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Hemodynamic Monitoring

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

maureen-cashman
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Hemodynamic Monitoring

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  1. Hemodynamic Monitoring Khaled O. Hadeli 12/7/99

  2. DO2 = CO x 13.4 x Hb x SaO2 DO2 = (SV x HR) 13.4 x Hb x SaO2

  3. MR

  4. RVF

  5. Hypovolemic shock

  6. Acute bronchospasm

  7. Busy Tracing

  8. Cardiac performance CO/CI CVP/RAP/RVP/PAP/ Pcwp RVEF SVR/PVR O2 transport parameters DO2 SvO2 VO2 O2ER PAC

  9. 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

  10. 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

  11. After-Load cont. • SVR = MABP-CVP/CO • PVR = MPBP-LAP/CO

  12. CLINICAL APPLICATIONS THE WEDGE PRESSURE

  13. The wedge pressure • Pcwp • LAP • LVED • LVEDV • Preload • SV--->CO

  14. Cardiac out put TEMP. TIME CO=Amount of indicator injected / Area under the curve

  15. DO2 = (SV x HR) 13.4 x HB x SaO2

  16. Complications • General • Delays in starting necessary treatment • Inaccurate measurements and false interpretations • Preoccupation with instrumentation

  17. 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%

  18. 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)

  19. 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

  20. 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

  21. 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

  22. Physician Knowledge of PAC PGY1 2-3 4-6 Staff Expert Iberti, JAMA 264:2928,1990

  23. 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

  24. RHC vs.. NO RHC Connors, JAMA 276;889,1996

  25. 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

  26. MEDIA • “…….1000$ procedure leads to increased mortality in our ICUs” • “…….are you safe if you stay in the ICU” • “ The pulmonary catheter cult”

  27. 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.

  28. 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

  29. 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

  30. 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

  31. PAC, a diagnostic toll or a therapeutic modality?

  32. In the critically ill patient hemodynamic monitoring is aimed to optimize which of the following? a. CO/CI b. Pcwp c. BP d. DO2

  33. 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.

  34. Current hemodynamic data • BP 130/90 HR 120 • CO 11 l/min • SaO2 93% on 60% Fio2 • Urine out put 10cc/hr • Pcwp 12

  35. 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

  36. 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

  37. A searchlight cannot be used effectively without a fairly thorough knowledge of the territory to be searched. Fergus Macartney, FRCP

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