Risk factors of HF
ACS especially MI, hypertension, DM, valvular diseases, smoking, obesity, thyroid diseases
Differentials for dyspnoea with/without chest pain
HF/ HF exacerbation
(PND better as slow fluid buildup, orthopnoea, nocturia, ankle oedema )
COPD exacerbation
Anaemia
(iron-deficiency, chronic disease, B12 deficiency)
Lung cancer
Pneumothorax
(young male, chest pain on inspiration, acute onset)
What is ejection fraction, afterload, preload?
Ejection fraction: percentage of the blood leaving the heart each time it contracts
Afterload/squeeze: the amount of pressure the heart must contract against to eject blood after systole
Preload/stretch: the amount of sarcomere stretches at the end of ventricular filling during diastole
What is the pathology of LHF?
MI → dec. aerobic respiration → dec. ATP → dec. function of myocardium → dec. contractility → inc. amount of blood retained in heart after systole → over time, inc. preload → ventricular remodelling → left ventricular dilation (eccentric hypertrophy)
What is the pathology of RHF?
thin walls –> accept a range of volume BUT sensitive to pressure
secondary to LHF due to inc afterload
cor pulmonale due to COPD
Symptoms
RHF vs LHF
LHF –> pulmonary circulation
orthopnoea
RHF --> systematic circulation peripheral oedema abdominal discomfort PND (fluid from peripheral oedema is drained via veins causing congestion)
Signs
RHF vs LHF
LHF
basal crackles
displaced apex beat
RHF peripheral oedema raised JVP ascites hepatosplenomegaly
Signs/symptoms for HF in general
Symptoms
- Fatigue, dizziness
- Impaired urine output (renal hypoperfusion)
Signs
- Hypotension, tachycardia
- Cool/cyanosed peripheries
- Slow capillary refill
Precipitant of symptomatic exacerbations
HEART FAILED HYPERTENSION endocarditis anaemia rheumatic heart disease Thyrotoxicosis FAILURE TO TAKE MED arrhythmia Infarction/ischaemia/infection Lung problems (COPE, pneumonia) Endocrine DIETARY: salt intake, fluid overload
What is systolic HFrEF?
Pathology?
Inability of ventricle to contract normally –> dec CO, SV –> dec EF <50%
- impairment of ventricular contractility: ACS
- inc afterload: hypertension, AS
What is diastolic HFpEF?
Pathology?
Inability of ventricle to relax and fill normally –> inc filling pressure EF >50%
- impaired ventricular relaxation/filling
ageing, tamponade
Diagnostic features of HFrEF
S3 (post S2) –> rapid ventricular filling in systole
displaced apex beat
dull percussion note over bases –> pleural effusion
investigations
- CXR: cardiothoracic ratio > 0.5
- previous infarcts, deformed valves
Diagnostic features of HFpEF
S4 (before S1): hard contraction of atrium in diastole
normal size heart on CXR
Complications of HF
- Sudden cardiac death (1/3 of death in HF)
- Anaemia
Chronic kidney failure: hypoperfusion –> drop in EPO production –> few RBC - Cardiorenal syndrome
Systolic: reduced CO hypoperfusion prerenal kidney failure - Arrhythmia
- Stroke (Blood stasis in dilated chambers)
- Hepatic congestions (receive 25% of CO –> hepatic hypoxia)
Inc ALT/AST, inc bilirubin, abdo discomfort
Investigations for HF
CBE
- Anaemia (resulting from hypoperfusion of kidney)
- Infection that exacerbates HF decompensation
Cardiac markers (TO RULE OUT MI) - Troponin T
ECG
- Previous MI –> infarcted area shows pathological Q wave, inverted T
- LV hypertrophy –> left axis deviation
EUC
- Sodium: dilutional hyponatremia
- Potassium: HyperK (impaired renal), hypoK (diuretics)
- GFR
LFT
- Inc ALT/AST, inc bilirubin –> RHF
Chest X-ray
- Pulmonary oedema (bat wings)
- Kerley B line (interstitial oedema) –> short linear markings at lung bases
- Cardiomegaly
- Dilated pulmonary vessels
- Effusions (blunting of costo-diaphragmatic recess)
- Thickening of fissures
Echo
systolic/diastolic function, valves, wall thickness, wall motion abnormalities
- transthoracic
transesophageal (invasive, emergency situations such as aortic dissection)
Approach for diagnosing HF
initial assessment
- EUC, LFT, CBE, ECG, CXR
HF diagnosed
echocardiogram to confirm HFrEF, HFpEF, valvular diseases
Management of acute pulmonary oedema as HF exacerbation
ABCDE + POND
Position: sit up, positive airway
- reduce V/Q mismatch, assist work of breathing
Oxygen (92-96% target)
Nitrates
- Smooth muscle relaxation –> venous dilation –> preload reduction
Diuretics (frusemide)
- Evidence of fluid overload pulmonary oedema
Behavioural management of HF
- Physical activity: physio, walking, light weightlifting
Avoid exercise preventing normal talking - Diet changes
Reduce sodium intake (3g max/day)
High fibre diet: constipation is common due to gut hypoperfusion - Fluid management: fluid overload causes acute decompensation
- Weight diary: every morning, same time and same clothes
Restricted to 1.5L per day
Weight gain or loss >2kg within 3 days seek help - Alcohol + caffeine
Limit to 1-2 standard drinks/day
Caffeine can exacerbate arrhythmia inc HR/BP - Smoking cessation
- Vaccination
Inc risk of especially resp infections causes acute decompensation
Influenza and pneumococcal vaccinations! - Travel
Inc risk of DVT
Approach to pharmacological management of HFpEF
No proven pharm
Treat associated underlying diseases
Approach to pharmacological management of HFrEF
reduce mortality: ACEi/ARB + beta blockers + potassium sparing diuretics
ACEi ARB (not effective as ACEi, use in patients with absolute contraindications of ACEi and severe side effects) loop diuretics cardio selective beta blockers potassium sparing diuretics
Repeat echo in 3-6 months to check efficacy of the medication If EF still < 40%, use SGLT2/ARNI instead of ACEi/ARB
SGLT2/ARNI CANNOT BE USED WITH ACE/ARB SO STOP ACE/ARB
ARNI: wait at least 36 hours after stoping ACE/ARB
MOA and side effect of ACEi
By blocking ACE enzymes, it prevents Angiotensin II formation and inhibit bradykinin breakdown –> reduce angiotensin II-induced vasoconstriction and sodium/fluid retention –> reduce preload and afterload
absolute contraindication
- history of intolerance
- history of hereditary/idiopathic angioedema
- pregnancy
- renal artery stenosis
Relative contraindication
- Hypotension < 90
- Hyperkalaemia > 6
- Renal impairment
side effect
- dry cough
- angioedema (swelling of tongue, face, throat)
- hyperkalaemia inhibiting aldosterone –> arrythmia
MOA and side effect of angiotensin II receptor blockers
ARB - sartan
used if ACEi is not tolerated
Competitively inhibit binding of angiotensin II –> reduce angiotensin II-induced vasoconstriction and sodium retention
Do not act on bradykinin
side effect
- hyperkalaemia inhibiting aldosterone –> arrythmia
MOA and side effect of loop diuretics (furosemide)
Act on luminal Na+/K+/2Cl- co-transporters in ascending loop of Henle –> sodium, potassium, chloride loss in urine
Dramatic diuresis: incontinence, nocturia, polyuria, high urea
Postural hypotension
Monitor Hyponatremia and hypokalaemia alkalosis
- Dehydration from excessive fluid loss (hydrogen ion loss alkalosis)
- Hypokalaemia alkalosis: As a result of excessive sodium loss, kidney tubules try to compensate sodium loss by losing potassium and hydrogen ions
- Hypotension from excessive fluid loss renal function
MOA and side effect of cardio selective beta blockers
Competitively blocks beta receptors in heart –> reduce contractility, bronchi relaxation, relax SMC of arteries
Do not use beta blockers during decompensation – the patient is already fluid overload, so reducing cardiac contractility would be detrimental, wait until stabilise
reduce mortality and risk of hospitalisation
