is keyed toward this new staging classification.
The Syndrome of Heart Failure
The traditional view that heart failure is a constellation of signs and symptoms caused by inadequate performance of the heart focuses on only one aspect of the pathophysiology involved in the syndrome. Currently, a complex blend of structural, functional, and biologic alterations are evoked to account for the progressive nature of heart failure and to explain the efficacy or failure of therapies used in clinical trials.10 For example, the rationale for the use of beta-blockers in a patient with a poorly contracting heart is based on a conceptual framework broader than that which suggests the treatment of congestion with diuretics or digoxin. The rationale for using beta-blockers is predicated on an understanding of the role of the sympathetic nervous system in promoting the release of renin and other vasoactive substances that trigger vasoconstriction, tachycardia, and changes in myocytes that lead to disadvantageous ventricular dilatation.
Heart failure has been described variously as: (1) an oedematous disorder, whereby abnormalities in renal haemodynamics and excretory capacity lead to salt and water retention; (2) a haemodynamic disorder, characterised by peripheral vasoconstriction and reduced cardiac output; (3) a neurohormonal disorder, predominated by activation of the renin-angiotensin-aldosterone system (RAAS) and adrenergic nervous system; (4) an inflammatory syndrome, associated with increased local and circulating proinflammatory cytokines; and (5) a myocardial disease, initiated by injury to the heart followed by pathological ventricular remodelling. In fact, these descriptions of heart failure pathophysiology are not mutually exclusive and all factor in the onset and progression of the clinical syndrome of heart failure. Moreover, development of heart failure generally proceeds in stages, from risk factors to end-stage or refractory disease (figure )
Indeed, recent reviews have combined several models that had been used previously to understand heart failure in order to illustrate more fully the cascade of mechanisms, as well as the opportunities for intervention. Thus, the hemodynamic model of heart failure emphasized the effect of an altered load on the failing ventricle and ushered in the era of vasodilators and inotropic agents. The neurohumoral model recognized the importance of activation of the renin–angiotensin–aldosterone axis and the sympathetic nervous system in the progression of cardiac dysfunction. More recently, efforts to antagonize the effects of circulating norepinephrine and angiotensin II have shifted with the recognition that these and other vasoactive substances are also synthesized within the myocardium and therefore act in an autocrine and paracrine manner, in addition to their actions in the circulation. For example, braiatriuretic peptide is produced by the ventricular myocardium in response to stretch; its vasodilatory and natriuretic effects counteract the opposing actions of angiotensin II and aldosterone. Other studies have scrutinized myocytes from failing hearts in an attempt to detect abnormal signaling, gene expression, or contractile protein structure. Table 1 details many of the factors that contribute to the heart–failure syndrome as it is currently understood.
Heart failure is usually associated with a structural abnormality of the heart. The initial injury might be sudden and obvious (eg, myocardial infarction) or insidious (eg, longstanding hypertension). In some instances, such as idiopathic dilated cardiomyopathy, it is unknown. Once the injury happens, a series of initially compensatory but subsequently maladaptive mechanisms ensue.
Compensatory mechanisms that are activated in heart failure include: increased ventricular preload, or the Frank-Starling mechanism, by ventricular dilatation and volume expansion; peripheral vasoconstriction, which initially maintains perfusion to vital organs; myocardial hypertrophy to preserve wall stress as the heart dilates; renal sodium and water retention to enhance ventricular preload; and initiation of the adrenergic nervous system, which raises heart rate and contractile function. These processes are controlled mainly by activation of various neurohormonal vasoconstrictor systems, including RAAS, the adrenergic nervous system, and non-osmotic release of arginine-vasopressin. These and other mechanisms contribute to the symptoms, signs, and poor natural history of heart failure. In particular, an increase in wall stress along with neurohormonal activation facilitates pathological ventricular remodelling; this process has been closely linked to heart failure disease progression. Management of chronic heart failure targets these mechanisms and, in some instances, results in reverse remodelling of the failing heart.
Because no single pathophysiological model can account for the host of clinical expressions of heart failure, current therapy often targets more than one organ system, as outlined in Figure 1. Additional pathophysiological concepts that have become clinically meaningful areas for investigation or treatment are described below.
Figure Primary Targets of Treatment in Heart Failure.
Treatment options for patients with heart failure affect the pathophysiological mechanisms that are stimulated in heart failure. Angiotensin-converting–enzyme (ACE) inhibitors and angiotensin-receptor blockers decrease afterload by interfering with the renin–angiotensin–aldosterone system, resulting in peripheral vasodilatation. They also affect left ventricular hypertrophy, remodeling, and renal blood flow. Aldosterone production by the adrenal glands is increased in heart failure. It stimulates renal sodium retention and potassium excretion and promotes ventricular and vascular hypertrophy. Aldosterone antagonists counteract the many effects of aldosterone. Diuretics decrease preload by stimulating natriuresis in the kidneys. Digoxin affects the Na+/K+–ATPase pump in the myocardial cell, increasing contractility. Inotropes such as dobutamine and milrinone increase myocardial contractility. Beta-blockers inhibit the sympathetic nervous system and adrenergic receptors. They slow the heart rate, decrease blood pressure, and have a direct beneficial effect on the myocardium, enhancing reverse remodeling. Selected agents that also block the alpha-adrenergic receptors can cause vasodilatation. Vasodilator therapy such as combination therapy with hydralazine and isosorbide dinitrate decreases afterload by counteracting peripheral vasoconstriction. Cardiac resynchronization therapy with biventricular pacing improves left ventricular function and favors reverse remodeling. Nesiritide (braiatriuretic peptide) decreases preload by stimulating diuresis and decreases afterload by vasodilatation. Exercise improves peripheral blood flow by eventually counteracting peripheral vasoconstriction. It also improves skeletal-muscle physiology.
Remodeling
Increased levels of circulating neurohormones are only part of the response seen after an initial insult to the myocardium. Left ventricular remodeling is the process by which mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape, and function. Remodeling occurs in several clinical conditions, including myocardial infarction, cardiomyopathy, hypertension, and valvular heart disease; its hallmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis. For example, after a myocardial infarction, the acute loss of myocardial cells results in abnormal loading conditions that involve not only the border zone of the infarction, but also remote myocardium. These abnormal loading conditions induce dilatation and change the shape of the ventricle, rendering it more spherical, as well as causing hypertrophy. Remodeling continues for months after the initial insult, and the eventual change in the shape of the ventricle becomes deleterious to the overall function of the heart as a pump (Figure 2A). In cardiomyopathy, the process of progressive ventricular dilatation or hypertrophy occurs without the initial apparent myocardial injury observed after myocardial infarction (Figure 2B).
Several trials involving patients who were studied after a myocardial infarction or who had dilated cardiomyopathy found a benefit from ACE inhibitors, beta-adrenergic antagonists, or cardiac resynchronization. Such beneficial effects were associated with so-called reverse remodeling, in which the therapy promoted a return to a more normal ventricular size and shape. The reverse-remodeling process is a mechanism through which a variety of treatments palliate the heart–failure syndrome.
Mitral Regurgitation
Another potential deleterious outcome of remodeling is the development of mitral regurgitation. As the left ventricle dilates and the heart assumes a more globular shape, the geometric relation between the papillary muscles and the mitral leaflets changes, causing restricted opening and increased tethering of the leaflets and distortion of the mitral apparatus. Dilatation of the annulus occurs as a result of increasing left ventricular or atrial size or as a result of regional abnormalities caused by myocardial infarction. The presence of mitral regurgitation results in an increasing volume overload on the overburdened left ventricle that further contributes to remodeling, the progression of disease, and symptoms. Correction of mitral regurgitation has been an appropriate focus of therapy.
Figure 2. Ventricular Remodeling after Infarction (Panel A) and in Diastolic and Systolic Heart Failure (Panel B).
At the time of an acute myocardial infarction — in this case, an apical infarction — there is no clinically significant change in overall ventricular geometry (Panel A). Within hours to days, the area of myocardium affected by the infarction begins to expand and become thinner. Within days to months, global remodeling can occur, resulting in overall ventricular dilatation, decreased systolic function, mitral-valve dysfunction, and the formation of an aneurysm. The classic ventricular remodeling that occurs with hypertensive heart disease (middle of Panel B) results in a normal-sized left ventricular cavity with thickened ventricular walls (concentric left ventricular hypertrophy) and preserved systolic function. There may be some thickening of the mitral-valve apparatus. In contrast, the classic remodeling that occurs with dilated cardiomyopathy (right side of Panel B) results in a globular shape of the heart, a thinning of the left ventricular walls, an overall decrease in systolic function, and distortion of the mitral-valve apparatus, leading to mitral regurgitation.
Arrhythmias and Bundle-Branch Block
The myocardial conduction system is vulnerable to the same pathophysiological processes that occur in the myocytes and interstitium, with altered conduction properties observed in response to ischemia, inflammation, fibrosis, and aging. Supraventricular arrhythmias, particularly atrial fibrillation, are often the precipitating events that herald the onset of either systolic or diastolic heart failure. Elevated ventricular end-diastolic pressure in a patient with hypertension or abnormal myocardial function leads to atrial stretch, which in turn incites electrical instability. Recognition of the presence of atrial fibrillation in a patient is critical, since several studies have now demonstrated the effectiveness of oral anticoagulant therapy for the prevention of stroke.
Abnormal myocardial conduction can also lead to delays in ventricular conduction and bundle-branch block. Left bundle-branch block is a significant predictor of sudden death and a common finding in patients with myocardial failure. Its presence also affects the mechanical events of the cardiac cycle by causing abnormal ventricular activation and contraction, ventricular dyssynchrony, delayed opening and closure of the mitral and aortic valves, and abnormal diastolic function. Hemodynamic sequelae include a reduced ejection fraction, decreased cardiac output and arterial pressure, paradoxical septal motion, increased left ventricular volume, and mitral regurgitation. Ventricular arrhythmias are thought to be secondary to a dispersion of normal conduction through nonhomogeneous myocardial tissue, which promotes repetitive ventricular arrhythmias.
The rate of sudden cardiac death among persons with heart failure is six to nine times that seen in the general population. Major innovations in medical and device-based therapy for the primary and secondary prevention of lethal ventricular arrhythmias have occurred during the past decade but are beyond the scope of this article. Increasing use of implantable cardioverter–defibrillators has unequivocally reduced mortality in a subgroup of patients with heart failure.
Diastolic Heart Failure
It is estimated that 20 to 50 percent of patients with heart failure have preserved systolic function or a normal left ventricular ejection fraction. Although such hearts contract normally, relaxation (diastole) is abnormal. Cardiac output, especially during exercise, is limited by the abnormal filling characteristics of the ventricles. For a given ventricular volume, ventricular pressures are elevated, leading to pulmonary congestion, dyspnea, and edema identical to those seen in patients with a dilated, poorly contracting heart. Characteristics of patients with systolic heart failure and those with diastolic heart failure are compared in Table 2. Patients with diastolic heart failure are typically elderly, often female, and usually obese and frequently have hypertension and diabetes. Mortality among these patients may be as high as that among patients with systolic heart failure, and the rates of hospitalization in the two groups are equal. The diagnosis of diastolic heart failure is usually made by a clinician who recognizes the typical signs and symptoms of heart failure and who is not deterred by the finding of normal systolic function (i.e., a normal ejection fraction) on echocardiography. Echocardiography may be useful in the detection of diastolic filling abnormalities.
See also European Society of Cardiology Guidelines for the Diagnosis and Treatment of Chronic Heart Failure
Heart failure is a clinical syndrome, with diagnosis based on a combination of typical symptoms and signs together with appropriate clinical tests. Presentation can be non-specific and mimicked by many other disease states, especially in elderly people. Unsurprisingly, sensitivity and specificity of frequent presenting symptoms of heart failure are rather poor. Signs of heart failure—such as raised jugular venous pulse, a third heart sound, basal pulmonary crackles, and sinus tachycardia—have somewhat greater specificity for a heart failure diagnosis than do symptoms, at least in some assessments.
Routine objective testing methods, such as electrocardiograms (ECGs) and chest radiographs, are also fairly non-specific. The ECG is, however, a reasonable rule-out test for systolic dysfunction—ie, this diagnosis is somewhat unlikely if the ECG is entirely normal.
Laboratory testing can provide useful information about cause of heart failure, disease severity, and prognosis. Such data are especially valuable if important comorbid disorders (eg, anaemia, hyponatraemia, renal dysfunction, and diabetes) are also present.
Echocardiography is a useful method to assist in diagnosis of heart failure. This modality can provide important information about left-ventricular dimensions and geometry, extent of systolic dysfunction, whether dysfunction is global or segmental, the status of valve apparatus, and estimates of pulmonary pressures. Echocardiography is most specific for diagnosis of left-ventricular systolic dysfunction. Conversely, assessment of diastolic dysfunction remains elusive, even with the advent of tissue doppler imaging, a technique that provides important information on patterns of diastolic relaxation and filling. Tissue doppler imaging can also provide data on ventricular dyssynchrony.
New imaging modalities such as MRI, especially with gadolinium contrast, provide great precision for assessment of ventricular structure and function.37 However, use of MRI to measure progression of established heart failure is limited by presence of device hardware in many patients.
Measurement of amounts in plasma of either B-type natriuretic peptide (BNP) or its precursor, N terminal-proBNP, has aided diagnosis of heart failure. In patients presenting with acute dyspnoea, area under the receiver-operating characteristic curve is 0·90, indicating relatively high sensitivity and specificity for this peptide compared with the gold standard of diagnosis by a cardiologist on the basis of available clinical information. Low BNP has very high negative predictive value, making it a useful rule-out test, particularly in populations in which frequency of heart failure is expected to be high. By contrast, use of BNP for community-based screening of presence of left-ventricular dysfunction can be complicated by low background disease prevalence.Clinical use of BNP for diagnosis of heart failure has been criticised, in that patients with high concentrations of this peptide typically have classic signs, symptoms, and laboratory values greatly indicative of the disorder—ie, an accurate diagnosis can be made on clinical grounds. For individuals in whom a diagnosis of heart failure is less clear, BNP amounts often fall within an uncertain grey zone. The usefulness of this peptide is lessened by the fact that amounts are raised with advanced age, female sex, and renal impairment and are lowered with obesity. Nevertheless, plasma BNP testing is emerging as a useful aid for diagnosis of heart failure.
Management of Heart Failure
Clinical Assessment
Breathlessness, fatigue, and even edema may be due to a host of noncardiac conditions and do not necessarily indicate the presence of heart failure. Nevertheless, the clinician must have a high index of suspicion that the source of a patient’s problems may be cardiac and must become adept at assessing patients for fluid overload and cardiac abnormalities. Measurement of serum braiatriuretic peptide may aid in the diagnosis of heart failure. Serial measurements of weight at office visits, combined with instructions for daily weighing at home, help to alert the clinician and the patient to the possibility of fluid retention. The patient should be evaluated regularly in an appropriate position (45-degree elevation), with notation of the jugular venous pressure. Hepatojugular reflux, presence of a gallop rhythm, and peripheral edema are key findings on physical examination that may indicate a need for additional diuretic therapy and may be prognostically important.
Treatment of Patients with Stage A Heart Failure
Control of risk factors in stage A (e.g., hypertension, coronary artery disease, and diabetes mellitus) has a favorable effect on the incidence of later cardiovascular events (Figure 3). Results from trials have shown that the effective treatment of hypertension decreases the occurrence of left ventricular hypertrophy and cardiovascular mortality, as well as reducing the incidence of heart failure by 30 to 50 percent. Guidelines have recommended that the target for diastolic blood pressure in patients considered to be at high risk, particularly those with diabetes, be below
Figure 3. Stages of Heart Failure and Treatment Options for Systolic Heart Failure.
Patients with stage A heart failure are at high risk for heart failure but do not have structural heart disease or symptoms of heart failure. This group includes patients with hypertension, diabetes, coronary artery disease, previous exposure to cardiotoxic drugs, or a family history of cardiomyopathy. Patients with stage B heart failure have structural heart disease but have no symptoms of heart failure. This group includes patients with left ventricular hypertrophy, previous myocardial infarction, left ventricular systolic dysfunction, or valvular heart disease, all of whom would be considered to have New York Heart Association (NYHA) class I symptoms. Patients with stage C heart failure have known structural heart disease and current or previous symptoms of heart failure. Their symptoms may be classified as NYHA class I, II, III, or IV. Patients with stage D heart failure have refractory symptoms of heart failure at rest despite maximal medical therapy, are hospitalized, and require specialized interventions or hospice care. All such patients would be considered to have NYHA class IV symptoms. ACE denotes angiotensin-converting enzyme, ARB angiotensin-receptor blocker, and VAD ventricular assist device.
Treatment of Stage B, C, or D Heart Failure with or without Symptoms
The goals of therapy for patients with heart failure and a low ejection fraction are to improve survival, slow the progression of disease, alleviate symptoms, and minimize risk factors. Modifications of lifestyle can be helpful in controlling the symptoms of heart failure. For example, basic habits of moderate sodium restriction, weight monitoring, and adherence to medication schedules may aid in avoiding fluid retention or alerting the patient to its presence. Moderation of alcohol intake is advised; avoidance of nonsteroidal antiinflammatory drugs (NSAIDs) is also important. NSAIDs have been associated with an increase in the incidence of new heart failure, decompensated chronic heart failure, and hospitalizations for heart failure. For selected patients, a regularly scheduled exercise program may have beneficial effects on symptoms. ACE inhibitors decrease the conversion of angiotensin I to angiotensin II, thereby minimizing the multiple pathophysiological effects of angiotensin II, and decrease the degradation of bradykinin. Bradykinin promotes vasodilatation in the vascular endothelium and causes natriuresis in the kidney. The beneficial effects of ACE inhibitors in heart failure and after a myocardial infarction include improvements in survival, the rate of hospitalization, symptoms, cardiac performance, neurohormonal levels, and reverse remodeling.
ACE inhibitors have not been unequivocally shown to reduce the incidence of sudden death. They are recommended for many patients with stage A heart failure and all patients with stage B, stage C, or stage D heart failure. But unresolved issues persist. First, underuse of ACE inhibitors by physicians for fear of potential side effects has been a concern. Yet side effects are fairly predictable and reversible and can usually be successfully managed. Second, the optimal dose of an ACE inhibitor is uncertain. Most randomized trials have showo difference in mortality between patients receiving high-dose ACE inhibitors and those receiving low-dose ACE inhibitors. Finally, it is uncertain whether there are any meaningful differences among the many ACE inhibitors available today. Table 3 details some common clinical problems with recommended approaches.
Beta-blockers have long been used for the treatment of hypertension, angina, and arrhythmias and for prophylaxis in patients who have had a myocardial infarction. This class of medication has had a remarkable effect on chronic heart failure. The primary action of beta-blockers is to counteract the harmful effects of the sympathetic nervous system that are activated during heart failure. The beneficial effects of these drugs have been demonstrated in trials involving patients with heart failure from various causes and of all stages. These effects include improvements in survival, morbidity, ejection fraction, remodeling, quality of life, the rate of hospitalization, and the incidence of sudden death.3,57 Beta-blockers should be used in all patients in stable condition without substantial fluid retention and without recent exacerbations of heart failure requiring inotropic therapy. There are a few populations of patients in whom beta-blockers should not be used or should be used only with extreme caution. Such patients include those with reactive airway disease, those with diabetes in association with frequent episodes of hypoglycemia, and those with bradyarrhythmias or heart block who do not have a pacemaker.
Although the short-term effects of beta-blockers may result in a temporary exacerbation of symptoms, their long-term effects are uniformly beneficial. Placebo-controlled trials involving long-term treatment have shown improved systolic function after three months of treatment and reverse remodeling after four months. In the United States, two beta-blockers are specifically approved for the treatment of heart failure: carvedilol and long-acting metoprolol. Currently, neither drug has proved to be consistently superior; both have shown significant clinical efficacy. Carvedilol is a nonselective -adrenergic antagonist with alpha-blocking effects; metoprolol is a selective 1-adrenergic antagonist with no alpha-blocking effects. A large trial comparing these drugs is nearing completion. However, the most frequently prescribed beta-blocker in the United States is atenolol; there have beeo studies to date on the use of atenolol in patients with heart failure. Drugs that antagonize the sympathetic nervous system through alternative pathways, such as clonidine or moxonidine, have been less clinically useful in patients with heart failure.
Available angiotensin-receptor antagonists block the effects of angiotensin II at the angiotensin II subtype 1 receptor. The recently published guidelines recommend that these drugs should not be used as first-line therapy for heart failure of any stage but should be used only in patients who cannot tolerate ACE inhibitors because of severe cough or angioedema. Several trials involving patients with heart failure have shown that angiotensin-receptor antagonists have efficacy similar to that of ACE inhibitors but are not superior. On the other hand, in a randomized trial of patients with symptomatic left ventricular systolic dysfunction, the addition of valsartan to ACE-inhibitor treatment reduced the rate of the combined end point of death or cardiovascular events and improved clinical signs and symptoms of heart failure. However, patients who were receiving beta-blockers, an ACE inhibitor, and the angiotensin-receptor blocker valsartan had more adverse events and increased mortality. More recently, the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was completed in patients with stage B heart failure — specifically, asymptomatic patients with hypertension and left ventricular hypertrophy on electrocardiography. Treatment with the angiotensin-receptor blocker losartan yielded improvements in cardiovascular morbidity and survival, as well as a decrease in the incidence of new-onset diabetes, as compared with treatment with the beta-blocker atenolol.64 Thus, accumulating data lend support to the contention that angiotensin-receptor antagonists are a reasonable alternative to ACE inhibitors.
Additional Therapy for Symptomatic Patients with Stage C or Stage D Heart Failure
There is evidence to support the use of spironolactone, an aldosterone antagonist, in patients with advanced symptoms of heart failure — specifically, NYHA class III or IV symptoms. In patients with advanced heart failure, circulating levels of aldosterone become elevated in response to stimulation by angiotensin II, and there is a decrease in the hepatic clearance of aldosterone due to hepatic congestion. Aldosterone stimulates the retention of salt, myocardial hypertrophy, and potassium excretion; spironolactone counteracts these responses. The beneficial effects of spironolactone in heart failure may also include a decrease in collagen synthesis that promotes organ fibrosis.
Since heart failure is a salt-avid syndrome resulting in intravascular volume overload, diuretics are a mainstay for controlling symptoms of congestion. Thiazide or loop diuretics are often prescribed, and combination therapy may be used to promote effective diuresis in advanced cases.
It is only within the past five years that a large, randomized, placebo-controlled study of digoxin for symptomatic patients with a low ejection fraction has been completed. There was no difference in mortality between patients receiving digoxin and patients receiving placebo, but there were decreases in the digoxin group in the rates of worsening heart failure and hospitalization. Recent data suggest that the maintenance of a low serum digoxin concentration (<0.09 ng per milliliter) is as effective in reducing the rate of cardiovascular events as the maintenance of a higher concentration and is associated with a lower rate of toxic effects.70 Elderly patients and those with renal insufficiency are more prone to toxic effects. There is a commonly observed and clinically important interaction between digoxin and amiodarone: digoxin levels can become markedly elevated after the introduction of amiodarone.
There are some patients who cannot tolerate either ACE inhibitors or angiotensin-receptor blockers, usually because of hyperkalemia or renal insufficiency. In such patients who remain symptomatic despite diuretic and beta-blocker therapy, treatment with the vasodilator combination of hydralazine and isosorbide dinitrate may be an option.
Nonpharmacologic Therapy
Cardiac resynchronization therapy is an innovative, pacemaker-based approach to the treatment of patients with heart failure who have a wide QRS complex on 12-lead electrocardiography. The purpose of resynchronization is to provide electromechanical coordination and improved ventricular synchrony in symptomatic patients who have severe systolic dysfunction and clinically significant intraventricular conduction defects, particularly left bundle-branch block.
A percutaneous, three-lead, biventricular pacemaker system is used; one lead is placed in the right atrium, one is placed in the right ventricle, and a third is passed through the right atrium, through the coronary sinus, and into a cardiac vein on the lateral wall of the left ventricle. This left ventricular lead constitutes the key difference between resynchronization therapy and standard dual-chamber pacing. Beneficial effects include reverse remodeling, resulting in decreased heart size and ventricular volumes, improved ejection fraction, and decreased mitral regurgitation. Clinical improvements in exercise tolerance, quality of life, and the rate of hospitalization have been documented. To date, however, resynchronization therapy has not been shown to enhance survival.
Revascularization and Surgical Therapy
Patients with heart failure of any stage who are at risk for coronary artery disease should be screened for myocardial ischemia. Revascularization, through either a catheter-based or a surgical approach, often improves ischemic symptoms, improves cardiac performance, and reduces the risk of sudden death.79,80 Patients with stage C or stage D heart failure, who have heretofore been considered unacceptable candidates for surgery, may in fact derive substantial benefit from bypass surgery and additional techniques designed to reduce myocardial wall stress. Procedures to eliminate or exclude areas of infarction, repair mitral regurgitation, or support the failing myocardium are undergoing clinical trials. Similarly, the role of mechanical devices that serve to support patients who are awaiting heart transplantation or are definitive therapy for end-stage (stage D) heart failure continues to evolve, and such devices offer great hope to many patients who are not eligible for cardiac transplantation.
The Future
Many common clinical problems encountered in patients with heart failure remain unresolved. The role of anticoagulant therapy in patients with systolic dysfunction and sinus rhythm is unclear; neither the type of therapy needed nor the appropriate duration of treatment is known. There may be an important adverse interaction between aspirin and ACE inhibitors that will be clarified in upcoming trials.85 The optimal care for patients with heart failure and preserved systolic function (diastolic heart failure) awaits further research. The value of revascularization in patients with symptoms of heart failure but without angina will be explored in an important trial that is slated to begin soon. How will we identify patients with familial cardiomyopathy at an earlier stage? How do we identify patients with the greatest risk of sudden death? What is the best way to prevent sudden death in a cost-effective manner? Who will be best served by mechanical cardiac-support devices? Can we afford optimal care for the growing number of patients with heart failure? These questions and many others will undoubtedly be answered in the years to come. Perhaps our most intensive investigations, however, should be reserved for efforts that have been shown to prevent this cardiac plague — the control of hypertension and vascular risk factors.
Acute Heart Failure
See also European Society of Cardiology Guidelines on the Diagnosis and Treatmnet of Acute Heart Failure
Epidemiology, aetiology, and clinical context
The combination of the aging of the population in many countries, and improved survival after acute myocardial infarction (AMI) has created a rapid growth in the number of patients currently living with chronic heart failure (CHF), with a concomitant increase in the number of hospitalizations for decompensated heart failure. Coronary heart disease is the aetiology of AHF in 60–70% of patients, particularly in the elderly population. In younger subjects, AHF is frequently caused by dilated cadiomyopathy, arrhythmia, congenital or valvular heart disease, or myocarditis. The causes and complications of AHF are described in Table.
The management of heart failure consumes 1–2% of health care expenditure in European countries, with around 75% relating to inpatient care. Advanced heart failure and related acute decompensation have become the single most costly medical syndrome in cardiology.
Patients with AHF have a very poor prognosis. Mortality is particularly high in patients with acute myocardial infarction (AMI) accompanied by severe heart failure, with a 30% 12 month mortality. Likewise, in acute pulmonary oedema a 12% in-hospital and 40% 1 year mortality have been reported.
About 45% of patients hospitalized with AHF will be rehospitalized at least once (and 15% at least twice) within twelve months. Estimates of the risk of death or rehospitalization within 60 days of admission vary from 30 to 60%, depending on the population studied.
Table Causes and precipitating factors in AHF
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Definitions, diagnostic steps, instrumentation and monitoring of the patient with AHF
Definition and clinical classification of AHF
Acute heart failure is defined as the rapid onset of symptoms and signs secondary to abnormal cardiac function. It may occur with or without previous cardiac disease. The cardiac dysfunction can be related to systolic or diastolic dysfunction, to abnormalities in cardiac rhythm, or to pre-load and after-load mismatch. It is often life threatening and requires urgent treatment.
AHF can present itself as acute de novo (new onset of acute heart failure in a patient without previously known cardiac dysfunction) or acute decompensation of chronic heart failure.
The patient with acute heart failure may present with one of several distinct clinical conditions (Table):
i. Acute decompensated heart failure (de novo or as decompensation of chronic heart failure) with signs and symptoms of acute heart failure, which are mild and do not fulfil criteria for cardiogenic shock, pulmonary oedema or hypertensive crisis.
ii. Hypertensive AHF: Signs and symptoms of heart failure are accompanied by high blood pressure and relatively preserved left ventricular function with a chest radiograph compatible with acute pulmonary oedema.
iii. Pulmonary oedema (verified by chest X-ray) accompanied by severe respiratory distress, with crackles over the lung and orthopnoea, with O2 saturation usually <90% on room air prior to treatment.
iv. Cardiogenic shock: Cardiogenic shock is defined as evidence of tissue hypoperfusion induced by heart failure after correction of pre-load. There is no clear definition for haemodynamic parameters, which explains the differences in prevalence and outcome reported in studies (Table), but cardiogenic shock is usually characterized by reduced blood pressure (systolic BP <90 mmHg or a drop of mean arterial pressure>30 mmHg) and/or low urine output (<0.5 ml/kg/h), with a pulse rate >60 b.p.m. with or without evidence of organ congestion. There is a continuum from low cardiac output syndrome to cardiogenic shock.
v. High output failure is characterized by high cardiac output, usually with high heart rate (caused by arrhythmias, thyrotoxicosis, anaemia, Paget’s disease, iatrogenic or by other mechanisms), with warm peripheries, pulmonary congestion, and sometimes with low BP as in septic shock.
vi. Right heart failure is characterized by low output syndrome with increased jugular venous pressure, increased liver size and hypotension.
Various other classifications of the acute heart failure syndrome are utilized in coronary care and intensive care units. The Killip classification is based on clinical signs and chest X-ray findings, and the Forrester classification is based on clinical signs and haemodynamic characteristics. These classifications have been validated in acute heart failure after AMI and thus are best applied to acute de novo heart failure. The third ‘clinical severity’ classification has been validated in a cardiomyopathy service and is based on clinical findings. It is most applicable to chronic decompensated heart failure.
The Killip classification was designed to provide a clinical estimate of the severity of myocardial derangement in the treatment of AMI:
· StageI—No heart failure. No clinical signs of cardiac decompensation;
· StageII—Heart failure. Diagnostic criteria include rales, S3 gallop and pulmonary venous hypertension. Pulmonary congestion with wet rales in the lower half of the lung fields;
· StageIII—Severe heart failure. Frank pulmonary oedema with rales throughout the lung fields;
· StageIV—Cardiogenic shock. Signs include hypotension (SBP90mmHg), and evidence of peripheral vasoconstriction such as oliguria, cyanosis and diaphoresis.
The Forrester AHF classification was also developed in AMI patients, and describes four groups according to clinical and haemodynamic status (Figure). Patients are classified clinically on the basis of peripheral hypoperfusion (filliform pulse, cold clammy skin, peripheral cyanosis, hypotension, tachycardia, confusion, oliguria) and pulmonary congestion (rales, abnormal chest X-ray), and haemodynamically on the basis of a depressed cardiac index (2.2 L/min/m2) and elevated pulmonary capillary pressure (>18 mmHg). The original paper defined the treatment strategy according to the clinical and haemodynamic status. Mortality was 2.2% in group I, 10.1% in group II, 22.4% in group III, and 55.5% in group IV.
Figure Clinical classification of the mode of heart failure (Forrester classification). H I-IV refers to haemodynamic severity, with reference figures for CI and pulmonary capillary pressures shown on the vertical and horizontal axes, respectively. C I-IV refers to clinical severity.
‘Clinical severity’ classification.
The clinical severity classification is based on observation of the peripheral circulation (perfusion) and on auscultation of the lungs (congestion). The patients can be classified as Class I (Group A) (warm and dry), Class II (Group B) (warm and wet), Class III (Group L) (cold and dry), and Class IV (Group C) (cold and wet). This classification has been validated prognostically in a cardiomyopathy service, and is therefore applicable to patients with chronic heart failure, whether hospitalized or outpatients.
AHF is a clinical syndrome, with reduced cardiac output, tissue hypoperfusion, increase in the pulmonary capillary wedge pressure (PCWP), and tissue congestion. The underlying mechanism may be cardiac or extra-cardiac, and may be transient and reversible with resolution of the acute syndrome, or may induce permanent damage leading to chronic heart failure. The cardiac dysfunction can be related to systolic or diastolic myocardial dysfunction (mainly induced by ischaemia or infection), acute valvular dysfunction, pericardial tamponade, abnormalities of cardiac rhythm, or pre-load/after-load mismatch. Multiple extra-cardiac pathologies may result in acute heart failure by changing the cardiac loading conditions for example (i) increased after-load due to systemic or pulmonary hypertension or massive pulmonary emboli, (ii) increased pre-load due to increased volume intake or reduced excretion due to renal failure or endocrinopathy, or (iii) high output state due to infection, thyrotoxicosis, anaemia, Paget’s disease. Heart failure can be complicated by co-existing end-organ disease. Severe heart failure can also induce multi-organ failure, which may be lethal.
Appropriate long-term medical therapy and, if possible, anatomical correction of the underlying pathology may prevent further AHF syndrome ‘attacks’ and improve the poor long-term prognosis associated with this syndrome.
The clinical AHF syndrome may be classified as predominantly left or right forward failure, left or right backward failure, or a combination of these.
Forward acute heart failure may be mild-to-moderate with only effort fatigue, up to severe with manifestations of reduced tissue perfusion at rest with weakness, confusion, drowsiness, paleness with peripheral cyanosis, cold clammy skin, low blood pressure, filliform pulse, and oliguria, culminating in the full blown presentation of cardiogenic shock.
This syndrome may be induced by a large variety of pathologies. An adequate history may indicate the main diagnosis for example (i) acute coronary syndrome with the relevant risk factors, past history, and suggestive symptoms; (ii) acute myocarditis with a recent history suggestive of acute viral infection; (iii) acute valvular dysfunction with a history of chronic valve disease or valve surgery, infection with the possibility of bacterial endocarditis, or chest trauma; (iv) pulmonary embolism with a relevant history and suggestive symptoms; or (v) pericardial tamponade.
Physical examination of the cardiovascular system may be indicative of the main diagnosis, for example by distended neck veins and paradoxical pulse (pericardial tamponade), muffled heart sounds related to myocardial systolic dysfunction, or the disappearance of artificial valve sounds or an appropriate murmur indicating a valvular problem.
In forward AHF immediate management should include supportive treatment to improve cardiac output and tissue oxygenation. This can be achieved with vasodilating agents, fluid replacement to achieve an optimal pre-load, short-term inotropic support and (sometimes) intra-aortic balloon counterpulsation.
Left-heart backward failure may be related to left ventricular dysfunction with varying degrees of severity, from mild-to-moderate with only exertional dyspnoea, to pulmonary oedema presenting with shortness of breath (dry cough, sometimes with frothy sputum), pallor or even cyanosis, cold clammy skin, and normal or elevated blood pressure. Fine rales are usually audible over the lung fields. Chest X-ray shows pulmonary congestion/oedema.
Pathology of the left heart may be responsible for this syndrome, including: myocardial dysfunction related to chronic existing conditions; acute insult such as myocardial ischaemia or infarction; aortic and mitral valve dysfunction; cardiac rhythm disturbances; or tumours of the left heart. Extra-cardiac pathologies may include severe hypertension, high output states (anaemia, thyrotoxicosis) and neurogenic states (brain tumours or trauma).
Physical examination of the cardiovascular system, including the apex beat, the quality of the heart sounds, the presence of murmurs, and auscultation of the lungs for fine rales and expiratory wheezing (‘cardiac asthma’) may be indicative of the main diagnosis.
In left heart backward failure patients should be treated mainly with vasodilation and the addition of diuretics, bronchodilators and narcotics, as required. Respiratory support may be necessary. This can either be with continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation, or in some circumstances invasive ventilation may be required following endotracheal intubation.
The syndrome of acute right heart failure is related to pulmonary and right heart dysfunction, including exacerbations of chronic lung disease with pulmonary hypertension, or acute massive lung disease (e.g. massive pneumonia or pulmonary embolism), acute right ventricular infarction, tricuspid valve malfunction (traumatic or infectious), and acute or sub-acute pericardial disease. Advanced left heart disease progressing to right-sided failure should also be considered, and similarly long-standing congenital heart disease with evolving right ventricular failure should be taken into account. Non-cardiopulmonary pathologies include nephritic/nephrotic syndrome and end-stage liver disease. Various vasoactive peptide-secreting tumours should also be considered.
The typical presentation is with fatigue, pitting ankle oedema, tenderness in the upper abdomen (due to liver congestion), shortness of breath (with pleural effusion) and distension of the abdomen (with ascites). The full-blown syndrome includes anasarca with liver dysfunction and oliguria.
History and physical examination should confirm the syndrome of acute right heart failure, indicate the suspected diagnosis and guide further investigation, which is likely to include ECG, blood gases, D-dimer, chest X-ray, cardiac Doppler-echocardiography, angiography or chest CT scan.
In right heart backward failure fluid overload is managed with diuretics, including spironolactone, and sometimes with a short course of low dose (‘diuretic dose’) of dopamine. Concomitant treatment may include: antibiotics for pulmonary infection and bacterial endocarditis; Ca++ channel blockers, nitric oxide, or prostaglandins for primary pulmonary hypertension; and anticoagulants, thrombolytics, or thrombectomy for acute pulmonary embolism.
The vicious circle in the acute failing heart
The final common denominator in the syndrome of AHF is a critical inability of the myocardium to maintain a cardiac output sufficient to meet the demands of the peripheral circulation. Irrespective of the underlying cause of AHF, a vicious circle is activated that, if not appropriately treated, leads to chronic heart failure and death. This is shown in Figure, and is described in detail elsewhere.
Figure Pathophysiology of the syndrome of acute heart failure.
Following acute critical events, LV deterioration occurs rapidly and requires urgent medical treatment. The pathophysiology of the syndrome of heart failure is summarized. Mechanical, haemodynamic and neurohormonal changes are similar but not identical to those observed in CHF. The time course of development or reversal of these changes varies considerably and strongly depends on the underlying cause of LV deterioration as well as pre-existing cardiovascular disease. However, changes develop rapidly and therefore AHF is considerably different to the syndrome of CHF.
In order for patients with AHF to respond to treatment the myocardial dysfunction must be reversible. This is particularly important in AHF due to ischaemia, stunning or hibernation, where a dysfunctional myocardium can return to normal when appropriately treated.
Myocardial stunning is the myocardial dysfunction that occurs following prolonged ischaemia, which may persist in the short-term even wheormal blood flow is restored. The intensity and duration of stunning is dependent on the severity and duration of the preceding ischaemic insult.
Hibernation is defined as an impairment of myocardial function due to severely reduced coronary blood flow although myocardial cells are still intact. By improving blood flow and oxygenation, hibernating myocardium can restore its normal function.
Hibernating myocardium and stunning can co-exist. Hibernation improves in time with reinstitution of blood flow and oxygenation, whilst stunned myocardium retains inotropic reserve and can respond to inotropic stimulation. Since these mechanisms depend on the duration of myocardial damage, a rapid restoration of oxygenation and blood flow is mandatory to reverse these pathophysiological alterations.
The diagnosis of AHF is based on the symptoms and clinical findings, supported by appropriate investigations such as ECG, chest X-ray, biomarkers, and Doppler-echocardiography (Figure). The patient should be classified according to previously described criteria for systolic and/or diastolic dysfunction (Figure), and by the characteristics of forward or backward left or right heart failure.
Figure Diagnosis of AHF.
Figure Assessment of LV function in AHF.
Clinical evaluation
Systematic clinical assessment of the peripheral circulation, venous filling, and peripheral temperature are important.
Right ventricular (RV) filling in decompensated heart failure may usually be evaluated from the central jugular venous pressure. When the internal jugular veins are impractical for evaluation (e.g. due to venous valves) the external jugular veins can be used. Caution is necessary in the interpretation of high measured central venous pressure (CVP) in AHF, as this may be a reflection of decreased venous compliance together with decreased RV compliance even in the presence of low RV filling.
Left sided filling pressure is assessed by chest auscultation, with the presence of wet rales in the lung fields usually indicating raised pressure. The confirmation, classification of severity, and clinical follow-up of pulmonary congestion and pleural effusions should be done using the chest X-ray.
Class I recommendation, level of evidence C
Again, in acute conditions the clinical evaluation of left-sided filling pressure may be misleading due to the rapidly evolving clinical situation. Cardiac palpation and auscultation for ventricular and atrial gallop rhythms (S3, S4) should be performed. The quality of the heart sounds, and the presence of atrial and ventricular gallops and valvular murmurs are important for diagnosis and clinical assessment. Assessment of the extent of arteriosclerosis by detecting missing pulses and the presence of carotid and abdominal bruits is often important, particularly in elderly subjects.
A normal ECG is uncommon in acute heart failure. The ECG is able to identify the rhythm, and may help determine the aetiology of AHF and assess the loading conditions of the heart. It is essential in the assessment of acute coronary syndromes. The ECG may also indicate acute right or left ventricular or atrial strain, perimyocarditis and pre-existing conditions such as left and right ventricular hypertrophy or dilated cardiomyopathy. Cardiac arrhythmia should be assessed in the 12-lead ECG as well as in continuous ECG monitoring.
Chest X-ray and imaging techniques
Chest X-ray and other imaging should be performed early for all patients with AHF to evaluate pre-existing chest or cardiac conditions (cardiac size and shape) and to assess pulmonary congestion. It is used both for confirmation of the diagnosis, and for follow-up of improvement or unsatisfactory response to therapy. Chest X-ray allows the differential diagnosis of left heart failure from inflammatory or infectious lung diseases. Chest CT scan with or without contrast angiography and scintigraphy may be used to clarify the pulmonary pathology and diagnose major pulmonary embolism. CT scan or transesophageal echocardiography should be used in cases of suspicion of aortic dissection.
A number of laboratory tests should be performed in AHF patients (Table). Arterial blood gas analysis (Astrup) enables assessment of oxygenation (pO2), respiratory adequacy (pCO2), acid–base balance (pH), and base deficit, and should be performed in all patients with severe heart failure. Non-invasive measurement with pulse oximetry and end-tidal CO2 can often replace Astrup (Level of evidence C) but not in very low output, vasocontricted shock states. Measurement of venous O2 saturation (i.e. in the jugular vein) may be useful for an estimation of the total body oxygen supply-demand balance.
Table Laboratory tests in patients hospitalized with AHF
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Other specific laboratory tests should be taken for differential diagnostic purposes or in order to identify end-organ dysfunction.
INR=international normalized ratio of thromboplastin time; TnI=troponin I; TnT=troponin T.
Plasma B-type natriuretic peptide (BNP) is released from the cardiac ventricles in response to increased wall stretch and volume overload and has been used to exclude and/or identify congestive heart failure (CHF) in patients admitted, for dyspnoea, to the emergency department. Decision cut points of 300 pg/mL for NT-proBNP and 100 pg/mL for BNP have been proposed, but the older population has been poorly studied. During ‘flash’ pulmonary oedema, BNP levels may remain normal at the time of admission. Otherwise, BNP has a good negative predictive value to exclude heart failure. Various clinical conditions may affect the BNP concentration including renal failure and septicaemia. If elevated concentrations are present, further diagnostic tests are required. If AHF is confirmed, increased levels of plasma BNP and NT-pro BNP carry important prognostic information. The exact role of BNP remains to be fully clarified.
Echocardiography is an essential tool for the evaluation of the functional and structural changes underlying or associated with AHF, as well as in the assessment of acute coronary syndromes.
Organization of the treatment of AHF
Best results are achieved if patients with AHF are treated promptly by expert staff in areas reserved for heart failure patients. An experienced cardiologist and/or other suitably trained staff should treat AHF patients. The diagnostic services should provide early access to diagnostic procedures such as echocardiography and coronary angiography, as needed.
Treatment of patients with AHF requires a treatment plan in the hospital system.
Class I recommendation, level of evidence B
Comparative studies have shown shorter hospitalization time in patients treated by staff trained in heart failure management. The treatment of AHF should be followed by a subsequent HF clinic programme when applicable and as recommended by ESC guidelines.
The care and informatioeeds of the acutely ill patient and his/her family will usually be addressed by expert nurses.
Heart failure staff nurses and cardiology/heart failure/intensive care specialists should be given the opportunity for continuing professional education.
Recommendations on the standard structure, nursing staff and equipment requirements in intensive cardiology care units and relevant step-down care units based on the expert opinion of the Working Group of Acute Cardiac Care are under preparation.
Instrumentation and monitoring of patients in AHF
Monitoring of the patient with AHF should be initiated as soon as possible after his/her arrival at the emergency unit, concurrently with ongoing diagnostic measures addressed at determining the primary aetiology. The types and level of monitoring required for any individual patient vary widely depending on the severity of the cardiac decompensation and the response to initial therapy. Local logistic issues may also be relevant. The guidelines on monitoring discussed here are based on expert opinion.
In all critically ill patients, BP measurements should be made routinely; blood pressure, temperature, respiratory rate, heart rate, the electrocardiogram and blood pressure is mandatory. Some laboratory tests should be done repeatedly i.e. electrolytes, creatinine and glucose or markers for infection or other metabolic disorders. Hypo– or hyperkalaemia must be controlled. These can all be monitored easily and accurately with modern automated equipment. If the patient becomes more unwell, the frequency of these observations will need to be increased.
ECG monitoring (arrhythmias and ST segment) is necessary during the acute decompensation phase, particularly if ischaemia or arrhythmia is responsible for the acute event.
Class I recommendation, level of evidence C
Maintenance of normal blood pressure is critical during the initiation of therapy, and consequently it should be measured regularly (e.g. every 5 minutes), until the dosage of vasodilators, diuretics or inotropes has been stabilized. The reliability of non-invasive, automatic plethysmographic measurement of blood pressure is good in the absence of intense vasoconstriction and very high heart rate.
Class I recommendation, level of evidence C
The pulse oximeter is a simple non-invasive device that estimates the arterial saturation of haemoglobin with oxygen (SaO2). The estimate of the SaO2 is usually within 2% of a measured value from a co-oximeter, unless the patient is in cardiogenic shock. The pulse oximeter should be used continuously on any unstable patient who is being treated with a fraction of inspired oxygen (FiO2) that is greater than in air. It should also be used at regular intervals (every hour) on any patient receiving oxygen therapy for an acute decompensation.
Class I recommendation, level of evidence C
Cardiac output and pre-load can be monitored non-invasively with the use of Doppler techniques (see Section 5.5.). There is little to no evidence to help choose which of these to monitor and it makes no difference as long as the limitations of individual monitoring devices are understood and the data are used appropriately.
Class IIb recommendation, level of evidence C
Arterial line.
The indications for the insertion of an in-dwelling arterial catheter are the need for either continuous beat-to-beat analysis of arterial blood pressure due to haemodynamic instability or the requirement for multiple arterial blood analyses. The complication rate for the insertion of a 20-gauge 2-inch radial artery catheter is low.
Class IIb recommendation, level of evidence C
Central venous pressure lines.
Central venous lines provide access to the central venous circulation and are therefore useful for the delivery of fluids and drugs and can also be used to monitor the CVP and venous oxygen saturation (SvO2) in the superior vena cava (SVC) or right atrium, which provides an estimate of oxygen transport.
Class II b recommendation, level of evidence C
Caution has to be advised, however, to avoid the over-interpretation of right atrial pressure measurements, as these rarely correlate with left atrial pressures, and therefore left ventricular (LV) filling pressures, in patients with AHF. CVP measurements are also affected by the presence of significant tricuspid regurgitation and positive end-expiratory pressure (PEEP) ventilation.
Class I recommendation, level of evidence C
The pulmonary artery catheter (PAC) is a balloon flotation catheter that measures pressures in the superior vena cava (SVC), right atrium, right ventricle and pulmonary artery as well as cardiac output. Modern catheters can measure the cardiac output semi-continuously as well as the mixed venous oxygen saturation and right ventricular end diastolic volume and ejection fraction.
Although the insertion of a PAC for the diagnosis of AHF is usually unnecessary, it can be used to distinguish between a cardiogenic and a non-cardiogenic mechanism in complex patients with concurrent cardiac and pulmonary disease. The PAC is also frequently used to estimate PCWP, cardiac output and other haemodynamic variables and therefore guide therapy in the presence of severe diffuse pulmonary pathology or ongoing haemodynamic compromise not resolved by initial therapy. PCWP is not an accurate reflection of left ventricular end–diastolic pressure (LVEDP) in patients with mitral stenosis (MS) aortic regurgitation (AR), ventricular interdependence, high airway pressure, or stiff LV, due to, for example, left ventricular hypertrophy (LVH), diabetes, fibrosis, inotropes, obesity, ischaemia. Severe tricuspid regurgitation, frequently found in patients with AHF, can overestimate or underestimate cardiac output measured by thermodilution.
Several retrospective studies assessing the use of the PAC in acute myocardial infarction demonstrated increased mortality with the PAC. These observations were partially explained by case-mix differences between the groups of the study. Similar observational findings have subsequently been reported in other groups of patients. A recent prospective randomized study enrolling a mixed group of critically ill patients failed to demonstrate a difference in outcome, although randomization to the PAC led to increased fluid resuscitation within the first 24 h. The PAC did not cause harm to patients, rather it was the use of the information derived from the catheter (sometimes in an inappropriate fashion) that was detrimental.
The use of a PAC is recommended in haemodynamically unstable patients who are not responding in a predictable fashion to traditional treatments, and in patients with a combination of congestion and hypoperfusion. In these cases it is inserted in order to ensure optimal fluid loading of the ventricles and to guide vasoactive therapies and inotropic agents. Because the complications increase with the duration of its use, it is critical to insert the catheter when specific data are needed (usually regarding the fluid status of the patient) and to remove it as soon as it is of no further help (i.e. when diuretic and vasodilating therapy have been optimized).
In AHF patients: Decreased CI: <2.2 L/min/m2; PCWP: low if <14 mmHg, high if >18–20 mmHg.
Class IIb recommendation, level of evidence C
In cardiogenic shock and prolonged severe low output syndrome it is recommended that the mixed venous oxygen saturation from the pulmonary artery be measured as an estimation of oxygen extraction (SpO2–SvO2). The aim should be to maintain SvO2 above 65% in patients with AHF.
General medical issues in the treatment of AHF
Infections: Patients with advanced AHF are prone to infectious complications, commonly respiratory or urinary tract infections, septicaemia, or nosocomial infection with Gram positive bacteria. An increase in C-reactive protein (CRP) and a decrease in general condition may be the only signs of infection—fever may be absent. Meticulous infection control and measures to maintain skin integrity are mandatory. Routine cultures are recommended. Prompt antibiotic therapy should be given when indicated.
Diabetes: AHF is associated with impaired metabolic control. Hyperglycaemia occurs commonly. Routine hypoglycaemic drugs should be stopped and glycaemic control should be obtained by using short-acting insulin titrated according to repeated blood glucose measurements. Normoglycaemia improves survival in diabetic patients who are critically ill.
Catabolic state: negative caloric and nitrogen balance is a problem in ongoing AHF. This is related to reduced caloric intake due to reduced intestinal absorption. Care should be undertaken to maintain calorie and nitrogen balance. Serum albumin concentration, as well as nitrogen balance, may help to monitor metabolic status.
Renal failure: a close interrelationship exists between AHF and renal failure. Both may cause, aggravate, and influence, the outcome of the other. Close monitoring of renal function is mandatory. Preservation of renal function is a major consideration in the selection of the appropriate therapeutic strategy for these patients.
Oxygen and ventilatory assistance
Rationale for using oxygen in AHF
The maintenance of an SaO2 within the normal range (95–98%) is important in order to maximize oxygen delivery to the tissues and tissue oxygenation, thus helping to prevent end-organ dysfunction and multiple organ failure.
Class I recommendation, level of evidence C
This is best achieved first by ensuring that there is a patent airway and then by administration of an increased FiO2. Endotracheal intubation is indicated if these measures fail to improve tissue oxygenation.
Class IIa recommendation, level of evidence C
Despite this intuitive approach to giving oxygen, there is little to no evidence available that giving increasing doses of oxygen results in an improved outcome. Studies have demonstrated that hyperoxia can be associated with reduced coronary blood flow, reduced cardiac output, increased blood pressure, increased systemic vascular resistance, and a trend to higher mortality.
The administration of increased concentrations of oxygen to hypoxaemic patients with acute cardiac failure is unquestionably warranted.
Class IIa recommendation, level of evidence C
use of increased concentrations of oxygen in patients without evidence of hypoxaemia is more controversial and may cause harm.
Ventilatory support without endotracheal intubation (non-invasive ventilation)
Two techniques are used for ventilatory support: CPAP or non-invasive positive pressure ventilation (NIPPV). NIPPV is a method of providing mechanical ventilation to patients without the need for endotracheal intubation. There is a strong consensus that one of these two techniques should be used before endotracheal intubation and mechanical ventilation. Utilization of non-invasive techniques dramatically reduce the need for endotracheal intubation and mechanical ventilation.
Application of CPAP can cause pulmonary recruitment and is associated with an increase in the functional residual capacity. The improved pulmonary compliance, reduced transdiaphragmatic pressure swings, and decreased diaphragmatic activity can lead to a decrease in the overall work of breathing and therefore a decreased metabolic demand from the body. NIPPV is a more sophisticated technique that requires a ventilator. Addition of a PEEP to the inspiratory assistance results in a CPAP mode (also known as bilevel positive pressure support, BiPAP). The physiological benefits of this mode of ventilation are the same as for CPAP but also include the inspiratory assist which further reduces the work of breathing and the overall metabolic demand.
Evidence for the use of CPAP and NIPPV in left ventricular failure
CPAP in patients with cardiogenic pulmonary oedema improves oxygenation, decreases symptoms and signs of AHF, and results in a decreased need for endotracheal intubation. The studies have been relatively small and therefore have not reported a statistically significant reduction in mortality. A systematic review following the first three trials suggested that CPAP was associated with a decreased need for intubation and a trend to decreased in-hospital mortality compared to standard therapy alone. Evidence was lacking, however, on the potential for CPAP to actually cause harm.
There have been three randomized controlled trials of the use of NIPPV in the setting of acute cardiogenic pulmonary oedema. NIPPV appears to decrease the need for endotracheal intubation, but this does not translate into a reduction in mortality or improvement in long-term function.
The use of CPAP and NIPPV in acute cardiogenic pulmonary oedema is associated with a significant reduction in the need for tracheal intubation and mechanical ventilation.
Class IIa recommendation, level of evidence A
There are insufficient data to demonstrate a significant reduction in mortality; however, the data do not trend in that direction.
Mechanical ventilation with endotracheal intubation in AHF
Invasive mechanical ventilation (with endotracheal intubation) should not be used to reverse hypoxaemia that could be better restored by oxygen therapy, CPAP, or NIPPV, but rather to reverse AHF-induced respiratory muscle fatigue. The latter is the most frequent reason for endotracheal intubation and mechanical ventilation. Respiratory muscle fatigue may be diagnosed by a decrease in respiratory rate, associated with hypercapnia and confused state of mind.
Invasive mechanical ventilation should only be used if acute respiratory failure does not respond to vasodilators, oxygen therapy, and/or CPAP, or NIPPV. Another consideration should be the need for immediate intervention in a patient with pulmonary oedema secondary to ST-elevation acute coronary syndrome.
Morphine and its analogues in AHF
Morphine is indicated in the early stage of the treatment of a patient admitted with severe AHF, especially if associated with restlessness and dyspnoea.
Class IIb recommendation, level of evidence B
Morphine induces venodilatation and mild arterial dilatation, and reduces heart rate. In most studies, iv boluses of morphine 3 mg were administered as soon as the intravenous line was inserted. This dosing can be repeated if required.
Anticoagulation is well established in acute coronary syndrome with or without heart failure. The same is true in atrial fibrillation. There is less evidence for the initiation of unfractionated heparin or low molecular weight heparin (LMWH) in AHF. A large placebo-controlled trial of enoxaparine 40 mg subcutaneoulsy in acutely ill and hospitalized patients, including a major group of heart failure patients, showed no clinical improvement but less venous thrombosis. There are no large comparative studies comparing LMWH to unfractionated heparin (given as 5000 IU twice or thrice daily). Careful monitoring of the coagulation system is mandatory in AHF as there is often concomitant liver dysfunction. LMWH is contraindicated if the creatinine clearance is below 30 mL/min or should be used with extreme care with monitoring of the anti-Factor Xa level.
Vasodilators in the treatment of AHF
Vasodilators are indicated in most patients with acute heart failure as first line therapy, if hypoperfusion is associated with an adequate blood pressure and signs of congestion with low diuresis, to open the peripheral circulation and to lower pre-load (Table).
Table Indications and dosing of vasodilators in AHF
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Nitrates
Nitrates relieve pulmonary congestion without compromising stroke volume or increasing myocardial oxygen demand in acute left heart failure, particularly in patients with acute coronary syndrome. At low doses they only induce venodilation, but as the dose is gradually increased they cause the arteries, including the coronary arteries, to dilate. With appropriate doses, nitrates exert balanced vasodilation of the venous and arterial sides of the circulation, thereby reducing LV pre-load and after-load, without impairing tissue perfusion. Their effect on cardiac output depends on pre-treatment pre-load and after-load and the ability of the heart to respond to baroreceptor-induced increases in sympathetic tone.
Initially nitrates may be given orally but intravenous nitrates are also well tolerated in AMI. Two randomized trials in AHF have established the efficacy of intravenous nitrates in combination with furosemide and have demonstrated that titration to the highest haemodynamically tolerable dose of nitrates with low dose furosemide is superior to high dose diuretic treatment alone.
Class I recommendation, level of evidence B
In one of these randomized studies furosemide and isosorbide dinitrate as bolus injections were tested and it was reported that intravenous high dose nitrate was more effective than furosemide treatment in controlling severe pulmonary oedema.
In practical use nitrates have a U-shaped curve effect. If given in sub-optimal doses vasodilators may have a limited effect in preventing AHF recurrences. However, administration of high doses may also reduce their effectiveness. One disadvantage of nitrates is the rapid development of tolerance especially when given intravenously in high doses, limiting their effectiveness to 16–24 h only. Nitrates should be given at doses aimed at achieving optimal vasodilation, leading to an increase in cardiac index (CI) and decrease in pulmonary wedge pressure. Inappropriate vasodilation may induce a steep reduction in blood pressure, which may result in haemodynamic instability.
Nitroglycerin can be administered orally or by inhalation [glyceryl trinitrate (GTN) spray 400 µg (2 puffs) every 5–10 min], or buccally (isosorbide dinitrate 1 or 3 mg), while monitoring blood pressure. The intravenous administration and dosing of nitrates (glycerylnitrate 20 µg/min increasing dose to 200 µg/min, or isosorbide dinitrate 1–10 mg/h) should be done with extreme caution, under careful blood pressure monitoring, titrating the dose administered against blood pressure decrease. One should be particularly cautious when administering nitrates to a patient with aortic stenosis, although this therapy may help in these complex situations. The dose of nitrates should be reduced if systolic blood pressure falls below 90–100 mmHg and discontinued permanently if blood pressure drops further. From a practical point of view a reduction of 10 mmHg in mean arterial pressure should be achieved.
Sodium nitroprusside (SNP) (0.3 µg/kg/min up-titrating carefully to 1 µg/kg/min up to 5 µg/kg/min) is recommended in patients with severe heart failure, and in patients with predominantly increased after-load such as hypertensive heart failure or mitral regurgitation.
Class I recommendation, level of evidence C
SNP should be titrated cautiously and usually requires invasive arterial monitoring and close supervision. Prolonged administration may be associated with toxicity from its metabolites, thiocyanide and cyanide, and should be avoided especially in patients with severe renal or hepatic failure. Controlled trials with SNP in AHF are lacking and its administration in AMI has yielded equivocal results. SNP should be tapered down to avoid rebound effects. In AHF caused by acute coronary syndromes, nitrates are favoured over SNP as SNP may cause ‘coronary steal syndrome’.
Recently, nesiritide, a new class of vasodilator, has been developed for the treatment of AHF. Nesiritide is a recombinant human brain or B-type natriuretic peptide (BNP) that is identical to the endogenous hormone. Nesiritide has venous, arterial, and coronary vasodilatory properties that reduce pre-load and after-load, and increase cardiac output without direct inotropic effects.
Systemic infusion of nesiritide in patients with CHF has beneficial haemodynamic actions, results in an enhanced sodium excretion, and suppression of the renin–angiotensin–aldosterone and sympathetic nervous systems. Nesiritide was compared to intravenous nitroglycerin and resulted in improvement in haemodynamics more effectively and with fewer adverse effects, although this did not translate into improvement in clinical outcome. Nesiritide may cause hypotension and some patients are non-responders.
Calcium antagonists are not recommended in the treatment of AHF. Diltiazem and verapamil, and dihydropyridines, should be considered contraindicated.
Angiotensin converting enzyme (ACE)-inhibitors in AHF.
Indications.
ACE-inhibitors are not indicated in the early stabilization of patients with AHF.
Class IIb recommendation, level of evidence C
However, as these patients are at high risk, ACE-inhibitors have a role in early management of AHF patients and AMI. There is still debate on the selection of patients and the timing of initiation of ACE-inhibitor therapy.
Effects and mechanism of action.
The haemodynamic effects of ACE-inhibitors result from decreased formation of AII and increased levels of bradykinin, which in turn decreases total peripheral vascular resistances and promotes natriuresis. Short-term treatment is accompanied by a decrease in angiotensin II (AII) and aldosterone and an increase in angiotensin I and plasma renin activity.
There have beeo efficacy studies of ACE-inhibitors in AHF to date. Studies with ACE-inhibitors in heart failure after myocardial infarction have focused on long-term effects. A recent meta-analysis found that mortality at 30 days was reduced from 7.6% in the placebo group to 7.1% in the ACE-inhibitor group [relative risk reduction 7% (95% CI 2–11%, P<0.004)]. This equates to about five fewer deaths per 1000 patients treated for 4–6 weeks [number needed to treat (NNT) to prevent one death=200]. The trials which selected high-risk patients found that ACE-inhibitors led to large relative and absolute reductions in mortality.
Intravenous ACE-inhibition should be avoided. The initial dose of the ACE-inhibitor should be low and increased progressively after early stabilization within 48 h with monitoring of blood pressure and renal function. The duration of therapy, when initiated, should be at least six weeks.
Class I recommendation, level of evidence A
ACE-inhibitors should be used with caution in patients with marginal cardiac output as they may significantly reduce glomerular filtration.The risk of intolerance to the ACE-inhibitors is increased by the concomitant administration of non-steroid anti-inflammatory agents, and in the presence of bilateral renal artery stenosis.
Indications.
Administration of diuretics is indicated in patients with acute and acutely decompensated heart failure in the presence of symptoms secondary to fluid retention.
Class I recommendation, level of evidence B
The symptomatic benefits and their universal clinical acceptance have precluded a formal evaluation in large-scale randomized clinical trials.
Effects and mechanisms of action.
Diuretics increase the urine volume by enhancing the excretion of water, sodium chloride and other ions, leading to a decrease in plasma and extracellular fluid volume, total body water and sodium, a reduction in right and left ventricular filling pressures and a decrease in peripheral congestion and pulmonary oedema. Intravenous administration of loop diuretics also exerts a vasodilating effect, manifested by an early (5–30 min) decrease in right atrial and pulmonary wedge pressure as well as pulmonary resistances. With high bolus doses (>1 mg/kg) there is a risk of reflex vasoconstriction. As opposed to chronic use of diuretics, in severe decompensated heart failure the use of diuretics normalizes loading conditions and may reduce neurohormonal activation in the short term. Especially in acute coronary syndromes diuretics should be used in low doses and preference given to vasodilator therapy.
Intravenous administration of loop diuretics (furosemide, bumetanide, torasemide), with a strong and brisk diuretic effect is the preferred choice in patients with AHF. Therapy can safely be initiated before hospital admission and the dose should be titrated according to the diuretic response and relief of congestive symptoms. Administration of a loading dose followed by continued infusion of furosemide or torasemide have been shown to be more effective than bolus alone. Thiazides and spironolactone can be used in association with loop diuretics, the combination in low doses being more effective and having with fewer secondary effects than the use of higher doses of a single drug. Combination of loop diuretics with dobutamine, dopamineor nitrates is also a therapeutic approach that is more effective and produces fewer secondary effects than increasing the dose of the diuretic.
Class IIb recommendation, level of evidence C
Table below lists the recommendations for the practical use of diuretics. Table gives the recommended doses of commonly used diuretics in heart failure.
Table Practical use of diuretics in AHF
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Table Diuretic dosing and administration
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HCTZ=hydrochlorothiazide.
Diuretic resistance.
Diuretic resistance is defined as the clinical state in which diuretic response is diminished or lost before the therapeutic goal of oedema relief has been achieved. Such resistance is associated with a poor prognosis. It is more frequent in patients with chronic, severe heart failure on long-term diuretic therapy, although it has also been reported with acute volume depletion after intravenous administration of loop diuretics. Diuretic resistance can be attributed to a number of factors . A number of therapeutic approaches to overcome diuretic resistance have been explored, and in clinical practice different strategies may be of value in a particular patient. Continuous infusion of furosemide is more effective than individual boluses.
Secondary effects, drug interactions.
Although diuretics can be used safely in the majority of patients, secondary effects are frequent and may be life-threatening. They include neurohormonal activation, especially of the angiotensin–aldosterone system and the sympathetic nervous system, hypokalaemia, hypomagnesaemia, and hypochloraemic alkalosis that may lead to severe arrhythmias, and nephrotoxicity and aggravation of renal failure. Excessive diuresis may reduce venous pressure, pulmonary wedge pressure and diastolic filling excessively, leading to a reduction in stroke volume and cardiac output, particularly in patients with severe heart failure and predominant diastolic failure or ischaemic RV dysfunction. Intravenous administration of acetazolamide (1 or 2 doses) may be helpful for the correction of alkalosis.
Some new compounds with diuretic and other effects are under investigation, including vasopressin V2 receptor antagonists, braiatriuretic peptides and adenosine receptor antagonists.
Indications and rationale for ß-blocking agents.
There has beeo study with ß-blocker therapy in AHF targeted to acutely improve the condition. On the contrary, AHF has been considered a contraindication for this treatment. Patients with more than basal pulmonary rales, or hypotension, have been excluded from trials early after AMI. In patients with AMI who are not in overt heart failure or hypotensive, ß-blockers limit infarct size, reduce life-threatening arrhythmias and relieve pain.
Intravenous administration should be considered in patients with ischaemic chest pain resistant to opiates, recurrent ischaemia, hypertension, tachycardia, or arrhythmia. In the Gothenburg metoprolol study, intravenous metoprolol or placebo was initiated early after an AMI and followed by oral therapy for three months. Fewer patients developed heart failure in the metoprolol group. In patients with signs of pulmonary congestion with basal rales and/or treatment with intravenous furosemide, metoprolol therapy had even greater effects and reduced mortality and morbidity. There is experience with the short acting ß-blocker esmolol mainly in the setting of cardiac surgery. One small study has compared celiprolol and esmolol in severe heart failure. Celiprolol reduced CI less at similar heart rate reduction, which was claimed to be due to differences in the vasodilation effect. The clinical importance of this difference is unclear. Invasive haemodynamic monitoring was carried out in the MIAMI trial on patients with elevated pulmonary wedge pressures up to 30 mmHg. These patients when treated with metoprolol showed a decrease in filling pressures.
In patients with overt AHF and more than basal pulmonary rales, ß-blockers should be used cautiously. Among such patients in whom ongoing ischaemia and tachycardia are present, intravenous metoprolol can be considered.
Class IIb recommendation, level of evidence C
However, in patients with an AMI who stabilize after developing AHF, ß-blockers should be initiated early.
Class IIa recommendation, level of evidence B
In patients with chronic heart failure, ß-blockers should be initiated when the patient has stabilized after the acute episode (usually after 4 days).
Class I recommendation, level of evidence A
The initial oral dose of bisoprolol, carvedilol, or metoprolol should be small and increased slowly and progressively to the target dose used in the large clinical trials. Up-titration should be adapted to individual response. ß-blockers may reduce blood pressure and heart rate excessively. As a general rule, patients on ß-blockers admitted to hospital due to worsening heart failure should be continued on this therapy unless inotropic support is needed but the dose could be reduced if signs of excessive dosage are suspected (i.e. bradycardia and hypotension).
Clinical indications.
Inotropic agents are indicated in the presence of peripheral hypoperfusion (hypotension, decreased renal function) with or without congestion or pulmonary oedema refractory to diuretics and vasodilators at optimal doses (Figure)
Figure Rationale for inotropic drugs in AHF
Class IIa recommendation, level of evidence C
Their use is potentially harmful as they increase oxygen demand and calcium loading and they should be used with caution.
In patients with decompensated CHF the symptoms, clinical course, and prognosis of the disease may become critically dependent on the haemodynamics. Thus, improvements in the haemodynamic parameters may become a goal of treatment and inotropic agents may be useful and life-saving in this setting. The beneficial effects of an improvement in the haemodynamic parameters is, however, partially counteracted by the risks of arrhythmias and, in some cases, myocardial ischaemia and by the possible long-term progression of myocardial dysfunction caused by an excessive increase in energy expenditure. The risk-benefit ratio may not, however, be the same for all the inotropic agents. Those acting through the stimulation of the ß1-adrenergic receptors which increase cytoplasmic myocardial cell Ca++ concentration may be associated with the greatest risk. Lastly, only a few controlled trials with inotropic agents in patients with AHF have been performed, and very few have assessed their effects on the symptoms and signs of heart failure and their long-term effects on prognosis.
At low doses (<2 µg/kg/min i.v.) dopamine acts only on peripheral dopaminergic receptors and lowers peripheral resistance both directly and indirectly. Vasodilation occurs predominantly in the renal, splanchnic, coronary, and cerebral vascular beds. At this dosage, its action may cause an improvement in renal blood flow, glomerular filtration rate, diuresis, and sodium excretion rate, with an increased response to diuretic agents, in patients with renal hypoperfusion and failure.
At higher doses (>2 µg/kg/min i.v.) dopamine stimulates the ß-adrenergic receptors both directly and indirectly with a consequent increase in myocardial contractility and cardiac output. At doses >5 µg/kg/min dopamine acts on -adrenergic receptors with an increase in the peripheral vascular resistance which, though potentially useful in hypotensive patients, may be deleterious in patients with AHF, as it may augment the LV after-load, pulmonary artery pressure, and pulmonary resistance.
Dobutamine is a positive inotropic agent acting mainly through stimulation of ß1-receptors and ß2-receptors to produce dose-dependent positive inotropic and chronotropic effects, and a reflex decrease in sympathetic tone, and thus vascular resistance. The resultant benefit may therefore differ from patient to patient. At low doses, dobutamine induces mild arterial vasodilatation, which augments stroke volume by reductions in after-load. At higher doses dobutamine causes vasoconstriction.
Heart rate is generally increased in a dose-dependent manner to a lesser extent than with other cathecholamines. However, in patients with atrial fibrillation, heart rate may be increased to undesirable rates, due to facilitation of atrioventricular (AV) conduction. Systemic arterial pressure usually increases slightly, but may remain stable, or decrease. Similarly pulmonary arterial pressure and capillary wedge pressure usually decrease, but may remain stable or even increase in some patients with heart failure.
The improved diuresis observed during dobutamine infusion in patients with heart failure is the result of increased renal blood flow in response to improved cardiac output.
Dopamine may be used as an inotrope (>2 µg/kg/min i.v.) in AHF with hypotension. Infusion of low doses of dopamine (2–3 µg/kg/min) may be used to improve renal blood flow and diuresis in decompensated heart failure with hypotension and low urine output. However if no response is seen the therapy should be terminated (Table)
Table Administration of positive inotropic agents
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Class of recommendation IIb, level of evidence C
Dobutamine is currently indicated when there is evidence of peripheral hypoperfusion (hypotension, decreased renal function) with or without congestion or pulmonary oedema refractory to diuretics and vasodilators at optimal doses (Table ).
Class IIa recommendation, level of evidence C
Dobutamine is used to increase the cardiac output. It is usually initiated with a 2–3 µg/kg/min infusion rate without a loading dose. The infusion rate may then be progressively modified according to symptoms, diuretic response, or haemodynamic monitoring. Its haemodynamic actions are proportional to its dosage, which can be increased to 20 µg/kg/min. The elimination of the drug is rapid after cessation of infusion, making it a very convenient inotropic agent.
In patients receiving ß-blocker therapy with metoprolol, dobutamine doses have to be increased as high as 15–20 µg/kg/min to restore its inotropic effect. The effect of dobutamine differs in patients receiving carvedilol: it can lead to an increase in pulmonary vascular resistance during the infusion of increasing doses of dobutamine (5–20 µg/kg/min).
Based on haemodynamic data alone, the inotropic effect of dobutamine is additive to that of phosphodieasterase inhibitors (PDEI); the combination of PDEI and dobutamine produces a positive inotropic effect greater than either drug alone.
Prolonged infusion of dobutamine (above 24–48 h) is associated with tolerance and partial loss of haemodynamic effects. Weaning from dobutamine may be difficult because of recurrence of hypotension, congestion, or renal insufficiency. This can sometimes be solved by very progressive tapering of dobutamine (i.e. decrease in dosage by steps of 2 µg/kg/min every other day) and optimization of oral vasodilator therapy such as with hydralazine and/or an ACE-inhibitor. It is sometimes necessary to tolerate some renal insufficiency or hypotension during this phase.
Infusion of dobutamine is accompanied by an increased incidence of arrhythmia originating from both ventricles and atria. This effect is dose-related and may be more prominent than with PDEI and should prompt strict potassium compensation during intravenous diuretic use. Tachycardia may also be a limiting parameter, and dobutamine infusion may trigger chest pain in patients with coronary artery disease. In patients with hibernating myocardium dobutamine appears to increase contractility in the short term at the expense of myocyte necrosis and loss in myocardial recovery. There are no controlled trials on dobutamine in AHF patients and some trials show unfavourable effects with increased untoward cardiovascular events.
Milrinone and enoximone are the two Type III phosphodiesterase inhibitors (PDEIs) used in clinical practice. In AHF, these agents have significant inotropic, lusitropic, and peripheral vasodilating effects with an increase in cardiac output and stroke volume, and a concomitant decline in pulmonary artery pressure, pulmonary wedge pressure, systemic and pulmonary vascular resistance. Their haemodynamic profile is intermediate between that of a pure vasodilator, like nitroprusside, and that of a predominant inotropic agent, like dobutamine. As their site of action is distal to the beta-adrenergic receptors, PDEIs maintain their effects even during concomitant ß-blocker therapy.
Type III PDEIs are indicated when there is evidence of peripheral hypoperfusion with or without congestion refractory to diuretics and vasodilators at optimal doses, and preserved systemic blood pressure.
Class of recommendation IIb, level of evidence C
These agents may be preferred to dobutamine in patients on concomitant ß-blocker therapy, and/or with an inadequate response to dobutamine.
Class of recommendation IIa, level of evidence C
In practical use milrinone is administered as a 25 µg/kg bolus over 10–20 min, followed by a continuous infusion at 0.375–0.75 µg/kg/min. Similarly, enoximone is administered as a bolus of 0.25–0.75 mg/kg followed by a continuous infusion at 1.25–7.5 µg/kg/min (Table ). Hypotension caused by excessive peripheral venodilation is an untoward effect observed mainly in patients with low filling pressures. It may be avoided by starting the infusion without any bolus. Thrombocytopaenia is uncommon with both milrinone (0.4%) and enoximone.
The data regarding the effects of PDEI administration on the outcome of patients with AHF are insufficient, but raise concerns about safety, particularly in patients with ischaemic heart failure.
Levosimendan has two main mechanisms of action: Ca++ sensitization of the contractile proteins responsible for a positive inotropic action, and smooth muscle K+ channel opening responsible for peripheral vasodilation. Some data suggest levosimendan may also have a phosphodioesterase inhibition effect. Levosimendan has a potent acetylated metabolite that is also a Ca++-concentration dependent Ca++ sensitizer. Its half-life is 80 h, which probably explains the prolonged haemodynamic effects of a 24 h levosimendan infusion.
Levosimendan is indicated in patients with symptomatic low cardiac output heart failure secondary to cardiac systolic dysfunction without severe hypotension (Table ).
Class of recommendation IIa, level of evidence B
Levosimendan is generally administered as a continuous intravenous infusion at a dose of 0.05–0.1 µg/kg/min preceded by a loading dose of 12–24 µg/kg, administered over 10 min. Its haemodynamic effects are dose-dependent and the infusion rate may be up-titrated to a maximal rate of 0.2 µg/kg/min. Most of the clinical data have been obtained with intravenous infusions lasting from 6 hto 24 h, but the haemodynamic effects persist for >48 h after the end of the infusion.
Levosimendan infusion in patients with acutely decompensated heart failure caused by left ventricular systolic dysfunction has been associated with a dose-dependent increase in the cardiac output and stroke volume, a decline in the pulmonary wedge pressure, systemic vascular resistance, and pulmonary vascular resistance, and a slight increase in the heart rate, and decrease in the blood pressure. An improvement in symptoms of dyspnoea and fatigue and a favourable outcome has been shown in randomized trials comparing levosimendan with dobutamine. Differently from dobutamine, the haemodynamic response to levosimendan is maintained, or even of greater magnitude, in the patients on concomitant ß-blocker therapy.
Tachycardia and hypotension are described with high-dose levosimendan infusion and it is not currently recommended in patients with a systolic blood pressure <85 mmHg. Levosimendan has not been associated with an increased frequency of malignant arrhythmias in comparative trials with either placebo, or dobutamine. Reductions in the haematocrit, haemoglobin, and plasma potassium, likely secondary to vasodilation and secondary neurohumoral activation, have been described and seem to be dose-dependent.
Vasopressor therapy in cardiogenic shock
When the combination of inotropic agent and fluid challenge fails to restore adequate arterial and organ perfusion despite an improvement in cardiac output, therapy with vasopressors may be required. Vasopressors may also be used, in emergencies, to sustain life and maintain perfusion in the face of life-threatening hypotension. Since cardiogenic shock is associated with high vascular resistances, any vasopressor should be used with caution and only transiently, because it may increase the after-load of a failing heart and further decrease end-organ blood flow.
Epinephrine is a catecholamine with high affinity for ß1, ß2, and receptors. Epinephrine is used generally as an infusion at doses of 0.05 to 0.5 µg/kg/min when dobutamine refractoriness is present and the blood pressure remains low. Direct arterial pressure monitoring and monitoring of haemodynamic response by PAC is recommended (Table ).
Norepinehrine is a catecholamine with high affinity for -receptors and is generally used to increase systemic vascular resistance. Norepinephrine-induced increases in heart rate are less than with epinephrine. The dosing is similar to epinephrine. Norepinephrine (0.2 to 1 µg/kg/min) is favoured in situations with low blood pressure related to reduced systemic vascular resistance such as septic shock. Norepinephrine is often combined with dobutamine to improve haemodynamics. Norepinehrine may reduce end-organ perfusion.
Cardiac glycosides inhibit myocardial Na+/K+ ATPase, thereby increasing Ca++/Na+ exchange mechanisms, producing a positive inotropic effect. In heart failure the positive inotropic effect following ß-adrenergic stimulation is attenuated and the positive force–frequency relationship is impaired. In contrast to ß-adrenoceptor agonists, the positive inotropic effect of cardiac glycosides is unchanged in failing hearts and the force–frequency relationship is partially restored. In chronic heart failure, cardiac glycosides reduce symptoms and improve clinical status, thereby decreasing the risk of hospitalization for heart failure without effects on survival. In AHF, cardiac glycosides produce a small increase in cardiac outputand a reduction of filling pressures. In patients with severe heart failure following episodes of acute decompensation, cardiac glycosides have been shown to be efficacious in reducing the re-occurrence of acute decompensation. Predictors for these beneficial effects are a third heart sound, extensive LV dilatation and distended jugular veins during the AHF episode.
However, in patients following myocardial infarction with heart failure, a substudy of the AIRE-Investigation has shown adverse effects on outcome after AMI accompanied by heart failure. Furthermore, following AMI an increase of creatinine kinase was more pronounced in patients receiving cardiac glycosides. In addition, for patients with myocardial infarction and AHF, the use of digitalis was a predictor for life-threatening pro-arrhythmic events. Therefore, inotropic support with cardiac glycosides cannot be recommended in AHF, in particular following myocardial infarction.
An indication for cardiac glycosides in AHF may be tachycardia-induced heart failure e.g. in atrial fibrillation with insufficient rate-control by other agents such as ß-blockers. Rigorous control of heart rate in tachyarrhythmia during the course of AHF can control heart failure symptoms. Contraindications to the use of cardiac glycosides include bradycardia, second and third degree AV-block, sick sinus syndrome, carotid sinus syndrome, Wolff–Parkinson–White syndrome, hypertrophic obstructive cardiomyopathy, hypokalaemia, and hypercalcaemia.
Underlying diseases and co-morbidities in AHF
There are several acute morbidities, which can cause de novo AHF or trigger decompensation in CHF. Coronary heart disease and acute coronary syndromes are the most frequent causes for AHF. Non-cardiac co-morbidities may also significantly complicate the therapy of AHF.
In acute coronary syndromes (unstable angina or myocardial infarction) complicated by AHF, coronary angiography is indicated (Figure). In AMI, reperfusion may significantly improve or prevent AHF. Emergency percutaneous coronary intervention (PCI), or on occasion surgery, should be considered at an early stage and performed as indicated. If neither PCI nor surgery are readily available or can only be provided after a long delay, early fibrinolytic therapy is recommended.
Figure Algorithm: AHF in AMI. IABP=intra-aortic balloon pump; VSR=ventricular septal rupture; PAC=pulmonary artery catheterization; TEE=trans-esophageal echocardiography; EF=ejection fraction; MR=mitral regurgitation; IVS=intraventricular septum; SAM=systolic anterior movement; RA=right atrium; RV=right ventricle; PCI=percutaneous coronary intervention; Qp:Qs=pulmonary circulation volume:systemic circulation volume.
All patients with AMI and signs and symptoms of heart failure should undergo an echocardiographic study to assess regional and global ventricular function, associated valve dysfunction (mainly mitral regurgitation) and to rule out other disease states (e.g. perimyocarditis, cardiomyopathy, and pulmonary embolism).
Class of recommendation I, level of evidence C
Special tests to provide evidence of reversible myocardial ischaemia are sometimes necessary.
In cardiogenic shock caused by acute coronary syndromes coronary angiography and revascularization should be performed as soon as possible.
Class I recommendation, level of evidence A
Temporary stabilization of the patient can be achieved by adequate fluid replacement, intra-aortic balloon counter-pulsation, pharmacological inotropic support, nitrates and artificial ventilation. Repeated blood samples for monitoring of electrolytes, glucose, renal function, and arterial blood gases should be taken, particularly in diabetic patients.
Metabolic support with high-dose glucose, insulin, and potassium cannot be recommended (except in diabetic patients) until the results from larger-scale studies in AMI become available.
Class II recommendation, level of evidence A
When the haemodynamic state continues to be unstable for several hours, the introduction of an in-dwelling PAC may be considered. Repeated measurements of mixed venous blood oxygen saturation from the PAC can be helpful.
Class II recommendation, level of evidence B
When all these measures fail to achieve stabilization of the haemodynamic status, mechanical support with a LV assist device should be considered, particularly if heart transplantation is contemplated.
In left heart failure/pulmonary oedema the acute management is similar to that for other causes of pulmonary oedema. Inotropic agents may be deleterious. Intra-aortic balloon counter-pulsation (IABC) should be considered.
The long-term management strategy should include adequate coronary revascularization and, where there is evidence of reduced LV function, long-term treatment with renin angiotensin aldosterone system (RAAS)-inhibition and ß-blockade should follow.
Acute right heart failure is usually related to acute RV ischaemia in acute coronary syndromes, particularly RV infarction with a characteristic electro- and echo-cardiogram. Early revascularization of the right coronary artery and its ventricular branches is recommended. Supportive treatment should focus on fluid-loading and inotropic support.
The initial treatment of AHF consists of:
· Oxygenation with face-mask or by CPAP (SPO2 target of 94–96%)
· Vasodilatation by nitrate or nitroprusside
· Diuretic therapy by furosemide or other loop diuretic (initially intravenous bolus followed by continuous intravenous infusion, wheeeded)
· Morphine for relief of physical and psychological distress and to improve haemodynamics
· Intravenous fluids should be given if the clinical condition is pre-load-dependent and there are signs of low filling pressure. This may require testing the response to an aliquot of fluid.
· Other complicating metabolic and organ-specific conditions should be treated on their own merits.
· Patients with acute coronary syndrome or other complicated cardiac disorders should undergo cardiac catheterization and angiography, with a view to invasive intervention including surgery.
· Appropriate medical treatment by ß-blocking agents and other medical therapy should be initiated as described in this report.
Further specific therapies should be administered based on the clinical and haemodynamic characteristics of the patient who does not respond to initial treatment. This may include the use of inotropic agents or a calcium sensitizer for severe decompensated heart failure, or inotropic agents for cardiogenic shock.
The aim of therapy of AHF is to correct hypoxia and increase cardiac output, renal perfusion, sodium excretion, and urine output. Other therapies may be required e.g. intravenous aminophylline or ß2-agonist for bronchodilation. Ultrafiltration or dialysis may be prescribed for refractory heart failure.
Patients with refractory AHF or end-stage heart failure should be considered for further support, where indicated including: intra-aortic balloon pump, artificial mechanical ventilation, or circulatory assist devices as a temporary measure, or as a ‘bridge’ to heart transplantation.
The patient with AHF may recover extremely well, depending on the aetiology and the underlying pathophysiology. Prolonged treatment on the ward and expert care are required. This is best delivered by a specialist heart failure team that can rapidly initiate medical management and attend to the informatioeeds of the patient and family.
