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Medicine Year 3 > Week 5 - Cardiology > Flashcards

Week 5 - Cardiology Flashcards

1
Q

Describe the flow of blood in secundum ASD

A

Shunts left to right when isolation (path of least resistance, from high to low pressure)

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2
Q

Describe catheter ablation in atrial fibrillation

A
  • Identification of triggers for paroxysmal AF in the pulmonary veins
  • Pulmonary vein isolation can be curative in up to 65-80% of patients with paroxysmal AF, 50-60% of patients with persistent AF
  • Radiofrequency current (‘burning’) or cryo-ablation (‘freezing’)
  • More effective in patients with structurally normal hearts or minimal heart disease
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3
Q

Describe the prevalence of hypertension

A

Increasing in prevalence (35-45%), estimated 1 billion worldwide

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4
Q

Describe the timing of coronary revascularisation in NSTEMI

A

Early coronary revascularisation (<24 hours) is of substantial benefit in high risk group. No benefit in lower risk groups.

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5
Q

Describe anticoagulation in AF

A
  • Atrial fibrillation with mechanical heart valves or moderate/severe mitral stenosis - Warfarin
  • All other atrial fibrillation - NOACs
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6
Q

Describe the classificaiton of endocarditis

A
  • Native valve endocarditis - most common
  • Endocarditis in IVDUs
  • Prosthetic valve endocarditis - more difficult to treat, higher mortality
    • Inserted for a variety of reasons, mainly to replace diseased valves
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7
Q

Describe the appearance of a normal ECG

A

Normal sinus rhythm, rate of 75bpm, normal waveform

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8
Q

How can the heart rate be determined from an ECG?

A

300 divided by the number of large squares between each QRS complex:

1 square = 300/min

2 squares = 150/min

3 squares = 100/min

4 squares = 75/min

5 squares - 60/min

6 squares = 50/min

OR - number of QRS complexes across ECG (10 sec) x 6

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9
Q

What signs may be seen on imaging in coarctation of the aorta?

A

Rib notching may be present on CXR due to retrograde flow from high pressure anterior intercostal arteries to low pressure posterior

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10
Q

What are the consequences of mitral regurgitation?

A
  • Volume overload - LA/LV
  • LV and LA dilatation
  • Pulmonary hypertension
  • Secondary right heart dilatation
  • Atrial fibrillation
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11
Q
A
  • What is the QRS rate?
    • Normal (300/5 = 60 bpm)
  • Are the QRS complexes regular?
    • Yes
  • Is the QRS broad or narrow?
    • Usually narrow
  • What is the P:QRS relation?
    • 1:1

= Normal Sinus Rhythm

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12
Q

Describe the classificatino of heart failure

A
  • New York Heart Association Functional Classification
    • Method of describing functional limitations in heart failure
  • Class I
    • No symptoms and no limitation in ordinary physical activity e.g. shortness of breath when walking, climbing etc.
  • Class II (mild)
    • Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity
  • Class III (moderate)
    • Marked limitation in activity due to symptoms, even during less-than-ordinary activity e.g. walking short distance (20-100m). Comfortable only at rest.
  • Class IV (severe)
    • Severe limitations. Experiences symptom even while at rest. Mostly bedbound patients.
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13
Q

List the types of MI based on their cause

A
  1. Spontaneous MI due to a primary coronary event (coronary artery plaque rupture and formation of an intraluminal thrombus), ischaemia/necrosis or area supplied by artery (acute coronary syndrome) CORONARY ARTERY IS THE PROBLEM
  2. Increased oxygen demand or decreased oxygen supply
  • Heart failure, sepsis, anaemia, arrhythmias, hypertension or hypotension (supply-demand imbalance)
  • CORONARY ARTERY IS NOT THE PROBLEM
  1. Sudden cardiac death, often proven on autopsy
  2. Iatrogenic
  • MI associated with percutaneous coronary intervention - angioplasty in coronary artery can cause infarction in area supplied by artery, arterial rupture/perforation can occur
  • MI stent thrombosis (stent reocclusion) documented by angiography or PM
  • MI associated with CABG
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14
Q

Compare amiodarone and dronedarone

A
  • Dronedarone
    • Same effect as amiodarone without iodine
    • Less potent
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15
Q

Describe the components of tetralogy of fallot

A
  • Ventricular septal defect
  • Right ventricular outflow tract obstruction
    • Often stenosis below the pulmonary valve due to large muscle mass
    • Narrowing of the pulmonary valve and outflow tract or area below the valve that creates an obstruction (blockage of blood flow) from the right ventricle to the pulmonary artery
  • Overriding aorta - aortic valve enlarged and appears to arise from both the left and right ventricles instead of the left ventricle as in normal hearts
  • Right ventricular hypertrophy
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16
Q

Which antihypertensive should be used in which patients?

A
  • Step 1
    • Aged under 55 years - ACE inhibitor or low-cost angiotensin II receptor blocker
    • Aged over 55 years or black person of African or Carribean origin of any age
      • Calcium channel blocker
  • Step 2
    • ACE inhibitor or low-cost angiotensin II receptor blocker and calcium channel blocker
  • Step 3
    • ACE inhibitor or low-cost angiotensin II receptor blocker and calcium channel blocker and thiazide-like diuretic
  • Step 4 - resistant hypertension
    • ACE inhibitor or low-cost angiotensin II receptor blocker and calcium channel blocker and thiazide-like diuretic and consider further diuretic or alpha- or beta-blocker
  • Take into account co-morbidities
    • Beta-blockers in heart failure/asymptomatic coronary heart disease
    • ACEI in heart failure
    • ACEI in diabetes mellitus
  • Often more than one drug will be required
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17
Q

What is seen on an ECG in pericarditis?

A

ST elevation in V1-6 - global ST elevation

= Pericarditis rather than STEMI

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18
Q

Describe the heart murmur heard in mitral stenosis

A

Low-pitched (‘rumbling’) mid-diastolic murmur, with pre-systolic accentuation in sinus rhythm due to atrial systole, best heard at the apex with patient lying on their left side

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19
Q

Describe the appearance of a STEMI on ECG

A
  • STEMI shows elevation of J point - junction of the termination of the QRS complex and the beginning of the ST segment.
  • 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
      • Always ask senior advice as to whether to treat as a STEMI or not
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20
Q

Describe the use of ACE inhibitors in heart failure

A

ACE inhibitors (e.g. enalapril, captopril) shown to improve outcomes compared with placebo (reduce mortality) in severe and less symptomatic patients.

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21
Q

Explain the complications of aortic valve disease including the effects on the L ventricle

A
  • Aortic stenosis
    • Angina, syncope, dyspnoea
    • Sudden death, heart failure - surgical valve replacement considered even in absence of severe symptoms
  • Aortic regurgitation
    • LV dilatation, heart failure will eventually occur
  • Challenge is to offer valve replacement before irreversible damage has occurred but delay appropriately in asymptomatic patients
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22
Q

Describe the modern techniques used for procedural intervention in valve dysfunction

A
  • TAVI
    • Reduces morbidity/mortality in those too unwell for conventional surgery
    • Catheter from leg to aorta, inflate balloon w/ valve, valve expands
    • Trials to prove its better than conventional
  • Mitraclip
    • Not well enough for mitral valve surgery, clips that keep mitral valve together
  • Valvuloplasty
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23
Q

Describe the pathophysiology of endocarditis

A
  • Vegetation = mass of platelets, fibrin, microcolonies of organisms, inflammatory cells and RBC debris
    • Vegetation hard to penetrate - hard treat.
  • Vegetation - biofilm = mass of organisms
    • Commonly associated with infections of prosthetic devices e.g. valves, hip replacements
  • Quorum Sensing:
    • Ability to detect and respond to cell population density by gene regulation
    • E.g. enables bacteria to restrict the expression of specific genes to the high cell densities at which the resulting phenotypes will be most beneficial
    • Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population
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24
Q

Why is heart failure important?

A
  • Common - prevalence = 1-2% of population, may be increasing. Incidence - 1 in 5 lifetime risk of HF.
  • Costly - 2% of all health care expenditure - mainly spent on hospital admissions (70% of expenditure on heart failure, also outpatient clinics and drugs)
  • Disabling - associated with a worse quality of life than almost any other medical condition. Because of symptoms (dyspnoea, fatigue) and frequent deterioration leading to hospital admission. Unemployment due to poor health.
  • Deadly - worse survival than most forms of cancer. 50% mortality within 5 years, is improving.
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25
Q

Which ECG leads show an inferior STEMI and which is the culprit coronary artery?

A
  • II, III, aVF leads
  • Right coronary artery
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26
Q

Describe the appearance of an inferior STEMI on ECG

A
  • ST elevation in inferior leads
  • Reciprocal ST depression in high lateral leads
  • Rhythm disturbance - R coronary artery supplies AV node, bradycardia (35bpm), no P wave for every QRS complex = dissociation between sinus node activity and ventricular contraction
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27
Q

List the risk factors for coronary artery disease

A
  • Non-modifiable
    • Increasing age
    • Sex
    • Ethnicity
    • Family history
    • PMHx/co-morbidities
  • Modifiable
    • Smoking
    • Obesity
    • Lack of physical activity
    • Diet
    • High cholesterol
    • HTN
    • Co-morbidities e.g. diabetes, metabolic syndrome
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28
Q

List the valves of the heart

A
  • 2 x semilunar valves (aortic and pulmonary) - 3 cusps, open by pressure, pressure closes valve to stop backflow
  • 2 x atrioventricular valves (mitral and tricuspid)
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29
Q

Describe the normal path of blood through the heart

A
  • Oxygen poor blood passes into the RA through the SVC and IVC (+ coronary sinus)
  • Passes through the right atrioventricular valve called the tricuspid valve into the right atrium and is pumped through the pulmonary valve into the pulmonary arteries and passes through the lungs
  • Blood is oxygenated, passes back into the heart through the pulmonary veins into the left atrium
  • Passes through the left atrioventricular valve i.e. mitral valve into the LV and is pumped through the aortic valve into the aorta and the remainder of the systemic system
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30
Q

What are the consequences of secundum ASDs?

A
  • Right heart volume loading - RV dilates in an effort to accommodate this extra volume
  • Can have no symptoms in early life, commonly diagnosed in adulthood
  • Dilation of RA - patients can get arrhythmias and present with palpitations, also often present with SOB, can have embolic stroke
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31
Q

Describe the function of the mitral valve

A
  • Controls blood flow into the left ventricle from the left atrium
  • Bi-leaflet valve tethered by the chordae tendineae to the papillary muscles
  • Opens when the left atrial pressure exceeds left ventricular pressure during diastole, when LV pressures are low because of ventricular muscle relaxation
  • Blood flow from LA to LV initially occurs passively down a pressure gradient, with further filling of the LV at end-diastole due to LA contraction
  • Closes when LV pressure exceeds LA pressure, during ventricular systole
  • The chordae tendineae/papillary muscles prevent the valve prolapsing into the LA
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32
Q

Describe the changes seen on ECG in ichaemic discomfort

A
  • Fully occluded coronary vessel = ST elevation MI (STEMI)
  • Partially occluded coronary vessel = no ST elevation MI (NSTEMI) or unstable angina
  • Full thickness infarction of myocardial wall = Q wave infarction
  • Partial thickness infarction of myocardial wall = non-Q wave infarction
  • Q wave persists after MI - always seen on ECG
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33
Q

Describe the prevalence of transposition of the great arteries

A

5% of CHD, affects males:females 4:1

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34
Q

Describe the use of angiotensin receptor neprilysin inhibitors in heart failure

A
  • Valsartan stops angiotensin II binding to receptor AT1 - stops vasoconstriction, sodium/water retention, fibrosis/hypertrophy
  • Sacubitril inhibits neprilysin which breaks down natriuretic peptides (cause vasodilation, natriuresis, diuresis, inhibition of pathologic growth/fibrosis)
  • Reduce mortality
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35
Q

Describe ongoing research in atrial fibrillation

A
  • Should we be screening asymptomatic people for AF?
    • Esp. high risk groups e.g. elderly patients
  • Better risk stratification
    • Prevention of stroke vs reduction in risk of bleeding on anticoagulant therapy
  • AF in patients with heart failure
    • Risks vs benefits of different treatment strategies
    • Persistent AF and HF better outcomes than paroxysmal AF and HF
  • New ablation techniques
  • Lifestyle and AF
    • Obesity, lack of physical activity as modifiable risk factors for AF
    • If lose >10% of body weight more likely to restore to sinus rhythm than those who lose weight/gain weight
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36
Q

What is congenital heart disease?

A
  • Abnormality of foetal heart development
  • Encompasses a wide variety of malformations all ranging in severity and treatment options, can affect the various structures of the heart + great vessels e.g. aortic coarctations
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37
Q

Describe the structure of the mitral valve

A
  • Mitral valve leaflets and chordae tendineae, connected to papillary muscle
  • Needs to be anchored to ventricle to prevent backflow
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38
Q

What is atrial fibrillation?

A
  • Arrhythmia characterised by rapid and irregular atrial contraction
  • Commonest sustained cardiac arrhythmia
  • Affects 1.5-2% of the population
    • 10% of octogenarians
  • Major risk factor for stroke
    • 5x increase in stroke risk - risk increases with age anyway
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39
Q

Describe the guidelines for management of a patient with suspected AHF

A
  • Urgent phase after first medical contact
      1. Cardiogenic shock?
        * Yes - circulatory support (pharmacological, mechanical)
    • No - 2. Respiratory failure?
      • Yes - ventilatory support (oxygen, non-invasive positive pressure ventilation (CPAP, BIPAP), mechanical ventilation)
    • Immediate stabilisation and transfer to ICU/CCU
  • Immediate phase (initial 60-120 minutes)
    • Identification of acute aetiology
      • C - acute Coronary syndrome
      • H - Hypertension emergency
      • A - Arrythmia
      • M - acute Mechanical cause
      • P - Pulmonary embolism
    • Yes - immidiate initiation of specific treatment (follow detailed recommendations in the specific guidelines)
    • No - diagnostic work-up to confirm ANF, clinical evaluation to select optimal management
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40
Q

Define systemic hypertension

A
  • Persistent elevation in arterial blood pressure >140/90mmHg
  • A BP level that increases the vascular risk in patients sufficient to require intervention
    • There is a linear relationship between blood pressure and CV events such as MI, stroke, heart failure and PVD
  • The threshold at which benefits of action (i.e. therapeutic intervention) exceed those of inaction
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41
Q

Outline the common causes of heart failure

A
  • Myocardial dysfunction e.g. MI, cardiomyopathy
  • Volume overload e.g. renal failure, severe mitral regurgitation
  • Obstruction to outflow e.g. 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)
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42
Q

Rank the valves in order of most to least commonly affected by infective endocarditis

A
  1. Mitral valve
  2. Aortic valve
  3. Tricuspid valve - most common site in IVDU (venous injection of organisms)
  4. Pulmonary valve (rarely infected)
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43
Q

What are the risk factors for stroke in AF?

A

Left ventricular systolic dysfunction, hypertension, previous TIA or stroke, diabetes, age and female gender

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44
Q

Describe the appearance of late pulmonary oedema on CXR

A
  • Alveolar oedema
    • Cotton-wool appearance
    • Consolidation - white lungs w/ tubes of air running through
    • Pleural effusions
  • Fluid not only leaking into interstitium from hugely distended vessels but into the alveolar sacs
  • ‘Bat wing’ pulmonary oedema - most change in peri-hilar vessels moving outwards
  • Loss of sharp costophrenic angle
  • Usually worse at base, better moving up - due to gravity
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45
Q

Describe the diagnosis of ventricular tachycardia

A
  • ECG features - assume its VT while get more information
  • If >35 y/o, previous MI (+ other risk factors) - VT
  • If <35 etc. higher suspicion of SVT w/ bundle branch etc.
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46
Q

List the forms of AF

A
  • Paroxysmal AF - terminates spontaneously, usually lasts less than 48 hours, but may recur
  • Persistent AF - remain in atrial fibrillation but sinus rhythm can be restored e.g. by cardioversion either electrically or with drugs
  • Permanent AF - chronic, sinus rhythm can’t be restored or may be inappropriate to try
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47
Q

What are pleural effusions?

A
  • Fluid within potential space between parietal and visceral fluid
  • Divided into transudates and exudates
    • Protein levels >30g/l, LDH>200IU consistent with exudate. pH <7.1 also suggests exudate
  • In CHF 70% of pleural effusions are bilateral
  • At least 175ml of fluid must be present to be seen in PA chest x-ray, 500ml on supine examination
  • Homogeneous lower zone opacity with a curvilinear upper border
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48
Q

How are echocardiographs used in the diagnosis of infective endocarditis?

A
  • Transthoracic
    • Non-invasive
    • Transducer placed at front of chest
    • 50% sensitivity
  • Transoesophageal
    • Invasive
    • Transducer placed in oesophagus
    • 85-100% sensitivity
  • Transthoracic performed first - if negative and high clinical suspicion remains, transoesophageal indicated
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49
Q

Describe the features of failed Fontan circulation

A
  • Early failure (3%)
    • Low cardiac output, pleural effusions, chylothoraces, ascites, hepatomegaly
  • Late failure (2-13%) - lymphatic dysfunction, protein-losing enteropathy
    • Ascites, peripheral oedema, pleural effusions, diarrhoea, malabsorption of fat, hypoalbuminaenia
  • Plastic bronchitis (<2%)
    • Tachypnoea, cough, wheezing, expectoration of bronchial casts
  • Primary ventricular dysfunction (7-10%)
    • Progressive exercise intolerance, AV valve insufficiency, hepatomegaly, ascites
  • Progressive increase in pulmonary resistance
    • Hypoxaemia
  • Hepato-renal insufficiency
  • Hepatic failure
    • Hepatomegaly, ascites, hepatocellular carcinoma
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50
Q

What is a bundle branch block?

A
  • Electrical impulses from AV node down bundle of His, divides into the left and right bundle branches, which eventually end in the Purkinje fibres
  • Left bundle branch block - activation of the left ventricle by the bundle branch/fascicles delayed, causes the left ventricle to contract later than the right ventricle
    • Supraventricular origin
    • QRS duration >120ms
    • QS or RS in V1, R in V6 (notched/M shaped)
  • Right bundle branch block
    • Septum depolarises left to right - R wave in V1, Q wave in V6
    • LV depolarised via left bundle - deep S in V1, tall R in V6
    • RV depolarises late - R wave in V1, S wave in V6
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51
Q

What causes primary hypertension?

A
  • No identifiable cause
  • Associated with several risk factors
  • Non-modifiable
    • Age
    • Gender
    • Ethnicity
    • Genetic factors
  • Modifiable
    • Diet
    • Physical activity
    • Obesity
    • Alcohol in excess
    • Stress
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52
Q

What causes bicuspid aortic valves?

A
  • Associated with aortic abnormalities
  • Genetic component (10%)
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53
Q

What is the function of the aortic valve?

A
  • Tricuspid semi-lunar valve
  • Controls blood flow from LV into the aorta
  • Opens when the systolic pressure in the LV exceeds the end-diastolic pressure in the aorta e.g. 80mmHg
  • Closes when the pressure falls towards the end of systole
  • Semi-lunar structure of the valve cusps results in closure of the valve, preventing regurgitation of blood back into LV
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54
Q

Describe rate control in the management of AF

A
  • Target heart rate <110/min
  • If still symptomatic, aim for heart rate <80/min
  • Patients w/out heart failure should be started on either a beta-blocker (e.g. bisoprolol or atenolol) or rate-limiting Ca+ antagonist
    • 2 classes of Ca+ antagonist - rate limiting e.g. Verapamil, Diltiazem (act on cardiac muscle to slow heart rate) or dihydropinidine group e.g. amlodipine (act on vascular muscle to cause vasodilation, lower BP but usually cause increase in HR) - don’t use in AF
  • Digoxin as second line
  • For patients w/ heart failure follow guidelines
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55
Q

How are chambers named in congenital heart defects?

A
  • Chambers are named by their morphological features NOT their position
  • RA - sinoatrial node, broad appendage
  • LA - narrow, long appendage
  • RV - trabeculated endocardium, insertion of chordae to IVS, moderator band
  • LV - smooth endocardium, ellipsoid cavity
  • AV valve goes with the ventricle

Will be some congenital heart defects where the morphological RA is on the left and the morphological LA is on the right side, same with ventricles. Can have a RA draining into a LV and LA which drains into a RV. Aortic and pulmonary valves stay with their relevant artery and can be connected to the wrong ventricle.

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56
Q

How is hypertension diagnosed?

A
  • Generally asymptomatic, discovered incidentally
  • Uncommonly - headache, visual disturbance
  • Diagnosis should not be made on single elevated BP reading
    • At least two readings, five minutes between readings over at least two visits
  • Out of office BP measurements
    • 24 hour ambulatory blood pressure monitoring
      • Portable measurement device, BP taken 20-30 minutes throughout the day, 2 hourly overnight
    • Home blood pressure monitoring
      • 2 readings, twice a day, taken over 4-7 days
  • Cut off values for diagnosing hypertension using office and out of office BP monitoring are different
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57
Q

Describe the differential diagnosis for regular broad complex tachycardia

A
  • Ventricular tachycardia
  • Supraventricular tachycardia with bundle branch block - originates from atria
  • Supraventricular tachycardia conducted over an AP
  • Ventricular pacing
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58
Q

Describe the pathogenesis of endocarditis in IVDU

A
  • Classed as separate entity due to tendency to involve right-sided valves
    • Right sided due to:
      • Particulate induced endothelial damage to right-sided valves
      • Increased bacterial loads in these patients
      • Direct physiologic effects of injected drugs
      • Deficient immune response caused by IVDU
  • Tricuspid valve endocarditis more common than aortic or mitral (do occasionally occur)
  • Underlying valve normal in 75-93%, repeated bouts of IE in an IVDU will lead to gradual increase in structural abnormalities of the valve
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59
Q

Describe the heart murmur heard in pulmonary regurgitation

A

Soft early diastolic murmur in pulmonary area

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60
Q

List the drugs used for pharmacological management of hypertension

A
  • Diurectics
    • Loop
    • Thiazide (1st line)
    • Potassium sparing
  • ACE-I/angiotensin II receptor blockers
  • Vasodilators
    • Calcium channel blockers
    • Beta blockers
    • Alpha blockers
  • Others
    • Methyldopa
    • Hydrolazone
    • Monoxidine
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61
Q

What are the complications of repaired tetralogy of fallot?

A
  • Significant pulmonary regurgitations
    • Leads to RV overload, RV dilation and eventually RV failure
    • Will often need pulmonary valve replacement later on in life
  • Arrhythmia
    • Increase in RV pressure causes rise in RA pressure, subsequently dilates and can trigger arrhythmias (more likely to be atrial flutter)
    • Particularly ventricular tachycardia (SVT with RBBB can be similar)
    • Can be treated with anti-arrhythmic agents such as amiodarone or beta-blockers
  • Pulmonary arterial/branch pulmonary artery stenosis
    • Will contribute to rising RV pressure with dilation and failure, can be improved with transcutaneous stenting
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62
Q

Describe abnormal axis seen on ECG

A
  • Left axis deviation -30 to -90 (predominantly negative QRS in II and aVF, predominantly positive QRS in I)
  • Right axis deviation +90 to +180 (predominantly negative QRS in II and I, predominantly positive QRS in III)
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63
Q

How does depolarisation of the heart relate to the shape of ECG waves?

A

Depolarisation travelling towards the lead, upward deflection:

Depolarisation travelling away from the lead, downward deflection:

Depolarisation travelling from superior to inferior:

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64
Q

What are the clinical features of heart failure?

A
  • Clinically causes breathlessness, effort intolerance, fluid retention (peripheral and pulmonary oedema) and is associated with frequent hospital admission and poor survival
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65
Q

Describe the systematic approach to interpreting an ECG

A
  • Before you get to the traces
    • Always ask for clinical context
    • Check the date, time and patient
    • Assess technical quality of the trace (artefact, speed, gain)
  • Look at the rhythm strip
    • Check the QRS rate/ECG intervals
    • Identify P/QRS/T and determine the rhythm
  • Look at the limb leads
    • Determine the QRS axis
  • Look across all leads
    • P/QRS/T morphology
  • Do not reply on automatic interpretation
  • Looking at old ECGs is very helpful
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66
Q

What is seen on examination in a secundum ASD?

A
  • Pulmonary flow murmur
  • Fixed, split second heart sound
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67
Q

What is a univentricular heart? What causes it?

A
  • CHD which results in only one effective pumping ventricle, caused by many types of CHD but rare
  • Tricuspid atresia is one of the commoner causes of univentricular heart (low incidence <1 per 10,000 live births)
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68
Q

Describe the pathophysiology of heart failure

A
  • Natural mechanisms increase perceived low circulating volume/pressure - in place as mechanisms to compensate for massive blood loss (adaptive response which has maladaptive outcome)
  • Natriuretic peptides released from heart in response to atrial stretch in fluid overload - increase natriuresis (kidneys excrete salt and water).
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69
Q

Describe the appearance of early pulmonary oedema on chest X-ray

A
  • Interstitial oedema - Kerley B lines
    • Thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lung
    • Short parallel lines at the lung periphery
    • Frequently observed at the costophrenic angle
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70
Q

Describe the anatomy and location of the tricuspid and pulmonary valves

A

Pulmonary valve -

  • Three leaflets
  • Lies between RV and pulmonary artery

Tricuspid Valve -

  • Three leaflets
  • Lies between RA and RV
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71
Q

List the initial investigations done in hypertension

A
  • U&Es
  • Glucose/HbA1c
  • Lipid profile
  • TFTs
  • LFTs
  • Urine dipstick +/- ACR/PCR
  • 12-lead ECG (?LVH)
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72
Q

What is the axis on an ECG?

A

Axis = overall direction of the electrical activity of the heart

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73
Q

Describe the heart murmur heard in aortic regurgitation

A

High-pitched (‘blowing’) early diastolic murmur, best heard at the left sternal edge (also heard in aortic area) with patient sitting forward in expiration

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74
Q

Explain the symptoms/signs of aortic regurgitation

A
  • LV volume rather than pressure overload - LV dilatation with increased volume to maintain normal stroke volume
  • Patient may be symptomatic even if severe
  • Main symptom = exertional dyspnoea
  • Heart failure will eventually occur
  • Signs
    • Auscultatory - early diastolic murmur
    • Large volume ‘collapsing’ pulse
    • Large pulse pressure
    • Displaced apex beat
    • Additional - pulsatile nail bed circulation, ‘pistol-shot’ femorals and head nodding
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75
Q

Describe the normal ECG intervals

A
  • PR interval <1 large square/<200ms
  • QRS <3 small squares/<120ms
  • QT interval <11 small squares/<440ms
    • Upper limit of normal for QT = 450/470 for male/female
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76
Q

What is coarctation of the aorta?

A

Accounts for 5-8% of all CHD and means narrowing of the aorta, typically located at the insertion point of the ductus arteriosus

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77
Q

What are the consequences of mitral stenosis?

A
  • Pressure overload
  • Dilated LA
  • Atrial fibrillation
  • Pulmonary hypertension
  • Secondary right heart dilatation
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78
Q

Describe Glagovian remodelling

A
  • Atherosclerotic progression = Glagovian remodelling
    • Initially with small plaque formation there is eccentric dilatation of coronary artery to compensate
    • Increased myocardial oxygen demand e.g. exercise - not wide enough to supply blood to myocardium = angina/MI
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79
Q

What is the function of the pulmonary valve?

A
  • Similar function to aortic valve between the RV and the pulmonary artery, although at lower pressures (systolic pressure in the PA may be 200mmHg, compared to 120mmHg in the aorta)
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80
Q

Describe impulse propagation through the heart

A
  • Heartbeat generated in Sino-Atrial node, in high R atrium = P wave
  • Impulse spreads down through atria, depolarisation of atrial muscle = atrial contraction (not captured in final waveform)
  • Impulse reaches Atrio-Ventricular (AV) node, only normal electrical connection between atria and ventricles
  • Impulse delayed in AV node to allow time for ventricular filling after atrial contraction = PR interval
  • Conduction to ventricles through bundle branches then Purkinje fibres, take impulse to ventricular myocardium
  • Ventricular contraction = QRS complex
  • Delay as ventricular action potentials in plateau phase = ST segment
  • Ventricular repolarisation = T wave
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81
Q

Describe the ECG seen in complete AV block

A
  • Impulse generated in SA node can’t propagate to the ventricles
  • Instead, AV nodes intrinsic rhythm dictates ventricular contraction
  • 2 rhythms seen on ECG
    • P waves with regular P-to-P interval - normal atrial sinus rhythm
    • QRS complexes with regular R-to-R interval - generated by AV nodes intrinsic rhythm
  • No correlation seen between two rhythms - lack of apparent relationship between P waves and QRS complexes = complete AV block
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82
Q

What must be decided when considering a patient for valve replacement?

A
  • Mechanical vs tissue valve
  • Durability (age/life expectancy)
  • Anticoagulation (compliance)
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83
Q

Describe the consequences of tetralogy of fallot

A
  • As with all CHD the severity varies greatly with each patient from mild sub-pulmonary stenosis to complete absence of the pulmonary valve, and from slight deviation of the aorta to predominantly overlying the right ventricle
  • As a result of the RVOT obstruction there is restricted flow into the pulmonary arteries, with remainder of the flow passing through the VSD into the systemic circulation via the aorta –> mixing of blood and drop in saturation
  • Perfusion of the pulmonary circulation dependent on the ductus arteriosus with flow from the high pressure aorta into the lower pressure pulmonary circulation - can delay closure of the ductus arteriosus with IV prostaglandins
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84
Q

Describe the structure of the mitral valve

A
  • Lies between LA and LV
  • 2 leaflets
    • Anterior and posterior
    • Anterolateral and posteromedial commissures between
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85
Q

Which device should be used in heart failure?

A
  • Broad QRS (ventricular desynchronisation) - CRT
  • Narrow QRS - ICD
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86
Q

Describe the types of valves which can be used in valve replacement

A
  • Mechanical e.g. tilting disc last longer but need life-long anti-coagulation
  • Tissue e.g. treated porcine valves, have reduced longevity and may require re-replacement but don’t need anticoagulation
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87
Q

Describe the normal physiology of cardiac conduction

A
  • Starts with sinus node - group of cells in the high right atrium
  • Activity spreads through atrium to AV node
  • AV node induces delay of up to 200ms to allow blood flow from the atrium –> ventricle
  • Conduction continues with the Bundle of His, splits into right and left bundle branches
  • Left bundle branch splits into anterior and posterior fascicle
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88
Q

What causes atrial fibrillation electrically?

A

Sinus node suppression - erratic chaotic activity from atria

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89
Q

What are the consequences of endocarditis?

A
  • Early manifestations of infection
    • Fever and murmur - IE until proven otherwise
      • Fever most common sign but maybe absent in elderly
      • Murmur present in 80-85%
        • Often absent in tricuspid endocarditis
      • Fatigue and malaise
  • Embolic events
    • Can take days-weeks to occur
    • Seen early in acute endocarditis
    • Small emboli
      • Petechiae
      • Splinter haemorrhages
      • Haematuria
    • Large emboli
      • CVA
      • Renal infarction
    • Right sides endocarditis - tricuspid valve involvement
      • Septic pulmonary emboli
        • Pleuritic chest pain and classical CXR appearance
  • Long-term effects
    • Immunological reaction
      • Splenomegaly
      • Nephritis
      • Vasculitic lesions of skin and eye
      • Clubbing
    • Tissue damage (seem more commony in acute endocarditis)
      • Valve destruction
      • Valve abscess
        • Aortic root abscess - high mortality, need surgical intervention
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90
Q

Describe the heart murmur heard in tricuspid regurgitation

A

Soft high-pitched (‘blowing’) pan-systolic murmur at left sternal edge, increased during inspiration

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91
Q

Describe the stages of change seen on CXR in heart failure

A
  1. Enlarged heart
  2. Early signs
  3. Late signs
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92
Q

What causes a broad/narrow QRS duration?

A
  • If QRS is broad - must be problem with conducting system below the AV node (His-Purkinje system) = ventricular tachycardia
  • If QRS is narrow - problem with conducting system above the AV node = supraventricular tachycardia
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93
Q

Define endocarditis

A
  • Infection of endocardium (lining of heart)
  • Formation of a vegetation
  • Results in damage to cusp of valves
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94
Q

Which patients with AF should be referred for specialist assessment?

A
  • Patients still symptomatic despite adequate rate control
  • Young age (<60)
  • Inadequate rate control despite beta-blocker (or Ca antagonist) and digoxin)
  • Structural heart disease on echo
  • AF and coexisting heart failure
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95
Q

What causes atrial flutter

A
  • Circular movement of electrical activity within the atrium
  • Rhythm is self-perpetuating
  • Commonly regular, with 2:1 AV conduction e.g. atrial rate 300bpm, ventricular rate 150bpm
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96
Q

Describe the presentation of coarctation of the aorta

A
  • Highly variable in severity - symptoms and time of presentation highly variable
    • Severe narrowing will present in early life with complications of poor lower limb perfusion e.g. cold feet, claudication of the legs, abdominal angina
    • May also develop complications of increased systemic pressure proximal to coarctation e.g. headache and nosebleeds
    • Discrepancies in limb BPs, lower limb should be greater than upper, in coarctation leg BP lower than arm BP due to impaired arterial supply
    • Radio-femoral delay on palpation, collaterals may create a continuous murmur heard on the back
  • Age at presentation depends on position and severity
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97
Q

Which ECG leads show a lateral STEMI and which is the culprit coronary artery?

A
  • I, aVL (+V5/6) leads
  • Left circumflex artery or left anterior descending artery
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98
Q

What is the function of the tricuspid valve?

A

Controls blood flow between the right atrium and right ventricle

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99
Q

Describe management of preserved EF

A
  • Still do not have evidence based treatment for HF with preserved ejection fraction
  • Same signs and symptoms as reduced EF
  • Spironolactone only treatment available, treat w/ diuretics and try to treat underlying cause
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100
Q

How is a heart murmur diagnosed?

A
  • Clinical diagnosis depends on the timing, location, radiation and pitch of the murmur
  • Aortic stenosis produces a systolic murmur, and aortic regurgitation is associated with a diastolic murmur
  • More specific analysis of the timing of the murmur may also indicate its origin
    • Blood flow across aortic valve increases to a peak during mid-systole and then declines, thus aortic stenosis produces a crescendo-decrescendo sound described as an ejection systolic murmur
    • Aortic regurgitation occurs during diastole, when pressure in the LV falls below that in the aorta, and is maximal in early diastole, with reduced flow across the valve as the LV fills - early diastolic murmur
  • Heart sounds and murmurs originating from each valve are best heard at specific sites on the on the surface of the thorax, and have characteristic radiation
    • Aortic stenosis is heard in the aortic area (2nd interspace on the right) and radiates into the neck
  • Stenotic murmurs are low pitched, and regurgitant murmurs are high-pitched
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101
Q

Describe the management of infective endocarditis

A
  • Medical
    • Antimicrobial therapy - most cases results in a cure
  • Surgical - indications =
    • Heart failure
    • Uncontrollable infection
      • Abscess, false aneurysm, enlarging vegetation (urgent)
      • Persisting fever and positive blood cultures >7 days
      • Infection cause by multi-drug resistant organisms
    • Prevention of embolism
      • Large vegetations (>10mm) and embolic episode
  • Earlier surgical interventions –> better outcomes
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102
Q

How can the rhythm of an ECG be determined?

A
  • What is the QRS rate?
  • Are the QRS complexes regular?
  • Is the QRS broad or narrow?
  • Are there P waves? - no P wave = atrial fibrillation/sinoatrial arrest
  • What is the P:QRS relation?
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103
Q

What are the most common causative agents in endocarditis?

A

Bacterial and fungal infections - bacterial more common

  • Bacterial -
    • Gram positive (stain purple)
      • Staphylococci (look like bunch of grapes)
        • Staph. Aureus - two types depending on antibiotic resistance, MRSA or MSSA (methicillin sensitive or resistant)
        • Coagulative negative staphylococci (CoNS) - usually found on skin
      • Streptococci
        • Strep. Viridans - most common cause of IE, usually oral
        • Enterococci - usually found in bowel
    • Gram negative (stain pink)
      • HACEK organisms
        • Haemophilus (haemophilus parainfluenzae)
        • Aggregatibacter (aggregatibacter actinomycetemcomitans, aggregatibacter aphrophilus)
        • Cardiobacterium hominis
        • Eikenella corrodens
        • Kingella (kingella kingae)
      • Enterobacteriaceae (aka coliforms) - E. Coli most common example (usually live in gut)
      • Pseudomonas auerginosa (uncommon rod, seen in IVDU)
    • Not classified as gram negative or positive - not culturable
      • Coxiella burnetii (Q fever) - transmission from sheep, cattle, goats
  • Fungal -
    • Candida species most common
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104
Q

List the main types of heart failure

A
  • HR - reduced ejection fraction
    • Younger
    • More often male
    • Coronary aetiology
  • HF - preserved ejection fraction
    • Older
    • More often female
    • Hypertensive aetiology
  • 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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105
Q

Describe the classification of heart failure based on warm/cold, dry/wet

A
  • Cold = hypoperfusion
  • Wet = congestion
  • Cold-dry
    • Hypoperfusion
      • Cold sweated extremities
      • Oliguria
      • Mental confusion
      • Dizziness
      • Narrow pulse pressure
  • Warm-wet
    • Congestion
      • Pulmonary congestion
      • Orthnopnoea/paroxysmal nocturnal dysnpnoea
      • Peripheral (bilateral) oedema
      • Jugular venous dilation
      • Congested hepatomegaly
      • Gut congestion, ascites
      • Hepatojugular reflux
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106
Q

How is an echocardiogram performed?

A

Probe is placed in an interspace, to the left of the sternum, and angled to cut across the aortic root

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107
Q

Give examples of single ventricle anomalies

A
  • Tricuspid atresia
  • Hypoplastic left heart syndrome
  • Double inlet left ventricle
  • Many of the heterotaxy defects
  • Some variations of double outlet right ventricle
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108
Q

Describe the structure of the aortic valve

A
  • Lies between LV and aorta
  • 3 cusps - trileaflet
    • Right, left, non-coronary
109
Q

Describe sinus node inhibition in the management of heart failure

A
  • Ivabradine inhibits activity of sinus node
  • Reduces hospitalisation but not mortality - not first line
110
Q

Describe triage and priorisisation of patients with NSTEMI

A
  • If patients stabilise post admission, WoS guidelines suggest
    • Low risk - discharge on medical treatment
    • Intermediate risk - discharge to be readmitted for angiogram within 1-2 weeks
    • High risk (GRACE > 140) - urgent inpatient angiogram
    • All via SCI gateway - E-referral
111
Q

Describe the appearance of supraventricular tachycardia on ECG

A
  • QRS rate = fast
  • QRS complexes regular
  • QRS narrow
  • P waves absent
  • No P:QRS relationship
112
Q

List the essential investigations which should be done in atrial flutter

A
  • ECG
  • Echocardiogram
  • Thyroid function tests
  • Liver function tests
113
Q

Describe the appearance of an anterior STEMI on ECG

A
  • ST elevation in V1-4
  • Reciprocal ST depression in inferior leads - significant MI
114
Q

How can the location of acute coronary occlusion be determined on ECG?

A
  • Anterior = V1-4
    • Anterior descending artery occlusion
  • Lateral = I, AVL, V5 + 6
    • Circumflex artery occlusion
  • Inferior = II, III, AVF
    • Right coronary artery occlusion
115
Q

What can cause aortic stenosis?

A
  • Thickening
  • Calcification
  • Rheumatic valve disease
  • Congenital
116
Q

What is an atrial septal defect?

A
  • Hole in the wall between the atria, 10% of congenital heart defects
  • Different types depending on where hole is
    • Secundum most common, primum far more complex and better thought of as ‘partial AVSD’
  • Sinus venosus and coronary sinus defects not technically of the atrial septum and less common
  • Patent foramen ovale - not an atrial septal defect, embryological remnant
  • Only need to close if signs of strain on heart
117
Q

List the risk factors for stroke and thrombo-emoblism in AF

A
  • Major risk factors -
    • Previous stroke
    • TIA or systemic embolism
    • Age >75 years
  • Clinically relevant non-major risk factors
    • CHF or moderate to severe LV systolic dysfunction (e.g. LV EF <40%)
    • Hypertension
    • Diabetes mellitus
    • Age 65-74 years
    • Female sex (AF more common in males but more risky in females - high risk of thromboembolic events esp. if other risk factors)
    • Vascular disease
118
Q

What causes aortic regurgitation?

A
  • Degeneration
  • Rheumatic valve disease
  • Aortic root dilation
  • Systemic disease
    • Marfan’s syndrome
    • Ehlers Danlos syndrome
    • Ankylosing spondylitis
    • Systemic lupus erythematous
  • Endocarditis
119
Q

Define a (heart) valve

A

A device for controlling the passage of fluid (blood) through a pipe or duct (blood vessels/heart chambers), especially an automatic device allowing movement in one direction only

120
Q

Describe the treatment of acute heart failure

A
  • Bilevel or continuous positive airway pressure - preload reduction
  • Dobutamine, dopamine, milrinone - increased inotropy
  • Furosemide - natriuresis
  • Nitrates, morphine - venodilation
  • Nitrates, nitroprusside, dobutamine - arterial vasodilation
  • Ultrafiltration - aqua/natriuresis
121
Q

How effective are beta-blockers in the management of heart failure?

A
122
Q

How prevalent is primary vs secondary hypertension?

A
  • Primary hypertension = 90-95% of cases
  • Secondary hypertension = 5-10% of cases, usually in <40y/o
123
Q

List the symptoms and signs of heart failure

A
  • Symptoms
    • Dyspnoea (orthopnoea, PND) and 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
124
Q

Describe the diagnostic evaluation of a patient with hypertension

A
  • Confirm the diagnosis - out of office blood pressure 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

Describe the use of SGLT2 inhibitors in heart failure

A
  • SGLT2 transporter reabsorbs glucose in kidney, inhibitors cause more excretion of glucose and water
  • Acts like a diuretic to reduce fluid overload
  • Beneficial in heart failure with and without diabetes - reduces mortality and hospitalisation
126
Q

What should be examined in a patient with hypertension?

A
  • BP measured both arms
  • Weight/BMI
  • Xanthelasma
  • Pulses
  • Oedema
  • Rashes
  • Heart - murmurs
  • Lungs - failure
  • Abdomen - renal masses
  • Vascular bruits - kidneys, carotids
  • Eyes
127
Q

What are the complications of uncontrolled hypertension?

A

Uncontrolled hypertension affects specific organ groups leading to end organ damage:

  • TIA, stroke (35-40%)
  • Cardiac
    • MI (20-25%)
    • LVH
    • CHD
    • HF (50%)
  • Renal failure (35-40%)
  • Peripheral vascular disease
  • Retinopathy
128
Q

Describe the risk scoring of acute coronary syndrome

A
  • GRACE score
    • At admission - age, HR, SBP, creatinine, CHF stage
    • At discharge - cardiac arrest at admission, ST-segment deviation, elevated cardiac enzymes/markers
129
Q

Where does coarctation of the aorta usually form?

A

Tends to form after LSA in a ‘juxta-ductal’ position

130
Q

How can valve dysfunction be treated?

A
  • Medication
    • LV bigger, mitral regurgitation
    • Medication can shrink LV
  • Intervention
    • Surgical
      • Valve repair
      • Valve replacement
    • Procedural
131
Q

What investigations should be done in heart failure?

A
  • ECG (MI, LVH, rhythm, rate, QRS duration)
  • CXR (exclude lung pathology, pulmonary oedema)
  • Echocardiogram (chamber size, systolic and diastolic function, valves) - CMRI alternative
  • Blood chemistry (U&Es, Cr, urea, LFTs, urate)
  • Haematology (Hb, RBW)
  • Natriuretic peptides (BNP, NT-proBNP)
132
Q

List the signs and symptoms of an MI

A
  • Symptoms:
    • Chest pain - band-like, tight (may be discomfort rather than pain)
    • Back pain
    • Jaw pain
    • Indigestion (‘heartburn’)
    • Sweatiness, clamminess - SNS activation
    • Shortness of breath
    • None (diabetes/dementia/silent MI)
    • Death
  • Signs:
    • Tachycardia - SNS activation
    • Distressed patient - feeling of ‘impending doom’, agitation
    • Heart failure (crackles, raised JVP)
    • Cardiogenic shock - output insufficient to meet demands, delirium, cold
    • Ventricular arrhythmia
    • None
133
Q

What are ECGs used for?

A

12-lead electrocardiograph (ECG) used to record the electrical activity of the heart from the skin

  • First line investigation for patients with chest pain, palpitations or blackouts
  • Live-saving in the management of arrhythmias and acute myocardial infarction
  • Can be better diagnostically than advanced/invasive tests
134
Q

What should be asked in a history of a patient with hypertension?

A
  • Risk factors
  • Family history
  • Relevant medical condition
    • CKD
    • OSA
    • Diabetes
  • Established complications
    • Stroke
    • IHD
    • PVD
    • Heart failure
  • Current and past BP medications
  • Other drugs
    • OCP
    • Steroids
    • NSAIDs
    • Cyclosporin
    • Herbal remedies
    • Liquorice
    • Illicit substances
135
Q

Describe the heart murmur heard in aortic stenosis

A

Low-pitched ejection systolic murmur, best heard in the aortic area, radiating to the neck

136
Q

Describe the diagnosis of infective endocarditis

A
  1. Blood cultures
  2. Echocardiograph
137
Q

What are the features of failing Fontan circulation?

A
  • Constitutional
    • Growth failure - inadequate cardiac output
    • Exercise intolerance - chronotropic incompetence, pronounced atrial distention
    • Depression - secondary to limitations on functional status
  • Haemodynamic
    • Obstruction - atriopulmonary, pulmonary arterial
    • Systemic venous - pulmonary venous return, atrioventricular valve inflow
    • Systemic outflow - ventricular outflow, aortic arch
    • AV valve function - >moderate regurgitation, >mild stenosis
    • Ventricular dysfunction - secondary: atrial dilation/distortion, AV valve or semilunar valve dysfucntion, chronic arrhythmias or antiarrhythmic medications, impaired myocardial perfusion due to coronary sinus hypertension
    • Thrombosis - systemic venous, atrial, pulmonary
  • Rhythm
    • Arrhythmias - sinus node dysfunction, predominant junctional rhythm, AV block, supraventricular tachycardia/atrial tachycardia, ventricular tachycardia
  • Pulmonary
    • Cyanosis - intracardiac right to left shunt, veno-venous collaterals, pulmonary arteriovenous malformations
    • Pleural effusions
  • Gastrointestinal
    • Ascites - secondary to portal hypertension related to obstruction, versus cirrhosis
  • Metabolic
    • Metabolic markers - declining albumin, thrombocytopaenia, hyperbilirubinaemia, coagulopathy
138
Q

How is a doppler ultrasound performed?

A
  • The probe is placed at the apex and the ultrasound directed towards the aortic valve
  • Valve movements shown as lines, flow away from probe i.e. across the valve during systole shown as downwards signal
  • Some flow also detected during diastole (blood entering ventricle from mitral valve)
139
Q

How is transposition of the great arteries treated?

A
  • Delay closure of foetal shunts w/ prostaglandins - buys time to perform surgery
  • Two methods of surgical correction - atrial and arterial switch
140
Q

Describe the pathogenesis of rheumatic heart disease

A
  1. Streptococcus pyogenes infection (e.g. strep throat)
  2. Infection partially/not treated
  3. Liberation of Streptolysin ‘O’ exotoxin
  4. Anti-Streptolysin O antibodies produced against Streptolysin
  5. Cross-reactivity of antibodies - cardiac valves have similar antigenic structure so antibodies attack valves
  6. Stenosis or regurgitation of valves
141
Q

Describe the pathogenesis of fluid overload in congestive heart failure

A
  • Heart not beating properly, backed up fluid, heart enlarges
  • Fluid overload, vessels get bigger
  • Big distended blood vessels –> fluid leaks out
  • Initially small amount of leakage then lots
142
Q

How prevalent is congenital heart disease?

A
  • 8 per 1000 live-born infants have significant cardiac malformations, some abnormality present in 1-2% e.g. bicuspid aortic valve
  • Becoming increasing common - people are surviving longer, children who would have died in infancy are now surviving to 30s/40s –> 60s/70s due to advances in treatment
    • Advances in treatment - development of specialist multidisciplinary congenital cardiac service in recognition of complexities of managing these patients
143
Q

What are the consequences of a univentricular heart?

A

Only one pumping chamber, foetal circulation relies on patent foramen ovale/ductus arteriosus for mixing of oxygenated and deoxygenated blood

144
Q

Describe the incubation period of infective endocarditis

A

Incubation period = 2 weeks

Longer in PVE

145
Q

List the stages of congestive heart failure and the features seen on CXR

A
  • Stage 1 - redistribution PCWP 13-18mmHg
    • Redistribution pulmonary vessels
    • Cardiomegaly
  • Stage 2 - interstitial oedema PCWP 18-25mmHg
    • Kerley lines
    • Peribronchial cuffing
    • Hazy contours of vessels
    • Thickened interlobar fissures
  • Stage 3 - alveolar oedema PCWP >25mmHg
    • Consolidation
    • Air bronchogram
    • Cotton-wool appearance
    • Pleural effusions
146
Q

How can a secundum ASD be treated?

A

Can be fixed surgically with a sternotomy or through the groin vessels with a transcatheter device if small enough

147
Q

List the lifestyle interventions which can by used to control hypertension

A
  • Exercise
  • Weight loss (10kg)
  • Reduction in sodium intake
  • Reduction in alcohol intake
  • DASH diet
  • Smoking cessation
148
Q

Describe the use of angiotensin receptor blockers in heart failure

A
  • An ARB is an alternative in patients intolerant of an ACE inhibitor due to cough
  • Need to stop ACE inhibitor when using ARB - already causes ACE inhibition, likely to cause angioedema and cou
149
Q

What is Fontan circulation?

A
  • Single functional ventricle used to support the systemic circulation by disconnecting it from the pulmonary valve and artery
  • The IVC and SVC are redirected and plumbed straight into the pulmonary arteries ultimately bypassing the heart altogether
  • Deoxygenated blood flows up the IVC directly into the pulmonary arteries without passing through any valves, blood oxygenated in the lungs and flows back to the left atrium as deoxygenated blood, through the mitral valve into the single ventricle, through the aortic valve into the aorta and remainder of the systemic circulation
150
Q

How are the ECG leads arranged on the body?

A
  • 10 leads - 1 per limb and 6 arranged around the heart
    • 2 intersecting planes - chest leads arranged in transverse plane from anterior right ventricle to apex of left ventricle
    • Limb leads in coronal plane full 360 degrees around heart, can be thought of as clock face with LVA at 5 o’clock
151
Q

Describe secondary prevention of MIs

A
  • Aspirin (lifelong) - shown to reduce risk of reinfarction, CV events and CV death
  • Ticagrelol/Clopidogrel - patients with ACS should receive DATP for six months
    • Longer duration used when risks of atherothrombotic events outweigh the risk of bleeding
    • Shorter duration used where risk of bleeding outweigh risk of atherothrombotic events
  • Beta-blocker - reduce risk of reinfarction and CV mortality including arrhythmic death and all cause mortality. Also reduce risk of symptomatic angina
  • ACEI - shown to reduce all cause mortality, MI and stroke
  • Statin - large RCT showed statins reduce risk of death, reinfarction and hospitalisation for ischaemia
  • Modification of risk factors e.g. smoking cessation
152
Q

How is hypertension managed?

A
  • Lifestyle measures
  • Pharmacological management
  • Device based therapies
    • E.g. renal denervation, baroreceptor stimulation
153
Q

Describe the pathogenesis of rheumatic valve disease

A
  • Acute rheumatic fever
    • Painful joints, fever, rash
  • 1-3% of streptococcus 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
154
Q

Describe the types of atrial fibrillation

A
  • Atrial fibrillation may be
    • Paroxysmal - intermittent, starting and stopping
    • Persistent - requiring intervention to terminate the arrhythmia, e.g. IV antiarrhythmic drug injection or DC cardioversion
    • Permanent
  • Often start off paroxysmal and become more persistent
155
Q

Describe antiarrythmic drugs used for rhythm control in AF

A
  • Class 1 (Na+ channel blockers)
    • E.g. Flecainide 100mg bd, Propafenone 150-300mg bd
  • Class 3 (K+ channel blockers, prolong action potential duration/QT interval)
    • E.g. Sotalol (beta blocker with additional class 3 activity) 80mg bd, amiodarone 200mg daily
  • Multichannel blockers
    • E.g. Dronedarone 400mg bd
  • Often used in combination with a beta blocker
156
Q

Describe the subsequent management of an NSTEMI

A
  • Monitor in coronary care unit for complications of MI
    • Aspirin
    • Clopidogrel or ticagrelor
    • Low molecular weight heparin or fondaparinux
  • Drugs for secondary prevention
    • ACE inhibitors (for all - if LVSD reduce mortality)
    • Beta blockers (for all - if LVSD reduce mortality)
    • Statins - for all
    • Eplerenone - only for diabetes and LVSD or clinical HF
  • Echocardiogram for LV function and cardiac structure
  • Cardiac rehabilitation
  • If LVSD at >9 months consider primary prevention ICD
157
Q

Describe the typical clinical history of pericarditis

A
  • Several days of
    • Fatigue
    • Flu-like symptoms
  • Acutely
    • Sharp chest pain worse on inspiration
  • On ECG
    • Clinical history not consistent with MI
    • Concave ST elevation
    • No specific territory (often global)
    • No reciprocal change
    • PR depression
158
Q

Describe the risk factor-based point scoring system for strokes

A

CHADS-VASc

  • Adjusted stroke rate according to CHADS-VASc score - stroke rate increases as CHAD-VASc score increases
159
Q

What causes thrombus/embolus formation in AF?

A
  • Atria don’t contract properly, stasis of blood –> risk of clot formation
  • Thrombus can become dislodged and embolise
  • 90% of emboli travel to the brain = stroke
160
Q

How is Fontan circulation created?

A
  • BT shunts
    • Tube graft placed from an artery (usually left subclavian or left innominate artery) to the pulmonary artery
  • Norwood procedure - 1st week of life
    • Right ventricle becomes the systemic or main ventricle pumping to the body
    • A new or ‘neo’ aorta is made from part of the pulmonary artery and the original, tiny aorta, which is reconstructed/enlarged to provide blood flow to the body
    • To provide blood flow to the lungs, a small tube graft is placed either from an artery to the lung vessels (called a modified BT shunt) of from the right ventricle to the lung vessels (called a Sano modification)
  • Bi-directional Glenn - 3-6 months
    • Superior vena cava is taken off the heart and sewn directly to the pulmonary artery
    • If a prior BT shunt was present, it is removed
    • If a pulmonary artery band was previously placed, it may be removed but can also be left in place in some situations
  • Fontan completion operation - 2-3 years
    • Inferior vena cava is taken off the heart and connected directly to the pulmonary arteries
    • Until now, the blood has bypassed the lungs and has been pumped directly to the body resulting in oxygen levels lower than normal
161
Q

Describe the foetal circulation in transposition of the great arteries

A
  • Shunts in foetal circulation allow for oxygenation of blood
  • When baby takes its first breath at birth, changes in pressure in the lungs/heart mean that the foramen ovale and ductus arteriosus close within a few hours
  • Loss of shunts is catastrophic for baby with TGA therefore we delay closing by giving the baby prostaglandins - buys time to perform surgery
162
Q

Which ECG leads show an anterior STEMI?

A
  • V1-2 septum, V3-4 apex, V5-6 anterior/lateral
  • Left anterior descending artery
163
Q

Describe the management of hypertension depending on the grade

A
  • High normal BP
    • Lifestyle advice
    • Consider drug treatment in very high risk patients with CVD, especially CAD
  • Grade 1 hypertension
    • Lifestyle advice
    • Immediate drug treatment in high or very high risk patients with CVD, renal disease or HMOD
    • Drug treatment in low moderate risk patients without CVD, renal disease or HMOD after 3-6 months of lifestyle intervention if BP not controlled
  • Grade 2 hypertension
    • Lifestyle advice
    • Immediate drug treatment in all patients
    • Aim for BP control within 3 months
  • Grade 3 hypertension
    • Lifestyle advice
    • Immediate drug treatment in all patients
    • Aim for BP control within 3 months
164
Q

Describe the appearance of atrial flutter on ECG

A
  • Rate variable
  • Regular narrow QRS
  • Sawtooth atrial activity 300bpm
  • Variable AV block
165
Q

Describe rhythm control in AF

A
  • Particularly for younger patients, and patients with ongoing symptoms despite good rate control
  • Options include
    • Direct current cardioversion (for persistent AF)
    • Antiarrhythmic drugs
    • Catheter ablation
166
Q

How common are secumdum ASDs?

A

80% of all ASDs

167
Q

List the signs of mixed aortic valve disease

A
  • Depend on severity of relative lesions
  • If both regurgitation and stenosis are severe, characteristic double waveform (‘bisferiens’) pulse may be found
168
Q

Describe the normal ECG waveform

A
169
Q

Compare the troponin and ECG changes in unstable angina, an NSTEMI and a STEMI

A
  • Unstable angina
    • Troponin normal
    • Normal ECG, ST depression possible
  • NSTEMI
    • Raised troponin
    • ECG can be normal, ST depression, T wave inversion
  • STEMI
    • Raised troponin
    • ST elevation, hyperacute T waves, new LBBB, T wave inversion, Q waves (after days)
170
Q

What are the complications of secundum ASD?

A
  • RV failure
  • Tricuspid regurgitation
  • Atrial arrhythmias
  • Pulmonary hypertension
  • Eisenmenger syndrome
171
Q

What are the treatment targets in hypertension treatment?

A
  • <140/90
  • <130/80 if tolerated
  • Easy to overshoot and cause symptomatic hypotension
172
Q

How are blood cultures used in the diagnosis of infective endocarditis?

A
  • Most important investigation in any patient suspected of having IE
  • Constant bacteraemia so no need to wait for fever to take samples
  • 3 sets of blood cultures required - if organism only found in one could be due to contamination
  • Volume most important factor in organism detection
    • 10mls/bottle required
  • Before antibiotics - antibiotics will get rid of organisms
  • Aseptic technique - reduce risk of contamination and risk of needle stick injury
173
Q

Describe the approach to analysing SVT on ECG

A
  • Look for P waves in V1
    • 1:1 AV = AVNRT or AVRT
    • A>V = flutter, atrial tachycardia
  • Block AVN
    • Adenosine given through vein in antecubital fossa, short-acting
    • Transiently blocks AV node, establish AV node activity
      • If no atrial activity = AVNRT or AVRT
      • If saw tooth atrial activity = atrial flutter or atrial tachycardia
174
Q

How is permanent AF treated?

A
  • Object of anti-arrhythmic therapy is to control the ventricular rate - achieved with Beta-blocker or calcium channel blocker (dilitiazem or verapamil) in combination w/ digoxin if necessary
  • Digoxin alone not very effective at controlling heart rate during exertion
  • If medical therapy fails then ablation of AV node can be considered thus severing the connection between the atrium and the ventricle
    • Backup activity sensing ventricular pacemaker required
175
Q

Describe the prevalence of AF

A
  • Increases with age
  • Incidence higher in males than females
176
Q

List the most common congenital heart defects

A
  • Acyanotic
    • L to R shunts
      • VSD 30%
      • Persistent ductus arteriosus 12%
      • ASD 10%
    • Outflow obstruction
      • Pulmonary stenosis 7%
      • Aortic stenosis 5%
      • Coarctation of the aorta 5%
  • Cyanotic
    • Tetralogy of the Fallot 5%
    • Transposition of the great arteries 5%
    • Atrioventricular septal defect (complete) 2%
177
Q

List the symptoms of mitral stenosis

A
  • Shortness of breath
  • Palpitation
  • Chest pain
  • Haemoptysis
  • Right heart failure symptoms
178
Q

What are the side effects associated with amidarone?

A
  • Contains iodine so affects thyroid gland
  • Can cause hypo or hyperthyroidism (can worsen AF)
  • Need to regularly test thyroid function
179
Q

Describe the risk of stroke associated with AF

A
  • Annual risk of ischaemic stroke in AF (without prior stroke or TIA) up to 5% per annum
  • With previous TIA/stroke - 12% per annum
  • With rheumatic heart disease, principally mitral stenosis - 17-20% per annum
  • Intermittent AF usually occurs in younger patients with less associated CVD so risk of stroke is lower (intermittency alone doesn’t appear to independently influence stroke risk)
180
Q

Describe the pathophysiology of hypertension

A
181
Q

What are the symptoms of aortic stenosis?

A
  • Shortness of breath
  • Presyncope
  • Chest pain
  • Reduced exercise capacity
182
Q

List the signs of transposition of the great arteries

A
  • Cyanotic spells
  • Ejection systolic murmur at upper left sternal edge
  • Single 2nd heart sound
  • Clubbing
183
Q

How is paroxysmal AF treated?

A
  • If well tolerated and occurs infrequently then no anti-arrhythmic therapy is required and the patient can be reassured
  • If the patient has symptoms requiring treatment and has no significant cardiac disease, anti-arrhythmic therapy is either a Beta-blocker or class 1C anti-arrhythmic agent such as flecainide
  • In patients with significant heart disease e.g. unstable coronary disease, recent heart attack or impaired LV function then class I agents e.g. flecainide are contra-indicated, associated with excess mortality
    • In those with severe LV dysfunction - amiodarone is agent of choice
  • In many patients the arrhythmia originates from the pulmonary veins, and ablation to electrically isolate the pulmonary veins may be beneficial
184
Q

What is unstable angina? How is it differentiated from an MI?

A
  • An acute coronary event without a rise in troponin - no myocardial necrosis
  • I.e. clinical presentation of an MI + ECG changes or tight narrowings on coronary angiography
  • Rare now with high sensitivity troponin
185
Q

Describe the antimicrobial therapy in infective endocarditis

A
  • Bactericidal agents at high doses
  • Treatment tailored to organism susceptibility
  • Duration of therapy
    • NVE: 4 weeks
    • PVE: 6 weeks
  • Intravenous therapy for duration in most cases - oral may not penetrate the avascular vegetations
186
Q

Describe the arterial switch method of correcting transposition of the great arteries

A
  • Disconnect the aorta and pulmonary artery, switch them and sew them back on
  • The aorta is now above the LV and the pulmonary artery is now above the RV
  • Special care needs to be taken with the coronary arteries which have to be reconnected to the aorta and if not carefully stitched back on can occlude and cause an MI or sudden death post-op
  • Patients often develop stenosis of the pulmonary artery later in life requiring stretching, stenting or in some cases further surgery
187
Q

Describe the appearance of a normal CXR

A
  • Heart less half the width of chest wall
  • Lungs black - full of air
  • Size of vessels in lungs normal
188
Q

Describe the nomenclature used to describe a normal heart

A
  • Sequential segmental arrangement
  • Each component named in turn - atria, ventricles, great vessels
  • Normal heart
    • Situs solitus - thoracic and abdominal organs in right place
    • Levocardia - heart points to left
    • Concordant AV connections - RA to RV, LA to LV
    • Concordant VA connections - RV to pulmonary artery, LV to aorta
189
Q

Describe the criteria used in endocarditis

A

Duke Criteria:

  • Developed to aid diagnosis of endocarditis
  • Major
    • Typical organism in 2 separate blood cultures
    • Positive echocardiogram or new valve regurgitation
  • Minor
    • Predisposition (heart condition or IVDU)
    • Fever >38 degrees
    • Vascular phenomena (e.g. septic emboli)
    • Immunological phenomena (e.g. Osler’s nodes)
    • Positive blood cultures (not meet major criteria)
  • Definite IE = 2 major, 1 major + 3 minor or 5 minor
190
Q

Describe the aims of the treatment of AF

A
  • Prevention of stroke
  • Symptom relief
  • Optimum management of concomitant CVD
  • Rate control
  • +/- correction of rhythm disturbance (not always necessary)
191
Q

Describe the atrial switch method of correcting transposition of the great arteries

A
  • Used to be done, now not performed
  • Redirect the venous blood to the appropriate side of the heart, create a channel for the deoxygenated venous blood to pass into the pulmonary artery via the LV and the atrial septum is cut away to allow the oxygenated venous blood by pass through the RA and into the aorta via the LV
  • Issues mainly related to the fact the RV has now become the systemic ventricle pumping blood around the body, which is it not designed to do - extra demand of the RV means it starts to fail and we get systemic ventricular failure
  • AV valve always follows the ventricle, almost all the patients develop regurgitation of the tricuspid valve, which worsens their systemic ventricular dysfunction
192
Q

What are the complications of coarctation of the aorta?

A
  • Upper body hypertension
  • Berry aneurysms
    • Thought to be due to systemic connective tissue disorder rather than direct consequence of coarctation
  • Claudication
  • Renal insufficiency
  • Accelerated coronary artery disease common - may suggest a more generalised artiopathy
  • Often associated with other congenital heart defects, in particular bicuspid aortic valve (need to screen)
193
Q

Describe the appearance of a posterior wall infarction on ECG

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
  • May be caused by left circumflex artery (usually) or right coronary artery occlusion
    • Often associated with inferior or lateral ST elevation
  • ST depression in anterior leads
  • Subtle ST elevation in inferior leads
194
Q

What is 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 (low filling pressure = low circulating blood volume)
  • Characterised by typical haemodynamic changes (e.g. systemic vasoconstriction) and neurohumoral action
195
Q

What are the complications of catheter ablation?

A

Ablation requires a hole to be made in the intratrial septum - complications e.g. thrombus, bleeding into pericardium (tamponade)

196
Q

What are the options for reperfusion therapy following an MI?

A
  • Primary PCI
    • Invasive procedure to open the blocked artery and treat the underlying atheromatous plaque by balloon angioplasty and stent placement
    • Can restore the coronary blood supply, minimise cardiac damage and improve outcomes
    • Superior to thrombolysis - short and long term mortality, sroke, reinfarction recurrent ischaemia and need for CABG
    • Risks of invasive procedure (e.g. vascular damage, stroke), only performed at specialist centres
    • SIGN recommend as treatment of choice if patient can recieve treatment within 120 minutes of ECG diagnosis - journey time of 40 minutes or less
  • Thrombolytic therapy
    • If pPCI not available (either due to contraindications or patient’s geographical location) - should recieve immediate thrombolytic therapy with PCR in due course
    • Fibrinolytic therapy to break up thrombus in coronary artery, risks of bleeding, including haemorrhagic stroke, contraindications include recent surgery, previous stroke, GI bleeding, bleeding disorders
197
Q

Describe the appearance of a left bundle branch block on ECG

A
  • I more positive than II
  • Broad QRS - >120ms
  • Dominant S in V1
  • Broad R wave with deep S wave and inverted T wave in V6
198
Q

Describe the diagnosis of atrial fibrillation

A
  • Irregular pulse
    • ‘Irregularly irregular’
    • Confirmed by 12-lead ECG
  • May require prolonged ambulatory ECG recordings to detect paroxysmal (intermittent) AF
199
Q

What is aortic stenosis? Describe the aetiology of aortic stenosis

A
  • Narrowing of the aortic valve
  • Incidence of AS increases with age
  • Aetiology
    • Age related calcification in 50%
    • Calcification of congenitally abnormal valve 30-40%
    • Rheumatic fever 10%
200
Q

What are the most common causative organisms by the type of endocarditis?

A
  • NVE:
    • Strep. Species - S. Viridans, then enterococci
  • IVDU:
    • Staph. Aureus
    • Higher incidence of gram negative and fungal infections - organisms injected into veins, more variety of causative organisms
  • PVE:
    • Staph - CoNS (best at forming biofilm)
    • Gram negative and fungal infection more common in this group
  • Streptococcal endocarditis, especially caused by Viridans present more indolently - subacute endocarditis (NVE)
  • Staph. Aureus, gram negative and fungal endocarditis present acutely, causing rapidly valve destruction (IVDU/PVE)
201
Q

What is atherosclerosis?

A
  • Deposition of lipids in BV wall forming atherosclerotic plaque, causes narrowing of the vessel
  • Risk of rupture of plaque and embolus leading to acute coronary syndrome + MI
202
Q

What are the symptoms of mitral regurgitation?

A
  • Shortness of breath
  • Palpitation
  • Right heart failure symptoms
203
Q

What additional investigations can be done in selected patients to aid the diagnosis of heart failure?

A
  • Coronary angiography
  • Exercise test
  • Ambulatory ECG monitoring
  • Myocardial biopsy
  • Genetic testing
204
Q

What are the consequences of aortic regurgitation?

A
  • Volume overload
  • LV dilatation
205
Q

Compare outcomes in primary PCI compared with thrombolysis

A

Compared to thrombolysis, primary PCI:

  • 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
206
Q

List the complications of MIs

A
  • Arrhythmias
    • VT/VF - DC cardioversion
    • AF (heart failure/LVSD or other structural complication)
  • Heart failure
    • Diuretics, inotropes, vasodilators
  • Cardiogenic shock
    • IABP (intra-aortic balloon pump, ventricular assist device)
  • Myocardial rupture
    • Septum - VSD (surgery)
    • Papillary muscle - mitral regurgitation (surgery)
    • Free wall - tamponade, usually fatal)
  • Psychological
    • Anxiety/depression
    • Cardiac rehabilitation
207
Q

What causes supra-ventricular tachycardia?

A
  • Due to re-entry circuit using an extra electrical pathway
  • Can be present within the AV node or as a connection between the atrium and ventricle (an accessory pathway or bypass tract)
  • SVT usually initiated by an atrial extra-systole which finds the accessory pathway refractory to accepting stimulation in the direction of atrium to ventricle
  • Electrical activity then passes through the normal conduction systems, then is able to conduct back from the ventricle to atrium through the accessory pathway
208
Q

What is atrial flutter?

A

Haemodynamically similar to atrial fibrillation, abnormal electrical activity around the tricuspid valve starts a re-entry circuit, causes supraventricular tachycardia.

Risk of thrombosis.

209
Q

Describe investigations of aortic valve lesions

A
  • ECG may show evidence of LVH
  • Chest X-ray will show cardiomegaly w/ AR, but may be normal in AS
  • Echocardiography most valuable
    • Allows imaging of valve, showing reduced valve opening and calcification
    • LV dimensions, hypertrophy and function can be measured
  • Doppler allows quantification of the degree of stenosis and assessment of the severity of AR
    • Colour doppler superimposes the blood flow onto the echo image, and is of value in identifying and assessing regurgitation
  • Exercise testing may be used w/ caution - in this case good for assessing coronary artery disease
  • Coronary angiography performed to determine coronary artery disease
  • Aortogram to confirm AR, shows calcification of valve
210
Q

Describe the heart murmur heard in pulmonary stenosis

A

Soft ejection systolic murmur pulmonary area

211
Q

What are the benefits of devices in the management of heart failure?

A

Reduces CV death and hospitalisation

212
Q

Which antibiotics are used for the common causative agents of bacterial endocarditis?

A
  • Streptococcus species - benzylpenicillin +/- gentamicin
  • Enterococcus species - amoxicillin or vancomycin +/- gentamicin
  • S. Aureus (MSSA) - flucloxicillin +/- gentamicin
  • S. Aureus (MRSA) - vancomycin +/- gentamicin
  • CoNS - vancomycin +/- gentamicin +/- rifampicin
  • Organisms often intrinsically resistant to gentamicin, but the penicillin/vancomycin acts by destroying the bacterial cell wall, which allows the gentamicin to exert its effect –> synergy
  • CoNS tends only to cause PVE, able to stick to valves very effectively, therefore often need 3 agents
  • Rifampicin v good at penetrating biofilm but using it alone results in resistance v quickly
213
Q

Describe the appearance of a high lateral STEMI on ECG

A
  • ST elevation in high lateral leads - I, aVL
  • Reciprocal ST depression in inferior leads
214
Q

Describe the pathology of valve stenosis

A

Stenosis results from fusion of valve cusps, fibrosis and calcification

215
Q

Describe the process of a transradial percutaneous intervention

A
  • Catheter up L arm through radial artery into heart
  • Coronary stent
216
Q

How can the risk of adverse outcomes be calculated in MI?

A

HEART Score - uses risk factors to predict risk of CV outcomes e.g. death, MI, stroke

217
Q

What is transposition of the great arteries?

A
  • Aorta and pulmonary artery switch places, aorta connected to right ventricle and pulmonary artery is connected to the left ventricle
  • Creates 2 separate circulation systems:
    • In the systemic circulation deoxygenated blood returns to the RA via the SVC and IVC, passes through the tricuspid valve and into the RV, then pumped through the aortic valve into the aorta and around the body without being oxygenated
    • In the pulmonary circulation, the oxygenated blood passes back into the left atrium via the pulmonary veins, through the mitral valve into the left ventricle, and is then pumped back into the pulmonary artery via the pulmonary valve
  • Without mixing the oxygenated and deoxygenated blood there is profound cyanosis
218
Q

Describe the treatment of low LVEF CHF

A

SIGN Guidelines -

  • Beta blocker and ACE inhibitor (if intolerant of ACE inhibitor give an angiotensin receptor blocker)
  • Ongoing symptoms (NHYA II-IV)
    • Mineralocorticoid receptor antagonist (added to ACE inhibitor or ARB)
  • Ongoing symptoms (NHYA II-IV)
    • Seek specialist advice
    • Sacubitril/valsartan (stop ACE inhibitors and ARBs, continue beta blocker and MRA)
  • Ongoing symptoms (NHYA II-IV)
    • Implantable cardioverter-defibrillator (ICD) or implantable cardiac resynchronisation therapy pacemaker/device (CRT-P/D) in selected patients, ivabradine (if sinus rhythm heart rate >75bpm)
  • Ongoing symptoms
    • Digoxin, hydralazine/isosorbide dinitrate (if intolerant to ACE inhibitor, ARB or sacubitril/valsartan due to renal dysfunction, hyperkalaemia or other side effects
  • Ongoing symptoms
    • Consider referral to the National Transplant Unit for assessment for LVAD/cardiac transplantation
      • V few patients get cardiac transplantation
      • Total artificial heart?
  • Diuretics:
    • Symptomatic relief - reduce peripheral/pulmonary oedema
    • Don’t alter outcomes
  • Hydralazine and isosorbide dinitrate used in African-American populations who sometimes don’t respond as well to other treatments
219
Q

Describe the treatment of coarctation of the aorta

A
  • Can be repaired both surgically and transcatheter
    • Surgical repair via thoracotomy - subclavian flap, end to end, jump graft
    • Non-surgical - transcatheter through femoral artery, fed up to the coarctation, balloon passed through and inflated to stretch the narrowed artery (may recur)
220
Q

What causes secondary hypertension?

A
  • Endocrine
    • Hyperaldosteronism
    • Phaeochromocytoma
    • Thyroid disorders
  • Vascular
    • Co-arctation of the aorta
  • Renal
    • Renal artery stenosis
    • Renal parenchymal disease
  • Drug
    • NSAIDs
    • Herbal remedies
    • Cocaine
    • Exogenous steroid use
  • Other
    • Obstructive sleep apnoea
221
Q

How can the CV risk be assessed in hypertension?

A
  • Based on BP category, presence of end organ damage, presence of diabetes, CV or renal disease
  • Various calculators available to calculate CV risk e.g. ASSIGN score
222
Q

List the complications of STEMI

A
  • Arrhythmias
    • Bradycardia - heart block may result from vagal overactivity (as in this scenario) or because of involvement of the conducting system in extensive anterior infarction
    • Ventricular arrhythmia - the risk of cardiac arrest because of ventricular fibrillation is greatest at the onset of chest pain and diminishes exponentially thereafter, making the first 24 hours the period of highest risk. Unfortunately, many patients die suddenly reaching hospital
    • Atrial arrhythmia - the most common is atrial fibrillation, which may be transient
  • Heart failure
    • Extensive infarction can result in severe LV dysfunction and heart failure
    • Can occur acutely, with the development of pulmonary oedema and HF may resolve with successful treatments
    • Mortality directly related to extent of LV damage, and heart failure is an indicator of poor prognosis
  • Valvular disease
    • Acute mitral regurgitation can be caused by rupture of papillary muscles
  • Cardiogenic shock
    • Severe LV damage can result in shock, with hypotension, heart failure and poor cardiac output - very poor prognosis
    • Revascularisation by urgent angioplasty has been shown to improve outcome, but mortality remains high
  • Myocardial rupture
    • Consequences of rupture depend on site of infarction
    • Rupture of free LV wall is usually fatal
    • Rupture of inter-ventricular septum can produce a ventricular septal defect, the consequences of which depend on the size of the defect
    • Papillary muscle rupture causes mitral regurgitation, which may cause heart failure
  • Pericarditis/Dressler’s syndrome
    • Causes chest pain and was usually self-limiting after several days, it is uncommon in this era of early reperfusion
  • LV mural thrombus
    • May embolise e.g. to brain causing stroke
  • Death
    • Risk of death significantly decreased by revascularisation
223
Q

What risks are associated with hypertension?

A
  • Independent risk factor for the development of coronary artery disease, cerebrovascular disease, peripheral artery disease and heart failure
    • CVD risk doubles for every 20mmHg increase in systolic and 10mmHg increase in diastolic pressure
224
Q

Describe the appearance of atrial fibrillation on ECG

A
  • Rate variable
  • Irregular, narrow QRS
  • No P waves - chaotic/absent atrial activity
225
Q

Describe the subsequent management of a STEMI

A
  • Monitor in coronary care unit for complications of MI
  • Drugs for secondary prevention
    • ACE inhibitors (for all - if LVSD reduce mortality)
    • Beta blockers (for all - if LVSD reduce mortality)
    • Statin - for all
    • Eplerenone - only for diabetes and LVSD or clinical HF
  • Echocardiogram for LV function and cardiac structure
  • Cardiac rehabilitation
  • If LVSD at >9 months consider primary prevention ICD
226
Q

Describe the hierarchy of pacemaking in the heart

A
  • SA intrinsic rate fires impulses at a higher speed than the AV node and atrial/ventricular foci - their impulses are overridden and the rhythm observed is that of the SA node
  • If the SA node fails, the intrinsic impulse firing of the other nodes/foci is seen as a a back-up but is much slower = bradycardia
  • AV node intrinsic rate = 40-60 bpm - ECG 1 has AV node action
  • Ventricular foci intrinsic rate = 20-40 bpm - ECG 2 has only ventricular foci action (broad QRS because problem in His-Purkinje system)
227
Q

Explain the symptoms/signs of aortic stenosis

A
  • May be asymptomatic even when severe, because the heart may compensate for the stenosis by generating high LV pressure, maintaining normal cardiac output
  • Results in LV hypertrophy
  • May be associated w/ chest pain, similar to angina pectoris, even in the absence of coronary artery disease
    • LVH produces increased demand for blood supply, combined with restricted cardiac output
    • Dizziness and syncope characteristically during exertion may occur, due to the inability of the cardiac output to increase in response to increased demand
  • In late stages, heart failure may develop
  • Signs
    • Auscultatory findings - ejection systolic murmur
    • An associated thrill (palpable murmur)
    • A slow-rising (‘plateau’) pulse
    • Reduced pulse pressure
    • Forceful non-displaced apex
228
Q
A
229
Q
A

QRS rate - fast (300/1.5 = 200bpm)

QRS complexes regular

QRS complex broad

P waves? P:QRS relationship?

= Regular broad complex tachycardia

230
Q

When should IE be suspected?

A
  • All patients w/ S. Aureus bacteraemia
  • IVDU with any positive blood cultures
  • All patients with prosthetic valves and positive blood cultures (40-50% will end up having IE)
231
Q

Describe the heart murmur heard in mitral regurgitation

A

High-pitched (‘blowing’) pan-systolic murmur, best heard at the apex, radiating to the axilla

232
Q

List the conditions which predispose to/encourage the progression of AF

A
  • Hypertension
  • Symptomatic heart failure (NYHA II-IV) including tachycardiomyopathy
  • Valvular heart disease
  • Cardiomyopathies including primary electrical cardiac disease
  • Atrial septal defect and other congenital heart defects
  • Coronary artery disease
  • Thyroid dysfunction and possibly subclinical thyroid dysfunction
  • Obesity
  • Diabetes mellitus
  • Chronic obstructive pulmonary disease and sleep apnoea
  • Chronic renal disease
233
Q

Describe the general epidemiology of endocarditis

A
  • Common - no formal registry so hard to accurately state figures
  • Rates vary according to - age of population, incidence of IVDU
  • Rate remained constant for 50 years
  • 3x more common in men
  • Increasingly elderly patients
    • 25-50% of cases occur in over 60s
234
Q

List common cardiac arrhythmias

A
  • Atrial fibrillation - chaotic rhythm of the atrium
  • Atrial flutter
  • Supra-ventricular tachycardia
  • Ventricular arrhythmias - include extra-systoles, ventricular tachycardia, ventricular fibrillation
235
Q

What pathology can affect the heart valves?

A
  • Valve leaflets
    • Calcification - happens with age
      • Cause of aortic stenosis - generally disease of the elderly
    • Thickening
    • Degeneration
    • Infection - endocarditis
    • Prolapse - leakage
  • Apparatus/annulus
    • Annular dilation
    • Annular calcification
    • Apparatus tethering/thickening/rupture
    • Regional wall motion abnormality

Stenosis = pressure overload

Regurgitation = volume overload

236
Q

How is a univentricular heart treated?

A
  • After birth patient will require surgery to survive
    • Aim of surgery is to create two functioning ventricles, however anatomy of some infants born with a univentricular heart will not allow this
    • In this situation Fontan circulation will be created
237
Q

What are the risk factors for NVE?

A
  • Underlying valve abnormalities in 55-75%
    • Aortic stenosis
    • Mitral valve prolapse
  • IVDU
  • No identifiable risk factors in 30%
238
Q

Which patients with AF should recieve catheter ablation?

A
  • Patients w/ highly symptomatic paroxysmal AF resistant to one or more antiarrhythmic drugs and little or no comorbidity should be referred to arrhythmia specialist for consideration of ablation
  • Patients w/ symptomatic AF (paroxysmal or persistent), symptomatic heart failure and left ventricular systolic dysfunction with a left ventricular ejection fraction of 25-35% should be referred to an arrhythmia specialist for consideration of ablation
  • Catheter ablation techniques for AF should focus on electrical isolation of the pulmonary veins
  • Early ablation strategy should be considered for highly symptomatic patients with little or no comorbidity
  • Any patient w/ highly symptomatic and persistent AF should be referred to an arrhythmia specialist and ablation may be useful in selected cases
  • Patients who present with typical atrial flutter should be offered radiofrequency catheter ablation
239
Q

What should be done for patients who present with AF for the first time?

A
  • 30-50% will spontaneously revert to sinus rhythm
  • First aim of treatment is rate control, in some patients continued long-term if likelihood of achieving sinus rhythm is low or patients are not symptomatic
  • In those who have no structural heart disease, duration of AF is short (less than 48 hours) and left atrium is small - consider immediate medical or electrical cardioversion
    • Immediate cardioversion may be achieved more successfully by infusion of class 1C drug e.g. flecainide
    • Amiodarone widely used but can be associated with severe thrombophlebitis if not administered through a central line
    • Digoxin no more effective than placebo in re-establishing sinus rhythm
    • Or immediate electrical cardioversion - highly successful in this case but requires general anaesthetic
  • In those who present with established atrial fibrillation of greater than 48 hours duration then full anticoagulation should be instituted, rate control achieved and patient considered for cardioversion in 4-6 weeks time
240
Q

List the general clinical features of endocarditis

A
  • 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
241
Q

Describe the diagnosis of heart failure

A
  • Signs and symptoms suggestive of heart failure
  • Clinical examination
    • Full blood count
    • Fasting blood glucose
    • Serum urea and electrolytes
    • Urinalysis
    • Thyroid function and chest X-ray
  • BNP/NT-proBNP, then ECG especially if BNP not available
    • Low BNP (or NT-proBNP) and normal ECG –> HF excluded, consider alternative cause for symptoms
    • Raised BNP (or NT-proBNP) or abnormal ECG –> HF possible, refer for echocardiography (ECG if not already done, to determine cause of HF and future management decisions)
  • Low natriuretic peptides means it is very unlikely they have HF
242
Q

What is a heart murmur?

A
  • Heart murmur = sound produced by turbulent blood flow
  • Timing of the turbulence during the cardiac cycle determines when the murmur is heard
  • Stenosis, or narrowing of a valve produces turbulent flow when blood passes through it in the correct direction, whereas regurgitation through the valve (also called incompetence) produces turbulence during a period of cardiac cycle when blood does not normally flow across the valve
243
Q

What investigations should be done in a suspected MI?

A
  • Troponin
    • Protein, part of the cardiac myocyte
      • Biomarker of myocyte necrosis - released into blood after myocyte death
    • 3 types - I, C, T
    • Recent years troponin test very sensitive, able to detect small Mis
    • Anything which puts strain on the heart can cause high troponin
    • Acutely
      • Acute heart failure
      • Tachy-arrhythmias
      • Pulmonary embolism
      • Sepsis
      • Apical ballooning syndrome (Takosubo cardiomyopathy)
    • Chronic
      • Renal failure - kidneys clear troponin from the blood
      • Chronic heart failure
      • Infiltrative cardiomyopathies e.g. amyloidosis, haemochromatosis, sarcoidosis
  • ECG - ST deviation
  • CXR + echocardiogram - evidence of acute HF/LV systolic dysfunction
  • Coronary angiogram - pathology of coronary arteries
244
Q

What are the consequences of aortic stenosis?

A
  • Increased LV cavity pressure
  • Pressure overload –> LV hypertrophy
245
Q

Describe the path of blood in the foetal heart

A
  • In-utero oxygenation is by the maternal placenta (foetus doesn’t breathe)
  • Lungs are not fully formed, vascular resistance in the pulmonary arteries is high, therefore blood from the IVC takes the path of least resistance and passes from the right atrium through the foramen ovale directly into the left atrium
  • Minority of blood will pass into right ventricle and through the pulmonary artery to the lungs, but nearly all of the blood from the pulmonary artery passes through the ductus arteriosus to the aorta
  • Foetal circulation has two shunts which allow mixing of the oxygenated and deoxygenated blood
246
Q

Describe the use of ambulatory ECG recording in the diagnosis of atrial fibrillation

A
  • Several types of devices -
    • 24 hour monitor
    • Hand held monitor - handheld ECG electrode attached to phone w/ app, gives 1 ECG trace (lead one - R arm to L arm)
    • Stand alone devices
    • Patches - can be worn for 2 weeks
247
Q

Why concentrate more on L heart disease?

A

Greater consequence for mortality than R heart disease

248
Q

Describe the anatomy of the conduction system of the heart

A
249
Q

Describe the treatment of tetralogy of fallot

A
  • BT shunt
    • Provides more long-term circulation to the pulmonary system
    • Performed a few days after birth
    • Connect the carotid or subclavian artery directly onto the pulmonary artery
    • Improves chances of survival through infancy following which they would later get definitive corrective surgery
    • Because subclavian artery is rerouted, patients will not have a recordable BP in that arm
  • Complete repair - possible with surgical advances
    • Performed within a few days of birth
    • Close VSD with a patch, resection of the RVOT obstruction and enlargement of the pulmonary artery with a patch
250
Q

What are single ventricle anomalies?

A
  • Non-specific
  • Common feature that only one of the two ventricles is of adequate functional size
  • All will generally undergo staged reconstructive procedures ultimately resulting in a ‘Fontan circulation’
251
Q

Describe the use of mineralocorticoid receptor antagonists in heart failure

A
  • E.g. spironolactone (Aldactone), eplerenone
  • Block final part of the renin-angiotensin system
  • Relative risk reduction in mortality compared to placebo in more and less symptomatic patients
252
Q

What are the issues with Fontan circulation?

A
  • Without an RV to actively pump the deoxygenated blood into the pulmonary circulation, the pulmonary circulation is now dependent on high systemic venous pressure and low pulmonary vascular resistance
  • Anything that causes an imbalance can cause catastrophic haemodynamic compromise:
    • PE - increases pulmonary vascular resistance (majority of patients on anticoagulation - switching from Warfarin to NOACs)
    • Arrhythmia - reduces systemic circulation and therefore systemic venous pressure crashes (patients should be cardioverted ASAP and this is usually via a DCCV)
    • Dehydration - reduce venous pressure and therefore all patients should be kept hydrated with IV fluids if fasting
    • Bleeding - reduce venous pressure, low threshold to transfuse
253
Q

What are the consequences of coarcation of the aorta?

A

Narrowing means the LV has to generate a higher pressure to push the blood through so the patient would develop left ventricular hypertension, could progress to LV failure

Blood will find alternative and easier means to reach the descending aorta and will develop collateral arteries

254
Q

What are the symptoms of aortic regurgitation?

A
  • Shortness of breath
  • Reduced exercise capacity
255
Q

What are the immediate treatments in an MI?

A
  • Morphine for pain relief, may cause nausea, hypotension and drowsiness
  • Antiemetics for nausea secondary to MI and/or morphine
  • Nitrates (GTN) to lower vascular resistance, improve blood flow to myocardium
  • Oxygen - there is no evidence that routine administration of oxygen improves outcomes, recommended only if oxygen saturation <94%
  • Dual antiplatelet therapy
  • Aspirin - antiplatelet, reduces rate of vascular events in patients with ACS
  • Ticagrelol/Clopidogrel - second antiplatelet. Ticagrelol has been shown to be superior to Clopidogrel however associated with increased risk of major bleeding in elderly patients
  • Reperfusion - time is muscle
256
Q

Which ECG leads show a posterior STEMI and which is the culprit coronary artery?

A
  • ST depression V1-3
  • Left circumflex or right coronary artery
257
Q

Describe the heart murmur heard in tricuspid stenosis

A

Rare, diastolic murmur at left sternal edge

258
Q

What additional tests should be done in younger patients with hypertension to screen for secondary cases?

A
  • Renin and aldosterone (primary hyperaldosteronism)
  • 24 hour urine catecholamines (phaeochromocytoma)
  • Echo
  • Renal ultrasound
  • MRA renal
259
Q

What heart murmurs are produced by congenital heart defects

A

Congenital heart disease may also produce murmurs e.g. pan-systolic murmur with ventricular septal defect, continuous ‘machinery’ murmur with patent ductus arteriosus. Atrial septal defect does not produce a murmur (because there is no turbulent flow) other than a flow murmur across the pulmonary valve.

260
Q

List the common and less common causes of heart failure

A
  • Common (in UK)
    • Coronary artery disease (MI)
    • Hypertension
    • Idiopathic i.e. unknown
    • Toxins (alcohol, increasingly chemotherapy related)
    • Genetic?
  • Less Common (in UK)
    • Valve disease
    • Infections (virus, Chaga’s - South America)
    • Congenital heart disease
    • Metabolic e.g. haemochromatosis, amyloid, thyroid disease
    • Pericardial disease e.g. TB
    • Endocardial disease
261
Q

Describe the normal physiological role of the renin-angiotensin system

A
  • The liver produces angiotensinogen in response to low sensed volume/pressure
  • Converted to angiotensin I by renin produced by the juxtaglomerular cells of the kidney
  • Converted to angiotensin II by angiotensin converting enzyme produced by the liver
  • Angiotensin II effects
    • Blood vessel - vasoconstriction, smooth muscle cell hypertrophy, superoxide generation, endothelin secretion, monocyte activation, inflammatory cytokines, reduced fibrinolysis
    • Kidney - sodium and water retention, efferent arteriolar vasoconstriction, glomerular and interstitial fibrosis
    • Heart - cellular hypertrophy, myocyte apoptosis, myocardial fibrosis, inflammatory cytokines, coronary vasoconstriction, positive inotropy (contractions), proarrhythmia
    • Adrenal gland - aldosterone secretion
    • Brain - vasopressin secretion, sympathetic activation
262
Q

Describe the ECG seen in second degree AV block

A
  • Failure of one or more (but not all) atrial impulses to conduct to the ventricles due to impaired conduction
  • Type 1 (Mobitz I/Wenckebach) - almost always disease of the AV node, regular cycle, progressive prolongation of PR intervals followed by a blocked P wave (dropped QRS complex), then cycle resets
    • Fixed ratio of number of P waves and QRS complexes per cycle
  • Type 2 (Mobitz II/Hay) - almost always disease of distal conduction system (His-Purkinje system)
    • Non-conducted P waves with no PR prolongation before/shortening after
    • Usually fixed number of non-conducted P waves for every conducted QRS complex
    • Can progress rapidly to complete heart block
263
Q

Describe the classification of hypertension

A
264
Q

List the symptoms of atrial fibrillation

A
  • May be asymptomatic
  • Palpitation (awareness of heartbeat)
  • Dyspnoea
  • Rarely - chest pain, syncope (transient loss of consciousness)
  • Patients may present with complications e.g. stroke
    • Stroke can occur in otherwise asymptomatic patients (risk of stroke not related to symptoms)
265
Q

How can the function of the heart valves be assessed?

A
  • History
  • Examination
  • Blood pressure
  • ECG
  • Echo
  • CT
  • MRI
  • Exercise tolerance test
  • CPET
  • Stress echo
  • Left heart catheterisation
  • Right heart catheterisation
266
Q

Describe the normal morphology of the P/QRS/T waves

A
  • Normal P wave is positive in the inferior leads
  • Normal ST segment is flat
  • Normal T wave has the same polarity as the QRS
267
Q

List the devices which can be used in heart failure

A
  • Implantable cardioverter defibrillator (ICD) - heart becomes dilated in HF, predisposition to abnormal rhythms which can be a cause of sudden death
  • Implantable cardiac resynchronisation therapy pacemaker/device (CRT-P/D) - dysfunction LV often becomes out of synch with RV, conventional pacemaker leads into R side, L lead through coronary sinus to LV to synchronise the heart
268
Q

What causes mitral stenosis?

A
  • Rheumatic valve disease
  • Calcification
269
Q

Describe the immediate management of STEMI

A
  • ABCD
  • Attached to defibrillator in ambulance - risk of ventricular arrhythmia
  • Aspirin 300mg PO
  • Unfractioned heparin 5000U IV
  • Morphine 5-10mg IV
  • Anti-emetics
  • Clopidogrel (in ambulance)
  • 600mg if for PPCI
  • 300mg if for thrombolysis (75mg if aged >75)
  • Ticagrelor 180mg (in hospital)
  • Activate PPCI team

Medicine Year 3 (15 decks)

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