Functional Hemodynamic IndicatorsArterial Pressure Waveform Technology

Donna Adkisson, RN, MSN

Blood Flow in the Heart 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

Left side of the Heart Out the aorta

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Anatomy & Physiology Review

Cardiac Cycle

Diastole – relaxation or filling

Preload coming into right side of the heart

70% of blood flows into the ventricles passively

Other 30% from atrial kick

Systole – contraction or pumping

Atrial Systole = Ventricular Diastole

30% of blood flows into the ventricles from the atrial contraction

Ventricular Systole

How well can the heart pump – Ejection or Stroke Volume

What is the heart pumping against - SVR

Anatomy & Physiology Review

Anatomy & Physiology Review

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Cardiac Output

CO = SV x HR

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.

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 Invasive

EKG NIBP Arterial Line LiDCO CVP PA catheter

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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 OutputCardiac IndexSVRStroke VolumeBlood PressureDO2Oxygen ConsumptionPreload Indicators

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Cardiac Output

Ways to clinically determine Cardiac Output:

Dilution method

Thermodilution

Green Dye

Lithium Dilution

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.

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CO = SV x HR

Stroke VolumeThe 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

Preload – volume Afterload – resistance (SVR) Contractility – Muscle compliance (EF)

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Ventricular Preload and Fluid Responsiveness

Fluid Resuscitation primary treatment of many shock states Fluid Resuscitation is not without risk Less than 50% of patients respond to a fluid bolus.

The heart performs more efficiently when appropriately filled.

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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Bridges, Elizabeth J. Arterial Pressure – Based Stroke Volume and Functional Hemodynamic Monitoring. Journal of Cardiovascular Nursing, March/April 2008;23(2): pp 105-112

Functional Hemodynamics

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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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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. 

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.

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.

Preload Indicators

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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

Best Preload Responsiveness - PPV

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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

Hemodynamic Monitoring

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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.

This is true to a defined point of stretch above which point contraction force will not increase further.

Frank Starling’s Law

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SV

Patient A is preload responsive

On steep part of curve

Set preload results in Significant increase in SV

Patient B is not preload responsive

An equal preloading does not result in a great increase in SV

This patient does not require fluid resuscitation

Frank-Sartling's Curve

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Preload

Str

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Preload

Preload

SV

SV

Patient B

Patient A

Frank Starling Curve

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Pulse Pressure Variation of 65% After ½ liter of volume down to 24% After another ½ liter of volume down to 10%

Pulse Pressure Variation of 124% 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% 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

Case Studies

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Afterload

Systemic Vascular Resistance

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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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

Drugs used to Effect SVR

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Vasoactive Drugs

Vasoactive Drugs: vasoconstructors

Isoproteranol – most widely used to ease breathing problems in asthma and COPD and tocontrol 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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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.

Drugs used to Effect SVR

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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

Is the power of contraction

Is independent of preload or afterload

At a constant preload positive inotropic agents > contractility > SV

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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

Drugs used to Effect Cardiac Output

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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.

Positive Inotropic Agents

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CO = SV x HR

Heart Rate

HR < 60 beats per minute

HR > 100 beats per minute

Bradycardia – pacemaker, Atropine, Epinephrine

Tachycardia – Cardioversion, Digoxin, Treat fever or shock causing ↑ HR

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Cardiac Output Decreases

Decrease in blood volume Increase in PPV or SVV

Decrease in ejection fraction Decrease in SV

Decrease in Heart Rate Bradycardia

Cardiac Output Increases

Vasodilation Decrease in SVR

Increase in Contractility Increase SV

Increase in Heart Rate Tachycardiac

Cardiac Output Changes

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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 > 10 to 13% → Give fluid

Decision Table

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Fluid replacement therapy

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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

The Old Way is Not Good Enough

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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

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

Vascular Complications Related to Pulmonary Artery Catheters

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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 catheter-associated infections.

New rules go into effect October 2008New rules go into effect October 2008

Cost Related to Line Infections

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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.

Cost Related to Line Infections

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