basic & advanced hemodynamic monitoring part 2

Advanced Hemodynamics PART 2

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

Grady Memorial Hospital, Atlanta GA, USA

[email protected] 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

Intravascular volume

Myocardial contraction and heart rate

Vasoactivity

4 factors that aec/ng the haemodynamic condi/ons

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

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.

Preparation

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

Preload

Stroke Volume

0 0

Cardiac Ouput Maximization

Cardiac Output Optimization Concept

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 Ohms 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

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

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

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

Systemic venoconstriction

Decrease right ventricular compliance

Obstruction of the great veins

Tricuspid regurgitation

Mechanical ventilation

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

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)

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,

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

Preload = CVP = PAOP= LAP = LVEDP All equal volume??!!!???

Is ventricular geometry

unchanged?

Is ventricular compliance unchanged?

Is there valve

disease?

Are intrathoracic or intra-abdominal

pressures elevated?

Catheter properly

positioned?

CVP is accurate ONLY when these potential sources of error have been eliminated

CVP Variability

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

responsiveness

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

INSP

EXP 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

2011 Lippincoi Williams & Wilkins, Inc. 3

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

Box. 1 No cap/on available.

Cardiac Output

Stroke volume

Cardiac Output

L/ min

ml/ beat

Compensatory Mechanisms

Heart rate

beats/min

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

Heart rate

Stroke volume

Cardiac Output

beats/min

L/ min

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

4

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.

RV Dysfunction in ICU

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 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

3

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

RA

LA

LV

Alveoli Sv02 :0.6 0.8

Sa02 :0.95 1.0 Scv02 :0.65- 0.85

Oxygenation Patterns with Normal Function

Cell

RV

St02 :0.80- 0.90

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%

VO2

75% StiO2

Managing Tissue Oxygenation

OxyHemoglobin Dissociation

OXYGEN Delivery

OXYGEN Consump/on

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 OxygenComponents 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


OXYGEN Delivery

OXYGEN Consump/on

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


OXYGEN Delivery

OXYGEN Consump/on

Dissociation must be measured in the venous compartment

Pv02

Sv02 Scv02

RA

LA

LV

Alveoli Sv02 :0.6 0.8

Sa02 :0.95 1.0 Scv02 :0.65- 0.85

Oxygenation Patterns with Normal Function

Cell

RV

OXYGEN release

OXYGEN Demand &

Consump/on

OXYGEN Delivery

Compensation in attempts to sustain Tissue Oxygen

COMPENSATION: Shin to the right Release oxygen to save the cells MEASURE: Scv02 Always Compensatory Always an EMERGENCY

PROBLEM Oxygen delivery inadequate for oxygen demand Primary failure

Sv02 Scv02 Low

Pv02

Compensation Oxygenation


OXYGEN Demand &

Consump/on

OXYGEN Delivery

OXYGEN release

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

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)

Sv02 Normal to High With Persistent Lactic Acidosis

Pv02


Cells do not need it!

OR

Cells need it but cannot get it!

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 is equivalent to SvO2

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:R74R82. 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

Heart rate

Stroke volume

Cardiac Output

beats/min

L/ min

ml/ beat


Why do we give volume

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

Volume expasion for hemodynamically unstable paQents

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

Systolic pressure

Diastolic pressure

Average pressure

Pulse pressure = systolic pressure - diastolic pressure

80

100

120

1 second

Pressure [m

mHg]

Aortic pulse wave

40

PPmax

PPmin

PPmax - PPmin

(PPmax + PPmin) /2

PP =

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

Use of Heart Lung Interactions to Diagnose Preload-Responsiveness

ValSalva maneuver Ventilation-induced changes in:

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

Sharpey-Schaer. Br Med J 1:693-699, 1955 Zema et al., D Chest 85,59-64, 1984 Magder et al. J Crit Care 7:7685, 1992

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

Michard et al. Am J Respir Crit Care Med 162:134-8, 2000

Jardin & Vieillard-Baron. Intensive Care Med 29:1426-34, 2003

Vieillard-Baron et al. Am J Respir Crit Care Med 168: 671-6, 2003

Preload

Stroke Volume

0

0

Normal

Heart Failure

Frank-Starling relationship

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

Venous Return RVEDV

RVSV

pulmonary venous return

LVEDV

LVSV

Pulmonary Vascular transit Time

Static Parameters vs. Dynamic Parameters

Airway pressure up Ventricular compliance and volume load down

Ventricular pressure up (resistance )

CVP, PA , PaOP

Preload

Stroke Volume

0

0

ExhalaQon

inspiraQon


Stroke volume varia/on occurring with ITP change

Preload

Stroke Volume

VariaQon opQmized


normal

hypovolemic

Preload

Stroke Volume

0 0

PP /POP Minimization

Preload Dependence Optimization Concept

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.

Preload Independent Preload Dependent

AP AP

= SVmax SV min (SVmax + SV min)/2

Dynamic change of SV inspira/on

Variation from Ventilation

SVV, PPV, and SPV are created by tidal volume-induced 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)

.

Stroke Volume

Ventricular preload

Preload-dependence

Preload-independence

Normal heart

Failing heart

SVV physiology

SVV

Normal Variation & Pulsus Paradoxus

Arterial Pressure

Time

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

F.Michard

Pulsus Paradoxus Expiration Inspiration

Reversed Pulsus Paradoxus

Arterial Pressure

Time

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

F. Michard

Expiration

Inspiration

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.

11

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.

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)

7

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

Preload

Stroke Volume

0 0

Cardiac Ouput Maximization

Cardiac Output Optimization Concept

EVLW

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

0

Volts

Io

Vo

Io

Vo

0

Amp.

Bioimpedance

Bioreactance

Perfusion Index Perfusion Index is an objective method for

measuring a patients peripheral perfusion Perfusion Index is an early indicator of

deterioration

Perfusion Index

Infrared

Satura/on

Red

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

What is a Normal PI ?

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

Photoplethysmography

Abso

rptio

n

Time

R IR

Photodetector

Pleth Waveform

Pleth Waveform

A-line versus Pulse Ox Pleth

McLean Method

Cardiac

Heart Rate

SV

SVV

PPV Systolic pressure

Echo Oxyhemoglobin Dissocia/on

Volume

IOS

PPV SVV SV

EVLW U/O ml/kg

Echo Oxyhemoglobin Dissocia/on

Vascular Tone

Respiratory Rate

PPV

SVV

PPV/SVV Diastolic pressure

Echo

Oxyhemoglobin Dissocia/on

Tissue 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


BPS 80 BPD 55

BPS 80 BPD 40

BPS 100 BPD 60


HR 127 133 113

RR 34 28 18




BPS 80 BPD 55

BPS 80 BPD 40

BPS 100 BPD 60

Sv02 45% Sv02 70% Sv02 65


HR 127 133 113

RR 34 28 18




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


HR 127 133 113

RR 34 28 18




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

basic & advanced hemodynamic monitoring part 2

Documents

pressure bag

sense pressure

cardiovascular system

pump pressure transducer

hemodynamic monitoring

monitoring device

catheter system

svv central venous pressure