Heart Failure Flashcards
Definition
CO inadequate for bodies requirements, despite adequate filling pressure.
Stage 1- heart disease but no dyspnoea from normal activity.
Stage 2- dyspnoea on normal activity.
Stage 3- dypnoea on less than normal activity, which is limiting.
Stage 4- dyspnoea at rest, all activity causes discomfort.
Acute- new onset or decompensation. Pulmonary and/or peripheral oedema without peripheral hypoperfusion.
Chronic- gradual. Venous congestion common.
Aetiology
Heart cant produce same force for given filling pressure due to muscle weakness or death.
Systolic failure, decreased ejection fraction.
Diastolic failure, increased EF.
IHD primary cause.
LVF-
Abnormal LV systolic function (increased capacity, reduced output)- CAD, HTN, aortic stenosis, MV or AV regurg, dilated cardiomyopathy (infection, alcohol, pregnancy, chemo, anaemia, thyrotoxicosis , idiopathic), infection, toxins, infiltrative, arrhythmia, neuro hormonal activation, fibrosis/necrosis/proteinase.
Preserved LV systolic function- impaired compliance eg ischaemia, DM. Tachyarrhythmia. Restrictive cardiomyopathy. High CO. High afterload. Hypervolaemia. RFs- female, old, HTN, obesity, DM.
RVF-
LVF, pulmonary disease, P/MVD, PE, pulmonary HTN, L to R shunt, endocarditis, RV MI.
Neuro hormonal activation due to reduced renal perfusion causes cycle of increasing afterload- RAS, SNS, NPs, ADH, endothelin, PG, NO, TNF etc. Tries to compensate but bad LT.
Symptoms
- LVF- causes pulmonary oedema by increase pulmonary VP Dyspnoea Fatigue Orthopnoea PND Nocturnal cough pink frothy sputum Wheeze Nocturia Cold peripheries Weight loss Muscle wasting - RVF- (caused by LVF often, also pulmonary stenosis and lung disease) Peripheral oedema Ascites Nausea Anorexia Epistaxis Back and face pulsation
Signs
Framingham major- PND, crepitations, S3/4 gallop, cardiomegaly, increased central VP, weight loss, neck V distension, acute pulmonary oedema, hepatojugular reflux.
Minor- ankle oedema, dyspnoea on normal exertion, tachy, decreased VC, nocturnal cough, hepatomegaly, pleural effusion.
Other- exhaustion, cool peripheries, cyanosis, narrow PP, pulsus alternans, displaced apex beat, RV heave, MV/AV murmur, wheeze, functional mitral regurg.
RHF- pitting oedema, pleural effusion, ascites, hepatic enlargement, raised JVP.
BNP biomarker of increased GFR ad decreased Na reabsorption.
Differentials
COPD, asthma Cirrhosis Nephrotic syndrome Venous insufficiency PE ARDS Pneumonia Heroin OD MI Pneumothorax
Management
Lifestyle and RF management Then HF tx pathway: -ACEi or ARB decrease preload and afterload -BB decrease workload -restrict dietary Na. diuretics to remove fluid from tissues and lungs eg loop furosemide, with K sparing spironolactone if required. Maybe add thiazide. -cardiac resynchronisation if BBB -reavascularisation, MV surgery -aldosterone antagonists -ionotrope, VAD, transplant
Aspirin reduce risk further damage
Nitrates venodilation to reduce preload eg isosorbide dinitrate+ hydralazine if ACEi and ARB intolerant.
Digoxin glycoside positive ionotrope rarely used for HF LT
Surgery- transplant, assistive devices, valve, revascularisation.
Biventricular pm
Implantable defect
Beta agonists eg dobutamine for acute but reversible HF eg following surgery, NOT for LT tx.
Complications
Congestive HF
Diagnosis
Basal crackles S3/4 with gallop rhythm Echocardiogram for cause Raised JVP ECG for previous damage CXR for cardio thoracic ratio, and other causes of dyspnoea BNP in plasma reflects myocyte stretch (over 100ng/L indicates HF) UE
ACEi notes
-ACEi eg ramipril- upregulates RAS but aldosterone escape.
AE- dry cough, renal failure, hyperK, angioedma.
Contra indicated- pregnancy, renovascular HTN.
BB notes
Low dose for stable HF only. Risk precipitating acute HF Caution in PVD and DM Contra indicated in asthma, COPD, HB. AE- bradycardia, decreased glucose tolerance as prevents glycogen mobilisation, reduced concentration, raynauds.
Loop diuretic notes eg furosemide.
Blocks NCCK thick ascending limb
Action in HF by diuretic effect and vasodilation.
AE- increase uric acid gout, hypoK, glucose intolerance, increase LDL, ototoxicity, myalgia.
DDI- with aminoglycosides= oto and nephrotoxicity.
Thiazide eg bendroflumethazide notes
Block NaCl in DT
AE- high risk hypoK, hyperuricaemia, glucose intolerance, high LDL, erectile dysfunction. NOT work in renal failure.
DDI- loop or thiazide+ digoxin= hypoK= increase digoxin toxicity.
BB+ thiazide= hyperglycaemia, hyperlipid, hyperuricaemia.
Loop or thiazide+ steroid= more hypoK
Thiazide+ carbamazepine= more hypoNa.
Aldosterone antagonist notes eg spironolactone
K sparing Reduce eNac rebasorption in CD Also reduce Na/K ATPase Used sometimes in HF WITH loops. AE- hyperK, painful gynaecomastia, androegenic x reactivity.
Normal volumes
SV 75ml
ESV 75ml
EDV 150ml
Ejection fraction 50%
Explanation
- HF is when your heart doesnt pump enough blood around the body. The body needs blood with oxygen in order to hav energy to move and things, so without enough blood you feel tired and SOB.
- as this continues the heart can grow and the walls can get thinner, making its pumping action even less efficient. Gradually you are able to do less and less activity.
- lifestyle involves stopping things that could have made it happen in the first place. So dont smoke or drink. Follow an exercise regime as part of management and eat healthily.
- also drug treatment to help the heart have to work less hard. For example reducing pressure in the vessels the heart has to pump against, reducing the force with which the heart pumps, and reducing the overall fluid in the body.
