Advanced Hemodynamics PART 2

B. McLean, MN, RN, CCRN, CCNS-BC, ANP-BC, FCCM

Grady Memorial Hospital, Atlanta

GA, USA
bamclean@mindspring.com
www.barbaramclean.com

Hemodynamic Monitoring Truth

No monitoring device, no matter how simple or
complex, invasive or non-invasive, inaccurate or
precise will improve outcome
Unless coupled to a treatment, which itself
improves outcome

Pinsky & Payen. Func/onal Hemodynamic Monitoring, Springer,

2004

4 factors that aec/ng the

haemodynamic condi/ons

Myocardial
contraction
and heart rate

Intravascular volume

Vasoactivity

Hemodynamic monitors
Traditional invasive monitors: Static Measures
Arterial line
CVP & ScvO2
PA catheter, CCO, SvO2

Functional variation: Dynamic measures

Pulse pressure variation
Stroke volume variation

Why are we monitoring?

Preload, contractility, afterload,
and oxygen transport are
commonly abnormal in the
critically ill
Inadequate resuscitation and
failure to restore cellular
oxygen delivery and organ
perfusion results in multiple
system organ dysfunction
syndrome (MODS) and death

Optimization of critical illness

reduces organ failure and
improves survival
Accurate assessment of
hemodynamic function and
goal-directed resuscitation is
essential to improving patient
outcome

Purpose of monitoring
Evaluate cardiovascular system
Pressure, flow, resistance

Evaluate blood flow and oxygen delivery

Establish baseline values and evaluate trends
Determine presence and degree of dysfunction

Implement and guide interventions

Provides criteria for determination of CV efficacy

Hemodynamic measures
Arterial pressure
Systolic, diastolic, PP, MAP, Cardiac output, SVV

Central venous pressure

Mean pressure, Oximetry

Pulmonary artery pressure

PA systolic, diastolic, mean

PAOP
Cardiac output
Oximetry

Arterial Pressure Monitoring

Indications
Patient in shock not rapidly responsive to therapy

Insertion Sites

Radial
Brachial
Axillary
Femoral
Dorsalis Pedis

Arterial Pressure Monitoring

Radial artery has the benefit of collateral
circulation from the ulnar artery
Allen Test used to evaluate the collateral
flow prior to radial artery cannulation

Invasive Monitoring Equipment

Flush solution
Continuous flush system (usually a pressure bag
or pump)
Pressure transducer and pressure tubing
Invasive catheter
Monitor

Transducers

Convert one form of energy to another

Sense pressure
Convert it to an electrical signal
Electrical signal causes monitor reading

Pressure monitoring system

Catheter placed in vessel
Fluid filled, low compliance, tubing-transducer kit
Amplifier-monitor
Oscilloscope
Printer

Phlebostatic Axis
Located at the intersection of the 4th ICS and
midway between the anterior and posterior
surfaces of the chest
Midaxillary line is NOT interchangeable with mid
anteroposterior level in all persons Bartz, et al,
1988

Phlebostatic Axis

As the pa/ent moves from at to upright, the phlebosta/c

level rotates on the axis and remains horizontal. This posi/on
conrmed by CT by Paolella, et al, 1988.

Phlebostatic Axis

The phlebosta/c axis moves to midchest at

the 4th ICS when pa/ent is in the lateral
posi/on.

Leveling, Referencing, Balancing

Placing the air-fluid interface of the catheter
system at the phlebostatic axis
This negates the weight effect of the fluid in the
catheter tubing (hydrostatic pressure)
Setting the correct reference point is the single
most important step in setting up a pressure
monitoring system. Gardner, 1993

Leveling
Air fluid interface is the point in the system that is
opened to air during zeroing
Inaccuracies are produced if the air-fluid interface
is above or below the phlebostatic axis 1.86
mmHg/inch
Phlebostatic axis determined by Windsor and
Burch (1945) as correct reference for
measurement of venous pressures

Zeroing
Opening the system to air to establish atmospheric
pressure as zero (0)
This negates all pressure contributions from the
atmosphere
Allows only pressure values that exist within the
heart or vessel to be measured

When to Zero
Before insertion
After disconnecting transducer from pressure cable
When values are in question
Ahrens, T. et al. Frequency requirements for zeroing
transducers in hemodynamic monitoring, Am J Crit Care,
1995;4:466-471

What can we see.

Arterial line
Real time SBP, DBP, MAP
Pulse pressure variation (PP)

PP (%) = 100 (PPmax - PPmin)/([PPmax + PPmin]/2)

>= 13% (in septic pts,) discriminate between fluid responder and
non respondaer (sensitivity 94%, specificity 96%)
Am J Respir Crit Care Med 2000, 162:134-138

Arterial Pressure Waveform

1. Systole
2. Dicro/c notch
3. Diastole

Summary
Perfusion is the goal
Perfusion =
oxygenation + flow
You cannot do it alone
Less invasive is better
Technology should make you a better clinician
(only as good as you can be)

Pressure monitoring
Principles
Unobstructed fluid filled system will reflect change in
pressure at distal tip of system (catheter) throughout the
system
Pressure change may be detected at proximal end of
system, transformed into electrical signal and displayed
as a waveform

Principles
Level the system
Level to remove effects of hydrostatic pressure
Pressure caused by weight of the fluid in the tubing

Level with left atrium

Transducer above pressure directed from
transducer to tip so measured pressures less than
actual
Transducer below pressure directed from tip to
transducer so measured pressures higher than actual
pressure

Preparation
Connect and prime tubing
system with solution
Typically NS
Use gravity flush to prevent
micro-bubbles all must be
removed
Apply pressure bag to
solution container and
inflate to 300 mmHg
Automatic delivery of solution
3-5 ml/hr.

Phlebostatic Axis

Arterial pressure
Continuous pressure evaluation
Tissue perfusion status

Trends in blood pressure

Efficacy of drugs, interventions
Frequent blood samples required

Arterial pressure
Placement of catheter

Radial
Brachial
Axillary
Femoral
Dorsalis pedis

Arterial waveform
Morphology (shape) of waveform

Depends on force generated by ventricle

Speed of ejection
Volume of blood ejected
Compliance of arterial vessels
Rate of forward blood runoff dependent on resistance to
forward flow or systemic vascular resistance

Measures
Systolic pressure
Reflects volume and speed of ejection, compliance of
aorta

Diastolic pressure
Reflects vascular resistance and competence of aortic
valve

Other?
Pulse pressure
Reflects difference in volume ejected from LV into arterial
vessels and volume that exits simultaneously
Function of SV and SVR
Wide PP increase in SV and decrease in SVR
Narrow PP Decreased SV and increased SVR

Mean Arterial Pressure (MAP)

Best indicator of tissue perfusion
Average driving pressure of blood during cardiac cycle
Time weighted diastole is longer

Arterial line
Advantages

Easy setup
Real time BP monitoring
Beat to beat waveform display
Allow regular sampling of blood for lab tests

Disadvantages
Invasive
Risk of haematoma, distal ischemia, pseudoaneurysm
formation and infection

Review of physiology

Increase venous pressure (preload) leads to a rise in stroke

volume and therefore cardiac output
End diastolic volume causes stroke volume
The energy of contraction of a cardiac muscle fiber,
like that of a skeletal muscle fiber, is proportional to
the initial fiber length at rest.
Stroke volume increase due to increased force of
contraction

Frank-Starling mechanism or
Starlings Law of the Heart

Cardiac Output Optimization Concept

Stroke
Volume

Cardiac Ouput Maximization

0
0

Preload

Current state of monitoring

Preload
Definition
The degree that the myocardial fiber is stretched prior to
contraction at end diastole
The more the fiber is stretched, the more it will contract.
However, if it is overstretched the amount of contraction
goes down.
(Think rubber band)

On right side of heart Right Ventricular End

Diastolic Volume which is reflected by Right Atrial
Pressure or Central Venous Pressure (CVP)
On left side, the LVEDV is reflected by the PCWP.

Afterload
Definition
The force against which the ventricles must work to pump
blood
The ventricular wall tension generated during systole
Determined by:
Volume and viscosity of blood
Vascular resistance
Heart valves

Vascular Resistance
Derivation of Ohm s Law
The resistance in a circuit is determined by the voltage
difference across the circuit and the current flowing
through the circuit.

Resistance = D Pressure

Flow
Vascular Resistance = D Blood Pressure (mmHg)

Cardiac Output (L/min)

Where D Blood Pressure is the highest pressure
in the circuit minus the lowest pressure in the
circuit.

Pulmonary Vascular Resistance (PVR)

Key Components:
Highest Pressure MPAP
Lowest Pressure LAP or PCWP
Flow Cardiac Output

Formula
PVR = (MPAP-PCWP)/CO x 80

Systemic Vascular Resistance (SVR)

Key Components
Highest Pressure MAP
Lowest Pressure RAP or CVP
Flow Cardiac Output

Formula
SVR = (MAP-CVP)/CO x 80

Contractility
Definition
The force generated by the myocardium when the
ventricular muscle fibers shorten.
Positive Inotropic effect ( force of contraction)
Negative Inotropic effect ( force of contraction)

Contractility is affected by:

Drugs
Oxygen levels within the myocardium
Cardiac muscle damage
Electrolyte imbalances

The Central Venous Catheter in Critical Care

Central venous pressure

Indication of RVEDV
Preload of RV
Indication of fluid volume state

Catheter insertion
Percutaneous technique
Seldinger technique
Exploring needle, guide or J wire, dilator, catheter system

2-3 cm above junction of SVC and atrium ideally

Most common sites

Internal jugular vein
Subclavian vein

Central Venous Line

Indications:

CVP monitoring
Advanced CV disease + major operation
Secure vascular access for drugs: TLC
Secure access for fluids: introducer sheath
Aspiration of entrained air: sitting craniotomies
Inadequate peripheral IV access
Pacer, Swan Ganz

Central Venous Line: RIJ

IJ vein lies in groove between sternal + clavicular
heads of sternocleidomastoid muscle
IJ vein is lateral + slightly anterior to carotid
Aseptic technique, head down
Insert needle towards ipsilateral nipple
Seldinger method: 22 G finder; 18 G needle,
guidewire, scalpel blade, dilator + catheter
Observe ECG + maintain control of guide-wire
Ultrasound guidance; CXR post insertion

CVP Monitoring
Reflects pressure at junction of vena cava +
RA
CVP is driving force for filling RA + RV
CVP provides estimate of:
Intravascular blood volume
RV preload

Trends in CVP are very useful

Measure at end-expiration
Zero at mid-axillary line

Zero @ Mid-Axillary Line

CVP Waveform Components

Component

Phase of Cycle

Event

a wave

End diastole

Atrial cont

c wave

Early systole

Isovol vent cont

x descent

Mid systole

Atrial relaxation

v wave

Late systole

Filling of atrium

y descent

Early diastole

Vent filling

Mark JB, CV Monitoring, in Miller 5th Edi/on, 2000, pg 1153

Right Atrial Pressure Tracing

a wave results from
atrial systole
c wave occurs with the
closure of the tricuspid
valve and the initiation of
atrial filling
v wave occurs with
blood filling the atrium
while the tricuspid valve
is closed

Timing of the positive deflections

a wave occurs after
the p wave during the
PR interval
c wave when
present occurs at the
end of the QRS
complex (RST
junction)
v wave occurs after
the T wave

Right Atrial Chamber

Height of the v wave is
related to the atrial
compliance and the
volume of blood returning
from the periphery
Height of the a wave is
related to the pressure
needed to eject forward
blood flow
The v wave is usually
smaller than the a wave in
the right atrium

Right atrial hemodynamic pathology

Elevated a wave
Tricuspid stenosis
Decreased RV
compliance
e.g. pulm htn, pulmonic
stenosis

Cannon a wave
AV asynchrony
atrium contracts
against a closed
tricuspid valve
e.g. AVB, Vtach

Absent a wave

Atrial fibrillation or
standstill
Atrial flutter

Elevated v wave

Tricuspid regurgitation
RV failure
Reduced atrial
compliance
e.g. restrictive
myopathy

Right atrial hemodynamic pathology

Note the Cannon a wave that is

occurring during AV dysynchrony
atrial contrac/on is occurring
against a closed tricuspid valve.

Note the large V wave that

occurs with Tricuspid
regurgita/on

Hemodynamic Pathology
Tricuspid Stenosis
Large jugular venous a
waves on noted on exam
Notable elevated a wave
with the presence of a
diastolic gradient >5mmHg gradient is
considered signficant

Limitation of CVP
Obstruction of the
great veins

Mechanical
ventilation

Decrease right
ventricular
compliance

Systemic venoconstriction

Tricuspid regurgitation

Central venous catheter

Advantages
Easy setup
Good for medications infusion

Disadvantages
Cannot reflect actual RAP in most situations
Multiple complications
Infections, thrombosis, complications on insertion, vascular
erosion and electrical shock

Michard F, Boussat S et al. Am J Respir Crit Care Med 2000;162:1348

Feissel M, Michard F, et al. Chest 2001; 119:86773
Tavernier B, Makho/ne O, et al. Anesthesiology1998;89:131321
Rex S, Brose S, et al. Br J Anaesth 2004;93:7828
Wiesenack C, Fiegl C, et al.. Eur J Anaesthesiol 2005;22:65865
Michard F. Anesthesiology 2005;103:419 28,

Static indicators have been shown to be poor predictors

of fluid responsiveness
central venous pressure(CVP)
pulmonary capillary wedge pressure (PCWP)
left ventricular end diastolic area

Dynamic indicators demonstrated to be better predictors

of fluid responsiveness in patients during mechanical
ventilation.
During positive pressure ventilation, the inspiratory right
ventricular stroke volume (SV) decrease is proportional
to the degree of hypovolemia and is transmitted to the
left heart after two or three beats (pulmonary transit time)

Neither CVP or Ppao reflect Ventricular Volumes or

tract preload-responsiveness

Kumar et al. Crit Care Med 32:691-9, 2004

Neither CVP or Ppao reflect Ventricular Volumes or

tract preload-responsiveness

Kumar et al. Crit Care Med 32:691-9, 2004

Marik PE: Techniques for assessment of intravascular

volume in critically ill patients.
J Intensive Care Med 2009; 24:329337
studies have shown that the CVP often does not
accurately reflect end-diastolic volume and right
ventricular preload.
Dynamic responses to volume challenge by using either
stroke volume variation or pulse pressure variation are
both highly sensitive and specific for preload
responsiveness in mechanical ventilated patients,
whereas the
passive straight leg test should be used in
spontaneously breathing patients

The CVP Assumption

Is ventricular
geometry
unchanged?

Is ventricular
compliance
unchanged?

Is there
valve
disease?

Catheter
properly
positioned?

Preload = CVP = PAOP= LAP = LVEDP

All equal volume??!!!???
CVP is accurate ONLY when these potential
sources of error have been eliminated

Are intrathoracic or
intra-abdominal
pressures elevated?

CVP Variability
CVP clearly has limitations
Respiratory variability may be an option
>1 mm change with inspiration consistent with fluid
responsiveness

INSP

EXP
Magder S ,et al, Respiratory varia/ons in right atrial pressure predict the response to
uid challenge, Journal of Cri/cal Care, Volume 7, Issue 2, June 1992, Pages 76-85

EXP

 Emerging data show that the choice, timing and amount

of fluid therapy may affect clinical outcomes
Early administration of fluid therapy in sepsis may
improve survival
Later fluid therapy in acute lung injury patients will
increase the duration of ventilator dependence without
achieving better survival

Complications
Pneumothorax
Incidence 0.5 to 6%
Intervention
None
Needle decompression
Tube thoracostomy

Sudden dyspnea, chest pain, absent breath sounds,

tachycardia, asymmetrical chest wall movement

The Pulmonary Artery Catheter in Critical Care

Connors et al 1996 JAMA

5734 adult ICU pa/ents 1989-1994, 5 ICUs at 15

ter/ary med centers
PA cath = 30 day mortality,
ICU LOS, costs of care

Harvey et al: PAC-Man 2005 Lancet - Game Over?

1014 pa/ents at 65
UK ins/tu/ons:
NO DIFFERENCE
between PA cath
versus no PA cath

Cochrane R & R: 2006

(Review and Reappraisal)

The PAC is a monitoring tool;

if it is used to direct therapy and there is no
improvement in outcome,
then the therapy does not help.

Pulmonary Artery Catheterization

Initially devised by Swan and Ganz.
Allows for view of Left Ventricular function by using
extrapolation of right heart measurements.
Catheter is floated into right side of the heart and
into a small pulmonary arteriole.
Catheter is then wedged and a pressure is
measured.
Pulmonary Capillary Wedge Pressure (PCWP) or
Pulmonary Occlusion Pressure (POP)

PCWP reflects Left Atrial Pressure (LAP) which

reflects Left Ventricular End Diastolic Pressure
(LVEDP) which reflects Left Ventricular End
Diastolic Volume (LVEDV)

Pulmonary arterial catheter

Indications for PAP monitoring

Shock of all types
Assessment of cardiovascular function and
response to therapy
Assessment of pulmonary status
Assessment of fluid requirement
Perioperative monitoring

Box. 1 No cap/on available.

Pulmonary artery catheter monitoring in 2011.

Richard, Chris/an; Monnet, Xavier; Teboul, Jean-Louis

Current Opinion in Cri/cal Care. 17(3):296-302, June
2011.
DOI: 10.1097/MCC.0b013e3283466b85
2011 Lippincoi Williams & Wilkins, Inc.

Cardiac Output

Compensatory Mechanisms
Heart
rate

beats
/min

Cardiac
Output

L/
min

Stroke
volume

ml/
beat

Heart Rate
heart rate increase in response to stress and tissue demands
for oxygen
maximum heart rate and VO2
baroreflex control of BP
increase in ejection fraction
dependence on Frank-Starling mechanism to maintain stroke volume

vagal tone increases

Stroke Volume
Range of normal at rest is 60 100 ml/b
Max. SV is 120 200 ml/b, depending on size, heredity, and
conditioning.
Increased SV due to complete filling of ventricles during
diastole and/or complete emptying of ventricles during systole
Rate of rise
Vascular tone

Cardiac Output: Heart Rate X Stroke Volume

Compensatory Mechanisms
Heart
rate

beats
/min

Cardiac
Output

L/
min

Stroke
volume

ml/
beat

Stroke Volume Index

Stroke index is defined as the amount of blood
pumped with each beat indexed to BSA
Normal 35-45 ml's/m2
Low values require treatment, especially if SvO2 is
low

Cardiac Output
Typically determined via thermodilution
A change in temperature of a known volume of cooled
infusate is used to calculate CO
How quickly or slowly the cooled infusate mixes with blood
determines the CO

Accuracy altered by conditions affecting the mixing of

infusate and blood
Tricuspid regurgitation, intracardiac shunts, cardiac
arrhythmias, positive pressure ventilation

Main circumstances in ICU

Positive pressure ventilation

Severe pulmonary embolism
ARDS
Sepsis induced RV dysfunction
Exacerbation of medical conditions leading to
chronic pulmonary hypertension
Right ventricle infarction
Pericardial diseases
RV failure after cardiac surgery
After cardiac transplant

Physiology of the normal pulmonary circulation

Low pressure system: PRV (syst) = 25 mmHg
versus PLV (syst) = 120 mmHg
The pressure in the pulmonary system depends on
cardiac output, resistance and compliance
Normally very compliant pulmonary vessels with large
diameter and thin wall
Normal RV afterload very low

alveolar hypoxia leads to pulmonary arterial

vasoconstriction and pulmonary vascular
resistance

RV Dysfunction in ICU

Management strategies for patients with

pulmonary hypertension in the
intensive care unit *.
Zamanian, Roham; Haddad, Francois;
Doyle, Ramona; Weinacker, Ann
Critical Care Medicine. 35(9):2037-2050,
September 2007.

Figure 2. Implica/ons of pulmonary hypertension on right ventricular (RV) func/on and hemodynamics. Development and progression of pulmonary
hypertension leads to right ventricular pressure overload, which impacts right ventricular systolic and diastolic func/on. Len ventricular (LV) dysfunc/on also 4
can result in the seong of right ventricular failure. The physiologic consequence of ventricular dysfunc/on in conjunc/on with development of arrhythmias,
tricuspid regurgita/on (TR), and worsening hypoxemia ul/mately lead to hypotension and circulatory collapse.

Effects of mechanical ventilation

Increased RV afterload due to positive pressure
ventilation
Hemodynamic failure frequently refractory in PAH
patient put on MV
In ARDS increase in mPAP while increasing tidal
volume and PEEP
Permissive hypercapnia is deleterious (increase in
mPAP)

Effect of MV on venous return

Effect of high PEEP on RV

Monitoring of right-sided heart function.

Jardin, Francois; Vieillard-Baron, Antoine
Current Opinion in Critical Care. 11(3):271-279, June 2005.

O2 requirements and blood supply to the RV

Less O2 requirements than the LV : myocardial
mass due toafterload
Vascularisation : 2/3 RCA, 1/3 left branches
RV perfused in both systolic and diastolic phases
low systolic pressure (25 mmHg) does not compress
vessel

Vicious cycle of auto-aggravation

Ventricular interdependence

During systole, LV protrudes in RV

Surrounding pericardium with limited distensibility
Compliance of one ventricle can modify the other =
Diastolic ventricular interaction

PA Catheter Pressures
Impacted by circumstances altering ventricular
compliance
Ischemia, LVH, hypertension, tamponade, AS

PEEP applied during mechanical ventilation

Once greater than 10 cm H2O pressures transmit across
vasculature and elevate PAWP

Changes during respiratory cycle

Intrathoracic pressure varies with inhalation/ exhalation,
impacting the PA catheter readings
Measure readings at end exhalation

Ventricular Function
Left ventricular function
Right ventricular function
Depressed right ventricular function was further
linked to more severely compromised left
ventricular function.

Nielsen et al. Intensive care med 32:585-94, 2006

Pulmonary artery catheter monitoring in 2011.

Richard, Christian; Monnet, Xavier; Teboul, Jean-Louis
Current Opinion in Critical Care. 17(3):296-302, June 2011.
3

Oxygenation Patterns with Normal

Function

Sv02 :0.6 0.8

Alveoli

RV

LA

RA

LV

Scv02 :0.65- 0.85

Cell

St02 :0.80- 0.90

Sa02 :0.95 1.0

What are the Normal Post Cell Reads?

60-80% sat
PA (mixed venous reading)
65-85% sat
central venous reading
75-85 %
thenar eminence
When all numbers low, failure to deliver oxygen
Not all patients are the same

SCVO2 Monitoring

Surrogate of global tissue hypoxia

Sepsis results in increased metabolic stress at the tissue level
Response is to increase cardiac output and/or O2 utilization
When O2 supply is overwhelmed by the disease, SCVO2 continues to
decrease (O2 demand > supply)
Thus, SCVO2 is proposed to be a marker of adequate O2 utilization at the
tissue level as a response to metabolic stress

Central Venous O2 Saturation (SCvO2)

Measures O2 saturation in the superior vena cava
May be measured continuously with available fiberoptic catheters or
intermittently with venous blood gases
More readily available as does not require a PA catheter
Reflects CvO2 of blood returned from upper body
SCvO2 typically higher than SvO2 but trend track in parallel

SvO2 v. ScvO2
100%

75%

StiO2

VO2

Managing Tissue Oxygenation

OxyHemoglobin
Dissociation

OXYGEN
Consump/on

OXYGEN
Delivery

Understanding Tissue Oxygen

Tissue Oxygenation
The single MOST important issue is tissue
oxygenation.
All physiologic components are designed to
maintain balanced tissue oxygen consumption
(demand).
What are the components of Oxygen
Consumption?

Oxygen delivery
Metabolic demand at the cellular level
Blood flow through the capillary
Ability to dissociate oxygen from hemoglobin

Understanding Tissue Oxygen

Components of Oxygen Delivery
1. Cardiac Output = Heart rate x stroke volume
2. Total hemoglobin (02 carrying capacity)
3. Saturation of hemoglobin
First line compensatory mechanism ( patient)
Increase the heart rate and stroke volume to increase delivery when
cells are hypermetabolic and/or when oxygen is not functionally
dissociating from its transporter, hemoglobin.

Understanding Tissue Oxygen

The amount of oxygen required by the cells
changes every second"
When demand/consumption increases, hemoglobin
releases oxygen more rapidly"
Shift to the right: release"

When demand/consumption decreases, hemoglobin

decreases release or latches on to oxygen"
Shift to the left: latched on"

Second compensatory mechanism: hemoglobin

more aggressively releases oxygen to dissolve in
the blood (partial pressure) to be used by the cells"

Understanding Tissue Oxygen

What is the purpose of saturating hemoglobin?
Hemoglobin is the transporter of oxygen
Each heme molecule binds 1.34 mLs of oxygen

When oxygen is bound it is not usable

Measure of bound oxygen in the arterial blood is the Sa02
(indirectly reflected by pulse oximetry Sp02)

Only oxygen dissolved in blood can be used

Measure of dissolved oxygen in the arterial blood is the
Pa02

The rate of oxygen use at the cell determines the Pa02

which in turn affects the dissociation

Understanding Tissue Oxygen

Oxygen dissociation as a compensatory response
Shifts in the bound oxygen mean that there is a
change in the way oxygen is
Taken up by the hemoglobin molecule at the alveolar
level (Sa02)
Depends on the partial pressure of alveolar gas (PA02)

Released related to the partial pressure of capillary

oxygen (Pa02, Pcap02)
Capillary oxygen depends on the tissue oxygen (Pti02)
Tissue oxygen goes down when cells are hypermetabolic
and/or the delivery is inadequate

Continuous SvO2 Monitoring

Incorporated into PA catheter
SvO2 changes rapidly when DO2 altered
May allow for rapid interventions as patients
condition changes

Global Tissue Hypoxia:

A More Sensitive Measure of Shock

OxyHemoglobin
Dissociation

OXYGEN
Consump/on

OXYGEN
Delivery

Understanding Tissue Oxygen

Tissue Oxygenation
There are two mechanisms designed to meet
oxygen consumption (demand)
Increase oxygen delivery
Increase the release (dissociation) of oxygen from
hemoglobin

In the best of critical situations, both delivery and

dissociation increase to maintain cells
failure of one mechanism will be supported by
compensation by the other

Managing Tissue Oxygenation

OxyHemoglobin
Dissociation

OXYGEN
Consump/on

OXYGEN
Delivery

Dissociation must be measured in the venous compartment

Sv02
Scv02

Pv02

Oxygenation Patterns
with Normal Function

Sv02 :0.6 0.8

Alveoli

RV

LA

RA

LV

Scv02 :0.65- 0.85

Cell
Sa02 :0.95 1.0

Compensation in attempts to sustain Tissue Oxygen

PROBLEM
Oxygen delivery inadequate for
oxygen demand
Primary failure

OXYGEN
release
COMPENSATION:
Shin to the right
Release oxygen to save the
cells

MEASURE:
Scv02
Always Compensatory
Always an EMERGENCY

OXYGEN
Delivery
OXYGEN
Demand &
Consump/on

Compensation Oxygenation

Sv02
Scv02
Low
Pv02

Compensation in attempts to sustain Tissue Oxygen

PROBLEM
Scv02 normal to in the face of
suspicion (HR, RR persistent
acidosis (LA))
MUST BE considered as failure to release
oxygen (in the presence of LA)

OXYGEN
release

OXYGEN
Demand &
Consump/on

OXYGEN
Delivery
COMPENSATION:
Cardiac output increases
Despite increase, /ssue
hypoperfusion persists (LA)

Compensation in attempts to sustain Tissue Oxygen

Sv02
Normal to
High
With
Persistent
Lactic
Acidosis

Cells do not
need it!
OR
Cells need it
but cannot
get it!

Pv02

Monitoring Venous Oxygenation

ScvO2 is usually less than SvO2 by about 23% but
two change in parallel
In septic shock ScvO2 often exceeds SvO2 by
about 8% -correlation between these two
parameters may worsen
ScvO2/SvO2 should not be used alone in
assessment of cardiocirculatory system

The Research

Chawla et al. Lack of equivalence between central and mixed

venous oxygen saturation. Chest 2004; 126:18911896
--------

53 critically ill patients that SvO2 was consistently

lower than ScvO2 (P < 0.0001), with a mean bias of
5.2 5.1%, ScvO2 was not a reliable surrogate
Tahvanainen J, Can central venous blood replace mixed venous
blood samples? Crit Care Med 1982; 10:758761 ------ ScvO2

equivalent to SvO2

is

Dueck MH et al. Trends but not individual values of central venous

oxygen saturation agree with mixed venous oxygen saturation
during varying hemodynamic conditions. Anesthesiology 2005;
103:249257

----- 70 neurosurgical patients, trends of ScvO2

and SvO2 are interchangeable

Why do we need dynamic fluid measures

What about other information?

With a thermaldilution, transpulmonary system, it is
possible to calculate and index:
Global end diastolic volume
Extravascular lung water
Measurements of extravascular lung water (EVLW) correlate
to the degree of pulmonary edema and have substantial
prognostic information in critically ill patients.
normal EVLW (defined as < 10mL/kg)

Mar/n GS, Eaton S, Mealer M, Moss M. Extravascular lung water in pa/ents with severe sepsis: aprospec/ve cohort study. Crit Care 2005;9:R74
R82.
Kuzkov VV, Kirov MY, Sovershaev MA, et al. Extravascular lung water determined with single transpulmonary thermodilu/on correlates with the
severity of sepsis-induced acute lung injury. CritCare Med 2006;34:16471653. [
Groeneveld AB, Verheij J. Extravascular lung water to blood volume ra/os as measures of permeability in sepsis-induced ALI/ARDS. Intensive Care
Med 2006;32:13151321.
Patroni/ N, Bellani G, Maggioni E, Mano A, Marcora B, Pesen/ A. Measurement of pulmonary edema in pa/ents with acute respiratory distress
syndrome. Crit Care Med 2005;33:25472554.

Newer Methodologies for Obtaining CO Data

The arterial pressure wave form results from
interactions of the vascular system and the ejected
SV
Analyzing the waveform allows for determination of
SV
CO then simply calculated by equation:
CO = HR x SV

Compensatory Mechanisms
Heart
rate

beats
/min

Cardiac
Output

L/
min

Stroke
volume

ml/
beat

Why do we give volume

Volume expasion for hemodynamically unstable paQents

Increase stroke volume (SV) and cardiac output (CO)

Only 50% of patients respond to a fluid challenge
Cumulative fluid balance may affect outcome
Whether the patient is responsive to fluid or not?
Optimal strategy of increasing CO and oxygen delivery

Newer Methodologies for Obtaining CO Data

Stroke volume variation
Determined with arterial pressure cardiac output monitors
Shown to predict volume responsiveness in mechanically
ventilated patients
An algorithm utilizing this concept follows

Aortic pulse wave

Pressure [mmHg]

Systolic pressure

120

100

80

Average pressure

1 second

Diastolic pressure

Pulse pressure = systolic pressure - diastolic pressure

Am J Respir Crit Care Med 2000; 162:134-138

PP =

PPmax
PPmin

40

PPmax - PPmin
(PPmax + PPmin) /2

Use of Heart Lung Interactions to Diagnose PreloadResponsiveness

ValSalva maneuver
Ventilation-induced changes in:

Right atrial pressure

Systolic arterial pressure
Arterial pulse pressure
Inferior vena caval diameter
Superior vena caval diameter

Perel et al. Anesthesiology 67:498-502, 1987

Sharpey-Schaer. Br Med J 1:693-699, 1955

Jardin & Vieillard-Baron. Intensive Care Med 29:1426-34, Zema et al., D Chest 85,59-64, 1984
2003
Michard et al. Am J Respir Crit Care Med 162:134-8, 2000 Magder et al. J Crit Care 7:7685, 1992
Vieillard-Baron et al. Am J Respir Crit Care Med 168: 671-6,
2003

Frank-Starling relationship
Stroke
Volume

Normal

Heart Failure

0
0

Preload

Fluid Responsiveness
% increase in stroke volume after volume
expansion.
Responders 15 %
Non Responders < 15%

The Goal is to Improve Oxygen Delivery

Respiratory Variations in LV Stroke Volume

Airway pressure up

Ventricular compliance and volume load down

Pulmonary Vascular transit Time

Venous Return

RVEDV

Ventricular pressure up
(resistance )

RVSV

pulmonary venous
return

LVEDV
LVSV

CVP, PA , PaOP

Static Parameters vs. Dynamic Parameters

Frank-Starling relationship
Stroke
Volume

ExhalaQon
Stroke volume varia/on occurring
with ITP change
inspiraQon

0
0

Preload

Frank-Starling relationship
Stroke
Volume

hypovolemic
opQmized

VariaQon
normal

Preload

Preload Dependence Optimization Concept

Stroke
Volume

PP /POP Minimization
0
0

Preload

Cardiopulmonary Interactions
The more sensitive a ventricle is to preload, the
more the stroke volume will be impacted by
changes in preload due to positive pressure
ventilation.
AP

AP

Preload Independent

Dynamic change of SV =
inspira/on

Preload Dependent

SVmax SV min
(SVmax + SV min)/2

Variation from Ventilation

SVV, PPV, and SPV are
created by tidal volumeinduced changes in venous
return.
presumes a constant R-R
interval and are measured
from diastole to systole
+ presure ventilation causes
changes in venous return,
which is accentuated in
hypovolemic patients
take advantage of the swings
in venous return in order to
determine the fluid
responsiveness of hypotensive
patients

Lose their
predictive value
under conditions of
varying R-R intervals
(atrial fibrillation),
tidal volume varies
from breath to breath
(with assisted and
spontaneous
ventilation)

When do measures become less reliable?

aortic insufficiency
Peripheral vascular disease
intra-aortic counterpulsation
cardiac arrhythmias
SIMV, other forms of ventilation that have limited
changes ( APRV,HFOV, ) or uncontrolled changes
(SIMV)

SVV physiology

Normal heart

Stroke
Volume

SVV

Preload-dependence

Failing heart

Preload-independence

Ventricular preload

Normal Variation & Pulsus Paradoxus

In a normal individual who is breathing spontaneously, blood
pressure decreases on inspiration
The exaggeration of this phenomenon is called pulsus paradoxus
F.Michard
Expiration

Pulsus Paradoxus

Inspiration

Arterial
Pressure
Time

Reversed Pulsus Paradoxus

Inspiration

Arterial
Pressure

Expiration

Time
A phenomenon that is the reverse of the conventional pulsus
paradoxus has been reported during positive pressure breathing
F. Michard

Calculate is variability

Assign PA label
Go to the wedge window
Edit and store trace
Move my cursor
High Systole: 154
Low Systole: 148
High diastole: 84
Low diastole: 80
High systole high diastole: MAX PP
Low systole low diastole: MIN PP
MAX PP= 154-84 = 70
MIN PP= 148-80= 68

MEAN PP Max + min/2= 69

MAX PP MIN PP/ mean PP
70-68=2/69
2% variation

Pulse Pressure Variation

Pulse pressure variation (PPV)
Calculated in the same manner as SVV,
Also predict preload responsiveness well.

A 13% PPV predicts a 15% increase in CO for a

500-mL volume bolus
ANY signal that gives pulse density
REQUIRED
Controlled variables
Ventilation
Heart rate

What are the Limitations of SVV?

Mechanical Ventilation
Currently, literature supports the use of SVV on patients
who are 100% mechanically (control mode) ventilated
with tidal volumes of more than 8cc/kg and fixed
respiratory rates.

Spontaneous Ventilation
Currently, literature does not support the use of SVV with
patients who are spontaneously breathing.

Arrhythmias
Arrhythmias can dramatically affect SVV. Thus, SVVs
utility as a guide for volume resuscitation is greatest in
absence of arrhythmias.

Emerging trends in minimally invasive haemodynamic monitoring and opQmizaQon of uid therapy.
Benington S; Ferris P; Nirmalan M

European Journal of Anaesthesiology. 26(11):893-905, 2009 Nov.

11

Are the pulse analysis techniques as accurate as

the PAC for monitoring CO?
Yes, (level of evidence, C)
but it depends.
Not all monitors are the same.
In stable patients they perform to a clinically acceptable level
and have other advantages.
Continuous data
Less invasive
Offer other variables.

In shocked patients the evidence is less clear.

A. Rhodes , personal communication ESICM 2010

Why are we concerned about too much volume or

volume that is in the wrong place?

What about other information?

With a thermodilution, transpulmonary system, it is
possible to calculate and index:
Intrathoracic blood volume
Pulmonary vascular permeability index
Increased capillary permeability during the first 48 h in
patients with sepsis was associated with a higher mortality
rate during the intensive care unit (ICU) stay than those with
decreased permeability 1, 2

1. Hotchkiss RS, Karl IE (2003) The pathophysiology and treatment of sepsis.N Engl J Med 348: 138150.
2. Abid O, Sun Q , Sugimoto K, Mercan D, Vincent JL (2001) Predic/ve value of microalbuminuria in medical ICU pa/ents: results of a pilot
study. Chest 120:19841988.

What does thermodilution do for me

Fluid responsiveness: PPV and SVV
CO measurement
Transpulmonary thermodilution
Pulse contour analysis

Extravascular lung water index (EVLWI): a good

surrogate assessment of pulmonary edema
Global end-diastolic volume index (GEDI): a
volumetric preload assessment
Cardiac function index: a calculated index of
cardiac function
Pulmonary vascular permeability index (PVPI)

Emerging trends in minimally invasive haemodynamic monitoring and opQmizaQon of uid therapy.
Benington S; Ferris P; Nirmalan M

European Journal of Anaesthesiology. 26(11):893-905, 2009 Nov.

What am I looking for?

Indices of hypovolemia: SVV > 13%
volume loading should decrease SVV. If not
Stop fluid administration
Inotropic support initiated

Goals for cardiocirculatory therapy

ScvO2 >70% or SvO2 >65%

MAP (mean arterial pressure) >65 mmHg
Cardiac Index >2.0 l/min/m2
CVP 815 mmHg (dependent on ventilation mode)
SVV < 13 %
ITBVI 8501000 ml/m2
GEDVI 640800 ml/m2
PAOP 1215 mmHg
Diuresis >0.5 ml/kgBW/h
Lactate <3 mmol/l

GMS German Medical Science 2010, Vol. 8, pp 1-25

Carl,M. Alms,A. et al

Cardiac Output Optimization Concept

EVLW
Stroke
Volume

Cardiac Ouput Maximization

0
0

Preload

Why do we need EVLWI

Diagnosis
Prognosis
Goal to aggressive therapy
Better guide to resuscitation in patients at risk for
pulmonary edema (anyone with high permeability
index)
Shock or severe sepsis
ALI
CHF

Case Presentation 1
54 year old man with fever and
abnormal liver function for liver biopsy
Biopsy well tolerated until 3 hours
afterwards when he developed
abdominal distension , with systolic
BP 60 and Hg 8.6

Case Presentation 1a

HR 128, RR 26
22% SVV what now?
EVLWI < 8
Next?

Volume responsive!

Case Presentation 1b

SVV 13%
BP 80/40
EVLWI > 12
Next?

Vasopressor

Case Presentation 1c

SVV 20%
EVLWI 10%
Next?

Volume, inotrope

Newer Methodologies for Obtaining CO Data

The arterial pressure wave form results from
interactions of the vascular system and the ejected
SV
Analyzing the waveform allows for determination of
SV
CO then simply calculated by equation:
CO = HR x SV

Newer Methodologies for Obtaining CO Data

Stroke volume variation
Determined with arterial pressure cardiac output monitors
Shown to predict volume responsiveness in mechanically
ventilated patients
An algorithm utilizing this concept follows

Hemodynamic Monitoring Truth

No monitoring device, no matter how simple or
complex, invasive or non-invasive, inaccurate or
precise will improve outcome
Unless coupled to a treatment, which itself
improves outcome

Pinsky & Payen. Func/onal Hemodynamic Monitoring, Springer,

2004

Volts

Amp.

Bioimpedance

Vo
Io

Bioreactance

Io
Vo

Perfusion Index
Perfusion Index is an objective method for
measuring a patients peripheral perfusion
Perfusion Index is an early indicator of
deterioration

Perfusion Index
Satura/on

Infrared
Red

What is a Normal PI ?
108 healthy, 37 critically ill adults (finger
sensors)
PI range: 0.3% to 10%, median 1.4%
ROC used to determine the cutoff value
1.4% PI best discriminated normal from
abnormal
Lima, et al. CCM 2002

Clinical Uses for PI

Normals have been suggested to be:
>1.4% adults, >1.27% neonates

1.Site selection (varies between patients and sites)

2.Chorioamnionitis (placental membrane/amniotic fluid
infection)
3.Effectiveness of Servoflorane anesthesia
4.Monitor onset/effectiveness of epidural anesthesia
5.Predict illness severity scores (good correlation)
6.Monitor/quantify peripheral perfusion
7.Detect shock states
8.PI trend may best reflect changes in condition

R IR

Absorption

Photoplethysmography

Pleth Waveform

Photodetector

Time

Pleth Waveform

A-line versus Pulse Ox Pleth

McLean Method
Heart Rate

IOS

Cardiac

Volume

SV
SVV
PPV
Systolic
pressure

PPV
SVV
SV
EVLW
U/O ml/kg
Echo
Oxyhemoglobin
Dissocia/on

Echo
Oxyhemoglobin
Dissocia/on

Tissue

Respiratory Rate

Vascular Tone
PPV
SVV
PPV/SVV
Diastolic pressure
Echo
Oxyhemoglobin
Dissocia/on

Anion Gap, Serum C02, Base, pH, Lac/c acid, Ketones, S/0

What do these patients have in common?

PaQent 1

PaQent 2

PaQent 3

HR 127

133

113

RR 34

28

18

Pa02 70
PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV

91
PaC02 35
0.70
PEEP 15
Rate 15 SIMV

100
PaC02 39
0.5
PEEP 20
Rate 10 SIMV

BPS 80
BPD 55

BPS 80
BPD 40

BPS 100
BPD 60

What do these patients have in common?

PaQent 1

PaQent 2

PaQent 3

HR 127

133

113

RR 34

28

18

Pa02 70
PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV

91
PaC02 35
0.70
PEEP 15
Rate 15 SIMV

100
PaC02 39
0.5
PEEP 20
Rate 10 SIMV

BPS 80
BPD 55

BPS 80
BPD 40

BPS 100
BPD 60

Sv02 45%

Sv02 70%

Sv02 65

What do these patients have in common?

PaQent 1

PaQent 2

PaQent 3

HR 127

133

113

RR 34

28

18

Pa02 70
PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV

91
PaC02 35
0.70
PEEP 15
Rate 15 SIMV

100
PaC02 39
0.5
PEEP 20
Rate 10 SIMV

BPS 80
BPD 55

BPS 80
BPD 40

BPS 100
BPD 60

PP 25
SVV 16%

PP 40
SVV 21%

PP 40
SVV 15%

Sv02 45%

Sv02 70%

Sv02 65

What do these patients have in common?

PaQent 1

PaQent 2

PaQent 3

HR 127

133

113

RR 34

28

18

Pa02 70
PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV

91
PaC02 35
0.70
PEEP 15
Rate 15 SIMV

100
PaC02 39
0.5
PEEP 20
Rate 10 SIMV

BPS 80
BPD 55

BPS 80
BPD 40

BPS 100
BPD 60

PP 25
PPV 16%

PP 40
PPV 21%

PP 40
PPV 15%

Sv02 45%

Sv02 70%

Sv02 65

AG 34

AG 41

AG 13

LA 6.1

LA 7.2

LA 2.8

Remember
A searchlight cannot be used effectively without a
fairly thorough knowledge of the territory to be
searched.

Fergus Macartney, FRCP