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Finals > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Acute coronary syndrome

Umbrella term for what?

A
  • STEMI
  • NSTEMI
  • Unstable angina
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2
Q

Acute coronary syndrome

Pathophysiology

A
  • RFs lead to initial endothelial damage (pro-inflammatory, pro-oxidant, proliferative and reduced NO bioavailability)
  • Gradual build-up of atherosclerotic plaques (LDLs) in walls of arteries
  • Monocytes migrate from blood and differentiate into macrophages -> phagocytose the oxidised LDL -> large foam cells
  • As macrophages die -> further inflammation
  • Smooth muscle proliferation and migration from tunic media into intima -> fibrous capsule covering fatty plaque

Leads to:

  • gradual narrowing -> angina
  • sudden occlusion -> MI
  • aneurysm -> rupture
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3
Q

Acute coronary syndrome

Risk factors

A
  • Male
  • Older age
  • Fx
  • Smoking
  • Alcohol
  • DM
  • HTN
  • Hypercholesterolaemia
  • Obesity
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4
Q

Acute coronary syndrome

Presentation

A
  • Central, constricting chest pain
  • May radiate to jaw or left arm
  • SOB
  • Palpitations
  • Sweating and clamminess
  • Nausea and vomiting
  • General observations (HR, BP, SpO2) may all be normal
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5
Q

Acute coronary syndrome

Who may have atypical MI?

A
  • Elderly
  • Diabetic
  • Females
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6
Q

Acute coronary syndrome

Mainstay investigations

A

First = ECG

  • STEMI = ST elevation or new LBBB
  • No ST elevation -> do Troponin

Troponin

  • Raised +/- other ECG signs (T wave inversion, pathological Q waves, ST depression) -> diagnose NSTEMI
  • Normal troponin and ECG -> unstable angina or other cause (e.g. MSK)
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7
Q

Acute coronary syndrome

Other investigations

A
  • Physical exam
  • FBC for anaemia
  • U&Es (prior to ACE-Is)
  • LFTs (prior to statins)
  • Lipid profile
  • TFTs
  • CXR (other causes of chest pain and pulmonary oedema)
  • ECHO (assess functional damage)
  • CT coronary angiogram (coronary artery disease)
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8
Q

Acute coronary syndrome

STEMI criteria

A

Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:

- 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
- 1.5 mm ST elevation in V2-3 in women
- 1 mm ST elevation in other leads
- New LBBB (LBBB should be considered new unless there is evidence otherwise)
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9
Q

Acute coronary syndrome

Initial management

A

MONA

Morphine
Oxygen if sats < 94%
Nitrates (SL or IV)
Aspirin 300 mg

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10
Q

Acute coronary syndrome

When should nitrates be used with caution?

A

In hypotensive patients

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11
Q

Acute coronary syndrome

Complications of MI

A

DREAD

Death
Rupture of heart septum or papillary muscles
E'Edema' (HF)
Arrhythmias, aneurysm
Dressler's syndrome
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12
Q

Acute coronary syndrome

Poor prognostic factors

A
  • Age
  • Development (or history) of heart failure
  • Peripheral vascular disease
  • Reduced systolic blood pressure
  • Killip class*
  • Initial serum creatinine concentration
  • Elevated initial cardiac markers
  • Cardiac arrest on admission
  • ST segment deviation

CARDIOGENIC SHOCK carries 30-day mortality of 81%

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13
Q

Acute coronary syndrome

Secondary prevention
Lifestyle

A
  • Stop smoking
  • Reduce alcohol consumption
  • Mediterrean diet
  • Cardiac rehab
  • Optimise Tx of other medical conditions (e.g. DM, HTN)
  • Sexual activity may resume 4 weeks after an uncomplicated MI. Reassure that sex does not increase likelihood of further MI.
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14
Q

Acute coronary syndrome

Secondary prevention
Medications

A

6 A’s

  • Aspirin 75 mg OD
  • Another antiplatelet (Clopidogrel or Ticagrelor) for up to 12 months
  • Atorvastatin 80 mg OD
  • ACE-I
  • Atenolol (or other beta-blocker)
  • Aldosterone antagonist (for those with clinical HF, e.g. Eplerenone) - initiate with 3-12 days and ideally after ACE-I
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15
Q

Acute coronary syndrome

STEMI management
Basic principle

A
  • PCI within 2 hours

- Thrombolysis within 12 hours if not PCI

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16
Q

Acute coronary syndrome

STEMI management
PCI process

A
  • Give within 120 minutes
  • If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
  • Catheter into patients brachial or femoral artery → feeds up to coronary arteries under XR guidance → injects contrast to identify blockage → balloon dilatation or device to remove blockage → stent to keep artery open
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17
Q

Acute coronary syndrome

STEMI management
PCI drugs

A

Further antiplatelet prior to PCI (dual antiplatelet therapy - aspirin + another drug)

- If NOT taking an oral anticoagulant → Prasugrel
- If taking an oral anticoagulant → Clopidogrel

Drug therapy during PCI:

- If undergoing with radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
- If undergoing with femoral access: bivaluridin with bailout GPI
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18
Q

Acute coronary syndrome

STEMI management
Thrombolysis process

A
  • Offered within 12 hours of onset if primary PCI not delivered within 120 minutes of the time when fibrinolysis could have been given
  • Injecting fibrinolytic medication → break down fibrin → rapidly dissolve the clot
  • Significant risk of bleeding
  • Repeat ECG after 60-90 minutes, if ECG changes have not been resolved → PCI
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19
Q

Acute coronary syndrome

STEMI management
Thrombolysis drugs

A

Streptokinase
Alteplase
Tenecteplase

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20
Q

Acute coronary syndrome

NSTEMI / Unstable angina management

Basic treatment

A 
BATMAN
B: Beta-blocker
A: Aspirin
T: Ticagrelor (or Clopi)
M: Morphine
A: Anticoagulant (Fondaparinux)
N: Nitrates

Oxygen if sats < 94%

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21
Q

Acute coronary syndrome

NSTEMI / Unstable angina management

When might you not use fondaparinux?

A
  • High bleeding risk
  • Having immediate angiography
  • Creatinine > 265

Give unfractionated heparin if either of the bottom two apply.

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22
Q

Acute coronary syndrome

NSTEMI / Unstable angina management
What score is used to assess recurrency risk?

A

GRACE score

Assesses 6 month risk of death or repeat MI after NSTEMI

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23
Q

Acute coronary syndrome

NSTEMI / Unstable angina management
GRACE Score

A
  • Age
  • HR/BP
  • Cardiac and renal function
  • Cardiac arrest on presentation
  • ECG changes
  • Troponin levels
0-3% = low risk
3-6% = intermediate risk
>6% = high risk

PCI > 3% within 72 hours!

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24
Q

Acute coronary syndrome

NSTEMI / Unstable angina management
Criteria for angiography (and maybe also PCI)

A
  • Clinically unstable, e.g. hypotensive
  • Within 72 hrs if GRACE score > 3%
  • If ischemia is subsequently experienced after admission
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25
Q

Acute coronary syndrome

NSTEMI / Unstable angina management
Conservative drug management

A

Dual antiplatelet therapy:

  • NOT at high risk of bleeding - Ticagrelor
  • IS at high risk of bleeding - Clopidogrel
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26
Q

Acute coronary syndrome

NSTEMI / Unstable angina management
PCI drugs

A
  • Unfractionated heparin (regardless of already having fondaparinux or not)
  • Further antiplatelet (dual therapy):
    If not on oral anticoagulant → Prasugrel or Ticagrelor
    If they are on oral anticoagulant → Clopidogrel
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27
Q

Dressler’s Syndrome

What is it? When?

A
  • Occurs 2-3 weeks after MI
  • Caused by a local immune response
  • Causes pericarditis
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28
Q

Dressler’s Syndrome

Features

A
  • Pleuritic chest pain
  • Low grade fever
  • Pericardial rub on auscultation
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29
Q

Dressler’s Syndrome

Diagnosis

A

ECG

  • Global ST elevation - saddle-shaped ST
  • T wave inversion

ECHO - pericardial effusion

Raised inflammatory markers

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30
Q

Dressler’s Syndrome

Management

A
  • NSAIDs (aspirin, ibuprofen)
  • Steroids if severe (e.g. Prednisolone)
  • May need pericardiocentesis to remove fluid
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31
Q

Dressler’s Syndrome

Complications

A
  • Pericardial effusion

- Pericardial tamponade (fluid constricts heart and prevents function) - rare

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32
Q

Hypertension

Definition

A
  • > 140/90 in clinic

- > 135/85 with ambulatory or home readings

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33
Q

Hypertension

Causes of secondary

A

ROPE
R: Renal: glomerulonephritis, chronic pyelonephritis, adult PCKD, renal artery stenosis
O: Obesity
P: Pregnancy/pre-eclampsia
E: Endocrine: Phaeochromocytoma, Cushing’s, Liddle’s, Congenital adrenal hyperplasia (11-beta hydroxylase deficiency), acromegaly, PRIMARY HYPERALDOSTERONISM (CONNS) - do renin:aldosterone blood test

Other causes:
- Coarctation of the aorta
Drugs: steroids, NSAIDs, COCP, MAOIs, leflunomide

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34
Q

Hypertension

Features

A

Does not typically present with symptoms unless VERY high (>200/120 mmHg):

  • Headaches
  • Visual disturbances
  • Seizures
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35
Q

Hypertension

Diagnosis

A
  • Check BP every 5 years to screen for HTN
  • Measure more often in borderline (140/90) or every year in T2DM
  • Gold-standard = 24-hour BP readings or home readings
  • Check in BOTH arms, if differ by > 20 → repeat readings, take highest reading
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36
Q

Hypertension

Monitoring checks

A
  • Fundoscopy - hypertensive retinopathy
  • Urine dipstick - renal disease (consequence or cause)
  • ECG - LVH or IHD
  • HbA1c - co-existing DM
  • Lipids - hyperlipidaemia
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37
Q

Hypertension

Management
Lifestyle

A
  • Low salt diet (< 6g/day), ideally 3g/day
  • Reduced caffeine intake
  • Stop smoking, drink less aclohol, eat balance diet, exercise more
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38
Q

Hypertension

Management
When to admit?

A
  • Retinal haemorrhage/papilloedema
  • New onset confusion
  • Chest pain
  • Signs of HF
  • AKI
  • If suspect phaeochromocytoma (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)
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39
Q

Hypertension

Management
Medications
Step 1

A

Patient < 55-years-oldor a background oftype 2 diabetes mellitus:

  • ACE inhibitor orAngiotensin receptor blocker (ACE-i orARB):(A)
  • Angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)

Patients >= 55-years-oldor ofblack African or African–Caribbean origin:

  • Calcium channel blocker(C)
  • ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line.
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40
Q

Hypertension

Management
BP targets

A

< 80 yrs
Clinic: 140/90
ABPM/HBPM: 135/85

> 80 yrs
Clinic: 150/90
ABPM/HBPM: 145/85

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41
Q

Hypertension

Complications

A
  • Ischaemic heart disease
  • Cerebrovascular accident (i.e. stroke or haemorrhage)
  • Hypertensive retinopathy
  • Hypertensive nephropathy
  • Heart failure
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42
Q

Hypertension

When might you suspect renal tubular acidosis as cause?

A

If very high BP and not responding to Tx

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43
Q

Hypertension

Management
Medications
Step 2

A
  • If already taking A, add C or D (thiazide-like Diuretic)
  • If already taking C, add A or D

For those of black African or Afro-Caribbean originally taking a CCB, add ARB in preference to ACE-I

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44
Q

Hypertension

Management
Medications
Step 3

A

Add a third drug:

  • If already taking (A+C), then add D
  • if already taking (A+D), then add C
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45
Q

Hypertension

Management
Medications
Step 4

A

Either add fourth drug or seek specialist advice

First, check:

  • Confirm elevated BP with ABPM/HBPM
  • Assess for postural hypotension
  • Discuss adherence

Then:
- If K+ < 4.5mmol/l: add low-dose spironolactone
If K+ > 4.5mmol/l: add alpha- (doxazosin) or beta-blocker (propanolol/atenolol)

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46
Q

Stable angina

Pathophysiology

A
  • Narrowing of the coronary arteries reduced blood flow to the myocardium
  • During times of high demand e.g. exercise, there is insufficient blood supply to meet demand
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47
Q

Stable angina

Features

A
  • Constricting chest pain
  • +/- radiation to jaw or arms
  • Brought on by exercise
  • Relieved by GTN
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48
Q

Stable angina

Investigations

A

CT coronary angiography = gold-standard

  • Inject contrast and take CT images timed to heart beat
  • Detailed view of coornary arteries, higlighting any narrowing

All patients should have baseline:

- Physical examination
- ECG
- FBC (check for anaemia)
- U&Es (prior to ACEi and other meds)
- LFTs (prior to statins)
- Lipid profile
- Thyroid function tests (check for hypo / hyper thyroid)
- HbA1C and fasting glucose (for diabetes)
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49
Q

Stable angina

Basic management

A 
RAMP:
R: Refer to cardiology
A: Advise them about diagnosis, management and when to call an ambulance
M: Medical treatment
P: Procedural or surgical interventions
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50
Q

Stable angina

Medical management

A

Immediate symptom relief:
- GTN, then again at 5 mins, if not relieved after further 5 mins then call ambulance

Long-term symptom relief:
- B-blockers
- CCBs
- Try monotherapy then dual therapy
- Others: isosorbide mononitrate ivabradine, nicorandil, ranolazine
BEWARE patint may develop tolerance to nitrates, necessitating a change in dose regime. Can use asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours

Secondary prevention:

  • Aspirin
  • Atorvastatin
  • ACE-I
  • Beta-blocker (already on for symptom relief)
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51
Q

Stable angina

Surgical management

A
  • PCI with coronary angioplasty

- CABG

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52
Q

Aortic dissection

Pathophysiology

A
  • Break or tear forms in the inner layer of the aorta → allows blood to flow between the layer of the wall of the aorta
  • 3 layers of aorta: intima, media, adventitia
  • In dissection → blood enters between the INTIMA and MEDIA → creation of a false lumen
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53
Q

Aortic dissection

Risk factors

A
  • Hypertension- heavy lifting/cocaine cause sudden increase in BP
  • Male
  • Older age
  • Smoking
  • Poor diet
  • Reduced physical activity
  • Raised cholesterol
  • Aortic conditions:
    • Biscuspid aortic valve
    • Coarctation of the aorta
    • Aortic valve replacement
    • CABG
  • Connective tissue disorders:
    • Marfan’s Syndrome
    • Ehlers-Danlos Syndrome
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54
Q

Aortic dissection

Classifications

A

The Stanford System:

  • Type A: Affects the ascending aorta, before the brachiocephalic artery
  • Type B: Affects the descending aorta, after the left subclavian artery

The DeBakey System:

  • Type I: Begins in ascending aorta and involves at least the aortic arch (if not whole aorta)
  • Type II: Isolated to ascending aorta
  • Type IIIa: Begins in descending aorta and involves only the section above the diaphragm
  • Type IIIb: Begins in the descending aorta and involves the aorta below the diaphragm
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55
Q

Aortic dissection

Features

A
  • Chest/back/abdo pain
    • Severe and sharp
    • Tearing in nature
    • Maximal at onset
    • Chest = more common in Type A
    • Back = more common in Type B
  • Radial pulse deficit
  • Difference in BP between arms (> 20 mmHg)
  • Aortic regurgitation
  • Diastolic murmur
  • Hypertension → hypotension as progresses (poor prognosis)
  • Collapse/syncope
  • Other features from involvement of specific arteries:
    • Coronary arteries → angina
    • Spinal arteries → paraplegia
    • Distal aorta → limb ischaemia
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56
Q

Aortic dissection

Investigations

A

CT angiography of chest, abdo and pelvis = investigation of choice

- Suitable for stable patients and for planning surgery
- False lumen = key finding
Transoesophageal echo (TOE)
    - More suitable for unstable patients
  • CXR: widened mediastinum
  • ECG: exclude other causes (e.g. MI), but may be normal and therefore falsely reassuring
    • Important to exclude MI as Tx for MI (thrombolysis) could cause fatal progression of dissection
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57
Q

Aortic dissection

General management

A
  • Surgical emergency!
  • Analgesia → morphine
  • BP and HR well controlled to reduce stress on aortic walls → beta-blockers
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58
Q

Aortic dissection

Management of Type A

A
  • Open surgery (midline sternotomy) to remove section of aorta with defect and replace with graft
  • Aortic valve may also need to be replaced during procedure
  • BP should be kept at 100-120 mmHg systolic whilst awaiting intervention
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59
Q

Aortic dissection

Management of Type B

A
  • Thoracic endovascular aortic repair (TEVAR)
  • Conservative management
  • Bed rest
  • Reduce BP → IV labetalol
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60
Q

Aortic dissection

Complications

A

Backward tear (rare):

  • Aortic valve regurgitation
  • Cardiac tamponade
  • MI: inferior pattern due to R coronary involvement

Forward tear:

  • Stroke
  • Unequal arm pulses and BP
  • Paraplegia
  • Renal failure
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61
Q

Aortic aneurysm

Types

A
  • True: All 3 layers of the arterial wall are involved

- False: Only a single layer of fibrous tissue forms the aneurysm wall

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62
Q

Aortic aneurysm

Risk factors

A
  • Males
  • Increased age
  • Smoking
  • Hypertension
  • Fx
  • Existing CVS disease
  • Diabetes
  • Connective tissue disorders (Marfans, Ehlers-Danlos)
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63
Q

Aortic aneurysm

Features

A
  • Most are asymptomatic
  • Usually incidental finding on US, Abdo XR, CT
  • Non-specific abdo pain
  • Pulsatile and expansile mass when palpated with two hands
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64
Q

Aortic aneurysm

Screening

A
  • All men are offered a screening US at 65 yrs old

- Patients with an aorta diameter above 3cm are referred to a vascular team (urgently if more than 5.5cm)

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65
Q

Aortic aneurysm

Investigations

A
  • US

- CT angiogram - more detailed picture and helps guide surgery, generally reserved for >5 cm

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66
Q

Aortic aneurysm

Management of unruptured aneurysm

A
  • Treat reversible RFs
  • Screening and surveillance: yearly for 3 - 4.4 cm, 3 monthly for 4.5 - 5.5 cm
  • Surgery: artificial graft, either open laparotomy or endovascular aneurysm repair (EVAR) via femoral artery
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67
Q

Aortic aneurysm

Management of ruptured aneurysm

A
  • Surgical emergency → 100% mortality without surgery
  • Permissive hypotension → lower than normal BP to reduce pressure
  • Haemodynamically unstable → directly to theatre, do not delay with imaging
  • Haemodynamically stable → CT angiogram first
  • In patients with co-morbidities that make the prognosis with surgery very poor, a discussion needs to be had with senior doctors, the patient and their family about palliative care
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68
Q

Aortic aneurysm

Prognosis

A
  • 80% mortality if ruptured
  • Poor prognosis if bleeds anteriorly into peritoneal cavity (about 20%)
  • 100% mortality if ruptures and no surgery
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69
Q

Aortic aneurysm

features of rupture aneurysm

A
  • Severe abdominal pain that may radiate to the back or groin
  • Haemodynamic instability (hypotension and tachycardia)
  • Pulsatile and expansile mass in the abdomen
  • Collapse
  • Loss of consciousness
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70
Q

Aortic aneurysm

Criteria for elective surgery

A
  • Symptomatic aneurysm
  • Diameter growing >1 cm per year
  • Diameter > 5.5 cm
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71
Q

Coarctation of the aorta

Epidemiology

A

More common in males (despite association with Turner’s syndrome)

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72
Q

Coarctation of the aorta

Features

A
  • Infancy: heart failure, poor feeding, grey floppy baby
  • Adult: hypertension
  • Radio-femoral delay
  • Mid systolic murmur, maximal over back
  • Apical click from the aortic valve
  • LV heave (due to LVH)
  • Notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Growth failure, tachycardia and tachypnoea in the context of weak femoral pulses = consider coarctation in babies

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73
Q

Coarctation of the aorta

Associations

A
  • Turner’s syndrome
  • Bicuspid aortic valve
  • Berry aneurysms
  • Neurofibromatosis
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74
Q

Coarctation of the aorta

What is it and pathophysiology

A

Congenital condition where there is a narrowing of the aortic arch, usually around the ductus arteriosus.

Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases the pressure in areas proximal to the narrowing, such as the heart and the first three branches of the aorta.

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75
Q

Coarctation of the aorta

Management

A
  • In babies: Prostaglandin E is used keep the ductus arteriosus open whilst awaiting surgery
  • Surgery is then performed to correct the coarctation and to ligate the ductus arteriosus
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76
Q

Cardiac arrest

Shockable rhythms

A
  • Ventricular fibrillation
  • Pulseless ventricular tachycardia
    (VF/pulseless VT)
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77
Q

Cardiac arrest

Non-shockable rhythms

A
  • Asystole
  • Pulseless-electrical activity
    (asystole/PEA)
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78
Q

Cardiac arrest

Chest compressions:ventilation ratio

A
  • Ratio of chest compressions to ventilation = 30:2
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79
Q

Cardiac arrest

Defibrillation

A
  • A single shock for VF/pulseless VT
  • Followed by 2 mins of CPR
  • If witnessed cardiac arrest in a monitored patient (e.g. cardiac ward) –> three quick successive (stacked) shocks instead
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80
Q

Cardiac arrest

Drugs
Delivery routes

A
  • IV access = first-line

- If not –> intraosseous route

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81
Q

Cardiac arrest

Drugs used and when

A

Adrenaline (1 mg):

  • Non-shockable: ASAP
  • Shockable: Once chest compressions have restarted after the third shock
  • Repeat adrenaline 1mg every 3-5 minutes

Amiodarone:

  • Shockable: 300 mg given after 3 shocks, further 150 mg after 5 shocks
  • Lidocaine used as alternative

Thrombolytic drugs

  • Given if PE is suspected
  • Prolonged CPR for 60-90 minutes if given
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82
Q

Cardiac arrest

Reversible causes

A

4 H’s:

  • Hypoxia
  • Hypovolaemia
  • Hyperkalemia, hypokalaemia, hypoglycaemia, hypocalcemia, acidaemia (and other metabolic disorders)
  • Hypothermia

4 T’s:

  • Toxins
  • Tamponade (cardiac)
  • Thrombus
  • Tension pnuemothorax (PEA)
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83
Q

Atrial flutter

Define

A

Form of supraventricular tachycardia characterized by a succession of rapid atrial depolarisation waves

  • Re-entrant rhythm
  • Electrical signal re-circulates in self-perpetuating loop due to extra electrical pathway
  • Goes round and round atrium without interruption
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84
Q

Atrial flutter

ECG findings

A
  • SAWTOOTH appearance
  • Atrial rate of 300 bpm
  • Ventricular rate of 150 bpm (signal conducts every second lap)
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85
Q

Atrial flutter

Associated conditions

A
  • Hypertension
  • Ischaemic heart disease
  • Cardiomyopathy
  • Thyrotoxicosis
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86
Q

Atrial flutter

Management

A
  • Rate/rhythm control with beta-blockers or cardioversion
  • Treat underlying reversible conditions (e.g. htn, thyrotoxicosis)
  • Radiofrequency ablation of the tricuspid valve - curative for most
  • Anticoagulation based on CHA2DS2VASc
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87
Q

Aortic stenosis

Pathophysiology

A
  • Outflow obstruction of the left ventricle
  • Pressure gradient builds between left ventricle and aorta
  • INCREASES the AFTERLOAD
  • Initially, LV function is maintained by compensatory pressure HYPERTROPHY
  • When compensatory mechanisms are exhausted → decline of LV function
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88
Q

Aortic stenosis

Features

A
  • Normally asymptomatic
  • Features tend to appear when 1/4 of size
  • normal size = 3-4cm

SAD
S: Syncope - exertional
A: Angina
D: Dyspnoea - exertional

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89
Q

Aortic stenosis

Murmur

A
  • EJECTION SYSTOLIC MURMUR
  • Crescendo-descendo character
  • Radiates to carotids
  • Loudness does not correlate with severity
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90
Q

Aortic stenosis

Other signs

A
  • Narrow pulse pressure
  • Slow rising pulse
  • Delayed ESM
  • Soft-absent S2
  • Thrill
  • LVH or failure
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91
Q

Aortic stenosis

Investigations

A
  • Transthoracic ECHO

- Valvular gradient (doppler-derived)

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92
Q

Aortic stenosis

Management

A
  • Asymptomatic → observe
    • Advise about dental hygiene
    • Consider IE prophylaxis in dental procedures
  • Symptomatic → valve replacement
    • TAVI (transcatheter aortic valve implantation)
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93
Q

Aortic stenosis

Criteria for surgery

A
  • Symptomatic with severe AS
  • Decreasing ejection fraction
  • Undergoing CABG with moderate AS

Consider in asymptomatic patients with valvular gradient > 40 mmHg and features such as LV systolic dysfunction

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94
Q

Aortic stenosis

Causes

A
  • DEGENERATIVE CALCIFICATION (most common >65 yrs)
  • CONGENITAL BISCUSPID (most common <65 yrs)
  • Rheumatic heart disease
  • William’s syndrome (supravalvular aortic stenosis)
  • Subvalvular: hypertrophic obstructive cardiomyopathy (HOCM)
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95
Q

Mitral regurgitation

Pathophysiology

A
  • Mitral valve does not close properly
  • Backflow of blood from LV → LA during systole
  • Compensatory mechanisms = LA enlargement and LVH
  • As it becomes more severe → body’s oxygen demand may exceed what the heart can supply → myocardium may thicken over time → may eventually feel more fatigued as a thicker myocardium becomes less efficient → finally results in congestive heart failure
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96
Q

Mitral regurgitation

Risk factors

A
  • Female
  • Low BMI
  • Age - idiopathic weakening
  • Renal dysfunction
  • Prior MI
  • Prior mitral stenosis or valve prolapse
  • Collagen disorders, e.g Ehler-Danlos, Marfans
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97
Q

Mitral regurgitation

Causes

A
  • IHD or post-MI: papillary muscles or chordae tendinae may be affected by cardiac insult
  • Mitral valve prolapse - due to myxomatous degeneration
  • Infective endocarditis: vegetations from organisms colonise the valve and prevent it from closing properly
  • Rheumatic fever: inflammation of the valves
  • Congenital
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98
Q

Mitral regurgitation

Features

A
  • Most are asymptomatic
  • Features tend to be due to LV failure, arrhythmias or pulmonary hypertension
    • Fatigue
    • Dyspnoea
    • Oedema
99
Q

Mitral regurgitation

Murmur

A
  • PAN-SYSTOLIC MURMUR
  • Heard best at apex and radiating into axilla
  • High-pitched
  • Whistling
  • Soft S1 sound
  • May hear a third heart sound (severe)
  • Displaced hyperdynamic apex beat
  • Loudness DOES correlate with severity
100
Q

Mitral regurgitation

Investigations

A
  • ECG: Broad P wave (left atrial enlargement)
  • CXR: Cardiomegaly (enlarged left atrium and ventricles)
  • ECHO: Crucial to diagnosis
101
Q

Mitral regurgitation

Management

A
  • Medical management
    • Nitrates
    • Diuretics
    • Positive inotropes
    • Intra-aortic balloon pump to increase CO
  • If HF → ACE-Inhibitors along with beta-blockers and spironolactone
  • Degenerative → repair (valvuloplasty) is more effective than replacement
102
Q

Mitral regurgitation

Criteria for surgery

A
  • Acute and severe
  • ANY symptoms (at rest or on exertion)
  • Asymptomatic but ejection fraction <60% (regardless of symptoms)
  • Asymptomatic but new-onset AF or raised pulmonary artery pressure (PAP)
103
Q

Aortic regurgitation

Pathophysiology

A
  • Leakage of blood from aorta into LV during diastole
  • Combined pressure and volume overload
  • Compensatory mechanisms: LV dilation and hypertrophy to maintain cardiac output
  • Progressive dilation may lead to HF
104
Q

Aortic regurgitation

Causes

A

Due to valve disease:

  • Rheumatic fever
  • Infective endocarditis
  • Bicuspid aortic valve
  • Idiopathic age related weakness
  • Connective tissue disorders, e.g. Ehler-Danlos, Marfan’s, SLE

Due to aortic root disease:

  • Aortic dissection
  • Spondyloarthropathies (AS)
  • Hypertension
  • Syphilis
105
Q

Aortic regurgitation

Features

A
  • Asymptomatic until 4th/5th decade
  • Exertional dyspnoea, orthopnoea, paroxysmal dyspnoea
  • Palpitations
  • Angina
106
Q

Aortic regurgitation

Murmur

A
  • EARLY DIASTOLIC, SOFT BLOWING MURMUR
  • Heard at the left sternal border
  • Can also cause Austin Flint murmur → heard at apex, early diastole, rumbling
107
Q

Aortic regurgitation

Other signs

A
  • Corrigan’s pulse - collapsing pulse
  • Wide pulse pressure
  • Displaced apex beat
  • HEAD BOBBING (de musset’s sign)
  • Quincke’s sign (nailbed pulsation)
108
Q

Aortic regurgitation

Investigations

A
  • ECG: LVH
  • CXR: Cardiomegaly (LV and aortic root enlargement)
  • ECHO
109
Q

Aortic regurgitation

Management

A
  • Infective endocarditis prophylaxis
  • ACE-Is
  • Serial ECHOs
  • Surgery → TAVI
110
Q

Aortic regurgitation

Surgery indications

A
  • Symptoms worse
  • Enlarging heart
  • ECG deterioration (T wave inversion in lateral leads)
111
Q

Mitral stenosis

Pathophysiology

A
  • Narrow mitral valve prevents proper filling during diastole from LA → LV
  • Raised LA pressure causes LA hypertrophy and dilation
  • Increased pressure in the lungs
  • Pulmonary hypertension
112
Q

Mitral stenosis

Causes

A
  • Rheumatic heart disease
  • Infective endocarditis
  • Mitral calcification
113
Q

Mitral stenosis

Other signs

A
  • Low volume pulse
  • Atrial fibrillation
  • Malar flush
  • Additional ‘a’ wave in JVP (pulmonary HTN)
114
Q

Mitral stenosis

Investigations

A
  • ECG: AF, LA enlargement, P-mitrale (broad, bifid P-waves in Lead 2)
  • CXR: LA enlargement
  • ECHO: A tight mitral valve would be <1 sq cm
115
Q

Mitral stenosis

Management

A
  • Anticoagulation in AF (Warfarin)
  • Monitor asymptomatic patients with serial ECHOs
  • Symptomatic → percutaneous mitral balloon valvotomy or mitral valve commissurotomy or replacement
116
Q

Mitral stenosis

Management

A
  • Anticoagulation in AF (Warfarin)
  • Monitor asymptomatic patients with serial ECHOs
  • Symptomatic → percutaneous mitral balloon valvotomy or mitral valve commissurotomy or replacement
117
Q

Myocarditis

Pathophysiology

A

inflammation of the myocardium

118
Q

Myocarditis

Causes

A
  • viral: coxsackie B, HIV
  • bacteria: diphtheria, clostridia
  • spirochaetes: Lyme disease
  • protozoa: Chagas’ disease, toxoplasmosis
  • autoimmune
  • drugs: doxorubicin
119
Q

Myocarditis

Features

A
  • Usually young patient with an acute history
  • Chest pain
  • Dyspnoea
  • Arrhythmias
120
Q

Myocarditis

Investigations

A

Bloods
↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP

ECG

  • Tachycardia
  • Arrhythmias
  • ST/T wave changes including ST-segment elevation and T wave inversion
121
Q

Myocarditis

Management

A
  • Treatment of underlying cause e.g. antibiotics if bacterial cause
  • Supportive treatment e.g. of heart failure or arrhythmias
122
Q

Myocarditis

Complications

A
  • Heart failure
  • Arrhythmia, possibly leading to sudden death
  • Dilated cardiomyopathy: usually a late complication
123
Q

Venous leg ulcers

Causes

A
  • Venous hypertension (secondary to chronic venous insufficiency) = MOST COMMON
  • Calf pump dysfunction
  • Neuromuscular disorders
124
Q

Venous leg ulcers

Pathophysiology

A
  • Form due to capillary fibrin cuff or leucocyte sequestration
125
Q

Chronic venous insufficiency

Features

A
  • Oedema
  • Brown pigmentation
  • Lipodermatosclerosis
  • Eczema
126
Q

Venous leg ulcers

Features

A
  • Occur in the GAITER area
  • Occur after minor injury to leg
  • Larger than arterial ulcers
  • More superficial than venous ulcers
  • Irregular, sloping border
  • More likely to bleed
  • Less painful
  • Pain = relieved by elevation
  • Pain = worse on lowering the leg
127
Q

Venous leg ulcers

What is deep venous insufficiency related to?

A

DVT

128
Q

Venous leg ulcers

What is superficial venous insufficiency related to?

A

Varicose veins

129
Q

Venous leg ulcers

Investigations

A
  • ABPI - assess for poor arterial flow, could impair healing
  • Bloods to look for infection (FBC/CRP)
  • Bloods for co-morbidities (HbA1c, FBC for anaemia, albumin for malnutrition)
  • Charcoal swabs to look for causative organism
  • Skin biopsy (if skin cancer suspected) - 2 week wait
  • Doppler US to look for reflux
  • Duplex US to look at anatomy/flow of veins
130
Q

Venous leg ulcers

Management

A
  • 4 LAYER COMPRESSION BANDAGING (after exclusion of arterial disease or surgery)
  • Oral pentoxifylline, a peripheral vasodilator, improves healing rate
  • Cleaning, debridement and dressing of wound
  • If fails to heal within 12 weeks or > 10 cm -> may need grafting
  • Tissue viability in complex/non-healing ulcers
  • Pain killers or pain team if painfuk
  • Diabetes team if diabetic
  • Abx if infection
131
Q

Arterial ulcers

Associations

A
  • PAD

- Absent pulses, pallor and intermittent claudication

132
Q

Arterial ulcers

Features

A
  • Occur distally, toes or dorsum of foot (heel)
  • Smaller than venous ulcers
  • Deeper than venous ulcers
  • Well-defined borders
  • Punched-out appearance
  • Pale due to poor blood supply
  • Less likely to bleed
  • Painful
  • Worse at night (when elevated)
  • Pain improved by lowering leg
  • May be areas of gangrene
  • Low ABPI measurements
  • Cold, no palpable pulses
133
Q

ABPI interpretation

A
  • Normal ABPI = 0.9 - 1.2
  • Values below 0.9 indicate arterial disease
  • Interestingly, values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)
134
Q

Arterial ulcers

Management

A
  • Same as PAD
  • Urgent referral to vascular to consider surgical revascularization
  • If the underlying arterial disease is treated, the ulcer should heal rapidly

Debridement and compression are NOT used in arterial ulcers

135
Q

Complication of diabetic foot ulcer?

A

Osteomyelitis

136
Q

What score is used for pressure ulcers?

A

Waterlow Score

137
Q

Tricuspid regurgitation

Signs

A
  • Pan-systolic murmur
  • Prominent/giant V waves in JVP
  • Pulsatile hepatomegaly
  • Left parasternal heave
138
Q

Tricuspid regurgitation

Causes

A
  • Right ventricular infarction
  • Pulmonary hypertension, e.g. COPD
  • Rheumatic heart disease
  • Infective endocarditis
  • Ebstein’s anomaly
  • Carcinoid syndrome
139
Q

Ebstein’s Anomaly

Pathophysiology

A
  • Congenital heart defect
  • Low insertion of the tricuspid valve
  • Results in large atrium and small ventricle
  • Sometimes referred to as atrialisation of the right ventricle
  • Poor flow from right atrium to right ventricle -> poor flow to pulmonary vessels
140
Q

Ebstein’s Anomaly

Associations

A
  • Patent foramen ovale (PFO) or atrial septal defect (ASD) is seen in at least 80% of patients, resulting in a shunt between the right and left atria
  • Wolff-Parkinson White syndrome
  • Exposure to lithium in-utero
141
Q

Ebstein’s Anomaly

Features

A
  • Cyanosis
  • SOB
  • Tachypnoea
  • Poor feeding if baby
  • Prominent ‘a’ wave in the distended jugular venous pulse,
  • Hepatomegaly
  • Tricuspid regurgitation
  • Pansystolic murmur, worse on inspiration
    right bundle branch block → widely split S1 and S2 (S3 and S4 = gallop rhythm)
  • Collapse/cardiac arrest
142
Q

JVP

‘a’ wave

A

= Atrial contraction

  • large if atrial pressure e.g.tricuspid stenosis, pulmonary stenosis,pulmonary hypertension
  • absent if inatrial fibrillation
143
Q

JVP

Cannon ‘a’ wave

A
  • caused by atrial contractions against a closed tricuspid valve
  • are seen incomplete heart block,ventricular tachycardia/ectopics, nodal rhythm, single-chamber ventricular pacing
144
Q

JVP

‘c’ wave

A
  • closure of the tricuspid valve

- not normally visible

145
Q

JVP

‘v’ wave

A
  • due to passive filling of blood into the atrium against a closed tricuspid valve
  • giant v waves in tricuspid regurgitation
146
Q

JVP

‘x’ descent

A

fall in atrial pressure during ventricular systole

147
Q

JVP

‘y’ descent

A

opening of tricuspid valve

148
Q

JVP

Non-pulsatile JVP

A

Vena cava obstruction

149
Q

JVP

Kussmaul’s sign

A
  • Paradoxical rise in JVP on inspiration

- Seen in constrictive paricarditis

150
Q

Ejection systolic murmur

Louder on expiration causes

A
  • Aortic stenosis

- Hypertrophic obstructive cardiomyopathy

151
Q

Ejection systolic murmur

Louder on inspiration causes

A
  • Pulmonary stenosis

- Atrial septal defect

152
Q

Pansystolic murmur

Causes

A

High-pitched and blowing in character

  • Mitral regurgitation
  • Tricuspid regurgitation- louder during inspiration

Harsh in character
- Ventricular septal defect

153
Q

Late systolic murmur

Causes

A
  • Mitral valve prolapse

- Coarctation of aorta

154
Q

Early diastolic murmur

Causes

A

High-pitched and blowing in nature

  • Aortic regurgitation
  • Graham-Steel murmur (pulmonary regurgitation)
155
Q

Mid-late diastolic murmur

Causes

A
  • Mitral stenosis (‘rumbling’ in character)

- Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

156
Q

Continuous machine-like murmur

Causes

A

Patent ductus arteriosus

157
Q

Ebstein’s Anomaly

Investigations

A

ECHO

158
Q

Ebstein’s Anomaly

Managegenmt

A
  • Treat arrhythmias and HF
  • Prophylactic Abx for infective endocarditis
  • Definitive surgical correction of defect
159
Q

Infective endocarditis

Risk factors

A

Things that can introduce infectious material:

  • IVDU
  • Poor dental hygiene
  • Dental treatment
  • IV cannula
  • Cardiac surgery
  • Recent piercings

Others:

  • Prosthetic valves
  • Valve disease (including rheumatic)
  • Congenital heart defects
  • Elderly
160
Q

Infective endocarditis

Causative organisms

A
  • STAPH. AUREUS = MOST COMMON (IVDUs, DM, surgery)
  • Strep viridans (poor dental hygeine, dental procedure)
  • Staph epidermidis (indwelling lines, prosthetic valve surgery). MOST COMMON if < 2 months of valve surgery.
  • Strep bovis (colorectal cancer)
  • Non-infective = SLE (Libman-Sacks), malignancy (marantic endocarditis)

Culture-negative causes:

  • Prior Abx therapy
  • Coxiella burnetti
  • Bartonella
  • Brucella
  • HACEK = Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
161
Q

Infective endocarditis

Modified Duke Criteria
Major criteria

A
  • Positive blood culture (x2 12 hrs apart, x3 for less specific like s.aureus) or positive serology for culture-negatives
  • Positive echocardiogram
  • New valvular regurgitation murmur
162
Q

Infective endocarditis

Modified Duke Criteria
Minor criteria

A
  • Predisposing heart condition or IVDU
  • Microbiological evidence does not meet major criteria
  • Fever > 38
  • Vascular phenomena - major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechia or purpura
  • Immunological phenomena - glomerulonephritis, Osler’s nodes, Roth spots
163
Q

Infective endocarditis

Modifed Duke Criteria
Pathological critera

A
  • Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
  • E.g. valve tissue, embolic fragments, intracardiac abscess content
164
Q

Infective endocarditis

Modifed Duke Criteria
Score interpretation

A

Infective endocarditis diagnosed if:

  • Pathological criteria positive, or
  • 2 major criteria, or
  • 1 major and 3 minor criteria, or
  • 5 minor criteria
165
Q

Infective endocarditis

Poor prognostic factors

A
  • Staph.aureus infection
  • Prosthetic valve
  • Culture negative endocarditis
  • Low complement levels
166
Q

Infective endocarditis

Management
Initial blind therapy

A

Own valve:
- Amoxicillin (consider adding low-dose gentamicin)

Penicillin allergic:
- Vancomycin + low-dose gentamicin

Prosthetic valve:
- Vancomycin + rifampicin + low-dose gentamicin

167
Q

Infective endocarditis

Specific Tx

A

Staphylococci:

  • Own valve: Flucloxacillin
  • Own valve and PA: Vanc + rifampicin
  • Prosthetic valve: Flucloxacillin + rifampicin + low-dose gent
  • Prosthetic and PA: Vanc + rifampicin + low-dose gent)

Streptococci:

  • Own valve: Benzylpenicillin
  • Own valve and PA: Vanc + low-dose gent
  • Prosthetic valve: Benzylpenicillin + low-dose gent
  • Prosthetic and PA: Vanc + low-dose gent

PA = penicillin allergy

168
Q

Infective endocarditis

Indications for surgery

A
  • Severe valvular incompetence
  • Aortic abscess (lengthened PR)
  • Infections resistant to Abx/fungal infections
  • HF
  • Recurrent emboli after Abx
169
Q

Infective endocarditis

Indications for prophylaxis

A
  • Any episode of infection in people at risk of IE
  • If a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
170
Q

DVT

Risk factors

A
  • Immobility
  • Recent surgery
  • Long haul travel
  • Pregnancy
  • Hormone therapy with oestrogen (combined oral contraceptive pill and hormone replacement therapy)
  • Malignancy
  • Polycythaemia
  • Systemic lupus erythematosus
  • Thrombophilia
171
Q

DVT

Thrombophilias

A
  • MAIN = ANTIPHOSPHOLIPID SYNDROME (recurrent VTEs and recurrent miscarriages, blood test fr antiphospholipid antibodies)
  • Factor V Leiden
  • Antithrombin deficiency
  • Protein C or S deficiency
  • Hyperhomocysteinaemia
  • Prothombin gene variant
  • Activated protein C resistance
172
Q

DVT

Features

A
  • Almost always unliateral
  • Bilateral symptoms are more likely to be chronic venous insufficiency or HF
  • Lower limb swelling
  • Dilated superficial veins
  • Tenderness to the calf
  • Oedema
  • Colour changes to the leg

To examine for leg swelling, measure the calf 10cm below the tibial tuberosty. >3 cm difference is significant.

173
Q

DVT

Diagnosis

A
  • WELLS SCORE

If Wells >=2 (DVT likely):

  • Proximal leg vein USS
  • If positive -> diagnosed
  • If negative -> D-Dimer
  • If USS can not be carried out within 4 hrs then give anticoagulation and do D-Dimer whilst waiting
  • If positive D-Dimer but negative scan and Wells+, stop anticoagulation and offer repeat USS 1 week later

If Wells < 1 (unlikely):

  • Perform a D-Dimer within 4 hrs
  • Give anticoagulation in interim if not within 4 hrs
  • Negative -> DVT unlikely
  • Positive -> proximal leg USS within 4 hrs
  • If USS not within 4 hrs, anticoagulate and do it within 24hrs
174
Q

DVT

Other things that may cause a raised D-Dimer

A
  • Pregnancy
  • Pneumonia
  • Malignancy
  • HF
  • Surgery
175
Q

DVT

Initial management

A
  • Apixaban or Rivoraxaban
  • Started immediately

If neither are suitable:
- LMWH followed by dabigatran or edoxaban
OR
- LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)

176
Q

DVT

When might you consider catheter-directed thrombolysis?

A
  • Symptomatic ileofemoral DVT

- Symptoms lasting < 14 days

177
Q

DVT

Management in active cancer

A

DOAC unless CI

178
Q

DVT

Management in renal impairment

A

If severe, e.g. < 15/min:

- LMWH, unfractionated heparin or LMWH followed by a VKA (Warfarin)

179
Q

DVT

Management in antiphospholipid syndrome

A
  • LMWH followed by VKA (Warfarin)
180
Q

DVT

How long do you continue anticoagulation for?

A
  • 3 months: Reversible cause (then review)
  • 3+ months (often 6 months, exact time based on HASBLED): Unclear cause, recurrent VTE, an irreversible underlying cause (e.g. thrombophilia)
  • 3-6 months: Active cancer (then review)
181
Q

DVT

Further management for recurrent PEs that are unsuitable for anticoagulation

A

IVC filter

- Catch blood clots travelling from the venous system

182
Q

DVT

What should you check for in patients with unprovoked DVT or PE that are about to finish anticoagulation?

A
  • Antiphospholipid syndrome (check antiphospholipid antibodies)
  • Hereditary thrombophilias (only if they have a first-degree relative also affected by a DVT or PE)
183
Q

DVT

What should you check in patients presenting with their first VTE without a clear cause?

A
  • Medical history
  • Baseline bloods
  • Physical examination for evidence of cancer
184
Q

PE

CTPA vs V/Q scanning in pregnancy

A

CTPA:

  • Slight increased risk of maternal breast cancer
  • Pregnancy makes breast cancer more sensitive to radiation

V/Q Scanning:
- Slight increased risk of childhood cancer compared with CTPA

185
Q

Antiphospholipid syndrome

Pathophysiology

A
  • Acquired disorder
  • Predisposes to venous and arterial thromboses, recurrent foetal loss and thrombocytopenia
  • May occur as primary disorder or secondary to other conditions, particularly SLE
186
Q

Antiphospholipid syndrome

Features

A
  • Venous/arterial thrombosis - stroke/MI/renal thrombosis
  • Recurrent foetal loss
  • Livedo reticularis (reddish/blue mottled rash, worse on cold)
  • Thrombocytopenia (low platelets)
  • Prolonged APTT (paradoxical)
  • Pre-eclampsia
  • Pulmonary hypertension
187
Q

Antiphospholipid syndrome

Associations

A
  • SLE
  • Other autoimmune disorders
  • Lymphoproliferative disorders
  • Phenothiazines (RARE)
  • VTEs
188
Q

Antiphospholipid syndrome

Diagnosis

A

Hx of thrombosis or pregnancy complication PLUs peristent antibodies:

  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies
189
Q

Antiphospholipid syndrome

Management
Primary, secondary and pregnancy

A

Primary thromboprophylaxis:
- Low-dose aspirin

Secondary thromboprophylaxis:

  • Initial VTE or arterial thrombosis -> lifelong warfarin, target INR 2-3
  • Recurrent VTE -> lifelong warfarin, target INR 3-4

Pregnancy:

  • LMWH plus aspirin to reduce risk of complications
  • Warfarin CI in pregnancy
190
Q

Antiphospholipid syndrome

Target INRs

A
  • Initial VTE/arterial thrombosis: 2-3

- Recurrent VTE: 3-4

191
Q

Haemochromatosis

Pathophysiology

A
  • Autosomal recessive
  • Disorder or iron absorption and metabolism
  • Mutation in HFE gene (human haemochromatosis protein)
  • Located on chromosome 6
192
Q

Haemochromatosis

Epidemiology

A
  • 1 in 10 people in Europe carry mutation
  • More common that CF
  • Usually presents after age of 40 yrs (iron overload becomes symptomatic)
  • Presents later in females due to loss of iron through menstruation
193
Q

Haemochromatosis

Features

A

Early on:

  • Fatigue
  • Erectile dysfunction
  • Arthralgia (esp. hands)

Others:

  • Bronze skin pigmentation
  • DM
  • Stigmata of chronic liver idisease
  • Cardiac failure (2nd to dilated cardiomyopathy)
  • Hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotropic hypogonadism)
  • Arthritis, especially of hands
  • Hair loss
  • Cognitive symptoms (memory and mood disturbances)
  • Amenorrhoea
194
Q

Haemochromatosis

Diagnosis

A
  • Serum ferritin level (HIGH - > 500ug/l)
  • Transferring saturation (HIGH >55% men, 50% women)
  • LOW TIBC
  • Genetic testing = gold-standard
  • Liver biopsy with Perl’s stain
  • CT abdo
  • MRI - liver deposits of iron, iron deposits in heart
195
Q

Haemochromatosis

Complications

A
  • T1DM
  • Cardiomyopathy (iron deposits in heart)
  • Hepatocellular carincoma
  • Hypothyroidism (iron in thyroid)
  • Cirrhosis
  • Chondrocalcinosis, pseudogout
  • Iron deposits in pituitary and gonads -> endocrine and sexual problems
196
Q

Haemochromatosis

Management

A
  • Venesection (weekly protocol of removing blood to decrease total iron) = first-line
  • Monitoring of serum ferritin and transferrin saturation: TS < 50%, SF < 50 ug/l
  • Desferrioxamine = second-line
  • Avoid alcohol
  • Genetic counseling
  • Monitor and treat complications
197
Q

Thoracic aortic aneurysm

Pathophysiology

A
  • Dilation of the thoracic aorta
  • Most commonly affected area = ascending aorta
  • Diameter is normally < 4.5 cm for ascending and 3.5 cm for descending
  • First symptoms may be when it ruptures (extremely high mortality)
198
Q

Thoracic aortic aneurysm

Features

A
  • Chest or back pain
  • Trachea or left bronchus compression may cause cough, shortness of breath and stridor
  • Phrenic nerve compression may cause hiccups
  • Oesophageal compression may cause dysphagia (difficulty swallowing food)
  • Recurrent laryngeal nerve compression may cause a hoarse voice
  • May result in aortic regurgitation
199
Q

Thoracic aortic aneurysm

Diagnosis

A
  • Echocardiogram

- CT or MRI angiogram

200
Q

Thoracic aortic aneurysm

Management

A
  • Reduce modifiable RFs
  • Surveillance to monitor size
  • TEVAR (thoracic endovascular aortic repair) - catheter via femoral artery to insert stent graft
  • Open surgery (remove damaged aorta and replace with synthetic graft)
201
Q

Thoracic aortic aneurysm

Complications

A
  • Aortic dissection
  • Rupture aneurysm
  • Aortic regurgitation (if aortic valve is affected)
202
Q

Thoracic aortic aneurysm

Rupture features

A
  • Severe chest pain or back pain
  • Haemodynamic instability (hypotension and tachycardia)
  • Collapse
  • Death (often patients do not reach hospital)

May be bleeding into:

  • Oesophagus, causing haematemesis (vomiting blood)
  • Airways or lungs, causing haemoptysis (coughing up blood)
  • Pericardial cavity, causing cardiac tamponade (compression of the heart)
203
Q

Thoracic aortic aneurysm

Rupture management

A

Emergency open surgery

Often patients do not reach hospital

204
Q

Peripheral arterial disease (PAD)

Pathophysiology

A
  • Narrowing of the arteries supplying the limbs and peripheries
  • Reducing the blood flow to these areas
  • Usually refers to lower limbs, resulting in symptoms of CLAUDICATION
205
Q

Peripheral arterial disease (PAD)

Umbrella term for what

A
  • Intermittent claudication
  • Critical limb ischaemia
  • Acute limb-threatening ischaemia
206
Q

Intermittent claudication

What is it

A
  • The symptom of ischaemia in a limb
207
Q

Intermittent claudication

Features

A
  • Occurs during exertion
  • Relieved by rest (within minutes)
  • Crampy, achey pain in the calf, thigh or buttock
  • Muscle fatigue when walking beyond a certain intensity (usually a predictable distance)
208
Q

All peripheral arterial disease (PAD)

Assessment

A
  • Check femoral, popliteal tibialis and dorsalis pedis pulses
  • ABPI
  • Duplex USS = First-line
  • MRA (MR angiography) or CTA prior to any intervention
  • Check for aterial/venous ulcers
209
Q

ABPI interpretation

A

ABPI = Ratio of systolic BP in ankle compared to arm
Taken manually using doppler probe
E.g. Ankle SBP of 80, arm SBP of 100 = 0.8 ratio

0.9 - 1.3 = Normal
0.6 - 09 = Claudication (mild PAD)
0.3 - 0.6 = Rest pain (mod-sev PAD)
< 0.3 = Impending (critical ischaemia)
> 1.3 can indicate calcification of the arteries (DM)

210
Q

Critical limb ischaemia

Features

A
  • Typically a burning pain
  • Worse at night when leg is raised, patients often hang legs out of bed to relieve pain
  • 1 or more of:
    • Rest pain in foot >2 weeks
    • Ulceration
    • Gangrene
211
Q

Acute limb-threatening ischaemia

Features

A

6 P’s

  • Pain
  • Pallor
  • Pulseless
  • Paralysis
  • Paraesthesia
  • Perishingly cold
212
Q

Intermittent claudication

Management

A
  • Lifestyle changes
  • Exercise training

Medicine:

  • Atorvastatin
  • Clopidogrel
  • Naftidofurly oxalate (peripheral vasodilator)

Surgery:

  • Endovascular angioplasty and stenting
  • Endarterectomy - cut open and remove atheromatous plaque
  • Bypass surgery
213
Q

Critical limb ischaemia

Management

A

Urgent referral to vascular team

Surgery:

  • Endovascular angioplasty and stenting
  • Endarterectomy - cut open and remove atheromatous plaque
  • Bypass surgery
  • Amputation if not possible to restore blood supply
214
Q

Acute limb-threatening ischaemia

Management

A

REVASCULARISE WITHIN 4-6 HRS

  • Endovascular thrombolysis
  • Endovascular thrombectomy
  • Surgical thrombectomy
  • Endarterectomy - cut open and remove atheromatous plaque
  • Bypass surgery
  • Amputation if not possible to restore blood supply
215
Q

PAD

Factors suggestive of thrombus

A
  • Pre-existing claudication with sudden deterioration
  • No obvious source for emboli
  • Reduced or absent pulses in contralateral limb
  • Evidence of widespread vascular disease (e.g. MI, stroke, TIA, previous vascular surgery)
216
Q

PAD

Factors suggestive of emboli

A
  • Sudden onset leg pain (< 24 hrs)
  • No Hx of claudication
  • Clinically obvious source of embolus (e.g. AF, recent MI)
  • No evidence of PAD (normal pulses in contralateral limb)
  • Evidence of proximal aneurysm (e.g. abdominal or popliteal)
217
Q

PAD

Buergers test

A

Part 1

  • Lying on back
  • Lift leg to 45 degrees at hip and hold for 1-2 mins
  • Pallor would indicate inadequate arterial supply
  • Buergers angle refers to angle in which the legs go pale

Part 2

  • Sit patient up and hang legs off bed
  • Blood will flow back into legs
  • In health patient -> legs will remain pink
  • In PAD they will go:
    • BLUE initially as ichaemic tissue deoxygenates the blood
    • DARK RED (RUBOR) after short time due to vasodilation in response to waste products of anaerobic respiration
218
Q

Acute pericarditis

Causes

A
  • Viral infections (Coxsackie)
  • Tuberculosis
  • Uraemia
  • Trauma
  • Post-MI
  • Dressler’s syndrome
  • Connective tissue disease (SLE, RA)
  • Hypothyroidism
  • Malignancy
219
Q

Acute pericarditis

Features

A
  • Sudden onset of SHARP pain
  • Worse on inspiration and lying flat
  • relief when leaning forwards (differentiate from MI)
  • Radiates to arm and trapezius ridge
  • Dyspnoea
  • Fever
  • Irritation of phrenic nerve (cough, hiccups)
  • Cardiac tamponade
220
Q

Acute pericarditis

Investigations

A

ECG:

  • Saddle-shaped ST elevation
  • Global/widespread changes (differentiate from MI)
  • PR depression = most specific marker!!

Trans-thoracic echo
- For ALL patients with suspected acute pericarditis

221
Q

Acute pericarditis

Management

A
  • Treat underlying cause
  • NSAIDs and COLCHICINE
  • Steroids if not improving
222
Q

Constrictive pericarditis

Causes

A
  • Any causes of acute pericarditis

- Especially TB

223
Q

Constrictive pericarditis

Features

A
  • Dyspnoea
  • RHF - raised JVP, ascites, oedema, hepatomegaly
  • JVP shows x and y descent
  • Pericardial knock (Loud S3)
  • Kussmaul’s sign = positive
224
Q

What is Kussmaul’s sign

A

Increased jugular venous pressure with inspiration

225
Q

Constrictive pericarditis

Pathophysiology

A

The heart is encased in rigid fibrotic pericardium -> prevents diastolic filling of ventricles

226
Q

Constrictive pericarditis

Investigations

A

CXR: pericardial calcification

227
Q

Constrictive pericarditis

Management

A

Surgical excision of the pericardium

228
Q

Constrictive pericarditis vs Cardiac tamponade

A

JVP:
- CT - absent Y descent
- CP - X+Y descent present
TAMponade = TAMpaX

Pulsus paradoxus:

  • CT - present
  • CP - absent

Kussmaul’s sign

  • CT - rare
  • CP - present

Characteristic features
- CP - pericardial calcification on CXR

229
Q

Cardiac tamponade

Pathophysiology

A

Accumulation of pericardial fluid under pressure

230
Q

Cardiac tamponade

Features

A

BECK’S TRIAD

  • Hypotension
  • Raised JVP
  • Muffled heart sound

Others:

  • Dyspnoea
  • Tachycardia
  • Absent Y descent on JVP
  • Pulsus paradoxus - large drop in BP during inspiration
231
Q

Cardiac tamponade

Investigations

A
  • ECG: electrical alternans

= Alternating QRS amplitude in any or all leads

232
Q

Cardiac tamponade

Management

A

Urgent pericardiocentesis

233
Q

Dilated cardiomyopathy

Pathophysiology

A
  • Most common type of cardiomyopathy
  • Dilated heart primarily causes systolic dysfunctions
  • All four chambers are dilated but left ventricle more than right ventricle
  • Deterioration of the heart muscle (myocardium) to contract
  • Electrical and mechanical functions are affected
  • Arrhythmia risk
  • Eccentric hypertrophy
  • Can be genetic –> Autosomal dominant
234
Q

Dilated cardiomyopathy

Causes

A
  • Idiopathic = most common
  • Myocarditis - Coxsackie B, HIV, dipththeria, Chagas disease
  • IHD
  • Peripartum (pregnancy)
  • HTN
  • Iatrogenic, e.g. doxorubicin
  • Substance abuse - alcohol, cocaine
  • Inherited - autosomal dominant, or Duchenne muscular dystrophy
  • Infiltrative (haemochromatosis, sarcoidosis)
235
Q

Dilated cardiomyopathy

Features

A
  • HF findings
  • Systolic murmur - stretching of valves may result in mitral and tricuspid regurgitation
  • S3
236
Q

Dilated cardiomyopathy

Investigations

A
  • CXR: balloon heart
  • ECHO
  • ECG: T wave flattening, poor R wave progression, tachycardia
  • BNP
  • Low sodium - poor prognostic factor
237
Q

Dilated cardiomyopathy

Management

A
  • Bed rest
  • HF meds: ACE-I, Beta-blockers, diuretics, digoxin
  • Bi-ventricular pacing
  • ICD
  • Heart transplant
238
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

Pathophysiology

A
  • Most common = mutation in beta-myosin heavy chain protein or myosin-binding protein C
  • Results primarily in diastolic dysfunction (LVH -> decreased compliance -> decreased CO)
  • Characterised by myofibrillar hypertrophy with chaotic and disorganised fashion myocytes (disarray) and fibrosis on biopsy
239
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

Features

A
  • Often asymptomatic
  • Exertional dyspnoea
  • Angina
  • Syncope (usually exertional)
  • Sudden death (due to ventricular arrhythmias)
  • Jerky pulse
240
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

Associations

A
  • Wolff-Parkinson-White syndrome

- Friedrich’s ataxia

241
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

Examination findings

A
  • Jerky pulse
  • Large ‘a’ waves
  • Double apex beat
  • Ejection systolic murmur
242
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

Investigations

A

ECHO - MR SAM ASH

  • MR = mitral regurgitation
  • SAM = systolic anterior motion of anterior mitral valve
  • ASH = asymmetric hypertrophy

ECG

  • LVH
  • Non-specific ST and T wave abnormalities
  • Progressive T wave inversion
  • Deep Q waves
  • AF occasionally
243
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

Management

A

ABCDE

  • A: Amiodarone
  • B: Beta-blocker or verapamil
  • C: Cadioverter defibrillator
  • D: Dual chamber pacemaker
  • E: Endocarditis prophylaxis (maybe?)

AVOID:

  • Nitrates
  • ACE-Is
  • Inotropes
244
Q

Causes of AF?

A
  • *SMITH**
  • S: Sepsis
  • M: Mitral valve pathology (stenosis)
  • I: Ischaemic heart disease
  • T: Thyrotoxicosis
  • H: Hypertension

Finals (21 decks)

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