Part 11

-CHF

-Cardiac arrhythmia

What Is Congestive Heart Failure?

Congestive heart failure, or heart failure, is a condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from "backing up" into the lungs.

In most cases, heart failure is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ. Heart failure is characterized by shortness of breath (dyspnea) and abnormal fluid retention, which usually results in swelling (edema) in the feet and legs.

Normal Blood Flow of the Heart

The heart consists of four chambers: the right atrium, the left atrium, the right ventricle, and the left ventricle, and four major valves: the mitral valve, the tricuspid valve, the aortic valve, and the pulmonary valve. Atria are relatively thin-walled chambers that receive blood from the circulatory system and from the lungs. Ventricles are muscular chambers that pump blood into the circulatory system and into the lungs.

Blood passes from the atria into the ventricles through two processes. During the "resting phase," when the ventricles are not contracting, the tricuspid and mitral valves open and allow some of the blood that has accumulated in the atria to flow passively through the valves into the ventricles. Then, the atria contract and actively pump blood out through the valves and into the ventricles. Once the ventricles fill with blood, they contract, pumping blood to the lungs and the rest of the body.

When the left ventricle cannot adequately pump blood out of the left atrium, or when one or more of the heart valves becomes leaky or narrowed (stenotic), blood can "back up" into the lungs, causing "left-sided" heart failure. When this occurs, the lungs become congested with fluid (called pulmonary edema), causing difficulty breathing and interfering with the movement of oxygen from the lungs into the bloodstream, causing fatigue.

When an abnormality or condition affects the flow of blood through the right ventricle, pressure in the blood vessels increases and fluid is forced from the blood vessels into body tissues. This "right-sided" heart failure causes swelling (edema), usually in the feet and legs, and sometimes, in the abdomen.

Incidence and Prevalence
According to the American Heart Association, nearly 5 million people experience heart failure and about 550,000 new cases are diagnosed each year in the United States. Heart failure becomes more prevalent with age and the number of cases is expected to grow as the overall age of the population increases.

The condition affects 1% of people aged 50 years and older and about 5% of those aged 75 years and older. African Americans experience heart failure twice as often as Caucasians. About 10% of patients diagnosed with heart failure die within 1 year, and about 50% die within 5 years of diagnosis.

Causes

Risk factors for heart disease (e.g., smoking, being overweight, eating a diet high in fat and cholesterol, living a sedentary lifestyle) also increase the risk for heart failure. Underlying conditions that increase the risk for heart failure include the following:

• Abnormal heart rhythm (arrhythmia)
• Abnormal heart valve(s), which may be congenital (present at birth) or caused by disease or infection (e.g., aortic stenosis, mitral regurgitation)
• Alcoholism and drug abuse
• Coronary heart disease (CHD; also called atherosclerosis)
• Damaged heart muscle, which may be caused by disease (e.g., cardiomyopathies) or inflammation (e.g., myocarditis)
• Diabetes
• High blood pressure (hypertension)
• Low red blood cell count (severe anemia)
• Lung disease
• Overactive thyroid gland (hyperthyroidism)
• Pneumonia
• Prior history of heart attack (myocardial infarction)
• Vitamin deficiency

The most common cause for heart failure is dysfunction of the left ventricle. Normally, every time the heart "beats," the left ventricle contracts and ejects approximately 60% of the blood in the chamber into the main artery (aorta). The percentage of blood pumped out of the left ventricle with each contraction is called the ejection fraction.

Measuring the ejection fraction is a way to determine left ventricle function. In patients with left ventricular dysfunction, the ejection fraction may be as little as 10%. An ejection fraction of approximately 40–45% indicates mild dysfunction; 30–40% indicates moderate dysfunction; and 10–25% indicates severe dysfunction.

Other Causes
Heart failure may develop during the last 3 months of pregnancy or several months after pregnancy. The cause of this is not well understood, but it may be due to an abnormal immune system response.

In some cases, the cause of heart failure is never identified (called idiopathic cardiomyopathy). Idiopathic cardiomyopathy may be due to a past, unidentified viral infection.

Signs and Symptoms

Symptoms of heart failure vary and include the following:

• Fatigue
• Increased heart rate, palpitations
• Loss of appetite
• Memory loss, confusion
• Nausea
• Persistent coughing or wheezing
• Shortness of breath (dyspnea)
• Swelling (edema) of the feet, legs, or abdomen

Treatment

Treatment for heart failure varies and involves reducing symptoms, treating the underlying cause of the condition when possible (e.g., antibiotics to treat pneumonia, restoring normal heart rhythm in patients with atrial fibrillation), and using medications to prevent further deterioration of heart function.

In mild cases, lifestyle modifications can help reduce symptoms such as fatigue, shortness of breath, and swelling (edema). These modifications may include dietary changes (e.g., restricted salt intake), abstaining from alcohol, and exercising regularly (only under the supervision of a physician).

Medications used to treat heart failure include the following:

• Angiotensin-converting enzyme (ACE) inhibitors (e.g., captopril [Capoten®], enalapril [Vasotec®], ramipril [Altace®], lisinopril [Prinivil®, Zestril®], quinapril [Accupril®], fosinopril [Monopril®], benazepril [Lotensin®], moexipril [Univasc®])
• Angiotensin II receptor blockers (ARBs; e.g., candesartan [Atacand®], irbesartin [Avapro®], losartan [Cozaar®], telmisartin [Micardis®], and valsartan [Diovan®]
• Beta-blockers (e.g., carvedilol [Coreg®], metoprolol [Lopressor®, Toprol XL®])
• Blood thinners (e.g., warfarin [Coumadin®])
• Diuretics (e.g., hydrochlorothiazide [HydroDIURIL®], chlorothiazide [Diuril®], furosemide [Lasix®], indapamide [Lozol®], bumetanide [Bumex®], spironolactone [Aldactone®], triamterene [Dyrenium®], metolazone [Zaroxolyn®], combination agents [Dyazide®])
• Inotropic agents (e.g., digoxin [Lanoxin®], dobutamine [Dobutrex®], dopamine)
• Other vasodilators (e.g., hydralazine [Apresoline®], isosorbide dinitrate [Isordil®], nitrates)

Angiotensin-converting enzyme (ACE) inhibitors help open (dilate) the arteries, making it easier for the heart to pump blood throughout the body. They usually are the treatment of choice for heart failure. Studies have shown that these drugs, which are often used to treat high blood pressure, can improve symptoms and reduce the risk for sudden death from heart failure.

ACE inhibitors usually are well tolerated and may be taken once a day, or 2 or 3 times daily. They are not used in patients with low blood pressure (hypotension) and may affect kidney function and potassium levels.

Side effects include the following:

  Chronic, nonproductive cough (occurs in about 10% of patients)

  Dizziness or weakness (caused by low blood pressure)

  Increased potassium levels

  Skin rashes

  Sudden swelling of the lips, face, and cheeks (if this occurs, the patient must seek medical attention immediately)

Angiotensin II receptor blockers (ARBs) may be used in patients who are unable to tolerate ACE inhibitors due to chronic cough, low blood pressure, or edema. These drugs, which help open (dilate) the arteries, are similar to ACE inhibitors, make it easier for the heart to pump blood, and may improve heart failure symptoms. Ongoing studies are investigating the use of ACE inhibitors with the use of ARBs in some patients with heart failure.

Angiotensin II receptor blockers generally are taken once a day, and they usually do not cause significant side effects. Rarely, they can impede kidney function.

Heart failure often causes the heart to pump harder to compensate for its weakened pumping ability. Beta-blockers help to relax the heart, reduce the vigor of its contractions, and reduce additional strain on the heart. These drugs often are used in combination with other drugs (e.g., ACE inhibitors, diuretics) to treat mild to moderate heart failure.

Beta-blockers are started at low doses that are gradually increased over a period of several months. During the first several weeks of treatment, some patients experience worsening symptoms due to a decrease in oxygen circulation in the body. Other side effects include low blood pressure, difficulty breathing, and nausea and weakness with exertion.

Heart failure increases the risk for stroke caused by blood clot (thrombus) formation and blood thinners (e.g., warfarin [Coumadin®]) often are prescribed to help reduce this risk. Blood thinners may cause nosebleeds and excessive bleeding and bruising.

In most cases, diuretics, commonly called "water pills," are prescribed to reduce fluid buildup in the body. These drugs cause the kidneys to excrete excess amounts of sodium and water into the urine, often reducing symptoms of heart failure (e.g., shortness of breath and swelling of the legs, ankles, and feet).

The correct diuretic dosage is based on the patient's weight. If not enough fluid is removed, heart failure symptoms do not improve and if too much fluid is removed, fatigue, low blood pressure, and impaired kidney function may occur. Diuretics usually are taken once (in the morning) or twice a day. In some cases, two diuretics are used to increase salt and fluid excretion.

Side effects include frequent urination and low potassium blood levels. Because of this, blood tests are performed periodically, and a potassium supplement is prescribed if blood levels are low.

Inotropic agents such as digoxin (Lanoxin®) and dopamine may be used in heart failure patients when ACE inhibitors and diuretics are ineffective. These drugs can help the heart pump more vigorously and can modestly increase the ejection fraction (percentage of blood pumped out of the left ventricle with each contraction), reducing heart failure symptoms.

Patients who are taking inotropic agents must undergo regular blood tests to monitor levels of the drug. They usually are well tolerated and side effects are rare when correct blood levels are maintained. Side effects include the following:

• Blurred vision
• Cardiac conditions (e.g., arrhythmias, heart block)
• Diarrhea
• Headaches
• Loss of appetite
• Low blood pressure (hypotension)
• Nausea and vomiting

Other vasodilators (e.g., hydralazine, isosorbide dinitrate, nitroglycerin) may be used in patients who are unable to tolerate ACE inhibitor therapy. Side effects include fainting or dizziness upon standing, headaches, and flushing.

Other treatments

, which often depend on the cause of heart failure, include the following:

• Coronary angioplasty
• Coronary artery bypass surgery
• Implantable cardiac defibrillator (ICD)
• Intra-aortic balloon pump (IABP)
• Left ventricular assist device (LVAD)
• Valve repair or valve replacement surgery

Cardiac arrhythmia

Cardiac arrhythmia is a group of conditions in which the muscle contraction of the heart is irregular or is faster or slower than normal. Cardiac dysrhythmia might be a more correct phrase to describe the condition, as arrhythmia would imply that there is "no rhythm," but this term is not used frequently.

Some arrhythmias are life-threatening medical emergencies that can cause cardiac arrest and sudden death. Others cause aggravating symptoms, such as an awareness of a different heart beat, or palpitation, which can be annoying. Some are quite benign and normal. Sinus arrhythmia is the mild acceleration followed by slowing of the normal rhythm that occurs with breathing. In adults the normal heart rate ranges from 60 beats per minute to 100 beats per minute. The normal heart beat is controlled by a small area in the upper chamber of the heart called the sinoatrial node or sinus node. The sinus node contains specialized cells that have spontaneous electrical activity that starts each normal heart beat.

Frequency too high or too low

A heart rate faster than 100 beats/minute is considered a tachycardia. This number varies with age, as the heartbeat of a younger person is naturally faster than that of an older person's. With exercise the sinus node increases its rate of electrical activity to accelerate the heart rate. The normal fast rate that develops is called sinus tachycardia. Arrhythmias that are due to fast, abnormal electrical activity can cause tachycardias that are dangerous. If the ventricles of the heart experience one of these tachycardias for a long period of time, there can be deleterious effects. Individuals may sense a tachycardia as a pounding sensation of the heart, known as palpitations. If a tachycardia lowers blood pressure it may cause lightheadedness or dizziness, or even fainting (syncope). If the tachycardia is too fast, the pump function of the heart is impeded, which may lead to a sudden death.

Most tachycardias are not dangerous. Anything that increases adrenaline or its effects on the heart will increase the heart rate and potentially cause palpitations or tachycardias. Causes include stress, ingested or injected substances (ie: caffeine, alcohol--see Holiday heart syndrome), and an overactive thyroid gland (hyperthyroidism). Individuals who have a tachycardia are often advised to limit or remove exposure to any causative agent.

A slow rhythm, known as bradycardia (less than 60 beats/min), is usually not life threatening, but may cause symptoms. When it causes symptoms implantation of a permanent pacemaker may be needed.

Either dysrhythmia requires medical attention to evaluate the risks associated with the arrhythmia.

Fibrillation

A serious variety of arrhythmia is known as fibrillation. The muscle cells of the heart normally function together, creating a single contraction when stimulated. Fibrillation occurs when the heart muscle begins a quivering motion due to a disunity in contractile cell function. Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation); ventricular fibrillation is imminently life-threatening.

Atrial fibrillation is the quivering, chaotic motion in the upper chambers of the heart, known as the atria. Atrial fibrillation is often due to serious underlying medical conditions, and should be evaluated by a physician. It is not typically a medical emergency.

Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest, and an individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.

CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the intervention which is most likely to restore a more healthy heart rhythm. It does this by applying an electric shock to the heart, after which sometimes the heart will revert to a rhythm that can once again pump blood.

Almost every person goes into ventricular fibrillation in the last few minutes of life as the heart muscle reacts to diminished oxygen or general blood flow, trauma, irritants, or depression of electrical impulses themselves from the brain.

Origin of impulse

When an electrical impulse begins in any part of the heart, it will spread throughout the myocardium and cause a contraction; see Electrical conduction system of the heart. Abnormal impulses can begin by one of two mechanisms: automaticity or reentry.

Automaticity

Automaticity refers to a cardiac muscle cell firing off an impulse on its own. Every cardiac cell has this potential: if it does not receive any impulses from elsewhere, its internal "pacemaker" will fire off an impulse after a certain amount of time. A single specialized location in the atrium, the sinoatrial node, has a higher automaticity (a faster pacemaker) than the rest of the heart, and therefore is usually the one to start the heartbeat.

Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus, and is by definition a pathological phenomenon. This may cause a single premature beat now and then, or, if the ectopic focus fires more often than the sinoatrial node, it can produce a sustained abnormal rhythm. Rhythms produced by an ectopic focus in the atria, or by the atrioventricular node, are the least dangerous dysrhythmias; but they can still produce a decrease in the heart's pumping efficiency, because the signal reaches the various parts of the heart muscle with slightly different timing than usual and causes a poorly coordinated contraction.

Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia. The resulting heart rhythm depends on where the first signal begins: if it is the sinoatrial node, the rhythm remains normal but rapid; if it is an ectopic focus, many types of dysrhythmia can result.

Re-entry

Re-entrant dysrhythmias occur when an electrical impulse travels in a circle within the heart, rather than moving outward and then stopping. Every cardiac cell is able to transmit impulses in every direction, but will only do so once within a short period of time. Normally the impulse spreads through the heart quickly enough that each cell will only respond once, but if conduction is abnormally slow in some areas, part of the impulse will arrive late and will be treated as a new impulse, which can then spread backward. Depending on the timing, this can produce a sustained abnormal rhythm, such as atrial flutter, a self-limiting burst of supraventricular tachycardia, or the dangerous ventricular tachycardia.

By analogy, imagine a room full of people all given these instructions: "If you see anyone starting to stand up, then stand up for three seconds and sit back down." If the people are quick enough to respond, the first person to stand will trigger a single wave which will then die out; but if there are stragglers on one side of the room, people who have already sat down will see them and start a second wave, and so on.

SADS

SADS, or sudden arrhythmia death syndrome, is a term used to describe sudden death due to cardiac arrest brought on by an arrhythmia. The most common cause of sudden death in the US is coronary artery disease. Approximately 300,000 people die suddenly of this cause every year in the US. SADS can also occur from other causes. Also, there are many inherited conditions and heart diseases that can affect young people that can cause sudden death. Many of these victims have no symptoms before dying suddenly.

Causes of SADS in young people are long QT syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia and hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia ("arrythmia"-causing, "right ventricle"-involving, pre-cancerous malformation(bad-growth)).

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