What Is Hemodynamic Monitoring?
There are both invasive and noninvasive techniques that can be used to determine the hemodynamic status of the patient. Taking a simple blood pressure with a cuff is a hemodynamic measurement. By taking a blood pressure, you can determine three homodynamic parameters. The systolic pressure, the diastolic pressure, and, using these two numbers, you can calculate the mean pressure. Hemodynamic monitoring can be much more involved than a simple blood pressure reading. It may involve actual measurements of pressures directly within the heart. For our purposes we will be primarily talking about the latter. That is, invasive homodynamic monitoring. With the arrival of our modern technology, and improvements in biomedical engineering, we are now able to monitor the hemodynamic status of patients continuously. Invasive hemodynamic monitoring allows the nurse to have access too much more information about the status of the patient that is available by simple physical examination. However, keep in mind that hemodynamic monitoring will never replace hands on patient assessment. Parameters said chest cardiac output (CO), cardiac index (CI), pulmonary artery wage pressures (PAWP), and cardiac index (CI) are just a few of the pressures which can be monitored to a special indwelling catheter, the Swan-Ganz or pulmonary artery catheter.
The primary purpose of invasive hemodynamic monitoring is the early detection, identification, and treatment of life-threatening conditions such as heart failure and cardiac tampanade. By using invasive hemodynamic monitoring the nurse is able to evaluate the patient’s immediate response to treatment such as drugs and mechanical support. The nurse can evaluate the effectiveness of cardiovascular function such as cardiac output, and cardiac index.
The nurse cares for the hemodynamicly unstable patient as well as the equipment required to conduct hemodynamic monitoring. It is essential that the nurse be able to interpret the data and make clinical decisions based on that data. The nurse must know how to detect and prevent complications of this clinical tool.
Indications for Hemodynamic Monitoring:
One of the obvious indications for hemodynamic monitoring is decreased cardiac output. This could be from dehydration, hemorrhage, G. I. bleed, Burns, or surgery. All types of shock, septic, cardiogenic, neurogenic, or anaphylactic may require invasive hemodynamic monitoring. Any deficit or loss of cardiac function: such as acute MI, cardiomyopathy and congestive heart failure may require invasive hemodynamic monitoring.
Components of a Hemodynamic Monitoring System.
There may be some small variations of the requirements of a hemodynamic monitoring system depending on the manufacturer requirement and the type of system employed by your institution. Generally there are three components of a hemodynamic monitoring system.
The amplifier is located inside the bedside monitor. It increases the size of signal from the transducer. There must be a recorder or monitor to display the signal and record information. A transducer is needed which changes the mechanical energy or the pressures of pulse into electrical energy. In addition to these three components there is some supplemental equipment which is required. Pressure tubing is necessary since changes in pressure from tubing distention will affect your readings. The tubing must have a continuous flush device as well as a manual one with transducer. There must be a pressure bag containing a heparin solution of 1000 units in 500 ml of normal saline. Some institutions require the transducer be mounted on an IV pole. There should be a pressure cable that carries information from the transducer to the amplifier.
The Pulmonary Artery Catheter (PA catheter, Swan, Swan-Ganz).
The pulmonary artery catheter normally has four ports. The proximal port can be used to measure central venous pressure and as an injectate port during the measurement of cardiac output. There is a distal port which bills to the pulmonary artery and which is connected to the pressure line. A balloon port is also present where a 1.5-ml special syringe is connected. This is used during the determination of pulmonary artery wedge pressure. No more than 1.5 ml of air should ever be injected into a pulmonary artery catheter during wage determination.
The pulmonary artery catheter has several functions. It allows for continuous bedside hemodynamic monitoring. So that vascular tone, myocardial contractility, and fluid balance can be assessed and managed. It measures pulmonary artery pressure, central venous pressure, and allows for hemodynamic calculations to be determined. Cardiac output can be determined using the thermodilution method. Transvenous pacing can be done. The administration of fluids is not recommended with a pulmonary artery catheter.
Pulmonary Artery Catheter Insertions.
The bedside monitor should be turned on 10 to 15 minutes before insertion. The pulmonary artery catheter should be selected based on physician’s preference and size of the patient. The introducer should be selected. The pressure monitoring system should be set up. This is the same monitoring system as used for an arterial line. The bedside monitor should zeroed and calibrated. Before insertion, the integrity of the pulmonary artery catheter should be checked. The insertion of the introducer is much the same as that of a central line placement. After insertion, the pulmonary artery catheter is attached to the pressure line. Then it is inserted through the introducer into the vena cava. When the pulmonary artery catheter enters the right atrium, a waveform and pressure registers on the monitor. The physician may request that the balloon be inflated at this time. The inflated blame will act as a “sail” to “float” the tip of the catheter into the pulmonary artery. The pressures and waveforms would change as the tip of the catheter enters the right ventricle and again as it enters the pulmonary artery and then again when the balloon is wedged in an artery that is too small to allow it to go any further.
Normally the right atrium will have a mean pressure of 2-6 mm Hg. The right ventricle will have a systolic pressure of 15 to 25 mm hg, while the right ventricle will have 0-8 mm Hg.
The pulmonary arterial pressure should have a systolic of between 20 to 30 mm Hg, a diastolic of 6 to 12 mm Hg. with a mean of 10 to 15 mm Hg. The pulmonary artery wedge pressure should have a mean of 6 to 15 mm Hg.
Insuring Accuracy of Hemodynamic Monitoring.
The transducer should be level with the phlebostatic axis to counter the effects of hydrostatic pressure. It should be at the same level as the bill right atrium. You can estimate this by intersecting lines from the fourth intercostal space, mid axillary line.
The transducer must be zeroed to negate atmospheric pressure. The reference port on the transducer should be open and the appropriate “zero” buttons on the bedside monitor should be pushed. This should be done every eight hours. Some institutions require ever for hours. When the monitor is turned on it should be allowed to warm up for 15 minutes.
The pressure in the continuous flush device must be maintained at 300 mm Hg. continuously. As a result of this, the devise will deliver a preset amount of flush solution through the pulmonary artery catheter continuously. This is designed to prevent clots from forming at the catheter tip. The pulmonary artery catheter should be fast flesh every eight hours. However, this may vary from institution to institution.
Manifestations of Altered Hemodynamics.
Altered hemodynamic signs and symptoms are varied. The symptoms can be anything from cardiac dysfunction, pulmonary edema, rales, increased jugular vein size, pulmonary edema, complete cardiovascular collapse, and profound shock. Symptoms can include weakness, pallor, confusion, cold clammy skin, diminished or absent pulses, cardiac arrhythmias, low arterial blood pressure, and decreased cardiac output. New murmurs and heart sounds may develop.
By obtaining additional information of left ventricular performance, treatment can be altered according to pressure measurements. This is known as a fluid challenge.
Preload (Pulmonary wedge pressure, PAWP, Wedge).
Preload is the degree of muscle fiber stretching present in the ventricles right before systole. It could be looked at as the amount of blood available to be ejected at systole. Central venous pressure or right atrial pressure affects right ventricular preload. Normally 2-8 mm Hg. This also measures right ventricular end diastolic pressure.
Left ventricular preload, on the other hand, is reflected by the pulmonary artery wedge pressure, which measures the left ventricular end diastolic pressure. The pulmonary diastolic pressure estimates it. The pulmonary wage pressure (PAWP) measures the additional fluid, which stretches the left ventricle just prior to contraction. This is determined by the volume of blood in the right ventricle at the end of filling. Normally this measurement is 4-12 mm Hg.
A decrease in preload may be caused by hypovolemia as a result of hemorrhage, surgery, diuresis, dehydration, vomiting and diarrhea. Resulting in a decrease filling time for the heart may also cause it. Consequently, the blood does not have time to enter the heart to be circulated resulting in hypovolemia. Another reasons for decreased preload may be vasodilation that causes pooling. Hypothermia and sepsis must also be considered.
An increase in preload may be caused by vasoconstriction as a result of sympathetic stimulation or hypothermia. It may also be caused by hypovolemia after heart surgery, renal problems, or heart failure. Generally, anything that changes circulating blood volume such as dehydration, hemorrhage, or hypervolemia will affect preload. Likewise, anything that changes about blood returning to the heart, such as vasoconstriction, vasodilation or exercise will affect it. And anything that changes the ventricular filling time such as congestive heart failure, cardiac tampanade, and increased or decreased heart rate will also affect preload.
Afterload (CVP, Central Venous Pressure).
Any resistance against which the ventricles must pump in order to eject its volume is called afterload. The resistance to the ventricular ejection, which is measured, by the pulmonary vascular resistance by the systemic vascular resistance, is afterload. Right side preload is normally 1-6 mm Hg. This central venous pressure (CVP) and right atrial pressure (RA) gives an indication of amount of blood returning to the right side of the heart. Vasodilation as a result of sepsis or hypothermia, low blood pressure, or the effective nitrates, will cause a decrease in afterload. On the other hand, vasoconstriction as a result of hypovolemia, hypothermia, aortic stenosis, hypertension or the affect of vasopressive agents may cause an increase in afterload.
Afterload can be managed by the manipulation of peripheral vascular resistance or systemic vascular resistance. By increasing the preload, the length of the fiber stretch will also increased thereby increasing the heart’s myocardial contractibility resulting in decreased afterload, causing an increase cardiac output.
Both mechanical and pharmaceutical agents may accomplish this. Frequently the administration of dopamine, which will increase preload, while simultaneously titrating Nipride to decrease afterload, is done. The nurse must carefully balance both of these vasotonic agents in order to assist the failing heart.
Remember, the greater the preload, the greater the stroke volume (SV), and therefore, the greater the cardiac output (CO). This is a direct relationship he can be measured by a pulmonary artery catheter (Swan-Gantz). The blood pressure (BP) is an indirect reflection of afterload; therefore BP usually equals afterload.
Cardiac output and afterload have an inverse relationship. That is, the lower the cardiac output the greater the afterload.
Systemic Vascular Resistance.
Systemic vascular resistance (SVR) can be calculated from the main arterial pressure (MAP), central venous pressure (CVP) and cardiac output (CO).
Afterload is not completely measured by vascular resistance. Blood viscosity and valvular resistance will all affect vascular resistance thus afterload. We can normally measured two types of vascular resistance, systemic vascular resistance (SVR) reflects left ventricular afterload. Normally systemic vascular resistance is 900 to 1300 dynes/second/cm2 times per second.
The left ventricle faces increased resistance to as in hypertension so the aim be aimed to reduce systemic vascular resistance. On the other hand of the patient was suffering from symptoms such a shock, the treatment would be aimed at improving cardiac output. Some other causes may be decreased pathologic response due to an inflammatory process, diseases due to increased collateral circulation, or neurogenic induced central vasodilation.
The pulmonary vascular resistance (PVR) is a reflection of right ventricular afterload. It is normally 40 to 220 dynes/second/cm2.
Cardiac Output (CO).
The cardiac output (CO) can be calculated if we know the heart rate and the stroke volume.
CO=HR*SV dynes/Cm2 Normal 4-8 L/min
Poor ventricular filling such as may be found in hypovolemia can cause a decrease in cardiac output. It may be due to poor emptying and as a result of decrease myocardial contractility. This is usually found with a myocardial infarction, cardiac ischemia, arrhythmias, or papillary muscle dysfunction. It can also be found with vasodilatation as a result of vasopressors or sepsis.
An increase in cardiac output may occur whenever there is an increase in oxygen demand, psychological stimulation, and a response to a systemic inflammation, hepatic disease, viral toxic doses, or neurogenic mediated vasodilation.
Tissue oxygenation may be maintained provided that cardiac parameters are adequate. If these parameters are abnormal, the nurse must suspect a threat to tissue oxygenation and consider interventions aimed at improving cardiac function. The numbers must be closely watched. Usually by the time the patient loses pulses, has a changing level of consciousness, or has a decrease in urinary output the situation may be irreversible. Therefore invasive cardiac monitoring through the use of pulmonary arterial catheter is essential. It is one of the most accurate tools for the early assessment of critical patients.
Before cardiac parameters can be obtained the cardiac monitor at the bedside must be programmed. These requirements may vary depending on the type of monitor available. Generally, the nurse must first program the monitor with the type of pulmonary artery catheter in use, the volume of injectate, the temperature of injectate, as well as a computation constant. Each of these requirements may vary slightly from manufacturer to manufacture. Keep in mind that those patients suffering from abnormal cardiac valves (tricuspid) are unstable cardiac rhythms may present inaccurate readings.
Restoring the patient’s normal cardiac output is the goal of treatment. The initial short-term goal should be aimed at regulating stroke volume. There are three factors that regulate stroke volume, preload, afterload, and contractility. The nurse must keep in mind that cardiac output changes are a symptom of a problem and not the actual problem itself. The underlying causes of decreased CO must always be identified and treated before cardiac output can return to normal.
Cardiac Index (CI).
The cardiac index is an adjustment of the cardiac output based on the size of the person’s body. It is the most and individualized cardiac parameter that the nurse can use. It is based on body surface area (BSA). The formula for calculating cardiac index is CI= CO/BSA. The normal value for this parameter is 2.5 to 4L/min/m2
Heart Rate (BPM, HR).
One of the most often overlooked hemodynamic parameters is the heart rate. Critical care patients should be continuously monitored for arrhythmias.
Cardiac dysrhythmias such as bradycardia or tachycardia will affect cardiac output and may make it difficult for the nurse to obtain accurate hemodynamic readings. Additionally, they are potentially life threatening. Persistent tachycardia may increase myocardial oxygen consumption. Normally the heart rate should the 60 to 100 beats per minute. Any rate greater than 120 beats per minute results in decreased cardiac output as a result of the decreased ventricular filling time. Dysrhythmias result in a decrease cardiac output due to a loss of synchronization of atrial and ventricular filling and injection. Bradycardia, that is a heart rate less than 60 beats per minute, are caused by vagel stimulation such as a valsalva maneuver or straining, heart blocks or conduction defects, and maybe caused by drugs. Hypoxia, fear, anxiety, hypovolemia, catecholamines or pain may cause tachycardia, rates greater than 100 beats per minute.
Stroke Volume (SV).
The volume of blood injected with each heartbeat is stroke volume. Whenever there is a condition with results in cardiac dysfunction stroke volume will eventually declined. This reduction in stroke volume might not be apparent initially. Therefore, it should be used in conjunction with additional hemodynamic parameters. Normally the stroke volume is 60 to 130 ml/beat ml. This parameter can be calculated by: SV=CO/HR
Any parameter that affects stroke volume will also affect cardiac output. These include preload, after load, and contractility.
Stroke Index (SI).
Stroke index (SI) like cardiac index (CI) is a more useful measure for determining hemodynamics that is based on the patient size. It can be calculated: SI=SV/BSA
Ejection Fraction (EF).
The ejection fraction is a measurement of how well the left ventricle, or the heart’s main pumping chamber, works. It is expressed as a percentage of blood that leaves the heart with each beat. Normally the left ventricle ejects 55 to 70 percent of the blood during each heartbeat. Generally, the lower the Ejection Fraction the more severe the symptoms
When heart muscle is destroyed by a heart attack, persistent hypertension, or viral infections can lower the Ejection Fraction and cause an enlarged heart. When the EF is to low Congestive Heart Failure may occur. This results in symptoms of heart failure that may include swollen ankles, fatigue, weakness, and shortness of breath.
Contractility is the ability of the cardiac muscle to contract. According to Starling’s Law, fluid volume expansion causes an increase in myocardial end diastolic fiber length. The greater the stretch of the muscle fibers, the greater the force of contraction and volume of blood ejected. This increases the force of the ventricular contraction. There is a direct relationship between contractility and cardiac output.
This is defined, as how much blood is pumped with each contraction in relation to how much blood is available to be pumped. The ejection fraction (EF) can change before the stroke volume in certain conditions, such as left ventricular failure and sepsis. The nurse must remember that contractility is not directly measured by hemodynamic monitoring, it is estimated by the stroke volume index (SVI) from cardiac calculations, and the ejection fraction which can be estimated via echocardiogram.
Fluids may be pushed until adequate central venous pressure (CVP) and pulmonary artery wage pressures (PAWP or Wedge) pressures are reached. This is assuming the patient is suffering from uncomplicated hypovolemia. This increase of fluids will return the patient to normal volemic state. However, if the central venous pressure and wedge pressure rises with fluid challenge and the patient remains hypotensive, the possibility of heart failure must be considered.
Central Venous Pressure.
The central venous pressure is a measurement of the pressure in the right atrium. This reflects the right ventricular diastolic pressure, or the ability of the right side of the heart to pump blood. This is a valuable tool for assessing the relationship between cardiac action, vascularity, and blood volume. However, keep in mind that the central venous pressure is not accurate for the measurement of left ventricular function and maybe the last parameter to change. Still, for those patients in whom fluids are a concern, it is a valuable diagnostic tool. On the basis of central venous pressure readings, decisions for the replacement are restrictions of fluids can be prescribed more accurately. The normal reading for central venous pressure is to 2-6 mm Hg.
One of the most frequent causes of a decrease in central venous pressure is hypovolemia, which results in an increased venous return. Most of the time with this condition, the stroke volume will also be low. You may also see this with neurogenic and anaphylactic shock
An increase in central venous pressure may result from over hydration causing increased venous return or right-sided heart failure. If the stroke volume is high, with an increase central venous pressure, right ventricular dysfunction is assumed. Cardiac tampanade, constrictive pericarditis, pulmonary hypertension, tricuspid stenosis and regurgitation may also cause increases in central venous pressure.
Right Ventricular Pressure (RV).
The right ventricular pressure (RV) can only be measured if a pulmonary artery catheter (Swan-Ganz) has been inserted into the right atrium and the tip of the catheter is advanced and allowed to travel through the tricuspid valve with blood into the right ventricle. The normal pressures within the right ventricle should be between 20 to 30 mm Hg systolic and less than five mm Hg diastolic.
Pulmonary Artery Pressure (PAP).
The catheter is allowed to move into the pulmonary artery. Remember that the pulmonary artery is always venous blood because it is leaving the right ventricle on its way to the lungs to receive oxygen. The waveform is distinctive the dicrotic notch should be present due to the pulmonary valve closure and left-sided heart function. Normally the pressure is 20-30 mm Hg systolic and 8 to 12 mm Hg diastolic.
The systolic pulmonary pressure may be increased from such things as a pulmonary embolus, pneumothorax, hypoxia, or acute respiratory distress syndrome. The diastolic pressure of the right ventricle may be increased by constrictive pericarditis or cardiac tampanade. A decrease in pulmonary artery pressure is also caused by hypovolemia and distributed shock.
Pulmonary Artery Wedge Pressure (PAWP, PACWP, Wedge).
The pulmonary artery catheter is inflated. As the pulmonary artery catheter makes its way into small capillary vessels and becomes wedged. The pulmonary artery wage pressures (PAWP) may be measured. Generally, this measurement is more important than the central venous pressure. If there is left ventricular dysfunctions, such as with a myocardial infarct or cardiomyopathy, a threat to tissue oxygenation and low cardiac output may exist. Left ventricular function may be assessed by using the pulmonary catheter wedge pressure, which would provide an indirect measurement of preload. With a normal stroke volume the wedge pressure should be for 4-12 mm Hg.
Nursing Considerations in Hemodynamic Monitoring.
To ensure accuracy of the hemodynamic values obtained from any transducer system, the nurse must level and zero the system as follows:
Leveling is performed to eliminate the effects of hydrostatic pressure on the transducer. It should be done before and after connecting the pressure system to the patient, with every change in bed height or changes in the elevation of the head of the bed, with any significant change in patient’s hemodynamic variables, and prior to zeroing and calibration.
Zeroing is performed to eliminate the effects of atmospheric pressure on the transducer. Zeroing should be performed before and after connecting the pressure system to the patient, with any leveling, and whenever there is a significant change in the hemodynamic variables.
All values should be rated at the end of expiration. The transducer should be leveled visibly with static axis. The transducer should be leveled, is a road, and calibrated every eight hours depending on institutional policy. Readings can be taken with ahead a bed elevated, as long as a transducer is leveled to the plane to static axis. Readings cannot be taken with a patient and a lateral position.
The same electrical equipment that is invaluable in critical care monitoring and resuscitation also may be a potential risk to the patient; the most hazardous of which is ventricular fibrillation. Respect of electrical safety monitoring guidelines is crucial. A defibrillator, emergency crash cart and medications must be readily available.
Patients who have a pulmonary artery catheter are subject to the same complications of other patients who have central venous liens. Among these are increased risk for infection, thrombosis, and emboli.
One complication that must to be avoided is a constant wedging of the pulmonary artery catheter. This occurs when the balloon is left inadvertently inflated. The catheter will migrate down straining to a smaller pulmonary vessel is can result in pulmonary artery ischemia and lung ischemia. It can also be a cause of pulmonary infarction, and pulmonary artery perforation. If this occurs it is considered an emergency. The nurse must rapidly capable import and a flight to blame if necessary. The patient should be repositioned usually from the side to the back. The patient should cost. The pulmonary artery catheter should be rapidly flashed. And the catheter may be pulled back slightly. Keep in mind that this is a complication that is preventable by being careful with the position of the syringe.
Ventricular irritation from the catheter is another hazard the nurse must be aware of. This occurs when the catheter floats back into the right ventricle or is looped through the ventricle. The hazard to the patient with this condition is ventricular dysrhythmias. If this happens the nurse must check waveform pressures. If the catheter tip is in the right ventricle the waveform will be taller with a diastolic of 0-5. Notify the physician if the catheter needs to be floated back into the pulmonary artery. Rarely the catheter will require pulling back slightly.
Air embolism may occur when the bowling ruptures. This can result in pulmonary embolism. When inflating the balloon the nurse must feel for resistance and watch for a dampened waveform. No resistances, along with no wedge are the indications of a ruptured balloon. The nurse should remove the syringe, close the port, and label the port that the balloon is ruptured.
A dampen waveform may be caused by kinks, bubbles, within the IV system, clots may be present, or the catheter may be against the vessel wall. The Nurse must check for air bubbles or air in the system. The cable and catheter should be checked for kinks. The pressure bag must be inflated to 300 mm Hg. Check for the ability to aspirate the line and flush line. The patient may cough, be repositioned, or the catheter may have to be repositioned.
At times the pulmonary artery line cannot be flushed. Again the nurse must check for kinks, adequate fluid and pressure within the flesh bag, and check to stopcocks for correct position.
If there is no waveforms the connections of the tubing, cables, and stopcocks should be checked. Check for blood or air within the system.
If the nurse keeps getting a low reading or a false high reading, the transducer should be leveled, zeroed, and calibrated. The connections should be checked. And in the air or blood within the system should be removed.
When the balloon will not wedge, the artery is too large for the inflated balloon to inflate. The pulmonary artery catheter might have migrated back into the ventricle. This would require repositioning by the physician. The balloon may have ruptured.
|Hemodynamic Parameters||Abbreviations||Normal Values|
|Mean Arterial Pressure||MAP||70-90 mm Hg|
|Right Atrial Pressure||RAP||2-6 mm Hg|
|Central Venous Pressure||CVP||2-8 mm Hg|
|Pulmonary Artery Systolic Pressure||PAS||20-30 mm Hg|
|Pulmonary Artery Diastolic Pressure||PAD||6-12 mm Hg|
|Pulmonary Artery Mean Pressure||PAM||10-15 mm Hg|
|Pulmonary Artery Wedge Pressure||PAWP, Wedge||8-12 mm Hg|
|Cardiac Output||CO||4-8 L/min|
|Cardiac Index||CI||2.5-4 L/min|
|Stroke Volume||SV||60-130 ml|
|Stroke Volume Index||SVI||40-50 ml/m2|
|Systemic Vascular Resistance||SVR||800-1200 dynes|
|Systemic Vascular Resistance Index||SVRI||2000-2400 dynes|
|Pulmonary Vascular Resistance||PVR||150-300 dynes|
Brunner, Charlotte, Little Rock Critical Care Course, “Hemodynamic Monitoring,” Lecture Notes, 1998.