INTRODUCTION Hemodynamic monitoring is a cornerstone of care for the hemodynamically unstable patient, but it requires a manifold approach and
d its use is both context and disease specific. One of the primary goals of hemodynamic monitoring is to alert the health care team to impending cardiovascular crisis before organ injury ensues; it is routinely used in this manner in the operating room during high-risk surgery. Another goal of hemodynamic monitoring is to obtain information specific to the disease processes, which may facilitate diagnosis and treatment and allow one to monitor the response to therapy. The effectiveness of hemodynamic monitoring depends both on available technology and on our ability to diagnose and effectively treat the disease processes for which it is used.
Hemodynamic Monitoring The pulmonary artery catheter is a balloon-tipped multi-lumen catheter that allows for invasive hemodynamic monitoring. The primary purpose of invasive hemodynamic monitoring is the early detection, identification, and treatment of critically ill or injured patients. By using invasive hemodynamic monitoring the nurse is able to evaluate the patient's immediate response to treatment such as drugs and mechanical support. Indications for Hemodynamic Monitoring
Because there is no specific criteria or rule as to who should be hemodynamically monitored, each patients circumstance must be evaluated individually. The risk vs. benefit of placing a pulmonary artery catheter, as well as the expense need to be considered. General indications for pulmonary artery pressure monitoring include:
Assessment of cardiovascular function (complicated MI, cardiogenic shock, papillary muscle rupture) Peri-operative monitoring of surgical patients with major systems dysfunction Shock of all type (septic, hypovolemic, any shock that is prolonged or origin is unknown) Assessment of pulmonary status Assessment of fluid status (dehydration, hemorrhage, GI bleed, burns) Therapeutic indications (aspiration of air emboli, cardiac pacing ) Diagnostic indications (aspiration of arterial blood ,pulmonary hypertension)
. CLINICAL CAVEATS FOR HEMODYNAMIC VARIABLES: BLOOD PRESSURE: Arterial blood pressure is not a single pressure but a range of pressure values from systole and diastole. Mean arterial pressure best approximates the organ perfusion pressure in noncardiac tissues, as long as venous or surrounding pressures are not elevated. Arterial pressure is commonly measured noninvasively on an intermittent basis using a sphygmomanometer. Indwelling arterial catheters permit continuous monitoring of arterial pressure. Because blood pressure is a regulated variable, a normal blood pressure does not necessarily reflect hemodynamic stability Organ systems also tend to autoregulate their blood flow such that organ-specific blood flow remains constant within a wide range of blood pressures if metabolic rate is unchanged, and varies with changes in local metabolic rate. The lower limit of this flow autoregulation, based on mean arterial pressure, varies between organs, patients (based on their underlying circulatory status, for example essential hypertension or peripheral vascular disease), their disease state, their metabolic activity, and associated vasoactive therapies. Thus, there is no threshold blood pressure value that defines adequate organ perfusion among organs, between patients, or in the same patient over time . However, because arterial pressure is a primary determinant of organ blood flow, hypotension (mean arterial pressure <65 mmHg) is always pathological.
CENTRAL VENOUS PRESSURE:
CVP is the back-pressure to systemic venous return. Because CVP is usually very low, defining the appropriate hydrostatic zero level is important in estimating CVP, but such physiological zeroing can be difficult. Few absolutes can be stated regarding static measures of CVP. If CVP is 10 mmHg or less then cardiac output will uniformly decrease when 10 cmH2O positive end-expiratory pressure is given to ventilator-dependent patients, whereas a CVP above 10 mmHg has no predictive value. Demonstration, using echocardiographic techniques, of more than 36% superior vena caval collapse during positive-pressure inspiration or complete inferior vena
cavalcollapse identifies individuals whose CVP is below 10 mmHg. However, there is no threshold value of CVP that identifies patients whose cardiac output will increase in response to fluid resuscitation. Importantly, CVP is only elevated in disease, but the clinical utility of CVP as a guide to diagnosis or therapy has not been demonstrated. PULMONARY ARTERY CATHETER: o The pulmonary artery catheter (PAC) permits LV filling pressures to be estimated by measuring Ppao. However, Ppao values do not correlate with LV end-diastolic volume, and neither do they predict preload responsiveness. Nevertheless, Ppao is the backpressure to pulmonary blood flow, and it can be used to identify the presence of a hydrostatic component to pulmonary edema and to assess pulmonary vascular resistance. o Using a rapid response thermistor, the PAC can be used to monitor RV end-diastolic volume based on measures of residual thermal signal. Measures of changes in RV enddiastolic volume are useful in cardiac surgery when trying to identify right-sided cardiac failure. If RV end-diastolic volume increases as cardiac output decreases, then the patient has corpulmonale. o Using a transthoracic measure of thermal decay, one can estimate intrathoracic blood volume, global cardiac volume, and lung water. Of these three measures, intrathoracic blood volume is presently the most widely used technique, although intrathoracic lung water measures may be of interest in the management of patients with acute lung injury. o Intrathoracic blood volume and its changes in response to fluid challenge reflect LV preload and changes in LV preload better than do more conventional measures, such as CVP or Ppao. However, the utility of any of these measures as static single-point values in predicting preload responsiveness or in improving outcome in unstable patients has not been documented. o Indicator dilution techniques using thermal, indocyanine green, and lithium can measure blood flow from both central venous and PAC. LV stroke volume can be estimated using a beat-to-beat based, algorithmic analysis of arterial pulse pressure. Several monitoring techniques use subtle variations in this concept to calculate stroke volume and cardiac output. o The overall accuracy of these techniques varies. Esophageal Doppler techniques can be used to measure descending aortic flow and to estimate both stroke volume and cardiac output. Because accurate measurement of cardiac output is less important than accurate documentation of trends in flow, these measures may have profound clinical utility if they are accurate and stable over time.
FUNCTIONAL HEMODYNAMIC MONITORING; DEFINING RESPONSE TO THERAPY:
o Although one may use hemodynamic monitoring to identify cardiovascular insufficiency before it results in clinical hypoperfusion or as a prognostic indicator of survival, its greatest potential role is in directing application of cardiovascular therapies that are of proven efficacy. o Monitoring conducted to evaluated the effect of treatment can be referred to as functional monitoring, because it implies a therapeutic application. Although trends in specific variables over time are useful in defining hemodynamic stability, their rapid change in response to application of a therapy has greater clinical utility. Some examples of functional monitoring variables. o The most common example of functional monitoring is in a therapeutic trial. Below we list the various types of functional monitoring presently validated. severely hypovolemic patients. Changes in central venous pressure during spontaneous breathing CHANGES IN LEFT VENTRICULAR OUTPUT DURING POSITIVE PRESSURE VENTILATION: If changes in both right and left ventricles induce changes in output, then one can use positive pressure ventilation to assess the dynamic and necessarily cyclic effect of ventilation on venous return by assessing dynamic swings in LV output. The greater the increase in tidal volume for the same lung compliance, the greater is the transient decrease in venous return and subsequently greater decrease in LV output. Changes in systolic arterial pressure during a programmed series of increasing tidal breaths quantify the degree of preload responsiveness. Furthermore, during fixed tidal volume positive pressure ventilation, variations in systolic pressure, pulse pressure, LV stroke volume, and aortic flow are robust measures of preload responsiveness.
STANDARDIZATION OF CARE: The application of evidence-based guidelines to clinical practice is rational. This approach often reduces health care costs by reducing practice variations, medical errors, and length of stay. Fluid optimization as an end-point of resuscitation reduces length of hospital stay and important complications in patients undergoing a variety of major surgical procedures that routinely require postoperative resuscitation, but the degree of this effect varies among patients. Cost-effectiveness analyses of specific types of treatment directed by hemodynamic monitoring, namely SvO2 monitoring to identify adequacy of treatment for hemodynamic instability andpreoptimization in high-risk surgery patients, have demonstrated benefit.
NORMAL HEMODYNAMIC VALUES:
Hemodynamic Parameters Mean Arterial Pressure Central Venous Pressure Pulmonary Artery Systolic Pressure Pulmonary Artery Diastolic Pressure Pulmonary Artery Mean Pressure Pulmonary Artery Wedge Pressure Cardiac Output Cardiac Index Stroke Volume Stroke Volume Index Systemic Vascular Resistance Systemic Vascular Resistance Index
Abbreviations
Normal Values
MAP CVP
70-90 mm Hg 2-8 mm Hg
PAS
20-30 mm Hg
PAD
6-12 mm Hg
MPAP
10-15 mm Hg
PAWP, Wedge
8-12 mm Hg
CO CI SV SVI
4-8 L/min 2.5-4 L/min 60-130 ml 40-50 ml/m2
SVR
800-1200 dynes
SVRI
150-300 dynes
CONCLUSION:
Fundamentally, one may ask just three questions regarding the cardiovascular system during resuscitation from shock will blood flow to the body increase with fluid resuscitation?; is arterial hypotension due to inadequate blood flow or loss of vasomotor tone, or both?; and is the heart capable of maintaining effective blood flow without going into failure? If the answer to the first question is 'yes', then treatment must include volume expansion.
