Don’t F*ck Finals

Don’t F*ck Finals

Don’t F*ck Finals!

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Multiple Sources

Sources include NICE, BMJ Best Practice & UpToDate.

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Here’s an excerpt from our Cardiology notes:

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❤️‍🩹 The Heart Wall
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Diagram: The Heart Wall
Blausen.com staff (2014), CC BY 3.0
Blausen.com staff (2014), CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.

Diseases by anatomy:

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Pericardium

This is a fluid-filled sac that surrounds and protects the heart, preventing friction during heart contractions.

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Pericarditis
‣
Acute pericarditis
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Causes
‣
What’s the most common cause of pericarditis?

Infection:

  • Viruses (more common): Coxackie B, CMV, echovirus, HIV, influenza
  • Although bacteria can also cause it:
    • Streptococcuus → Rheumatic heart disease
    • Tuberculosis
    • Pneumococcus
    • Haemophilus
‣
What is Dressler’s syndrome?
  • Pericarditis occurring 1–4 weeks—although can be longer—after an MI secondary to myocardial or pericardial damage. Occurs in ~ 7% of MI patients.
    • ‣
    What blood tests can be useful?
    • ESR
    • Antimyocardial antibodies as it is an autoimmune reaction against damaged myocardial tissue.
‣
What other things can cause it?
  1. Secondary immune processes (e.g. rheumatic fever, post-cardiotomy syndrome)
  2. Metabolic disorders (e.g. uraemia, myxoedema)
  3. Radiotherapy
  4. Cardiac surgery
  5. Percutaneous cardiac interventions
  6. Malignancy
  7. Rheumatology: SLE, RA, sarcoidosis, vasculitis (Behçet's)
‣
What are the classic presenting features in exams?
  1. Sharp chest pain relieved by leaning forwards, and worse when lying flat
  2. Friction rub heard on auscultation of the heart
  3. Fever
‣
What are the key investigations?
  • ECG:
    • ‣
    What does the following ECG show?
    ‣
    Answer
    • 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.
    James Heilman, MD, CC BY-SA 3.0
    James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
  • 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).
‣
How do you manage uncomplicated pericarditis?

BMJ Best Practice:

  1. NSAIDs
    • Ibuprofen 600mg PO for (+ PPI)
    • PPI for gastroprotection
    • Aspirin is preferred for patients developing pericarditis after a myocardial infarction
  2. Colchicine (if idiopathic or viral pericarditis) to prevent recurrent pericarditis, improve response, and increase remission rates.
  3. Lifestyle: Restrict strenuous physical activities
  4. If not resposive: Consider corticosteroids
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Constrictive pericarditis

This results from pericardial scarring.

‣
What often causes it?
  • Acute pericarditis leading to inflammation & scarring
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How would they present?
  • 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
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How is it treated?

Relieve pressure on the heart exerted by the pericardium, and treat underying cause.

  • Pericardiectomy.
  • NSAIDs, steroids, diuretics and other medications can be useful.
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Cardiac tamponade

Accumulation of fluid within the pericardial space → ↑ intra-pericardial pressure → Restriction of cardiac filling → ↓ cardiac output.

‣
What is Beck's triad?
  1. Quiet heart sounds
  2. Hypotension
  3. Raised JVP
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What examination findings suggest this? (2)
  1. Kussmaul's sign: JVP rises with inspiration
  2. Pulsus paradoxus: Drop in systolic BP with inspiration
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What is shown on this ECG:
‣
Answer
  • 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
CardioNetworks: Vdbilt, CC BY-SA 3.0
CardioNetworks: Vdbilt, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
What other invetigations will you need?
  1. Bloods
    • FBC: ? inflammatory cause
    • ESR
    • Troponin
  2. CXR: Enlarged cardiac shadow
  3. Transthoracic echocardiogram, looking for:
    • Pericardial effusion (and size of it).
    • Chamber collapse and respiratory variation of ventricular filling.
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How would you manage these patients:
‣
Haemodynamically stable (pre-tamponade)
  • Anti-inflammatory treatment, gastroprotection and observation.
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Haemodynamically unstable patient with tamponade
  • Pericardiocentesis
    • Send fluid for culture and cytology to identify cause
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Haemopericardium
  • Surgical drainage.
  • Blood is associated with malignancy or traumatic effusion.
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Myocardium

This is the middle muscular layer of the heart, made up of cardiomyocytes.

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Ischaemic heart disease
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Acute coronary syndrome (ACS)
‣
Classifying ACS
‣
ACS cases

The following patients have chest pain at rest and the following:

‣
ST elevation present on the ECG.
  • STEMI
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New LBBB present on ECG.
  • STEMI
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No ECG changes. No dynamic rise in troponin.
  • Unstable angina
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T-wave inversion in V1-3. Dynamic rise in troponin.
  • NSTEMI

We classify ACS using symptoms, ECG & cardiac biomarkers.

‣
STEMI

ST elevation OR new LBBB is present on the ECG.

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Coronary artery anatomy
Servier Medical Art. Annotations by Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D., CC BY 3.0
Servier Medical Art. Annotations by Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D., CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
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Management

Acute:

‣
What medications would you give immediately?
  1. Morphine
  2. Oxygen (if SpO₂ < 95%)
  3. Nitrates (GTN spray)
  4. Aspirin 300mg STAT
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What is the gold-standard treatment?
  • Primary PCI
    • ‣
    Within what time limits is this appropriate?
    • Has to be available within 2 hours of presentation.
    ‣
    What is it?
    • 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.
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What is the other definitive treatment option?
  • Thrombolysis (e.g. with alteplase)
    • If PCI not available within 2 hours of presentation, thrombolysis is indicated.

Long-term:

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What medications do we need to consider for secondary prevention?

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:

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ST elevation is found in the following leads, what artery is affected:
‣
II, III, aVF
  • RCA - Inferior
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V1-2
  • Proximal LAD - Septal
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V3-4
  • LAD - Anterior
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V5-6
  • Distal LAD, LCx, RCA - Apex
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I, aVL
  • LCx - Lateral
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V7-9
  • 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
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What is present on the following ECG:
‣
Diagnosis
  • ST elevation in II, III, aVF → Inferior MI
Glenlarson, CC BY-SA 3.0
Glenlarson, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0/, via Wikimedia Commons. No changes were made.
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NSTEMI

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.

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How is it acutely managed?

BATMAN

  1. Beta-blockers
  2. Aspirin 300mg STAT
  3. Ticagrelor 180mg STAT (OR prasugrel OR clopidogrel 300mg)
  4. Morphine for pain
  5. Anticoagulant: Fondaparinux (but need to assess bleeding risk)
  6. Nitrates (e.g. GTN)
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What are the principles underlying this management?
  1. Slow heart down to reduce demand of muscles → Beta-blockers
  2. Prevent more platelet aggregation → Dual antiplatelet therapy
  3. Control pain for patient comfort and to prevent tachycardia → Morphine
  4. Break down clot → Anticoagulant
  5. Stop coronary artery spasm → Nitrates
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Unstable angina

Chest pain is present at rest. There are no ECG changes and there is not a dynamic rise in troponin.

General:

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Investigations
‣
What ECG changes are you looking for?
  1. ST elevation
  2. Bundle branch blocks
  3. ST depression
  4. T-wave inversion (but this is normal in aVR)
  5. Pathological Q waves (although this is a late sign)
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When looking at serum troponin, what is key for diagnosis of MI?
  • Ensuring you have serial troponins. Troponins can be released from the myocardium during ischaemia, but also from elsewhere. Dynamic rise is key for diagnosis.
    • ‣
    When do we measure troponin to test for this dynamic rise?
    1. Baseline (arrival to hospital/onset of pain)
    2. 6–12 hours after onset of symptoms
    ‣
    What else can cause raised troponin?
    1. CKD
    2. Sepsis
    3. Pulmonary embolism
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What other bloods may be useful?
  1. FBC
    2. ‣
    Why might anaemia be relevant?
    • Anaemia could contribute to a type 2 MI. This is cardiac ischaemia due to:
      • increased demand (tachycardia) or,
      • reduced supply (anaemia/hypotension).
  2. LFT
    3. ‣
    Why?
    • Baseline for starting statin therapy
  3. U&E
    4. ‣
    Why?
    • Need to know renal function for CT angio with contrast and if we’re going to start an ACEi
  4. TFT
  5. Lipid profile
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Complications
‣
What score is used to stratify their risk?
  • 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:

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New pan-systolic murmur and acute HF.
  • Interventricular septal rupture → VSD (HF makes this more likely)
  • Papillary muscle rupture → Mitral regurgitation
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Muffled heart sounds, pulsus paradoxus, raised JVP.
  • Cardiac tamponade
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3 weeks later presents with chest pain and fever. Raised ESR.
  • Dressler's syndrome: Immune response following MI causing pericarditis.
    • ‣
    Management?
    • NSAIDs (e.g. aspirin / ibuprofen)
    • Steroids (e.g. prednisolone)
    • Pericardiocentesis
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Stable angina

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 are symptoms classically relieved?
  1. When using GTN spray.
  2. When resting.
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How are they investigated?
  1. CT coronary angiogram (Gold standard)
    • Contraindicated if patient has poor renal function due to the contrast needed to carry this out.
  2. Stress echocardiogram / Myocardial perfusion SPECT / MRI
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What makes up the medical management?
  • Short-term relief:
    1. GTN spray (nitrates stimulate vasodilation)
  • Long-term relief:
    1. Bisoprolol
    2. Amlodipine/nifedipine & bisoprolol
    3. Isosorbide mononitrate
    4. Ivabradine/nicorandil
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What surgical management can be used?
  1. Percutaneous coronary intervention (PCI)
    • Balloon dilation of the artery +/- stent insertion.
  2. 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.
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Heart failure

There are two ways to classify this:

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Left-sided HF (LHF/LVF)

HFrEF vs HFpEF:

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Heart failure with reduced ejection fraction (HFrEF)

Systolic failure (EF < 40%) → Impaired contraction.

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Ischaemic cardiomyopathy
  • MI → Muscle hypoxia → Muscle ischaemia → Cardiac muscle dysfunction
‣
Dilated cardiomyopathy
  1. Idiopathic
  2. Alcoholic
    3. ‣
    What other drugs can cause DCM?
    1. Cocaine
    2. Doxorubicin
    3. Cyclophosphamide
    4. Clozapine
  3. Infiltrative
    4. ‣
    What are the causes?
    1. Haemochromatosis
    2. Sarcoidosis
    3. Amyloidosis
  4. Infective
    5. ‣
    What are the causes?
    1. Secondary to myocarditis
    2. HIV
    3. Lyme disease
    4. Chagas disease: Caused by Trypanzoma cruzi parasite prevalent in Central/South America
  5. Takotsubo
    6. ‣
    What causes this?
    • Stress-induced. Psychological stress → LV ballooning.
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Heart failure with preserved ejection fraction (HFpEF)

Diastolic failure (EF > 50%) → Impaired filling.

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Hypertrophic cardiomyopathy
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How is it inherited & what is it?
  • Autosomal dominant
  • Genetic abnormality in the proteins making up the heart sarcomere leading to septal hypertrophy
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How does it lead to HF?
  • Impaired outflow → LV hypertrophy → Low preload volume
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How many of these patients have HOCM?
  • 25%
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How does HOCM cause sudden death?
  • Ventricular arrhythmia
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How do they commonly present?
  • Young patient presenting with exertional syncope. Can have chest pain and SOB.
  • Unexplained syncope is a poor prognostic factor
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How are they managed?
  1. Exercise restriction, β-blockers
  2. ICD for those at risk of sudden cardiac death
  3. Surgical: Myomectomy or septal ablation
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Restrictive cardiomyopathy

Deposits within the heart cause it to become stiff → Less heart muscle compliance → Poor filling.

  1. Amyloidosis: Amyloid deposits within the heart.
    2. ‣
    What features suggest this?
    1. ECHO shows "sparkling appearance"
    2. Renal dysfunction due to amyloid deposition
  2. Haemochromatosis
  3. Sarcoidosis
  4. Post-radiation fibrosis

Acute vs Chronic:

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Acute LVF

Acute decompensation of the LV → Back-pressure into the lungs → Pulmonary oedema (transudative mechanism) → Impaired gas exchange.

‣
What are the symptoms & signs?
  1. Rapid onset SOB
  2. Worsened SOB lying back
  3. T1RF
  4. ↓ SpO₂
  5. Bibasal crackles (pleural effusion)
‣
How do you manage them?
  1. Ensure they’re sat up.
  2. Diuretics to clear the fluid from their lungs.
  3. Oxygen to make sure they maintain saturations.
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Chronic heart failure
‣
What are the classic symptoms?
  1. 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.
  2. 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?’
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What are the steps in HFrEF management?
  1. Ramipril/valsartan & bisoprolol
  2. Spironolactone
    • If causes GI upset/gynaecomastia → Switch to eplerenone
  3. Hydralazine/isosorbide dinitrate
  4. Digoxin/ivabradine
  5. Surgical: Cardiac resynchronisation therapy or transplant
    6. ‣
    What are the 3 indicatons that need to be present for this?
    1. LBBB
    2. EF < 30%
    3. NYHA III
‣
What can be used for symptomatic management?
  • Furosemide 40mg OD
‣
How is HFpEF managed?
  1. Lifestyle advice.
  2. Manage underlying cause, if possible.
  3. Low-dose furosemide to manage oedema.
  4. Ramipril if hypertensive.
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Right-sided HF (RHF)
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Cor pulmonale

This is right-sided HF secondary to respiratory disease.

‣
What respiratory diseases cause this?
  1. COPD
  2. ILD
  3. PE
  4. CF
‣
Why does respiratory disease cause RHF?
  • 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)
‣
What symptoms/signs may suggest this?
  • Symptoms: SOB, syncope, chest pain.
  • Signs: Raised JVP, peripheral oedema, murmurs, hepatomegaly, ascites
‣
What are the common causes?
  1. LV failure causing backpressure and increased afterload
  2. Pulmonary stenosis
  3. Pulmonary hypertension (as discussed in cor pulmonale)
‣
How would you manage them?
  1. Treat the underlying cause of hypoxia & pulmonary hypertension (see Respiratory)
  2. Manage symptoms, e.g. oedema

General:

‣
How are the symptoms classified?

NYHA classification:

  1. No limitation to daily life
  2. Slight limitation on physical activity
  3. Marked physical activity limitation, comfortable at rest
  4. Symptoms at rest
‣
Investigations
‣
What are the common CXR findings?

ABCDE

  1. Alveolar oedema
  2. Kerley B lines
  3. Cardiomegaly
  4. Upper lobe Diverson
  5. Pleural Effusions

Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
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What blood test do you need before doing an echocardiogram?
  • BNP (if > 2000 → urgent referral to cardiology)
‣
What diagnosis do the following echocardiogram results suggest:
‣
Asymmetric hypertrophy, diastolic dysfunction
  • Hypertrophic cardiomyopathy
‣
Regional wall motion abnormality, EF < 55%
  • Ischaemic cardiomyopathy (CAD)
‣
LV dilation, EF < 55%
  • Dilated cardiomyopathy
‣
Apical ballooning of LV
  • Takotsubo cardiomyopathy
‣
Myocarditis

Inflammation of the myocardium → Infiltration of lymphocytic cells → Myocardial necrosis & degeneration.

‣
What is the classic exam question?
  • Presents with shortness of breath and mild palpitations, had an upper respiratory infection (viral picture) a couple of months ago.
‣
What are the causes?
  1. Coxackie viruses (A/B)
  2. Lyme disease
  3. SLE
  4. Drug-associated
‣
What features differentiate it from pericarditis?
  1. Marked troponin elevation
  2. No relief on sitting forward or pericardial rub on examination

‣
How do you definitively diagnose it?
  • Cardiac biopsy (only perform if this information would alter the treatment plan as it’s risky).
‣
Cardiac myxoma

Noncancerous tumor that arises from connective tissue, commonly located in the atria, affecting blood flow and electrical conduction.

‣
What are the classic features?
  1. Fever
  2. Weight loss
  3. Clubbing
  4. Audible tumour 'plop' - Variable with position
‣
How would you investigate?
  1. ECG: May reveal AF
  2. Echocardiogram: Help to visualise lesion and blood flow
  3. CXR: Cardiomegaly, pulmonary oedema
‣
How would you manage it?
  • Open heart surgery to remove the tumour.
‣
Endocardium (Valves)

The lining of the heart’s chambers.

‣
Heart valves
‣
Diagram: Heart valves
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.
‣
Name the 4 heart valves.
‣
Aortic
‣
Aortic stenosis

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.

‣
What murmur would you hear?
  • Ejection systolic (crescendo-decrescendo)
‣
What are the causes of this?
  1. Mechanical stress over time
    • Risk factor that makes this worse is a biscuspid aortic valve
  2. Rheumatic heart disease
‣
What is the classic triad of symptoms?
  1. Syncope (insufficient oxygen supply to brain)
  2. Exertional dyspnoea (back pressure into lungs)
  3. Angina (insufficient oxygen supply to heart)
‣
What are the other differentials for this type of murmur?
  1. Hypertrophic cardiomyopathy
    • Louder standing, quieter supine due to LV outflow obstruction.
    • Heard louder on LLSE due to septum causing obstruction not the valve
  2. Aortic flow murmur
    • Hyperdynamic circulation due to infection, anaemia, thyrotoxicosis or pregnancy
‣
Aortic regurgitation

Widening of the aortic valve → Backflow through the valve during diastole → Increased preload within the LV → Dilation of LV.

‣
What murmur would you hear?
  • Early diastolic, louder leaning forward and on LLSE
‣
What can cause this?
  1. Degenerative
  2. Rheumatic fever
  3. Connective tissue disease (e.g. Marfan’s)
  4. Endocarditis
  5. Aortic root dilatation
‣
Mitral
‣
Mitral stenosis
‣
What murmur would you hear?
  • Mid-diastolic murmur with opening ‘snap’.
‣
What are the other common features?
  1. Malar flush
  2. AF
  3. P-mitrale on ECG (Bifid P-wave) due to atrial hypertrophy
‣
What are the causes?
  • Rheumatic fever (most common): Inflammation → Leaflet fusion
  • Age-related calcification
  • Systemic disease: RA/SLE
  • Congenital
‣
Mitral regurgitation (most common valvular condition)
‣
What murmur would you hear in prolapse?
  • Pan-systolic murmur / Late-systolic murmur
‣
What are the causes?
  • 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
‣
What are the complications?
  • Pulmonary hypertension → RVF
  • Left atrial dilatation → Pacemaker cell irritation → AF
‣
Pulmonary

These are less commonly tested, but covered in paediatric cardiology, where they are more relevant.

  1. Pulmonary stenosis
  2. Pulmonary regurgitation
‣
Tricuspid
  1. Tricuspid stenosis
  2. Tricuspid regurgitation

Investigations & Management:

‣
What investigations are useful in assessing valvular pathology?
  1. ECG: Looking for ventricular hypertrophy,
  2. Echocardiogram: Flow across valves (regurgitation, pressure gradients), calcification of the valves, atria/ventricular size.
  3. CXR: Cardiomegaly
‣
What management should you consider?
  • Often you watch and ensure that hypertension is managed well.

Surgical:

  1. Valve replacement
    • Transcatheter aortic/mitral valve replacement via femoral artery catheter
    • Bioprosthetic valve replacement
  2. Balloon valvuloplasty for stenotic valves (inflate a balloon in the valve to open it)
‣
Endocarditis

Infection of the endocardium +/- heart valves.

‣
Infective
‣
What organisms can cause this?
  1. S. aureus (IVDU)
  2. S. viridans (Dental hygiene)
  3. S. epidermis (Prosthetic valve surgery/infected catheter)
  4. S. bovis (from GI tract)
‣
What signs & symptoms are you looking for?
  • Roth spots (eyes)
  • Osler nodes (painful finger lesions)
  • Janeway lesions (painless palm lesions)
  • Anaemia
  • Splinter haemorrhages
‣
What criteria are used to diagnose this and what are the constituents?

Duke's criteria:

  1. Pathological criteria positive, OR
  2. 2 major criteria, OR
  3. 1 major & 3 minor criteria, OR
  4. 5 minor criteria

Major criteria:

  1. Two positive blood cultures
  2. Persistent bacteraemia from two blood cultures taken > 12 hours apart
  3. Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
  4. Positive echocardiogram
  5. New valvular regurgitation

Minor criteria:

  1. Predisposing heart condition or intravenous drug use
  2. Microbiological evidence does not meet major criteria
  3. Fever > 38ºC
  4. Vascular phenomena: Major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  5. Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

Investigations & Management:

‣
How do you investigate?
  1. 3 sets of blood cultures from 3 different sites at 3 different times
  2. ECG
  3. CXR
  4. Transoesophageal echocardiogram → Valvular pathology
‣
How do you manage it?
  1. Medical: IV antibiotics
    • Central line infection: IV vancomycin
  2. Surgical: Valve repair
    3. ‣
    When is this indicated?
    1. Severe sepsis despite antibiotics
    2. Heart failure
    3. Haemodynamic instability
‣
Non-infective
  1. Rheumatic fever
    2. ‣
    What is this caused by?
    • Group A haemolytic Streptococci → Autoimmune inflammatory disease
      • Streptococci proteins cross-react with myocardial, valvular, joint and brain proteins
    ‣
    How do they present?
    • 2-4 weeks following a throat infection, they develop SOB, fever & chest pain. Pericardial rub and joint pain.
    ‣
    How do you investigate it?
    • Anti-Streptolysin O (ASO) titre
    ‣
    How is this managed?
    1. STAT IV benzylpenicillin - Covers this group A beta-haemolytic streptococcal infection
    2. PO Pen V for 10 days
  2. Libman-Sacks endocarditis
    • SLE/RA antigen-antibody complexes settle in endocardium → Endocardial damage → Valve regurgitation
  3. Non-bacterial thrombotic endocarditis
    • Damage to valve exposes collagen → Platelets & fibrin adhere to form clots → Mitral valve regurgitation.
‣
Heart sounds
‣
Diagram: Heart sounds
Madhero88, CC BY-SA 3.0
Madhero88, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.

What are the causes of:

‣
Loud S2
  1. HTN
  2. Pulmonary HTN
  3. Hyperdynamic states
  4. ASD
‣
Soft S2
  • Aortic stenosis
‣
Fixed split S2
  • ASD
‣
Widely split S2
  1. Deep inspiration (increased VR causes tricuspid to close after mitral)
  2. RBBB
  3. Pulmonary stenosis
  4. Severe MR

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