Heart Failure

Question 1

What is heart failure?

Answer 1

Heart failure is a clinical syndrome in which the heart is unable to deliver sufficient blood to the rest of the body due to cardiac dysfunction.

Question 2

How is heart failure defined?

Answer 2

Heart failure is defined as a collection of symptoms and signs characteristic of a specific disease.

Question 3

What are the most common causes of heart failure?

Answer 3

The most common cause of heart failure is cardiomyopathy, which is a disease of the heart muscle. Other causes include ischemic heart disease, hypertension, inherited factors, alcohol excess, viral infections, toxins, metabolic disorders, and unknown causes.

Question 4

How prevalent is heart failure in the UK?

Answer 4

In the UK, there are approximately 200,000 new diagnoses of heart failure per year, with an average of 500 new diagnoses per day. The mean age at presentation is 77 years. There are around 650,000 patients on GP registers and 900,000 patients living with heart failure. The 5-year mortality rate is 50%.

Question 5

What are the three clinical syndromes of heart failure?

Answer 5

The three clinical syndromes of heart failure are chronic heart failure, characterized by peripheral edema; acute heart failure, characterized by pulmonary edema; and cardiogenic shock, characterized by low blood pressure.

Question 6

What is LV systolic heart failure?

Answer 6

LV systolic heart failure refers to left ventricular weakness, often accompanied by dilation or thinning of the left ventricle. It is also known as dilated cardiomyopathy. The causes of LV systolic heart failure include ischemic heart disease (acute myocardial infarction or chronic ischemia), hypertension, inherited factors, alcohol excess, viral infections, toxins, metabolic disorders, and unknown causes.

Question 7

How can we measure left ventricular (LV) function?

Answer 7

There is no single perfect measure of LV function since it depends on factors such as preload (venous return) and afterload (blood pressure). However, a measurement of LV contractility that is independent of loading is isovolumic dP/dt. Another commonly used measure is the LV ejection fraction.

Question 8

What is ejection fraction?

Answer 8

Ejection fraction is a measure of LV function that represents the percentage of blood pumped out of the LV during each contraction. It is calculated by subtracting the end-systolic volume from the end-diastolic volume and dividing the result by the end-diastolic volume.

Question 9

What are the hemodynamic characteristics of systolic heart failure?

Answer 9

Systolic heart failure is characterized by decreased LV contractility, resulting in reduced stroke volume. This leads to increased LV diastolic pressure and increased LV end-diastolic volume, causing LV dilation. Systolic heart failure is typically defined by a left ventricular ejection fraction (LVEF) of less than 40%. A normal LVEF range is considered to be 55-70%.

Question 10

What are the two theories of heart failure pathophysiology?

Answer 10

The “Forward” theory and the “Backward” theory. The “Forward” theory emphasizes the effects of a low cardiac output on the body’s reactions, while the “Backward” theory emphasizes the effects of elevated pressures transmitted through the circulation.

Question 11

What are the symptoms of heart failure?

Answer 11

The symptoms of heart failure include breathlessness (exertional, orthopnea, paroxysmal nocturnal dyspnea), fatigue, and leg swelling (edema).

Question 12

What is the NYHA severity classification for heart failure?

Answer 12

The NYHA (New York Heart Association) severity classification is used to assess the functional status of heart failure patients.

Class 1: Asymptomatic
Class 2: Mild symptoms with ordinary day-to-day activities
Class 3: Moderate symptoms with minor exertion
Class 4: Symptoms at rest

Question 13

What are the signs of heart failure?

Answer 13

The signs of heart failure include elevated Jugular Venous Pressure (JVP), edema (ankle, shins, thighs, genitals, trunk), ascites, pleural effusions, lung crackles (inspiration, bases), low volume pulse, low blood pressure, tachycardia, increased respiratory rate, displaced apex beat, murmur (functional mitral regurgitation), and liver enlargement (hepatomegaly).

Question 14

What investigations are commonly performed for heart failure?

Answer 14

There are several investigations performed for heart failure:

ECG: Rarely normal in heart failure patients, may show tall complexes (indicating left ventricular hypertrophy), broad complexes (indicating left bundle branch block), or T wave inversion.
Brain Natriuretic Peptide (BNP): Released by the left atrium in response to increased left atrial pressure. It is sensitive for heart failure and used as a screening test, although it is not specific.
Echocardiogram: Assess LV dimensions and function, LV ejection fraction, and estimate intra-cardiac pressures.
Cardiac MRI: Assess LV dimensions and function, LV ejection fraction, and characterize myocardial pathology.
Cardiac catheterization: Assess LV dimensions and function, and directly measure intra-cardiac pressures. It may also involve coronary angiography.

Question 15

What are the characteristics of acute left heart failure?

Answer 15

Acute left heart failure often presents with elevated left heart pressures that are transmitted back to the pulmonary capillaries. When the pulmonary capillary pressure exceeds 25 mmHg, pulmonary edema occurs. In severe cases, the ability to maintain cardiac output may be compromised, resulting in cold, clammy skin, a thready pulse, and a systolic blood pressure (SBP) below 90 mmHg. This condition is known as cardiogenic shock.

Question 16

What are the mechanisms of right heart failure?

Answer 16

Right heart failure occurs due to increased left atrial (LA)/pulmonary venous pressures, which are transmitted to the pulmonary arteries/right ventricle/right atrium. This leads to increased venous return (preload) and cardiac output. The renin/angiotensin/aldosterone system is activated, resulting in renal sodium and water retention. There is also sympathetic activation and increased contractility. Pulmonary edema and peripheral edema (swelling) are common manifestations of right heart failure.

Question 17

What are the characteristics of right-sided heart failure?

Answer 17

Right-sided heart failure typically presents as a chronic condition, often resulting from left heart disease. Although there are elevated left heart pressures, the left atrium dilates and the left atrial/pulmonary venous pressure remains below 25 mmHg. The elevated pressure is transmitted back to the pulmonary arteries, right ventricle, right atrium, and superior/inferior vena cava. Signs of right-sided heart failure include elevated jugular venous pressure (JVP), leg edema, and the presence of pleural effusions or ascites.

Question 18

What is cor pulmonale?

Answer 18

Cor pulmonale refers to right-sided heart failure that is caused by chronic lung disease. It can occur due to various causes such as chronic obstructive pulmonary disease (COPD), lung fibrosis, and pulmonary hypertension. In cor pulmonale, there are elevated pulmonary artery pressures, which are transmitted back to the right ventricle, right atrium, and superior/inferior vena cava. Clinical manifestations include elevated JVP, leg edema, and the presence of pleural effusions or ascites.

Question 19

What is the role of preload in heart failure?

Answer 19

Preload refers to the volume of blood that fills the ventricles during diastole. In heart failure, increased preload leads to elevated left atrial/pulmonary venous pressures, which can result in pulmonary edema and peripheral edema. It also increases the venous return, contributing to cardiac output.

Question 20

What is the renin-angiotensin-aldosterone system (RAAS)?

Answer 20

The renin-angiotensin-aldosterone system is a hormonal cascade that plays a crucial role in regulating blood pressure and fluid balance. In heart failure, low cardiac output activates the RAAS, leading to increased release of renin. This initiates a series of reactions that ultimately result in the production of angiotensin II, which causes vasoconstriction and stimulates the release of aldosterone. Aldosterone promotes sodium and water retention in the kidneys, further contributing to fluid overload.

Question 21

What is the role of neuro-endocrine activation in heart failure?

Answer 21

In heart failure, low cardiac output activates neuro-endocrine systems, including the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system. This activation helps to compensate for reduced cardiac function. The RAAS is involved in fluid balance and vasoconstriction, while sympathetic activation increases heart rate and contractility. These mechanisms aim to maintain perfusion to vital organs but can also contribute to the progression of heart failure over time.

Question 22

What happens during RAAS activation in heart failure?

Answer 22

In heart failure, low cardiac output leads to reduced renal perfusion, which triggers the activation of the renin-angiotensin-aldosterone system (RAAS). This activation results in increased release of renin, angiotensin, and aldosterone. The subsequent effects include salt and water retention, increased preload (volume of blood in the ventricles during diastole), and increased cardiac output. However, these compensatory mechanisms can also lead to fluid overload, resulting in edema, ascites, and pleural effusions. Additionally, angiotensin-mediated vasoconstriction increases afterload.

Question 23

What is the role of sympathetic activation in heart failure?

Answer 23

Sympathetic activation is a compensatory response in heart failure aimed at maintaining cardiac output. It increases sympathetic nerve activity, leading to enhanced contractility and heart rate. This helps to improve cardiac output initially. However, chronic sympathetic activation can have detrimental effects, including increased afterload and vasoconstriction, which contribute to pulmonary edema and peripheral edema (swelling).

Question 24

What happens during neuro-endocrine activation in heart failure?

Answer 24

In heart failure, low cardiac output triggers neuro-endocrine activation, which includes the activation of the sympathetic nervous system and increased circulating catecholamines (such as adrenaline and noradrenaline). This leads to increased contractility and heart rate, aiming to improve cardiac output initially. However, it also activates the renin-angiotensin-aldosterone system (RAAS), leading to increased afterload and catecholamine cardiotoxicity. Prolonged sympathetic activation can cause structural and functional changes in cardiomyocytes, leading to left ventricular (LV) dilation, adverse remodeling, and worsened LV systolic dysfunction.

Question 25

What are the effects of sympathetic activation on the heart?

Answer 25

Sympathetic activation increases heart rate and contractile force through beta-1 adrenergic receptor stimulation. In the short term, this can increase cardiac output. However, in the longer term, it exacerbates heart failure and is often compared to “flogging a dying horse,” as it puts further strain on an already compromised heart.

Question 26

What are the effects of sympathetic activation on the arterial system?

Answer 26

Sympathetic activation causes vasoconstriction through alpha-1 adrenergic receptor stimulation. This leads to an increase in systemic vascular resistance (SVR) and consequently increases afterload. In the short term, it helps maintain arterial blood pressure. However, in the longer term, it increases the workload on a weakened heart, comparable to making a dying horse run uphill.

Question 27

What is diastolic heart failure?

Answer 27

Diastolic heart failure, also known as heart failure with preserved ejection fraction (HFpEF), is a type of heart failure where the left ventricular (LV) systolic function is good (ejection fraction >40%). It is characterized by a chronic heart failure syndrome but with normal LV volume and increased LV stiffness (reduced compliance). Despite the preserved ejection fraction, the cascade of increased pressures and the associated symptoms and complications are similar to other forms of heart failure, although LV dilation is less prominent.

Question 28

What are the mechanisms of diastolic heart failure?

Answer 28

In diastolic heart failure, increased LV stiffness (reduced compliance) plays a key role. This leads to increased left atrial/pulmonary venous pressures, increased pulmonary artery/right ventricle/right atrial pressures, and increased venous return (preload). The neuro-endocrine and sympathetic activations, as well as renal sodium and water retention, are similar to other forms of heart failure, leading to symptoms such as pulmonary edema and peripheral edema.

Question 29

What are the specific causes and associated conditions of LV diastolic heart failure?

Answer 29

LV diastolic heart failure is commonly seen in elderly patients and often associated with conditions such as hypertension, diabetes, and atrial fibrillation. It is characterized by increased LV stiffness and is classified as a restrictive cardiomyopathy. Specific causes can include amyloid heart disease, sarcoidosis, severe LV hypertrophy, hypertension, and hypertrophic cardiomyopathy.

Question 30

What are the therapeutic options for managing chronic heart failure with fluid retention?

Answer 30

For fluid retention in chronic heart failure, various medications can be used:

Loop diuretics (e.g., Furosemide) help in promoting diuresis and reducing fluid overload.
Angiotensin-converting enzyme (ACE) inhibitors (e.g., Ramipril) and angiotensin II receptor blockers (ARBs) (e.g., Losartan, Candesartan) target the renin-angiotensin-aldosterone system, reducing the production and effects of angiotensin II, which helps in fluid balance.
Aldosterone antagonists (e.g., Spironolactone) inhibit the effects of aldosterone, leading to reduced sodium and water retention.
Beta blockers (e.g., Bisoprolol) act on the sympathetic system, reducing sympathetic activity and improving overall heart function.

Question 31

What are the advanced therapeutic options for managing chronic heart failure?

Answer 31

In advanced stages of chronic heart failure, additional therapeutic options include:

SGLT-2 inhibitors (e.g., Dapagliflozin), which reduce glucose reabsorption in the kidney, leading to osmotic diuresis and improved fluid balance.
Neprilysin inhibitors (e.g., Sacubatril) are often used in combination with an angiotensin antagonist (e.g., Valsartan) to inhibit the degradation of natriuretic peptides, promoting diuresis and vasodilation.
If heart rate remains high despite optimal medical therapy, Ivabradine may be considered as a selective sinus node inhibitor to lower heart rate.

Question 32

What is the management approach for acute heart failure?

Answer 32

The management approach for acute heart failure can be remembered using the acronym “PODMAN”:

P: Position the patient in an upright or semi-upright position to help alleviate respiratory distress.
O: Administer supplemental oxygen to improve oxygenation.
D: Initiate diuretic therapy, typically with intravenous furosemide, to reduce fluid overload.
M: Consider administering morphine for pain relief and to reduce anxiety and respiratory distress.
Administer anti-emetic medication to control nausea and vomiting.
N: Administer nitrates, such as GTN spray or intravenous isosorbide mononitrate, to promote vasodilation and reduce preload.
Non-invasive ventilation, such as continuous positive airways pressure (CPAP), may also be used to support respiratory function.
Note: Beta-blockers should not be given in acute heart failure.