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Flashcards in Heart Failure Deck (15):
1

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.

2

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.

3

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

4

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.

5

Differentials

COPD, asthma
Cirrhosis
Nephrotic syndrome
Venous insufficiency
PE
ARDS
Pneumonia
Heroin OD
MI
Pneumothorax

6

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.

7

Complications

Congestive HF

8

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

9

ACEi notes

-ACEi eg ramipril- upregulates RAS but aldosterone escape.
AE- dry cough, renal failure, hyperK, angioedma.
Contra indicated- pregnancy, renovascular HTN.

10

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.

11

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.

12

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.

13

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.

14

Normal volumes

SV 75ml
ESV 75ml
EDV 150ml
Ejection fraction 50%

15

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.