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Cardiology Flashcards

1
Q

What is the difference between stable and unstable angina?

A

Stable angina usually by exertion

Unstable can occur at any time, may be more severe, and may not be relived by rest/ GTN

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2
Q

What basic investigations would you want to do for a px with probable angina?

A 
FBC to check for anaemia
U&Es for renal function
Fasting blood glucose if no known diabetes/ HbA1c if known diabetes
LFTs baseline before commencing statins
Serum lipids for hyperlipidaemia
TFT
Troponins and cardiac enzymes
12 lead ECG
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3
Q

What ECG changes could show in a px with angina?

A

ST depression
T wave inversion
LBBB

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4
Q

How would you manage a px with angina?

A

Conservative: reduce IHD risk factors eg weight loss, dietary advice, smoking cessation, exercise, optimise HTN and diabetes

Medical: GTN spray PRN, Aspirin OD, statin (atorvastatin), beta blocker, Ca2+ channel blocker

Surgical: PCI or CABG

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5
Q

Give an example of a Ca2+ channel blocker relatively selective for myocardium

A

Verapamil

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6
Q

What are some side effects of Ca2+ channel blockers?

A

Cause vasodilation and reduce HR and FOC so…

Headaches
Constipation
Flushing
Bradycardia
Reflex tachycardia
Ankle oedema
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7
Q

What are some modifiable and non modifiable risk factors for an MI?

A

Non-modifiable: age, male, ethnicity (south Asians), family history, premature menopause

Modifiable: smoking, diabetes Mellitus, hypertension, obesity, hyperlipidaemia

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8
Q

What does ST elevation in leads 1 to 4 indicate?

A

Anteroseptal STEMI of LAD

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9
Q

Where would ECG changes present for a lateral STEMI?

A

In V5-6 (Cx/ LAD)

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10
Q

What leads would an inferior MI show ECG changes in and what artery would be affected?

A

II, III, aVF

Right coronary artery

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11
Q

A high lateral MI would show ECG changes in which leads?

A

I and aVL

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12
Q

What ECG changes can appear for an MI?

A

ST elevation
T wave inversion
New LBBB
Pathological Q waves

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13
Q

How do the levels of different cardiac enzymes change in the blood over time?

A

Troponins: start to rise 3-12 hours post onset of pain, peak at 24-48 hours, return to baseline within 5-14 days

CK-MB: starts to rise 3-12 hours post onset of pain, peaks at 24 hours, returns to baseline after 48-72 hours

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14
Q

What is the initial management of a px suffering from an MI?

A

MONA
= morphine, oxygen, nitrates (GTN spray), Aspirin

Also establish IV access
Do FBC, troponins, CK-MB, lipids, U&Es
12 lead ECG

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15
Q

What medications would a patient be on post MI?

A 
Aspirin (for life)
Clopidogrel (for one year)
Statin
ACEi
Beta blocker

Can’t drive for 4 weeks

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16
Q

What is the most common type of AVRT?

A

Wolf Parkinson White syndrome

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17
Q

What is the accessory pathway called in Wolf Parkinson White syndrome?

A

Bundle of Kent

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18
Q

Why are P waves not visible in AVNRT?

A

As the atria and ventricles contract at a similar time so the atrial depolarisation is masked by the ventricular depolarisation

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19
Q

What are the pathways involved in AVNRT?

A

Slow alpha pathway

Faster beta pathway

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20
Q

What is the definitive treatment of AVRT or AVNRT?

A

Radio frequency ablation of the accessory pathway/ slow alpha pathway

Can also use vagal manoeuvres (carotid sinus massage or valsalva manoeuvre) to activate the vagus nerve and block the AVN

Medication to slow AVN conduction

If not, cardioversion

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21
Q

What ECG changes are seen in Wolff Parkinson White syndrome?

A

Shortened PR <120ms

Delta waves

Long QRS (as ventricle contract early)

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22
Q

How long is one small square on an ECG?

A

0.04 seconds

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23
Q

How long is one large square on an ECG?

A

0.2 seconds

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24
Q

How would you calculate a regular rate on an ECG?

A

300/ number of squares in RR interval

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25
Q

How would you calculate an irregular rate on an ECG?

A

The number of QRS complexes in 30 large squares x 10

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26
Q

What should the normal axis on an ECG be?

A

-30 to +90 degrees

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27
Q

Left axis deviation will cause which leads to become more positive and negative?

A

1 and aVL will be more positive
2 and 3 more negative

(So leads 1 vs 2 and 3 are ‘leaving’ each other)

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28
Q

Right axis deviation will cause which leads to become more positive and negative?

A

Leads 3 and aVF will become more positive
Lead 1 more negative

So leads 1 and 3 “reaching” each other

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29
Q

Where would you place the ECG leads v1 to v6?

A 
V1 4th ICS RSE
V2 4th ICS LSE
V3 in between V2 and V4
V4 5th ICS MCL
V5 5th ICS anterior axillary line 
V6 5th ICS mid axillary line
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30
Q

How long should the PR interval be?

A

3 to 5 squares (0.12 to 0.2 seconds)

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31
Q

What does a lengthened PR interval indicate?

A

1st degree heart block
Delay in conduction between the atria and ventricles
Delay usually in the AVN

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32
Q

How would Mobitz type 1 heart block show on an ECG?

A

Progressive lengthening of the PR intervals, followed by a missed QRS, which then resets and repeats

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33
Q

What type of heart block in Wenckebachs phenomenon?

A

Type 2.1

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34
Q

How does Mobitz type 2 heart block present on an ECG?

A

Constant PR but occasionally dropped QRS

Usually a bundle branch problem

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35
Q

What is 3rd degree heart block?

A

When there is no relationship between P waves and QRS complexes so no beats are conducted from the atria to the ventricles
Often due to fibrosis of the bundle of His
Causes the ventricles to contract at their own intrinsic rate (very slow, hence urgent pacing required)

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36
Q

Increased height of the QRS complex indicates what?

A

Ventricular hypertrophy (R or L depending on lead)

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37
Q

Increased width of the QRS complex indicates what?

A

Bundle branch block

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38
Q

Why do LBBB show a W shape in lead 1 and an M shape in lead 6?

A

As the bundle branch block means the depolarisation is reversed so the RBBB is depolarised first and then goes through the septum to the left heart

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39
Q

Tall T waves indicate what?

A

Hyperkalaemia

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40
Q

Prolonged QTc is associated with which ventricular tachycardia?

A

Torsades des pointes

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41
Q

What do U waves indicated?

A

Severe hypokalaemia or hypocalcaemia

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42
Q

What arrhythmia will present with loss of the isoelectric baseline and a saw tooth pattern?

A

Atrial flutter

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43
Q

What is the first line anti hypertensive drug for for 47 year old Caucasian patient?

A

ACEi

if under 55 and not Afro Caribbean

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44
Q

What is the first line anti hypertensive drug for a 40 year old Afro Caribbean patient?

A

Calcium channel blocker

Either if aged over 55 or if Afro Caribbean

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45
Q

What is the second line drug treatment for hypertension?

A

ACEi + CCB

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46
Q

When would a thiazide diuretic by contraindicated?

A

Gout
Hypokalaemia
Hyponatraemia

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47
Q

What are some ADRs of ACEi?

A

Dry cough
Angio-oedema
Renal failure
Hyperkalaemia

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48
Q

For a hypertensive patient on an ACEi and CCB but still not responding adequately to treatment, what other drug would you add?

A

Thiazide like diuretic

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49
Q

How do thrombolytic drugs work?

A

Activate plasminogen to plasmin which degrades fibrin

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50
Q

What are some examples of thrombolytic drugs?

A

Alteplase

Streptokinase

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51
Q

What does the CHADS-VASc score determine?

A

Whether to anticoagulate a px with AF
If 0, no anticoag
If 1, anticoag if male. If 2, anticoag if female.

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52
Q

What are some causes of systolic heart failure?

A

IHD
MI
Cardiomyopathy

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53
Q

What are some symptoms/ signs seen in left sided heart failure?

A 
Dyspnoea
Dizziness
Pink/ white frothy sputum (due to pulmonary oedema)
Fatigue
Orthopnoea
Cold peripheries 
PND
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54
Q

What are some symptoms and signs seen in right sided heart failure?

A

Dyspnoea
Oedema
Ascites
Raised JVP

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55
Q

What is usually raised in the blood in heart failure?

A

BNP

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56
Q

What signs could indicated heart failure on a chest x Ray?

A 
Cardiomegaly 
Kerley B lines
Pleural effusion
Batwing shadowing
Dilated prominent upper lobe vessels
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57
Q

What does a third heart sound heard in early diastole indicate?

A

Normal in young people and athletes
Indicates congestive heart failure in older people

Caused by a sudden deceleration of blood flow into the LV from the LA

58
Q

How is heart failure managed?

A
  1. Conservative (smoking cessation, exercise, weight loss, diet
  2. Pharmacological
    ACEi and Beta blocker 1st line
    Loop diuretic e.g. furosemide for symptomatic relief (can then add thiazide if needed)

2nd line add spironolcatone (K sparing so monitor U&Es)

Consider digoxin if still symptomatic

59
Q

What are some side effects of ACEi?

A 
Dry cough
Hyperkalaemia
Fatigue
Dizziness
Headaches
60
Q

What are some side effects of furosemide?

A

Hyponatraemia
Hypokalaemia
Otoxtoxicity
Gout

61
Q

What does the NYHA scale measure?

A

New York heart association classifies heart failure 1 to 4, 4 being dyspnoea at rest and 1 being dyspnoea only on exertion

62
Q

Which murmurs are heard best on expiration?

A

Left sided murmurs

Intrathoracic pressure increases, so pulmonary vessels constrict and blood is forced from pulmonary veins into LA

63
Q

What are some causes of mitral stenosis?

A

Rheumatic fever
Old age and calcification
Congenital
Prosthetic valve

64
Q

When is mitral stenosis heard?

A

Mid diastolic murmur

65
Q

What are some causes of aortic stenosis?

A

Age related calcification
Congenital bicuspid valve
Williams syndrome
Rheumatic fever

66
Q

What are some symptoms of aortic stenosis?

A 
Angina
Heart failure
Syncope
(Classic triad)
Also: dyspnoea, dizziness
67
Q

Where does an aortic stenosis murmur radiate to?

A

Right carotid

68
Q

What type of murmur is an aortic stenosis murmur?

A

Ejection systolic

69
Q

Where would you hear an aortic stenosis murmur?

A

2nd ICS, RSE

70
Q

Which murmur has a characteristic slow rising pulse with narrow pulse pressure?

A

Aortic stenosis

71
Q

What may you see on an ECG for a px with aortic stenosis?

A

LVH

T wave inversion

72
Q

Which murmurs are heard during systole?

A

Aortic stenosis

Mitral regurgitation

73
Q

When is aortic regurgitation heard?

A

Early diastolic murmur

74
Q

What are some causes of aortic regurgitation?

A 
Infective endocarditis
Aortic dissection
Chest trauma
Congenital
Connective tissue disorders e.g.  Marfans, Ehlers Danlos
Rheumatic fever
Hypertension
75
Q

Which murmur also has a collapsing pulse with a wide pulse pressure?

A

Aortic regurgitation

76
Q

Which valve incompetency has an early diastolic murmur?

A

Aortic regurgitation

77
Q

When is aortic regurgitation best heard?

A

During expiration

With px sat forwards

78
Q

Which valve incompetency can be treated with ACEi?

A

Aortic regurgitation

To reduce systolic HTN

79
Q

Why are aortic murmurs heard best with the patient sat forwards?

A

As this brings the aortic valve closer to the chest wall

80
Q

Why are mitral murmurs heard loudest with the patient on their left side?

A

Brings the apex closer to the chest wall

81
Q

What does S1 represent?

A

Start of systole

Mitral and tricuspid Valves are closed

82
Q

Peripheral pulse is felt at the same time as which heart sound?

A

S1

83
Q

What does S2 represent?

A

Start of diastole and end of systole

Closure of aortic and pulmonary valves

84
Q

What are some causes of carcinogenic shock?

A
  • post MI
  • serious arrhythmias
  • acute worsening of AF
85
Q

Cardiac tamponade is an example of which type of shock?

A

Mechanical shock

86
Q

What is Beck’ triad?

A

Signs of cardiac tamponade

Raised JVP, muffled heart sounds, low BP

87
Q

What are some signs of distributive shock?

A

Tachycardic

Warm, red extremities (due to widespread vasodilation, where hypovolaemic shock has cold, pale extremities)

88
Q

Where is mitral stenosis best heard?

A

With the bell at the apex
Px lay on their side
During expiration

89
Q

What are some signs and symptoms associated with mitral valve stenosis?

A 
Malar flush
AF
Pink frothy sputum (pulmonary HTN)
Breathlessness
Raised JVP
Enlarged LA on CXR
ECG can show AF
90
Q

How can mitral stenosis be treated?

A

Diuretics to reduce preload and pulmonary venous congestion
If in AF: anticoagulate and rate control

If still symptomatic: ballon valvuloplasty, open mitral valvotomy, or valve replacement

91
Q

Which valve defect has a mid diastolic murmur?

A

Mitral stenosis

92
Q

What are some causes of mitral regurgitation?

A 
Infective endocarditis
Rheumatic fever
Papillary muscle rupture post-MI
Cardiomyopathy
Mitral valve prolapse
CT disorder eg Ehlers Danlos, Marfans 
Congenital
93
Q

When is a mitral regurgitation murmur?

A

Pan systolic murmur

Heard at the apex and radiates to the axilla

94
Q

Patients with a 10 year cardiovascular risk greater than what value should receive a statin?

A

> 10%

95
Q

What are some side effects of statins?

A 
Myopathy (myalgia, myosotis, rhabdomyolysis, asymptomatic raised CK)
Liver impairment (so check LFTs at baseline, 3month and 12 month)
96
Q

What ECG features are present in hypokalaemia?

A 
U waves
Small/ absent T waves
Prolonged PR interval
ST depression
Long QT

“You have no Pot and no T, but a long PR and a long QT”

97
Q

Rheumatic fever can develop 2-4 weeks after an infection by what?

A

Streptococcal pyogenes throat infection

98
Q

What features indicate a diagnosis of infective endocarditis until proven otherwise?

A

Fever and a new murmur

99
Q

Janeway lesions and Osler’s nodes together are pathognomic for which condition?

A

Infective endocarditis

100
Q

What are common causative organisms of infective endocarditis?

A

Staph aureus

Strep viridans

101
Q

What is the difference between janeway lesions and oslers nodes?

A

Janeway lesions: non tender haemorrhagic legions on palms/ soles of feet, due to septic emboli depositing bacteria in small vessels (microabscesses)

Osler’s nodes: small tender red raised lesions on pulp of the phalanges, due to immune complex deposition

102
Q

How will AVRT and AVNRT present on ECG?

A

Narrow complex tachycardia
Regular
No P waves

103
Q

What is the accessory pathway in WPW?

A

Bundle of Kent

104
Q

How would you treat a narrow complex tachycardia that has a regular rhythm?

A

Vagal manoeuvres

If unsuccessful, IV adenosine

105
Q

How should atrial fibrillation be managed?

A

1) rate control: beta blocker or CCB
If unsuccessful/ px still symptomatic: rhythm control
2) cardioversion (if more than 48hrs wait few weeks to anticoag before cardioversion)
If drug tx for long term rhythm control is needed: amiodarone

Anticoagulation based on CHA2DS2-VASc score

106
Q

What are some examples of broad complex tachycardias?

A

Ventricular tachycardia
Ventricular fibrillation
Torsades de pointes
Wolff Parkinson white

107
Q

What causes ventricular tachycardia?

A 
Low K
Low Mg
Coronary heart disease
Cardiomyopathy
Cocaine
Caffeine
108
Q

How can vebtricular tachycardia show on ECG?

A

Broad complex
Regular
May have capture beats or fusion beats

109
Q

What are capture beats and fusion beats?

A

Can be seen with ventricular tachycardia

Capture beat: normal QRS with VT complexes
Fusion beat: when normal sinus rhythm gets through and fuses with VT

110
Q

What is ventricular fibrillation?

A

Heart is quivering instead of pumping due to disorganised electrical activity so CO is insufficient and can result in cardiac arrest with LOC and no pulse

111
Q

How is ventricular fibrillation treated?

A

Defibrillation and CPR

112
Q

What are some causes of Torsades de Pointes?

A

Long QTc due to drugs (amiodarone, erythromycin, citalopram), diarrhoea, low Mg, low K, low Ca

113
Q

How is Torsades de Pointes treated?

A

Magnesium Sulfate

Also stop any precipitating drugs

114
Q

In what syndrome can delta waves be seen on an ECG?

A

Wolff Parkinson White syndrome

115
Q

What is sick sinus syndrome?

A

Malfunction of the SAN often due to age,often causing bradycardia or can cause the heart to alternative between tachy and Brady

116
Q

How are bradycardias treated?

A

Pacemaker

Can give atropine too

117
Q

When are beta blockers contraindicated?

A

In asthma: bronchoconstriction
With verapamil: bradycardia, heart block, congestive heart failure
Sick sinus syndrome

118
Q

How does pericarditis appear on an ECG?

A

PR depression

Widespread ST elevation

119
Q

An inferior MI will show ECG changes in which leads? Which artery is affected?

A

II, III, aVF

Right coronary artery

120
Q

What is the GRACE tool?

A

Used to determine mortality risk for px with NSTEMI or STEMI

121
Q

For a px with a STEMI, how would manage this?

A

Morphine, O2 if sats <94%, Nitrates, aspirin, clopidogrel
PCI (angioplasty and stent to reopen the blocked vessel, done via a catheter inserted into the radial or femoral artery)

To prevent further events: Aspirin, clopidogrel, beta blocker, ACEi, statin

122
Q

What type of drug is indapamide?

A

A thiazide like diuretic

Third line for HTN

123
Q

What are the typical symptoms for pericarditis?

A

Sharp pleuritic chest pain (can radiate to L shoulder)
Relieved by sitting forwards!
+/- fever

124
Q

ST saddle shaped elevation on ECG is indicative of what?

A

Pericarditis

125
Q

A pericardial friction rub is indicative of what?

A

Pericarditis

126
Q

What can pericarditis lead to?

A

Pericardial effusion (which could lead to cardiac tamponade)

127
Q

What are some causes of pericarditis?

A 
Idiopathic
Viral (cocksackie, HIV, Epstein Barr)
Infective (TB, pneumococcal)
MI (Dresslers syndrome)
Trauma
Autoimmune (SLE, rheumatic fever)
128
Q

What is cardiac tamponade?

A

A type of pericardial effusion that leads to reduced ventricular filling (so reduces CO and can lead to shock)

129
Q

What is Becks triad?

A

= raised JVP, low BP, muffle heart sounds

Indicates cardiac tamponade

130
Q

What can cause low voltage QRS complexes on ECG?

A

Pericardial effusion (& cardiac tamponade)

Also obesity, pleural effusion, pneumothorax

131
Q

How is cardiac tamponade treated?

A

Supportive: fluids etc

Pericardiocentesis

132
Q

What is aortic dissection?

A

When blood accumulates within the tunica intima and media after damage to the tunica intima

133
Q

How would you manage a suspected aortic dissection?

A

Beta blocker to keep BP 100-110
Cross match blood
Surgical stenting

134
Q

What are common causative organisms for infective endocarditis?

A

Staph aureus most common
Strep viridans 2nd
Staph epidermis common for prosthetic valves

135
Q

What criteria is used to diagnose infective endocarditis?

A

Dukes criteria

Diagnosis confirmed if 2 major or 1 major + 3 minor or 5 minor

136
Q

What is dukes criteria?

A

Used to diagnose infective endocarditis (“BE FIVE PM”)
Major:
B: Blood culture +ve with typical bacteria on 2 occasions
E: Echo showing new valvular regurgitation/ vegetation
Minor:
F: fever >38
I: immune phenomena e.g. Roth’s spots, Osler’s nodes
V: vascular phenomenon e.g. janeway lesion
E: echo findings (that don’t meet major criteria)
P: predisposition e.g. IVDU, prosthetic valve, valvular heart disease
M: microbiological evidence (that doesn’t meet major criteria)

137
Q

Why are delta waves seen in AVRT?

A

As the conduction of the ventricles via the accessory pathway produces pre excitation of the ventricles (as the accessory pathway conducts more rapidly than the AVN), and this early ventricular activation is manifested as a delta wave (a slurred upstroke at the start of the QRS)

138
Q

ECG U waves are pathognomonic for what?

A

Hypokalaemia

Also small/ absent T, prolonged PR, long QT

139
Q

When should surgery be considered for aortic stenosis?

A

When symptomatic

Or if asymptomatic but valvular gradient >40mmHg

140
Q

What does the GRACE score measure?

A

Estimated 6 month mortality for NSTEMI or STEMI

Medicine (7 decks)

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