evaluating the cardiovascular status. The pediatricheart rate is influenced by age and disease process.Neonates have the added influence of gestational ageand weight. Additional influences on heart rate includecentral nervous system dysfunction, autonomicdysfunction, stress, drugs, sepsis, anemia,hyperthermia, and endocrine dysfunction (e.g. thyroid).Since cardiac output equals stroke volume times heartrate, monitoring changes in heart rate can reflect anacute change in the patient’s condition or trendimpending problems.

Patients in respiratory failure frequently have anincrease in heart rate to improve cardiac output and tocompensate for decreased oxygenation. Although,increasing heart rate is an effective mechanism forincreasing cardiac output, there is a point whenincreasing the heart rate will cause the cardiac outputto decrease as the decreased time for ventricular fillingand coronary blood flow effect cardiac efficiency.

Bradycardia can be associated with episodes of apnea

Introduction

There is an inextricable link between hemodynamiccharacteristics and response to ventilation settings.Therefore, a careful evaluation of cardiovascularfunction in critically ill patients with pulmonarydisease is an important aspect of their ventilatorymanagement. It is also then important to understandand utilize those tools and measurements that willenhance our understanding of these inter-relationships.

Matching Ventilation/Perfusion

The goal of breathing is to match alveolar ventilationwith pulmonary perfusion to obtain an ideal V/Qbalance as it is the major determinant of PaO2 andPaCO2. While our ventilation management determinesthe "V" component, there are three major determinantsof pulmonary "Q". They are myocardial function, thepulmonary blood volume, and pulmonary vascularresistance (PVR).

There are many factors which play a role in PVR. Thelung is not a passive participant in PVR but plays anactive role affecting PVR by lung volume (Figure 1).The lung parenchyma not only tethers the airways, buttethers the extra alveolar vessels. At low lung volume,there is a reduction in radial traction reducing thecross-sectional area of the extra alveolar vascular bed,increasing PVR in these vessels. As lung volumeincreases, PVR falls to its minimal level at an optimumlung volume. However, if mean airway pressure (Paw)continues to increase lung volume resulting in overdistention of the alveoli, this results in compression ofthe intra-alveolar vessels which lack perivascularsupport resulting in a rise of PVR. Because of this directaction by the ventilator on a major component ofhemodynamic performance, it is therefore important totrack hemodynamic responses while changing Paw.

Clinical Cardiovascular Monitoring Heart Rate

Monitoring the heart rate is an essential element for

ritical Care ReviewCURRENT APPLICATIONS AND ECONOMICS

Managing Hemodynamics During High Frequency Oscillatory VentilationStephen Minton, MD

lung volume (cc)

vasc

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0.12

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Figure 1.

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and hypoxia. Other physiologic dysfunctionsassociated with a decrease in heart rate include cardiacischemia, mechanical defects, hypovolemia, andincreased vascular resistance. On rare occasions, it hasbeen seen secondary to a reflex response to high PEEPor Paw.

Blood Pressure

Arterial blood pressure is the dynamic measurement ofthe force of blood against the wall of the arteryreflected during systole (tension during LV contraction),and diastole (relaxation pressure during ventriculardiastole). Pulse pressure, the difference between thesystolic and diastolic, reflects the ventricular ejectionamplitude. Normal values vary in the pediatric patientby age, sex, and method of monitoring. Neonateshave the additional effects of gestational age, birthweight, and postnatal age to consider.

Hypotension may result from true low blood volume,low effective blood volume secondary to peripheralvasodilatation, or left ventricular dysfunction.Hypotension induced reduction in oxygenation deliverymay result in tissue hypoxia and elevation of lactic acidlevels. Hypertension, or an elevated blood pressure,can be the result of increased peripheral vascularresistance or fluid overload. Pulse pressure can beincreased with the left-to-right shunt from a patentductus arteriosus (PDA) or decreased by shock,hypovolemia, or heart failure.

In the pediatric population, considerable informationcan be obtained from the arterial pressure tracing. Theshape of the tracing, pulse pressure, and location ofthe dicrotic notch, all give pertinent hemodynamicinformation about the patient.

Central Venous Pressure

Central venous pressure (CVP) is the pressure obtainedfrom a catheter inserted into the superior vena cava orthe right atrium. It is crucial when using this pressureto be certain of the catheter’s placement (Fig 2). In theneonate, slight displacement of the catheter from theright atrium can result in fictitious measurements.These errors can result from placing the catheteracross the foramen ovale into the left atrium, or byplacing it too far into the right atrium with partialobstruction from the intra-atrial septum. If the catheteris not inserted far enough, the pressure may reflecthepatic pressures. Both an AP and lateral chest x-rayfor placement is very helpful. In our nursery, wedocument UVC placement with ultrasonography.

About 70% of the time, the correct placement isapproximately T9 on AP chest x-ray. With normalcardiac status, CVP reflects right atrium pressure,which correlates with right ventricular pressure. CVP isused to evaluate pre-load to the right ventricle. Itallows us to evaluate hemodynamic states such asintravascular volume, intra-thoracic pressure, andresponse to volume replacement.

The normal range for CVP in the neonate and pediatricpatient varies, ranging from 0-8 mmHg. However, inour experience, we cannot usually use high frequencyoscillatory ventilation (HFOV) effectively if the CVP’s inthe 0-3 mmHg range, but may require CVP’s of 5-8mmHg to allow increasing Paw above the criticalopening pressure of the lung.

CVP’s decrease in hypovolemia or with any mechanismcausing delayed venous return to the right heart.Increasing levels of Paw without blood volumeexpansion can also cause decreases in venous return.Increases in CVP’s are seen in right heart failure,hypervolemia, or myocardial dysfunction.

While the validity of CVP in the critically ill ormechanically ventilated patient has been questioned, inour experience, if the CVP is placed in the appropriateposition (entrance of right atrium), it is very valuable inevaluating right ventricular preload.

Pulmonary Artery Occlusion or “Wedge” Pressure

Pulmonary artery occlusion or “wedge” pressure isused for measuring the preload for the left ventricle.The Swan-Ganz catheter introduction by right heart

Figure 2.

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catheterization into the pulmonary artery (PA) is thestandard method in pediatrics and adults for evaluatingpulmonary vascular hemodynamics. The indicationsfor a PA catheter include discriminating cardiac andnoncardiac causes of pulmonary infiltrates, titration offluid therapy, evaluation of pharmacologicinterventions in pulmonary hypertension, and todetermine the etiology of hypotension.

To obtain a pulmonary capillary wedge pressure(PCWP), the distal lumen of the catheter is used.Balloon inflation isolates the distal tip of the catheterfrom upstream pulmonary arterial pressure creating astatic, nonflowing column of blood distal to theballoon. Without flow there is no pressure drop alongthe column of fluid. The pressure at the catheter tipmeasures pressure in the pulmonary vein. Becausethere is normally minimal resistance in the pulmonaryveins, the pressure measured approximates thepressure in the left atrium.

Oxygen Delivery

Oxygen tension (PaO2) is the partial pressure of oxygenin the arterial blood. PaO2 is affected by FiO2, alveolarventilation, diffusion defects, V/Q mismatch, and shunt(intrapulmonary or intracardiac). Oxygen is carried bythe blood in two ways. Although we frequently focuson PaO2, this dissolved oxygen (0.0031 ml/torr) is onlya small fraction (< 5%) of O2 carried in the blood. Theremaining and most significant portion is carriedbound with the hemoglobin (Hb) as determined by theO2 saturation. Each gram of Hb can carry 1.34 ml of O2

and therefore, the arterial oxygen content (CaO2) or thetotal amount of oxygen carried is dramatically effectedby changes in hemoglobin.

Normal CaO2 is approximately 20 ml O2/dl blood(Vol%). To emphasize the difference between PaO2 andCaO2 (CaO2 = O2 carried by Hb + dissolved O2),consider the aspects of varying Hb concentration onthe following patients:

Patient 1: The CaO2 for a child with a Hb of15 gm, PaO2 of 100 torr and O2 Satof 97%:= (15 x 1.34 x 0.97) + (0.0031 x 100)= 19.50 ml O2/dl + 0.31 ml O2/dl= 19.81 ml O2/dl

Patient 2: The CaO2 for a child with a Hb of8 gm, PaO2 of 100 torr and O2 Satof 97%:

CaO2 = O2 carried by Hb + dissolved O2

= (8 x 1.34 x 0.97) + (0.0031 x 100)= 10.40 ml O2/dl + 0.31 ml O2/dl= 10.71 ml O2/dl

These two examples demonstrate the dramatic fall inblood oxygen content that occurs with the fall in Hb.Although both patients have the same PaO2 and O2

Sat, the second patient must almost double cardiacoutput to maintain the same oxygen delivery as thefirst patient.

Oxygen Extraction

The Arterial-Venous Difference (A-VDO2)

The Arterial-Venous difference (A-VDO2) is the amountof O2 extracted by the tissues and is commonly used inthe ICU as an indirect measurement of cardiac output.The A-VDO2 is derived from oxygen contentcalculations from arterial and mixed venous blooddrawn simultaneously. The normal CaO2 isapproximately 20 Vol% while the CvO2 is 15 Vol%.Therefore only 5 ml O2 in each 100 ml is extracted forutilization by the tissues. An increase in the A-VDO2

indicates that either tissue extraction has increased orcardiac output has decreased. Conversely, a decreasein the A-VDO2 usually indicates an increase in cardiacoutput. Ideally, a true venous sample should be drawnfrom the pulmonary artery. If drawn from the rightatrium, there is an increased probability for poorvenous mixing and loss of data reliability.

Cardiac Output In Pediatric Patients

Methods used to directly measure cardiac output inpediatric patients include the Fick equation, dyeindicator-dilution and most commonly by the use ofthermal dilution. The thermal dilution technique utilizesinjection of chilled 0.9% sodium chloride into theright atrium while the temperature of the blood isconstantly measured in the pulmonary artery with a thermistor-tipped catheter. The warming of the salinereflect the blood flow heat transfer. This is an accuratemethod of determining cardiac output that allowsrepeated measurements, however, consideration mustbe given when administering volume to infants andsmall children relative to the potential for fluidoverload. The newest thermal dilution technologyreplaces cold boluses as an indicator with pulses ofenergy from a thermal filament in the catheter. Thiseliminates the potential of fluid overload and canprovide continuous measurements.

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Cardiac performance can also be assessed clinically byobservation of indirect signs, frequently presented asthe signs of poor organ perfusion. Signs andsymptoms of low cardiac output include cool and paleextremities (skin), oliguria (renal), and decreased levelof consciousness (CNS). Variables that may be usedindirectly to measure the adequacy of cardiac outputinclude: systemic blood pressure, right atrial pressure(CVP), left atrial pressure (LAP), urine output, blood pHand lactate levels, and arterial venous oxygendifference (A-VDO2).

Because pediatric patients have greater variation insize, it is important to normalize cardiac output by thecardiac index (CI = cardiac output per square meter ofbody surface area). The CO in children is higher perkilogram of body weight than the adult, resulting in ahigher CI. When comparing the child’s cardiac functionto the adult, it is important to note that the rangeof increase in stroke volume is much smaller andtherefore a child’s cardiac output is more directlyproportional to heart rate. Tachycardia in thepediatric patient is the most efficient way to increasecardiac output.

Echocardiographic Evaluation of

Cardiovascular Function

The heart is a parallel pump that delivers blood intotwo circuits, the right heart to the lungs and the leftheart to the systemic circulation. It is critical that theseparallel pumps work in sync to meet the metabolicdemands of the body for oxygen and nutrients and theremoval of the byproducts of metabolism. In theneonate where signs and symptoms of respiratorydistress, sepsis, and metabolic derangements maymimic those of congenital heart disease, it may bemore difficult to arrive at a correct hemodynamicinterpretation at the bedside without more advancedtechnology. In complex heart-lung interactions,the only true methods to evaluate myocardialfunction are with an echocardiogram and pulmonaryartery catheter.

Left Ventricular Performance

The stroke volume component of CO is affectedby cardiac preload, myocardial contractility andafterload. Stroke volume will rise when preloador myocardial contractility improves and fall whenafterload increases.

The measurement of left ventricular end-diastolicvolume (LVED) reflects preload. This volume effects the

stretch of the myocardial fiber length. Preloaddecreases with blood loss, inadequate fluidmaintenance and during positive pressure ventilation.Fluid volume replacement will usually correct adecreased preload in a healthy myocardium. Fluidoverload increases preload and can be treated withdiuretics. Preload can be evaluated using CVP andcircumferential fiber shortening (VCFc).

Afterload is the resistance to blood flow from theventricle and is effected by aortic pressure, radius ofthe ventricle, peripheral vascular resistance and theviscosity of the blood. It increases with hypertensionand an enlarged ventricle. Decreases in afterload areseen with anemia, vasodilation and central shunting ofblood volume. Pharmacologic agents such asNitroprusside that alter vascular tone will also changeright and left ventricular afterload. Left ventricularafterload can be evaluated measuring left ventricularposterior wall stress. Laplace’s Law states that wallstress of a chamber is equal to the pressure times thecavity diameter/wall thickness. Combining bloodpressure with left ventricular wall thickness and cavitydimensions allows calculation of peak systolic wallstress (PSS).

The force of contraction of the heart, reflected in theefficiency of myocardial fiber shortening, is calledcontractility. Left Ventricular Shortening Fraction (LVSF)and Ventricular Ejection Fraction (VEF) are bestestimated when the left ventricle is circular. In thepremature infant, there is intraventricular septalflattening causing distortion of the shape of the leftventricle and a decrease in circularity. This results in ashortening fraction in the neonate which canunderestimate the differences in regional ventricularfunction. Decrease in contractility occurs with hypoxia,acidosis, with certain drugs and glucose abnormalities.Inotropic drugs will usually improve contractility andcardiac output once preload deficits have beencorrected. Common inotropic agents utilized toimprove contractility include Dopamine, Dobutamine,Epinephrine, Isoproterenol, Norepinephrine andAmrinone. The ratio of PSS and VCFc allows betterevaluation of myocardial function by reducing theeffect of preload and postload. Other echocardiographicmeasures that may assist in evaluation of leftventricular function include Left Ventricular CardiacOutput calculated from the velocity time integral aorticvalve area and heart rate, Left Ventricular Volume, andLeft Ventricular Systolic Time Interval (LVSTI) as anindex of LVS function.

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Right Ventricular Performance

In the neonate, the right heart is more difficult toevaluate echocardiographically. The right ventricle liesdirectly beneath the sternum, has an irregular crescentshape, and trabeculated walls. Useful right ventricularperformance measurements include right ventricularafterload (estimated by measuring right ventricular enddiastolic diameter-RVEDD), Right Systolic Time Interval(RSTI), and Right Ventricular Output (calculated fromthe velocity time integral x pulmonary valve area xheart rate).

Pulmonary Artery Pressure

Echocardiography is also an ideal noninvasive methodfor estimating pulmonary artery pressure andevaluating the degree of pulmonary arteryhypertension. Right ventricular systolic time intervalscan reflect elevated pulmonary vascular resistance.Echocardiography can be used to measure the velocityand direction of flow across the PDA. Use of thetricuspid regurgant jet across the tricuspid valve andCVP in a simplified Bernoulli’s equation gives anestimate of the Systolic Pulmonary Artery Pressure(SPAP). This method has been shown to be morereliable than the other echocardiographic methods.

Ductus Venous

The ductus venous can be assessed ultrasonographicallyfor flow pattern. The flow pattern reflects theportocaval pressure gradient and the pressure on theright side of the heart and in the pulmonary arteries.

Shunts

Patterns of flow across a Patent Foramen Ovale (PFO)or ductus arteriosus can be recorded by color flow andpulsed-wave Doppler studies. The size of the defect,direction of shunt, and velocity can be estimated.Contrast echocardiography to evaluate PFO flow usingan agitated saline flush can be performed if color flowis unsatisfactory.

Hemodynamics In High Frequency Oscillatory

Ventilation

Abnormal respiratory function treated with assistedmechanical ventilation can alter lung volume,pulmonary vascular resistance, or intrathoracicpressure. All of these can have significant effects onnormal and abnormal circulatory function. Duringconventional mechanical ventilation (CMV) increasingthe tidal volume can decrease venous return.Increasing PEEP is associated with decreased cardiacoutput, although cardiac function has generally been

observed to be normal with PEEP.

The decreased cardiac output with PEEP appears to bedue to decreased venous return. Administration offluids can usually overcome the decreased venousreturn and restore cardiac output.

The decreased venous return with increasing PEEP canbe explained in Figure 3. As lung volume increaseswith PEEP, intrathoracic pressure increases by anamount determined by chest wall compliance and thelung volume. This effect is transmitted to the rightatrium, where it decreases venous return. As PEEPincreases from zero to 20 (PEEP 20 = cardiac functioncurve with PEEP 20), there is a progressive rightwardshift in the cardiac function curves (ZEEP = cardiacfunction curve with zero end expiratory pressure; PEEP10 and PEEP 20 = cardiac function curve with 10 and 20cmH20 PEEP). The point of intersection between thecardiac function and venous return curves shifts fromPoint A to B to C. Point D is a theoretical point ofintersection between the original venous return curveand the cardiac function curve on PEEP, which wouldhave been the situation had mean circulatory pressurenot increased with PEEP. Thus, increased meancirculatory pressure buffered the effects of increasedPEEP on cardiac output and venous return. There isalso a decrease in the downward slope of the venousreturn curve with PEEP which suggests an increase inthe resistance to venous return as well. In addition,Fessler demonstrated a vascular waterfall in theInferior Vena Cava (IVC) associated with mechanicalcompression of the lower lobes of the right lung on the

PEEP 10 PEEP 20ZEEP

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Figure 3. Effects of PEEP on the Determinants of

Venous Return

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IVC causing a flow limitation. Veddeng found PEEPapplied to the right lung alone limits cardiac outputmore than PEEP to the left lung alone. This effect maybe explained on the basis of either direct mechanicalcompression by the inflating lung on the right ventricleand right atrium with greater increases in right atrialpressure and hence greater decreases in venous returnor exceeding a critical closing pressure of the inferiorvena cava.

There have been relatively few studies in the literatureconcerning cardiovascular effects of HFOV, especiallyin immature subjects.

The ventilatory strategy used in all pathophysiologiesexcept gross air leak is an optimum lung volumestrategy. Because the tidal volumes are very small inHFOV, the lung volumes remain near constant. Meanairway pressure is increased on the inflation limb ofthe pressure volume above the critical openingpressure of the lung. Lung volume is maintained abovethe critical closing pressure of the lung on the deflationlimb of the hysteresis curve. This results in a higher“PEEP” than seen in CMV. However, because in CMVthere is an expiration time with a lower pressure(usually a low PEEP), it is more forgiving in its effect onvenous return for the same blood volume than thehigher “PEEP” seen in HFOV. Although when HFOVPaw is similar to that of CMV, several authors found nosignificant differences in cardiac output, organ bloodflow, or metabolic status.

Traverse, et al, found impairment of hemodynamics onHFOV in the cat model. They found that cardiac outputdecreased and pulmonary vascular resistanceincreased with increasing Paw. Although the responsewas diminished in animals with decreased respiratorysystem compliance, it was not eliminated.

Kinsella, et al, investigated the hemodynamicconsequences of ventilator strategies for HFOV andCMV in the baboon model of HMD using the radiolabeled microsphere technique. Measuring cardiacoutput and organ blood flow at three time points (3, 8,and 23 hours) showed no significant differences in leftventricular output, effective systemic flow, organ bloodflow, or central venous pressure. The HFOV strategyresulted in significant improvement in oxygenationduring the 24 hours of treatment without adverse effecton left ventricular output, cerebral blood flow, orcentral venous pressure.

Nicol, et al, studied changes in aortic blood flow andblood pressure in normal and surfactant deficientrabbits under varying ventilator strategies ofConventional Tidal Volume Ventilation (CMV), InverseRatio Ventilation (IRV), High Frequency PositivePressure Ventilation (HFV) and High FrequencyOscillatory Ventilation (HFOV). Each strategy was alsostudied at PEEP (Paw) levels of 0, 5 and 10 cmH2O. Inthe injured lungs, when 10 cmH2O of distendingpressure was applied, PaO2 increased with all modes,but the aortic blood flow was significantly reduced(p<0.05) with a 40% reduction in calculated oxygendelivery during CMV and IRV as compared to HFV orHFOV. They concluded that hemodynamic stability isbetter maintained during HFV or HFOV when highPEEP levels are required for oxygenation.

Minton, et al, compared the hemodynamics in 100newborn infants with birth weights less than 2500grams with RDS randomized to either CMV andsurfactant or HFOV and surfactant. The strategy usedon HFOV was an optimum lung volume strategy. Theyfound no difference in cardiac output or right and leftventricular hemodynamics if close attention was paidto blood volume expansion.

We have subsequently reported on 299 patients onHFOV who underwent 1420 echocardiograms in thefirst 21 days of life. In these patients (GA 22.5 to 42weeks and BW 310 to 5200 grams) we found a slightincrease in cardiac output with advancing gestationage and birth weight increasing from 280 cc at 23weeks to 300 cc at 41 weeks. Mean cardiac output was314 cc/kg/mm with a standard deviation of 28cc/kg/mm. There did not appear to be any effects onleft or right hemodynamics, cardiac output, orincidence of patent ductus arteriosus or foramen ovaleshunting in these patients. The cardiovascular effectsof a patent ductus arteriosus (in a premature baboonmodel of HMD treated with CV or HFOV) were studiedby Yoder, et al. There were no significant differencesbetween the two forms of ventilation when MAP, HR,CO, or modes of ventilation were compared.

Gutierrez, et al, evaluated eight of their pediatricpatients who had been managed with HFOV for severerespiratory failure and had pulmonary artery cathetersin place. With significant 50% increases in meanairway pressures from CMV to HFOV (20.9 cmH2O to30 cmH2O), the only observed effect was a meanreduction in heart rate of 20 beats/min. Oxygen

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delivery, cardiac index, and mean systemic arterialblood pressure did not change significantly followingthe change to HFOV with the exception of one patient.

Blood Volume Expansion and Inotropic Support

Venous return is influenced by the blood volume and areduction will cause a decrease in cardiac output andhypotension. It is important to correct hypovolemia byfluid replacement. Decreases in cardiac output mayalso occur in patients with normal volume status andinotropic drugs may be used to improve theirmyocardial function.

Measurement of the left atrial pressure (LAP) providesthe most accurate guide to fluid replacement and is theearliest indicator of hypovolemia. CVP reflects theright ventricular end diastolic pressure. Although CVPis often a poor correlate of left-sided filling pressure,its measurement is important in the assessment of right-sided pressure of the patients with right-sidedobstructive lesions.

Preload is best assessed by the measurement of LAP.If filling pressures are low, volume should beadministered using normal saline, lactated Ringer’s,Plasmatate, plasma, 5% albumin, or blood transfusion.In the neonate, usual fluid replacement is administeredwith 5-10% glucose at a rate of 80-100 ml/kg/day.When cardiac output is compromised, a fluid challengemay be required until stabilization occurs.

Once the preload is optimized, cardiac output andsystemic blood pressure should be measured again. Ifthe output is still low, but the BP is now elevated, aperipheral vasodilator should be used to decreaseventricular afterload (nitroprusside + nitroglycerin).Preload should be carefully monitored during theinfusion of vasodilators as sudden peripheralvasodilatation may increase the need for volumeadministration. If the cardiac output and bloodpressure remain low after preload optimization, thencontractility should be increased by the use of inotropicagents. Several drugs that are used have bothinotropic and vasoactive properties.

RAP of less than 6 mm Hg may be challenged withfluid bolus of 10 ml/kg. Pressures between 6-10 mmHgmay require a fluid bolus of 5 ml/kg and pressures ofgreater than 10 mmHg may respond to a bolus of 3ml/kg. All volume is infused over 30-60 minutes. If theRAP continues to be within 2 mmHg of the originalmeasurement repeat the fluid bolus. The bolus can be

repeated times three until cardiac output improveswhich will be reflected by an increase in RAP greaterthan 2 mmHg than the original pressure. If there is noimprovement, an echocardiogram should beperformed for spatial anatomy, myocardial function,and chamber dimensions.

Inotropic Support

Dopamine

1. Low Dose: 2-5 µg/kg/min IV. Low dose Dopamineincreases renal perfusion and has a minimal effect onheart rate and cardiac output.

2. Intermediate Dose: 5-15 µg/kg/min IV. Effectsinclude increases in renal perfusion, heart rate, cardiaccontractility and cardiac output.

3. High Dose: >20 µg/kg/min IV. High doses increasesystemic vascular resistance and supports arterial BP.High doses of Dopamine decreases renal perfusion.

4. Maximum Dose: 20-50 µg/kg/min IV.

Dobutamine

1. Continuous IV infusion: 2.5-15 µg/kg/min.Dobutamine is an effective beta adrenergic andincreases arterial BP and myocardial contractility.Tachycardia and hypertension may occur.

2. Maximum Dose: 40 µg/kg/min.

Intractable Shock

Patients on HFOV that experience intractable shock inthe face of maximum inotropic support and adequatefluid administration should be considered foralternative treatment. These alternatives includetransitioning the patient back to conventionalmechanical ventilation or transfer to an ECMO facility.

In our experience, careful selection of mean airwaypressures to optimize lung inflation, adequate fluidadministration with appropriate inotropic agent anduse of all the monitoring techniques described in thisarticle, has limited cases of intractable shock to ahandful in more than 600 infants we have treated withthe SensorMedics 3100A.

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REFERENCES1 Arnold JH et al. High frequency oscillatory ventilation inpediatric respiratory failure. Crit Care Med 1993;21:272-8.

2 Arnold JH et al. Prospective, randomized comparison ofhigh frequency oscillatory ventilation and conventionalmechanical ventilation in pediatric respiratory failure. CritCare Med 1994;22:1530-9.

3 Berglund JE, Haldén E, Jakobson S, Svensson J. PEEPventilation does not cause humorally mediated cardiac outputdepression in pigs. Intensive Care Med 1994;20:360-364.

4 Berglund JE, Haldén E, Jakobson S. The effect of PEEPventilation on cardiac function in closed chest pigs. Ups JMed Sci 1994;99:167-178.

5 Blumer J. Pediatric Intensive Care (3rd Ed).

6 Boyton BR, Waldemar CA, Jobe AH. New therapies forneonatal respiratory failure (Reference Book). CambridgeUniversity Press, 1994.

7 Clark RH, Null DM. High frequency oscillatory ventilation(Book Chapter). Neonatology for the Clinician. 1993 Chapter24, pp. 289-309.

8 Dally EK, Schroeder JS. Bedside Hemodynamic Monitoring(Reference Book). Mosby, 1985.

9 Dantzker DR, Scharf SM. Cardiopulmonary Critical Care(Reference Book). WB Saunders, 1998.

10 Fessler HE, Brower RG, Shapiro EP, Permutt S. Effects ofpositive end-expiratory pressure and body position onpressure in the thoracic great veins. Am Rev Resp Dis 1993;148:1657-1664.

11 Fessler HE, Brower RG, Wise RA, Permutt S. Effects ofpositive end-expiratory pressure on the canine venous returncurve. Am Rev Resp Dis 1992;146:4-10.

12 Goldsmith JP. Assisted Ventilation of the Neonate(Reference Book). WB Saunders, 1998.

13 Gutierrez JA et al. Hemodynamic effects of high frequencyoscillatory ventilation in severe pediatric respiratory failure.Intensive Care Med 1995;21:505-10.

14 Hazinski T. Nursing Care of the Critically III Child (2nd Ed).

P/N 770118-006 Copyright © SensorMedics Corporation 1999

SensorMedics Corporation22705 Savi Ranch ParkwayYorba Linda, CA 92887-4645Telephone: (800) 520-4368 • (714) 283-1830Fax: (714) 283-8493http://www.sensormedics.com

SensorMedics BVRembrandtlaan 1b3723 BG BilthovenThe NetherlandsTelephone: (31) 30 2289711Fax: (31) 30 2286244

15 Johnson KB. The Harriet Lane Handbook (ReferenceBook). Mosby, 1993.

16 Kinsella, JP, Gerstmann DR, Clark RH et al. High frequencyoscillatory ventilation versus intermittent mandatoryventilation: Early hemodynamic effects in the prematurebaboon with hyaline membrane disease. Pediatric Research1991; 29:160-166.

17 Minton SD. Echocardiographic comparison of highfrequency oscillatory ventilation to conventional mechanicalventilation in neonate with respiratory distress syndromeduring the first twenty-four hours of life (Abstract). Soc CritCare Med 1996.

18 Minton SD, Gerstmann DR, Stoddard RA. Use of highfrequency oscillatory ventilation in newborns (CourseSyllabus). 1995 Utah Valley Regional Medical Center AdvanceTraining Course, Provo, Utah.

19 Morrow WR, Taylor AF, Kinsella JP, et al. Effect of ductalpatency on organ blood flow and pulmonary function in thepreterm baboon with hyaline membrane disease. Critical CareMedicine 1995; 23:179-186.

20 Nicol ME, Dritsopoulou A, Wang C, et al. Ventilationtechniques to minimize circulatory depression in rabbits withsurfactant deficient lungs. Pediatr Pulmonol 1994; 18:317-322.

21 Sprung CL. The Pulmonary Artery Catheter (ReferenceBook). University Park Press, 1993.

22 Traverse JH et al. Impairment of hemodynamics withincreasing mean airway pressure during high frequencyoscillatory ventilation. Pediatr Res 1988;23:628-31.

23 Veddeng OJ, Mybre ES, Risow C, Smiseth OA. Selectivepositive end-expiratory pressure and intracardiac dimensionsin dogs. J Appl Physiol 1992;73:2016-2020.

24 Weil MMH, Henning RJ. New concepts in the diagnosisand fluid treatment of circulatory shock. Anesth Analg 1979;58:124-131.

25 West JB. Pulmonary Pathophysiology (Reference Book).Williams & Wilkins, 1977.

26 Yoder BA, Kuehl TJ, deLemos RA, et al. Patent ductusarteriosus during high frequency ventilation for hyalinemembrane disease. Critical Care Medicine 1987:15:587-590.

ABOUT THE AUTHOR...

Stephen D. Minton, MD

Dr. Minton is the Director of Newborn Services and Medical Director of the Perinatal Center at Utah Valley RegionalMedical Center in Provo, Utah as well as the Medical Director of Newborn Nurseries at Orem Community Hospital inOrem, Utah. He has been a staff Neonatologist at UVRMC since 1979 and participates in numerous Neonatal andPediatric Committees and Programs. He is also a member of several medical associations, community activities, andinvolved in clinical research studies for the improvement of managing the critically ill.