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Cardiology Flashcards

1
Q

What is hereditary hypertrophic cardiomyopathy?

A

Autosomal dominant condition = massive left ventricular hypertrophy –> diastolic dysfunction –> sub aortic stenosis. Causes ventricular arrhythmias particularly in young athletes.

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2
Q

What are the risk factors for AAA (and which one carries the most risk) ? (5)

A

SMOKING, Hypertension, family history, increasing age, male gender

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3
Q

What is the most common cause of right sided heart failure?

A

Left sided heart failure ( Ischemia, hypertension, dilated cardiomyopathy, restrictive cardiomyopathy)

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4
Q

A ECG has tall QRS complexes across it and high amplitude R waves on the left leads - what is most likley to be the cause?

A

Left ventricular Hypertrophy.

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5
Q

What ECG changes are associated with pericarditis?

A

PR segment depression and widespread ST elevation with reciprocal changes in aVR
Can also have sinus tachycardia due to pain.
As well as flattened T waves in the first 3 weeks.

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6
Q

Which of the valves is most likely to be affected in infective endocarditis?

A

Tricuspid valve - likely to get tricuspid regurgitation. Because the infective organism is most likely to enter through the right atrium therefore the tricuspid valve is the first valve it meets.

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7
Q

What are the differential diagnoses of pleuritic chest pain? (11)

A 
Aortic Dissection 
Pneumothorax 
Pleural Effusion 
Pneumonia 
Pericarditis (cardiomegaly) 
Pulmonary Embolism 
MI
Viral Pleurisy 
Costochondritis 
Muscle sprain/strain 
Fracture
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8
Q

A patient presents with pleuritic chest pain what would be the next steps in getting a diagnosis?

A

Bloods - troponin, D-dimer
CT chest
ECG

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9
Q

A pansystolic murmur heard best at the lower sternal border and apex following a LAD infarct is indicative of what condition?

A

Ventricular Septal Defect

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10
Q

In the majority of the population which artery supplies the AV node?

A

Right coronary artery - AVN branch

Less common artery is the left circumflex branch

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11
Q

What is the pathophysiology of cardiovascular disease?

A

Endothelial cells - unusual adhesion molecules appear
Macrophages are attracted and LDL accumulates
Macrophages take up the oxidised LDL = foam cells
The foam cells die and release their lipid core
Cytokines and Growth factor (PDGF) are released which causes smooth muscle proliferation in order to repair it.

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12
Q

What is the difference between stable and unstable angina - Symptoms?

A 
Stable = chest pain that goes on rest and is only brought on exertion 
Unstable = chest pain that comes on at rest and is brought on spontaneously.
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13
Q

What is the difference between stable and unstable angina - Pathophysiology?

A 
stable = Smooth muscle cells are in repair function 
Unstable = inflammation is worse than the repair can do so the fibrous cap becomes weak and vulnerable to becoming a thrombus.
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14
Q

What 6 drugs can be used as secondary prevention of cardiovascular disease to prevent an acute coronary event?

A 
ACEI 
Aspirin 
Clopidogrel 
B-blocker 
Omega 3
Statin
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15
Q

What are the 3 forms of cardiovascular disease?

A

Coronary heart disease - angina
Cerebrovascular disease
Peripheral vascular disease

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16
Q

What needs to be present to be defined as a MI?

A

Troponin rise (99th percentile) (falls can actually occur)
And
Symptoms of ischaemia
ECG changes - ST change, LBBB, T wave change, pathological Q waves

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17
Q

What are the clinical features of STEMI/NSTEMI/Unstable angina?

A

All similar
Chest pain - jaw, arms and back (over 15 mins)
Nausea and vomiting
Sweating
Dyspnoea
Upper abdominal pain (women and elderly)
Not relieved by GTN

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18
Q

What is the immediate action for a possible MI?

A 
ECG 
Morphine 
Oxygen (if sats low) 
Nitrates 
Aspirin
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19
Q

What is the difference in terms of pathology between a STEMI and a NSTEMI?

A 
STEMI = complete occlusion of carotid artery resulting in immediate myocardial death 
NSTEMI = Partial occlusion of a carotid artery
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20
Q

A ECG for possible MI has ST elevation in V1-V4. What area of the heart is this and what artery is most likely to be occluded?

A

Anterior - Left anterior descending artery

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21
Q

A ECG for possible MI has ST elevation in II, III, AvF. What area of the heart is this and what artery is most likely to be occluded?

A

Inferior - Right coronary artery

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22
Q

A ECG for possible MI has ST elevation in I, AvL, V5-6. What area of the heart is this and what artery is most likely to be occluded?

A

Anterolateral - circumflex

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23
Q

A ECG for possible MI has ST elevation in I, AvL, V2-6. What area of the heart is this and what artery is most likely to be occluded?

A

Anterior - extensive = Left coronary artery

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24
Q

A ECG for possible MI has tall R waves in V1-3. What area of the heart is this and what artery is most likely to be occluded?

A

Posterior - right coronary artery

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25
Q

What are the first and second line management of a MI (after MONA) and what are the possible side effects?

A

1st line = Primary PCI - has to be done within 12 hrs of symptom onset
2nd line = Thrombolysis - increased risk of bleeding and some may need a rescue angioplasty

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26
Q

What is the management of NSTEMI’s?

A

Beta-blockade (HR to be around 50-60)
ACEI
Atorvastatin
- if medium/high risk then angioplasty within 96 hrs

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27
Q

What is the Grace score?

A

The mortality risk for up to 6 months after a NSTEMI

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28
Q

How is unstable angina diagnosed?

A

Absence of a high troponin and a normal ECG

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29
Q

What is the treatment of unstable angina?

A

Beta-blockade (HR to be around 50-60)
ACEI
Atorvastatin

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30
Q

What are risk factors for AF?

A 
Increased age 
Increased BP
DMII 
Obesity 
Smoking 
Sleep apnoea 
CAD
Valve disease 
CKD
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31
Q

What are possible reversible causes of AF?

A

ETOH, Hyperthyroidism, electrolyte abnormalities, sepsis

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32
Q

How may AF present?

A

Mostly asymptomatically

Acute - palpitations, syncope, chest pain, dyspnoea

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33
Q

What is the main finding of AF - on a ECG?

A

Irregularly irregular pulse
No P waves
Irregular QRS but normal shape

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34
Q

What investigations may be carried out for a patient with AF?

A

ECG

Bloods - U+Es, TFT, troponin, CMP (calcium, magnesium, phosphate)

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35
Q

How would you treat acute AF (under 48hrs)?

A

Treat underlying cause
Anti-coagulate (patient dependent)
DC or drug cardioversion

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36
Q

How would you treat chronic AF?

A

Underlying cause, ECHO, Control ventricular rate
B-blocker or non-dihydropyridine CCB (verampil)
+digoxin or amiodarone (2nd line)
Anti-coagulate - CHADS-VASc and HASBLED
- apixaban (1st line)
- Dabigatran (2nd line)

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37
Q

What is the mechanism of apixiban?

A

Factor Xa inhibitor

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38
Q

What is the mechanism of dabigatran?

A

Thrombin inhibitor

39
Q

What is paroxysmal AF and how is it treated?

A

Occasional spells of AF
B-blocker (elderly) or CCB (Young)
2nd line = digoxin

40
Q

What things can increase the risk of getting a DVT?

A 
Stasis 
Dehydration 
Oestrogen 
Surgery 
AF 
PMH of DVT/PE 
Previous MI 
Malignancy 
Varicose veins 
Virchow's triad
41
Q

What is Virchows triad?

A

Stasis + Vessel wall injury + hypercoagulation

42
Q

What are the signs/symptoms of DVT?

A

Red and swollen leg (calf) + tenderness
Pitting oedema
Fever

43
Q

What is Well’s score used for?

If it is 2+ what should you do? But if it is 1 or less what should be done?

A

Diagnose and plan management for DVT.
2+ = compression ultrasound but treat as a DVT
1 or less = D.Dimer test
- if that is then negative explore other causes. If positive then do a compression ultrasound

44
Q

What are the differential diagnosis for a DVT? (swollen calf)

A

Cellulitis
Ruptured bakers’ cyst
Superficial thrombophlebitis
Injury –> muscle haematoma

45
Q

What is the sign on the ECG of a PE?

A

S1-Q3-T3 (increased waves - S/Q and inverted T wave) plus sinus tachycardia

46
Q

What is the initial treatment of a DVT?

A

Low molecular weight heparin - used for first 5 days until INR is 2-3

47
Q

What is the long term management of a DVT?

A

Continue with heparin or apixaban or change to warfarin or dabigatran. Used for at least 3 months usually long term however.

48
Q

What are the signs of a PE?

A 
Pyrexia 
Cyanosis 
Tachypnoea 
Tachycardia 
Hypotension 
Raised JVP
Pleural rub/effusion 
SIgns of risk factors - DVT, travel, recent surgery 
AF (rare)
49
Q

What are the symptoms of PE?

A 
Pleuritic chest pain 
Breathlessness 
Cough 
Haemoptysis 
Syncope/dizzy
50
Q

What scoring system is used to diagnose PE?

A

Wells score
4 or under = D-dimer test
4+ = CTPA

51
Q

PE differential diagnosis?

A 
Acute coronary syndrome 
Pneumonia 
Pericarditis 
MSK - back pain 
Embolus 
Dissection aortic aneurysm 
Anxiety 
Syncope 
COPD exacerbation
52
Q

What investigations should be done for a PE?

A 
CTPA 
Chest X-ray
ECG (S1Q3T3) 
VQ scan - much less accurate though 
ABG = metabolic acidosis 
High troponin
53
Q

What is the treatment for a PE?

A

Low molecular weight heparin and oral warfarin.

If the PE is massive then thrombolysis could be the best option (alteplase - fibrinolytic)

54
Q

What is left sided heart failure and what are the likely symptoms (specific)?
What can left sided cause?

A

Left ventricle is unable to pump blood around the body.
Pulmonary hypertension and oedema.
Due to the pulmonary hypertension LSHF can cause RSHF

55
Q

What is right sided heart failure and what are the likely symptoms (Specific)?
What is the most likely cause?

A 
Right ventricle unable to pump blood around the body. Systemic venous hypertension. 
Peripheral oedema 
Raised JVP
Hepatic congestion 
Most commonly due to COPD
56
Q

What is cardiac output and how can it be altered?

A 
CO=HR x Stroke volume 
HR
Preload 
Contractility 
Afterload
57
Q

What are the risk factors for heart failure?

A 
Hypertension 
Infection/immune 
Genetics 
Heart attack 
Volume overload 
Infiltration 
Structural
58
Q

A patient has suspected heart failure, what would you be looking for on the examination?

A 
Tachycardia 
Hypotension - narrow pulse pressure 
Raised JVP 
Displaced apex beat - LV dilatation 
RV heave 
Gallop rhythm 
aortic stenosis 
pedal and sacral oedema 
crackles and wheeze 
pleural effusion 
ascites 
hepatomegaly
59
Q

Symptoms such as exertional dyspnoea, exercise tolerance, orthopnoea causing them to sleep with more pillows, nocturnal breathlessness and cough is indicative of what condition ?

A

Heart failure

60
Q

What is the treatment of a acute NSTEMI?

BATMAN

A 
Beta Blocker 
Aspirin 
Ticagrelor  
Morphine 
Anticoagulant  
Nitrates
61
Q

What is the secondary treatment for a NSTEMI? (6)

A

Aspirin
2nd antiplatelet - ticagrelor/clopidogrel
Atorvastatin
ACEI
Beta blocker
Aldosterone antagonist - if chronic heart failure

62
Q

What murmur is collapsing pulse associated with?

A

Aortic regurgitation

63
Q

What murmur is heard best listening to the bell?

A

Mitral stenosis - is a lower pitched sound

64
Q

What is the first line treatment for chronic heart

A

Beta-blocker and ACE inhibitor (ARB if ACEI not good)

+ Mineralocorticoid receptor antagonist if they aren’t effective (spironolactone)

65
Q

What are the arrhythmias for a cardiac arrest and which ones are shockable?

A

Ventricular tachycardia and ventricular fibrillation = shock

Asystole and pulselessness electrical activity = non-shockable

66
Q

How does the treatment of unstable and stable tachycardia differ?

A

Unstable = up to 3 synchronised shocks and Iv amiodarone
Stable = Narrow complex - βblocker or SVT = vagal manoeuvre and adenosine
Wide complex = Vt - amiodarone infusion

67
Q

What is the pathophysiology of supraventricular tachycardia? And how would you manage it acutely?

A

Electrical re-entry from the ventricles to the atria

Acute = vasalva manoeuvre and carotid sinus massage

68
Q

In which patients should adenosine not be used?

A

Asthma, COPD, HF, Heart block, hypotension (severe)

69
Q

What is Wolff-parkinson White syndrome?

A

Bundle of kent between the atria and ventricle allowing ventricle to atria activity.

70
Q

A ECG shows short PR interval, Wide QRS and delta waves. What is the most likely diagnosis?

A

Wolff-parkinson White syndrome

71
Q

What is the treatment for Wolff-parkinson White syndrome?

A

Radiofrequency ablation

72
Q

What is torsades de pointes?

A

Polymorphic VT (spiralling around the baseline) with QT prolongation.

73
Q

How would ventricular ectopics present and what would they show on a ECG?

A

presents with palpitations

Abnormal broad QRS complexes that come on a otherwise normal ECG

74
Q

What would you want to check if a patient presents with ventricular ectopics?

A

Anaemia, electrolytes and thyroid function

75
Q

What is 1st degree heart block?

A

PR interval over 0.2 seconds

76
Q

What is the difference between mobitz type 1 and type 2 heart block and what degree are they?

A

2nd degree
Mobitz type 1 = gradual lengthening of the PR interval until a QRS is dropped
Mobitz type 2 = Missing QRS complexes usually in a set ratio (2:1 - 2 p waves to 1 QRS complex)

77
Q

A ECG shows no relationship between P waves and QRS complexes - what is the cause/diagnosis?

A

3rd degree heart block/Complete.

78
Q

What drug is given in asystole?

A

Atropine

79
Q

Sodium channel blockers are what type of antiarrhythmic and what are the 3 different classes?

A

Class 1
a - disopyramidine = prolongs AP and mid decrease in VMAX
B - lidocaine - shortens AP and small decrease in Vmax
C - flecainide - no change to AP and big decrease in VMax

80
Q

How do beta-blockers work as a anti-arrhythmic?

A

Blocks the A/NA affect on β1 receptors to slow down the sodium efflux. This suppresses the abnormal pacemaker and increases the refractory period = decreased HR.

81
Q

What are Class III anti-arrhythmics?

A

Potassium channel blocker - amiodarone

extends the action potential.

82
Q

Verapamil is what type of drug and what class of antiarrhythmic?

A

Class IV - calcium channel blocker - non-dihydropyridine

83
Q

How do calcium channel blockers work?

A

Shortens phase 2 by blocking voltage gated calcium channels = reduced contractility

84
Q

What effect does adenosine have on the AV/SA node?

A

Negative chronotropic effect.

85
Q

What does atropine solve?

A

Bradycardia

86
Q

What can digoxin be used for?

A

Atrial fibrillation - increased vagal activity

Heart failure - increased contractility

87
Q

When should the Digoxin concentration be taken? And what should be monitored whilst on digoxin?

A

6 hours after 1st dose

monitor electrolytes and renal function

88
Q

A ejection systolic murmur is heard loudest over the right sternal edge and it radiates to the carotid arteries. What would you do to make it louder, what is the most likely diagnosis and what is the most common cause?

A

Expire and sit forward
Aortic stenosis
Calcification

89
Q

A early diastole murmur is heard loudest over the right sternal edge. it is heard loudest when the patient sits forward and expires. What is the most likely diagnosis and what other signs may you find?

A 
Aortic regurgitation 
- corrigans sign = visible carotid pulse 
De mussets sign = head bobbing 
collapsing pulse 
displaced apex
90
Q

A ejection systolic murmur is heard loudest over the left sternal border and during inspiration. What is the most likely diagnosis and where may it radiate to?

A

Pulmonary stenosis

radiates to left shoulder

91
Q

A pansystolic murmur heard loudest at the apex. What would you do to hear it louder and what is the most likely diagnosis?

A

Mitral regurgitation

roll onto left side

92
Q

For what murmur would you ideally use the bell for (due to its low pitch)?

A

Mitral stenosis

mid diastolic - roll onto left side

93
Q

A pansystolic murmur is heard loudest over the left sternal border. What is it commonly related to and what is the most likely diagnosis ?

A

Tricuspid regurgitation

right ventricular dilation (right sided heart failure)

94
Q

What is likely to be seen in the JVP with a patient who has complete heart block?

A

Cannon A waves

Medicine (26 decks)

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