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Heart failure is a complex clinical syndrome that results from a functional or structural heart disorder impairing ventricular filling or ejection of blood to the systemic circulation. It is by definition a failure to meet the systemic demands of circulation. Heart failure remains a highly prevalent disorder worldwide with a high morbidity and mortality rate. It has an estimated prevalence of 26 million people worldwide and contributes to increased healthcare costs worldwide.

The etiology of heart failure varies the treatment plan to some degree; however, most of the treatment recommendations are based on the presence of heart failure alone, regardless of the cause. Classification of heart failure is based on symptoms and calculated left ventricular ejection fraction LVEF. Heart failure due to left ventricular dysfunction is categorized into heart failure with reduced ejection fraction HFrEF , heart failure with preserved ejection fraction HFpEF , and heart failure with mid-range ejection fraction HFmrEF.

The latter may consist of mixed left ventricular dysfunction a combination of systolic and diastolic heart failure.

Heart failure can severely decrease the functional capacity of a patient and increase mortality risk. It is imperative to diagnose and effectively treat the disease to prevent recurrent hospitalizations, improve quality of life, and enhance patient outcomes.

An interprofessional team approach is warranted to optimize patient care. Congestive heart failure is caused by structural abnormalities of the heart, functional abnormalities, and other triggering factors. Historically, an overwhelming majority of the cases were due to coronary artery disease and myocardial infarction. Over time, coronary artery disease and diabetes mellitus have become the predominant predisposing factors for heart failure. Other structural causes of congestive heart failure CHF include hypertension, valvular heart disease, uncontrolled arrhythmia, myocarditis, and congenital heart disease.

Diastolic heart failure with impaired ventricular filling can be caused by restrictive cardiomyopathies and constrictive pericarditis, in addition to the etiologies identified above. It is important to identify etiologies of decompensated heart failure, as they contribute to most of the morbidity and mortality associated with the disease. The most common cause of decompensated congestive heart failure is inappropriate drug treatment, dietary sodium restriction, and decreased physical activity.

Uncontrolled hypertension is the second most common cause of decompensated heart failure. Another group of diseases associated with "congestive heart failure" leads to high-output cardiac failure. This, by definition, is not an impairment in cardiac function but a failure of the heart to meet the increased systemic demands due to extracardiac diseases.

Common etiologies of this type of congestive heart failure include severe anemia, thyrotoxicosis, obesity, nutritional deficiencies thiamine deficiency, etc. The above-mentioned list of etiologies is not an all-inclusive list but a broad categorization of various etiologies.

Approximately 6. This has not translated to improved quality of life or a decrease in the number of hospitalizations for patients with heart failure. This translates to 9. Age is a major determinant of HF. Regardless of the cause or the definition used to classify patients with heart failure HF , the prevalence of HF increases steeply with age. According to the American Heart Association, heart failure is still the primary cause of hospitalization in the elderly population and accounts for 8.

International statistics regarding the epidemiology of HF are similar to those of the United States. The incidence increases dramatically with age, and metabolic risk factors along with a sedentary lifestyle are major risk factors. Ischemic cardiomyopathy, along with hypertension, is a major cause of HF in developing countries. The theoretical cause of this is thought to be due to the higher prevalence of tuberculous, pericardial disease, and lung disease.

There is a lack of robust data to verify these claims. The adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. In the initial stages of congestive heart failure, cardiac physiology attempts to adapt via several compensatory mechanisms to maintain cardiac output and meet the systemic demands.

These include the Frank-Starling mechanism, changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility.

With increased wall stress, the myocardium attempts to compensate via eccentric remodeling, which further worsens the loading conditions and wall stress. A decrease in cardiac output stimulates the neuroendocrine system with a release of epinephrine, norepinephrine, endothelin-1 ET-1 , and vasopressin. They cause vasoconstriction leading to increased afterload. There is an increase in cyclic adenosine monophosphate cAMP , which causes an increase in cytosolic calcium in the myocytes.

This increases myocardial contractility and further prevents myocardial relaxation. An increase in afterload and myocardial contractility with impaired myocardial relaxation leads to increased myocardial oxygen demand.

This paradoxical need for increased cardiac output to meet myocardial demand eventually leads to myocardial cell death and apoptosis. As apoptosis continues, a decrease in cardiac output with increased demand leads to a perpetuating cycle of increased neurohumoral stimulation and maladaptive hemodynamic and myocardial responses. A decrease in cardiac output also stimulates the renin-angiotensin-aldosterone system RAAS , leading to increased salt and water retention, along with increased vasoconstriction.

This further fuels the maladaptive mechanisms in the heart and cause progressive heart failure. In addition to this, the RAAS system releases angiotensin II, which has been shown to increase myocardial cellular hypertrophy and interstitial fibrosis.

This maladaptive function of angiotensin II has been shown to increase myocardial remodeling. In HFpEF, there is a decrease in myocardial relaxation and an increase in the stiffness of the ventricle due to an increase in ventricular afterload.

This perpetuates a similar maladaptive hemodynamic compensation and leads to progressive heart failure. The most commonly reported symptom is shortness of breath. Further qualification of this symptom is essential to help elucidate potential causes of heart failure and to determine the plan of care for the patient.

Shortness of breath must further be classified to determine if it is related to exertion, positional changes orthopnea , and whether it is acute or chronic.

Other commonly reported symptoms of HF include chest pain, palpitations, anorexia, and fatigue. Some patients may present with a recumbent cough which may be due to orthopnea. Physical examination of patients with heart failure requires a comprehensive assessment.

The general appearance of patients with severe, chronic heart failure or those with acutely decompensated heart failure will include anxiety, diaphoresis, and poor nutritional status. The classical finding of pulmonary rales translates to heart failure of moderate to severe intensity.

Wheezing may be present in acute decompensated heart failure. As the severity of pulmonary congestion increases, frothy and blood-tinged sputum may be seen. It is important to note that the absence of rales does not exclude pulmonary congestion. Jugular venous distention is another classical finding which must be assessed in all patients with HF.

A paradoxical increase in jugular venous distention with respiration Kussmaul sign may be seen. Peripheral edema is present in severe heart failure and will be seen if a substantial degree of volume overload is present. Cardiac findings in patients with HF include S3 gallop, pulsus alternans, and accentuation of P2. An S3 gallop is the most significant and early finding associated with HF. The commonly used Framingham Diagnostic Criteria for Heart Failure requires the presence of 2 major criteria or 1 major and 2 minor criteria to make the diagnosis of heart failure.

This diagnostic tool is highly sensitive for the diagnosis of heart failure but has a relatively low specificity. The Framingham Diagnostic criteria are as follows:. Cardiac-specific testing and prognostic factors for HF are outlined below. Serum sodium levels have prognostic value as predictors of mortality in patients with chronic HF. They also play a role in the prediction of short-term mortality for patients admitted with decompensated heart failure.

The highest mortality risk was seen in patients in the lowest quintile of serum sodium levels on presentation. BNP is an independent predictor of increased left ventricular end-diastolic pressure, and it is used for assessing mortality risk in patients with heart failure.

According to the American Heart Association AHA and the American College of Cardiology ACC recommendations from and , predischarge natriuretic peptide levels are strong predictors of the risk of death and hospital readmission in patients with HF. In patients with true clinical presentation of HF, natriuretic peptides should not be used to drive treatment plans. It is important to remember that BNP and NT-proBNP levels can be elevated in patients with renal dysfunction, atrial fibrillation, and in older patients.

Conversely, BNP levels can be falsely low in patients with obesity, hypothyroidism, and advanced heart failure due to myocardial fibrosis. Chest radiographs are used to assess the degree of pulmonary congestion and cardiac contour to determine the presence of cardiomegaly. Findings indicative of congestive heart failure on chest radiographs include enlarged cardiac silhouette, edema at the lung bases, and vascular congestion.

In florid heart failure, Kerley B lines may be seen on chest radiographs. Echocardiography is the most commonly used test for the diagnosis of HF.

It can assess for systolic and diastolic dysfunction and help elucidate the presence of focal wall motion abnormalities or valvular pathology. Traditional 2D transcutaneous echocardiography is the most commonly utilized form of testing. However, in patients with severe obesity, pregnancy, or mechanical ventilation, it may be difficult to obtain adequate acoustic windows. Transesophageal echocardiography TEE is an alternative for these patients. Adequate rate control in patients with tachyarrhythmias is necessary to obtain adequate echocardiographic images.

Computed tomography CT and magnetic resonance imaging MRI in patients with HF are used principally for the diagnosis of congenital cardiac abnormalities. Radionuclide multiple-gated acquisition MUGA scan is a reliable imaging technique for the evaluation of left ventricular LV and right ventricular RV function. MUGA scan is, in fact, the most accurate scan to assess for ejection fraction EF and is used in patients when there is a disparity of EF measurements from other studies.

Electrocardiogram ECG -gated myocardial perfusion imaging is another diagnostic tool for assessing the EF, regional wall motion, and regional wall thickening. EF measurement with this study may be affected in patients with an irregular heart rate, low count density, and extracardiac radiotracer uptake.

ECG-gated images are also useful in recognizing artifactual defects seen on SPECT imaging, such as breast tissue and diaphragmatic attenuation. Iobenguane scanning is scintigraphic imaging using iobenguane I injection.

Iobenguane I is a norepinephrine analog. The test can show the amount of norepinephrine uptake in the cardiac sympathetic nervous system. Improved reuptake of norepinephrine is associated with a better prognosis. Other tests used in evaluating patients with HF include cardiac catheterization, stress testing, and electrocardiograms.

However, they are used in patients with HF to determine the underlying cause of the disease. They do not play any specific role in the diagnosis of HF or its prognostication. The goal of therapy for chronic CHF is to improve symptom management and quality of life, decrease hospitalizations, and decrease overall mortality associated with this disease. The goal of pharmacologic therapy is to give all indicated agents rather than single agents because the aggregate effect of these therapies is better than monotherapy from any of the agents.

The nitrate and hydralazine combination is also indicated to reduce mortality and morbidity in African American patients with symptomatic HFrEF, currently receiving optimal medical therapy.

Ivabradine selectively inhibits the funny current I-f in the sinoatrial node. Vericiguat is an agent that stimulates the intracellular receptor for endogenous NO, which is a potent vasodilator. Digoxin may be considered in symptomatic patients in sinus rhythm despite adequate goal-directed therapy to reduce the all-cause rate of hospitalizations, but its role is limited.

In patients with refractory HF, despite optimized pharmacologic therapy, intravenous vasodilator therapy and intravenous inotropes have been considered in the past. In patients with HFpEF, none of the current therapies have a definitive improvement in mortality or hospitalization.

However, medical management with the above therapies is indicated. Patients with progressive HF or those with acute, severe refractory HF may be considered for heart transplantation. It is also important to address potential triggers for HF exacerbation once the diagnosis of HF is made. These include:. They note that the trend correlates with a shift from coronary heart disease as the underlying cause of heart failure deaths to metabolic diseases and other noncardiac causes of HF such as obesity, diabetes, malignancies, chronic pulmonary diseases, and renal disease.

It determines the day risk of mortality, hospital readmission, and acute coronary syndrome in patients who presented to the emergency department with symptoms of HF to help arrive at safe disposition planning. Skeletal muscle wasting can occur in severe biventricular failure and may reflect some disuse but also increased catabolism associated with increased cytokine production.

Significant weight loss cardiac cachexia is an ominous sign associated with high mortality. In older people, presenting complaints may be atypical, such as confusion, delirium, falls, sudden functional decline, nocturnal urinary incontinence, or sleep disturbance. Coexisting cognitive impairment and depression may also influence assessment and therapeutic interventions and may be worsened by the HF.

General examination may detect signs of systemic or cardiac disorders that cause or aggravate heart failure eg, anemia, hyperthyroidism Hyperthyroidism Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form In LV failure, tachycardia and tachypnea may occur.

Patients with severe LV failure may appear visibly dyspneic or cyanotic, hypotensive, and confused or agitated because of hypoxia and poor cerebral perfusion. Some of these less specific symptoms eg, confusion are more common in older patients. Central cyanosis affecting all of the body, including warm areas such as the tongue and mucous membranes reflects severe hypoxemia. Peripheral cyanosis of the lips, fingers, and toes reflects low blood flow with increased oxygen extraction.

If vigorous massage improves nail bed color, cyanosis may be peripheral; increasing local blood flow does not improve color if cyanosis is central. These abnormal heart sounds also can occur in HFpEF. Pulmonary findings include early inspiratory basilar crackles that do not clear with coughing and, if pleural effusion is present, dullness to percussion and diminished breath sounds at the lung base s.

Nontender peripheral pitting edema digital pressure leaves visible and palpable imprints, sometimes quite deep in the feet and ankles. Visible elevation of the jugular venous pressure, sometimes with large a or v waves that are visible even when the patient is seated or standing see figure.

In severe cases of heart failure, peripheral edema can extend to the thighs or even the sacrum, scrotum, lower abdominal wall, and occasionally even higher. Severe edema in multiple areas is termed anasarca.

Edema may be asymmetric if patients lie predominantly on one side. Large V waves in the jugular veins are usually indicative of significant tricuspid regurgitation which is often present in RV failure. A paradoxical increase in the jugular venous pressure during inspiration Kussmaul sign is indicative of right-sided heart failure and can occur in RV failure, restrictive cardiomyopathy Restrictive Cardiomyopathy Restrictive cardiomyopathy is characterized by noncompliant ventricular walls that resist diastolic filling; one most commonly the left or both ventricles may be affected.

With hepatic congestion, the liver may be palpably enlarged or tender, and hepatojugular or abdominal-jugular reflux may be detected see Approach to the Cardiac Patient Neck veins. Precordial palpation may detect the left parasternal lift of RV enlargement, and auscultation may detect the murmur of tricuspid regurgitation or the RV S3 along the left sternal border; both findings are augmented upon inspiration.

Clinical findings eg, exertional dyspnea or fatigue, orthopnea, edema, tachycardia, pulmonary crackles, S3, jugular venous distention suggest heart failure but are usually not apparent early.

Alpha-1 antitrypsin deficiency and various occupational Initial diagnosis is usually based on chest x-ray and clinical findings. Causes, symptoms, treatment, preventive measures, and Suspicion for heart failure should be high in patients with a history of myocardial infarction Acute Myocardial Infarction MI Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Chest x-ray, ECG, and an objective test of cardiac function, typically echocardiography, should be done see figure.

Blood tests, except for BNP levels, are not used for diagnosis but are useful for identifying cause and systemic effects 1 Diagnosis references Heart failure HF is a syndrome of ventricular dysfunction. Eur Heart J 42 36 , 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 reflect 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. Careful examination of the cardiac silhouette on a lateral projection can identify specific ventricular and atrial chamber enlargement.

The x-ray may also suggest alternative diagnoses eg, COPD, pneumonia, idiopathic pulmonary fibrosis Idiopathic Pulmonary Fibrosis Idiopathic pulmonary fibrosis IPF , the most common form of idiopathic interstitial pneumonia, causes progressive pulmonary fibrosis. Symptoms and signs develop over months to years and include Symptoms can include cough, chest discomfort or pain, weight loss This patient has bilateral pleural effusions arrows.

The normally sharp costophrenic angles are obscured by fluid in this patient. Kerley B lines arrows are horizontal lines in the lung periphery that extend to the pleural surface. They denote thickened, edematous interlobular septa often due to pulmonary edema. The patient also has cephalization black arrows whereby upper lobe pulmonary vessels become more prominent. These findings are often seen in patients with heart failure. Lateral chest x-ray in a patient with fluid in major 1 and minor 2 fissures as well as a loculated effusion 3 seen along right posterior chest wall.

ECG findings are not diagnostic, but an abnormal ECG, especially 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. Echocardiography Echocardiography This photo shows a patient having echocardiography.

This image shows all 4 cardiac chambers and the tricupsid and mitral valves. Echocardiography uses ultrasound waves to produce an image of Intracardiac thrombi, tumors, and calcifications within the heart valves, mitral annulus, and aortic wall abnormalities can be detected. Localized or segmental wall motion abnormalities strongly suggest underlying coronary artery disease Overview of Coronary Artery Disease Coronary artery disease CAD involves impairment of blood flow through the coronary arteries, most commonly by atheromas.

Clinical presentations include silent ischemia, angina pectoris, acute Doppler or color Doppler echocardiography accurately detects valvular disorders and shunts. The combination of Doppler evaluation of mitral inflow with tissue Doppler imaging of the mitral annulus can help identify and quantify LV diastolic dysfunction and LV filling pressures.

It is important to re-emphasize that heart failure 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 important but currently is routinely reported only in specialized centers.

Radionuclide imaging Radionuclide Imaging of the Heart Radionuclide imaging uses a special detector gamma camera to create an image following injection of radioactive material. This test is done to evaluate Cardiac valvular disorders Cardiomyopathy Standard imaging tests include Echocardiography Chest x-ray CT MRI read more provides accurate images of cardiac structures and is becoming more widely available.

Cardiac MRI using late gadolinium enhancement imaging LGE, also called fibrosis or scar imaging is useful to evaluate the cause of myocardial disease and to detect focal and diffuse myocardial fibrosis.

Cardiac amyloidosis, sarcoidosis, hemachromatosis, and myocarditis are causes of HF that can be detected with or suspected by cardiac MRI findings.

Serum BNP levels are often high in heart failure; this finding may help when clinical findings are unclear or other diagnoses eg, COPD need to be excluded. It may be particularly useful for patients with a history of both pulmonary and cardiac disorders. 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 heart failure. Sonographic "comet tail artifact" on thoracic ultrasonography corresponds to the x-ray finding of Kerley B lines.

Coronary angiography or CT coronary angiography is indicated when coronary artery disease Overview of Coronary Artery Disease Coronary artery disease CAD involves impairment of blood flow through the coronary arteries, most commonly by atheromas.

Cardiac catheterization with intracardiac pressure 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 done when an infiltrative cardiomyopathy, or acute giant cell myocarditis is strongly suspected but cannot be confirmed with noninvasive imaging eg, cardiac MRI.

Generally, patients with heart failure have a poor prognosis unless the cause is correctable. Specific factors that suggest a poor prognosis include hypotension, low ejection fraction, presence of coronary artery disease, troponin release, elevation of BUN, reduced GFR, hyponatremia, and poor functional capacity eg, as tested by a 6-minute walk test.

HF usually involves gradual deterioration, interrupted by bouts of severe decompensation, and ultimately death, although the time course is being lengthened with modern therapies. However, death can also be sudden and unexpected, without prior worsening of symptoms. All patients and family members should be taught about disease progression and the risk of sudden cardiac death. For some patients, improving quality of life is as important as increasing quantity of life.

All patients should be reassured that symptoms will be relieved, and they should be encouraged to seek medical attention early if their symptoms change significantly. Involvement of pharmacists, nurses, social workers, and clergy when desired , who may be part of an interdisciplinary team or disease management program already in place, is particularly important in end-of-life care The Dying Patient Dying patients can have needs that differ from those of other patients.

So that their needs can be met, dying patients must first be identified. Before death, patients tend to follow 1 of Sometimes device therapy eg, implantable cardioverter-defibrillator, cardiac resynchronization therapy, mechanical circulatory support. Immediate inpatient treatment is required for patients with acute or worsening heart failure due to certain disorders eg, acute myocardial infarction Acute Myocardial Infarction MI Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery.

Patients with mild exacerbations of previously diagnosed HF can be treated at home. The most common The plaques contain lipids, inflammatory cells, smooth muscle Treatment involves dietary and lifestyle changes, drugs Drugs for Heart Failure Heart failure HF is a syndrome of ventricular dysfunction see Heart Failure.

Drug treatment of heart failure HF involves symptom relief with Diuretics Nitrates Digoxin read more , devices, and sometimes percutaneous coronary interventions or surgery. Treatment is tailored to the patient, considering causes, symptoms, and response to drugs, including adverse effects. There are currently several evidence-based therapies for chronic HFrEF 1 Treatment references Heart failure HF is a syndrome of ventricular dysfunction. Drug treatment of heart failure HF involves symptom relief with Diuretics Nitrates Digoxin read more for detailed information on drug treatment and the specific drugs and classes.

General measures, especially patient and caregiver education and diet and lifestyle modifications, are important for all patients with heart failure. Patient and caregiver education are critical to long-term success. The patient and family 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 health 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 most effective in the sickest patients. Dietary sodium restriction helps limit fluid retention. Monitoring daily morning weight helps detect sodium and water accumulation early.

Intensive case management, particularly by monitoring drug adherence and frequency of unscheduled visits to the physician or emergency department and hospitalizations, can identify 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 diet appropriate for their disorder. Regular light activity eg, walking , tailored to symptoms, is generally encouraged. Activity prevents skeletal muscle deconditioning, which worsens functional status; however, activity does not appear to improve survival or decrease hospitalizations. Rest is appropriate during acute exacerbations.

Formal exercise cardiac rehabilitation Cardiovascular Rehabilitation Rehabilitation may benefit some patients who have coronary artery disease or heart failure or who have had a recent myocardial infarction or coronary artery bypass surgery, particularly those Patients should have annual influenza vaccination Influenza Vaccine Based on recommendations by the World Health Organization and the Centers for Disease Control and Prevention CDC , vaccines for influenza are modified annually to include the most prevalent If causes such as hypertension, persistent tachyarrhythmia, severe anemia, hemochromatosis, uncontrolled diabetes, thyrotoxicosis, beriberi, alcohol use disorder, or toxoplasmosis are successfully treated, patients may dramatically improve.

Significant myocardial ischemia should be treated aggressively; treatment may include revascularization by percutaneous coronary intervention Percutaneous Coronary Interventions PCI Percutaneous coronary interventions PCI include percutaneous transluminal coronary angioplasty PTCA with or without stent insertion. Primary indications are treatment of Angina pectoris Coronary artery bypass grafting CABG Management of extensive ventricular infiltration eg, in amyloidosis has improved considerably.

Newer treatments for amyloidosis Treatment Amyloidosis is any of a group of disparate conditions characterized by extracellular deposition of insoluble fibrils composed of misaggregated proteins. Because arrhythmias can worsen heart failure, it is important to identify and treat the cause of any arrhythmia Overview of Arrhythmias The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial Sinus tachycardia, a common compensatory change in heart failure, usually subsides when HF treatment is effective.

If it does not, associated causes eg, hyperthyroidism Hyperthyroidism Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Risk factors for pulmonary embolism are If sinus tachycardia persists despite correction of causes, a beta-blocker, given in gradually increasing doses, may help selected patients.

However, lowering heart rate with a beta-blocker can be detrimental to patients with advanced HFpEF eg, restrictive cardiomyopathy Restrictive Cardiomyopathy Restrictive cardiomyopathy is characterized by noncompliant ventricular walls that resist diastolic filling; one most commonly the left or both ventricles may be affected.

Atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Beta-blockers are the treatment of choice, although rate-limiting calcium channel blockers may be used cautiously if systolic function is preserved. Routine conversion to and maintenance of sinus rhythm has not been shown to be superior to rate control alone in large clinical trials.

However, it is best to make this determination on a case-by-case basis because some patients improve significantly with restoration of normal sinus rhythm. If rapid atrial fibrillation does not respond to drugs, permanent pacemaker insertion with complete or partial ablation of the atrioventricular node, or other atrial fibrillation ablation procedures Ablation procedures for atrial fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm.

Isolated ventricular premature beats Ventricular Premature Beats VPB Ventricular premature beats VPB are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells.

They are extremely common in both healthy However, optimization of HF treatments and correction of electrolyte abnormalities especially potassium and magnesium reduce the risk of ventricular arrhythmias. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic Amiodarone , beta-blockers, and dofetilide are the drugs of choice because other antiarrhythmics have adverse proarrhythmic effects when LV systolic dysfunction is present.

Serum digoxin level and INR international normalized ratio level should be routinely monitored. However, drug toxicity can occur even at therapeutic levels. Because long-term use of amiodarone can cause adverse effects, a low dose mg orally once a day is used when possible; blood tests for liver function and thyroid-stimulating hormone are done every 6 months.

If chest x-ray is abnormal or dyspnea worsens significantly, chest x-ray and pulmonary function tests are done yearly to check for pulmonary fibrosis. For sustained ventricular arrhythmias, amiodarone may be required; to reduce risk of sudden death, a loading dose of to mg orally twice a day is given for 1 to 3 weeks until rhythm control is adequate, then dose is decreased over 1 month to a maintenance dose of mg orally once a day.

Use of an implantable cardioverter-defibrillator Implantable Cardioverter-Defibrillators ICD The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. A clinical trial that included HFrEF patients with nonischemic cardiomyopathy demonstrated no mortality benefit from prophylactic primary prevention ICD placement 4 Treatment references Heart failure HF is a syndrome of ventricular dysfunction.

CRT is a mode of pacing that synchronizes contraction of the left ventricle by simultaneously pacing its opposing wall, thereby improving stroke volume. CRT devices are effective but expensive, and patients should be appropriately selected. An implantable device that remotely monitors invasive hemodynamics eg, pulmonary artery pressure may help guide heart failure management in highly selected patients.

For example, drug eg, diuretic titration based on readings from one 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 as a surrogate for pulmonary capillary wedge pressure and hence left atrial pressure in HF patients. Further evidence will help guide how this technology should be implemented. Ultrafiltration venovenous filtration can be useful in selected hospitalized patients with severe cardiorenal syndrome and volume overload refractory to diuretics. However, 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 chance of recovery eg, acute HF following myocardial infarction or in those who need a bridge to a more permanent solution such as cardiac surgery eg, to fix severe valvular disease or to revascularize multivessel coronary artery disease , an LV assist device, or heart transplantation.

Other forms of temporary mechanical circulatory support for patients with acute HF and cardiogenic shock include surgically placed devices such as extracorporeal membrane oxygenation ECMO, typically venoarterial cannulation and centrifugal flow ventricular assist devices that can support either the LV, the RV, or both and can also be combined with an oxygenator to provide full cardiopulmonary support. Percutaneously placed devices such as intravascular microaxial ventricular assist devices are available for both LV and RV support.

Selection of temporary mechanical circulatory support devices is based mainly on availability and local medical center experience. They are commonly used to maintain patients with severe HF who are awaiting transplantation and are also used as "destination therapy" ie, as a long-term or permanent solution in some patients who are not 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. Coronary artery bypass grafting Coronary artery bypass grafting CABG Coronary artery disease CAD involves impairment of blood flow through the coronary arteries, most commonly by atheromas.

Thus, the decision to revascularize a HF patient with multivessel coronary artery disease should be made on a case-by-case basis. If HF is primarily due to a valvular disorder Overview of Cardiac Valvular Disorders Any heart valve can become stenotic or insufficient also termed regurgitant or incompetent , causing hemodynamic changes long before symptoms. Patients with primary mitral regurgitation are more likely to benefit than patients with mitral regurgitation secondary to LV dilation, in whom poor myocardial function is likely to continue postoperatively.

Surgery is preferably done before myocardial dilation and damage become irreversible. Heart transplantation Heart Transplantation Heart transplantation is an option for patients who have any of the following and who remain at risk of death and have intolerable symptoms despite optimal use of drugs and medical devices Some older patients about 60 to 70 years with otherwise good health are also typically considered if they meet other criteria for transplantation.

Human organ donation remains low. Anemia is common among patients with chronic heart failure and is frequently multifactorial. Anemia is associated with worse symptoms and outcomes in HF and so reversible causes should be sought and treated. Iron deficiency Iron Deficiency Anemia Iron deficiency is the most common cause of anemia and usually results from blood loss; malabsorption, such as with celiac disease, is a much less common cause.

Symptoms are usually nonspecific Oral iron replacement is often less effective due to poor absorption and other reasons, thus intravenous iron replacement is preferred. Presence of an undiagnosed thyroid disorder, anemia, or supervening arrhythmia eg, atrial fibrillation with rapid ventricular response, intermittent ventricular tachycardia.

Also, drugs used to treat other disorders may interfere with HF treatment. Nonsteroidal anti-inflammatory drugs NSAIDs , thiazolidinediones eg, pioglitazone for diabetes, and short-acting dihydropyridine or nondihydropyridine calcium channel blockers can worsen heart failure and should be avoided unless no alternative exists; patients who must take such drugs should be followed closely. Circulation 1 �90, N Engl J Med 13 �, N Engl J Med 24 �, Heart failure HF involves ventricular dysfunction that ultimately leads to the heart not providing tissues with adequate blood for metabolic needs.

In heart failure with reduced ejection fraction HFrEF , the ventricle contracts poorly and empties inadequately; ejection fraction is low. Treatment includes education and lifestyle changes, control of underlying disorders, a variety of drugs, and sometimes implantable devices CRT, ICDs. The following are some of the major English-language heart failure guidelines that may be useful.

View Patient Education. Increasing heart rate. Frank-Starling principle Normally top curve , as preload increases, cardiac performance also increases.

Overview of Heart Failure. Increased diastolic volume and pressure. Increased LV end-diastolic pressure at rest or during exertion. Causes of Heart Failure Type. The most common classification of heart failure currently in use stratifies patients into. A: High risk of HF but no structural or functional cardiac abnormalities or symptoms.

Diffuse, sustained, and laterally displaced apical impulse. Enlarged and sometimes pulsatile liver palpable below the right costal margin. Sometimes only clinical evaluation.

Imaging in Patients With Heart Failure. Diet and lifestyle changes. The primary goal is to diagnose and to correct or treat the disorder that led to heart failure. Electrolytes are normalized. Surgical closure of congenital or acquired intracardiac shunts can be curative. After treatment, symptoms often persist. Reasons include.

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It can also cover your viva questions and will help you to score very high. Concept of Physics by H. Cardiovascular diseases claim more lives each year than all forms of cancer and Chronic Lower Respiratory Disease combined.

In , I was diagnosed with Congestive Heart Failure and became yet another such statistic. However, by making certain lifestyle changes, improving my diet, and following a very specific whole food supplement protocol, I was able to fully recover!

I invite you to join me on my personal journey as I battled congestive heart failure from utter despair to full recovery. I share the details of my personal experience with you and tell you exactly what I did to regain my health. If you or a loved one have been diagnosed with congestive heart failure, you need to read this book.

It could literally save your life or the life of a loved one. Download Link. Assessment Symptoms of heart failure include those due to excess fluid accumulation dyspnea, orthopnea, edema, pain from hepatic congestion, and abdominal distention from ascites and those due to a reduction in cardiac output fatigue, weakness most pronounced with physical exertion.

Apical impulse: Laterally displaced past the midclavicular line, usually indicative of left ventricular enlargement. S3 gallop: A low-frequency, brief vibration occurring in early diastole at the end of the rapid diastolic filling period of the right or left ventricle. It is the most sensitive indicator of ventricular dysfunction. Evaluation Tests used in the evaluation of patients with HF include: Electrocardiogram ECG : Important for identifying evidence of acute or prior myocardial infarction or acute ischemia, rhythm abnormalities, such as atrial fibrillation.

Blood test: Cardiac troponin T or I , complete blood count, serum electrolytes, blood urea nitrogen, creatinine, liver function test, and brain natriuretic peptide BNP. Medical Management Diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, angiotensin receptor neprilysin inhibitor, hydralazine plus nitrate, digoxin, and aldosterone antagonists can produce an improvement in symptoms and are indicated for patients with HF based on their functional classification and severity of symptoms.

Nursing Management The nursing care plan for patients with HF should include: [4] Relieving fluid overload symptoms. When To Seek Help Prompt assessment by the medical team is indicated in the following situations: Worsening symptoms of fluid overload. Monitoring Patients with HF require frequent monitoring of vital signs, including oxygen saturation.

Coordination of Care Heart failure is a serious disorder best managed by an interprofessional team that includes the primary care physician, emergency department physician, cardiologist, radiologist, cardiac nurses, internist, and cardiac surgeons. Health Teaching and Health Promotion Nursing care plans for patients with HF must include patient education to improve clinical outcomes and reduce hospital readmissions. Discharge Planning Discharge planning for patients with HF must include patient education on medication management, medication compliance, low-sodium diet, fluid restriction, activity and exercise recommendations, smoking cessation, and learning to recognize the signs and symptoms of worsening HF.

Review Questions Access free multiple choice questions on this topic. Comment on this article. Figure congestive heart failure. Image courtesy S Bhimji MD. References 1. Savarese G, Lund LH. Card Fail Rev. Diagnosis of heart failure: the new classification of heart failure. Vnitr Lek. Ziaeian B, Fonarow GC. Epidemiology and aetiology of heart failure. Nat Rev Cardiol. Impact of risk factors for major cardiovascular diseases: a comparison of life-time observational and Mendelian randomisation findings.

Open Heart. J Am Coll Cardiol. The pathophysiology of heart failure. Cardiovasc Pathol. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med. Diagnosis and evaluation of heart failure. Am Fam Physician. Clinical predictors of heart failure in patients with first acute myocardial infarction. Am Heart J. Curr Heart Fail Rep. Int J Cardiovasc Imaging. Calibrated scintigraphic imaging procedures improve quantitative assessment of the cardiac sympathetic nerve activity.

Sci Rep. Use of isosorbide dinitrate and hydralazine in African-Americans with heart failure 9 years after the African-American Heart Failure Trial. Am J Cardiol. Eur J Heart Fail. Imamura T, Narang N. ESC Heart Fail. Adv Exp Med Biol. J Card Fail. Freedom from congestion predicts good survival despite previous class IV symptoms of heart failure. Disposition of acute decompensated heart failure from the emergency department: An evidence-based review.

Am J Emerg Med. Long-term management of end-stage heart failure. Best Pract Res Clin Anaesthesiol. Heart failure. Cardiovasc Drugs Ther. Eur Heart J. In: StatPearls [Internet]. In this Page.

Bulk Download. Related information. Similar articles in PubMed. Circ Heart Fail.

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Congestive Heart Failure (CHF) - Causes of CHF - Pathophysiology of CHF - Heart Failure - Part-1

WebDec 16, �� (PDF) Congestive Heart Failure Home Cardiovascular Disease Heart Diseases Heart Failure Biological Science Anatomy Cardiovascular System Congestive . WebCONGESTIVE HEART FAILURE: THE BASICS By understanding some basics about congestive heart failure (CHF) and its symptoms, you will be better prepared to care for . WebJul 19, �� Overcoming Congestive Heart Failure PDF Free Download. In this blog post, we are going to share a free PDF download of Overcoming Congestive Heart .