Heart Failure
Original Editors - Students from Glasgow Caledonian University's Cardiorespiratory Therapeutics Project.
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Definition/Description[edit | edit source]
Heart failure is a complex clinical syndrome of symptoms and signs that suggest impairment of the heart as a pump supporting physiological circulationCite error: Invalid <ref> tag; name cannot be a simple integer. Use a descriptive title. It occurs when the heart becomes less efficient at pumping blood around the body at the right pressure in order to sustain bodily functions to a high standard. It commonly is a result of myocardial muscle dysfunction or loss, and is characterised by left ventricle dilation or hypertrophy, elevated cardiac filling pressure and/or inadequate peripheral oxygen delivery, at rest or during stress.
The condition can be acute, transient, or chronic:
- Acute is the first presentation of heart failure or a sudden onset of heart failure
- Transient is when heart failure is recurrent or episodic
- Chronic is heart failure that is persistent, worsening, or decompensate. It usually offset at first by compensatory mechanisms to maintain tissue perfusion, but eventually cardiac function declines and symptoms develop.
Heart failure can be classified into three different types:
Left Ventricular Failure (LVF): this is the most common form of heart failure, gradually pushing up pressure in the left atrium and pulmonary vascular system. The resulting pulmonary hypertension may force fluid into the alveoli creating a pulmonary oedema. This can cause compensatory mechanisms:
- Fast acting neural systems increase sympathetic acting, raising heart rate and myocardial contractility
- The slower response of the retin-antiogtensin mechanism promotes the retention of sodium and water by the kidney, increasing preload and encouraging myocardium to contract
The compensatory mechanisms raise the workload of the left ventricle further because angiotensin is an arterial vasoconstrictor and increases the afterload. Other factors that can increase the workload of the left ventricle are increased volume load as in aortic valve regurgitation, or increased resistance to flow such as with systemic hypertension.
Right Ventricle Failure (RVF): this generally occurs secondary to cardiopulmonary disorders such as pulmonary hypertension, right ventricle infraction, congenital heart disease, pulmonary embolism or COPD. It is usually irreversible unless the ventricles is underloaded e.g. by lung transplant for pulmonary hypertension. Enlargement of the right ventricle that has resulted from lung disease is referred to as cor pulmonale and is caused by hypoxic vasoconstriction and pulmonary hypertension.
Congestive Cardiac Failure (CCF): combination of LVF and RVF with congestion in the pulmonary and systemic circulations
Helpful Terminology:
- Stroke volume: volume of blood ejected by the ventricle in one contraction, usually 70ml
- End diastolic volume: volume of blood in the ventricle at the end of filling, just before it contracts, usually 120ml
- Ejection fraction: stroke volume expressed as a percentage of end diastolic volume, normally >55%
- Systolic heart failure: reduced or weakened pumping action of the heart, with ejection fraction <55%
- Diastolic heart failure: low compliance of myocardium, but with normal contraction and normal ejection fraction
- Preload: degree of stretch applied to the ventricle before contraction
- Afterload: load that the ventricle must overcome to eject blood
Epidemiology[edit | edit source]
It is estimated that around 800,000 people in the UK suffer from heart failure, a number which will continue to rise due to an ageing population, improved survival rates following a heart attack, and more effective treatments. The prevalence of heart failure doubles with each decade. The British Heart Foundation statistics estimate the incidence and prevalence of heart failure in the UK, using the Clinical Practice Research data, show that both rise steeply with age. The British Heart Foundation reports that 0.9% of men and 0.7% of women in the UK suffer from heart failure, rising to 13.1% of men and 11.9% of women aged over 75 years old.
Heart failure is the leading cause of hospitalisation in the elderly population and accounts for one million inpatient bed-days. Survival rates for heart failure patients are variable, dependent on the age and severity of disease of the patient, and the quality of care they receive. Outcomes are consistently poor for patients who receive suboptimal care, but input from heart failure specialists and prescription of evidence-based heart failure therapies have a significant impact on prognosis and life expectancy. The National Heart Failure Audit has reported around one in ten patients dying in hospital, and of those who survive between one-quarter and one-third dying within the year of their admission. However these mortality rates are beginning to reduce, reflecting more consistent implementation of guidelines for recommended practice.
Aetiology[edit | edit source]
It is rare for heart failure to be derived from one cause, it is normally multi-factorial. A number of health conditions increase your chances of developing heart failure but in general it is causes by an excess workload placed on the heart. Excess workload on the heart involves on or both ventricles and is thought to relate to oxidative stress and inflammation which leads to one or more of the following:
- Impaired contractibility of the myocardium e.g. after acute coronary syndromes
- Increased afterload e.g. with hypertension or aortic valve stenosis
- Increased preload e.g. with mitral or aortic valve regurgitation
In addition anaemia, overactive thyroid gland (hyperthyroidism), pulmonary hypertension, diabetes, chronic renal impairment, chronic obstructive pulmonary disease (COPD), and asthma are reported as potential causes of heart failure.
Below is a table from The British Society for Heart Failure outlining the medical history of patients admitted to hospital with heart failure.
Pathophysiology[edit | edit source]
In response to increased load, the left ventricular myocardium hypertrophies.The greater size and number of myocytes raises myocardial oxygen demand and increases diffusion distance for oxygen. Some muscel fibres become ischaemic, leading to pathcy fibrosis, stiffness and reduced contractability. The workload may cause the ventricle to stretch and dilate, leading to further force being required to maintain cardiac output. Systolic failure is by reduced ejection fraction and diastolic failure is by reduced end-diastolic volume. Metabolic effects include loss of bone mineralisation, skeletal muscel and fat.
The stiffness and reduced contractibility push up end-diastolic pressure, which is transmitted back along the pulmonary veins to the pulmonary capillaries, which causes fluid to be forced into the interstitial spaces and, if severe, into the alveoli, causing pulmonary oedema. The increased pulmonary vascular pressure raises the afterload of the right ventricle, in the same way as chronic systemic hypertension raises the afterload of the left ventricle. Hypertrophy, pathcy fibrosis, stiffness and reduced contractibility of the righht ventricular myocardium then ensuses, as with left ventricle, and congestive cardiac failure develops.
Investigations[edit | edit source]
This may well include any investigations used to gain a diagnosis or that you might need to gain information about your patient assessment.
Clinical Manifestations[edit | edit source]
Clinical manifestations (the signs and symptoms your patient may well present to you on an examination) ensure you relate this back to the underlying pathophysiology.
Physiotherapy and Other Management[edit | edit source]
Physiotherapy and other management. Other health professionals will be treating your patient. What is their input?
Prevention[edit | edit source]
Brief consideration of how this pathology could be prevented and the physiotherapy role in health promotion in relation to prevention of disease or disease progression.
Resources
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add appropriate resources here
Recent Related Research (from Pubmed)[edit | edit source]
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References[edit | edit source]
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