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MRCP part 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Mortality in endocarditis according to organisms

A
  • Staphylococci 30%
  • Bowel organisms - 15%
  • Streptococci 5%
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2
Q

Poor prognostic factors of endocarditis

A
  • Staphyloccocus aureus
  • Prosthetic valve
  • Culture negative endocarditis
  • Low complement levels
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3
Q

Rx of endocarditis

A

Initial blind therapy

  • Native valve
    • Amoxicillin
  • Pen allergic
    • Vancomycin** + **low-dose gentamicin
  • Prosthetic valve
    • Vancomycin** + **low-dose gentamicin** + **rifampicin

Native valve endocarditis caused by streptococci

  • Fully-sensitive (e.g. viridans)
    • Benzylpenicillin
    • If pen allergic: vancomycin** + l**ow-dose gentamicin
  • Less-sensitive
    • Benzypenicillin** + **low-dose gentamicin
    • If pen allergic: vancomycin** + **low-dose gentamicin

Endocarditis caused by staphylocci

  • Native valve
    • Flucloxacillin
    • Pen allergic or MRSA: vancomycin** + **low-dose gentamicin
  • Prosthetic valve
    • Flucloxacillin** + **rifampicin** + **low-dose gentamicin
    • Pen allergic: Vancomycin** + **rifampicin** + **low-dose gentamicin
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4
Q

Indications for surgery in endocarditis

A
  • Severe valvular incompetence
  • Aortic abscess (lengthening of PRi)
  • Infections resistant to antibiotics
  • Cardiac failure refractory to standard medical treatment
  • Recurrent emboli after ABx Rx
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5
Q

Rx of ventricular tachycardia

A

1st line - Amiodarone

2nd line - Lidocaine

3rd line - Procainamide

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6
Q

Mx of pulseless VT or VF

A
  • Compressions with a shock of at least 150 J
  • Compressions 30:2 for 2 min
  • After 3rd shock (increasing voltage) - 1 mg adrenaline IV and then the same after every shock
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7
Q

Cardiac catheterisation and oxygen saturation levels

A

Rules

  • Deoxygenated blood returns to the R heart - SpO2 ~ 70%
    • RA, RV, PA
  • The lungs oxygenate blood to 98-100% - L right Z 100%
    • LA, LV, Aorta

Conditions

  • ASD
    • Oxygenated blood in LA mixes with deoxygenated in the RA
      • R heart - 85%, L heart - 100%
  • VSD
    • Oxygenated blood in LV mixes with deoxygenated in the RV
      • RA - 70%
      • RV, PA - 85%
      • LA, LV, Aorta - 100%
  • Patent Ductus Arteriosus
    • PDA connects higher pressure Aorta with lower pressure PA
      • ​RA, RV - 70%
      • PA - 85%
      • LA, LV, Aorta - 100%
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8
Q

Management of HOCM

A

AD disorder of muscle tissue caused by defects in the genes encoding contractile proteins

  • 1 in 500

Rx

  • Amiodarone
  • Beta-blockers or Verapamil for Sx
  • Cardioverter defibrillator
  • Dual chamber pacemaker
  • Endocarditis prophylaxis

Drugs to avoid

  • Nitrates
  • ACE-inhibitors
  • Inotropes
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9
Q

Mx of high INR

A

Major bleeding

  • Stop warfarin
  • IV vitamin K 5mg
  • Prothrombin complex concentrate
    • If N/A then FFP

INR > 8.0, minor bleeding

  • Stop warfarin
  • IV vitamin K 1-3 mg
  • Repeat dose of vit K if INR still too high after 24h
  • Restart warfarin when INR < 5.0

INR > 8.0, no bleeding

  • Stop warfarin
  • Vitamin K 1-5 mg IV preparation orally
  • Repeat dose of vitamin K if INR still high after 24h
  • Restart warfarin when INR < 5.0

INR 5.0 - 8.0, minor bleeding

  • Stop warfarin
  • IV vitamin K 1-3 mg
  • Restart when INR < 5.0

INR 5.0 - 8.0, no bleeding

  • Withhold 1 or 2 doses of warfarin
  • Reduce subsequent maintenance doses
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10
Q

Treatment of PE

A

LMWH or fondaparinux initially after PE has been diagnosed

  • Except for massive PE where thrombolysis is considered

LMWH/fondaparinux for at least 5 days or until INR is 2.0 or above for at least 24h (whichever is longer)

  • i.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range

Warfarin / DOACs for at least 3 months

Unprovoked PE - anticoagulation for at least 6 months

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11
Q

Normal JVP waveform

A

The a wave

  • Atrial contraction

The c wave

  • Invisible flicker in the x descent due to closure of the tricuspid valve
  • Just before the start of ventricular systole

The x descent

  • Downward movement of the heart > atrial stretch > drop in pressure

The v wave

  • Passive filling of blood into the atrium against a closed tricuspid valve

The y descent

  • Opening of the tricuspid valve
  • Passive movement of blood from the RA to the RV (S3 when audible)
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12
Q

Causes of raised JVP (normal waveform)

A
  • Heart failure
  • Fluid overload
  • Severe bradycardia
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13
Q

Causes of raised JVP - Kussmaul’s sign

A

Normally, JVP increases upon inspiration (up), drops with expiration (down)

Kussmaul’s sign

  • Opposite of what occurs in health
  • = Right heart chambers cannot increase in size to accommodate increased venous return

Causes

  • Pericardial disease (constriction)
  • Fluid in the pericardial space
    • Pericardial effusion
    • Cardiac tamponade
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14
Q

Raised JVP with loss of normal pulsations

A

Causes

  • SVC syndrome
    • Obstruction
      • Mediastinal malignancy
        • Bronchogenic malignancy > head, neck &/or arm swelling
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15
Q

a wave in diseases

A

Absent

  • Atrial fibrillation - no co-ordinated contraction

Large

  • Tricuspid stenosis
  • Right HF
  • Pulmonary HTN

Cannon

  • AV dissociation - allowing the atria & ventricles to contract at the same time
    • Atrial flutter & atrial tachycardias
    • Third-degree (complete) heart block
    • Ventricular tachycardia & ventricular ectopics
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16
Q

v waves in diseases

A

Giant

  • Tricuspid regurgitation
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17
Q

x descent in diseases

A
  • Downward movement of the heart > atrial stretch & a drop in P

Steep

  • tamponade
  • cardiac constriction

If steep x descent only > tamponade

18
Q

y descent in diseases

A
  • Opening of tricuspid valve with passive movement of blood from RA to RV

Steep

  • Cardiac constriction

Slow

  • Tricuspid stenosis
19
Q

JVP waveforms in diseases

A

Atrial fibrillation

  • Loss of a-wave

Tricuspid regurgitation

  • Large c-V wave

R HF, Pulmonary HTN

  • Raised JVP
  • Prominent a-wave

Constriction

  • Prominent and deep x and y descents

Tamponade

  • Prominent x descent only
  • y descent slow or absent
20
Q

Absent radial pulse

A
  • Iatrogenic - post-catheterisation or arterial line
  • Blalock-Taussig shunt for congenital heart disease (e.g. ToF)
  • Aortic dissection with subclavian involvement
  • Trauma
  • Takayasu’s arteritis
  • Peripheral arterial embolus
21
Q

Collapsing pulse

A
  • Aortic regurgitation
  • Arteriovenous fistula
  • PDA
  • Other large extracardiac shunts
22
Q

Slow rising pulse

A
  • Aortic stenosis
    • delayed percussion wave
23
Q

Bisferiens

A
  • A double shudder due to mixed aortic valve disease with significant regurgitation
24
Q

Jerky

A

hypertrophic obstructive cardiomyopathy

25
Q

Alternans

A
  • Occur in severe left ventricular dysfunction
    • Reduced EF > elevated end-diastolic volume
    • This may sufficiently stretch the myocytes (Frank-Starling physiology) to improve the EF of the next HB
    • This leads to pulses that alternate weak and strong
26
Q

Paradoxical (pulsus paradoxus)

A
  • An excessive reduction in the pulse with inspiration
    • Drop in BP >10 mmHg
      • Left ventricular compression
      • Tamponade
      • Constrictive pericarditis
      • Severe asthma as venous return is compromised
27
Q

Hyperkalaemia on ECG

A
  • Tall T waves
  • Prolonged PR interval
  • Flattened/absent P waves
28
Q

Very severe hyperkalaemia on ECG

A
  • Wide QRS
  • Sine wave pattern
  • Ventricular tachycardia / VF / asystole
29
Q

Hypokalaemia ECG

A
  • Flat T waves, occasionally inverted
  • Prolonged PR interval
  • ST depression
  • Tall U waves
30
Q

What heart defect can present with acute ischaemic stroke?

A

Patent foramen ovale

  • Present in 20% of population
  • May allow embolus (e.g. from DVR) to pass from R side of the heart to the L side > paradoxical embolus
31
Q

Target INR for prosthetic valves

A

Aortic - 3.0

Mitral - 3.5

32
Q

Pulmonary arterial hypertension

A

PAH = a resting mean pulmonary artery pressure ≥ 25 mmHg

  • More common in females
  • Typically 30-50 yoa
  • RF
    • HIV
    • Cocaine
    • Anorexigens (e.g. fenfluramine)
    • 10% inherited - AD
  • Features
    • Progressive exertional dyspnoea
    • Exertional syncope, exertional chest pain, peripheral oedema
    • Cyanosis
    • Right ventricular heave, loud P2, ^JVP with prominent ‘a’ waves, tricuspid regurgitation
  • Management
    • Anticoagulants, oxygen
    • Acute vasodilator testing (central to deciding on the appropriate Mx strategy)
      • To decide which pts show a significant fall in pulmonary arterial P after administration of vasodilators
        • E.g. IV epoprostenol, inhaled NO
      • If +ve response to acute vasodilator testing (minority of pts)
        • Oral Ca channel blockers
    • If negative response to acute vasodilator testing (majority)
      • Prostacyclin analogues
        • Treprostinil, iloprost
      • Endothelin receptor antagonists
        • Bosentan, ambrisentan
      • Phosphodiesterase inhibitors
        • Sildenafil
33
Q

Describe the JVP

A

‘a’ wave = atrial contraction

  • large if atrial pressure
    • tricuspid stenosis
    • pulmonary stenosis
    • pulmonary hypertension
  • absent if in AF

Cannon ‘a’ waves

  • caused by atrial contractions against a closed tricuspid valve
  • are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single-chamber ventricular pacing

‘c’ wave

  • closure of tricuspid valve
  • not normally visible

‘v’ wave

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

‘x’ descent = fall in atrial pressure during ventricular systole

‘y’ descent = opening of tricuspid valve

34
Q

Treatment of Hypertension

A

Clinic reading ≥ 140/90 mmHg

  • Offer ABPM or HBPM
    • < 135/85 mmHg
      • Not hypertensive > monitor
    • ≥ 135/85 mmHg
      • Stage 1 hypertension
        • Treat if < 80 yrs & any of the following
          • Target organ dmg
          • Established CVS disease
          • Renal disease
          • Diabetes
          • 10-yr CVS risk ≥10%
    • ≥ 150/95 mmHg
      • Stage 2 hypertension
        • Treat all patients, regardless of age
35
Q

Anteroseptal - V1-V4

A

Left anterior descending

36
Q

Inferior - II, III, aVF

A

Right coronary

37
Q

Anterolateral - V4-V6, aVL

A

Left anterior descending

Left circumflex

38
Q

Lateral - I, aVL +/- V5-6

A

Left circumflex

39
Q

Posterior - Tall R waves V1-V2

A

Usually left circumflex, also right coronary

40
Q

Acute pericarditis

A

Features

  • Chest pain - can be pleuritic
    • Often relieved by sitting forwards
  • Other Sx
    • Non-productive cough
    • Dyspnoea
    • Flu-like Sx
    • Pericardial rub
    • Tachypnoea
    • Tachycardia

Causes

  • Viral infections (Coxsackie)
  • Tuberculosis
  • Uraemia (causes ‘fibrinous’ pericarditis)
  • Trauma
  • Post-MI > Dressler’s syndrome
  • Connective tissue disease
  • Hypothyroidism
  • Malignancy

Ix

  • ECG changes
    • Widespread ST elevation
    • Saddle-shaped ST elevation
    • PR depression - most-specific ECG marker for pericarditis
  • All pts with suspected acute pericarditis should have
    • Transthoracic echocardiography

Mx

  • Treat the underlying cause
  • Comb of NSAIDs & colchicine
41
Q

Modified Duke criteria

A

(Modified) Duke criteria

  • The Duke criteria help to diagnose infective endocarditis. To confirm the diagnosis, one of the following requirements must be met:
    • Two major criteria
    • One major and three minor criteria
    • Five minor criteria

Major diagnostic criteria

  • Two separate blood cultures positive for typical pathogens (see “Etiology” above)
  • Evidence of endocardial involvement in echocardiography
  • A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)

Minor diagnostic criteria

  • Predisposition: underlying heart disease or IV drug abuse
  • Fever ≥ 38°C (100.4F)
  • Vascular abnormalities
  • Immunologic disorder

Microbiology

MRCP part 1 (4 decks)

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