 Discuss the possible causes of heart failure.  Distinguish left heart failure from right heart failure in terms of etiology and physiologic effects.  Describe how right heart failure may result from left heart failure.  Discuss the physiologic mechanisms that become active to compensate for heart failure.

 What are the clinical manifestations of heart failure? Why does each occur?  Discuss the different approaches that might be used to treat heart failure.

 The heart is a four-chambered pump consisting of two atria (the right atrium, which receives blood returning to the heart from the systemic circulation, and the left atrium, which receives oxygenated blood from the lungs)  and two ventricles (a right ventricle, which pumps blood to the lungs, and a left ventricle, which pumps blood into the systemic circulation).

 The cardiac cycle is divided into two major periods: systole, when the ventricles are contracting, and diastole, when the ventricles are relaxed and filling.

 Heart failure (HF) is a clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body.  Heart failure can result from any disorder that reduces ventricular filling (diastolic dysfunction) and/or Reduces myocardial contractility (systolic dysfunction).

 Heart failure is a condition in which the heart is no longer pumping blood effectively.  Depending upon the cause, heart failure may be classified as low output failure or high-output failure.  Low-output failure is a reduced pumping efficiency of the heart that is caused by factors that impair cardiac function such as myocardial ischemia, myocardial infarction or cardiomyopathy.

 With high output failure, the cardiac output is normal or elevated but still cannot meet the metabolic and oxygen need of the tissues )uncommon(.  Common causes of high-output failure include hyperthyroidism (hypermetabolism) and anemia (reduced oxygen- carrying capacity), conditions in which even greatly elevated cardiac output cannot keep up with the increased metabolic requirements of the tissues.

- Heart failure is very common - Heart failure affects nearly 5 million Americans - An estimated 400,000 to 700,000 new cases are diagnosed each year

Heart failure results after injury to the heart. Risk factors include: High blood pressure Heart attack High cholesterol Damage to heart valves Diabetes Obesity Advancing age

Think FACES... - F atigue - A ctivities limited - C hest congestion - E dema or ankle swelling - S hortness of breath

 Classically, the manifestations of heart failure can be divided into those occurring as a result of left heart failure (left atrium and ventricle) and right heart failure (right atrium and ventricle).

 The left side of the heart is responsible for pumping oxygenated blood from the lungs out to the peripheral tissues of the body.  The most common causes of left heart failure include  myocardial infarction,  cardiomyopathy and  chronic hypertension.  Left heart failure is also referred to as congestive heart failure due to the pulmonary congestion of blood that accompanies the condition

 Manifestations of left heart failure include the following: 1. Decreased stroke volume, increased left- ventricular end-diastolic volume (LVEDV), increased preload. 2. Congestion of blood in the pulmonary circulation leading to increased pulmonary pressure and pulmonary edema. 3. Dyspnea, cough, frothy sputum; “rales” or crackling sounds that may be heard through a stethoscope as a result of fluid accumulation in the lungs

4. Orthopnea, the accumulation of fluids and dyspnea that are often worse at night or when the patient lies in the supine position because blood and fluids from the lower limbs may redistribute into the pulmonary circulation. 5. Poor perfusion of systemic circulation that may lead to cyanosis. 6. Generalized fatigue and muscle weakness

 Stroke volume — The volume of blood pumped by one ventricle during one contraction.  Preload — The degree to which the myocardium is stretched by venous return. Determined by LVEDV.  LVEDV (left-ventricular end-diastolic volume) — The amount of blood that fills the left ventricle during relaxation.  Ejection fraction — The fraction of the blood contained in the ventricle at the end of diastole that is expelled during its contraction (the stroke volume divided by end-diastolic volume).

 Afterload — The pressure the heart must overcome to pump blood out into the aorta.  Orthopnea — Difficulty breathing when lying down.  Cyanosis — Bluish discoloration of the skin and mucous membranes due to inadequate amounts of oxygen in the blood.

“Ejection Fraction” refers to the fraction of blood the heart pumps out with each beat. - Healthy heart = 60% or more - Heart failure = 40% or less

 Right heart failure often arises as a consequence of left heart failure. As a result of the increased pulmonary pressure that accompanies left heart failure, the resistance to blood flow now faced by the right ventricle is significantly increased as it pumps blood to the lungs.  Over time, the increased workload on the right ventricle leads to dilation and eventual failure of the right heart. Right heart failure may also result from chronic obstructive pulmonary disease, cystic fibrosis or adult respiratory distress syndrome.

Manifestations of right heart failure include the following: 1. Increased right ventricular workload. 2. Venous congestion and distention 3. Peripheral edema, ascites 4. Swelling of the liver with possible injury and eventual failure 5. Gastrointestinal symptoms

 Recently, the American Heart Association issued guidelines for treating heart failure based upon whether patients experience systolic failure or diastolic failure.  With systolic failure, there is a decreased ejection of blood from the heart during systole.  With diastolic failure, filling of the ventricles during diastole is impaired.

 Decreased myocardial contractility  Decreased ejection fraction  Most commonly caused by conditions that impair contractility such as ischemic heart disease, myocardial infarction and cardiomyopathy  Symptoms mainly those of reduced cardiac output

 Approximately 20 to 40% of patients with heart failure  Preserved left ventricular systolic function but reduced ventricular filling that may be associated with impaired ventricular relaxation  Associated with conditions such as cardiomyopathy  Symptoms primarily those of blood congestion and may include marked dyspnea and fatigue

 The signs and symptoms of heart failure may not appear in the early stages as a result of a number of compensatory mechanisms that combine to maintain cardiac output. This early stage of heart failure is termed compensated heart failure.  The compensatory responses are only effective in the short term and will eventually be unable to maintain cardiac output for a long period of time.  Decompensated heart failure occurs when cardiac output is no longer adequately maintained and overt symptoms of heart failure appear.

Compensatory mechanisms include the following: 1. Increased cardiac output — The normal heart responds to increases in preload or LVEDV by increasing stroke volume and cardiac output. The more the heart is stretched by filling, the greater its responsive strength of contraction ( Frank–Starling Principle)

 With heart failure there are chronic increases in preload that continually distend the ventricular muscle fibers. Over time, the compensatory Frank– Starling mechanism becomes ineffective because the cardiac muscle fibers stretch beyond the maximum limit for efficient contraction.  In addition, the oxygen requirements of the distended myocardium exceed oxygen delivery. At this point, further increases in preload are not matched by an increase in cardiac output.

2. Increased sympathetic activity — The decrease in cardiac output that accompanies heart failure will lead to decreases in blood flow and blood pressure that activate the sympathetic nervous system. The result of sympathetic activation is an increase in circulating levels of catecholamines that cause peripheral vasoconstriction as well as an increase in heart rate and force of cardiac contraction (positive chronotropic and positive inotropic effects).

Unfortunately, the failing myocardium becomes dependent on circulating levels of catecholamines to help it maintain cardiac output. Over time, the failing myocardium becomes less responsive to the stimulatory effects of these catecholamines and function continues to deteriorate.

 3. Activation of renin–angiotensin system— As a result of decreased cardiac output, blood flow to the kidneys will be significantly reduced.  The kidneys respond to this reduction in blood flow by releasing the enzyme renin. Renin ultimately leads to the production of angiotensin II in the plasma and the release of aldosterone from the adrenal gland.  Angiotensin II is a powerful vasoconstrictor that increases systemic blood pressure while aldosterone acts on the kidney tubules to increase salt and water retention, a second factor that will increase systemic blood pressure.

Other hormones that appear to be increasingly active during heart failure are antidiuretic hormone (ADH) from the pituitary gland and atrial natriuretic factor (ANF) that is released in response to atrial dilation. ANF may have a beneficial effect on CHF since it acts as a natural diuretic.

4. Ventricular hypertrophy — Faced with a chronic increase in workload, the myocardium responds by increasing its muscle mass. Although increased muscle mass can increase cardiac output in the short term, contractility eventually suffers as the metabolic demands of the hypertrophied myocardium continue to increase and the efficiency of contraction decreases.

 Dyspnea with exertion, orthopnea, nocturnal dyspnea  Rales, cough, hemoptysis  Distention of jugular vein, liver enlargement, ascites  Peripheral and pulmonary edema  ECG (“EKG” or “ECG”), chest x-ray for cardiac hypertrophy, Echocardiogram (“echo”)  Cardiac catheterization to assess hemodynamic function

 Class I: No limitations  Class II: Slight limitation of physical activity  Class III: Marked limitation of physical activity  Class IV: Symptomatic at rest. Symptoms of CHF are present at rest.

Treatment for heart failure can be directed to reducing the workload on the failing heart and/or to enhancing cardiac contractility. Treatment may include the following: 1. Restriction of physical activity to reduce cardiac workload 2. Reduction of preload through: Salt and fluid restriction Venous dilation with vasodilator drugs The use of diuretic drugs to reduce fluid volume

3. Reduction of afterload through:  The use of arterial vasodilators  The inhibition of angiotensin II formation by ACE inhibitor drugs 4. Blunting the effects of the catecholamines and adrenergic input with β -adrenergic receptor antagonists 5. Increasing contractility (positive inotropic agents):  Digitalis glycosides — digoxin  Inhibitors of heart-specific phosphodiesterases — amrinone, milrinone

- No, currently there is not a cure - BUT, early diagnosis and proper treatment can: - Slow the progression of disease - Keep you out of the hospital - Save your life!

Experts recommend: - Diuretics - help control symptoms - Digoxin - helps control symptoms - ACE Inhibitors - can slow disease progression - Beta Blockers - can slow disease progression This combination of medications has been proven to save lives and keep people out of the hospital.

 To achieve improvement in symptoms :  Diuretics  Digoxin  ACE inhibitors  To achieve improvement in survival:  ACE inhibitors  ß blockers (for example, carvedilol and bisoprolol)  Oral nitrates plus hydralazine

Doctors usually treat heart failure with a combination of medications. Depending on your symptoms, you might take one or more of these drugs. They include:  Angiotensin-converting enzyme (ACE) inhibitors. These drugs help people with heart failure live longer and feel better. ACE inhibitors are a type of vasodilator, a drug that widens blood vessels to lower blood pressure, improve blood flow and decrease the workload on the heart. Examples include enalapril, lisinopril and captopril.

 Angiotensin II receptor blockers (ARBs). These drugs, which include losartan and valsartan, have many of the same benefits as ACE inhibitors. They may be an alternative for people who can't tolerate ACE inhibitors.  Digoxin (Lanoxin). This drug, also referred to as digitalis, increases the strength of your heart muscle contractions. It also tends to slow the heartbeat. Digoxin reduces heart failure symptoms and improves your ability to live with the condition.

 Beta blockers. This class of drugs slows your heart rate and reduces blood pressure. Examples include carvedilol, metoprolol and bisoprolol. These medicines also reduce the risk of some abnormal heart rhythms. Beta blockers may reduce signs and symptoms of heart failure and improve heart function.

 Diuretics. Often called water pills, diuretics make you urinate more frequently and keep fluid from collecting in your body. Commonly prescribed diuretics for heart failure include furosemide.The drugs also decrease fluid in your lungs, so you can breathe more easily.  Because diuretics make your body lose potassium and magnesium, your doctor may also prescribe supplements of these minerals. If you're taking a diuretic, your doctor will likely monitor levels of potassium and magnesium in your blood through regular blood tests.

 Aldosterone antagonists. These drugs include spironolactone and eplerenone.They're primarily potassium-sparing diuretics, but they have additional properties that help the heart work better, may help people with severe heart failure live longer. Unlike some other diuretics, spironolactone can raise the level of potassium in your blood to dangerous levels, so talk to your doctor if increased potassium is a concern.

YES! - See your physician regularly - Limit your salt intake - Weigh yourself each day - Contact your healthcare provider if your weight changes more than 2-3 pounds in one day - Take your medications - Exercise at levels recommended by your physician

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