Flashcards in Heart Failure Deck (15):
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.
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.
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.
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.
- LVF- causes pulmonary oedema by increase pulmonary VP
Nocturnal cough pink frothy sputum
- RVF- (caused by LVF often, also pulmonary stenosis and lung disease)
Back and face pulsation
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.
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
-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.
Beta agonists eg dobutamine for acute but reversible HF eg following surgery, NOT for LT tx.
S3/4 with gallop rhythm
Echocardiogram for cause
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)
-ACEi eg ramipril- upregulates RAS but aldosterone escape.
AE- dry cough, renal failure, hyperK, angioedma.
Contra indicated- pregnancy, renovascular HTN.
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
Reduce eNac rebasorption in CD
Also reduce Na/K ATPase
Used sometimes in HF WITH loops.
AE- hyperK, painful gynaecomastia, androegenic x reactivity.
Ejection fraction 50%