They retain sodium and water.
It leads to myocardial dysfunction.
Vegetations.
Prosthetic valve.
Indwelling catheters.
They increase cardiac output and systemic blood pressure.
It is released into the kidneys to retain sodium and water.
Embolization.
Skin, wound, lung, or GU infection.
They contribute to myocardial dysfunction and ventricular remodeling.
Valvular heart disease, inflammation, and thrombus formation.
It contributes to hypertrophy and dilation of the ventricle.
Endocardial damage.
They are associated with hypertrophy and dilation of the ventricle.
Bacterial endocarditis of the mitral valve.
Renin-angiotensin-aldosterone system and sympathetic nervous system.
They contribute to ventricular remodeling.
Injection drug use.
They activate vasomotor regulatory centers in the medulla.
Abscesses, petechiae, splinter hemorrhages, Osler nodes, and Janeway lesions.
Angiotensin II, aldosterone, catecholamines, and cytokines.
Endocardial damage.
In the left ventricle, aortic arch, and carotid sinus.
Murmurs, regurgitant valve, and heart failure.
The pathogenesis of infective endocarditis.
A lesion in combination with old rheumatic valvulitis.
Dental, GU, or cardiac procedures.
It increases systemic blood pressure.
Fever, night sweats, malaise, and weight loss.
Fibrin and thrombus formation.
It gets activated.
Release of angiotensin II and aldosterone.
Bacterial adherence.
Bacteremia.
The impaired myocardium may be unable to deliver the increased output, leading to depletion of cardiac reserves and low-output failure.
Dysrhythmias range in severity from occasional 'missed' or rapid beats to serious disturbances that impair the pumping ability of the heart, contributing to heart failure and death.
The myocardium relies on getting enough fuel, having adequate mitochondrial function, and using an effective creatine kinase system for efficient ATP production.
Angiotensin II mediates remodeling of the ventricular wall, contributing to sarcomere death, loss of the normal collagen matrix, and interstitial fibrosis.
There may be evidence of underlying coronary disease, hypertension, or valvular disease.
The inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure.
Myocardial fibrosis is associated with autonomic dysfunction and dysrhythmias.
Metabolic acidosis occurs when the body's cells switch to anaerobic metabolism.
In the United States, beriberi is usually caused by malnutrition secondary to chronic alcoholism.
Dysrhythmias can be caused by either an abnormal rate of impulse generation by the SA node or other pacemaker, or the abnormal conduction of impulses through the heart’s conduction system, including the myocardial cells themselves.
Baroreceptors stimulate the SNS to cause vasoconstriction and the hypothalamus to produce antidiuretic hormone.
Individuals most often present with dyspnea on exertion and fatigue.
Beta-blockers, ACE inhibitors, ARBs, and aldosterone blockers.
Pressure will rise in the systemic venous circulation, resulting in jugular venous distention, peripheral edema, and hepatosplenomegaly.
TNF-α is elevated in heart failure and contributes to myocardial hypertrophy and remodeling.
Many new medications used to treat diabetes and insulin resistance have deleterious side effects on cardiac functioning.
PPAR-gamma agonists (thiazolidinediones) are contraindicated because of increased fluid retention at the renal tubule.
Cardiac output increases to maintain blood pressure and prevent metabolic acidosis.
Decreased systemic vascular resistance (SVR) triggers increased cardiac output in beriberi.
It causes a stretching of the myocardium that can lead to dysfunction of the sarcomeres and decreased contractility.
Pathologic hypertrophy results in an increase in oxygen and energy demand.
Activation of the RAAS causes increases in preload and afterload, and direct toxicity to the myocardium.
It shows pulmonary congestion without cardiomegaly.
Outcomes can be as poor as those with systolic heart failure.
Management of the left ventricular dysfunction.
TNF-α induces myocyte apoptosis and may contribute to weight loss and weakness in individuals with heart failure.
The heart muscle exhibits progressive changes in myocyte myofilaments, decreased contractility, myocyte apoptosis and necrosis, abnormal fibrin deposition in the ventricle wall, myocardial hypertrophy, and changes in the ventricular chamber geometry.
It causes varying degrees of valvular dysfunction.
Common causes of high-output failure are anemia, septicemia, hyperthyroidism, and beriberi.
In overwhelming septicemia, the heart may not be able to raise its output enough to compensate for vasodilation, leading to inadequate blood supply to body tissues despite high cardiac output.
A dysrhythmia, or arrhythmia, is a disturbance of heart rhythm.
Contractility of the myocardium is compromised, leading to an energy-starved state that contributes to changes in myocytes and ventricular remodeling.
The consequences include decreased contractility, changes in myocardial compliance, and ventricular dilation.
Signs and symptoms of heart failure, normal left ventricular ejection fraction, and evidence of diastolic dysfunction.
Myocardial fibrosis is implicated in endothelial dysfunction and prothrombotic effects.
Calcium transport is critical to normal contractile function in myocytes.
ACE inhibitors, aldosterone blockers, and beta-blockers are routinely used in the management of heart failure.
Pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop, and evidence of underlying CAD or hypertension.
To monitor hemodynamics or to document underlying coronary disease.
Heart transplant.
Intravenous inotropic drugs.
Hypertrophy and ischemia.
Human recombinant ANP and ularitide.
Decreased compliance of the left ventricle and abnormal diastolic relaxation (lusitropy).
Hyperthyroidism accelerates cellular metabolism through the actions of elevated levels of thyroxine from the thyroid gland.
Ventricular remodeling results in the deposition of collagen between myocytes, disrupting muscle integrity, decreasing contractility, and making the ventricle more likely to dilate and fail.
Aldosterone contributes to the pathogenesis of heart failure by promoting fibrosis and inflammation.
By echocardiography, which demonstrates poor ventricular filling with normal ejection fractions.
It most often results from left heart failure when the increase in left ventricular filling pressure is severe enough.
The right ventricle will dilate and fail.
It is most commonly caused by pulmonary hypertension resulting from diffuse hypoxic pulmonary disease such as COPD, cystic fibrosis, and ARDS.
Arginine vasopressin causes both peripheral vasoconstriction and renal fluid retention.
Insulin resistance causes abnormal myocyte fatty acid metabolism and generation of ATP, contributing to decreased myocardial contractility and remodeling.
In the failing heart, increased demand for oxygen and energy is coupled with a decreased ability to use fatty acids as an energy source.
No, unless other comorbid conditions such as CAD are present.
Janeway lesions are nonpainful hemorrhagic lesions on the palms and soles.
Diuretics.
Approximately 50%.
Diabetes.
Increasing contractility and reducing preload and afterload.
Ischemic heart disease and hypertension are the most important predisposing risk factors.
If anemia is severe, even maximum cardiac output does not supply the cells with enough oxygen for metabolism.
Disturbed metabolism, bacterial toxins, and the inflammatory process cause systemic vasodilation and fever in septicemia.
Thiamine deficiency leads mainly to peripheral vasodilation, which decreases systemic vascular resistance (SVR).
Nearly 75% of cases of heart failure have antecedent hypertension.
Increased PVR can result in resistance to ventricular emptying and more workload for the left ventricle, leading to hypertrophy of the myocardium.
The physiologic response to increased workload (exercise) is intermittent and increases muscle mass without distorting cardiac architecture, whereas sustained afterload leads to pathologic hypertrophy mediated by angiotensin II and catecholamines.
In response to metabolic acidosis, heart rate and stroke volume increase in an attempt to circulate blood faster.
Thiamine deficiency impairs cellular metabolism in all tissues, including the myocardium, leading to insufficient contractile strength.
The result is the progressive worsening of left heart failure.
There may be evidence of pulmonary edema, such as inspiratory crackles on auscultation and pleural effusions.
Treating hypertension or valvular disease.
Natriuretic peptides, such as atrial and BNPs, may have a protective effect by decreasing preload.
Diabetes contributes to heart failure through disturbed calcium metabolism, oxidative stress, changes in fatty acid and glucose metabolism, and mitochondrial dysfunction.
PPAR genes control fatty acid oxidation and are important in heart failure associated with insulin resistance and diabetes.
An ECG and serum troponin.
Serum BNP levels.
Gene and stem cell therapies.
Abnormalities in an intracellular protein component of the myocyte cytoskeleton called titin.
An increase in wall tension.
Myocardial infarction is the most common cause of decreased contractility.
92% to 98%.
Ularitide.
Adenovirus, sendai virus, and adeno-associated virus (AAV).
Anemia decreases the oxygen-carrying capacity of the blood.
Cardiac output increases to meet the body's increased demand for oxygen and prevent metabolic acidosis.
Normal heart rhythms are generated by the SA node and travel through the heart’s conduction system, causing the atrial and ventricular myocardium to contract and relax at a regular rate.
Hypertensive hypertrophic cardiomyopathy is the weakness of the cardiac muscle due to hypertension-induced hypertrophy.
It is reflected back into the pulmonary circulation and results in pulmonary edema.
Improving ventricular relaxation and prolonging diastolic filling times to reduce diastolic pressure.
Right ventricular MI, cardiomyopathies, and pulmonic valvular disease.
Arginine vasopressin exacerbates heart failure by causing hyponatremia and edema.
Heart failure activates the SNS and RAAS, which contribute to insulin resistance.
Several genes, including the peroxisome proliferator-activated receptor (PPAR) family of genes, are activated to alter the ability of myocytes to use lipids and glucose as fuel sources.
Infective endocarditis may involve the lungs, eyes, kidneys, bones, joints, and CNS.
Amiodarone or ICDs.
Sudden onset of severely debilitating symptoms indicates acute disease.
Preload and contractility.
Pericardial effusion and left heart failure are the most common complications.
Changes in myocardial structure such as molecular alterations in collagen.
Preload, afterload, and mortality.
Genetic changes in kinases, phosphatases, and cellular calcium cycling are being explored.
Decreased.
S3.
They are safe and have minimal immunogenicity but are not efficient at delivering genes to tissues.
Even an abnormally elevated cardiac output may be inadequate to meet the body's needs.
Conditions such as renal failure and mitral valvular disease can increase LVEDV and potentially improve cardiac output up to a certain point.
Increased peripheral vascular resistance (PVR), such as that seen with hypertension, is the most common cause of increased afterload.
As cardiac output falls, renal perfusion diminishes, activating the RAAS, which increases PVR and plasma volume, further increasing afterload and preload.
Symptoms worsen with tachycardia, such as during exercise.
Aerobic and weight training improve endurance and quality of life.
No, the compensatory mechanisms of natriuretic peptides are inadequate in heart failure.
Receptors on myocytes for damaging advanced glycation end-products (RAGE) are up-regulated in injuries to the heart, including ischemia and reperfusion injury.
Energy starvation and high levels of catecholamines lead to altered fatty acid oxidation and decreased effective ATP generation and use, resulting in decreased myocardial contractility and structural changes in the myocardium.
The use of certain medications.
Signs and symptoms are caused by infection and inflammation, systemic spread of microemboli, and immune complex deposition.
Cardiac resynchronization therapy.
The criteria include persistent bacteremia, new heart murmurs, vascular complications, and appropriate electrocardiographic and echocardiographic findings.
Calcium-sensitizing inotropic drugs (e.g., levosimendan).
Treatment with cART can cause hyperlipidemia and atherosclerotic disease.
It becomes noncompliant and poorly lusitropic, unable to accept filling with blood without significant resistance and an increase in wall tension.
Decreased.
Preload, or LVEDV, increases with decreased contractility or when there is an excess of plasma volume.
It improves preload and contractility, but the results of this therapy have been mixed.
Systolic congestive heart failure is characterized by a complex constellation of neurohumoral, inflammatory, and metabolic processes.
Pulmonary hypertension and right ventricular failure may develop.
The resistance to right ventricular emptying increases.
Endothelin is a potent vasoconstrictor associated with a poor prognosis in individuals with heart failure.
Measurement of levels of RAGE in plasma or serum may correlate with the degree of heart failure.
Potential therapies include PPAR agonists, which have been shown to enhance fatty acid oxidation, improve endothelial cell function, and decrease myocardial fibrosis and hypertrophy in animal models of heart failure.
Through the use of pharmacogenetics that can identify those genotypes most likely to respond favorably to specific treatment options.
Heart size and evidence of pulmonary congestion.
Interrupting the worsening cycle of decreasing contractility, increasing preload, and increasing afterload, as well as blocking the neurohormonal mediators of myocardial toxicity.
Other drugs may be necessary to treat left heart failure secondary to valvular dysfunction, and surgical intervention to repair or replace the valve may be required.
Acute coronary bypass or PCI.
Heart failure is defined as the pathophysiologic condition in which the heart is unable to generate an adequate cardiac output such that there is inadequate perfusion of tissues or increased diastolic filling pressure of the left ventricle, or both.
Only in those who do not tolerate ACE inhibitors.
Normal.
Yes, it is probable.
The effectiveness and safety of recent gene therapy trials.
Methods such as antegrade or retrograde coronary infusion, intravenous infusion, direct myocardial injection, and pericardial injection.
It increases heart rate and peripheral vascular resistance.
An S4 gallop may arise.
The inability of the heart to adequately supply the body with blood-borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility.
TNF-α down-regulates the synthesis of the vasodilator nitric oxide (NO).
The interaction of these processes results in a gradual decline in myocardial function.
Trimetazidine is a partial fatty-acid-oxidation inhibitor that may decrease hospitalization for cardiac causes, improve clinical symptoms and cardiac function, and reduce left ventricular remodeling in people with CHF.
Infective endocarditis may be acute, subacute, or chronic.
The classic findings are fever, new or changed cardiac murmur, and petechial lesions of the skin, conjunctiva, and oral mucosa.
Coronary bypass surgery or PCI.
Increase contractility and can help raise the blood pressure in hypotensive individuals.
Hypertension-induced myocardial hypertrophy and myocardial ischemia with resultant ventricular remodeling.
The intra-aortic balloon pump (IABP).
Nearly 10% of Americans older than age 65 have symptomatic heart failure.
Symptoms and survival.
Diagnosis of heart failure, prognosis in HF, monitoring treatment of HF, and treatment of HF.
It reduces total cardiovascular events, mortality, and hospital readmission with heart failure.
It catalyzes cAMP formation and beta-adrenergic receptor function.
Many new and potentially lifesaving gene therapies for individuals with intractable heart failure.
Catecholamines cause direct toxicity to myocytes, induction of myocyte apoptosis, myocardial remodeling, down-regulation of adrenergic receptors, facilitation of dysrhythmias, and potentiation of autoimmune effects on the heart muscle.
It often reveals evidence of left ventricular hypertrophy.
Because contractility and ejection fraction are not affected.
Arginine vasopressin is also known as antidiuretic hormone.
Changes in calcium ion channels, intracellular transport mechanisms in the sarcoplasmic reticulum, and calcium cycling are implicated in decreased myocardial contractility and heart failure.
The heart relies on the efficient production of adenosine triphosphate (ATP) and has very little capacity for energy storage.
The inotropic drug digoxin.
Osler nodes are painful erythematous nodules on the pads of the fingers and toes.
Oxygen, nitrates, and morphine administration.
Two different antibiotics may be given simultaneously to eliminate the offending microorganism and prevent the development of drug resistance.
The risk is estimated at only 1 case per 1.1 million dental procedures.
In the aorta just distal to the aortic valve; it is inflated during diastole to improve coronary perfusion and deflated during systole to reduce afterload.
Approximately 20% of asymptomatic individuals older than age 40 have some evidence of myocardial dysfunction.
Pressure and volume overload of the cardiac chambers.
93% to 98%.
It is manufactured from Escherichia coli using recombinant deoxyribonucleic acid (DNA) technology.
Nonviral and viral.
IL-6 is elevated in individuals with severe heart failure and cardiogenic shock and may contribute to further deleterious immune activation.
These changes reduce myocardial function and cardiac output, leading to increased morbidity and mortality.
Dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema.
To confirm decreased cardiac output and cardiomegaly.
Acute myocardial ischemia.
Antimicrobial therapy is generally given for 4 to 6 weeks.
Individuals with valvular heart disease received prophylactic antibiotics for dental, genitourinary, or gastrointestinal procedures.
High risk individuals include those with a history of infective endocarditis, prosthetic valves, cyanotic congenital heart disease, and heart transplant with valvular defect.
Sustained activation of the RAAS and the SNS.
Male>female.
Ventricular remodeling is a process mediated by inflammatory, immune, and neurohumoral changes that result in disruption of the normal myocardial extracellular structure, causing dilation of the myocardium and progressive myocyte contractile dysfunction over time.
Pulmonary congestion with cardiomegaly.
Sarcoendoplasmic reticulum calcium ATPase (SERCA2a) and S100A1.
Pulmonary vascular congestion and inadequate perfusion of the systemic circulation.
In selected individuals, particularly those with intracardiac thrombi or atrial fibrillation.
Other manifestations include weight loss, back pain, night sweats, and heart failure.
Heart failure with preserved ejection fraction.
ACE inhibitors and intravenous beta-blockers.
Aortic valvular disease, mitral valve disease, pericardial diseases, and cardiomyopathies.
Other conditions include cardiomyopathy, myocarditis, tuberculous pericarditis, infective and nonbacterial endocarditis, heart block, pulmonary hypertension, and non-antiretroviral drug-related cardiotoxicity.
ACE inhibitors and beta blockers.
Other risk factors include age, obesity, diabetes, renal failure, valvular heart disease, cardiomyopathies, myocarditis, congenital heart disease, and excessive alcohol use.
Inhibits myocardial fibrosis and hypertrophy and enhances diastolic function.
Serum levels of BNP are correlated with morbidity and mortality, and risk for future acute exacerbations.
Pulmonary capillary wedge pressure and cardiac output, but not mortality.
No, it has not been shown to improve survival.
CNS, splenic, renal, pulmonary peripheral arterial, coronary, and ocular emboli may lead to a wide variety of signs and symptoms.
Pulmonary congestion despite a normal stroke volume and cardiac output.
Malignancies such as lymphoma and Kaposi sarcoma are often seen.
Salt restriction, loop diuretics, and aldosterone-blockers such as spironolactone and eplerenone.
Female>male.
Increased.
Nesiritide is the first of a new class of drugs, human B-type natriuretic peptide (hBNP), and it was approved in August 2001.
Homing of stem cells to infarcted myocardium.
Changes in calcium transport from myocytes and may be related to the activity of sarcoplasmic reticulum–calcium adenosine triphosphatase (ATPase).
Numerous genetic polymorphisms, including genes for cardiomyopathies, myocyte contractility, and neurohumoral receptors, have been linked to an increased risk for heart failure.
When contractility is decreased, stroke volume falls, and left ventricular end-diastolic volume (LVEDV) increases, causing dilation of the heart and an increase in preload.
Pulmonary congestion without cardiomegaly.
MicroRNAs and genes that code for critical neurohumoral factors, including insulin-like growth factor-1 (IGF-1), growth hormone, and B-type natriuretic peptide.
Causes arterial and venous dilation, natriuresis, and suppression of the renin-angiotensin-aldosterone system and the sympathetic nervous system.
Yes, it is possible.
S4.
They are more efficient at delivering genes to cells, but safety concerns persist.
