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Medicine Phase 2a > Cardio: Good set > Flashcards

Cardio: Good set Flashcards

1
Q

What are the types of IHD?

A

Stable angina

Acute Coronary Syndromes (ACS)
- Unstable angina
- NSTEMI
- STEMI

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2
Q

What are the modifiable risk factors for IHD?

A

Smoking
Obesity
Sedentary lifestyle
Diet

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3
Q

What are the clinical modifiable risk factors for IHD?

A

Hypertension
Diabetes
Hyperlipidaemia
Depression

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4
Q

What are the non-modifiable risk factors for IHD?

A

Age
Genetics/Family history - black
Gender (M>F risk)

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5
Q

What are the psychosocial risk factors for IHD?

A

High demand, low control jobs (high stress),
Low social interaction and support

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6
Q

What are the types of angina?

A

Stable angina: induced by effort, relived by rest

Unstable angina: angina of increasing frequency or severity, occurs on minimal exertion or at rest, associated with an increased risk of MI

Decubitus angina: precipitated by lying flat

Variant (Prinzmetal) angina: caused by coronary artery spasm

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7
Q

What is definition of angina?

A

Symptomatic reversible myocardial ischaemia

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8
Q

What are the main causes of angina?

A

Atheroma
Hypertension
Vasculitis
Anaemia

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9
Q

What is the presentation of angina?

A

Classical features
Constricting/heavy, central, tight chest pain radiating to jaw, neck, shoulders or arm
Precipitated by exertion
Relived by rest or GTN

Other features
Levine’s sign (clenched fist over the chest to cope with the pain)
Associated symptoms: Dyspnoea, Nausea, Sweatiness, Faintness

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10
Q

What are the classifications of Stable Angina?

A

Classification: Classical Features
All 3 features = typical angina,
2 features = atypical angina,
0-1 features = non-anginal chest pain

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11
Q

What are features that make angina less likely?

A

Pain that is continuous, pleuritic or worse with swallowing
Pain associated with palpitations, dizziness or tingling

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12
Q

What precipitating features can lead to angina?

A

Demand:
Emotion
Cold weather
Heavy meals
HTN
Tachyarrhythmia
VHD
Hyperthyroidism

Supply:
anaemia
Hypoxia
Polycythaemia
Hypothermia
Hypo/Hypervolaemia

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13
Q

What baseline investigations may you do for stable angina?

A
  • ECG – usually normal, may show ST depression and T wave inversion
  • FBC (check for anaemia)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • Lipid profile
  • Thyroid function tests
  • HbA1C and fasting glucose
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14
Q

What is the gold standard investigation for stable angina?

A

CT coronary angiogram

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15
Q

What is the treatment for stable angina?

A

1: Lifestyle changes

2: Pharmacological

  • Secondary Prevention:
    • Aspirin (75mg OD)
    • Atorvastatin (80mg OD)
    • ACEi
  • Symptomatic relief: GTN spray
  • Anti-anginal Medications:
  1. Beta Blockers (bisoprolol) OR Rate limiting CCB (verapamil)
  2. Switch
  3. Combine (BB + CCB - but would be amlodipine not verapamil as this can cause asystole)
  4. Add 3rd drug (isosorbide dinitrate)

3: Interventional (revascularisation)

  • Percutaneous Coronary Intervention (PCI)
  • Coronary Artery Bypass Graft (CABG)
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16
Q

What are the conditions under ACS?

A

Unstable angina
NSTEMI
STEMI

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17
Q

What is the pathology of ACS?

A

Plaque Rupture –> Thrombosis –> Inflammation –> Infarction

Rarer causes:
Emboli
Coronary artery Spasm
Vasculitis

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18
Q

Define Myocardial Infarction

A

Reduced blood supply to myocardial cells resulting in cell death releasing troponin

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19
Q

Define unstable Angina?

A

ACS defined by the absence of biochemical evidence of myocardial damage

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20
Q

What are the main features of unstable angina presentation?

A

Cardiac chest pain at rest (lasting >20mins)
Cardiac chest pain with crescendo pattern (gradual increase)
New onset angina

Associated symptoms
Nausea, Sweatiness, Dyspnoea, Palpitations

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21
Q

What are the investigations for Unstable angina?

A

ECG – ST depression (when in pain)
Cardiac enzymes – normal troponin
FBC – anaemia (precipitating factors)
Coronary angiogram - GS

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22
Q

What is the treatment of Unstable Angina?

A

Risk factor modification:

  • High dose statin e.g. Atorvastatin
  • ACE-I (unless CI)

Reduce cardiovascular events:

  • Antiplatelet agents: Aspirin and Clopidogrel (DAPT)
  • Anti-coagulants: Fondaparinux or LMWH

PRN symptomatic relief:

  • Nitrates (PO or IV) – for recurrent chest pain

Anti-anginal medications:

  • Beta-blockers e.g. Bisoprolol
  • CCB e.g. Amlodipine (if beta-blockers CI)
  • Nitrates e.g. Isosorbide dinitrate

Revascularisation:

  • Percutaneous coronary intervention (PCI – ‘stenting’)
  • Coronary artery bypass graft (CABG) surgery
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23
Q

What is the presentation of an MI?

A

Acute central chest pain lasting >20mins radiating to jaw, neck, shoulders or arm
Unremitting, usually severe but may be absent, Occurs at rest, 1/3 at night

Associated symptoms
Nausea, Sweatiness, Dyspnoea, Palpitations

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24
Q

What are the investigations for an STEMI?

A

ECG
Acute changes:
Hyperacute T-waves,
ST elevation or new LBBB

Hours/days:
T-wave inversion and pathological Q waves (deep and wide)

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25
Q

What are the investigations for an NSTEMI?

A

ECG:
ST depression, T wave inversion, non-specific changes or normal

Cardiac Enzymes:
Troponin (sensitive marker for myocyte injury, not ACS specific)

Bloods – FBC, U&E, Glucose, Lipids
Other – CXR, Echo

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26
Q

What ECG cords are associated with a circumflex MI?

A

Lateral:
Lead I
aVL
V4-V6

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27
Q

What ECG cords are associated with an LAD MI?

A

Anteroseptal:
V1-V3

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28
Q

What ECG cords are associated with an Inferior MI?

A

Lead II
Lead III
Lead aVF

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29
Q

What is the Pre-hospital management of an MI?

A

Aspirin 300mg and GTN

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30
Q

What is the acute Hospital management of an MI?

A

MONAC:
Morphine
Oxygen (if hypoxic under 94%)
Nitrates (GTN)
Aspirin
Clopidogrel

+/- Heparin

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31
Q

What is the NSTEMI acute management?

A

B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. <95%)

Estimate 6 month mortality with GRACE:
Low risk = Ticagrelor
High Risk = PCI within 72 hours + Prasugrel + Heparin

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32
Q

What is the STEMI acute management?

A
  1. STEMI identified
  2. Aspirin (300mg)
  3. PCI possible within 120 mins within 12 hours of STEMI onset?
    3a (yes). Prasugrel + Unfractionated Heparin + PCI
    3b (No). Fibrinolysis if within 12 hours STEMI onset. (IV alteplase) + Ticagrelor
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33
Q

What is the Long term management of an MI?

A

BACAS:
Beta blocker
Aspirin
Clopidogrel
ACEi
Statin

Risk factor modification.

High risk of emboli - Give warfarin (3-6 months)

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34
Q

What are the complications of MI?

A

Death
Arrythmias
Ruptured Septum
Tamponade
Heart Failure

Valve disease - ruptured papillary muscles
Aneurysm of Ventricles
Dressler’s Syndrome
Embolism
Reoccurrence of ACS

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35
Q

What are some differential Diagnoses for Chest pain?

A

Cardiac: MI, Angina, Aortic Dissection, Pericarditis
Resp: PE, Pneumonia, Pneumothorax, Pleurisy, Cancer
MSK: Rib fracture, costrochondritis
GI: GORD
Psychological: Anxiety, Panic Attack

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36
Q

Define Heart Failure

A

‘A state where the heart is unable to pump enough blood to satisfy the needs of metabolizing tissues”

CO is inadequate for body’s requirements (CO=HR x SV)

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37
Q

What is the aetiology of HF?

A

Ischemic Heart Disease
Valvular Heart Disease (commonly AS)
Hypertension
Arrhythmias (commonly AF)
Cardiomyopathy

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38
Q

What are the risk factors for HF?

A

65 and older
African descent
Men
Obesity
Previous MI

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39
Q

What are the classifications of HF?

A

Reduced EF (<40%) - often Systolic failure
Mid Range EF (40-49%)
Preserved EF (>50%) - often Diastolic Failure

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40
Q

What are the cardinal Symptoms of HF?

A

Shortness of Breath
Fatigue
Ankle swelling

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41
Q

What are the signs symptoms of Left ventricular failure?

A

Causes Pulmonary Congestion:
Symptoms:

  • Exertional dyspnoea
  • Fatigue
  • Paroxysmal nocturnal dyspnoea (PND)
  • Nocturnal cough – (+/-) pink frothy sputum

Signs:

  • Cardiomegaly (displaced apex beat)
    3rd and 4th heard sounds
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42
Q

What are the signs symptoms of Right ventricular failure?

A

Causes Systemic Congestion:
Symptoms:

  • Peripheral oedema
  • Ascites

Signs:

  • Raised JVP
  • Hepatomegaly
  • Pitting oedema
  • Weight gain (fluid)
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43
Q

What system is used to classify HF?

A

NYHA:
Stage 1 - No limitation (asymptomatic)
Stage 2 - Slight limitation (mild HF)
Stage 3 - Marker Limitation (symptomatic HF)
Stage 4 - Severe Symptomatic HF

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44
Q

What are the investigations for HF?

A

Blood tests:
NT-pro B-type Natriuretic peptide (BNP) – secreted by ventricles in response to increased myocardial wall stress
Cardiac enzymes: Creatinine kinase, troponin I, troponin T

Others:
FBC (anaemia), LFTs (hepatomegaly), U&Es, BNP, TFTs, Glucose (DM)
CXR – ABCDE
ECG

Echocardiography – Gold standard

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45
Q

What is seen on CXR in HF?

A

ABCDE:
Alveolar Oedema (Batwings)
Kerley B Lines (interstitial Oedema)
Cardiomegaly
Dilation of upper Lobe Vessels
Pleural Effusions

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46
Q

What is the Management of HF?

A
  1. Lifestyle Management
  • Education
  • Smoking cessation
  • Reduce alcohol
  • Reduce salt intake
  • Exercise and Obesity control
  1. Symptomatic Management:
  • Diuretics - Loop (furosemide)
  1. Disease Altering Medication (ABAL):
  • 1st Line - ACEi (ramipril) + - Beta Blockers (bisoprolol)
  • 2nd Line - Aldosterone Antagonist (Eplerenone)
  • 3rd Line - Ivabradine, ARNI, Hydralazine, Digoxin
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47
Q

What is the acute Treatment of HF?

A
  • IV Furosemide – reduce fluid afterload
  • Oxygen
  • Nitrates e.g., GTN (spray or tablets)
  • Severe: consider inotropic drug (e.g., dobutamine) or vasopressors (e.g., norepinephrine) or mechanical circulatory assistance
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48
Q

What is the Chronic Treatment of HF?

A

ABCD

  • ACE-I (e.g., Ramipril)/ARB (e.g., Candesartan, Valsartan)
  • Beta-blockers (e.g., Atenolol)
  • CCB and other vasodilators (e.g., Amlodipine, Hydralazine)
  • Diuretics and Digoxin (loop – Furosemide, aldosterone antagonist – Spironolactone)
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49
Q

When should you avoid using ACE inhibitors?

A

In patients with valvular heart disease

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50
Q

Why is Eplerenone preferred over Spironolactone?

A

Spironolactone causes gynaecomastia

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51
Q

What are the causes of Acute left ventricular failure and pulmonary oedema?

A

Iatrogenic (aggressive IV fluids in frail elderly patient with impaired LV function)
Sepsis
Myocardial Infarction
Arrhythmias

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52
Q

What is the Treatment of Acute left ventricular failure and pulmonary oedema?

A

Pour SOD (acute LVF):

Pour away (stop) their IV fluids
Sit up
Oxygen – oxygen saturations are falling (<95%)
Diuretics – Furosemide

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53
Q

What is Cor Pulmonale?

A

Right heart failure and abnormal enlargement (of the right ventricle) caused by chronic pulmonary arterial hypertension

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54
Q

What are the causes of Cor Pulmonale?

A

COPD
Bronchiectasis
PF
Chronic Asthma
PE
Pulmonary Vasculitis
etc

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55
Q

How does Cor Pulmonale Present?

A

Symptoms:

  • Dyspnoea
  • Fatigue
  • Syncope

Signs:

  • Cyanosis
  • Tachycardia
  • Raised JVP
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56
Q

What are the investigations for Cor Pulmonale?

A

GS - right heart catheterisation

Bloods: FBC (Hb and haematocrit ↑ – secondary polycythaemia)
ABG: hypoxia +/- hypercapnia
CXR: enlarged right atrium and ventricle, prominent pulmonary arteries
ECG: P-pulmonale, Right axis deviation, Right ventricular hypertrophy/strain

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57
Q

What is the treatment for Cor Pulmonale?

A

Treat underlying cause
Treat respiratory failure – acute situation give 24% oxygen
Treat cardiac failure – Diuretic e.g., Furosemide
Heart-lung transplant (if young patient)

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58
Q

What is the most important risk factor for premature death and CVD?

A

Hypertension

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59
Q

Define White Coat Hypertension

A

Elevated clinic BP but normal ABPM

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60
Q

Define Malignant Hypertension

A

Rapid rise in BP leading to vascular damage
(fibrinoid necrosis is pathological hallmark)

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61
Q

What are the causes of Hypertension?

A

Primary/Essential Hypertension (95%) – cause unknown

Secondary Hypertension
R – Renal disease - Renal Artery Stenosis, CKD, Tubular Necrosis
O – Obesity
P – Pregnancy
E – Endocrine - Acromegaly, Cushing’s, Conns, Phaeochromocytoma

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62
Q

What are the risk factors for Hypertension?

A

Family history
Old age
Male
Afro-Caribbean
Lack of physical activity
Unhealthy diet (high salt intake, alcohol, smoking)
Obesity
Diabetes mellitus
Stress

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63
Q

What is the presentation of Malignant Hypertension?

A

Headaches
Visual Disturbances

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64
Q

What are some complications of malignant Hypertension?

A

Eyes - Retinopathy
Cardiac - LVH, HF, IHD, PVD
Kidney - Renal failure, Proteinuria
Neurological - Headache, Nausea, Vomiting, Stroke/TIA
GU - Impotence

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65
Q

What is the treatment for Malignant Hypertension?

A

Hypertensive Urgency: (no end organ damage)
oral Nifedipine
Oral Nifedipine and Oral Amlodipine

Hypertensive Emergency (end organ damage):
IV Labetalol
IV GTN

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66
Q

What are the investigations for Hypertension?

A

High BP in clinic
24 hr Ambulatory BP monitoring (ABPM)

Multiple home BP monitoring (twice daily for 4-7 days)

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67
Q

What are the tests for End organ damage in new hypertension diagnosis?

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage

Bloods for HbA1c, renal function and lipids

Fundoscopy examination for hypertensive retinopathy

ECG for cardiac abnormalities

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68
Q

What are the stages of Hypertension?

A

Stage 1: (low risk)
Clinical = 140/90 to 160/100mmHg
Home = 135/85 to 150/95mmHg

Stage 2: (high risk)
Clinical = >160/100mmHg
Home = >150/95mmHg

Severe:
Clinical systolic >180mmHg or Clinical diastolic >110 mmHg

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69
Q

When should you consider starting Hypertension treatment?

A

Stage 1 - Treat if >80yrs or if signs of end organ target damage or QRISK2 score 10%

Stage 2 - start Treatment

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70
Q

What is the life style management of hypertension?

A

Weight loss
Reduce alcohol intake
Reduce salt intake
Stop smoking
Regular exercise
Stress reduction

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71
Q

What is the pharmacological management of hypertension in under 55 years or DM?

A
  1. ACE inhibitor / ARB
  2. Add CCB
  3. Add Thiazide Diuretic
  4. Resistant Hypertension
    4a. If K+ < 4.5 - Add Spironolactone
    4b. If K+ > 4.5 - Add alpha or beta blocker
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72
Q

What is the pharmacological management of hypertension in over 55 years or Afro-Caribbean?

A
  1. CCB
  2. Add ACE inhibitor / ARB
  3. Add Thiazide Diuretic
  4. Resistant Hypertension
    4a. If K+ < 4.5 - Add Spironolactone
    4b. If K+ > 4.5 - Add alpha or beta blocker
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73
Q

What are the heart sounds?

A

S1 = mitral and tricuspid valve closure
S2 = aortic and pulmonary valve closure
S3 = in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with MR and HF
S4 = Contraction of atria forcing blood against a stiff non-compliant ventricle

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74
Q

What are the Systolic Heart Valve Murmurs?

A

ASMR
Aortic Stenosis:

  • Crescendo-decrescendo Ejection Systolic Murmur
  • Loudest at Aortic Area, Radiates to Carotids

Mitral Regurgitation:

  • Pansystolic High-Pitched “Blowing Murmur”
  • Loudest at Apex and Radiates to Axilla
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75
Q

What are the Diastolic Heart Valve Murmurs?

A

ARMS:
Aortic Regurgitation:

  • High-Pitched “Blowing” Early Diastolic Decrescendo Murmur
  • Best Heard Sitting Forward

Mitral Stenosis:
- Opening Snap then Delayed Rumbling Mid-Diastolic Murmur

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76
Q

What is the murmur of a Patent Ductus Arteriosus?

A

Continuous Machine Like Murmur

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77
Q

What is the Aetiology of Mitral Stenosis?

A

Rheumatic Heart Disease
Infective Endocarditis

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78
Q

What is the murmur Like in Mitral Stenosis?

A

Mid-diastolic, low pitched “rumbling” murmur
Loud S1 due to thick valves

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79
Q

What are the associations of Mitral Stenosis?

A

Malar flush
Atrial fibrillation

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80
Q

What are the complications of Mitral Stenosis?

A

Left atrial Hypertrophy
Can lead to AF

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81
Q

What is the Aetiology of Mitral Regurgitation?

A

Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective Endocarditis
Rheumatic Heart Disease
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

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82
Q

What is the murmur like in Mitral Regurgitation?

A

Pan-systolic, high pitched “whistling” murmur
Radiates to left axilla

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83
Q

What are the complications of Mitral Regurgitation?

A

Left atrial dilatation
Congestive cardiac failure

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84
Q

What is the Aetiology of Aortic Stenosis?

A

Bicuspid Aortic Valve >70 yrs
Idiopathic age-related calcification >70 yrs
Rheumatic Heart Disease

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85
Q

What is the murmur like in Aortic Stenosis?

A

Crescendo-decrescendo ejection-systolic, high-pitched murmur
Radiates to the carotids

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86
Q

What are the associations of Aortic Stenosis?

A

Slow rising pulse
Narrow pulse pressure
Exertional syncope
Breathlessness

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87
Q

What are the complications of Aortic Stenosis?

A

Left Ventricular Hypertrophy

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88
Q

What is Aortic Sclerosis?

A

Senile degeneration of the heart valve
Ejection systolic murmur but no carotid radiation and normal pulse

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89
Q

What is the Aetiology of Aortic Regurgitation?

A

Idiopathic age-related weakness
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

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90
Q

What is the murmur like in Aortic Regurgitation?

A

Early Diastolic
Soft Murmur

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91
Q

What are the associations of Aortic Regurgitation?

A

Corrigan’s pulse (collapsing Water- hammer pulse)
Wide pulse pressure
“Austin-Flint” murmur – heard at the apex and is an early diastolic “rumbling” murmur

Quince
De Musset

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92
Q

What are the complications of Aortic regurgitation?

A

left Ventricular Dilation

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93
Q

What is the investigation for heart valve defects?

A

Echocardiogram

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94
Q

What is the aetiology of Rheumatic Heart Fever?

A

Group A Beta-haemolytic Streptococcus (GABHS) – Streptococcus pyogenes infection

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95
Q

What is the pathology of Rheumatic heart Fever?

A

Type 2 Hypersensitivity Reaction (autoantibodies against cells of joints/heart/skin/nervous system)

Results in:
leaflet thickening
commissural fusion
shortening and thickening of the tendinous cords

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96
Q

Define Tachycardia?

A

A heart rate >100 BPM

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97
Q

Define Bradycardia?

A

A heart rate <60 bpm

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98
Q

How can tachycardias be classified?

A

Narrow Complex Tachycardias (QRS <120ms)
Broad Complex Tachycardias (QRS >120ms)

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99
Q

What are the narrow complex tachycardias?

A

Often occur Above the ventricles (supra ventricular)
In Atria:
Sinus Tachycardia
Atrial Fibrillation (Irregular Irregular Rhythm)
Atrial Flutter (Regular Irregular Rhythm)
Focal Atrial Tachycardia

In Atrioventricular Node:
AV Re-entry Tachycardia (AVRT)
AV nodal Re-entry Tachycardia (AVNRT)

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100
Q

What are the broad complex tachycardias?

A

Ventricular Tachycardia (Regular Irregular Rhythm)
Ventricular Fibrillation (Irregular Irregular Rhythm)

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101
Q

What are the types of Bradycardia?

A

SAN Dysfunction (followed by QRS):
Sinus Bradycardia
1st Degree heart Block

AVN Dysfunction (not followed by QRS):
2nd Degree Heart Block (Mobitz Type I and II)
3rd Degree Heart Block

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102
Q

What is Sinus Tachycardia?

A

> 100 bpm + Sinus Rhythm

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103
Q

What is the Aetiology of Sinus Tachycardia?

A

Physiological response to exercise and excitement
Anaemia, Infection, Fever, HF, Thyrotoxicosis, Acute PE, Hypovolemia, Atropine

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104
Q

What is the ECG in Sinus Tachycardia?

A

P waves piggyback onto the T waves = camel hump T waves

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105
Q

What is the treatment of Sinus Tachycardia?

A

Correct the cause
Beta Blockers to slow sinus rate e.g., atenolol

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106
Q

What is a supraventricular Tachycardia?

A

Any tachycardia that arises from the atrium or atrioventricular junction

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107
Q

What are the 4 Main types of SVT?

A

Atrial fibrillation
Atrial flutter
Atrioventricular nodal re-entry tachycardia (AVNRT)
Atrioventricular reciprocating tachycardia (AVRT)

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108
Q

What is the 1st Line management in SVT?

A

Vagal Manoeuvres (Valsalva Manoeuvre + Carotid Sinus Massage)
Adenosine if doesnt work

109
Q

What is the most common arrhythmia?

A

Atrial Fibrillation

110
Q

What is the pathology of AF?

A

Atrial activity is chaotic and mechanically ineffective (atrial activation 300-600/min)
AVN conducts only a proportion of atrial impulses, with an irregular ventricular response
HR 120-180bpm
Blood pools in atria leading to increased risk of clotting and Thrombo-embolic events

111
Q

What is the Aetiology of AF?

A

SMITH:
Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension

112
Q

What are the types of AF?

A

First detected episode

Recurrent – 2 or more episodes of AF

  • Paroxysmal – terminate spontaneously (usually <24 hours)
  • Persistent – not self-terminating (usually last >7 days)

Permanent – continuous AF which cannot be cardioverted or cardioversion deemed inappropriate

113
Q

What is the presentation of AF?

A

Symptoms:
Palpitations, SOB, Syncope

Signs:
Irregularly irregular pulse

114
Q

What are the complications of AF?

A

Emboli - Due to the pooling of blood in the atria which can lead to thrombus formation.

115
Q

What are the investigations of AF?

A

ECG:
Irregularly irregular rhythm
Absent P waves
Narrow QRS

Bloods – Cardiac enzymes, TFTs
Echo

116
Q

What is the Treatment of Acute AF?

A

Cardioversion (electrical/amiodarone) – usually 1st line
Correct electrolyte imbalances + Rate control + Anti-coagulate

117
Q

What is the treatment of Chronic AF?

A

Rate control
1st Line: Beta blockers (atenolol) or rate limiting CCB (diltiazem)
If Sedentary Lifestyle then Digoxin

If this doesnt work then Combine any two.

Then assess Stroke Risk with CHA2DS2VASc and ORBIT

If risk then Add anticoagulation (DOAC 1st or Warfarin with metal valve)

118
Q

How does amiodarone work?

A

Amiodarone works by increasing the duration of ventricular and atrial muscle action by inhibiting Na,K-activated myocardial ATPase – which means nerve impulses take longer to initiate contraction – it is an anti-arrhythmic mediation.

119
Q

What is first line control of AF and when is it not used?

A

Rate Control:

  • BB (1st), CCB (Diltiazem)
  • If Sedentary then Digoxin

Used Unless: RANCH:
Reversible cause of AF
Ablation for atrial flutter
New onset <48 hours
Clinical Judgement
Heart Failure secondary to AF

120
Q

When is Rhythm Control used in AF?

A

If Rate Control is not working (ie. Rate still bad or still have Sx)
OR RANCH (reversible, Aflu, New onset, Clin Judge, Heart Failure)

AF < 48 hrs or Severely Haemodynamically unstable
Immediate DC Cardioversion: (electrical first then Amiodarone)

AF > 48 hrs and they are stable:
Delayed Cardioversion: after 3 weeks of anti-coagulation

If all medical management has failed or is CI:
Then ABLATION

121
Q

What are the options for Cardioversion?

A

Pharmacological:
Flecainide - pill in pocket
Amiodarone (drug of choice in patients with structural heart disease)

Electrical: defibrillator

122
Q

What are the Class I, II, III, IV anti arrhythmic Drugs?

A

Class I: Sodium channel Blockers (Flecainide, quinidine, Lidocaine)
Class II: Beta Blockers
Class III: Amiodarone
Class IV: CCB (Verapamil or Diltiazem)

123
Q

What score is used to calculate risk of stroke in AF?

A

CHA2DS2VASc Score:
Congestive HF
Hypertension (>140/90)
Age >75 (+2)
Diabetes Mellitus
Stroke or TIA prior (+2)
Vascular Disease
Age 65-74
Sex (Female Gender)

0 = No anticoagulation
1 = Consider anticoagulation in males (not females)
2 = Oral Anticoagulation (DOAC (1st Line) then Warfarin)

124
Q

What score is used to assess Bleeding risk in AF?

A

ORBIT:
Older age (>74)
Reduced haemoglobin (anaemia)
Bleeding history
Insufficient Kidney Function
Treatment with antiplatelet

> 4 = High Risk

125
Q

What is the target INR on warfarin?

A

2-3 (2.5)

126
Q

What Thromboprophylaxis is best for patients with arrhythmias and a metallic heart valve?

A

Warfarin is preferred.

127
Q

What is Atrial Flutter?

A

Regular Irregular heart rhythm

128
Q

What is the pathology of Atrial Flutter?

A

Type of SVT caused by a re-entrant circuit within the right atrium
Ventricular rate determined by the AV conduction ratio: 2:1 (commonest), 3:1, 4:1, variable rate

So the atria only contract to the ventricles every 2nd turn due to AVN delay

129
Q

What is the ECG in Atrial Flutter?

A

‘Sawtooth’ pattern (F wave)
Regular atrial rate

130
Q

What is the treatment of Atrial Flutter?

A

Rate control (beta-blockers), Rhythm control (DC cardioversion) and Anticoagulation (warfarin)

Radiofrequency catheter ablation – curative for most patients

131
Q

What is the pathology of an AVNRT?

A

AV nodal re-entry tachycardia (AVNRT):
Circuits from within the AVN (‘ring’ of conduction tissue)
ECG: Absent P waves (or seen immediately before QRS)

132
Q

What is the pathology of an AVRT?

A

AV reciprocating tachycardia (AVRT):
Accessory pathway connecting the atria and ventricles
Wolff-Parkinson-White syndrome (WPW) – bundle of kent

133
Q

What is the acute treatment of an AVNRT/AVRT?

A

Stable:
Vagal Manoeuvres (Valsalva + Carotid Sinus Massage)
If doesnt work then adenosine

Unstable
Electrical Cardioversion

134
Q

What is the Long Term treatment of an AVNRT/AVRT?

A

Beta Blockers
Radio-frequency Ablation

135
Q

What is the ECG of Wolf Parkinson White Syndrome (WPW)?

A

Short PR interval (due to early depolarization of ventricle)
Wide QRS complex
Slurred start to the QRS (delta wave)
ST changes

136
Q

What are some associations with WPW?

A

HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD

137
Q

What is the management of WPW?

A

Definitive: Radiofrequency Ablation

Medical Therapy: Sotalol, Amiodarone, Flecainide

138
Q

Why do you get the delta wave in WPW?

A

Bundle of kent accessory pathway allows the transfer of conduction to the ventricles slightly faster than AVN and therefore the delta wave is the early contraction of the ventricles

139
Q

What are broad complex tachycardias associated with?

A

Prolonged QT syndrome

140
Q

What is Ventricular Tachycardia?

A

Ventricle does not fully depolarize through the Purkinje fibres leading to rapid electrical conduction around the ventricles

Due to re-entrant circuit due to scarring from past ischemia/infarction OR triggered by long QT or digoxin toxicity

141
Q

What is the ECG in V-Tach?

A

broad complex tachycardia with wide QRS complex

142
Q

What is the treatment of V-Tach?

A

Stable - Amiodarone
Unstable Electrical DC and IV Amiodarone

143
Q

What is Ventricular Fibrillation?

A

No pattern of ECG due to the fibrillation of the ventricles.
They do not contract and no blood is ejected meaning this is a life threatening situation

144
Q

What is the Treatment of V-Fib?

A

Defibrillation + IV amiodarone

145
Q

What are the causes of Sinus Bradycardia?

A

Athlete

Extrinsic:
- Vasovagal attacks
- Drugs (BB, Digoxin, Amiodarone
- Hypothermia
- Hypothyroidism
- Raised ICP

Intrinsic:
- Acute ischaemia
- Infarction of SAN

146
Q

What is the treatment for Sinus Bradycardia?

A

Extrinsic: Treat Underlying cause
Intrinsic - Atropine

147
Q

Define 1st Degree heart Block?

A

PR interval is prolonged (over 0.20s)

148
Q

Define 2nd Degree Heart Block?

A

Mobitz type I: Progressive PR interval prolongation, until a P wave fails to conduct and a QRS is dropped

Mobitz type II: PR interval is constant, but QRS complexes are regular missed

149
Q

Define 3rd Degree Heart Block?

A

Complete Heart Block
Ventricular contraction completely independent of atria contractions

150
Q

What are the features of complete Heart Block?

A

Syncope
Heart failure
Regular bradycardia (30-50 bpm)
Wide pulse pressure
JVP: cannon waves in neck
Variable intensity of S1

151
Q

What is the treatment of heart Block?

A

Stable: Observe

Unstable / Risk of Asystole ( Type II Mobitz, 3rd degree):

  • IV Atropine 500mcg
  • Permanent implantable pacemaker
152
Q

What are the causes of LBBB?

A

myocardial infarction
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

153
Q

What is the ECG of LBBB?

A

WiLLiaM
Slurred S wave in V1
R wave in V6

154
Q

What are the causes of RBBB?

A

Normal
PE
IHD
ASD
VSD
Cor pulmonale

155
Q

What is the ECG of RBBB?

A

MaRRoW:
R wave in V1
Slurred S wave in V6

156
Q

What is Long QT Syndrome?

A

Inherited condition associated with delayed repolarization of the ventricles
May lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/ sudden death

157
Q

What are the causes of Long QT?

A

Romano Ward Syndrome
Amiodarone
TCA/SSRIs
Hypocalcaemia, Hypokalaemia, Hypomagnesaemia
MI

158
Q

What is the management of long QT?

A

Avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)

Beta-blockers (sotalol may exacerbate)

Implantable cardioverter defibrillators – high risk cases

159
Q

What is Torsades De Pointes (Twisting of the Tips)

A

Form of polymorphic ventricular tachycardia associated with a long QT interval
where the QRS will twist around the base line

Either terminate spontaneously (revert back to sinus rhythm) or progress into ventricular tachycardia (cardiac arrest)

160
Q

What is the management of Torsades De Pointes?

A

Correct the Cause (EG. Electrolyte Disturbances)
Magnesium Infusion
Defibrillation if V-Tach occurs

161
Q

What are the Cardiac Arrest Rhythms? Which are shockable?

A

Shockable:
Ventricular Tachycardia
Ventricular Fibrillation

Non-Shockable:
Pulseless Electrical Activity
Asystole

162
Q

What are the indications for a pacemaker?

A

Symptomatic bradycardias
Mobitz Type 2 AV block
Third degree heart block
Severe heart failure (biventricular pacemakers)
Hypertrophic obstructive cardiomyopathy (ICDs)

163
Q

What are the types of Aneurysms?

A

True = Abnormal dilations that affect all 3 layers (intimal, media, adventitia)
False = A collection of blood in the adventitia only

Due to inflammation and MMPs breaking down structural proteins within the walls

164
Q

What is the presentation of an Abdominal Aortic Aneurysm?

A

Unruptured:

  • Asymptomatic (usually), Pulsatile on palpation

Ruptured:

  • Intermittent or continuous abdominal/epigastric pain (radiates to back, iliac fossae or groins)
  • Collapse/Shock
  • Expansive abdominal mass
165
Q

What are the complications of an Abdominal Aortic Aneurysm?

A

Rupture
Thrombosis
Embolism
Death
Hypovolaemic Shock

166
Q

What are the investigations for an aortic aneurysm?

A

1st Line: Abdominal Ultrasound
GS: CT angiography

167
Q

What is the treatment for an Aortic Aneurysm?

A

Ruptured: IMMEDIATE Surgery
Unruptured AAA: Elective surgical repair (Open repair via a laparotomy or EVAR)
Unruptured TAA: Elective surgical repair (TEVAR or Open repair)

168
Q

What is the Screening for AAA?

A

All males at age of 65yrs can have screening via Aortic USS

High Risk if Symptomatic, Aortic Diameter >5.5cm

169
Q

What is Pathology of an Aortic Dissection?

A

Tear in the intima
Blood flows between intima and media
False Lumen Forms
Splits the aortic Media

As Dissection spreads it leads to occlusion of the branches of the aorta

170
Q

What is the presentation of an Aortic Dissection?

A

Sudden, severe, tearing chest pain (+/-) Radiating to the back
Unequal arm pulses, Absent pulses

171
Q

What are the Investigations for aortic Dissection?

A

CT (/MRI) Angiogram - False lumen and intimal Flap
CXR – widened mediastinum

ECG to rule out STEMI

172
Q

What is the treatment of an Aortic Dissection?

A

Type A: Control BP (IV labetalol) + Surgery (Open Surgery)
Type B: Control BP (IV labetalol) + Conservative management

173
Q

What are the two types of PVD?

A

Chronic Limb Ischaemia
Acute Limb Ischaemia

174
Q

What is the classification of Chronic Limb Ischaemia?

A

Fontaine Classification:
1. Asymptomatic
2. Intermittent Claudication
3. Ischaemic Rest Pain (Chronic Ischaemia)
4. Ulceration/Gangrene (Critical Ischaemia)

175
Q

What is the Cause and pathology of Chronic Limb Ischaemia?

A

Atherosclerosis in lower limb arterial vessels leading to reduced blood supply and ischaemia.

At lower stages it reduces blood supply when demand increases (exercise). As it Progresses it will reduce blood supply at rest (pain at rest)

176
Q

What are the risk factors for Chronic Limb Ischaemia?

A

smoking, DM, HTN, hypercholesteraemia, obesity

177
Q

What is the presentation of Chronic Limb Ischaemia?

A

Intermittent claudication: Cramping pain in calves, thighs and buttocks induced by exercise (e.g., walking) and is relieved by rest

Critical ischemia: Ulceration, Gangrene and Foot pain at rest
e.g., burning pain at night relived by hanging legs over side of bed

Signs: Buerger’s angle <20o, absent femoral/popliteal/foot pulses, punched out ulcers, CRT >15s

178
Q

What is Leriche Syndrome?

A

Occlusion in the distal aorta or proximal common iliac artery

Clinical triad:
Thigh/buttock claudication
Absent femoral pulses
Male impotence

179
Q

What is Intermittent Claudication?

A

Cramping pain that is induced by exercise and relived by rest

Caused by: Inadequate blood supply to muscle –> anaerobic metabolism –> lactic acid production causing pain

180
Q

What is Critical Limb Ischaemia?

A

Triad of ischemic rest pain, arterial insufficiency ulcers, and gangrene
Blood supply barely adequate to allow basal metabolism
No reserve available for increased demand
Rest pain that is typically NOCTURNAL

181
Q

What are the investigations for Chronic Limb Ischaemia?
How is Severity of PVD determined?

A

Colour duplex ultrasound – 1st line
CT angiogram – gold standard

Ankle-brachial pressure index (ABPI)
Normal = 0.9-1.2;
Mild PAD = 0.6-0.9;
Moderate-Severe PAD = 0.3-0.6;
Critical ischemia = <0.3

182
Q

What is the treatment for Intermittent Claudication?

A

Lifestyle changes (smoking cessation), Optimise treatment of co-morbidities, Exercise training

Medical: Atorvastatin, Clopidogrel, Naftidrofuryl oxalate

Surgical: Endovascular angioplasty and stenting, Endarterectomy, Bypass surgery

183
Q

What is the treatment for Critical Limb Ischaemia?

A

Urgent referral and Analgesia

Urgent revascularisation: Endovascular angioplasty and stenting, Endarterectomy, Bypass surgery, Amputation (if unable to restore blood supply)

184
Q

What is the cause of Acute Limb Ischaemia?

A

Thrombosis in situ
Emboli
Graft/angioplasty occlusion
Trauma

185
Q

What is the pathology of Acute Limb Ischaemia?

A

Complete occlusion of the lower limb vessels leading to ischaemia and infarction.

Often due to Thrombosis in situ or Emboli

186
Q

What is the presentation of Acute Limb Ischaemia?

A

6Ps
Pale
Pulseless
Painful
Paralysed
Paraesthetic – numbness and tingling in an extremity (‘pins and needles’)
‘Perishingly cold’

187
Q

What are the investigations for Acute Limb Ischaemia?

A

Surgical emergency and may require urgent open surgery or angioplasty

Handheld arterial Doppler examination (ABI if doppler signals absent)

188
Q

What is the Treatment of Acute Limb Ischaemia?

A

Initial management:
Analgesia, IV fluids, Oxygen
IV Unfractionated Heparin (5000 Units)

Revascularisation within 4-6 hrs
Definitive management: (Treat underlying clot:)
Endovascular thrombolysis, Endovascular thrombectomy, Surgical thrombectomy

Other surgical options:
Endarterectomy, Bypass surgery, Amputation

189
Q

What is the risk of Acute Limb Ischaemia?

A

If not revascularised within 4-6 hours then lose limb.

190
Q

What are Varicose Veins?

A

Distended Superficial Veins measuring >3mm in diameter

Often Due to Primary Mechanical Factors (95%)
Secondary to obstruction.

191
Q

What is the presentation of Varicose Veins?

A

Pain/ache, Heaviness, Cramps, Itching/Burning, Oedema

192
Q

What are the tests to check for Varicose Veins?

A

Tap Test
Cough Test
Trendelenburgs Test
Perthes Test

193
Q

What is the Treatment of Varicose Veins?

A

Conservative management: Compression stockings

Surgical options: Endothermal ablation, Sclerotherapy, Stripping

194
Q

What are some complications of Varicose Veins?

A

Prolonged/heavy bleeding after trauma, Superficial thrombophlebitis, DVT, Chronic venous insufficiency

195
Q

What is Shock?

A

Circulatory failure resulting in inadequate organ perfusion

(Systolic <90mmHg with evidence of hypoperfusion)

196
Q

What are the different Types of Shock?

A

Septic - Inflammation with any organism –> acute vasodilation from Cytokines

Anaphylactic - Type I IgE mediated Hypersensitivity Rxn –> Histamine Release

Neurogenic - Spinal Cord Injury

Hypovolaemic - Bleeding, Trauma, Ruptured AA, GI Bleed

Cardiogenic - Pump failure, Inadequate Filling

197
Q

What is Sepsis?

A

overwhelming and life-threatening inflammatory response to a severe infection, which can lead to tissue damage, organ failure, and death

198
Q

Define Septicaemia?

A

when bacteria enter the bloodstream, and cause blood poisoning which triggers sepsis

199
Q

Define Septic Shock

A

life-threatening condition that is characterised by low blood pressure despite adequate fluid replacement, and organ dysfunction or failure

200
Q

How is Sepsis Treated?

A

SEPSIS 6: (BUFALO)
Blood Cultures (Out)
Urine Output (Out)
Fluids (In)
Antibiotics (In)
Lactate (Out)
Oxygen (In)

201
Q

What are the 4 anatomical cardiac abnormalities in Tetralogy of Fallot?

A

Ventricular Septal Defect (VSD)
Pulmonary Stenosis
Right Ventricular Hypertrophy (RVH)
Overriding Aorta

202
Q

What is the Pathology of Tetralogy of Fallot?

A

Right to left Shunt
Reduced Oxygenation of blood
Causes Cyanosis

203
Q

What are the risk factors for Tetralogy of Fallot?

A

Rubella infection
Increased age of the mother (over 40 years)
Alcohol consumption in pregnancy
Diabetic mother

204
Q

What is the presentation of Tetralogy of Fallot?

A

Symptoms:

  • Infants: Cyanotic, Paroxysmal hypercyanotic spells
  • Toddlers: May squat

Signs:

  • Clubbing
  • Pulmonary stenosis murmur
  • Tet Spells: Intermittent symptomatic periods precipitating a cyanotic episode
205
Q

What are the investigations of Tetralogy of Fallot?

A

CXR - Boot Shaped Heart
Echocardiography - GS

206
Q

What is the Treatment of Tetralogy of Fallot?

A

Prostaglandin E Infusion (Alprostadil) (Prevents Closure of PDA shunt to allow oxygenated blood to enter the aorta)

Surgery

207
Q

What is a Ventricular Septal Defect and what are the associations?

A

Hole in the ventricles.

Associated with Downs, Turners

208
Q

What is the presentation of an VSD?

A

Asymptomatic (typical/early)

Symptoms :

  • SoB, Poor feeding, Failure to thrive

Signs:

  • Loud pan-systolic murmur with a systolic thrill +/- left parasternal heave
  • Heard at left lower sternal edge
  • Smaller hole = louder murmur/thrill
  • Signs of pulmonary hypertension
209
Q

What are the Investigations of a VSD?

A

Echocardiogram

210
Q

What is the Treatment of VSD?

A

Treat heart failure if present
Surgical repair (transvenous or open) – if severe HF or pulmonary hypertension
Antibiotic prophylaxis should be considered during surgical procedures (IE risk)

Majority will close spontaneously

211
Q

What is an atrial Septal Defect?

A

Connection between Atria:
Ostium secundum defect: (85%)
Defect in the region of the foramen ovale

Partial atrioventricular septal defect (ostium primum) (15%)
More serious ASD
Affects endocardial cushion tissue, located in lower atrial septum
AVSD are often seen in Down’s syndrome

212
Q

What is the presentation of ASD?

A

Recurrent chest infections and heart failure

Symptoms:

  • Chest pain, Palpitations, Dyspnoea

Signs
- Wide fixed split S2
- Pulmonary systolic flow murmur – mid-systolic, crescendo-decrescendo

213
Q

What are the investigations of an ASD?

A

Echocardiogram

214
Q

What is the treatment of an ASD?

A

Cardiac catherization or Open-heart surgery
Anticoagulants (aspirin, warfarin and NOACs) used to reduce the risk of clots and stroke in adults

215
Q

What are the complications of an ASD?

A

SAPE:
Stroke in the context of venous thromboembolism
Atrial fibrillation or atrial flutter
Pulmonary hypertension and right sided heart failure
Eisenmenger syndrome

216
Q

What is Eisenmenger’s Syndrome?

A

Reversal of Left to Right Shunt to a right to left shunt due to increased pressure in pulmonary vasculature leading to RV hypertrophy and increased RV pressure.

Complication of ASD, PDAs and VSDs

217
Q

What is the result of Eisenmenger’s Syndrome?

A

Marked cyanosis
Clubbing
Heart failure
Others: syncope, high RBC, organ damage

218
Q

What is a Patent Ductus Arteriosus (PDA)?

A

Duct still being present 1 month after the child should have been born

219
Q

What is the presentation of a PDA?

A

Symptoms:
Heart failure – Breathlessness
Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)
Infants – poor feeding, failure to thrive

Signs:
Continuous ‘machinery’ murmur in left infraclavicular area
Wide pulse pressure or bounding peripheral pulse
large volume, bounding, collapsing pulse

220
Q

What is the Treatment of PDA?

A

Monitored until 1 year of age using echocardiograms
Medical: Diuretics
Medical Closure: Indomethacin or Ibuprofen
Cardiac catheter: Device closure (usually at 1 yr)
Surgical: Ligation (rarely)

221
Q

What is Coarctation of the Aorta?

A

Aorta is narrowed at the site of the ductus arteriosus
Associations: Bicuspid aortic valve, Turner’s syndrome

222
Q

What is the presentation of Coarctation of the Aorta?

A

Symptoms:
Heart failure – if severe

Signs:

  • Radio-femoral delay
  • Weak femoral pulse (bilaterally) – may be only indication in neonate
  • Hypertension – Right arm hypertension
  • Systolic murmur (best heard over the scapula)
  • Scapular bruit
223
Q

What are the complications of Coarctation of the Aorta?

A

Premature coronary artery disease
Congestive Cardiac Failure (CCF)
Hypertensive encephalopathy
Intracranial haemorrhage

224
Q

What are the investigations of Coarctation of the Aorta?

A

CT or MRI-aortogram
CXR – may show rib notching

225
Q

What is the Treatment of Coarctation of the Aorta?

A

Prostaglandin E – if risk of HF/death shortly after birth

Surgery – risk of aortic aneurysm after surgical repair
Balloon dilation +/- stenting

226
Q

What is the pathology of HOCM?

A

Septal Cardiac Hypertrophy which leads to Left Ventricular outflow obstruction

227
Q

What is the epidemiology of HOCM?

A

1 in 500

228
Q

What are the Gene mutations in HOCM?

A

Autosomal Dominant Sarcomere Protein Gene Mutations

229
Q

What is the Presentation of HOCM?

A

Angina
Dyspnoea
Palpitations
Sudden Death (most common cause of sudden death in young adults)

230
Q

What is the treatment of HOCM?

A

Amiodarone (prevent AF)
Beta-Blockers for Symptoms

231
Q

What is the pathology of DCM?

A

Dilated left Ventricle leading to systolic dysfunction as the ventricular walls are thin and cannot contract

232
Q

What are the gene mutations in DCM?

A

Cytoskeletal Gene mutations

233
Q

What is the Presentation of DCM?

A

heart Failure symptoms:
Dyspnoea, Fatigue, Oedema

234
Q

What is the Treatment of DCM?

A

Diuretics for fluid overload
Beta blockers
ACEi
Anticoagulation (LMWH)

235
Q

What is the pathology of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

A

Myocardium is Replaced by fibrous and fat tissue leading to conduction problems between the atria and ventricles.

This causes arrhythmias

236
Q

What are the Gene mutations in ARVC?

A

Desmosome Gene Mutations

Naxos disease - AR condition with ARVC + wooly hair and Palmerplanterkeratoderma

237
Q

What is the Presentation of ARVC?

A

Arrythmias
Palpitations
Syncope

238
Q

What is the Treatment of ARVC?

A

Sotalol
Amiodarone

239
Q

What is Pericarditis?

A

Inflammation of the pericardium

240
Q

What is the aetiology of pericarditis?

A

Idiopathic (80-90%)
Infection – Viral (most common): enterovirus, adenovirus, Coxsackie; Bacterial: TB
Autoimmune – Rheumatoid arthritis, Scleroderma
Dressler’s syndrome (post-MI)

241
Q

What are the symptoms of pericarditis?

A

Central (pleuritic) chest pain worse in inspiration or lying down.
Relieved by sitting forward

Fever
Dyspnoea

242
Q

What are the signs of pericarditis?

A

Pericardial Rub
Tachypnoea
Tachycardia

243
Q

What are the investigations for pericarditis?

A

ECG: Concave saddle-shaped ST elevation, PR depression (most specific), Sinus tachycardia
Bloods: FBC, ESR, U&E, Cardiac enzymes (troponin may be raised)
Echo
Others: CXR

244
Q

What is the Treatment for Pericarditis?

A

NSAIDs or Aspirin
Colchicine (if relapse or continuing symptoms as reduces risk of recurrence)
Additional used in the short term treatment of gout
Treat underlying cause

245
Q

What are the requirements for a clinical diagnosis of pericarditis?

A

Clinical diagnosis made with 2 of 4 from:
Chest Pain (85-90%)
Friction rub (33%)
ECG changes (60%)
Pericardial effusion (up to 60% usually mild)

246
Q

What are the major complications of pericarditis?

A

Pericardial Effusion - Fluid accumulation in the pericardium
Pericardial Tamponade - Severe effusion that prevents heart diastolic filling and function (reducing CO)
Chronic Constrictive Pericarditis - Fibrotic rigid pericardium from persistent inflammation

247
Q

What is the presentation, Investigation and treatment of a pericardial effusion?

A

Px: Dyspnoea and Chest pain
Ix: Echo
Tx: Pericardiocentesis

248
Q

What is the presentation, Investigation and treatment of a pericardial tamponade?

A

Px: Becks Triad (falling BP, Rising JVP, Muffled Heart Sounds)
Ix: Echo
Tx: Pericardiocentesis

249
Q

What is the presentation, Investigation and treatment of a chronic constrictive pericarditis?

A

Presentation: Symptoms of right heart failure, Dyspnoea
Treatment: Surgical excision

250
Q

What is infective endocarditis?

A

Infection and inflammation of the endocardial lined structure (commonly the heart valves)

251
Q

What are the causes of Infective Endocarditis?

A

Staphylococcus aureus (now the most common) – IVDU, dermatitis, DM
Streptococcus viridans – new cardiac murmur
Staphylococcus epidermitis – metallic valve replacement

252
Q

What are the risk factors for Infective Endocarditis?

A

Old age
IVDU
Prosthetic valves
Congenital heart disease
Others: Poor dental hygiene, Skin and soft tissue infection, IV cannula, Cardiac surgery, Pacemaker

253
Q

What is the presentation of Infective Endocarditis?

A

Fever + non-specific Symptoms
May have IE signs
New onset murmur

254
Q

What are the associated signs and symptoms with Infective Endocarditis?

A

FROM JANE:
Fever
Roth Spots - Retinal Haemorrhages
Osler Nodes - painful spots on digits
Murmur

Janeway lesions - PAINLESS finger, palms and soles spots
Anaemia (normocytic)
Nail Bed Haemorrhages (splinter Haemorrhages)
Emboli (cardiogenic)

+ Clubbing

255
Q

What are the investigations for Infective Endocarditis?

A

Blood cultures – 1st line (from 3 sites, on 3 occasions)
Echocardiogram – vegetations on heart valves
Others: Bloods (normochromic, normocytic anemia), ECG, Urinalysis (hematuria), CXR

256
Q

What is the diagnostic Criteria for Infective Endocarditis?

A

Modified Dukes Criteria (BE FEVER)
Definite IE: 2 major OR 1 Major + 3 minor OR 5 Minor
Possible IE: 1 Major + 1 Minor OR 3 Minors

Major (BE):
Blood Cultures - Positive IE organisms > 12 hours apart
Evidence of endocardial involvement (ECHO)

Minor (FEVER):
Fever > 38 degrees
Evidence from microbio - Positive organisms not typical IE
Vascular Phenomena - Emboli, Janeway Lesions
Evidence from Immunology - Roth Spots, Osler Nodes, GN
Risk Groups - Predisposing factors (IVDU, prosthesis, valvular disease)

257
Q

What is the treatment for Infective Endocarditis?

A

Antibiotics
Staphylococci:
Native: IV Flucloxacillin (allergic/MRSA: Vancomycin + Rifampicin)
Prosthetic: IV Flucloxacillin + Rifampicin + Gentamicin

Streptococci:
High-sensitivity: IV Benzylpenicillin
Low-sensitivity: IV Benzylpenicillin + Gentamicin

Blind therapy:
Native: IV Amoxicillin +/- Gentamicin
Prosthetic: Vancomycin + Rifampicin + Gentamicin
Surgery – severe incompetence, aortic abscess, resistance, CF, recurrent emboli

258
Q

What are some poor prognostic factors for Infective Endocarditis?

A

Staphylococcus aureus
Prosthetic valve (especially ‘early’, acquired during surgery)
Culture negative endocarditis
Low complement levels

259
Q

What are the classifications of Carotid Artery Stenosis?

A

Mild – less than 50% reduction in diameter
Moderate – 50 to 69% reduction in diameter
Severe – 70% or more reduction in diameter

260
Q

What is the presentation of Carotid Artery Stenosis?

A

Usually asymptomatic, diagnosed after a TIA or stroke
Carotid bruit – may be heard on examination

261
Q

What are the investigations for Carotid Artery Stenosis?

A

Carotid ultrasound – usually the initial investigation to diagnose and assess carotid artery stenosis
CT or MRI angiogram – may be used to assess stenosis in more detail before surgical interventions

262
Q

What is the treatment for Carotid Artery Stenosis?

A

Conservative management (modifiable risk factors and medical therapy)

Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
- Lipid-lowering medications (e.g., atorvastatin)

Surgical interventions – significant stenosis
- Carotid endarterectomy
- Angioplasty and stenting

263
Q

What is Buerger Disease?

A

Thromboangiitis Obliterans:
Inflammatory condition that causes thrombus formation in the small and medium-sized blood vessels in the distal arterial system (affecting the hands and feet)

264
Q

Who do Buerger Disease typically affect?

A

Men aged 25-35 (diagnostic criteria involves <50 yrs)
Strong association with smoking

265
Q

What is the presenation of Buergers Disease?

A

Painful, blue discolouration to the fingertips or tips of the toes
Pain is often worse at night

266
Q

What is the Investigations of Buergers Disease?

A

Angiograms - Corkscrew Collaterals

267
Q

What is the treatment for Buergers Disease?

A

Completely stop smoking – main component of treatment
Other specialist treatments: Intravenous Iloprost (a prostacyclin analogue that dilates blood vessels)

268
Q

What are some complications of Buergers Disease?

A

Ulcers
Gangrene
Amputation

269
Q
A

Medicine Phase 2a (20 decks)

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