1
Q
Describe the ECG waveform:
A
- P waves represent atrial depolarisation
- PR interval represents time taken for electrical activity to travel from atria to ventricles
- QRS complex represents depolarisation of the ventricles
- ST segment is an isoelectric line that represents time between depolarisation and re-polarisation of the ventricles (ie contraction)
- T wave represents ventricular re-polarisation
- QT interval is the time it takes ventricles to depolarise and re-polarise
2
Q
Where are ECG electrodes placed?
A
6 chest electrodes: - V1 at 4th IC space, right sternal edge - V2 at 4th IC space, left sternal edge - V3 midway between V2 and V4 - V4 at 5th IC space on the midclavicular line - V5 left anterior axillary line, same horizontal level as V4 - V6 left mid-axillary line, same horizontal level as V4,5 Limb electrodes: - LA - RA - LL - RL
3
Q
Outline the systematic approach to ECG interpretation:
A
- Before you get traces:
- always ask for clinical context
- check date, time and patient
- assess technical quality (artefact/speed/gain) - Look at the rhythm strip
- check the QRS rate/ECG intervals
- identify P/QRS/T and determine rhythm - Look at the limb leads
- determine the QRS axis - Look across all leads
- P/QRS/T morphology
4
Q
What is a normal cardiac rhythm?
A
- Normal QRS rate
- Regular QRS complexes
- Usually narrow QRS
- P waves present
- 1:1 P:QRS relation
5
Q
How do you recognise abnormal cardiac rhythms?
A
What is the QRS rate? Are the QRS complexes regular? Is the QRS broad or narrow? Are there P waves What is the P:QRS relation
6
Q
What does acute MI look like on ECG?
A
ST elevation in acute coronary occlusion
Reciprocal ST depression
7
Q
Describe the hierarchy of evidence in cardiology:
A
Classes of recommendations;
- Class I; evidence and/or general agreement that a given treatment or procedure is beneficial, useful and effective
- Class II; conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of the given procedure
-class IIa; weight of evidence/opinion is in favour of usefulness/efficacy
- class IIb; usefulness/efficacy is less well established by evidence/opinion
- Class III; evidence or general agreement that the given treatment or procedure is not useful/effective, and in some cases may be harmful
Also level of evidence A,B or C
8
Q
Describe the pathophysiology of HF:
A
- Failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of tissues
- Characterised by haemodynamic changes (e.g. systemic vasoconstriction) and neurohumeral activation
- Common causes include coronary artery disease (MI and muscle atrophy), hypertension (compensatory hypertrophy and dilatation of ventricular myocardium), toxins and degenerative valve disease
9
Q
What are the main types of heart failure?
A
HF-REF
- younger
- more often male
- coronary aetiology
HF-PEF
- older
- more often female
- hypertensive aetiology
Chronic
- present for a period of time
- may have been acute or may become acute
Acute
- usually admitted to hospital
- worsening of chronic
- new onset ('de novo')
10
Q
Describe the clinical presentation of HF:
A
Symptoms: - dyspnoea (orthopnoea, PND) & cough - ankle swelling (also legs/abdomen) - fatigue/tiredness Signs: - peripheral oedema (ankles, legs, sacrum, abdomen) - elevated JVP - third heart sound - displaced apex beat (cardiomegaly) - pulmonary oedema (lung crackles) - pleural effusion
11
Q
What is the New York Heart Association functional classification of HF?
A
NYHA
Class I: no symptoms and no limitation in ordinary physical activity, e.g. SOB when walking, climbing stairs
Class II: mild symptoms (mild SOB and/or angina) and slight limitation during ordinary activity
Class III: marked limitation in activity due to symptoms even during less-than-ordinary activity (e.g. walking short distances, comfortable only at rest)
Class IV: severe limitations. Experiences symptoms even while at rest- mostly bed-bound patients
12
Q
What are the main drugs used to treat HF?
A
- Beta-blocker and ACE inhibitor (renin-angiotensin system blockade)
- Mineralocorticoid receptor antagonist
- Sacubutril/valsartan (angiotensin II receptor antagonist)
- Ivabradine (acts on If ion current in SA node)
- Digoxin (inhibition of Na/K ATPase mainly in myocardium)
- Diuretics to treat oedema
13
Q
What are some non-pharmacological treatments of HF?
A
- Implantable defibrillator
- Heart transplantation
- Ventricular assist devices
14
Q
What are the radiological signs of HF in stage 1?
A
- Redistribution of pulmonary vessels; upper zone vessels are greater than equivalent lower zone vessels
- Cardiomegaly, measured from midline to each widest side of heart
15
Q
What are the radiological signs in stage 2 HF?
A
- Interstitial oedema
- sub-pleural pulmonary oedema
- fluid can accumulate in the loose CT beneath the visceral pleura
- seen as a sharply defined band of increased density
- sub-pleural pulmonary oedema
- Kerley lines
- B lines
- septal lines
- seen at the bases perpendicular to the pleural surface
- if transient or rapidly developing, almost diagnostic of interstitial pulmonary oedema
- Peribronchial cuffing
- normally walls of bronchi are invisible
- when fluid collects in peribronchial interstitial space the bronchial walls become visible
- Hazy contours of vessels
- vessels not only enlarge but lose their defined margin due to surrounding oedema
- Thickened interlobar fissures
16
Q
What are the radiological signs in stage 2 HF?
A
- Interstitial oedema
- sub-pleural pulmonary oedema
- fluid can accumulate in the loose CT beneath the visceral pleura
- seen as a sharply defined band of increased density
- sub-pleural pulmonary oedema
- Kerley lines
- B lines
- septal lines
- seen at the bases perpendicular to the pleural surface
- if transient or rapidly developing, almost diagnostic of interstitial pulmonary oedema
- Peribronchial cuffing
- normally walls of bronchi are invisible
- when fluid collects in peribronchial interstitial space the bronchial walls become visible
- Hazy contours of vessels
- vessels not only enlarge but lose their defined margin due to surrounding oedema
- Thickened interlobar fissures
17
Q
What are the radiological signs in stage 3 HF?
A
- Alveolar oedema
- represents spill of fluid from interstitium into alveolar spaces resulting in airspace opacity
- bilateral usually
- if unilateral, predisposition for right lung
- Bat’s wing or butterfly distribution
- rapid change
- Pleural effusions
- transudates and exudates
18
Q
What are the radiological signs in stage 3 HF?
A
- Alveolar oedema
- represents spill of fluid from interstitium into alveolar spaces resulting in airspace opacity
- bilateral usually
- if unilateral, predisposition for right lung
- Bat’s wing or butterfly distribution
- rapid change
- Pleural effusions
- transudates and exudates
- Consolidation
- Air bronchogram
- Cottonwool appearance
- Pleural effusions
19
Q
What abnormalities affect heart valves?
A
Valve leaflets: calcification, thickening, degeneration, infection, prolapse
Apparatus/annulus: annular dilatation, annular calcification, apparatus tethering/thickening/rupture, regional wall motion abnormality
20
Q
What is the difference between stenosis and regurgitation?
A
Stenosis= pressure overload Regurgitation= volume overload
21
Q
What is the pathogenesis of aortic stenosis?
A
- Causes: thickening, calcification, rheumatic valve disease, congenital
- Increased LV cavity pressure
- Pressure overload- LV hypertrophy
- Symptoms: SOB, presyncope, syncope, chest pain, reduced exercise capacity
22
Q
What is the pathogenesis of aortic regurgitation?
A
- Causes: degeneration, rheumatic valve disease, aortic root dilatation, systemic disease (Marfan’s syndrome, Ehlers Danlos syndrome, Anklyosing Spondylitis, SLE), endocarditis
- Volume overload with LV dilatation
- Symptoms: SOB, reduced exercise capacity
23
Q
What is the pathogenesis of mitral stenosis?
A
- Causes: rheumatic valve disease, pressure overload, dilated LA, atrial fibrillation, pulmonary hypertension, secondary right heart dilatation
- Symptoms: SOB, palpation, chest pain, haemoptysis, right heart failure symptoms
24
Q
What is the pathogenesis of mitral regurgitation?
A
- Causes: multifactorial (leaflets, annulus, apparatus), volume overload (LA/LV), LV and LA dilatation, pulmonary hypertension, secondary right heart dilatation, AF
- Symptoms: SOB, palpitation, right heart failure symptoms
25
How are common valvular lesions investigated?
- History
- Examination
- Blood pressure
- ECG
- Exercise tolerance test
- CPET
- Stress echo
- Echo, CT, MRI
- Left heart catheterisation/right heart catheterisation
26
What is bicuspid aortic valve?
- 1-2% prevalence
- Prone to premature dysfunction
- Associated with aortic abnormalities
- Genetic component (~10%)
27
How are common valvular lesions treated?
- Medication
- Intervention
- surgical
- valve repair
- valve replacement (mechanical vs tissue valve)
- procedural
- TAVI
- Mitraclip
- Valvuloplasty
28
What are the clinical features of endocarditis?
- Classified as native valve endocarditis (NVE), endocarditis in IVDUs or prosthetic valve endocarditis (PVE)
-
29
Discuss microbiology of organisms in IE:
- NVE most commonly caused by S. viridans of Streptococcus species
- IVDU IE most commonly caused by S. aureus, gram negative organisms (not HACEK) and fungi
- PVE most commonly caused by CoNS of staphylococcus species, gram negative organisms and fungi
30
What are the general clinical features of endocarditis?
- Classified as native valve endocarditis (NVE), endocarditis in IVDUs or prosthetic valve endocarditis (PVE)
- Common- 3 times more common in men and increasing in elderly patients
- Acute
- toxic presentation
- progressive valve destruction and metastatic infection developing in days to weeks
- most commonly caused by S. aureus
- Subacute
- Mild toxicity
- Presentation over weeks to months
- Rarely leads to metastatic infection
- Most commonly Strep. viridans or enterococcus
31
Outline the diagnosis of IE:
- 3 sets of blood cultures required, before antibiotics
- Diagnosis with echo (transthoracic- 50% sensitivity- or transoesophageal- 85-100% sensitivity)
- Duke criteria required: 2 major, 1 major and 3 minor or 5 minor
32
Describe clinical features of IE:
1. Early manifestations of infection
- Incubation period = 2 weeks
- longer in PVE
- Fever + murmur = IE until proven otherwise
- fever is most common sign, may be absent in elderly
- murmur present in 80-85%
- fatigue and malaise
2. Embolic events
- Can take days-weeks to occur, seen earlier in acute endocarditis
- Small emboli: petechiae, splinter haemorrhages, haematuria
- Large emboli: CVA, renal infarction
- Right sided endocarditis- septic pulmonary emboli
3. Long term effects
- Immunological reaction: splenomegaly, nephritis, vasculitic lesion of skin and eye, clubbing
- Tissue damage: valve destruction, valve abscess
33
Discuss treatment of IE:
- Medical; antimicrobial therapy
- treatment tailored to organism susceptibility
- NVE: 4 week duration
- PVE: 6 week duration
- Indications for surgical intervention
1. HF
2. Uncontrollable infection
- abscess
- persisting fever + positive blood cultures >7days
- infection caused by multi-drug resistant organisms
3. Prevention of embolism
- large vegetations + embolic episode
34
What can chest Xray be used for in cardiology?
- Cardiac silhouette
- size
- position
- Pulmonary vasculature
- Great vessels
- Pulmonary oedema
- Pleural effusions
35
Describe the use of echocardiography in cardiology:
```
Indications
- structure + function of heart
- valve assessment
- pericardial assessment
- assess inducible ischaemia (stress)
Pros
- cheap, available portable, no radiation
Cons
- requires good acoustic window
- user dependent
```
36
Describe the use of nuclear perfusion imaging in cardiology:
```
Indications
- assess ischaemia
- assess ejection fraction
Pros
- availability
Cons
- radiation
- no structural assessment
```
37
Describe the use of cardiac CT:
```
Indications
- coronary artery anatomy
- great vessel anatomy
Pros
- good 'rule out' for CAD
- low risk
Cons
- radiation dose
- requires low heart rate
- no functional assessment of ischaemia
```
38
Describe the use of invasive angiography in cardiology:
```
Indications
- ischaemia
- primary PCI
- valve assessment
- assessment ventricular pressure (R+L)
Pros
- gold standard, option for intervention during same procedure and availability
Cons
- radiation
- risks- CVA, MI, contrast reaction, bleeding, death
```
39
Describe the use of CMRI in cardiology:
```
Indications
- assess structure and function
- perfusion/stress
- assess great vessels
- tissue characterisation
- infiltrative cardiomyopathies
- previous infarction
Pros
- gold standard LV assessment
- reproducible
- no radiation
Cons
- cost
- availability
- claustrophobia
- pacemakers
```
40
What is troponin?
Part of the cardiac myocyte, release into blood stream is a marker of cardiac necrosis
41
What are the types of MI?
Type 1: spontaneous MI due to a primary coronary event
Type 2: increased oxygen demand or decreased oxygen supply (HF, sepsis, anaemia, arrhythmias, hypertension, or hypotension)
Type 3: sudden cadmic death
Type 4a: associated with PCI
Type 4b: MI stent thrombosis documented by angiography or PM
Type 5: MI associated with CABG
42
What is unstable angina?
Acute coronary event without a rise in troponin
| - ie clinical presentation of an MI + ECG changes, or tight narrowings on coronary angiography
43
What are the different ECG patterns in STEMI?
ST elevation reflects occlusion of a coronary artery
- occurs in regional patterns
Posterior infarct
- location means ST elevation not seen
Left bundle branch block
- if new can indicate infarction
- if old can obscure ST elevation during an infarct
44
Which locations of ST elevation on ECG correspond to which occluded coronary arteries?
ST elevation correlates to the territory of occluded artery
```
Inferior= RCA (mostly) or LCx
Posterior= Cx (mostly) or RCA
Lateral= LCx
Anteroseptal= LAD
```
45
Describe posterior infarct:
Posterior infarct may be caused by LCx (or RCA)
| - often associated with inferior or lateral ST elevation
46
How is STEMI immediately managed?
- DRS ABCD
- Put in ambulance attached to defibrillator
- Aspirin PO
- Unfractionated heparin IV
- Morphine + anti-emetics
- Clopidogrel, in ambulance
- Ticagrelor, in hospital
- Activate PPCI team at GJNH
47
How is STEMI subsequently managed?
- Monitor in coronary care unit for complications of MI
- Drugs for secondary prevention:
- ACE inhibitors
- beta-blockers
- statins
- eplerenone; only for diabetics and LVSD or clinical HF
- Echo for LV function and cardiac structure
- Cardiac rehabilitation
- If LVSD >9 months consider primary prevention ICD
48
What are the complications of MI?
- Arrhythmias
- VT/VF
- AF (HF/LVSD)
- HF
- diuretics, inotropes, vasodilators
- Cardiogenic shock
- IABP (intra-aortic balloon pump, ventricular assist device)
- Myocardial rupture
- septum- VSD, surgery
- papillary muscle- mitral regurgitation, sugary
- free wall- tamponade, usually fatal
- Psychological
- anxiety/depression
- cardiac rehabilitation
49
How does subsequent management of NSTEMI differ from STEMI?
Given aspirin; clopidogrel or ticagrelor; LMWH or fondaparinux
50
What are the symptoms of MI?
- Chest pain
- Back pain
- Jaw pain
- Indigestion
- Sweatiness, clamminess
- SOB
- None (in diabetes/dementia)
- Death
51
What are the signs of MI?
- Tachycardia
- Distressed patient
- HF (crackles/raised JVP)
- Shock
- Arrhythmia
- None
52
What is ASD?
- Hole in the atrial wall; 4 main types: primum, secundum, sinus venosus and coronary sinus
- May lead to;
- RV dilatation and failure
- tricuspid regurgitation
- atrial arrhythmias
- pulmonary hypertension
- eisenmenger syndrome
53
What is coarctation of the aorta?
- Narrowing of the aorta, usually after the LSA, forms in a juxta-ductal position
- Highly variable severity; can cause limb cyanosis if pre-ductal and may cause upper body hypertension, Berry aneurysms, claudication and renal insufficiency
54
How is coarctation of aorta treated?
Surgical repair via thoracotomy;
- subclavian flap
- end to end
- jump graft
55
What is transposition of the great arteries?
Aorta and PAs switched position- cyanotic lesion. Incompatible with life unless surgically treated immediately after birth
56
How is transposition of great arteries treated?
Surgery:
- atrial switch
- systemic RV
- dilatation RV, tricuspid regurgitation, HF and atrial arrhythmias
- arterial switch
- systemic LV
- coronary artery complications
57
What comprises the teratology of Fallot?
1. VSD
2. Overriding aorta
3. RVOT obstruction
4. RV hypertrophy
58
How is teratology of Fallot treated and what are the complications of repair?
```
BT shunt (obsolete) or complete repair
Complications:
- significant pulmonary regurgitation
- RV dilatation +/- dysfunction
- arrhythmia
- particularly ventricular tachycardia
- pulmonary arterial/branch PA stenoses
```
59
What is Fontan circulation?
- Single functional ventricle is used to support systemic circulation, with IVC and SVC plumbed into the pulmonary arteries bypassing the heart altogether
- Dependent on high systemic venous pressure and low pulmonary vascular resistance, anything that causes an imbalance can cause catastrophic haemodynamic compromise (PE, arrhythmia, dehydration or bleeding)
60
What causes hypertension?
Genetic influences and environmental factors causing:
- defects in renal sodium homeostasis
- functional vasoconstriction
- defects in vascular smooth muscle growth and structure
Increasing both cardiac output, and total peripheral vascular resistance causing hypertension
61
How is hypertension investigated?
Diagnosis should be made over at least two readings, five minutes between readings over at least 2 visits
Also out of office BP measurement;
- 24 hour ambulatory BP measurement
- home BP pressure monitoring
Also need to investigate for end-organ damage: U&Es, glucose/HbA1c, lipid profile, TFTs, LFTs, urine dipstick, ECG
62
What are the complications of hypertension?
End-organ damage: cardiovascular or renal disease
63
What are the pharmacological treatments for hypertension?
```
Diuretics
- loop
- thiazide
- potassium sparing
ACE inhibitors
Vasodilators
- calcium chanel blockers
- beta blockers
- alpha blockers
Others
- e.g. methyldopa, hydralazine, monoxidine
```
Often more than one drug required- A then A+C then A+C+D
64
What is AF, and what causes it?
```
Cardiac arrhythmia, random contraction of the atrium
Conditions predisposing;
- hypertension
- HF
- valvular heart disease
- cardiomyopathies
- atrial septal defect and other congenital heart defects
- coronary artery disease
- thyroid dysfunction
- obesity
- diabetes mellitus
- COPD
- chronic renal disease
```
65
What investigations are used in the diagnosis of AF?
- Irregularly irregular pulse
| - Confirmed with 12 lead ECG
66
What investigations are used in the diagnosis of AF?
- Irregularly irregular pulse
| - Confirmed with 12 lead ECG, echo, TFTs, LFTs
67
How can AF be treated pharmacologically?
Rate control:
- Target HR <110/min, if still symptomatic aim for <80/min
- Patients without HF should be started on a beta-blocker or rate limiting Ca++ antagonist
- Digoxin as a second line
Rhythm control:
- Particularly for younger patients, and patients with ongoing symptoms despite good rate control
- Class 1 (Na+ channel blockers)
- Class 3 (K+ channel blockers, prolong action potential duration/QT interval)
- amiodarone
- Multichannel blockers
- dronedarone
- Often used in combination with a beta-blocker
68
What are the complications of AF and how can they be treated?
Significant risk of stroke, especially if pt has had previous stroke, TIA or age >75
Treated with anti-coagulation; warfarin or NOAcs
Phase 3
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