Determinants of CO
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Determinants of Cardiac OutputDeterminants of Cardiac Output
Carol Wesley MSN, CCRN
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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
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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
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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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