Monitoring - CVP and Cardiac Output

Monitoring - CVP and Cardiac Output is a topic covered in the Clinical Anesthesia Procedures.

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CVP. CVP is measured by coupling the intravascular space to a pressure transducer using a fluid-filled tubing.

  1. Pressure is monitored at the level of the vena cava or the right atrium. The transducer apparatus is placed at the level of the coronary sinus.
    1. Indications
      1. Measurement of right heart filling pressures to assess intravascular volume and right heart function
      2. Drug administration to the central circulation
      3. Intravenous access for patients with poor peripheral access
      4. Indicator injection for cardiac output determination
      5. Access for insertion of pulmonary artery catheter (PAC)
    2. Waveform. The CVP tracing contains three positive deflections—the a, c, and v waves—and two negative slopes—the x and y descents (Fig. 10.2). The waves correspond to atrial contraction, isovolemic ventricular contraction including tricuspid bulging, and right atrial filling, respectively. The x descent corresponds to atrial relaxation and systolic collapse. The y descent corresponds to early ventricular filling and diastolic collapse.
    3. Analysis
      1. Range. The CVP is read between the a and c waves at end-expiration, thus minimizing the interaction of respiration. The normal CVP is 2 to 6 mm Hg.
      2. Decreases in CVP. When a CVP decrease is associated with an increase in blood pressure, without changes to the systemic vascular resistance, the CVP has fallen because of increased cardiac performance. If blood pressure is decreased, decreased CVP is due to decreased intravascular volume or venous return.
      3. Increases in CVP. When this increase is associated with increased blood pressure, without changes to the systemic vascular resistance, the cause of increased CVP is an increase in volume or venous return. With an associated decrease in blood pressure, the increased CVP is due to decreased cardiac performance.
    4. Pathology and CVP
      1. Cannon a waves are caused by the atrium contracting against a closed tricuspid valve, as during atrioventricular dissociation.
      2. Large v waves are caused by regurgitant flow during ventricular contraction, as with tricuspid regurgitation.
    5. Positive-pressure ventilation affects both cardiac output and venous return. According to the Starling rule, the transmural pressure, which is the difference between the atrial pressure and extracardiac pressure, correlates with the cardiac output. At low levels of PEEP, the CVP increases with increased PEEP. At high levels of PEEP (over about 15 cm H2O), CVP increases as the cardiac output is depressed because of impaired right ventricular output.
  2. Procedure: CVP
    1. Locations. Common locations include the following veins: internal jugular (IJ), subclavian, external jugular, axillary, cephalic, and femoral.
    2. Materials include a saline bag under pressure, fluid-filled tubing, and transducer. The transducer is placed at the level of the coronary sinus.
      1. Multiple lumen catheters are directly inserted and are available with one to four lumens to provide access for multiple drugs, pressure monitoring, and blood sampling.
      2. An introducer is a large-bore catheter with a septum valve. A special multiple lumen catheter or a PAC is then placed through the introducer as described below.
      3. Ultrasound can be used to identify anatomy, assist catheter insertion, and verify placement.
    3. Complications
      1. Dysrhythmias, caused by the guide wire irritating the endocardium, are temporary and resolve with withdrawal of the wire.
      2. Arterial puncture can cause significant vessel damage and bleeding if the dilator or catheter is placed into the artery. Before dilation, intravenous position should be verified by color, blood gas, or pressure measurement through the finder needle, thin-walled needle, or 18-gauge catheter. If an artery is punctured before dilatation, the needle should be removed and pressure applied for at least 5 minutes (10 minutes in the case of coagulopathy) and a new site chosen. If the catheter is placed in the artery, it should remain in place and a vascular surgeon should be consulted.
      3. The guide wire should not feel tethered with dilator placement, as this may signify venous damage or puncture of the posterior wall. Do not continue to advance a guide wire if it does not pass easily.
      4. Pneumothorax, hemothorax, hydrothorax, chylothorax, or pericardial tamponade may become evident with vital sign changes. They are in part ruled out with chest radiography. The risk of pneumothorax is highest with subclavian vein insertion.
      5. Infection and air embolism may occur at any time before removal of the catheter. The risk of infection is higher with femoral venous placement. To reduce the chance of air embolism upon catheter removal, the site is occluded with the patient performing a Valsalva maneuver. The Trendelenburg position helps to prevent air entrainment at neck and subclavian sites.
    4. For the internal jugular Seldinger technique, the right side is preferred because the vessels run a straighter course to the right atrium (Fig. 10.4). (;
      1. Position and preparation. There are three positions for placement of the CVP catheter into the IJ: anterior, medial, and posterior based on the location of insertion relative to the sternocleidomastoid muscle. The most common is the medial position. The patient is supine or in the Trendelenburg position with the head extended and turned toward the contralateral side of insertion. To reduce catheter-related infections, sterile drapes should cover the patient from head to toe, the procedurist should wear sterile gown and gloves, and the neck should be prepped with chlorhexidine.
      2. Landmarks include the suprasternal notch, clavicle, lateral border of sternocleidomastoid (SCM) muscle, and angle of the mandible. For insertion, locate the midpoint between the mastoid process and the sternal attachment of the SCM. Ultrasound is routinely used for visualizing anatomy and locating the vein (Fig. 10.3).
      3. Placement can vary based upon the needle insertion site in relation to the patient's neck anatomy (Fig. 10.4). While aspirating, a finder needle is inserted at a 45° angle to the skin and advanced toward the ipsilateral nipple until venous blood is aspirated. Once the vein is located, the syringe is removed and a guide wire is passed through the needle or catheter.
      4. Intravenous position must be verified by ultrasound, color, blood gas, or pressure measurement. The needle or catheter is then removed, and the site enlarged laterally with a scalpel.
      5. For triple and quadruple lumen catheters, a dilator is often not necessary when accessing the internal jugular vein. With countertraction, a rigid dilator is advanced over the wire with gentle twisting; the guide wire should still be easily mobile, indicating preserved intravascular position.
      6. The dilator is removed while maintaining the guide wire, and a central catheter or introducer is inserted over the wire. Alternatively, an introducer and dilator are inserted simultaneously. The wire is removed, the ports are aspirated and flushed, and the catheter is secured to the skin.
      7. A chest radiograph is required to confirm the position and exclude complications, such as pneumothorax. The tip of the catheter should be at the junction of the superior vena cava (SVC) and right atrium and should not encounter the wall of the SVC at a right angle.
    5. The SCV ( may be easily accessed as the vessel passes under the clavicle at the midclavicular line. It is one of the most common central venous line locations. Although the artery is not compressible in case of puncture, coagulopathy is not a contraindication to placement. The SCV is often preferred for patient comfort, and the left SCV is often chosen because of the natural course of the brachial cephalic vein into the SVC.
      1. Landmarks include the clavicle, suprasternal notch, and lateral border of the SCM as it inserts onto the clavicle. The insertion site is medial to the midclavicular line.
      2. The thin-walled needle is placed at the insertion site and aimed at the suprasternal notch. It is used to identify the clavicle, and the tip is then “walked” posteriorly under the clavicle. The key to avoid a pneumothorax is to always keep the needle parallel to the floor during insertion. Total insertion of the catheter should not be greater than 16 to 17 cm, as this may place the tip in the right atrium.
    6. Femoral vein is one of the most easily accessible central veins and using it does not carry a risk of pneumothorax. Limitations include hip immobility and limited utility during cardiopulmonary resuscitation.
      1. Landmarks include the femoral artery, inguinal ligament, anterior superior iliac spine (ASIS), and pubic tubercle. The femoral vein is immediately medial to the femoral artery. If the artery is not palpable, the vein is reliably located one third of the distance from the pubic tubercle to the ASIS. In either case, the insertion point is just inferior to the inguinal ligament, 1 to 2 cm medial to the artery.
      2. Placement uses the Seldinger technique.
    7. External jugular vein is cannulated similarly to an internal jugular vein placement described in section II.D.2.b. It runs obliquely across the SCM, along a line running from the angle of the mandible to the midpoint of the clavicle. Occlusive pressure at the inferior portion of the vein near the clavicle may ease cannulation. Because the vessel bends to join the SCV, threading of a guide wire may be difficult and should not be forced. For this reason, internal jugular cannulation may be easier for central catheter placement.
    8. Basilic vein may be used to access the central circulation with a long catheter. Passing the guide wire into the SCV may be difficult but may be facilitated by abducting the ipsilateral arm and turning the head toward the side of insertion.
  3. Pulmonary artery catheterization and pulmonary artery occlusion pressures. The PAC gives information about ventricular function and vascular volume by measuring CVP, pulmonary artery pressure (PAP), pulmonary artery occlusion pressure (PAOP), mixed venous sampling, and cardiac output.
    1. Mechanism. The PAC is inserted through a central venous introducer catheter. It passes through the vena cava, right atrium, and right ventricle and into the pulmonary artery. Transducers are connected to separate ports to allow CVP and PAP measurements. Inflating the balloon at the tip of the catheter allows measurement of PAOP, or “wedge” pressure, reflecting the left atrial pressure and left ventricular preload. To minimize the effect of alveolar pressure on PAOP, the tip should rest in West zone III, where pulmonary venous pressure is greater than alveolar pressure. Fortunately, the tip usually ends up in this location.
    2. Indications
      1. Unexplained hypotension
      2. Access for cardiac pacing
      3. Surgical procedures with significant physiologic changes (e.g., open aortic aneurysm repair, and lung or liver transplant)
      4. Acute myocardial infarction with shock
    3. PA and PAOP
      1. Waveform. The PAP waveform is similar in shape to the systemic arterial waveform. Because of the location, the waveform is smaller and precedes the systemic waveform. With the balloon inflated, the PAC will measure the PAOP recording, which is similar to the CVP waveform, with a and v waves. This waveform approximates the left atrial pressures and is slightly delayed because of the interposed lung.
      2. Range. The normal PAP is 15 to 30 mm Hg systolic and 5 to 12 mm Hg diastolic. The normal range for PAOP is 5 to 12 mm Hg. At end expiration, this approximates the left atrial pressure and correlates with the left ventricular end diastolic volume.
    4. PAOP analysis is used to assess the left heart performance. A basic model of left heart function is given by the relationship between the end-systolic pressure–volume curve and end-diastolic pressure–volume curve. Because the left ventricular end-diastolic pressure (LVEDP), which correlates with the left ventricular end-diastolic volume, is known, the following deductions are possible (Fig. 10.5).
      1. Increase in PAOP can be due to an increase in end-diastolic volume, decrease in compliance, or both.
      2. Decrease in PAOP can be due to a decrease in end-diastolic volume, increase in compliance, or both.
    5. Pathology and PAOP
      1. Large a waves may be due to either left ventricular hypertrophy (LVH) or atrioventricular dissociation. LVH will decrease the compliance of the left ventricle and will elevate the LVEDP. Thus, the PAOP should be measured at the peak of the a wave. During atrioventricular dissociation, pressure should be measured before the a wave.
      2. Large v waves are the result of mitral regurgitation.
      3. Right heart dilatation can cause shifting of the interventricular septum into the left ventricle, effectively decreasing the left ventricular end-diastolic compliance. Thus, LVEDP will be elevated.
      4. Pulmonary embolism may cause an elevation of the PAP without a concomitant elevation of the PAOP.
    6. Materials/catheter types. Most catheters are available with or without bonded heparin. Types of PACs include the following:
      1. Venous infusion (VIP, VIP+) catheters provide extra ports for infusion and sampling.
      2. Paceports allow placement of cardiac pacing wires.
      3. Continuous cardiac output catheters perform frequent automated determinations of cardiac output by using frequent low-heat pulses to obtain a thermodilution curve; the values are usually an average over time.
      4. Oximetric catheters monitor mixed venous O2 saturation.
      5. Right ventricular ejection fraction catheters use a rapid response thermistor to calculate the right ventricular ejection fraction in addition to cardiac output.
  4. Procedure: pulmonary artery catheter
    1. Locations and preparation are similar to those of the central venous catheter described in section II.D.2. The PAC is invariably placed through an introducer catheter. The operator typically dons a fresh pair of sterile gloves between the introducer and PAC placement.
    2. Technique. The PAC is prepared and examined as follows:
      1. Sheath placement is done before balloon examination and placed at 70 cm. The sheath allows movement of the PAC to adjust to the optimum position while maintaining sterility.
      2. Balloon examination includes inflating the balloon with 1.5 mL of air. The balloon should be symmetrical, inflate and deflate smoothly, and the tip of the PAC should not protrude past the balloon.
      3. All ports are flushed to ensure patency and are attached to calibrated pressure transducers. Raising and lowering the PAC distal end should produce changes on the pressure tracing and serve as a quick test of the system before insertion.
      4. Placement (Fig. 10.6). The PAC is held so that it follows a natural curve through the heart during passage through the introducer. Once the 20-cm mark is reached, the balloon is inflated with 1.5 mL of air, and the CVP waveform is confirmed. As the catheter is advanced, the waveform will change to a right ventricular waveform and then to a pulmonary artery waveform (with a diastolic pressure step-up and down-sloping diastolic plateau). The PAC is advanced until a PAOP waveform is seen, and the balloon is then deflated. The waveform should return to a pulmonary artery tracing upon deflation. If it does not, then the PAC should be withdrawn about 5 cm with the balloon deflated, the balloon should be reinflated, and the PAC should be advanced until a PAOP tracing is encountered. The balloon should remain deflated normally.
      5. Securing the sheath to the introducer proximally and at the 70-cm mark distally ensures the ability to manipulate the PAC aseptically. The introducer and PAC are secured to the patient, and an occlusive dressing is applied.
    3. Distances. From the right internal jugular vein, each location appears “on the tens.” The right atrium is reached at 20 cm, the right ventricle is reached at 30 cm, the pulmonary artery is reached at 40 cm, and the PAOP should be at 50 cm. For subclavian vein placement, subtract 5 cm from these distances; for femoral vein placement, add 20 cm to these distances.
    4. During PAC insertion, difficulty in passing the catheter into the right ventricle and pulmonary artery may be encountered because of balloon malfunction, valvular lesions, a low-flow state, or a dilated right ventricle. The monitoring equipment should be rechecked for calibration and scale. Inflating the balloon with a full 1.5 mL of air, slow PAC advancement, and large inspirations by the patient to augment venous return may be helpful. The PAC may have to be withdrawn to a depth of 20 to 30 cm, rotated slightly, and readvanced.
    5. Complications
      1. Pneumothorax during placement of the PAC is the most common complication.
      2. Dysrhythmias are possible because of direct stimulation of the atrium, ventricle, and pulmonary outflow tract in 50% to 70% of placements. They are usually transient and resolve spontaneously with continued passage or with withdrawal of the PAC. Complete heart block and ventricular tachycardia are possible (up to 0.3% of placements) and should be treated appropriately.
      3. Right bundle branch block is a specific risk in patients with either a left bundle branch block or a first-degree heart block, as this may result in complete heart block. In this event, the PAC should be withdrawn and temporary pacing initiated.
      4. Pulmonary artery rupture or infarction is possible from overinflation or prolonged inflation of the balloon or from direct pressure by the PAC. Thus, the balloon should be slowly inflated, and volume to achieve PAOP should be monitored. Furthermore, the PAP should be monitored by default; if a persistent PAOP appears, the catheter should be pulled back immediately and repositioned.
      5. Pacemakers do not contraindicate PAC placement, although fluoroscopic guidance should be used if the pacemaker is less than 6 weeks old.
      6. Balloon rupture may occur with overinflation with more than the recommended 1.5 mL.
      7. Valve damage, thrombus formation, and infection can occur with PACs. Knotting of the catheter can happen when the catheter will not pass through the pulmonary valve and turns back on itself in the right ventricle.
  5. Cardiac output is typically 4 to 8 L/minute, while the cardiac index (CO/body surface area [BSA]) is 2.4 to 4.0 L/min/m2. CO is conventionally measured with a PAC using thermodilution. The risks of PAC placement have generated interest in alternative CO methods such as pulse contour analysis, whole body dilution techniques, esophageal Doppler, Fick methods, and impedance cardiography.
    1. Thermodilution with a PAC is the gold standard for CO measurement. A known volume of cold saline is injected into the CVP port. The resulting temperature change is monitored by the thermistor located at the PAC tip. The area under the temperature–time curve correlates with cardiac output.
      1. CO should be measured at end expiration. Changes in intrathoracic pressure affect the CO measurement. Negative intrathoracic pressure during the inspiration phase of spontaneous breathing increases venous return and left ventricular transmural pressure. Positive intrathoracic pressure during the inspiration phase of positive-pressure ventilation decreases venous return and left ventricular transmural pressure.
      2. Tricuspid regurgitation often causes CO and cardiac index to be underestimated by prolonging the time and increasing the area under the CO curve. Though underestimation is the most common error, values may be overestimated as well.
      3. Errors in CO measurement may also be caused by injectate spillage, very slow injection, use of the wrong catheter constant, and intracardiac shunt.
    2. Pulse contour analysis determines stroke volume and cardiac output by computer analysis of the arterial pulse pressure waveform. This method assumes aortic pulse pressure is proportional to stroke volume. The effects of vascular tone are included in the calculation as a conversion factor calculated from heart rate, MAP, and vessel compliance. The advantage is that central venous access is not needed. Available systems utilize patient demographics and physical characteristics for arterial impedance estimation (FloTrac System, Edwards Lifesciences, Irvine, CA) or injected indicators for calculation (see below). Limitations include:
      1. Nonlinearity of aortic compliance changes. The compliance of the aorta changes nonlinearly with pressure. This may limit the accuracy of stroke volume estimates.
      2. Resonance and damping may occur, as with use of any arterial catheter for invasive blood pressure monitoring.
      3. Does not accurately track changes in stroke volume. Limited ability to clinically assess changes in SV after a volume challenge or the use of vasopressors.
    3. Whole body dilution techniques were originally done using indocyanine green dye dilution. Currently available methods combine the use of an indicator dilution CO measurement for calibration and pulse contour analysis, examples include PiCCO and LiDCO.
      1. Transpulmonary thermodilution (PiCCO) requires a central venous catheter and a specialized femoral arterial catheter with a thermistor. A cold saline bolus is injected through the central venous catheter. The femoral arterial thermistor records the temperature changes downstream. Analysis of the curve yields estimates of cardiac output and blood volume in the heart.
      2. Lithium dilution (LiDCO) may be used with a radial or brachial artery catheter with a lithium sensor at the tip. A known concentration and volume of lithium chloride solution is injected through a central or peripheral vein. An arterial lithium concentration–time curve is generated. CO is calculated from the area under the curve.
      3. Limitations of dilution techniques. Intracardiac shunt and aortic insufficiency may cause CO to be underestimated.
    4. Esophageal Doppler measures descending thoracic aortic blood flow (ABF) with a Doppler beam and sensor positioned at a known angle in the esophagus. This measures ABF, but not CO, directly. Since ABF is roughly 70% of CO, CO may be estimated while avoiding the invasive risks of PAC placement. The probe requires minimal training to place and may be left in place for days. However, it cannot be performed easily on awake patients and does not provide direct information about cardiac filling pressures.
    5. Modified Fick techniques. NICO (Philips Respironics, Pittsburgh, PA) uses sensors in the breathing circuit attached to an intubated patient to measure flow, airway pressure, and CO2 concentration. During periods of rebreathing, CO2 elimination is calculated from these measurements. The Fick principle is applied to calculate cardiac output, which is proportional to the change in CO2 elimination divided by the change in end-tidal CO2.
    6. Thoracic Bioimpedance uses skin electrodes placed along the neck and thorax to measure changes in voltage and impedance. Because blood is a stronger conductor than muscle, bone, and skin, changes in thoracic blood volume during the cardiac cycle result in impedance changes. Ohm's law is applied to use the change in impedance to determine CO. This method is completely noninvasive and the electrodes require minimal training to place. A large body habitus and fluid overload may result in inaccurate measurements.
    7. Thoracic Bioreactance (NICOM device, Cheetah Medical, Portland, OR) uses outer electrodes that apply an electric current of known frequency across the thorax and inner electrodes that record the signal after it interacts with the pulsatile blood flow within the thorax resulting in a time delay, or phase shift. The volume of pulsatile blood (stroke volume) that caused the specific time delay can be calculated and continually detected to create the NICOM signal. The continual, dynamic sensing results in less signal distortion than bioimpedance systems. Although further studies are needed, the CO as measured by bioreactance has been shown to be highly correlated with that measured by thermodilution.
  6. Echocardiography
    1. Mechanism. Echocardiography is performed with ultrasonic waves to create a two-dimensional image of the heart and surrounding structures. This may be done from a transthoracic or transesophageal approach, depending on the targeted structures, patient compliance, and conditions during placement. It provides independent assessments of the same parameters that a PAC measures, but it also reveals cardiac valve function, ventricular contractility, diastolic function, and intracardiac structures.
    2. Indications
      1. Hypotension of unknown cause
      2. Uninterpretable PAC values
      3. Suspected intracardiac masses or vegetations
      4. Valvular abnormalities
      5. Shunts
      6. Air embolism
      7. Pericardial disease
      8. Thoracic aneurysm/dissection
    3. Methods
      1. Transthoracic echocardiogram can be performed with the patient awake and provides good visualization of right heart structures and qualitative estimates of contractile performance, although visualization of the left heart is limited and may not be allowed by the surgical location.
      2. Transesophageal echocardiogram requires that the patient be topically, locally, or generally anesthetized, but it may be performed intraoperatively and allows superior visualization of the left heart.

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TY - ELEC T1 - Monitoring - CVP and Cardiac Output ID - 728188 ED - Pino,Richard M, BT - Clinical Anesthesia Procedures UR - PB - Wolters Kluwer ET - 9 DB - Anesthesia Central DP - Unbound Medicine ER -