Pathophysiology
Cardiac failure is when the heart is unable to pump out enough blood to meet the body’s demands/metabolic requirements. Let’s first recap some of the cardiac physiology:
Our cardiac output is defined as:
A normal at-rest adult has a cardiac output of about 5-6L per minute. So if the heart rate is 60bpm then this would equate to 83-100ml of blood being ejected with each pump of the ventricles. However, this does not mean that all the blood in the ventricles is being ejected.
To simplify things, let’s imagine the total volume within the ventricle is 100ml. A normal contraction of the ventricle would then eject about 50-70ml of this initial volume. The ejection fraction would then be 50-70% which is considered the normal range. Anything <40% is considered heart failure.
The formula for ejection fraction is:
🔢 Classification
Let’s discuss different types of heart failure based off of 4 factors:
- Ejection fraction
- Side
- Time
- Output
Ejection fraction
Heart failure often but not always results in a reduced ejection fraction, therefore we can classify it as reduced or preserved ejection fraction.
- Heart failure with reduced ejection fraction (HF-rEF)
- Ischaemic heart disease - less perfusion to myocardium leads to its damage and impaired contraction.
- Myocardial infarction - leads to scar tissue formation which is unable to contract.
- Dilated cardiomyopathy - initially it compensates as it increases the preload and contractile strength (according to Frank-Starling law of the heart). However, eventually the muscle wall becomes too thin and weak
Approximately 50% of heart failure patients have rEF. It was previously known as systolic heart failure as it occurs as a result of the ventricular myocardium being unable to contract normally which results in a reduced ejection fraction and reduced cardiac output.
It is when our left ventricular ejection fraction (LVEF) is <40%.
Causes of HF-rEF:
- Heart failure with preserved ejection fraction (HF-pEF)
- Restrictive cardiomyopathy - stiffening of the heart walls leading to impaired stretching and as a result they are unable to fill up with blood.
- Ventricular hypertrophy (hypertrophic obstructive cardiomyopathy) - often with long-standing hypertension. When afterload increases, it makes it harder for the ventricles to pump blood into our arterial system. As a result the myocardial cells undergo hypertrophy and this encroaches on the ventricular space → less filling space → reduced end-diastolic volume.
- Constrictive pericarditis - as the heart is unable to stretch.
- Cardiac tamponade - similarly as there is pressure on the heart, it stretches less and can’t fill efficiently.
Approximately 50% have this other type of HF. It is when the LVEF >50%. It was previously known as diastolic heart failure.
It occurs as a result of impaired filling of the ventricles. So our heart is able to pump out the blood efficiently, however, there is not enough blood to pump out in the first place. Hence the CO is low but the EF remains normal.
Heart failure with mid-range ejection fraction (HF-mrEF) is also possible but much rarer. It is usually due to structural heart diseases and/or diastolic dysfunction.
Time
- Chronic heart failure
- Dyspnoea - as fluid backs up into the lungs causing pulmonary oedema that impairs gaseous exchange.
- Orthopnoea - due to fluid backing up even more when lying down as there is gravitational force which drags it down.
- Paroxysmal nocturnal dyspnoea - shortness of breath that awakens the patient. It is relieved by sitting upright.
- Bibasal fine crackles - due to the fluid backup.
- Cardiac wheeze - aka cardiac asthma. It is not really asthma, it is just a type of coughing and wheezing that may occur with HF.
- Nocturnal cough
- Pink frothy sputum - this is because with the pressure from fluid buildup, the pulmonary vessels may have microhaemorrhages which cause blood to leak into the alveoli. Macrophages then invade into the alveoli to form haemosiderin laden macrophages which are also known as heart failure cells. However, as the blood loss isn’t very significant, we get a pinkish colour instead of the red seen in haemoptysis.
- Weight loss (cardiac cachexia) - however, this may be obscured by weight gained secondary to oedema.
- Oedema:
- Left-sided HF → pulmonary oedema.
- Right-sided HF
This is a slow progression of HF. Fluid backs up from the left side of the heart → the pulmonary veins → lungs. This is known as congestion and that is why it is sometimes referred to as congestive heart failure.
→ Peripheral oedema such as pitting oedema of the legs, sacral oedema after lying down.
→ It can also lead to back flow into the liver and spleen causing hepatosplenomegaly. In the liver this can then lead to what we refer to as cardiac cirrhosis (congestive hepatopathy) as we increase venous pressure and pressure in the hepatic sinusoids.
→ Raised JVP is also a common finding due to elevated pressure in the SVC causing back flow of blood through the internal jugular vein.
→ Ascites if fluid collects in the peritoneum.
We can classify the severity of chronic HF using the New York Heart Association (NYHA) classification:
Class | Severity | Physical activity limitation |
Class I | None | No limitation. Normal physical exercise does not cause unwarranted fatigue, dyspnoea, and palpitations. |
Class II | Mild | Slight limitation of physical activity. Comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea. |
Class III | Moderate | Marked limitation of physical activity. Comfortable at rest but less than ordinary activity results in symptoms. |
Class IV | Severe | Unable to carry out any physical activity without discomfort. Symptoms of HF are present at rest with increased discomfort with any physical activity. |
- Acute heart failure
- Cardiac ischaemia
- Viral myopathy
- Toxins
- Valvular disease
- Breathlessness
- Reduced exercise tolerance
- Oedema
- Fatigue
- ACS
- Hypertensive crisis
- Acute arrhythmia
- Valvular disease
- Cyanosis
- Tachycardia
- Elevated JVP
- Displaced apex beat
- Bibasal crackles
- Wheeze
- S3 heart sound
Acute HF exclusively refers to a new-onset acute HF or new-onset decompensation of chronic HF (acute-on-chronic). Decompensation is when there is failure of an organ to compensate for the functional overload resulting from a disease.
If it is acute HF without a history of HF then we call it de-novo acute HF. If it is acute HF with a history of HF then we can call it decompensated acute HF (more common).
Side
- Left ventricular failure (LVF)
- Aortic regurgitation - causes increased LV preload and increases the amount of blood that the left ventricle has to pump out and as a result it works harder → hypertrophy and eventually weakness of the muscle → ventricular failure.
- Aortic stenosis or hypertension - leads to increased LV afterload which also makes it more difficult for the heart to pump → ventricular failure.
- Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, bibasal fine crackles
- Poor tolerance to exercise
- Nocturnal cough
- Pink frothy sputum
- Nocturia
- Cold peripheries
- Weight loss
- Right ventricular failure (RVF)
- Pulmonary hypertension - causes an increased RV preload. The most common cause of this is portal hypertension, and the most common cause of portal hypertension is left-sided heart failure, so ultimately LHF is the most common cause of RHF.
- Pulmonary regurgitation and tricuspid regurgitation - both cause the heart to pump harder and eventually weaken which can then lead to RVF.
- Peripheral oedema
- Increased JVP
- Hepatomegaly
- Weight gain
LVF is more common than RVF. It may lead to pulmonary hypertension and pulmonary oedema. It also can then ultimately lead to right ventricular failure. As blood gets backed up in the pulmonary circuit, it is then unable to flow through our systemic circuit.
Output
- High-output heart failure (HOHF)
- Anaemia
- AV malformation
- Paget’s disease
- Pregnancy
- Thyrotoxicosis
- Thiamine deficiency (Wet Beri-Beri)
A rare type of HF in which the cardiac output is higher than normal due to an increased peripheral demand. This leads to a high venous return which will then cause systolic failure as time passes which then leads to a reduced CO eventually.
🔍 Investigations
Before doing any investigations, we need to take a full history and perform CVS exam.
For acute heart failure, an A-E approach should be taken.
- ⭐️ NT-proBNP - this is a pro-hormone secreted by cardiomyocytes (mainly in the left ventricular myocardium) in response to stretch. It is converted to BNP which promotes natriuresis to then decrease fluid volume and decrease stretch of the heart.
- 🏆 Transthoracic echo - to assess their function and exclude valve disease.
- ECG
- CXR
- Blood tests:
- FBC (anaemia and high lymphocytes are poor prognostic indicators), LFT (abdominal congestion), creatinine and blood urea nitrogen (BUN) [to rule out renal disease], HbA1C (DM has 3-5x increased risk of developing HF), TFT, lipid profile, ferritin and transferrin saturations (to assess for iron overload cardiomyopathy).
- Monitor urine output
- Take daily weights
Normal levels of BNP - <100pg/mL
Normal levels of NT-proBNP - <400mg/mL
If NT-proBNP is 400 - 2000 → refer to HF specialist + transthoracic echo within 6 weeks.
If NT-proBNP is >2000 → urgent specialist referral + transthoracic echo within 2 weeks.
💡 What affects BNP?
Increases BNP | Decreases BNP |
Left ventricular hypertrophy | Obesity |
Ischaemia | Diuretics |
Tachycardia | ACEIs |
Right ventricular overload | B-blockers |
Hypoxaemia | ARBs |
GFR < 60ml/min | Aldosterone antagonists |
Sepsis | |
COPD | |
Diabetes | |
Age >70 | |
Liver cirrhosis |
BNP has a good specificity for heart failure. Therefore, a positive proBNP is not diagnostic for heart failure, a negative proBNP is pretty good at ruling out heart failure.
🧰 Management
We will take a look at the management of acute heart failure first and then we will discuss the management of chronic heart failure:
Acute HF management
Acute heart failure is a medical emergency and the patient needs to be stabilised first and then post-stabilisation requires continuous management:
Stabilisation
- IV diuretics - such as furosemide or bumetanide, for example. with either bolus or infusion approaches. If they are already on a diuretic, then increase their dosage.
- Consider oxygen - aim to keep SpO2 (94-98%).
- Consider vasodilators - if there is concomitant myocardial ischaemia, severe hypertension, regurgitan aortic or mitral valve disease.
For stabilisation, do not routinely offer sodium nitroprusside (although NICE does indicate its usage for hypertensive emergencies and acute HF), opiates, nitrates, inotropes, vasopressors for HF.
Non-pharmacological management for stabilisation:
- Respiratory failure → CPAP to reduce work of breathing
- Hypotensive → difficult to manage as the IV diuretics can exacerbate the hypotension.
- If they have potential reversible cardiogenic shock and LVF → give inotropes such as dobutamine.
- If there is end-organ hypoperfusion or inotropes did not work → give vasopressors such as norepinephrine.
- Mechanical circulatory assistance Is also an option.
Management after stabilisation:
- Continue medication for HF:
- B-blockers - only stop B-blockers if HR is <50, or if there is 2º or 3º heart block, or shock.
- ACEIs/ARB + aldosterone antagonist
Chronic HF management
- 🥇 ACEI + B-blocker + lifestyle modification
- ACEI - ramipril, captopril, enalapril for example.
- B-blockers - bisoprolol, carvedilol, nebivolol are the licensed for HF.
- 🥈 Aldosterone antagonist
- Spirinolactone and eplirenone
- 🥉 Specialist medication should only be initiated by a specialist. These options include ivabradine, sacubitril/valsartan, hydralazine with nitrates, digoxin and cardiac resynchronisation therapy.:
- Ivabradine - a negative chronotrope that slows the heart rate by inhibiting the Na+ funny channels to slow the rate of SA node depolarisation thus improving myocardial perfusion and decreasing oxygen demand.
- NVHA II-IV with systolic dysfunction +
- In sinus rhythm with HR >75bpm +
- Already on ACEI, ß-blocker and aldosterone antagonist +
- LVEF <35%
- 🥉 Sacubitril-valsartan (entresto) is recommended only in people:
- NYHA II-IV symptoms +
- LVEF <35% +
- Who are already taking a stable dose of ACEIs or ARBs as it replaces them.
- 🥉 Hydralazine/nitrate
- Indicated especially in Afro-Caribbean patients with moderate-severe heart failure NYHA III-IV
- 🥉 Digoxin
- Recommended for worsening or severe heart failure with reduced EF as it is a positive inotrope.
- It's also useful in those with AF, as it is a neagtive chronotrope. It improves morbidity but worsens mortality.
- Loop diuretics can be used to relieve symptoms of congestion and fluid retention such as breathlessness and oedema.
- Offer influenza vaccine and pneumococcal vaccine
⚠️ Remember that ACEIs and aldosterone antagonists both cause hyperkalaemia and potassium level monitoring should be monitored.
Aldosterone antagonists and ACEIs can cause hyperkalaemia through blockage of angiotensin II (which prevents aldosterone secretion) or aldosterone receptor antagonism. Aldosterone causes the Na+/K+ antiporter to excrete potassium in exchange for sodium (and subsequently water). Thus by inhibiting aldosterone activity potassium is not excreted → hyperkalaemia.
⚠️ Stop ACEI 36 hours prior to starting sacubitril-valsartan as it can cause bradykinin accumulation.
- Refer to HF specialist
- Loop diuretics should be prescribed for fluid retention symptoms (low-medium dose):
- Bumetanide
- Furosemide