Week 5 Flashcards

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
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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
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3
Q

Outline the systematic approach to ECG interpretation:

A
  1. Before you get traces:
    - always ask for clinical context
    - check date, time and patient
    - assess technical quality (artefact/speed/gain)
  2. Look at the rhythm strip
    - check the QRS rate/ECG intervals
    - identify P/QRS/T and determine rhythm
  3. Look at the limb leads
    - determine the QRS axis
  4. Look across all leads
    - P/QRS/T morphology
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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
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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
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6
Q

What does acute MI look like on ECG?

A

ST elevation in acute coronary occlusion

Reciprocal ST depression

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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

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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
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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')
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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
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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

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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
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13
Q

What are some non-pharmacological treatments of HF?

A
  • Implantable defibrillator
  • Heart transplantation
  • Ventricular assist devices
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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
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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
  • 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
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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
  • 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
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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
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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
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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

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20
Q

What is the difference between stenosis and regurgitation?

A
Stenosis= pressure overload
Regurgitation= volume overload
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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
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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
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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
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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
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25
Q

How are common valvular lesions investigated?

A
  • History
  • Examination
  • Blood pressure
  • ECG
  • Exercise tolerance test
  • CPET
  • Stress echo
  • Echo, CT, MRI
  • Left heart catheterisation/right heart catheterisation
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26
Q

What is bicuspid aortic valve?

A
  • 1-2% prevalence
  • Prone to premature dysfunction
  • Associated with aortic abnormalities
  • Genetic component (~10%)
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27
Q

How are common valvular lesions treated?

A
  • Medication
  • Intervention
    • surgical
      • valve repair
      • valve replacement (mechanical vs tissue valve)
    • procedural
      • TAVI
      • Mitraclip
      • Valvuloplasty
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28
Q

What are the clinical features of endocarditis?

A
  • ## Classified as native valve endocarditis (NVE), endocarditis in IVDUs or prosthetic valve endocarditis (PVE)
29
Q

Discuss microbiology of organisms in IE:

A
  • 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
Q

What are the general clinical features of endocarditis?

A
  • 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
Q

Outline the diagnosis of IE:

A
  • 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
Q

Describe clinical features of IE:

A
  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
Q

Discuss treatment of IE:

A
  • 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
      1. Prevention of embolism
    • large vegetations + embolic episode
34
Q

What can chest Xray be used for in cardiology?

A
  • Cardiac silhouette
    • size
    • position
  • Pulmonary vasculature
  • Great vessels
  • Pulmonary oedema
  • Pleural effusions
35
Q

Describe the use of echocardiography in cardiology:

A
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
Q

Describe the use of nuclear perfusion imaging in cardiology:

A
Indications
- assess ischaemia
- assess ejection fraction
Pros
- availability
Cons
- radiation
- no structural assessment
37
Q

Describe the use of cardiac CT:

A
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
Q

Describe the use of invasive angiography in cardiology:

A
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
Q

Describe the use of CMRI in cardiology:

A
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
Q

What is troponin?

A

Part of the cardiac myocyte, release into blood stream is a marker of cardiac necrosis

41
Q

What are the types of MI?

A

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
Q

What is unstable angina?

A

Acute coronary event without a rise in troponin

- ie clinical presentation of an MI + ECG changes, or tight narrowings on coronary angiography

43
Q

What are the different ECG patterns in STEMI?

A

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
Q

Which locations of ST elevation on ECG correspond to which occluded coronary arteries?

A

ST elevation correlates to the territory of occluded artery

Inferior= RCA (mostly) or LCx
Posterior= Cx (mostly) or RCA
Lateral= LCx
Anteroseptal= LAD
45
Q

Describe posterior infarct:

A

Posterior infarct may be caused by LCx (or RCA)

- often associated with inferior or lateral ST elevation

46
Q

How is STEMI immediately managed?

A
  • 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
Q

How is STEMI subsequently managed?

A
  • 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
Q

What are the complications of MI?

A
  • 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
Q

How does subsequent management of NSTEMI differ from STEMI?

A

Given aspirin; clopidogrel or ticagrelor; LMWH or fondaparinux

50
Q

What are the symptoms of MI?

A
  • Chest pain
  • Back pain
  • Jaw pain
  • Indigestion
  • Sweatiness, clamminess
  • SOB
  • None (in diabetes/dementia)
  • Death
51
Q

What are the signs of MI?

A
  • Tachycardia
  • Distressed patient
  • HF (crackles/raised JVP)
  • Shock
  • Arrhythmia
  • None
52
Q

What is ASD?

A
  • 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
Q

What is coarctation of the aorta?

A
  • 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
Q

How is coarctation of aorta treated?

A

Surgical repair via thoracotomy;

  • subclavian flap
  • end to end
  • jump graft
55
Q

What is transposition of the great arteries?

A

Aorta and PAs switched position- cyanotic lesion. Incompatible with life unless surgically treated immediately after birth

56
Q

How is transposition of great arteries treated?

A

Surgery:

  • atrial switch
    • systemic RV
      • dilatation RV, tricuspid regurgitation, HF and atrial arrhythmias
  • arterial switch
    • systemic LV
      • coronary artery complications
57
Q

What comprises the teratology of Fallot?

A
  1. VSD
  2. Overriding aorta
  3. RVOT obstruction
  4. RV hypertrophy
58
Q

How is teratology of Fallot treated and what are the complications of repair?

A
BT shunt (obsolete) or complete repair 
Complications:
- significant pulmonary regurgitation
   - RV dilatation +/- dysfunction
- arrhythmia
  - particularly ventricular tachycardia
- pulmonary arterial/branch PA stenoses
59
Q

What is Fontan circulation?

A
  • 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
Q

What causes hypertension?

A

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
Q

How is hypertension investigated?

A

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
Q

What are the complications of hypertension?

A

End-organ damage: cardiovascular or renal disease

63
Q

What are the pharmacological treatments for hypertension?

A
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
Q

What is AF, and what causes it?

A
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
Q

What investigations are used in the diagnosis of AF?

A
  • Irregularly irregular pulse

- Confirmed with 12 lead ECG

66
Q

What investigations are used in the diagnosis of AF?

A
  • Irregularly irregular pulse

- Confirmed with 12 lead ECG, echo, TFTs, LFTs

67
Q

How can AF be treated pharmacologically?

A

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
Q

What are the complications of AF and how can they be treated?

A

Significant risk of stroke, especially if pt has had previous stroke, TIA or age >75

Treated with anti-coagulation; warfarin or NOAcs