HEMODYNAMIC MONITORINGDaniel Saddawi-Konefka, MD, MBA, and Jonathan E. Charnin, MD CH

APTER6

1. What is the purpose of hemodynamic monitoring?Oxygen and fuels are brought to the tissues and waste products are removed by the flow ofblood. The goal of hemodynamic monitoring is to assess whether the circulatory system hasadequate performance in this regard to sustain organ function and life. Notably, hemodynamicmonitoring provides data to guide therapy but is not by itself therapeutic.

2. Howdomanual blood pressure cuffs differ from automatic bloodpressure cuffs?Manual auscultation of the blood pressure assigns systolic value to the pressure measuredwhen the first Korotkoff sound is heard and diastolic value to the pressure measured when thefourth Korotkoff sound disappears. Automatic blood pressure cuffs measure oscillations inpressure, caused by blood flow across a range of blood pressures; they determine only the meanblood pressure, which is determined by the point of greatest oscillation. With use of proprietaryalgorithms, the systolic and diastolic blood pressures are calculated. Both methods aresusceptible to error with poor cuff size (which should cover two thirds of the limb segment),motion artifact, arrhythmia, and extremes of blood pressure.

3. How are arterial lines calibrated, and what factors affect readings?Arterial lines generate blood pressure readings using pressure transducers. To yield usefulinformation, the transducers must first be zeroed and leveled (positioned appropriately). Second,the system should be monitored for damping and resonance.

Zeroing and leveling eliminate the effects of atmospheric pressure and hydrostatic pressure,respectively, on blood pressure readings. Atmospheric pressures are set to zero so that reportedvalues are relative pressures. If the system is not zeroed appropriately, measurements willcontinuously offset by a fixed amount. Errors can also occur if the transducer is physicallylowered so that it will read a higher pressure and vice versa (potential energy is replaced bypressure to maintain energy in the fluid; read about Bernoulli’s equation for more). Therefore it iscrucial to position the transducer at the height of interest (e.g., external acoustic meatus toapproximate pressure at the circle of Willis).

Damping is the tendency of an oscillating system to decrease oscillation amplitude. In the caseof an arterial line, the systolic and diastolic readings tend to converge around the meanpressure. Damping results from medium or large air bubbles in the circuit, compliant tubingbetween the transducer and cannulation site, loose connections, or kinks. Resonance or whipcauses falsely increased systolic readings and falsely decreased diastolic readings. It occurs whenthe system’s frequency of oscillation (i.e., heart rate) matches the system’s natural frequency ofvibration causing whip in the signal. The classic example of this (though not easy to accomplish) isbreaking a wine glass by singing a note of the same frequency as the wine glass’s resonantfrequency.

4. In what situations should arterial line placement be considered?n Inability to obtain noninvasive blood pressures.n Hemodynamic instability. Patients who need monitoring because of extremely high bloodpressure, extremely low blood pressure, or extremely volatile blood pressure.

39

n Need for rigorous blood pressure control. Patients who need blood pressure kept within a tightrange (e.g., status post aortic aneurysm repair).

n Need for frequent arterial blood sampling. Patients with severe ventilation compromise,oxygenation compromise, or other condition where it is useful to follow serial laboratory valueswith an arterial line.Choice of cannulation site is important because each site has unique benefits and risks.

The radial artery is often chosen given the convenient location and good collateral supply to thehand. In patients with severe vasoconstriction, however, a femoral line may be preferablebecause the radial pressure may underestimate central arterial pressure.

5. How do arterial tracings differ between proximal and distal cannulation sites?Arterial tracings become more peaked with higher systolic pressures but similar meanpressures as one transduces sites progressively distal from the aorta. The dicrotic notchrepresenting aortic valve closure is seen in the aorta and its largest branches but becomes lost inperipheral arteries. A smaller second wave of pressure during diastole represents pressure wavesreflecting off the peripheral resistance arterioles. This phenomenon can sometimes cause apulse-oximeter to double count the pulse.

6. List indications for central line placement.Central lines are indicated for monitoring the central venous pressure, infusing concentratedvasopressors, delivering total parenteral nutrition, sampling central venous blood for analysis,and obtaining venous access when peripheral access cannot be obtained.

7. Describe the central venous waveform components. Which part of the waveformcycle should be reported as the central venous pressure?Central venous pressures have predictable waveforms. These waveforms have upwarddeflections representing atrial contraction (“a” wave), ventricular contraction that causesthe tricuspid valve to bulge into the atrium (“c” wave), and passive venous return of blood duringdiastole (“v” wave). (Note the somewhat counterintuitive fact that ventricular contractioncoincides with the “c” wave, not the “v” wave.) The downslope after the “c” wave is called the “x”descent, and the downslope after the “v” wave is called the “y” descent. See Figure 6-1.

Central venous pressure should reflect the end-diastolic distention of the ventricle. Therefore thepressure measured should be immediately before systole. This corresponds to the valleyimmediately before the “c” wave and immediately after the “a” wave. In addition, becauseintrathoracic pressure (which is transmitted to the central veins) varies with respiration, pressuresshould be measured at end-expiration to minimize this effect on measurements.

8. List the indications for pulmonary artery catheter (PAC) placement.Indications to place a PAC include monitoring pulmonary artery pressures, measuring cardiacoutput by using thermodilution, assessing left ventricular filling pressures, and allowingsampling of true mixed-venous blood.

9. Describe complications of central line or PAC placement.Central line complications include pneumothorax, arterial puncture, line infection, arrhythmia,hematoma, and deep venous thrombosis. Rarer complications include thoracic duct injury andcardiac tamponade.

All the aforementioned central line complications can also arise during PAC placement. Inaddition, PAC placement can result in transient right bundle branch block through directmechanicalirritation of the right ventricle; therefore, PACs are relatively contraindicated in patients withleft bundle branch blocks because of the potential for complete heart block. Lastly, pulmonaryarterial rupture, which is usually fatal, can occur if care with the balloon tip is not taken.

40 CHAPTER 6 HEMODYNAMIC MONITORING

10. Describe normal pressures and waveforms encountered as a PAC is advanced.The inflated balloon on the distal tip will advance with the flow of blood through the superiorvena cava, right atrium, right ventricle, and ultimately the pulmonary artery. Different waveformsare obtained at each position as illustrated below.

The right atrial pressures are similar to central venous pressures described in question 7.Right ventricular pressures will have systolic components that are in phase with (i.e., occursynchronously with) systemic arterial systolic pressures and have low diastolic pressures thatincrease during diastole. Systolic pulmonary arterial pressures will also be in phase withsystemic arterial systolic pressures and have similar waveforms that gradually decrease duringdiastole. The pulmonary artery occlusion pressure (PAOP)—or wedge pressure if no balloon isused—reflects the left atrial pressure and thereby left ventricular filling. Because the wedgepressure reflects the left atrial pressures, it may have “a,” “c,” and “v” waves, although inpractice these may difficult to identify. Large “v” waves due to mitral regurgitation can occur onthe PAOP trace, but these large “v” waves will occur during late systole and early diastole. SeeFigure 6-2.

DiastoleSystoleDiastole

SVC

IVC

PA

RARV

a

c x yv

a

Figure 6-1. Central venous waveform components. IVC, Inferior vena cava; PA, pulmonaryartery; RA, right atrium; RV, right ventricle; SVC, superior vena cava.

CHAPTER 6 HEMODYNAMIC MONITORING 41

11. Normally, central venous pressures gauge right ventricular end-diastolic volumeand pulmonary arterial occlusion pressures gauge left ventricular end-diastolicvolume. What factors alter these relationships?Physiologic or pathologic conditions that affect the relationship between measured pressuresand ventricular volumes can be understood by appreciating the following concepts:n Transducers measure atrial pressures as surrogates for ventricular end-diastolic volumes.In patients with severely stenotic valves, pressures will be elevated and therefore overestimatethe volumes.

& Volumeventricle ¼ Complianceventricle�ðPinside ventricle � Poutside ventricleÞ

From this it becomes clear that:□ A less compliant ventricle will have less volume for the same pressure (e.g., left ventricularhypertrophy).

□ Volume depends on the relationship between pressure inside and pressure outside theventricle. In cases where the pressures externally compressing the ventricle are high (e.g.,high positive end-expiratory pressure [PEEP], increased intraabdominal pressures), thepressures inside the ventricles will overestimate the volumes. This is also the case withintraventricular dependence where a severely dilated right ventricle could compress theleft ventricle.

12. Describe how thermodilution with a PAC can be used to determinecardiac output.The principle of thermodilution cardiac output is that a bolus of cold injectate will lower thetemperature of the blood as it flows through the right side of the heart. Cold salinesolution is bolused proximal to the right side of the heart, and the temperature is measured by thedistal tip of the catheter in the pulmonary artery. Higher blood flow (i.e., cardiac output)means the cold is diluted in a larger volume of blood, and smaller temperature changes willbe measured. Conversely, low cardiac output shows high temperature change with thebolus, because the cold bolus comprises a much higher portion of the flow that passes thetemperature probe.

30

20

10

0

mm

Hg

Right atrium Right ventricle Pulmonary artery Wedge pressure

Figure 6-2. Normal pressures and waveforms when a PAC is advanced.

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The modified Stewart-Hamilton equation describes this:

CO ¼ Tbody � Tinjectate� ��V1�K1

AUC

where CO is cardiac output, Tbody is the temperature of the body, Tinjectate is the temperature of theinjectate, V1 is the volume of the injectate, K1 represents properties specific to the catheterand measuring system, and AUC is the area under the curve of the temperature change. Insimple terms, the equation relates that flow (a volume per time) is equal to quantity (of cold) pertime divided by concentration (in this case a temperature concentration). Again, even moresimply:

Flow ðL=minÞ ¼ Quantity per timeð‘‘temperature’’=minÞConcentrationð‘‘temperature’’=LÞ

13. How is a fluid challenge useful in the intensive care unit (ICU) setting?Determining volume status (i.e., which side of the Frank-Starling curve a patient is on) in the ICUcan be very difficult but remains important to thoughtfully optimize hemodynamics. A time-honored test is to give a fluid bolus and look for a change in hemodynamics. If a bolus has asalutary effect (increase in blood pressure or cardiac output), then the patient is likely on theascending portion of the Frank-Starling curve, and another fluid bolus may be indicated toimprove hemodynamics. If a fluid bolus produces minimal effect, then it is likely that the patientis near the top of the Frank-Starling curve. If a fluid bolus causes deterioration in the bloodpressure or cardiac output, then the patient may be volume overloaded on the descending portionof the curve.

A similar test of volume status is the passive leg raise. To perform this test, blood pressure orcardiac output is measured with the patient supine. The patient’s legs are then passivelyelevated, delivering a reversible autotransfusion of approximately 500 mL of blood (i.e., bloodrushes to the central veins from the legs because of hydrostatic pressure). If the passiveleg raise improves hemodynamics, additional volumemay be indicated. If the effect is negative, itcan be quickly reversed by lowering the legs, which is an advantage over the fluid bolus techniquewhere the bolus cannot be quickly removed.

14. Can arterial lines tell us anything more than pressure?Arterial lines can be used to assess both fluid responsiveness and cardiac output. With theubiquity of arterial lines in ICUs, these techniques can be very useful.n Fluid responsiveness: If central veins are not adequately filled (i.e., with a patient withhypovolemia), changes in intrathoracic pressure during positive-pressure variation can resultin highly significant effects on cardiac output and blood pressure. Variation in pulsepressure or systolic pressure of greater than 10% to 12% is predictive of positive fluidresponsiveness. Note that this technique holds only for sedated patients (with no spontaneousrespirations) receiving positive-pressure ventilation with regular cardiac rhythm.

n Cardiac output: As the arterial pulse pressure waveform reflects the stroke volume, algorithmshave been developed to continuously monitor cardiac output through waveform analysis.These techniques are challenged by nonlinearity of pressure to volume translation, dampingand resonance issues, and flow-independent systemic vascular resistance changes.

15. What are transpulmonary thermodilution and transpulmonary lithium dilution?Similar to thermodilution with PACs (see question 12), these techniques use the Stewart-Hamilton equation to approximate cardiac output using temperature (in the case ofthermodilution) or lithium concentration (in the case of lithium dilution). Boluses (of either coldinjectate or lithium) are injected in central veins, and temperatures or lithium concentrations are

CHAPTER 6 HEMODYNAMIC MONITORING 43

measured in arterial lines. Commercial applications typically use these techniques to calibratesome form of arterial waveform analysis to provide a continuous determination of cardiac output(e.g., the PiCCO and LiDCO devices).

16. What is impedance cardiac output?With impedance cardiac output, current is applied across the chest and the impedance(resistance) is calculated. With each heartbeat, the impedance decreases (as the low-resistanceblood-filled aorta expands). Combining the impedance change and heart rate allows estimation ofthe cardiac output. Limitations of this technique in the critically ill have resulted in lack ofwidespread adoption.

17. How is Fick’s principle used to measure cardiac output?Fick’s principle allows highly accurate calculation of cardiac output. Total oxygen consumption,VO2, in the tissues must equal the delivered oxygen less the returned oxygen. Delivered oxygen isequal to cardiac output multiplied by arterial oxygen content (Ca, determined in a systemicartery). Returned oxygen is equal to cardiac output multiplied by mixed venous oxygencontent (Cv, determined in the pulmonary artery). Oxygen consumption can also be measureddirectly with a closed-loop spirometer. Setting these two equal to each other allows us togenerate the following equation:

VO2 ¼ ðCO�CaÞ � ðCO�CvÞRearranging, cardiac output is calculated as

CO ¼ VO2

Ca � Cv

In this equation, oxygen content of blood, C, is calculated as

C ¼ Hgb�1:34 SpO2 þ 0:003�PO2

where Hgb is hemoglobin (measured in grams per deciliter), SpO2 is hemoglobin saturation withoxygen (measured as a percentage), and PO2 is the partial pressure of oxygen in blood(measured in millimeters of mercury).

18. How is cardiac output measured with transesophageal aortic Doppler?Doppler technology relies on frequency change of sound waves as they reflect off movingobjects. With transesophageal aortic Doppler, the Doppler probe lies in the esophagus andreflects sound from the blood pumping through the aorta, and the velocity of blood in theaorta is determined. By assuming an aortic diameter (based on height, weight, age, sex) ormeasuring the diameter directly, a flow can be calculated (flow¼ area� velocity time integral�heart rate). Because this calculates flow only in the descending aorta, a certain percentage(typically around 30%) is added to determine total cardiac output.

19. Describe some of the general applications of bedside ultrasound examinationto monitor hemodynamics in the ICU.Ultrasound scan provides real-time noninvasive data, and its utility in critical care is tremendousand growing. To cover ICU ultrasound applications in detail is beyond the scope of this chapter,but certain key points bear mentioning. Ultrasound can be used to directly assess cardiacoutput and function (stroke volume, contractility/ventricular function, valvular function) withtransthoracic or transesophageal echocardiography. Fluid responsiveness can be gauged bymeasuring the change in inferior vena cava diameter during a respiratory cycle, similar toassessing systolic pressure variation, in a patient receiving mechanical ventilation. The presence

44 CHAPTER 6 HEMODYNAMIC MONITORING

of pulmonary edema can be seen, but not quantified, by ultrasound examination of the lung.Technical limitations make the usefulness of ultrasound quite variable. Also, it is a very operator-dependent technology, and specific training coupled with frequent practice is required.

20. Is it possible to look more directly at tissue perfusion?Many methods to assess tissue perfusion (the ultimate gauge of adequate hemodynamics) havebeen and are being developed. Although many more exist than are covered in this chapter, someincluden Gastric tonometry: Carbon dioxide accumulation in gut mucosa typically results fromdecreased perfusion. Therefore measurement of gastric carbon dioxide via nasogastric ororogastric tube can provide a gauge for whether tissue perfusion is adequate.

n Tissue oxygenation (StO2): Tissue oxygenation is a measure of the ratio of oxygenated tononoxygenated hemoglobin in a sample of tissue. It differs from arterial oxygenation (SpO2),which represents systemic arterial oxygenation, in that tissue oxygenation is a localmeasurement at the microcirculation level. Think of this as a pulse oximeter for muscle ordeeper tissues.

n Confocal microscopy: With use of confocal techniques, these microscopes can lookunder the skin or mucosa of the tongue. Confocal microscopes can actually watch red bloodcells moving through capillaries. This technology is not currently being used for bedsidemonitoring, but it is often cited as a research tool when studying perfusion.

KEY POINTS: HEMODYNAMIC MONITORING

1. Hemodynamic monitoring is our way of attempting to determine whether tissue perfusion isadequate; it provides data to guide therapy but is not by itself therapeutic.

2. Arterial transducers must first be zeroed and leveled to eliminate the effects of atmosphericpressure and hydrostatic pressure on readings. In addition, system readings should bemonitored for damping (where readings erroneously converge to the mean pressure) andresonance (where readings erroneously diverge from the mean pressure).

3. Central lines have predictable waveforms with upward deflections during atrial contraction(the “a” wave), ventricular contraction (the “c” wave), and passive venous return (the “v” wave).To gauge end-diastolic volume, the pressure reported should be at the valley immediatelypreceding the “c” wave.

4. Fluid responsiveness in critically ill patients can be assessed with fluid challenge, the passiveleg raise test, systolic pressure variation, pulse pressure variation, ultrasound examination ofthe inferior vena cava, and several other methods.

BIBLIOGRAPHY

1. Brennan J, Blair J, Goonewardena S, et al: Reappraisal of the use of inferior vena cava for estimating right atrialpressure. J Am Soc Echocardiogr 20:857-861, 2007.

2. Chatterjee K: The Swan-Ganz catheters: past, present and future: a viewpoint. Circulation 119:147-152, 2009.

3. Cholley B, Payen D: Noninvasive techniques for measurements of cardiac output. Curr Opin Crit Care11:424-429, 2005.

4. Isakow W, Shuster D: Extravascular lung water measurements and hemodynamic monitoring in the critically ill:bedside alternatives to the pulmonary artery catheter. Am J Physiol Lung Cell Mol Physiol 291:1118-1131, 2006.

5. Jensen M, Sloth E, Larsen K, et al: Transthoracic echocardiography for cardiopulmonary monitoring in intensivecare. Eur J Anesthesiol 21:700-707, 2004.

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6. Karamanoglu M, O’Rourke M, Avolio A, et al: An analysis of the relationship between central aortic and peripheralupper limb pressure waves in man. Eur Heart J 14:160-167, 1993.

7. Monnet X, Rienzo M, Osman D: Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med34:1402-1407, 2006.

8. Munis J, Lozada L: Giraffes, siphons and starling resistors: cerebral perfusion pressure revisited. J NeurosurgAnesthesiol 12:290-296, 2000.

9. Pittman J, Ping J, Mark J: Arterial and central venous pressure monitoring. Int Anesthesiol Clin 42:13-30, 2004.

10. Seneff M: Arterial line placement and care. In Irwin RS, Rippe JM (eds): Irwin and Rippe’s Intensive CareMedicine, 6th ed. Philadelphia, Lippincott Williams & Wilkins, 2008, pp 36-45.

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