hemodynamic monitoring
DESCRIPTION
Hemodynamic Monitoring. Khaled O. Hadeli 12/7/99. DO2 = CO x 13.4 x Hb x SaO2 DO2 = (SV x HR) 13.4 x Hb x SaO2. MR. RVF. Hypovolemic shock. Acute bronchospasm. Busy Tracing. Cardiac performance CO/CI CVP/RAP/RVP/PAP/ Pcwp RVEF SVR/PVR. O2 transport parameters - PowerPoint PPT PresentationTRANSCRIPT
Hemodynamic Monitoring
Khaled O. Hadeli
12/7/99
DO2 = CO x 13.4 x Hb x SaO2
DO2 = (SV x HR) 13.4 x Hb x SaO2
MR
RVF
Hypovolemic shock
Acute bronchospasm
Busy Tracing
PAC
• Cardiac performance– CO/CI
– CVP/RAP/RVP/PAP/ Pcwp
– RVEF
– SVR/PVR
• O2 transport parameters– DO2
– SvO2
– VO2
– O2ER
Physiology of cardiac performance
• Pre-Load– contractility: Frank-
Starling Law, ( within physiologic limits the strength of muscle contraction is directly related to the length of the muscle fiber)
– compliance
After-Load
• It is the opposing force that determines the force of muscle contraction needed to initiate muscle shortening
• Laplace Law: T=Pr
T=Pr/t
After-Load cont.
• SVR = MABP-CVP/CO
• PVR = MPBP-LAP/CO
CLINICAL APPLICATIONS
THE WEDGE PRESSURE
The wedge pressure
• Pcwp• LAP• LVED• LVEDV• Preload Preload • SVSV--->--->CO CO
Cardiac out put
TEMP.
TIME
CO=Amount of indicator injected // Area under the curve
• DO2 = (SV x HR) 13.4 x HB x SaO2
Complications
• General– Delays in starting necessary treatment
– Inaccurate measurements and false interpretations
– Preoccupation with instrumentation
Complications
• Related to central venous cannulation– arterial puncture/hematoma 8%– pnemothorax 2-4%– others ( hemothorax, brachial plexus damage,
air embolism, phrenic nerve damage, sheared cath…etc.) <1%
Complications
• Related to passage of catheter– Arrhythmia 13- 70% (1%)– RBBB– Cardiac perforation & tamponade (1%)– Over wedging leading to Pulmonary infarction
(pt with severe MR)
Complications
• Related to presence of the cath. In circulation– Infection
• colonization 40%
• sepsis 4-6%
– Thrombotic• autopsy 66%
• clinical <1%
– Pulmonary• infarction <1 - 7%
• artery rupture <1%
– Cardiac• endocardial damage
35%
• valve damage <1%
• endocarditis 0 - 7%
– Mechanical• Balloon rupture <4%
• knotting <1%
Limitation of Hemodynamic monitoring
• Cost
• Incorrect measurement of data– calibration, damping, zeroing– transient respiratory muscle activity– reliance on digital readout– failure to wedge– non zone-III region
Cont.
• Incorrect interpretation of data– ventricular compliance– valve disease– SCDs and false reading of CO
• Improper therapeutic strategies - poor application of data on over zealous goals/targets
Physician Knowledge of PAC
0
10
20
30
40
50
60
70
80
90
100
PGY1 2-3 4-6 Staff Expert
Iberti, JAMA 264:2928,1990
Open Vs. Closed ICUs
Significant improvement in mortality subsequent to the presence of CCM specialist in the ICU
despite increased use of PAC
Reynolds et. Al. JAMA1988:260;3446-50
0
20
40
60
80
100
120
0 5 10 15 20 25 30
days
% a
live
NO RHCRHC
RHC vs.. NO RHC
Connors, JAMA 276;889,1996
Is it time to pull the PAC?
• Moratorium on the use of PAC until a (RCT) provides more evidence*
• ATS consensus statement against the moratorium, but use with caution untill (RCT) provides more evidence
*Dalen et.al. JAMA 1996:276;916-8
MEDIA
• “…….1000$ procedure leads to increased mortality in our ICUs”
• “…….are you safe if you stay in the ICU”
• “ The pulmonary catheter cult”
PAC use
1,000,000 RHC every year
2 Billion Dollars / year(1990)*
• CT surgery 30%
• high risk surgery 10%
• cardiac cath. Lab 25%
• MICU 15%
• others20%
*Shoemaker et al.
Why do we need PAC
• In cardiac cases (AMI) clinical criteria where predictive of pcwp and CO in 81% & 85% of the subjects, respectively
• In ICU the estimates of pcwp & CO where 42%-44%. And another study 30%-50%.
• In ICU the planned therapy was changed in 50% of patients after PAC was placed
Potential impact on therapy
• Hemodynamic profiles predicted in 56%
• PAC derived profiles changed therapy in 50%
• No change in over all mortality!
• Improvement in mortality of Pts. With shock not responding to usual measures
Mimoz et.al.CCM 1994;22:573-9
PAC in ARDS
• Optimize intervascular volume
• Improved survival with high DO2*– Mean DO2 491ml/min/m2 in nonsurvivors– Mean DO2 718 ml/min/m2 in survivors
• No benefit and some possible harm from non specific augmentation of DO2 in pts with ARDS**
*Russell et a.
**Gattinoni/Hayes, NEJM 1995/1994
PAC, a diagnostic toll or a therapeutic modality?
In the critically ill patient hemodynamic monitoring is aimed to optimize which of the following?
a. CO/CI
b. Pcwp
c. BP
d. DO2
CASE
A 65yr old male 4 days post-op developed sudden onset of fever, chills and SOB. Vitals show HR 130, BP 85/55 mmHg, RR40/min, PaO2 40mmHg.
He was intubated and given 500cc NS, started on vasoactive therapy, and referred to MICU.
Current hemodynamic data
• BP 130/90 HR 120
• CO 11 l/min
• SaO2 93% on 60% Fio2
• Urine out put 10cc/hr
• Pcwp 12
• Your immediate action should be:
A. give volume
B. diurese
C. leave volume status as is
• And / Or
A. give more vasopressor therapy
B. Taper vasopressor therapy
C. leave vasoactive therapy as is
Recommendations
• PAC should be used when there is a question of diagnosis and management
• Like all information it must be adequately processed
• DON’T FORGET– what we measure is not always what we think it
is– DO2 = SV x HR x 13.4 x Hb x SaO2
A searchlight cannot be used effectively without a fairly thorough knowledge of the
territory to be searched.
Fergus Macartney, FRCP