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CP1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

ECG Lead Position - Limb Leads

A

aVR - Right arm (wrist)
aVL - Left arm (wrist)
aVF - Left Leg
Neutral - Right leg

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2
Q

ECG Lead I

A

Information between (-) aVR and (+) aVL

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3
Q

ECG Lead II

A

Information between (-) aVR and (+) aVF

often used for the rhythm strip

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4
Q

ECG Lead III

A

Information between (-) aVL and (+) aVF

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5
Q

ECG Lead Position - Chest Leads

A 
V1	4th ICS, right sternal edge.
V2	4th ICS, left sternal edge.
V3	midway between V2 and V4
V4	5th ICS, midclavicular line
V5	5th ICS, anterior axillary line
V6	5th ICS, mid-axillary line
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6
Q

ECG - Isoelectric Line

A

the imaginary line that forms the baseline of the ECG trace through the entire strip.

We measure the amplitude (height) of waves and deviation of segments from this reference point

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7
Q

ECG Square Sizes

A

Large Squares are 5mm x 5mm

Small Squares are 1mm x 1mm

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8
Q

ECG Calibration

A

Must be properly calibrated.

Normal calibration:

Amplitude (height) = 10mm/mV
=> 1 small square = 0.1mV
=> 1 large square = 0.5 mV

Duration (speed) - 25mm/s
=> 1 small square = 0.04 sec
=> 1 large square – 0.2 sec

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9
Q

What does the P-wave on an ECG represent and what are its normal parameters?

A

represents atrial depolarisation

Normal Parameters:
=> Duration – <0.12 secs (3 small squares)
=> Amplitude – <0.25 mV (2.5 small squares)
=> Direction – Upright in leads I, AvF, V3-V6

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10
Q

What does the PR segment on an ECG represent and what are its normal parameters?

A

= the distance between the P-wave and the QRS complex

represents the delay at the AV Node

Normal Parameters:
=> Amplitude – 0.0mV (i.e. isoelectric line)

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11
Q

What does the PR interval on an ECG represent and what are its normal parameters?

A

represents atrial depolarisation and delay at AV Node

Normal Parameters:
=> Duration – 0.12-0.20 secs (3-5 small squares)

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12
Q

What does the QRS complex on an ECG represent and what are its normal parameters?

A

represents ventricular depolarisation

Normal Parameters:
=> Duration – <0.12 secs (3 small squares)

=> Amplitude
>0.5 mV (in ≥1 limb lead)
>1mV (in ≥1 chest lead)
Upper Limit: 3.0mV (6 big squares)

=> Direction
Positive in I, II, V4-V6
Negative in aVR, V1 and V2

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13
Q

What does the QT interval on an ECG represent and what are its normal parameters?

A

represents the whole ventricular action potential

Normal Parameters:
=> Duration:
- Males: <0.40 secs (2 big squares)
- Females: <0.44 secs (11 small, or 2 big 1 small)

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14
Q

What does the ST segment on an ECG represent and what are its normal parameters?

A

represents the “Plateau Phase” of ventricular action potential

Normal Parameters:
=> Amplitude – Isoelectric, slanting up to the T-wave

=> Direction:
Elevation of up to 2mm normal in chest leads
Not normally depressed >0.5mm

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15
Q

What does the T-wave on an ECG represent and what are its normal parameters?

A

represents ventricular repolarisation

Normal Parameters:
=> Normally rounded and asymmetrical (gradual upslant)
=> Amplitude – >0.2 mV (2 small squares) in leads V3 and V4
=> Direction – Same as QRS in at least 5 of 6 limb leads.

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16
Q

What is an approach to interpreting ECGs?

A

Confirm patient demographics
Indication for test
Calibration

Rate
Rhythm
Axis

Abnormalities:

  • P-wave
  • PR interval
  • QRS complexes
  • ST segments
  • T-waves
  • QT interval
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17
Q

what is the normal cardiac axis?

A

-30° to 90°

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18
Q

what indicates normal cardiac axis on ECG?

A

QRS up in Lead I

QRS up in aVF

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19
Q

what indicates left axis deviation on an ECG?

what conditions are associated with this?

A

QRS up in Lead I
QRS down in aVF

essential hypertension or valvular heart disease

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20
Q

what indicates right axis deviation on an ECG?

A

QRS down in Lead I
QRS up in aVF

COPD and pulmonary hypertension

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21
Q

what indicates extreme axis deviation on an ECG?

A

QRS down in Lead I

QRS down in aVF

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22
Q

what would absence of P-waves indicate?

A

atrial fibrillation (alongside irregularly irregular rhythm)

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23
Q

What would cause prolongation or shortening of the PR interval?

A

PROLONGATION:
1st Degree Heart block
2nd Degree Mobitz Type I heart block

SHORTENING:
pre-excitation syndromes

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24
Q

what is counted as a narrow QRS complex? what does this represent?

A

<3mm

normal => represents fast, synchronised ventricular depolarisation

relies on the fast-conduction pathways

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25
Q

what is counted as a broad QRS complex? what does this represent?

A

> 3mm

caused by:

Abnormal depolarisation (e.g. bundle branch blocks, ventricular ectopic beats)

Pre-excitation (accessory pathways)

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26
Q

when is the ST segment elevated?

what does this indicate?

A
  • 1mm in the limb leads (Leads I, II, III, aVR, aVL, aVF)
  • 2mm in the chest leads (V1-V6).

must occur in 2+ adjacent leads

ST Elevation Myocardial Infarction (STEMI)

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27
Q

when is the ST segment depressed?

what does this indicate?

A

Any depression >0.5mm in 2+ leads is abnormal

Indicates ischaemia

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28
Q

what are “Tall and Tented” T-waves on an ECG?

what could this indicate?

A

Tall – at least ½ the amplitude of the preceding QRS complex)

Tented – look as if they’ve been pinched from above - i.e. a pointed peak, narrow base

Caused by hyperkalaemia.

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29
Q

Inverted T-waves

A

normal in Lead aVR (where everything should be negative)

can be a normal variant in Leads V1 and III

T-wave Inversion in other leads is a non-specific sign for Ischaemia, Bundle Branch Blocks, Pulmonary Embolism (PE), Hypertrophic Cardiomyopathy (HCM) etc.

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30
Q

Flattened T-waves

A

another non-specific sign, of ischaemia, or of electrolyte imbalance (e.g. Hypokalaemia)

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31
Q

Long QT Syndrome

A

carries a risk of life-threatening Arrhythmias

Some medications prolong the QT Interval, so should be carefully monitored, and avoided altogether in patients with Long QT Syndrome

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32
Q

1st degree heart block

A

a PR interval >200ms (5 small squares or 1 big square)

prolongation remains fixed in length, and P-waves remain associated with QRS complexes

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33
Q

2nd degree heart block, mobitz I

A

“Wenckebach”

PR-interval progressively elongates, eventually culminating in the non-conduction of one P-wave, before the cycle begins again with a minimally-prolonged/normal PR interval

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34
Q

2nd degree heart block, mobitz II

A

Intermittent conduction and non-conduction of P waves without PR-interval prolongation (can be no pattern, or fixed ratio)

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35
Q

3rd degree heart block

A

Total dissociation between atrial and ventricular activity

e.g. Atrial rate of 60bpm, and an overlying, but independent Ventricular rate of 27 bpm.

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36
Q

which heart blocks require a pacemaker?

A

2nd degree (Mobitz II) and 3rd degree heart blocks carry a high risk of asystole, and require pacemaker implantation

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37
Q

which heart blocks don’t normally require a pacemaker?

A

1st degree and 2nd degree (Mobitz I) heart blocks tend to be asymptomatic, and don’t tend to require pacing

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38
Q

Normal cardiac conduction pathway

A

Triggered at the SA node (right atrium)

AP spreads through the atria, causing atrial contraction.

AP reaches the AV node, delayed for a short time.

AV Node triggers the AP to travel rapidly down the septum via the bundle of His and the bundle branches.

At the apex of the heart, the AP spreads rapidly through the ventricles via the Purkinje Fibres, causing synchronised depolarisation

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39
Q

what is the purpose of the delay in conduction at the AV node?

A

to allow the ventricles to fill fully

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40
Q

What is the firing rate of the SA Node?

A

60 - 100 bpm

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41
Q

what is the firing rate of the ventricular cardiomyocytes?

A

10-40 bpm

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42
Q

what would indicate whether the arrhythmia is supra ventricular or ventricular?

A

SV - narrow QRS complex

V - broad QRS complex

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43
Q

Cardiac accessory pathways

A

AP is able to bypass the AV Node

triggers early depolarisation of part of the ventricle (seen as a Delta Wave on the ECG)

AP propagates slowly, as it spreads cell-to-cell through the heart muscle

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44
Q

Distribution of ST elevation in anterior MI?

A

Anterior zone supplied by left anterior descending (LAD) artery

elevated in Leads V1-V4

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45
Q

Distribution of ST elevation in lateral MI?

A

Lateral zone is supplied by the Left Circumflex (LCx) Artery

elevated in Leads V5, V6, I and aVL

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46
Q

Distribution of ST elevation in inferior MI?

A

inferior zone is supplied by the Right Coronary Artery (RCA)

elevated in Leads II, III and aVF

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47
Q

Distribution of ST elevation in anterolateral MI?

A

when the Left Coronary Artery is occluded

affecting both the Anterior and Lateral zones as LAD and LCx branches affected

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48
Q

What might an ECG look like days/months after a STEMI?

A

may have a deep Q-wave (indicating tissue death)

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49
Q

Atrial flutter vs. Atrial fibrillation on an ECG

A

quivering baseline, no P-waves = atrial fibrillation

sawtooth pattern = atrial flutter

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50
Q

Causes of LVH

A
  • Hypertension (most common cause)
  • Aortic stenosis
  • Aortic regurgitation
  • Mitral regurgitation
  • Coarctation of the aorta
  • Hypertrophic cardiomyopathy
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51
Q

what are the two shockable cardiac arrhythmias?

A

Ventricular Tachycardia

Ventricular Fibrillation

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52
Q

What is cardiac failure?

A

a clinical syndrome, characterised by typical signs and symptoms

associated with abnormality of cardiac structure or function

leading to failure of the heart to deliver oxygen at a rate meeting the requirements of the metabolising tissues.

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53
Q

What are the types of heart failure?

A
  1. LV heart failure
  2. RV heart failure
  3. Biventricular failure
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54
Q

LV Heart failure

A

Poor output of the impaired LV leads to an increase in left atrial and pulmonary venous pressure

This causes pulmonary oedema, as the increased pulmonary venous pressure prevents the reuptake of fluid at the level of the capillaries.

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55
Q

RV Heart failure

A

RV output fails

Predominantly due to lung disease (cor pulmonale) and pulmonary valvular stenosis.

This typically leads to peripheral oedema

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56
Q

Biventricular Heart Failure

A

LVF and RVF may be present at the same time

Either:

i. Disease (e.g. IHD) has affected both sides of the heart
ii. LVF leads to pulmonary congestion which can then lead to RVF (termed “congestive heart failure”)

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57
Q

What are the most common causes of heart failure?

What are other causes?

A

IHD
Dilated cardiomyopathy
Hypertension

Other cardiomyopathies
Valvular disease
Congenital heart disease
Cor pulmonale
Alcohol/drugs
AF/heart block
Anaemia
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58
Q

what is ejection fraction ?

A

a measurement of how much blood the left ventricle pumps out with each contraction

expressed as a percentage

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59
Q

what is Stroke volume ?

A

the amount of blood pumped by the left ventricle of the heart in one contraction

expressed in mL

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60
Q

What is cardiac output?

How can it be worked out?

A

the amount of blood the heart pumps through the circulatory system in a minute

expressed in litres per minute

CO = Heart Rate (HR) × Stroke Volume (SV))

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61
Q

what is systolic dysfunction ?

A

insufficient pumping action or impaired contraction

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62
Q

what is diastolic dysfunction?

A

insufficient filling of the ventricle due to decreased compliance and impaired relaxation

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63
Q

Signs of LV failure

A

Fatigue

Exertional dyspnoea, Paroxysmal nocturnal dyspnoea, Orthopnoea

Pulmonary oedema/congestion
=> Inspiratory crepitations initially in lung bases, then throughout lungs if untreated.
=> Cough

“Gallop rhythm” – three distinct heart sounds.

Cardiomegaly, laterally displaced apex beat.

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64
Q

Signs of RV failure

A 
Fatigue
Breathlessness
Anorexia/nausea (due to hepatomegaly)
Raised peripheral venous pressure and JVP.
Organomegaly – liver and spleen. 
Cardiomegaly
Peripheral oedema
Ascites
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65
Q

what are the maladaptive compensatory mechanisms in cardiac failure?

A

Reduced CO leads to activation of the SNS and RAAS.

RAAS activation leads to vasoconstriction (increasing afterload) and sodium/water retention (increasing preload) thus further increasing BP and cardiac work.

SNS activation initially maintains cardiac output but prolonged stimulation leads to myocyte apoptosis and necrosis

chronic heart failure => desensitisation of the myocytes to the SNS and the ventricles enlarge (however they contract less efficiently).

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66
Q

NYHA classification of heart failure

A

Class I – no limitation of physical activity.

Class II – slight limitation of activity (breathlessness/ fatigue with moderate exercise)

Class III – marked limitation of activity (breathlessness with minimal exercise)

Class IV – severe limitation of activity (dyspnoea at rest)

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67
Q

Cardiac Failure - Investigations

A

Bloods - FBC, U&Es, LFTs, thyroid function, (cardiac enzymes in acute failure).

BNP

CXR - any cardiomegaly? pulmonary oedema?

ECG - any ischaemia, HTN, or arrhythmias?

Echo - if ECG or BNP are abnormal, gold standard for diagnosis.
=> EF <45% is diagnostic of heart failure

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68
Q

B-type natriuretic peptide in heart failure

A

A normal level of BNP will exclude heart failure, so this a good screen for breathlessness

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69
Q

what is acute on chronic/decompensated part failure?

A

chronic heart failure with a sudden deterioration

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70
Q

Cardiac failure - goals of treatment

A
  • Identify/treat any cause (valvular disease, IHD, etc.)
  • Reduce cardiac workload
  • Increased cardiac output
  • Counteract maladaptation
  • Relieve symptoms
  • Prolong quality of life – reduce hospitalisation.
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71
Q

Acute heart failure - management

A

Sit the patient up!
High flow oxygen

IV diuretics at escalating doses.

Consider IV nitrates (caution in hypotension and heart failure secondary to severe aortic stenosis)

Consider non-invasive ventilation

Consider inotropic support

Consider device therapy (intra-aortic balloon pump, etc)

Consider referral for Left ventricular assist device or cardiac transplantation.

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72
Q

Chronic heart failure - management

A

Lifestyle advice

1st line therapy – ACEi and beta-blocker

Add diuretic if symptomatic oedema.

2nd line therapy – Aldosterone antagonists (e.g. spironolactone) / ATRA / hydralazine plus nitrate.

3rd line therapy – Cardiac resynchronisation therapy/ digoxin/ ivabradine

Consideration of cardiac transplant.

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73
Q

Cardiac Failure - Lifestyle advice

A

Obesity control,

dietary modification (salt and fluid restriction if severe heart failure).

Smoking cessation

Bed rest important following exacerbation, but generally low-level exercise is recommended.
=> Avoid strenuous exercise.

Vaccination – against pneumococcal disease and influenza.

Sex – avoid Viagra (can cause hypotension).

74
Q

What role does an ACEi have in cardiac failure?

When would its use be avoided?

A

Works to reverse the neurohormonal adaptation

Should NOT be used with NSAIDs (risk of renal damage)
Avoided in patients with SBP <100 – risk of severe hypotension

75
Q

What role does a beta-blocker have in cardiac failure?

What is important to note about initial effects?

When should beta-blockers be avoided?

A

Used to block the SNS activity causing maladaptation.
Also anti-arrhythmic effects

Symptoms initially become worse!!

Contraindicated in asthma, caution in COPD

76
Q

What role do diuretics have in cardiac failure?

A

Mainly for symptomatic relief of pulmonary oedema (also venodilate)

77
Q

Digoxin

A

Positive ionotrope and negative chronotrope
=> increases force of contraction but decreased heart rate

Impairs AVN conduction, increases vagal activity.

Contra-indicated in heart block and bradycardia.

Dose titrated to make sure HR does not go <60bpm.

78
Q

Typical presentation of IHD

A

described as chest “discomfort” rather than pain.

Pain tends to be retrosternal
(can range from anywhere from umbilicus to the jaw)

Feels like a pressure or weight on the chest.

Pain normally lasts <10 minutes.

Exacerbating factors – inclines, cold weather, heavy meals.

Pain unrelated to respiration/position

79
Q

characteristics of “Typical” angina

A
  1. Constricting discomfort in the front of the chest or in the neck, jaw, shoulder, or arm.
  2. Precipitated by physical exertion
  3. Relieved by rest or nitrates within 5 min.
80
Q

How is angina graded?

A

According to its association with exertion.

I - only with strenuous exertion
II - with moderate exertion
III - with mild exertion
IV - at rest

81
Q

What are some risk factors for IHD?

A 
Hypertension
Hypercholesterolaemia
Diabetes
Smoking 
Family History – presence of premature CAD
82
Q

What investigations should be done for chest pain?

A

ECG

Bloods - FBC, U&Es, glucose, HbA1c, Lipids, TSH (cardiac enzymes)

CXR

Echo

83
Q

what can be identified on an echocardiogram?

A

LV function

Regional wall motion abnormalities – IHD/previous MI

Valve disease

Cardiomyopathy

84
Q

General management of IHD

A

Address modifiable risk and lifestyle factors

If patient has significant co-morbidities – consider treating medically

if patient is very high risk with symptoms despite treatment – proceed directly to invasive assessment

85
Q

IHD - managing lifestyle factors

A

Smoking cessation,

Mediterranean diet, weight control (aim for BMI <25),
Sensible alcohol intake.

Diabetes control,
Hypertension control,
Dyslipidaemia control,

Physical exercise – 30-60 minutes per day.

Influenza vaccine

86
Q

IHD - medical treatment

A

ANGINA SYMPTOMS:

  • Short-acting GTN – used sublingually (can also use LA)
  • Beta-blocker first line (HR 55-60bpm)
  • Dihydropyridine CCB (e.g. amlodipine) – 2nd line if BB not tolerated.
  • Combination of BB and CCB

OTHER:

  • Low-dose aspirin (or clopidogrel)
  • Dual anti-platelet therapy
  • potentially low-dose rivaroxaban in combination with aspirin
  • Statin for lipid profile
  • ACEi for those with diabetes, HTN or HF
87
Q

What is important to remember with use of a long-acting nitrate?

A

a “nitrate free period” will be needed

this is to avoid down-regulation of nitrate receptors and reduced efficacy of the drug

88
Q

what is dual anti-platelet therapy

A

A combination of two anti-platelet drugs

usually aspirin + clopidogrel

there are some newer anti-platelet therapies too

89
Q

IHD - Revascularisation

A

Used for patients with increased mortality because a large area of myocardium is at risk (>10%) on functional testing.

Options are PCI or CABG

90
Q

When is PCI favoured?

A

Tends to be favoured for a discrete narrowing/stenosis.

Favoured in advanced age/frailty/reduced life expectancy as it is less invasive than CABG

91
Q

When is CABG favoured?

A

Favoured in diffuse CAD – 3 vessels affected.

Used for patients with re-stenosis of stents and patients that may need other cardiac pathologies treated at the same time (e.g. valvular disease, aortic aneurysm).

92
Q

What does the “Lub” /S1 heart sound indicate?

A

Indicates the start of systole

Due to the increase in ventricular pressure and the closure of the mitral and tricuspid valves

will be heard WITH pulse.

93
Q

when would you hear a “split” heart sound?

A

If there is pathology on one side of the heart and there is a delay in closure of one valve

94
Q

What does the “dub” /S2 heart sound indicate?

A

Due to the closure of the aortic and pulmonary valves.

Occurs before diastole

95
Q

Valve stenosis

A

narrowing of the valve that does not fully open, causes turbulent blood flow

96
Q

Valve regurgitation/incompetence

A

valve does not shut properly and the blood regurgitates back through the valve

97
Q

Aortic stenosis

A

Narrowing of the aortic valve, causing obstruction of blood flow across the valve

98
Q

Aortic Stenosis - causes

A
  • Congenital – bicuspid aortic valve (BAV).
  • Rheumatic fever
  • Age-related calcification.
99
Q

Aortic Stenosis - common signs/symptoms

A
  • Angina – SoB, chest pain
  • Arrythmias (cardiac remodelling can lead to altered conduction)
  • Exertional Syncope
  • Left ventricular failure
100
Q

Aortic Stenosis - On Examination

A

PALPATION
Pulse - small volume, slow rising, narrow pulse pressure.
Heaves - as left ventricle has to push hard to get blood out of stenosed valve

AUSCULTATION
Crescendo-decrescendo ejection systolic murmur
May have radiation to carotids (sitting forward on expiration)

101
Q

Aortic Stenosis - investigations

A
  • ECG – may show LVH
  • CXR – any cardiomegaly?
  • Echo – to see how thick the valves are and possible calcification
  • Cardiac Catheterisation – to assess pressure gradient across the valve.
102
Q

Aortic Stenosis - management

A

Acute – balloon valvuloplasty

Chronic – aortic valve replacement

103
Q

Aortic Regurgitation

A

Leakage of blood from the aorta back into the left ventricle during diastole.

Due to imperfect closing of the aortic valve

104
Q

Aortic Regurgitation - Causes

A
  • Hypertension
  • Aortic dissection
  • Weak connective tissue – e.g. Marfan’s syndrome.
  • Infection
105
Q

Aortic Regurgitation - Common signs/symptoms

A
  • Angina – SoB, chest pain
  • Fatigue
  • Palpitations
  • Chest pains
  • Fainting/syncopal episodes
106
Q

Aortic Regurgitation - on examination

A

PALPATION
Pulse - wide volume, collapsing pulse
Displaced Apex beat

AUSCULTATION
Crescendo diastolic murmur at left sternal edge.

107
Q

Aortic Regurgitation - investigations

A
  • ECG – may show LVH
  • CXR – any cardiomegaly?
  • Echo – determine degree of regurgitation
  • Cardiac Catheterisation – to assess pressure gradient across the valve.
108
Q

Aortic Regurgitation - management

A

Acute – haemodynamic support

Chronic:

  1. Medical management – reduce BP, reduce cardiac contractility.
  2. Aortic valve replacement – if symptoms worsening.
109
Q

Mitral Stenosis

A

Narrowing of mitral valve causing obstruction to blood flow

110
Q

Mitral Stenosis - Causes

A
  • > 95% of causes due to Rheumatic fever
  • Congenital
  • Old-age degenerative
  • SLE
111
Q

Mitral Stenosis - Causes

A
  • > 95% of causes due to Rheumatic fever
  • Congenital
  • Old-age degenerative
  • SLE
112
Q

Mitral Stenosis - Common signs/symptoms

A
  • SoB
  • Fatigue
  • Atrial fibrillation – due to left atrium dilation.
  • Haemoptysis – due to any back flow into the pulmonary circulation.
113
Q

Mitral Stenosis - on examination

A

INSPECTION
Malar Flush

PALPATION
Pulse – small volume
Parasternal heave

AUSCULTATION
Mid-diastolic murmur – heard at apex (normally 5th ICS, mid-clavicular line).

Added sounds – due to blood flow turbulence and opening snap.

Can accentuate the murmur by asking the patient to lie in the left lateral position and listen as they breathe out.

114
Q

Mitral Stenosis - investigations

A
  • ECG – may show AF
  • CXR
  • Echo – determine the degree of stenosis
  • Cardiac Catheterisation – to assess pressure gradient across the valve
115
Q

Mitral Stenosis - management

A

Acute – haemodynamic support

Chronic

  1. Medical management – diuretics
  2. Percutaneous balloon valvotomy – widen stenosed valve.
116
Q

Mitral regurgitation

A

Leakage of blood from the left ventricle to the left atrium during systole.

Due to imperfect closing of the mitral valve leaflets

117
Q

Mitral regurgitation - causes

A
  • Left ventricular dilatation
  • Cardiomyopathy
  • Old-age degenerative
  • Infection – vegetations from infective endocarditis
  • Autoimmune
118
Q

Mitral regurgitation - common signs/symptoms

A
  • SoB
  • Fatigue
  • Peripheral oedema – due to LVF
  • Faint/dizziness
119
Q

Mitral regurgitation - on examination

A

PALPATION
Pulse - possible AF
Parasternal Heave

AUSCULTATION
Pan-systolic murmur

120
Q

Mitral regurgitation - investigations

A
  • ECG – may show AF
  • CXR
  • Echo – determine degree of regurgitation
  • Cardiac catheterisation – to assess pressure gradient across the valve.
121
Q

Mitral regurgitation - management

A

Acute – haemodynamic support

Chronic:

  1. Medical management – ACEi, beta-blockers.
  2. Mitral valve replacement – if symptoms worsening.
122
Q

Congenital causes of valvular heart disease

A

atria/ventricular septal defects,

Marfan’s syndrome,

abnormal valves – e.g. bicuspid aortic valve

123
Q

Rheumatic causes of valvular heart disease

A

Rheumatic fever

Seronegative spondyloarthropathies

124
Q

Degenerative causes of valvular heart disease

A

Small defects which slowly escalate to larger defects over time.

e.g. Plaque which gets progressively worse, leading to stenosis

125
Q

Cardiac remodelling causes of valvular heart disease

A

Heart may change shape due to changes over time.

Disruption to anatomy, can lead to regurgitant valves

126
Q

Infective endocarditis as a cause of valvular disease

A

Bacteria from the bloodstream can deposit on the valves.

Vegetations develop, leading to (permanent) valvular disruption.

In the acute infective phase, these patients deteriorate very rapidly

127
Q

why does valvular disease ultimately lead to heart failure?

A

Stenosis – the heart has to work harder to force blood through the valve.

Regurgitation – the heart has to work harder to pump enough blood forward against blood that leaks back through the valve.

128
Q

Tissue valve Vs. mechanical valve replacement

A

Mechanical valve is less likely to need to be replaced again

Mechanical valve has increased risk of blood clots - lifelong anticoagulation (warfarin) needed
(Tissue valve would only need life-long aspirin)

Mechanical valve has audible clicking noise.

129
Q

When is the optimal timing for a valve replacement?

A

just as decompensation is starting to develop

Avoid replacing too early or too late

130
Q

What is cardio-thoracic ratio?

On what CXR projection can this be officially assessed?

What should this be?

A

the ratio of the width of the heart versus the width of the chest at the same level

On a PA projection

should be <50% (>50% is cardiomegaly)

131
Q

A systematic approach to interpreting CXRs

A
  1. Patient demographics
  2. Projection and technical adequacy.
  3. Tubes and lines
  4. A – airways
  5. B – Bones
  6. C – cardiac and mediastinal contours (cardio-thoracic ratio).
  7. D – diaphragm
  8. E – everything else: pleural spaces, lungs, etc.
  9. Review areas where pathology can be easily missed – lung apices, below the diaphragm, lung hila.
132
Q

Causes of acute chest pain - lungs

A

Pleurisy (LRTI)

Pneumothorax

Tension PTX !

133
Q

Causes of acute chest pain - cardiac

A

ACS !

Stable angina

Pericarditis

Aortic Dissection !

Coronary spasm

134
Q

Causes of acute chest pain - MSK

A

Costochondritis
Varicella Zoster
Muscular Strain

135
Q

Causes of acute chest pain - Other

A

Anxiety

136
Q

Causes of acute chest pain - GI

A

GORD

Duodenitis/Gastritis

Boerhaave’s Oesophageal Perforation !

Cholecystitis

Peptic Ulcer Disease

Oesophageal Spasm

137
Q

What conditions are considered acute coronary syndromes (ACS)?

A

STEMI
NSTEMI
Unstable angina

138
Q

what is atheroma and what does it lead to?

A

= an abnormal accumulation of material within the walls of the coronary arteries

reduces the size of the lumen and thereby reduces blood flow to the myocardium => ischaemic damage

predisposes to thrombus and aneurysm formation

139
Q

Percutaneous coronary intervention (PCI)

A

involves the use of a balloon to inflate the vessel, and sometimes addition of a stent.

140
Q

pharmacotherapy for coronary interventions

A

the patient will need to have dual anti-platelet therapy (aspirin and clopidogrel) before undergoing PCI

to prevent peri-procedural thrombosis (due to the plastic catheters in the arteries temporarily) unfractionated heparin is normally given

141
Q

What is infective endocarditis?

A

an infection of the endocardial surface of the heart, or mainly an infectious vegetation on a heart valve

described as “pyrexia, with a new/changing murmur”

142
Q

Causes of infective endocarditis

A

Damaged Endothelium
=> Damaged valves
=> Prosthetic valves
=> Congenital heart disease

High levels of sustained bacteria
=> IV drug users
=> Infected intravascular devices
=> Untreated abscess/collection elsewhere

143
Q

Most common infective organism - native valves

A

~80% are caused by various staphylococci or streptococci

e.g. Strep. viridans, Strep. mitis, Staph. aureus

144
Q

Most common infective organism - prosthetic valves

A

Coagulase negative staphylococcus (such as Staph. epidermidis).

Usually <2 months after surgery.

After 2 months – tend to revert to the normal causative organisms

145
Q

Most common infective organism - IV drug users

A

Staph. aureus is especially common

tends to be right-sided heart disease, as this is the side that the bacteria reach first from the periphery

146
Q

Other infective organisms/causes of endocarditis

A

Strep. bovis – found in association with bowel malignancy.

Enterococcus – has there been manipulation of GU/GI tract?

Difficult to grow organisms / “Culture negative endocarditis”

Non-infectious endocarditis – SLE

147
Q

Signs/Symptoms of endocarditis

A

Fever + new/changing murmur

Microscopic haematuria

Splenomegaly

Osler’s Nodes – tender red nodules in fingers due to immune complex deposition.

Clubbing

Splinter haemorrhages

Roth’s Spots – pale areas with surrounding haemorrhage on retina.

Janeway lesions – painless palmar/plantar macules.

Petechial rash

Digital infarcts

148
Q

Investigations for infective endocarditis

A

Bloods – FBC, CRP/ESR, U&E

Blood cultures – ideally take 3 sets, 1 hour apart, different sites, before antibiotics.

Urinalysis – proteinuria and microscopic haematuria.

ECG – at regular intervals (?MI)

CXR – any evidence of heart failure/abscesses/emboli

Transthoracic Echocardiography – in all patients, but negative echo does not rule out endocarditis.

149
Q

Duke’s Criteria - Major

A

Positive culture (typical organism in two cultures).

Endocardial involvement on echo (vegetations, abscess, new regurgitation

150
Q

Duke’s Criteria - Minor

A

Predisposition – e.g. heart condition, IVDU

Fever >38C

Vascular phenomena

Immunologic phenomena

Positive blood culture/echo but not sufficient for “major” criteria.

151
Q

What criteria are required for a diagnosis of infective endocarditis?

A 
2 major and 1 minor criteria
or 
1 major and 3 minor criteria
or
5 minor criteria
152
Q

Management of infective endocarditis

A

MEDICAL
Antibiotics – correct choice, strength, frequency, and duration.

SURGICAL
Excision of infected or damaged valve and replacement with prosthetic (ideally after no longer bacteraemic)
Draining of metastatic abscesses

SOCIAL
Manage pre-disposing factors (e.g. IV drug use)

153
Q

Is prophylaxis used for infective endocarditis?

A

Not routinely anymore

Sometimes for high-risk patients undergoing dental procedures.

154
Q

Cardiovascular exam - inspection of hands (and arms)

A

HANDS
Temperature – cool could mean poor cardiac output/hypovolaemia

Clubbing

Peripheral cyanosis

Janeway Lesions, Osler’s Nodes.

Xanthomata – deposition of yellowish cholesterol-rich material, indicating hyperlipidaemia

Capillary refill time – hypovolaemia

Tar staining

ARMS
Track marks (IV drugs?)
Scars (e.g. CABG)

155
Q

Cardiovascular exam - inspection of face and neck

A

EYES
conjunctival pallor, xanthelasma, corneal arcus

MOUTH
central cyanosis, anaemia, dental hygiene

NECK
Palpate carotid pulse
Assess JVP

156
Q

Where would you auscultate the aortic valve?

A

Right 2nd ICS, near the sternal edge

157
Q

Where would you auscultate the pulmonary valve?

A

Left 2nd ICS, near the sternal edge

158
Q

Where would you auscultate the mitral valve?

A

Left 5th ICS at the mid-clavicular line

159
Q

Where would you auscultate the tricuspid valve?

A

Left 4th/5th ICS, near the sternal edge

160
Q

How do you feel for ventricular heave?

What would this indicate?

A

Palpate over left sternal edge with heel of hand and fingers to look for chest wall moving with each heartbeat

volume or pressure overload (hypertrophy)

161
Q

How do you feel for thrills?

what would this indicate?

A

feel gently with fingertips in 2nd and 3rd ICS

turbulence of blood over the valves - palpable murmurs

162
Q

Where would you palpate the apex beat?

A

Left 5th ICS at the mid-clavicular line; palpate with flat hand.

163
Q

How would you “complete” a cardiovascular examination?

A

Peripheral vascular exam
Peripheral pulses
ECG
Measure BP

164
Q

What are causes of ankle swelling?

A 
Heart failure (worse later in the day)
Drugs (especially amlodipine)
Venous diseases
Renal causes
Hypoalbuminaemia
165
Q

What is useful to ask about a patient’s palpitations?

A

Get them to tap out the rhythm!

Ask about any triggers? (e.g. caffeine, exercise, anxiety, etc.)

Frequency and duration

Associated features?

Any history of thyroid disease?

166
Q

What are some relevant PMH conditions to ask about in a history about a cardiovascular complaint?

A

MI, HTN, CVA, Diabetes

Previous surgery and details of procedures

Rheumatic fever

Recent dental work

167
Q

What are some relevant aspects of family history to ask about in a history about a cardiovascular complaint?

A

Any ischaemic heart disease?

Any sudden cardiac death? (particularly < 40 years)

168
Q

unstable angina

A

atheromatous plaque is ruptured and thrombus forms, causing partial occlusion of the vessel and supply ischaemia

Pain occurs at rest or progresses rapidly over a short period of time.

169
Q

In what acute coronary syndromes will cardiac enzymes be elevated?

A

STEMI

NSTEMI

170
Q

What is the difference between a STEMI and NSTEMI?

A

STEMI

  • complete occlusion of vessel
  • transmural ischaemia
  • ST-elevation/hyperacute T waves

NSTEMI

  • partial occlusion of vessel
  • subendocardial ischaemia
  • normal/inverted T waves/ ST depression
171
Q

At what time after an MI would microscopic changes be visible?

A

at 12-24 hours

172
Q

At what time after an MI does the acute inflammatory reaction to dead muscle occur?

What does this look like?

A

at 24-72 hours

The area becomes soft and pale.

173
Q

Early complications of MI

A

Sudden death due to cardiac dysrhythmia

Sudden death due to acute left ventricular failure

Rupture of myocardium -> haemopericardium

Rupture of papillary muscle -> acute valve failure ->LVF

Mural thrombus on infarct -> embolism -> stroke & others

Fibrinous Pericarditis & extension of MI

174
Q

Late complications of MI

A

Chronic LVF

Ventricular Aneurysm

175
Q

what is aortic dissection?

A

A tear in the intima of the aorta, causing a false lumen in the tunica media into which blood can enter.

176
Q

How does aortic dissection present?

A

Sudden “tearing” chest pain

Radiation to the back

There can be occlusion of aortic branches, with symptoms depending on which branch is affected.

177
Q

Risk factors for aortic dissection

A 
Hypertension
Connective tissue disorders
Vascular inflammation
Trauma
Surgery
Smoking/drugs
178
Q

Long-term management of MI

A

Beta-blocker
ACEi- Ramipril
Dual Antiplatelet – Aspirin and Ticagralor
Increase statin dose
Smoking cessation
Cardiac rehabilitation
Return to exercise, driving & work advice

179
Q

Immediate Management of MI

A

Analgesia (morphine?)
Oxygen, if required

GTN

Aspirin/anti-platelets

PCI?

180
Q

Possible causes of loss of consciousness

A 
ACS – STEMI, NSTEMI or Unstable Angina 
Tachy/bradycardia
Aortic dissection
Postural hypotension
Simple faint – vaso-vagal
Pulmonary Embolism (PE)
Hypoglycaemia
Intracranial haemorrhage
181
Q

When does blood flow to the coronary arteries occur?

A

During diastole

CP1 (12 decks)

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