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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
  • Men > 440 milliseconds
  • Women > 460 milliseconds
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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? (4)

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)?

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
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51
Q

Investigation of MR

A
  • ECG may show a broad P wave, indicative of atrial enlargement
  • Chest x-ray- Cardiomegaly may be seen on , with an enlarged left atrium and ventricle
  • Echocardiography is crucial to diagnosis and to assess severity
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52
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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53
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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54
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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55
Q

Mitral stenosis

A
  • obstruction of blood flow across the mitral valve from the left atrium to the left ventricle.
  • Increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.
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56
Q

mitral stenosis features

A
  • Dyspnoea: ↑ Left atrial pressure → pulmonary venous hypertension
  • Haemoptysis: Pink frothy sputum or sudden haemorrhage (ruptured bronchial veins)
    Heart Sounds:
  • Mid-late diastolic murmur (expiration)
  • Loud S1
  • Opening snap (mobile mitral leaflets)
    Other Signs:
  • Low volume pulse
  • Malar flush
  • Atrial Fibrillation: From left atrial enlargement
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57
Q

Features of severe MS

A

length of murmur increases
opening snap becomes closer to S2

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58
Q

CXR MS findings

A

left atrial enlargement may be seen

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59
Q

Echo MS findings (4)

A
  • Calcification
  • Thickened valve
  • Enlarged LA
  • Subvalvular thickening
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60
Q

Management of MS

A
  1. Atrial Fibrillation

Anticoagulation:
Moderate/severe MS: Warfarin recommended
Mild MS: DOACs may be suitable (emerging consensus)
2. Asymptomatic Patients

Regular echocardiogram monitoring
No percutaneous/surgical intervention recommended
3. Symptomatic Patients

Procedures:
Percutaneous mitral balloon valvotomy
Mitral valve surgery (commissurotomy or replacement)

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61
Q

Mitral valve prolapse association (10)

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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62
Q

Features of mitral prolapse

A
  • 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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63
Q

Target INR for mechanical valves

A

Target INR
aortic: 3.0
mitral: 3.5

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64
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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65
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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66
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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67
Q

Syncope evaluation

A
  • Postural Blood Pressure:
  • A fall in systolic BP > 20 mmHg, diastolic BP > 10 mmHg, or systolic BP < 90 mmHg is considered diagnostic.
  • ECG: Perform for all patients.
  • Other Tests: Based on clinical features.
  • Further Investigations: Not required for patients with typical features, no postural drop, and normal ECG.
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68
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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69
Q

Late systolic murmur

A

mitral valve prolapse
coarctation of aorta

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70
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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71
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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72
Q

Continuous machine-like murmur

A

patent ductus arteriosus

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73
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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74
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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75
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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76
Q

Ejection murmurs

A

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

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77
Q

Still’s murmur

A

Low-pitched sound heard at the lower left sternal edge

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78
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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79
Q

Infective endocarditis
diagnosis requirments

A

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

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80
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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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 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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83
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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84
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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85
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

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86
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

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87
Q

Left anterior descending

A

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

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88
Q

Left circumflex

A

Part of posterior Left Lateral Ventricle •Left Atrium

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89
Q

Right coronary r

A

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

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90
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)

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91
Q

Hypertension

A

Systolic >140mmHg or Diastolic >90mmHg

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92
Q

Primary vs secondary hypertension

A

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

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93
Q

Stage 1 hypertension

A

Systolic 140-159mmHg or Diastolic 90-99mmHg

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94
Q

Stage 2 hypertension

A

Systolic 160 – 179mmHg or Diastolic 100 – 109mmhg

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95
Q

Stage 3 hypertension

A

Systolic >180mmHg or Diastolic >110mmHg

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96
Q

HOCM definition

A
  • dynamic obstruction of mitral valve leaflet during systole
  • pressure overload of LV
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97
Q

Symptoms of HOCM

A

angina, dyspnoea, syncope, palpitations and sudden death.

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98
Q

Inotropes in HOCM

A

CONTRADICTED
use direct alpha agonist in emergency

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99
Q

Treatment of HOCM

A

beta-blockade or Verapamil

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100
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

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101
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.

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102
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.

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103
Q

Positive vs negative deflection

A
  • Depolarisation- negative deflection
  • Repolarisation - positive deflection
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104
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

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105
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

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106
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.

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107
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.
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108
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.

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109
Q

Gas gangrene causative agent

A

Clostridial myonecrosis

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110
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
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111
Q

Necrotising fascitis

A

Necrotizing Fasciitis

  • A severe form of gangrene affecting the fascia and subcutaneous tissues.
  • Caused by mixed bacterial infections, commonly 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.
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112
Q

Managment of gangrene

A
  • surgical intervention
  • antibiotics (penicillin and clindamycin for gas gangrene)
  • supportive care
  • hyperbaric oxygen
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113
Q

Pathophysiology of aortic dissection

A

Tear in the tunica intima of the wall of the aorta

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114
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
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115
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
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116
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
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117
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

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118
Q

S1

A
  • closure of mitral and tricuspid valves
  • soft if long PR or mitral regurgitation
  • loud in mitral stenosis
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119
Q

S2

A
  • closure of aortic and pulmonary valves
  • soft in aortic stenosis
  • splitting during inspiration is normal
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120
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
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121
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
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122
Q

Left second intercostal space, at the upper sternal border

A

Pulmonary valve

123
Q

Right second intercostal space, at the upper sternal border

A

Aortic valve

124
Q

Left fifth intercostal space, just medial to mid clavicular line

A

Mitral valve

125
Q

Left fourth intercostal space, at the lower left sternal border

A

Tricuspid valve

126
Q

Causes of a loud S2

A

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

127
Q

Causes of soft S2

A

aortic stenosis

128
Q

Causes of fixed split S2

A

atrial septal defect

129
Q

Causes of widely split S2

A
  • deep inspiration
  • RBBB
  • pulmonary stenosis
  • severe mitral regurgitation
130
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
131
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.
132
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

133
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

134
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
135
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
136
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:

137
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

138
Q

not appropriate for DAPT

A

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

139
Q

tricuspid regurgitation signs

A

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

140
Q

tricuspid regurgitation signs

A

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

141
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

142
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

143
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%
144
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

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

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

147
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
148
Q

CTPA changes in PE

A

peripheral emboli affecting subsegmental arteries may be missed

149
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
150
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

151
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

152
Q

what is used as a first line in patients with PAD

A

Clopidogrel

153
Q

what should be encourage patients with PAD to do?

A

supervised exercise training

154
Q

myocarditis

A

inflammation of the myocardium.
Common on younger patients

155
Q

causes of myocarditis

A
  • viral: coxsackie B, HIV
  • bacteria: diphtheria, clostridia
  • spirochaetes: Lyme disease
  • protozoa: Chagas’ disease, toxoplasmosis
  • autoimmune
  • drugs: doxorubicin
156
Q

presentation of myocarditis

A
  • usually young patient with an acute history
  • chest pain
  • dyspnoea
  • arrhythmias
157
Q

blood investigation for myocarditis

A

↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP

158
Q

ECG investigation for myocarditis

A

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

159
Q

management of myocarditis

A

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

160
Q

complications of myocarditis

A

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

161
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

162
Q

test for all patients with suspected active pericarditis?

A

Transthoracic echocardiogrpahy

163
Q

blood tests for acute pericarditis

A

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

164
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
165
Q

how long does pericarditis last?

A

4-6 weeks

166
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

167
Q

beck’s triad

A
  • hypotension
  • raised JVP
  • muffled heart sounds
  • Linked to cardiac tamponade
168
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
169
Q

what is Kussmaul’s sign

A
  • paradoxical increase in jugular venous pressure (JVP) when a person inhales
170
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

171
Q

JVP C waves

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

not normally visible

172
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
173
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.

174
Q

JVP x descent

A

Caused by atrial relaxation and the tricuspid valve moving downward

fall in atrial pressure during ventricular systole

175
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

176
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

177
Q

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

A
178
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

179
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)

180
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

181
Q

irreversible complications of haemochromatosis

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

182
Q

Reversible features of haemochromatosis

A

Cardiomyopathy
Skin pigmentation

183
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

184
Q

Investigations for haemochromators

A

transferrin saturation
Ferritin
Genetic testing for HDE mutation

185
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

186
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

187
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

188
Q

Still’s murmur

A

Low-pitched sound heard at the lower left sternal edge

189
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)

190
Q

Right-sided valves

A

Tricuspid and pulmonary

191
Q

Left sided valves

A

Mitral
Aortic

192
Q

Mitral and aortic valves are…

A

Left sided valves

193
Q

Atrial natriuretic peptide

A

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

194
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

195
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

196
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

197
Q

Factors affecting stroke volume

A

Cardiac size
Contractility
Preload
Afterload

198
Q

Factors affecting stroke volume

A

Cardiac size
Contractility
Preload
Afterload

199
Q

Factors affecting stroke volume

A

Cardiac size
Contractility
Preload
Afterload

200
Q

Endothelia promotes the release of

A

angiotensin II
ADH
hypoxia
mechanical shearing forces

201
Q

Endothelia promotes the release of

A

angiotensin II
ADH
hypoxia
mechanical shearing forces

202
Q

Endothelia inhibits

A

nitric oxide
prostacyclin

203
Q

Endothelia is increased in

A

primary pulmonary hypertension
myocardial infarction
heart failure
acute kidney injury
asthma

204
Q

Endothelia is increased in

A

primary pulmonary hypertension
myocardial infarction
heart failure
acute kidney injury
asthma

205
Q

Pulse pressure

A
206
Q

LEFV

A

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

207
Q

LEFV

A

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

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
A

paradoxical rise in JVP during inspiration seen in constrictive pericarditis.

211
Q

non-pulsatile JVP

A

superior vena caval obstruction

212
Q

risk factors for infective endocarditis are

A
  • Intravenous drug use
  • Structural heart pathology
  • Chronic kidney disease (particularly on dialysis)
  • Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
  • History of infective endocarditis
213
Q

Causes of infective endocarditis

A
  • Streptococcus (notably the viridans group of streptococci)
  • Enterococcus (e.g., Enterococcus faecalis)
  • Rarer causes include Pseudomonas, HACEK organisms and fungi
214
Q

What to look for in infective endocarditis examination.

A
  • Splinter haemorrhages
  • Petechiae
  • Janeway lesions
  • Osler’s nodes
  • Roth spots
  • Splenomegaly
  • Finger clubbing
215
Q

Drug managment of infective endocarditis

A

Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin)

  • 4 weeks for with native heart valves
  • 6 weeks for patients with prosthetic heart valves
216
Q

Prophylaxis of infective endocarditis

A

none

217
Q

Structural pathology can increase the risk of endocarditis

A
  • Valvular heart disease
  • Congenital heart disease
  • Hypertrophic cardiomyopathy
  • Prosthetic heart valves
  • Implantable cardiac devices (e.g., pacemakers)
218
Q

What is the definition of acute coronary syndrome (ACS)?

A

ACS is a very common and important presentation in medicine characterized by chest pain, dyspnoea, nausea, vomiting, sweating, and palpitations.

ACS includes conditions such as STEMI, NSTEMI, and unstable angina.

219
Q

List the features of acute coronary syndrome (ACS).

A
  • Chest pain, classically on the left side of the chest
  • May radiate to the left arm or neck
  • Dyspnoea
  • Nausea and vomiting
  • Sweating
  • Palpitations

Atypical presentations are more likely in elderly, diabetic, or female patients.

220
Q

What are the classifications of acute coronary syndrome (ACS)?

A
  • ST-elevation myocardial infarction (STEMI)
  • Non ST-elevation myocardial infarction (NSTEMI)
  • Unstable angina

STEMI is characterized by ST-segment elevation and elevated biomarkers, while NSTEMI has ECG changes without ST elevation.

221
Q

What is the initial drug therapy for all patients with ACS?

A
  • Aspirin 300mg
  • Oxygen (if O2 saturation < 94%)
  • Morphine (for severe pain)
  • Nitrates (sublingually or intravenously)

Morphine should be used with caution due to potential adverse outcomes.

222
Q

What criteria must be met to diagnose STEMI?

A

Clinical symptoms consistent with ACS for ≥ 20 minutes with persistent ECG features in ≥ 2 contiguous leads.

Specific ST elevation measurements vary by age and sex.

223
Q

What are the two types of coronary reperfusion therapy for STEMI?

A
  • Percutaneous coronary intervention (PCI)
  • Fibrinolysis

PCI is preferred if symptoms onset is within 12 hours and can be delivered within 120 minutes.

224
Q

What is the recommended dual antiplatelet therapy prior to PCI for STEMI patients?

A
  • Aspirin + Prasugrel (if not on oral anticoagulant)
  • Aspirin + Clopidogrel (if on oral anticoagulant)

Dual antiplatelet therapy is crucial for preventing thrombotic events.

225
Q

What is the management for NSTEMI/unstable angina?

A
  • Antithrombin treatment (fondaparinux or unfractionated heparin)
  • Risk assessment using the GRACE score

The GRACE score considers age, heart rate, blood pressure, ECG findings, and troponin levels.

226
Q

What are the poor prognostic factors for patients with acute coronary syndrome?

A
  • Age
  • History of heart failure
  • Peripheral vascular disease
  • Reduced systolic blood pressure
  • Elevated initial cardiac markers
  • Cardiac arrest on admission

These factors influence risk stratification and management decisions.

227
Q

What are the potential complications following a myocardial infarction (MI)?

A
  • Cardiac arrest
  • Cardiogenic shock
  • Chronic heart failure
  • Tachyarrhythmias
  • Bradyarrhythmias
  • Pericarditis
  • Left ventricular aneurysm
  • Left ventricular free wall rupture
  • Ventricular septal defect
  • Acute mitral regurgitation

Each complication has specific management strategies.

228
Q

What is the recommended lifestyle advice post-myocardial infarction?

A
  • Mediterranean diet
  • 20-30 minutes of exercise daily
  • Sexual activity may resume after 4 weeks

Patients should avoid omega-3 supplements and ensure safe use of PDE5 inhibitors.

229
Q

What is the screening protocol for abdominal aortic aneurysm (AAA) in males aged 65?

A
  • < 3 cm: Normal, no further action
  • 3 - 4.4 cm: Small aneurysm, rescan every 12 months
  • 4.5 - 5.4 cm: Medium aneurysm, rescan every 3 months
  • ≥ 5.5 cm: Large aneurysm, refer within 2 weeks

AAA screening is crucial due to high mortality from ruptured aneurysms.

230
Q

What medications should all patients post-myocardial infarction be offered?

A
  • Dual antiplatelet therapy
  • ACE inhibitor
  • Beta-blocker
  • Statin

These medications are aimed at improving long-term outcomes.

231
Q

What is the management of fibrinolysis for patients with STEMI?

A
  • Antithrombin drug should be given
  • ECG should be repeated after 60-90 minutes

Persistent myocardial ischemia after fibrinolysis necessitates consideration of PCI.

232
Q

True or False: Ventricular fibrillation is the most common cause of death following a myocardial infarction.

A

True

It’s important to manage patients according to the ALS protocol.

233
Q

What is the screening method for an abdominal aortic aneurysm in males aged 65?

A

A single abdominal ultrasound

234
Q

What is the interpretation and action for an aorta width of < 3 cm?

A

Normal

No further action is required.

235
Q

What is the action for a small aneurysm (aorta width 3 - 4.4 cm)?

A

Rescan every 12 months

236
Q

What is the recommended action for a medium aneurysm (aorta width 4.5 - 5.4 cm)?

A

Rescan every 3 months

237
Q

What should be done for a large aneurysm (aorta width ≥ 5.5 cm)?

A

Refer within 2 weeks to vascular surgery for probable intervention

238
Q

What is the estimated prevalence of abdominal aortic aneurysms found during screening?

A

1 per 1,000 screened patients

239
Q

What characterizes low rupture risk in abdominal aortic aneurysms?

A

Asymptomatic, aortic diameter < 5.5 cm

240
Q

What is the management for high rupture risk abdominal aortic aneurysms?

A

Refer within 2 weeks to vascular surgery for probable intervention

241
Q

What is the primary cause of abdominal aortic aneurysms?

A

Failure of elastic proteins within the extracellular matrix

242
Q

What are the major risk factors for the development of aneurysms?

A
  • Smoking
  • Hypertension
243
Q

Name three main patterns of presentation in patients with peripheral arterial disease.

A
  • Intermittent claudication
  • Critical limb ischaemia
  • Acute limb-threatening ischaemia
244
Q

What are the features of acute limb-threatening ischaemia?

A

1 or more of the 6 P’s: * pale * pulseless * painful * paralysed * paraesthetic * ‘perishing with cold’

245
Q

What initial investigations should be performed for acute limb-threatening ischaemia?

A

Handheld arterial Doppler examination

246
Q

What does an ankle-brachial pressure index (ABI) of < 0.5 suggest?

A

Critical limb ischaemia

247
Q

What is the management approach for a ruptured abdominal aortic aneurysm?

A

Immediate vascular review with a view to emergency surgical repair

248
Q

What is aortic regurgitation (AR)?

A

Leaking of the aortic valve causing blood to flow in reverse during ventricular diastole.

249
Q

What are the causes of aortic regurgitation due to valve disease?

A
  • Rheumatic fever
  • Calcific valve disease
  • Connective tissue diseases
  • Bicuspid aortic valve
  • Spondylarthropathies
  • Hypertension
  • Syphilis
  • Marfan’s, Ehler-Danlos syndrome
250
Q

What are the features of symptomatic aortic stenosis?

A
  • Chest pain
  • Dyspnoea
  • Syncope / presyncope
  • Murmur
251
Q

What does a narrow pulse pressure indicate in aortic stenosis?

A

Severe aortic stenosis

252
Q

What is the most common cause of aortic stenosis in older patients?

A

Degenerative calcification

253
Q

What are the two main options for valve replacement?

A
  • Biological (bioprosthetic) valves
  • Mechanical valves
254
Q

What is the major disadvantage of biological (bioprosthetic) valves?

A

Structural deterioration and calcification over time

255
Q

What is the target INR for patients with mechanical aortic valves?

A

3.0

256
Q

What is the target INR for patients with mechanical mitral valves?

A

3.5

257
Q

What is the management of stable angina?

A
  • Lifestyle changes
  • Medication
  • Percutaneous coronary intervention
  • Surgery
258
Q

What medications should all patients with stable angina receive?

A
  • Aspirin
  • Statin
259
Q

What should be done if a patient is still symptomatic after monotherapy with a beta-blocker?

A

Add a calcium channel blocker

260
Q

What is nitrate tolerance?

A

Reduced efficacy of nitrates due to regular use

261
Q

What should patients taking standard-release isosorbide mononitrate do to minimize nitrate tolerance?

A

Maintain a daily nitrate-free time of 10-14 hours

262
Q

What are the features of pulmonary oedema on a chest x-ray?

A
  • Interstitial oedema
  • Bat’s wing appearance
  • Upper lobe diversion
  • Kerley B lines
  • Pleural effusion
  • Cardiomegaly may be seen if there is cardiogenic cause

The features help in diagnosing pulmonary oedema and can indicate underlying cardiac issues.

263
Q

What is the first-line investigation for heart failure according to NICE guidelines?

A

N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test

This guideline was updated in 2018, moving away from relying on a history of myocardial infarction.

264
Q

What should be arranged if NT-proBNP levels are ‘high’?

A

Specialist assessment within 2 weeks

This includes transthoracic echocardiography.

265
Q

What are the normal levels of B-type natriuretic peptide (BNP)?

A

< 100 pg/ml (29 pmol/litre)

Normal levels help in differentiating heart failure from other conditions.

266
Q

List factors that can increase BNP levels.

A
  • Left ventricular hypertrophy
  • Ischaemia
  • Tachycardia
  • Right ventricular overload
  • Hypoxaemia
  • GFR < 60 ml/min
  • Sepsis
  • COPD
  • Diabetes
  • Age > 70
  • Liver cirrhosis

Understanding these factors is crucial for interpreting BNP levels accurately.

267
Q

What is the first-line treatment for heart failure according to NICE?

A

Both an ACE-inhibitor and a beta-blocker

Clinical judgement is advised when determining which one to start first.

268
Q

What are examples of beta-blockers licensed to treat heart failure in the UK?

A
  • Bisoprolol
  • Carvedilol
  • Nebivolol

These medications are important for managing heart failure symptoms.

269
Q

What is the standard second-line treatment for heart failure?

A

Aldosterone antagonist

Examples include spironolactone and eplerenone.

270
Q

What is the role of SGLT-2 inhibitors in heart failure management?

A

Reduce glucose reabsorption and increase urinary glucose excretion

Examples include canagliflozin, dapagliflozin, and empagliflozin.

271
Q

What is the significance of cardiac resynchronisation therapy?

A

Indicated for patients with heart failure and wide QRS complex

It improves symptoms and reduces hospitalisation in NYHA class III patients.

272
Q

What does the New York Heart Association (NYHA) Class I indicate?

A

No symptoms and no limitation in ordinary physical exercise

This classification helps in assessing the severity of heart failure.

273
Q

What is acute heart failure (AHF)?

A

A life-threatening emergency characterized by sudden onset or worsening of heart failure symptoms

AHF may present with or without a history of pre-existing heart failure.

274
Q

What are common precipitating causes of acute heart failure?

A
  • Acute coronary syndrome
  • Hypertensive crisis
  • Acute arrhythmia
  • Valvular disease

Understanding these causes aids in timely intervention.

275
Q

What are the symptoms of acute heart failure?

A
  • Breathlessness
  • Reduced exercise tolerance
  • Oedema
  • Fatigue
  • Chest signs (e.g., bibasal crackles)

These symptoms are critical for diagnosis.

276
Q

What is the recommended treatment for all patients with acute heart failure?

A

IV loop diuretics (e.g., furosemide or bumetanide)

Diuretics help manage fluid overload effectively.

277
Q

What is high-output heart failure?

A

A situation where a ‘normal’ heart is unable to pump enough blood to meet metabolic needs

Causes include anemia, arteriovenous malformation, and pregnancy.

278
Q

Fill in the blank: The most common cause of decompensated heart failure is _______.

A

Acute coronary syndrome

This condition often leads to worsening symptoms in patients with existing heart failure.

279
Q

What are signs of right-sided heart failure?

A
  • Peripheral oedema
  • Raised jugular venous pressure
  • Hepatomegaly
  • Weight gain due to fluid retention
  • Anorexia (‘cardiac cachexia’)

Identifying these signs is crucial for diagnosis and management.

280
Q

What is the strongest risk factor for developing infective endocarditis?

A

A previous episode of endocarditis

281
Q

What types of patients are affected by infective endocarditis?

A
  • Previously normal valves (50%)
  • Rheumatic valve disease (30%)
  • Prosthetic valves
  • Congenital heart defects
  • Intravenous drug users (IVDUs)
  • Recent piercings
282
Q

Which valve is most commonly affected in infective endocarditis?

A

The mitral valve

283
Q

What is the most common cause of infective endocarditis?

A

Staphylococcus aureus

284
Q

What type of patients is Staphylococcus aureus particularly common in?

A

Acute presentation and intravenous drug users (IVDUs)

285
Q

Historically, which organism was the most common cause of infective endocarditis?

A

Streptococcus viridans

286
Q

What are the two most notable viridans streptococci?

A
  • Streptococcus mitis
  • Streptococcus sanguinis
287
Q

What is the link between Streptococcus viridans and infective endocarditis?

A

Linked with poor dental hygiene or following a dental procedure

288
Q

Which organisms are commonly associated with culture-negative endocarditis?

A
  • Coxiella burnetii
  • Bartonella
  • Brucella
  • HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
289
Q

What are poor prognostic factors for infective endocarditis?

A
  • Staphylococcus aureus infection
  • Prosthetic valve (especially early)
  • Culture negative endocarditis
  • Low complement levels
290
Q

What is the mortality rate according to organism for staphylococci?

A

30%

291
Q

What antibiotic is suggested for initial blind therapy in native valve endocarditis?

A

Amoxicillin, consider adding low-dose gentamicin

292
Q

What is the recommended antibiotic therapy for prosthetic valve endocarditis caused by staphylococci?

A

Flucloxacillin + rifampicin + low-dose gentamicin

293
Q

Which procedure is indicated for severe valvular incompetence in endocarditis?

A

Surgery

294
Q

According to NICE guidelines, which procedures do not require antibiotic prophylaxis?

A
  • Dental procedures
  • Upper and lower gastrointestinal tract procedures
  • Genitourinary tract procedures
  • Upper and lower respiratory tract procedures
295
Q

What is the typical cause of acute mesenteric ischaemia?

A

An embolism resulting in occlusion of an artery supplying the small bowel

296
Q

What are the common features of acute mesenteric ischaemia?

A
  • Severe abdominal pain of sudden onset
  • Symptoms out-of-keeping with physical exam findings
297
Q

What is the management for acute mesenteric ischaemia?

A

Immediate laparotomy

298
Q

What condition may chronic mesenteric ischaemia be thought of as?

A

‘Intestinal angina’

299
Q

What are common predisposing factors for bowel ischaemia?

A
  • Increasing age
  • Atrial fibrillation
  • Other causes of emboli (endocarditis, malignancy)
  • Cardiovascular disease risk factors (smoking, hypertension, diabetes)
  • Cocaine use
300
Q

What is the preferred investigation for diagnosing mesenteric ischaemia?

A

CT scan

301
Q

What does ischaemic colitis describe?

A

An acute but transient compromise in the blood flow to the large bowel

302
Q

What may be seen on abdominal x-ray in cases of ischaemic colitis?

A

‘Thumbprinting’ due to mucosal oedema/haemorrhage

303
Q

What is the management for ischaemic colitis?

A
  • Usually supportive
  • Surgery may be required in cases of generalised peritonitis, perforation, or ongoing haemorrhage

UKMLA Prep (39 decks)

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