Heart Failure Handout

Heart Failure
Inability of the heart to pump adequate
amounts of blood to meet the body's
metabolic demands
Remember not a diagnosis it’s a
SYNDROME, need to treat underlying
o AF/complete heart block
Hyperdynamic circulation
o Anaemia, pagets diease, thyroid
Pericardial disease
o Constructive pericarditis, pericardial
Alcohol, Drugs, Chemotherapy
Right heart problems
o Pulmonary hypertension
o PE
o Right ventricle infarct
Inability of the left ventricle to pump adequate
amount of blood leading to pulmonary circulation
congestion and pulmonary oedema. Usually results
in RHF due to pulmonary hypertension.
Inability of the right ventricle to pump adequate
amount of blood leading to systemic venous
congestion, therefore peripheral oedema and
hepatic congestion and tenderness
Low output: heart failure resulting from reduced
cardiac output
High Output: heart failure that occurs in normal or
high cardiac output due to metabolic demand and
supply mismatch, either due to reduced blood
oxygen carrying capacity e.g. anaemia increase
body metabolic demand e.g. thyrotoxicosis
Acute: aute onset of symptom presentation usually
due to acute event i.e. MI, persistent arrhythmia,
mechanical event (ruptured valve, ventricular
NB :
CO = SV x HR
Starlings curve: the greater the volume of blood
entering the heart during diastole (end diastole
volume) the greater the volume of blood ejected
during systolic contraction (stroke volume)
Normal physiological changes
 Ventricular dilation
 Myocyte hypertrophy
 Increased ANP secretion
 Sympathetic stimulation
 Peripheral vasoconstriction
Compensatory Mechanisms
Normal heart: If CO low, venous return will increase
increasing (preload) allowing increased end diastolic
volume, returning CO back to normal
Mild myocardial depression: CO maintained but
increased venous pressure and sinus tachycardia,
this however reduces ejection fraction
Moderate Myocardial Dysfunction: CO only
maintains as above but unable to maintain CO
during exercise, increasing venous pressure in
peripheries leads to symptoms
Chornic: slow symptoms presentation usually due
to slow progressive underlying disease
Severe Heart Failure: CO not maintained at rest
despite increased venous pressure and tachycardia
Acute on Chronic: acute deterioration of a chronic
condition, usually following an acute event.
CXR – Aleveloar oedema, Kerly B lines
(septal lines) Cardiomegaly, Upper lobe
Diversion, pleural Effusion
3 main: ischemic heart disease 70%, non ischemic
dilated cardiomyopathy 25%, hypertension 5%
ECG – ischeamia, bundle branch block,
L/RVH, pericardial disease, arrhythmias
Other causes:
Bloods – FBC, U&Es, LFTs, thyroid function
tests, BNP, NTpro BP
ECHO – LV function (ejection fraction),
systolic and diastole function, valve disease,
ventricular wall thickness
Valve disease
o Mitral/aortic/tricuspid
Congenital heart disease
Lung function tests – to exclude other
causes of breathlessness if main symptom
Angiography – assess extent of IHD
Symptom control
Patient education and self care
Low level exercise – encourage the use of cardiac
Low salt diet
Smoking cessation
Alcohol reduction
Vaccination as increase risk of infections – flu and
Monitor weight
Dobutamine, think about when haemodynamically
unstable with acute LVF, hypotension to support
myocardial function, dopamine to enhance renal
perfusion and prevent renal failure. Digoxin may
benefit patients with severe heart failure in spite of
therapy with treatments above and with rapid AF.
GTN or ISMN help to reduce preload and afterload,
but with chornic use, patient can develop tolerance.
Increase risk of stroke and thromboemboli in severe
heart failure, may benefit from Warfarin use
especially with co-existing AF.
Long term Care
IV furosemide start with 40mg and titre up if
necessary, may need higher doses in chronic kidney
disease patients, possible infusions if slow progress,
sit up high flow oxygen, if deteriorating may need
CPAP. May benefit from morphine IV 2.5-10mg do
not offer routinely. May need GTN infusion only if
systolic BP >100, do not offer routinely. When
stabilised, consider switching to bumetanide if
furosemide not working well. Thiazides no longer
recommended due to effects on renal function.
Inform GP’s of changes to medication and future
Involve specialists for treatment of underlying
Involve specialist cardiac heart failure nurses
Discuss driving: especially if HGV’s
Refer to cardiac Rehabilitation
measurements of urine, daily weight, daily renal
function checks.
Prognostic control
ACE inhibitors
Trials have shown to improve symptoms and
prognosis. Start low dose 2.5mg ramipril/lisionpril,
check U&E’s in 1-2 weeks time and titre up if
tolerated 2-4 weeks later to max to 10mg. Good in
EF <40 % even if not symptomatic. If side effects
persist use Angiotensin II receptor antagonists
Beta – blocker
E.g. bisoprolol initiated in confirmed left systolic
dysfunction after diruetics and ACE-I therapy. Start
1.25mg and titre up to 10mg depending on heart
Aldosterone antagonists
E.g. spironolactone, 30% reduction in all cause
mortality when added to above treatement in
moderate to severe heart failure. Start at 25mg
Muscle under perfusion causing muscle weakness
and atrophy causing fatigue, exercise intolerance
and dyspnoea
Increase risk of thromboembolism and stroke
development. This is due to blood stasis,
arrhythmias commonly AF a nd existing atheromas.
Arrhythmias usually results from increase in fibrous
tissue deposition during tissue remodeling postinsults. Arrhythmias themselves lead to HF therefore
they worsen the situation when they exist.
Ventricular Tachycardia (VT) is common in
advanced HF, which may evolve into ventricular
arrhythmias and cardiac arrest. Beta-blockers
treatments are used to minimize these VT, hence
sudden death
Increased risks of infections that can initiate an
acute-on-chronic event