Aetiology and Pathophysiology of Heart Failure

• 
  Rachel Corston-Jackson
  

Heart Failure

The heart is a diverse organ and the diseases associated with it are caused by many different organs when they become dysfunctional or diseased. It is for this reason that heart failure is more diverse than just the stopping or failure of the heart as there are many types and causes of heart failure. Therefore, this essay will discuss the subject heart failure in the human body by addressing its aetiology and pathophysiology, the signs and symptoms associated with it, as well as the risk factors and causal agents linked to heart failure, and lastly, the relevant tests and treatment options available to heart failure patients to improve their quality of life.

Aetiology:

Heart failure, sometimes called congestive heart failure, refers to when the heart isn’t pumping blood as well as it should (American Heart Association, 2014). It is a chronic disease characterised by the failure of the heart as a pump and is the result of any structural or functional cardiac disorders (Butler, 2012). This doesn’t mean that the heart stops beating, however, the American Heart Association (2014) warns that heart failure can get worse if it’s not treated. The heart does not stop altogether but keeps working, despite the fact that the demands of blood and oxygen of the heart and body far exceed supply (Butler, 2012). This is caused a variety of disorders such as coronary artery disease, heart attacks, cardiomyopathy, and congenital birth defects (Butler, 2012).

Coronary artery disease (CAD), as stated by Butler (2012) is a disease characterised by a narrowing or blockage of the arteries which restricts blood and oxygen supply to the heart, resulting in a reduced preload in the ventricles and reduced ventricular stretch. When low ventricular stretch occurs it results in a decreased force of cardiac contraction and a low stroke volume. The effects of low stroke volume include low blood pressure and can lead to the body’s organs and tissues becoming deprived of adequate oxygen and nutrients which may cause the body to go into a state of shock.

The second cardiovascular disorder which can cause heart failure is a heart attack. A heart attack according to the Heart Foundation (2015) occurs when ‘a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle’. Damage to the heart muscle occurs during a heart attack, and becomes scarred, the damaged area does not function properly, resulting in a reduced cardiac output and low blood pressure. When this happens the heart compensates by undergoing a remodelling process where it changes in size, shape or structure, and according to Butler (2012) the remodelling is more likely to occur in the left ventricle as it has a thicker muscle mass.

The third form of heart failure mentioned above is cardiomyopathy, which is caused by infections, alcohol abuse, or pregnancy and is characterised by damage to the heart muscle. The type of cardiomyopathy which presents during pregnancy is called peripartum cardiomyopathy (Demir, Tufenk, Karakaya, Akilli, & Kanadas, 2013). It is a form of dilated cardiomyopathy and involves systolic dysfunction of the heart. Onset is usually around the last month of pregnancy and five months postpartum, hence the name. One common symptom of peripartum cardiomyopathy is sinus tachycardia which according to Demir et al. (2013) can be treated with a drug called Ivabradine. This brings me to the next section which is the pathophysiology of heart failure.

Pathophysiology:

Heart failure is a complex problem and is characterised by many signs and symptoms. Symptoms include; shortness of breath, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced ability to exercise, peripheral oedema, loss of appetite and more (Nicholson, 2014). Signs include; Tachycardia, tachypnoea, an abnormal pulse, and displaced apex beat, third heart sounds, a raised jugular venous pressure, lung crepitation, weight changes, hepatomegaly and more (Nicholson, 2014).

The common symptoms which will be focused on here include shortness of breath (S.O.B), paroxysmal nocturnal dyspnoea, fatigue, and a lack of appetite (Butler, 2012). The American Heart Association (2014) states that S.O.B during activity, at rest, or while sleeping, can have a sudden onset, often causing the patient to wake. They describe S.O.B as being caused by the blood when it “backs up” in the pulmonary veins because the heart can’t keep up with the supply. The result is stated to be that the kidneys develop a reduced capacity to dispose of sodium and water, and that excess fluid leaks into the lungs causing a pulmonary oedema and around the lungs causing pleural effusion. The clinical sign which indicates that this has occurred, aside from S.O.B, is the presence of lung crepitations (Butler, 2012). A lung crepitation, according to Butler, is a crackling sound produced during inhalation and exhalation due to fluid accumulation inside the lungs and predominantly occurs in the lower lung fields. The American Heart Association states that peripheral oedemas can also occur as a result of the venous blood backing up and is characterised by swelling in the ankles, feet and abdomen resulting in ill-fitting shoes and weight gain due to the excess fluid accumulation.

The build-up of fluid which causes S.O.B also leads to paroxysmal nocturnal dyspnoea (PND) (Butler, 2012; Nicholson, 2014). PND usually occurs at night, according to the American Heart Association, and is characterised by sudden awakening from sleep after only a few hours, with a feeling of breathlessness, suffocation and severe anxiety. On chest auscultation, the bronchospasm associated with a heart failure exacerbation can be difficult to distinguish from an acute asthma exacerbation (Dumitru & Baker, 2014).

Other symptoms of heart failure included fatigue. Fatigue and weakness according to Dumitru & Baker (2014) are often accompanied by a feeling of leaden limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Essentially the heart produces a decreased volume of blood and cannot meet the needs of body tissues so the body diverts blood away from less vital organs, particularly muscles in the limbs, and sends it to the heart and brain (American Heart Association, 2014). The American Heart Association (2014) and Nicholson (2014) both link this diversion of blood to vital organs to the loss of appetite and feelings of nausea often experienced by people with heart failure due to the fact that the digestive system receives less blood and cannot function correctly.

The common signs that will be discussed here are hepatomegaly, third heart sounds, tachycardia and a displaced apex beat. Hepatomegaly, an enlargement of the liver which can occur with right heart failure (Nicholson, 2014), and is caused by the blood backing up from the heart into the inferior vena cava, such congestion increases pressure in the inferior vena cava and other veins that carry blood to it, including the hepatic veins (Orfanidis, 2013).Once this occurs the pressure may build to a point where the liver becomes engorged with blood and malfunctions. The common symptoms of hepatomegaly are nausea, abdominal pain or fullness, swelling of the feet and legs, and shortness of breath, all of which are also seen in heart failure (Butler, 2012).

The third heart sound (S3) is a low-pitched sound that occurs when the ventricles fill rapidly and is one of the more specific signs of heart failure and auscultating to determine the presence of it can help healthcare professionals to diagnose heart failure (Santhosh, 2009). S3 is commonly present in conjunction with tachycardia, which is a high resting heart rate and is common as a haemodynamic compensatory response (Nicholson, 2014). The final sign of heart failure listed above is a displaced apex beat. A displaced apex beat means ‘the point of maximal impulse on the precordium can be displaced down and to the left laterally and commonly occurs when the heart is dilated (Nicholson, 2014, p. 33)’. Each sign and symptom of heart failure is linked to a causal agent such as a previous history of Myocardial Infarctions (MI).

Risk factors/causal agents:

The term ‘heart failure’ includes many conditions and disease, thus it has many causal agents including; Family history, narrowed arteries, high blood pressure, coronary artery disease, myocardial infarctions, valve disorders, peripartum, ischemic heart disease, diabetes, obesity, kidney disease, hypothyroidism, toxins (alcohol), and infection (Butler, 2012; Nicholson, 2014). The causal agents which will be discussed here are narrowed arteries, high blood pressure, obesity, diabetes and infection.

Family history is an important indicator of increased risk in relation to heart failure, it is however not to be considered on its own but in relation to other risk factors such as narrowed arteries (Goldberg, 2014). Narrowed arteries can refer to vasoconstriction or atherosclerosis. Atherosclerosis is a plaque formation is medium or large sized arteries in response to damage of the tunica intima (National Health Council, 2014). These plaque formations cause increased resistance to laminar blood flow resulting in turbulent flow and high blood pressure (Foss & Farine, 2013). Blood pressure alone is characterised as the force exerted on blood vessel walls by a volume of blood as it passes through (Heart Foundation, Blood Pressure, 2010). High blood pressure on the other hand is known as hypertension, and is defined by the Heart Foundation (2010) as chronically elevated blood pressure resulting in stain on the heart and blood vessels. Hypertension is visually manifested by jugular venous distention on the right side of the neck (Nicholson, 2014). Foss & Farine (2013) state that the elevated blood pressure is detected in the blood vessels by baroreceptors located in the carotid sinus and aortic arch. The baroreceptors are said to then stimulate vasomotor nerves to increase the diameter of the blood vessels to increase blood flow and reduce blood pressure.

Another cause of high blood pressure is obesity. This is due to the fact that overweight or obese people have a greater the volume of tissue and fat that requires a constant blood supply, this results in an increase in blood vessel length (Foss & Farine, 2013). Foss & Farine (2013) state that the longer the blood vessels become the more distance the blood will have to travel which increases the resistance, the body will compensate for this by increasing the blood pressure throughout the body by increasing the stroke volume of the heart. This increase in blood pressure is to ensure both adequate blood supply to all blood vessels and adequate venous return. If the high weight threshold is maintained then high blood pressure will continue, causing hypertension and heart strain (Heart Foundation, Blood Pressure, 2010).

A second effect that obesity can have on the heart is diabetes mellitus. Diabetes is a disorder of the metabolism where the glucose produced from the breakdown of food is no effectively absorbed into the cells for fuel. Diabetes is characterised by an inadequate production of the hormone called insulin which is produced in the pancreas and must be present to allow glucose to enter the cells (Goldberg, 2014). When insulin production is low the glucose remains in the blood and has many effects, such as increasing the susceptibility to infection (Foss & Farine, 2013). The long term effects of low insulin and high glucose levels in the blood include atherosclerosis, which is an increase in deposits of fatty materials on the insides of the blood vessel walls (Goldberg, 2014). These deposits affect blood flow by reducing the diameter of the blood vessels and raising blood pressure, increasing the chance of clogging and hardening of blood vessels (Goldberg, 2014).

Relevant tests:

There are many tests which can help determine if a patient has heart failure or is at risk, such as; checking blood pressure, chest x-rays, blood tests, 12-lead electrocardiogram and respiratory function tests. Checking blood pressure regularly is part of a standard visit to the doctor or nurse, because it helps to establish a pattern of high, normal or low blood pressure. Long term high blood pressure has been linked to heart strain, and in conjunction with other health issues such as atherosclerosis can result in heart failure. (Heart Foundation, Blood Pressure, 2010).

Another test which can contribute to the diagnosis of heart failure is a chest x-ray. Chest x-rays may be performed to look for signs of a pulmonary oedema which can cause symptoms such as S.O.B and paroxysmal nocturnal dyspnoea (Butler, 2012). A pulmonary oedema is commonly caused by a disrupted flow of blood to and from the heart. Respiratory function tests are also performed, to exclude respiratory causes for dyspnoea, such as asthma and chronic obstructive pulmonary disease (COPD) (Butler, 2012).

Another direct test of the heart is via a 12-lead electrocardiogram (ECG), the results of an ECG may show evidence of left or right ventricular hypertrophy, CHD, or arrhythmias commonly associated with heart failure such as atrial fibrillation (Butler, 2012). If no abnormality is present then the patient is unlikely to have heart failure (Nicholson, 2014). Further tests for signs of heart failure include blood tests for glucose (Butler, 2012; Nicholson, 2014). Checking glucose levels can be performed at home and is a vital component in the management of diabetes because if the blood glucose level remains high it can lead to atherosclerosis, and later, heart failure. High glucose levels are managed by first testing the blood then administering the appropriate amount of insulin to help absorption of the glucose into the cells and thus lower the blood glucose levels.

Treatment strategy:

Education on self-management strategies is a vital aspect of patient empowerment and care both at hospital and in their own home (Cockayne, Pattenden, Worthy, Richardson, & lewin, 2014). Heart failure patients require education how they can manage their symptoms and to ensure they can recognise the warning sign associated with acute situations (Nicholson, 2014). Patient education commonly includes information on how to maintain good control of comorbid conditions such as diabetes. Control of diabetes at home begins with the monitoring blood glucose levels and commonly results in injecting oneself with insulin (Goldberg, 2014). Cockayne et al. (2014) state that ensuring patients understand the importance of adhering to the medication regime designed for their optimal health is a vital part of patient education.

Another important aspect of patient education and self-management is providing an explanation on how to improve health habits and adopt a healthier lifestyle (Nicholson, 2014). The most commonly required lifestyle change to improve health outlooks for patients is to advise that they limit any consumption of alcohol and tobacco smoke as both produce detrimental effects on the heart, such as, causing pulmonary blockages and narrowing of airways, which will affect the oxygen supply to the blood, tissues and organs (Nicholson, 2014). Other important lifestyle changes according to Nicholson (2014) and Butler (2012) include advice on losing weight if the patient is obese, because obesity results in long, narrow blood vessels and high blood pressure which increases the patient’s risk of heart failure. The management of weight for patients with heart failure includes recommendations for specific dietary changes such as a low sodium intake or a low refined sugar intake (Butler, 2012). It may also include guidelines for increased daily exercise which is shown to have positive effects on heart failure symptoms according to Nicholson.

Butler (2012) states that for women there is another important lifestyle factor to consider in the self-management of heart failure symptoms, the use of contraception. Contraception is important for women who experience heart failure and its symptoms because if a woman with heart failure were to become pregnant it would increase her risk of heart failure and morbidity during pregnancy and birth.

The use of pharmacology in the management and treatment of heart failure symptoms is multifaceted. The use of angiotensin-converting enzyme (ACE) inhibitors is said to be one of the most valuable drug therapies in heart failure according to Butler and is intended to decrease the effects of compensatory mechanisms which are maladaptive so as to improve heart failure symptoms and increase the rate of survival, particularly when taken in conjunction with beta-blockers. Beta-blockers work by reducing heart rate and the myocardial oxygen demand (Nicholson, 2014). The use of ACE inhibitors means that it is important to closely monitor the blood chemistry of the patient, and that the side effects are commonly limited to a dry, persistent cough (Butler, 2012). If the patient cannot tolerate ACE inhibitors due to the dry, persistent cough then the use of angiotensin-II receptor blockers (ARBs) will be considered as this drug has similar properties to the ACE inhibitor and will also require the monitoring of blood chemistry. (Butler, 2012).

Other pharmacological treatments include the use of vasodilators and diuretics. Vasodilators are used to improve cardiac output and often used in cases of heart failure where the patient cannot tolerate ACE inhibitors or ARBs (Butler, 2012). Diuretics are used to increase fluid loss in order to reduce the size and occurrence of peripheral oedemas and pulmonary oedemas, resulting in a reduced level of breathlessness (Nicholson, 2014).

The last treatment option to be discussed here is the use of device therapy. Device therapy as stated by Butler (2012) refers to an implantable cardiac defibrillator (ICD) and a biventricular pacemaker. Biventricular pacemakers are implanted to restore ventricular synchrony and reduce symptoms in the event ventricular failure. ICDs on the other hand addresses the problem of cardiac death by delivering an electric shock to the heart to restore normal rhythm and function.

In conclusion, heart failure is a complex and multifaceted health problem which encompasses many heart problems like coronary artery disease, heart attacks and cardiomyopathy. Because heart failure is such a large problem it has many symptoms including S.O.B, fatigue and oedemas, and also many signs like tachycardia and lung crepitation. Each sign and symptom of heart failure is associated with a causal agent or risk factor such as hypertension in relation to obesity and diabetes. Heart failure cannot be cured, however the symptoms can be managed through patient education and self-management, pharmacology, and as a last resort, device therapy.

1 | Page

• 
  Rachel Corston-Jackson
  

Heart Failure

The heart is a diverse organ and the diseases associated with it are caused by many different organs when they become dysfunctional or diseased. It is for this reason that heart failure is more diverse than just the stopping or failure of the heart as there are many types and causes of heart failure. Therefore, this essay will discuss the subject heart failure in the human body by addressing its aetiology and pathophysiology, the signs and symptoms associated with it, as well as the risk factors and causal agents linked to heart failure, and lastly, the relevant tests and treatment options available to heart failure patients to improve their quality of life.

Aetiology:

Heart failure, sometimes called congestive heart failure, refers to when the heart isn’t pumping blood as well as it should (American Heart Association, 2014). It is a chronic disease characterised by the failure of the heart as a pump and is the result of any structural or functional cardiac disorders (Butler, 2012). This doesn’t mean that the heart stops beating, however, the American Heart Association (2014) warns that heart failure can get worse if it’s not treated. The heart does not stop altogether but keeps working, despite the fact that the demands of blood and oxygen of the heart and body far exceed supply (Butler, 2012). This is caused a variety of disorders such as coronary artery disease, heart attacks, cardiomyopathy, and congenital birth defects (Butler, 2012).

Coronary artery disease (CAD), as stated by Butler (2012) is a disease characterised by a narrowing or blockage of the arteries which restricts blood and oxygen supply to the heart, resulting in a reduced preload in the ventricles and reduced ventricular stretch. When low ventricular stretch occurs it results in a decreased force of cardiac contraction and a low stroke volume. The effects of low stroke volume include low blood pressure and can lead to the body’s organs and tissues becoming deprived of adequate oxygen and nutrients which may cause the body to go into a state of shock.

The second cardiovascular disorder which can cause heart failure is a heart attack. A heart attack according to the Heart Foundation (2015) occurs when ‘a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle’. Damage to the heart muscle occurs during a heart attack, and becomes scarred, the damaged area does not function properly, resulting in a reduced cardiac output and low blood pressure. When this happens the heart compensates by undergoing a remodelling process where it changes in size, shape or structure, and according to Butler (2012) the remodelling is more likely to occur in the left ventricle as it has a thicker muscle mass.

The third form of heart failure mentioned above is cardiomyopathy, which is caused by infections, alcohol abuse, or pregnancy and is characterised by damage to the heart muscle. The type of cardiomyopathy which presents during pregnancy is called peripartum cardiomyopathy (Demir, Tufenk, Karakaya, Akilli, & Kanadas, 2013). It is a form of dilated cardiomyopathy and involves systolic dysfunction of the heart. Onset is usually around the last month of pregnancy and five months postpartum, hence the name. One common symptom of peripartum cardiomyopathy is sinus tachycardia which according to Demir et al. (2013) can be treated with a drug called Ivabradine. This brings me to the next section which is the pathophysiology of heart failure.

Pathophysiology:

Heart failure is a complex problem and is characterised by many signs and symptoms. Symptoms include; shortness of breath, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced ability to exercise, peripheral oedema, loss of appetite and more (Nicholson, 2014). Signs include; Tachycardia, tachypnoea, an abnormal pulse, and displaced apex beat, third heart sounds, a raised jugular venous pressure, lung crepitation, weight changes, hepatomegaly and more (Nicholson, 2014).

The common symptoms which will be focused on here include shortness of breath (S.O.B), paroxysmal nocturnal dyspnoea, fatigue, and a lack of appetite (Butler, 2012). The American Heart Association (2014) states that S.O.B during activity, at rest, or while sleeping, can have a sudden onset, often causing the patient to wake. They describe S.O.B as being caused by the blood when it “backs up” in the pulmonary veins because the heart can’t keep up with the supply. The result is stated to be that the kidneys develop a reduced capacity to dispose of sodium and water, and that excess fluid leaks into the lungs causing a pulmonary oedema and around the lungs causing pleural effusion. The clinical sign which indicates that this has occurred, aside from S.O.B, is the presence of lung crepitations (Butler, 2012). A lung crepitation, according to Butler, is a crackling sound produced during inhalation and exhalation due to fluid accumulation inside the lungs and predominantly occurs in the lower lung fields. The American Heart Association states that peripheral oedemas can also occur as a result of the venous blood backing up and is characterised by swelling in the ankles, feet and abdomen resulting in ill-fitting shoes and weight gain due to the excess fluid accumulation.

The build-up of fluid which causes S.O.B also leads to paroxysmal nocturnal dyspnoea (PND) (Butler, 2012; Nicholson, 2014). PND usually occurs at night, according to the American Heart Association, and is characterised by sudden awakening from sleep after only a few hours, with a feeling of breathlessness, suffocation and severe anxiety. On chest auscultation, the bronchospasm associated with a heart failure exacerbation can be difficult to distinguish from an acute asthma exacerbation (Dumitru & Baker, 2014).

Other symptoms of heart failure included fatigue. Fatigue and weakness according to Dumitru & Baker (2014) are often accompanied by a feeling of leaden limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Essentially the heart produces a decreased volume of blood and cannot meet the needs of body tissues so the body diverts blood away from less vital organs, particularly muscles in the limbs, and sends it to the heart and brain (American Heart Association, 2014). The American Heart Association (2014) and Nicholson (2014) both link this diversion of blood to vital organs to the loss of appetite and feelings of nausea often experienced by people with heart failure due to the fact that the digestive system receives less blood and cannot function correctly.

The common signs that will be discussed here are hepatomegaly, third heart sounds, tachycardia and a displaced apex beat. Hepatomegaly, an enlargement of the liver which can occur with right heart failure (Nicholson, 2014), and is caused by the blood backing up from the heart into the inferior vena cava, such congestion increases pressure in the inferior vena cava and other veins that carry blood to it, including the hepatic veins (Orfanidis, 2013).Once this occurs the pressure may build to a point where the liver becomes engorged with blood and malfunctions. The common symptoms of hepatomegaly are nausea, abdominal pain or fullness, swelling of the feet and legs, and shortness of breath, all of which are also seen in heart failure (Butler, 2012).

The third heart sound (S3) is a low-pitched sound that occurs when the ventricles fill rapidly and is one of the more specific signs of heart failure and auscultating to determine the presence of it can help healthcare professionals to diagnose heart failure (Santhosh, 2009). S3 is commonly present in conjunction with tachycardia, which is a high resting heart rate and is common as a haemodynamic compensatory response (Nicholson, 2014). The final sign of heart failure listed above is a displaced apex beat. A displaced apex beat means ‘the point of maximal impulse on the precordium can be displaced down and to the left laterally and commonly occurs when the heart is dilated (Nicholson, 2014, p. 33)’. Each sign and symptom of heart failure is linked to a causal agent such as a previous history of Myocardial Infarctions (MI).

Risk factors/causal agents:

The term ‘heart failure’ includes many conditions and disease, thus it has many causal agents including; Family history, narrowed arteries, high blood pressure, coronary artery disease, myocardial infarctions, valve disorders, peripartum, ischemic heart disease, diabetes, obesity, kidney disease, hypothyroidism, toxins (alcohol), and infection (Butler, 2012; Nicholson, 2014). The causal agents which will be discussed here are narrowed arteries, high blood pressure, obesity, diabetes and infection.

Family history is an important indicator of increased risk in relation to heart failure, it is however not to be considered on its own but in relation to other risk factors such as narrowed arteries (Goldberg, 2014). Narrowed arteries can refer to vasoconstriction or atherosclerosis. Atherosclerosis is a plaque formation is medium or large sized arteries in response to damage of the tunica intima (National Health Council, 2014). These plaque formations cause increased resistance to laminar blood flow resulting in turbulent flow and high blood pressure (Foss & Farine, 2013). Blood pressure alone is characterised as the force exerted on blood vessel walls by a volume of blood as it passes through (Heart Foundation, Blood Pressure, 2010). High blood pressure on the other hand is known as hypertension, and is defined by the Heart Foundation (2010) as chronically elevated blood pressure resulting in stain on the heart and blood vessels. Hypertension is visually manifested by jugular venous distention on the right side of the neck (Nicholson, 2014). Foss & Farine (2013) state that the elevated blood pressure is detected in the blood vessels by baroreceptors located in the carotid sinus and aortic arch. The baroreceptors are said to then stimulate vasomotor nerves to increase the diameter of the blood vessels to increase blood flow and reduce blood pressure.

Another cause of high blood pressure is obesity. This is due to the fact that overweight or obese people have a greater the volume of tissue and fat that requires a constant blood supply, this results in an increase in blood vessel length (Foss & Farine, 2013). Foss & Farine (2013) state that the longer the blood vessels become the more distance the blood will have to travel which increases the resistance, the body will compensate for this by increasing the blood pressure throughout the body by increasing the stroke volume of the heart. This increase in blood pressure is to ensure both adequate blood supply to all blood vessels and adequate venous return. If the high weight threshold is maintained then high blood pressure will continue, causing hypertension and heart strain (Heart Foundation, Blood Pressure, 2010).

A second effect that obesity can have on the heart is diabetes mellitus. Diabetes is a disorder of the metabolism where the glucose produced from the breakdown of food is no effectively absorbed into the cells for fuel. Diabetes is characterised by an inadequate production of the hormone called insulin which is produced in the pancreas and must be present to allow glucose to enter the cells (Goldberg, 2014). When insulin production is low the glucose remains in the blood and has many effects, such as increasing the susceptibility to infection (Foss & Farine, 2013). The long term effects of low insulin and high glucose levels in the blood include atherosclerosis, which is an increase in deposits of fatty materials on the insides of the blood vessel walls (Goldberg, 2014). These deposits affect blood flow by reducing the diameter of the blood vessels and raising blood pressure, increasing the chance of clogging and hardening of blood vessels (Goldberg, 2014).

Relevant tests:

There are many tests which can help determine if a patient has heart failure or is at risk, such as; checking blood pressure, chest x-rays, blood tests, 12-lead electrocardiogram and respiratory function tests. Checking blood pressure regularly is part of a standard visit to the doctor or nurse, because it helps to establish a pattern of high, normal or low blood pressure. Long term high blood pressure has been linked to heart strain, and in conjunction with other health issues such as atherosclerosis can result in heart failure. (Heart Foundation, Blood Pressure, 2010).

Another test which can contribute to the diagnosis of heart failure is a chest x-ray. Chest x-rays may be performed to look for signs of a pulmonary oedema which can cause symptoms such as S.O.B and paroxysmal nocturnal dyspnoea (Butler, 2012). A pulmonary oedema is commonly caused by a disrupted flow of blood to and from the heart. Respiratory function tests are also performed, to exclude respiratory causes for dyspnoea, such as asthma and chronic obstructive pulmonary disease (COPD) (Butler, 2012).

Another direct test of the heart is via a 12-lead electrocardiogram (ECG), the results of an ECG may show evidence of left or right ventricular hypertrophy, CHD, or arrhythmias commonly associated with heart failure such as atrial fibrillation (Butler, 2012). If no abnormality is present then the patient is unlikely to have heart failure (Nicholson, 2014). Further tests for signs of heart failure include blood tests for glucose (Butler, 2012; Nicholson, 2014). Checking glucose levels can be performed at home and is a vital component in the management of diabetes because if the blood glucose level remains high it can lead to atherosclerosis, and later, heart failure. High glucose levels are managed by first testing the blood then administering the appropriate amount of insulin to help absorption of the glucose into the cells and thus lower the blood glucose levels.

Treatment strategy:

Education on self-management strategies is a vital aspect of patient empowerment and care both at hospital and in their own home (Cockayne, Pattenden, Worthy, Richardson, & lewin, 2014). Heart failure patients require education how they can manage their symptoms and to ensure they can recognise the warning sign associated with acute situations (Nicholson, 2014). Patient education commonly includes information on how to maintain good control of comorbid conditions such as diabetes. Control of diabetes at home begins with the monitoring blood glucose levels and commonly results in injecting oneself with insulin (Goldberg, 2014). Cockayne et al. (2014) state that ensuring patients understand the importance of adhering to the medication regime designed for their optimal health is a vital part of patient education.

Another important aspect of patient education and self-management is providing an explanation on how to improve health habits and adopt a healthier lifestyle (Nicholson, 2014). The most commonly required lifestyle change to improve health outlooks for patients is to advise that they limit any consumption of alcohol and tobacco smoke as both produce detrimental effects on the heart, such as, causing pulmonary blockages and narrowing of airways, which will affect the oxygen supply to the blood, tissues and organs (Nicholson, 2014). Other important lifestyle changes according to Nicholson (2014) and Butler (2012) include advice on losing weight if the patient is obese, because obesity results in long, narrow blood vessels and high blood pressure which increases the patient’s risk of heart failure. The management of weight for patients with heart failure includes recommendations for specific dietary changes such as a low sodium intake or a low refined sugar intake (Butler, 2012). It may also include guidelines for increased daily exercise which is shown to have positive effects on heart failure symptoms according to Nicholson.

Butler (2012) states that for women there is another important lifestyle factor to consider in the self-management of heart failure symptoms, the use of contraception. Contraception is important for women who experience heart failure and its symptoms because if a woman with heart failure were to become pregnant it would increase her risk of heart failure and morbidity during pregnancy and birth.

The use of pharmacology in the management and treatment of heart failure symptoms is multifaceted. The use of angiotensin-converting enzyme (ACE) inhibitors is said to be one of the most valuable drug therapies in heart failure according to Butler and is intended to decrease the effects of compensatory mechanisms which are maladaptive so as to improve heart failure symptoms and increase the rate of survival, particularly when taken in conjunction with beta-blockers. Beta-blockers work by reducing heart rate and the myocardial oxygen demand (Nicholson, 2014). The use of ACE inhibitors means that it is important to closely monitor the blood chemistry of the patient, and that the side effects are commonly limited to a dry, persistent cough (Butler, 2012). If the patient cannot tolerate ACE inhibitors due to the dry, persistent cough then the use of angiotensin-II receptor blockers (ARBs) will be considered as this drug has similar properties to the ACE inhibitor and will also require the monitoring of blood chemistry. (Butler, 2012).

Other pharmacological treatments include the use of vasodilators and diuretics. Vasodilators are used to improve cardiac output and often used in cases of heart failure where the patient cannot tolerate ACE inhibitors or ARBs (Butler, 2012). Diuretics are used to increase fluid loss in order to reduce the size and occurrence of peripheral oedemas and pulmonary oedemas, resulting in a reduced level of breathlessness (Nicholson, 2014).

The last treatment option to be discussed here is the use of device therapy. Device therapy as stated by Butler (2012) refers to an implantable cardiac defibrillator (ICD) and a biventricular pacemaker. Biventricular pacemakers are implanted to restore ventricular synchrony and reduce symptoms in the event ventricular failure. ICDs on the other hand addresses the problem of cardiac death by delivering an electric shock to the heart to restore normal rhythm and function.

In conclusion, heart failure is a complex and multifaceted health problem which encompasses many heart problems like coronary artery disease, heart attacks and cardiomyopathy. Because heart failure is such a large problem it has many symptoms including S.O.B, fatigue and oedemas, and also many signs like tachycardia and lung crepitation. Each sign and symptom of heart failure is associated with a causal agent or risk factor such as hypertension in relation to obesity and diabetes. Heart failure cannot be cured, however the symptoms can be managed through patient education and self-management, pharmacology, and as a last resort, device therapy.

1 | Page

• 
  Rachel Corston-Jackson
  

Heart Failure

The heart is a diverse organ and the diseases associated with it are caused by many different organs when they become dysfunctional or diseased. It is for this reason that heart failure is more diverse than just the stopping or failure of the heart as there are many types and causes of heart failure. Therefore, this essay will discuss the subject heart failure in the human body by addressing its aetiology and pathophysiology, the signs and symptoms associated with it, as well as the risk factors and causal agents linked to heart failure, and lastly, the relevant tests and treatment options available to heart failure patients to improve their quality of life.

Aetiology:

Heart failure, sometimes called congestive heart failure, refers to when the heart isn’t pumping blood as well as it should (American Heart Association, 2014). It is a chronic disease characterised by the failure of the heart as a pump and is the result of any structural or functional cardiac disorders (Butler, 2012). This doesn’t mean that the heart stops beating, however, the American Heart Association (2014) warns that heart failure can get worse if it’s not treated. The heart does not stop altogether but keeps working, despite the fact that the demands of blood and oxygen of the heart and body far exceed supply (Butler, 2012). This is caused a variety of disorders such as coronary artery disease, heart attacks, cardiomyopathy, and congenital birth defects (Butler, 2012).

Coronary artery disease (CAD), as stated by Butler (2012) is a disease characterised by a narrowing or blockage of the arteries which restricts blood and oxygen supply to the heart, resulting in a reduced preload in the ventricles and reduced ventricular stretch. When low ventricular stretch occurs it results in a decreased force of cardiac contraction and a low stroke volume. The effects of low stroke volume include low blood pressure and can lead to the body’s organs and tissues becoming deprived of adequate oxygen and nutrients which may cause the body to go into a state of shock.

The second cardiovascular disorder which can cause heart failure is a heart attack. A heart attack according to the Heart Foundation (2015) occurs when ‘a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle’. Damage to the heart muscle occurs during a heart attack, and becomes scarred, the damaged area does not function properly, resulting in a reduced cardiac output and low blood pressure. When this happens the heart compensates by undergoing a remodelling process where it changes in size, shape or structure, and according to Butler (2012) the remodelling is more likely to occur in the left ventricle as it has a thicker muscle mass.

The third form of heart failure mentioned above is cardiomyopathy, which is caused by infections, alcohol abuse, or pregnancy and is characterised by damage to the heart muscle. The type of cardiomyopathy which presents during pregnancy is called peripartum cardiomyopathy (Demir, Tufenk, Karakaya, Akilli, & Kanadas, 2013). It is a form of dilated cardiomyopathy and involves systolic dysfunction of the heart. Onset is usually around the last month of pregnancy and five months postpartum, hence the name. One common symptom of peripartum cardiomyopathy is sinus tachycardia which according to Demir et al. (2013) can be treated with a drug called Ivabradine. This brings me to the next section which is the pathophysiology of heart failure.

Pathophysiology:

Heart failure is a complex problem and is characterised by many signs and symptoms. Symptoms include; shortness of breath, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced ability to exercise, peripheral oedema, loss of appetite and more (Nicholson, 2014). Signs include; Tachycardia, tachypnoea, an abnormal pulse, and displaced apex beat, third heart sounds, a raised jugular venous pressure, lung crepitation, weight changes, hepatomegaly and more (Nicholson, 2014).

The common symptoms which will be focused on here include shortness of breath (S.O.B), paroxysmal nocturnal dyspnoea, fatigue, and a lack of appetite (Butler, 2012). The American Heart Association (2014) states that S.O.B during activity, at rest, or while sleeping, can have a sudden onset, often causing the patient to wake. They describe S.O.B as being caused by the blood when it “backs up” in the pulmonary veins because the heart can’t keep up with the supply. The result is stated to be that the kidneys develop a reduced capacity to dispose of sodium and water, and that excess fluid leaks into the lungs causing a pulmonary oedema and around the lungs causing pleural effusion. The clinical sign which indicates that this has occurred, aside from S.O.B, is the presence of lung crepitations (Butler, 2012). A lung crepitation, according to Butler, is a crackling sound produced during inhalation and exhalation due to fluid accumulation inside the lungs and predominantly occurs in the lower lung fields. The American Heart Association states that peripheral oedemas can also occur as a result of the venous blood backing up and is characterised by swelling in the ankles, feet and abdomen resulting in ill-fitting shoes and weight gain due to the excess fluid accumulation.

The build-up of fluid which causes S.O.B also leads to paroxysmal nocturnal dyspnoea (PND) (Butler, 2012; Nicholson, 2014). PND usually occurs at night, according to the American Heart Association, and is characterised by sudden awakening from sleep after only a few hours, with a feeling of breathlessness, suffocation and severe anxiety. On chest auscultation, the bronchospasm associated with a heart failure exacerbation can be difficult to distinguish from an acute asthma exacerbation (Dumitru & Baker, 2014).

Other symptoms of heart failure included fatigue. Fatigue and weakness according to Dumitru & Baker (2014) are often accompanied by a feeling of leaden limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Essentially the heart produces a decreased volume of blood and cannot meet the needs of body tissues so the body diverts blood away from less vital organs, particularly muscles in the limbs, and sends it to the heart and brain (American Heart Association, 2014). The American Heart Association (2014) and Nicholson (2014) both link this diversion of blood to vital organs to the loss of appetite and feelings of nausea often experienced by people with heart failure due to the fact that the digestive system receives less blood and cannot function correctly.

The common signs that will be discussed here are hepatomegaly, third heart sounds, tachycardia and a displaced apex beat. Hepatomegaly, an enlargement of the liver which can occur with right heart failure (Nicholson, 2014), and is caused by the blood backing up from the heart into the inferior vena cava, such congestion increases pressure in the inferior vena cava and other veins that carry blood to it, including the hepatic veins (Orfanidis, 2013).Once this occurs the pressure may build to a point where the liver becomes engorged with blood and malfunctions. The common symptoms of hepatomegaly are nausea, abdominal pain or fullness, swelling of the feet and legs, and shortness of breath, all of which are also seen in heart failure (Butler, 2012).

The third heart sound (S3) is a low-pitched sound that occurs when the ventricles fill rapidly and is one of the more specific signs of heart failure and auscultating to determine the presence of it can help healthcare professionals to diagnose heart failure (Santhosh, 2009). S3 is commonly present in conjunction with tachycardia, which is a high resting heart rate and is common as a haemodynamic compensatory response (Nicholson, 2014). The final sign of heart failure listed above is a displaced apex beat. A displaced apex beat means ‘the point of maximal impulse on the precordium can be displaced down and to the left laterally and commonly occurs when the heart is dilated (Nicholson, 2014, p. 33)’. Each sign and symptom of heart failure is linked to a causal agent such as a previous history of Myocardial Infarctions (MI).

Risk factors/causal agents:

The term ‘heart failure’ includes many conditions and disease, thus it has many causal agents including; Family history, narrowed arteries, high blood pressure, coronary artery disease, myocardial infarctions, valve disorders, peripartum, ischemic heart disease, diabetes, obesity, kidney disease, hypothyroidism, toxins (alcohol), and infection (Butler, 2012; Nicholson, 2014). The causal agents which will be discussed here are narrowed arteries, high blood pressure, obesity, diabetes and infection.

Family history is an important indicator of increased risk in relation to heart failure, it is however not to be considered on its own but in relation to other risk factors such as narrowed arteries (Goldberg, 2014). Narrowed arteries can refer to vasoconstriction or atherosclerosis. Atherosclerosis is a plaque formation is medium or large sized arteries in response to damage of the tunica intima (National Health Council, 2014). These plaque formations cause increased resistance to laminar blood flow resulting in turbulent flow and high blood pressure (Foss & Farine, 2013). Blood pressure alone is characterised as the force exerted on blood vessel walls by a volume of blood as it passes through (Heart Foundation, Blood Pressure, 2010). High blood pressure on the other hand is known as hypertension, and is defined by the Heart Foundation (2010) as chronically elevated blood pressure resulting in stain on the heart and blood vessels. Hypertension is visually manifested by jugular venous distention on the right side of the neck (Nicholson, 2014). Foss & Farine (2013) state that the elevated blood pressure is detected in the blood vessels by baroreceptors located in the carotid sinus and aortic arch. The baroreceptors are said to then stimulate vasomotor nerves to increase the diameter of the blood vessels to increase blood flow and reduce blood pressure.

Another cause of high blood pressure is obesity. This is due to the fact that overweight or obese people have a greater the volume of tissue and fat that requires a constant blood supply, this results in an increase in blood vessel length (Foss & Farine, 2013). Foss & Farine (2013) state that the longer the blood vessels become the more distance the blood will have to travel which increases the resistance, the body will compensate for this by increasing the blood pressure throughout the body by increasing the stroke volume of the heart. This increase in blood pressure is to ensure both adequate blood supply to all blood vessels and adequate venous return. If the high weight threshold is maintained then high blood pressure will continue, causing hypertension and heart strain (Heart Foundation, Blood Pressure, 2010).

A second effect that obesity can have on the heart is diabetes mellitus. Diabetes is a disorder of the metabolism where the glucose produced from the breakdown of food is no effectively absorbed into the cells for fuel. Diabetes is characterised by an inadequate production of the hormone called insulin which is produced in the pancreas and must be present to allow glucose to enter the cells (Goldberg, 2014). When insulin production is low the glucose remains in the blood and has many effects, such as increasing the susceptibility to infection (Foss & Farine, 2013). The long term effects of low insulin and high glucose levels in the blood include atherosclerosis, which is an increase in deposits of fatty materials on the insides of the blood vessel walls (Goldberg, 2014). These deposits affect blood flow by reducing the diameter of the blood vessels and raising blood pressure, increasing the chance of clogging and hardening of blood vessels (Goldberg, 2014).

Relevant tests:

There are many tests which can help determine if a patient has heart failure or is at risk, such as; checking blood pressure, chest x-rays, blood tests, 12-lead electrocardiogram and respiratory function tests. Checking blood pressure regularly is part of a standard visit to the doctor or nurse, because it helps to establish a pattern of high, normal or low blood pressure. Long term high blood pressure has been linked to heart strain, and in conjunction with other health issues such as atherosclerosis can result in heart failure. (Heart Foundation, Blood Pressure, 2010).

Another test which can contribute to the diagnosis of heart failure is a chest x-ray. Chest x-rays may be performed to look for signs of a pulmonary oedema which can cause symptoms such as S.O.B and paroxysmal nocturnal dyspnoea (Butler, 2012). A pulmonary oedema is commonly caused by a disrupted flow of blood to and from the heart. Respiratory function tests are also performed, to exclude respiratory causes for dyspnoea, such as asthma and chronic obstructive pulmonary disease (COPD) (Butler, 2012).

Another direct test of the heart is via a 12-lead electrocardiogram (ECG), the results of an ECG may show evidence of left or right ventricular hypertrophy, CHD, or arrhythmias commonly associated with heart failure such as atrial fibrillation (Butler, 2012). If no abnormality is present then the patient is unlikely to have heart failure (Nicholson, 2014). Further tests for signs of heart failure include blood tests for glucose (Butler, 2012; Nicholson, 2014). Checking glucose levels can be performed at home and is a vital component in the management of diabetes because if the blood glucose level remains high it can lead to atherosclerosis, and later, heart failure. High glucose levels are managed by first testing the blood then administering the appropriate amount of insulin to help absorption of the glucose into the cells and thus lower the blood glucose levels.

Treatment strategy:

Education on self-management strategies is a vital aspect of patient empowerment and care both at hospital and in their own home (Cockayne, Pattenden, Worthy, Richardson, & lewin, 2014). Heart failure patients require education how they can manage their symptoms and to ensure they can recognise the warning sign associated with acute situations (Nicholson, 2014). Patient education commonly includes information on how to maintain good control of comorbid conditions such as diabetes. Control of diabetes at home begins with the monitoring blood glucose levels and commonly results in injecting oneself with insulin (Goldberg, 2014). Cockayne et al. (2014) state that ensuring patients understand the importance of adhering to the medication regime designed for their optimal health is a vital part of patient education.

Another important aspect of patient education and self-management is providing an explanation on how to improve health habits and adopt a healthier lifestyle (Nicholson, 2014). The most commonly required lifestyle change to improve health outlooks for patients is to advise that they limit any consumption of alcohol and tobacco smoke as both produce detrimental effects on the heart, such as, causing pulmonary blockages and narrowing of airways, which will affect the oxygen supply to the blood, tissues and organs (Nicholson, 2014). Other important lifestyle changes according to Nicholson (2014) and Butler (2012) include advice on losing weight if the patient is obese, because obesity results in long, narrow blood vessels and high blood pressure which increases the patient’s risk of heart failure. The management of weight for patients with heart failure includes recommendations for specific dietary changes such as a low sodium intake or a low refined sugar intake (Butler, 2012). It may also include guidelines for increased daily exercise which is shown to have positive effects on heart failure symptoms according to Nicholson.

Butler (2012) states that for women there is another important lifestyle factor to consider in the self-management of heart failure symptoms, the use of contraception. Contraception is important for women who experience heart failure and its symptoms because if a woman with heart failure were to become pregnant it would increase her risk of heart failure and morbidity during pregnancy and birth.

The use of pharmacology in the management and treatment of heart failure symptoms is multifaceted. The use of angiotensin-converting enzyme (ACE) inhibitors is said to be one of the most valuable drug therapies in heart failure according to Butler and is intended to decrease the effects of compensatory mechanisms which are maladaptive so as to improve heart failure symptoms and increase the rate of survival, particularly when taken in conjunction with beta-blockers. Beta-blockers work by reducing heart rate and the myocardial oxygen demand (Nicholson, 2014). The use of ACE inhibitors means that it is important to closely monitor the blood chemistry of the patient, and that the side effects are commonly limited to a dry, persistent cough (Butler, 2012). If the patient cannot tolerate ACE inhibitors due to the dry, persistent cough then the use of angiotensin-II receptor blockers (ARBs) will be considered as this drug has similar properties to the ACE inhibitor and will also require the monitoring of blood chemistry. (Butler, 2012).

Other pharmacological treatments include the use of vasodilators and diuretics. Vasodilators are used to improve cardiac output and often used in cases of heart failure where the patient cannot tolerate ACE inhibitors or ARBs (Butler, 2012). Diuretics are used to increase fluid loss in order to reduce the size and occurrence of peripheral oedemas and pulmonary oedemas, resulting in a reduced level of breathlessness (Nicholson, 2014).

The last treatment option to be discussed here is the use of device therapy. Device therapy as stated by Butler (2012) refers to an implantable cardiac defibrillator (ICD) and a biventricular pacemaker. Biventricular pacemakers are implanted to restore ventricular synchrony and reduce symptoms in the event ventricular failure. ICDs on the other hand addresses the problem of cardiac death by delivering an electric shock to the heart to restore normal rhythm and function.

In conclusion, heart failure is a complex and multifaceted health problem which encompasses many heart problems like coronary artery disease, heart attacks and cardiomyopathy. Because heart failure is such a large problem it has many symptoms including S.O.B, fatigue and oedemas, and also many signs like tachycardia and lung crepitation. Each sign and symptom of heart failure is associated with a causal agent or risk factor such as hypertension in relation to obesity and diabetes. Heart failure cannot be cured, however the symptoms can be managed through patient education and self-management, pharmacology, and as a last resort, device therapy.

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• 
  Rachel Corston-Jackson
  

Heart Failure

The heart is a diverse organ and the diseases associated with it are caused by many different organs when they become dysfunctional or diseased. It is for this reason that heart failure is more diverse than just the stopping or failure of the heart as there are many types and causes of heart failure. Therefore, this essay will discuss the subject heart failure in the human body by addressing its aetiology and pathophysiology, the signs and symptoms associated with it, as well as the risk factors and causal agents linked to heart failure, and lastly, the relevant tests and treatment options available to heart failure patients to improve their quality of life.

Aetiology:

Heart failure, sometimes called congestive heart failure, refers to when the heart isn’t pumping blood as well as it should (American Heart Association, 2014). It is a chronic disease characterised by the failure of the heart as a pump and is the result of any structural or functional cardiac disorders (Butler, 2012). This doesn’t mean that the heart stops beating, however, the American Heart Association (2014) warns that heart failure can get worse if it’s not treated. The heart does not stop altogether but keeps working, despite the fact that the demands of blood and oxygen of the heart and body far exceed supply (Butler, 2012). This is caused a variety of disorders such as coronary artery disease, heart attacks, cardiomyopathy, and congenital birth defects (Butler, 2012).

Coronary artery disease (CAD), as stated by Butler (2012) is a disease characterised by a narrowing or blockage of the arteries which restricts blood and oxygen supply to the heart, resulting in a reduced preload in the ventricles and reduced ventricular stretch. When low ventricular stretch occurs it results in a decreased force of cardiac contraction and a low stroke volume. The effects of low stroke volume include low blood pressure and can lead to the body’s organs and tissues becoming deprived of adequate oxygen and nutrients which may cause the body to go into a state of shock.

The second cardiovascular disorder which can cause heart failure is a heart attack. A heart attack according to the Heart Foundation (2015) occurs when ‘a coronary artery becomes suddenly blocked, stopping the flow of blood to the heart muscle’. Damage to the heart muscle occurs during a heart attack, and becomes scarred, the damaged area does not function properly, resulting in a reduced cardiac output and low blood pressure. When this happens the heart compensates by undergoing a remodelling process where it changes in size, shape or structure, and according to Butler (2012) the remodelling is more likely to occur in the left ventricle as it has a thicker muscle mass.

The third form of heart failure mentioned above is cardiomyopathy, which is caused by infections, alcohol abuse, or pregnancy and is characterised by damage to the heart muscle. The type of cardiomyopathy which presents during pregnancy is called peripartum cardiomyopathy (Demir, Tufenk, Karakaya, Akilli, & Kanadas, 2013). It is a form of dilated cardiomyopathy and involves systolic dysfunction of the heart. Onset is usually around the last month of pregnancy and five months postpartum, hence the name. One common symptom of peripartum cardiomyopathy is sinus tachycardia which according to Demir et al. (2013) can be treated with a drug called Ivabradine. This brings me to the next section which is the pathophysiology of heart failure.

Pathophysiology:

Heart failure is a complex problem and is characterised by many signs and symptoms. Symptoms include; shortness of breath, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, reduced ability to exercise, peripheral oedema, loss of appetite and more (Nicholson, 2014). Signs include; Tachycardia, tachypnoea, an abnormal pulse, and displaced apex beat, third heart sounds, a raised jugular venous pressure, lung crepitation, weight changes, hepatomegaly and more (Nicholson, 2014).

The common symptoms which will be focused on here include shortness of breath (S.O.B), paroxysmal nocturnal dyspnoea, fatigue, and a lack of appetite (Butler, 2012). The American Heart Association (2014) states that S.O.B during activity, at rest, or while sleeping, can have a sudden onset, often causing the patient to wake. They describe S.O.B as being caused by the blood when it “backs up” in the pulmonary veins because the heart can’t keep up with the supply. The result is stated to be that the kidneys develop a reduced capacity to dispose of sodium and water, and that excess fluid leaks into the lungs causing a pulmonary oedema and around the lungs causing pleural effusion. The clinical sign which indicates that this has occurred, aside from S.O.B, is the presence of lung crepitations (Butler, 2012). A lung crepitation, according to Butler, is a crackling sound produced during inhalation and exhalation due to fluid accumulation inside the lungs and predominantly occurs in the lower lung fields. The American Heart Association states that peripheral oedemas can also occur as a result of the venous blood backing up and is characterised by swelling in the ankles, feet and abdomen resulting in ill-fitting shoes and weight gain due to the excess fluid accumulation.

The build-up of fluid which causes S.O.B also leads to paroxysmal nocturnal dyspnoea (PND) (Butler, 2012; Nicholson, 2014). PND usually occurs at night, according to the American Heart Association, and is characterised by sudden awakening from sleep after only a few hours, with a feeling of breathlessness, suffocation and severe anxiety. On chest auscultation, the bronchospasm associated with a heart failure exacerbation can be difficult to distinguish from an acute asthma exacerbation (Dumitru & Baker, 2014).

Other symptoms of heart failure included fatigue. Fatigue and weakness according to Dumitru & Baker (2014) are often accompanied by a feeling of leaden limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Essentially the heart produces a decreased volume of blood and cannot meet the needs of body tissues so the body diverts blood away from less vital organs, particularly muscles in the limbs, and sends it to the heart and brain (American Heart Association, 2014). The American Heart Association (2014) and Nicholson (2014) both link this diversion of blood to vital organs to the loss of appetite and feelings of nausea often experienced by people with heart failure due to the fact that the digestive system receives less blood and cannot function correctly.

The common signs that will be discussed here are hepatomegaly, third heart sounds, tachycardia and a displaced apex beat. Hepatomegaly, an enlargement of the liver which can occur with right heart failure (Nicholson, 2014), and is caused by the blood backing up from the heart into the inferior vena cava, such congestion increases pressure in the inferior vena cava and other veins that carry blood to it, including the hepatic veins (Orfanidis, 2013).Once this occurs the pressure may build to a point where the liver becomes engorged with blood and malfunctions. The common symptoms of hepatomegaly are nausea, abdominal pain or fullness, swelling of the feet and legs, and shortness of breath, all of which are also seen in heart failure (Butler, 2012).

The third heart sound (S3) is a low-pitched sound that occurs when the ventricles fill rapidly and is one of the more specific signs of heart failure and auscultating to determine the presence of it can help healthcare professionals to diagnose heart failure (Santhosh, 2009). S3 is commonly present in conjunction with tachycardia, which is a high resting heart rate and is common as a haemodynamic compensatory response (Nicholson, 2014). The final sign of heart failure listed above is a displaced apex beat. A displaced apex beat means ‘the point of maximal impulse on the precordium can be displaced down and to the left laterally and commonly occurs when the heart is dilated (Nicholson, 2014, p. 33)’. Each sign and symptom of heart failure is linked to a causal agent such as a previous history of Myocardial Infarctions (MI).

Risk factors/causal agents:

The term ‘heart failure’ includes many conditions and disease, thus it has many causal agents including; Family history, narrowed arteries, high blood pressure, coronary artery disease, myocardial infarctions, valve disorders, peripartum, ischemic heart disease, diabetes, obesity, kidney disease, hypothyroidism, toxins (alcohol), and infection (Butler, 2012; Nicholson, 2014). The causal agents which will be discussed here are narrowed arteries, high blood pressure, obesity, diabetes and infection.

Family history is an important indicator of increased risk in relation to heart failure, it is however not to be considered on its own but in relation to other risk factors such as narrowed arteries (Goldberg, 2014). Narrowed arteries can refer to vasoconstriction or atherosclerosis. Atherosclerosis is a plaque formation is medium or large sized arteries in response to damage of the tunica intima (National Health Council, 2014). These plaque formations cause increased resistance to laminar blood flow resulting in turbulent flow and high blood pressure (Foss & Farine, 2013). Blood pressure alone is characterised as the force exerted on blood vessel walls by a volume of blood as it passes through (Heart Foundation, Blood Pressure, 2010). High blood pressure on the other hand is known as hypertension, and is defined by the Heart Foundation (2010) as chronically elevated blood pressure resulting in stain on the heart and blood vessels. Hypertension is visually manifested by jugular venous distention on the right side of the neck (Nicholson, 2014). Foss & Farine (2013) state that the elevated blood pressure is detected in the blood vessels by baroreceptors located in the carotid sinus and aortic arch. The baroreceptors are said to then stimulate vasomotor nerves to increase the diameter of the blood vessels to increase blood flow and reduce blood pressure.

Another cause of high blood pressure is obesity. This is due to the fact that overweight or obese people have a greater the volume of tissue and fat that requires a constant blood supply, this results in an increase in blood vessel length (Foss & Farine, 2013). Foss & Farine (2013) state that the longer the blood vessels become the more distance the blood will have to travel which increases the resistance, the body will compensate for this by increasing the blood pressure throughout the body by increasing the stroke volume of the heart. This increase in blood pressure is to ensure both adequate blood supply to all blood vessels and adequate venous return. If the high weight threshold is maintained then high blood pressure will continue, causing hypertension and heart strain (Heart Foundation, Blood Pressure, 2010).

A second effect that obesity can have on the heart is diabetes mellitus. Diabetes is a disorder of the metabolism where the glucose produced from the breakdown of food is no effectively absorbed into the cells for fuel. Diabetes is characterised by an inadequate production of the hormone called insulin which is produced in the pancreas and must be present to allow glucose to enter the cells (Goldberg, 2014). When insulin production is low the glucose remains in the blood and has many effects, such as increasing the susceptibility to infection (Foss & Farine, 2013). The long term effects of low insulin and high glucose levels in the blood include atherosclerosis, which is an increase in deposits of fatty materials on the insides of the blood vessel walls (Goldberg, 2014). These deposits affect blood flow by reducing the diameter of the blood vessels and raising blood pressure, increasing the chance of clogging and hardening of blood vessels (Goldberg, 2014).

Relevant tests:

There are many tests which can help determine if a patient has heart failure or is at risk, such as; checking blood pressure, chest x-rays, blood tests, 12-lead electrocardiogram and respiratory function tests. Checking blood pressure regularly is part of a standard visit to the doctor or nurse, because it helps to establish a pattern of high, normal or low blood pressure. Long term high blood pressure has been linked to heart strain, and in conjunction with other health issues such as atherosclerosis can result in heart failure. (Heart Foundation, Blood Pressure, 2010).

Another test which can contribute to the diagnosis of heart failure is a chest x-ray. Chest x-rays may be performed to look for signs of a pulmonary oedema which can cause symptoms such as S.O.B and paroxysmal nocturnal dyspnoea (Butler, 2012). A pulmonary oedema is commonly caused by a disrupted flow of blood to and from the heart. Respiratory function tests are also performed, to exclude respiratory causes for dyspnoea, such as asthma and chronic obstructive pulmonary disease (COPD) (Butler, 2012).

Another direct test of the heart is via a 12-lead electrocardiogram (ECG), the results of an ECG may show evidence of left or right ventricular hypertrophy, CHD, or arrhythmias commonly associated with heart failure such as atrial fibrillation (Butler, 2012). If no abnormality is present then the patient is unlikely to have heart failure (Nicholson, 2014). Further tests for signs of heart failure include blood tests for glucose (Butler, 2012; Nicholson, 2014). Checking glucose levels can be performed at home and is a vital component in the management of diabetes because if the blood glucose level remains high it can lead to atherosclerosis, and later, heart failure. High glucose levels are managed by first testing the blood then administering the appropriate amount of insulin to help absorption of the glucose into the cells and thus lower the blood glucose levels.

Treatment strategy:

Education on self-management strategies is a vital aspect of patient empowerment and care both at hospital and in their own home (Cockayne, Pattenden, Worthy, Richardson, & lewin, 2014). Heart failure patients require education how they can manage their symptoms and to ensure they can recognise the warning sign associated with acute situations (Nicholson, 2014). Patient education commonly includes information on how to maintain good control of comorbid conditions such as diabetes. Control of diabetes at home begins with the monitoring blood glucose levels and commonly results in injecting oneself with insulin (Goldberg, 2014). Cockayne et al. (2014) state that ensuring patients understand the importance of adhering to the medication regime designed for their optimal health is a vital part of patient education.

Another important aspect of patient education and self-management is providing an explanation on how to improve health habits and adopt a healthier lifestyle (Nicholson, 2014). The most commonly required lifestyle change to improve health outlooks for patients is to advise that they limit any consumption of alcohol and tobacco smoke as both produce detrimental effects on the heart, such as, causing pulmonary blockages and narrowing of airways, which will affect the oxygen supply to the blood, tissues and organs (Nicholson, 2014). Other important lifestyle changes according to Nicholson (2014) and Butler (2012) include advice on losing weight if the patient is obese, because obesity results in long, narrow blood vessels and high blood pressure which increases the patient’s risk of heart failure. The management of weight for patients with heart failure includes recommendations for specific dietary changes such as a low sodium intake or a low refined sugar intake (Butler, 2012). It may also include guidelines for increased daily exercise which is shown to have positive effects on heart failure symptoms according to Nicholson.

Butler (2012) states that for women there is another important lifestyle factor to consider in the self-management of heart failure symptoms, the use of contraception. Contraception is important for women who experience heart failure and its symptoms because if a woman with heart failure were to become pregnant it would increase her risk of heart failure and morbidity during pregnancy and birth.

The use of pharmacology in the management and treatment of heart failure symptoms is multifaceted. The use of angiotensin-converting enzyme (ACE) inhibitors is said to be one of the most valuable drug therapies in heart failure according to Butler and is intended to decrease the effects of compensatory mechanisms which are maladaptive so as to improve heart failure symptoms and increase the rate of survival, particularly when taken in conjunction with beta-blockers. Beta-blockers work by reducing heart rate and the myocardial oxygen demand (Nicholson, 2014). The use of ACE inhibitors means that it is important to closely monitor the blood chemistry of the patient, and that the side effects are commonly limited to a dry, persistent cough (Butler, 2012). If the patient cannot tolerate ACE inhibitors due to the dry, persistent cough then the use of angiotensin-II receptor blockers (ARBs) will be considered as this drug has similar properties to the ACE inhibitor and will also require the monitoring of blood chemistry. (Butler, 2012).

Other pharmacological treatments include the use of vasodilators and diuretics. Vasodilators are used to improve cardiac output and often used in cases of heart failure where the patient cannot tolerate ACE inhibitors or ARBs (Butler, 2012). Diuretics are used to increase fluid loss in order to reduce the size and occurrence of peripheral oedemas and pulmonary oedemas, resulting in a reduced level of breathlessness (Nicholson, 2014).

The last treatment option to be discussed here is the use of device therapy. Device therapy as stated by Butler (2012) refers to an implantable cardiac defibrillator (ICD) and a biventricular pacemaker. Biventricular pacemakers are implanted to restore ventricular synchrony and reduce symptoms in the event ventricular failure. ICDs on the other hand addresses the problem of cardiac death by delivering an electric shock to the heart to restore normal rhythm and function.

In conclusion, heart failure is a complex and multifaceted health problem which encompasses many heart problems like coronary artery disease, heart attacks and cardiomyopathy. Because heart failure is such a large problem it has many symptoms including S.O.B, fatigue and oedemas, and also many signs like tachycardia and lung crepitation. Each sign and symptom of heart failure is associated with a causal agent or risk factor such as hypertension in relation to obesity and diabetes. Heart failure cannot be cured, however the symptoms can be managed through patient education and self-management, pharmacology, and as a last resort, device therapy.

1 | Page