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Heart valve disease
https://t.me/med1917
Causes
Pathogenesis Example
Congenital Abnormal valve formation
Slow degeneration over time Mitral valve prolapse
Degenerative
Infective
Cardiac remodelling Causes dilated valve rings Functional: mitral regurgitation
Calcification (with age) Aortic stenosis
Post-MI ischaemia / papillary muscle rupture Mitral regurgitation
Direct infection Bacterial endocarditis
Immune-mediated damage Rheumatic fever (rare)
Bicuspid aortic valve → aortic stenosis or regurgitation
Pathological: connective tissue disease
Chapter 1: Cardiology 5
Investigations of valve disease
1. Hx & examination: murmurs, signs of HF, AF
2. ECG: AF, ventricular hypertrophy (large R wave), atrial hypertrophy (bifid P wave)
3. CXR: size of heart & vessels, calcification, pulmonary oedema
4. Echo: dimensions of chambers, valve morphology, LV function, wall defects
5. Doppler: shows regurgitation (measures pressure gradient across valve)
Medical management of valve disease
1. Slow rate of structural remodelling/deterioration: ACEis (for mitral
regurgitation)
2. Symptom control: diuretics (if heart failure), beta-blockers & anticoagulation
(if AF/palpitations)
3. Periodic surveillance: if non-severe aortic stenosis (with echo)
3
Tricuspid/pulmonary disease = RARE
Causes: IVDU, rheumatic fever
General principles of management:
1. Mild disease: no treatment
2. Moderate disease: medical Tx (surgical if
having concomitant cardiac surgery)
3. Severe disease: surgical repair/replacement
(TAVI/TAVR)
Mitral valve disease
Mitral stenosis Mitral regurgitation
Causes Rheumatic fever (rare in Western countries) Degenerative (MVP), endocarditis, LV remodelling/dilation,
Papillary dysfunction (MI)
Pathogenesis LA can’t empty = pulmonary HTN
→ can result in secondary RHF
Symptoms Asymptomatic if mild
→ Dyspnoea & haemoptysis (pulmonary HTN)
→ Fatigue, weakness, peripheral oedema (RHF)
→ Palpitations (RA hypertrophy)
Signs
Treatment 1. Percutaneous mitral balloon commissurotomy
→ Malar flush
→ Irregular pulse / AF
→ JVP
MID-DIASTOLIC MURMUR
2. Surgery: replacement
(loud S1 ‘opening SNAP’)
LV can’t fill = blood in LA & pulmonary HTN
Results in CO so LV works harder = LV dilation
Asymptomatic for a long time
→ Dyspnoea & orthopnoea (pulmonary HTN)
→ Fatigue, weakness ( CO)
→ Palpitations (AF)
→ Irregular pulse / AF
→ Laterally displaced apex (LV hypertrophy)
PANSYSTOLIC MURMUR
1. Surgical repair or replacement
(repair > replacement if favourable anatomy)
(soft H1)
SURGICAL OPTIONS FOR MITRAL VALVE DISEASE3:
1. Percutaneous mitral balloon commissurotomy (PMC)/valvuloplasty
→ 1st line in mitral stenosis if no contraindications
2. Mitral valve repair: repair leaflets & insert supportive ring & new chordae
→ Preferred to replacement if possible
3
2021 ESC/EACTS Guidelines for the management of valvular heart disease; Eur. Heart J. 43:561.
Contraindications for PMC:
• Only mild MS (mitral valve area >1.5cm2)
• LA thrombus
• Moderate/severe mitral regurgitation
• Severe calcification
• Severe aortic valve disease needing surgery
Medicine
6 Chapter 1: Cardiology
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3. Mitral valve replacement: mechanical or biological
→ Mechanical mitral valves at HIGHER RISK OF THROMBOSIS than mechanical
aortic valves
→ Mechanical mitral valves are potentially MORE DURABLE than bioprosthetic
valves
Aortic valve disease
Aortic stenosis Aortic regurgitation
Causes CALCIFICATION (common), congenital bicuspid valve Endocarditis, syphilis, rheumatic fever, CTD
Pathogenesis LV can’t empty = LV hypertrophy
Results in LHF, angina & arrhythmia
Symptoms
Signs
Treatment Aortic valve replacement (TAVR/TAVI)
→ Syncope
→ Angina + Arrhythmia
→ Dyspnoea (exertional)
→ Slow rising pulse
→ Narrow pulse pressure
EJECTION SYSTOLIC MURMUR
+ Soft S2 (AV closure)
+ Systolic thrill
→ If symptomatic + severe stenosis on echo
→ If asymptomatic & severe stenosis
(radiates to neck)
blood in LV & CO
Results in LV dilation
Asymptomatic for a long time
→ Angina
→ Dyspnoea
→ Collapsing pulse
→ Wide pulse pressure
→ Quincke’s sign: nailbed pulsation
→ De Musset’s sign: head bobbing
EARLY DIASTOLIC MURMUR
Surgical valve replacement
→ If significantly enlarged aorta
→ If severe regurgitation + LVEF <55%
Those with heart valve disease often have concurrent
IHD which should be treated AT SAME TIME AS
VALVE OPERATION
DOACs contraindicated in mechanical
heart valves
Cardiac catheterisation/angiography
Procedure:
1. For imaging of coronary arteries:
Catheter through right radial/femoral artery → contrast medium injected → X-ray series taken
2. For assessment of right heart & pulmonary artery pressures:
Catheter through femoral vein
Risks: bleeding, bruising, allergy to contrast medium, pericardial effusion/tamponade, death (very rare)
Indications:
1. Diagnosis: CAD, valve disease, cardiomyopathy, congenital heart disease, pulmonary HTN
2. Treating conditions with a transcatheter approach: PCI*, TAVI, closure of PFO/ASD, some cases of mitral regurgitation (using Mitraclip)
SURGICAL OPTIONS FOR AORTIC VALVE DISEASE3:
1. Surgical aortic valve replacement: via sternotomy (usual option for severe
aortic stenosis/regurgitation)
→ if younger, fit, healthy patient or need cardiac surgery for concurrent coronary
artery disease
2. Transcatheter aortic valve replacement/implantation (TAVR/TAVI):
→ catheter through femoral artery (transfemoral) or apex of heart (transapical)
→ balloon dilation to deploy valve
→ if older/frailer (contraindications for open heart surgery)
Mechanical vs. biological valves
→ Mechanical require lifelong anticoagulation: WARFARIN (INR 2.5–3.5)
→ Biological: increasing durability to 10–15y & only need anticoagulation for 3m
(unless needed for comorbidity like AF)
*Percutaneous coronary intervention (PCI) = using catheter + balloon & stents to open a blocked/narrow vessel
Medicine
Infective endocarditis
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Infection of endocardial heart surface (especially heart valves)
Chapter 1: Cardiology 7
Pathophysiology
→ Damaged endocardium allows bacterial adhesion
→ Become encased in fibrin mesh → protected while multiply
→ Form vegetations that damage valves & chordae
Risk factors
1. Abnormal structure + commensal organisms
• prosthetic valve, valve disease, congenital defect
• commensals (skin/GI tract) enter circulation to reach valves (e.g. following
dental treatment)
• more insidious onset
2. Normal structure + pathogenic organisms
• IVDU, open heart surgery, septicaemia
• pathogenic organisms can infect normal valves
• acute, fulminating onset
Clinical presentation
Murmur & Microscopic haematuria
M
A Anaemia
J Janeway lesions (spots on palms)
O Osler’s nodes (nodules on fingers)
R Roth spots (eyes)
P Pyrexia
E Emboli
N
Nail splinter haemorrhages
ANTIBIOTIC PROPHYLAXIS NO LONGER
ROUTINELY GIVEN when undergoing
invasive procedures or dental work.
Check with cardiologist for individual patients at
high risk.
→ febrile illness + new murmur
Causative organisms: (rarely fungi)
• Strep. viridans (in dental/URT disease)
• Staph. aureus (IVDU)
• Strep. epidermis (in prosthetic valves)
• Enterococci
• Strep. bovis (in bowel pathology)
• Candida (immunosuppressed)
Common valves affected
→ usually LHS (mitral > aortic)
→ tricuspid valve in IVDU
Complications:
1. Systemic emboli: brain/kidneys
2. Valvular incompetence & CCF
3. Glomerulonephritis: immune complexes
deposit in kidneys
Investigations
1. Hx & examination: for risk factors, fever, new murmur
2. Bedside tests: urine dip & ECG (haematuria, MI due to emboli)
3. Routine bloods: FBC, CRP/ESR, U&Es (infection, anaemia)
4. Triple blood cultures: from 3 different sites → before ABX
5. Transthoracic (TTE) & transoesophageal echo (TOE) → diagnostic
6. Other imaging: CXR & CT (signs of HF/emboli)
Diagnosis
Major criteria
• +ve blood culture of typical organism
at 2 separate sites
• Echo shows endocardial involvement
Minor criteria
• Predisposing risk factors (prosthetic valve, IVDU)
• Fever >38°C
• Vascular phenomena (Janeway lesions/emboli)
• Immunological phenomena
(glomerulonephritis/Osler’s)
• +ve blood culture not meeting major criteria
Duke’s criteria
Diagnosis made if:
→ 2 major OR
→ 1 major + 3 minor OR
→ 5 minor
TTE first, then TOE if:
1. High clinical suspicion
2. Positive findings on TTE
3. Poor image quality
4. Suspected aortic root abscess
Management
MANAGEMENT: microbiology advice
1. IV ABX: 6 weeks
→ Should respond in 48h ( fever & CRP/ESR)
• usually penicillin-based (± gentamicin)
• teicoplanin, vancomycin if prosthetic valves
2. Surgery if:
• persistent bacteraemia after 72h ABX
• heart failure results
• valvular obstruction / unstable valve
• conduction disturbance
• repeated emboli
4
4
2015 ESC Guidelines for the management of infective endocarditis; Eur. Heart J. 36:3075
Medicine
8 Chapter 1: Cardiology
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Congestive cardiac failure
Abnormality of structure or function causing inadequate pumping
Pathophysiology
Compensatory changes occur to maintain CO & BP → leads to hypertrophy &
dilation → cardiac failure
1. Activated SNS: TPR & HR (vasoconstriction increases afterload)
2. Activated RAAS: TPR & fluid retention (increases preload & afterload)
3. ADH secretion: fluid retention (increases preload)
Causes of heart failure
Systolic HF
insufficient pumping function
Ejection fraction EF <40% EF >50%
Causes
1. IHD (CAD → MI → LV dysfunction)
2. Myocarditis → dilated cardiomyopathy
3. Cor pulmonale / COPD = RH failure
Diastolic HF
poor filling due to compliance / impaired relaxation
(HF with preserved EF → HFpEF)
1. Chronic hypertension
2. Restrictive/hypertrophic cardiomyopathy
3. Fibrosis/amyloidosis/sarcoidosis
Symptoms
Right-sided failure
= systemic congestion
Symptoms • Dyspnoea & fatigue
• Peripheral oedema & ascites
• Hepatomegaly
Signs
Common signs Cyanosis, decreased BP, narrow pulse pressure, displaced apex, RV heave
New York Heart Association classification of HF
Class I: no limitation of activity (no dyspnoea/fatigue)
Class II: slight limitation (dyspnoea/fatigue on
moderate activity)
Class III: marked limitation (only comfortable at rest)
Class IV: symptoms at rest
Goals of treatment:
1. Treat any underlying cause e.g. IHD
2. Cardiac workload (afterload)
3. Cardiac output (stroke volume)
4. Counteract maladaptation
5. Symptom relief
Ramipril Bisoprolol
1st line: ACEi + BB (ARB if ACEi not tolerated)
2nd line: spironolactone + nitrate
3rd line: digoxin (resynchronisation if wide QRS)
Medicine
• JVP, hepatomegaly, ascites
• Pitting oedema & face engorged
• Pleural effusions
Cardiac cachexia: metabolic demands + appetite
Left-sided failure
= pulmonary congestion
• Fatigue & reduced exercise tolerance
• Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
• Nocturnal cough = pink, frothy sputum
• Cardiomegaly: displaced apex
• Tachycardia: 3rd heart sound, gallop rhythm
• Pulmonary oedema: bibasal crackles
Investigations
1. Careful Hx & examination
2. Bloods: FBC, U&Es, LFT, TFT
3. BNP: strong –ve predictive value (ifnormal = unlikely HF)
4. ECG: may show cause e.g. ischaemia, arrhythmia, HTN
5. CXR: cardiomegaly, pulmonary oedema
6. Echo: show structure abnormalities & measure EF → only if ECG/BNP is abnormal
→ Possible further tests: cardiac MRI, cardiac catheterisation, stress echo
Management
ACUTE HEART FAILURE = emergency (due to pulmonary oedema)
• ABCDE: sit patient upright, high flow O2, IV diuretics (furosemide)
• Consider IV nitrates if no improvement (caution if SBP <100 / aortic stenosis)
• Consider CPAP & inotropes if needed
CHRONIC HEART FAILURE
1. Lifestyle: smoking cessation, alcohol & salt reduction,
exercise, BMI optimisation
2. Symptom relief: diuretics (furosemide)* & med R/V (NSAIDs)
3. Counteract maladaptation: medications (renal monitoring)
4. Consider IHD risk: statin + aspirin 75mg if high
5
NICE (2018) Chronic heart failure in adults [NG106]
4. Constrictive pericarditis
5. Haemochromatosis
6. Aging
Usually LHS & RHS HF
occur simultaneously
so there is
symptoms
falsely low BNP if on ACEi, BB, diuretic
5
do not prescribe RL CCB in HF
overlap of
*daily weights if
inpatient
Acute pulmonary oedema
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Increased fluid in pulmonary interstitium
Causes
• LEFT VENTRICULAR FAILURE: post-MI or IHD (most common cause)
• Other cardiac causes: valve disease, arrhythmias, hypertension
• Acute respiratory distress: trauma, drugs, malaria
• Fluid overload
• Neurogenic: head injury
Clinical presentation
• Dyspnoea, orthopnoea, PND (sat up, leaning forward)
• Productive cough with pink, frothy sputum
• Distressed, pale, sweaty
Clinical signs
Chapter 1: Cardiology 9
Differentials:
∙ Asthma/COPD
∙ Pneumonia
∙ Pneumothorax
∙ Interstitial lung disease
• HR, RR, JVP
• Gallop rhythm (3rd heart sound)
• Fine crackles ± wheeze
Investigations
1. Careful Hx & examination
2. Bedside: ECG (tachycardia, LVH, arrhythmias)
3. Bloods: FBC, U&Es, CRP, glucose, troponin, ABG*
4. Imaging: CXR ± echo (clarify cause e.g. valve disease / MI)
Management
EMERGENCY → begin treatment before investigations
As for acute heart failure (see above)
• ABCDE: sit patient upright, high flow O2 (if hypoxia)
• IV diuretics (furosemide / loop diuretic = 1st line)
• GTN spray x2 puffs (caution if SBP <90)
• Consider IV nitrates if no improvement (caution if SBP <100 / aortic stenosis)
• Consider CPAP & inotropes if needed
6
Features on CXR
*Initially T1RF (hyperventilation) then T2RF
(impaired gas exchange)
Monitor:
∙ BP, pulse
∙ O2 sats, ABG, RR
∙ JVP
∙ Urine output
∙ ECG
• Batwing oedema
• Kerley B & septal lines = thickened fissures
• Upper vessel engorgement (cephalisation)
• Cardiomegaly
• Fluid in costophrenic angles (small pulmonary effusions)
6
BMJ Best Practice (2021, updated 2022) Acute heart failure
Cardiomegaly
Fig. 1.3 Pulmonary oedema CXR.
Medicine
10 Chapter 1: Cardiology
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Syncope
RED FLAGS in red suggest possible
life-threatening cause
PATHOPHYSIOLOGY: transient reduction in cerebral blood flow
CARDIAC NEURALLY-MEDIATED ORTHOSTATIC
• Elderly: sinoatrial disease,
AV nodal disease / heart
block
• Young: long QT syndrome,
Brugada syndrome
• Structural heart disease
e.g. HCM causing ventricular
arrhythmias
Symptoms: occurs on
exertion, palpitations, SOB,
chest pain
Sudden, transient loss of consciousness with spontaneous & rapid resolution
• Vasovagal
• Situational (cough,
micturition, defecation)
• Carotid sinus syndrome
(CSS)
Symptoms: light-headedness,
nausea, pallor, sweating, visual
disturbance
Provoked by: hot environment,
pain, emotion, prolonged
standing, pressure on carotid
baroreceptors (CSS)
• Autonomic failure
• Volume depletion
Symptoms: occurs on
standing, dizziness, weakness,
tachycardia, preceding
melaena/haematemesis
Causative drugs:
antihypertensives, diuretics,
vasodilators
Postural drop on LSBP:
SBP drop of ≥20
or DBP drop ≥10
Red flag differentials:
• Myocardial ischaemia
• Arrhythmias
• Aortic dissection
• Occult haemorrhage
• Severe hypoglycaemia
• Massive PE
• Subarachnoid haemorrhage
Investigations
• Thorough history – preceding symptoms, DHx, PMHx, FHX + RED FLAGS
• Physical examination – including lying & standing blood pressure (LSBP), HR, RR
• 12-lead ECG – check for arrhythmias / hear t block / ischaemia
• Bloods – Hb (anaemia), U&Es, troponin, glucose, d-dimer
• CT head – if any concern of head injury / stroke / TIA
• Ambulatory ECG recording (7d)
7
Management
CARDIAC SYNCOPE
• ILR (implantable loop recorder) – placed substernal subcutaneous, under local
anaesthetic
• ICD / pacemaker implant
• Anti-arrhythmic therapy (VT ablation in selected patients)
VASOVAGAL SYNCOPE
1. Patient education: avoid triggers (prolonged standing, warm environments,
etc.)
2. Physical counter-pressure manoeuvres: muscle tensing / leg crossing /
squatting
3. Volume expansion: increase salt & fluid intake (beware may be
contraindicated in some patients)
4. Medication: fludrocortisone, midodrine → only occasionally used
in the elderly
8
Medicine
7
BMJ Best Practice (2021) Assessment of syncope
8
BMJ Best Practice (2021) Neurally mediated reex syncope
Atrial fibrillation
1. Absent P waves 2. Irregular R-R interval 3. Rapid rate
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Rapid, irregular heart rhythm due to uncoordinated contraction of the atria
1. Paroxysmal: recurrent, sudden, self-limiting episodes of palpitations →
sometimes Tx with ‘pill in pocket’ e.g. flecainide
2. Persistent: AF >7 days → needs beta-blocker to rate control & cardioversion
to ‘reset’ rhythm
3. Permanent: long-term AF → RATE CONTROL vs. rhythm control
Causes
• Cardiac: HTN, heart failure, IHD, valve disease
• Respiratory: PE, chest infection, lung cancer
• Systemic: sepsis, thyrotoxicosis, alcohol/caffeine, electrolytes
Investigations*
1. Systems examination:
▶ Irregularly irregular pulse
▶ Signs of underlying disease, e.g. murmur/HF
2. 12-lead ECG: if normal do 24h ambulatory ECG
Fig. 1.4
3. Bloods: 4. CXR/ECHO: investigate cause
▶ FBC, TFTs, U&Es, LFTs, glucose
▶ Alcohol levels (if suspicious)
Management
9
A) RATE & RHYTHM CONTROL
1. Rate control: target HR 60–80 → beta-blocker (or RL CCB if BB contraindicated)
2. Rhythm control: if new onset <48h, reversible cause, HF → flecainide/
amiodarone or DCCV (direct current cardioversion)
Long-term side-effects: hepatotoxic, phototoxic, thyrotoxic, lung fibrosis
Rate control
BB or RL CCB
+ digoxin
BB/flecainide/
amiodarone
Rhythm control
B) STROKE PREVENTION (ANTICOAGULATION)
1. Assess risk with CHA2DS2-VASc score: anticoagulate females if score ≥2
or men if ≥1
→ DOAC (rivaroxaban, apixaban, edoxaban, dabigatran) = more predictable
& ICH risk
→ Warfarin (if mechanical valve/mitral stenosis or low eGFR) = needs close
monitoring
2. Assess bleeding risk with ORBIT* score: ≥3 needs closer anticoag. monitoring
*Consider app on mobile phone, to enable rhythm
recording by patient during symptoms
DO NOT COMBINE BB + RL CCB
* NOT digoxin as monotherapy unless immobile
(often combined with digoxin*)
Cardioversion
or
Selected patients with Sx
Ablation
despite optimal medical Tx
Causes: Mrs SMITH has AF
Sepsis
Mitral valve stenosis
IHD
Thyrotoxicosis
Hypertension
DCCV in HAEMODYNAMICALLY
UNSTABLE (acute HF/chest
pain/hypotension)
Chapter 1: Cardiology 11
Complications
• STROKE • Vascular dementia
• LV function • quality of life
• Peripheral embolism
Symptoms
• SOB • Palpitations
• Syncope • Chest pain
Warfarin: vit K antagonist (reversible)
INR: NSAIDs, cranberry juice, SSRIs, ABX
INR: AEDs, rifampicin, barbiturates, SJW, smoking
NB: warfarin = teratogenic INR aim: 2–3
CHADSVaSc score
C Congestive HF 1
H HTN 1
A2Age >74y 2
Age 65–74y 1
D Diabetes 1
S2Previous stroke/TIA 2
Va Vascular disease 1
Sc Sex category = female 1
5 Predictors of ORBIT score
Age ≥75y 1
eGFR <60 1
Treatment with antiplatelet 1
Bleeding history 2
Hb <130 (females) <140 (males),
haematocrit or Hx of anaemia
*ORBIT score now recommended by NICE over HASBLED score to
calculate bleeding risk for those with AF
Follow-up
• In 1y to check for Sx of AF
• Annual R/V of stroke & bleed risk
Safety-net
• Signs of MI/stroke
(LOC, severe chest pain/SOB, dizzy)
• If HR >150 or SBP <90
Advise may need to inform DVLA (if symptomatic)
2
C) LIFESTYLE
• Weight loss, diet, exercise
• alcohol, caffeine, smoking
9
NICE (2021) Atrial brillation [NG196]
• Optimise RFs: BP, renal function, etc.
For elective electrical cardioversion (not
emergency): ANTICOAGULATE before with LMWH
or 3 weeks other agent
Medicine
12 Chapter 1: Cardiology
Single Double Triple Quadruple
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Miscellaneous cardiac conditions
Coronary artery bypass graft → most common cardiac surgery
Gold standard conduit:
Left internal mammary artery (LIMA) attached to
left anterior descending (LAD)
Can also use other arteries/veins:
• great saphenous vein
• radial artery
• right internal mammary artery
Fig. 1.5 Types of CABG.
INDICATIONS:
Bypass narrowings in coronary arteries if:
• Left main stem stenosis
• Diabetes with multivessel disease
• 2–3 vessel disease & impaired left ventricle
TECHNIQUES:
What to do in a cardiac trauma
→ Ix: echo (for haemopericardium), ECG
± troponin
→ Tx: emergency clamshell thoracotomy
if witnessed cardiac arrest
Complications of cardiac trauma:
• Silent arrhythmias
• Cardiac contusion
• Cardiac wall rupture
1. On pump: arrest heart & use cardiopulmonary bypass machine
2. Off pump: performed on beating heart → careful positioning & stabilisers
Cardiac trauma
TYPES:
1. Blunt trauma: deceleration injuries (e.g. road traffic accident)
2. Penetrating trauma: e.g. anterior stab wound (usually right ventricle
damaged)
Atrial myxoma → most common primary tumour of heart
Causes of constrictive pericarditis:
• TB
• Cardiac surgery
• Post-MI (rare)
Causes of acute pericarditis:
• Post-MI (Dressler’s)
• Viral infection / TB
• Hypothyroidism
• CTD
• Trauma
Pain on inspiration & relief sitting forward
SYMPTOMS: secondary to mass
→ Intermittent syncope
→ SOB
→ Fever, malaise, cachexia
MANAGEMENT: surgical resection
→ Minimally invasive right
thoracotomy
affects women aged 30–40y
LOCATION: 80% in left atrium → may hear ‘succession splash’ as ‘plops’
in & out of ventricle
Constrictive pericarditis → chronic pericarditis causes thick & fibrous
pericardium & constriction
SYMPTOMS:
→ Progressive dyspnoea
→ Fatigue/weakness
→ Peripheral oedema
→ Pleural effusions
MANAGEMENT: pericardiectomy
→ Surgical resection of pericardium
between the 2 phrenic nerves
→ Usually via sternotomy incision
Acute pericarditis → acute inflammation of the pericardium
SYMPTOMS:
→ Pleuritic chest pain
→ Pericardial rub + tachypnoea +
tachycardia
± non-productive cough, SOB, flu Sx
INVESTIGATIONS:
1. ECG = saddle ST elevation globally
2. Bloods
3. Transthoracic echo to r/o myocarditis
MANAGEMENT: NSAID + colchicine
Medicine
Myocarditis → group of disorders causing non-ischaemic inflammation of
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the myocardium
Chapter 1: Cardiology 13
SYMPTOMS: commonly preceded by viral illness
• Fatigue
• Dyspnoea
• Chest pain (in 35%)
• Palpitations/arrhythmia
• Congestive heart failure:
▶ orthopnoea, JVP, HR
INVESTIGATIONS:
• 12-lead ECG – non-specific ST/T wave abnormalities
• CXR – may show pulmonary oedema if CHF
• CK-MB, troponin – elevated
• B-type natriuretic peptide – elevated
• Echo – global motion abnormalities
• Endomyocardial biopsy – inflammatory infiltrate
COMPLICATIONS:
• Arrhythmias
• Dilated cardiomyopathy
• Fulminant heart failure
• Cardiogenic shock / sudden cardiac death
MANAGEMENT10:
Haemodynamically stable:
• supportive care + treat underlying cause
Haemodynamically stable + evidence of LHF:
• ACEi + beta-blocker ± diuretic ± nitrate + treat underlying cause
Haemodynamically unstable:
• IV arterial vasodilator + invasive haemodynamic monitoring ± inotrope
+ Anticoagulation if arrhythmia or
evidence of LV thrombus
Differentials:
• ACS
• Pericarditis
Risk factors:
• HIV
• autoimmune disease
• drugs (anti-epileptics, penicillins, digoxin,
lithium, heavy metals)
• smallpox vaccine
• preceding viral illness
• peripartum/postnatal
Other causes of dilated cardiomyopathy:
Idiopathic, genetic, drugs, stress (takotsubo),
post-viral
Specific Tx of underlying causes:
Autoimmune/hypersensitivity: steroids
Giant cell myocarditis: steroids + other
immunosuppressant
Avoid NSAIDs & alcohol if history of myocarditis
Pulmonary hypertension → proliferation and remodelling of the small
pulmonary arteries causing increased pulmonary vascular resistance (PVR)
SYMPTOMS:
• Fatigue
• Dyspnoea
• Peripheral oedema
SIGNS:
• Loud 2nd heart sound
• Tricuspid regurgitation murmur
• Cyanosis
INVESTIGATIONS:
• CXR – enlarged main pulmonary artery & hilar vessels
• ECG – RV hypertrophy (tall R wave, small S wave in V1)
• Transthoracic Doppler echo – estimates pulmonary artery pressure
• Right heart catheterisation – measures mean pulmonary arterial pressure
• Nocturnal oximetry – >70% patients desaturate during sleep
• 6-minute walk test – estimate of disease severity
10
BMJ Best Practice (2021) Myocarditis
Complications of pulmonary hypertension:
∙ RV failure ∙ Tachyarrhythmias
Diagnosis if mean pulmonary arterial
pressure >25mmHg at rest
Medicine
14 Chapter 1: Cardiology
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CAUSES:
Cause of pulmonary hypertension Specific investigations
Idiopathic Diagnosis of exclusion
Lung disease e.g. COPD, ILD, OSA ABG, PFTs, high resolution CT
Chronic embolic/thrombotic disease V/Q scan, CTPA
Connective tissue disease e.g. scleroderma, SLE, RA ANA, anti-centromere antibodies, rheumatoid factor
Cardiac shunts e.g. atrial/ventricular septal defect Transoesophageal Doppler, echo
Portal hypertension in liver disease LFTs, abdo USS
→ Refer to pulmonary hypertension centre
for consideration of secondary pulmonary
vasodilator therapies
MANAGEMENT
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: management of underlying cause if present
1. General supportive therapy: supervised exercise training, reduced sodium
intake plus oral anticoagulants (warfarin)
± diuretics if fluid overload
± oxygen if hypoxic
± digoxin if supraventricular
arrhythmias
2. Calcium channel blockers: in idiopathic pulmonary hypertension
→ 2nd line options: prostanoids, endothelin receptor antagonists (bosentan),
phosphodiesterase inhibitors (sildenafil)
Medicine
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BMJ Best Practice (2021) Idiopathic arterial hypertension
Соседние файлы в папке Библиотека им академика М.И. Перельмана