heart failure Flashcards
preload
stretch that the cardiac muscle fibres at the end of diastole
- reflects the volume of blood in the ventricles
- determined by venous return (the amount of blood returning to the heart)
- and the ventricular compliance - the ability of the ventricle to stretch and accommodate blood
baso blood volume
afterload
- resistance the heart must overcome to eject blood during systole
- related to the pressure in the aorta and systemic vasculature
like trying to push open a heavy door
define heart failure
inability of the heart to deliver blood at a rate of commensure with the requirements of the matabolism, tissues, despite normal or increased filling pressures
epidemiology
common
costly
disabling
deadly
phenotypes of HF (5)
- HR w reduced ejection fraction
- HR w preserved ejection fraction
other:
- HF due to severe vulvar disease
- HF w pulmonary hypertension
- HF due to PV systolic dysfunction
new york heart association classification
class I - asymptomatic
class II - slight limitation - mild HF
class III - marked limitation - symptomatically moderate HF
class IV - inability to carry out everyday activities without physical dyscomfort - symptomatically severe HF
ways to classify HF
- acute or chronic
- left and right sided
- systolic or diastolic
what ejection fracture counts as abnormal?
below 50%
in chronic HF, how does the body compensate for the decreased blood around the body?
- baroreceptors sense lower BP - inc RAAS - inc water retention and vasoconstriction to inc BP to compensate for low volume
- inc in SNS - release of adrenaline to inc heart rate and contractility
this will then fail
- cardiac remodelling - hypertrophy, dilation of chambers - this can make the walls thinner
right sided HF pathology
- cant pump blood towards the lungs very well
- backs up from where it came from - the systemic circulation
- this leads to systemic congestion and oedema
right sided HF causes?
any increase in pulmonary pressure makes it harder for the right side of the heart to beat
- left-sided HF
- chronic lung disease
- Pulm hypertension
- R sided MI
- COPD
left-sided HR pathology
- cant pump blood towards the body
- backs up onto lungs
- pulmonary congestion and oedema
left sided HR causes
- causes prevent blood flow
- CAD
- hypertension
- MI
- valve disease
acute HF pathology
- rapid onset of symptoms
- often life threatening
- no time for the body to compensate eg RAAS and SNS and cardiac remodelling
acute HF causes
anything sudden:
- STEMI / NSTEMI
- hypertensive crisis
- severe tachycardia or bradycardia
- pulmonary embolism
- severe infection / sepsis
- acute valve dysfunction
acute HF symtpoms
- severe dyspnea
- pink frothy sputum
- hypoxia and cyanosis
- severe hypertension and cardiogenic shock
- rapid weight gain from fluid overload
acute HF treatment
emergency:
- diuretics
- oxygen
- vasodilator
- inotropes
chronic HF pathology
- develops gradually over time allowing the body to compensate
- bc its gradual, symptoms are persistant
- RAAS and SNS and cardiac remodelling occurs but this can acc worsen HF and will eventually fail
chronic HF causes
- CAD
- long term hypertension
- dilated cardiomyopathy - weak, enlarged heart muscle
- valvar HD
- diabetes, obesity, alcohol abuse
chronic HF symptoms
- fatigue and exersize intolerance
- dyspnoea
- orthopneoa and PND
- peripheral oedema and weight gain
- ascites
chronic HF treatments
- lifestyle changes
- beta blockers
- ace inhibitors
- diuretics
- ARNI
- implantable devices
signs of HF
Tachycardia
Tachypnoea (raised respiratory rate)
Hypertension
Murmurs (indicating valvular disease)
3rd heart sound
Bilateral basal crackles (indicating pulmonary oedema)
Raised jugular venous pressure (caused by a backlog on the right side of the heart)
Peripheral oedema
risk factors of HF
Age (65+)
Smoking
Obesity
Previous MI
Male sex
diagnostic tests
Blood Test (High NT-proBNP)
ECG
Chest x-ray (see image for results)
ECHO – analyse chamber dimensions (GOLD STANDARD)
features on xray
A - Alveolar Bat Wing
B - B lines
C - Cardiomegaly
D - Dilated upper vessels
E - Effusion (pleural)
first line treatment
First Line
ABAL mnemonic
A- Ace inhibitor
B- Beta blocker
A – Aldosterone antagonist (only given when A+B don’t control the symptoms)
L- Loop diuretics
dont give ace inhibitors to those w valvar disease
check U&Es because drugs can cause hyperalkaemia
when should you not give someone aceI?
if they have valvular disease
when should you check patients U&E during treatment
diuretics
ace
aldosyterone antagonists
Blood results with heart failure? (2)
BNP (brain natriuretic peptide) = key marker
High >400ug/ml
Level correlates with extent of damage
So more severe heart failure = higher bnp
It is released from stressed ventricles in response to increase mechanical stress
*might also measure NT ProBNP (inactive BNP) and levels are 5x higher so increase of >2000 ug/ml
what are some things that can increase cardiac work making HF worse?
-obesity
-htn
-pregnancy
-hyperthyroid
-arrhythmias
Management of cor pulmonale? (3) (RHF due to pulm abnormality)
Management involves treating the symptoms and underlying cause
Long term oxygen therapy often used
Prognosis is poor unless reversible underlying cause
Normal physiology of heart/Frank Starling Law
Normally- increased preload= increased afterload= increased cardiac output (frank starling law)
Other symptoms of heart failure (5)
-orthopnoea (dyspnoea worse lying flat, pillows)
-increased JVP
-bibasal crackles (pul oedema)
-hypotensive
-tachycardic
Respiratory causes of cor pulmonale? (5)
-COPD is most common cause
-pulmonary embolism
-interstitial lung disease
-cystic fibrosis
-primary pulmonary hypertension
Natriuretic peptides
reduce fluid volume
induce vasodilation
take pressure off the heart
which blood marker is elevated in HF?
Brain natriuretic peptide (BNP)
what drugs do you NOT give?
CCB
