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UKMLA Prep > Cardiovascular > Flashcards

Cardiovascular Flashcards

presentations and conditions

1
Q

Shockable rhythms

A

Ventricular tachycardia
Ventricular fibrillation

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2
Q

Non shockable rhythms

A
  • pulseless electrical activity
    -asystole
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3
Q

Narrow complex tacycardia

A
  • QRS less than 0.12
  • equal to 3 small squares on ecg

Sinus tachycardia (treatment focuses on the underlying cause)
Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)
Atrial fibrillation (treated with rate control or rhythm control)
Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)

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4
Q

Management of life-threatening features of narrow complex tachycardia

A
  • synchronised DC cardio version under sedation or GA

IV amioadrome is given if shocks are unsuccessful

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5
Q

Broad complex tachycardia

A
  • QRS greater than 0.12 or 3 small squares
  • VT
    -polymorphic ventricular tachycardia (Rosales de pointes)
    -AF with bundle branch block
    -SVT with bundle branch block
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6
Q

Management of torsades de pointes

A

IV magnesium

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7
Q

Management of AF

A
  • Rate control drugs
  • Anticoagulant
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8
Q

Ventricular tachycardia management

A

IV amiodarone

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9
Q

Atrial flutter

A
  • re-enterant rhythm
  • self perpetuating loop
    -300bpm regular regular
    -sawtooth appearance
    -CHA2DS2VASC score
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10
Q

Prolonged QT number in men vs women

A

More than 440 milliseconds in men
More than 460 milliseconds in women

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11
Q

Causes of long QT syndrome

A
  • Long QT syndrome (an inherited condition)
  • Drugs: such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
  • Electrolyte imbalances, hypokalaemia, hypomagnesaemia and hypocalcaemia
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12
Q

Management of prolonged QT interval

A
  • Stopping and avoiding medications
  • Correcting electrolyte disturbances
  • Beta blockers (not sotalol)
  • Pacemakers or implantable cardioverter defibrillators
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13
Q

Type 1 heart block

A
  • slow conduction to the AV node.
  • typically results in increased PR interval
  • greater than 0.2 seconds
  • regular HR
  • can be asymptomatic

Manamgment
- monitoring
-identify underlying cause
Pacing

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14
Q

Acute NSTEMI tx- Batman

A

Bisoprolol
Aspirin (300mg)
T icagreloe
M Orphine
Anti coax
Nitrates

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15
Q

LCA

A

Anterolateral
I, avL
V3-6

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16
Q

LAD

A

Anterior
V1-v4

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17
Q

Circumflex

A

Lateral
I, AVL
V5-v6

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18
Q

RCA

A

Inferior
II, III, AVF

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19
Q

First degree heart block

A

AV node issue
Takes longer for signals to get to ventricles
PR elongation seen

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20
Q

Type 1 Wenckebach

A

progressive lengthening of the PR interval until a beat is dropped

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21
Q

Type 2 mobitz

A

occasional dropped beats occur without a progressive lengthening of the PR interval.

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22
Q

3rd degree heart block

A

complete heart block, there is a complete block of electrical signals between the atria and ventricles.

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23
Q

pulseless VT after 5 shock administered

A

Amiodarone 150mg

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24
Q

What are the long-term preventive measures for patients with a history of acute limb-threatening ischemia?

A

Antiplatelet therapy (e.g., aspirin or clopidogrel)
Statins
Smoking cessation
Control of hypertension and diabetes

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25
Q

What happens if acute limb-threatening ischemia is not treated promptly?

A

Delayed treatment can lead to irreversible tissue damage, necrosis, and limb loss.

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26
Q

What are the main revascularization options for acute limb-threatening ischemia?

A

Surgical thrombectomy or bypass, and endovascular options such as angioplasty or stenting.

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27
Q

What is the initial management of acute limb-threatening ischemia?

A
  • Immediate anticoagulation with heparin to prevent clot propagation
  • analgesia for pain
  • vascular surgery consultation for revascularization (e.g., thrombectomy or bypass).
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28
Q

How is acute limb-threatening ischemia diagnosed?

A

Diagnosis is made clinically, often confirmed with imaging (Doppler ultrasound, CT angiography) to assess the blood flow and locate the obstruction.

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29
Q

What are the most common causes of acute limb-threatening ischemia?

A

Embolism (from the heart, such as in atrial fibrillation)
Thrombosis in situ (usually from pre-existing peripheral arterial disease)
Trauma to the vessels

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30
Q

What is the pathophysiology behind peripheral arterial disease (PAD)?f

A

atherosclerosis, where plaque buildup narrows and hardens the arteries, reducing blood flow to the limbs. This can lead to ischemia, especially during exertion.

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31
Q

Main risk factors PAD (5)

A
  • smoking, diabetes
  • hypertension
  • hyperlipidemia
  • advanced age
  • history of cardiovascular disease.
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32
Q

ABPI and PAD

A

normal ABPI is 1.0–1.4. An ABPI <0.9 indicates PAD, with <0.5 suggesting severe disease

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33
Q

Classification system for ALI?

A

Rutherford classification

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34
Q

What is the Rutherford classification for acute limb ischemia (ALI)?

A
  1. Viable: No immediate threat to the limb.
  2. Threatened: Limb salvageable with immediate treatment.
  3. Irreversible: Limb cannot be salvaged, amputation needed.
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35
Q

Imaging used for ALI

A

Doppler ultrasound is used to assess blood flow, while CT angiography or MR angiography is used to locate the blockage and plan revascularization.

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36
Q

What are the major complications of untreated acute limb ischemia?

A

Complications include irreversible tissue damage, gangrene, limb loss (amputation), and potentially life-threatening reperfusion injury after delayed revascularization.

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37
Q

What is reperfusion injury, and why is it a concern in acute limb ischemia?

A

Reperfusion injury occurs when blood flow is restored to ischemic tissues, causing oxidative stress, inflammation, and further tissue damage. It can result in compartment syndrome or systemic complications.

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38
Q

What is the long-term management for patients who have undergone revascularization for acute limb ischemia?

A

Long-term management includes antiplatelet therapy (aspirin or clopidogrel), statins for cholesterol control, lifestyle changes (e.g., smoking cessation, exercise), and management of diabetes and hypertension.

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39
Q

When is amputation indicated in patients with acute limb ischemia?

A

Amputation is indicated when the limb is non-viable due to irreversible tissue damage, and there is no possibility of salvaging the limb through revascularization.

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40
Q

Definitive management of ALI (5)

A

intra-arterial thrombolysis
surgical embolectomy
angioplasty
bypass surgery
amputation: for patients with irreversible ischaemia

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41
Q

Initial management ALI

A

ABC approach
analgesia: IV opioids are often used
intravenous unfractionated heparin is usually given to prevent thrombus propagation, particularly if the patient is not suitable for immediate surgery
vascular review

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42
Q

Factors suggesting thrombus

A

pre-existing claudication with sudden deterioration
no obvious source for emboli
reduced or absent pulses in contralateral limb
evidence of widespread vascular disease (e.g. myocardial infarction, stroke, TIA, previous vascular surgery)

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43
Q

Factors suggesting embolus

A

sudden onset of painful leg (< 24 hour)
no history of claudication
clinically obvious source of embolus (e.g. atrial fibrillation, recent myocardial infarction)
no evidence of peripheral vascular disease (normal pulses in contralateral limb)
evidence of proximal aneurysm (e.g. abdominal or popliteal)

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44
Q

Features of DVT

A

lower limb pain (often calf pain) and tenderness along the line of the deep veins:
swelling
erythema
pitting oedema
distension of superficial veins

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45
Q

What criteria is used to assess for DVT

A

Well’s score

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46
Q

Major criteria for Well’s

A

Active cancer (treatment ongoing or within the last 6 months)
Paralysis, paresis, or recent plaster immobilization of the leg
Bedridden for ≥3 days or major surgery within 4 weeks
Localized tenderness along the distribution of the deep venous system
Entire leg swollen
Calf swelling by >3 cm compared to the asymptomatic leg
Pitting edema (greater in the symptomatic leg)
Collateral superficial veins (non-varicose)

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47
Q

What are the risk categories based on the Wells Score for DVT?

A

High risk: ≥3 points (high probability of DVT)
Moderate risk: 1-2 points (moderate probability)
Low risk: ≤0 points (low probability)

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48
Q

Major criteria and scores for Well’s

A

Signs and symptoms of DVT (3 points)
Heart rate >100 bpm (1.5 points)
Immobilization for ≥3 days or surgery within 4 weeks (1.5 points)
Previous DVT or PE (1.5 points)
Hemoptysis (1 point)
Active cancer (treatment within the last 6 months or palliative) (1 point)
PE more likely than an alternative diagnosis (3 points)

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49
Q

How to use well’s score

A

High/Moderate risk: Perform Doppler ultrasound and D-dimer testing.
Low risk: D-dimer testing; if negative, DVT is unlikely.

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50
Q

Risk factors for Mitral regurgitation (7)

A

Female sex
Lower body mass
Age
Renal dysfunction
Prior myocardial infarction
Prior mitral stenosis or valve prolapse
Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome

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51
Q

Risk factors for Mitral regurgitation (7)

A

Female sex
Lower body mass
Age
Renal dysfunction
Prior myocardial infarction
Prior mitral stenosis or valve prolapse
Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome

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52
Q

Investigation of MR

A

ECG may show a broad P wave, indicative of atrial enlargement
Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle
Echocardiography is crucial to diagnosis and to assess severity

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53
Q

MR signs

A

pansystolic murmur described as ‘blowing’. It is heard best at the apex and radiating into the axilla.

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54
Q

Symptoms of MR

A
  • typically asymptomatic

Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.

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55
Q

Causes of MR (5)

A

-Following coronary artery disease or post-MI

  • Mitral valve prolapse
  • Infective endocarditis
  • Rheumatic fever
  • Congenital
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56
Q

Mitral stenosis

A

obstruction of blood flow across the mitral valve from the left atrium to the left ventricle. This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.

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57
Q

mitral stenosis features

A

dyspnoea
↑ left atrial pressure → pulmonary venous hypertension
haemoptysis
due to pulmonary pressures and vascular congestion
may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
mid-late diastolic murmur (best heard in expiration)
loud S1
opening snap
indicates mitral valve leaflets are still mobile
low volume pulse
malar flush
atrial fibrillation
secondary to ↑ left atrial pressure → left atrial enlargement

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58
Q

Features of severe MS

A

length of murmur increases
opening snap becomes closer to S2

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59
Q

CXR MS findings

A

left atrial enlargement may be seen

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60
Q

Echo MS findings

A

Calcification
Thickened valve
Enlarged LA
Subvalvular thickening

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61
Q

Management of MS

A

patients with associated atrial fibrillation require anticoagulation
currently warfarin is still recommended for patients with moderate/severe MS
there is an emerging consensus that direct-acting anticoagulants (DOACs) may be suitable for patients with mild MS who develop atrial fibrillation
asymptomatic patients
monitored with regular echocardiograms
percutaneous/surgical management is generally not recommended
symptomatic patients
percutaneous mitral balloon valvotomy
mitral valve surgery (commissurotomy, or valve replacement)

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62
Q

Mitral valve prolapse association

A

congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease

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63
Q

Features of mitral prolapse

A

patients may complain of atypical chest pain or palpitations
mid-systolic click (occurs later if patient squatting)
late systolic murmur (longer if patient standing)
complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

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64
Q

Target INR for mechanical valves

A

Target INR
aortic: 3.0
mitral: 3.5

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65
Q

Orthostatic syncope

A

primary autonomic failure: Parkinson’s disease, Lewy body dementia
secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
drug-induced: diuretics, alcohol, vasodilators
volume depletion: haemorrhage, diarrhoea

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66
Q

Cardiac syncope

A

arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
others: pulmonary embolism

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67
Q

Reflex syncope (neurally mediated)

A

vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
situational: cough, micturition, gastrointestinal
carotid sinus syncope

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68
Q

Syncope evaluation

A

cardiovascular examination
postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
ECG for all patients
other tests depend on clinical features
patients with typical features, no postural drop and a normal ECG do not require further investigations

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69
Q

Features of ACS

A

chest pain
classically on the left side of the chest
may radiate to the left arm or neck
this may not always be present. Being elderly, diabetic or female makes an atypical presentation more likely
dyspnoea
nausea and vomiting
sweating
palpitations

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70
Q

Late systolic murmur

A

mitral valve prolapse
coarctation of aorta

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71
Q

Early diastolic murmur

A

aortic regurgitation (high-pitched and ‘blowing’ in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)

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72
Q

Mid late diastolic murmur

A

mitral stenosis (‘rumbling’ in character)
Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

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73
Q

Continuous machine-like murmur

A

patent ductus arteriosus

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74
Q

Holosystolic (pansystolic) murmur

A

mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)

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75
Q

Ejection systolic murmur

A

louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy
louder on inspiration
pulmonary stenosis
atrial septal defect
also: tetralogy of Fallot

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76
Q

Characteristics of an innocent ejection murmur include:

A

soft-blowing murmur in the pulmonary area or short buzzing murmur in the aortic area
may vary with posture
localised with no radiation
no diastolic component
no thrill
no added sounds (e.g. clicks)
asymptomatic child
no other abnormality

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77
Q

Ejection murmurs

A

Due to turbulent blood flow at the outflow tract of the heart

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78
Q

Still’s murmur

A

Low-pitched sound heard at the lower left sternal edge

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79
Q

Venous Hume

A

Due to the turbulent blood flow in the great veins returning to the heart. Heard as a continuous blowing noise heard just below the clavicles

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80
Q

Infective endocarditis

A

pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria

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81
Q

Right atrium

A

Receives deoxygenated blood from the body via vena cava
•Blood flows through tricuspid valve à right ventricle
•SA node in the upper part
•AV node near base of tricuspid valve

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82
Q

Right atrium

A

Receives deoxygenated blood from the body via vena cava
•Blood flows through tricuspid valve à right ventricle
•SA node in the upper part
•AV node near base of tricuspid valve

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83
Q

Right ventricle

A

Receives blood from right atrium à pulmonary valve à pulmonary trunk à pulmonary artery
•Has rough internal wall muscle fibres (trabeculae) à papillary muscles à attach to tricuspid valve

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84
Q

Left atrium

A

Receives oxygenated blood from lungs via 4 pulmonary veins (open superiorposteriorly) •Blood à mitral valve (bicuspid) à left ventricle

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85
Q

Left ventricule

A

Thickest walled chamber
•Blood pumped through aortic valve to aorta •Aortic valve = tricuspid with right, left and posterior cusps
•Small sinuses lie above the cusps à gives rise to the coronary arteries

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86
Q

Left coronary artery

A

Left Coronary Artery
or main stem
•Lies behind and lateral to pulmonary trunk •Two main branches: -
1.Circumflex artery - gives off left marginal branch
2.Left Anterior Descending - a.k.a. Anterior interventricular artery

87
Q

Right coronary artery

A

Descends between pulmonary trunk and right atrium in the anterior atrioventricular groove
•Two main branches
1.Right Marginal Branch 2.Posterior Interventricular Branch

88
Q

Left anterior descending

A

Anterior Left & Right Ventricle •Anterior 2/3 Ventricular Septum
•Anterior Apex
•Bundle of His & Bundle Branches

89
Q

Left circumflex

A

Part of posterior Left Lateral Ventricle •Left Atrium

90
Q

Right coronary r

A

Posterior 1/3 Intraventricular Septum •Right Ventricle & interior wall of Left
Ventricle
•AV Node and Atrial Septum

91
Q

Coronary artery

A

1/3rd drained by Thebesian veins, venae cordis minimae à drains directly
into cardiac cavity
•2/3rd drained by veins accompanying arteries
•4 Veins that drain directly into the coronary sinus (large posterior venous dilatation) then into right atrium
•Great Cardiac Vein •Middle Cardiac Vein •Small Cardiac Vein •Oblique Vein
•Oxygen tension in the coronary sinus = approx 40% (3.5 – 4.0kPa)

92
Q

Hypertension

A

Systolic >140mmHg or Diastolic >90mmHg

93
Q

Primary vs secondary hypertension

A

Primary = cause unknown
•Secondary = as a result of another disease, e.g. Phaeochromocytoma

94
Q

Stage 1 hypertension

A

Systolic 140-159mmHg or Diastolic 90-99mmHg

95
Q

Stage 2 hypertension

A

Systolic 160 – 179mmHg or Diastolic 100 – 109mmhg

96
Q

Stage 3 hypertension

A

Systolic >180mmHg or Diastolic >110mmHg

97
Q

HOCM definition

A
  • dynamic obstruction of mitral valve leaflet during systole
  • pressure overload of LV
98
Q

Symptoms of HOCM

A

angina, dyspnoea, syncope, palpitations and sudden death.

99
Q

Inotropes in HOCM

A

CONTRADICTED
use direct alpha agonist in emergency

100
Q

Treatment of HOCM

A

beta-blockade or Verapamil

101
Q

Restrictive cardiomyopathy

A

Stiff ventricles à impaired filling and diastolic dysfunction •Very hazardous anaesthetic à cardiac arrest can occur
•Consider anaesthetising with Ketamine
•Aims
•Sinus rhythm
•Adequate volume loading – maintain elevated Right heart pressures •High normal SVR
•AVOID myocardial depression

102
Q

Limb leads ECG

A

II, III, aVF: inferior leads. Look at the inferior surface of the heart
I, aVL: lateral leads. Look at the left lateral surface of the heart
aVR: right arm lead. looks at the right atrium of the heart.

103
Q

ECG chest leads

A

V1, V2: septal leads. View the right ventricle of the heart and septum between ventricles.
V3, V4: anterior leads. View the anterior wall of the left ventricle
V5, V6: lateral leads. Look at the anterior and lateral wall of the left ventricle.

104
Q

Positive vs negative deflection

A

Depolarisation- negative deflection
Repolarisation - positive deflection

105
Q

Normal ECG wave

A

P-waves: atrial depolarisation
QRS complexes (<120 ms): ventricular depolarisation. If first deflection is down it is a Q-wave, if the first deflection is up it is an R-wave.
T-waves: ventricular repolarisation.
U-waves: sometimes seen, origin disputed. May be pathological if follows abnormal T-wave

106
Q

Normal ecg segments

A

PR-interval (120-200 ms): time taken for the electrical impulse to travel between the atria and ventricles.

ST-segment: should be isoelectric (i.e. on the baseline). Can be depressed or elevated (changes typical in ischaemia).

QT-interval*: varies with heart rate, long QT has many causes but may predispose to polymorphic ventricular tachycardia.

normal QT interval is 350-440 ms in men and 350-460 ms in women

107
Q

Pathophysiology of gangrene

A

Arterial occlusion: Atherosclerosis, thrombosis, or embolism can obstruct blood flow.

Infection: Bacteria, especially in wet and gas gangrene, can exacerbate tissue necrosis through toxin production.

Trauma: Severe injuries can compromise blood supply and introduce pathogens.

Chronic conditions: Diabetes mellitus and other chronic diseases can predispose individuals to gangrene by impairing vascular function and immune response.

108
Q

Dry gangrene

A
  • Caused by chronic ischaemia, usually due to peripheral arterial disease (PAD).
  • Appearance:
    1. Characterised by dry, shrivelled, and blackened tissue (‘mummified’).
    2. Clear demarcation between healthy and necrotic tissue.
    3. Typically painless due to nerve damage.
  • Often develops slowly and is usually not associated with infection.
109
Q

Wet Gangrene

A

-Results from a sudden lack of blood supply combined with bacterial infection.
Appearance
1. Swollen, moist, and blistered tissue with a foul odour.
2. Rapid spread and marked systemic symptoms such as fever and malaise.
3. Severe pain and erythema around the affected area.
- Progresses rapidly and can lead to systemic sepsis.

110
Q

Gas gangrene causative agent

A

Clostridial myonecrosis

111
Q

Gas gangrene

A
  • production of gas and toxins
    Appearance:
  • Severe pain and swelling at the site of –infection.
  • Crepitus due to gas production by Clostridium bacteria.
  • Rapid onset of systemic symptoms, including tachycardia, hypotension, and shock.
  • Requires urgent medical intervention due to rapid progression and high mortality
112
Q

Necrotising fascitis

A

A severe form of gangrene involving the fascia and subcutaneous tissues.
Caused by mixed bacterial infections, often including Streptococcus pyogenes and Staphylococcus aureus.
Appearance:
Intense pain disproportionate to the visible signs.
Rapid progression of erythema, swelling, and tissue necrosis.
Systemic signs of sepsis, such as fever, tachycardia, and hypotension

113
Q

Managment of gangrene

A
  • surgical intervention
  • antibiotics (penicillin and clindamycin for gas gangrene)
  • supportive care
  • hyperbaric oxygen
114
Q

Pathophysiology of aortic dissection

A

Tear in the tunica intima of the wall of the aorta

115
Q

Aortic dissection associations

A
  • hypertension: the most important risk factor
  • trauma
  • bicuspid aortic valve
  • collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
  • Turner’s and Noonan’s syndrome
  • pregnancy
  • syphilis
116
Q

classification of aortic dissection- standord classification

A

type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases

117
Q

DeBakey classification

A

type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

118
Q

Features of aortic dissection

A
  • tearing chest pain (ore common with A)
  • upper back pain more common with type B
  • Pulse deficit
  • weak or absent carotid, brachial, or femoral pulse
  • variation (>20 mmHg) in systolic blood pressure between the arms
  • aortic regurgitation
  • hypertension
    coronary arteries → angina
    spinal arteries → paraplegia
    distal aorta → limb ischaemia

-majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads

119
Q

S1

A
  • closure of mitral and tricuspid valves
  • soft if long PR or mitral regurgitation
  • loud in mitral stenosis
120
Q

S2

A
  • closure of aortic and pulmonary valves
  • soft in aortic stenosis
  • splitting during inspiration is normal
121
Q

S3

A
  • caused by diastolic filling of the ventricle
  • considered normal if < 30 years old (may persist in women up to 50 years old)
  • heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
122
Q

S4

A
  • may be heard in aortic stenosis, HOCM, hypertension
  • caused by atrial contraction against a stiff ventricle
    therefore coincides with the P wave on ECG
  • in HOCM a double apical impulse may be felt as a result of a palpable S4
123
Q

Left second intercostal space, at the upper sternal border

A

Pulmonary valve

124
Q

Right second intercostal space, at the upper sternal border

A

Aortic valve

125
Q

Left fifth intercostal space, just medial to mid clavicular line

A

Mitral valve

126
Q

Left fourth intercostal space, at the lower left sternal border

A

Tricuspid valve

127
Q

Causes of a loud S2

A

hypertension: systemic (loud A2) or pulmonary (loud P2)
hyperdynamic states
atrial septal defect without pulmonary hypertension

128
Q

Causes of soft S2

A

aortic stenosis

129
Q

Causes of fixed split S2

A

atrial septal defect

130
Q

Causes of widely split S2

A

deep inspiration
RBBB
pulmonary stenosis
severe mitral regurgitation

131
Q

Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)

A

LBBB
severe aortic stenosis
right ventricular pacing
WPW type B (causes early P2)
patent ductus arteriosus

132
Q

TIA definition

A

brief period of neurological deficit due to a vascular cause, typically lasting less than an hour.

a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

133
Q

TIA feature

A

unilateral weakness or sensory loss.
aphasia or dysarthria
ataxia, vertigo, or loss of balance
visual problems
sudden transient loss of vision in one eye (amaurosis fugax)
diplopia
homonymous hemianopia

Resolves in 1hr

134
Q

24hr of onset of TIA what to give

A

be given aspirin 300 mg immediately unless contraindicated
assessed urgently within 24 hours by a stroke specialist clinician

135
Q

exclusion diagnosis of TIA

A

hypoglycaemia
intracranial haemorrhage
all patients on anticoagulants or with similar risk factors should be admitted for urgent imaging to exclude haemorrhage

136
Q

who should assess for TIA

A
  • stroke specialist
  • no CT scan unless other concern
  • MRI (including diffusion-weighted and blood-sensitive sequences) is preferred to determine the territory of ischaemia, or to detect haemorrhage or alternative pathologies
    Should be done same day as specialist seen
137
Q

Tia medication

A

antiplatelet therapy

patients within 24 hours of onset of TIA or minor ischaemic stroke and with a low risk of bleeding, the following DAPT regimes should be considered:

138
Q

DAPT REGIMES

A

clopidogrel (initial dose 300 mg followed by 75 mg od) + aspirin (initial dose 300 mg followed by 75 mg od for 21 days) followed by monotherapy with clopidogrel 75 mg od

ticagrelor + clopidogrel is an alternative

139
Q

not appropriate for DAPT

A

clopidogrel 300 mg loading dose followed by 75 mg od should be given

140
Q

tricuspid regurgitation signs

A

pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

141
Q

tricuspid regurgitation signs

A

pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

142
Q

causes of tricuspid regurgitation

A

right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein’s anomaly
carcinoid syndrome

143
Q

vasovagal syncope

A

the most common cause of syncope and may account for up to 50% of cases of syncope
often referred to as ‘fainting’
typically occurs in the sitting or standing position and may be triggered by emotion, pain or stress
the patient may feel warm/hot prior to loss of consciousness or feel ‘light-headed’
brief myoclonic jerks can occur during uncomplicated vasovagal syncope

144
Q

clinical signs of PE

A

Tachypnea (respiratory rate >20/min) - 96%
Crackles - 58%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%

145
Q

ECG changes PE

A

large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

146
Q

ECG changes PE

A

large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

147
Q

chest X ray changes in PE

A

a chest x-ray is recommended for all patients to exclude other pathology
however, it is typically normal in PE
possible findings include a wedge-shaped opacification

148
Q

v/Q scan change PE

A

sensitivity of around 75% and specificity of 97%
other causes of mismatch in V/Q include old pulmonary embolisms, AV malformations, vasculitis, previous radiotherapy
COPD gives matched defects

149
Q

CTPA changes in PE

A

peripheral emboli affecting subsegmental arteries may be missed

150
Q

drugs for PAD

A

naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE

151
Q

surgical revascularization

A

surgical bypass with an autologous vein or prosthetic material
endarterectomy
open surgical techniques are typically used for long segment lesions (> 10 cm), multifocal lesions, lesions of the common femoral artery and purely infrapopliteal disease

152
Q

endovascular revascularization

A

percutaenous transluminal angioplasty +/- stent placement
endovascular techniques are typically used for short segment stenosis (e.g. < 10 cm), aortic iliac disease and high-risk patients

153
Q

what is used as a first line in patients with PAD

A

Clopidogrel

154
Q

what should be encourage patients with PAD to do?

A

supervised exercise training

155
Q

myocarditis

A

inflammation of the myocardium.
Common on younger patients

156
Q

causes of myocarditis

A

viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin

157
Q

presentation of myocarditis

A

usually young patient with an acute history
chest pain
dyspnoea
arrhythmias

158
Q

blood investigation for myocarditis

A

↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP

159
Q

ECG investigation for myocarditis

A

tachycardia
arrhythmias
ST/T wave changes including ST-segment elevation and T wave inversion

160
Q

management of myocarditis

A

treatment of underlying cause e.g. antibiotics if bacterial cause
supportive treatment e.g. of heart failure or arrhythmias

161
Q

complications of myocarditis

A

heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication

162
Q

ECG changes of myocarditis

A

the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis

163
Q

test for all patients with suspected active pericarditis?

A

Transthoracic echocardiogrpahy

164
Q

blood tests for acute pericarditis

A

inflammatory markers
troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis

165
Q

features of acute pericarditis

A

chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
pericardial rub

166
Q

how long does pericarditis last?

A

4-6 weeks

167
Q

Links with pericarditis ( causes)

A

viral infections (Coxsackie)
tuberculosis
uraemia
post-myocardial infarction
early (1-3 days): fibrinous pericarditis
late (weeks to months): autoimmune pericarditis (Dressler’s syndrome)
radiotherapy
connective tissue disease
systemic lupus erythematosus
rheumatoid arthritis
hypothyroidism
malignancy
lung cancer
breast cancer
trauma

168
Q

beck’s triad

A

hypotension
raised JVP
muffled heart sounds

Linked to cardiac tamponade

169
Q

features of cardiac tamponade

A

dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans

170
Q

features of cardiac tamponade

A
171
Q

what is Kussmaul’s sign

A

paradoxical increase in jugular venous pressure (JVP) when a person inhales

172
Q

JVP A waves
Cannon ‘a’ waves

A
  • caused by atrial contraction against a closed tricuspid valve
  • A waves can be identified by timing with the carotid pulse. It occurs before the pulse

are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

173
Q

JVP C waves

A

Caused by the tricuspid valve bulging into the right atrium during ventricular systole.

not normally visible

174
Q

V wave

A

Caused by the right atrium filling with blood in late systole and early diastole.
The V wave occurs towards the end of the carotid pulse.

due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation

175
Q

V wave

A

Caused by the right atrium filling with blood in late systole and early diastole. The V wave occurs towards the end of the carotid pulse.

176
Q

JVP x descent

A

Caused by atrial relaxation and the tricuspid valve moving downward

fall in atrial pressure during ventricular systole

177
Q

JVP Y descent

A

Caused by the tricuspid valve opening and blood flowing into the right ventricle. The Y descent is usually not as deep or brisk as the X descent

opening of tricuspid valve

178
Q

what is pulses paradous?

A

condition where there is an abnormal drop in systolic blood pressure when a person inhales. It’s a sign of an underlying heart or lung condition, and can be detected by measuring blood pressure during both inhalation and exhalation. A drop of more than 10 mm Hg is considered pulsus paradoxus

179
Q

JVP, PP, kussmaul’s signs and features (cardiac tamponade vs constrictive pericarditis)

A
180
Q

Cause of a pericardial effusion include:

A

infectious pericarditis: viral, tuberculosis, pyogenic spread from septicaemia and pneumonia
uraemia
idiopathic
post myocardial infarction (including Dressler’s syndrome)
malignancy
heart failure
nephrotic syndrome
hypothyroidism
trauma

181
Q

presenting features of haemochromatosis

A

early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)

182
Q

Hameochromatosis

A

Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6

183
Q

irreversible complications of haemochromatosis

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

184
Q

Reversible features of haemochromatosis

A

Cardiomyopathy
Skin pigmentation

185
Q

Management of haemochromators

A

venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line

186
Q

Investigations for haemochromators

A

transferrin saturation
Ferritin
Genetic testing for HDE mutation

187
Q

Features of DVT

A

lower limb pain (often calf pain) and tenderness along the line of the deep veins:
swelling
erythema
pitting oedema
distension of superficial veins

188
Q

Characteristics of an innocent ejection murmur

A

soft-blowing murmur in the pulmonary area or short buzzing murmur in the aortic area
may vary with posture
localised with no radiation
no diastolic component
no thrill
no added sounds (e.g. clicks)
asymptomatic child
no other abnormality

189
Q

Venous hums

A

Due to the turbulent blood flow in the great veins returning to the heart. Heard as a continuous blowing noise heard just below the clavicles

190
Q

Still’s murmur

A

Low-pitched sound heard at the lower left sternal edge

191
Q

Which location is it most likely for a traumatic aortic rupture to occur?

A

Proximal descending aorta distal to origin of left subclavian artery (aortic isthmus)

192
Q

Right-sided valves

A

Tricuspid and pulmonary

193
Q

Left sided valves

A

Mitral
Aortic

194
Q

Mitral and aortic valves are…

A

Left sided valves

195
Q

Atrial natriuretic peptide

A

natriuretic, i.e. promotes excretion of sodium
lowers BP
antagonises actions of angiotensin II, aldosterone

196
Q

Basics of ANP

A

secreted mainly from myocytes of right atrium and ventricle in response to increased blood volume
secreted by both the right and left atria (right&raquo_space; left)
28 amino acid peptide hormone, which acts via cGMP
degraded by endopeptidases

197
Q

Three types of troponin

A

troponin C: binds to calcium ions
troponin T: binds to tropomyosin, forming a troponin-tropomyosin complex
troponin I: binds to actin to hold the troponin-tropomyosin complex in place

198
Q

Three types of troponin

A

troponin C: binds to calcium ions
troponin T: binds to tropomyosin, forming a troponin-tropomyosin complex
troponin I: binds to actin to hold the troponin-tropomyosin complex in place

199
Q

Factors affecting stroke volume

A

Cardiac size
Contractility
Preload
Afterload

200
Q

Factors affecting stroke volume

A

Cardiac size
Contractility
Preload
Afterload

201
Q

Factors affecting stroke volume

A

Cardiac size
Contractility
Preload
Afterload

202
Q

Endothelia promotes the release of

A

angiotensin II
ADH
hypoxia
mechanical shearing forces

203
Q

Endothelia promotes the release of

A

angiotensin II
ADH
hypoxia
mechanical shearing forces

204
Q

Endothelia inhibits

A

nitric oxide
prostacyclin

205
Q

Endothelia is increased in

A

primary pulmonary hypertension
myocardial infarction
heart failure
acute kidney injury
asthma

206
Q

Endothelia is increased in

A

primary pulmonary hypertension
myocardial infarction
heart failure
acute kidney injury
asthma

207
Q

Pulse pressure

A
208
Q

LEFV

A

Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) * 100%

209
Q

LEFV

A

Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) * 100%

210
Q

LEFV

A

Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) * 100%

211
Q

LEFV

A

Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) * 100%

212
Q
A

paradoxical rise in JVP during inspiration seen in constrictive pericarditis.

213
Q

non-pulsatile JVP

A

superior vena caval obstruction

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