Heart Failure Definition 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 diagnosis Types o AF/complete heart block Hyperdynamic circulation o Anaemia, pagets diease, thyroid disease Pericardial disease o Constructive pericarditis, pericardial effusion Alcohol, Drugs, Chemotherapy Right heart problems o Pulmonary hypertension o PE o Right ventricle infarct Pathophysiology Left 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. Right Inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion, therefore peripheral oedema and hepatic congestion and tenderness Terms 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 aneurysm) NB : CO = SV x HR MAP = CO x TPR 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. Investigations 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 Causes Valve disease o Mitral/aortic/tricuspid Congenital heart disease o ASD/VSD Arrhythmias Lung function tests – to exclude other causes of breathlessness if main symptom Angiography – assess extent of IHD Symptom control Intropes Management General Patient education and self care Low level exercise – encourage the use of cardiac rehabilitation Low salt diet Smoking cessation Alcohol reduction Vaccination as increase risk of infections – flu and pneumonccal 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. Nitrates GTN or ISMN help to reduce preload and afterload, but with chornic use, patient can develop tolerance. Anticoagulation Medical Increase risk of stroke and thromboemboli in severe heart failure, may benefit from Warfarin use especially with co-existing AF. Acute 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 considerations Involve specialists for treatment of underlying causes Involve specialist cardiac heart failure nurses Discuss driving: especially if HGV’s Refer to cardiac Rehabilitation Basic: fluid restriction, daily input/output measurements of urine, daily weight, daily renal function checks. Chronic 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 rate 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 Complications 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