Hemodynamic monitoring
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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

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Hemodynamic Monitoring

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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

DO2

SvO2

VO2

O2ER

PAC


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

  • SV--->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)


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%

Complications


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

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


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


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