Heart Failure

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Heart failure (HF) is an abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolizing tissues (ESC 2012).
HF is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood (ACCF/AHA 2013):

It describes the clinical syndrome that heart develops when the heart cannot maintain an adequate cardiac output, or can do so at the expense of elevated filling pressure.

Terminology related to left ventricular ejection fraction

HFrEF and HFpE

The incidence of heart failure increases with advancing age.
US - Average annual incidence is 2-4% between 35 and 64 years, and 10% in patients over 65 years.
Heart failure accounts for 5% of admissions to hospital medical wards with over 100,000 each year in the UK. The cost of managing heart failure in the UK exceeds £600 million.
The prognosis of heart failure has improved over the past 10 years, but the mortality rate is still high with approximately 50% of patients dead at 5 years.
Black men have the highest incidence rate (1000 person-years) for heart failure and the greatest five-year mortality rate when compared to whites. White women represent the lowest incidence.

All patients with HF, regardless of their symptoms, have a poor prognosis.

Within 3 years, 34% of NYHA class I and II patients, and 42% of NYHA class III and IV patients die.

Patients with HF often suffer from co-morbid conditions:

Co-morbidities frequently accompany HF, with 74% of patients in the ESC Heart Failure Pilot Study reporting at least one co-morbid condition.

Common comorbidities of HF

Hypertension - Three quarters of all HF patients have pre-existing hypertension.
Coronary heart disease
Valvular disease - Congenital or acquired - infective, degenerative
Infections
Cardiomyopathies:
- Idiopathic cardiomyopathy
- Alcoholic cardiomyopathy
- Toxin-related cardiomyopathy e.g. adriamycin
- Post-partum cardiomyopathy
- Hypertrophic obstructive cardiomyopathy
- Tachyarrhythmia-induced cardiomyopathy
Infiltrative disorders (e.g. amyloidosis)
Congenital heart disease
Pericardial disease
Hyperkinetic states:
- Anemia
- Arterio-venous fistula
- Beriberi
Abuse of drugs such as Alcohol, cocaine, and chemotherapy (trastuzamab, imatinib)
Hyperdynamic Circulation

Anaemia (SEVERE)
Thyrotoxicosis
Haemochromatosis
Piaget's disease

Tricuspid Incompetence
Arrhythmias

Atrial fibrillation
Bradycardia (complete heart block, the sinus syndrome)

Pericardial Disease

Constrictive pericarditis
Pericardial effusion

Infections

Chagas’ disease
Viral myocarditis

Connective Tissue Disease

such as systemic lupus erythematosus

NOTE: Heart damage from obstructive sleep apnoea (a condition of sleep wherein disordered breathing overlaps with obesity, hypertension, and/or diabetes) is regarded as an independent cause of heart failure.

CO = HR X SV
BP = CO X TPR

CO = perfusion

Cardiac output is a function of:

Preload (the volume and pressure of blood in the ventricle at the end of diastole or venous return)
Afterload (the load or resistance against which the ventricle pumps)
Myocardial Contractility (this initial three form the basis of Starling's law)
Heart rate

Compensatory Mechanisms

Increasing cardiac output via the Frank–Starling mechanism
Increasing ventricular volume and wall thickness through ventricular remodeling

Frank-Starling Mechanism

"Stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant."

Persistent neurohormonal imbalance results in continued disease progression

Decline in systolic function leads to activation of three major neurohormonal systems

Angiotensin II - Role in BP/ Organ Damage

Cardiac Abnormalities

Ventricular dilatation
Myocyte hypertrophy
Increase collagen synthesis
Altered myocardial gene expression (due to hemodynamic overload)

The structural cardiac abnormalities that occur in patients with hypertension, including LV hypertrophy (LVH) or MI, contribute to a higher number of adverse CV outcomes. Initially, concentric LV hypertrophy compensates for pressure overload and normalizes systolic wall stress. This adaptive hypertrophy is accompanied by structural modifications of the cardiac muscle, including alterations in gene expression, loss of cardiomyocytes, defective vascular development, and fibrosis. Thus, the compensatory response transits from HF to progressive contractile dysfunction.

Within the heart, failure-induced changes have been documented in Ca²⁺ handling:

In transcription factors that lead to hypertrophy and fibrosis
In mitochondrial function which is critical for energy production in the overworked heart

Remodeling

Term applied to dilatation (other than that due to passive stretch) and other slow structural changes that occur in the stressed myocardium.
It may lead to proliferation of connective tissue cell as well as abnormal myocytes.
Ultimately, myocytes in the failing heart die at a faster rate through apoptosis.

Laplace’s Law

"Laplace’s law as applied to vessels states that 'transluminal pressure varies inversely with vessel radius and is directly proportional to tension that develops in the vessel walls.' This means that the pressure pushes against the wall making them to stretch = tension, as the size of the vessel decreases, the tension in the wall decreases."

The NP system- ANP and BNP are formed by cleavage of precursor molecules

The heart is an endocrine organ, releasing NPs in response to mechanical stretch, which counter some effects of the RAAS

Effects of the NP system- NPs mediate a wide range of physiological effects via NP receptors

Symptoms

Cough & Breathlessness - Quantify breathlessness
Easy fatigability (Reduced exercise tolerance), dyspnea on exertion
Orthopnea
Paroxysmal Nocturnal Dyspnea
Leg swelling - Characteristic
Abdominal swelling

Signs

General examination: Pedal edema
CVS: Tachycardia, Elevated jugular venous pressure, S3, murmurs
Abdomen: Tender hepatomegaly, splenomegaly, features of pericardial effusion
Hepato-jugular reflux, ascites
RS: Tachypnea, features of pleural effusion, pulmonary edema

HFrEF vs HFpEF
Systolic vs Diastolic HF
High output vs Low output HF
Forward vs Backward HF

Framingham’s Criteria:

Major Criteria:

Paroxysmal nocturnal dyspnea
Weight loss of 4.5kg in 5 days in response to treatment
Neck vein distention
Acute pulmonary edema
Hepato-jugular reflux
3rd heart sound gallop
Central venous pressure >16cm water
Circulation time of 25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy

Minor criteria:

Nocturnal cough
Dyspnea in ordinary exertion
A decrease in vital capacity by one-third the maximal value recorded
Pleural effusion
Tachycardia
Hepatomegaly
Bilateral ankle edema

Diagnosis of heart failure
Type of heart failure
HFrEF	Requires 3 conditions to be satisfied:
	1. Symptoms typical of HF
	2. Signs typical of HF*
	3. Reduced LVEF
HFpEF
	1. Symptoms and signs typical of HF
	2. Elevated BNP or NT-proBNP
	3. Normal LVEF and LV not dilated
	4. Relevant structural heart disease (LV hypertrophy/LA enlargement) and/or diastolic dysfunction

NYHA Functional Class
NYHA Class	Functional Capacity
I	Patient without limitation of physical activity
II	Patient with slight limitation of physical activity, in which ordinary physical activity leads to fatigue, palpitation, dyspnea or angina pain; they are comfortable at rest
III	Patient with marked limitation of physical activity, in which less than ordinary activity results in fatigue, palpitation, dyspnea, or angina pain; they are comfortable at rest
IV	Patient who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or the anginal syndrome even at rest; the patient's discomfort increases if any physical activity is undertaken

ACC/AHA Stages

STAGE A

High risk for HF but without structural heart disease or symptoms of HF.

Examples: Patients with hypertension, atherosclerotic disease, diabetes, obesity, etc.

STAGE B

Structural heart disease without symptoms or signs of heart failure.

Examples: Patients with previous MI, LV remodeling, asymptomatic valvular disease.

STAGE C

Structural heart disease with prior or current heart failure.

Examples: Patients with known structural heart disease.

STAGE D

Refractory heart failure requiring specialized interventions.

Examples: Patients who have marked symptoms at rest despite maximal medical therapy.

Classification of HF: ACC/AHA stage vs NYHA functional class
ACC/AHA HF stage	NYHA functional class
A At high risk of HF but without structural heart disease or symptoms	None
B Structural disease but without HF	I Asymptomatic
C Structural disease with prior or current HF symptoms	II Symptomatic witd moderate exertion
C Structural disease with prior or current HF symptoms	III Symptomatic witd minimal exertion
D Refractory HF requiring specialized interventions	IV Symptomatic at rest

Initial diagnosis of HF

INVESTIGATIONS include:

Echocardiography
Chest X-ray
ECG

Other tests, such as radionuclide ventriculography, MRI, computed tomography may also be carried out to provide information on the nature and severity of cardiac abnormality.