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DPD interactive cases > Cardiovascular (1) > Flashcards

Cardiovascular (1) Flashcards

1
Q

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

A

ECG
Troponins (Can do high sensitivity assays at 6hr, most sensitive at 12)
Echocardiogram

NB: can do troponin at 3 hr and monitor incrementally

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2
Q

What is the next step in the management of a patient whose troponins are i) negative ii) positive

A

i) -ve: Exercise tolerance test

ii) +ve: coronary angiography (with dye)

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3
Q

List possible causes of chest pain of cardiac origin (3)

A

Ischaemic heart disease
Pericarditis
Aortic dissection

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4
Q

List possible causes of chest pain of respiratory origin (3)

A

PE
Pneumonia
Pneumothorax

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5
Q

List possible causes of chest pain of GI origin (3)

A

Oesophageal spasm
Oesophagitis/Gastritis
Candida

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6
Q

List one cause of chest pain of musculoskeletal origin

A

Costochondritis

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7
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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8
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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9
Q

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

List 2 signs of AD

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

O/E: Difference in BP in 2 arms, Early DM: AR

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10
Q

List some specific respiratory symptoms that you should ask a patient about when taking a history. (5)

A 
Wheeze 
Breathlessness
Haemoptysis
Cough
Weight loss
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11
Q

What is a common and major risk factor for gastritis?

A

Excessive alcohol

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12
Q

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

A

Oral candidiasis

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13
Q

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

a. STEMI
b. NSTEMI

A

a. STEMI
Go to cathlab immediately for percutaneous coronary intervention + Angiogram/Angioplasty
Give aspirin + clopidogrel
b. NSTEMI
Go to cathlab within 24 hours
Give aspirin + clopidogrel + fondaprinux/LMWH

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14
Q

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

A 
a. Anterior
Left Anterior Descending 
V1-V4
b. Inferior
Right Coronary Artery
II, III, aVF
c. Lateral
Left Circumflex 
I, aVL, V5/V6
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15
Q

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

A

Left Main Stem

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16
Q

How long after an MI does the troponin level peak?

A

24-48 hours

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17
Q

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

A

5-14 days

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18
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: No warning vs Aura
During: Tongue biting
After: Confusion

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19
Q

What are the three main cardiac causes of collapse?

Give another one

A

Arrhythmia
Outflow Obstruction
Postural Hypotension

Vasovagal syncope (increased vagal discharge leads to bradycardia and collapse – it can be precipitated by certain conditions)

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20
Q

List the main causes of collapse.

A

Hypoglycaemia
Cardiac reasons - 4
Neurological - seizure

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21
Q

List some features of seizures.

A

Tongue biting
Aura
Wetting themselves
Being confused after the seizure

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22
Q

Define syncope.

A

Collapse caused by hypoperfusion of the brain

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23
Q

List some investigations for arrhythmias.

A

ECG
24 hr tape
Cardiac monitor

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24
Q

State two causes of left-ventricular outflow obstruction.

A

Aortic stenosis

Hypertrophic obstructive cardiomyopathy (HOCM)

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25
Q

List two signs of aortic stenosis

A

Slow-rising pulse (+ low volume if severe)

Ejection-systolic murmur

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26
Q

What is the main investigation for outflow obstruction

A

Echocardiogram

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27
Q

What is the main investigation for postural hypotension?

A

Lying/standing blood pressure (20mmHg significant)

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28
Q

List some causes of Long QT Syndrome; how do you tell?

A 
Congenital (mutations of K+ channels) - FHx of sudden death
Hypomagnesaemia
Hypokalaemia
Drugs 
Longer than half of RR interval
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29
Q

List three causes of pan-systolic murmur

A

Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

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30
Q

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

A

Left-sided murmurs are louder on EXPIRATION (Aortic, mitral valves)
Right-sided murmurs are louder on INSIPRATION (Tricuspid, pulmonary)

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31
Q

State an important non-cardiac feature of tricuspid regurgitation

A

Hepatomegaly – due to backpressure causing hepatic congestion –> Increased JVP, pulsatile liver

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32
Q

List three causes of a raised JVP

A

Tricuspid regurgitation
Right heart failure
Constrictive pericarditis

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33
Q

List two causes of tricuspid regurgitation

A

Damage to valve leaflets (e.g. by bacteria); IVDU infective endocarditis
Right ventricular dilation of valve ring (valve root enlarges)

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34
Q

List two causes of right heart failure.

A

Left heart failure
Pulmonary hypertension
(E.g. COPD: Chronic hypoxia –> chronic vasoconstriction –>pulmHTN)

35
Q

List some causes of constrictive pericarditis and define it

A

Infection (e.g. TB)
Inflammation (e.g. connective tissue disease - lupus, sarcoid)
Malignancy
Thickening/calcification of pericardium

36
Q

List four causes of a systolic murmur.

A

Aortic stenosis
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

37
Q

Where are Systolic murmurs loudest and its radiation

A

Aortic stenosis – loudest in aortic area and radiates to the carotids
Mitral regurgitation – loudest in mitral area and radiates to the axilla
Tricuspid regurgitation: L sternal border
VSD: L sternal border, parasternal thrill

38
Q

Describe how you would differentiate aortic stenosis and mitral regurgitation by associated signs

A

Aortic stenosis – slow-rising pulse (thrill under thumb), ejection systolic murmur, soft S2
Mitral regurgitation – displaced apex beat (hyperdynamic)

39
Q

State four broad causes of palpitations.

A

Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Ventricular tachycardia

40
Q

State three causes of sinus tachycardia.

A
  • Physiological:
    Shock (Sepsis)
    Hypovolaemia
  • Endocrine (e.g. hyperthyroidism, phaeochromocytoma)
41
Q

What is supraventricular tachycardia?

A

Regular narrow complex tachycardia with no p waves (depol. from AVN, not SAN
SVT refers to AVRT and AVNRT

42
Q

Explain the difference between AVNRT and AVRT.

A

AVNRT – a local circuit forms around the AV node (Slow and fast pathways, one with shorter refractory period)
AVRT – a circuit forms between the atria and ventricles via an accessory pathway

43
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)

44
Q

What is the name of the accessory pathway in AVRT?

A

Bundle of Kent

45
Q

How is AVRT definitively treated?

A

Radiofrequency ablation of the accessory pathway

46
Q

Describe the ECG morphology of atrial fibrillation.

A

Irregularly irregular with no p waves

47
Q

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

A

Thyrotoxicosis

Alcohol

48
Q

List some causes of atrial fibrillation.

A

Myocardium (Heart Muscle): ischaemic heart disease, rheumatic heart disease, hypertensive heart disease
Endocardium: Valvular heart disease
Pericardium: Pericarditis
Lung: pneumonia, PE, cancer

49
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

50
Q

Describe the ECG morphology of ventricular tachycardia.

A

Regular broad complex tachycardia (assume VT until proven)

51
Q

State three causes of VT.

A

Ischaemia
Electrolyte abnormalities (Hypomagnesaemia
Hypokalaemia)
Long QT syndrome (look at old ECGs) - congen mutation?

52
Q

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

A

If they are haemodynamically unstable

53
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

54
Q

Describe the management of a patient with SVT who is not haemodynamically compromised. (AIM: restore to sinus rhythm)

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

Adenosine slows the AVN
Warn pt. they may feel like they’re going to die

55
Q

In which patients is adenosine contraindicated?

A

Asthmatics

56
Q

What are the two main aims of management of AF?

A

Rate control

Reduce risk of stroke

57
Q

Describe the criteria for cardioversion of patients with acute fast AF (rhythm control)

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 (Warfarin, Rivaroxaban, Apixiban)

58
Q

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

A

Beta-blockers

Digoxin

59
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)

60
Q

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

A

IV Amiodarone

Treat underlying cause

61
Q

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

A

Implantable cardioverter defibrillator (ICD)

62
Q

Which variant of VT requires defibrillation?

A

Pulseless VT

63
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

64
Q

What is the definitive diagnostic test for left ventricular hypertrophy?

A

Echocardiography

65
Q

Describe the ECG morphology of first-degree heart block.

A

Fixed prolonged PR interval

66
Q

Describe the ECG morphology of Mobitz type 2 heart block.

A

Fixed prolonged PR interval with a dropped QRS every few beats

67
Q

Describe the ECG morphology of complete heart block.

A

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

68
Q

State three ECG signs of ischaemia.

A

ST depression
Pathological Q waves
T wave inversion

69
Q

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

A

S waves and R waves

Axis deviation

70
Q

What is responsible for these heart sounds:

S1, S2, Fixed wide splitting of S2, S3, S4?

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)

71
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 (low pitched)

72
Q

Click b/t S1 and S2 is a sign of?

A

Mitral Valve Prolapse

73
Q

Describe the steps in the management of acute heart failure.

A 
Sit up 
Oxygen 60-100%
GTN infusion (VD, less preload)
Furosemide (IV) - gut oedema = wont absorb
CPAP later if not oxygenating well
74
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

75
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
76
Q

What are the two non-shockable rhythms?

A

Pulseless electrical activity (PEA)
Asystole
(Just do CPR + Adrenaline and correct causes)

77
Q

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

A 
Hypoxia
Hypothermia
Hypovolaemia
Hypokalaemia
Toxic
Thromboembolic
Tamponade
Tension pneumothorax
78
Q

Describe the appearance of pericarditis on ECG.

A

Diffuse ST elevation (in all leads)

ST elevation is saddle-shaped

79
Q

List causes of pleuritic chest pain.

A 
PE
Pneumothorax
Pneumonia
Pericarditis 
Pleural pathology 
NOTE: and subphrenic pathology (e.g. hepatic abscess)
80
Q

Atrial Flutter: what does it look like?

A

Chaotic atrial activity
No p waves, narrow QRS
Saw-tooth baseline
Variable block (if 2:1 block = 150bpm)

81
Q

What to check for if you think there is an Arrythmia/Conductive defectis?

A

Rate, rhythm
PR - prolonged?
QRS: Narrow, Broad, L/RBBB?
QT interval (long QT –> VT)

82
Q

What to do if hypothermic pt is in VT?

A

Hypothermia affects metabolism of drugs –> cardiotoxic, and shock will not work. warm patient and give CPR

83
Q

In HF what crackles do you hear?

A

Fine, end inspiratory crackles

DPD interactive cases (8 decks)

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