Cardio - Miscellaneous Flashcards

1
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM)

A
  • autosomal dominant disorder of muscle tissue caused by defects in the genes encoding sarcomere
  • often asymptomatic
  • exertional dyspnoea
  • angina and syncope (typically following exercise)
    due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
  • sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
  • ejection systolic murmur +/- systolic thrill at LLSE
  • AF commonly seen
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2
Q

HOCM - investigations

A

Echo findings

  • mitral regurgitation
  • systolic anterior motion of the anterior mitral valve leaflet
  • asymmetric hypertrophy

ECG

  • left ventricular hypertrophy
  • non-specific ST segment and T-wave abnormalities
  • progressive T wave inversion may be seen
  • deep Q waves
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3
Q

HOCM - management

A

Management - ABCDE

  • Amiodarone
  • Beta-blockers or verapamil for symptoms
  • Cardioverter defibrillator
  • Dual chamber pacemaker
  • Endocarditis prophylaxis*

Drugs to avoid

  • nitrates
  • ACE-inhibitors
  • inotropes
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4
Q

Dilated Cardiomyopathy

A
  • most common form of cardiomyopathy (90%)

Classic causes include

  • alcohol
  • Coxsackie B virus
  • wet beri beri (thiamine deficiency with cardiovascular involvement)
  • doxorubicin (chemotherapy agent)
  • dilated heart leading to systolic dysfunction
  • left ventricle more so than right ventricle
  • eccentric hypertrophy (sarcomeres added in series)

Features

  • classic findings of heart failure
  • systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
  • S3
  • ‘balloon’ appearance of the heart on CXR
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5
Q

Restrictive cardiomyopathy

A

Classic causes include
amyloidosis
post-radiotherapy
Loeffler’s endocarditis

  • the walls of the heart are stiff but not thickened, causing diastolic HF
  • decreased exercise tolerance, fatigue, jugular venous distention, peripheral edema, and ascites. Arrhythmias and conduction blocks are common.
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6
Q

Other causes of dilated and restrictive cardiomyopathy

A

“mixed” - many patients will have a genetic predisposition to cardiomyopathy which is then triggered by the secondary process, hence the ‘mixed’ dilated and restrictive category
(there’s a lot of overlap so this classification is not as widely used now)

Causes

  • idiopathic: the most common cause
  • myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas
  • ischaemic heart disease
  • peripartum
  • amyloidosis
  • hypertension
  • drugs, alcohol
  • inherited (familial or syndromic)
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7
Q

Abdominal Aortic Aneurysm (AAA)

A
  • True aneurysm = all 3 layers of the arterial wall are involved; False aneurysm = only a single layer of fibrous tissue forms the aneurysm wall.
  • commonest in elderly men - UK is introducing the aneurysm screening program = abdominal aortic ultrasound in all men aged 65 years
  • RF: HTN, diabetes, smokers, connective tissue diseases (e.g. marfan’s)
  • Most AAA are an incidental finding.
  • Symptoms most often relate to rupture or impending rupture (The risk is related to aneurysm size) - abdominal, back, and groin pain are typical
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8
Q

AAA - investigations

A
  • Ultrasound remains the definitive test for initial diagnosis and screening
    (all men get offered on at age 65)
    Aorta width < 3 = normal
    Aorta width 3 - 4.4 cm (small aneurysm) - rescan in 12 months
    Aorta width 4.5 - 5.4 (medium aneurysm) - rescan in 3 months
    Aorta width 5.5 or more (large aneurysm) - refer to vascular surgery within 2 weeks
  • most vascular surgeons will subject patients with an aneurysm size of 5cm or greater to CT scanning of the chest, abdomen and pelvis with the aim of delineating anatomy and planning treatment

Indications for surgery

  • aneurysm is between 5.5cm and 6cm.
  • symptomatic aneurysm
  • rupture
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9
Q

AAA - management

A

Low risk –> conservative, US monitoring
High risk –> refer for probable intervention

  • Abdominal aortic aneurysm repair: aneurysm dissected and aorta clamped –> longitudinal aortotomy –> atherectomy –> graft insertion –> suture, clamps off
  • Post operatively: ITU (Almost all)
    (Increasingly patients are now being offered endovascular aortic aneurysm repair.)

Complications:

  • Embolic- gut and foot infarcts
  • Cardiac - re-perfusion injury, effects of cross clamp
  • Wound problems
  • graft infection and aorto-enteric fistula
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10
Q

Aortic Dissection - features

A
  • tear in the tunica intima of the wall of the aorta
  • RF: HTN, trauma, bicuspic aortic valve, marfan’s
  • chest pain: typically severe, radiates through to the back and ‘tearing’ in nature
    (anterior chest pain- ascending aorta, back pain - descending aorta)
  • aortic regurgitation, SOB, pulse deficit (in different arms), radio-radial delay

Stanford classification
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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11
Q

Aortic Dissection - investigations

A
  • CXR: change in morphology, mediastinal widening, intimal calcification
  • CT angiography with contrast
  • CT chest
  • Echo (transoesophageal): shows the false lumen
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12
Q

Aortic Dissection - management

A
Type A
surgical management (open or endovascular aortic repair), but BP should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B

  • conservative management: bed rest, opioids
  • reduce BP: IV labetalol to prevent progression

Complications of backward tear

  • aortic incompetence/regurgitation
  • MI: inferior pattern often seen due to right coronary involvement

Complications of forward tear

  • unequal arm pulses and BP
  • stroke
  • renal failure
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13
Q

Acute Pericarditis

A
  • causes: viral infections (Coxsackie), TB, uraemia (causes ‘fibrinous’ pericarditis), post-MI (Dressler’s syndrome), connective tissue disease, hypothyroidism

Features

  • chest pain: may be pleuritic. Is often relieved by sitting forwards
  • other symptoms include non-productive cough, dyspnoea and flu-like symptoms (viral prodrome)
  • O/E: pericardial rub, tachypnoea, tachycardia
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14
Q

Acute Pericarditis - Ix and Management

A

Investigations

  • ECG changes: global/widespread, ‘saddle-shaped’ ST elevation; PR depression: most specific ECG marker for pericarditis
  • all patients with suspected acute pericarditis should have transthoracic echocardiography

Management

  • treat the underlying cause
  • a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
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15
Q

Constrictive Pericarditis

A
  • causes: any cause of pericarditis, particularly TB

Features

  • dyspnoea
  • right heart failure: elevated JVP, ascites, oedema, hepatomegaly
  • pericardial knock - loud S3
  • Kussmaul’s sign is positive

CXR
pericardial calcification

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16
Q

Cardiac Tamponade

A

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

Classical features - Beck’s triad:

  1. hypotension
  2. raised JVP
  3. muffled heart sounds

Other features:

  • dyspnoea, tachycardia
  • pulsus paradoxus - an abnormally large drop in BP during inspiration
  • Kussmaul’s sign - much debate about this
  • ECG: electrical alternans

Management: urgent pericardiocentesis

17
Q

Brugada Syndrome

A
  • inherited autosomal dominant cardiovascular disease which may present with sudden cardiac death
  • more common in Asians
  • 20-40% mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

ECG

  • convex ST elevation (V1-V3) + a negative T wave
  • partial RBBB
  • the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases

Managment: implantable cardioverter-defibrillator

18
Q

Acute Chest Pain - differentials

A
  • ACS
  • PE
  • penumothorax
  • aortic dissection
  • Pericarditis
  • GORD
  • MSK chest pain: often worse on movement/palpation; May be precipitated by trauma or coughing.
  • Perforated peptic ulcer
  • Boerhaaves syndrome: oesophageal rupture as a result of repeated episodes of vomiting.
19
Q

IE - causes

A
  • strongest risk factor is a previous episode of IE
  • 50% have previously normal valves - the mitral valve is most commonly affected
  • 30% associated with rheumatic valve disease

Other groups:

  • prosthetic valves, indwelling vascular catheters
  • congenital heart defects
  • intravenous drug users

Pathogens

  • Streptococcus viridans most common in developing countries
  • Staphylococcus aureus most common overall. Also particularly common in acute presentation and IVDUs
  • Staphylococcus epidermidis commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery
  • Streptococcus bovis a/w colorectal cancer
20
Q

IE - features

A

(Based on Modified Duke Criteria)

Pathological criteria: Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (e.g. valve tissue)

Major Criteria: 2 positive blood cultures, positive echo or new valve regurgitation

Minor Criteria

  • predisposing heart condition or IVDU
  • fever > 38ºC
  • vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  • Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots

(diagnosis with 1 isolated pathological or 2 majors, 1 major + 3 minor, or 5 minor)

21
Q

IE - management

A

Abx:

  • initial –> amoxicillin +/- gentamicin
  • prosthetic valve –> vancomycin +/- gentamicin
  • Staph –> flucloxacillin
  • Strep viridans –> Benzylpenicillin

Indications for surgery

  • severe valvular incompetence
  • aortic abscess (often indicated by a lengthening PR interval)
  • infections resistant to antibiotics/fungal infections
  • cardiac failure refractory to medical treatment
  • recurrent emboli after antibiotic therapy
22
Q

Thrombophilias

A
  • Factor V Leiden
  • Prothrombin gene mutation
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin III deficiency
    *

Acquired:

  • antiphospholipid syndrome
  • COCP use
  • Clinical relevance: Consider doing a thrombophilia screen in cases of PE aged <40 years, recurrent VTE or a positive family history