Pharmacotherapy/Treatment Of Congestive Heart Failure (CHF)

Heart failure is a situation whereby the heart works less efficiently. Blood and nutrients move through the heart and body at a slower rate thereby increasing the pressure in the heart. It occurs when the heart chamber expands more to hold more blood or become too stiff and thick. If the kidney responds to this condition, salt and water is retained in the arms, legs, ankles, feet, lungs and other organs. This is known as congestive heart failure (CHF).

Congestive HF or decompensated HF occurs in patients where there is increased blood pressure resulting from weak pumps in heart failure reduced ejection fraction (HFrEF) also called systolic HF and stiff pumps in heart failure preserved ejection fraction (HFpEF) also called diastolic HF. In either case, there is a backfill of pressure in the lungs as the ventricle cannot eject enough blood out of the left ventricle. This leads to increased pulmonary pressure that pushes fluid out of capillaries and into alveolar space (causing pulmonary oedema). This additional fluid in the alveolar spaces slows diffusion of oxygen and carbon dioxide, leading to dyspnoea (shortness of breath).

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Orthopnoea can also be present in decompensated HF; this is a feeling of breathlessness when lying flat, which is caused as more venous blood flows back into the heart and into pulmonary circulation when the patient assumes a supine posture, again leading to raised pulmonary pressures and migration of fluid into alveolar space. Rales, or ‘crackles’, are heard when listening to the chest through a stethoscope, at least in the lung bases. Similar to the mechanism of pulmonary congestion, when there is either a rise in the pulmonary artery pressure and/or impairment of the right ventricle, back pressure would lead to fluid accumulation in the liver, legs, sacrum and peritoneal cavity, causing ascites.

Symptoms Of CHF

1. Congested lungs causing shortness of breath or difficulty breathing at rest or when lying down

2. Dry or hacking cough due to fluid buildup in the lungs

3. Edema and weight gain

4. Urinary urgency at night

5. Bloating and loss of appetite

6. Nausea

Causes

1. Coronary artery disease; block arteries

2. Heart attack

3. Condition that overworked the heart

4. Cardiomegaly

Type

Systolic dysfunction (systolic heart failure): when the cause of the heart failure is as a result of dysfunction of the ventricles contraction. There is left and right systolic dysfunction named according to the position of the ventricles affected. Left systolic dysfunction is more common than right.

Diastolic dysfunction (diastolic heart failure): this occurs when the cause of the heart failure is as a result of dysfunction of the ventricles that do not properly relax and become stiff. There is also right or left dysfunction.

Right sided heart failure causes edema. HF is more in men than women but complications occur more in women than men.

Classification

Acute HF: symptoms appear suddenly and go away fairly quickly. It commonly occurs after a heart attack or problem with a heart valve that controls the flow of blood in the heart.

Chronic HF: same symptoms with acute but persist longer. This is more common than acute.

Stages

There are five stages of HF. They are;

Stage I: There is high risk of HF but no structural heart disease or symptoms. There is no limitation of physical activity.

Stage II: there is the presence of structural heart disease but no symptoms of heart failure. At this stage, there are slight limitations of physical activity.

Stage III: structural heart disease with symptoms. There are marked limitations of physical activity.

Stage IV: it is becoming more severe. Symptoms appear even at rest. This is termed refractory HF requiring intervention.

Risk Factors

1. Anemia

2. Hyperthyroidism

3. Hypothyroidism

4. Emphysema

5. Unhealthy living like smoking, sedentary lifestyle, high cholesterol diet, etc

Diagnosis

There are so many test uses to determine if one is having HF. However, most of them only analyse information from symptoms to come to a conclusion. The best is the use of echocardiograms. It is an ultrasound that determines the movement, structure and function of the heart. Others are;

1. Electrocardiogram (EKG or ECG) uses electrical impulses to analyse the heart

2. Chest x-ray check for the size and fluid buildup

3. Cardiac catheterization (coronary angiogram) check for the presence of coronary artery disease

4. Stress test also determined coronary artery disease

5. Ejection fraction (EF): Determine systolic or heart failure

6. Blood test/B-type natriuretic peptide (BNP) test: BNP increase in the presence of HF and reduce in normal heart. However, presence does not indicate stage of HF.

Pathophysiology Of Congestive Heart Failure (CHF)

Pathophysiology of CHF

Frank Starling law of heart states that the stroke volume increases in response to an increase in volume of blood filling the heart (end diastolic volume) when other factors remain constant. Let us illustrate using an elastic band (rubber band). The greater the band is apart, the greater the recoil. But it will lose its elasticity if it crosses it elastic point and break if it crosses it's breaking point.

Before we continue, let us define some terms. It will help us understand the concept better. HF is often classified based on EF. In HF, the cardiac output or ejection fraction is reduce.

EF=end diastolic volume-end systolic volume/end diastolic volume.

Also, cardiac output=amount ejected every beat (stroke volume)×heart rate

Heart failure reduced ejection fraction (HFrEF) is identified when the EF is less than 40 percent. Normal EF is between 55-70 percent. Heart failure with preserved ejection fraction (HFpEF) can be harder to diagnose and is defined as EF less than 50 percent with other markers of HF (e.g diastolic dysfunction or structural heart disease). 

In HFrEF, stroke volume is typically reduced (reduced cardiac output). In HFpEF, EF is normal, diastolic dysfunction is often present, lowering the diastolic volume. Patients with HFpEF are often older, female with history of hypertension, valvular disease and ischemic heart disease.

Natriuretic peptides are released from the myocardium in response to ventricular wall stress, hypertrophy and fluid overload. Two main types of these substances are brain natriuretic peptide (BNP) and N-terminal pro b-type natriuretic peptide (NT-proBNP). They increase in HF.

Impact Of Compensatory Mechanism

A reduction in cardiac output in both HFrEF and HFpEF leads to compensatory mechanisms being activated to reduce the unbalance. They strain the heart in the long run. The main systems activated in response to reduce systemic perfusion are renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system (SNS) and natriuretic peptide system (NPS). Others are parasympathetic activation, vasopressin, endothelium and other strategies.

A reduction in cardiac output triggers RAAS, which leads to salt and water retention, increased circulating blood volume which increases preload with the aim to increase atrial pressure and increase stroke volume to improve cardiac output.

SNS is activated through the release of catecholamine which increases heart rate and force of contraction (beta I and II receptors). It also leads to the RAAS system activating when chronic NPS affects the kidney, heart and CNS and tends to oppose the effect of RAAS and SNS.

Pharmacotherapy/Treatment Of Congestive Heart Failure

Treatment depends on the stage and the cause. Treatment plans adopt both pharmacology and non pharmacological approaches (drugs and lifestyle changes). Lifestyle changes are recommended for every stage. There is no cure but symptoms can improve depending on response to therapy.

Stage I: lifestyle changes are enough. However, if drugs should be added, it should be based on the cause. Hypertension in the presence of coronary artery disease (CAD) and diabetes should be treated with angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB). Hypertension can also be treated with beta blockers (BB).

Stage II: lifestyle changes along with ARB and ACEI. Aldosterone antagonist is necessary in the event of a heart attack or diabetes and EF of less than 35 percent. Surgery is recommended in case of CAD, heart attack and valve repair.

Stage III: Treatment procedure is same with stage II with additional suggestions such as the use of hydralazine/nitrate combination when other treatments fail. Others are medications to slow heart rate, diuretic, cardiac resynchronization therapy (biventricular pacemaker) and Implantable cardioverter-defibrillators (ICD) therapy.

Stage IV: Treat using the methods for the previous stages. But when they fail, heart transplant, ventricular assistance device, heart surgery, continuous infusion or intravenous (IV) inotropic drugs, palliative or hospice care can be used.

Others

Coronary bypass surgery (alternative entry), angioplasty using catheter to blow open an artery or pacemaker are some other procedures available. Ventricular assist devices (VAD) help pump blood.

Symptoms e.g pulmonary edema is treated with oxygen therapy, sublingual or IV nitroglycerin and IV furosemide and morphine sulphate.

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Treatment of those with HFrEF have reduced mortality and morbidity. Treatment is management of underlying commodities (HBP, Ischemic heart disease and diabetes). This is not so with HFpEF although both have similar symptoms. HFrEF can be treated with ACEI or ARB with BB as the first line.

Diuretic use when there is fluid overload does not treat the cause but has mortality benefits. Furosemide 40-80 mg morning and night is first line therapy among the loop diuretics. Alternatively, brunettemide can be used. 2.5-5 mg thiazide (metolazone) daily can be added for synergistic effect.

Spironolactone is recommended in symptomatic patients with an EF of less than 35 percent. Urea and electrolyte level should be monitored within one week of initiating therapy, then monthly for three months, then every trimester for a year and then quarterly thereafter.

BB should be avoided in acute CHF but very good in clinically stable patients. Calcium channel blockers (CCB) is good except in systolic HF. Secubril is a neprilutic inhibitor. Adding it with valsartan (avoid the ACEI) helps improve treatment. HF patients should avoid naproxen and ibuprofen.