Transcript 5. Massive Pulmonary Embolism
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 management of 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 ~ 90% No haemodynamic
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RV dysfunction in 25-40% Goldhaber et al; Circ 1997 Acute syncope, haemodynamic instability, shock, arrest ~ 10% Major PE / “Haemodynamically unstable” PE 7 x mortality Wood, KE. Chest 2002
“Massive” PE; A Misnomer Clot size is not the only predictor Poor LV function Good LV function PE Size
Factors influencing survival 399 patients in PIOPED followed for a year Mortality predicted by: Underlying Cancer Prior LV Failure Underlying COPD Hazard Ratio 3.8
Hazard Ratio 2.7
Hazard Ratio 2.2
(Carson et al; N Engl J Med 1992.)
Major (High-risk)* PE Defined as PE with: Hypotension - SBP < 90 mm Hg (or
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>40 mm Hg) Cardiogenic shock (organ perfusion defects) Cardiac Arrest (PEA) (MAPPET Registry) n=102 n=316 Syncope is an underemphasized feature n=407 n=126 * ECS
The Shock Index Shock Index = HR (beats/ min) SBP (mm Hg) >1 high risk / <1 low risk More sensitive & specific than SBP in predicting All Death Fatal PE & Recurrent fatal PE RIETE Registry Eur Respir J 2007; 30: 1111–1116
Shock Index & Mortality Both the Shock index and SBP were independent predictors of mortality RIETE Registry Eur Respir J 2007; 30: 1111–1116
Diagnosis of Major PE Though Multi-slice CT Pulmonary Angiography may be the gold standard of diagnosis, patients may be too unstable for the test Alternative testing?
RV Pressure Load & Failure (From Wood, KE. Chest 2002)
Normal: RV : LV area <0.5
RV Dimensions Absolute values irrelevant; error-prone Compare ratio of RVED to LVED area in apical 4-chamber view Moderate dilation RV : LV >0.6 & <1.0
Severe dilation RV : LV >1.0
ECG Change in Septal Kinetics LV Pres.
RV Pres.
Septal Kinetics: RVF Vent Septum RV LV RV LV
Septal Kinetics; B-mode Eccentricity 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 diagnosis No echocardiographic parameter for diagnosis of has sufficient sensitivity to allow its use 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 with Shock Index >1 & No RVF on Echo had PE on CTPA
Haemodynamically Unstable PE Shock Index >1 2-D Echo Other causes: AMI, aortic dissection tamponade, valve Emboli in PA; in transit Non Contributory No PE Treat: ’Lysis, embolectomy Yes In Extremis?
Major PE: ’Lysis?
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) 1. Wan et al, Circulation 2004.
2. Kucher et al, Circulation 2006.
Long term Effects of ’Lysis ’Lysis Heparin RV pressures at 6 months are less than if Rx with heparin alone Chest. 2009; 136: 1202-10.
Which Agent for ’Lysis?
Alteplase infusions result in best clinical outcomes 100 mg over 2 hours is the recommendation Capstick & Henry; Eur Resp J 2005
Treatment of Major PE Circ 2011; 123: 1788-1830 Risk of bleeding to be considered; recent surgery, stroke, haemorrhage Surgical embolectomy vs.
Catheter embolectomy
Cardiac arrest in PE Patients 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
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LV output declines After 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 PE and CI <2.5 L/min No hypotension 1 bolus ; 500 ml dextran Cardiac index better RVEDI 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 45 Pulse pressure variation during MV is increasingly used to judge “volume responsiveness” 0 120 70 PPmax PPmin Airway Pressure Arterial Pressure
Pulse Pressure variation Positive pressure ventilation
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return to right heart venous ++ ++ A + + + + + + B
Pulse Pressure Variation “In Series” effect on LV function
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of RV load has a delayed ( out-of-phase ) effect on LV RV output Determines LV preload & LV output
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
AC Guyton Circ Res 1954; 2:326–332 Classical Observation
“Auto-aggravation” Coronary ischemia is presumed to be the final arbiter of the lethal decline (From Wood, KE. Chest 2002)
Haemodynamic Support Avoid excessive fluid loading Consider inotropes Dobutamine (with care) Noradrenaline Raise systemic vascular pr.
Noradrenaline ____________________________________________________________ Avoid BP drop at intubation Etomidate for sedation
Inotropes?
Dobutamine: Aim; Improving RV contractility Doses: <5
m
g / Kg / min 5-10
m
g / Kg / min
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PVR and HR, no
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CO on PVR Better than noradrenaline in RVD Crit Care Med 2007; 35: 2037-50 Hypotension in RV shock patients
Systolic Interdependence: Isolated heart preparations: Change in load (pr./ vol.) in one ventricle alters 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
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RV/LV separation in 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% 125mm Hg 15mm Hg LV contribution to RV syst pr.: 65% 0 75mm Hg 0 15mm Hg RV contribution to LV syst pr.: 5% 0 RV contribution to RV syst pr.: 35% 0 Since LV significantly contributes to RV output Santamore W; Chest 1995; 107:1134-45
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LV function affects the RV output
Vasoconstriction A strategy to improve systolic function Canine model of pulmonary constriction Coronary blood-flow controlled by roller-pump Control PHT PHT + Aortic Cons While
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coronary flow coincides with the deterioration, the cycle of auto aggravation may proceed independent of coronary ischemia Aortic constriction
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septal shift & systolic interdependence
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LV output Allows better right heart pressure generation via Circulation 1995; 92: 546-554
Haemodynamic Support Avoid excessive fluid loading Impaired systolic interdependence Raise systemic vascular pr.
Noradrenaline ____________________________________________________________ Avoid BP drop at intubation Etomidate for sedation ________________________________ Consider inotropes Dobutamine (with care) Rx Thrombus ’lysis, thrombectomy