major pulmonary embolism: early care & cautions ram e. rajagopalan, mbbs, ab (int. med &...
TRANSCRIPT
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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
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Goals of this talk
To discuss the acute managementof Major Pulmonary Embolism
with a focus on the patho-physiology of haemodynamic
alterations
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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
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“Massive” PE; A MisnomerClot size is not the only predictor
RIP
Mor
talit
y
PE Size
Good LV function
Poor LV function
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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.)
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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)
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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 =
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Shock Index & Mortality
Both the Shock index and SBP were independent predictors of mortality
RIETE RegistryEur Respir J 2007; 30: 1111–1116
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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?
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(From Wood, KE. Chest 2002)
RV Pressure Load & Failure
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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
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Change in Septal Kinetics
ECG
LV Pres.RV Pres.
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Septal Kinetics: RVF
RV
LV
Vent SeptumRV
LV
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Septal Kinetics; B-modeEccentricity Index
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RV Dysfunction
ECHO features include:- Mc Connell sign- RV dilatation (RV/LV >1)- Flattening of IV septum - No phasic collapse of
IVC- Tricuspid regurgitation
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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, ……..
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ECHO in Major PE
Eur Heart J 2003; 24: 366-76
No patient withShock Index >1 &No RVF on Echohad PE on CTPA
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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
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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)
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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.
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Which Agent for ’Lysis?
Alteplase infusions result in best clinical outcomes100 mg over 2 hours is the recommendation
Capstick & Henry; Eur Resp J 2005
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Treatment of Major PE
Risk of bleeding to be considered;recent surgery, stroke, haemorrhage
Surgical embolectomyvs.Catheter embolectomy
Circ 2011; 123: 1788-1830
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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
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Major PE: Titrating Fluid
Should hypotension in Major PE be resuscitated with fluid boluses?
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(From Wood, KE. Chest 2002)
“RV Failure”
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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
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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
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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
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Pulse Pressure variation
+
+ +
+
+
+
B
- -
-
--
-
++
++
A
Positive pressure ventilation K venous return to right heart
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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
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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
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Classical Observation
Circ Res 1954; 2:326–332
AC Guyton
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(From Wood, KE. Chest 2002)
“Auto-aggravation”
Coronary ischemia is presumed to be the final arbiter of the lethal decline
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Haemodynamic SupportAvoid excessive fluid loading
Consider inotropes Dobutamine (with care)NoradrenalineRaise systemic vascular pr.
Noradrenaline____________________________________________________________
Avoid BP drop at intubation Etomidate for sedation
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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
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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
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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
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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
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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
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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)
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Thank youfor yourattention……