Heart failure Flashcards
What is normal circulation?
The body has 2 circulations and each pump is linked to the vessels in front and behind.
therefore what happens on one side will affect the other
What is cardiac output?
volume of blood leaving either side of the heart per minute - inadequate in heart failure
What does stroke volume depend on?
depends on preload, afterload, and contractility
contractility- the intrinsic muscle strength
These three factors will affect cardiac output as well.
Preload- venous return (will be inadequate in heart failure)
After load- resistance (will be excessive in heard failure which will compromise the ejection fraction).
How do you calucluate cardiac output?
CO = SV x HR
WHat is the ejection fraction?
Stroke volume/ end diastolic volume
(as a %)
>55% normal, 45-54% mildly reduced, 30-44% moderately reduced, <30% severely reduced
Stroke volume= end diastolic volume - end systolic volume
How do you measure the ejection fraction?
transthoracic echocardiogram
This is a chest ultrasound
The data you need to use to calculate the ejection fraction comes up on the side.
What is heart failure?
clinical syndrome caused by inability of heart to supply blood to tissues. Insufficient to meet metabolic needs, or achieved at expense of filling pressures; causes inadequate organ perfusion and congestion in lungs/legs; often compensate with tachycardia.
The heart cannot keep up with the demand.
Why is the heart in a state of tachycardia when it is in heart failure?
It is a compensation mechanism to maintain the cardiac output.
Remember CO= SV x HR
(taccy increases the HR)
What is dilated cardiac myopathy?
Thinning of the ventricular walls- they are therefore less able to produce a sufficient pressure to pump.
What are the different types of heart failue?
- Left vs Right heart failure
- Chronic vs acute heart failure
- Heart failure with reduced ejection fraction (HFrEF) vs Heart failure with preserved ejection fraction (HFpEF)
Left vs right sided heart failure
Left: to do with an issue with the left ventricle. It is a filling or ejection issue. There is congestion. Blood backs up into the lungs ( through the pulmonary veins)- it does not go through the heart. There is increased pressure in the lungs (pulmonary hypertension). Hydrostatic pressure increases in the vessels and fluid leaks out causing oedema. Symptoms: coughing, wheezing, breathlessness
This increases the load on the right ventricle (pulmonary artery) as it needs to contract against a higher load.
Right: similar thing an issue with the right ventricle so that it is not able to fill/ ejection issue. Increased afterload (resistance) because of the pulmonary hypertension. Secondary to left heart failure.
Acute vs chronic heart failure
Chronic- slow onset. Due to infection, pulmonary embolism, myocradial infarction or surgery.
Acute: same as chronic but rapid onset
Reserved vs preserved ejection fraction
Reduced: abnormal systolic function. Ventricle is unable to contract and pump blood into the aorta and pulmonary artery. Can be due to think ventricle walls, valve issue (stenosis) or damage/destruction of ventricular myocytes. As the systolic volume increases, the stroke volume decreases. Even though there is a increased HR, there is a reduced CO and ejection fraction. Weaker ejection leads to higher diastolic pressure.
Preserved: diastolic dysfunction. The ventricles contract normally but there is a filling issue as the ventricles are more stiff, impaired relaxation or impaired filling. There is a reduced end diastolic volume. Hypertrophies- smaller amount of space for blood fill up. Becuase EDV is inherently reduced, the reduced stroke volume is masked when looking at ejection fraction. it is preserved.
Epidemiology of heart failure
Number of heart failure tends to rise above 60 and peaks around 75.
It will tail away again as people die.
What are the causes of heart failure?
- Valve disease- mitral/tricuspid (AV) problems mean ventricles cannot fill with blood, pulmonary/aortic valve means cannot expel blood (systolic issue)
- IHD (ischaemic heart disease)- narrowing of coronary arteries deprive the heart of oxygen. Less of the heart has to form the same function- it has to work harder and needs more oxygen- this just makes things worse.
- Myocardial infarction- significant occlusion of the coronary arteries leads to death of the heart muscle.
- Hypertension- increases afterload to much work harder (need more oxygen which not supplied so die), so muscle grows inward (reducing space for filling). Ventricles will hypertrophy CO decreases
- Dilated cardiomyopathy- systolic dysfunction- dilated LV reduced generatable pressure, reducing ejection
- Hypertrophic cardioyopathy- ventricles hypertrophy inwards, increasing thickness of LV. Reduced internal volume and impedes filling.
Majority of heart failure is caused by?
Coronary heart disease- occulsion of the coronary arteries
Clinical features of heart disease
Patient: breathlessness, fatigue, weight loss, anorexia, orthopnoea
Clinical- tachycardia, pitting oedema, increased jugular venous pressure, ascites (Increased fluid in peritoneal cavity)
Investigations- chest x-ray will see an enlarged heart, ECG to measure ejection fraction
Hallmark signs of heart failure
- Raised jugular venous pressure- increased pressure in the right side of the heart therefore pressure backs up into systemic veins (especially jugular vein) JVP rises and there is pulsation in the neck
- Pitting oedema- fluid accumulation in tissues (lower extremities), leads to a pitting effect when physically depressed) WIll be visible fro a short period
- Ascites- fluid build up in the peritoneal cavity
What is B-type natriuretic peptide (BNP)?
natriuresis- sodium excretion
BNP is released from the ventricular myocytes in response to stretch. It is a marker for heart failure.
If it is greater than 100 for people under 70 years of age, there is indication that they have heart failure. (greater than 300 for over 70)
BNP causes vasodilation of vessels, and it will reduce BP 9reduced aldosterone secretion), reducing afterload and ventricles don’t have to work as hard.
It also reduces aldosterone secretion- reduces sodium absorbtion, therefore reduce in water absorption less fluid accumulation. It does this by inhibiting renin secretion (RAAS).
All of this results in reduced extracellular fluid
And a reduced pressure :)
Lifestyle changes to reduced risk of HF?
- Weight loss
- Stop smoking
- Less alcohol
- More exercise
Medication for HF
First line: ACE Inhibitors (reduce afterload and block aldosterone production) and Beta Blockers (bisoprolol/carvedilol NOT atenolol/metoprolol - reduce HR but don’t change afterload). Beta blockers slow the heart down so it requires less energy and oxygen to function.
Diuretics can also lead to fluid loss to reduce BP- it is also an aldosterone antagonist.
Second line: ivabradine (if HR>70) to cause vasodilation. It also inhibits the enzyme that breaks down BNP.
Sacubitril (inhibits enzyme to break down BNP)/valsartan (stops aldosterone being produced)
Last thing- cardiac resynchronisation therapy for more efficient contraction
The timeline for medication with HF
what do diuretics and ace inhibitors do?
They reduce the load so the heart has to put less effort into pumping
Why are beta blockers good?
They slow the heart rate down, reducing the speed saves energy makes it easier
Non-pharmacological treatments
- Fluid control- haemofiltration, peritoneal dialysis and haemodialysis
- Devices- intra-aortic balloon pumping, resynchronisation, total artificial heart (TAD)
- Surgical- coronary artery bypass graft, valve surgery, transplantation
What is the law of LaPlace?
It’s to do with wall stress.
Pressure x Radius / 2 x wall thickness
If the wall thickness increases, the wall stress decreases
This is seen in the compensatory mechanism of ventricular hypertrophy. Reduces wall stress in response to acute load, but then leads to dilated cardiomyopathy as ventricle volume has reduced - increasing wall stress; thin wall can no longer contract with enough force to eject blood. Its not a good cycle. The hypertrophy is only a SHORT TERM SOLUTION.
Neural and hormonal changes
There is a benefical physiological and pathophysiological response.
Benefical to do with BNP- allows for vasodiation and lowers BP, decreases aldosterone levels. BNP is good stuff.
Pathophysiological response0 reduced renal perfusion as the heart is beating less effectively. This activates RAAS which will increase BP.
Living with heart failure
- Breathlessness
- Fatigue
This is becuase the heart is damaged and is a less effective pump.
There is marked neurohormonal activation
Quality of life is poor
Life expectancy is reduced.
What is the NYHA classifcation of HF?
New York Heart association. Functional. HF based on patient physical limitations.
Progression of HF
Becomes more severe till death, and coronary events (e.g. MI) speeds up process of dying
