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Cardiology Flashcards

1
Q

Coronary Artery Anatomy

A

1) Left Coronary Artery

  • Left Anterior Descending a.
  • Left Circumflex a.

2) Right Coronary Artery –> AV nodular a. and Post. Interventricular a.

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2
Q

Conduction System of Heart

A
  1. Sinoatrial node (pacemaker)
  2. Atrioventricular node
  3. Bundle of His
  4. Bundle Branches
  5. Purkinji fibres
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3
Q

2 Major Cardiac Biomarkers

A
  • Troponin - peak 1-2days, elevated up to 2 weeks (MI, CHF, PE, myocarditis). Check at presentation and 8 hours later.
  • CK-MB - peak 1 day, elevated 3 days (MI, myocarditis, pericarditis)
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4
Q

Left HF Symptoms and Signs

A

Symptoms:

  • Venous congestion –> Dyspnoea, orthopnoea, PND, Nocturnal cough
  • Low CO –> Poor exercise tolerance, fatigue, weight loss, Nocturia

Signs:

  • Venous congestion –> Inspiratory crepitations
  • Low CO –> Pulsus alternans, Systemic Hypotension, Cool extremities, slow cap refill, peripheral cyanosis, Mitral regurgitation, S3 gallop
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5
Q

Coronary Angiography Contraindication

A

Coronary angiography is a radiographic visualisation of the coronary vessels after injection of radiopaque contrast media. Contraindicated in severe renal failure

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6
Q

Right HF Symptoms and Signs

A

Symptoms:

  • Venous Congestion –> peripheral oedema, ascites, fatigue, anorexia

Signs:

  • Venous Congestion –> Peripheral oedema, elevated JVP with abdominojugular reflex and Kussmauls sign, hepatomegaly, pulsatile liver
  • Low CO –> Tricuspid regurg
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7
Q

Causes of Heart Failure

A

Left Heart Failure:

  1. Ischaemic Heart Disease
  2. Hypertension
  3. Valvular Heart Disease
  4. Cardiomyopathy
  5. Myocarditis
  6. Alcoholism
  7. Infections - endocarditis
  8. congenital heart disease
  9. pericardial disease
  10. amyloidosis, haemochromatosis, sarcoidosis

Right Heart Failure:

  1. Left Heart Failure
  2. Cor pulmonale
  3. PE
  4. … And all the causes for LHF
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8
Q

Investigations in HF

A

Imaging:

  1. Transthoracic Echocardiogram
  2. ECG
  3. CXR

Bloods:

  1. BNP
  2. FBC
  3. LFTs
  4. UEC
  5. TFTs
  6. Lipid profile
  7. HbA1c
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9
Q

Findings on CXR in HF

A

A - Alveolar oedema

B - Kerley B lines

C - Cardiomegaly

D - Dilated prominent upper lobe veins

E - Pulmonary Effusions

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10
Q

Acute Treatment of HF

A

LMNOPP

L) Loop diuretic (frusemide)

M) Morphine

N) Nitroglycerin

O) Oxygen

P) Positive airway pressure

P) Positioned sitting upright with feet over edge

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11
Q

Chronic HF Treatment

A

Lifestyle Modification –> Stop Smoking, exercise –> Treat cause of HF —> Treat exacerbating factors Fluid management (Limit intake) and reduce sodium intake

  1. ACE-I —> Captopril 6.25 mg orally, times daily
  2. Beta-Blocker –> Bisoprolol 1.25mg daily (or carvediol, nebivolol, metorolol succinate
  3. Aldosterone antagonist –> Spironolactone 25mg orrally, daily
  4. Loop Diuretic –> Frusemide 20-40mg daily
  5. Can also add… Digoxin + Nitrate
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12
Q

Ischaemic Heart Disease Risk Factors

A
  • HTN
  • Dyslipidaemia
  • Smoking
  • Diabetes
  • Obesity
  • Age
  • Family History
  • Male
  • Depression
  • CKD, SLE, RA Metabolic syndrome
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13
Q

Stable vs Unstable Angina

A

Stable Angina - Induced by effort, relieved by rest

Unstable Angina - Characterised by prolonged (>20 min) angina at rest; new onset of severe angina; angina that is increasing in frequency; longer in duration; or lower in threshold

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14
Q

The 3 typical features of angina

A
  1. Constricting/ heavy discomfort to the chest, jaw, neck, shoulders or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved within 5 minutes of rest or GTN
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15
Q

Investigations for angina

A

Lab tests:

  1. Hb
  2. fasting glucose
  3. fasting lipid profile
  4. troponin

Imaging:

  1. Coronary angiogram (gold standard)
  2. ECG (rule out MI)
  3. CXR (HF, Valve disease, pericardial disease, aortic dissection)
  4. Echo - Stress testing
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16
Q

Long Term Treatment for Angina

A

1) Anti-Angina Medication

  • Beta-Blocker - reduce myocardial demand (Atenolol 25mg daily)
  • Calcium Channel Blocker Antagonist (Verapamil 120mg orally daily)

2) Address exacerbation factors (Anaemia, tachycardia, thyrotoxicosis)
3) Secondary prevention of CVD - Stop smoking, exercise - Antiplatelet - Address BP (ACE-I) - Address Hyperlipidaemia
4) Symptom Relief - Glyceryl trinitrate 400mcg
5) Revascularisation considered if medical therapy inadequate - CABG - Percutaneous coronary intervention

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17
Q

Most common coronary branch affected in MI

A

LAD = 50-40%

RCA = 30-40%

LCx = 15-20%

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18
Q

2 types of MI

A

1) STEMI = transmural full thickness necrosis
2) NSTEMI = sub-endocardial (Troponin rise with no ST elevation)

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19
Q

Clinical features of an MI

A
  • Retrosternal pain acute in onset
  • Radiating to the left side of the chest, left arm, neck, lower jaw
  • Dyspnoea
  • Diaphoresis, syncope, palpitations, N + V
  • New murmur
  • *Note women and diabetes less likely to experience pain
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20
Q

Potential ECG findings for an MI

A
  • ST elevation > 1mm in chest leads and > 2mm in limb leads in at least 2 cont. leads
  • ST depression in leads V1-4 should consider posterior STEMI
  • Flat or inverted T waves
  • Pathogenic Q waves (occurs later)
  • New onset LBBB
  • Dominant R waves in V1-3
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21
Q

Investigations for potential MI

A

1) ECG
2) Troponin
3) Coronary Angiogram

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22
Q

Treatment of MI

A

Morphine, Oxygen, Nitrate

1) Dual Antiplatelet (continue for 12 months)

  • Aspirin 300mg orally then 100mg daily
  • Clopidogrel 600mg orally, then 75mg daily

2) Restore coronary Perfusion (If STEMI or new LBBB)

  • < 90 min (PCI) Percutaneous Intervention i
  • > 120 min (TPA) fibrinolysis - Alteplase

3) Beta-Blocker - Atenolol 25mg daily (Not in decompensated HF)
4) High Dose Statin - 40-80mg atorvastatin daily
5) ACE-I - Captopril 6.25 mg daily

Also modify risk factors - stop smoking, exercise, diabetes, HTN Tx

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23
Q

If you give a patient GTN and it improves chest pain does it mean its cardiac?

A

Not necessarily - GTN will improve indigestion as well. Give gaviscon - if symptoms improve then its indigestion.

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24
Q

Risk factors for essential Hypertension

A
  • OSA
  • Diabetes
  • Obesity
  • Metabolic Syndrome
  • FHx
  • Age > 65yo
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25
Q

Complications of HTN

A
  • CAD
  • LVH
  • Cerebrovascular accident
  • HF
  • PAD
  • CKD
  • Retinopathy
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26
Q

Investigations for Hypertension

A
  1. ECG – may show evidence of LVH or old infarction
  2. Lipid panel – may show high LDL, low HDL or high triglycerides
  3. Urinalysis – may show proteinuria (end organ damage)
  4. FBC – anaemia accompanies chronic renal failure, polycythaemia may be seen with phaeochromocytoma
  5. TSH
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27
Q

First Line Medications for Hypertension

A
  1. ACE-I (Captopril 12.5-50mg TD)
  2. ARB (Candesartan 8-32mg OD)
  3. Ca Channel Blocker (Amlodipine 5-10mg OD)
  4. Thiazide Diuretic (Hydrochlorothiazide 12.5-50mg OD)
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28
Q

The Definition of Shock

A

Shock is most commonly defined as the life-threatening failure of adequate oxygen delivery to the tissues and may be due to decreased blood perfusion of tissues, inadequate blood oxygen saturation, or increased oxygen demand from the tissues that results in decreased end-organ oxygenation and dysfunction.

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29
Q

The 3 different types of shock

A
  1. Loss of intravascular fluid —> hypovolemic shock
  2. Inability of the heart to circulate blood —> cardiogenic shock
  3. Redistribution of body fluid —> distributive shock
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30
Q

Causes of hypovolemic shock

A

Haemorrhagic fluid loss:

  1. Trauma (External or Internal haemorrhage)
  2. Upper GI bleed (Variceal bleeding)
  3. Postpartum haemorrhage

Non-haemorrhagic fluid loss:

  1. Diarrhoea, Vomit
  2. Increased insensible fluid (Burn, SJS)
  3. Third Space fluid loss
  4. Renal fluid loss
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31
Q

Causes of Cardiogenic shock

A
  • MI - Arrhythmias
  • Tension pneuomothorax
  • Cardiac tamponade
  • Constrictive pericarditis
  • PE
  • Restrictive cardiomyopathy
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32
Q

Signs of Shock

A
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33
Q

Causes of Distributive Shock

A

1) Septic Shock (Abnormal Response to infection –> capillary leakage and vasodilation)
2) Neurogenic Shock (Loss of sympathetic vascular tone –> vasodilation)

  • Spinal cord Injury
  • Traumatic brain injury
  • Cerebral haemorrhage
  • Severe pain

3) Anaphylactic shock (Degranulation of mast cells –> histamine release –> vasodilation and capillary leakage)

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34
Q

Definition of Cardiac Arrest

A

Cardiac arrest is the abrupt loss of heart function, breathing and consciousness. Sudden cardiac arrest differs from a heart attack, when blood to a part of the heart is blocked. However, a heart attack can sometimes trigger an electrical disturbance that leads to sudden cardiac arrest.

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35
Q

Causes of Cardiac Arrest (Reversible causes and cardiac causes)

A

Reversibe Causes:

  1. Hypoxia
  2. Hypovolaemia
  3. Hyperkalaemia/ Hypokalaemia
  4. Hypothermia
  5. Hydrogen Ion (acidosis)
  6. Thrombosis (MI)
  7. Thromboembolism (PE)
  8. Tension Pneumothorax
  9. Table and toxins
  10. Cardiac Tamponade

Common Cardiac Causes

  1. Ischaemic Heart Disease (MI and CAD)
  2. Cardiomyopathy
  3. Prolonged QT from medications + Brugada Syndrome
  4. Congenital Heart Disease
  5. Valvular heart disease
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36
Q

4 Specific cardiac rhythms of cardiac arrest

A

Shockable

  1. Ventricular fibrilation
  2. Ventricular tachycardia

Non-Shockable

  1. Asystole
  2. Pulseless electrical activity (PEA)
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37
Q

Investigations for Cardiac Arrest

A
  1. ECG – May show QT interval, ST-segment or T wave changes; conduction abnormalities; ventricular hypertrophy
  2. FBC – Low haematocrit in haemorrhage (Hypovolaemia)
  3. Serum electrolytes – could show abnormality
  4. ABG – May show respiratory acidosis; metabolic acidosis; resp. acidosis with renal comp., metabolic acidosis with resp comp.
  5. Cardiac biomarkers – may be elevated (troponin)
  6. Toxicology
  7. CXR – may show pneumothorax or other disorder of longs leading to hypoxia
  8. Echocardiogram – May show valvular abnormalities, myocardial scarring, cardiomyopathy, pericardial effusion
  9. Coronary angiography – may show signs of CAD
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38
Q

What makes the first and second heart sounds?

A
  1. First Heart Sound - Mitral and Tricuspid valves closing (Soft in MR, louder in MS)
  2. Second Heart Sound - Aortic and Pulmonary valves closing (Softer in more severe aortic stenosis, louder in systemic and pulmonary hypertension)
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39
Q

Causes of 3rd and 4th heart sounds

A

3rd Heart Sound (Precedes S1) –> LVH

4th Heart sound (Procedes S2) –> Severe HTN

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40
Q

Intensity of Murmurs

A
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41
Q

Dynamic Manouvres for Heart Murmurs

A

Left lateral position

  • Get patient to roll onto left side which brings apex of heart closer to chest wall, auscultate over mitral area and in axilla

Inspiration

  • Get patient to fully inspire and listen over the tricuspid and pulmonary areas. Inspiration will increase venous return and blood blow to right side of heart

Valsalva

  • Valsalva manoeuvre and listen over left sternal edge (systolic murmur with hypertrophic cardiomyopathy) and apex (late systolic murmur with mitral valve prolapse)

Deep expiration

  • Get patient to lean forward in full expiration and listen to the base of the heart to accentuate aortic regurgitation and pericardial rub
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42
Q

Causes of Aortic Stenosis

A
  1. Degenerative calcification
  2. Rheumatic Endocarditis
  3. Congenital (Unicuspid/ Bicuspid Valve)
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43
Q

Signs of Aortic Stenosis

A
  • Slow Rising Pulse
  • Narrow Pulse Pressure
  • LV Heave
  • Severe AS - soft S2

Ejection Systolic Murmur - hear at hase, left sternal edge and aortic area, radiates to carotid

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44
Q

Aortic Regurgitation causes

A

Acute:

  1. Infective Endocarditis
  2. Aortic Dissection type A

Chronic

  1. Bicuspid aortic valve
  2. Connective tissue disease (Marfans)
  3. Rheumatic fever
  4. Rheumatic Disease (RA, SLE)
45
Q

Aortic Regurgitation Signs

A
  • Bounding pulse – Collapses when raise arm
  • De Messet’s sign – head bobbing with pulse
  • Corrigan’s sign – visible carotid pulse
  • Quinicke’s sign - capillary nailbed pulsation in fingers
  • Meller’s sign – systolic pulsation of the uvula
  • Traube’s sign – booming shoud herd over femorals

Early Decrescendo Diastolic Murmur - Exacerbated by dynamic manouvre

46
Q

Mitral Regurgitation Causes

A
  1. Mitral valve prolapse
  2. Dilated cardiomyopathy
  3. Ischaemic heart disease (post MI)
  4. Rheumatic fever
47
Q

Signs of Mitral Regurgitation

A
  • AF
  • Displaced apex

Pansystolic Murmur – loudest at 5th intercostal mid-clavicular line, radiating to axilla. Loudest at apex when rolled to the side and louder on expiration.

48
Q

The 3 Microangiopathic complications of diabetes

A
  1. Diabetic nephropathy - Decreased GFR and albuminuria also glomerulosclerosis, arteriosclerosis, pyelonephritis
  2. Retinopathy - Proliferative (increased number of blood vessels covering retina) and Non-proliferative (plaques on retina). Also cataracts and glaucoma
  3. Neuropathies - Peripheral neuropathy (glove and stocking) and Autonoic neuropathy (erectile dysfunction, abnormal sweating, dysregulation of BP)
49
Q

Macroangiopathic complications of diabetes

A
  1. Atherosclerosis due to endothelial dysfunction, pro-inflam/coagulant cytokines
  2. Ischaemic Heart Disease
  3. Cerebrovascular Disease
  4. Peripheral Vascular Disease
  5. Diabetic Foot
  6. Hypertension
50
Q

Virchows Triad

A
  1. Hypercoaguable state - cancer, pregnancy
  2. Endothelial Injury - trauma, surgery
  3. Stasis - immobilisation
51
Q

Causes/ Risk factors of DVT

A
  1. Previous VTE
  2. Active Malignancy
  3. HRT + Oral contraceptive Pill
  4. Immobility (Long Flight)
  5. Recent Surgery
  6. Hypercoaguability - Protein S and C def., Anti-thrombin def., Factor V leiden
  7. Smoking
  8. Older age
  9. Obesity
52
Q

3 Complications of DVT

A
  1. PE
  2. Post-Thrombotic Syndrome - manifest years post DVT –> erythema, swelling and ulceration
  3. Paradoxical embolism (PFO –> CVA)
53
Q

Investigations to order for a DVT

A

Blood Tests

  1. APTT (Activated Partial Thromboplastin Time) [Heparin]
  2. INR [warfarin]
  3. D-dimer
  4. bHCG (Women of Childbearing age)
  5. FBC - haematological malignancy, thrombocytopenia
  6. UEC - baseline for meds
  7. LFTs - baseline for meds

Imaging

  1. Venous Duplex U/S or Doppler Venous flow testing
  2. CT
54
Q

Treatment for DVT

A
  1. Anticoagulant therapy
  • Apixaban (CrCl more than 25 mL/min) 10 mg orally, twice daily for 7 days, then decrease to 5 mg twice daily.
  • For patients with proximal DVT with major risk factor no longer present treat for 3 months
  1. Physical activity – early ambulation
  2. Compression stockings
55
Q

Prophylaxis for DVT

A
  • Pharmacotherapy –> LMW Heparin - dalteparin (CrCl 30 mL/min or more) 5000 units subcutaneously, once daily
  • Graduated compression stocking
  • Intermittent pneumatic compression devices
  • Calf exercises, Increase mobility
56
Q

Well’s Criteria for DVT

A
57
Q

DVT symptoms

A
  • Unilateral Pain and tenderness
  • Oedema, erythema, warmth
  • mild fever
  • engorged superficial veins
58
Q

Stages of Peripheral Arterial Disease

A
  1. Asymptomatic PAD
  2. Intermittent Claudication - pains, cramps, parasthesia distal to arterial occlusion
  3. Pain at rest - typically in distal metatarsals, worse at night
  4. Critical Limb Ischaemia - presence of resting pain, ulcer, gangrene (indicative of limb-threatening arterial occlusion)
59
Q

Signs and Symptoms of Peripheral Arterial Disease (6 P’s and other leg signs)

A

The 6 P’s

  • Pulse - Absent/ Diminished
  • Pallor
  • Parasthesia
  • Perishingly cold
  • Paralysed
  • Pain

And…

  • Decreased perspiration
  • Decreased hair
  • Brittle nails
  • Atrophied Skin
  • End-stage –> gangrene, ulcers
60
Q

Definition of Peripheral Arterial Disease

A

PAD is characterized by narrowing and, in final stages occlusion of the peripheral arteries due to atherosclerotic plaques. PAD is defined by abnormal ankle brachial index of < 0.9.

61
Q

Investigations in Peripheral Arterial Disease

A
  1. ABI - Systolic BP ankle: SBP brachial
    > 1.3 = medial sclerosis with incompressible vascular wall
    1-1.3 = normal
    0.91-0.99 = Borderline
    0.4-0.9 = mild to moderate PAD (Claudication)
    < 0.4 = severe PAD
  2. Imaging
    Digital subtraction angiography
    Colour-coded duplex U/S
  3. Exercise testing ABI (if normal resting ABI)
62
Q

Treatment For Peripheral Arterial Disease

A
  1. Conservative
    Smoking Cessation
    Foot care
    Graduated walking program
  2. Medications to reduce CVD risk
    Long term antiplatelet - aspirin 100mg oral
    Statin
    Anti-HTN (Statin)
    Hyperglycaemic Control
  3. Revascularisation (Critical Limb Ischaemia)
  4. Amputation (Gangrene)
63
Q

Symptoms and Signs of Acute Pulmonary Oedema

A
  • Dyspnoea, PND and orthopnoea
  • Pink Frothy sputum
  • Peripheral oedema
  • Morning Cough

Signs

  • Crackles
  • Cardiogenic wheeze
  • Displaced apex beat
  • Other signs of Left Heart Failure
64
Q

Treatment of Acute Pulmonary Oedema

A
  1. Oxygen - 10-15L/min viahudson mask
  2. Diuretics (reduces fluid overload) - Frusemide 20-80mg IV bolus
  3. Glyceryl Trinitrate 400ug (reduce preload)
  4. CPAP or BIPAP
  5. Morphine (Anxiety and stress) - 1-2.5mg IV
  6. If in AF –> Amiodarone 300mg IV
  7. Dobutamine - Inotropic effects and vasodilation
65
Q

infective Endocarditis Risk Factors

A

Pre-existing conditions:

  • Prosthetic heart valves
  • Cyanotic congenital heart disease
  • Previous infective endocarditis
  • Mitral valve prolapses with significant regurgitation
  • Acquired valvular dysfunction in indigenous patients e.g. Rheumatic fever
  • Surgically constructed pulmonary-systemic shunts

Bacteraemia

  • Infected peripheral venous catheters, surgery, dental procedures
  • Non-sterile venous injections (IVDU)
  • Bacterial infections of various organs (UTI)
66
Q

Main Pathogens in Infective Endocarditis

A
  1. Staphylococcus aureus
  2. Streptococcus mutans & sanguinis (Predamaged calces)
  3. Staphylococcus epidermidis
  4. Enterococcus faecalis
67
Q

Signs Of Infective endocarditis

A

Constitutional symptoms

  • Fever, chills
  • Tachycardia
  • General malaise, weakness, night sweats, weight loss
  • Dyspnoea, cough, pleuritic chest pain
  • Arthralgias, myalgias

Cardiac Manifestations

  • New heart murmur (MR, MS, AR, AS)
  • Signs of progressive heart failure e.g. dyspnoea, oedema
  • Signs of acute cardiac decompensation e.g. pulmonary oedema
  • Arrhythmias e.g. Third-degree AV block

Extra cardiac manifestations

These manifestations are mainly caused by bacterial micro embolisms or precipitation of immune complexes

  • Petechiae –> splinter haemorrhages
  • Janeway lesions – asymptomatic haemorrhages on palms and soles
  • Osler nodes – painful, nodulous haemorrhages on pads of fingers and toes
  • Roth spots – retinal haemorrhages
  • Acute renal failure –> haematuria and anuria
  • Neurological manifestations e.g. seizures, paresis
  • Pulmonary embolism –> Dyspnoea
  • Clubbing
68
Q

Investigations in Infective Endocarditis

A
  1. Lab tests
  • Blood culture
  • Leucocytosis – raised WCC
  • Raised ESR and CRP
  1. Echocardiogram
  • Valve vegetation’s, new regurgitation, abscess
  • Transoesophageal echo to confirm findings

Also… ECG, FBC, urinalysis

69
Q

Dukes criteria (IE)

A

Major

  • Two separate blood cultures positive for typical pathogen, blood cultures persistently positive > 12 hours apart, 3 or more separate cultures > 1 hour apart prior to antibiotic therapy
  • Echocardiogram evidence
  • New valvular regurgitation

Minor

  • Predisposition (underlying heart disease or IVDU)
  • Fever > 38
  • Vascular abnormalities – arterial emboli, intracranial infarction
  • Immunologic disorder e.g. Osler node, Roth spot, glomerulonephritis
  • Microbiology – positive blood culture for atypical pathogen
70
Q

Treatment for Infective Endocarditis

A

Native valve endocarditis

  • IV benzylpenicillin + flucloxacillin

Prosthetic valve endocarditis

  • IV vancomycin + IV gentamicin
71
Q

Clinical features of Chronic Venous Insufficiency

A
  1. Oedema formation
  2. Telangiectasia
  3. Yellow-brown or red-brown skin pigmentation
  4. Statis dermatitis - scaly, pruritic rash
  5. Varicose veins
  6. Lipodermatosclerosis
  7. Restless legs
  8. Pruritis, tingling and numbness
  9. Generalised or localised pain (worsened by heat and standing)
72
Q

3 Main types of ulcers and their characteristics

A
  1. Venous Ulcers - Shallow with irregular borders, characteristically located over medial malleolus. Associated with other featured of chronic venous insufficiency
  2. Arterial Ulcers - small deep lesions and well defined borders and necrotic tissue. most commonly occur distally at sites of pressure. Likely to have intermittent claudication. Associated with cold limb, hair loss, skin atrophy, diminished pulses.
  3. Neuropathic Ulcers - Variable in size and depth, with punched out appearance. Occur in sites of pressure. Additionally they have peripheral neuropathy with warm feet and good pulses.
73
Q

Investigation for ulcers

A
  1. Ankle-brachial index - to exclude peripheral artery disease
  2. HbA1c - peripheral neuropathy in diabetes
  3. Duplex U/S - underlying venous insufficiency
  4. Microbilogy swabs and cultures - if infection suspected (erythematous or purulent)
  5. X-ray - osteomyelitis (Neuropathic)
  6. Serum B12 (Neuropathic)
74
Q

Definition of Abdominl Aortic Aneurysm

A

AAA is a focal dilation of the abdominal aorta to more than 1.5 times its normal diameter. Dilation is of all 3 layers of the aortic wall (intima, media and adventitia) to >50% of the normal diameter

75
Q

Clinical features of AAA

A
  • Lower back pain
  • Pulsatile abdominal mass
  • Bruit on auscultation
  • Peripheral thrombosis and distal atheroembolic phenomena (blue toe syndrome and livedo reticularis)
  • Decreased ankle brachial index

Ruptured:

  • throbbing abdominal or low back pain radiating to flank, buttocks
  • grey turner sign (ecchymosis of affected flank)
  • Cullen sign (Periumbilical ecchymosis)
  • hypovolaemic shock
  • nausea and vomiting
  • syncope
76
Q

Investigations for AAA

A
  1. U/S –> Determines presence, size and extent. Can detect thrombus or free peritoneal blood in case of rupture
  2. CT with contrast –> Determines AAA rupture, suprarenal involvement and visceral artery involvement
  3. Arteriography
77
Q

Treatment for AAA

A

1) Conservative - reduce cardiovascular risk factors
2) Surgical - elective repair for asymptamatic AAA over 5.5 cm or emergency repair if symptomatic

  • Endovascular aneurysm repair
  • Open repair
78
Q

Treatment for AF

A

Anticoagulation

  • Concurrent MS or mechanical valve –> Warfarin
  • Non-valvular –> NOAC e.g. apixiban 5mg oral TD

Rate control

  • Beta-blocker e.g. atenolol 25mg
  • Ca-channel blocker e.g. verapamil 180 OD
  • Amiodarone 200mg OD

Rhythm control

  • Synchronised direct current electrical cardioversion
  • Amiodarone 300mg IV
79
Q

Classifications of AF

A
  1. Haemodynamic stability
  2. Heart rate - slow or rapid
  3. Onset - paroxysmal, persistent, long standing
  4. Mitral valve involement
80
Q

Complications of AF

A
  • Acute LHF –> pulmonary oedema
  • Life threatening ventricular tachycardia
  • Thromboembolic events –> stroke/ TIA, renal infarct
  • The relative stagnation of blood in the atria due to ineffective atrial emptying promotes clot formation
81
Q

What layers are involved in an aortic dissection?

A

Tear in the inner later of the aorta which leads to a progressively growing haematoma between the intima-media space.

82
Q

Causes of aortic dissection

A
  1. Hypertension
  2. Trauma (Deceleration injury in MVAs)
  3. Connective tissue disease (Marfans, Ehlers-Danlos syndrome)
  4. Bicuspid aortic valve
  5. Coarctation of the aorta
83
Q

Clinical features of aortic dissection

A
  • Sudden and severe tearing/ ripping pain in anterior chest or back (interscapular or retrosternal pain)
  • Migrates as the dissected wall propagates caudally
  • ­ BP (If hypotensive consider shock from blood loss or cardiac tamponade)
  • Asymmetrical BP and pulse readings between limbs
  • Syncope, diaphoresis, confusion
  • Heart murmur
84
Q

Group A strept supporative and non-supporative complications

A

Non-supportive

  • Rheumatic fever
  • Scarlet fever
  • Post-streptococcal glomerulonephritis

Supportive

  • Peritonsillar abscess
  • Parapharyngeal abscess
  • Otitis media
  • Sinusitis
85
Q

Clinical features of Rheumatic Fever (JONES criteria)

A
  • Joints - migratory polyarthritis
  • Love Heart “O” - pericarditis
  • Nodules (Subcutaneous nodules)
  • Erythema marginatum - centrifugally expanding pink rash with well defined borders and centrally clearing
  • Sydenham chorea - involuntary, irregular movements of limbs, neck, head. Muscle weakness and slurred speech.
86
Q

Treatment of rheumatic fever

A
  1. Antibiotics – oral penicillin
  2. Therapy for arthritis and fever – NSAIDs
  3. Therapy for Heart Failure – diuretics and conventional therapy
  4. Therapy for myocarditis – monitor and treat arrhythmias
87
Q

Rheumatic Heart Disease refers to which two clinical entities

A
  • Acute pericarditis as a sequela of GAS infection
  • Chronic cardiac valvular changes as a complication of acute rheumatic fever
88
Q

What are the three major types of cardiomyopathy

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive
89
Q

Causes of dilated cardiomyopathy

A
  1. Idiopathic (50%)
  2. Secondary cause
    • CAD
    • HTN
    • Valvular heart disease – AS, AR, MR
    • Peripartum
  3. Infections
  • Coxsackie B virus myocarditis
  • Rheumatic heart disease
  • Chagas disease
  • Viral hep, HIV
  1. Genetic predisposition
    * Haemochromatosis
  2. SLE
  3. Toxin – alcohol, cocaine, cardiotoxic drugs (doxorubicin)
  4. Malnutrition – B1 (Thiamine), selenium def.
  5. Chronic tachycardia – AF
  6. Metabolic - thyroid disease
90
Q

Causes of hypertrophic cardiomyopathy

A
  1. Primary hypertrophic cardiomyopathy (60-90%)
  2. Secondary hypertrophic cardiomyopathy
  • Friedreich ataxia, Fabry disease, Noonan syndrome, amyloidosis
    iii. Pressure related hypertrophy – chronic hypertension

Hypertrophic obstructive cardiomyopathy is one of the most frequent causes of sudden cardiac death in young patients, especially young athletes

  • 70% obstructive type
  • 30% non-obstructive type
91
Q

Cause of restrictive cardiomyopathy

A

Idiopathic

Secondary to endomyocardial fibrosis (Puppy LEASH)

  • Post radiation fibrosis
  • Loffler endocarditis
  • Endocardial fibroelastosis
  • Amyloidosis
  • Sarcoidosis
  • Haemochromatosis
92
Q

Causes of myocarditis

A

Infectious

Viral

  • Coxsackie B1-5
  • Parvovirus B19
  • Human Herpesvirus 6
  • Adenovirus
  • HCV, HIV, EBV, CMV, ECHOVIRUS

Bacterial

  • Beta-haemolytic Streptococcus group A (Rheumatic fever)
  • Corynebacterium diphtheria (diphtheria)
  • Borrelia burgdorferi
  • Mycobacterium (TB)
  • Mycoplasma

Non-infectious

  • Connective tissue diseases (SLE)
  • Vasculitis syndromes (Kawasaki disease)
  • Toxic myocarditis – radiation therapy, medications (Sulfonamides), chemotherapy, alcohol, cocaine
93
Q

Clinical features of myocarditis

A
  • Preceding (1-2 weeks) of flulike symptoms – fever, arthralgia, myalgia, URTI (viral cause)
  • Fatigue, weakness, dyspnoea, nausea, vomiting
  • Cardiac arrhythmia – often sinus tachycardia
  • Chest pain – indicated pericardial involvement
  • Auscultation - Brief systolic murmur, HF –> S3 gallop, Pericarditis –> pericardial friction rub
94
Q

Investigations for Suspected Myocarditis

A
  • Holter monitor
  • Lab tests - raised troponin, ESR + CRP, Leukocytosis, raised BNP, viral serology
  • Imaging - CXR - cardiomegaly, pulm congestion, Echo - exclude other causes, myocardial biopsy
95
Q

Causes of Thrombophlebitis

A

Stasis

  • Immobility
  • varicose veins

Hypercoaguability

  • Oral contraceptive, HRT
  • Factor V leiden, protein C or S def.
  • cancer

Vessel wall damage

  • Cannulation
  • IVDU
  • surgery
  • Inflammatory vascular disease
  • previous vein thrombosis
96
Q

Treatment of thrombophlebitis

A
  1. First line

Initial treatment doses of low molecular weight heparin (LMWH), unfractionated heparin (UFH), or fondaparinux followed by warfarin to target INR 2.5. Rivaroxaban, dabigatran, apixaban, or edoxaban can also be used for initial treatment.

  1. Second line

Oral NSAIDs can be used as an alternative to anticoagulants, especially if the superficial vein thrombophlebitis (SVT) is short in length and far removed from the saphenofemoral junction. NSAIDs can alleviate symptoms and may prevent SVT extension and recurrence. However, there are not adequate data to support a decreased incidence of venous thromboembolism with NSAIDs.

97
Q

When should Familial hypercholesterolaemia be suspected?

A

FH should be suspected when untreated fasting LDL cholesterol levels are above 5mmol/L

98
Q

Causes of Hyperlipidaemia

A

Acquired

  • Obesity
  • Diabetes mellitus
  • Physical inactivity
  • Alcoholism
  • Hypothyroidism
  • Nephrotic syndrome
  • Cholestatic liver disease
  • Cushing’s disease
  • Drugs: OCP, metoprolol, high dose diuretic

Congenital

  • Hyperchylomicronemia
  • Familial hypercholesterolemia (mutation of LDL receptor leading to increased LDL)
  • Familial hypertriglyceridemia
99
Q

Acyanotic Congenital Heart Defects

A

ASD, VSD, PDA, PFO, Coarct of aorta, Endocardial cushion defect

100
Q

What is Eisenmenger syndrome?

A
  1. Prolonged pulmonary hypertension due to left-to-right shunt causes reactive constriction with permanent remodelling of pulmonary vessels –> irreversible pulmonary hypertension
  2. Right ventricle hypertrophies to compensate for pulmonary hypertension –> Right ventricular pressure becomes higher and eventually exceeds left ventricular pressure –> reversal of blood flow, associated with onset of cyanosis either at rest of during exercise
101
Q

Pathophysiology of acyonitic heart defects

A
  • The left chambers of the heart are a high-pressure pump system and the right chambers of the heart are a low-pressure pump system.
  • Heart defects may lead to the formation of connections between the two systems (shunts), allowing blood to flow along the pressure gradient from high to low pressure.
  • The shunts are classified according to the direction of blood flow as left-to-right shunts or right-to-left shunts.
  • Left-to-right shunt: Oxygenated blood from the lungs is shunted back into the pulmonary circulation via an ASD, VSD, or PDA → pulmonary hypertension and right ventricular pressure overload → right-sidedheart hypertrophy (cardiomegaly on x-ray) and heart failure, but no cyanosis
  • Right-to-left shunt: blood flows from the right to the left heart via a shunt → deoxygenated blood enters the systemic circulation → cyanosis
102
Q

General features of acyanotic congenital heart disease

A
  • Exercise intolerance – fatigue, exertional tachycardia, pallor
  • Exertional dyspnoea, tachypnea
  • Recurrent bronchopulmonary infections
  • Failure to thrive
  • Right sided HF –> Hepatic venous congestion with hepatomegaly
  • -> Peripheral oedema is rarely seen in infants
  • Left-sided HF –> Tachypnoea, pulmonary oedema
  • -> Low CO –> decreased BP, pallor, cool extremities, poor growth, syncope
103
Q

Complication of ASD

A

Paradoxical embolism –> Stroke

104
Q

Causes of congenital heart diseases

A
  • Genetic defects (e.g. trisomies)
  • Maternal infections (e.g. rubella)
  • Maternal consumption of drugs or alcohol during pregnancy
105
Q

Cyanotic Congenital Heart disease

A

Tetrology of fallot, Transposition of great arteries and coarctation of aorta in newborns

106
Q
A
107
Q

4 defects in teratology of fallot

A
  1. RV outflow obstruction
  2. RVH
  3. VSD
  4. overriding aorta
108
Q

You see a patient on the ward post MI complaining of shortness of breath - what are your differentials

A
  1. Heart failrue secondary to IHD
  2. PE
  3. Infection - Hospital acquired pneumonia
  4. Medications e.g. beta-blockers
109
Q

What type of STEMI would you not give GTN for?

A

Inferior STEMI as reduced preload

Medicine (11 decks)

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