I ment and assessment of pressures

Transcription

1 lnvasive.... monitoring Patricia C Seifert, RN Patricia C Seifert, RN, BA, CNOR, is head nurse in cardiac surgery at the Fairfax Hospital, Falls Church, Va. An AD graduate of Northern Virginia Community College School of Nursing, Annandale, Va, she received her bachelor s degree from Trinity College, Washington, DC. The author gratefully acknowledges the assistance of Edward A Lefrak, MD, in the preparation of this manuscript. nvasive hemodynamic monitoring is the direct intravascular measure- I ment and assessment of pressures and forces inherent in circulating blood. The hydrodynamic pressures within arteries and veins are converted to electrical signals by a transducer, which is connected to a pressure monitor. The monitor processes and amplifies the electrical signals into a continuous waveform, which is displayed on an oscilloscope. Pressure values can also be digitally displayed, depending on the monitor used. Continuous pressure monitoring is valuable in situations where systemic circulation may be compromised. Candidates for hemodynamic monitoring include patients with 0 acute myocardial infarction 0 right or left heart failure 0 cardiac valvular disease 0 ventricular septa1 rupture 0 cardiac tamponade 0 cardiogenic shock 0 cardiac surgery 0 respiratory distress syndromes high risk general surgery All these patients suffer from an alteration in systemic circulation that, if not reversed at an early stage, results in cellular death. Maintaining cardiac function and thus ensuring an adequate cardiac output is the therapeutic goal for these high-risk patients. Since hemodynamic alterations may occur suddenly, in-, traoperative invasive monitoring is necessary for detecting early changes. Trends, rather than isolated readings, should be noted and evaluated in conjunction with the more traditional assessment of temperature, color, urine output, electrolyte, and arterial blood gas values. Hemodynamic monitoring is particularly useful during surgery for congenital heart disease. Pressures during cardiopulmonary bypass are generated by 416 AORN.Journal, September 198,?, Vol38. No 3

2 Fig 7. The setup is shown for the insertion of the hemodynamic monitoring catheters. The numbers correspond to the numbered items in the photo: (1) pressure tubing; (2) J guide wire; (3) introducer with dilator and flush line; (4) pulmonary artery (four-lumen) thermodilution catheter; (5) temperature sensor for thermodilution cardiac output determinations; (6) balloon inflated on distal the bypass pump and do not accurately represent cardiac function. When evaluating the efficacy of the surgical repair, it is particularly useful to compare pre- and postcardiopulmonary bypass pressures. Hemodynamic monitoring. Before the widespread clinical application of invasive hemodynamic monitoring in the tip for wedge pressure; (7) cardiac output computer attachment; (8) plastic sheath for pulmonary artery catheter; (9) RAICVP (proximal) port (attach to CVP manometer); (10) pulmonary artery (distal) port (attach to transducer); (1 1) balloon inflation port with syringe attached; (1 2) three-way stopcocks; (1 3) needle guard; (1 4) CVP catheter. 1970s, it was difficult to determine rapidly and accurately the etiology of decreased tissue perfusion. Before the introduction of the flow-directed, balloon-tipped pulmonary artery catheter by H J C Swan and William Ganz in 1970, left ventricular function was difficult to measure outside the cardiac catheterization laboratory (Figs 1 and AORN Journal, September 1983, Vol38, No 3 417

3 Fig 2. The transducer setup consists of (1) transducer; (2) transducer dome; (3) port for blood samples; (4) stopcock; (5) pressure tubing to patient; (6) stopcock; (7) flush line; (8) protective cap. 2).l Physicians and nurses relied on central venous pressure (CVP) measurements to assess left ventricular function. When the CVP was low in the presence of low systemic blood pressure, volume replacement was often given. In those patients with low circulating blood volume, this was appropriate. But in a patient with normal blood volume and impaired left ventricular function, the infusion was an additional strain on a compromised left ventricle. In some cases, this treatment led to congestive heart failure and pulmonary edema. Clinicians no longer rely on isolated CVP measurements to assess the status of the patient s circulatory system. Since the heart is composed of two separate pumps which communicate with the lungs, the CVP does not correlate with left heart performance in the presence of impaired left ventricular function. Because the pulmonary vasculature is very compliant, there can be a considerable increase in pulmonary blood flow before there is significant congestion. This capacity of the lungs to accept increased flow illustrates why the CVP can be a delayed sign of left ventricular failure. The increase in pulmonary artery pressure associated with the backup of blood caused by left ventricular dysfunction precedes increased right-sided pressure, as reflected in the CVP.2 A competent pulmonic valve prevents regurgitation from the pulmonary vasculature so that increased pulmonary vascular resistance (PVR) and pulmonary congestion may become evident before the increased pressures affect the right ventricle and right atrium. Monitoring pulmonary pressures provides a more precise indication of the patient s pulmonary and left ventricular status. The ability to measure various pulmonary pressures in the OR with the pulmonary artery catheter is a significant advance in the care of high-risk patients. The pulmonary artery catheter can measure pulmonary systolic, diastolic, and mean pressures from the distal lumen, pulmonary wedge pressure from the inflation of the balloon lumen, and right atrial pressure from the proximal lumen. The waveforms will differ depending on the location of the lumen in the patient s circulatory system (Fig 3). When the pulmonary artery waveform is shown on the monitor, the nurse is assured of correct catheter position. The pulmonary capillary wedge waveform appears only when the balloon is temporarily inflated to take the wedge pressure. Measuring these various pressures provides an assessment of the left ventricle s ability to eject an adequate cardiac output. 418 AORN Journal, September 1983, Vol38, No 3

4 Fig 3 Typical waveforms E E 3 0) C E t I mmhg Pressure tracings seen on the monitor utilizing a flow directed pulmonary artery catheter. The pulmonary artery waveform is continuously displayed on the monitor except when the catheter is deliberately wedged. Cardiac output. The cardiac output is the amount of blood (in liters) ejected by the left ventricle per minute. (See Table 1 for normal values.) It is the product of the heart rate times the stroke volume. Stroke volume, the amount of blood ejected with each contraction, represents the difference between the volume of blood at the end of ventricular diastole and that at the end of systole. During systole, the ventricle does not eject the entire amount of blood received during diastole. Thus when the stroke volume is viewed as the percentage of the volume ejected, it is referred to as the ejection fraction. This value is commonly used as the indicator of ventricular function. Since patients vary in size, metabolic requirements differ. The cardiac output and the stroke volume can be corrected for the differences in body size by computing the cardiac index and the stroke volume index by dividing each of them by the patient s body surface area. The four determinants of cardiac output are: heart rate, preload, afterload, and contractility. When the cardiac output or index is insufficient to meet the patient s metabolic needs, it is due to a derangement of one or more of these factors. The heart rate is easily evaluated by conventional electrocardiographic monitoring. The nurse responsible for the patient understands the underlying physiology of the remaining three determinants and uses invasive hernodynamic values for her assessment. Preload. Preload is the amount of blood in the ventricle at the end of diastole. This is also referred to as the left ventricular end diastolic volume (LVEDV) or filling pressure. Because it is technically easier to determine pressure rather than volume, LVEDP usu- AORN Journal, September 1983, Vol38, No 3 419

5 Table 1 Normal resting values Cardiac index (CI) Cardiac output (CO) Ejection fraction (EF) Left ventricular end diastolic volume (LVEDV) Left atrial pressure (LAP) Left ventricular end diastolic pressure (LVEDP) Left ventricular stroke work index (LVSWI) Mean arterial pressure (MAP) Pulmonary artery pressure systolic/diastolic/mean (PAP S/D/M) Pulmonary artery wedge pressure (or pulmonary capillary wedge pressure) (PAWP or PCWP) Right atrial pressure (RAP) Stroke volume (SV) Stroke volume index (SVI) Systemic vascular resistance (SVR) 2.5 to 4.0 Umin/m2 4.0 to 8.0 Umin 60% to 70% 90 to 180 ml 8 to 12 mm Hg (mean) 5 to 12 mm Hg 60? 15 g/m2/beat 70 to 90 mm Hg 25/12/16 mm Hg 4 to 12 mm Hg (mean) 1 to 5 mm Hg (mean) 60 to 130 ml/beat 35 to 70 ml/beatlm* 15 to 20 units or 900 to 1440 dynes/se~/cm-~ Adapted from C 0 Brantigan, Hemodynamic monitoring: Interpreting values, American Journal of Nursing 82 (1982) 86; E K Daily, J S Schroeder, Techniques in Bedside Hemodynamic Monitoring, 2nd ed (St Louis: C V Mosby, 1981) 186; J A Kaplan, Hemodynamic Monitoring and Ischemic Heart Disease (Irvine, Calif: Edwards Laboratories, 1979). ally indicates pre10ad.~ Either of these values reflects the length or stretch of the myocardial fibers during diastole. Since the heart is composed of two pumps, it is necessary to differentiate between the right and the left preload. The CVP obtained from a catheter in the superior vena cava measures the preload of the right side of the heart because it represents the amount of venous return and therefore the filling pressure of the right ventricle. The preload of the left ventricle is determined with the pulmonary artery catheter by inflating the balloon at its distal tip, causing it to wedge in a peripheral branch of the pulmonary artery. There are no valves between the pulmonary artery and the left atrium, therefore when the mitral valve is open during ventricular diastole, the pulmonary ar- tery wedge pressure (PAWP or PCWP) reflects both left atrial pressure and left ventricular end diastolic pressure. Only in the presence of chronic problems such as mitral valve disease and obstructive lung disease do pulmonary pressures not reflect left ventricular function. The greater the preload and subsequent myocardial fiber stretch, the more the fibers shorten and with greater force, producing an increase in the stroke volume. At a certain point, the ventricle begins to fail. This relationship between volume, stretch, and subsequent contraction, Frank Starling s law of the heart, is a fundamental principle of cardiac performance. Stroke volume and preload are also influenced by the circulation and dis- 420 AORN Journal, September 1983, Vol38, No 3

6 Fig 4. Patient in operating room with hemodynamic pressure monitoring equipment. (Photos courtesy of Kip Seymour of the Fairiax Hospital, Falls Church, Va.) tribution of blood volume, and atrial contraction.* When circulating blood volume is depleted during hemorrhage, venous return and preload are decreased. Cardiac output suffers because one of its main determinants is reduced. Body position and venous tone can affect the distribution ofblood throughout the body. Veins can dilate and sequester significant amounts of blood, thereby decreasing the amount of venous return to the heart. Atrial contraction substantially contributes to ventricular filling, providing up to 30%: of the end diastolic volume. The loss of this atrial kick, which occurs during atrial fibrillation, can seriously compromise ventricular filling. Optimal cardiac output depends on all the variables that affect filling pressure and preload. Afterload. The third determinant of cardiac output is the afterload. This is the impedance or resistance the heart must overcome to pump blood into the systemic circulation. Impedance to flow is created by the arterial circuitry more accurately known as the systemic vascular resistance. Stated another way, afterload is the left ventricular wall tension during systole. The ventricle must create a pressure greater than the pressure in the aorta to open the aortic valve and eject blood into the systemic circulation. The narrower or more constricted the arterioles, or the greater the aortic pressure, the greater the tension and pressure required by the ventricle to overcome the resistance. This tension and pressure is the afterload. Since afterload is not a direct measure observed on pulmonary or radial artery waveforms, it is inferred by calculating the systemic vascular resistance. The systemic vascular resistance is obtained when the pressure differences between arterial and venous circuits are divided by the cardiac outp~t.~ Calculations can be done in the OR. AORN Journal, September 1983, Vol38, No

7 Table 2 Monitoring complications Equipment complications 1. Dampened arterial waveforms resulting in abnormally low pressure readings Cause Catheter obstructed or clotted at distal tip Air in transducer or tubing Leak in tubing system Incorrect calibration or gain control Precautions and treatment Attempt aspiration of clot. If successful, flush with heparinized solution. If unsuccessful, may have to remove catheter Aspirate catheter and flush air out of system Check connections, transducer domes and stopcocks. Replace defective parts Recalibrate and check monitor settings. Check that transducer level with heart 2. Arterial pressure tracing Catheter kinked or more than 20 mm Hg higher impinging on arterial than cuff pressure wall Transducer not calibrated or zeroed correctly Transducer not at right atrial level Check for kinks in tubing; splint arm if necessary, reposition Recalibrate, rezero Reposition and rezero 3. Pulmonary catheter will not Catheter out of Check chest x-ray film to assess proper "wedge" when balloon position position inflated Insufficient air in balloon Deflate and reinflate slowly Balloon rupture Patient complications Pulmonary catheters 1. Arrhythmias: PAC's or Irritation of PVC'S endocardium during catheter insertion Proximal migration of catheter into right ventricle If air not recoverable or no resistance to inflation, discontinue inflation and notify physician Monitor ECG during insertion. Be prepared to defibrillate; administbr lidocaine if necessary Secure catheter at insertion site to prevent migration. Pulmonary catheter that has fallen back into right ventricle must be removed 422 AORN Journal, September 1983, Vol38, No 3

8 ~ Adapted from R S Baigrie, C D Morgan, Hemodynamic monitoring: Catheter insertion techniques, complications and troubleshooting, Canadian Medical Association Journal 121 (1979) 885; S M Lalli, The complete Swan-Ganz, RN(September 1978) Patient complications 2. Pulmonary artery rupture and hemorrhage 3. Air embolism 4. Pulmonary thromboembolism 5. Infection, endocarditis Cause Overinflation of balloon or excessive wedging Balloon left inflated Migration of catheter into wedge position Balloon rupture Thrombus dislodged from catheter tip Inadequate sterile technique, irritation to insertion site, vascular or endocardia1 injury Precautions and treatment Inflate only with appropriate amount of air. Take PCWP measurements only when necessary Inflate only long enough to obtain wedge tracing. Recognize difference between pulmonary artery and pulmonary wedge pressure tracing Secure catheter at insertion site to prevent migration. If it has already migrated, reposition by pulling catheter back into pulmonary artery Do not overinflate balloon. If air unrecoverable or no resistance to inflation, discontinue and notify physician. Obtain wedge pressure only as necessary. In patients with intracardiac shunts, use COZ for inflation. In the event balloon ruptures air embolism is prevented with Con Maintain patency with heparin flush solution. If thrombus suspected, try to aspirate, do not flush. May require anticoagulation therapy Prepare sterile field and use sterile technique. Prevent overmanipulation of catheter. Change dressings, tubing, and stopcocks daily. Alert physician to signs of infection. If insertion site painful and inflamed, culture and apply topical antibiotic ointment Arterial catheters 1. Arterial thrombosis Irritation of vessel wall, hypercoagulation, inadequate flushing of lines and catheters Prevent overmanipulation. Flush lines and catheters routinely. May require anticoagulation therapy. Catheter removal may be indicated 2. Bleeding from insertion site Vessel trauma or improper fixation at insertion site Inspect insertion site. Apply local pressure and secure fixation site. Notify physician AORN Journal, September 1983, Vol38, No 3 423

9 The formula used is: Systemic vascular resistance = MAP-CVP (in mm Ha) Cardiac output ^^ I, "U Intraarterial pressure monitoring is particularly useful for observing the mean arterial pressure. Since diastole is twice as long as systole, mean arterial pressure is not exactly the average of systolic and diastolic blood pressures. It is calculated by most monitors and can be shown on the digital display. If a cuff is used to assess blood pressure, the nurse calculates the mean by using the formula: Mean arterial pressure = Systolic pressure $ (2x) diastolic pressuree Mean arterial pressure represents the basic driving pressure or perfusion pressure of the body. This value is especially crucial for myocardial perfusion because coronary blood flow occurs mainly in diastole. If systolic blood pressure is normal but diastolic pressure is low, coronary perfusion suffers. Intraoperative arterial blood pressures may be altered by surgical factors. The use of hypothermia causes peripheral vasoconstriction. Therefore, radial artery blood pressures may not accurately reflect the central aortic pressure and coronary perfusion pressure. When this occurs, a femoral arterial pressure line may be inserted in the groin for a more precise indication of vital organ perfusion. When the patient has reached normothermia, radial and femoral pressures will be similar. Contractility. The fourth determinant of cardiac output is the contractility or inotropic state of the heart. It is independent of changes in both the stretch of the myocardial fibers (preload) and the resistance to ejection (afterload). Con- 3 tractility cannot be directly measured but is calculated using information from the arterial and pulmonary catheters. Inotropic agents such as digitalis, calcium, dobutamine hydrochloride, and epinephrine increase contractility and result in an increase in cardiac output. In conditions where there is loss of functioning ventricular muscle, as in myocardial infarction or left ventricular aneurysm, or when agents such as barbiturates, beta blockers, or calcium channel blockers are given, there will be a decrease in contractility and a reduction in cardiac output. The heart's ability to pump is reflected by the calculated left ventricular stroke work index. If contractility is low and is the etiology of the decreased cardiac output, inotropic support is administered. Equipment. Monitoring systems require special handling and maintenance. Repair services must be available, and persons using the equipment should be familiar with the proper operation of the machinery. Monitor complications are not uncommon (Table 2). The equipment must be properly calibrated and maintained. Heparinized flush solutions provide catheter patency and reduce the incidence of blood clot formation. Summary. The use of indwelling arterial and pulmonary pressure catheters has made the assessment of physiologic alterations rapid and precise. This has resulted in improved patient care and confirmed the value of continuous hemodynamic measurements for high-risk patients. 0 Notes 1. H J C Ganz, W Swan et al, "Catheterization of the heart in man with use of a flow-directed balloontipped catheter," New England Journal of Medicine 283 (1970) A C Guyton, Textbook of Medical Physiology, 6th ed (Philadelphia: W 6 Saunders, 1981) AORN Journal, September 1983, Vol38, No 3

10 3. P W Armstrong, R S Baigrie, eds, Hemodynamic Monitoring in the Critically Il (Hagerstown, Md: Harper & Row, 1980) Ibid, E K Daily, J S Schroeder, Techniques in Bedside Hernodynamic Monitoring, 2nd ed (St Louis: C V Mosby, 1981) Ibid. Suggested reading Brantigan, C 0. Hernodynamic monitoring: Inter- preting values. American Journal of Nursing 82 (1982) 86. Lalli, S M. The complete Swan-Ganz. RN (September 1978) Palmer, P N. Advanced hernodynamic assessment. Dimensions of Critical Care Nursing 1 (1 982) 139. Rettig, F M. Appraisal of intracardiac monitoring. AORN Journal 29 (1979) 839. Shipley, S B. Pitfalls and perils of intracardiac monitoring. AORN Journal 29 (1 979) 845. Ectopic pregnancy rates rise; deaths decline The numbers and incidence of ectopic pregnancies are on the rise in the United States, according to a recent report by the Centers for Disease Control in the Journal of the American Medical Association (JAMA). Ectopic pregnancies occur when a fertilized ovum fails to reach the uterus, developing in the ovary, fallopian tube, or other extrauterine location instead. The number of these potentially life-threatening pregnancies has risen from 17,800 in 1970 to 42,000 in During the same period, the incidence more than doubled, from 4.5 per 1,000 to 9.4 per 1,000. Fortunately, earlier detection and improved treatment have reduced death rates from ectopic pregnancies by 75%. David A Eschenbach, MD and Janet R Daling, MD, pointed out in an accompanying JAMA editorial that the increase in ectopic rates has occurred among a wide variety of populations in many industrial countries. In the US, as of 1975, the ectopic pregnancies accounted for 5% of reproductive deaths. There is also a 50% infertility rate after an ectopic pregnancy. Even when a pregnancy occurs, there is a 10% to 15% risk of subsequent ectopic pregnancy in women who have had a prior ectopic pregnancy. Acute salpingitis (pelvic inflammatory disease) appears to increase a woman s ectopic pregnancy rate by sevenfold. Other causes are gonorrhea, gravidity, changes in contraceptive methods, induced abortion, cesarean section, fertility induced by ovulatory drugs, pelvic surgery, and fetal diethylstilbestrol (DES) exposure. Drs Eschenbach and Daling called for further studies, saying multiple factors may have accounted for the increasing ectopic rates, including but not limited to an increased maternal age, increased salpingitis rate, changes in contraceptive practices, and an increase in early detection. Testing service acts in new role Educational Testing Service, which generally develops and administers tests for licensing of various health fields, will only administer the National Council Licensure Examination in Texas and Massachusetts. It is estimated that 4,800 registered and practical nursing candidates will take the Massachusetts examination. The test was given to approximately 1,500 nurses in the Fort Worth-Galveston area in February and will be given again in July. Educational Testing Services and its division, Center for Occupational and Professional Assessment (COPA), assess the qualifications for licensure and credentials in more than 60 state licensing and certification agencies and provide test administration, development, scoring, and record management services to many health field professions. Test administration and scoring are done according to a state s needs. AORN Journal, September 1983, Vol38, No 3 425