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Functional Hemodynamic Indicators
Arterial Pressure Waveform Technology
Donna Adkisson, RN, MSN
Anatomy & Physiology Review
Blood Flow in the Heart
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From the body
Right side of the Heart
To the lungs for Oxygenation
 Air in via trachea
 Bronchus
 Bronchioles
 Alveoli
 Capillaries
 Oxygen in
 Carbon Dioxide out
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Left side of the Heart
Out the aorta
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Anatomy & Physiology Review
Anatomy & Physiology Review
Cardiac Cycle
Diastole – relaxation or filling
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Preload coming into right side of the heart
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70% of blood flows into the ventricles passively
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Other 30% from atrial kick
Systole – contraction or pumping
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Atrial Systole = Ventricular Diastole
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30% of blood flows into the ventricles from the atrial
contraction
Ventricular Systole
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How well can the heart pump – Ejection or Stroke
Volume
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What is the heart pumping against - SVR
Cardiac Output
CO = SV x HR
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Cardiac output is the volume of blood pumped by the heart per minute. For an average
size of adult (70 kg) at rest this would be about 5 liters/min. During severe exercise it
can increase to over 30 liters/min.
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Cardiac output is frequently necessary to assess the state of a patient's circulation.
The simplest measurements, such as heart rate and blood pressure, may be adequate
for many patients, but if there is a cardiovascular abnormality then more detailed
measurements are needed.
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Hemodynamic Monitoring
Hemodynamic Monitoring is an important
aspect of patient care in:
 Operating Rooms
 Critical Care Units
Hemodynamic Monitoring ranges from:
Non-Invasive
EKG
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NIBP
Invasive
Arterial Line
LiDCO
CVP
PA catheter
Functional Hemodynamic Monitoring
Transpulmonary Thermodilution (TPTD)
– Based on the Stewart-Hamilton equation
 LiDCOplus
 Pulse Power analysis to derive Stroke Volume
 Calibrated with Bolus dilution of lithium
 PiCCO
 Pulse contour analysis
 Temperature change sensed by thermistor-tipped arterial catheter
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Functional Hemodynamic Monitoring
Non-Calibrated
 LiDCOrapid
 Pulse Power analysis to derive Stroke Volume
 Same algorithm as the LiDCOplus
 FloTrac
 Proprietary sensor attached to arterial line
 Algorithm applied to analysis has been changed
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Hemodynamic Monitoring including:
Cardiac Output
Cardiac Index
SVR
Stroke Volume
Blood Pressure
DO2
Oxygen Consumption
Preload Indicators
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Cardiac Output
Ways to clinically determine Cardiac Output:
 Dilution method
 Thermodilution
 Green Dye
 Lithium Dilution
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Arterial Wave Form Analysis
Blood sample to calculate the Fick equation
Continuous Cardiac Output
TEE/EsopheagealDoppler
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Continuous Cardiac Output?
Sampling to get a 3 to 5 minute average
 PA catheter
Beat to Beat Continuous
 Arterial wave form analysis
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Beat-to-Beat Continuous Cardiac Output
Pulse Power waveform analysis continuously assesses the
patient's hemodynamic status by analyzing and processing
the arterial pressure signal obtained from the primary blood
pressure monitor.
• 0
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CO = SV x HR
Stroke Volume
The volume of blood per stroke of the heart
Effected by:
Amount of Blood coming into the heart – Preload
How well the heart works – Contractility
How much pressure or resistance the heart has to work against – Afterload
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CO = SV x HR
Stroke Volume
SV = Preload + Afterload + Contractility
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Preload – volume
Afterload – resistance (SVR)
Contractility – Muscle compliance (EF)
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Ventricular Preload and Fluid Responsiveness
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Fluid Resuscitation primary treatment of many shock states
Fluid Resuscitation is not without risk
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Less than 50% of patients respond to a fluid bolus.
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The heart performs more efficiently when appropriately filled.
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The term preload refers to maximum stretch on the heart's muscle fibers
at the end of diastolic filling. The degree of stretch is determined by the
volume of blood contained in the ventricle at that time.
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Ventricular Preload and Fluid Responsiveness
Commonly used static preload measurement are not sensitive or
specific predictors of a patient's ability to respond to fluid bolus
 CVP
 PAOP
Functional Hemodynamic Indices are more sensitive and specific
predictors of fluid responsiveness
 Reflect the effect of positive pressure
ventilation on preload and SV
 Pulse Pressure Variation
 Stroke Volume Variation
 Systolic Pressure Variation
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Functional Hemodynamics
Bridges, Elizabeth J. Arterial Pressure
– Based Stroke Volume and Functional
Hemodynamic Monitoring. Journal
of Cardiovascular Nursing,
March/April 2008;23(2): pp 105-112
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Preload
Systolic and Pulse pressure variation can be measured
 intermittently from the arterial line via the beside monitor
 continuously using
 PPV, SVV or SPV
 LiDCO system – plus or rapid
 FloTrac
 SVV
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Preload Indicators
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Systolic pressure variation (SPV) may reflect variations in pleural pressure and
changing LVSV. PPV reflects only changes in transmural aortic pressure and
therefore changes in LVSV on a beat-to-beat basis.
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Michard et al (1999) found PPV gave a more accurate measure of cardiac index
when compared to SPV, which it turn was a better measure than CVP and PAW.
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PPV was superior to SPV in predicting preload responsiveness proving to have
better precision with less variance.
Note: SPV and PPV do not require the patient to be in apnoea.
In fact they depend on positive pressure breathing.
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Best Preload Responsiveness - PPV
Michard F., Boussat S, Chemla D, et al.
Relation between respiratory changes in arterial
pulse pressure and fluid responsiveness in septic
patients with acute circulatory failure. American
Journal of Respiratory and Critical Care
Medicine. Jul 2000;162(1):134-138
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Hemodynamic Monitoring
Arterial Waveform Analysis
Preload indicator - looks at the variation from inspiration
to expiration of the patient
 PPV - Pulse Pressure Variation
» Greater than 10 to 13% patient
preload responsive
 SVV - Stroke Volume Variation
» Greater than 10 to 13% patient
preload responsive
 SPV - Systolic Pressure Variation
» Greater than 5mmHg patient
preload responsive
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Frank Starling’s Law
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The greater the ventricle is filled during diastole, the
more the muscle fibres are stretched, the greater is
the force of contraction.
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This is true to a defined point of stretch above which
point contraction force will not increase further.
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Frank Starling Curve
Frank-Sartling's Curve
90
Patient A is preload responsive
Patient B
80
SV
SV
Stroke Volume
70
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On steep part of curve
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Set preload results in
Significant increase in SV
Preload
60
50
Patient B is not preload responsive
40
Patient A
30
SV
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An equal preloading does not
result in a great increase in SV
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This patient does not require
fluid resuscitation
20
10
Preload
0
1
3
5
7
9
11
Preload
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13
15
17
19
Case Studies
Pulse Pressure Variation of 65%
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After ½ liter of volume down to 24%
After another ½ liter of volume down to 10%
Pulse Pressure Variation of 124%
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Patient on Epinephrine & Levophed drips
2 units of Albumin given
Within 24 hours, patient off all drips
Extubated
Pulse Pressure Variation of 38%, CO 2.8, EF 15%
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Pulmonary Edema & Peripheral Edema
500cc IV fluid, Lasix (times 4)
8 hours later: PPV 16%, CO 3.9
no increase in Pulmonary or Peripheral Edema
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Afterload
Systemic Vascular Resistance
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The amount of pressure the heart must work against
Decreases as CO & CI increases
Can be controlled with medications
 Vasoconstrictor – Increases SVR & BP
 Vasodialators – Decreases SVR & BP
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Drugs used to Effect SVR
Vasoactive Drugs – can be a vasoconstrictor or vasodialators
 Vasoconstrictors – increase SVR (afterload) and blood pressure, but
vary in their effect on cardiac output. The pure a agonists leave the output
of the normal heart unchanged, but may significantly reduce it in the failing
heart. As the beta activity of the vasoconstrictor is increased, so cardiac
output also tends to increase
 Vasodilators – Used to dilate arteries, Decrease SVR, Decrease BP
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Vasoactive Drugs
Vasoactive Drugs: vasoconstructors
 Isoproteranol – most widely used to ease breathing problems in asthma and COPD and to
control irregular heartbeat until a pacemaker can be implanted.
 Phenylephrine – Neo-Synephrine: used to treat shock and low blood pressure.
 Ephedrine – used to counteract the hypotensive effects of anesthesia. Also useful as a pressor
agent in hypotensive states following sympathectomy, or following overdosage drugs used for
lowering blood pressure in the treatment of arterial hypertension.
 Metaraminol – Aramine: used to raise the blood pressure and stimulate the heart in treating
patients with shock.
 Milrinone – Primacor : short-term treatment of patients with acute decompensated heart failure.
 Vasopressin – an alternative to noradrenaline in the treatment of hypotension effective in
combating milrinone-induced hypotension.
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Drugs used to Effect SVR
Vasodilators - Used to dilate arteries, Decrease SVR, Decrease BP
 Sodium Nitroprusside is the most potent of the 'mixed' vasodilators.
Reliably reduces both afterload and preload.
 Nitroglycerine acts predominantly on the venous side of the
circulation to reduce preload. The reduction in preload is
accompanied by a decrease in LV wall tension with a secondary
reduction in myocardial oxygen, also a specific coronary arterial
vasodilator and spasmolytic.
 Adenosine can be used for its vasodilatory effects. Because of its
short plasma half life (< 5 seconds), the drug has a particular role
as a relatively specific pulmonary vasodilator.
 Hydralazine acts exclusively on the arterial side of the circulation
to reduce afterload.
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Contractility
Muscle Compliance (EF)
 The ability of the muscle fiber to stretch and contract
Medications that can assist with contractility
 Epinephrine
 Dobutamine
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Contractility
Contractility
Myocardial
Contractility
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Is the power of contraction
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Is independent of preload or afterload
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At a constant preload
 positive inotropic agents > contractility > SV
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Drugs used to Effect Cardiac Output
Vasoactive Drugs – can be a vasoconstrictor or iontrope
 Vasoconstrictors: increase SVR (afterload) and blood
pressure, but vary in their effect on cardiac output. The
pure a agonists leave the output of the normal heart
unchanged, but may significantly reduce it in the failing
heart. As the beta activity of the vasoconstrictor is
increased, so cardiac output also tends to increase
 Inotrope: is an agent that alters the force or energy of
muscular contractions
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Positive Inotropic Agents
Inotrope:
is an agent that alters the force or energy of muscular contractions
 Adrenaline – Epinephrine (Epi or Adrenalin): used to treat shock, as a
heart stimulant.
 Noradrenaline – Norepinephrine (Levophed): used to increase the
output of the heart and raise blood pressure as part of the treatment of
shock.
 Dopamine – used for the correction of hemodynamic imbalances present
in the shock syndrome due to myocardial infarctions, trauma, endotoxic
septicemia, open heart surgery, renal failure, and chronic cardiac
decompensation as in congestive failure.
 Dobutamine – Dobutrex and generic forms: used to stimulate the heart
during surgery or after a heart attack or cardiac arrest.
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CO = SV x HR
Heart Rate
HR < 60 beats per minute
HR > 100 beats per minute
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Bradycardia – pacemaker, Atropine, Epinephrine
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Tachycardia – Cardioversion, Digoxin,
Treat fever or shock causing ↑ HR
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Cardiac Output Changes
Cardiac Output Decreases
 Decrease in blood volume
 Increase in PPV or SVV
 Decrease in ejection fraction
 Decrease in SV
 Decrease in Heart Rate
 Bradycardia
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Cardiac Output Increases
 Vasodilation
 Decrease in SVR
 Increase in Contractility
 Increase SV
 Increase in Heart Rate
 Tachycardiac
Decision Table
Does my patient need an increase in SV or CO?
↓Yes
Is the arterial trace accurate?
↓Yes
Is the patient fully ventilated?
↓Yes
Is the tidal volume > 8ml/kg
↓Yes
Is the cardiac rhythm regular
↓Yes
What is the PPV or SVV
< 10% → No fluid
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> 10 to 13% → Give fluid
Fluid replacement therapy
Non responder
Responder
Stroke volume
increases < 10%
Stroke volume
increases > 10%
100 - 200 ml
fluid challenge
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The Old Way is Not Good Enough
Hemodynamic monitoring has traditionally involved the
placement of a pulmonary artery catheter
Minimally invasive Cardiac Output Monitoring eliminates
the complications of the pulmonary artery catheter
Which includes:
Complications Related to Catheter
Vascular Complications
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Complications Related to
Pulmonary Artery Catheters
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Tachyarrhytmias
Right bundle branch block ( 0.05-5% )
Complete heart block ( with preexisting left bundle branch block )
Cardiac perfuration
Thrombosis and embolism
Pulmonary infarction due to persistent wedging ( 0-1.4% )
Catheter-related sepsis
PA rupture ( 0.2% chance )
Knotting of the catheter
Endocarditis, bland and infective
Pulmonic valve insufficiency
Balloon fragmentation and embolization
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Vascular Complications Related
to Pulmonary Artery Catheters
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Accidental arterial puncture
Pneumothorax
Braquial plexus lesion
Horner syndrome
Phrenic nerve lesion
Gaseous embolism
Hemorrhage
Infections
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Cost Related to Line Infections
Cost for Prolonged Bloodstream Infections can top $50,000
7 to 21 extra hospital days for Bloodstream Infections
New Medicare Regulations
Hospitals will no longer receive higher payments
for the additional costs associated with treating
patients for hospital-acquired infections
Payments will be withheld from hospitals for
care associated with treating vascular catheterassociated infections.
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New rules go into
effect October 2008
Cost Related to Line Infections
CDC reports that there are 248,678 cases of central line
associated bloodstream infections every year.
Institute for Healthcare Improvement estimates that
approximately 14,000 people die every year from
central line-related bloodstream infections.
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