Heart Failure
Brief outline to heart failure outlining:
Epidemiology
Aetiologies
Pathophysiology
Neurohormonal effects of decreases cardiac output
The clinical findings
Investigation of suspected heart failure
Treatment of heart failure
Heart failure is a clinical syndrome (a collection of symptoms – what patient
complains of and signs – what you can see) caused by the inability of the heart to
supply sufficient blood flow to meet the body’s needs.
When the pump is not working, this may be because its weak, because the valves
are leaky or narrow or due to blockage in the rest of the system.
There are lots of classifications of heart failure, firstly it can be classified due to
impaired left ventricular ejection fraction, this measures the function of pumping.
It may not be the heart is weak, it could be that there is a valve issue or the heart is
very stiff.
There is also classification of left ventricular heart failure or right ventricular heart
failure. This is not a particularly good question as it is usually a combination of
both.
A very common classification system is the NYHA classification, this separates the
heart syndromes into degrees of severity. There are four classes.
Class one is when you have a damaged heart but no symptoms/signs
Class four is when you are completely breathless even at rest and probably on ICU
with very severe heart failure.
Between are moderate levels of severity.
UK Heart Failure Epidemiology
The prevalence is 1-2% and rising (1 million)
It is estimated there will be a 50% increase in patients by 2030
It is currently the commonest cause of emergency admission for those over 65,
consequently there is a high readmission rate. As a result heart failure takes up
1.8% of total NHS health care costs. It also takes up 70% of the cost of hospital
admissions.
Below the age of 65, heart failure is very rare, but above this age its prevalence
increases rapidly. Survival of patients with heart failure is improving.
Heart specialist nurses are also very important in looking after patients.
Anatomy revision –
, The LV pumps blood into the aorta, if there are any problems on the left side of the
heart be it: left ventricular weakness, aortic stenosis or mitral regurgitation it will
result in a back pressure into the LA. The LA pressure will go up and this eventually
feeds back into the lungs, so you get leakage of fluid into the alveoli = pulmonary
oedema.
The RV pumps blood into the pulmonary artery, and RA drains blood from SVC and
IVC. When there is RV failure commonly due to pulmonary hypertension, you get
increased pressure in RA which feeds back down IVC and SVC and you get oedema
starting in legs working its way up. You get ascities, a raised JVP.
Cardiac cycle =
1. Atrial contraction -> P
2. Ventricular contraction -> just after QRS
3. Passive filling during ventricular relaxation
Physiology
Cardiac Output = CO = SV x HR
SV = Volume pumped out in each heart beat
^ can work out by looking at End diastolic volume and end systolic volume and
subtracting the latter from the former.
Preload = End diastolic ventricular pressure that stretches the ventricle to its
largest volume prior to contraction
Frank-Starling Law
As you increase the filling of the ventricle (EDV) the contractility increases and you
get a larger stroke volume. This pretty much a linear relationship, however
Brief outline to heart failure outlining:
Epidemiology
Aetiologies
Pathophysiology
Neurohormonal effects of decreases cardiac output
The clinical findings
Investigation of suspected heart failure
Treatment of heart failure
Heart failure is a clinical syndrome (a collection of symptoms – what patient
complains of and signs – what you can see) caused by the inability of the heart to
supply sufficient blood flow to meet the body’s needs.
When the pump is not working, this may be because its weak, because the valves
are leaky or narrow or due to blockage in the rest of the system.
There are lots of classifications of heart failure, firstly it can be classified due to
impaired left ventricular ejection fraction, this measures the function of pumping.
It may not be the heart is weak, it could be that there is a valve issue or the heart is
very stiff.
There is also classification of left ventricular heart failure or right ventricular heart
failure. This is not a particularly good question as it is usually a combination of
both.
A very common classification system is the NYHA classification, this separates the
heart syndromes into degrees of severity. There are four classes.
Class one is when you have a damaged heart but no symptoms/signs
Class four is when you are completely breathless even at rest and probably on ICU
with very severe heart failure.
Between are moderate levels of severity.
UK Heart Failure Epidemiology
The prevalence is 1-2% and rising (1 million)
It is estimated there will be a 50% increase in patients by 2030
It is currently the commonest cause of emergency admission for those over 65,
consequently there is a high readmission rate. As a result heart failure takes up
1.8% of total NHS health care costs. It also takes up 70% of the cost of hospital
admissions.
Below the age of 65, heart failure is very rare, but above this age its prevalence
increases rapidly. Survival of patients with heart failure is improving.
Heart specialist nurses are also very important in looking after patients.
Anatomy revision –
, The LV pumps blood into the aorta, if there are any problems on the left side of the
heart be it: left ventricular weakness, aortic stenosis or mitral regurgitation it will
result in a back pressure into the LA. The LA pressure will go up and this eventually
feeds back into the lungs, so you get leakage of fluid into the alveoli = pulmonary
oedema.
The RV pumps blood into the pulmonary artery, and RA drains blood from SVC and
IVC. When there is RV failure commonly due to pulmonary hypertension, you get
increased pressure in RA which feeds back down IVC and SVC and you get oedema
starting in legs working its way up. You get ascities, a raised JVP.
Cardiac cycle =
1. Atrial contraction -> P
2. Ventricular contraction -> just after QRS
3. Passive filling during ventricular relaxation
Physiology
Cardiac Output = CO = SV x HR
SV = Volume pumped out in each heart beat
^ can work out by looking at End diastolic volume and end systolic volume and
subtracting the latter from the former.
Preload = End diastolic ventricular pressure that stretches the ventricle to its
largest volume prior to contraction
Frank-Starling Law
As you increase the filling of the ventricle (EDV) the contractility increases and you
get a larger stroke volume. This pretty much a linear relationship, however
