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Heart Failure (Pathophysiology: (SNS: Carotid sinus detected decreased CO …
Heart Failure
Classification:
Stage 3: Clinical heart failure
Stage 4: Advanced heart failure requiring intervention e.g. pacemakers, transplant
Stage 2: Presence of structural disease e.g. decreased ejection fraction but asymptomatic
Stage 1: Risk factors with no structural abnormalities e.. DM
American College of Cardiology/American Heart Association classification
Long term management:
Other drugs to consider: Digoxin (increases contractility (blocks Na/K pump --> blocks Na/Ca pump--> no Ca leaves cell --> increased intracellular Ca) and vagal tone)
Diuretic (frusemide): Loop (stops reabsoprtion in the ascending loop) +/- thiazide (prevents reabsoprtion in the DCT) is preferred, spironalactone later on
Non pharmacological: 2 g of salt per day, 2L of water per day, daily weights and a 2kg difference in 2 consecutive days warrants medical review, vaccinations, smoking cessation, exercise, ETOH reduction, healthy diet, control of risk factors/comorbidities
Cardio selective beta-blocker (carvidelol (a1), bisoprolol, metoprolol): decreases HR and afterload, further interrupting the neurohormonal response
Drugs to avoid: antiarrythmics, CCB (non-dihydropyradines), NSAIDs, metformin, glitazones, steroids
ACE/ARB (enalapril): interrupting the neurohormal response
Pathophysiology:
SNS:
Carotid sinus detected decreased CO -->Increased HR and contractility also increases RAAS stimulation
RAAS:
Decreased CO sensed by kidneys --> Juxtaglomerular cells increase renin production --> converts angiotensinogen to angiotensin 1 --> angiotensin 2 (via ACE) --> increase water reabsorption at the kidneys, (via aldosterone) increased thirst, vasoconstriction and SNS activation
Neuro hormonal mechanisms
ADH:
Decreased CO is sensed by the hypothalamus --> posterior pituitary secretes ADH --> increase water reabsorption in the DCT and collecting duct
ANP/BNP:
ANP is released from the atria in response to increased atrial stretch early in disease course. With chronic heart failure, high ventricular filling pressure --> ventricular cells secreting both ANP and BNP. Role: To oppose SNS and RAAS
Chronic neurohormonal activation --> chronic excessive preload and afterload --> remodelling of heart with loss of myocardial cells, fibrosis and LVH
Frank starling: increase preload (stretch) --> increased contractility. In HF, chronic dilation and hypertrophy --> inability of myocytes to contract normally --> failure of mechanism
Investigations:
CXR: alveolar oedema, bat wing sign, cardiomegaly, dilated upper lobe vessels, effusion
Echo: valvular disease, pulmonary hypertrophy and distinguish systolic vs diastolic heart failure
Bloods: FBC, trops, BNP, UEC, LFT, TFT, lipids
BNP: 30-80 (possible HF, consider other causes e.g. renal failure), >80 (heart failure)
Hypervolaemic, hyponatraemia; hypokalaemia (meds)
Elevated AST/ALT (passive liver congestion)
ECG: LVH, RVH, BBB's, all low voltage (poor contractility)
Types:
Systolic/Diastolic
Systolic: IHD, DCMO
Diastolic: ventricular hypertrophy, HOCM, HTN
Left/Right
Left: IHD
Right: Secondary to left, cor pulmonale, IHD, CMO
Output
High (increased metabolic demand): Hyperthyroidism,
Low (based on SV and HR): HTN, hypertrophy, regurg, HOCM, brady/tachycardias
Clinical Features:
Risk Factors: Female, HTN, DM, ETOH, obesity, smoking, age, Hx of IHD/valvulardisease/AFib/thyroid dysfunction, CKD, OSA, FHx
LHF sx: PND, orthopnoea, SOB +/- exertional, cough, pink frothy sputum, nocturia, wheeze, crackles, loud P2
Common sx: tachycardia, tachypnoea, fatigue, cyanosis, confusion, chest pain, S3, S4, cool peripheries
RHF: ankle oedema, sacral oedema, abdominal fullness, ascites, raised JVP, hepato/spleomegaly, facial engorgement, nausea, anorexia, right ventricular heave, hepatojugular reflex
Definition:
Failure of the heart to generate enough cardiac output to meet the minimum metabolic demands of the body tissues despite normal filling pressure
Acute decompensation:
Causes: systemic infection, IHD, acute or progressive valve disease, myocarditis, poorly controlled HTN
Characterised by acute SOB, with elevated filling pressures (more preload) +/- pulmonary oedema
Management: Loop diuretics (for fluid overload), morphine (relieve anxiety/discomfort), nitrates (if SBP >100), oxygen (+/- CPAP), position the patient upright; if in AF: add digoxin; if low BP: call ICU
Dromotropy: conductivity of AV node
Chronotropy: HR
Inotropy: contractility
SE of digoxin: sinus bradycardia/arrest, hyperkalaemia --> cardiac toxicity; renally excreted (careful in kidney disease), long half life