Heart failure topic Flashcards
Definition of heart failure
Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired
- Having heart failure means that for some reason, your heart is
not pumping blood around the body as well as it used to.
How does blood flow through the heart?
- Oxygen-poor blood from the body returns to the right atrium of the heart. Blood from the upper body returns through the superior vena cava. Blood from the lower body returns through the inferior vena cava.
- As the atrium is filled with blood, it contracts, the tricuspid valve opens and blood is pumped into the right ventricle
- When the right ventricle is filled, the tricuspid valve closes to prevent backflow of blood into the atrium.
- The right ventricle contracts, pulmonary valve opens and blood is pumped into the pulmonary artery and into your lungs
- The pulmonary valve closes to prevent backflow into the ventricles
- Oxygen rich blood from the lungs returns through the pulmonary veins to the left atrium of the heart. As the left atrium is filled with blood, it contracts, the mitral valve opens and blood is pumped into the left ventricle of your heart.
- This happens at the same time as the right atrium pumps blood into the right ventricle on the other side of the heart.
- As the left ventricle is full, the mitral valve closes, the left ventricle contracts and the aortic valve opens, the left ventricle contracts and oxygen- rich blood is pumped to the aorta to reach all parts of the body.
- This happens at the same time as the right ventricle pumps blood into the pulmonary artery on the other side of the heart.
- The aortic valve closes to prevent backflow back into the heart.
- Meanwhile the atria have filled with blood and the cycle repeats again.
What are the causes of heart failure?
- ischaemic heart disease
- hypertension
- valve disease
- diabetes
- cardiomyopathies
- alcohol, drugs and pregnancy
what does ejection fraction mean?
a measure of how well the heart is pumping. a measure of the amount of blood pumped out of the ventricle compared to the total amount of blood in the ventricle each time that the heart contracts
what does a low ejection fraction mean?
the lower the ejection fraction, the worse the pumping ability of the heart. a normal EJ is around 60-70%. a person with HF their EJ is around 30%
what does left ventricular systolic dysfunction mean
the heart contracts in the systole mode of the heart and if this is impaired, then this will be associated with reduced ejection fraction and reduced emptying of the heart.
what is heart failure with preserved ejection fraction
– Impaired LV relaxation (diastolic)
– Preserved ejection fraction- impaired relaxation of the heart itself. So when you measure the ejection fraction of the heart it will appear normal
• Common in HTN particularly in the elderly (females) and other comorbidities such as AF, chronic obstructive airways disease, diabetes etc
• In these patients they may have all the signs and symptoms of heart failure but when you measure their ejection fraction, it is within normal range. This is known as heat failure with preserved ejection fraction
what are the precipitants of heart failure
• Non- compliance * – Medication- diuretics to manage the fluid overload, they may have stopped taking their disease modifying agents in patients with HfrEF – Fluid intake • Infection – E.g. Chest ( HR and demand on heart) • Arrhythmias – Tachyarrhythmia's (e.g. AF) –loss of atrial component to cardiac output – Bradyarrhythmias – rate too slow to provide enough cardiac output • XS Etoh / fluid – Fluid / Cardiomyopathy • Anaemia • Check thyroid and renal function
what are the signs of HF
• Hypotension • Cold peripheries • Raised JVP • 3rd heart sound • Lung crackles/ wheeze • Fluid retention – L-lung- becomes congested – R-peripheral /ascites
Definition of heart failure
the inability of the heart to meet the circulatory demands.
OR
The ability to do so only at abnormally high cardiac filling pressures. If you increase the amount of blood returning to the heart then the stroke volume and the cardiac output will increase. However for a given stroke volume, a failing heart requires much more blood to be returned to the ventricles than a healthy heart.
what are the two classifications of heart failure
HFPED stands for heart failure with preserved with ejection fraction and HFREF stands for heart failure with reduced ejection fraction
what is heart failure with preserved ejection fraction?
In patients who have heart failure with preserved ejection fraction have a normal ejection fraction range between 60-70%. they have heart failure because the volume of the ventricles is reduced. This is because the left ventricles muscles cells have become larger and there is marked fibrosis.
because the chamber the left ventricle is smaller the ventricle will hold less blood even though the ejection fraction is preserved
what is heart failure with reduced ejection fraction?
with reduced fraction, the cross section of the ventricles is different. the ventricles are enlarged because lots of blood returning to the ventricles. but there is a dysfunction in the ability of the heart to contract . therefore there is less than 35% of blood returning to the ventricles
what factors predisposes people to have reduced ejection fraction
being male, having a heart attack previously, having cardiac problems
what factors predisposes people to have preserved ejection fraction
aging, prolonged untreated high blood pressure and diabetes
what is the frank starling curve?
describes how the heart is able to move blood through the body in a regulated way by pumping out as much blood as it receives.
the law states that increased filling of the ventricles results in a greater contraction force and therefore a higher cardiac output
in Hf the mechanism fails as the ventricles is filled with blood to the point where the heart muscles contractions become less efficient.
describe the intrinsic mechanism
This mechanism is important in allowing the heart to increase stroke volume in response to an increase in diastolic volume is based around the sensitivity of this protein Troponin C to calcium Muscles require calcium to contract and the calcium is involved in the contractile process because it binds to troponin C and when they bind, it pulls the protein tropomyosin out of the way because there is a change in troponin C and it pulls the myosin binding site out of the way
The actin and the myosin can interact and the muscle can contract
Calcium binding causes a confirmation or change which pulls tropomyosin away from the myosin binding site
As we increase the diastolic volume, troponin c is able to move this tropomyosin protein at increasingly lower concentrations of calcium. So by stretching the muscle fibres, sensitises troponin c to calcium. At far lower concentrations of intracellular calcium, the tropomyosin will be removed allowing contraction to occur.
- The whole process is sensitised by blood returning and stretching the ventricles
ANOTHER EXPLANTION
• At rest, when end-diastolic volume is relatively low, there is very little stretch on the muscle fibres in the ventricle and therefore sarcomere length is relatively short and has a high degree of overlap of the myosin and actin filaments in the heart myocytes
• If this heart muscle cell wanted to contract, it can only move a relatively small distance
• As we increase stroke volume, sarcomere length increases and we have a much larger distance that the muscle fibres can contract over
• The more blood that returns to the heart, the more it stretches the sarcomere and therefore the more contraction is possible, allowing the heart to pump out the same amount of blood that enters the heart
• Eventually, these muscle fibres get stretched far too much and therefore the degree of the overlap of the actin and the myosin will not be optimal and you will start to damage the fibres and they will start to lose their efficiency – so the stroke volume will eventually start to decline
ANOTHER EXPLANATION
At the beginning of the cardiac contraction cycle, calcium ions enter cardiomyocytes via L-type calcium channels, leading to further calcium release from the sarcoplasmic reticulum (SR). High concentrations of Ca2+ causes calcium binding to Troponin C, moving Troponin I out of the way of the actin-myosin binding site, allowing for an interaction between the two. The interaction between actin & myosin leads to force generation (muscle contraction). When the conc of Ca2+ drops, troponin returns to its standard conformation.
Actin-myosin filaments stretch when the heart fills with blood. The more these fibres stretch, the contraction of the heart becomes stronger, increasing stroke volume. However, if the fibres stretch too far, they break, and the heart fails to contract. With greater stretch of the fibres, Troponin becomes more sensitive to calcium; his means a smaller concentration of calcium illicit a response. the length of contraction & relaxation is longer, but the force of contraction is reduced. This means that the volume of blood that fills the right ventricle increases, but the stroke volume decreases. This leads to accumulation of blood, increasing the risk of thrombosis, pulmonary congestion a transient ischaemic event (TIA).
Describe extrinsic mechanism?
RAS, sympathetic nervous system and natriuretic system
Sign and symptoms of heart failure?
- Elevated pulmonary capillary wedge pressure is a marker to see how well gaseous exchange occurs.
- Crackles due to fluid build-up in the lungs.
- Wheezing and capillaries can be ruptured In the lung leading to blood in the sputum
- The patient is likely to be breathing faster than normal because of the lack of oxygen into the body. They can become restless and confused because of poor perfusion to the brain.
- They may have a faster heart rate than normal because the heart is beating harder because body is not getting the oxygen and nutrients it needs and also because the cardiac output is reduced and this will activate the barro receptors to drive the sympathetic system to cause tachycardia.
causes of heart failure
- acute MI and associated cardiovascular risk factors (obesity, diabetes, cigarette smoking)
- hypertension
- valve disease
- cardiomyopathies (genetic)
- toxins (alcohol, cytotoxic; doxorubicin)
- viruses/bacteria (e.g. viral myocarditis HIV and SLE; systemic lupus erythematosus)
- Arrhythmias (AF)
- Right-sided failure: Chronic pulmonary problems (anything that will increase pulmonary blood pressure). If there is not enough oxygen in a tissue because of a mucus in the airway or because of a tumour, this will disrupt gaseous exchange. The bloods vessels in the airway clamp off or constrict so the blood supply to that damaged are is reduced and blood going to the lungs is redistributed to parts of the lung that are healthy and where gas exchange is happening naturally. But because you have constricted some parts of the vasculature, there is an increase in blood pressure in the lungs leading to damage to the RHS of the heart.
how do you measure raised JVP
Vertical height from the sternal angle to the top of the pulsating column of blood in the internal jugular vein. 45 degrees. Measuring how high that jugular venous pulse is above the sternal angle. Around 6 cm in healthy and in HF is about 4cm
what are the initial steps to diagnose HF?
signs and symptoms
- 2D doppler Echocardiography (ejection fraction <35%)
- raised JVP
- BNP levels >100pg/ml suggests heart failure. Levels >400pg/ml poor prognosis
describe the sympathetic response to heart failure?
in the face of reduced cardiac output, the arterial baroreceptors located in the aortic arch and carotid sinus will sense changes in the blood pressure, leading to a release in norepinephrine and adrenaline that in turn stimulate the beta-1 receptors located in the SA node, myocardium and the ventricular conduction. stimulation of these receptors increases the heart rate and cardiac contractility leading to a greater stroke volume. when the heart rate and the stroke volume increase, the cardiac output will also increase to maintain adequate blood pressure and therefore perfusion of vital organs
Describe the activation of renin angiotensin aldosterone system?
- In addition to the Renin-angiotensin system also gets activated when there is a decrease in cardiac output.
- Cardiac output is reduced which leads to a reduction in renal blood flow(barro-receptors in the renal artery) which will stimulate the release of renin from the juxtaglomerular cells.
- Renin will start to activate the RAS which leads to the production of angiotensin 2
- Angiotensin 2 can constrict veins through the action on the AT-1 receptors which is linked to the production of IP3 on the smooth muscles which drives calcium release which will cause the muscles to contract and the veins to constrict. This will increase preload and increase stroke volume and cardiac output.
- The RAS system through the actions of angiotensin 2 on the adrenal gland will release aldosterone. Aldosterone works on the distal convoluted tubules cells to increase the expression of ENaC in the luminal membrane and sodium-potassium ATPase in the apical membrane and as a consequence there is more salt and water retention.
- This will increase blood volume which will increase venous return and increase cardiac output
- Angiotensin 2 will also increase blood pressure by constricting arteries in the same way it constricts veins through the activation of AT-1 receptors and this will increase after load
- The direct effects of aldosterone and angiotensin and the effects of increased after load will lead to the remodelling of the heart by increasing the size of the heart muscle fibres and also there is an increase in the connective tissue that is present in the heart. This remodelling makes the heart less efficient.
How does beta blockers work for the treatment of HF?
works by binding to the beta-1 receptors in the heart and blocking the action of norepinephrine therefore reducing heart rate and contractility thereby decreasing cardiac output and blood pressure. a decreased heart rate allows diastolic filling time so the stroke volume is not reduced.
- also via blocking the beta-1 receptors of the renal juxtaglomerular complex, certain beta blockers can also decrease the renin secretion, therefore reducing the severity of angiotensin 2 induced vasoconstriction as well as aldosterone
