Heart failure Flashcards
What is dilated cardiomyopathy?
thinner ventricle wall less able to produce enough pressure to generate good CO
What is inadequate in heart failure?
CO = volume of blood leaving either side of heart per minute (LV) CO = SV x HR
heart cannot keep up with metabolic demand of tissues
inadequate perfusion of organs (brain, liver, kidney)
causes congestion on lungs and legs (fluid build up)
What does SV depend on?
preload - reduced with reduced VR
afterload - compromised with excessive TPR
contractility
How to measure EF?
transthoracic echocardiogram EF = SV/EDV x 100% normal >55% mildly reduced 45-54% moderately 30-44% severely <30%
Describe biventricular heart failure?
LEFT
associated with LV ejection or filling issue
blood backs up into lungs and causes congestion/pulmonary hypertension
increase pressure causes pulmonary oedema
–> respiratory symptoms of breathlessness, cough, wheeze, dizzy, cyanosis
RIGHT RV increased afterload of pulmonary circulation due to pulmonary hypertension so RV must work harder need more O2 that is not present heart failure secondary to LV
What is the difference between acute and chronic heart failure>
ACUTE
rapid onset
similar symptoms to CHF but more severe onset and worsening
typically caused by viral myocarditis
CHRONIC
slow onset
due to infection, PE, surgery, MI
What is HFrEF?
abnormal systolic function with impaired ventricular contraction despite increase HR, reduced CO
increase diastolic pressure due to weak ejection
EF DECREASE, ESV INCREASE, EDV NORMAL/INCREASE
weakness due to damage/destruction of ventricular myocytes
- dilated cardiomyopathy, aortic stenosis, valve issue
What is HFpEF?
abnormal diastolic function with normal ventricular contraction but increased ventricular stiffness, impaired relaxation/filling
EDV reduced, EF same, SV reduced
due to hypertrophy (inwards to less space for blood in chambers)
How does HF change with age?
number of cases rises >60
peaks at 75-84 before decreasing again before death
What are the causes of heart failure?
valve disease - hard mitral/tricuspid reduces ven filling, hard aortic/pulm reduced ejection and leads to congestion
ischaemic heart disease - narrow coronary arteries lead to ischaemia, worsen HF
MI - death of cardiac myocytes due to occlusion
hypertension - increase afterload, ventricle work harder, hypertrophy and decrease CO
dilated cardiomyopathy - thinner ven wall, cannot generate pressures to force blood out, decrease CO
hypertrophic cardiomyopathy - decrease ven volume, decrease filling and CO
What are most cases the cause of HF?
34% - coronary artery disease
15% - cardiomyopathy/hypertension
12% - valve disease
10% - neoplasia, myocarditis
What are the neural and hormonal changes as a result of heart failure?
BNP released when ventricular myocytes stretch that leads to vasodilation, decrease BP, decrease hypertrophy, decrease aldosterone levels
BUT
heart beats less effectively
decrease renal perfusion that activates RAAS to increase aldosterone production
- to increase vasoconstriction and increase BP, increase Na retention and fluid retention
- increase SNS to increase vasospasm, HR and cardiac fibrosis
What are signs to the patient of heart failure?
exertional breathlessness fatigue orthopnoea (breathless on lying) paroxysmal nocturnal dyspnoea anorexia SOB weight loss
What are clinical signs of heart failure?
tachycardia (compensation for low CO)
reduce pulse volume
pitting oedema (RHF - blood backs up in SVC in legs)
increase JVP
hepatomegaly
ascites (fluid accumulated in peritoneal cavity)
RHF = peripheral oedema LHF = breathlessness
What investigations are done for HF?
X ray - enlarged heart echocardiogram - measure EF ambulatory ECG - arrhythmia exercise test angiogram BNP - B type natiuretic peptide BNP (natiuresis is Na excretion from myocytes responding to stretch) HF = BNP >100pg/ml (<70y) or >300pg/ml (>70y)
