Struktur Lewis Hf

In HFrEF (too called systolic HF), global LV systolic dysfunction predominates. The LV contracts poorly and empties inadequately, leading to

Many defects in free energy utilization, energy supply, electrophysiologic functions, and contractile element interaction occur, with abnormalities in intracellular calcium modulation and military camp production.

In HFpEF (also called diastolic heart failure), LV filling is impaired, resulting in

Global contractility and hence ejection fraction remain normal (≥ 50%).

International societies have put forth the concept of HF with mildly reduced ejection fraction (HFmrEF), in which patients take an LV ejection fraction of 41 to 49%. It is unclear whether this group is a distinct population or consists of a mixture of patients with either HFpEF or HFrEF.

In heart failure that involves left ventricular dysfunction, CO decreases and pulmonary venous pressure level increases. When pulmonary capillary pressure exceeds the oncotic pressure level of plasma proteins (nearly 24 mm Hg), fluid extravasates from the capillaries into the interstitial infinite and alveoli, reducing pulmonary compliance and increasing the work of breathing. Lymphatic drainage increases but cannot recoup for the increase in pulmonary fluid. Marked fluid accumulation in alveoli (pulmonary edema

Pulmonary Edema

Pulmonary edema is astute, severe left ventricular failure with pulmonary venous hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, wheezing, and sometimes claret-tinged…

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) significantly alters ventilation-perfusion (V/Q) relationships: Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, decreasing systemic arterial oxygenation (PaO2) and causing dyspnea. However, dyspnea may occur earlier Five/Q abnormalities, probably because of elevated pulmonary venous pressure and increased work of breathing; the precise mechanism is unclear.

In middle failure that involves correct ventricular dysfunction, systemic venous pressure increases, causing fluid extravasation and consequent edema, primarily in dependent tissues (anxiety and ankles of ambulatory patients) and abdominal viscera. The liver is well-nigh severely afflicted, but the stomach and intestine besides get congested; fluid aggregating in the peritoneal crenel (ascites) tin can occur. RV failure commonly causes moderate hepatic dysfunction, with usually small-scale increases in conjugated and unconjugated bilirubin, PT (prothrombin time), and hepatic enzymes (particularly alkaline phosphatase and gamma-glutamyl transpeptidase [GGT]). The impaired liver breaks downwardly less
aldosterone, further contributing to fluid accumulation. Chronic venous congestion in the viscera can cause anorexia, malabsorption of nutrients and drugs, protein-losing enteropathy (characterized past diarrhea and marked hypoalbuminemia), chronic gastrointestinal blood loss, and rarely ischemic bowel infarction.

In HFrEF, left ventricular systolic function is grossly impaired; therefore, a higher preload is required to maintain CO. As a result, the ventricles are remodeled over fourth dimension: During remodelling, the LV becomes less ovoid and more spherical, dilates, and hypertrophies; the RV dilates and may hypertrophy. Initially compensatory, remodelling ultimately is associated with agin outcomes because the changes somewhen increment diastolic stiffness and wall tension (ie, diastolic dysfunction develops), compromising cardiac performance, especially during physical stress. Increased wall stress raises oxygen demand and accelerates apoptosis (programmed cell death) of myocardial cells. Dilation of the ventricles tin also crusade mitral or tricuspid valve regurgitation (due to annular dilation) with further increases in end-diastolic volumes.

With reduced CO, oxygen delivery to the tissues is maintained by increasing oxygen extraction from the claret and sometimes shifting the oxyhemoglobin dissociation curve (see figure
) to the right to favor oxygen release.

Reduced CO with lower systemic claret pressure activates arterial baroreflexes, increasing sympathetic tone and decreasing parasympathetic tone. As a event, center rate and myocardial contractility increment, arterioles in selected vascular beds constrict, venoconstriction occurs, and sodium and water are retained. These changes compensate for reduced ventricular performance and help maintain hemodynamic homeostasis in the early on stages of eye failure. However, these compensatory changes increase cardiac work, preload, and afterload; reduce coronary and renal perfusion; cause fluid accumulation resulting in congestion; increase potassium excretion; and may cause cardiomyocyte necrosis and arrhythmias.

Equally cardiac office deteriorates, renal blood catamenia decreases (due to low cardiac output). In addition, renal venous pressures increment, leading to renal venous congestion. These changes both result in a subtract in GFR (glomerular filtration rate), and blood flow inside the kidneys is redistributed. The filtration fraction and filtered sodium decrease, but tubular resorption increases, leading to sodium and water retention. Blood flow is further redistributed away from the kidneys during do, but renal blood period improves during balance.

The renin-angiotensin-aldosterone-vasopressin
(antidiuretic hormone [ADH]) system causes a cascade of potentially deleterious long-term effects. Angiotensin Ii worsens heart failure by causing vasoconstriction, including efferent renal vasoconstriction, and past increasing aldosterone product, which enhances sodium reabsorption in the distal nephron and too causes myocardial and vascular collagen degradation and fibrosis. Angiotensin II increases
norepinephrine
release, stimulates release of
vasopressin, and triggers apoptosis. Angiotensin 2 may be involved in vascular and myocardial hypertrophy, thus contributing to the remodeling of the center and peripheral vasculature, potentially worsening HF. Aldosterone tin can exist synthesized in the middle and vasculature independently of angiotensin II (mayhap mediated by
corticotropin, nitric oxide, costless radicals, and other stimuli) and may have deleterious effects in these organs.

Heart failure that causes progressive renal dysfunction (including renal dysfunction caused by drugs used to care for HF) contributes to worsening HF and has been termed the cardiorenal syndrome.

In conditions of stress, neurohumoral responses help increase heart function and maintain blood force per unit area and organ perfusion, only chronic activation of these responses is detrimental to the normal balance between myocardial-stimulating and vasoconstricting hormones and between myocardial-relaxing and vasodilating hormones.

The heart contains many neurohumoral receptors (blastoff-1, beta-i, beta-ii, beta-iii, angiotensin II type 1 [AT1] and type two [AT2], muscarinic, endothelin, serotonin,
adenosine, cytokine, natriuretic peptides); the roles of all of these receptors are not yet fully divers. In patients with eye failure, beta-one receptors (which constitute 70% of cardiac beta receptors) are downregulated, probably in response to intense sympathetic activation. The result of downregulation is impaired myocyte contractility and increased heart rate.

Plasma
norepinephrine
levels are increased, largely reflecting sympathetic nerve stimulation as plasma
epinephrine
levels are not increased. Detrimental effects include vasoconstriction with increased preload and afterload, direct myocardial damage including apoptosis, reduced renal blood catamenia, and activation of other neurohumoral systems, including the renin-angiotensin-aldosterone-vasopressin
arrangement.

Vasopressin
is released in response to a autumn in blood force per unit area via various neurohormonal stimuli. Increased
vasopressin
decreases renal excretion of free water, possibly contributing to hyponatremia in heart failure.
Vasopressin
levels in patients with HF and normal blood pressure vary.

Atrial natriuretic peptide is released in response to increased atrial book and pressure; brain (B-blazon) natriuretic peptide (BNP) is released from the ventricle in response to ventricular stretching. These peptides enhance renal excretion of sodium, only in patients with HF, the effect is blunted by decreased renal perfusion pressure, receptor downregulation, and perhaps enhanced enzymatic deposition. In addition, elevated levels of natriuretic peptides exert a counter-regulatory event on the renin-angiotensin-aldosterone organisation and catecholamine stimulation.

Considering endothelial dysfunction occurs in HF, fewer endogenous vasodilators (eg, nitric oxide, prostaglandins) are produced, and more endogenous vasoconstrictors (eg, endothelin) are produced, thus increasing afterload.

The declining eye and other organs produce tumor necrosis factor (TNF) alpha. This cytokine increases catabolism and is mayhap responsible for cardiac cachexia (loss of lean tissue
≥
x%), which may accompany severely symptomatic HF, and for other detrimental changes. The failing center also undergoes metabolic changes with increased free fatty acid utilization and decreased glucose utilization; these changes may get therapeutic targets.

Age-related changes in the center and cardiovascular arrangement lower the threshold for expression of heart failure. Interstitial collagen within the myocardium increases, the myocardium stiffens, and myocardial relaxation is prolonged. These changes lead to a pregnant reduction in diastolic left ventricular function, even in salubrious older people. Modest reject in systolic role also occurs with aging. An age-related decrease in myocardial and vascular responsiveness to beta-adrenergic stimulation further impairs the ability of the cardiovascular system to respond to increased work demands.

Equally a result of these changes, peak practise chapters decreases significantly (about 8%/decade afterwards age xxx), and CO at peak exercise decreases more than modestly. This decline can be slowed by regular physical exercise. Thus, older patients are more than decumbent than are younger ones to develop HF symptoms in response to the stress of systemic disorders or relatively modest cardiovascular insults. Stressors include infections (particularly pneumonia), hyperthyroidism, anemia, hypertension, myocardial ischemia, hypoxia, hyperthermia, renal failure, perioperative IV fluid loads, nonadherence to drug regimens or to low-salt diets, and employ of certain drugs (particularly NSAIDs [nonsteroidal anti-inflammatory drugs]).

• 1. Heidenreich PA, Bozkurt B, Aguilar D, et al: 2022 AHA/ACC/HFSA Guideline for the Management of Centre Failure: A written report of the American College of Cardiology/American Middle Association Articulation Commission on Clinical Do Guidelines.
  Circulation
  145:e876–e894, 2022, doi: 10.1161/CIR.0000000000001062

Chest x-ray findings suggesting heart failure include an enlarged cardiac silhouette, pleural effusion, fluid in the major fissure, and horizontal lines in the periphery of lower posterior lung fields (Kerley B lines). These findings reverberate chronic elevation of left atrial pressure and chronic thickening of the intralobular septa due to edema. Upper lobe pulmonary venous congestion and interstitial or alveolar edema may also be present. Conscientious examination of the cardiac silhouette on a lateral projection can identify specific ventricular and atrial bedroom enlargement. The x-ray may too suggest alternative diagnoses (eg, COPD, pneumonia, idiopathic pulmonary fibrosis

Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF), the most common class of idiopathic interstitial pneumonia, causes progressive pulmonary fibrosis. Symptoms and signs develop over months to years and include…

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, lung cancer

Lung Carcinoma

Lung carcinoma is the leading cause of cancer-related death worldwide. About 85% of cases are related to cigarette smoking. Symptoms can include coughing, chest discomfort or pain, weight loss…

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).

ECG findings are not diagnostic, but an abnormal ECG, specially showing previous myocardial infarction, left ventricular hypertrophy, left bundle branch block, or tachyarrhythmia (eg, rapid atrial fibrillation

Atrial Fibrillation

Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may grade…

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), increases suspicion for HF and may help identify the cause. An entirely normal ECG is uncommon in chronic HF.

Echocardiography

tin can aid evaluate chamber dimensions, valve function, LVEF, wall motion abnormalities, LV hypertrophy, diastolic function, pulmonary artery pressure level, LV and RV filling pressures, RV function, and pericardial effusion. Intracardiac thrombi, tumors, and calcifications inside the heart valves, mitral annulus, and aortic wall abnormalities tin exist detected. Localized or segmental wall movement abnormalities strongly advise underlying coronary artery disease

Overview of Coronary Artery Illness

Coronary artery disease (CAD) involves impairment of blood menstruum through the coronary arteries, nearly ordinarily by atheromas. Clinical presentations include silent ischemia, angina pectoris, astute…

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merely can likewise exist present with patchy myocarditis

Myocarditis

Myocarditis is inflammation of the myocardium with necrosis of cardiac myocytes. Myocarditis may be caused by many disorders (eg, infection, cardiotoxins, drugs, and systemic disorders such…

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. Doppler or color Doppler echocardiography accurately detects valvular disorders and shunts. The combination of Doppler evaluation of mitral arrival with tissue Doppler imaging of the mitral annulus can aid place and quantify LV diastolic dysfunction and LV filling pressures. Measuring LVEF can distinguish between predominant HFpEF (EF
≥
50%) and HFrEF (EF
≤
40%). It is important to re-emphasize that middle failure tin can occur with a normal LVEF. Speckle-tracking echocardiography (which is useful in detecting subclinical systolic dysfunction and specific patterns of myocardial dysfunction) may become of import but currently is routinely reported merely in specialized centers.

Serum BNP levels
are frequently high in eye failure; this finding may help when clinical findings are unclear or other diagnoses (eg, COPD) demand to be excluded. It may be peculiarly useful for patients with a history of both pulmonary and cardiac disorders. NT-pro-BNP, an inactive moiety created when pro-BNP is cleaved, can be used similarly to BNP. All the same,
a normal BNP level does not exclude the diagnosis of heart failure,
particularly in patients with HFpEF and/or obesity. In HFpEF, BNP levels tend to be nearly 50% of those associated with HFrEF (at like degree of symptoms), and up to thirty% of patients with acute HFpEF have a BNP level below the normally used threshold of 100 pg/mL (100 ng/L). Obesity, which is becoming an increasingly common comorbidity in HF, is associated with reduced BNP production and increased BNP clearance, resulting in lower levels.

Besides BNP, recommended blood tests include complete blood count, creatinine, BUN (blood urea nitrogen), electrolytes (including magnesium and calcium), glucose, albumin, ferritin, and liver tests. Thyroid function tests are recommended for patients with atrial fibrillation and for selected, especially older, patients.

Thoracic ultrasonography
is a noninvasive method of detecting pulmonary congestion in patients with middle failure. Sonographic “comet tail antiquity” on thoracic ultrasonography corresponds to the x-ray finding of Kerley B lines.

Cardiac catheterization with intracardiac pressure level measurements (invasive hemodynamics) may be helpful in the diagnosis of restrictive cardiomyopathies and constrictive pericarditis. Invasive hemodynamic measurements are also very helpful when the diagnosis of HF is equivocal, particularly in patients with HFpEF. In addition, perturbing the cardiovascular system (eg, exercise testing, volume challenge, drug challenges [eg,
nitroglycerin,
nitroprusside]) can be very helpful during invasive hemodynamic testing to help diagnose HF.

Endocardial biopsy is sometimes washed when an infiltrative cardiomyopathy, or astute behemothic cell myocarditis is strongly suspected just cannot be confirmed with noninvasive imaging (eg, cardiac MRI).

• 1. McDonagh TA, Metra M, Adamo Thou, et al: 2021 ESC Guidelines for the diagnosis and handling of acute and chronic heart failure: Developed past the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Lodge of Cardiology (ESC) with the special contribution of the Center Failure Association (HFA) of the ESC.
  Eur Heart J
  42(36):3599-3726, 2021. doi: 10.1093/eurheartj/ehab368

• 2. Heidenreich PA, Bozkurt B, Aguilar D, et al: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A report of the American College of Cardiology/American Centre Association Joint Committee on Clinical Practice Guidelines.
  Apportionment
  145:e876–e894, 2022, doi: ten.1161/CIR.0000000000001062

General measures,
especially patient and caregiver education and diet and lifestyle modifications, are important for all patients with eye failure.

Patient and caregiver instruction are critical to long-term success. The patient and family unit should be involved in treatment choices. They should be taught the importance of drug adherence, warning signs of an exacerbation, and how to link cause with effect (eg, increased salt in the diet with weight gain or symptoms).

Many centers (eg, specialized outpatient clinics) have integrated wellness care practitioners from different disciplines (eg, HF nurses, pharmacists, social workers, rehabilitation specialists) into multidisciplinary teams or outpatient heart failure management programs. These approaches can improve outcomes and reduce hospitalizations and are virtually effective in the sickest patients.

Dietary sodium restriction
helps limit fluid retention. All patients should eliminate common salt in cooking and at the table and avert salted foods; the most severely sick should limit sodium to
<
2 g/twenty-four hours by consuming simply low-sodium foods.

Monitoring daily morning weight
helps observe sodium and water accumulation early on. If weight increases
>
two kg over a few days, patients may be able to conform their diuretic dose themselves, merely if weight gain continues or symptoms occur, patients should seek medical attending.

Intensive instance management,
particularly by monitoring drug adherence and frequency of unscheduled visits to the physician or emergency section and hospitalizations, can place when intervention is needed. Specialized HF nurses are valuable in education, follow-up, and dosage adjustment according to predefined protocols.

Patients with atherosclerosis or diabetes should strictly follow a nutrition appropriate for their disorder. Obesity may cause and e’er aggravates the symptoms of HF; patients should attain a body mass index (BMI) ≤ 30 kg/m^two
(ideally 21 to 25 kg/chiliad^two).

CRT
is a style of pacing that synchronizes contraction of the left ventricle by simultaneously pacing its opposing wall, thereby improving stroke volume. CRT may relieve symptoms and reduce heart failure hospitalizations for patients who have HF, LVEF
<
35%, and a widened QRS circuitous with a left bundle co-operative block pattern (>
0.15 second—the wider the QRS, the greater potential benefit). CRT devices are effective but expensive, and patients should be appropriately selected. Many CRT devices also incorporate an ICD in their mechanism.

An implantable device that remotely monitors invasive hemodynamics (eg, pulmonary artery pressure) may assist guide heart failure management in highly selected patients. For example, drug (eg, diuretic) titration based on readings from 1 of these devices was associated with a marked reduction in HF hospitalization in one clinical trial that included patients with both HFrEF and HFpEF. The device uses the pulmonary artery diastolic pressure equally a surrogate for pulmonary capillary wedge pressure level (and hence left atrial pressure) in HF patients. However, information technology has been evaluated simply in NYHA (New York Centre Association) class Three patients who had recurrent HF exacerbations. Further show will aid guide how this technology should be implemented.

Ultrafiltration
(venovenous filtration) tin can be useful in selected hospitalized patients with severe cardiorenal syndrome and volume overload refractory to diuretics. All the same, ultrafiltration should not be used routinely because clinical trials do not show long-term clinical benefit.

An
intra-aortic counterpulsation balloon pump
(IABP) is helpful in selected patients with acute HF who have a good risk of recovery (eg, acute HF following myocardial infarction) or in those who need a bridge to a more than permanent solution such as cardiac surgery (eg, to fix astringent valvular affliction or to revascularize multivessel coronary artery disease), an LV assist device, or eye transplantation. Other forms of temporary mechanical circulatory support for patients with acute HF and cardiogenic shock include surgically placed devices such every bit
extracorporeal membrane oxygenation
(ECMO, typically venoarterial cannulation) and
centrifugal catamenia ventricular assist devices
that tin back up either the LV, the RV, or both and tin can besides exist combined with an oxygenator to provide full cardiopulmonary support. Percutaneously placed devices such as
intravascular microaxial ventricular help devices
are available for both LV and RV support. Option of temporary mechanical circulatory support devices is based mainly on availability and local medical center experience.

Durable or ambulatory
LV assist devices
(LVADs) are longer-term implantable pumps that augment LV output. They are commonly used to maintain patients with severe HF who are awaiting transplantation and are also used as “destination therapy” (ie, every bit a long-term or permanent solution) in some patients who are non transplant candidates.

Surgery may be appropriate when certain underlying disorders are present. Surgery in patients with advanced HF should be done in a specialized center.

Surgical closure of built or acquired intracardiac shunts tin be curative.

Afterward treatment, symptoms often persist. Reasons include

Also, drugs used to care for other disorders may interfere with HF handling. Nonsteroidal anti-inflammatory drugs (NSAIDs), thiazolidinediones (eg,
pioglitazone) for diabetes, and short-acting dihydropyridine or nondihydropyridine calcium channel blockers tin can worsen heart failure and should be avoided unless no alternative exists; patients who must accept such drugs should exist followed closely.

• one. McDonagh TA, Metra M, Adamo Thou, et al: 2021 ESC Guidelines for the diagnosis and handling of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of astute and chronic heart failure of the European Order of Cardiology (ESC) with the special contribution of the Centre Failure Association (HFA) of the ESC.
  Eur Heart J
  42(36):3599-3726, 2021. doi: 10.1093/eurheartj/ehab368

• 2. Heidenreich PA, Bozkurt B, Aguilar D, et al: 2022 AHA/ACC/HFSA Guideline for the Management of Middle Failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.
  Circulation
  145:e876–e894, 2022, doi: 10.1161/CIR.0000000000001062

• iii. Shah SJ, Kitzman D, Borlaug B, et al: Phenotype-specific handling of heart failure with preserved ejection fraction: A multiorgan roadmap.
  Circulation
  134(ane):73–90, 2016. doi: x.1161/CIRCULATIONAHA.116.021884

• 4. Kober Fifty, Thune JJ, Nielsen JC, et al: Defibrillator implantation in patients with nonischemic systolic heart failure.
  N Engl J Med
  375(13):1221–2130, 2016. doi: 10.1056/NEJMoa1608029

• v. Stone GW, Lindenfield J, Abraham WT, et al: Transcatheter mitral-valve repair in patients with heart failure.
  N Engl J Med
  379(24):2307–2318, 2018. doi: 10.1056/NEJMoa1806640