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Cardiology Flashcards

1
Q

Causes of stable angina

A 
Atherosclerosis
Anaemia
Aortic stenosis 
Tachyarrhythmias
Arteritis
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2
Q

Risk factors for stable angina

A 
Smoking 
Diet high in saturated fats and salt
Obesity
Lack of exercise
Type A personally
Alcohol
HTN
DM
Cholesterol high
Older age
Male
Fix ( MI<55yo)
Genetic - hyperlipidaemia
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3
Q

Symptoms of stable angina

A

central chest pain (tight/heavy), brought on by exertion and relived by rest or GTN spray. Can radiate to one/both arms, neck, jaw or teeth.

o Precipitants for pain: exercise, emotion, cold weather, heavy meals

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4
Q

5 types of angina

A 
Stable - induced by effort
Unstable - at rest
Decubitus
Prinzmetals/variant
Syndrome X/microvascular
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5
Q

What is decubitus angina?

A

angina on laying down

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6
Q

What is prinzmetals/variant angina?

A

coronary spasm causes angina at rest (ST^ on ECG). Tx = Calcium channel blocker + long-acting nitrate e.g. ivabradine

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7
Q

What is syndrome X/microvascular angina?

A

Angina symptoms & ST^ on exercise test but no evidence of coronary atherosclerosis on angiography.

?cause is abnormal dilator responses of coronary microvasculature. Difficult to treat.

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8
Q

Ix for stable angina

A
  1. Gold standard = angiography
  2. ECG = usually normal [may be evidence of previous MI - ST↓, flat/inverted T waves]
  3. Bloods = FBC (look for anaemia), U&E, lipids, glucose, ESR, TFTs
  4. ? Exercise ECG / ? Stress echocardiogram / ? myocardial perfusion scan
  5. Screen for risk factors – hypercholesterolaemia, HTN, DM
  6. Look for valve disease on examination
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9
Q

Mx for stable angina

A
  1. Lifestyle changes
  2. Medical
     Anti-anginals:
    • Glyceryl trinitrate (GTN) sublingual + either:
    o Beta-blocker (atenolol)
    o [or CCB if BB is contraindicated (verapamil)]
    • 2nd line: BB + dihydropyridine CCB (amlodipine)
    • 3rd line:
    o Isosorbide mononitrate
    o Slow-release nitrate: ivabradine / nicorandil / ranolazine
     Prevention
    • Aspirin
    • ACEi (if angina + DM)
    • Statins
    • Antihypertensives
  3. Non-medical: REVASCULARISATION (percutaneous coronary intervention or coronary artery bypass grafting)
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10
Q

Complications of stable angina

A

MI, stroke

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11
Q

Types of ACS

A
  1. Unstable angina – angina at rest, no ECG changes/troponin elevation
  2. NSTEMI (non ST elevation myocardial infarction)– some obstruction of coronary artery with ^troponin/CK-MB but no ECG changes
  3. STEMI (ST elevation myocardial infraction)– obstruction of coronary artery causing infarction of heart muscle - ^ST on ECG & raised markers of myocardial damage (troponin)
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12
Q

Unstable angina pathology

A

Myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury or necrosis.

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13
Q

Unstable angina symptoms

A
  • Chest pain
  • Marked sweating
  • Epigastric pain
  • Dyspnoea
  • Syncope
  • Back pain

that is:
• prolonged (>20 mins) angina at rest,
• new onset severe angina,
• angina that is increasing in frequency/longer in duration/lower in threshold,
• or angina that occurs after a recent episode of MI.

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14
Q

Ix for unstable angina

A

No ST elevation on ECG + normal troponin levels = unstable angina

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15
Q

Acute management of unstable angina

A
  1. O2: aim for SpO2 94-98%
  2. 300mg aspirin
  3. GTN (spray, tablet or IV if pain continues)
  4. Analgesia: Morphine 5-10mg IV
  5. Anti-emetic: metoclopramide 10mg IV
  6. Anticoagulation – fondaparineux 2.5mg SC
  7. Assess cardiovascular risk & if high risk refer for PCI intervention
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16
Q

Long term management for unstable angina

A
  1. Beta blocker – anti-anginal medication. Bispoprolol
  2. GTN
  3. Dual antiplatelet therapy: aspirin + clopidogrel
  4. Consider:
    a. ACEi (linsopril 2.5mg)
    b. Statin
    c. Aldosterone antagonist in heart failure e.g. eplerenone/spironolactone
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17
Q

What is an NSTEMI?

A

An acute ischaemic event causing myocyte necrosis. Encompasses a broad spectrum of ischaemic injury to the myocardium which is detected by elevation of troponin.

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18
Q

ECG changes for NSTEMI

A

may show ischaemic changes including ST depression, T wave changes or transient ST elevation OR may be normal.

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19
Q

Symptoms NSTEMI

A
  • Central constricting chest pain with pain radiating to jaw or arms
  • Nausea and vomiting
  • Sweating
  • Impending doom
  • SOB
  • Palpitations
  • If diabetic/elderly – syncope, delirium, post op oliguria/hypotension
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20
Q

Ix for NSTEMI

A

Possible ECG changes –

  • ST segment depression: worse prognosis
  • Deep T wave inversion
  • Pathological Q waves
  • Transient ST elevation

High sensitivity troponin (hs-cTn) – elevated

Other Ix to consider:

  • CXR
  • FBC
  • U&E
  • LFT
  • BMs
  • CRP
  • Echo
  • Coronary angiography
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21
Q

What score is used to assess the need for PCI in NSTEMI?

A

GRACE Score

  • The score gives a 6 month risk of death or repeat MI after having an NSTEMI
    o <5% low risk
    o 5-10% medium risk
    o >10% high risk
  • Medium – high risk = early PCI (within 4 days of admission)
  • Includes: age, heart rate, systolic BP, creatinine, cardiac arrest at admission, ST segment deviation on ECG, abnormal cardiac enzymes and the presence of certain symptoms (CHF, rales, pulmonary oedema, cardiogenic shock)
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22
Q

Mx for NSTEMI

A

BATMAN

  • B = beta blockers
  • A = aspirin 300mg
  • T = ticagrelor 180mg (or clopidogrel 300mg)
  • M = Morphine (titrated to control pain)
  • A = Anticoagulant = fondaparinux
  • N = Nitrates (GTN)
    o Give fondaparinux if no immediate PCI planned
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23
Q

Secondary prevention following NSTEMI

A

6 As

  • Aspirin 75mg OD
  • Another antiplatelet = clopidogrel or ticagrelor for up to 12 months
  • Atorvastatin 80mg OD
  • ACEi e.g., ramipril
  • Atenolol or another beta-blocker
  • Aldosterone antagonist for those with heart failure (eplerenone)
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24
Q

STEMI pathology

A

Cardiac myocytes die due to ischaemia as a coronary artery is blocked

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25
Q

Symptoms of STEMI

A
  • Chest pain - >20 mins, doesn’t respond to GTN, radiates down L arm/neck/jaw
  • Pale, clammy, sweating
  • In elderly or diabetic = dyspnoea, fatigue, pre-syncope, syncope
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26
Q

Criteria for a STEMI

A
  • ST elevation >2mm (2 little squares) in 2 contiguous chest leads or >1mm (1 little square) in 2 contiguous limb leads (i.e. territorial)
  • Symptoms of ACS for >20 mins with persistent ECG features in 2 or more contiguous leads:
    • 2.5mm ST elevation in V2-3 in men under 40
    • 2 mm ST elevation in V2-3 in men over 40
    • 1.5 mm ST elevation in V2-3 in women
    • 1mm ST elevation in other leads
    • New LBBB
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27
Q

Posterior STEMI ECG changes and artery blocked?

A

Left circumflex and right coronary arteries blocked.

ST depression V1-V3
Tall broad R waves V1-V3
Dominant R wave in V2
Inverted T wave in aVR

Posterior infarction is confirmed by putting on posterior chest leads - V7-V9

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28
Q

Ix in STEMI

A
  • ECG
  • Cardiac enzymes
  • Bloods
  • Transthoracic echocardiography (TTE)
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29
Q

Anterior STEMI ECG changes and what artery is blocked?

A

Left anterior descending artery blocked

ST elevation in V1 - V4

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30
Q

Anterolateral STEMI ECG changes and what artery is blocked?

A

Left coronary artery blocked (that branches into LAD and circumflex artery)

ST elevation in lead I, aVL and V3-V6

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31
Q

Lateral STEMI ECG changes and what artery is blocked?

A

Circumflex artery blocked

ST elevation in Lead I, aVL and V5-6

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32
Q

Inferior STEMI ECG changes and what artery is blocked?

A

Right coronary artery blocked

ST elevation in II, II and aVF

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33
Q

What score is used to decide whether to admit someone from ED with ACS?

A 
-	HEART Score
•	History
•	ECG
•	Age
•	Risk factors
•	Troponin
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34
Q

Initial management of STEMI

A
  • MONA – initial management of STEMI
    • Morphine: only if needed and give with metoclopramide as it delays the absorption of antiplatelet drugs
    • Oxygen: only to maintain sats
    • Nitrates: sublingual or IV (used in cation in hypotensive patients)
    • Aspirin: 300mg stat
  • In ED:
    • Cardiac monitoring
    • Load with P2Y12 inhibitor – ticagrelor or prasugrel
    • 2nd line = clopidogrel
    • Anticoagulation – fondaparinux
    • Don’t give a beta blocker or ACEi at this stage without a specialist
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35
Q

Definitive management of STEMI

A
  • Primary PCI within 12 hours – better than thrombolysis, majority of patients come straight from ambulance.
  • thrombolysis - CI if after 24 hours from pain onset & other CIs remembered with AGAINST. Use streptokinase, alteplase or tenectaplase.
  • If no repercussion therapy = fondaparinux
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36
Q

Follow up after a STEMI

A

• Clinic 1 month later
• Transthoracic echocardiogram
• Cardiac rehabilitation programme in community
• Smoking cessation
* DVT prophylaxis until fully mobile
* Statin
• GP to up titrate secondary prevention e.g. ramipril and bisoprolol
* Clopidogrel for up to 1 year
* continue aspirin 75mg
• Don’t drive for 1 week after PCI, 4 weeks if no PCI

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37
Q

What are 3 cardiac enzymes and protein markers used to Ix ACS?

A

o Serum troponin T = most important cardiac-specific marker for myocardial necrosis. The levels remain elevated for up to 10 days.
o Myoglobin is the first to rise.
o CK-MB = useful to look for reinfarction as it returns to normal after 2-3 days (while troponin T stays elevated for 10 days)

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38
Q

MI complications

A
  1. Death
  2. Heart failure
  3. Pericarditis – ECG shows saddle shaped ST elevation +/- PR depression
  4. Rupture – myomalacia cordis (means softening of the heart muscle)
  5. Arrhythmias: SVT, VT, VF, Sinus bradycardia, AV block, Ventricular bradycardia
  6. Aneurysm – ventricular
  7. Embolism
  8. Dressler’s syndrome
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39
Q

What are the 3 types of rupture seen following an MI?

A

a. L ventricular free wall rupture – seen in 3% of Mis. Occurs 1-2 weeks after MI. Presentation = acute HF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Mx = pericardiocentesis & thoracotomy
b. Papillary muscle or chordae rupture: mitral regurgitation
c. Septum rupture

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40
Q

What is Dressler’s syndrome and how does it present?

A

a. AKA post myocardial infarction syndrome
b. 2-3 weeks after MI
c. Localised auto-immune response against antigenic proteins formed as the myocardium recovers that causes pericarditis
d. Presentation = pleuritic chest pain, low grade fever, pericardial rub, pericardial effusion and pericardial tamponade

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41
Q

What are the ECG changes, echo results and inflammatory markers seen with Dressler’s syndrome?

A

Global ST elevation and T wave inversion
Echo = pericardial effusion
Raised CRP and ESR

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42
Q

Mx for Dressler’s syndrome

A

NSAIDs, prednisolone, pericardiocentesis to remove fluid from around heart

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43
Q

What is an abdominal aortic aneurysm?

A

AAA is a permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior diameter of that segment, given the patients sex and body size.

Commonly adopted threshold = diameter of 3cm or more

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44
Q

Pathology for AAA

A

They occur primarily because of elastic proteins within the extracellular matrix.
Aneurysms typically represent dilation of all layers of the arterial wall.
Most are caused by degenerative disease.
Most are infrarenal (e.g., below the origin of the renal arteries)

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45
Q

Risk factors for AAA

A
  • SMOKING
  • HTN & diabetes
  • Family hx
  • Male sex (men have a higher prevalence of AAA but women have a higher rate of AAA rupture than men)
  • Syphilis
  • Connective tissue diseases e.g., Elhers Danlos type 1, Marfan’s syndrome
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46
Q

Symptoms of AAA (not ruptured)

A
  • Palpable pulsative abdominal mass
  • Abdominal, flank or back pain
  • Hypotension
  • Frequently asymptomatic, presence of symptoms indicates rupture/impending rupture
  • LOC
  • Pallor
  • Abdominal distention
  • Fever
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47
Q

Symptoms of ruptured AAA

A

sudden collapse

persistent severe central abdominal pain with developing shock (mortality is 80%).

Grey Turners sign (flank bruising) if theres retroperitoneal bleeding

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48
Q

Ix for AAA

A
  • For diagnosis = AORTIC USS
  • Other Ix to consider:
    o Cross match
    o Clotting screen
    o ESR / CRP
    o FBC
    o Blood cultures
    o CT angiography for planning surgery

ECG = right coronary artery occlusion (inferior ECG changes: leads II, III and aVF)

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49
Q

Screening for AAA

A

– NHS screening for AAA for men over 65 yo, by abdominal USS. Findings dictate management:

  1. <3cm = no further follow up
  2. 3cm – 4.4 cm = yearly USS screening
  3. 4.5cm – 5.4 cm = 3 monthly USS screening
  4. > 5.4 cm = urgent two week wait referral to vascular surgeons
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50
Q

Mx for ruptured or symptomatic AAA

A

a. If there’s rupture: 20% rupture anteriorly into the peritoneal cavity (poor prognosis) & 80% rupture posteriorly into the retroperitoneal space

b. Surgical repair – endovascular aneurysm repair (EVAR) or open surgical repair
c. Resuscitation measures
d. Perioperative antibiotic therapy
e. Analgesia
f. VTE prophylaxis

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51
Q

Mx for incidental finding of asymptomatic AAA <5.5cm

A

a. Surveillance

b. Aggressive cardiovascular risk management

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52
Q

Mx for incidental finding of asymptomatic AAA >5.5cm or rapidly growing

A

a. Elective surgical repair
b. Preoperative cardiovascular risk reduction
c. Perioperative antibiotic therapy
d. Analgesia
e. VTE prophylaxis

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53
Q

What is aortic dissection?

A

Aortic dissection = separation in the aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.
TEAR IN THE TUNICA INTIMA OF THE WALL OF THE AORTA

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54
Q

How is aortic dissection classified?

A

Classification is anatomical, with 2 systems most used:

  1. Stanford
    a. Type A = ascending aorta involved. 2/3rds cases.
    b. Type B = ascending aorta NOT involved. Is descending aorta distal to L subclavian artery. 1/3rd cases.
  2. DeBakey
    a. Type I = involves ascending aorta, dissection extends into the arch and beyond
    b. Type II = limited to ascending aorta, proximal to brachiocephalic artery
    c. Type IIIa = involves descending thoracic aorta, distal to L subclavian artery, proximal to coeliac artery
    d. Type IIIb = involves descending thoracic aorta and abdominal aorta
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55
Q

Causes of aortic dissection (congenital)

A
  • Connective tissue disorders e.g., Marfan’s syndrome, Ehlers Danlos syndrome, osteogenesis imperfecta
  • Turner’s syndrome
  • Noonan’s syndrome
  • Bicuspid aortic valve
  • Metabolic disorders
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56
Q

Causes of aortic dissection (acquired)

A
  • Arterial hypertension
  • Syphilitic aortitis
  • Pregnancy
  • Trauma
  • Iatrogenic – surgical aortic cannulation, aortic cross-clamp
  • Cocaine use
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57
Q

Symptoms of aortic dissection

A
  • Severe chest pain (tearing, maximal at onset) // asymptomatic
  • Cardiac tamponade = Beck’s triad (raised JVP, muffled heart sounds, hypotension)
  • Aortic regurgitation = diastolic murmur, wide pulse pressure, signs of heart failure
  • Back and abdominal pain
  • SOB
  • Syncope / collapse
  • Different BP L and R arm (>20 mmHg systolic)
  • Neurological deficit
  • Horner’s syndrome (miosis, ptosis, anhidrosis)
  • Absent peripheral pulses
  • Hypertension
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58
Q

What is Beck’s triad?

A

Raised JVP, muffled heart sounds and hypotension

Due to cardiac tamponade

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59
Q

Ix for aortic dissection

A
  1. CXR = widened mediastinum & L sided pleural effusion
  2. ECG = no changes / non-specific changes
  3. CT angiography CAP (definitive Ix)
     False lumen = diagnostic
     Good for planning surgery
  4. Transoesophageal echocardiography (TOE)
     Good if patient too risky to take to CT scanner
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60
Q

MX for aortic dissection (by Stanford type)

A
  1. Stanford type A
    a. Emergency surgery in suitable patients
    b. Get BP 100-120mmHg whilst awaiting surgery
  2. Stanford type B
    a. Uncomplicated = medical management – BP management (IV labetalol) and appropriate analgesia
    b. Emergency surgery in Stanford type B with:
    i. Intractable pain
    ii. Rupture or impending rupture
    iii. End organ damage / limb ischaemia
    iv. Rapid progression
    v. Marfan’s syndrome
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61
Q

Complications of aortic dissection

A
  • Backwards tear = aortic incompetence / regurgitation, MI

- Forwards tear = unequal arm pulses and BP, stroke, renal failure

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62
Q

When can you hear a third heart sound?

A

heard after S2.

Normal in young healthy people. Is caused by rapid ventricular filling that causes the chordae tendinae to pull to their full length and twang.

In older patients = HF.

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63
Q

When can you hear a fourth heart sound?

A

Heard directly before S1.
Always abnormal.

Stiff/hypertrophic ventricle = turbulent flow from an atria against a non-compliant ventricle.

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64
Q

How should you assess a murmur?

A

Assessing a murmur: SCRIPT
S = site – where the murmur is loudest
C = character – soft/blowing/crescendo/decrescendo/crescendo-decrescendo
R = radiation – over carotids or into L axilla?
I = intensity – what grade is the murmur
P = pitch – high or low pitched? – indicates velocity
T = timing – is it systolic or diastolic

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65
Q

How do you grade a murmur?

A
  1. Difficult to hear
  2. Quiet
  3. Easy to hear
  4. Easy to hear with palpable thrill
  5. Hear with stethoscope barely touching chest
  6. Hear with stethoscope off the chest
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66
Q

What valve lesion causes left atrial hypertrophy?

A

Mitral stenosis

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67
Q

What valve lesion causes L ventricular hypertrophy?

A

Aortic stenosis

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68
Q

What valve lesion causes L atrial dilation?

A

Mitral regurgitation

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69
Q

What valve lesion causes L ventricular dilation?

A

Aortic regurgitation

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70
Q

Causes of mitral stenosis

A

Rheumatic heart disease

Infective endocarditis

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71
Q

Murmur heard in mitral stenosis and other findings on examination

A

Mid-diastolic low pitched rumbling murmur

Loud S1
Palpable tapping apex beat

Malar flush
AF

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72
Q

Causes of mitral regurgitation

A

Idiopathic weakening of the valve with age
IHD
Infective endocarditis
Rheumatic heart disease
Connective tissue disorder – Elhers-Danlos/Marfan

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73
Q

Murmur heard in mitral regurgitation and other findings on examination

A

Pansystolic high pitched whistling murmur that radiates to L axilla

Possible S3
CCF

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74
Q

Causes of aortic stenosis

A

Age related calcification
Rheumatic heart disease
Bicuspid aortic valve

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75
Q

Murmur heard in aortic stenosis and other findings on examination

A

Ejection systolic high pitched murmur with crescendo-decrescendo character

Murmur radiates to carotids

Slow rising pulse and narrow pulse pressure
Exertional syncope
S4 - if ventricles hypertrophied

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76
Q

Causes of aortic regurgitation

A

Idiopathic age related weakness
Connective tissue disorder – Elhers-Danlos / Marfans
Stanford type A aortic dissection
Bicuspid aortic valve

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77
Q

Murmur heard in aortic regurgitation and other findings o/e

A

Early diastolic soft murmur

Austin-Flint murmur: heard at the apex, is an early diastolic rumbling murmur

Collapsing pulse (Corrigan’s pulse)	
HF
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78
Q

Symptoms of aortic stenosis

A
  • Chest pain / angina
  • SOB
  • Syncope
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79
Q

Ix for aortic stenosis

A

Ix = ECHOCARDIOGRAM + DOPPLER

  • ECG = L ventricle hypertrophy (deep S waves in V1 and V2, tall R waves in V5 and V6) / LV strain (tall R waves, ST depression, T wave inversion in V4-6) / LBBB or complete AV block (due to septal calcification)
  • CXR = small heart, dilated ascending aorta, calcified AV especially on lateral films.
  • Bloods = FBC, U&E, lipids, glucose
  • Cardiac catheterisation and angiography
  • Exercise stress test
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80
Q

Mx for aortic stenosis

A
  • Asymptomatic = observation
  • Symptomatic = valve replacement
  • If asymptomatic but valvular gradient >40 mmHg and there’s features like L ventricular systolic dysfunction = valvular replacement
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81
Q

Indications for valve replacement in aortic stenosis

A
  1. Severe symptomatic AS
  2. Severe asymptomatic AS with reduced ejection fraction (<50%)
  3. Severe AS undergoing CABG or other valve operation
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82
Q

Types of valves used to replace stenosed aortic valve

A
  1. Bioprosthetic valves – can come from pigs (porcine bioprosthetic). Lifespan of 10 years
  2. Mechanical valves – 20+ years lifespan & require anticoagulation with warfarin (target INR 2.5-3.5)
     Starr Edwards Valve – ball in cage valve, highest risk of thrombus formation
     Tilting disc valve – a single tilting disc
     St Jude valve – two metal tilting discs, bileaflet valve, least risk of thrombus formation
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83
Q

What are the problems with mechanical heart valves?

A

o Thrombus formation
o Infective endocarditis (caused by gram positive cocci e.g. staphylococcus, streptococcus or enterococcus)
o Haemolysis causing anaemia – blood is churned up in the valve

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84
Q

What heart sounds occur with mechanical heart valves?

A

• Mechanical heart valves cause a click:
o Click replaces S1 for metallic mitral valve
o Click replaces S2 for metallic aortic valve

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85
Q

What mx for patients unfit for valve replacement?

A
  1. Balloon valvuloplasty
     High complication rate
     Restenosis occurs in 6-12 months
  2. Transcatheter aortic valve implantation (TAVI)
     Insert catheter into femoral artery, feed a wire under x-ray guidance to location of aortic valve, inflate a balloon to stretch the stenosed valve then implant a bioprosthetic valve.
     Long term outcomes unclear
     No warfarin required
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86
Q

Symptoms of aortic regurgitation

A 
SOB
fatigue
weakness
orthopnoea
PND
pallor
mottled extremities
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87
Q

What is Quincke’s sign

A

Nailed pulsation seen in aortic regurgitation

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88
Q

Signs of severe aortic regurgitation

A
  1. Wide pulse pressure and collapsing pulse
  2. S3
  3. Long murmur
  4. Austin Flint murmur
  5. Decompensation = LVF
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89
Q

What is De Musset’s sign?

A

Head bobbing seen in Aortic Regurgitation

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90
Q

Ix for AR?

A
  • Transthoracic echocardiography (TTE): can see abnormal aortic valve leaflets & regurgitant jet
  • Bloods: BNP (HF) and blood cultures (if suspecting infective endocarditis)
  • ECG: no specific signs but rules out other differentials
  • CXR – to look for pulmonary oedema or aortic dissection causing AR. Chronic AR can cause cardiomegaly.
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91
Q

Mx for AR

A

• Manage HTN and HF
• Do surgical valve replacement if:
1. Acute severe AR e.g., after aortic dissection
2. Symptomatic chronic AR
3. Asymptomatic chronic severe AR with reduced LVEF (<55%) or cardiac surgery happening for other reasons

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92
Q

Murmur heard with tricuspid regurgitation and other signs on examination

A

o Pansystolic murmur
o Prominent/giant V waves in JVP
o Pulsatile hepatomegaly
o L parasternal heave

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93
Q

Causes of tricuspid regurgitation

A 
o	Right ventricular infarction
o	Pulmonary HTN e.g., COPD
o	Rheumatic heart disease
o	Infective endocarditis
o	Ebstein’s anomaly – congenital heart defect where tricuspid valve leaflets are malformed
o	Carcinoid syndrome
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94
Q

What causes arterial ulcers?

A

Insufficient blood supply to the skin due to peripheral arterial disease

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95
Q

Characteristics of arterial ulcers

A

Distal, affect the toes/dorsum of the foot
Associated with peripheral arterial disease – absent pulses, pallor, intermittent claudication
Smaller and deeper
Well defined borders
Punched out appearance
Pale colour (due to poor blood supply)
Less likely to bleed
Painful
Pain worse at night when horizontal
Pain worse on elevating and improved by lowering leg

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96
Q

Ix for arterial and venous ulcers

A

ABPI – used to assess for arterial disease

Blood tests –

  • FBC: infection, anaemia
  • CRP: infection
  • HbA1C
  • Albumin: malnutrition

Charcoal swabs – if infection suspected

Skin biopsy – if squamous cell carcinoma is suspected (TTW)

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97
Q

Mx for arterial ulcers

A

Urgent referral to vascular surgeons for surgical revascularisation

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98
Q

Cause of venous ulcers

A

Occur due to pooling of blood and waste products in the skin secondary to venous insufficiency

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99
Q

Characteristics of venous ulcers

A

Occur in gaiter area (between top of foot and bottom of calf muscle)
Chronic venous changes = hyperpigmentation, venous eczema, lipodermatosclerosis
Occur after minor injury to leg
Larger & more superficial
Irregular, gently sloping borders
More likely to bleed
Less painful
Pain relieved by elevation and worse on lowering leg

100
Q

Mx for venous ulcers

A

Refer to vascular surgery if mixed type suspected

Refer to tissue viability/specialist leg ulcer clinics

Dermatology if suspecting SCC

Wound care from nurses:

  • Cleaning the wound
  • Debridement of the wound
  • Dressing the wound
Compression therapy (after arterial disease excluded with ABPI)
Pentoxifylline (oral) – can improve healing

Abx for infections
Analgesia for pain

101
Q

What causes foot ulcers in diabetics?

A
  • Diabetic neuropathy – unlikely to realise they’ve injured their feet
  • Damage to small & large blood vessels (PAD) = impaired blood supply
  • Raised blood sugar, immune system changes and autonomic neuropathy = ulceration & poor healing
102
Q

Complications of diabetic foot ulcers

A

osteomyelitis, cellulitis, gangrene

103
Q

Presentation of diabetic foot ulcers

A
  • Neuropathy

- Ischaemia – absent foot pulses, reduced ABPI, intermittent claudication

104
Q

What foot screening should diabetics get?

A

Screen on annual basis

  • Palpate dorsalis pedis and posterior tibial pulses
  • 10g monofilament on sole of foot for neuropathy
105
Q

What causes pressure ulcers?

A

Reduced mobility with prolonged pressure on areas = reduced blood supply, reduced lymphatic drainage & deformation of tissues under pressure

106
Q

Risk factors for pressure ulcers

A
  • Malnourished
  • Incontinent
  • Lack of mobility
  • Pain
107
Q

How are pressure ulcers graded?

A

1 – non-blanchable erythema of intact skin
2 – partial thickness skin loss
3 – Full thickness skin loss with damage/necrosis of subcutaneous tissue that can extend to underlying fascia
4 – extensive destruction, tissue necrosis or damage to muscle/bone/supporting structures

108
Q

How can pressure ulcers be prevented?

A
  • Risk assessment
  • Regular repositioning
  • Special inflating mattresses
  • Regular skin checks
  • Protective dressings and creams
109
Q

Score used to assess risk of pressure ulcers

A 
Waterlow score  
•	BMI
•	Nutritional status
•	Skin type
•	Mobility
•	Continence
110
Q

Mx for pressure ulcers

A
  • Hydrocolloid dressings to keep wound moist
  • Don’t swab, give abx on clinical findings
  • Tissue viability nurse
  • Surgical debridement
111
Q

What is cardiac arrest?

A

a sudden state of circulatory failure due to a loss of cardiac systolic function.

112
Q

What are the 4 specific cardiac rhythm disturbances seen in cardiac arrest?

A
  1. Ventricular tachycardia
  2. Pulseless ventricular tachycardia
  3. Pulseless electrical activity
  4. Asystole
113
Q

Risk factors for cardiac arrest

A
  • Coronary artery disease
  • L ventricular dysfunction
  • Hypertrophic cardiomyopathy (HCM)
  • Long QT syndrome
  • Acute medical or surgical emergency
  • Illicit substances
114
Q

Symptoms of cardiac arrest

A
  • Unresponsive
  • Absent or agonal respiration
  • Absence of pulse
  • Cardiac rhythm disturbances: VT, pulseless VT, PEA, asystole
115
Q

Ix for cardiac arrest

A 
•	Continuous cardiac monitoring: will show shockable or non-shockable rhythm 
1.	Shockable = VT or pulseless VT
2.	Non-shockable = asystole or PEA
•	FBC: look for haemorrhage 
•	U&E: hyperkalaemia/hypokalaemia
•	ABG
•	Cardiac biomarkers / echocardiogram
116
Q

ECG changes for VT

A

= monomorphic: regular, broad complex tachycardia with uniform QRS complexes in each lead. Polymorphic: QRS complexes vary in shape and amplitude.

117
Q

What is pulseless electrical activity?

A

no breathing, no pulse despite appearance of organised electrical activity on ECG

118
Q

Mx for cardiac arrest

A
  • CPR (see algorithm in notes) – 30 compressions to 2 breaths, with compression depth of at least 5 cm and allowing for full chest wall recoil
  • Defibrillation if pulseless VT or VT, attempted as soon as possible for witnessed arrest or after 5 cycles of CPR for unwitnessed arrest. Give one shock and follow with CPR if perfusing rhythm not restored.
  • Adrenaline – 1mg IV/IO every 3-5 minutes.
  • Amiodarone – for pulseless VT or VT that’s unresponsive to defibrillation
  • Magnesium – for cardiac arrest due to Torsades de pointes
119
Q

Define heart failure

A

clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body. Usually, a result of structural or functional heart disease but also the term is sometimes used more broadly e.g., high output heart failure.

120
Q

What are the ways in which heart failure can be defined?

A

By ejection fraction
By left right
By chronic / acute
+ High output heart failure

121
Q

What is LVEF, how is it measured and what is considered reduced?

A

L ventricular ejection fraction
Measured with echocardiography
Reduced LVEF = <35-40%

122
Q

What is heart failure with preserved ejection fraction? (HF-pEF)

A
  1. Heart failure with preserved ejection fraction (HF-pEF)
    o Normal left ventricular ejection fraction (LVEF)
    o 50% of patients with HF
    o The overlap isn’t perfect, but patients with HF-pEF have diastolic dysfunction (impaired ventricular filling during diastole)
123
Q

Causes of HF-pEF?

A

 Hypertrophic obstructive cardiomyopathy (HOCM)
 Restrictive cardiomyopathy
 Cardiac tamponade
 Constrictive pericarditis

124
Q

What Is heart failure with reduced ejection fraction? HF-rEF

A

o Abnormal left ventricular ejection fraction (LVEF)
o 50% of patients with HF
o The overlap isn’t perfect, but patients with HF-rEF typically have systolic dysfunction (impaired myocardial contraction during systole)

125
Q

Causes of HF-rEF

A

 Ischaemic heart disease
 Dilated cardiomyopathy
 Myocarditis
 Arrhythmias

126
Q

What sided HF do people usually develop?

A

Left sided

127
Q

Causes of L sided HF?

A
  • Increased L ventricular afterload = arterial HTN / aortic stenosis
  • Increased L ventricular preload = AR
128
Q

Symptoms of L HF?

A

• Pulmonary oedema =

  1. Dyspnoea
  2. Orthopnoea
  3. Paroxysmal nocturnal dyspnoea
  4. Bibasal fine crackles
129
Q

Cause of Right sided HF?

A
  • Increased R ventricular afterload = tricuspid regurgitation
130
Q

Symptoms of RHF?

A
  • Peripheral oedema: ankle/sacral oedema
  • Raised JVP
  • Hepatomegaly
  • Weight gain due to fluid retention
  • Anorexia (cardiac cachexia)
131
Q

What is high output HF?

A

A normal heart is unable to pump enough blood to meet the metabolic needs of the body

132
Q

Causes of high output HF?

A
  • Anaemia
  • Ateriovenous malformation
  • Paget’s disease
  • Pregnancy
  • Thyrotoxicosis
  • Thiamine deficiency
133
Q

What is acute HF?

A

Life threatening emergency
Sudden onset or worsening of the symptoms of HF
AHF without hx of HF = de-novo AHF
Decompensated AFH is more common – most have hx of HF

134
Q

Causes of acute HF?

A 
•	Iatrogenic – aggressive IV fluids
•	Sepsis
•	MI
•	Arrhythmias
* HTN crisis
135
Q

symptoms of acute HF?

A
  • Rapid onset breathlessness
  • Cough – frothy white/pink sputum
  • Look unwell
136
Q

Signs of acute HF?

A
  • Increased RR
  • Reduced O2 sats
  • Tachycardia
  • S3
  • Bilateral bibasal crackles
  • Hypotension in severe cases with shock
  • Cyanosis
    If there’s also right sided heart failure = raised JVP & peripheral oedema
137
Q

Ix for acute HF

A
  • Clinically, if it looks like acute HF then treat before waiting for investigations
  • ECG – ischaemia/ arrhythmias
  • ABG
  • Bloods – infection, kidney function, BNP, troponin
  • Echocardiography – measure ejection fraction (above 50% = normal)
  • CXR: alveolar oedema, Kelley B lines, Cardiomegaly, dilated upper lobe vessels, pleural effusion
138
Q

What is BNP and what can cause it to be raised?

A

o B type natriuretic peptide – hormone released from heart ventricles when myocardium is stretched beyond the normal range. High result = heart is overloaded in HF.

Other causes of raised BNP:
	Tachycardia
	Sepsis
	PE
	Renal impairment 
	COPD
139
Q

What is cardiomegaly?

A

diameter of the widest part of the heart is more than half the diameter of the widest part of the lung fields

140
Q

Mx for acute HF

A

Continue normal medication for HF e.g., b blockers and ACEi

Pour SOD

  • Pour away (stop) their fluids
  • Sit up
  • Oxygen
  • Diuretics – IV furosemide 40mg
    • monitor fluid balance
      In severe acute pulmonary oedema/cardiogenic shock:
  • IV opiates (vasodilation) – not routinely used now
  • NIV CPAP
  • Inotropes e.g., dobutamine [need to be on ICU]
  • Vasopressor e.g., noradrenaline [need to be on ICU]
141
Q

Presentation of chronic HF

A
  • SOB worse on exertion
  • Cough – frothy white/pink sputum
  • Orthopnoea
  • Cardiac wheeze
  • Paroxysmal nocturnal dyspnoea: sudden waking at night feeling acutely SOB, with a cough and wheeze
  • Peripheral oedema
  • Weight loss – cardiac cachexia
  • R sided HF = raised JVP, ankle oedema, hepatomegaly
142
Q

Ix for chronic HF

A
  • Clinical picture
  • BNP blood test – N-terminal pro-B-type natriuretic peptide NT-proBNP
  • Echocardiogram
  • ECG
  • CXR
143
Q

CXR findings in HF

A

ABCDE

  1. A – alveolar oedema (bat wing opacities)
  2. B – kerley B lines
  3. C – cardiomegaly
  4. D – dilated upper lobe vessels
  5. E – pleural effusion
144
Q

Causes of chronic HF

A
  • Ischaemic heart disease
  • Valvular heart disease (commonly AS)
  • HTN
  • Arrhythmias (commonly AF)
145
Q

Classification of chronic HF

A

New York Heart Association Classification of chronic HF:
6. NYHA class I
 No symptoms
 No limitation on exercise
7. NYHA class II
 Mild symptoms
 Slight limitation of physical activity – get fatigue/palpitations/dyspnoea on exercising
8. NYHA class III
 Moderate symptoms
 Marked limitation of physical activity – comfortable at rest but little activity causes symptoms
9. NYHA class IV
 Severe symptoms
 Unable to carry out any physical activity without discomfort with symptoms present at rest

146
Q

Mx of chronic HF

A
  1. 1st line = ACEi + b blocker
    a. Start one drug at a time
    b. B blockers = bisoprolol, carvedilol and nebivolol
  2. 2nd line = aldosterone antagonist (for HF-rEF)
    a. Spironolactone and eplerenone
  3. 3rd line = one of these started by a specialist:
    a. Ivabradine
    b. sacubitril-valsartan
    c. hydralazine + nitrate
    d. digoxin
    e. Cardiac resynchronisation therapy
  4. Loop diuretics (furosemide) can improve symptoms
  5. Offer annual influenza vaccine and one off pneumococcal vaccine
  6. Surgical tx for severe AS or MR
  7. Stop smoking
  8. Optimise co-morbidities
  9. Exercise as tolerated
  10. Monitor U&Es because ACEi and aldosterone antagonists can cause hyperkalaemia

Remember with ABAL = ACEi, b blocker, aldosterone antagonist, loop diuretic

147
Q

What is HTN defined as?

A

Hypertension = high blood pressure: 140/90 in clinic or 135/85 with ambulatory or home readings.

148
Q

Causes of secondary HTN

A

remember causes with ROPE:
o R = renal disease. Most common. Think renal artery stenosis if BP very high/doesn’t respond to Tx. Glomerulonephritis, chronic pyelonephritis, adult polycystic kidney disease.
o O = Obesity
o P = Pregnancy induced HTN / Pre-eclampsia
o E = endocrine. Hyperaldosteronism (Conn’s syndrome) – do renin:aldosterone ratio blood test. Pheochromocytoma, Cushing’s, Liddle’s syndrome, congenital adrenal hyperplasia, acromegaly.

o Other causes: Glucocorticoids, NSAIDs, coarctation of the aorta, COCP.

149
Q

Symptoms of HTN

A
  • Asymptomatic
  • Symptoms when very high (>200/120)
    o Headaches
    o Visual disturbances
    o Seizures
150
Q

How should BP be measured if HTN is suspected?

A
  • 1st = 24-hour blood pressure ambulatory monitoring – 2 measures per hour & average calculated from at least 14 readings (>135/85)
  • 2nd = home blood pressure readings – take 2 readings at least 1 minute apart, in the morning and evening for 4-7 days
  • 3rd = clinic reading (>140/90)
151
Q

What is stage 1 HTN?

A

Clinic reading = >140/90

Ambulatory/home reading = >135/85

152
Q

What is stage 2 HTN?

A

Clinic reading = >160/100

Ambulatory/home reading = >150/95

153
Q

What is stage 3 HTN?

A

Clinic reading >180/120

154
Q

When should HTN be screened for?

A

Screen for HTN every 5 years (or annually in T2DM)

155
Q

What IX for HTN?

A
  • Check for end organ damage / cause:
    o Fundoscopy – to check for hypertensive retinopathy
    o Urine dipstick / U&Es – to check for renal disease (cause or consequence) – urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria
    o ECG – to check for LV hypertrophy or IHD
    o HbA1C – to check for co-existing DM
    o Lipids - hyperlipidaemia
156
Q

Practice drawing out the flow chart for when to offer medical management for HTN

157
Q

Complications of HTN

A
  • IHD
  • CVA
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Heart failure
158
Q

Lifestyle changes for HTN

A

a. Stop smoking
b. Healthy diet
c. Reduce alcohol
d. Reduce caffeine and salt intake
e. Regular exercise

159
Q

Who should get medical management for their HTN?

A

a. All patients with stage 2 HTN
b. All patients under 80yo with stage 1 HTN who also have a Q-risk score of 10% or more, diabetes, renal disease, CVD or end organ damage

160
Q

Practice drawing flow chart for medical management of HTN

161
Q

What medication for patients with HTN who are younger than 55, not black or have T2DM?

A

a. ACEi or ARB
b. ACEi/ARB + CCB/thiazide like diuretic
c. ACEi/ARB + CCB + thiazide like diuretic
d. ACEi/ARB + CCB + thiazide like diuretic + spironolactone (if K<4.5) or alpha/beta blocker (if K>4.5)

162
Q

What medication for patients with HTN who are over 55 or black? (no T2DM)

A

a. CCB
b. CCB + ACEi/ARB/thiazide like diuretic
c. ACEi/ARB + CCB + thiazide like diuretic
d. ACEi/ARB + CCB + thiazide like diuretic + spironolactone (if K<4.5) or alpha/beta blocker (if K>4.5)

163
Q

What antihypertensive drugs cause electrolyte disturbances?

A

Monitor U&Es regularly: spironolactone + ACEi = hyperkalaemia (+ thiazide like diuretics can cause electrolyte imbalances)

164
Q

Example ACEi and side effects

A

Ramipril 1.25-10mg OD
Lisinopril 10mg OD

Dry cough
Angioedema
Hyperkalaemia

165
Q

Example B blockers used in HTN and SEs

A

Bisoprolol 5-20mg OD
Metoprolol 50mg OD
Carvedilol 6.25mg BD

Bradycardia
Fatigue
Erectile dysfunction
Bronchoconstriction = CI in asthma

166
Q

Example CCBs used in HTN and SEs

A

Amlodipine 5-10mg OD
Nifedipine 30-60mg OD

Flushing
Headaches
Peripheral oedema
Gingival hyperplasia

167
Q

Example thiazide like diuretics used in HTN and SEs

A

Indapamide 2.5mg OD
Hydrochlorothiazide 12.5-25mg OD

Hypokalaemia
Hyponatraemia
Can exacerbate diabetes, gout and SLE

168
Q

Example ARBs used in HTN and SEs

A

Candesartan 8-32mg OD
Losartan 25-50mg OD

Hyperkalaemia

169
Q

Example alpha blockers used in HTN and SEs

A

Doxazosin
Prazosin
Terazosin

GI disturbance
Dizziness, palpitations ad headache
Sexual dysfunction

170
Q

Example potassium sparing diuretic used in HTN and SEs

A

Spironolactone

Hypovolaemia
Hyponatraemia
Hyperkalaemia
Gynaecomastia

171
Q

Target BP readings for patients having their HTN managed

A

<80 yo = <140/90

>80 yo = <150/90

172
Q

Definition of infective endocarditis

A

an infection involving the endocardial surface of the heart, including valvular structures, the chordae tendineae, sites of septal defects or the mural endocardium.

173
Q

When should you worry about infective endocarditis?

A

Fever + new murmur = endocarditis until proven otherwise

Any fever >1 week in those with risk factors = do blood cultures

174
Q

Risk factors for infective endocarditis

A
  • History of infectious endocarditis
  • Artificial prosthetic heart valves
  • Congenital heart disease
  • Post heart transplant
  • Skin breaches – dermatitis, IV lines, wounds
  • IVDU: typically causing a tricuspid lesion
  • Renal failure
  • Immunosuppression
175
Q

Bacterial causes of infective endocarditis

A
  • Staphylococcus aureus: most common (IVDU especially)
  • Streptococcus viridians: poor dental hygiene/developing world
  • Staphylococcus epidermidis: indwelling lines/prosthetic valve surgery
  • Streptococcus bovis: colorectal cancer = need colonoscopy
176
Q

Non infective causes of endocarditis

A
  1. SLE

2. Malignancy – marantic endocarditis

177
Q

Rare culture negative causes of infective endocarditis

A

HACEK – culture negative

  1. Haemophilus
  2. Actinobacillus
  3. Cardiobacterium
  4. Eikenella
  5. Kingella
178
Q

Symptoms of infective endocarditis

A

• Septic signs = fever, rigors, night sweats, malaise, weight loss, anaemia, splenomegaly and clubbing
• New murmur / change to pre existing murmur
• Immune complex deposition:
1. Vasculitis
2. Microscopic haematuria
3. Glomerulonephritis
4. AKI
5. Roth spots – boat shaped retinal haemorrhages with pale centre
6. Osler’s nodes – painful pulp infarcts in fingers and toes
• Embolic phenomena:
1. Abscesses in brain, heart, kidney, spleen, gut
2. Janeway lesions – painless palmar or plantar macules

179
Q

Ix for infective endocarditis

A 
-	Blood cultures
o	3 sets at different times from different sites at peak of fever
-	Blood tests
o	Normochromic, normocytic anaemia
o	Neutrophilia 
o	High ESR/CRP
o	RF positive (immunological phenomenon)
-	Urinalysis 
o	Microscopic haematuria
-	CXR
o	Cardiomegaly 
o	Pulmonary oedema
-	Regular ECGs
o	Look for heart block
-	Echocardiography 
o	TTE may show vegetations 
-	CT
o	To look for emboli e.g., in spleen or brain
180
Q

What criteria is used to diagnose infective endocarditis?

A

Modified Duke Criteria for infective endocarditis

- Can diagnose if 2 major or 1 major + 3 minor or all 5 minor

181
Q

Major criteria for infective endocarditis by the Modified Duke Criteria

A

o Positive blood culture –
 Typical organism in 2 separate cultures or
 Persistently +ve blood cultures from 2 blood cultures taken >12 hours apartor
 Single positive blood culture for Coxiella burnetiid

o Endocardium involved –
 Positive echocardiogram (vegetation, abscesses, pseudoaneurysm, dehiscene of prosthetic valve)
 Abnormal activity around prosthetic valve on PET/CT/SPECT/CT
 Paravalvular lesions on cardiac CT

182
Q

Minor criteria for infective endocarditis by the Modified Duke Criteria

A

o Predisposition – cardiac lesion, IVDU etc
o Fever >38
o Vascular phenomenon e.g., emboli, Janeway lesions, clubbing, splenomegaly, petechiae, purpura
o Immunological phenomenon e.g., glomerulonephritis, Osler’s nodes
o Positive blood culture that doesn’t meet major criteria

183
Q

What initial blind abx therapy is given for infective endocarditis?

A

a. Initial blind therapy = amoxicillin [vancomycin if pen allergic]
b. Initial blind therapy if prosthetic valve = vancomycin + rifampicin + low dose gentamicin

184
Q

What abx for infective endocarditis caused by staphylococci?

A

i. Native valve = flucloxacillin [vancomycin + rifampicin if pen allergic]
ii. Prosthetic valve = flucloxacillin + rifampicin + low dose gentamicin [vancomycin instead of flucloxacillin if pen allergic]

185
Q

What abx for infective endocarditis caused by streptococci?

A

i. Benzylpenicillin [vancomycin + low dose gentamicin if pen allergic]

186
Q

Indications for surgery in infective endocarditis

A

i. Severe valvular incompetence
ii. Aortic abscess = lengthening PR interval
iii. Infections resistance to abx
iv. Fungal infection
v. Cardiac failure refractory to medical treatment
vi. Recurrent emboli after abx

187
Q

Poor prognostic factors in infective endocarditis

A
  • Staphylococcus aureus
  • Prosthetic valve
  • Culture negative endocarditis
  • Low complement levels
188
Q

What is mesenteric ischaemia?

A

lack of blood flow through the mesenteric vessels supplying the intestines which results in intestinal ischaemia.

189
Q

What is the blood supply to the gut?

A
  1. Coeliac artery: foregut [stomach, part of duodenum, biliary system, liver, pancreas, spleen]
  2. Superior mesenteric artery: midgut [distal duodenum to first ½ transverse colon]
  3. Inferior mesenteric artery: hindgut [second ½ transverse colon to rectum]
190
Q

What is chronic mesenteric ischaemia also known as?

A

Intestinal angina

191
Q

Pathology of chronic mesenteric ischaemia

A

narrowing of mesenteric blood vessels by atherosclerosis

192
Q

Symptoms of chronic mesenteric ischaemia

A
  • Intermittent abdominal pain: central, colicky, after eating (starts 30 mins after eating and lasts for 1-2 hours)
  • Weight loss due to food avoidance
  • Abdominal bruit on auscultation
193
Q

Risk factors for chronic mesenteric ischaemia

A
  • Increased age
  • Family hx
  • Smoking
  • DM
  • HTN
  • High cholesterol
194
Q

Diagnosis of chronic mesenteric ischaemia

A

CT angiography

195
Q

Mx for chronic mesenteric ischaemia

A
  • Reducing modifiable risk factors
  • Secondary prevention = statins and antiplatelets
  • Revascularisation to improve blood flow to intestines
    o Endovascular procedure e.g., percutaneous mesenteric artery stenting
    o Open surgery – endartectomy, reimplantation or bypass grafting
196
Q

Pathology of acute mesenteric ischaemia

A

rapid blockage in blood flow through the superior mesenteric artery caused by a thrombus that has developed inside the artery or is an embolus from another site.

197
Q

Important risk factor for acute mesenteric ischaemia

A

Atrial fibrillation

198
Q

Symptoms of acute mesenteric ischaemia

A
  • Acute non specific abdominal pain that is disproportionate to examination findings
  • Shock
  • Peritonitis
  • Sepsis
  • Necrotic bowel tissue = perforation
199
Q

Diagnosis of acute mesenteric ischaemia

A

contrast CT + metabolic acidosis + raised lactate (ischaemia)

200
Q

Mx for acute mesenteric ischaemia

A
  • Remove necrotic bowel

- Remove/bypass the thrombus in the blood vessel = open surgery or endovascular procedure

201
Q

Definition of myocarditis

A

Definition = inflammation of the myocardium.

Is often associated with pericardial inflammation = myopericarditis

202
Q

causes of myocarditis

A
  • Idiopathic (50% of cases)
  • Viral: coxsackie B, HIV
  • Bacteria: diphtheria, clostridia
  • Spirochaetes: Lyme disease
  • Protozoa: Chagas’ disease, toxoplasmosis
  • Autoimmune
  • Drugs: doxorubicin
  • Toxins: cocaine, lithium, alcohol, lead, arsenic
203
Q

Presentation of myocarditis

A
  • Young patient
  • Acute history
  • Chest pain – ACS like symptoms
  • HF symptoms – dyspnoea
  • Arrhythmias
  • Palpitations
  • Tachycardia
  • Soft S1
  • S4 gallop
204
Q

Ix for myocarditis

A
  1. Bloods
    a. Raised inflammatory markers in 99%
    b. Raised cardiac enzymes
    c. Raised BNP
  2. ECG
    a. Tachycardia
    b. ST changes – elevation
    c. T wave inversion
    d. Arrhythmias – atrial
    e. Transient AV block
    f. QT prolongation
  3. Echocardiogram
    a. Diastolic dysfunction
    b. Regional wall abnormalities
  4. Cardiac MR
205
Q

Gold standard for diagnosis of myocarditis

A

Endomyocardial biopsy

206
Q

Mx for myocarditis

A
  • Treat underlying cause e.g., abx for bacterial causes
  • Supportive tx: HF and arrhythmias
  • Avoid exercise, can precipitate arrhythmia
207
Q

complications of myocarditis

A
  • HF
  • Arrhythmia – possibly leading to sudden death
  • Dilated cardiomyopathy (late complication, even years)
208
Q

Define acute pericarditis and what is the classic clinical triad seen

A

inflammation of the pericardium, acute form is new onset inflammation lasting <4-6 weeks. Clinical triad: chest pain, pericardial friction rub, and serial ECG changes.

209
Q

what are the 2 types of acute pericarditis

A
  1. Fibrinous (dry)

2. Effusive (with purulent, serous, or haemorrhagic exudate)

210
Q

Risk factors for acute pericarditis

A
  • Male aged 20-50
  • Transmural MI
  • Cardiac surgery
  • Neoplasm
  • Viral/bacterial infection
211
Q

Causes of acute pericarditis

A
  • Viral: coxsackie
  • TB
  • Uraemia – causes fibrinous pericarditis
  • Trauma
  • Most MI = Dressler’s syndrome
  • Connective tissue disease
  • Hypothyroidism
  • Malignancy
212
Q

Symptoms of acute pericarditis

A
  • Chest pain – pleuritic chest pain, relieved by sitting forwards
  • Non-productive cough
  • Dyspnoea
  • Flu like symptoms: fever, myalgias
  • Pericardial rub: grating to and fro sound produced by friction of the heart against the pericardium
  • Tachypnoea
  • Tachycardia
213
Q

Ix for acute pericarditis

A

ECG

TTE - to look for pericardial effusion

214
Q

ECG changes seen in acute pericarditis

A

 Global saddle shaped ST elevation

 Global PR depression (most specific marker for pericarditis)

215
Q

Mx for acute pericarditis (what do you do for idiopathic/viral cause)?

A
  • Treat underlying cause

- Acute idiopathic/viral pericarditis = NSAIDs + COLCHICINE

216
Q

What is peripheral arterial disease?

A

= a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower extremity arteries.

217
Q

What is intermittent claudication?

A

symptom of ischaemia in a limb, occuring during exertion and relieved by rest.

218
Q

What is critical limb ischaemia?

A

end stage of peripheral arterial disease, there is inadequate blood supply to the limb to allow it to function normally at rest.

219
Q

What is acute limb ischaemia?

A

rapid onset of ischaemia in a limb, caused by a thrombus.

220
Q

What is gangrene?

A

the death of the tissue, due to inadequate blood supply

221
Q

Cause of PAD?

A
  • Atherosclerosis (typically asymptomatic until 50% stenosis)
  • Vasculitis
  • Fibromuscular dysplasia
222
Q

Risk factors for PAD?

A
  • Smoking
  • Blood pressure
  • DM
  • Hyperlipidaemia
  • Reduced exercise
  • FH and PMH
  • Male
  • Older age
  • Genetics
223
Q

Presentation of PAD - intermittent claudication

A
  1. Cramping pain after walking a fixed distance
  2. Pain rapidly relived by rest
  3. Calf pain = superficial femoral disease (commonest)
  4. Buttock pain = iliac disease
  5. Muscle fatigue when walking beyond a certain intensity
224
Q

Presentation of PAD - critical limb ischaemia

A
  1. Rest pain in foot for more than 2 weeks
  2. Ulceration
  3. Gangrene
  4. Hang legs out of bed at night to ease pain
  5. 6 Ps:
     Pain
     Pallor
     Pulseless
     Paralysis
     Paraesthesia
     Perishing cold
225
Q

What are the 6 Ps

A 
	Pain
	Pallor
	Pulseless
	Paralysis 
	Paraesthesia 
	Perishing cold
226
Q

Presentation of acute limb ischaemia

A

Rapid onset of 6 Ps

227
Q

What is Leriche syndrome?

A
  1. Thigh/buttock pain
  2. Absent femoral pulses
  3. Male impotence
228
Q

What do the scores of the ankle brachial pressure index show?

A

a. 1 = normal
b. 0.6-0.9 = claudication
c. 0.3-0.6 = rest pain
d. <0.3 impending
e. >1.3 = calcification of the arteries that makes them difficult to compress – common in diabetics

229
Q

Ix for PAD

A
  1. ABPI
  2. Duplex USS
  3. Angiography (CT / MRI)
230
Q

Mx for PAD

A 
-	Lifestyle
o	Stop smoking 
o	Optimise management of HTN, DM
o	Exercise training 
-	Medical treatments
o	Atorvastatin 
o	Clopidogrel 
o	Naftidrofuryl oxalate – peripheral vasodilator 
-	Surgery
o	Endovascular angioplasty and stenting 
o	Endartectomy 
o	Bypass surgery 
o	Amputation
231
Q

Mx for acute limb ischaemia

A 
o	Endovascular thrombolysis 
o	Endovascular thrombectomy 
o	Surgical thrombectomy 
o	Endartectomy 
o	Bypass surgery
o	Amputation
232
Q

Define pulmonary embolism

A

thrombus formation in the pulmonary arteries, usually due to DVT that has embolised.

233
Q

RFs for PE

A
  • Immobility
  • Recent surgery
  • Long haul flight
  • Pregnancy
  • Hormone therapy with oestrogen
  • Malignancy
  • Polycythaemia
  • SLE
  • Thrombophilia
234
Q

Presentation of PE

A 
o	Chest pain - pleuritic
o	ECG can look like an MI
o	Troponin can look like an MI
o	SOB
o	Cough +/- haemoptysis 
o	Hypoxia
o	Tachycardia 
o	Raised RR
o	Low grade fever
o	Haemodynamic instability
o	Signs of DVT 
o	ABG = respiratory alkalosis (high RR = blow off CO2)
235
Q

What score is used to assess the severity of PE?

A

PESI score (PE severity index) = helps to decide whether to admit a patient

236
Q

Diagnosis of PE

A
  • CTPA if Wells score predicts likely PE
  • D-dimer if Wells score predicts unlikely PE
  • Ventilation perfusion (VQ) scan
237
Q

Tx for PE

A
  • Oxygen, analgesia, monitoring
  • Anticoagulate: DOAC or LMWH (dalteparin)
  • Thrombolysis
  • Long term anticoagulation with DOAC or warfarin
    o 3 months if obvious cause
    o 3+ months if unlear cause
    o 6 months if active cancer
238
Q

Mx for acute pulmonary oedema

A
  • High flow O2
  • Sit forwards
  • Decide if shocked or not - ^BP, need critical care input
  • Vasodilation – 5mg IV diamorphine stat & GTN either sublingual or as IV infusion
  • Diuresis e.g. furosemide 80mg IV stat (vasodilates before diuresis)
  • Consider CPAP
  • Treat underlying cause
    o ?ACS treatment
    o Is there a STEMI?
    o Discuss with cardiology
239
Q

Define pulmonary embolism

A

thrombus formation in the pulmonary arteries, usually due to DVT that has embolised.

240
Q

RFs for PE

A
  • Immobility
  • Recent surgery
  • Long haul flight
  • Pregnancy
  • Hormone therapy with oestrogen
  • Malignancy
  • Polycythaemia
  • SLE
  • Thrombophilia
241
Q

Presentation of PE

A 
o	Chest pain - pleuritic
o	ECG can look like an MI
o	Troponin can look like an MI
o	SOB
o	Cough +/- haemoptysis 
o	Hypoxia
o	Tachycardia 
o	Raised RR
o	Low grade fever
o	Haemodynamic instability
o	Signs of DVT 
o	ABG = respiratory alkalosis (high RR = blow off CO2)
242
Q

What score is used to assess the severity of PE?

A

PESI score (PE severity index) = helps to decide whether to admit a patient

243
Q

Diagnosis of PE

A
  • CTPA if Wells score predicts likely PE
  • D-dimer if Wells score predicts unlikely PE
  • Ventilation perfusion (VQ) scan
244
Q

Tx for PE

A
  • Oxygen, analgesia, monitoring
  • Anticoagulate: DOAC or LMWH (dalteparin)
  • Thrombolysis
  • Long term anticoagulation with DOAC or warfarin
    o 3 months if obvious cause
    o 3+ months if unlear cause
    o 6 months if active cancer
245
Q

Mx for acute pulmonary oedema

A
  • High flow O2
  • Sit forwards
  • Decide if shocked or not - ^BP, need critical care input
  • Vasodilation – 5mg IV diamorphine stat & GTN either sublingual or as IV infusion
  • Diuresis e.g. furosemide 80mg IV stat (vasodilates before diuresis)
  • Consider CPAP
  • Treat underlying cause
    o ?ACS treatment
    o Is there a STEMI?
    o Discuss with cardiology

Finals Revision (18 decks)

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