Heart, Men's Health, Age related illnesses, Women's Health | May 9, 2014 | Author: The Super Pharmacist
The primary function of the heart is to pump oxygenated blood to all the organs and tissues of the body. When this pumping action weakens, for whatever reason, blood does not circulate normally, and the body organs are deprived of the oxygen and nutrients they require in order to function.
There is limited Australian data on the incidence and prevalence of heart failure in Australia. Based on overseas findings, it is estimated that at least 300,000 Australians have chronic heart failure (or about 4% of the population aged 45 or more), with 30,000 new cases diagnosed each year).
Heart failure is usually a long-term, chronic condition that gradually worsens, but it may have sudden onset as well. Heart failure can affect either the left or the right side of the heart but usually affects both sides. The most common risk factors for heart failure are ischaemic coronary artery disease and hypertension.
De-oxygenated blood returns to the right side of the heart from all the body organs via the veins. It flows from the right atrium into the right ventricle and into the lungs where carbon dioxide is released and oxygen is absorbed.
The oxygenated blood then travels to the left side of the heart, first into the left atrium, then into the left ventricle.
The left ventricle pumps the oxygenated blood into the aorta and general arterial circulation.
As blood flow to the kidneys decreases, the kidneys filter less fluid out of the circulation and produce less urine. This results in salt (sodium) and water retention and an increase in the circulating blood volume. An excess of fluid remains in the circulation and accumulates in body tissues such as the lungs, the liver, and even the legs. This excess fluid causes congestion of the body organs and tissues and, hence, the term, congestive heart failure.
Heart failure causes stimulation of the adrenergic nervous system, which results in increased production of the hormone adrenaline by the adrenal medullary glands. This is the same hormone that is released in the body of a person who is feeling a strong emotion (such as excitement, fear, or anger) and that causes the heart to beat faster among other effects.
The kidneys respond to decreased blood flow by increasing their production of another hormone called "renin." Renin is responsible for a number of biochemical reactions called the renin-angiotensin system. These sequence of reactions result in increased production of a compound called angiotensin II.
Angiotensin II causes several important physiological effects:
The interrelationship between cardiac hypertrophy (enlargement and thickening of the heart muscles) and heart failure has long been recognised. Cardiac hypertrophy (most commonly due to hypertension) frequently leads or contributes to heart failure. On the other hand, the failing heart almost always shows hypertrophy.
Cardiac hypertrophy results from microscopic structural changes in the heart that include growth in the size (not the number) of cardiac muscle cells, fibrosis (the formation of excess fibrous connective tissue leading to stiffness or decreased compliance) of the heart wall, cellular disarray, and cell death.
Heart failure most commonly involves the left side of the heart.
Common causes of left heart failure include:
In left heart failure, blood backs up in to the lungs, fluid seeps out of the blood vessels into the lung tissue and even into the air spaces. This prevents the lungs from taking in an adequate supply of oxygen and decreases the amount of oxygenated blood available to supply the needs of the body's organs.
Because of the congestion of the lungs, shortness of breath (dyspnea) is a common presenting symptom of left heart failure.
As heart failure first develops, shortness of breath on exertion may simply appear to be an aggravation of normal breathlessness that occurs during activity.
However, as left heart failure worsens, exercise tolerance declines progressively with dyspnea occurring even during light activity.
With further worsening of left heart failure, shortness of breath occurs in the recumbent position and is relieved with elevation of the head with pillows (orthopnea). On lying down, the blood that was pooled in the lower extremities returns to the heart, which is unable to pump out the extra volume and leads to backup of fluid in the lungs and shortness of breathe. The number of pillows needed to alleviate dyspnea increases with worsening left heart failure until the patient cannot lie down and must sleep in a sitting position.
Reduced blood flow to the kidneys results in reduced urination (oliguria). Increased urination occurs at night due to a relative increase in cardiac output in the recumbent position as blood that was pooled in the extremities returns to the heart (nocturia). Cardiac output refers to the amount of blood pumped by the heart in the course of one minute.
Fatigue and weakness, especially in the arms and legs, are also common symptoms of heart failure. The fatigue and weakness is caused by reduced output of blood from the heart and subsequent poor circulation in the limbs.
In right heart failure, the right ventricle loses the strength to pump blood into the lungs. A “backup” of blood occurs in the venous system leading to the heart. The major cause of right heart failure is left heart failure. Chronic lung disease, including chronic bronchitis and emphysema, can also cause right heart failure. Other causes include pulmonary embolism, primary pulmonary hypertension, and cardiac valvular disease (e.g., mitral stenosis).
The primary symptom of right heart failure is swelling (oedema) of the lower extremities. Since less blood is returning to the heart, blood backs up and excess fluid leaks out of the veins leading to the heart.
The fluid retention in right heart failure affects the abdominal cavity, leading to increased abdominal girth called ascites.
Shortness of breath may occur, but is not as prominent as in left heart failure.
Congestion of the hepatic and gastrointestinal venous circulation can cause anorexia, bloating, nausea, and constipation. Fatigue and weakness may occur during activity because the heart is not pumping enough blood to the body organs.
Exercise. Patients with chronic heart failure who are medically stable benefit from regular physical activity. This may include walking at home for 10-30 minutes/day, cycling, and stretching exercises. Patients should not exercise to a level that precludes participating in normal conversation.
Weight loss. In patients who are overweight, a weight reduction diet is recommended. A diet low in saturated fat is especially important in patients who have coronary artery disease.
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Salt restriction. Dietary sodium restriction may be indicated.
Keep track. Patients are encouraged to keep a diary of fluid intake and monitor their daily weight to prevent excess fluid retention.
Current guidelines or the pharmacologic management of chronic heart failure call for the use of:
Diuretics (e.g., furosemide, thiazide) increase the body's excretion of sodium and fluid through the kidneys and thus help reduce the excess fluid retention that occurs in heart failure. Inhibitors of the renin-angiotensin system include the angiotensin-converting-enzyme inhibitors (also called ACE inhibitors; e.g. ramipril) and the angiotensin receptor blockers (also called ARBs; e.g. irbesartan).
Current scientific evidence has established a significant reduction in mortality due to heart failure with the use of beta-blockers. Beta-blockers (e.g. atenolol) are judged to work by decreasing heart rate thereby giving the heart more time to fill completely with each beat. Other drugs used in the treatment of chronic heart failure are:
Angiotensin II acts on the adrenal gland to stimulate the production of the steroid hormone, aldosterone. Aldosterone acts to promote sodium absorption by the kidneys and secondary fluid retention by the body. Aldosterone antagonists (e.g., spironolactone) are used to block these effects. Hydralazine is typically used in combination with nitrates (e.g., isosorbide dinitrate) in the treatment of chronic heart failure. The combined effect of these agents lowers blood pressure, which allows the heart to pump out blood more effectively. Select calcium channel blockers (e.g. amlodipine) also aid in the treatment of heart failure by lowering arterial blood pressure. Inotropes such as digoxin are drugs that increase cardiac contractility and thus improve the pumping function of the heart.
Inthosepatients who have been resuscitated from an episode of spontaneous life-threatening arrhythmia (heart rhythm disturbance) or in select patients who are at high risk of such an arrhythmia, the implantable cardioverter-defibrillator (ICD) reduces the risk of sudden cardiac death. An ICD is a small electronic device, about the size of a stopwatch, that is placed under the skin usually just above the collarbone.
It consists of a pulse generator and wires, called leads. The pulse generator contains a battery and a tiny computer. Leads are tiny wires implanted through a vein from the generator to specific locations in the heart.
The ICD device is programmed to detect the development of a cardiac arrhythmia and correct it by delivering a brief and specifically timed electrical impulse to the heart.
The ICD is designed to deliver two levels of electrical energy:
Cardiac resynchronisation therapy (CRT), also called biventricular pacing, may be helpful in patients where the electrical impulses in the heart muscle do not travel through the heart quickly and evenly. For example, instead of contracting simultaneously, one ventricle may contract a fraction of a second before or after the other.
This lack of co-ordination significantly interferes with the efficiency of the heart's pumping action. CRT uses a special kind of pacemaker, called a biventricular pacemaker, where two wires are inserted in the lower chambers of the heart.
By delivering simultaneous electrical impulses to both lower heart chambers (the right and left ventricles), it causes the heart to beat in a more synchronized, efficient manner.
Biventricular pacemakers improve the symptoms of heart failure in about 50% of people who have been treated with medications but still have significant heart failure symptoms.
AIHW: Field B. (2003). Heart failure...what of the future? Bulletin no. 6. AIHW Cat. No. AUS 34. Canberra: AIHW. Accessed 28 April 2014: http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=6442453166
Nazareno J. (2013). Anatomy and physiology: cardiovascular system. Nurses Information and Trends Updates. Accessed 28 April 2014: http://nurseinfos.com/2013/12/03/anatomy-and-physiology-cardiovascular-system/
Klabunde RE. (2007). Cardiovascular Physiology Concepts: Pathophysiology of heart failure. Accessed 28 April 2014: http://www.cvphysiology.com/Heart%20Failure/HF003.htm
Harrison-Bernard L. The renal renin-angiotensin system. Adv Physiol Educ 33: 270–274, 2009. Accessed 28 April 2014: http://advan.physiology.org/content/ajpadvan/33/4/270.full.pdf
WebMD: Systolic heart failure: topic overview. Accessed 28 April 2014: http://www.webmd.com/heart-disease/heart-failure/tc/systolic-heart-failure-topic-overview
Dumitru I. (2014). Heart failure clinical presentation. Medscape. Accessed 28 April 2014: http://emedicine.medscape.com/article/163062-clinical
WebMD: Right-sided heart failure: topic overview. Accessed 28 April 2014: http://www.webmd.com/heart-disease/heart-failure/tc/right-sided-heart-failure-topic-overview
Dumitru I. (2014). Heart failure clinical presentation: predominant right-sided heart failure. Medscape. Accessed 28 April 2014: http://emedicine.medscape.com/article/163062-clinical#aw2aab6b3b3
Adnan MM. (n.d.). Edema. MBBS Medicine (Humanity First). Accessed 28 April 2014. http://medicinembbs.blogspot.com/2011/02/edema.html
Gibbs CR, Jackson G, Lip GY. ABC of heart failure: non-drug management. BMJ. Feb 5, 2000; 320(7231): 366–369.
Krum H. Guidelines for management of patients with chronic heart failure in Australia.National Heart Foundation of Australia and Cardiac Society of Australia & New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel. Med J Aust 2001; 174 (9): 459-466.
Mayo Clinic: Implantable cardioverter-defibrillators. Accessed 28 April 2014: http://www.mayoclinic.org/tests-procedures/implantable-cardioverter-defibrillator/basics/definition/prc-20015079
Lee DS, Green LD, Liu PP. Effectiveness of implantable defibrillators in preventing arrhythmic events and death. J Am Coll Cardiol. 2003 May 7;41(9):1573-82.
Shea JB, Sweeney MO. Cardiac resynchronisation therapy: a patient guide. Circulation.2003; 108: e64-e66.