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Cardiology Flashcards

2
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A
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4
Q

What are the types of IHD?

A

Stable angina

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

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6
Q

What are the modifiable risk factors for IHD?

A

Smoking
Obesity
Sedentary lifestyle
Diet

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8
Q

What are the clinical modifiable risk factors for IHD?

A

Hypertension
Diabetes
Hyperlipidaemia
Depression

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10
Q

What are the non-modifiable risk factors for IHD?

A

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

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12
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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14
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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16
Q

What is definition of angina?

A

Symptomatic reversible myocardial ischaemia

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17
Q

What are the main causes of angina?

A

Atheroma
Hypertension
Vasculitis
Anaemia

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19
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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21
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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23
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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25
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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26
Q

What is the gold standard investigation for stable angina?

A

CT coronary angiogram

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28
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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30
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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32
Q

What are the conditions under ACS?

A

Unstable angina
NSTEMI
STEMI

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34
Q

What is the pathology of ACS?

A

Plaque Rupture –> Thrombosis –> Inflammation –> Infarction

Rarer causes:
Emboli
Coronary artery Spasm
Vasculitis

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35
Q

Define Myocardial Infarction

A

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

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37
Q

Define unstable Angina?

A

ACS defined by the absence of biochemical evidence of myocardial damage

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38
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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40
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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42
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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44
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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46
What are the investigations for an STEMI?
ECG Acute changes: Hyperacute T-waves, ST elevation or new LBBB Hours/days: T-wave inversion and pathological Q waves (deep and wide)
48
What are the investigations for an NSTEMI?
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
50
What ECG cords are associated with a circumflex MI?
Lateral: Lead I aVL V4-V6
52
What ECG cords are associated with an LAD MI?
Anteroseptal: V1-V3
54
What ECG cords are associated with an Inferior MI?
Lead II Lead III Lead aVF
56
What is the Pre-hospital management of an MI?
Aspirin 300mg and GTN
57
What is the acute Hospital management of an MI?
MONAC: Morphine Oxygen (if hypoxic under 94%) Nitrates (GTN) Aspirin Clopidogrel +/- Heparin
59
What is the NSTEMI acute management?
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
60
What is the STEMI acute management?
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
61
What is the Long term management of an MI?
BACAS: Beta blocker Aspirin Clopidogrel ACEi Statin Risk factor modification. High risk of emboli - Give warfarin (3-6 months)
63
What are the complications of MI?
Death Arrythmias Ruptured Septum Tamponade Heart Failure Valve disease - ruptured papillary muscles Aneurysm of Ventricles Dressler's Syndrome Embolism Reoccurrence of ACS
65
What are some differential Diagnoses for Chest pain?
Cardiac: MI, Angina, Aortic Dissection, Pericarditis Resp: PE, Pneumonia, Pneumothorax, Pleurisy, Cancer MSK: Rib fracture, costrochondritis GI: GORD Psychological: Anxiety, Panic Attack
66
Define Heart Failure
‘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)
68
What is the aetiology of HF?
Ischemic Heart Disease Valvular Heart Disease (commonly AS) Hypertension Arrhythmias (commonly AF) Cardiomyopathy
70
What are the risk factors for HF?
65 and older African descent Men Obesity Previous MI
72
What are the classifications of HF?
Reduced EF (<40%) - often Systolic failure Mid Range EF (40-49%) Preserved EF (>50%) - often Diastolic Failure
74
What are the cardinal Symptoms of HF?
Shortness of Breath Fatigue Ankle swelling
75
What are the signs symptoms of Left ventricular failure?
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
77
What are the signs symptoms of Right ventricular failure?
Causes Systemic Congestion: Symptoms: - Peripheral oedema - Ascites Signs: - Raised JVP - Hepatomegaly - Pitting oedema - Weight gain (fluid)
79
What system is used to classify HF?
NYHA: Stage 1 - No limitation (asymptomatic) Stage 2 - Slight limitation (mild HF) Stage 3 - Marker Limitation (symptomatic HF) Stage 4 - Severe Symptomatic HF
80
What are the investigations for HF?
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
82
What is seen on CXR in HF?
ABCDE: Alveolar Oedema (Batwings) Kerley B Lines (interstitial Oedema) Cardiomegaly Dilation of upper Lobe Vessels Pleural Effusions
84
What is the Management of HF?
1. Lifestyle Management - Education - Smoking cessation - Reduce alcohol - Reduce salt intake - Exercise and Obesity control 2. Symptomatic Management: - Diuretics - Loop (furosemide) 3. Disease Altering Medication (ABAL): - 1st Line - ACEi (ramipril) + - Beta Blockers (bisoprolol) - 2nd Line - Aldosterone Antagonist (Eplerenone) - 3rd Line - Ivabradine, ARNI, Hydralazine, Digoxin
86
What is the Chronic Treatment of HF?
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)
87
What is the acute Treatment of HF?
- 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
89
When should you avoid using ACE inhibitors?
In patients with valvular heart disease
91
Why is Eplerenone preferred over Spironolactone?
Spironolactone causes gynaecomastia
93
What are the causes of Acute left ventricular failure and pulmonary oedema?
Iatrogenic (aggressive IV fluids in frail elderly patient with impaired LV function) Sepsis Myocardial Infarction Arrhythmias
95
What is the Treatment of Acute left ventricular failure and pulmonary oedema?
Pour SOD (acute LVF): Pour away (stop) their IV fluids Sit up Oxygen – oxygen saturations are falling (<95%) Diuretics – Furosemide
97
What is Cor Pulmonale?
Right heart failure and abnormal enlargement (of the right ventricle) caused by chronic pulmonary arterial hypertension
99
What are the causes of Cor Pulmonale?
COPD Bronchiectasis PF Chronic Asthma PE Pulmonary Vasculitis etc
100
How does Cor Pulmonale Present?
Symptoms: - Dyspnoea - Fatigue - Syncope Signs: - Cyanosis - Tachycardia - Raised JVP
102
What are the investigations for Cor Pulmonale?
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
104
What is the treatment for Cor Pulmonale?
Treat underlying cause Treat respiratory failure – acute situation give 24% oxygen Treat cardiac failure – Diuretic e.g., Furosemide Heart-lung transplant (if young patient)
106
What is the most important risk factor for premature death and CVD?
Hypertension
108
Define White Coat Hypertension
Elevated clinic BP but normal ABPM
109
Define Malignant Hypertension
Rapid rise in BP leading to vascular damage (fibrinoid necrosis is pathological hallmark)
111
What are the causes of Hypertension?
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
113
What are the risk factors for Hypertension?
Family history Old age Male Afro-Caribbean Lack of physical activity Unhealthy diet (high salt intake, alcohol, smoking) Obesity Diabetes mellitus Stress
115
What is the presentation of Malignant Hypertension?
Headaches Visual Disturbances
117
What are some complications of malignant Hypertension?
Eyes - Retinopathy Cardiac - LVH, HF, IHD, PVD Kidney - Renal failure, Proteinuria Neurological - Headache, Nausea, Vomiting, Stroke/TIA GU - Impotence
119
What are the investigations for Hypertension?
High BP in clinic 24 hr Ambulatory BP monitoring (ABPM) Multiple home BP monitoring (twice daily for 4-7 days)
121
What are the tests for End organ damage in new hypertension diagnosis?
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
123
What are the stages of Hypertension?
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
125
When should you consider starting Hypertension treatment?
Stage 1 - Treat if >80yrs or if signs of end organ target damage or QRISK2 score 10% Stage 2 - start Treatment
127
What is the life style management of hypertension?
Weight loss Reduce alcohol intake Reduce salt intake Stop smoking Regular exercise Stress reduction
129
What is the pharmacological management of hypertension in under 55 years or DM?
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
131
What is the pharmacological management of hypertension in over 55 years or Afro-Caribbean?
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
133
What is the treatment for Malignant Hypertension?
Hypertensive Urgency: (no end organ damage) oral Nifedipine Oral Nifedipine and Oral Amlodipine Hypertensive Emergency (end organ damage): IV Labetalol IV GTN
135
What are the Systolic Heart Valve Murmurs?
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
137
What are the Diastolic Heart Valve Murmurs?
ARMS: Aortic Regurgitation: - High-Pitched “Blowing” Early Diastolic Decrescendo Murmur - Best Heard Sitting Forward Mitral Stenosis: - Opening Snap then Delayed Rumbling Mid-Diastolic Murmur
138
What are the heart sounds?
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
140
What is the murmur of a Patent Ductus Arteriosus?
Continuous Machine Like Murmur
142
What is the Aetiology of Mitral Stenosis?
Rheumatic Heart Disease Infective Endocarditis
144
What is the murmur Like in Mitral Stenosis?
Mid-diastolic, low pitched “rumbling” murmur Loud S1 due to thick valves
146
What are the associations of Mitral Stenosis?
Malar flush Atrial fibrillation
148
What are the complications of Mitral Stenosis?
Left atrial Hypertrophy Can lead to AF
149
What is the Aetiology of Mitral Regurgitation?
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
150
What is the murmur like in Mitral Regurgitation?
Pan-systolic, high pitched “whistling” murmur Radiates to left axilla
151
What are the complications of Mitral Regurgitation?
Left atrial dilatation Congestive cardiac failure
152
What is the Aetiology of Aortic Stenosis?
Bicuspid Aortic Valve >70 yrs Idiopathic age-related calcification >70 yrs Rheumatic Heart Disease
153
What is the murmur like in Aortic Stenosis?
Crescendo-decrescendo ejection-systolic, high-pitched murmur Radiates to the carotids
154
What are the associations of Aortic Stenosis?
Slow rising pulse Narrow pulse pressure Exertional syncope Breathlessness
155
What are the complications of Aortic Stenosis?
Left Ventricular Hypertrophy
156
What is Aortic Sclerosis?
Senile degeneration of the heart valve Ejection systolic murmur but no carotid radiation and normal pulse
157
What is the Aetiology of Aortic Regurgitation?
Idiopathic age-related weakness Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
158
What is the murmur like in Aortic Regurgitation?
Early Diastolic Soft Murmur
159
What are the associations of Aortic Regurgitation?
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
160
What are the complications of Aortic regurgitation?
left Ventricular Dilation
161
What is the investigation for heart valve defects?
Echocardiogram
162
What is the aetiology of Rheumatic Heart Fever?
Group A Beta-haemolytic Streptococcus (GABHS) – Streptococcus pyogenes infection
163
What is the pathology of Rheumatic heart Fever?
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
164
Define Tachycardia?
A heart rate >100 BPM
165
Define Bradycardia?
A heart rate <60 bpm
166
How can tachycardias be classified?
Narrow Complex Tachycardias (QRS <120ms) Broad Complex Tachycardias (QRS >120ms)
167
What are the narrow complex tachycardias?
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)
168
What are the broad complex tachycardias?
Ventricular Tachycardia (Regular Irregular Rhythm) Ventricular Fibrillation (Irregular Irregular Rhythm)
169
What are the types of Bradycardia?
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
170
What is Sinus Tachycardia?
>100 bpm + Sinus Rhythm
171
What is the Aetiology of Sinus Tachycardia?
Physiological response to exercise and excitement Anaemia, Infection, Fever, HF, Thyrotoxicosis, Acute PE, Hypovolemia, Atropine
172
What is the ECG in Sinus Tachycardia?
P waves piggyback onto the T waves = camel hump T waves
173
What is the treatment of Sinus Tachycardia?
Correct the cause Beta Blockers to slow sinus rate e.g., atenolol
174
What is a supraventricular Tachycardia?
Any tachycardia that arises from the atrium or atrioventricular junction
175
What are the 4 Main types of SVT?
Atrial fibrillation Atrial flutter Atrioventricular nodal re-entry tachycardia (AVNRT) Atrioventricular reciprocating tachycardia (AVRT)
176
What is the 1st Line management in SVT?
Vagal Manoeuvres (Valsalva Manoeuvre + Carotid Sinus Massage) Adenosine if doesnt work
177
What is the most common arrhythmia?
Atrial Fibrillation
178
What is the pathology of AF?
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
179
What is the Aetiology of AF?
SMITH: Sepsis Mitral Valve Pathology (stenosis or regurgitation) Ischemic Heart Disease Thyrotoxicosis Hypertension
180
What are the types of AF?
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
181
What is the presentation of AF?
Symptoms: Palpitations, SOB, Syncope Signs: Irregularly irregular pulse
182
What are the complications of AF?
Emboli - Due to the pooling of blood in the atria which can lead to thrombus formation.
183
What are the investigations of AF?
ECG: Irregularly irregular rhythm Absent P waves Narrow QRS Bloods – Cardiac enzymes, TFTs Echo
184
What is the Treatment of Acute AF?
Cardioversion (electrical/amiodarone) – usually 1st line Correct electrolyte imbalances + Rate control + Anti-coagulate
185
What is the treatment of Chronic AF?
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)
186
How does amiodarone work?
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.
187
What is first line control of AF and when is it not used?
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
188
When is Rhythm Control used in AF?
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
189
What are the options for Cardioversion?
Pharmacological: Flecainide - pill in pocket Amiodarone (drug of choice in patients with structural heart disease) Electrical: defibrillator
190
What are the Class I, II, III, IV anti arrhythmic Drugs?
Class I: Sodium channel Blockers (Flecainide, quinidine, Lidocaine) Class II: Beta Blockers Class III: Amiodarone Class IV: CCB (Verapamil or Diltiazem)
191
What score is used to calculate risk of stroke in AF?
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)
192
What score is used to assess Bleeding risk in AF?
ORBIT: Older age (>74) Reduced haemoglobin (anaemia) Bleeding history Insufficient Kidney Function Treatment with antiplatelet >4 = High Risk
193
What is the target INR on warfarin?
2-3 (2.5)
194
What is Atrial Flutter?
Regular Irregular heart rhythm
195
What is the pathology of Atrial Flutter?
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
196
What is the ECG in Atrial Flutter?
‘Sawtooth’ pattern (F wave) Regular atrial rate
197
What is the treatment of Atrial Flutter?
Rate control (beta-blockers), Rhythm control (DC cardioversion) and Anticoagulation (warfarin) Radiofrequency catheter ablation – curative for most patients
198
What is the pathology of an AVNRT?
AV nodal re-entry tachycardia (AVNRT): Circuits from within the AVN (‘ring’ of conduction tissue) ECG: Absent P waves (or seen immediately before QRS)
199
What is the pathology of an AVRT?
AV reciprocating tachycardia (AVRT): Accessory pathway connecting the atria and ventricles Wolff-Parkinson-White syndrome (WPW) – bundle of kent
200
What is the acute treatment of an AVNRT/AVRT?
Stable: Vagal Manoeuvres (Valsalva + Carotid Sinus Massage) If doesnt work then adenosine Unstable Electrical Cardioversion
201
What is the Long Term treatment of an AVNRT/AVRT?
Beta Blockers Radio-frequency Ablation
202
What is the ECG of Wolf Parkinson White Syndrome (WPW)?
Short PR interval (due to early depolarization of ventricle) Wide QRS complex Slurred start to the QRS (delta wave) ST changes
203
What are some associations with WPW?
HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD
204
What is the management of WPW?
Definitive: Radiofrequency Ablation Medical Therapy: Sotalol, Amiodarone, Flecainide
205
Why do you get the delta wave in WPW?
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
206
What are broad complex tachycardias associated with?
Prolonged QT syndrome
207
What is Ventricular Tachycardia?
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
208
What is the ECG in V-Tach?
broad complex tachycardia with wide QRS complex
209
What is the treatment of V-Tach?
Stable - Amiodarone Unstable Electrical DC and IV Amiodarone
210
What is Ventricular Fibrillation?
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
211
What is the Treatment of V-Fib?
Defibrillation + IV amiodarone
212
What are the causes of Sinus Bradycardia?
Athlete Extrinsic: - Vasovagal attacks - Drugs (BB, Digoxin, Amiodarone - Hypothermia - Hypothyroidism - Raised ICP Intrinsic: - Acute ischaemia - Infarction of SAN
213
What is the treatment for Sinus Bradycardia?
Extrinsic: Treat Underlying cause Intrinsic - Atropine
214
Define 1st Degree heart Block?
PR interval is prolonged (over 0.20s)
215
Define 2nd Degree Heart Block?
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
216
Define 3rd Degree Heart Block?
Complete Heart Block Ventricular contraction completely independent of atria contractions
217
What are the features of complete Heart Block?
Syncope Heart failure Regular bradycardia (30-50 bpm) Wide pulse pressure JVP: cannon waves in neck Variable intensity of S1
218
What is the treatment of heart Block?
Stable: Observe Unstable / Risk of Asystole ( Type II Mobitz, 3rd degree): - IV Atropine 500mcg - Permanent implantable pacemaker
219
What are the causes of LBBB?
myocardial infarction hypertension aortic stenosis cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
220
What is the ECG of LBBB?
WiLLiaM Slurred S wave in V1 R wave in V6
221
What are the causes of RBBB?
Normal PE IHD ASD VSD Cor pulmonale
222
What is the ECG of RBBB?
MaRRoW: R wave in V1 Slurred S wave in V6
223
What is Long QT Syndrome?
Inherited condition associated with delayed repolarization of the ventricles May lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/ sudden death
224
What are the causes of Long QT?
Romano Ward Syndrome Amiodarone TCA/SSRIs Hypocalcaemia, Hypokalaemia, Hypomagnesaemia MI
225
What is the management of long QT?
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
226
What is Torsades De Pointes (Twisting of the Tips)
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)
227
What is the management of Torsades De Pointes?
Correct the Cause (EG. Electrolyte Disturbances) Magnesium Infusion Defibrillation if V-Tach occurs
228
What are the Cardiac Arrest Rhythms? Which are shockable?
Shockable: Ventricular Tachycardia Ventricular Fibrillation Non-Shockable: Pulseless Electrical Activity Asystole
229
What are the indications for a pacemaker?
Symptomatic bradycardias Mobitz Type 2 AV block Third degree heart block Severe heart failure (biventricular pacemakers) Hypertrophic obstructive cardiomyopathy (ICDs)
230
What are the types of Aneurysms?
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
231
What is the presentation of an Abdominal Aortic Aneurysm?
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
232
What are the complications of an Abdominal Aortic Aneurysm?
Rupture Thrombosis Embolism Death Hypovolaemic Shock
233
What are the investigations for an aortic aneurysm?
1st Line: Abdominal Ultrasound GS: CT angiography
234
What is the treatment for an Aortic Aneurysm?
Ruptured: IMMEDIATE Surgery Unruptured AAA: Elective surgical repair (Open repair via a laparotomy or EVAR) Unruptured TAA: Elective surgical repair (TEVAR or Open repair)
235
What is the Screening for AAA?
All males at age of 65yrs can have screening via Aortic USS High Risk if Symptomatic, Aortic Diameter >5.5cm
236
What is Pathology of an Aortic Dissection?
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
237
What is the presentation of an Aortic Dissection?
Sudden, severe, tearing chest pain (+/-) Radiating to the back Unequal arm pulses, Absent pulses
238
What are the Investigations for aortic Dissection?
CT (/MRI) Angiogram - False lumen and intimal Flap CXR – widened mediastinum ECG to rule out STEMI
239
What is the treatment of an Aortic Dissection?
Type A: Control BP (IV labetalol) + Surgery (Open Surgery) Type B: Control BP (IV labetalol) + Conservative management
240
What are the two types of PVD?
Chronic Limb Ischaemia Acute Limb Ischaemia
241
What is the classification of Chronic Limb Ischaemia?
Fontaine Classification: 1. Asymptomatic 2. Intermittent Claudication 3. Ischaemic Rest Pain (Chronic Ischaemia) 4. Ulceration/Gangrene (Critical Ischaemia)
242
What is the Cause and pathology of Chronic Limb Ischaemia?
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)
243
What are the risk factors for Chronic Limb Ischaemia?
smoking, DM, HTN, hypercholesteraemia, obesity
244
What is the presentation of Chronic Limb Ischaemia?
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
245
What is Leriche Syndrome?
Occlusion in the distal aorta or proximal common iliac artery Clinical triad: Thigh/buttock claudication Absent femoral pulses Male impotence
246
What is Intermittent Claudication?
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
247
What is Critical Limb Ischaemia?
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
248
What are the investigations for Chronic Limb Ischaemia? How is Severity of PVD determined?
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
249
What is the treatment for Intermittent Claudication?
Lifestyle changes (smoking cessation), Optimise treatment of co-morbidities, Exercise training Medical: Atorvastatin, Clopidogrel, Naftidrofuryl oxalate Surgical: Endovascular angioplasty and stenting, Endarterectomy, Bypass surgery
250
What is the treatment for Critical Limb Ischaemia?
Urgent referral and Analgesia Urgent revascularisation: Endovascular angioplasty and stenting, Endarterectomy, Bypass surgery, Amputation (if unable to restore blood supply)
251
What is the cause of Acute Limb Ischaemia?
Thrombosis in situ Emboli Graft/angioplasty occlusion Trauma
252
What is the presentation of Acute Limb Ischaemia?
6Ps Pale Pulseless Painful Paralysed Paraesthetic – numbness and tingling in an extremity (‘pins and needles’) ‘Perishingly cold’
253
What are the investigations for Acute Limb Ischaemia?
Surgical emergency and may require urgent open surgery or angioplasty Handheld arterial Doppler examination (ABI if doppler signals absent)
254
What is the Treatment of Acute Limb Ischaemia?
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
255
What is the risk of Acute Limb Ischaemia?
If not revascularised within 4-6 hours then lose limb.
256
What is the pathology of Acute Limb Ischaemia?
Complete occlusion of the lower limb vessels leading to ischaemia and infarction. Often due to Thrombosis in situ or Emboli
257
What are Varicose Veins?
Distended Superficial Veins measuring >3mm in diameter Often Due to Primary Mechanical Factors (95%) Secondary to obstruction.
258
What is the presentation of Varicose Veins?
Pain/ache, Heaviness, Cramps, Itching/Burning, Oedema
259
What are the tests to check for Varicose Veins?
Tap Test Cough Test Trendelenburgs Test Perthes Test
260
What is the Treatment of Varicose Veins?
Conservative management: Compression stockings Surgical options: Endothermal ablation, Sclerotherapy, Stripping
261
What are some complications of Varicose Veins?
Prolonged/heavy bleeding after trauma, Superficial thrombophlebitis, DVT, Chronic venous insufficiency
262
What is Shock?
Circulatory failure resulting in inadequate organ perfusion (Systolic <90mmHg with evidence of hypoperfusion)
263
What are the different Types of Shock?
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
264
What is Sepsis?
overwhelming and life-threatening inflammatory response to a severe infection, which can lead to tissue damage, organ failure, and death
265
Define Septicaemia?
when bacteria enter the bloodstream, and cause blood poisoning which triggers sepsis
266
Define Septic Shock
life-threatening condition that is characterised by low blood pressure despite adequate fluid replacement, and organ dysfunction or failure
267
How is Sepsis Treated?
SEPSIS 6: (BUFALO) Blood Cultures (Out) Urine Output (Out) Fluids (In) Antibiotics (In) Lactate (Out) Oxygen (In)
268
What are the 4 anatomical cardiac abnormalities in Tetralogy of Fallot?
Ventricular Septal Defect (VSD) Pulmonary Stenosis Right Ventricular Hypertrophy (RVH) Overriding Aorta
269
What is the Pathology of Tetralogy of Fallot?
Right to left Shunt Reduced Oxygenation of blood Causes Cyanosis
270
What are the risk factors for Tetralogy of Fallot?
Rubella infection Increased age of the mother (over 40 years) Alcohol consumption in pregnancy Diabetic mother
271
What is the presentation of Tetralogy of Fallot?
Symptoms: - Infants: Cyanotic, Paroxysmal hypercyanotic spells - Toddlers: May squat Signs: - Clubbing - Pulmonary stenosis murmur - Tet Spells: Intermittent symptomatic periods precipitating a cyanotic episode
272
What are the investigations of Tetralogy of Fallot?
CXR - Boot Shaped Heart Echocardiography - GS
273
What is the Treatment of Tetralogy of Fallot?
Prostaglandin E Infusion (Alprostadil) (Prevents Closure of PDA shunt to allow oxygenated blood to enter the aorta) Surgery
274
What is a Ventricular Septal Defect and what are the associations?
Hole in the ventricles. Associated with Downs, Turners
275
What is the presentation of an VSD?
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
276
What are the Investigations of a VSD?
Echocardiogram
277
What is the Treatment of VSD?
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
278
What is an atrial Septal Defect?
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
279
What is the presentation of ASD?
Recurrent chest infections and heart failure Symptoms: - Chest pain, Palpitations, Dyspnoea Signs - Wide fixed split S2 - Pulmonary systolic flow murmur – mid-systolic, crescendo-decrescendo
280
What are the investigations of an ASD?
Echocardiogram
281
What is the treatment of an ASD?
Cardiac catherization or Open-heart surgery Anticoagulants (aspirin, warfarin and NOACs) used to reduce the risk of clots and stroke in adults
282
What are the complications of an ASD?
SAPE: Stroke in the context of venous thromboembolism Atrial fibrillation or atrial flutter Pulmonary hypertension and right sided heart failure Eisenmenger syndrome
283
What is Eisenmenger's Syndrome?
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
284
What is the result of Eisenmenger's Syndrome?
Marked cyanosis Clubbing Heart failure Others: syncope, high RBC, organ damage
285
What is a Patent Ductus Arteriosus (PDA)?
Duct still being present 1 month after the child should have been born
286
What is the presentation of a PDA?
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
287
What is the Treatment of PDA?
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)
288
What is Coarctation of the Aorta?
Aorta is narrowed at the site of the ductus arteriosus Associations: Bicuspid aortic valve, Turner’s syndrome
289
What is the presentation of Coarctation of the Aorta?
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
290
What are the complications of Coarctation of the Aorta?
Premature coronary artery disease Congestive Cardiac Failure (CCF) Hypertensive encephalopathy Intracranial haemorrhage
291
What are the investigations of Coarctation of the Aorta?
CT or MRI-aortogram CXR – may show rib notching
292
What is the Treatment of Coarctation of the Aorta?
Prostaglandin E – if risk of HF/death shortly after birth Surgery – risk of aortic aneurysm after surgical repair Balloon dilation +/- stenting
293
What is the pathology of HOCM?
Septal Cardiac Hypertrophy which leads to Left Ventricular outflow obstruction
294
What is the epidemiology of HOCM?
1 in 500
295
What are the Gene mutations in HOCM?
Autosomal Dominant Sarcomere Protein Gene Mutations
296
What is the Presentation of HOCM?
Angina Dyspnoea Palpitations Sudden Death (most common cause of sudden death in young adults)
297
What is the treatment of HOCM?
Amiodarone (prevent AF) Beta-Blockers for Symptoms
298
What is the pathology of DCM?
Dilated left Ventricle leading to systolic dysfunction as the ventricular walls are thin and cannot contract
299
What are the gene mutations in DCM?
Cytoskeletal Gene mutations
300
What is the Presentation of DCM?
heart Failure symptoms: Dyspnoea, Fatigue, Oedema
301
What is the Treatment of DCM?
Diuretics for fluid overload Beta blockers ACEi Anticoagulation (LMWH)
302
What is the pathology of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?
Myocardium is Replaced by fibrous and fat tissue leading to conduction problems between the atria and ventricles. This causes arrhythmias
303
What are the Gene mutations in ARVC?
Desmosome Gene Mutations Naxos disease - AR condition with ARVC + wooly hair and Palmerplanterkeratoderma
304
What is the Presentation of ARVC?
Arrythmias Palpitations Syncope
305
What is the Treatment of ARVC?
Sotalol Amiodarone
306
What Thromboprophylaxis is best for patients with arrhythmias and a metallic heart valve?
Warfarin is preferred.
307
What is Pericarditis?
Inflammation of the pericardium
308
What is the aetiology of pericarditis?
Idiopathic (80-90%) Infection – Viral (most common): enterovirus, adenovirus, Coxsackie; Bacterial: TB Autoimmune – Rheumatoid arthritis, Scleroderma Dressler's syndrome (post-MI)
309
What are the symptoms of pericarditis?
Central (pleuritic) chest pain worse in inspiration or lying down. Relieved by sitting forward Fever Dyspnoea
310
What are the signs of pericarditis?
Pericardial Rub Tachypnoea Tachycardia
311
What are the investigations for pericarditis?
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
312
What is the Treatment for Pericarditis?
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
313
What are the requirements for a clinical diagnosis of pericarditis?
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)
314
What are the major complications of pericarditis?
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
315
What is the presentation, Investigation and treatment of a pericardial effusion?
Px: Dyspnoea and Chest pain Ix: Echo Tx: Pericardiocentesis
316
What is the presentation, Investigation and treatment of a pericardial tamponade?
Px: Becks Triad (falling BP, Rising JVP, Muffled Heart Sounds) Ix: Echo Tx: Pericardiocentesis
317
What is the presentation, Investigation and treatment of a chronic constrictive pericarditis?
Presentation: Symptoms of right heart failure, Dyspnoea Treatment: Surgical excision
318
What is infective endocarditis?
Infection and inflammation of the endocardial lined structure (commonly the heart valves)
319
What are the causes of Infective Endocarditis?
Staphylococcus aureus (now the most common) – IVDU, dermatitis, DM Streptococcus viridans – new cardiac murmur Staphylococcus epidermitis – metallic valve replacement
320
What are the risk factors for Infective Endocarditis?
Old age IVDU Prosthetic valves Congenital heart disease Others: Poor dental hygiene, Skin and soft tissue infection, IV cannula, Cardiac surgery, Pacemaker
321
What is the presentation of Infective Endocarditis?
Fever + non-specific Symptoms May have IE signs New onset murmur
322
What are the associated signs and symptoms with Infective Endocarditis?
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
323
What are the investigations for Infective Endocarditis?
Blood cultures – 1st line (from 3 sites, on 3 occasions) Echocardiogram – vegetations on heart valves Others: Bloods (normochromic, normocytic anemia), ECG, Urinalysis (hematuria), CXR
324
What is the diagnostic Criteria for Infective Endocarditis?
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)
325
What is the treatment for Infective Endocarditis?
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
326
What are some poor prognostic factors for Infective Endocarditis?
Staphylococcus aureus Prosthetic valve (especially 'early', acquired during surgery) Culture negative endocarditis Low complement levels
327
What are the classifications of Carotid Artery Stenosis?
Mild – less than 50% reduction in diameter Moderate – 50 to 69% reduction in diameter Severe – 70% or more reduction in diameter
328
What is the presentation of Carotid Artery Stenosis?
Usually asymptomatic, diagnosed after a TIA or stroke Carotid bruit – may be heard on examination
329
What are the investigations for Carotid Artery Stenosis?
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
330
What is the treatment for Carotid Artery Stenosis?
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
331
What is Buerger Disease?
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)
332
Who do Buerger Disease typically affect?
Men aged 25-35 (diagnostic criteria involves <50 yrs) Strong association with smoking
333
What is the presenation of Buergers Disease?
Painful, blue discolouration to the fingertips or tips of the toes Pain is often worse at night
334
What is the Investigations of Buergers Disease?
Angiograms - Corkscrew Collaterals
335
What is the treatment for Buergers Disease?
Completely stop smoking – main component of treatment Other specialist treatments: Intravenous Iloprost (a prostacyclin analogue that dilates blood vessels)
336
What are some complications of Buergers Disease?
Ulcers Gangrene Amputation

Phase 2a Practice (12 decks)

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