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1a. CARDIOVASCULAR > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

— shock —
Name the five main types of shock.

A

Hypovolaemic, neurogenic, cardiogenic, vasoactive, obstructive

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2
Q

Give some causes of obstructive shock.

A

Anything that increases intrathoracic pressure - tension pneumothorax, cardiac tamponade, aortic stenosis, pressure

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3
Q

Describe neurogenic shock.

A

Loss of sympathetic innervation - heart rate decreases

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4
Q

How must shock be treated?

A

ABCDE, O2, volume replacement if blood loss, inotropes for cardiogenic

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5
Q

— angina —
Describe the aetiology and presentation of angina pectoris.

A
  • the clinical manifestation of myocardial ischaemia, where myocardial oxygen demand exceeds supply
  • chest pain (central, retrosternal, crushing, tight, band across the chest) radiating to the arm, neck, or jaw present on exertion and relieved by rest and GTN
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6
Q

Describe the investigation of angina pectoris.

A

assess the typicality of chest pain according to the three typical symptoms:
- constricting discomfort in the front of the chest, neck, shoulders, jaw, or arms
- precipitated by physical exertion
- relieved by rest/GTN within ~5min
all 3 = typical angina; 2 = atypical angina

ECG is typically normal.
- 1st line: coronary CT angiography (CCTA)
- 2nd line: non-invasive functional testing (e.g. exercise ECG, MPS with SPECT, MR stress imaging)
- 3rd line: invasive coronary angiography

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7
Q

Describe the management of angina pectoris.

A

non-pharmacological:
- explain precipitants (exertion, emotional stress, exposure to cold, heavy meals)
- safety-netting: seek help if 2 GTN sprays do not relieve pain
- lifestyle advice

pharmacological:
- immediate relief: GTN
- prevention: beta-blockers, CCBs (dihydropyridines)
- cardiovascular risk: 4A’s (atorvastatin, aspirin, atenolol/beta-blocker, ACE inhibitor)

prevention of symptoms:
- monotherapy (B/CCB)
- second-line therapy:
– B + CCB (dihydropyridine)
– long-acting nitrate, ivabradine, nicorandil, or ranolazine (particularly if B/CCB contraindicated)
- third-line: add a third agent only when awaiting revascularisation via PCI/CABG

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8
Q

ADDITIONAL CARDS HERE
— syncope —
Define and broadly categorise the aetiologies of syncope.

A
  • syncope is a transient loss of consciousness (TLOC) and postural tone, followed by spontaneous recovery
  • three main types of ‘true syncope’: cardiovascular (arrhythmia, valve disease, MI, PE); cerebrovascular (vertebrobasilar insufficiency), and blood flow + tone (vasovagal, orthostatic, situational, carotid sinus)
  • mimics of syncope: seizures, metabolic (hypoglycaemia, hypoxia), panic attacks
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9
Q

Describe the aetiology and presentation of vasovagal syncope.

A
  • accounts for 50% of cases of syncope
  • parasympathetic drive takes over (sympathetic withdrawal) in response to stimuli e.g. prolonged standing, heat, stress etc.
  • summarised by the 3P’s: Posture, Provoking, Prodrome
  • prodrome: blurred vision, sweating, nausea, dizziness, weakness -> bradycardia, hypotension, TLOC
  • consciousness is regained within a few minutes
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10
Q

— DVT & PE —
Describe Virchow’s triad.

A

Virchow’s triad describes the three broad categories of factors that are thought to contribute to thrombosis.
- Hypercoagulability: cancer, thrombophilia, inflammatory disease etc.
- Vessel wall/endothelial injury: surgery, chemical irritation, inflammation etc.
- Stasis of blood: immobility, varicose veins, venous obstruction etc.

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11
Q

Describe the risk factors and presentation of DVT/PE (it may help to consider Well’s score).

A
  • immobility (surgery, trauma, paralysis, bedridden)
  • tachycardia (>100bpm)
  • previous diagnosis of DVT/PE
  • malignancy
  • haemoptysis
  • unilateral leg swelling, pitting oedema
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12
Q

Describe how the scoring systems used for DVT/PE should be considered for their diagnosis.

A
  • The 2-level DVT Well’s score should be calculated for all possible cases of DVT.
  • If the risk of PE is low, consider the PE rule-out criteria (PERC); if all of these criteria are absent the probability of a PE is <2%
  • For a moderate-high risk of PE, calculate the 2-level PE Well’s score to guide further investigation
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13
Q

Describe the interim assessment and management of DVT.

A
  • interim coagulation: NICE now advocate use of a DOAC (apixaban, rivaroxaban). if DOACs are unsuitable, use a LWMH + dabigatran, edoxaban, or warfarin
  • DVT likely (Well’s 2+, or d-dimer positive): proximal leg vein USS
  • DVT unlikely (Well’s <2): d-dimer; if negative, consider stopping interim anticoagulation and repeating USS 6-8 days later
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14
Q

Describe the interim assessment and management of PE.

A
  • interim coagulation: NICE now advocate use of a DOAC (apixaban, rivaroxaban). if DOACs are unsuitable, use a LWMH + dabigatran, edoxaban, or warfarin
  • PE likely (Well’s >4): immediate CTPA or V/Q scan
  • PE unlikely (Well’s =<4): d-dimer
  • PE (confirmed) + haemodynamic instability: offer thrombolytic therapy
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15
Q

Describe the long-term management of DVT & PE.

A
  • VTE is provoked (e.g. major surgery, immobilisation): 3 months DOAC therapy
  • VTE unprovoked: 6 months DOAC therapy
  • VTE + malignancy: 6 months DOAC therapy
  • Repeated episodes, despite optimal DOAC therapy: consider use of IVC filters
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16
Q

— hypertension —
Describe the aetiologies of hypertension.

A

90-95% of cases are idiopathic (primary hypertension). Secondary causes are rare and include
* renal: CKD, PCKD, Liddle’s syndrome
* vascular: renal artery stenosis, aortic coarctation
* endocrine: phaeochromocytoma, Conn’s syndrome, Cushing’s syndrome
* drugs: HRT, COCP, steroids, NSAIDs, alcohol, nicotine, drugs
* other: OSA, pregnancy

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17
Q

Describe the classification and categories of hypertension.

A

SBP, DBP, ABPM
* stage 1: >140, >90, >135/85
* stage 2: >160, >100, >150/95
* stage 3: >180, >110, >180/110

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18
Q

Which tests should be used in the diagnosis of hypertension?

A

Proteinuria (protein in the urine), bloods, fundoscopy, 12-lead ECG

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19
Q

Describe the drug management of hypertension.

A

Adding another low dose drug is 5x more effective than titrating one drug upward.

Step 1
* ACEi/ARB: age <55 or diabetic of any age
* CCB: age >55 or Afro-Caribbean of any age

Step 2
* Add the other agent (e.g. A + C), or a thiazide-like diuretic (D) if the other agent is unsuitable
* ARBs > ACEi in Afro-Caribbean patients
* non-rate-limiting CCBs (the ‘pines) are preferred in patients with gout

Step 3
* Triple therapy (A + C + D)
* Thiazide-like diuretics are preferred to thiazide diuretics due to lower incidence of electrolyte abnormalities

Step 4
* This is defined as resistant hypertension and requires adding a fourth agent and/or seeking specialist advice
* if K+ <4.5mmol/l: add spironolactone
* if K+ >4.5mmol/l: add alpha or beta-blocker

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20
Q

Describe the initial assessment and management of a clinical BP reading indicating stage 3/malignant hypertension.

A
  • clinic reading >180/110
  • assess for signs of end-organ damage (ocular, cardiac, neurological, endocrine) and admit for same-day specialist assessment if present
  • if signs of end-organ damage are absent, arrange urgent investigations (FBC, urine albumin/creatine ratio, ECG etc.). if results indicate organ damage, start antihypertensives immediately; if no damage identified, repeat clinic BP measurement within 7 days
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21
Q

How may drug non-concordance be assessed in hypertensives?

A

No drugs in the urine

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22
Q

— ACS —
Which one sole presenting complaint constitutes acute coronary syndrome?

A

Central, crushing, heavy, pressured chest pain

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23
Q

How would acute coronary syndrome be differentiated?

A

12 lead ECG to assess for ST elevation, then troponin testing

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24
Q

ADDITIONAL CARDS HERE
What specific level of ST elevation/depression is required to diagnose STEMI?

A

> 1 mm elevation in standard limb leads (I, II, III), > 2 mm depression in augmented (aVL, aVR, aVF)

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25
Q

Describe the management of NSTEMI.

A
  • aspirin 300mg
  • calculate 6 month mortality using a tool such as GRACE
  • if PCI is not imminent, give fondaparinux
  • mortality low (<3%): ticagrelor
  • mortality high (>3%): prasugrel or ticagrelor, angiography within 72hr to assess if PCI is needed
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26
Q

Describe the drug treatment of STEMI, when balloon time is < 120 minutes.

A
  • aspirin 300mg
  • prasugrel
  • PCI + drugs (UFH + GpIIb/IIIa inhibitor if radial access used for PCI)
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27
Q

What do ticagrelor, prasugrel, and clopidogrel do?

A

Stop ADP binding to platelets

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28
Q

Describe PCI.

A
  • non-surgical invasive technique utilising either ballooning or stents to improve blood supply to ischaemic tissue
  • access is via the femoral or radial artery; if the radial artery is used, GpIIb/IIIa inhibitors (eg abciximab) must be given
  • stenting is preferred
  • ballooning is now no longer preferred as the artery may return to the stenotic state, but may be useful for bridging therapies to eg CABG
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29
Q

Describe the mechanisms and indication for CABG.

A
  • Graft creates an anastamosis (left internal mammary artery or long saphenous vein) to coronary vessels
  • left main coronary disease >50% occlusion
  • 3 vessel disease >70%
  • 2 vessel disease (LAD + another)
  • 1 vessel >70% with optimal management of angina
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30
Q

Which drug(s) should be given between thrombolysis and PCI?

A

Enoxaparin or UFH

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31
Q

— complications after MI —
Describe the complications that may arise after MI and their timecourse,

A
  • hyperacute (0-24hr): arrhythmia (e.g. VF), pericarditis
  • acute (3-14 days): VSD, tamponade
  • subacute (1-2 weeks): LV free wall rupture, LV aneurysm
  • 2-6 weeks: Dressler’s syndrome
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32
Q

— bradyarrhythmia —
Which three arrhythmias are bradycardic?

A

Sinus bradycardia, sick sinus syndrome, tachy-brady syndrome

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33
Q

Describe sick sinus syndrome.

A

Can result in sinus arrest, escape beats, and tachy-brady syndrome

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34
Q

Describe the types of AV block.

A

1st deg - prolonged PR interval, all get through. 2nd - mobitz I - PR interval increases until beat skipped, mobitz II - every nth beat is missed. 3rd deg - complete block, bradycardia and low CO

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35
Q

Describe the ECG patterns that may be seen in right bundle branch block.

A

rSR’ on V1-V2, broad S wave on I, V5, V6

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36
Q

Describe the ECG patterns that may be seen in left bundle branch block.

A

I, aVL, V6 - broad R, ST depression. V1-V3 - broad QS

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37
Q

Describe hemiblock.

A

Causes axis deviation - left anterior -> left, posterio-inferior -> right.

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38
Q

Describe bifasicular block.

A

Same as right BBB + a deep S wave on III, aVF.

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39
Q

Describe AVNRT.

A

Micro-reentry (within AVN itself). ECG shows no clear P waves with rapid QRS complexes.

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40
Q

Describe AVRT. What is it otherwise known as?

A

Macro-reentry (branching the atria and ventricles). P waves occur AFTER the QRS complex. Wolff-Parkinson-White syndrome

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41
Q

What would atrial fibrillation show on the ECG?

A

F waves - i.e. never isoelectric. Irregularly irregular rhythm

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42
Q

What would atrial flutter show on the ECG?

A

Saw tooth pattern, limited transmission to ventricles (e.g. QRS complex)

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43
Q

Name the six main supraventricular tachyarrhythmias.

A

AVNRT, AVRT, AF, atrial flutter, atrial tachycardia, atrial ectopic beats

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44
Q

Describe how supraventricular tachyarrhythmias should be treated.

A

Haemodynamic instability -> emergency cardioversion. Stability -> vagal maneuvres then adenosine if that doesn’t work.

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45
Q

Which two ventricular tachyarrhythmias are life-threatening and may lead to cardiac arrest? Describe the main clinical sign

A

Ventricular fibrillation, ventricular tachycardia. Pulseless

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46
Q

Describe Brugada syndrome.

A

Idiopathic ST elevation with pseudo-RBBB. No structural cause

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47
Q

Describe long QT syndrome.

A

Long QT interval (!), which may result in torsades de pointes. Can be acquired (by ie. bradycardia) or congenital (i.e. Jervell-Lange-Nielsen, Romano Ward syndromes)

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48
Q

Which three ventricular tachyarrhythmias may be normal/transient?

A

Normal heart ventricular tachycardia, non-sustained ventricular tachycardia, ventricular premature beats?

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49
Q

— Vascular —
Describe the classification of PAD (peripheral arterial disease).

A
  • intermittent claudication (IC): ABPI 0.4-0.85, ‘leg angina’ (leg pain on exertion, pain-free at rest)
  • critical limb ischaemia, acute limb-threatening ischaemia (ABPI 0-0.4). pain at rest
50
Q

Describe the presentation and main differentials of intermittent claudication (IC).

A
  • calf pain on exertion at a variable walking distance with relief on rest
  • the main differential is neurogenic claudication, and care must be taken to differentiate this from arterial claudication
  • spinal stenosis: key differentiators include lack of smoking/cardiovascular risk factors, inconsistent claudication distance, normal pulses, and improvement of pain when walking uphill (‘shopping trolley’ test; bending forwards creates more space for the cauda equina)
  • Guillain-Barre: following an acute illness such as gastroenteritis
51
Q

Describe the management of intermittent claudication (IC).

A
  • atorvastatin + clopidogrel (aspirin if clopidogrel C/I)
  • NICE guidelines indicate first-line management is supervised exercise therapy (SET), 2hr/wk for 3mo
  • second-line is surgical management, but only when risk factors have been modified and SET has failed to improve symptoms
    – percutaneous transluminal angioplasty (PTA) with bare-metal stents for short-segment stenosis (<10cm)
    – surgical revascularisation for long-segment stenosis (>10cm); options include surgical bypass or endarterectomy
    – naftidrofuryl oxalate is an alternative to revascularisation after SET
  • if revascularisation is not feasible, above-ankle amputation is required
52
Q

Describe the aetiologies of acute limb-threatening ischaemia (ALTI).

A
  • either embolic or thrombotic
  • embolic: 80% of cases are associated with AF. pain is typically sudden onset with no history of claudication and evidence of obvious source (e.g. MI, AF)
  • thrombotic: atherosclerosis, aneurysm, graft/stent occlusion, iatrogenic
53
Q

Describe the classification of acute limb-threatening ischaemia (ALTI).

A
  • severity is classified via the Rutherford classification
  • I (viable): normal CRT and sensation, positive ADS + VDS
  • IIa/b (marginally threatened/immediately threatened): slow/absent/partial CRT and sensation, reduced ADS
  • III (irreversible): absent CRT, complete sensation and paralysis, reduced ADS and VDS
    [CRT: capillary refill time, ADS: arterial Doppler signal, VDS: venous Doppler signal]
54
Q

Describe the assessment and management plan of acute limb-threatening ischaemia (ALTI).

A
  • oxygen, analgesia, fluid resuscitation, reverse Trendelenberg, UFH, referral to vascular service
  • II(a), marginally threatened: rest pain, no paralysis and only mild sensory loss -> CT-angiogram (CTA) to plan revascularisation -> lysis or revascularisation surgery
  • II(b), immediately threatened: often due to emboli especially if contralateral pulses are normal -> CTA may help guide revascularisation but must not delay management -> immediate surgery
  • III (irreversible): paralysis, insensate legs -> primary amputation (revascularisation is futile and dangerous)
55
Q

Describe the classification of acute thoracic aortic syndrome (ATAS).

A

ATAS are a group of conditions affecting the thoracic aorta, and include
- aortic dissection
- intramural haematoma (IMH)
- penetrating aortic ulcer (PAU)

56
Q

Describe the risk factors for ATAS.

A
  • increasing age, male sex, hypertension, diabetes
  • bicuspid aortic valve, aortic hypoplasia
  • pre-existing aortic disease (aneurysm, atherosclerosis, arteritis)
  • collagen disorders (Marfan’s, Ehlers-Danlos)
  • Turner’s syndrome, Noonan’s syndrome
  • pregnancy
  • syphilis
  • iatrogenic (cardiac catheterisation, CABG, valve replacement)
57
Q

Describe the pathology, presentation, and classification of aortic dissection.

A
  • splitting of the tunica media, creating a false lumen which fills with blood
  • sharp chest pain (ripping) radiating to the back; pain may be absent in diabetics. other signs include different BP in each arm and weak pulses in downstream arteries
  • classified by Stanford (type A: ascending aorta; type B: descending aorta)
  • CTA is the investigation of choice; others include TOE and MRA
58
Q

Describe the management of aortic dissection.

A
  • all hypertensive patients require beta-blockade, including while awaiting surgical intervention, with a target SBP of 100-120mmHg
  • Stanford A: management is surgical via arch replacement (synthetic graft)
  • Stanford B (uncomplicated): management is medical in HDU, with beta-blockade -> + nicardipine -> + hydralazine
  • Stanford B (complicated); rapid expansion, rupture, hypotension/shock, ischaemic, refractory hypertension. first-line is thoracic endovascular aortic repair (TEVAR)
59
Q

What causes varicose veins?

A

High pressure in the saphenous vein by obstruction/valve incompetence forces blood into superficial veins. This creates dilated and tortous veins

60
Q

Describe the 6 venous skin changes observed with varicose veins.

A
  • eczema: most often at medial gaiter area
  • haemosiderin deposits (iron deposits due to extravasation of RBCs - appears brown),
  • lipodermoscoliosis (cherry red, concave calves with fibrosis and thickening of the skin; ‘inverted champagne bottle leg’),
  • atrophie blanche: pale, smooth scarring associated with telangiectasia
  • corona phlebectatica: ‘ankle/malleolar flare’ with high risk of ulceration
  • ulceration
61
Q

Describe the management of varicose veins and their complications.

A

having varicose veins alone is not a reason to refer to secondary care. referral is indicated only if symptomatic or associated with changes, including:
- symptoms: heavy/aching legs, itching/burning, oedema, cramps, restless legs
- skin changes: venous eczema etc.
- superficial vein thrombosis, thrombophlebitis
- venous ulcer >2 weeks

conservative management:
- weight loss, physical activity, leg elevation
- emollients for venous eczema, debridement, dressings and compression stockings (after exclusion of arterial disease)
- thrombophlebitis: NSAIDs + fondaparinux

surgical management:
- endothermal ablation, via either radiofrequency ablation (RFA) or endovenous laser ablation (EVLA)
- ultrasound-guided foam sclerotherapy (UGFS)

62
Q

Which scoring system is used to identify risk for pressure ulcers?

A

Waterlow risk assessment score
(others include Braden, Walsall, Maelor scores)

63
Q

— further vascular cards —

A
64
Q

— congestive heart failure —
Name and describe the two main types of heart failure, in combination with the ejection fraction.

A
  • ejection fraction is a measure of the heart’s systolic contractile function and = stroke volume / end-diastolic volume. in healthy adults, the ejection fraction is >50%
  • HFrEF (ventricular pump failure)
  • HRpEF (ventricular filling failure)
65
Q

What are the main presenting complaints of heart failure?

A
  • left-sided: pulmonary oedema (dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea)
  • right-sided: peripheral oedema, hepatomegaly, ascites, raised JVP
66
Q

Describe the classical CXR findings of congestive heart failure.

A

remember ABCDE
- alveolar oedema (perihilar/batwing opacification)
- Kerley B lines (interstitial oedema)
- cardiomegaly (CTR >50%)
- dilated upper lobe vessels
- effusions (e.g. pleural effusion)

67
Q

Describe the investigation pathway of a patient with suspected heart failure.

A
  • blood tests: FBC, U&Es, HbA1c, LFTs and TFTs
  • CXR, ECG
  • measure NT-proBNP to assess severity and guide waiting time for transthoracic echo
    – <400ng/l: heart failure unlikely
    – 400-2000: echo <6 weeks
    – >2000: echo <2 weeks
  • transthoracic echo: exclude valve disease, assess systolic function
68
Q

Which drugs should be used in HFrEF?

A
  • loop diuretic (e.g. furosemide)
  • 1st line: A + B (ACE/ARB + beta-blocker)
  • 2nd line: spironolactone, SGLT2 inhibitor
  • 3rd line: ivabradine, sacubitril valsartan (replaces ACE/ARB), hydralazine + nitrate, digoxin, amiodarone
69
Q

Describe the presentation of acute heart failure.

A

acute heart failure may arise in two ways:
- de novo, due to an acute cardiac condition (e.g. MI, acute valve disease, arrhythmia, tamponade)
- chronic heart failure becomes overwhelmed, particularly with poor adherence to medication or concurrent illness/anaemia

presentation is similar to chronic heart failure, including
- fatigue, oedema, cough, dyspnoea, orthopnoea
- tachycardia, tachypnoea, hypertension, S3 (gallop rhythm)
- typically left-sided (pulmonary oedema) which causes hypoxia and hyponatraemia

70
Q

Describe the management of acute heart failure.

A

consider OMFG - O2, morphine, furosemide, GTN (nitrates)
- loop diuretics (IV), such as furosemide or bumetanide, for all patients
- O2 [only with evidence of hypoxia, e.g. SpO2 <94%], escalating to CPAP with respiratory failure
- nitrates only have a role with concomitant ischaemia, hypertension, or valve regurgitation
- morphine should no longer be used routinely, as some studies have suggested increased morbidity
- regular medication (A+B) should be continued, with beta-blockers discontinued only with bradycardia, heart block, or shock

if care must be escalated to level 2 (e.g. HDU), consider
- inotropes (e.g. dobutamine)
- vasopressors (e.g. noradrenaline)
- mechanical circulatory devices

71
Q

— arrhythmia —
Which heart rhythms are shockable?

A

VF/pulseless VT

72
Q

Which rare treatment for cardiac arrest may be effective if the patient has it in front of you and the defib is a long way away?

A

Precordial thump

73
Q

What are the main associations of all valvular heart disease?

A

Exertional dyspnoea, syncope/dizziness, JVP, oedema, cardiomegaly/LVH (displaced apex), hepatic congestion

74
Q

Which two scales are used to give a quick overview of a patient’s murmur?

A

NYHA, Murmur grading

75
Q

Describe the NYHA scale.

A

I - no limitation, II - slight limit, III - marked limitation of less than normal activity, IV - severe limitation

76
Q

Describe the murmur grading scale.

A

1/6 - very faint. 2/6 - soft, all positions, 3/6 - loud, no thrill, 4/6 - loud, thrill, 5/6 - very loud, thrill, 6/6 - heard without stethoscope, thrill

77
Q

Which valvular disease is most common?

A

Aortic stenosis

78
Q

Describe aortic stenosis as a murmur and its main symptoms.

A

Ejection systolic murmur, radiates to carotids. Dyspnoea, chest pain, syncope.

79
Q

What are the primary treatment options for aortic stenosis?

A

Valve replacement (mechanical v bio-prosthetic), TAVI (transcatheter aortic valve implantation - only if patient can’t have sternotomy)

80
Q

Describe mitral regurgitation as a murmur and its primary symptoms.

A

Pansystolic, radiates to axilla. Insidious dyspnoea, oedema, fatigue

81
Q

What are the main treatment options for mitral regurg?

A

Repair prolapse, replace degenerated (very poor only), mitroclip in infancy, ACEi/diuretics

82
Q

Describe mitral stenosis as a murmur and its main symptoms.

A

Mid-diastolic, located to apex. Dyspnoea, fatigue, palpitation (AF only)

83
Q

What is the pathology of mitral stenosis?

A

Rheumatic fever

84
Q

What are the treatment options for mitral stenosis?

A

Diuretics, treat AF. Surgery, balloon valvuloplasty. Warfarin if also AF.

85
Q

Describe aortic regurg as a murmur and its main symptoms and signs.

A

Early diastolic radiating to left sternal edge. Dyspnoea, collapsing pulse, wide pulse pressure, displaced apex

86
Q

What are the main treatment options for aortic regurg?

A

ACEi, valve replacement.

87
Q

Which conditions can cause constant murmurs?

A

Patent ductus arteriosus, septal defects.

88
Q

What may trigger TdP in long QT syndrome?

A

Exercise, loud noises, sleep, medication

89
Q

What should be used to treat long QT syndrome?

A

B-blockers, avoid stimulation

90
Q

What may trigger Brugada syndrome?

A

Sleep, fever, excessive food/alcohol

91
Q

What should be used to treat Brugada syndrome?

A

Anti-pyretics, ICDs, avoid triggers

92
Q

— endocarditis —
What is bacteraemia?

A

Presence of bacteria in the blood

93
Q

Which four main organisms are associated with ICDs?

A

Staph aureus, staph epidermidis, corynebacterium sp., propionibacterium acnes

94
Q

Describe the pathology which causes infective endocarditis.

A

Damage to valves, turbulent blood flow displaces fibrin and bacteraemia settles.

95
Q

How may infective endocarditis spread in the body?

A

Bacteraemia is friable.

96
Q

What are the main gram positive bacteria which cause infective endocarditis?

A

Staph aureus, viridans, enterococcus sp, staph epidermidis

97
Q

What are the main gram negative bacteria which cause infective endocarditis?

A

HACEK - haemophilus, aggregatobacter, cardiobacterium, eikelleum, kingella

98
Q

What are the atypical organisms that cause IE?

A

Bartonella, coxiella burnetti, chylamydia, fungi

99
Q

Describe the viridans organisms which cause IE.

A

Alpha-haemolytic (green) - strep mitis, strep salivarius, strep mutans, strep sanguinis

100
Q

What are the major Duke criteria?

A

2 seperate positive blood cultures, endocardial involvement (i.e. new valve disease)

101
Q

What are the minor Duke criteria?

A

Predisposition, fever, vascular phenomena, immunologic phenomena, minor microbiological evidence

102
Q

Describe the necessary Duke criteria required to define ‘definitive’ vs ‘possible’ IE.

A

Definitive - 2M, 1M + 3m, 5m. Possible - 1M + 1m, 3m

103
Q

How is acute IE presented?

A

Overwhelming sepsis, cardiac failure

104
Q

What are some of the features of sub-acute IE?

A

Fever, malaise, weight loss, tiredness, dyspnoea, splinter haemorrhage, hepatomegaly, Roth spots, Janeway lesions, Osler Nodes etc

105
Q

Describe the scan use to diagnose IE?

A

Transthoracic echo if suspicion, transoesophageal echo if transthoracic has high risk

106
Q

Describe the empirical treatment of IE.

A

Native (i.e. viridans) - amoxicillin, gentamicin
Prosthetic valve - vancomycin, gentamycin, add in rifampicin day 3
PWIDs - flucloxacillin

107
Q

Describe the specific treatment of the major bacteria of IE.

A

Staph aureus (not MRSA) - flucloxacillin
Viridans - benzylpenicllin, gentamicin
Enterococcus - amoxicillin/vancomycin, gentamicin
Staph epidermidis - vancomycin, gentamicin, rifampicin

108
Q

Name three non-infective causes of endocarditis.

A

Rheumatic heart disease, non-bacterial thrombotic, Libman-Sacks (lupus)

109
Q

— inflammatory cardiac —
What is myocarditis and what are its main causes?

A

Inflammation of the myocardium - coxsackie A/B and echovirus

110
Q

Describe what histology of rheumatic heart disease and myocarditis may show.

A

Aschoff bodies

111
Q

Name two causes of non-infectious pericarditis.

A

Dressler’s (post-MI) and uraemic (liver failure)

112
Q

— cardiac tumours —
What is a carcinoid tumour?

A

One of the neuroendocrine cells

113
Q

What signs may indicate a carcinoid tumour?

A

Excess chemical secretion, flushing, nausea, vomiting, right side heart valve disease

114
Q

Although cardiac tumours are rare, which is the most common primary tumour?

A

Atrial myxoma

115
Q

Describe the important aspects of history taking in syncope.

A
  • prodromal symptoms: e.g. sweating, nausea etc. (vasovagal) / Deja vu or jamais vu (epilepsy)
  • events immediately prior to TLOC (eg during exertion suggests HOCM)
  • movement during TLOC: myoclonal jerks do NOT exclude vasovagal syncope
  • tongue biting (epilepsy)
  • recovery: immediate (vasovagal) vs confused (epilepsy)
  • medical or family history of heart disease
  • drug history (precipitants, eg diuretics)
116
Q

Describe the initial investigations for syncope.

A
  • cardiovascular and respiratory examinations
  • 12-lead ECG
  • bloods (e.g. TFTs, FBC)
117
Q

Name the red flag factors for urgent referral to a cardiologist regarding syncope.

A
  • ECG abnormalities: complete RBBB/LBBB, any QTc or ST/T wave abnormalities
  • heart murmur
  • heart failure, new onset dyspnoea
  • TLOC during exertion or sudden cardiac death family history
118
Q

Describe the investigations used for syncope.

A
  • exertional syncope: exercise testing unless contraindicated (HOCM, suspected aortic stenosis); if no diagnostic result available assume arrhythmic cause
  • arrhythmic cause suspected: offer ambulatory ECG based on frequency of symptoms ->
    — several times a week: Holter monitor
    — 1-2 weekly: external event recorder
    — <2 weekly: implantable event recorder
  • vasovagal syncope affecting QOL: consider a tilt table test
119
Q

Describe the initial management of a patient with ACS.

A

MOVE MONA 120:
- monitor vital signs
- oxygen (if SpO2 <94%)
- venous access
- ECG
- morphine (significant pain only)
- oxygen (if SpO2 <94%)
- nitrates (if hypertensive with chest pain; contraindicated in hypotension)
- aspirin
- for a diagnosis of STEMI where PCI cannot be performed within 120 minutes of ECG-based diagnosis, thrombolyse

120
Q

name the coronary territories, and the association between ECG leads and coronary arteries.

A
  • anterior: V1-4, LAD artery
  • inferior: II, III, aVF, right coronary
  • anterolateral: I, aVL, V1-6, proximal LAD
  • lateral: I, aVL, V5-6, left circumflex
  • posterior: ST depression in V1-3, left/right circumflex
121
Q

Describe the management of a STEMI patient who has undergone thrombolysis therapy.

A
  • transfer to a PCI centre immediately after administering therapy
  • assess for success of thrombolysis at the PCI centre;
    — significant improvement in symptoms
    — >50% resolution of ST elevation
    — haemodynamic stability
  • routine early angiography (<24hr) is recommended whether successful or not
  • if unsuccessful, perform rescue PCI

1a. CARDIOVASCULAR (3 decks)

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