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CV Flashcards

1
Q

Why do we have to see the same waveform 12 times on a standard ECG?

A

The 12 leads provide important spatial information about the heart

They all view the electrical activity of the heart from a different position

allows you to localise pathology to a particular heart region

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2
Q

What is the normal cardiac axis?

A

-30 to +90

(2pm - 6pm)

Most positive deflection in lead II

most negative deflection in aVR

If leads I and II are positive, the axis is normal

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3
Q

What can left axis deviation suggest?

A

conduction abnormality

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4
Q

What can right axis deviation suggest?

A

pulmonary embolus/congenital heart defect

If the right ventricle becomes hypertrophied, it has more effect on the QRS complex than the left ventricle, and the average depolarization wave – the axis – will swing towards the right

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5
Q

What would you see in left axis deviation?

A

overall electrical activity becomes distorted to the left

between -30° and -90°

positive lead I and aVL
negative lead II and III

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6
Q

What would you see in right axis deviation?

A

overall direction of electrical activity is distorted to the right

between +90º and +180º

Negative QRS in lead I, positive in aVF

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7
Q

What is the ECG paper speed?

A

25 mm/s

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8
Q

How many large squares would you find in a second on ECG?

A

5 (one square = 0.2s)

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9
Q

First degree heart block

A

slowing in AV nodal conduction

prolonged PR interval

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10
Q

second degree heart block

A

intermittent failure of AV nodal conduction

two types:
1) Mobitz I: PR interval steadily increases until a QRS complex is missed. the pattern resets

2) Mobitz II: regular skipping of QRS. e.g. P – QRS – P – P – QRS (this is 2:1). Most beats are normal but there is occasionally atrial depolarisation without ventricular depolarisation.

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11
Q

third degree heart block

A

complete failure of AV nodal conduction

No impulse conduction from atria to ventricles. No relationship between P:QRS.

ventricles are excited by a slow ‘escape rhythm’, from a depolarizing focus below the AV node

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12
Q

Which ECG leads are inferior?

A

II, III and aVF

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13
Q

Which ECG leads are anterior?

A

V1-V4

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14
Q

Which ECG leads are lateral?

A

I, aVL, V5, V6

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15
Q

What is an ECG lead?

A

imaginary line between 2 ECG electrodes.

Each lead provides a different view of the electrical activity of the heart

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16
Q

Which plane are the limb leads in?

A

Coronal

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17
Q

Which plane are the chest leads in?

A

Transverse

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18
Q

Which lead usually provides the rhythm strip on an ECG?

A

Lead II

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19
Q

What’s the normal range of the PR interval?

A

<1 large square

<200ms

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20
Q

What’s the normal range of the QRS complexl?

A

< 3 small squares

< 120ms

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21
Q

sinus rhythm

A

normal heart rhythm, starts in the sinoatrial node

Rhythm = activation sequence of the heart

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22
Q

What does a narrow QRS indicate?

A

that the rhythm is arising from the AVN or above

i.e. the rhythm is using the specialized conducting system (His-Purkinje system) to depolarize the ventricles (the fast route to depolarize all ventricular muscle in a short period of time)

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23
Q

What is heart failure?

A

failure of cardiac output to meet the physiological demands of the body

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24
Q

Name 4 causes of heart failure

A

MI
hypertension
toxins (alcohol, chemotherapy)
valve disease

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25
Q

what is systolic heart failure?

A

heart failure with reduced ejection fraction. inability of the ventricle to contract normally

Usually has a coronary cause
Affects younger male patients

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26
Q

what is diastolic heart failure?

A

heart failure with preserved ejection fraction

Inability of the ventricle to relax and fill normally, causing increased filling pressures

older
more often female
hypertensive aetiology

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27
Q

How do compensatory changes lead to heart failure?

A

haemodynamic changes cause compensatory changes in the heart and cardiovascular system

these physiological changes occur to maintain cardiac output and peripheral perfusion

chronic activation increases cardiac workload, causing progressive damage

as heart failure progresses, these mechanisms are overwhelmed and become pathological

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28
Q

What neurohumoral adjustments are seen in heart failure?

A

ischaemic injury causes decreased efficiency of the heart –> perceived hypotension

neurohumoral adjustments act to maintain arterial pressure and perfusion of vital organs

Noradrenaline increases cardiac contractility and peripheral vasoconstriction

RAAS (activated by reduced renal perfusion) increases blood volume -> fluid overload

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29
Q

What is the significance of BNP in heart failure?

A

distinguishes HF from other forms of dyspnoea

secreted by the ventricles in response to myocardial wall stress

Levels are increased in patients with heart failure, and levels correlate with the severity of heart failure

Low BNP excludes heart failure

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30
Q

Treatment of hear failure (reduced ejection fraction)

A

1) start with a beta blocker/ACEi (ARB if intolerant)
2) with ongoing symptoms, add a MR antagonist
3) sacubitril/valsartan (stop ACEi)
4) devices/ivabradine
5) digoxin
6) LVAD or transplant

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31
Q

What is the most evidence-based therapy in heart failure?

A

Beta-blockers

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32
Q

Mechanism of action: sacubitril

A

inhibits neprilysin, an enzyme that breaks down natriuretic peptides

this increases the number of natriuretic peptides in the body

this increases natriuresis

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33
Q

LCZ696

A

contains bothan ARB (valsartan) and a neprilysin inhibitor

blocks the unwanted effects of ANG-II and upregulates the beneficial system (natriuretic peptides)

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34
Q

What is an implantable cardioverter-defibrillator (ICD)

A

a device implantable inside the body

able to perform cardioversion, defibrillation, and pacing of the heart

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35
Q

ivabradine

A

selectively inhibits the pacemaker If current

Blocking this channel reduces cardiac pacemaker activity

This slows heart rate at the SAN

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36
Q

How would you manage inadequately perfused patients?

A

give them positive inotropes

e.g. adrenaline/dopamine

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37
Q

How would you manage congested patients?

A

treat the fluid overload with diuretics

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38
Q

NYHF classification

A

I - No symptoms and no limitation in ordinary physical activity
II - dyspnoea during normal activities but comfortable at rest
III- dyspnoea limits normal activities
IV - dyspnoea at rest, essentially bedbound

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39
Q

CXR signs in LV failure

A

remember: ABCDE

A = alveolar oedema (perihilar - bat's wings)
B = kerley B lines (interstitial oedema)
C = cardiomegaly 
D = dilated upper lobe vessels
E = pleural Effusion
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40
Q

Infective endocarditis

A

Infection of endocardium

Results in formation of a vegetation - a mass of platelets, fibrin, microorganisms, and inflammatory cells

Results in damage to cusp of valves

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41
Q

Which valve is most commonly affected by infective endocarditis?

A

mitral valve

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42
Q

Which valve is most commonly affected by IE in PWIDs?

A

tricuspid

causes:

(1) particulate-induced endothelial damage to right-sided valves
(2) increased bacterial loads in these patients
(3) direct physiologic effects of the injected drugs
(4) deficient immune response caused by IVDU

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43
Q

Classification of infective endocarditis

A

1) Native valve endocarditis (NVE) = most common type
2) Endocarditis in PWIDs
3) Prosthetic valve endocarditis (PVE)

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44
Q

What is the most common cause of infective endocarditis in PWIDs?

A

staph aureus

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45
Q

What is the most common cause of infective endocarditis in native valve endocarditis?

A

Strep viridans

presents more indolently, causing Subacute disease

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46
Q

What is the most common cause of infective endocarditis in prosthetic valve endocarditis?

A

CoNS

remember: CoNS because a prosthetic valve is a con

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47
Q

List some risk factors for infective endocarditis

A

underlying valve abnormalities (aortic stenosis/mitral valve prolapse)

IVDU

Rheumatic heart disease

Dental work

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48
Q

Acute infective endocarditis

A

patient presents very unwell

progressive valve destruction
metastatic infection developing rapidly → i.e. septic emboli

commonly caused by S. aureus

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49
Q

Subacute infective endocarditis

A

presents indolently over weeks to months in an insidious manner

rarely leads to metastatic infection

commonly caused by Strep. viridans

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50
Q

What is the most common cause of IE

A

Strep. viridans

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51
Q

What should you be worried about in a patient who has Fever + murmur?

A

Fever + murmur = IE until proven otherwise

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52
Q

what embolic events can occur in infective endocarditis?

A

Small emboli:

  • Petechiae
  • Splinter haemorrhages
  • Haematuria

Large emboli:

  • CVA
  • Renal infarction

Right sided endocarditis (in PWID)
-Septic pulmonary emboli

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53
Q

What are possible long term effects of infective endocarditis?

A

can be categorised into immunological damage and direct tissue damage

Immunological reaction:

  • Splenomegaly
  • Nephritis
  • Vasculitic lesions of skin & eye
  • Clubbing

Tissue damage:

  • Valve destruction
  • Valve abscess
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54
Q

What are 3 cases in which you should be suspicious of infective endocarditis?

A

1) patients with S.aureus bacteraemia
2) Any PWID with a positive blood culture
3) patients with prosthetic valves and positive blood cultures

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55
Q

How should you investigate infective endocarditis?

A

1) blood culture

2) echocardiography (transthoracic)

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56
Q

What are the guidelines for blood cultures in suspected infective endocarditis?

A
  • 3 sets of blood cultures of 10ml in each bottle (20ml total)
  • different peripheral sites
  • before antibiotic administration
  • aseptic technique crucial
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57
Q

What are the Duke criteria?

A

used to diagnose infective endocarditis

Major criteria:

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

Minor: FIIVE

  • Fever >38 ̊C
  • IVDU or other predisposition (heart condition)
  • Immunological phenomena (eg. oslers nodes)
  • Vascular phenomena (eg. septic emboli)
  • positive blood culture
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58
Q

How many of the Duke criteria do you need to be diagnosed with IE?

A

Definite IE is defined as:

  • 2 major
  • 1 major + 3 minor
  • 5 minor
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59
Q

What are 3 Indications for surgical intervention in IE?

A

1) Heart Failure
2) Uncontrolled Infection
3) prevention of embolism

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60
Q

How long will antimicrobial therapy be given for in IE?

A

4 weeks for NVE

6 weeks for PVE

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61
Q

What antibiotics would you use to treat IE caused by streptococcus species?

A

high doses of benzyl penicillin plus gentamicin

give IV

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62
Q

What antibiotics would you use to treat IE caused by enterococcus species?

A

amoxicillin or vancomycin +/- gentamicin

give IV

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63
Q

should you avoid beta blockers in patients with AF?

A

no

beta blockers work at the AV node to slow conduction

they are first line for rate management in AF

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64
Q

What do blunted costophrenic angles indicate?

A

pleural effusion

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65
Q

What is the difference between transudate and exudate?

A

Transudate is fluid pushed through the capillary due to high pressure within the capillary.

Exudate is fluid that leaks around the cells of the capillaries caused by inflammation. (Higher protein content)

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66
Q

Name three causes of transudate

A

LVF, Cirrhosis, Nephrotic syndrome

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67
Q

Name three causes of exudate

A

PE, Bacterial Infection, Bronchial Cancer

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68
Q

What is the difference between interstitial oedema and alveolar oedema?

A

interstitial oedema - occurs at lower pulmonary venous pressures. Fluid collects in interlobar fissures and septa (Kerley B lines)

alveolar oedema - occurs at higher pressures (>30 mm Hg). Causes areas of consolidation and mottling of the lung fields, and pleural effusion.

Continued fluid leakage into the interstitium, which cannot be compensated by lymphatic drainage.

Interstitium is overloaded and the fluid has nowhere else to go
Causes spill of fluid from interstitium into alveoli (alveolar oedema) and leakage into the pleural space (pleural effusion).

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69
Q

symptoms of MI

A 
Crushing central chest pain
Back pain
Jaw pain – lower jaw
Indigestion
Sweatiness, clamminess
Shortness of breath
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70
Q

Possible signs of MI

A 
Tachycardia (HR > 100bpm)
Distressed patient 
crackles/ raised JVP
Low BP
Sweaty, clammy
Arrhythmia
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71
Q

What is troponin?

A

marker of cardiac necrosis

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72
Q

definition of MI

A

Any elevation in troponin in clinical setting consistent with myocardial ischaemia.

E.g. chest pain, breathlessness, etc.

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73
Q

Type 1 Spontaneous MI

A

due to a primary coronary event

e.g. coronary artery plaque rupture and formation of thrombus

Chest pain, ECG changes, raised troponin

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74
Q

Type 2 MI

A

Increased oxygen demand or decreased oxygen supply
Not a primary problem in the coronary arteries

Troponin increases due to another cause of heart stress

e.g. PE, Heart failure, sepsis, anaemia, arrhythmias, hypertension, or hypotension

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75
Q

Type 3 MI

A

sudden cardiac death

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76
Q

Type 4 MI

A

Iatrogenic

4a MI associated with percutaneous coronary intervention

4b MI Stent thrombosis

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77
Q

Type 5 MI

A

Iatrogenic

associated with CABG

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78
Q

What should you suspect in a patient who is Breathless with high troponin levels?

A

PE

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79
Q

Name 3 causes of Chronic elevation of troponin

A

renal failure (reduced excretion)

infiltrative cardiomyopathies, e.g. sarcoidosis

chronic heart failure

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80
Q

What is unstable angina?

A

An acute coronary event without a rise in troponin

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81
Q

What ECG findings do you expect in a Posterior infarct?

A

Location of the infarct means that an ST elevation is not seen

There are no ECG leads directly over the back of the heart

Can be diagnosed by looking for reciprocal ST elevation

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82
Q

What is the significance of Left bundle branch block in MI?

A

NEw - can indicate infarction

old - can obscure ST elevation on ECG

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83
Q

What is the general pattern of ECG manifestation of ischaemia?

A

1) ST elevation
2) pathological Q wave
3) T wave inversion
4) normalisation with persistent Q wave

other factors

  • change in heart axis
  • broad QRS complex
  • ST depression
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84
Q

Which artery is likely to be blocked with ST elevation in the anterior leads?

A

LAD

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85
Q

Which artery is likely to be blocked with ST elevation in the lateral leads?

A

left circumflex artery

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86
Q

Which artery is likely to be blocked with ST elevation in the inferior leads?

A

right coronary artery

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87
Q

Which leads will show reciprocal ST depression when there is ST elevation in anterior leads?

A

reciprocal ST depression in inferior leads

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88
Q

What does ST elevation in aVR indicate?

A

occlusion of the left main coronary artery

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89
Q

Which leads will show reciprocal ST depression when there is ST elevation in lateral leads?

A

reciprocal ST depression in inferior leads

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90
Q

Which leads will show reciprocal ST depression when there is ST elevation in the inferior leads?

A

‘Reciprocal’ ST depression in high lateral leads (I and aVL)

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91
Q

Which leads will show a STEMI with right coronary artery occlusion?

A

inferior leads (II, III, and aVF)

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92
Q

What kind of STEMI doesn’t cause ST elevation?

A

posterior wall infarction

you would see anterior ST depression

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93
Q

Immediate Management of STEMI (common exam Q!)

A

ABCD
“CRITICAL TRANSFER PATHWAY”
Emergency transfer to heart centre. Put patient in an ambulance attached to defibrillator

Aspirin 300mg PO

Unfractionated heparin 5000U intravenously

Morphine 5-10mg intravenously
give anti-emetics to counter the nausea from morphine

Clopidogrel (in ambulance)
600mg if for PPCI
300mg if for Thrombolysis (75mg if aged > 75)

Ticagrelor 180mg (in hospital) 
given with aspirin

Activate PPCI team at GJNH

94
Q

Advantages of PCI over thrombolysis

A 
Improves survival
Reduces strokes (thrombolytic drugs significantly increase the risk)
Reduces the chance of further MI
Reduces the chance of further angina 
Speeds up recovery
Shortens the time spent in hospital
95
Q

Difference between Primary angioplasty and rescue angioplasty

A

Primary angioplasty = straight to cath lab without thrombolysis.
Rescue angioplasty = angioplasty following failed thrombolysis

96
Q

Subsequent management of STEMI (EXAM QUESTION)

A

Monitor in Coronary Care Unit for complications of MI

Drugs for secondary prevention (ABCDE)

  • ACE inhibitors
  • Beta blocker
  • Cholesterol - Statin
  • Dual antiplatelet (Aspirin + Ticagrelor)
  • Eplerenone – only for diabetes/ LVSD/ clinical HF
  • MR antagonist

Echocardiogram
Cardiac rehabilitation
If LVSD at >9 months post MI consider primary prevention ICD
defibrillator

97
Q

Complications of MI (COMMON EXAM QUESTION)

A 
Arrhythmias
Heart Failure
Cardiogenic shock
Myocardial rupture (papillary rupture causes mitral regurg. Free wall rupture causes tamponade)
Psychological
98
Q

GRACE Score

A

Used to risk stratify NSTEMI patients

What is the risk of the person with the NSTEMI dying in hospital and over the first 6 months?

Used to decide who to send for angiogram

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

99
Q

ticagrelor

A

P2Y12 receptor inhibitor

platelet aggregation inhibitor

recommended as dual antiplatelet therapy following MI in addition to aspirin for 12 months unless there are contraindications

100
Q

What ECG findings do you expect with Pericarditis?

A 
Clinical history not consistent with MI
Concave ST elevation
No specific territory (often global)
No reciprocal change
PR depression
101
Q

Systemic Hypertension

A

persistent elevation in arterial blood pressure >140/90mmHg

This is the BP level that increases the vascular risk in patients sufficiently to require intervention

This is the threshold at which benefits of action (i.e. therapeutic intervention’) exceed those of inaction

diagnosis should not be made on a single elevated BP reading

at least two readings, five minutes between readings over at least two visits

102
Q

Causes of Hypertension

A

complex and multifactorial

genetic factors - family history

lifestyle - obesity, physical inactivity, diet

RAAS overactivity - increase in salt/water retention

Sympathetic overdrive - vasoconstriction

103
Q

Grade 1 hypertension

A

systolic: 140-159
diastolic: 90-99

104
Q

Grade 2 hypertension

A

systolic: 160-179
diastolic: 100-109

105
Q

Grade 3 hypertension

A

systolic: 180+
diastolic: 110+

106
Q

isolated systolic hypertension

A

systolic: 140+
diastolic: below 90

Occurs in older patients as vessels become stiffer and less compliant with age

107
Q

Primary Hypertension

A

no identifiable cause

108
Q

Risk factors for Primary Hypertension

A 
Non-modifiable:
•	Age
•	Gender
•	Ethnicity
•	Genetic factors
Modifiable:
•	Diet – high salt, low fruit and veg
•	Physical activity 
•	Obesity
•	Alcohol in excess 
•	Stress
109
Q

Secondary Hypertension

A

an identifiable cause of the raised BP

5-10% of cases

5 categories:

1) endocrine - hyperaldosteronism, phaeochromocytoma
2) renal - renal artery stenosis
3) drugs - NSAIDs, cocaine
4) vascular - coarctation of aorta
5) other - OSA

110
Q

Examples of HTN end organ damage

A 
stroke
retinopathy
renal failure
peripheral vascular disease
heart failure
111
Q

Effect of beta blockers on HTN

A

Decrease blood pressure via blockade of b1 sympathetic tone on heart and reduction in renin release from kidney

Results in a decrease in heart rate and stroke volume = overall decrease in cardiac output

112
Q

adverse Effects of beta blockers

A

(a) Exacerbate asthma (block b2 adrenoceptors in the lungs, blocks effectiveness of salbutamol = absolute contraindication)
(b) Intolerance to exercise because of limited capacity to increase CO
(c) Hypoglycaemia – problematic for diabetics

113
Q

Name 2 ACEi

A

captopril and enalapril

114
Q

NAme 2 ARB

A

Losartan and candesartan

115
Q

Effect of Ca channel blockers on HTN

A

Reduce peripheral resistance
o Block of Ca2+ entry into vascular smooth muscle causes vasodilation

Reduce cardiac output
o Block of Ca2+ entry into cardiac muscle causes a reduction in heart rate and stroke volume

116
Q

Resistant HTN

A

patients who are on 3 drugs including a diuretic and their blood pressure still fails to respond

117
Q

HTN management under 55y

A

ACEi/ARB

ACEi/ARB + Ca channel blocker

ACEi/ARB + Ca channel blocker + thiazide-like diuretic

ACEi/ARB + Ca channel blocker + thiazide-like diuretic + other therapy (beta/alpha blocker)

118
Q

HTN management >55y or Black

A

Ca channel blocker

ACEi/ARB + Ca channel blocker

ACEi/ARB + Ca channel blocker + thiazide-like diuretic

ACEi/ARB + Ca channel blocker + thiazide-like diuretic + other therapy (beta/alpha blocker)

119
Q

atrial fibrillation

A

commonest sustained cardiac arrhythmia

causes an irregularly irregular pulse
irregular pattern persists when the pulse quickens in response to exercise

120
Q

symptoms of AF

A
  • May be asymptomatic
  • Palpitation
  • Dyspnoea – breathlessness

Rarely:
o chest pain
o syncope (collapse, transient loss of consciousness)

121
Q

Conditions predisposing to AF

A 
o	Rheumatic heart disease
o	Alcohol intoxication
o	Thyrotoxicosis
o	Hypertension 
o	Heart failure
o	diabetes
o	COPD/OSA
122
Q

types of AF

A

1) Paroxysmal (intermittent, starting & stopping)
o most episodes last less than 24 hours
o stops spontaneously within 7 days

2) Persistent
o Episodes of AF that last more than 7 days and may require either pharmacologic or electrical intervention to terminate

3) Permanent
o both patient and clinician have decided to abort any further strategies to try and restore sinus rhythm

123
Q

What would you see on ECG with AF?

A
  • Irregular baseline between the QRS complexes
  • No distinct P waves
  • QRS complexes are narrow but at irregular intervals

ventricles will have a variable rate depending on how many impulses are getting through the AV node and bundle branches

124
Q

Atrial Flutter

A

arrhythmia due to re-entry around the tricuspid valve on the right side of the heart

Not the same as AF but similar

Often associated with AF

125
Q

AF vs Atrial flutter

A
  • both abnormal heart rhythms.
  • In AF the atria beat irregularly.
  • In atrial flutter, the atria beat regularly but faster than usual and more often than the ventricles
126
Q

What can cause saw tooth pattern on ECG?

A

atrial flutter

seen in leads II, III, aVF

127
Q

what is the Haemodynamic Significance of AF/atrial flutter?

A

both cause a loss of cardiac output

Because the atria are not beating in a coordinated fashion, both predispose to thrombosis within the atria

128
Q

What are the objectives of AF treatment?

A

1) Prevention of stroke
2) Symptom relief
3) Optimum management of cardiovascular disease
4) Rate control
5) +/- Correction of rhythm disturbance (if appropriate)

NB: if there is an obvious underlying condition (e.g. thyrotoxicosis), treat that

129
Q

What are Essential investigations in AF?

A
  • ECG – confirm arrhythmia
  • Echocardiogram – look for structural heart disease
  • Thyroid Function Tests – rule out thyrotoxicosis
  • Liver Function Tests
130
Q

What is the target HR n AF?

A

under 110 bpm

131
Q

How is rate control achieved in AF?

A

by drugs that block the AV node plus administration of oral anticoagulants

first line: bisoprolol or verapamil (BB/CCB)

second line: digoxin

Heart failure: amiodarone

132
Q

How would you achieve rate control in AF patients with heart failure?

A

amiodarone

don’t use calcium channel blockers

133
Q

CHA2DS2VASc score

A

used to assess the risk of stroke in AF patients. Maximum score of 9

CHF
HTN
Age >75 (2)
Diabetes
Stroke (2)
Vascular disease
Age >65
Sex (F)

Do not give anticoagulant to patients with CHADSVASc score of 0. (risk>benefit)

o 2 or more -> treat with NOAC
o 1 -> consider anticoagulant therapy

134
Q

Which DOAC should be avoided in renal failure?

A

dabigatran

135
Q

“Rhythm control” for patients with AF

A

Particularly used for younger patients, and patients with ongoing symptoms despite good rate control

Options:
o Direct current cardioversion (for persistent AF)
o Anti-arrhythmic drugs – E.g. amiodarone
o Catheter ablation

136
Q

congenital heart disease

A

abnormality of foetal heart development

also encompasses the great vessels

137
Q

Atrial Septal Defect

A

Acyanotic heart lesion – does not affect saturation because blood shunts from left to right

Different types:

1) Secundum - Found in the same region where you would normally find the foramen ovale (but not the same as a patent FO!)
2) Primum - often affects the ventricles

138
Q

What kind of heart failure will you see with an ASD?

A

right ventricular HF

this is because blood shunts from left to right (path of least resistance), cause volume overload in the right heart.

The right ventricle dilates in compensation, but becomes overwhelmed

139
Q

Why does an ASD predispose to arrhythmias?

A

volume overload causes dilation of the RA

Because of this stretching, the RA becomes vulnerable to arrhythmias -> AF/atrial flutter

140
Q

What are possible consequences of ASD?

A
  • RV failure
  • Atrial arrhythmias
  • Pulmonary hypertension
  • Eisenmenger syndrome

Tricuspid regurgitation:
- RV dilates, this stretches the valve, so the leaflets no longer touch each other properly –> regurgitation

141
Q

what is Eisenmenger syndrome?

A

process in which a long-standing left-to-right cardiac shunt caused by a congenital heart defect causes pulmonary hypertension

This results in eventual reversal of the shunt into a cyanotic right-to-left shunt

142
Q

What are methods of ASD correction?

A
  • Surgical - sternotomy

* Transcatheter – through the groin

143
Q

Coarctation of the Aorta

A
  • congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.
  • Acyanotic heart lesion – does not affect saturation
144
Q

What kind of heart failure may be seen with coarctation of the aorta?

A

LV hypertrophy occurs because the heart has to pump harder to overcome the increased afterload

If this is not corrected, it leads to LV failure over time

Blood will try and find alternative ways to bypass the narrowing (as it follows the path of least resistance), leading to the development of collateral circulation

145
Q

Symptoms of coarctation of the aorta

A

Symptoms of poor peripheral perfusion:
• Cold feet
• Claudication of the legs
• Abdominal angina (pain on eating)

• Upper body hypertension, Berry aneurysms, claudication and renal insufficiency may ensue

  • Pre-coarctation hypertension – blood pressure will be very high before the coarctation, causing:
  • Headaches
  • Nose bleeds
146
Q

What examination findings would you expect with coarctation of the aorta?

A

Discrepancies in the limb blood pressures:
• Normally, BP is higher in the legs than in the arms
• This is reversed in aortic coarctation

Radiofemoral delay:
• Delay between the radial pulse and femoral pulse

Continuous murmur:
• Because the narrowing causes turbulent blood flow
• Heard on both the front and the back of the chest

147
Q

Which valve defect is associated with coarctation of the aorta?

A

bicuspid aortic valve

148
Q

Treatment of coarctation of the aorta?

A
  • Simple follow up for mild cases
  • Transcatheter approach – balloon angioplasty

Surgical repair via thoracotomy:
• resection and end to end anastomosis
• Jump graft

149
Q

Name 2 congenital cyanotic heart defects

A

1) tetralogy of fallot

2) transposition of the great arteries

150
Q

Transposition of the great arteries

A

aorta and pulmonary artery switch

males more commonly affected

This creates 2 separate circulation systems. Without mixing of the oxgenated and deoxygenated blood there is profound cyanosis

The foetus is able to survive this condition because of the connections (ductus arteriosus and foramen ovale) that allow it to bypass the normal circulation

151
Q

Management of transposition of the great arteries

A

Immediate administration of IV prostaglandins at birth

These maintain the patency of the foetal connections, allowing mixing of the blood

This buys time to perform corrective surgery

152
Q

Methods of surgical correction in transposition of the great arteries

A

1) arterial switch (better method) -> gives more anatomically correct result but coronary arteries have to be reattached -> complications
2) atrial switch. RV has to pump blood to systemic circulation -> leads to RV failure

153
Q

Tetralogy of Fallot

A

1) Ventricular septal defect
2) Overriding aorta
3) Obstruction of the right ventricular outflow tract

4) Right ventricular hypertrophy
• This is the net effect of all the other factors

154
Q

Why does Tetralogy of Fallot result in low oxygenation of blood?

A

mixing of oxygenated and deoxygenated blood in the left ventricle via the ventricular septal defect (VSD)

preferential flow of the mixed blood from both ventricles through the aorta because of the obstruction to flow through the pulmonary valve.

155
Q

Tetralogy of Fallot – operative strategy

A

give IV prostaglandins at birth to maintain the patency of the ductus arteriosus

BT shunt - redirect blood flow to the lungs

Complete repair:

  • Close VSD using a patch
  • Cut away extra muscle causing obstruction of the RVOT
  • Use a patch to enlarge pulmonary artery
156
Q

Univentricular Heart

A

congenital heart condition which results in only one effective pumping ventricle

heart relies on a PFO and PDA for mixing of the blood

• Tricuspid atresia

157
Q

Fontan circulation

A

single functional ventricle is 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, bypassing the heart altogether

158
Q

Problems with Fontan circulation

A

Without a RV the to pump blood into the pulmonary circulation, the heart relies on a sufficiently high systemic venous pressure to drive blood directly into the pulmonary arteries.

And the pulmonary vascular resistance needs to be low for optimal flow into the lungs.

This balance is very vulnerable and any change is difficult to adapt to -> can lead to haemodynamic collapse

159
Q

commonest causes of haemodynamic collapse in Fontan patients

A

PE - increases pulmonary vascular resistance

arrhythmia - reduces your systemic circulation and therefore reduces systemic venous pressure (preload)

dehydration - reduced venous pressures

160
Q

What does Acute Coronary Syndromes encompass?

A

STEMI
NSTEMI
unstable angina

share a common mechanism –rupture or erosion of the fibrous cap of a coronary artery plaque.

161
Q

Left-Ventricular Ejection Fraction

A

Measurement of how much blood is being pumped out of the left ventricle of the heart with each contraction

Most commonly used objective measure of LV function

Normal ejection fraction is >50%

162
Q

What imaging modality would you use to detect valve abnormality?

A

echocardiogram

doppler

163
Q

Which heart valves can be assessed using TTE?

A

LV, RV and aortic valve can easily be viewed with this method

164
Q

Which imaging modality is best for visualising the mitral valve?

A

transoesophageal echocardiography

165
Q

What is the purpose of Functional Stress Testing?

A

Aim is to compare the heart at rest and under stress.

Often used to determine if there is coronary artery narrowing.

Ischaemia is observed under stress because the blocked coronary artery loses its ability to vasodilate

166
Q

Percutaneous Coronary Intervention

A

o Coronary revascularisation technique

o Non-surgical widening of the coronary artery, using a balloon catheter to dilate the artery from within

167
Q

What is the gold standard test for assessing coronary arteries?

A

CT angiography

168
Q

Which form of imaging provides most accurate assessment of ejection fraction?

A

MRI

169
Q

what does pink frothy sputum on coughing suggest?

A

pulmonary oedema (transudate)

170
Q

What are the two types of systolic murmur?

A

ejection systolic murmur - aortic stenosis, pulmonary stenosis

pansystolic murmur - mitral regurgitation, tricuspid regurg, VSD

171
Q

What are the types of diastolic murmurs?

A

early diastolic - aortic/pulmonary regurgitation

mid-diastolic - mitral/tricuspid stenosis

172
Q

Annulus

A

base of a heart valve that supports the valve’s leaflet

173
Q

Rheumatic valve disease

A

cardiac inflammation and scarring triggered by an autoimmune reaction to infection with group A streptococci (strep pyogenes)

Antibody cross reactivity

174
Q

Aortic stenosis

A

obstruction of blood flow across the aortic valve due to pathological narrowing.

175
Q

Aortic stenosis symptoms

A

long subclinical period

  • Shortness of breath
  • Presyncope
  • Syncope
  • Chest pain
  • Reduced exercise capacity
176
Q

Aortic stenosis: murmur characteristics

A

systolic ejection murmur

crescendo decrescendo

radiates to carotids

177
Q

Aortic stenosis causes

A
  • Thickening
  • Calcification (due to degenerative changes)
  • Rheumatic valve disease
  • Congenital (unicuspid or bicuspid valve)
178
Q

Aortic regurgitation

A

diastolic flow of blood from the aorta into the left ventricle

Regurgitation is due to incompetence of the aortic valve or any disturbance of the valvular apparatus (eg, leaflets, annulus of the aorta)

179
Q

Aortic regurgitation causes

A
  • Degeneration
  • Rheumatic valve disease
  • Aortic root dilatation
Systemic disease
o	Marfan’s syndrome
o	Ehlers Danlos syndrome 
o	Ankylosing Spondylitis
o	SLE
180
Q

Aortic regurgitation symptoms

A
  • Shortness of breath

* Reduced exercise capacity

181
Q

Mitral stenosis

A

obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve apparatus

left atrial pressure increases. This leads to transudation of fluid into the lung interstitium and dyspnea

182
Q

Mitral stenosis causes

A
  • Rheumatic valve disease - most common cause

* Pressure overload

183
Q

Mitral stenosis symptoms

A 
o	Shortness of breath
o	Palpitation
o	Chest pain
o	Haemoptysis - if the bronchial veins rupture
o	Right heart failure symptoms
184
Q

Mitral regurgitation

A

abnormal reversal of blood flow from the left ventricle to the left atrium.

caused by disruption in any part of the mitral valve apparatus

185
Q

Mitral regurgitation causes

A

rheumatic fever

ruptured chordae tendinea

186
Q

Mitral regurgitation symptoms

A
  • Shortness of breath
  • Palpitation
  • Right heart failure symptoms
187
Q

The absence of P-waves and an irregular rhythm would suggest a diagnosis of

A

AF

In atrial fibrillation the atria no longer conduct electricity from the SA in an orderly fashion. Therefore P-waves are lost. As a result of disordered atrial activity only occasional waves of depolarisation pass through to the AV node and cause ventricular activation. This causes the typical irregular rhythm.

188
Q

What view of the heart do leads I, aVL, V5 and V6 represent?

A

Lateral

189
Q

What would it suggest if lead I became negative and lead III became more positive than lead II?

A

Right axis deviation

190
Q

The duration of the PR interval is noted to be increasingly prolonged. In addition QRS complexes appear to be dropped at regular intervals. What diagnosis would this suggest?

A

Second degree heart block

Mobitz type I

191
Q

If a rhythm is described as sinus, what does this indicate?

A

that a P-wave precedes each QRS-complex.

192
Q

What is often the earliest ECG change seen during myocardial infarction?

Tall P-waves
Tall peaked T-waves
ST-depression
ST elevation

A

Tall peaked T-waves

193
Q

What kind of ECG changes should you look for in suspected MI?

A 
ST elevation/depression
QRS broadening
Inverted T wave
Arrhythmia
Bradycardia/Tachycardia
194
Q

What tests would you perform on a patient who presents with suspected MI?

A

ECG
CXR - rule out other causes of chest pain
Troponin (rises 6-12 hours after onset of chest pain)

195
Q

Percutaneous Coronary Intervention

A

invasive procedure to open the blocked artery and treat the underlying atheromatous plaque by balloon angioplasty and stent placement

treatment of choice for MI if the patient can receive treatment within 90 minutes

196
Q

What is administered during thrombolysis?

A

Tenectaplase - fibrinolytic therapy to break-up thrombus in coronary artery

Heparin - anticoagulation to prevent further thrombosis

NB: patient should be immediately transferred to the Intervention Centre, to allow prompt “Rescue Angioplasty” if necessary, should reperfusion not occur with thrombolysis.

197
Q

Treatment of bradycardia

A

Atropine

competitive antagonist of the muscarinic acetylcholine receptors. i.e. anticholinergic drug

increases heart rate and improves atrioventricular conduction by blocking parasympathetic influences on the heart

198
Q

How would you manage a patient with bradycardia who is not responding to atropine?

A

temporary pacing, either trans-cutaneous or transvenous

199
Q

ectopic rhythm

A

an irregular heart rhythm due to a premature heartbeat

200
Q

What do Q waves represent?

A

transmural infarction

201
Q

What further tests should be done following PCI?

A 
Troponin
Cholesterol
Glucose
ECG
CXR
202
Q

What is the role of Beta-blockers in the secondary prevention of MI?

A

cardio-selective beta-blocker = bisoprolol

Blocks the action of endogenous catecholamines, adrenaline and noradrenaline, on β-adrenergic receptors

Blunts any increase in the rate and force of the heartbeat, particularly during exertion → protective effect on the heart muscle, which may reduce the risk of developing complications

203
Q

Which drugs would you prescribe to a patient for secondary prevention of MI?

A

ramipril (ACEi)

bisoprolol (beta blocker)

simvastatin (cholesterol)

aspirin (long term) and ticagrelor (6/12) = dual antiplatelet therapy

204
Q

What are troponins?

A

regulatory proteins for contraction that are released from ischaemic and dying myocytes

function as a cardiac marker

NB: will not increase until 6-12 hours after onset of chest pain

The amount by which troponin rises correlates with outcome (higher troponin = greater mortality)

205
Q

Unstable Angina

A

history of acute coronary syndrome (e.g. rest pain) but with no detectable troponin rise

should be investigated with exercise testing and coronary angiography

206
Q

Absolute Contraindications to thrombolytic therapy

A

History of intracranial bleed or neoplasm, or recent (<4 weeks) head trauma.

Recent (<3 weeks) surgery (including dental surgery) and major trauma.

Ischaemic stroke (<6 months).

Active internal bleeding (<1 month).

Suspected aortic dissection.

Acute pancreatitis.

Bleeding disorder

Refractory hypertension (SBP >160 or DBP >100)

NB: Diabetic retinopathy is not a contraindication to fibrinolysis

207
Q

Atherosclerosis

A

1) CV risk factors cause endothelial damage. This triggers leucocyte infiltration -> oxidative stress
2) LDL is deposited in tunica intima and oxidised -> fatty streak
3) macrophages engulf the oxidised lipid -> foam cells. Release pro-inflammatory cytokines -> VSMC proliferation and formation of a fibrous cap
4) lumen gradually narrows and plaque may rupture

208
Q

What happens when a plaque ruptures?

A

As the plaque grows, pressure increases, and the plaque may rupture

Rupture leads to thrombosis → coagulation occurs to stop the plaque from spilling its contents into the lumen

This forms a thrombus, which can impede blood flow and cause serious complications → acute clinical events (e.g. MI)

209
Q

What are the possible causes of acute arterial occlusion in a limb?

A

Thrombosis – pre-existing plaque disease. History of intermittent claudication

Embolism - more likely diagnosis in the absence of a previous history of PVD

210
Q

long-term management of peripheral vascular disease

A

aspirin

antihypertensive - not beta blockers! lowering systemic BP will impair blood flow to limbs

statin

lifestyle changes

211
Q

Resins

A

bind cholesterol-containing bile salts in the gut & prevent reabsorption

212
Q

Intermittent claudication (IC)

A

pain in the leg brought on by walking and relieved by rest.

most common in the calf muscles but can affect the thigh or buttock

local manifestation of a systemic disorder - atheroma. indicator of widespread vascular disease

Pain at rest is a later symptom. This pain is experienced in the toes (most distal).

213
Q

What are the features of critical ischaemia in the imminently non-viable limb?

A

“six Ps”:

Pain
pale 
paralysis
pulse deficit
paresthesia
Perishingly cold
214
Q

Describe how to investigate and treat acute limb ischaemia

A

priority is imaging to demonstrate vascular disease and site of obstruction = MRI/CTA/arteriogram

majority can be treated by treating HTN, avoiding beta-blockers, stopping smoking, reducing weight and exercise

Patients can be treated by angioplasty/stenting or surgical bypass

215
Q

What do forceful/displaced apex beats suggest?

A

o Forceful = hypertrophy of left ventricle to overcome the pressure gradient

o Displacement would suggest more of an overload problem

216
Q

classic triad of symptoms in patients with aortic stenosis

A

Angina: precipitated by exertion and relieved by rest

dyspnoea on exertion, and shortness of breath

Syncope: Often occurs upon exertion when systemic vasodilatation in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline

217
Q

What will cause a murmur that radiates to the carotid arteries?

A

Aortic stenosis

218
Q

What will cause a murmur that radiates to the axilla?

A

Mitral regurgitation

219
Q

Which are Ejection systolic murmurs?

A

Aortic and pulmonary stenosis

220
Q

Which are Pansystolic murmurs?

A

Mitral and tricuspid regurgitation

This is because systole occurs during ventricular contraction

Or VSD

221
Q

what type of murmurs are heard louder while sitting forward?

A

Aortic valve

Sitting forward brings the aortic valve closer to the chest wall, thus aortic murmurs are heard louder while sitting forward

222
Q

what type of murmurs are heard louder in the left lateral decubitus position?

A

Mitral valve
Left lateral decubitus position brings the apex closer to the chest wall, thus mitral valve murmurs are heard loudest in this position

223
Q

what type of murmurs are heard louder on inspiration?

A

Right-sided valve lesions (pulmonary and tricuspid valves) are heard loudest during inspiration

Intrathoracic pressure reduces, so more blood flows into the right heart chambers

224
Q

what type of murmurs are heard louder on expiration?

A

Left-sided heart valve lesions (aortic and mitral valves) are heard loudest during expiration

Intrathoracic pressure increases, forcing pulmonary vessels to constrict, so blood is forced from pulmonary veins into the left atrium and through the left side of the heart

225
Q

Aortic stenosis causes

A

age-related calcification (commonest cause)

Bicuspid aortic valve

226
Q

Aortic regurgitation causes

A

Prosthetic aortic valve failure
Connective tissue disease
Infective endocarditis

NB: Heard loudest at left sternal edge

227
Q

Treatment of atrial fibrillation

A

Both rate control and rhythm control must be considered

Rate control - digoxin, amiodarone

Rhythm control - amiodarone. NB dangerous drug and very toxic to veins -> thrombophlebitis. Use large cannula. Amiodarone is slow to work. Use direct electric cardioversion if necessary

Anticoagulant therapy - heparin - to manage the stroke risk

228
Q

Treatment of heart failure

A

1) oral diuretic - FURESOMIDE - symptom control only.
2) ACEi - RAMIPRIL
3) Beta blocker - CARVERDILOL
4) Aldosterone antagonist - SPIRONOLACTONE

229
Q

Treatment of atrial fibrillation

A

Anticoagulation - Apixaban for CHA2DS2-VASc score 2+

Rate and rhythm control - Amiodarone

230
Q

Assessment of valve dysfunction

A

● History
● Examination
● Blood pressure
● ECG

● Exercise Tolerance Test
● Cardiopulmonary Exercise Testing (CPET)
● Stress echo

● Echo
● CT
● MRI

● Left heart catheterisation
● Right heart catheterisation

231
Q

What antibiotics would you use to treat IE caused by CoNS?

A

high doses of vancomycin plus gentamicin

+/- rifampicin

give IV

232
Q

What antibiotics would you use to treat IE caused by S. aureus?

A

high doses of flucloxacillin (vancomycin for MRSA) plus gentamicin

give IV

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