Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Heart Failure Definition: Clinical syndrome resulting from inability to maintain adequate cardiac output. Incidence: 1-2%>/=65 years, 10%>/=75 years Pathophysiology: Inadequate cardiac output stimulates compensatory mechanisms which are initially beneficial but then become maladaptive… Neurohormonal activation - increase vasoconstrictors- provoke salt + water retention – increase cardiac afterload – decrease LV emptying and depress CO further – greater neuroendocrine activation etc Ventricular dilatation – impaired systolic function + fluid retention increases ventricular volume – mechanically inefficient, if energy supply limited e.g coronary disease – further contractile failure and neuroendocrine activation Left Heart Failure: Breathlessness- worse when lying down (orthopnoea), especially in middle of night (paroxysmal nocturnal dyspnoea) Tacchypnoea, tachycardia, 3rd heart sound (gallop rhythm) Bibasilar inspiratory pulmonary crepitations- if severe cyanosis, pink frothy sputum, extensive crepitations Right heart failure: Fluid retention in legs and in severe cases ascites Increased JVP + peripheral oedema Chronic heart failure: Cardiomegaly and secondary mitral/tricuspid regurg Skeletal muscle loss (cardiac cachexia) Classification: Acute heart failure- largely synonymous with LH failure, results from sudden failure to maintain CO, insufficient time for compensatory mechanisms to develop and pulmonary oedema predominates. Chronic heart failure- CO declines gradually, features relating to compensatory mechanisms dominate, CHF results in secondary pulmonary hypertension + RH failure = congestive cardiac failure Aetiology: LH failure inadequate LV filling (mitral stenosis, LVH, pericardial constriction) pressure overload (aortic stenosis, hypertension) volume overload (aortic/mitral regurg) high output (beri beri, thyrotoxicosis) LV muscle disease (MI, cardiomyopathy, myocarditis) RH failure Any cause of LH failure Pulmonary hypertension (PE, lung disease) ASD Provoking/exacerbating factors- arrhythmias, drug issues (non compliance or fluid retaining eg NSAIDs), anaemia, infection Investigations: Bedside tests- ECG (old MI, LVH, arrhythmias) Blood tests - BNP Electrolytes, renal function, FBC for anaemia, TFTs Imaging - CXR= Alveolar oedema, kerley B lines, Cardiomegaly, Diversion to upper lobes, pleural Effusion Echo (transthoracic or transoesophageal)– LV function, ejection fraction, regional wall abnormalities, valvular disease Special tests – nuclear isotope scanning, cardiac catheterisation Management: Conservative Smoking cessation Alcohol cessation Weight loss/ diet and exercise Cardiac rehabilitation Medical Acute- sit up, high flow oxygen, ABC, furosemide, GTN infusion Chronic – ACEi/ARB, beta blockers, aldosterone antagonist, digoxin See NICE guidelines algorithms on page 4 and 6 http://www.nice.org.uk/nicemedia/live/13099/50526/50526.pdf Surgical Cardiac resynchronisation therapy (CRT) ICD Transplant Complications: Thromboembolism- DVT/PE esp in severe CHF, risk reduced by warfarin AF- complicates CHF, deteriorates, rate control + warfarin Progressive pump failure- may respond to increasing doses of diuretics, heart transplant may be an option in some patients Ventricular arrhythmias- common and may cause syncope or sudden death (25-50% of deaths in CHF), Tx amiodarone, implantable defibrillators