Major Pulmonary Embolism: Early Care & Cautions Ram E. Rajagopalan, MBBS, AB (Int. Med & Crit. Care)...
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Transcript of Major Pulmonary Embolism: Early Care & Cautions Ram E. Rajagopalan, MBBS, AB (Int. Med & Crit. Care)...
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……