H Ηχωκαρδιολογία στην καθηµερινή κλινική ιατρική πράξη

ΠΝΕΥΜΟΝΙΚΗ ΕΜΒΟΛΗ

Ε.Γ.ΔΑΛΑΜΑΓΚΑ ΚΑΡΔΙΟΛΟΓΟΣ

Διδάκτωρ Ιατρικής Σχολής ΑΠΘ

ΜΕΤΕΚΠΑΙΔΕΥΤΙΚΑ ΜΑΘΗΜΑΤΑ ΗΧΩΚΑΡΔΙΟΛΟΓΙΑΣ-ΑΠΕΙΚΟΝΙΣΗΣ ΚΕΒΕ 2013

Pulmonary embolism still a big challenge….

….in terms of diagnosis because of

its unspecified clinical characteristics.

Pulmonary embolism •  Pulmonary embolism is a relative common cardiovascular

emergency. •  By occluding the pulmonary arterial bed it may lead to acute

life-threatening but potentially reversible RV failure. •  PE is a difficult diagnosis that may be missed because of non

specific clinical presentation. •  However, early diagnosis is fundamental, since immediate

treatment is highly effective.

Pathophysiology •  The consequences of acute PE are primarily hemodynamic and

become apparent when 30-50% of the pulmonary arterial bed is occluded by thromboemboli.

•  Sudden death may occur, usually in the form of

electromechanical dissociation. •  Or, the patient presents with syncope and/or systemic

hypotension, which might progress to shock and death due to acute RV failure.

•  Rightward bulging of the IVS may further compromise the

cardiac output as a result of diastolic LV dysfunction. Eur Heart Journal 2008 (29), 2276-2315

Diagnosis •  Chest Xray is usually abnormal and the most frequent findings

( plate-like atelecatsis, pleural effusion, or elevation of a hemidiaphragm) are non specific.

•  But chest X ray is useful in excluding other causes of SOB and chest pain.

•  PE is associated with hypoxaemia, but up to 20% of pts have normal PaO2 and a normal alveolar- arterial oxygen gradient (D(A-a)O2).

•  ECG signs of RV strain, such as T wave inversion in V1-V4, a QR pattern in V1,the classic S1Q3T3 type and RBBB may be helpful.

•  Normal D- dimer level renders acute PE or VTE unlikely,( the negative predictive value of D-dimer is high).

•  Grade the level of evidence of diagnostic procedures •  Clinical assessment : high risk / non high risk •  Severity of PE ~ early mortality risk

Eur Heart Journal 2008 (29), 2276-2315

Eur Heart Journal 2008 (29), 2276-2315

Eur Heart Journal 2008 (29), 2276-2315

ECHO: Limited sensitivity 60-70% Eur Heart Journal 2008 (29), 2276-2315

Role of ECHO in “high risk” pulmonary embolism

•  Differential Diagnosis -cardiogenic shock -acute valvular dysfunction -tamponade -aortic dissection

•  Screen for right heart thrombi in transit •  Detect indirect signs, which are highly suggestive of PE

Screen for right heart thrombi in transit Direct visualization of thrombus in PE

•  Thrombus can form anywhere in the venous system and be visualized anywhere en route to the lungs-IVC,SVC,RA,RV,PA

•  Thrombi visualized proximal to PA not diagnostic of PE, but point to the process

•  DDX of thrombi: tumors, myxomas •  Pulmonary arteries can be visualized to the bifurcation

Recognising normal right heart structures

•  The moderator band

•  Eustachian valve

•  Chiari network

RV dysfunction Echo criteria for diagnosis of PE

•  Acute RV dilatation Increased RV/LVEDD ratio •  RV impairement (depressed contractility) Mc Connell sign •  Raised pulmonary systolic pressure Increased TR velocity Decreased pulmonary acceleration time •  Disturbed RV ejection pattern 60/60 sign •  Pressure overload •  Impaired myocardial performance RV MPI

The RV as a window to the pulmonary Vasculature: The healthy Right Ventricle

•  The normal RV is accustomed to low pulmonary resistance •  Normal right ventricular pressures are low and compliance is

high •  Unlike the left ventricle, the normal right ventricle does a poor

job at acutely responding to sudden increases in afterload.

•  PE results in an acute increase in pulmonary vascular resistance

•  A previously normal RV is unable to accutely accommodate this additional load

•  The RV dilates acutely, but cannot acutely increase pressure. •  Depending on the size of the PE, this can result in mild right

ventricular dysfunction to frank right ventricular failure. •  The RV that has been subject to increased load for grater

periods of time will hypertrophy and better handle the increased load.

The RV in Pulmonary Embolism

Pathophysiology of Acute PE

RV Afterload

RV Dilatation/ Dysfunction

RV Cardiac Output

LV preload

LV Output

RV ischemia/ infarction

Pulmonary Embolism

Pulmonary Resistance

RV Wall Tension

RV O2 Demand

Coronary Perfusion

Hypotension

RV O2 Supply

Am Heart J 1995,:130:1276-82

Review standart 2D right heart views

RV dilatation in PE

•  Is the RV diameter greater than the LV diameter in the 4 chamber view?

•  Normal RV diameter- 0.9-2.6 cm in 4C •  Mean RV diameter in PE: >2.7cm •  Series of 261pts with acute PE Mean RV EDD= 4.1cm, RV/LV ratio=0.9

PLAX, 4C

Relative RV: LV ratio 1:3 RV/LV EDD >0.55

EurHeartJ 1996

Quantification of RV size

Reference range RVIT 2.7-3.3cm RVSAX 2-2.8cm RVLAX 7.1-7.9cm RVAd 11-28 cm²

Clinical application •  Practical?

•  Reproducible?

Lang, JASE 2005

Moderate RV dilatation >o.6

Major RV dilatation ≥1

RV fractional area change

RVFAC= (RVAd-RVAs /RVAd) x 100

RVAd (cm²) 11-28 RVAs (cm²) 7.5-16

RV FAC % 32-60

-Good correl of RVFAC with RVEF from cMRI

-Utilized in numerous studies

-Feasible in clinical practice?

normal

TAPSE tricuspid annular plane systolic excursion

-Good correl of RVFAC with RVEF -simple -reproducable -but load dependant

Normal 1.6-2 Mild 1.1-1.5

Moderate 0.6-1 Severe <0.5cm

McConnell sign

Patients without previous / with known cardiorespiratory diseases •  Sensitivity 77% •  Specificity 94% •  Positive predictive value 71% •  Negative predictive value 96%

Distinct regional RV dysfunction

•  Mid-free wall hypokinesia/akinesia •  Normal apical motion

•  Not seen in chronic PHT •  But also seen in acute RV infarction

Am J Cardiol 1996

RV impairement (depressed contractility)

McConnell's sign : Mechanisms 1.  In acute PE, the tethering of the right ventricular apex to a

contracting and often hyperdynamic left ventricle may account for the preserved wall motion at the apex.

2.  The right ventricle may be assuming a more spherical shape to equalize regional wall stress when subjected to an abrupt increase in afterload.

3. There may be localized ischemia of the right ventricular

free wall as a result of increased wall stress.

RV systolic pressure

RVsyst pressure= 4 (TRVmax)²+estimated RAP

•  RVSP PHT 35-55 mild 55-85 moderate >85 severe

60/60 sign TV PG<60mmHg

Tacc<60ms

98% specificity 48% sensitivity

Tacc normal>140ms Correlates with RVSP, MPAP,PVR

Pressure overload

Pressure loading systolic “D” shaped LV

Volume loading= diastolic D shaped LV+ TR/PR or L-R shunt ↑diastolic press= diastolic D shaped LV +RV impairement

Proposed echocardiographic measurements

•  RV dimensions •  RV fractional area change •  Right atrial size and pressure •  TAPSE •  Eccentricity index •  TEI index •  TDI measurements of TV annulus •  RV diastolic assessment •  Presence of pericardial effusion •  RV diastolic filling patterns

…concomitant echo signs of pressure overload are required To prevent the false diagnosis of acute PE in pts with RV free-wall

Hypo/akinesis due to RV infarction, which may mimic the McConnell sign.

RV overload criteria

•  Presence of ≥1 of four signs: 1.  Right sided cardiac thrombus 2.  RV diastolic dimension (parasternal view) > 30mm,

or RV/LV ratio>1 3.  Systolic flattening of the IVS 4.  Acceleration time <90ms or TR>30mmHg σε

απουσία RVH

Prognostic significance of RV dysfunction

Acute Pressure Overload

RV dysfunction

Preexcisting CV

disease

Recurrent PE

Other serious comorbidity

(cancer)

Presence of a

PFO

Poor prognosis

Determinants of an adverse early outcome

•  In patients with suspected high risk PE presenting with shock or hypotension, the absence of echocardiographic signs of RV overload or dysfunction practically excludes PE as a cause of hemodynamic instability.