Transcript What is the role of the pulmonary artery catheter in the ICU?

RIGHT VENTRICULAR DYSFUNCTION
University of British Columbia
October 15th, 2009
• Case 1: 54 year old female referred from another
institution with large pericardial effusion NYD and
shock liver. The amount of fluid around the heart is
large – enough to make her tachycardic with a soft
blood pressure but she remains alert, mentating
normally, pink, warm, dry.
• Vital signs: HR: 100-110, BP: 100-110, RR: 24, SpO2:
93% on 4L
• On the bedside monitor you notice both electrical
alternans (on telemetry) and pulse pressure variation
(on arterial line and SpO2 tracing).
1.What are the most sensitive and practical
indicators of fluid responsiveness that we can
derive from the bedside? - Rob
Sensitive and Practical Indicators of fluid responsiveness that we can
derive from the bedside
•
Physical Exam
– Capillary refill, blood pressure, heart rate, presence of peripheral cyanosis/skin mottling,
extremity temperature, passive leg raising, JVP, urine output
•
Static Measures of Intravascular Volume
–
–
–
–
–
–
•
CVP
PAOP
RVEDV (PAC with thermistor)
LVEDA (TEE)
IVC Diameter (Subcostal echo)
Transpulmonary thermodilution (GEDV)
Dynamic Indices of Intravascular Volume
–
–
–
–
–
PPV (arterial waveform analysis)
SVV (Pulse contour analysis)
Aortic Flow Velocity/Stroke Volume (Esophageal Doppler)
Chest wall echo (LV)
Changes (dynamic) in IVC/SVC Diameter
Fluid Responsiveness assessment – Physical Exam
• Physical Exam
–
–
–
–
–
–
–
–
Capillary refill
Blood pressure
Heart rate
Peripheral cyanosis/skin mottling
Extremity temperature
Passive leg raising
JVP
Urine output
Fluid Responsiveness Indicators – Static Measures of Intravascular
Volume
•
•
•
•
•
•
CVP
PAOP
RVEDV (PAC with thermistor)
LVEDA (TEE)
IVC Diameter (Subcostal echo)
Transpulmonary thermodilution (GEDV)
Fluid Responsiveness Indicators – Dynamic Measures of Intravascular
Volume
•
•
•
•
•
PPV (arterial waveform analysis)
SVV (Pulse contour analysis)
Aortic Flow Velocity/Stroke Volume (Esophageal Doppler)
Chest wall Echo (LV)
Changes (dynamic) in IVC/SVC Diameter
2009 Meta-analysis
Marik et al., Crit Care Med 2009 in press
• PPV and SVV measured during volumecontrolled mechanical ventilation predicted
with a high degree of accuracy those patients
likely to respond to a fluid challenge as well as
the degree to which the stroke volume is likely
to increase
– PPV: Sens 89% Spec 88% Thresold: 12%
– SVV: Sens 82% Spec 86% Threshold: 13%
Limitations of SVV
• Mechanical Ventilation
– If not on 100% control with tidal volumes > 8cc/kg
• Spontaneous Ventilation
– Irregular rate and tidal volumes
• Arrhythmias
• PEEP
– Increasing PEEP may cause an increase in SVV
• Vasodilation therapy
– Vasodilatory therapy may increase SVV
Esophageal Doppler
• Measures blood flow velocity in the
descending aorta
• Cardiac output calculated based on diameter
of aorta, distribution of the cardiac output (to
the descending aorta) and the measured flow
velocity of blood in the aorta.
• The duration of the aortic velocity signal
corrected for HR (flow time corrected) is
considered a static indicator of cardiac preload
Esophageal Doppler
• Cardiac output: 86% correlation with PAC and changes
in cardiac output correlated with therapeutic
interventions1
• Patients undergoing femur fracture repair randomized
to intraoperative intravascular volume optimized with
or without Doppler2
– Doppler: More rapid post-operative recovery and shorter
hospital stays.
• Similar study in trauma patients3
– Lower lactates
– Lower incidence of infectious complications
– Decreased ICU and hospital LOS
1Dark
and Singer Int Care Med 2004; 30: 2060-2066
et al BMJ 1997; 315: 909-912
3Chytra et al., Crit Care 2007; I 1: R24
2Sinclair
Esophageal Doppler
• Disadvantages
– Waveform is very much operator dependent
– Steep learning curve
– Not suitable for all patients
– Inability to obtain continuous reliable
meaurements
– Correlation better in studies where the
investigator was not blinded to the results of the
cardiac output obtained with a PAC
2. What is the role of bedside Intensivistperformed echo in this/similar settings (TTE
and Esophageal Doppler)? - Marius
Assessing fluid responsiveness using
TTE and esophageal doppler
TTE: Fully ventilated patients
• Fluid responsiveness can be measured in
patients being fully ventilated by measuring
the change in IVC diameter (ΔDIVC) with
inspiration.
• Rationale: insufflation-induced changes in
venous return are more marked in
hypovolemic states.
Measuring IVC collapsibility
Performance of ΔDIVC
• Feissel et al. Intensive Care Med (2004) 30:1834–1837
– ΔDIVC > 12% had a 93% PPV and 92% NPV for volume
responsiveness.
• Septic patients, sedated, on volume control with a Vt ≥ 8
cc/kg
• Vol. responsiveness described an increase in CO ≥ 15%
following an 8 cc/kg bolus of 6% hydroxyethylstarch over 20
min
• IVC measured approx. 3 cm from RA
• ΔDIVC = (Max DIVC – Min DIVC) / MeanDIVC
Performance of ΔDIVC
• Barbier et al. Intensive Care Med (2004) 30:1740–1746
– ΔDIVC > 18% had a 90% sensitivity and 90% specificity
for volume responsiveness
• Fully ventilated ICU patients on volume control with a Vt of
8.5 ± 1.5 cc/kg
• Vol. responsiveness defined as an increase in CO ≥ 15%
following a 7 cc/kg bolus of 4% gelatin over 30 min
• IVC examined just upstream of the origin of the suprahepatic
vein
• ΔDIVC = (Max DIVC – Min DIVC) / MinDIVC
Esophageal doppler and fully
ventilated patients
• Esophageal doppler measures aortic blood flow in the descending aorta.
• Owing to various heart-lung interactions, volume responsive patients
being fully mechanically ventilated tend to show variations in aortic blood
flow related to inspiration.
• These interactions are mediated by two factors:
– An increase in pleural pressure leading to:
• A decreased RV preload
– An increase in transpulmonary pressure leading to:
• An increased RV afterload
• An increased LV preload
• A decreased LV afterload
Hemodynamic effects of mechanical
ventilation
Esophageal doppler
• Monnet et al. Intensive Care Med (2005) 31:1195–1201
• A respiratory variation in aortic flow before
volume expansion of at least 18% predicted fluid
responsiveness with a sensitivity of 90% and a
specificity of 94%
• Fully mechanically ventilated patients (8±2 cc/kg) being
considered for fluid bolus
• Fluid responsiveness defined as an increase in aortic flow ≥
15% with a 500 cc NS bolus given over 10 min.
• ΔABF = (ABFmax – ABFmin) / ABFmean
Spontaneously breathing patients
• Predicting fluid responsiveness in spontaneously
breathing patients poses a greater challenge
• Reasons:
• Tidal volumes and respiratory rates are variable
• Intrathoracic pressure is negative during inspiration
• Intrathoracic pressure swings are lower than during
mechanical ventilation
• Options:
• Measuring IVC diameter (no good studies)
• Response to passive leg-raising
Measuring IVC diameter
• Yanagawa et al. Journal of Trauma 2007; 63:1245–1248
– An expiratory IVC diameter < 1cm in
spontaneously breathing trauma patients
predicted recurrent hypotension after successful
fluid resuscitation (SBP > 90)
Passive leg-raising
– Given the increase in RV filling induced by passive leg
raising does not depend on respiratory changes, it
has been studied as a marker for fluid responsiveness
in spontaneously breathing patients.
– Leg raising is thought to “bolus” the patient without
actually giving volume, the effects of which can be
measured in real time by esophageal doppler or echo.
Spontaneously breathing patients
Passive leg-raising and TTE
• Lamia et al. Intensive Care Med (2007) 33:1125–1132
– A PLR-induced increase in stroke volume ≥ 12.5%
predicted volume responsiveness with a 77%
sensitivity and a 100% specificity
• Spontaneously breathing ICU patients (including PSV)
• Volume responsiveness = 15% or more increase in
stroke volume after a 500 cc NS bolus over 15 min.
• Stroke volume = VTIAo x AVA
Passive leg-raising and TTE
• Maizel et al. Intensive Care Med (2007) 33:1133–1138
– A PLR-induced increase in CO or SV ≥ 12% predicted
volume responsiveness with a 69% sensitivity and
89% specificity
• Spontaneously breathing patients with hypotension, acute
renal failure, or clinical signs of volume depletion
• Volume responsiveness = An increase in CO ≥ 12% following
a 500 cc NS bolus over 15 min
• SV = VTIAo x AVA
Passive leg-raising and esophageal
doppler
• Monnet et al. Critical Care Medicine (2006) 34:1402-1407
– PLR-induced increase of aortic blood flow ≥10%
predicted fluid responsiveness with a sensitivity of
97% and a specificity of 94%
• Spontaneously breathing and deeply sedated patients
undergoing mechanical ventilation
• Volume responsiveness = a rise in aortic blood flow ≥
15% following a 500 cc NS bolus given over 10 min.
3. Discuss the role of the PAC in the ICU. When
is it useful? - Todd
What is the role of the pulmonary artery
catheter in the ICU?
• Who knows?
– Everyone should have one.
– Nobody should have one.
– We should use them, but only use the information
they provide if it confirms what we already think.
– We should use them, but only for true mixed
venous oxyhemoglobin values.
Some light bathroom reading…
• BCMJ, vol. 51, No. 7, Sept 2009. 302-307 (3
UBC cardio fellows)
• First right-heart cath by Forssman in 1929
(urethral catheter in his own arm…)
• Further development (and Nobel Prize), with
main limitation being the difficulty in passing
the catheter without flouroscopy.
• Swan’s major contribution was envisioning the
balloon-tipped, flow-directed catheter, which
he developed with Ganz in 1970.
Hemodynamic monitoring
• Central venous pressure (directly measured)
• Cardiac output (directly measured); Cardiac
index (calculated)
• Mixed venous O2 saturation (directly
measured)
• Pulmonary artery occlusion pressure (directly
measured, but with caveats)
• Systemic vascular resistance (calculated)
Controversy
• Does routine use of this device in critically ill
patients improve outcomes?
– Apparently not.
JAMA meta-analysis
• No clear benefit nor harm from routine PA
catheter use in critically ill patients.
– Many trials excluded patients in whom PA
catheterization would be specifically indicated (i.e.
lung transplant)
– ESCAPE trial specifically looked at refractory CHF
with reduced LVEF, and found that despite
effectively reaching target hemodynamic values,
outcomes didn’t improve.
Why?
•
•
•
•
•
Risks of insertion
Risks of catheterization of right heart/PA
Risk of “wedging”
Risks associated with interpretation of data…
Right Heart Cath as a marker for an aggressive
(read: risky) style of care?
– As a marker for sick patients who aren’t improving
with less invasive hemodynamic monitoring
• Timing?
When do you use it?
• Over time the patient becomes less alert. Her
respiratory effort is failing. You have to intubate her.
• Outline your approach to the induction of a patient
with a hemodynamically compromising pericardial
effusion (assuming you can’t tap the effusion first). Noemie
• How would you change your approach if the
hemodyamic compromise was, in fact, secondary to
a submassive/massive pulmonary embolism? Or a
large anterior mediastinal mass? - Noemie
Question 4 & 5
Approach to the induction of a patient with:
1. a hemodynamically compromising pericardial
effusion.
2. a submassive/massive pulmonary embolism.
3. a large anterior mediastinal mass.
Pericardial Tamponade Physiology
•  pericardial fluid   pericardial pressure
•  End diastolic pressure
• Early closure of AV valves
•  SV and  CO
Concerns about intubation
• Induction:
– Medication used
– Sympathetic drive
• PPV:
–  venous return   CO
– PEEP
Induction
•
•
•
•
•
No right answer…Multiple case reports
Good IV access, Fluid bolus
Avoid hypotension! Pressors and inotrope ready
Awake intubation with topical anesthetic?
Medication
– Ketamine ad etomidate suggested as drugs of choice b/c
don’t cause significant SVR
– Avoid propofol
Ventilation
• Try to avoid intubation if
possible
• Pericardiocenthesis!
• Avoid high PEEPs and
can try spontaneous
ventilation
British journal of anesthesiology 1979;51:409-415
Massive PE
• Complications of PPV
–  RV afterload
–  venous return
• IV, pressors and inotrope at bedsie
• Avoid hypotension to maintain good coronary
perfusion
Massive PE
• How to intubate?
– Maintain spontaneous ventilation to avoid  RV
afterload
– Ketamine/midaz
– Topical anesthetic with fibreoptic scope
– Aggressive management of blood pressure to
maintain coronary perfusion
Approach to the Mediastinal Mass
• Possible Complications to think prior to intubation:
–
–
–
–
Progressive airway obstruction
Lung volume loss
PA and/or cardiac compression
SVC obstruction
– POTENTIAL FOR CATASTROPHIC AIRWAY!
Canadian Journal of Anesthesia 1989;36(6):681-688
Approach to Induction
• Positon: flat or sitting dpdg on pathology
• Awake fibreoptic intubation with topical anesthesia
• Avoid muscle relaxant!!
• Maintain spontaneous ventilation during induction if
possible
Canadian Journal of Anesthesia 1989;36(6):681-688
• Case 2: 43 year old female, smoker and on HRT,
presents to the ED with shortness of breath and CP
and diagnosed with “submassive PE”.
• What is “submassive PE”, or what are the thresholds
to treat with thrombolytics? What is the current
standard treatment? - Rob
Submassive PE
• Hemodynamic stable patients with evidence of right
ventricular strain or dysfunction
– 40-50% of those with acute PE1,2,3
– Higher mortality - those with RV hypokinesis, even in the presence of
normal SBP had a 2x mortality1
– Another study described a 5% mortality rate in those with RV hypokinesis
(those without RV dysfunction had a 0% rate)35
• 162 patients
• 31% had RV dysfunction
1Goldhaber
et al Lancet 1999 353: 1386-1389
et al Circulation 2000; 2817-2822
3Ribiero et al., Am Heart J 1997; 479-487
2Grifoni
Submassive PE
• Konstantinides1
–
–
–
–
–
256 hemodynamically stable patients
Proven PE + RV hypokinesis or PHT
Got either r-tPA + heparin or placebo + heparin
30 day follow up
End points: In-hospital death or “escalation of care”
•
•
•
•
•
Vasopressor requirement
Embolectomy
Thrombolytics
Intubation
CPR
1Konstantinides
et al NEJM 2002
Konstantinides1 Results
•
•
•
•
11% vs. 25% deterioration rate favouring lytic group
RR reduction: 55% (NNT: 8)
No difference in all cause mortality (3.4% vs. 2.2%)
Significant Criticism
– Allowed treating MD to administer rescue lytics which could have driven
the composite end point to statistical significance
• 2008 ACCP Recs2:
– Selected high –risk patients without hypotension, judged to have a low
risk of bleeding should get thrombolytic therapy
1Konstantinides
2Kearon
et al NEJM 2002
et al Chest: 2008 454S-545S
• Case 3: 27 year old male presents with massive
hemoptysis to MSJ ER. Brutal CT chest with TB –
there is significant burden of disease with
consolidative process, cavitation/necrosis, and what
appears to be only ~ 25% “healthy” or aerating lung.
His right sided pressures are through the roof.
• Outline an approach to PHTN. - Neil
• What are the current therapies available in the ICU
setting? And in this patient what are the
risks:benefits of inhaled vs systemic pulmonary
vascular vasodilators? - Neil