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My MRCP > Cardio: Infective Endocarditis, Myocardial, Pericardial Disease > Flashcards

Cardio: Infective Endocarditis, Myocardial, Pericardial Disease Flashcards

1
Q

Define Infective Endocarditis

A

Infection of the lining of the heart

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2
Q

What is non-infective Endocarditis [2] and what causes it [5]?

A

Non-Bacterial Thrombotic Endocarditis [1]
The formation of a sterile Fibrin-platelet vegetation due to some disruption of the valve endothelium. [1]

  • Turbulent Flow
  • Electrodes/Catheters
  • Rheumatic Carditis
  • Degenerative Disease
  • Local inflammation
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3
Q

How do we classify cases of endocarditis [3]

A

Acute/Subacute/Chronic pattern
Causative organism
If prosthetic is it early or late? (<1yr or >1yr)

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4
Q

How can Infective endocarditis be acquired? [4]

A
  • IVDA
  • Community Acquired
  • Nosocomial
  • Healthcare Related but Non-Nosocomial
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5
Q

How do the IE organisms reach the circulation? [3]

A

From Extra Cardiac Infection

  • Invasive Procedures
  • Gingival Disease
  • Daily livinig (e.g. brushing teeth & defecating)
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6
Q

What are the risk factors for IE? [7]

A 
Male (though women have worse prognosis)
Elderly
Recent invasive procedures
IVDA
Prosthetic Valves
Any Heart Defect/Disease
Immunocompromised
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7
Q

Name 3 main symptoms and 4 others

A

FEVER - MALAISE - FATIGUE

also chills - arthralgia - weight loss - headache

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8
Q

What are the clinical signs of IE?
General [6]
Vascular [3]
Immunological [3]

A

General:
CHF - New Murmur - Splenomegaly - Emboli - Anaemia

Vascular:
Janeway Lesions (blood seeped into palms/soles)
Splinter Haemorrhages
Vasculitic Rash (feet, purple/red spots from burst capillaries)

Immunological:
Roth Spots (Retinal Haemorrhage)
Osler’s Nodes (Red raised painful spots of fingers, palms & soles)
Nephritis

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9
Q

When could the clinical signs be absent from IE? [3]

A

In the elderly, immunocompromised or post antibiotic treatment

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10
Q

What does the mnemonic FROM JANE stand for?

A
  • Fever
  • Roth Spots
  • Oslers Nodes
  • Malaise
  • Janeway Lesions
  • Anaemia
  • Nephritis & Nail haemorrhages
  • Emboli
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11
Q

What investigations are done on a suspected IE case? [7]

A 
FBC(neutrophilia)/CRP/ESR
U + Es
Blood Cultures
Urinalysis
ECG
CXR
ECHO
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12
Q

What are we looking for an ECG? [2]

A

A conduction delay caused by IE forming an abscess over part of the bundle of his or purkinje fibres. [1]
Wide QRS [1]

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13
Q

What shows up on a CXR in IE? [2]

A

Heart Failure and Pulmonary Abscesses

Cardiomegaly

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14
Q

What kind of ECHO do we use for Infective Endocarditis?

What do you do if TTE is negative but clinical suspicion is high?

A

A Trans-Thoracic Echo (TTE) is 1st line, TOE is 2nd line

TOE is used if TTE is -ve but your still suspicious OR if TTE is +ve for a better view of abscess/vegetation/complications

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15
Q

What do we do if both TTE & TOE are -ve but we’re still suspicious of IE? [1]

A

Repeat them 7-10 days later or earlier if theres a new complication

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16
Q

How many blood cultures do we take for IE? [1]

How would this change if they’re in septic shock? [1]

A

3 from different sites with 6 hours between them

Or if they’re in septic shock then just 2 from different sites with 1 hour between them.

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17
Q

In a patient with IE, what can cause false negative picture in blood cultures? [3]

A
  1. Recent antibiotics
  2. Fastidious Organisms have different diets so wont grow on blood culture (Nutritionally varied Strep - HACEK gram -ve bacilli - Brucella - Fungi)
  3. Nor would Intracellular Bacteria (Coxiella Burnetii - Bartonella - Chlamydia)
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18
Q

What are the common complications of IE? [6]

A
  • Heart Failure, Atrioventricular Heart Block
  • Fistula Formation
  • Leaflet Perforation
  • Uncontrolled Infection, Abscess Formation
  • Embolism
  • Prosthetic valve endocarditis (PVE) & PV dysfunction
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19
Q

What criteria are needed to have a sure diagnosis of IE? [3]

A

Definite diagnosis with:
2 Major
1M + 3m
5m

of the Modified Duke Criteria

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20
Q

What are the Major Duke criteria? [5]

A
  • IE causing organisms in 2 seperate blood cultures
  • IE organisms found in persistant blood cultures
  • +ve blood culture for Coxiella Burnetii
  • +ve ECHO
  • New Murmur
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21
Q

What are the minor Duke Criteria? [5]

A
  • Predisposition (IVDA or Heart Condition)
  • Fever
  • Vascular Signs
  • Immunologic Signs
  • Microbiological evidence that doesnt meet the major duke critera (serology or blood culture)
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22
Q

Name 3 top micro-organisms implicated in IE

A
  • Staphylococcus aureus
  • Streptococcus viridans
  • coagulase-negative Staphylococci such as Staphylococcus epidermidis
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23
Q

How do we empirically treat IE? (ie before the blood cultures come back) [3]

A

We use 2 IV antibiotics at once, AFTER the bloods are taken. [1]
Standard is Amoxicillin + low dose gentamicin

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24
Q

What do we use to empirically treat IE if the patient is severely septic, allergic to penicillin or infected with MRSA? [2]

Antibiotic if gram-negative suspected?

A

Vancomycin (replacing the amoxicillin) + low dose gentamicin

Gram negative: Meropenum and vancomycin

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25
Q

Antibiotic regimen
* Native valve endocarditis caused by staphylococci
* Prosthetic valve endocarditis caused by staphylococci

A
  • Flucloxacillin
  • Flucloxacillin + rifampicin + low-dose gentamicin
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26
Q

When do we use surgery as well as antibiotics?

A

The complications are indicators surgery is now necessary

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27
Q

How do we treat fungal IE? [2]

In what patients does Fungal IE occur?

A

With dual antifungals, often for life. And usually valve replacement too.

In PVE/IVDA/immunocompromised patients.

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28
Q

When is amoxicillin replaced with vancomycin in empirical IE treatment? [3]

A

If the patient has severe sepsis, is allergic to penicillin or has MRSA

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29
Q

What is the HACEK group of organisms [6]

A

All gram-negative [1]

Haemophilus influenza
Actinobacillus
Cardiobacterium
Eikenella
Kingella
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30
Q

Streptococcus viridans - associated with one risk factor

A

they are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure

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31
Q

Risk factor: coagulase-negative Staphylococci such as Staphylococcus epidermidis

A

commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.

32
Q

Streptococcus bovis - risk factor

A

associated with colorectal cancer

33
Q

What is myocarditis [1]

A

Inflammation of the heart muscle

34
Q

What causes myocarditis? [5]

A

Infection (Coxsackie virus, fungal, bacterial or parasitic)
Cocaine
Chemo & other drugs
Autoimmune e.g. rheumatic fever and SLE, sarcoid
Idiopathic 50%

35
Q

How does myocarditis present? [5]

A
  • Prodrome - days to weeks
  • Palpitations caused by sinus, tachy, vent extrasystole, VT, VF
  • Chest pain mimics angina
  • SOBOE from sudden heart failure
  • Syncope
36
Q

Investigations [3]

A

Bloods - troponin
ECG - AV block, bundle branch block, Q waves, ST depression, TWI.
ECHO
Encomyocardial biopsy

37
Q

How do we treat myocarditis? [4]

A

Mostly its self limiting
Exclude reversible causes like MI
In-patient monitoring
Immunosuppressant drugs - steroids, azathioprine, interferon B

38
Q

Causative organisms
Virus [7]
Bacterial [9]
Protozoa

A

Virus:
flu, hepatitis, mumps, rubella, coxsackie, polio, HIV

Bacterial
clostridium, diphtheria, TB, tetanus, meningococci, mycoplasma, brucellosis, psittacosis, spirochetes

Protozoa: Chagas

39
Q

Drugs that cause myocarditis [4]

A

Cyclophosphamide, Herceptin
Penicillin, chloramphenicol sulphonamides
Methyldopa, spironolactone
Phenytoin, carbamazepine

40
Q

Signs on cardiac examination [3]

A

Tachycardia
Soft 1 murmur
S4 gallop

41
Q

What are the 3 types of cardiomyopathy?

A

Restrictive - Stiffening of Myocardium
Hypertrophic - hypertrophy of myocardium
Dilated - Dilation of ventricles

42
Q

What causes DCM? [4] What is the most common cause

Complication and prognosis?

A
  • Genetics e.g. Muscular Dystrophy
  • Doxorubicin/alcohol/chemicals
  • Coxsackie B virus
  • Idiopathic*

Cx: sudden cardiac death
Pro: 40% mortality in 2y

43
Q

How does DCM present?
Symptoms [6]
Signs [8]

A
  • Fatigue
  • Dyspnoea/Orthopnea/PND
  • Peripheral edema
  • Cough
  • LHF: Weak Pulses, pleural effusion
  • RHF: Raised JVP, Ascites, jaundice, hepatomegaly
  • Tachycardia, hypotension
  • S3 gallop, mitral/tricuspid regurg
  • Displaced apex beat
44
Q

DCM investigations and results
4 first line
2 others

A
  • Bloods: FBC, U&E and creatinine (low Na+ indicates poor prognosis), LFT, BNP confirms HF
  • ECG: tachycardia, non-specific T wave changes, poor R wave progression, LVH. LBBB
  • Echo: dilated hypokinetic heart with low ejection fraction (may have MR, TR or mural thrombus)
  • CXR - Pulm congestion + Cardiomegaly

Cardiac MRI
Endomyocardial biopsy - Visibally stretched fibres

45
Q

How do we treat DCM? [6]

A 
Bed rest
Diuretics, ACEi, BB (reduce strain)
Digoxin (increase contractility)
Warfarin (reduce thrombus risk)
Biventricular pacing, ICD 
Heart transplant
46
Q

What causes RCM? [7]

A 
Amyloidosis
Sarcoidosis
Haemochromatosis
Fibrosis - MI, drugs, radiation, idiopathic
Genetic mutations causing familial
Diabetes
Loffler's endocarditis
47
Q

How does RCM present? [5]

A

Symptoms are similar to constrictive pericarditis, SOB, fatigue
Right ventricular failure predominates

  • Cough, Chest Pain
  • Oedema, Ascites, Hepatomegaly
  • Raised JVP
  • Tachycardia
  • Audible S3/4
48
Q

How do we test for RCM? [6] which one is gold standard

A

*Right ventricular biopsy: gold standard with +ve Congo red staining, may show sarcoidosis, amyloidosis

Serum Fe (Haemochromatosis)
ECHO - biatrial enlargement and patchy fibrosis from infiltrative disease
MRI (ddx from constrictive pericarditis)
CXR (pulm congestion + normal heart size)
ECG (AF)

Note: normal heart size and normal ejection fraction in ECHO

49
Q 
How do we treat RCM?
Treat the cause
Rx 3
Devices 1
Definitive treatment 1
A

Rx

  1. Warfarin (AF)
  2. B-blockers - ACEI - Diuretic -> Reduce strain on heart
  3. Amiodarone (arrhythmia’s)

ICD
Heart Transplant

50
Q

What is THE cause of HCM? [3]

Pathogenesis [3]

A

Familial hypertrophic cardiomyopathy
Autosomal dominant
Strong genetic components
Leading cause of sudden cardiac death in the young
Missense mutations [1] of beta-myosin chains [1] which affect sarcomeric proteins [1]

51
Q

How does HCM present?
Symptoms [7]
Signs [5]

A

Asymptomatic until the valve is occluded or the heart cant pump enough blood anymore:

  • Fatigue
  • Chest Pain, angina
  • Dyspnoea
  • Palpitations
  • Tachycardia
  • Presyncope
  • Exertional Arrythmias
  • Notched/bifid Pulse
  • Raised JVP
  • Audible S4
  • Double apex beat
  • Systolic ejection murmur worse on valsalva
52
Q

How do we test for HCM?

6 investigations

A 
ECG
ECHO
CXR
Cardiac catheterisation (MR)
Exercise testing with respiratory gas mask (risk stratification)
Genetic Testing
Biopsy - myocyte dissaray
53
Q 
How do we treat HCM?
Rx 4
Lifestyle modification 1
Devices 1
Surgical methods 3
A

Lifestyle mods: reduce exercise/stress

Rx:
Warfarin + Beta blockers (reduce contractility)
Verapamil
Amiodarone

Devices: Dual chamber pacing (ICD)

Surgical:
1. Septal myomectomy/ablation
(reduces outflow gradient)
2. Surgical mitral repair
3. Heart transplant
54
Q

What should we see on ECG for HCM? [4]

A 
LVH
Progressive T wave inversion
Deep Q waves (inferior and lateral leads)
AF, WPW
Ventricular ectopic, VT
55
Q

What would we see on ECHO for HCM? [4]

A
  • asymmetrical septal hypertrophy
  • non-dilated small LV cavity with hyper contractile posterior wall
  • mid-systolic closure of aortic valve
  • systolic anterior movement of mitral valve
56
Q 
Arrhythmogenic right ventricular dysplasia
Ax 
Pathophys
Symptoms [3]
Sign
A
  • AD mutation in genes coding for desmosome components

Patho: right ventricular myocardium replaced with fatty and fibro-fatty tissue

Sy: palpitations, syncope, sudden cardiac death
Late sign is RHF

57
Q

Arrhythmogenic right ventricular dysplasia
Mx
Sequelae

A 
Soltalol
Catheter ablation
ICD
Manage HF
Seq: SCD
58
Q

Cardiac myxoma
Ep
Ax
Pathophys

A

Ep: F>M
Ax: benign cardiac tumour that is usually sporadic but can be familial (Carney complex)
Px: 75% in left atrium, usually attached to fossa ovalis

59
Q

Cardiac myxoma
Symptoms [5]
Signs [5]
Mimics [2]

A

Sy:
- SOB, fatigue, weight loss, palpitations, PUO

Si:
- irregular pulse (AF), finger clubbing, emboli, mid-diastolic murmur and “tumour plop”

mimics IE and mitral stenosis

60
Q

Cardiac myxoma
Investigations
Management

A

Ix:

  • ECG (AF)
  • echo (pedunculated heterogeneous mass attached to fossa ovalis region of interatrial septa)

Mx: surgical excision

61
Q

What is the difference between acute pericarditis, Constrictive Pericarditis and Cardiac Tamponade?

A

Acute pericarditis = Inflammation of the pericardium

Constrictive Pericarditis = Fibrosing of the pericardium leading to the heart being encased in a rigid sac

Cardiac Tamponade = Increase in pericardial fluid -> Increase in intrapericardial pressure -> Lower ventricle filling and reduced Cardiac Output

62
Q

What causes acute pericarditis? [4]
List 2 types of infective causes
List 3 auto-immune causes of pericarditis

A

MI
Neoplastic
Radiation
Myxoedema
Infective
- Viral
- Bacterial eg TB
Autoimmune
- RA, SLE
- Scleroderma
- Dressler’s syndrome

63
Q

How does acute pericarditis present? [4]

A

Central Chest Pain [1] eased by leaning forward [1]
Pericardial Rub
~ Fever

64
Q

Acute pericarditis investigations [5]

When do we decide to admit?

A
  • ECG - Saddle shaped (concave) ST elevation
  • CXR - May show a pericardial effusion (follow with ECHO)
  • Bloods - FBC, ESR, U+E, Cardiac enzymes e.g. troponin
  • Blood cultures & Viral Serology

the majority of patients can be managed as outpatients
patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient

65
Q

How do we treat acute pericarditis? [2]

A
  • strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers
  • a combination of NSAIDs and colchicine for idiopathic or viral pericarditis
66
Q

What causes constrictive pericarditis? [3]

A

Often unkown - TB - Post-pericarditis

67
Q

How does constrictive pericarditis present?
Symptoms [3]
Signs [3]

A 
Fatigue
 - Dyspnoea 
- weakness 
- Peripheral Oedema (symptoms of RHF)
Raised JVP on inspiration (Kussmaul's signs) 
- Ascites (abdominal swelling) 
- quiet heart sounds
68
Q

How do we test for constrictive pericarditis? [4]

A

ECG - low voltage complexes
CXR = May see small heart and calcification
CT/MRI - IF CXR unclear
ECHO
Cardiac Catheterization

69
Q

How do we treat constrictive pericarditis? [1]

A

Surgical Excision

70
Q

What causes cardiac tamponade? [3]

A

Any pericarditis
Aortic Dissection
Warfarin

71
Q

How does cardiac tamponade present?
Symptoms [4]
Signs [3]

A

Cardiogenic Shock:

  • Dizziness
  • Weakness/collapse
  • Dyspnoea, Cough
  • Central Chest Pain
Becks Triad: 
- muffled Heart Sounds
- Raised JVP 
- drop in BP, increase HR
Pulsus paradoxus
Kussmaul breathing
72
Q

How do we diagnose Cardiac Tamponade? [4]

Describe what you might see that would confirm the diagnosis

A

CXR: Over 250ml will show a big globular heart
ECG: Low voltage QRS complexes, QRS alternans
ECHO: Larger pericardium +/- collapsed ventricles (mainly right heart in diastole)
Aspirate some fluid and send for M,C & S

73
Q

How do we treat Cardiac Tamponade? [4]

A

Treat the cause
URGENT drainage of the fluid (pericardiocentesis
Percutaneous balloon pericardiotomy
Pericardial resection

74
Q

Restrictive cardiomyopathy

A
  • amyloidosis (e.g. secondary to myeloma) - most common cause in UK
  • haemochromatosis
  • post-radiation fibrosis
  • Loffler’s syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrate
  • endocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young children
  • sarcoidosis
  • scleroderma
75
Q

What features suggest restrictive cardiomyopathy rather than constrictive pericarditis

A
  • prominent apical pulse
  • absence of pericardial calcification on CXR
  • the heart may be enlarged
  • ECG abnormalities e.g. bundle branch block, Q waves

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