Cardiology

Front 1

Define Heart Failure

Back 1

"HF is the inability of the heart to pump blood at a rate sufficient to meet the metabolic requirements of the tissues, caused by an abnormality of any aspect of cardiac function and with adequate filling pressure"

It is characterised by typical haemodynamic changes, such as systemic vasoconstriction and neurohormonal activation. Clinically, it causes breathlessness, effort intolerance, fluid retention and frequent hospital admission. It is associated with poor survival.

Front 2

What are the causes of heart failure?

Back 2

1. Coronary artery disease (MI)
2. Hypertension
3. Idiopathic
4. Toxins (e.g. alcohol, chemotherapy)
5. Genetic
6. Valvular disease
7. Congenital heart disease
8. Infection (virus, chaga's)
9. Metabolic (e.g. haemochromatosis, amyloid, thyroid disease)
10. Pericardial disease (e.g. TB)
11. Endocardial disease

Front 3

What are the symptoms of heart failure?

Back 3

1. Dyspnoea (PND, orthopnoea)
   
2. Cough
3. Ankle, leg and abdominal swelling/oedema
4. Fatigue/tiredness
5. Pink frothy sputum

Front 4

What are the signs of heart failure?

Back 4

1. Peripheral oedema
   
2. Elevated JVP
3. Third heart sound
4. Displaced apex beat
5. Pulmonary oedema (lung crackles)
6. Pleural Effusion

Front 5

What are the radiological signs you might find in a heart failure patient's CXR?

Back 5

1. Kerley B lines (interstitial oedema)
2. Dilated, prominent upper lobe vessels
3. Alveolar oedema (bat's wings)
4. Cardiomegaly
5. Pleural effusion

Front 6

What is the management for ACUTE heart failure?

Back 6

1. Sit patient upright
2. Oxygen (100% if no pre-existing lung disease)
3. Diamorphine
4. Furosemide
5. GTN spray (2 puffs)
6. Nitrate infusion (if systolic BP >100mmHg - e.g. isosorbide dinitrate)
7. Consider CPAP, further furosemide dose or increasing nitrate infusion if patient worsens

Front 7

What is the management for CHRONIC heart failure?

Back 7

1. Lifestyle changes (stop smoking, eat less salt, treat the cause, treat and avoid exacerbating causes)
2. Diuretics e.g. Furosemide
3. ACEi e.g. Ramipril
4. Beta blocker e.g. Carvedilol
5. Spironolactone (if still symptomatic despite standard therapy incl. ACEi, BB and those with AF)
6. Digoxin (decreases HR, use if still symptomatic despite ACEi, beta blocker or if AF)
7. Vasodilators e.g. hydralazine/isosorbide dinitrate (use in patients who are intolerant to ACEi and ARBs, can be added to standard therapy in black patients
8. Ivabradine (sinus node inhibition)

Front 8

What is the pathogenesis of atherosclerosis?

Back 8

1. Occurs more commonly in areas of turbulent blood flow, like bends/bifurcations in arteries
2. Endothelial damage leads to endothelial cells up regulating adhesion molecules which promote inflammatory cell recruitment, mainly monocytes and T-cells which migrate to the intima. They initiate local inflammatory responses
3. LDL and vLDLs bind to endothelial cells and translocate into the intima, where they become oxidised.
4. The oxidised form of LDLs are taken up by lipid laden macrophages which become foam cells. This results in the formation of the fatty streak (early sign of atherosclerosis)
5. Macrophages release pro inflammatory cytokines that cause smooth muscle cell migration into the initima to synthesise extra cellular matrix, which eventually forms a fibrous plaque with a fibrous capsule composed of the smooth muscle cells, surrounded by a dense connective tissue and extra/intracellular lipids. This is a stable plaque.
6. Macrophages also synthesise MMPs and collagenases which break down the fibrous cap. This leads to the formation of an unstable plaque, which may rupture, fissure or erode, and ultimately cause a thrombus to form.

Front 9

What are statins and their MoA?

Back 9

Statins are HMG-CoA reductase inhibitors which inhibit the biosynthesis of cholesterol in hepatocytes in a dose-dependent manner.

HMG-CoA catalysis the rate limiting step of cholesterol formation, and the resulting reduction in cholesterol stimulates the up regulation of sterol regulatory element binding protein (SREBP), a transcription factor, which increases the LDL receptors on hepatocytes which remove more LDL and therefore cholesterol, from the blood.

Front 10

What strategies could be suggested to lower lipid levels?

Back 10

1. Loose weight
2. Stop smoking
3. Healthy diet
4. Exercise
5. Statins (cholesterol should be <5mmol/l)
6. HDL raising drugs
7. BP control
8. Salt reduction

Front 11

After 24h ambulatory BP monitoring, when would you initiate anti-hypertensive treatment?

Back 11

1. <135/85 = treat if signs of end organ damage or if CV risk >20%/10yrs (140/90 clinically)
2. >150/95 = treat immediately (>160/100 clinically)

Aim for <140/90 (or 130/80 in diabetics, 150/90 elderly >80yrs)

Front 12

What are the symptoms/signs of hypertension

Back 12

1. Usually asymptomatic
2. Look for signs of end-organ damage - LVH, Retinopathy, proteinuria
3. Radio femoral delay
4. Weak femoral pulses (coarctation of aorta)
5. Palpable kidneys
6. Cushing's disease

Malignant hypertension = headaches +/- visual disturbance, with bilateral retinal haemorrhages and exudates and papilloedema

Front 13

How does hypertension affect the cardiovascular and renal systems?

Back 13

1. Accelerates arteriosclerosis and atherosclerosis formation, implications in aortic aneurysm and aortic dissection
2. Decreases renal blood flow and damage to renal vasculature -> ischaemia
3. Increases pressure load -> LVH

Therefore, hypertension increases the risk of LVH, IHD and stroke

Front 14

What is the management of hypertension?

Back 14

1. Lifestyle changes
2. Mono therapy - >55yrs/black then CCB or thiazide; <55yrs ACEi (or ARB if intolerant to ACEi. No ACEi in pregnancy!). Consider beta blocker if women of child-bearing potential or contraindication to ACEi/ARB
3. Combination therapy - ACEi + CCB/diuretic
4. Multiple therapy - ACEi + CCB + thiazide
5. Additional drug e.g. higher dose thiazide, +spironolactone or beta/alpha blockers

Front 15

What are the risk factors for Infective Endocarditis?

Back 15

• Underlying valvular abnormalities - e.g. aortic stenosis/age-related calcification, rheumatic fever
• IVDU
• Prosthetic valves

Front 16

What are the typical causative organisms of infective endocarditis?

Back 16

• Staph aureus (IVDU)
• Strep viridans (Native valve)
• Strep spp and CoN staphylococci (prosthetic valves)

Front 17

What are the treatments for infective endocarditis?

Back 17

1. Antibiotic therapy (S.aureus (MSSA) - Flucloxacillin + Gentamicin; S. aureus (MRSA) or CoNS - Vancomycin + Gentamicin; Enterococcus spp - Amoxicillin or vancomycin +/- gentamicin; Strep. spp - Benzylpenicillin + gentamicin)
2. Surgery - if heart failure or uncontrollable infection/abscess, or if large vegetations to prevent emboli

Front 18

What are the signs and symptoms of infective endocarditis?

Back 18

1. Early manifestations - Fever + Murmur, Fatigue, malaise
2. Embolic events - splinter haemorrhages, haematuria, petechiae, septic pulmonary emboli, CVA, renal infarction
3. Long term effects - (immunological: splenomegaly, nephritis, vasculitic lesions of skin and eye, clubbing) (tissue damage: valve destruction/abscess) Osler's nodes, Janeway's lesions

Front 19

How would you diagnose infective endocarditis?

Back 19

Think IE if:

- s. aureus bacteraemia

- IVDU and positive blood cultures

- All patient with prosthetic valves and positive blood cultures

1. 3 x Blood cultures 10ml bottles, aseptic and before antibiotics
2. ECHO - TTE or TOE
3. Duke's criteria