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Y3 Cardiovascular > Cardiology - DPD > Flashcards

Cardiology - DPD Flashcards

1
Q

List three important investigations to carry out in the acute setting when a patient presents with chest pain.

A

ECG
Troponins
Echocardiogram

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2
Q

What is the next step in the management of a patient whose troponins are: Negative

A

Exercise tolerance test

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3
Q

What is the next step in the management of a patient whose troponins are:Positive

A

Coronary angiography

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4
Q

List possible causes of chest pain from each of the following systems:
Cardiac

Respiratory

Gastro

Musculoskeletal

A 
Cardiac
Ischaemic heart disease 
Pericarditis 
Aortic dissection
Respiratory
PE
Pneumonia
Pneumothorax
GI
Oesophageal spasm
Oesophagitis/Gastritis 
Musculoskeletal
Costochondritis
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5
Q

List the symptoms, associated symptoms and risk factors of ischaemic heart disease.

A 
Symptoms: 
Central, crushing chest pain
Associated Symptoms:
Nausea
Sweating
Risk Factors:
Smoking 
Diabetes mellitus 
Hypertension
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6
Q

List the symptoms and associated symptoms of pericarditis.

A

Symptoms:
Pleuritic pain (worse on inspiration), which is better when leaning forward
Associated Symptoms:
Preceding flu-like symptoms

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7
Q

List the symptoms, associated symptoms and risk factors of aortic dissection.

A 
Symptoms:
Tearing pain between the shoulder blades 
Associated Symptoms:
Based on where blood supply is being lost (e.g. if dissection spread up the carotid arteries it can cause stroke)
Risk Factors: 
Hypertension
Marfan’s Syndrome
Ehlers-Danlos Syndrome
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8
Q

List some specific respiratory symptoms that you should ask a patient about when taking a history.

A 
Wheeze 
Breathlessness
Haemoptysis
Cough
Weight loss
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9
Q

What is a common and major risk factor for gastritis?

A

Excessive alcohol

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10
Q

Which upper GI infection are immunocompromised patients at risk of developing?

A

Oral candidiasis

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11
Q

Following ECG, describe the management of a patient with a:
STEMI

NSTEMI

A

STEMI:
Go to cathlab immediately for percutaneous coronary intervention
Give aspirin + clopidogrel

NSTEMI
Go to cathlab within 24 hours
Give aspirin + clopidogrel + fondaprinux

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12
Q

State the artery affected and the ECG leads showing ST elevation in myocardial infarction affecting the following parts of the heart:
Anterior
Lateral
Inferior

A 
Anterior
Left Anterior Descending 
V1-V4
Inferior
Right Coronary Artery
II, III, aVF
Lateral
Left Circumflex 
I, aVL, V5/V6
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13
Q

Which common artery do the left circumflex and left anterior descending coronary arteries originate from?

A

Left Main Stem

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14
Q

How long after an MI does the troponin level peak?

A

24-48 hours

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15
Q

How long after an MI does the troponin level return to normal?

A

5-14 days

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16
Q

Describe how collapse caused by a cardiac condition is different from collapse caused by a neurological condition.

A

The sequence of events before, during and after the collapse is important
Before:
Cardiac – no warning
Neurological – there may be an aura
During:
Cardiac – no tongue biting
Neurological – there may be tongue biting
After:
Cardiac – the patient will not be confused
Neurological – patients tend to be confused

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17
Q

What are the three main cardiac causes of collapse?

A

Arrhythmia
Outflow Obstruction
Postural Hypotension

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18
Q

List the main causes of collapse.

A

Hypoglycaemia (DO NOT EVER FORGET GLUCOSE)
Cardiac
Vasovagal syncope (increased vagal discharge leads to bradycardia and collapse – it can be precipitated by certain conditions)
Arrhythmia
Outflow obstruction
Postural hypotension
Neurological - seizure

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19
Q

List some features of seizures.

A

Tongue biting
Aura
Wetting themselves
Being confused after the seizure

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20
Q

Define syncope.

A

Collapse caused by hypoperfusion of the brain

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21
Q

List some investigations for arrhythmias.

A

ECG
24 hr tape
Cardiac monitor

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22
Q

State two causes of left-ventricular outflow obstruction.

A

Aortic stenosis

Hypertrophic obstructive cardiomyopathy (HOCM)

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23
Q

List two signs of aortic stenosis.

A

Slow-rising pulse

Ejection-systolic murmur

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24
Q

What is the main investigation for outflow obstruction?

A

Echocardiogram

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25
Q

What is the main investigation for postural hypotension?

A

Lying/standing blood pressure

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26
Q

List some causes of Long QT Syndrome.

A

Congenital (mutations of K+ channels)
Hypomagnesaemia
Hypokalaemia
Drugs

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27
Q

List three causes of pan-systolic murmur.

A

Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

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28
Q

How do you differentiate between left-sided murmurs and right-sided murmurs?

A

Left-sided murmurs are louder on EXPIRATION

Right-sided murmurs are louder on INSIPRATION

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29
Q

State an important non-cardiac feature of tricuspid regurgitation.

A

Hepatomegaly – due to backpressure causing hepatic congestion

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30
Q

List three causes of a raised JVP.

A

Tricuspid regurgitation
Right heart failure
Constrictive pericarditis

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31
Q

List two causes of tricuspid regurgitation.

A

Damage to valve leaflets (e.g. by bacteria)

Right ventricular dilation

32
Q

List two causes of right heart failure.

A

Left heart failure

Pulmonary hypertension

33
Q

List some causes of constrictive pericarditis.

A

Infection (e.g. TB)
Inflammation (e.g. connective tissue disease)
Malignancy

34
Q

List four causes of a systolic murmur.

A

Aortic stenosis
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

35
Q

Describe how you would differentiate between these causes of systolic murmur

A

Where is it loudest and where does it radiate?
Aortic stenosis – loudest in aortic area and radiates to the neck
Mitral regurgitation – loudest in mitral area and radiates to the axilla
Associated signs
Aortic stenosis – slow-rising pulse, ejection systolic murmur
Mitral regurgitation – displaced apex beat

36
Q

State four broad causes of palpitations.

A

Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Ventricular tachycardia

37
Q

State three causes of sinus tachycardia.

A

Shock
Hypovolaemia
Endocrine (e.g. hyperthyroidism, phaeochromocytoma)

38
Q

What is supraventricular tachycardia?

A

Regular narrow complex tachycardia with no p waves

SVT refers to AVRT and AVNRT

39
Q

Explain the difference between AVNRT and AVRT

A

AVNRT – a local circuit forms around the AV node

AVRT – a circuit forms between the atria and ventricles via an accessory pathway

40
Q

What key feature can be spotted on the ECG of a patient with AVRT who has been restored to sinus rhythm?

A

Delta wave (slurred upstroke on the QRS complex)

41
Q

What is the name of the accessory pathway in AVRT?

A

Bundle of Kent

42
Q

How is AVRT definitively treated?

A

Radiofrequency ablation of the accessory pathway

43
Q

Describe the ECG morphology of atrial fibrillation.

A

Irregularly irregular with no p waves

44
Q

State two important causes of atrial fibrillation that must be considered in young people.

A

Thyrotoxicosis

Alcohol

45
Q

List some causes of atrial fibrillation.

A

Heart Muscle: ischaemic heart disease, rheumatic heart disease, hypertensive heart disease
Valvular heart disease
Pericarditis
Lung: pneumonia, PE, cancer

46
Q

Why do respiratory conditions cause AF?

A

AF originates in the part of the right atrium that is close to the pulmonary vasculature – so changes in the levels of oxygen, carbon dioxide and pressure can impact on the myogenic cells within the right atrium

47
Q

Describe the ECG morphology of ventricular tachycardia.

A

Regular broad complex tachycardia

48
Q

State three causes of VT.

A

Ischaemia
Electrolyte abnormalities
Long QT syndrome

49
Q

Under what circumstance would you DC cardiovert a patient with SVT?

A

If they are haemodynamically unstable

50
Q

What is the difference between cardioversion and defibrillation?

A

Cardioversion is synchronized with the cardiac cycle – the electrical impulse is delivered at a certain point during the cardiac cycle
Defibrillation is not synchronized

51
Q

Describe the management of a patient with SVT who is not haemodynamically compromised.

A

Start with manoeuvres (e.g. valsalva, immerse face in cold water, blow into a syringe)
If that doesn’t work give ADENOSINE, and put the patient on a cardiac monitor
6 mg rapid IV bolus
If that doesn’t work, give 12 mg
If that doesn’t work, give another 12 mg

52
Q

In which patients is adenosine contraindicated?

A

Asthmatics

53
Q

What are the two main aims of management of AF?

A

Rate control

Reduce risk of stroke

54
Q

Describe the criteria for cardioversion of patients with acute fast AF.

A

Cardioversion should only occur if the patient has presented within 48 hours of onset of symptoms or if they have presented after 48 hours and have been anticoagulated for 3-4 weeks
If the onset is > 48 hours then you will need to anticoagulate them for 3-4 weeks before cardioversion is possible

55
Q

Which two drugs are regularly used for rate control in AF?

A

Beta-blockers

Digoxin

56
Q

Under what conditions would digoxin not be particularly effective as a drug for rate control?

A

If the patient is acutely unwell (e.g. pneumonia)

57
Q

Which drug is used to treat ventricular tachycardia without haemodynamic compromise?

A

IV Amiodarone

58
Q

State some causes of ventricular tachycardia.

A

Hypomagnesaemia

Hypokalaemia

59
Q

What is the treatment of choice for patients who experience recurrent VTs?

A

Implantable cardioverter defibrillator (ICD)

60
Q

Which variant of VT requires defibrillation?

A

Pulseless VT

61
Q

Describe the appearance of left ventricular hypertrophy on ECG.

A

Deep S wave in V1/V2
Tall R wave in V5/V6
If S wave + R wave = > 7 large squares then it is left ventricular hypertrophy by voltage criteria

62
Q

What is the definitive diagnostic test for left ventricular hypertrophy?

A

Echocardiography

63
Q

Describe the ECG morphology of:
first-degree heart block.
mobitz type 2 heart block
complete heart block

A

first degree: Fixed prolonged PR interval

type 2: Fixed prolonged PR interval with a dropped QRS every few beats

complete heart block:
Complete dissociation between the atria (p waves) and ventricles (QRS complexes)
QRS complexes will be broad
Bradycardia

64
Q

State three ECG signs of ischaemia.

A

ST elevation
Pathological Q waves
T wave inversion

65
Q

What features of an ECG would suggest ventricular strain or hypertrophy?

A

S waves and R waves

Axis deviation

66
Q

What is responsible for the following heart sounds?

A 
S1
Closure of the mitral valve 
S2
Closure of the aortic valve 
Fixed wide splitting of S2
Atrial septal defect 
S3
Rapid ventricular filling (sign of heart failure) 
S4
Ventricular hypertrophy (caused by atria contracting against stiff ventricles
67
Q

Describe how you would distinguish between fixed wide splitting of S2 and S3

A

Fixed wide splitting of S2 is heard better with the diaphragm
S3 – better with the bell and light pressure

68
Q

Describe the relationship of S3 and S4 to S1 and S2.

A

S3 comes just after S2

S4 comes just before S1

69
Q

Describe the steps in the management of acute heart failure.

A 
Sit up 
Oxygen 
GTN infusion
Diamorphine 
Furosemide (IV)
70
Q

Why are the three drugs mentioned above used in acute heart failure?

A

GTN, diamorphine and furosemide are all venodilators – they reduce venous return to the heart, hence reducing preload

71
Q

Describe the ALS protocol for VT and pulseless VF.

A 
Shock
CPR (2 mins) 
Assess rhythm
Adrenaline every 3-5 mins 
Correct reversible causes
72
Q

What are the two non-shockable rhythms?

A

Pulseless electrical activity (PEA)

Asystole

73
Q

State the 4Hs and 4Ts – reversible causes of cardiac arrest.

A 
Hypoxia
Hypothermia
Hypovolaemia
Hypokalaemia
Toxic
Thromboembolic
Tamponade
Tension pneumothorax
74
Q

Describe the appearance of pericarditis on ECG.

A

Diffuse ST elevation (in all leads)

ST elevation is saddle-shaped

75
Q

List causes of pleuritic chest pain.

A 
PE
Pneumothorax
Pneumonia
Pericarditis 
Pleural pathology 
NOTE: and subphrenic pathology (e.g. hepatic abscess)

Y3 Cardiovascular (43 decks)

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