Download The Right Heart

THE RIGHT HEART
Casey Buckingham
Advanced Clinical Physiologist
Aims
 To explain the normal Right Heart anatomy &
Abnormalities that occur.
 To review relevant measurements,
calculation & new BSE (2008) /ASE (2010)
guidelines.
Abnormalities
 Pulmonary Valve Disease
 Tricuspid Valve Disease
 Ebstien’s Anomaly
 Carcinoid
 Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC)
Normal Right Heart
 Pyramid shape divided into Inflow (Base) and
Outflow (Sides)
 Inflow and Outflow separated by Crista Supra
Ventricularis
 Crescent shape in cross section seen to wrap
around the LV
Right Ventricle
 Thinned wall (<5mm) and smaller than left
(~ 0.6)
 Tricuspid valve more apically displaced than
Mitral ( up to 1cm)
 Inner walls irregular and are lined by small
bundles of muscles called Trabeculae Caunae
 Large muscle band noted at Apex Moderator
Band
Coronary Artery Supply to Right
Heart
RV Dimension Apical 4ch (BSE
2008)
Basal RV dimension(RVD1)
Normal 2 – 2.8cm Mild 2.9 – 3.3cm Mod 3.4 –
3.8cm Severe > 3.9cm
Mid RV dimensions (RVD2)
Normal 2.7 – 3.3cm Mild 3.4 – 3.7cm Mod 3.8 –
4.1cm Severe >4.2cm
Base to Apex (RVD3)
Normal 7.1 -7.9 Mild 8 – 8.5 Mod 8.6 – 9.1
Severe >9.2cm
RV Apical 4ch Measurements
RVOT Diameters SAX (BSE
2008)
 RVOT at AOV level (RVOT 1)
Normal 2.5 – 2.9cm Mild 3 – 3.2cm Mod 3.3 –
3.5cm Severe >3.6cm
RVOT at PV annulus (RVOT2)
Normal 1.7 – 2.3cm Mild 2.4 – 2.7cm Mod 2.8 –
3.1cm Severe >3.2cm
Main PA diameter (PA1)
Normal 1.5 – 2.1cm Mild 2.2 – 2.5cm Mod 2.62.9cm Severe >3cm
RV Para-sternal SAX
Measurements
RV Dilation
 Mild – Increased 60 to 100 % of LV
 Moderate – Equal to LV
 Severe – Exceeds LV
RV Systolic Function
• Assessment similar to LV :
• ‘’Eyeball’’
• RWMA – Normal/Hypo/Dys/Akinetic
• TAPSE – Normal 16 – 20mm
Mild 11 – 15mm
Mod 6 – 10mm
Severe < 5mm
RV TAPSE
 Distance of systolic excursion along the
longitudinal plane at peak systole
Assessment of RVH
Normal <5mm
Right Atrium
 Assists in the filling of the RV.
 Thinned walled with relatively smooth body.
 Retrosternal – sometimes difficult to image.
 RAA trabeculated, broad based & triangular
in shape (seldom seen on TTE)
 Dimensions roughly similar to LA.
RA Normal Variants
 Crista Terminale.
 Eustachian Valve.
 Chiari Network.
RA Dimensions
 Primary TTE window to assess RA size Apical
4ch.
 Maximal long axis distance – centre of
Annulus to centre of the Superior wall.
 Mid minor distance – Mid level of the
Anterolateral wall (Free wall) to the IA
septum, perpendicular to the long axis.
Upper reference limits are 4.4cm & 5.3cm
RA Dimensions
RA Area
 Measure end systole = largest volume.
 Lateral aspect of TV annulus to the Septal
aspect – follow endocardium
 Excluding IVC/SVC & RAA
 Good indicator for RV diastolic dysfunction.
 Should be applied in the assessment of RV or
LV dysfunction.
 Upper reference limit of 18cm2
Tricuspid Valve
• Annulus apically displaced 1cm
• Septal, Anterior, Posterior (which is also the
Inferior or medial, depending which books
you read!!!)
• Open of the TV precedes opening of the MV.
• Varies with inspiration, measure over 4 – 5
beats.
• Normal velocities 0.4 to 0.8m/s
Causes of TR
• Rheumatic – 20 to 30 % near always occurring
•
•
•
•
•
•
with MV or +/- AOV disease.
Prolapse – associated with Marfans & MVP
Congenital - Ebsteins.
Endocarditis – IVDU.
Carcinoid – Free flowing, low velocity.
Functional – Annular dilation due to PHT caused
by left sided problems *Most common*
Physiological – Mild TR seen in 75% of healthy
individuals.
Classification
• Mild – Flow disturbance in sys localized to
area adjacent to TV closure plane <5cm2
• Moderate – Fills between 5 – 10 cm2 of RA
• Severe - >10cm2 of a dilated RA with IVC &
SVC systolic flow reversal. Vena contracta
width >0.7cm (89% sensitive 93% specific)
• Vena contracta – Moderate <0.7cm & Severe
>0.7cm.
TR Doppler Profile
• Maximum velocity = Maximum pressure
difference across the TV NOT severity of
regurgitation.
• Severe TR + Normal RVSP = Low velocity.
• Mild TR + PHT = High max velocity
• Intensity of CW = Regurgitant severity.
• Curve = time of instantaneous pressure
difference across TV
Measurements Obtainable
• Systolic Pulmonary Pressure – PA pressure or
•
•
•
•
RVSP
Measure Peak TR velocity
Apply simplified Bernoulli equation
Then add estimated RA pressure (IVC)
RVSP = 4 (vTR) 2 + RAP
• **In absence of RVOT /Pulmonary
obstruction**
RVSP/PA Pressure
Assessment of RAP
• Assess in sub-costal view.
• End expiration.
• Proximal to junction of hepatic veins which
lie 0.5cm to 3cm ostium of RA.
• Assess inspiratory collapse ‘’Sniff’’ – unable to
perform adequate ‘’sniff’’ IVC collapse <20%
with quiet inspiration = increased RAP
•
**Specific values not ranges**
Assessment of RAP
PA pressure + RA pressure
Small
Normal
Mild
Moderate
18 – 25mmHg
IVC <1.5cm &
seen to
collapse + 05mmHg
18 – 25mmHg
IVC 1.5cm to
2.5cm & seen
to collapse.
Normal
RA/Hepatic
vein size +
5mmHg to
10mmHg
30 – 40mmHg
IVC 1.5 to
2.5cm & >50%
collapse.
Normal
RA/Hepatic
vein size +5 –
10mmHg
40 – 70mmHg
IVC >2.5cm
with <50%
collapse with
dilation of
RA/Hepatic
veins +10 15mmHg
Severe
> 70mmHg
IVC > 2.5cm
with no resp
collapse &
significant
dilation of the
RA/Hepatic
veins +
>20mmHg
Tricuspid Stenosis
• Nearly always Rheumatic in origin
• Usually accompanied by Mitral stenosis.
• 2D – Thickening & shortening of TVL with
reduced excursion.
• Commissural fusion prevents tip separation,
dissociation of tip & body results in Doming in
diastole.
Doppler Assessment of TS
• Transvalvular flow velocity - Mean PG & PHT
• Use mean gradient of CW in Apical 4ch.
• Normal: TVA > 7cm2
• Moderate: Mean PG 2 to 5mmHg & TVA 7 to
1cm2.
• Severe: Mean PG >5mmHg & TVA <1cm2
Symptoms
 Usually gradual onset
 Systemic venous congestion leading to
abdominal discomfort & swelling.
 Dyspnoea may be present.
 Prominent pulsation in neck – increased JVP.
 Eventually leads to HF or other complications
including stroke or infection.
Other Causes
• Carcinoid heart disease.
• Congenital Tricuspid Atresia
• Infective endocarditis
• RA myxoma
**All obstruct so mimic TS**
Pulmonary Valve
 Tricuspid
 Annulus distal to RVOT
 Similar dimensions to Aortic root (develops
same time as Aorta)
 Not easily visualised on 2D – assess with CFM
& Doppler for accurate assessment.
 Normal forward flow 0.7 to 1.4m/s
Pulmonary Stenosis
• Most often congenital , 7.6% of CHD
• May occur with other congenital lesions –
ccTGA & TOF
• Mild PS may be asymptomatic but if occur
include; SOB, CP, fainting or exertional
syncope & sudden death
• 2D – thickening of leaflets with systolic
bowing
• Doppler – 4v2 **PVA not suggested**
PS (BSE 2008)
Mild
< 40 mmHg
Moderate
40 – 75mmHg
Severe
>75mmHg
Pulmonary Regurgitation
• Incidental, benign finding in most normal
•
•
•
•
individuals.
Congenital PVD – mild untreated or residual
after surgery
Common complication post surgical or
percutaneous relief of PS.
Secondary to dilation of PV ring due to PHT or
Marfan’s.
Leads to progressive RV dilation & dysfunction,
VT & sudden death.
Assessment
• Diastolic flow in RVOT
• Width of flow –semiquantive index of severity
• Holodiastolic flow reversal may be noted in
MPA
• Even if only mild, peak velocity reflects the
PA to RVDP difference.
PR (BSE 2008)
 Jet size CFM (cm)
Mild - Narrow <1cm Mod – Intermediate Severe
– Wide, large.
CW jet / Deceleration rate
Mild – Soft/Slow Mod – Dense/Variable Severe –
Dense / Steep.
Regurg Fraction (%)
Mild - <40% Mod – 40 to 60% Severe - >60%
Ebstein’s Anomaly
 Congenital defect
 One or more TVL are Apically displaced, most
often the septal leaflet
 Degree of displacement varies >1cm.
 Functional TR & enlarged RH
 Atrialization of RV
 ASD & WPW frequently associated.
Adult Presentation
 Fatigue
 Exertional dyspnoea
 Cyanosis
 TR and / or RHF
 Palpitations
Carcinoid
 Release of 5HAA from hepatic metastases
 Incidence of approx 1 in 75,000
 Slow growing, usually up to 20 years or more
before symptoms develop.
 Typically occurs in 5th – 7th decade of life.
 Cardiac involvement occurs in 50% of
patients – worsens prognosis & contributes
significantly to morbidity & mortality.
 Usually only tumours that invade the liver
result in pathological changes of the heart
Carcinoid Heart Disease
• Fibrous deposits on endocardium of RH
•
•
•
•
interfacing with the myocardium & (R) sided
valves.
Valves are thickened & retracted, eventually
becoming immobile & remain in a semi open
position ‘’drumstick’’ appearance
Free flow TR – short abrupt asymmetrical
Doppler due to reduced time to Peak velocity.
Dilated & overloaded RH
Results in RHF
Treatment
 Surgical intervention.
 Regular follow up
 Peri operative mortality around 35%
ARVC
 Infiltrative cardiomyopathy.
 Male to Female 3:1 ratio
 After HOCM next cause in SCD in young




persons (5% in < 65yr-olds)
Progressive replacement of normal
myocardium with fatty infiltration either
Adipose or Collagen.
LV & IV septum may be affected.
Hereditary
3 phases : Concealed - Electrical - Failure.
Echo Features
• Dilation & global dysfunction of RV.
• Localised aneurysmal bulges of outflow or
inflow tracts which are thinned & akinetic.
• Thickened, hyper reflective moderator band
• Normal or mildly impaired LV.
• New criteria – Increased Anteroposterior
diastolic dimension of outflow tract in (PLAX)
>3cm
Symptoms
 Abdominal pain.
 Fatigue.
 Reduced ET with SOBOE
 Dizziness.
 Palpitations.
 Syncope.
Test
 Echo.
 MRI – Gold standard non – invasive diagnosis.
 Endomyocardial biopsy.
 Contrast echo – to identify aneurysmal
segments.
Treatment
 Antiarrhythmic & anticoagulation drugs.
 ICD – primary prevention.
 RFA.
 Cardiac transplant.
Pressure Overload
 Acute rise in Pulmonary vascular resistance
 Pulmonary valve or RVOT obstruction.
 Increased Left sided pressures = increase PA
pressures.
 RV free wall & Septal hypertrophy.
 Exaggerated Septal motion in systole Concaved/flattened IV septum in systole
Volume Overload
• Dilation of RV
• Paradoxical septal motion ‘’D’’ shaped in
diastole.
• Augmentation of systolic function
• LV systolic & diastolic impairment.
• Septal hypertrophy = LV compliance.
• Left to right shunts = 30%
• Pure volume overload well tolerated.