Cardiovascular Disease Flashcards
(121 cards)
1
Q
— shock —
Name the five main types of shock.
A
Hypovolaemic, neurogenic, cardiogenic, vasoactive, obstructive
2
Q
Give some causes of obstructive shock.
A
Anything that increases intrathoracic pressure - tension pneumothorax, cardiac tamponade, aortic stenosis, pressure
3
Q
Describe neurogenic shock.
A
Loss of sympathetic innervation - heart rate decreases
4
Q
How must shock be treated?
A
ABCDE, O2, volume replacement if blood loss, inotropes for cardiogenic
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
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
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
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
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
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.
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
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
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
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
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
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
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
18
Q
Which tests should be used in the diagnosis of hypertension?
A
Proteinuria (protein in the urine), bloods, fundoscopy, 12-lead ECG
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
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
21
Q
How may drug non-concordance be assessed in hypertensives?
A
No drugs in the urine
22
Q
— ACS —
Which one sole presenting complaint constitutes acute coronary syndrome?
A
Central, crushing, heavy, pressured chest pain
23
Q
How would acute coronary syndrome be differentiated?
A
12 lead ECG to assess for ST elevation, then troponin testing
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)
25
Describe the management of NSTEMI.
- 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
26
Describe the drug treatment of STEMI, when balloon time is < 120 minutes.
- aspirin 300mg
- prasugrel
- PCI + drugs (UFH + GpIIb/IIIa inhibitor if radial access used for PCI)
27
What do ticagrelor, prasugrel, and clopidogrel do?
Stop ADP binding to platelets
28
Describe PCI.
- 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
29
Describe the mechanisms and indication for CABG.
- 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
30
Which drug(s) should be given between thrombolysis and PCI?
Enoxaparin or UFH
31
--- complications after MI ---
Describe the complications that may arise after MI and their timecourse,
- 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
32
--- bradyarrhythmia ---
Which three arrhythmias are bradycardic?
Sinus bradycardia, sick sinus syndrome, tachy-brady syndrome
33
Describe sick sinus syndrome.
Can result in sinus arrest, escape beats, and tachy-brady syndrome
34
Describe the types of AV block.
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
35
Describe the ECG patterns that may be seen in right bundle branch block.
rSR' on V1-V2, broad S wave on I, V5, V6
36
Describe the ECG patterns that may be seen in left bundle branch block.
I, aVL, V6 - broad R, ST depression. V1-V3 - broad QS
37
Describe hemiblock.
Causes axis deviation - left anterior -> left, posterio-inferior -> right.
38
Describe bifasicular block.
Same as right BBB + a deep S wave on III, aVF.
39
Describe AVNRT.
Micro-reentry (within AVN itself). ECG shows no clear P waves with rapid QRS complexes.
40
Describe AVRT. What is it otherwise known as?
Macro-reentry (branching the atria and ventricles). P waves occur AFTER the QRS complex. Wolff-Parkinson-White syndrome
41
What would atrial fibrillation show on the ECG?
F waves - i.e. never isoelectric. Irregularly irregular rhythm
42
What would atrial flutter show on the ECG?
Saw tooth pattern, limited transmission to ventricles (e.g. QRS complex)
43
Name the six main supraventricular tachyarrhythmias.
AVNRT, AVRT, AF, atrial flutter, atrial tachycardia, atrial ectopic beats
44
Describe how supraventricular tachyarrhythmias should be treated.
Haemodynamic instability -> emergency cardioversion. Stability -> vagal maneuvres then adenosine if that doesn't work.
45
Which two ventricular tachyarrhythmias are life-threatening and may lead to cardiac arrest? Describe the main clinical sign
Ventricular fibrillation, ventricular tachycardia. Pulseless
46
Describe Brugada syndrome.
Idiopathic ST elevation with pseudo-RBBB. No structural cause
47
Describe long QT syndrome.
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)
48
Which three ventricular tachyarrhythmias may be normal/transient?
Normal heart ventricular tachycardia, non-sustained ventricular tachycardia, ventricular premature beats?
49
--- Vascular ---
Describe the classification of PAD (peripheral arterial disease).
- 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
Describe the presentation and main differentials of intermittent claudication (IC).
- 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
Describe the management of intermittent claudication (IC).
- 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
Describe the aetiologies of acute limb-threatening ischaemia (ALTI).
- 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
Describe the classification of acute limb-threatening ischaemia (ALTI).
- 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
Describe the assessment and management plan of acute limb-threatening ischaemia (ALTI).
- 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
Describe the classification of acute thoracic aortic syndrome (ATAS).
ATAS are a group of conditions affecting the thoracic aorta, and include
- aortic dissection
- intramural haematoma (IMH)
- penetrating aortic ulcer (PAU)
56
Describe the risk factors for ATAS.
- 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
Describe the pathology, presentation, and classification of aortic dissection.
- 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
Describe the management of aortic dissection.
- 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
What causes varicose veins?
High pressure in the saphenous vein by obstruction/valve incompetence forces blood into superficial veins. This creates dilated and tortous veins
60
Describe the 6 venous skin changes observed with varicose veins.
- 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
Describe the management of varicose veins and their complications.
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
Which scoring system is used to identify risk for pressure ulcers?
Waterlow risk assessment score
(others include Braden, Walsall, Maelor scores)
63
--- further vascular cards ---
64
--- congestive heart failure ---
Name and describe the two main types of heart failure, in combination with the ejection fraction.
- 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
What are the main presenting complaints of heart failure?
- left-sided: pulmonary oedema (dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea)
- right-sided: peripheral oedema, hepatomegaly, ascites, raised JVP
66
Describe the classical CXR findings of congestive heart failure.
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
Describe the investigation pathway of a patient with suspected heart failure.
- 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
Which drugs should be used in HFrEF?
- 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
Describe the presentation of acute heart failure.
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
Describe the management of acute heart failure.
*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
--- arrhythmia ---
Which heart rhythms are shockable?
VF/pulseless VT
72
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?
Precordial thump
73
What are the main associations of all valvular heart disease?
Exertional dyspnoea, syncope/dizziness, JVP, oedema, cardiomegaly/LVH (displaced apex), hepatic congestion
74
Which two scales are used to give a quick overview of a patient's murmur?
NYHA, Murmur grading
75
Describe the NYHA scale.
I - no limitation, II - slight limit, III - marked limitation of less than normal activity, IV - severe limitation
76
Describe the murmur grading scale.
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
Which valvular disease is most common?
Aortic stenosis
78
Describe aortic stenosis as a murmur and its main symptoms.
Ejection systolic murmur, radiates to carotids. Dyspnoea, chest pain, syncope.
79
What are the primary treatment options for aortic stenosis?
Valve replacement (mechanical v bio-prosthetic), TAVI (transcatheter aortic valve implantation - only if patient can't have sternotomy)
80
Describe mitral regurgitation as a murmur and its primary symptoms.
Pansystolic, radiates to axilla. Insidious dyspnoea, oedema, fatigue
81
What are the main treatment options for mitral regurg?
Repair prolapse, replace degenerated (very poor only), mitroclip in infancy, ACEi/diuretics
82
Describe mitral stenosis as a murmur and its main symptoms.
Mid-diastolic, located to apex. Dyspnoea, fatigue, palpitation (AF only)
83
What is the pathology of mitral stenosis?
Rheumatic fever
84
What are the treatment options for mitral stenosis?
Diuretics, treat AF. Surgery, balloon valvuloplasty. Warfarin if also AF.
85
Describe aortic regurg as a murmur and its main symptoms and signs.
Early diastolic radiating to left sternal edge. Dyspnoea, collapsing pulse, wide pulse pressure, displaced apex
86
What are the main treatment options for aortic regurg?
ACEi, valve replacement.
87
Which conditions can cause constant murmurs?
Patent ductus arteriosus, septal defects.
88
What may trigger TdP in long QT syndrome?
Exercise, loud noises, sleep, medication
89
What should be used to treat long QT syndrome?
B-blockers, avoid stimulation
90
What may trigger Brugada syndrome?
Sleep, fever, excessive food/alcohol
91
What should be used to treat Brugada syndrome?
Anti-pyretics, ICDs, avoid triggers
92
--- endocarditis ---
What is bacteraemia?
Presence of bacteria in the blood
93
Which four main organisms are associated with ICDs?
Staph aureus, staph epidermidis, corynebacterium sp., propionibacterium acnes
94
Describe the pathology which causes infective endocarditis.
Damage to valves, turbulent blood flow displaces fibrin and bacteraemia settles.
95
How may infective endocarditis spread in the body?
Bacteraemia is friable.
96
What are the main gram positive bacteria which cause infective endocarditis?
Staph aureus, viridans, enterococcus sp, staph epidermidis
97
What are the main gram negative bacteria which cause infective endocarditis?
HACEK - haemophilus, aggregatobacter, cardiobacterium, eikelleum, kingella
98
What are the atypical organisms that cause IE?
Bartonella, coxiella burnetti, chylamydia, fungi
99
Describe the viridans organisms which cause IE.
Alpha-haemolytic (green) - strep mitis, strep salivarius, strep mutans, strep sanguinis
100
What are the major Duke criteria?
2 seperate positive blood cultures, endocardial involvement (i.e. new valve disease)
101
What are the minor Duke criteria?
Predisposition, fever, vascular phenomena, immunologic phenomena, minor microbiological evidence
102
Describe the necessary Duke criteria required to define 'definitive' vs 'possible' IE.
Definitive - 2M, 1M + 3m, 5m. Possible - 1M + 1m, 3m
103
How is acute IE presented?
Overwhelming sepsis, cardiac failure
104
What are some of the features of sub-acute IE?
Fever, malaise, weight loss, tiredness, dyspnoea, splinter haemorrhage, hepatomegaly, Roth spots, Janeway lesions, Osler Nodes etc
105
Describe the scan use to diagnose IE?
Transthoracic echo if suspicion, transoesophageal echo if transthoracic has high risk
106
Describe the empirical treatment of IE.
Native (i.e. viridans) - amoxicillin, gentamicin
Prosthetic valve - vancomycin, gentamycin, add in rifampicin day 3
PWIDs - flucloxacillin
107
Describe the specific treatment of the major bacteria of IE.
Staph aureus (not MRSA) - flucloxacillin
Viridans - benzylpenicllin, gentamicin
Enterococcus - amoxicillin/vancomycin, gentamicin
Staph epidermidis - vancomycin, gentamicin, rifampicin
108
Name three non-infective causes of endocarditis.
Rheumatic heart disease, non-bacterial thrombotic, Libman-Sacks (lupus)
109
--- inflammatory cardiac ---
What is myocarditis and what are its main causes?
Inflammation of the myocardium - coxsackie A/B and echovirus
110
Describe what histology of rheumatic heart disease and myocarditis may show.
Aschoff bodies
111
Name two causes of non-infectious pericarditis.
Dressler's (post-MI) and uraemic (liver failure)
112
--- cardiac tumours ---
What is a carcinoid tumour?
One of the neuroendocrine cells
113
What signs may indicate a carcinoid tumour?
Excess chemical secretion, flushing, nausea, vomiting, right side heart valve disease
114
Although cardiac tumours are rare, which is the most common primary tumour?
Atrial myxoma
115
Describe the important aspects of history taking in syncope.
- 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
Describe the initial investigations for syncope.
- cardiovascular and respiratory examinations
- 12-lead ECG
- bloods (e.g. TFTs, FBC)
117
Name the red flag factors for urgent referral to a cardiologist regarding syncope.
- 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
Describe the investigations used for syncope.
- 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
Describe the initial management of a patient with ACS.
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
name the coronary territories, and the association between ECG leads and coronary arteries.
- 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
Describe the management of a STEMI patient who has undergone thrombolysis therapy.
- 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
