Initial treatment may require hospitalization with a diuretic, oxygen, and other drugs such nitroglycerine paste. A diuretic (“water-pill”) such as the drug furosemide (Lasix®) Pleural effusion (fluid around the lungs) may require thoracocentesis, which is insertion of a small needle in order to drainsome of the fluid.
What is the treatment for dilated cardiomyopathy and heart failure?
Treatment of dilated cardiomyopathy is essentially the same as treatment of chronic heart failure (CHF). CHF is a complex clinical syndrome for which many treatment modalities have emerged. Research into the biochemical alterations that occur in persons with cardiomyopathies has led to the development of many medications designed to affect ...
What are the treatment options for heart failure?
Feb 12, 2001 · Amiodarone reduced the risk for death and hospitalization for heart failure in heart failure patients in the Grupo de Estudio de la Sobrevidea en la Insuficiencia Cardiaca en Argentina (GESICA). 113 However, in the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF STAT), 114 amiodarone did not improve all-cause mortality in patients with …
What is the best treatment for NYHA Class I heart failure?
Dilated cardiomyopathy is the main cause of heart failure leading to heart transplant. Its prognosis is variable and depends on the etiology, the patient's age at onset, and the severity. The management of dilated cardiomyopathy is aimed at minimizing symptoms and preventing disease progression; it …
How are ventricular arrhythmias treated in patients with end-stage heart failure?
The goal of drug therapy in patients with diastolic dysfunction is to control symptoms by reducing ventricular filling pressure without reducing cardiac output. Diuretic drugs and nitrates are the drugs of choice for symptomatic patients. Calcium channel blockers, β-blockers and ACE inhibitors may be of benefit.
What can you do for dilated cardiomyopathy?
What is the most common treatment for congestive heart failure?
What is the first line treatment for heart failure?
What is the first drug of choice for congestive heart failure?
What is the treatment for severe heart failure?
In cases of severe acute heart failure, emergency medical services (EMS) personnel may initiate treatment with oxygen, nitrates, and furosemide en route to the hospital. Cardiac monitoring, continuous pulse oximetry, and electrocardiography (ECG) may also be performed by units with advanced life support (ALS) certification. Further ventilatory support or even intubation may be indicated if the patient is in extremis.
Why are loop diuretics used in heart failure?
They are the mainstay of diuretic therapy because they produce significantly more natriuresis than other diuretics, particularly in the setting of decreased glomerular rate. They provide symptomatic relief without prolonging life or altering disease course.
What is the systolic blood pressure for heart failure?
The systolic blood pressure must be less than 120 mm Hg (preferably < 110 mm Hg).
Is dilated cardiomyopathy the same as CHF?
Treatment of dilated cardiomyopathy is essentially the same as treatment of chronic heart failure (CHF). CHF is a complex clinical syndrome for which many treatment modalities have emerged. Research into the biochemical alterations that occur in persons with cardiomyopathies has led to the development of many medications designed to affect these alterations. Some therapeutic interventions treat symptoms, whereas others treat factors that affect survival.
Is beta blocker safe for heart failure?
Several trials have shown that beta-blockers are both safe and effective in the treatment persons with any class of heart failure and that adding beta-blockers to outpatient management of chronic heart failure (CHF) yields great reductions in mortality rates.
Can anticoagulants be used in patients?
Anticoagulants may be used in selected patients .
Does enalapril reduce CHF?
The Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) group in 1987 showed that the addition of enalapril to the conventional treatment of CHF yielded a 31% reduction in mortality rate at 1 year. [ 94] A similar study by Studies of Left Ventricular Dysfunction (SOLVD) investigators in 1991 revealed a 16% risk reduction. [ 95] Losartan, an angiotensin II receptor blocker (ARB), also has been effective in decreasing mortality rates.
How to diagnose heart failure in infants?
The infant or child with heart failure is generally tachypneic, with a respiratory rate (taken while asleep) greater than ∼60 breaths/min at <2 years old and >40 breaths/min at ≥2 years old. The tachypnea generally is unlabored and requires close inspection because the infant may appear to be comfortable. The presence of retractions may indicate associated pulmonary infection or impending cardiovascular collapse. There is usually accompanying sinus tachycardia. Hepatomegaly is usually present, whereas splenomegaly is not. The patient may be diaphoretic and, depending on the state of the circulation, mottled in the presence of impending circulatory collapse. Such infants may be diagnosed incorrectly as having sepsis. The pulse volume should be examined in all four extremities and both carotid arteries. Blood pressure readings should be obtained in all four extremities. Infants with obstruction to systemic ventricular outflow, such as that found in critical aortic stenosis, may have diffusely reduced pulse volume, whereas in coarctation of the aorta or interruption of the aortic arch, there may be differential pulse volume between the arms and legs. If the coarctation involves the left subclavian artery, and there is a retroesophageal right subclavian artery originating below the coarctation site, the only normal pulses may be the carotids.
Why is functional capacity important in congestive heart failure?
Assessment of functional capacity in patients with congestive heart failure is important, for functional capacity has a direct impact on patient well-being and quality of life. Improvement of functional capacity is therefore a major goal of therapy in patients with heart failure. Also, functional capacity is a predictor of mortality in patients with heart failure, even after controlling for the prognostic information contained in various laboratory tests. Risk assessment of patients is essential to the choice of therapy, particularly surgical approaches.
What is the clinical presentation of acute heart failure?
The clinical presentation of acute heart failure ranges from the sudden appearance of dyspnea to frank cardiogenic shock. The management of acute heart failure differs for the various patient groups residing within the clinical spectrum of this condition; thus, this topic is approached by separately discussing the management of each of the major clinical groups.
What is an extensive evaluation and major intervention in patients with a concomitant terminal illness?
Extensive evaluation and major intervention in patients with a concomitant terminal illness , those afflicted with an irreversible underlying cause or those who are not candidates for corrective intervention or heart transplantation
What is the task force of the American College of Cardiology and the American Heart Association?
The task force of the American College of Cardiology and the American Heart Association shall develop guidelines relative to the role of new therapeutic approaches and of specific noninvasive and invasive procedures in the diagnosis and management of cardiovascular disease.
Which hormones are associated with heart failure?
Other vasoconstrictor hormonal factors that appear to be increased in heart failure include endothelin and vasopressin. In addition to the activation of the vasoconstrictor hormonal system, the activity of several hormonal systems with vasodilator activity is also altered in patients with chronic heart failure.
Can you be admitted to the hospital for acute heart failure?
Patients presenting with acute heart failure usually should be admitted to the hospital. Initial diagnostic testing for patients with acute heart failure should be limited to those tests necessary to exclude etiologies requiring special therapeutic procedures. Further diagnostic testing generally can be deferred until hemodynamic stability and improvement have been attained.
What is the objective of DHF treatment?
The initial objective of the treatment of DHF is to achieve hemodynamic and symptomatic improvement. In addition, other targets should be sought, including the preservation and/or improvement of the renal function, prevention of myocardial damage, modulation of the neurohormonal and/or inflammatory activation, and management of comorbidities that could cause or contribute to the progression of the syndrome(21).
Why is DHF diagnostic study important?
Although the diagnosis of DHF is made based on data from history and physical examination, diagnostic studies are important because, in addition to confirming the diagnosis, they also provide data on the degree of cardiac remodeling, the presence of systolic and/or diastolic dysfunction, etiology, cause of decompensation, presence of comorbidities, and risk stratification (Figure 2). Among the diagnostic studies available, the following are specially helpful.
What are the symptoms of DHF?
The presence of congestion can be inferred in 70% to 80% of DHF cases, by means of signs of tachypnea, pulmonary crackles, third heart sound, increased jugular venous pressure, leg edema, tender hepatomegaly, hepatojugular reflux, pleural effusion and ascites. The presence of poor perfusion is related to the findings of tachypnea, hypotension, pulsus alternans, prolonged capillary filling time, cyanosis, and abnormal level of consciousness.
What is a DHF?
Decompensated heart failure (DHF) is defined as a clinical syndrome in which a structural or functional change in the heart leads to its inability to eject and/or accommodate blood within physiological pressure levels, thus causing a functional limitation and requiring immediate therapeutic intervention (1). It has an irrefutable epidemiological importance, and clinical peculiarities that directly influence treatment. The objective of this study is to guide clinicians on the current management of DHF.
Why is history important in DHF?
In patients with DHF, findings from history taking and physical examination are important not only for providing the diagnosis of the syndrome, but also the time of onset of symptoms, information on the etiology, causes of decompensation (Chart 1) and prognosis.
What causes HF at rest?
Other important causes include: infection, pulmonary embolism, use of medications such as antiinflammatory drugs, and tachy- or bradiarrhythmias. It is usually related to pulmonary and/or systemic congestion, with evident hypervolemia. In addition to seeking the cause of decompensation, volume management with diuretics is crucial.
Why is it important to identify the cause of a chagasic ischemic cardiomyopathy?
Identifying the cause is important, since it can help to choose specific therapies (myocardial revascularization in ischemic cardiomyopathy), to infer the prognosis (greater severity of chagasic and ischemic cardiomyopathies)(1,7), and to guide the pharmacological treatment of decompensation.
How successful is AF ablation?
111 – 115 A range of 8 to 26 studies was evaluated with 354 to 1838 patients included. The single-procedure success rate of ablation ranges from 36% to 73% and the multiprocedure success ranges from 54% to 82%. Complications occurred in 4% to 7% of patients. The net improvement in EF was 11% to 13%. In 1 analysis, they found that the presence of coronary disease resulted in no improvement in EF. 112 Another analysis 114 also showed a net improvement in exercise capacity and quality of life. The most recent analysis showed that 55% of HF patients undergoing ablation in the studies received PVI alone, whereas the remaining patients received PVI plus substrate modification. 115 The majority of those receiving substrate modification received the so-called 7 scheme, whereas the remaining (<10%) received ablation of complex electrograms.
How many randomized trials have been conducted for AF ablation?
To date, there have only been 5 randomized trials assessing efficacy of AF ablation in HF patients ( Table 2 ). 84, 116 – 119 In contrast to the observational studies, all the patients received optimal HF medical therapy. However, with the exception of the recently published AATAC trial (Ablation vs. Amiodarone for Treatment of Atrial Fibrillation in Patients With Congestive Heart Failure and Implanted ICD/CRTD), 119 all included a very small number of patients. There is also some variability in the trial designs because 3 studies compared ablation with rate control, 116 – 118 1 with AV nodal ablation and biventricular pacing, 84 and 1 with amiodarone. 119 Given this mixed picture, it is difficult to make any definitive conclusions on the benefits of catheter ablation.
How does HFrEF affect the atrial structure?
In human patients, HF exerts a prominent effect on atrial structure, with left atrial (LA) enlargement, increased LA pressure, and functional mitral regurgitation. 17 LA voltage abnormalities are recorded in patients with persistent AF which are most prominent in areas associated with high atrial stress. 18 The stress induced by structural changes, and the vasoconstrictive neurohormonal milieu of HF, as well, produce atrial fibrosis, 19, 20 which has been shown to be ameliorated in animal models by angiotensin II–converting enzymes, and as other antifibrotic and anti-inflammatory agents, as well. 21 – 23 All these changes are not only profibrillatory, but cumulative and progressive.
How does AF affect HFrEF?
AF can facilitate the development of HFrEF by several mechanisms. The increase in resting heart rate shortens diastolic filling time that may result in a reduction in cardiac output. The irregular ventricular response results in a 25% reduction in cardiac output 5, 6 because filling during long cycles does not sufficiently compensate for the reduced filling in short cycles. The loss of atrial contribution to ventricular filling is also detrimental, at least conceptually. At issue is whether atria that are destined to fibrillate have already lost the potential for meaningful contractile function. It is theoretically possible that adaptation to AF may improve atrial reservoir and conduit function to compensate, but these functions may also deteriorate during AF, particularly in light of progressive atrial fibrosis. 7 In addition, AF-induced reduction in cardiac output leads to increases in plasma epinephrine and endothelin, augmenting the typical neurohormonal vasoconstrictor excess observed in HF. 8 – 10 AF can cause functional mitral annular enlargement with resultant mitral regurgitation, even in patients without structural heart disease. 11 Finally, AF may result in tachycardia-related cardiomyopathy, which in its full-blown form is related to rapid ventricular rates during AF and is reversible with appropriate rate control therapy. 12 – 14 Several observations suggest that a subtle form of tachycardia-related cardiomyopathy and a contribution of the hemodynamic effects described above are much more frequent, evidenced by improvement in left ventricular function after successful AF ablation, even in patients with reasonable rate control before ablation. 15, 16
Can HFrEF be treated with AF?
Guideline-directed pharmacological therapy for HFrEF is important; however, although there are various treatment modalities for AF, there is no clear consensus on how best to treat AF with concomitant HFrEF. This in-depth review discusses the available data for the treatment of AF in the setting of HFrEF, focuses on areas where more investigation is necessary, examines the clinical implications of randomized and observational clinical trials, and presents suggestions for individualized treatment strategies for specific patient groups.
Can HFrEF be coexisting?
In summary, AF and HFrEF commonly coexist, and incident AF has a profoundly negative effect on mortality and hospitalization in HFrEF. It would certainly appear that the optimal time for intervention in patients with HFrEF is early after AF onset.
Can HFrEF be treated with a pharmacological treatment?
There is no compelling evidence to suggest that usual pharmacological therapy for the treatment of HFrEF would not naturally extend to patients with concomitant AF. Nonetheless, 1 meta-analysis suggested that β-blockers, the cornerstone of guideline-directed medical therapy, were not as helpful in patients with AF as those without. 33 However, in legacy pharmacological trials of HF therapy, patients with AF are typically older, have more comorbidities and longer duration of HF symptoms, all of which may dampen their response to interventions. This observation does demonstrate the lack of data regarding the specific effect of guideline-directed medical therapy for HFrEF for patients with AF. On the other hand, retrospective analyses of large randomized trials have demonstrated that angiotensin-converting enzyme inhibitors, 34, 35 angiotensin II receptor blockers, 36, 37 β-blockers, 38 and eplerenone 39 all reduce the rate of incident AF in patients with HFrEF.
