JC M WCS 5

JC M WCS 5

FEVER & HEART MURMUR
Prof. Chu-Pak Lau

Cardiology

Fri 25-09-02
VALVULAR HEART DISEASE

PATHOPHYSIOLOGY

Valvular Stenosis - hypertrophy and mitral dilatation occurs as the chamber fails (no apex displacement)
Valvular regurgitation - chamber dilatation (early downward + lateral displacement of apex)

SYMPTOMS

Left heart failure - progressive exertional dyspnoea (quantitative assessment - NY)
Right heart failure

Ankle oedema

Hepatic pain - late cirrhosis + ascites

Chest pain – myocardial ischaemia ( demand, obstructed arterial flow)

Palpitations – commonly atrial fibrillation

Low output – easy fatigability

Complications

Thromboembolism (in atrial fib)

Preg problems ( IV volume ® fluid o'load ® heart failure complicating preg)

INVESTIGATIONS

ECG - chamber enlargement, rhythm (atrial fib?)
CXR - size of heart, pulmonary venous congestion
Echocardiogram (US) - (1) Valvular architecture (2) Chamber size and function
Doppler - assess valvular gradient - frequency shift of RBC as crossing valve (bet LV and aorta)
Cardiac catheterisation (rarely needed due to ECHO + Doppler)

Associated coronary artery disease
Pressure gradient - eg. aortic stenosis
Inject contrast to assess regurgitant lesion (view regurgitant jet)

TREATMENT

Mechanical problem = mechanical solution
Surgical if symptomatic

Valvular replacement
Valvuloplasty - valve mod - eg. mitral regurgitation
Valvotomy - expand valve - eg. mitral stenosis

Non-surg - anti-coagulationTx (heart failure, atrial fib)

Note: RF Jones Criteria

High probability of acute RF if 2 major or one major/ one minor present (if supported by evidence of Group A Strep infection)
Major manifestation

Carditis
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules

Minor manifestation

Clinical: Previous RF or RHD, Arthralgia, Fever

Laboratory: Acute phase reactants - ESR, C-reactive protein, leukocytosis, Prolonged P-R interval

Supporting evidence of streptococcal infection

Titre of anti-streptococcal Ab (ASO) (anti-streptolysin O), others

+ve Throat culture for Group A Streptococcus

Recent scarlet fever

Hx of RF in mitral stenosis/ regurgitation common
eg 1. Mitral stenosis

Haemodynamics

Obstruction to LV inflow

LA pressure (blood stored in LA)

Pulmonary venous pressure ® upper lobe venous diversion (reflex constriction of lower venules show on CXR) ® thickness pulmonary vascular beds ® pulmonary arterial hypertension ( arterial pressure transmitted to R side)

Right heart failure - sequelae

Clinical features

Respiratory symptoms

SOB on exertion - pressure, limit ADL, slowly progressive

PND

Frequent chest infection - pressure inside lung

Haemoptysis

Ruptured venule of pressure (eg. bronchial communicating venule)

Pulmonary oedema (frothy pink sputum)

DVT + pulmonary embolism

Chronic RV failure - Congestive cardiac failure

Ankle oedema
Hepatic congestion
Later: liver cirrhosis

Atrial Fibrillation: press/ size

Systemic Embolisation - LA + stasis of Blood (atrial fib) ® LA clots (embolisation to limbs)

SIGNS

Malar flush (pulmonary hypertension)

Small, irregular pulse volume (if in AF)

Loss of a wave in AF

JVP if RHF

Parasternal heath/tapping apex/

Palpable HS1 (extreme stage)

MS alone ® apex not displaced (LV not that enlarged)s

Loud HS1 and HS2 (pulmonary HT)

OS - opening snap (fast opening of mitral valve due to press, heard after 2^nd HS at left sternal border, high-pitch \ bell

Mid diastolic rumble, presystolic accentuation (louder at end of diastole, if no sound - Pt do PA, then check again)

Signs of complications

Respiratory symptoms – consolidation, pleural effusion
Embolisation – peripheral vessels (check peripheral pulse), stroke

INVESTIGATIONS

LA (straight L heart border)

Double atrial shadow - RA + LA enlarged

Upper lobe venous blood diversion - due to pulmonary HT

Kerley’s A and B lines - septal lines present in chest

If SR (sinus rhythm), P mitral
AF
RVH

Echocardiogram

Valve thickened + dooming (valve cannot open completely)
Measure size of MV opening (significant MS if <1.5cm²) - haemodynamics

Cardiac catheterisation: unnecessary if pure MS, to see associated coronary artery disease

Mitral Stenosis 2D Echo (VIDEO)

Check morphology of valve

Focus on leaflet mobility + calcification

Commissure and valvular involvement

Determine area of valve

LA size?

Thrombus?

Assoc. abn - other valves, ASD

Eg. 19/F with MS

Diastole frame: mitral leaflet thickened at septum, tethered to each other, "Hockey stick appearance" to anterior mitral leaflet

Pathology: thickened mitral leaflet and cords, diastolic orifice "fish mouth" appearance (stenotic mitral valve)

LV hypertrophy + flattening of ventricular septum ® sign of pulmonary HT

In normal mitral valve, anterior leaflet has "M" shape, leaflet thin, move away from each other in diastole (MS: ¯ diastolic separation of anterior and posterior leaflets)

In MS, anterior and posterior parts of leaflet thickened, posterior moves towards anterior leaflet in diastole, tethered because of commissural fusion

Limitations of 2D Echo: inadequate short axis image, not good for densely calcified leaflet/ previous commisurotomy

Doppler paraapical and apical transducer position: apical four chamber format - Doppler spectrum - peak velocity ¯ \ avoid aliasing (?), prolonged deceleration time

Alternative: duplex exam in continuous mode, calibration at 1 m/s

CLINICAL SEVERITY

Symptom
Signs

Pulmonary HT
Duration of murmur
Interval between HS1 and OS

TREATMENT OF MS

Medical

Diuretics

Digoxin if in AF

Anticoagulation: used early (1) Hx of embolisation - definite indication (2) Paroxysmal or sustained AF - chance emboli 17x cf. normal AF

Antibiotics (1) Prophylaxis against recurrence of rheumatic fever, IBE (2) Pt young/ RF ® monthly penicillin injection

Curative (Symptomatic)

Valvotomy (closed or open) / valvuloplasty (Balloon) (1) Closed: open valve and expand with instrument (2) Open: open heart surgery (need cardiopulmonary bypass)

If in SR (also AF), no clots in LA, valve pliable (¯ Ca++ in) – CMV/balloon (closed mitral valvotomy), Otherwise, OMV (open mitral valvotomy, under direct vision), No significant MR required.

MVR (replacement) - no MR, prevent otherwise produce another heart lesion

If valve calcified or badly destroyed - mechanical, tissue

EG 2. MITRAL REGURGITATION

AETIOLOGY

Rheumatic - degen calcification in elderly

Mitral valvular prolapse: floppy valve , prolonged chordae (valve redundancy - excessively long, 1-2% population), systolic murmur, generally benign, if murmur then req ABX prophylaxis, also atypical chest pain

Rupture chordae tendinae - infection, degen D 's

Papillary muscle dysfunction: ischaemia or MI

Left ventricular dilatation (due to heart failure of any cause): enlarged MV ring leading to regurgitation

SIGNS & SYMPTOMS

Acute rupture of chordae – acute LV failure b/c LV has no time to adapt to the increased volume (LV immediately builds up load
Chronic MR : SOB & HF (similar to MS, progressive)

PHYSICAL EXAMINATION

LV dilatation
HS1 not increase, HS2 obscured/ muffled by pansystolic murmur, HS3 usual, Pansystolic murmur loudest at apex and radiating to axilla (except mid systolic murmur of MVP)
Pulmonary hypertension (late)

INVESTIGATIONS:

CXR: similar to MS

TREATMENT

Treatment: if symptomatic or progressive left ventricular dilatation, for valvular repair (often) or MVR (if calcified)

SUMMARY

Lesion	Aetiology	Symptoms	Signs	Ix	Medical Tx	Surgery
Tricuspid regurg	Rheumatic 2^nd to RV dil	R heart failure Cirrhosis	Giant V save Pulsatile liver Pansystolic murmur	Echo- Doppler ECG CXR	Diuretics	MV surg Tricuspid anuloplasty Replacement
Aortic stenosis	Rheumatic Congenital Calcific	Angina Heart failure Syncope Sudden death	Small vol pulse LVH ¯ aortic 2^nd HS ESM (aortic area to neck)	As for TR Severe is AV grad > 50 mmHg, AV area < 1cm² Cath for CAD	None	Symp/sig AV gradient In conjunction with CABG if gradient > 30 mmHg 3 AV replacement Balloon Valvuloplasty only palliative
Aortic regurg	Rheumatic SBE Congenital (Marfan, Sero-ve, Rheumatoid D Disease, Traumatic aortic dissection)	Heart failure complicns	Collapsing pulse LV dilatation Early blowing diastolic Murmur in LSB	As above Cath for CAD	VD Improve fwd flow + ¯ regurgitation Hydrallazine + nifedipine + ACE	Symptomatic or EF < 50% or LVES > 5.5cm or LVED > 7.5cm AV replacement

INFECTIVE ENDOCARDITIS

Follows valvular problem

Microbial infection of the endocardial lining of the heart (or blood vessels) - not necessarily endocardium (eg. arteriovenous fistula)

PREDISPOSING CARDIAC LESIONS (usu. valve esp. turbulence)

High-pressure to low pressure through a narrow orifice

VSD > ASD ( from LV ® RV). If ASD, ¯ RV + LV pressure (10-12 mmHg) \ ¯ bacterial seeding b/c ¯ turbulence

AR > AS (AS: slow flow)

MR > MS

Common

Less Common

Virtually Never

Aortic valve disease

(Bicuspid or Rheumatic)

Mitral valve disease (eg. MR)

Prosthetic valves (after replacement)

Congenital Heart Disease (Coarctation, VSD, TOF)

AV fistula

Mural thrombosis

Secundum ASD (¯ pressure)

Pulmonary valve stenosis (¯ flow)

OTHER

Tricuspid and other valves in IVI drug addicts
Patients with indwelling central lines (difficult to Tx b/c multi-drug-resistant organisms)

PORTALS OF ENTRY (prevention)

Often not available, but may involve:

Dental procedures (detected 10-20% IE Pt)
UTI
Respiratory infection
Biliary tract disease
Pelvic sepsis - eg. septic abortion
Mainlining drug addicts
Indwelling catheter

SIGNS & SYMPTOMS

Systemic infection ® fever, chills, rigours, malaise, wt loss (esp. chronic), heart (chest pain - obstruct aorta + coronary BF)

Intravascular disease ® heart failure, embolism (ab pain), stroke, cold extremities

Immunological reactions ® arthralgia, myalgia, tenosynovitis (embolic or immunologic features)

Examination	Investigations
Fever Pallor Wt loss Splenomegaly	Anaemia Leucocytosis (* WCS)* ESR (> 80ml/ 1^st hr) * Blood culture (most important) Abn CSF
Changing murmurs (D vegetation size) Signs of heart failure	RBC in urine CXR
Petechiae (emboli to skin) Roth spots (emboli to eye; red-yellow ctr) Osler's nodes (fingertip, painful) Janeway lesions (painless) Splinter haemorrhages (nail bed) Strokes, ETC	Echocardiography Arteriography (rare) Liver-spleen scans (PET: infective lesion)
Arthritis Uraemia Vascular phenomena Finger clubbing (immune related)	Proteinuria, casts (immunological) Polyclonal Ig RF (rheumatoid factor) ¯ Complements, IC

* ESR > 80 ml/ 1^st hr ® IE, multiple myelitis, TB, chronic rheumatic diseases
DIAGNOSIS

Clinical features: persistent fever, heart murmur

Blood cultures

3 venous cultures (taken at different sites and separated by at least half an hour) - (1) Dx yield - 95% chance (2) IE: want persistent bacteraemia \ need 3 bottles (3) Exclude contamination (If Pt very bad condition, 3 cultures different sites then immediate Tx)

May take additional 3 cultures if initial ones are negative especially in patients receiving antibiotics before.

Arterial and marrow cultures – usually not helpful b/c bacteria not systemic

Other investigation (not diagnostic)

Echocardiograms – vegetations (false negative, false positive)
Transoesphageal echocardiogram – better delineation of vegetation (from back of heart)

TREATMENT

Initiate treatment (according to the likely incriminated organisms) while pending for cultures (several days)
Principles

Eradicate source of infection - eg. dental extraction

Bactericidal agents b/c host defence ¯

IV Tx and high dose antibiotics b/c bacteria are ‘protected’ by fibrin in the vegetations

Adequate duration of treatment b/c bacteria multiple slowly

Surgery and complications management (examine teeth - eg. check for dental abscess)

Aetiological agents (depends on valve, portal)

Native valve: (1) Streptococcus viridians (dental portal) (2) S. Boris (GIT - assoc. w/ colon polyps or ca colon) (3) R. Sided : Staphylococcus aureus (main-lining addicts) (4) Pseudomonas aeruginosa (ICU PT, IVDU)

Prosthetic value (1) < 2m of surgery ; coagulase – negative endocarditic (surgical contamination, usu. skin flora - eg. staph aureus ® repeated op for valve debridement) (2) > 2m: similar to native valve

ABX Tx (1) Long duration (2) Dose (3) IV

Penicillin G - 12 mega unit/day - 4w (prolonged action, diffuse into valve)

Penicillin G - 12 mega unit/day - 2w + Gentamicin 60mg ivi Q8h (allow P to act quickly)

Vancomycin - 30mg/24h - 2w (P allergy, toxicity)

(Megaunit = 10⁶)

Need microbiologist's input with atypical

CLINICAL ASSESSMENT OF PROGRESS

Note: systemic infection takes 1-2w to respond (even with Tx)

Physical signs, BW: sudden = fluid o'load? (slow wt gain = good)

Urine testing (Gn), Renal function and CBP twice weekly

ESR may take weeks to decrease to N level

Echocardiogram (complications?), Listen to heart each day (deterioration?)

Fever may take 1-2 week to decrease

BRITISH HEART FOUNDATION RECOMMENDATIONS / AHA RECOMMENDATIONS (1997)

Dental Extraction	Standard	Penicillin with 1m Penicillin Allergy
1hr pre- After 8hr	Amoxycillin 2G PO No need	Clindamycin 600mg or Clarithromycin 500mg
Parenteral Tx if Dental procedure under GA High risk group - prosthetic valve, previous IE

Dental extraction - commonest (incl. scaling, filing)

Penicillin within 1m ® resistance

Principle: B4 bacteraemia give ABX (bactericidal)

mortality for IE

Native - 1^st time = 95% cure

Debilitated (ICU, elderly) = 50% cure \ prevention important

Eg. PDA - ligate PD, avoid catheterisation (aseptic if must)

Parenteral Tx (esp. hi-risk Pt)	Standard	Penicillin Tx within 1m Penicillin Allergy
Before	Amoxycillin 1g IMI or Ampicillin 1g IVI	Vancomycin 1g IVI o' 30min
6hr later	+ Gentamicin 120mg IMI/IVI (IVI if warfarin) 0.5g Amoxycillin PO	+ Gentamicin 120mg IVI

Warfarin: haematoma with IMI \ IVI

Dentist: can do IMI but not IVI

OTHER PROCEDURES (Eg. Urinary tract and obstetric practices)

Follow recommendation as for parenteral treatment in dental procedures (penicillin + Gentamicin w/ Amoxycillin 6hr later) (Reference : Dajani AS et al. JAMA 1997; 277:1794-1801