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