Major Pulmonary Embolism: Early Care & Cautions

Ram E. Rajagopalan, MBBS, AB (Int. Med & Crit. Care)

Consultant & Head, Dept. Critical Care Medicine SUNDARAM MEDICAL FOUNDATION,

Chennai

Goals of this talk

To discuss the acute managementof Major Pulmonary Embolism

with a focus on the patho-physiology of haemodynamic

alterations

Is all PE the same?Clinical Syndromes:

Dyspnea with or without pleuritic pain, haemoptysis

Acute syncope, haemodynamic instability, shock, arrest

~ 90%

~ 10%

Major PE / “Haemodynamically unstable” PE7 x mortality

Wood, KE. Chest 2002

No haemodynamic DRV dysfunction in 25-40%

Goldhaber et al; Circ 1997

“Massive” PE; A MisnomerClot size is not the only predictor

RIP

Mor

talit

y

PE Size

Good LV function

Poor LV function

Factors influencing survival

399 patients in PIOPED followed for a year

Mortality predicted by:Underlying Cancer Hazard Ratio 3.8Prior LV Failure Hazard Ratio 2.7Underlying COPD Hazard Ratio 2.2

(Carson et al; N Engl J Med 1992.)

Major (High-risk)* PEDefined as PE with: Hypotension - SBP < 90 mm Hg (or K >40 mm Hg)

Cardiogenic shock (organ perfusion defects)

Cardiac Arrest (PEA)

Syncope is an underemphasized feature

* ECS

n=407n=316

n=102

n=126

Mor

talit

y (%

)

(MAPPET Registry)

The Shock Index

HR (beats/ min) SBP (mm Hg)

>1 high risk / <1 low risk

More sensitive & specificthan SBP in predicting

All DeathFatal PE &Recurrent fatal PE

RIETE RegistryEur Respir J 2007; 30: 1111–1116

Shock Index =

Shock Index & Mortality

Both the Shock index and SBP were independent predictors of mortality

RIETE RegistryEur Respir J 2007; 30: 1111–1116

Diagnosis of Major PE

Though Multi-sliceCT Pulmonary Angiography may be the gold standard of diagnosis, patients may be

too unstable for the test

Alternative testing?

(From Wood, KE. Chest 2002)

RV Pressure Load & Failure

RV DimensionsAbsolute values irrelevant; error-proneCompare ratio of RVED to LVED areain apical 4-chamber view

Normal:RV:LV area <0.5

Moderate dilationRV: LV >0.6 & <1.0

Severe dilationRV:LV >1.0

Change in Septal Kinetics

ECG

LV Pres.RV Pres.

Septal Kinetics: RVF

RV

LV

Vent SeptumRV

LV

Septal Kinetics; B-modeEccentricity Index

RV Dysfunction

ECHO features include:- Mc Connell sign- RV dilatation (RV/LV >1)- Flattening of IV septum - No phasic collapse of

IVC- Tricuspid regurgitation

Warning: Echo diagnosisNo echocardiographic parameter has sufficient sensitivity to allow its use for diagnosis of PE in stable patients irrespective of severity of symptoms

But, in shock, ……..

ECHO in Major PE

Eur Heart J 2003; 24: 366-76

No patient withShock Index >1 &No RVF on Echohad PE on CTPA

In Extremis?

Haemodynamically Unstable PE

Shock Index >1 Other causes: AMI, aortic dissectiontamponade, valve2-D Echo

Emboli in PA; in transitNon

Contributory

No PE

Treat: ’Lysis, embolectomy

Yes

Major PE: ’Lysis?

1. Wan et al, Circulation 2004.2. Kucher et al, Circulation 2006.

Meta-analysis of studies that included major PE:

“Real-world” registry data: ICOPER; 108 major PE (4.5%)68% got only heparin; 46% mortality (vs. 55% with ’lysis, NS)

& 12% recurrence (vs. 12% after ’lysis)

Long-term Effects of ’Lysis

RV pressures at 6 months are less than if Rx with heparin alone

’Lysis Heparin

Chest. 2009; 136: 1202-10.

Which Agent for ’Lysis?

Alteplase infusions result in best clinical outcomes100 mg over 2 hours is the recommendation

Capstick & Henry; Eur Resp J 2005

Treatment of Major PE

Risk of bleeding to be considered;recent surgery, stroke, haemorrhage

Surgical embolectomyvs.Catheter embolectomy

Circ 2011; 123: 1788-1830

Cardiac arrest in PEPatients will present with PEA identified easily by RV distension (Strongly presumptive)

ECHO during arrest is a valuable tool

Case studies identify improved survival if thrombolysis is done during CPR

The only controlled trial of ’lysis in CPR showed no benefit

But AHA/ ERC/ ILCOR recommends lysis (Alteplase 50 mg) during CPR & continued compression up to >1 hour

Major PE: Titrating Fluid

Should hypotension in Major PE be resuscitated with fluid boluses?

(From Wood, KE. Chest 2002)

“RV Failure”

Ventricular Interdependence

With rising RV pressure:the shared IV septum &pericardial restraint

influence LV function as well

Septum “flattens”LV Dimensions K

LV output declinesAfter Greyson CR;Crit Care Med 2008; 36: S57–65

Volume Loading?

Physio-illogical! – RV has poor Starling response; Ventricular interdependence worsens LV function

Mercat et al;Patients with acute PEand CI <2.5 L/minNo hypotension1 bolus; 500 ml dextran

Cardiac index betterRVEDI increases

Crit Care Med 1999; 27: 540-44

Best response with small RV ; use RV size as goal?Not acceptable in RV shock

Pulse Pressure Variation

Pulse pressure variation during MV is increasingly used to judge “volume responsiveness”

Arterial Pressure

Airway Pressure

PPmax

PPmin

45

0

120

70

Pulse Pressure variation

+

+ +

+

+

+

B

- -

-

--

-

++

++

A

Positive pressure ventilation K venous return to right heart

Pulse Pressure Variation“In Series” effect on LV function

RV outputDetermines LV preload

& LV outputArterial Pressure

Airway Pressure

PPmax

PPmin

45

0

120

70Arterial Pressure

Airway Pressure

PPmax

PPmin

45

0

120

70

D of RV load has a delayed (out-of-phase)effect on LV

In-phase variation in RV Failure

From: Vieillard-Baron. Curr Opin Crit Care 2009; 15: 254-60

Pulse pressure variation in RV failure is a marker of interdependence; not fluid responsiveness

Classical Observation

Circ Res 1954; 2:326–332

AC Guyton

(From Wood, KE. Chest 2002)

“Auto-aggravation”

Coronary ischemia is presumed to be the final arbiter of the lethal decline

Haemodynamic SupportAvoid excessive fluid loading

Consider inotropes Dobutamine (with care)NoradrenalineRaise systemic vascular pr.

Noradrenaline____________________________________________________________

Avoid BP drop at intubation Etomidate for sedation

Inotropes?

Dobutamine:Aim; Improving RV contractility

Doses:<5mg / Kg / min K PVR and J CO5-10mg / Kg / min J HR, no D on PVR

Better than noradrenaline in RVD

Hypotension in RV shock patientsCrit Care Med 2007; 35: 2037-50

Systolic Interdependence:

Isolated heart preparations:Change in load (pr./ vol.) in one ventriclealters diastolic & systolic pr. in the other

Acute fluid removal via VAD Instantaneous change in both LV & RV pressures

Not a result of in-series HD change

Systolic Interdependence:Magnitude?

RV pressure has a biphasic peak;one of which coincides with LV pressure

J RV/LV separationin a paced, electrically- isolated model allows mathematical estimation of LV contribution to RV systolic function

Santamore W; Chest 1995; 107:1134-45

Systolic Interdependence:Magnitude?

LV contribution to LV syst pr.:

95%

RV contribution to LV syst pr.:

5%

LV contribution to RV syst pr.: 65%

RV contribution to RV syst pr.: 35%

Santamore W;Chest 1995; 107:1134-45

Since LV significantly contributes to RV outputKLV function affects the RV output

15mm Hg

15mm Hg

125mm Hg

75mm Hg

0

0 0

0

Vasoconstriction A strategy to improve systolic function

Circulation 1995; 92: 546-554

Control PHT PHT + Aortic Cons

Canine model of pulmonary constrictionCoronary blood-flow controlled by roller-pump

Aortic constriction K septal shift & J LV outputAllows better right heart pressure generation via systolic interdependence

While K coronary flow coincides with the deterioration,

the cycle of auto- aggravation may proceed independent of coronary ischemia

Impaired systolicinterdependence

Haemodynamic SupportAvoid excessive fluid loading

Rx Thrombus ’lysis, thrombectomy

Raise systemic vascular pr.Noradrenaline____________________________________________________________

Avoid BP drop at intubation Etomidate for sedation________________________________

Consider inotropes Dobutamine (with care)

Thank youfor yourattention……