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Phase 3 > Wk5 - Cardiology > Flashcards

Wk5 - Cardiology Flashcards

1
Q

An ECG is a recording of the…

A

electrical activity of the heart from the skin.

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2
Q

A systematic approach to any ECG…

A 
1. Before you get to the traces:
Always ask for clinical context
Check date, time and patients
Assess tehcnical quality (artefact/speed/gain)
2. Look at the rhythm strip:
Check the QRS rate/ECG intervals
Identify P/QRS/T and determine the rhythm
3. Look at the limb leads:
Determine the RS axis
4. Look across all leads
P/QRS/T morphology
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3
Q

How to determine heart rate on an ECG

A

300 divided by the number of large squares between each QRS complex
e.g. 1 square = 300/min
2 sqaures = 150/min
3 squares = 100/min

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4
Q

Normal ranges for ECG intervals

A

PR interval <1 large square (<200ms)
QRS complex <3 small squares (<120ms)
QT interval <11 small squares (<440ms)

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5
Q

What questions to ask yourself when determining the ryhtym on an ECG

A 
Whats 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

P/QRS/T morphology

A

The normal P wave is positive in the inferior leads
The normal ST segment is flat
The normal T wave has the same polarity as the QRS (goes in the same direction)

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7
Q

Describe classes of guideline recommendations

A

Class I - evidence/agreement that a given treatment or procedure is beneficial, useful, effective - It is recommended
Class II - Conflicting evidence and/or divergence of opinion anout the usefulness/efficacy of a treatment or procedure
Class IIa - weight of evidence/opinion is in favour of usefulness/efficacy - should be considered
Class IIb - usefulness/efficacy is less well established by evidence/opinion
Class III - evidence or general agreement that the treatment or procedure is not useful/effective, and in some cases may be harmful

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8
Q

What is a clinical trial?

A

A clinical trail is an evaluation of a new therapeutic intervention (drug, device, procedure, surgery) in human volunteers.
Human volunteers may be healthy or patients with a disease.
Designed to provide an unbiased, accurate, estimate of the effect of treatment

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9
Q

Definition of heart failure

A

Failure of the heart to pump blood (oxygen) at a rate sufficient to meet the metabolic requirements of the tissues - caused by an abnormality of any aspect of cardiac function and with adequate cardiac filling pressure.

It is characterised by typical haemodynamic changes (e.g. systemic vasoconstriction) and neurohumoral activation

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10
Q

Causes of heart failure

A 
Coronary artery disease (MI)
Hypertension
'Idiopathic'
Toxins (alcohol, chemotherapy)
Valve disease
Infections (virus, Chaga's)
Congenital heart disease
Pericardial disease
Endocardial disease
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11
Q

What are the 4 main types of heart failure

A

HF-REF (systolic HF)
HF-PEF (diastolic HF)
Chronic (congestive)
Acute (decompensated)

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12
Q

Describe HF-REF HF and HF-PEF HF

A

Systolic (HF-REF):
Younger, more often in male, coronary aetiology

Diastolic (HF-PEF)
Older, more often female, hypertensive aetiology

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13
Q

Describe chronic vs acute HF

A

Chronic (congestive)
Present for a period of time, may have been acute or may become acute

Acute (decompensated)
Usually admitted to hospital, worsening of chronic, new onset (de novo)

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14
Q

Pathophysiology of HF

A

Myocardial injury ->
Left ventricular systolic dysfunction ->
Perceived reduction in circulating volume and pressure ->
Neurohumoral activation (SNS, RAAS, Natriuretic peptides) ->
Systemic vasoconstriction, Renal sodium and water retention

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15
Q

Symptoms of HF

A

Dyspnoea (orthopnoea, PND) & cough
Ankle swelling (also legs/abdomen)
Fatigue/tiredness
SOB

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16
Q

Signs of HF

A 
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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17
Q

Describe the different classes of HF

A

I - no symptoms, no limitation in N physical activity
II - mild sympotms (mild SOB/angina) and slight limitation during normal activity
III - Marker limitation in activity due to symptoms (e.g. walking short distances (20-100m). COmfortable only at rest
IV - Severe limitations. Experiences symptoms even while at rest. Bedbound

II, III, IV patients have pulmonary hypertension

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18
Q

Investigations for HF

A

ECG, CXR (to exclude lung pathology, pulmonary oedema), echocardiogram, blood chemsitry (U&Es, LFTs etc.), Haematology (HB), Natriuretic peptides (BNP)

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19
Q

Diagnosing HF

A

Signs or symptoms
Clinical examination (fbc, fasting glucose, serum u&e, urinalysis, thyroid function, chest x-ray)
Natriuretic peptides - BNP/NT-proBMP (then ECG, especially if BNP not available)
Low BNP and normal ECG -> HF excluded
Raised BNP or abnormal ECG -> HF possible -> refer for echocardiography (then do ECG if not already done)

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20
Q

Treatment for chronic HF (NHYA II-IV) & MoA

A

Beta blocker AND ACE inhibitor (if cant take ACEi give ARB) - if ongoing symptoms:
MRA (added to ACEi or ARB) - if ongoing symtpoms seek specialist advice:
Sacubitril/valsartan (stop ACEi and ARBs; continue BB and MRA) - ongoing symptoms:
ICD or CRT-P/CRT-D in selected patients
Ivabradine (if sinus rhythm heart rate >75bmp)
Digoxin
Hydralazine/isosorbide dinitrate - ongoing symptoms:
Consider referral to the National Transplant Unit for assessment for LVAD/ cardiac transplantation (either Cardiac Resynchronisation Therapy (CRT) or Implatable Cardioverter-Defibrillator (ICD))

ACEi - inhibits the conversion of angiotensin I to angiotensin II. This action subsequently inhibits release from the adrenal cortex, depressing sodium and fluid retention, thereby dec. blood volume.
BB - inhibits sympathetic stimulation of the heart and renal vasculature. Blockade of the SAN reduces heart rate and blockade of the receptors in the myocardium reduces cardiac contractility. Also inhibits release of renin.
Digoxin - Inc, vagal parasympathetic activity and inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly. In an effort to remove Na+, more Ca2+ is brought into the cell by the action of Na+/Ca2+ exchangers. The buildup of Ca2+ is responsible for the inc. force of contraction and dec. rate of conduction through the AV node

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21
Q

What is given in patients with HF to help with pulmonary oedema and peripheral oedema?

MOA of thiazide diuretics?
MOA of loop diuretics?

A

Diuretics

MOA of Thiazide diuretics (e.g. Bendroflumethazide):

  • Inhibits Na+/Cl- transporter at the distal convoluted tubule and collecting duct
  • Increases Na+, Cl- and water excretion

MOA of Loop diuretics (e.g. Furosemide)

  • Na+/Cl-/K+ symporter antagonists
  • Act on the thick ascending loop of Henle
  • Increases secretion of Na+, K+, Cl- and water
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22
Q

Features of angiotensin receptor neprilysin inhibition (ARNI): LCZ696

A

LCZ696 is made up of sacubitril (a neprilysin blocker) and valsartan (an ARB)

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23
Q

What does the drug If Ivabradine do?

A

Inhibits the sinus node; reducing sinus rate and reducing hospitalisation

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24
Q

Ventricular assist devices

A

Pulsatile-Flow LVAD

Continuous-Flow LVAD

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25
Q

Signs of HF on xray in relation to stages of HF

A 
Stage 1 (PCWP 13-18mmHg) - Redistribution pulmonary vessels, cardiomegaly
2 (PCWP 18-25mmHg) - Kerley lines, peribronchial cuffing, hazy contours of vessels, thickened interlobar fissures
3 (PCWP>25mmHg) - consolidation, air bronchogram, cottonwool appearance
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26
Q

Stage 1 of congestive HF - redistribution

A

In N chest xray vessels in lower zones are larger than equivalent vessles in upper zones.
Redistribution = upper zone vessels are equal to or greater than equivalent lower zone vessels = pulmonary hypertension

Artery to bronchus ratio -

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27
Q

Cardiothoracic ratio

A

Measure widest diameter of heart and compare with diameter of the lungs (diaphragm)
Cardiothoracic ratio should be less than 0.5

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28
Q

Peribronchial cuffing is a form of what type of oedema?

A

Interstitial oedema

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29
Q

Interstitial oedema - different types

A

Kerley B line - septal lines (fluid leakage into interlobular septa); seen at bases perpendicular to the pleural surface and measure 1-2cm
Kerley A lines - caused by distension of the anastomotic channels between the peripheral and central lymphatics; Oblique lines longer thn Kerley B lines
Kerley C lines - reticular opacities at the lung bases
Peribronchial cuffing - fluid collects in peribronchial interstitial space and the bronchial walls become visible
Hazy contour of vessels - vessels enlarge and lose their defined margin due to surrounding oedema
Subpleural pulmonary oedema - fluid accumulating in the loose connective tissue beneath the visceral pleura; Seen as a sharply defined band of increased density - can sometimes resemble a pleural effusion

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30
Q

When is redistribution, alveloar vs interstitial oedema seen on xray with congestive HF?

A

Stage 1 - redistribution
Stage 2 congestive HF - intersitial oedema
Stage 3 - alveolar oedema

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31
Q

Describe features of alveolar oedema

A

Represents spill of fluid from interstitium into alveolar spaces resulting in airspace opacity.
Bilaterally usually
If unilateral predisposition for right lung
‘Bats wing’ or ‘butterfly’ distribution - prehilar shadowing that is predominantly in central positions and fades out
Rapid change

Pleural effusions - fluid between parietal and visceral layers; divided into transudates and exudates; Protein levels >30g/l, LDH>200IU consistent with exudate. pH <7.1 also suggest exudate.
Exudates:
Common: PE, Bacterial infection, Bronchial Ca
Uncommon: Fungal/viral infection, lymphoma
Transudates:
Common: LVF, cirrhosis, nephrotic syndrome
Uncommon: Fungal/viral infection, lymphoma

Subpulmonic effusion - difficult to detect as mimics contour of diaphragm. Principal sign is elevation of hemidiaphragm

In CHF 70% of pleural effusions are bilateral

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32
Q

What age are you when valves stop growing?

A

~14 years old - loose their blood supply

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33
Q

Definition of a valve

A

A device for controlling the passage of fluid through a pipe or duct, especially an automatic device allowing movement in one direction only

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34
Q

What can go wrong with valve leaflets?

A

Calcification, thickening, degeneration, infection, prolapse

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35
Q

What can go wrong with valve apparatus/annulus

A

Annular dilatation
Annular calcification
Apparatus tethering/thickening/rupture
Regional wall motion abnormality

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36
Q

Rheumatic valve disease

A

Acut rheumatic fever - painful joints, fever, rash
1-3% of strep pyogenes throat infections
Antibody cross reactivity affecting connective tissue

Cardiac injury generated by recurrent inflammation and fibrinous repair and scarring
Less prevalent in antibiotic age

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37
Q

Aortic valve

A

Lies between LV and aorta
3 cusps - trileaflet
Right, left, coronary

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38
Q

Aortic stenosis - & symptoms

A

Increased LV cavity pressure
Pressure overload - LV hypertrophy
Symptoms - SOB, presyncope, syncope, chest pain, reduced exercise capacity

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39
Q

Most common causes of aortic stenosis

A

Age related calcification in ~50%
Calcification of congenitally abnormal valve ~30-40%
Rheumatic fever ~10%

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40
Q

Most common causes of aortic regurgitation

A 
Degeneration
Rheumatic valve disease
Aortic root dilatation
Systemic disease - Marfan's syndrome, Ehlers Danlos syndrome, Ankylosing spondylitis, SLE
Endocarditis
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41
Q

Aortic regurgitation - & symptoms

A

Volume overload
LV dilatation
Symptoms: SOB, reduced exercise capacity

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42
Q

Bicuspid aortic valve

A

1-2%
Prone to premature dysfunction
Associated with aortic abnormalities
Genetic component (~10%)

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43
Q

Mitral valve

A

Lies between LA and LV
2 leaflets
Anterior and posterior

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44
Q

Commonest causes of mitral stenosis

A

Rheumatic valve disease, pressure overload, dilated LA, AF< pulmonary hypertension, secondary right heart dilatation

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45
Q

Symptoms of mitral stenosis

A

SOB, palpitation, chest pain, haemoptysis, right heart failure symptoms

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46
Q

Mitral regurgitation casues

A

Volume overload (LA/LV), LV and LA dilatation, pulmonary hypertension, secondary right heart dilatation, atrial fibrillation

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47
Q

Symptoms of mitral regurgitation

A

SOB, palpitations, right HF symptoms

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48
Q

Why concentrate on left heart disease?

A

Right heart disease is of childhood
Left - adulthood, progressive
Can live on with right heart disease in utero - due to foramen ovale and not supplying blood to the lungs

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49
Q

Tricuspid valve

A

Pulmonic valve - 3 leaflets, lies between RV and pulmonary artery
Tricuspid valve - three leaflets, lies between RA and RV

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50
Q

Treatment of valve disease

A

Medication - no medication that stops it from progressing but can control oedema, AF, hypertension etc.

Intervention: Surgical & Procedural

Surgical:
Valve repair (most often done with mitral valve (e.g. prolapse) as aortic stenosis involves calcification.
Valve replacement: Mechanical vs tissue valve

Procedural intervention:
TAVI (mainly aortic stenosis)
Mitraclip
Valvulopasty

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51
Q

Definition of endocarditis

A

Infection of endocardium (lining of the heart)
Formation of a vegetation
Results in damage to cusp of valves

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52
Q

Classification of endocarditis

A

Native valve endocarditis (NVE)
Endocarditis in IVDUs
Prosthetic valve endocarditis (PVE)

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53
Q

Risk factors for NVE (native valve endocarditis)]

Most common pathogen causing infective endocarditis?

A

Underlying valve abnormalities in 55-75% (aortic stenosis, mitral valve prolapse (MVP)
No identifiable risk factors in 30%

Strep viridans, staph aureus, enterococci, coxiella burnetti, haemophilus species, kingella species (HACEK)
Candidas albicans

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54
Q

Describe how an individual becomes infected with rheumatic heart disease

A

Involves strep pyrogens, which contains the toxin Streptolysin “O” exotoxin.
When an individual becomes infected with Streptococcus pyogenes (GAS) - the exotoxin from Strep. pyogenes is released.
This exotoxin then attracts antibodies (Anti-Streptolysin O (ASO) antibodies) which attack the Streptolysin.
The structure of cardiac valves is very similar to the toxin so the antibodies attack the valves as well –> stenosis or regurgitation

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55
Q

Endocarditis in IVDU

A

Tricuspid valve endocarditis more common than aortic or mitral.
Underlying valve normal in 75-93%

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56
Q

Clinical features of infective endocarditis

Acute vs Subacute

A

Acute:
Toxic presentation (are sick and can be toxic)
Progressive valve destruction & 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
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57
Q

Early manifestations of infective endocarditis

A

Incubation period = 2 weeks (longer in PVE)
Fever + murmur = IE until proven otherwise (fever may be absent in the elderly; murmure present in 80-85% (often present in tricuspid endocarditis))
Fatigue and malaise

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58
Q

Embolic events of infective endocarditis

A 
Can take days-weeks to occur
Seen earlier in acute endocarditis
Small emboli (Petechiae, splinter haemorrhages, haematuria)
Large emboli (CVA (possible stroke), renal infarction)
Right sided endocarditis (septic pulmonary emboli)
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59
Q

Long term effects of infective endocarditis

A 
Oslers nodes (painful palpable lesions, found on hands and feet)
Immunological reaction (splenomegaly, nephritis, vasculitic lesions of skin and eye, clubbing)
Tissue damage (valve destruction, valve abscess)
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60
Q

When to think IE?

A

All patients with S.aureus bacteraemia (SAB)
IVDU with any positive blood cultures
All patients with prosthetic valves and positive blood cultures

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61
Q

Diagnosing IE (the most important investigation)

A 
3 sets of blood cultures are done - constant bacteraemia so no need to wait for fever
Volume is most important factor in organism detection - 10mls/bottle required
Done before antibiotics are given
Aseptic technique (to avoid blood contamination)

Need to do echocrardiogram as well

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62
Q

Diagnosing IE from echocardiography

A

TTE is done first as there are risks associated with TOE.

Transthoracic (TTE):
Non-invasive
Transducer placed at front of chest
50% sensitivity

Transoesophageal (TOE):
Invasive
Transducer placed in oesophagus
85-100% sensitivity

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63
Q

Diagnosing IE using Duke Criteria

A

Major:
Typical organism in 2 separate blood cultures
Positive echocardiogram or new valve regurgitation

Minor:
Predisposition (heart condition or IVDU)
Fever >38 degrees C
Vascular phenomena (e.g. oslers nodes)
Positive blood cultures (not meet major criteria)

Need 2 major criteria, or 1 major and 3 minor, or 5 minor

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64
Q

Management of IE

A

Medical - Antimicrobial therapy
indications for surgical intervention:
1. Heart failure
2. Uncontrollable infection (abscess, persisting fever + positive blood cultures >7 days, infection caused by multi-drug resistant organisms
3. Prevention of embolism (large vegetations and embolic episode

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65
Q

Management of IE - using antimicrobial therapy

A

Intravenous therapy for duration in most cases
NVE: 4 weeks
PVE: 6 weeks

Streptococcus - Benzylpenicillin +/- Gentamicin
Enterococcus - Amoxicillin or Vancomycin +/- Gentamicin
S.aureus (MSSA) - Flucloacillin +/- Gentamicin
S.aureus (MRSA) - Vancomycin +/- Gentamicin
CoNS - Vancomycin +/- Gentamicin +/- Rifampicin

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66
Q

Options for cardiovascular imaging

A 
CXR
ECG
Ultrasound (TTE, TOE)
Ionising radiation - nucelar, CT, invascve angiography
MRI
67
Q

Describe briefly transoesophageal echo

A

TEE probe is places into mouth and down oesophagus - can also placed in stomach

Patient lies flat on bed on left hand side

68
Q

Indications of echocardiography

A

Structure and function of heart
Valve assessment
Pericardial assessment
Assess inducable ischaemia (stress)

69
Q

Pros and cons of echocardiography

A

Pros: cheap, available, portable, no radiation

Cons: requires good acoustic window, user dependent

70
Q

Indications for nuclear perfusion imaging

A

Assess ischaemia

Assess ejection fraction

71
Q

Pros and cons of nuclear perfusion imaging

A

Pros - availablity

Cons - radiaiton, no structural assessment

72
Q

How long does someone need to hold their breath for for a cardiac CT?

A

6-12 seconds

73
Q

Coronary artery calcium scan

A

Non-contrast study
Used in asymptomatic patients
Coronary calcium present in direct proportion to extent of atherosclerosis
Minority (20%) of plaque is calcified

74
Q

Indications for cardiac CT

A

Coronary artery anatomy

Great vessel anatomy

75
Q

Pros and cons for cardiac CT

A

Pros:
Good ‘rule out’ for CAD
Low risk

Cons:
Radiation dose
Requires low heart rate
No functional assessment of ischaemia

76
Q

Indications for invasive angiography

A

Ischaemia
Primary PCI
Valve assessment
Assessment ventricular pressure R+L

77
Q

Pros and cons of invasive angiography

A

Pros:
Gold standard
Option for intervention during same procedure
Availability

Cons:
Radiation
Risks - CVA, MI, contrast reaction, bleeding, death

78
Q

Indications for CMR (cardiac MRI)

A

Assess structure and function
Perfusion/stress
Assess great vessels
Tissue characterisation - infiltrative cardiomyopathies, previous infarction

79
Q

Pros and Cons fro CMR

A

Pros:
Gold standard LV assessment
Reproducable
No radiation

Cons:
Cost
Availability
Clostrophobia
Pacemakers
80
Q

What is atrial fibrillation?

A

The commonest sustained cardiac arrhythmia.
AF is a supraventricular tachyarrhythmia.
Increases risk of stroke - 5 fold

81
Q

Symptoms of AF

A

Asymptomatic (may still be at risk of stroke, systemic embolism)
Palpitation (awareness of heartbeat)
Dyspnoea (due to dec. cardiac output)
Rarely chest pain, syncope (due to either very fast or slow heart rates)
Complications e.g. stroke

82
Q

Diagnosing AF

A

Having an ‘irregularly irregular’ pulse - confirm with 12-lead ECG (not always easy as AF may not be there all the time)

May require prolonged ambulatory ECG recordings to detect paroxysmal AF

83
Q

What are the 3 different types of AF

A

Paroxysmal AF: Recurrent AF that terminates spontaneously within 7 days
Persistent AF: Lasts longer than 7 days
Long-standing persistent AF: continuous AF >1 years in duration
Permanent AF: refractory to cardioversion and sinus rhythm cannot be restored or maintained, such that AF is accepted as a final rhythm. A decision has been made by the patient and physician not to pursue restoration of sinus rhythm by any means, including catheter or surgical ablation.

84
Q

Features of AF seen on ECG

A

Rate variable
Irregular, narrow QRS complex
No P waves

85
Q

Features of atrial flutter seen on ECG

A

Rate variable
Regular/irregular narrow QRS complex
Sawtooth appearance - seen in II, III and aVF
Atria are contracting about 250-300 bpm (with variable number of beats getting through to the ventricles)
Variable degrees of AV block

86
Q

Risk of atrial flutter

A

Blood clot can form in atria - either travels down to legs or to brain
Most emboli go to brain –> causing a stroke

87
Q

What gender is AF seen in more?

A

Slightly more prevalent in males

88
Q

Conditions predisposing to, or encouraging progression of AF

A 
Hypertension
CAD
Symptomatic HF (NYHA II-IV)
Valvular heart disease
Atrial septal defect and other congenital heart defects
Obesity
Thyroid dysfunction - thyrotoxicosis (particularly hyperthyroidism)
Diabetes mellitus
COPD and sleep apnoea
Chronic renal disease
89
Q

Investigations for AF

A

ECG (to confirm arrhythmia)
Echocardiogram (to look for structural problems - e.g. left ventricular hypertrophy, valvular heart disease)
Thyroid function tests
Liver function tests

90
Q

Rate control for AF? (treatment)

A

Target HR <100/min
If still symptomatic, aim for HR <80/minPatients without HF should be started on either a beta blocker (eg. Bisoprolol or atenolol) or rate-limiting Ca++ antagonist (Verapamil).
Digoxin as second-line.
For patients with HF, follow heart failure guidelines

91
Q

What are the 2 types of Ca++ antagonists

A

Dihydropyridine group e.g. amlodipine, nifedipine - cause relaxation of vascular smooth muscle, good for hypertension, although may cause a reflex tachycardia (due to them relaxing blood vessels)

Non-dihydropyridines - These work predominantly on calcium channels in the heart, particularly in SA node and AV node, slow the atrial rate, ventricular rate and sinus rhythm - e.g. Verapamil and Diltiazem - These slow the heart rate in AF

It is the non-dihydropyridines that are used in management of AF

92
Q

For patient with AF, we want to assess their risk for stroke. What are the major risk factors for stroke?
Clinically relevant risk factors?

A

Previous stroke
TIA or systemic embolism
Age >= 75 years

CHF (congestive HF) or moderate to severe LV systolic dysfunction
Hypertension
Diabetes mellitus
Age 65-74 years
Female sex
Vascular disease (CHD, PHD)
93
Q

What is the scoring system used to determine a patients risk of having a stroke when they have AF?

A

Chadsvasc - maximum score is 9

Age >= 75 = 2 points
Stroke/TIA/thrombo-embolsim = 2 points

Everything else = 1 point

Score 9 = 15.2% risk

94
Q

The 4 new oral anticoagulant drugs used in AF

A

Used when Chassvasc score >=2 (considered when score is 1)
Apixaban - direct factor Xa inhibitor
Rivaroxaban - direct factor Xa inhibitor
Dabigatran (prodrug) - direct thrombin inhibitor
Edoxaban - diret factor Xa inhibitor

Reduce stroke/ systemic embolism
Reduce intracranial haemorrhage
Increased risk of GI bleeding

95
Q

Preventing stroke in patients with AF who have mechanical heart valves or moderate or sever mitral stenosis

MOA of warfarin

A

VKA - Warfarin (as apposed to new oral anticoagulants)

MOA of Warfarin:
Inhibits vitamin K epoxide reductase.
Prevents recycling of vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X.
Prevents thrombus formation.

96
Q

Trying to maintains sinus rhythm for patients with AF

A

Options include:
Direct current cardioversion (for persistent AF)
Antiarrhythmic drugs)
Catheter ablation)

97
Q

Types of antiarrhythmic drugs to use for patients with AF - to try maintain sinus rhythm

A 
Class 1 (NA+ channel blockers) - e.g. Flecainide, Propafenone
Class 3 (K+ channel blockers) - Sotalol (beta blocker with additional class 3 activity), Amiodarone
Multichannel blockers e.g. Dronedarone

These drugs often used in comination with a b-blocker

98
Q

Catheter ablation in AF

A 
Pulmonary vein isolation can be curative in 65-80% f paradoxysmal AF, 50-60% of persistent Af
Radiofrequency current (burning) or cyro-ablation (freezing)
99
Q

Symptoms of MI

A 
Chest pain, back pain, jaw pain (lower jaw)
Indigestion
Sweatiness, calmminess
SOB
None - silent MI (diabetes/dementia)
Death
100
Q

Signs for MI

A 
Tachcardia (HR>100)
Distress patient
HF (crackles/raised JVP)
Shock (cold, grey, BP low, HR high)
Arrhythmia
None
101
Q

What is troponin?

A

Part od the cardiac myocyte
Damage to the heart (necrosis) –. troponin leaks into the bloodstream and can be detected.
Elevated troponin levels signifies MI

102
Q

Universal definition of MI

A

Any elevation in troponin in clinical setting consistent with myocardial ischaemia (e.g. chest pain, SOB)

Isolated troponin elevation does not equal MI

103
Q

Different types of MI

A

1 - spontaneous MI due to a primary cornoary event (coronary artery plaque rupture and formation of a thrombus) - the coronary artery is the problem
2 - increased oxygen demand or decreased oxygen supply (HF, sepsis, anaemia, arrhythmias, hypertension, or hypotension (Heart is stressed due to other reasons -> increasing troponinllevels ) - is secondary - the cornoary artery is not the problem
3 - Sudden cardiac death
4a - MI associated with percutaneous cornoary intervention
4b - MI stent thrombosis documented by angiography or PM (induced by cardiologists)
5 MI associated with CABG (induced by cardiac surgeons)

104
Q

Non coronary causes of elevated troponin

A 
Causes of type 2 MIs:
COngestive HF - acute
Tachy-arrhythmias
Pulmonary embolism
Sepsis
Apical ballooning syndrome (Takosubo cardiomyopathy)

Chronic elevation of troponin (.e. not an MI)
Renal failure
Chronic HF
Infiltrative cardiomyopathies e.g. amyloidosis, haemochromatosis, sarcoidosis

105
Q

What is unstable angina?

A

An acute coronary event without a rise in troponin i.e. clinical presentation of an MI + ECG changes or tight narrowing on coronary angiography

Advanced CAD - lumen narrows

Rare now with high sensitivity troponin

106
Q

What is the main difference between STEMi MI and NSTEMI MI

A

NSTEMI - does not obstruct the lumen

STEMI - fully occludes the lumen

107
Q

Different ECG patterns in STEMI

A

ST elevation - reflects occlusion of a coronary artery
Posterior infarct
Left bundle branch block - if new can indicate infarction, if old can obscure ST elevation during an infarct

108
Q

Posterior wall infarction

A

No ECG leads look directly at the posterior wall of the heart
Anterior leads are directly opposite and will see the opposite of any current generated at the posterior wall i.e. posterior ST elevation = anterior ST depression
Posterior infacrt may be caused by l. circumflex artery or r coronary artery

109
Q

Immediate management of STEMI

A

ABCD
Put in ambulance attached to defibrillator - immediate transfer to cardiac centre
Aspirin 300mg PO
Unfractionated heparin 5000U iv (prevents progression of blood clot)
Morphine 5-10mg iv (doesnt change the process - is just a pain killer)
Anti-emetics
Clopidogrel (in ambulance) - reduces mortality risk) - 600mg if for PPCI, 300mg if for thrombolysis (75mg if aged >75 y/o)
Ticagrelor 180mg (in hospital)
Activate PPCI team at GJNH

110
Q

Compared to thrombolysis, primary PCI

A 
Improves survival
Reduces strokes
Reduces the chance of further MI
Reduces the chance of further angina
Speeds up recovery
Shortens the time spent in hospital
111
Q

Subsequent management of STEMI

A

Monitor in coronary care unit for complications of MI
Drugs fro secondary prevention - ACEi, beta blockers, statins, Eplerenone 9only for diabetes and LVSD or clinical HF

Echocardiogram for LV function and cardiac structure
Cardiac rehabiltation
If LVSD at >9 months consider primary prevention ICD

112
Q

Complications of MI

A

Arrhythmias - VT/VF-DC cardioversion, AF
HF - diuretics, inotropes, vasodilators
Cardiogenic shock - IABP (intra-aortic balloon pump, ventricular assist device)
Myocardial rupture - septum - VSD-surgery, papillary muscles - mitral rgurgitation-surgery, free wall - tamponade-surgery

Pschological - anxiety/depression, cardiac rehabilitation

113
Q

NSTEMI subsequent management

A

Monitor in coronary care unit for complications of MI
ASpirin
Clopidogrel or ticagrelor
LMWH or fondaparinux

Drugs for secondary prevention:
ACEi, BB< Statins, Eplerenone - only fir diabetes and LVSD or clinical HF

Echocardiogram for LV function and cardiac struture
Cardiac rehabilitation

114
Q

What type of scoring is used to assess risks of acute coronary events post-MI

A

GRACE - global registry of acute coronary events

115
Q

Systemic hypertension

A

Persistent elevation in arterial BP >140/90mmHg
A BP level that increases the vascular risk in patients sufficient to require intervention - there is a linear relationship between BP and CV events such as MI, stroke, HF and PVD .
Independent risk factor for the development of coronary artery disease, cerebrovascular disease, peripheral artery disease and HF

116
Q

Pathophysiology of Hypertension

A

Genetic influences + envrionmental factors –>

  1. Defects in renal sodium hemostasis - inc. CO
  2. Functional vasoconstriction - inc. vascular reactivity
  3. Defects in vascular smooth muscle growth and structure - inc. vascular wall thickness
      1. = inc. total peripheral resistance

Inc. CO + inc. total peripheral resistance = Hypertension

117
Q

Effect of hypertension on risk of CV mortality

A

Cardiovascular disease risk doubles for every 20mmHg increase in systolic and 10mmHg increase in diastolic pressure.

118
Q

Classification of hypertension

A

High normal: 130-139 S, 85-89 D
Grade 1 hypertension: 140-159 S, 90-99 D
2 - 160-179 S, 100-109 D
3 - >= 180 S, >=110 D

Isolated systolic hypertension (more common in older patients) - >=140 S, <90 D

119
Q

What are the 2 types of hypertension?

A

Primary and secondary

120
Q

Features of primary hypertension

A

90-95% of cases
No identifiable cause
Non-modifiable risk factors - age, gender (males more likely before 50, equal after 50), ethnicity (african, carribean), genetic factors
Modifiable - diet, physical activity, obesity, alcohol in excess (associated with inc. in BP), stress

121
Q

Features of secondary hypertension - causes

A

5-10% of cases
Causes:
Endocrine - hyperaldosteronism, phaechromocytoma, thyroid, Cushings syndrome
Vascular - co-arctation of aorta
Renal - renal artery stenosis, renal parenchymal disease
Drug - NSAIDs, herbal remedies, cocaine, exogenous steroid use
Other - obstructive sleep apnoea

122
Q

Why do we treat hypertension?

A 
Uncontrolled hypertension affects specific organ groups leading to end organ damage e.g.
TIA, stroke,
Retinopathy
PVD
Renal failure
LVH, CHD, HF
123
Q

Diagnosis of hypertension

A

Generaly asymptomatic, discovered incidentally
Uncommonly - headaches, visual disturbance
Need at least 2 readings, 5 mins between readings, over at least 2 visits
Out of office BP monitoring:
24 hour ambulatory BP monitoring - portable measurement device, BP taken 20-30 mins, throughout the day, 2 hourly overnight)
Home BP measurement - 2 readings, twice a day, taken over 4-7 days

124
Q

Diagnosis evaluation of patient with hypertension

A

Confirm the diagnosis - out of office BP monitoring
Assess cardiovascular risk
Determine the presence of end organ damage or associated complications (e.g. IHD, CKD, PVD, CVA)
Assess presence of secondary hypertension

125
Q

Management of hypertension

A

Lifestyle measures
Pharmacological management
Device based therapies e.g. renal denervation, baroceptor stimulation

126
Q

Summary of antihypertensive drug treatment

A

Aged under 55 years Step 1: ACEi or ARB

2: ACEi + Calcium channel blocker
3: ACEi, CCB + Thiazide-like diuretic

Resistant hypertension A+C+D + consider further diuretuc or alpha-or beta-blocker

Aged over 55 years or black person of African or Caribbean origin of any age - start with CCB - then follow same steps (i.e. dont give ACEi)

127
Q

Take into account co-morbidities when choosing an anti-hypertensive drug for treating hypertension

A

Beta blockers in HF/asymptomatic CHD

ACEi in HF or DM

128
Q

What is congenital heart disease

A

An abnormal formation of the foetal heart e.g. atrial septal defect

129
Q

Prevalence of congenital heart disease

A

Its becoming increasingly more common
People are surviving longer
Prevalence is increasing
More patients are surviving with congenital heart disease

130
Q

Features of atrial septal defect

A

Relatively common (~10% CHD)
Can occur in different parts of the septum:
- Secundum is the most common ACHD
- Primium is associated with other endocardial cushion defects such as cleft valves, inlet type VSD etc.
- Sinus Venous account for 10%
- Coronary Sinus very rare

Tx = corrective closure

131
Q

Secundum atrial septum defect (ASD)

A

About 80% od ASDs
Shunts left to right when in isolation - the more shunting you have the more risk you are at of AF and pulmonary hypertension
RV will have to dilate to accomodate extra V of blood - can lead to RV failure
Examination: pulmonary flow murmur; fixed, split second heart sound
May lead to: RV failure, tricuspid regurgitation, atrial arrhythmias, pulmonary hypertension, Eisenmenger syndrome.

Can present with palpitations, systolic ejection murmur, SOB, RV failure (pitting oedema). Can rarely present with a stroke - so a young person with a stroke - most likely ASD.

132
Q

Treatment of ASD

A

A device is put in place using a catheter. The device is attached to the catheter and inserted through the femoral vein.
When the device is released from the catheter, it opens up and seals the hole. Over time, tissue grows over the implant and it becomes part of the heart

133
Q

Features of coarctation of the aorta

A

5-8% of ASD
Coarctation of the aorta is the narrowing in the proximal descending aorta (just at aortic arch) - can be pre-ductal or post-ductal.
Tends to form after LSA in a ‘juxta-ductal’ position
Age at presentation depends on position and severity
Pre-ductal may cause lower limb cyanosis
LV has to pump harder –> LV hypertrophy –> LV failure if not corrected
Colateral vessels will develop to try bypass the narrowing
Poor peripheral perfusion, claudication of legs, abdominal angina)
Pre-coarctation hypertension –> headaches, mood swings

Examination - differences in limb BPs - higher BP in arms than legs (N other way around), radio-femoral delay
Narrowing (coarctation) - turbulent blood flow = continuous murmur heard on front and back of chest

134
Q

Treatment of coarctation of aorta

A

Trans-catheter or surgical
[Transcatheter - balloon passed through femoral artery - stretches open narrowing]
Surgical repair via thoracotomy - subclavian flap, end to end, jump graft

135
Q

Features of transposition of great arteries

A

Transposition of the great arteries (~5% of CHD) - the aorta is connected to the RV and the pulmonary artery is connected to the LV - the opposite of a normal heart’s anatomy.
2 separate circuits are formed - one that circulates deoxygenated blood from the body back to the body, and another that recirculates oxygenated blood from the lungs back to the lungs.
TGA - ‘blue-baby syndrome’
2 circulations that don’t mix - not compatible
Foetus survive this as they receive oxygenated blood from the placenta - R side of heart via IVC.
They survive due to foramen ovale and ductus arteriosus.
When takes first breath - changes in pressure in heart and lungs.
In first few hours - foramen oval and ductus arteriosus closes - so the baby would die.
Needs to be given iv prostaglandins - maintains the patency of these structures - gives more time to perform corrective surgery

136
Q

Describe the foetal circulation

A

In-utero oxygenation is by the maternal placenta
Pulmonary circulation is minimal and at high resistance
Oxygenated blood returns to RA via IVC
It then bypassess the RV/PA via the foramen ovale
Of the blood that is pumped to the PA via the RV, most passes to the aorta via the ductus arteriosus

137
Q

Treatment of transposition of the great arteries

A

Arterial switch is now the procedure of choice - cut the pulmonary artery and aorta just above the valves and reconnect them
Move pulmonary artery and RV back onto LV
Coronary arteries can sometimes be affected - can cause MI

138
Q

Name 2 types of cyanotic lesions

A

Transposition of great arteries

Tetralogy of Fallot

139
Q

What are the 4 components of tetralogy of fallot

A

Ventricular septal defect
Overiding aorta
RVOT obstruction
Right ventricular hypertrophy (as working harder)

these babies will also be given IV prostaglandins after birth

140
Q

Operative strategy for tetralogy of Fallot

A

2 options BT shunt; complete repair
BT shunt:
Gortex tube connects subclavian artery to the pulmonary artery to improve blood supply to the lungs.
Can’t detect a BP with this on the side of the shunt

Complete repair:
VSD is closed off with a patch
Lung arteries are underdeveloped –> patch used to enlarge the pulmonary arteries

141
Q

Complications associated with tetralogy of Fallot

A

Valve often starts to become damaged -> regurgitation
Most patients will need a pulmonary valve replacement in later years
RV dilatation +/- dysfunction (–>RV failure)

Dilated RA occurs –. arrhythmia - can develop flutter - can cause ventricular tachycardia

Pulmonary arteries where underdeveloped during gestation –> often become stenosed

142
Q

Features of univentricular heart

A

Rare within CHD
One functioning ventricle reliant on shunts for mixing of the blue and red blood
Foetus can cope due to foramen ovale and ductus arteriosus
The aim of surgery will always be to create 2 functioning ventricles
If not feasible then a Fontan circulation will be created

143
Q

Commonest cause of univentricular heart

A

Tricuspid atresia

144
Q

Treatment of univentricular heart - extracardiac fontan

A

Extracardiac Fontan:
IVC and SVC are directly plumbed into the pulmonary arteries bypassing the heart altogether.
A small fenestration allows blood flow between the RA and conduit

145
Q

Issues with Fontan circulation

A

Pulmonary circulation is dependent on high systemic venous pressure and low pulmonary vascular resistance
Anything that causes an imbalance can cause catastrophic haemodynamic compromise. (e.g. PE, arrhythmia (due to de.BP), dehydration (deu to dec.BP), bleeding)
These patients are anticoagulated

If risk for dehydration - need IV fluids

146
Q 
What does not correlate with an increased troponin level?
a. 
Myocardial Infarction
b. 
Pulmonary Embolism
c. Congestive Heart Failure
d. Unstable angina 
Unstable angina. Unstable angina is defined by - an acute coronary event without rise in troponin level ; All the other answers may lead to an acute elevated troponin level
e. Sepsis
A

Unstable angina. Unstable angina is defined by - an acute coronary event without rise in troponin level ; All the other answers may lead to an acute elevated troponin level

147
Q

Cardiovascular imaging MCQ: What is the most accurate method for assessing left ventricular ejection fraction?

Select one:

a. Transthoracic echocardiography
b. Transoesophageal echocardiography
c. Cardiac magnetic resonance imaging
d. Cardiac CT
e. Angiography

A

Cardiac MRI

148
Q

What is the most common organism responsible for endocarditis in an intravenous drug user?

Select one:

a. Enterococcus species
b. Coagulase-negative Staphylococci
c. Staphylococcus aureus
d. Candida albicans
e. Pseudomonas aeruginosa

A

Staphylococcus aureus is the most common cause of native valve endocarditis in intravenous drug users, commonly causing tricuspid (also known as “right sided”) endocarditis. Coagulase-negative Staphylococci are the most common cause of prosthetic valve endocarditis.

149
Q

In the different types of bradyarrhythmias, which type of rhythm has no P waves present?
Select one:
a. Junctional bradycardia
b. Second degree atrioventricular block
c. Sinus bradycardia
d. Third degree (complete) atrioventricular block
e. First degree atrioventricular block

A

Junctional bradycardia

150
Q

Which arrhythmia can be described as having P waves present and constant PR intervals, but QRS complexes dropped intermittently?

Select one:

a. First degree heart block
b. Second degree heart block - Mobitz type 1
c. Junctional bradycardia
d. Third degree (complete) heart block
e. Second degree heart block - Mobitz type 2

A

Second degree heart block

151
Q

Which of the following treatments should all patients with heart failure and a reduced ejection fraction receive (assuming there is no contraindication to the drug or therapy)?

Select one:

a. ACE inhibitor and betablocker
b. ACE inhibitor and beta-blocker and diuretics
c. ACE inhibitor and mineralocorticoid receptor antagonist
d. ACE inhibitor and betablocker and an implantable cardioverter defibrillator (ICD)
e. ACE inhibitor and beta-blocker and mineralocorticoid receptor antagonist and diuretics

A

ACE inhibitors and beta-blockers

152
Q

A 45-year old Caucasian man had several elevated blood pressure readings on visits to his GP. His average home blood pressure reading was 168/94 mmHg. He had no significant past medical history and aside from blood pressure, examination was normal.

What is the most appropriate management?

Select one:

a. Commence amlodipine
b. Give lifestyle advice only
c. Commence bisoprolol
d. Observe and return in 3 months
e. Commence ramipril

A

Commence Ramipril

153
Q

Tx of AF

A
  • Amiodarone 200mg tid was started to prevent recurrence of AF. The dose will be reduced to 200mg maintenance. Amiodarone has many side effects, including photosensitivity, hyper- or hypo- thyroidism, abnormal liver function tests, neurological symptoms, and (rarely) pulmonary fibrosis
  • Anticoagulation – after discussing the benefits and risks, he was started on apixaban, a new oral anti-coagulant (NOAC). This carries a risk of bleeding, which has to be balanced against the risk of embolic complications, in particular stroke, associated with AF. Although his rhythm has reverted to sinus rhythm, there is a high likelihood of recurrent AF. NOACs have been shown to be at least as effective as warfarin, with reduced risk of intracranial haemorrhage. Risk of stroke is increased with cardiac failure, hypertension, age >75 years, diabetes, or previous embolic stroke. His CHA2DS2-VASc score is at least 2 (Cardiac failure; Hypertension; possible neurological episode).
154
Q

Most common causes of HF

Name a drug used to slow the ventricular rate in atrial fibrillation and describe the mechanism by which it does so.

A

Myocardial dysfunction e.g. MI, cardiomyopathy
Volume overload e.g. renal failure; severe mitral regurgitation
Obstruction to outflow e.g. aortic stenosis
Obligatory high output e.g. severe anaemia
Compromised ventricular filling e.g. restrictive cardiomyopathy
Altered rhythm e.g. AF with fast ventricular rate (‘tachycardiomyopathy’)

Digoxin slows ventricular rate in AF:
Increases vagal parasympathetic activity and inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly.
In an effort to remove Na+, more Ca2+ is brought into the cell by the action of Na+/Ca2+ exchangers.
The buildup of Ca2+ is responsible for the increased force of contraction and reduced rate of conduction through the AV node.

155
Q

Revise the nature and MOA of drugs used to treat HF

A

• Diuretic – for treatment of the symptoms of fluid overload in heart failure
• ACE inhibitors - these drugs antagonise the actions of the renin-angiotensin-aldosterone system and act as vasodilators. They may therefore reverse some of the major pathophysiological mechanisms in heart failure. They have been shown to improve symptoms and survival in heart failure. May cause cough, hypotension or renal dysfunction (particularly in the presence of renal vascular disease). The dose may have to be up-titrated gradually.
• Angiotensin-receptor blockers – also shown to improve outcome in heart failure. May be used in place of ACE inhibitors e.g. if cough a problem.
• Angiotensin-receptor neprilysin inhibitors – these drugs have been shown to improve outcomes in heart failure and are recommended in the guidelines for patients who are still symptomatic despite ACEI or ARB. They should be given in place of an ARB or ACEI and must not be given with an ACEI due to the risk of angioedema.
• Beta-blocker – also well established to improve outcome of patients with heart faiure, but may cause deterioration in the short term. They have to be started at a low dose, with subsequent increases in dose at intervals of at least a couple of weeks. This is often supervised as an out-patient by the Heart Failure Liaison nurses.
Mineralocorticoid receptor antagonists – Spironolactone is an mineralocorticoid receptor antagonist (aldosterone blocker)which has been shown to reduce mortality in patients with heart failure. It has the added advantage of being a potassium-sparing diuretic, although its diuretic action is mild. Blood biochemistry must be monitored because the most common adverse effect is hyperkalaemia, often exacerbated by the potassium retaining actions of other drugs, in particular ACE inhibitors

156
Q

Revise the normal physiology of cardiac conduction and describe common arrhythmias

A

Cardiac conduction system starts with a sinus node in a group of cells in the high right atrium. The activity spreads tthrough the atrium to the AV node. The AV node induces a delay of up to 200 milliseconds to allow blood flow to travel from the atrium into the ventricle. The cardiac conduction system continues with the Bundle of His before splitting into the right and left bundle branches. The left bundle branch then splits into an anterior and posterior fascicle.

157
Q

Describe the common cardiac arrhythmias

A

Atrial fibrillation. This is a chaotic rhythm of the atrium. There is effectively no co-ordinated electrical activity. Ventricular rhythm is irregular and the rate is determined by AV nodal refractoriness. Rate is controlled with AV nodal blocking drugs e.g. beta-blocker, calcium channel blockers (diltiazem and verapamil).

Atrial Flutter. This is a circular movement of electrical activity within the atrium. Basically the rhythm is self-perpetuating, chasing its tail. It is commonly regular, with 2:1 AV conduction e.g. atrial rate 300 bpm, ventricular rate 150 bpm.

Supra-ventricular tachycardia. This is due to a re-entry circuit using an extra electrical pathway. This can be present within the AV node or as a connection between the atrium and ventricle (an accessory pathway or bypass tract). The SVT is usually initiated by an atrial extra-systole which finds the accessory pathway refractory to accepting stimulation in the direction of atrium to ventricle. The electrical activity then passes through the normal conduction systems, and then is able to conduct back from the ventricle to the atrium through the accessory pathway. A circus movement is then initiated.

Ventricular arrhythmias:
These include extra-systoles, ventricular tachycardia, ventricular fibrillation

158
Q

List 6 risk factors for PVD (PVD causes claudication)

A

Male
Aged 40 and over
Smokers
Hypertensive
Diabetic
History of angina, infarction, cerebral ischaemia
Metabolic syndrome - ‘prediabetic’ group of people

159
Q

2 specific tests for peripheral arterial disease

Define ‘intermittent claudication’, state precisely where in the body it occurs and its aetiology

A

Ankle-brachial index
Aortograms

Intermittent claudication = severe cramping pain often in calf/thigh or buttock caused by an occlusion in the femoral artery which is made worse on physical exertion and alleviated on rest.

160
Q

Describe the clinical manifestations of PVD, including intermittent claudication

A 
Intermittent claudication (IC) is pain in the leg brought on by walking and relieved by rest. It is most common in the calf muscles but can affect the thigh or buttock. It is unusual for the pain to be anterior.
IC is a benign symptom. It is a local manifestation of a systemic disorder - atheroma. Less than 10% of all claudicants will come to amputation. The doctor needs to be aware that disabling claudication (symptoms which seriously restrict lifestyle), and deteriorating claudication (walking distance reducing) are both indications for referral to a specialist. The main prognostic implication of intermittent claudication is that it is an indicator of widespread vascular disease, and patients with PVD are at risk of cardiac, renal and cerebrovascular events.
161
Q

Features of a critically ischaemic limb

A 
Pale
Painful
Pulselessness
Paretic
Perishingly cold
Paraesthetic

The 6 P’s

162
Q

What vessel is most likely the cause of acute limb ischaemia

A

Femoral artery

163
Q

Virchows triad that predisposes to thrombus formation

A
  1. Endothelial damage or altered endothelial function
  2. Slowing (stasis) and perturbation of blood flow
  3. Changes in composition of blood
164
Q

Causes of acute arterial occlusion (acute limb ischaemia)

A

Thrombosis

Embolism

Phase 3 (15 decks)

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