Determinants of CO

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Determinants of Cardiac OutputDeterminants of Cardiac Output

Carol Wesley MSN, CCRN



ObjectivesObjectives

y Define Cardiac Output (CO) & thecomponents of CO

y Explain the effects of preload, afterload,

contractility, and heart rate on CardiacOutputy Describe the effects of various

medications on the determinants of Cardiac Output.

y Discuss hemodynamic terminologyy Discuss ways to measure CO (invasive &

noninvasive)

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Why Measure Cardiac Output?Why Measure Cardiac Output?

Cardiac output reflects the heart·s ability tomeet the metabolic demands of the

body·s organs and tissues

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What is Cardiac Output?What is Cardiac Output?

y The total volume of blood pumped by theheart per minute (mL blood/min)

y

Cardiac output is a function of: heart rate stroke volume

Normal value: 4.5- 6.5 L/min.CI= CO/ BSA

Normal Value: 2.8 L/min/m2

Avg body has 5 L of blood volume

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Cardiac OutputCardiac Output

TheThe amount of blood amount of blood

ejected by theejected by the ventricleventriclein one minute (L/Min).in one minute (L/Min).

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Cardiac output is a function of:Cardiac output is a function of:

heart rate

stroke volume

Normal value: 4.5- 6.5 L/min.

CI= CO/ BSA

Normal Value: 2.8 L/min/m2

Avg body has 5 L of blood volume

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Measurement of Cardiac OutputMeasurement of Cardiac Output

y Non-invasive

Perfusion

Patient History

Bioimpedeance cardiac output measurementy Invasive

Pulmonary Artery (PA) catheter

x Normal Cardiac Output 4-8 liters/minute

Cardiac Indexx CI= CO/BSA

x Normal Cardiac Index 2.5-4.0 L/min/m2

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ardiac Output (CO)Stroke volume (SV) x Heart Rate (HR)

Stroke Volume Heart Rate

Components of Cardiac OutputComponents of Cardiac Output

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Relationship of Determinants toRelationship of Determinants to

COCO

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Control of HRControl of HR

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Control of SVControl of SV

yThe amount of bloodejected by theventricle with eachsystolic contraction

y Stroke volume is

increased by 2

mechanisms:

increase in

sympathetic systemactivity

increase in end-

diastolic volumeSV = CO

HR

Normal Stroke Volume = 60-130 ml

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In other words«In other words«

Stroke VolumeStroke Volume = the difference between

end-diastolic volume (EDV) and end systolic

volume (ESV)

SV = EDV - ESV

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Ejection FractionEjection Fraction

Ejection Fraction is the Stroke Volume

Expressed as a percentage

EF = Stroke Volume

End-Diastolic Volume (EDV)

Normal EF ~ 70%

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Influences onInfluences on Stroke VolumeStroke Volume

Influences on Stroke VolumeInfluences on Stroke Volume

Preload

Afterload

Contractility

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Hemodynamic TerminologyHemodynamic Terminology

y Preload

y After load

y Contractility

y SVR

y PVR

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PreloadPreload

y Preload ² those pressures

and volumes that cause

myocardial muscle wall

stretching and wall tension

²

before ventricles eject volume

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Measuring PreloadMeasuring Preload

y Clinical Indicators

(1) Left Ventricular Preload = PCWP (PAOP)

(2) Right Ventricular Preload = CVP (RAP)

y Patient Assessment PCWP= pulmonary capillary wedge pressure

PAOP= pulmonary artery occlusion pressure

CVP= central venous pressure

RAP= right atrial pressure

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Frank Starling·s LawFrank Starling·s Law

The Starling Law

The greater amount of stretch imposed on the

ventricle by the end diastolic volume, the greater

the force of the subsequent myocardial

contraction

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Representation of StarlingRepresentation of Starling

Function CurveFunction Curve

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Factors Influencing PreloadFactors Influencing Preload

y Absolute blood volume

y Blood volume distribution

y Atrial kick

y Ventricular compliance

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PreloadPreload

Increased preload due to:Increased preload due to:Circulating volumeCirculating volumeUse of vasoconstrictorsUse of vasoconstrictorsMitral and aortic valve insufficiencyMitral and aortic valve insufficiency

Use of vasodilators decrease preloadUse of vasodilators decrease preload

Measured by RA pressure, End diastolic pressureMeasured by RA pressure, End diastolic pressure

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AfterloadAfterload

y Impedance or pressure against which theventricle ejects blood.

y Those forces that must be overcome to

eject blood from the ventricle ² what it is

pushing against.

Measured by MAP

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Measuring AfterloadMeasuring Afterload

Systemic Vascular Resistance (SVR)Systemic Vascular Resistance (SVR)

Resistance to ejection from the left side of the heartSVR = MAP - RAP X 80

CO

Normal = 800-1200 dynes/sec/cm5

MAP= Mean arterial pressure

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SVR (cont)SVR (cont)

y Causes of Increased SVR

Peripheral vasoconstriction

hypothermia

Causes of DecreasedSVR

Anesthetic agents

(residual affects) Allergic reaction

(protamine)

Sepsis

Hyperthermia

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Measuring AfterloadMeasuring Afterload

Pulmonary Vascular Resistance (PVR)Pulmonary Vascular Resistance (PVR)

Resistance to ejection from right side of the heart

PVR = PAP (Mean) - PCWP X 80CO

Normal = 50 - 250 dynes/sec/cm5

PAP= pulmonary artery pressure

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Factors Affecting AfterloadFactors Affecting Afterload

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Ventricular outflow obstruction

Ventricular dilation

SNS input

Pathologic conditions/ Compensatory Mechanisms

Temperature

Blood Viscosity

Medications



ContractilityContractility

y The ability of the myocardium to contract

and empty

No direct measurement

Best measurement is ejection fraction

Increase of sympathetic nervous system

increases contractility

Dopamine, Epinephrine, Dobutamine increasecontractility

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Measurements of ContractilityMeasurements of Contractility

y Cannot measure directly

(Measured with PA Catheter in place)

yy Stroke Work IndexStroke Work Index (SWI)(SWI)-- measures of the work

performed by the ventricle per contraction at a

constant End Diastolic Volume

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StrokeWork Index (SWI)StrokeWork Index (SWI)--

Left Ventricular Stroke Work Index (LVS WI)

SV x (MAPSV x (MAP -- PAD) x 0.0136PAD) x 0.0136BSABSA

= 38-85g/m2

/beat Right Ventricular Stroke Work Index (RVS WI)

SV x (Mean PAPSV x (Mean PAP--RAP) x 0.0136RAP) x 0.0136BSABSA

=7-12g/m2/beatBSA= body surface area

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Factors Affecting ContractilityFactors Affecting Contractility

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Ventricular Muscle Mass

Neurohumoral Input

HR

Oxygenation Status

Chemical or Pharmacological effects

Pathologic Conditions



Left Ventricular (LV) Function CurveLeft Ventricular (LV) Function Curve

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Manipulating Cardiac OutputManipulating Cardiac Output

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Adrenergic Receptors and CVAdrenergic Receptors and CV

Effects of StimulationEffects of Stimulation

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Medications Used to Stimulate or Block Medications Used to Stimulate or Block

CNS ReceptorsCNS Receptors

y Alpha (E)

1. Agonist: neosynephrine (Levophed)

2. Antagonist:P

hentolamine (R

egitine)y Beta ( F)

1. Agonist: Isoproterenol (Isuprel);

Dobutamine

2. Antagonist: beta blockers

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Medications Used to Stimulate or Block Medications Used to Stimulate or Block

CNS ReceptorsCNS Receptors

y Combination (E and F)

1. Agonist: epinephrine, norepinephrine, dopamine

2. Antagonist: labetalol

y Dopaminergic

1. Agonist: dopamine2. Antagonist: none

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Assessing COAssessing CO

y PA Catheter

CCO

Oximetric

x SVO2

y Noninvasive

measurements

y Minimally invasive

monitoring

Vigelo

x Arterial based CO

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PA cathetersPA catheters

y Swan ganz catheter

y Oximetric catheter

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MIXED VENOUS OXYGENMIXED VENOUS OXYGEN

SATURATIONSATURATION (SVO2)(SVO2)

Pa Catheter w/ fiberoptic oximetry system

SVO2 (normal 60-80%)

Fick's equation:

SvO2 = SaO2 -VO2 / 13.9 x Q x [Hb]

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Noninvasive MonitoringNoninvasive Monitoring

y Impedance

Cardiography (ICG)

provides parameters

including:

Cardiac Output /

Stroke Volume

Systemic Vascular

Resistance

Contractility Fluid Status

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Impedance Cardiography (ICG)Impedance Cardiography (ICG)

y Measures the beat-to-beat changes of

thoracic impedance using 4 dual sensors

applied on the neck and thorax in order

to calculate stroke volume.y Measures the impedance changes of the

thorax caused from the pumping heart to

monitor cardiac parameters

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Uses for ICGUses for ICG

y Establish baselinehemodynamic status toaid diagnosis, disposition,and treatment plan

y Trend and detect

changes for earlierintervention

y Identify appropriatetreatment options

y Monitor drug titration to

optimize therapy

Critical Care Specific

Decrease usage of PAcatheter (PAC)

- Replace PACs wherenoninvasive CO, SVR, andfluid trending can be utilized

instead

y If invasive procedurescontraindicated / not routinelyused

-Valve dysfunction-Thrombolytic therapy- High infection risk

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Minimally Invasive MonitoringMinimally Invasive Monitoring

y Vigileo

Uses the patient·s arterial

pressure waveform to

continuously measure cardiacoutput

Continuously computes stroke

volume from arterial pressure

signal

Displays hemodynamic parameters

(such as SVR

sensor measures the variations of the arterial pressure which isproportional to stroke volume

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VigileoVigileo

y Cardiac output is displayed

on a continuous basis by

multiplying the pulse rate

and calculated stroke

volume as determined from

the pressure waveform.

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Review and case studyReview and case study

y Causes of CO

x Hypovolemia

x Cardiogenic shock

x Late septic shock x Hypoperfusion

x Arrhythmias

x Metabolic acidosis

(severe)

y Causes of CO

x Hypoxia

x Use of + inotropes

x Early septic shock x Renal failure

x anemia

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Physical Assessment & COPhysical Assessment & CO

y Physical findings of

CO

BP

Tachycardia

Pulsus alterans

UO

y Physical findings of

CO

Tachycardia

body temp

Flushed warm skin

Tachypnea

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Hemodynamic Findings r/t COHemodynamic Findings r/t CO

y Hemodynamic

findings of CO

PAP

PCWP

SVR

y Hemodynamic

findings of CO

PCWP

SVR

PAP

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Case StudyCase Study

Read your case study««questions for

discussion:

y Define the following:

CO, CI, preload, afterload, PAP, PCWP

y Describe the benefits of using a PA

catheter during HFy Discuss the pathophysiology of HF

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ReferencesReferences

y Alspach, J.G. Instructor·s resource manual for theAACN core curriculum for critical care nursing.5th Ed. Saunders, 2001.

y Kinney, Dunbar, Brunn, Molter, CicciuAACNClinical Reference for Critical Care Nursing, 4th

Ed. Mosby, 1998

y PACEP.org

y

Urden, L.D. et al. Thelan·s Critical Care Nursing:Diagnosis and Management. Fourth Edition. St.Louis, MO. Mosby, Inc. 2002.

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Determinants of CO

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