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Here’s an excerpt from our Cardiology notes:
Diseases by anatomy:
This is a fluid-filled sac that surrounds and protects the heart, preventing friction during heart contractions.
Infection:
- Viruses (more common): Coxackie B, CMV, echovirus, HIV, influenza
- Although bacteria can also cause it:
- Streptococcuus → Rheumatic heart disease
- Tuberculosis
- Pneumococcus
- Haemophilus
- Pericarditis occurring 1–4 weeks—although can be longer—after an MI secondary to myocardial or pericardial damage. Occurs in ~ 7% of MI patients.
- ESR
- Antimyocardial antibodies as it is an autoimmune reaction against damaged myocardial tissue.
- Secondary immune processes (e.g. rheumatic fever, post-cardiotomy syndrome)
- Metabolic disorders (e.g. uraemia, myxoedema)
- Radiotherapy
- Cardiac surgery
- Percutaneous cardiac interventions
- Malignancy
- Rheumatology: SLE, RA, sarcoidosis, vasculitis (Behçet's)
- Sharp chest pain relieved by leaning forwards, and worse when lying flat
- Friction rub heard on auscultation of the heart
- Fever
- ECG:
- Widespread saddle ST elevation, not confined to a specific lead, showing that ischaemia is occurring to all areas of the myocardium due to pericardial compression.
- Bloods: FBC, U&E, CRP, ESR, troponin
- CXR: Rule out differentials (pneumonia, malignancy, etc.).
- Transthoracic echocardiogram: Looking for thickening of pericardial layers, pericardial effusion and resultant effects of it (tamponade/restriction).
BMJ Best Practice:
- NSAIDs
- Ibuprofen 600mg PO for (+ PPI)
- PPI for gastroprotection
- Aspirin is preferred for patients developing pericarditis after a myocardial infarction
- Colchicine (if idiopathic or viral pericarditis) to prevent recurrent pericarditis, improve response, and increase remission rates.
- Lifestyle: Restrict strenuous physical activities
- If not resposive: Consider corticosteroids
This results from pericardial scarring.
- Acute pericarditis leading to inflammation & scarring
- Symptoms: Fluid overload, exertional dyspnoea
- OE: Right HF
- Raised JVP, Kussmaul's sign (↑JVP), pulsus paradoxus (pulse wave volume decreases during inspiration).
- Kussmaul's is specific to this, differentiates it from tamponade
Relieve pressure on the heart exerted by the pericardium, and treat underying cause.
- Pericardiectomy.
- NSAIDs, steroids, diuretics and other medications can be useful.
Accumulation of fluid within the pericardial space → ↑ intra-pericardial pressure → Restriction of cardiac filling → ↓ cardiac output.
- Quiet heart sounds
- Hypotension
- Raised JVP
- Kussmaul's sign: JVP rises with inspiration
- Pulsus paradoxus: Drop in systolic BP with inspiration
- Electrical alterans (alternating tall and short QRS complexes)
- Fluid filled pericardium → Heart moving backwards and forwards during contractions → Wandering baseline
- Small QRS: Difficulty contracting due to pressure
- Bloods
- FBC: ? inflammatory cause
- ESR
- Troponin
- CXR: Enlarged cardiac shadow
- Transthoracic echocardiogram, looking for:
- Pericardial effusion (and size of it).
- Chamber collapse and respiratory variation of ventricular filling.
- Anti-inflammatory treatment, gastroprotection and observation.
- Pericardiocentesis
- Send fluid for culture and cytology to identify cause
- Surgical drainage.
- Blood is associated with malignancy or traumatic effusion.
This is the middle muscular layer of the heart, made up of cardiomyocytes.
The following patients have chest pain at rest and the following:
- STEMI
- STEMI
- Unstable angina
- NSTEMI
We classify ACS using symptoms, ECG & cardiac biomarkers.
ST elevation OR new LBBB is present on the ECG.
Acute:
- Morphine
- Oxygen (if SpO₂ < 95%)
- Nitrates (GTN spray)
- Aspirin 300mg STAT
- Primary PCI
- Has to be available within 2 hours of presentation.
- Insertion of catheter into brachial or femoral artery → Fed through arterial system into coronary arteries under XR guidance → Inject contrast to visualise the blockage → Balloon dilatation of artery +/- stent.
- Thrombolysis (e.g. with alteplase)
- If PCI not available within 2 hours of presentation, thrombolysis is indicated.
Long-term:
Antiplatelets (preventing thrombus formation on plaques):
- Aspirin 75mg OD
- Another antiplatelet: clopidogrel / ticagrelor for ~ 12 months
Lipid lowering (helping reduce atheromatous plaques):
- Atorvastatin 80mg OD
Antihypertensives (lowering BP to prevent damage to endothelium and high pressures pushing clots off plaques):
- ACE inhibitor
- Atenolol / bisoprolol
- Aldosterone antagonist (if in HF)
Cases:
- RCA - Inferior
- Proximal LAD - Septal
- LAD - Anterior
- Distal LAD, LCx, RCA - Apex
- LCx - Lateral
- LCx/RCA - Posterolateral
- V1-3: Reciprocal ST depression
- V5-6: May see ST elevation as LCx affected
- May see some inferior ST elevation depending on size of infarction
- ST elevation in II, III, aVF → Inferior MI
Chest pain is present at rest. There is no ST elevation. There are either other ECG changes suggesting ischaemia (T-wave inversion or ST depression) or a dynamic rise in troponin.
BATMAN
- Beta-blockers
- Aspirin 300mg STAT
- Ticagrelor 180mg STAT (OR prasugrel OR clopidogrel 300mg)
- Morphine for pain
- Anticoagulant: Fondaparinux (but need to assess bleeding risk)
- Nitrates (e.g. GTN)
- Slow heart down to reduce demand of muscles → Beta-blockers
- Prevent more platelet aggregation → Dual antiplatelet therapy
- Control pain for patient comfort and to prevent tachycardia → Morphine
- Break down clot → Anticoagulant
- Stop coronary artery spasm → Nitrates
Chest pain is present at rest. There are no ECG changes and there is not a dynamic rise in troponin.
General:
- ST elevation
- Bundle branch blocks
- ST depression
- T-wave inversion (but this is normal in aVR)
- Pathological Q waves (although this is a late sign)
- Ensuring you have serial troponins. Troponins can be released from the myocardium during ischaemia, but also from elsewhere. Dynamic rise is key for diagnosis.
- Baseline (arrival to hospital/onset of pain)
- 6–12 hours after onset of symptoms
- CKD
- Sepsis
- Pulmonary embolism
- FBC
- Anaemia could contribute to a type 2 MI. This is cardiac ischaemia due to:
- increased demand (tachycardia) or,
- reduced supply (anaemia/hypotension).
- LFT
- Baseline for starting statin therapy
- U&E
- Need to know renal function for CT angio with contrast and if we’re going to start an ACEi
- TFT
- Lipid profile
- GRACE score provides a risk of death or repeat MI within the next 6-months. Medium/high risk individuals are considered for early PCI.
- Low Risk < 5%
- Medium Risk 5-10%
- High Risk > 10%
What complication has occurred:
- Interventricular septal rupture → VSD (HF makes this more likely)
- Papillary muscle rupture → Mitral regurgitation
- Cardiac tamponade
- Dressler's syndrome: Immune response following MI causing pericarditis.
- NSAIDs (e.g. aspirin / ibuprofen)
- Steroids (e.g. prednisolone)
- Pericardiocentesis
This is coronary artery narrowing, causing exertional chest pain as the vessels supplying the heart cannot keep up with the oxygen demands of the muscle.
- When using GTN spray.
- When resting.
- CT coronary angiogram (Gold standard)
- Contraindicated if patient has poor renal function due to the contrast needed to carry this out.
- Stress echocardiogram / Myocardial perfusion SPECT / MRI
- Short-term relief:
- GTN spray (nitrates stimulate vasodilation)
- Long-term relief:
- Bisoprolol
- Amlodipine/nifedipine & bisoprolol
- Isosorbide mononitrate
- Ivabradine/nicorandil
- Percutaneous coronary intervention (PCI)
- Balloon dilation of the artery +/- stent insertion.
- Coronary artery bypass graft (CABG)
- Take a blood vessel from another part of the body, plumbing it into the coronary artery above and below the narrowed area or blockage.
- Better in > 65y, diabetics, 3 vessel disease.
- Usually use the great saphenous vein or the radial artery.
There are two ways to classify this:
HFrEF vs HFpEF:
Systolic failure (EF < 40%) → Impaired contraction.
- MI → Muscle hypoxia → Muscle ischaemia → Cardiac muscle dysfunction
- Idiopathic
- Alcoholic
- Cocaine
- Doxorubicin
- Cyclophosphamide
- Clozapine
- Infiltrative
- Haemochromatosis
- Sarcoidosis
- Amyloidosis
- Infective
- Secondary to myocarditis
- HIV
- Lyme disease
- Chagas disease: Caused by Trypanzoma cruzi parasite prevalent in Central/South America
- Takotsubo
- Stress-induced. Psychological stress → LV ballooning.
Diastolic failure (EF > 50%) → Impaired filling.
- Autosomal dominant
- Genetic abnormality in the proteins making up the heart sarcomere leading to septal hypertrophy
- Impaired outflow → LV hypertrophy → Low preload volume
- 25%
- Ventricular arrhythmia
- Young patient presenting with exertional syncope. Can have chest pain and SOB.
- Unexplained syncope is a poor prognostic factor
- Exercise restriction, β-blockers
- ICD for those at risk of sudden cardiac death
- Surgical: Myomectomy or septal ablation
Deposits within the heart cause it to become stiff → Less heart muscle compliance → Poor filling.
- Amyloidosis: Amyloid deposits within the heart.
- ECHO shows "sparkling appearance"
- Renal dysfunction due to amyloid deposition
- Haemochromatosis
- Sarcoidosis
- Post-radiation fibrosis
Acute vs Chronic:
Acute decompensation of the LV → Back-pressure into the lungs → Pulmonary oedema (transudative mechanism) → Impaired gas exchange.
- Rapid onset SOB
- Worsened SOB lying back
- T1RF
- ↓ SpO₂
- Bibasal crackles (pleural effusion)
- Ensure they’re sat up.
- Diuretics to clear the fluid from their lungs.
- Oxygen to make sure they maintain saturations.
- Paroxysmal nocturnal dyspnoea: Suddenly waking up in the middle of the night feeling short of breath, gasping.
- Stood up → Fluid sits in the bases of the lungs → Space for gas exchange in apex.
- Lying back → Fluid spreads across more of the lungs → Reduced gas exchange area.
- Orthopnoea: Shortness of breath when lying back, they may sleep sat up.
- History: ‘How many pillows do you use at night to prop yourself up?’
- Ramipril/valsartan & bisoprolol
- Spironolactone
- If causes GI upset/gynaecomastia → Switch to eplerenone
- Hydralazine/isosorbide dinitrate
- Digoxin/ivabradine
- Surgical: Cardiac resynchronisation therapy or transplant
- LBBB
- EF < 30%
- NYHA III
- Furosemide 40mg OD
- Lifestyle advice.
- Manage underlying cause, if possible.
- Low-dose furosemide to manage oedema.
- Ramipril if hypertensive.
This is right-sided HF secondary to respiratory disease.
- COPD
- ILD
- PE
- CF
- Disease → Hypoxia → Pulmonary hypertension → Increased RV afterload (pushing against a greater pressure)
- Hypertrophy of the RV → Increased O₂ demand → Higher likelihood of ischaemia
- RV dilatation → Tricuspid regurgitation → Increased preload → More RV dilatation (🔄 deadly cycle)
- Symptoms: SOB, syncope, chest pain.
- Signs: Raised JVP, peripheral oedema, murmurs, hepatomegaly, ascites
- LV failure causing backpressure and increased afterload
- Pulmonary stenosis
- Pulmonary hypertension (as discussed in cor pulmonale)
- Treat the underlying cause of hypoxia & pulmonary hypertension (see Respiratory)
- Manage symptoms, e.g. oedema
General:
NYHA classification:
- No limitation to daily life
- Slight limitation on physical activity
- Marked physical activity limitation, comfortable at rest
- Symptoms at rest
ABCDE
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Upper lobe Diverson
- Pleural Effusions
- BNP (if > 2000 → urgent referral to cardiology)
- Hypertrophic cardiomyopathy
- Ischaemic cardiomyopathy (CAD)
- Dilated cardiomyopathy
- Takotsubo cardiomyopathy
Inflammation of the myocardium → Infiltration of lymphocytic cells → Myocardial necrosis & degeneration.
- Presents with shortness of breath and mild palpitations, had an upper respiratory infection (viral picture) a couple of months ago.
- Coxackie viruses (A/B)
- Lyme disease
- SLE
- Drug-associated
- Marked troponin elevation
- No relief on sitting forward or pericardial rub on examination
- Cardiac biopsy (only perform if this information would alter the treatment plan as it’s risky).
Noncancerous tumor that arises from connective tissue, commonly located in the atria, affecting blood flow and electrical conduction.
- Fever
- Weight loss
- Clubbing
- Audible tumour 'plop' - Variable with position
- ECG: May reveal AF
- Echocardiogram: Help to visualise lesion and blood flow
- CXR: Cardiomegaly, pulmonary oedema
- Open heart surgery to remove the tumour.
The lining of the heart’s chambers.
Thickening, calcification and stiffening of the aortic valve → Valve does not open sufficiently → Increased afterload as LV has to push against a higher pressure to maintain cardiac output.
- Ejection systolic (crescendo-decrescendo)
- Mechanical stress over time
- Risk factor that makes this worse is a biscuspid aortic valve
- Rheumatic heart disease
- Syncope (insufficient oxygen supply to brain)
- Exertional dyspnoea (back pressure into lungs)
- Angina (insufficient oxygen supply to heart)
- Hypertrophic cardiomyopathy
- Louder standing, quieter supine due to LV outflow obstruction.
- Heard louder on LLSE due to septum causing obstruction not the valve
- Aortic flow murmur
- Hyperdynamic circulation due to infection, anaemia, thyrotoxicosis or pregnancy
Widening of the aortic valve → Backflow through the valve during diastole → Increased preload within the LV → Dilation of LV.
- Early diastolic, louder leaning forward and on LLSE
- Degenerative
- Rheumatic fever
- Connective tissue disease (e.g. Marfan’s)
- Endocarditis
- Aortic root dilatation
- Mid-diastolic murmur with opening ‘snap’.
- Malar flush
- AF
- P-mitrale on ECG (Bifid P-wave) due to atrial hypertrophy
- Rheumatic fever (most common): Inflammation → Leaflet fusion
- Age-related calcification
- Systemic disease: RA/SLE
- Congenital
- Pan-systolic murmur / Late-systolic murmur
- Weakening of valve with age
- LVF secondary to dilatation of the ventricle
- Endocarditis
- Papillary muscle rupture secondary to MI
- Connective tissue diseases
- Marfan's syndrome
- Ehlers-Danlos syndrome
- Pulmonary hypertension → RVF
- Left atrial dilatation → Pacemaker cell irritation → AF
These are less commonly tested, but covered in paediatric cardiology, where they are more relevant.
- Pulmonary stenosis
- Pulmonary regurgitation
- Tricuspid stenosis
- Tricuspid regurgitation
Investigations & Management:
- ECG: Looking for ventricular hypertrophy,
- Echocardiogram: Flow across valves (regurgitation, pressure gradients), calcification of the valves, atria/ventricular size.
- CXR: Cardiomegaly
- Often you watch and ensure that hypertension is managed well.
Surgical:
- Valve replacement
- Transcatheter aortic/mitral valve replacement via femoral artery catheter
- Bioprosthetic valve replacement
- Balloon valvuloplasty for stenotic valves (inflate a balloon in the valve to open it)
Infection of the endocardium +/- heart valves.
- S. aureus (IVDU)
- S. viridans (Dental hygiene)
- S. epidermis (Prosthetic valve surgery/infected catheter)
- S. bovis (from GI tract)
- Roth spots (eyes)
- Osler nodes (painful finger lesions)
- Janeway lesions (painless palm lesions)
- Anaemia
- Splinter haemorrhages
Duke's criteria:
- Pathological criteria positive, OR
- 2 major criteria, OR
- 1 major & 3 minor criteria, OR
- 5 minor criteria
Major criteria:
- Two positive blood cultures
- Persistent bacteraemia from two blood cultures taken > 12 hours apart
- Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
- Positive echocardiogram
- New valvular regurgitation
Minor criteria:
- Predisposing heart condition or intravenous drug use
- Microbiological evidence does not meet major criteria
- Fever > 38ºC
- Vascular phenomena: Major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
- Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
Investigations & Management:
- 3 sets of blood cultures from 3 different sites at 3 different times
- ECG
- CXR
- Transoesophageal echocardiogram → Valvular pathology
- Medical: IV antibiotics
- Central line infection: IV vancomycin
- Surgical: Valve repair
- Severe sepsis despite antibiotics
- Heart failure
- Haemodynamic instability
- Rheumatic fever
- Group A haemolytic Streptococci → Autoimmune inflammatory disease
- Streptococci proteins cross-react with myocardial, valvular, joint and brain proteins
- 2-4 weeks following a throat infection, they develop SOB, fever & chest pain. Pericardial rub and joint pain.
- Anti-Streptolysin O (ASO) titre
- STAT IV benzylpenicillin - Covers this group A beta-haemolytic streptococcal infection
- PO Pen V for 10 days
- Libman-Sacks endocarditis
- SLE/RA antigen-antibody complexes settle in endocardium → Endocardial damage → Valve regurgitation
- Non-bacterial thrombotic endocarditis
- Damage to valve exposes collagen → Platelets & fibrin adhere to form clots → Mitral valve regurgitation.
What are the causes of:
- HTN
- Pulmonary HTN
- Hyperdynamic states
- ASD
- Aortic stenosis
- ASD
- Deep inspiration (increased VR causes tricuspid to close after mitral)
- RBBB
- Pulmonary stenosis
- Severe MR
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