Hemodynamic Monitoring

Hemodynamic monitoring is the assessment of the patient’s circulatory status. It includes measurements of heart rate, intra-arterial pressure, pulmonary artery and pulmonary capillary wedge pressures, central venous pressure, cardiac output, and blood volume. Concepts of preload and afterload can overload busy nurses who care for patients with cardiovascular problems. Because of the complexity of these patients’ diseases, hemodynamic monitoring is an essential component of quality patient care. Hemodynamics refers to the forces, such as preload and afterload that affect circulating blood throughout the body. Nurses assess the stability of these forces when they take blood pressures or palpate a pulse. Although the interaction of these forces is quite complicated, the concepts are easily understood by substituting the word stretch for preload and resistance for afterload. Preload and afterload are closely related and reflect the heart’s effectiveness in managing blood flow in and out of its chambers. The purpose of this module is to review the concepts associated with hemodynamic monitoring.

Monitoring hemodynamic status through skin electrodes gained a good deal of attention in the 1960s when NASA began using the technique to evaluate the effects of zero gravity on astronauts in space. Although it worked well in healthy adults, impedance cardiography (ICG) was not consistently accurate on the critically ill at least in part because motion artifact and critical care equipment interfered with the signals. Advanced computer technology and signal processing have given ICG the precision needed to accurately assess high acuity patients. The pulmonary artery catheter (PAC) is the clinical standard for hemodynamic monitoring in intensive care units.

Dr. Swan and Dr. Ganz first inserted PACs in critical care units in the 1970’s. The Swan-Ganz catheter is a flow-directed, balloon-tipped, 4- to 5-lumen catheter. It is inserted percutaneously at the bedside and allows for continuous monitoring of pulmonary artery pressure as well as periodic measurement of pressures in the distal branches of the pulmonary artery. Recent studies have questioned the outcomes of patients with PACs related to increased mortality even when numbers were adjusted for the severity of illness. In 1996, the Pulmonary Artery Consensus Conference was held to respond to the controversy regarding the use of PACs. Six studies were conducted over the past twelve years to assess the knowledge of critical care nurses regarding PACs with a mean score of 31–65 %. The mean score for physicians was 61%. Several hemodynamic parameters are derived or calculated from other variables. Most bedside monitors perform the calculations necessary to attain these values; however, the nurse should know which variables are included in the calculations to understand how hemodynamics interact and to interpret the derived parameters.

The delivery of oxygen to tissues and organs depends largely on the delicate interplay between blood volume, vessel tone and the heart’s pumping action. Hemodynamic monitoring is a way of assessing each part of that process. The key parameters obtained from pulmonary catheters used for hemodynamic monitoring are cardiac output and stroke volume. These blood flow parameters are the first to be assessed when monitoring hemodynamic data. If these parameters are adequate, tissue oxygenation is generally adequate; if they are abnormal, a threat to tissue oxygenation may exist which requires treatment. Normal hemodynamic parameters can be found below:

Cardiac output is the heart rate times the stroke volume and is the amount of blood pumped by the ventricles each minute. Stroke volume is the amount of blood ejected with each cardiac contraction/heart beat. Understanding heart rate and stroke volume is essential for knowing how to treat abnormal cardiac output. An adequate cardiac output is essential to supply oxygen and nutrients to major organs and peripheral tissues. For example, a reduction in cardiac output may diminish blood flow to the brain and result in an altered level of consciousness and impaired cognition. Alterations in heart rate, contractility, preload, and afterload can affect cardiac output. Abnormal cardiac output is most commonly related to a problem with stroke volume. The stroke volume is extremely important because it will typically fall once blood volume becomes too low or left ventricle becomes too weak to eject blood. Clinical conditions, such as sepsis or with exercise, the stroke volume can be increased; however, low stroke volume is more commonly found during hemodynamic monitoring.

Cardiac index is the cardiac output adjusted to body size and is a better parameter to use than the cardiac output. Some patients are able to tolerate a low cardiac index without clinical problems. Tracking trends in the cardiac index is more useful than monitoring single data points since temporary changes in values may not be clinically significant. Monitoring both cardiac index and tissue oxygenation parameters will increase the accuracy in identifying a clinically dangerous event. The stroke index, like the cardiac index, is a more useful measure that individualizes the stroke volume based on the patient’s size. In any condition in which the heart begins to malfunction, the stroke index will decline; in certain circumstances such as left ventricular failure and sepsis, the stroke index may not initially decline because of the heart’s compensatory mechanisms. If a patient with coronary artery disease begins to have left ventricular dysfunction, the left ventricle will dilate, causing left ventricular end diastolic volume (LVEDV) to increase.

The ejection fraction is defined as the amount of blood pumped with each contraction in relation to the amount of blood available to be pumped. Although the increase in LVEDV might prevent a drop in stroke index, dysfunction can still be detected by observing a drop in the ejection fraction. Because changes in the ejection fraction (and end diastolic volumes) can provide early warning of ventricular dysfunction, they are ideal monitoring parameters. Typically, monitoring of these parameters is not routinely available. The stroke volume or index thus becomes the single most important piece of information regarding cardiac function in the absence of ejection fraction monitoring.

Preload is the force that stretches the muscle fibers of a resting heart – how much they are stretched just prior to contraction. The amount of blood present within the right and left atria and ventricles prior to contraction and the condition of the myocardium determine the stretch or preload of the heart muscle. The greater the volume of blood in a heart chamber, the greater the preload. As the blood volume in the left ventricles increases, the cardiac muscle stretches and up to a point, ejects its volume more effectively. Ideally, an adequately filled and stretched left ventricle should briskly contract, snap like a rubber band, to send blood on its way. However, there is also a point at which this stretch is so extreme that the output is diminished. The relationship between fiber stretch and contractile force is known as the Frank Starling’s Law of the Heart.

Starling’s mechanism states that, up to a point, the more a cardiac muscle is stretched in diastole, the more forcefully it contracts in the next systole. If the muscle stretches too much the contraction becomes weaker. It is difficult to measure preload in clinical practice and so it is estimated from the ventricular filling pressure. If the ventricular pressure is increased beyond normal it is assumed that the left ventricle is weakening. If the pressure exceeds 18 mm Hg the ventricle is near failure level. If the ventricular filling pressure is too low (< 8 mm Hg) then it is assumed that the blood volume is low. Optimal cardiac output is dependent upon volume, heart rate, and achieving the appropriate amount of stretch. For example, a hemorrhaging trauma victim may have a ventricle that is under-filled. The cardiac output would be reduced because of two mechanisms: inadequate blood in the ventricle available for pumping and a smaller force of contraction due to less muscle fiber stretch. However, compensatory mechanisms are triggered by the sympathetic nervous system response to a shock state – an increased heart rate and contractility as well as other mechanisms would temporarily sustain cardiac output. Replacing lost volume though would further preload, thus enhancing cardiac muscle stretch and subsequent contraction, the optimum effect of the Starling mechanism.

For the patient in heart failure who is volume overloaded, the ventricle has the opposite problem. Increased ventricular volume raises pressure within the ventricles, thereby augmenting myocardial stretch or preload and subsequent contraction. Initially, this serves as a compensatory mechanism with cardiac function reaching the maximum beneficial stretch described by Starlings mechanism, thus cardiac output is optimized. If fluid overload continues, the pressure within the ventricle rises beyond the point of beneficial stretch leading to less effective cardiac contraction (the stretched rubber band without the snap) and decreasing cardiac output.

Measuring preload can easily be evaluated by monitoring the effects of the effects of a physiologic fluid challenge on the stroke volume. Begin with the head of the bed elevated; then gently place the patient supine. Gravity moves blood from the lower torso and extremities toward the heart, giving the patient a fluid bolus. The normal response to this is a moderate rise in stroke volume and cardiac output. A large rise indicates hypovolemia, from bleeding, dehydration, or some other fluid loss. No change or a decrease in the stroke volume indicates volume overload, or poor cardiac function. Preload should be assessed on admission, and any time the cardiac index decreases. Checking the response to a change in position will help detect hypovolemia or left heart dysfunction early so interventions can be started quickly.

Right ventricular preload – the central venous pressure (CVP) or right atrial pressure (RAP) – also can be measured by a catheter placed in the right atrium. However, clinicians usually focus on preload of the left ventricle (LV), which is the largest and last chamber to eject blood to most of the body. A PAC indirectly measures LV preload or LVEDP, when inserted into the pulmonary artery and wedged in a pulmonary capillary. End-diastolic represents the moment in the cardiac contraction-relaxation cycle when the ventricle contains the greatest volume of blood, just before it contracts and ejects its volume. The volume and the stretch or amount of tension placed on the heart muscles at that point determines the pressure. The wedged pulmonary catheter reflects LVEDP because at end-diastole, the mitral valve is open and this creates communication between the left ventricle, the left atria, and the pulmonary vascular bed. In other words, “the doors are all open” from the LV to the pulmonary capillary.

Afterload is the tension that the ventricular muscle must generate in order to overcome resistance to ejection. Sources of resistance include blood pressure, systemic vascular resistance (SVR), and the condition of the aortic valve. When arterial vasoconstriction raises the systemic vascular resistance as in shock or the aortic valve is very stiff or tight as in aortic stenosis, the ventricle has to generate a tremendous amount of pressure – or afterload – to overcome that resistance. It is like opening a door against a strong wind – it requires a lot of energy.

Sympathetic stimulation causes vasoconstriction of certain arteries, arterioles and veins in turn raising blood pressure. This increases cardiac workload. The ventricle now has to generate enough tension to raise the pressure within the ventricle above the pressure in the aorta to force the aortic valve open. Only then can the ventricle eject the blood. Think about having a 60ml syringe with a 25-gauge needle on the end and trying to eject the contents of the syringe as quickly as possible. It takes a tremendous amount of force to empty the syringe because the diameter of the needle is small and acts as resistance to flow.

Aortic stenosis can occur congenitally, after infections such as rheumatic fever or with age as calcium is deposited on the valve leaflets. These have the effect of creating an obstruction to the outflow of blood from the left ventricle. Valves open because the pressure generated on one side of the valve (left ventricle) exceeds the pressure on the other side (aorta). A stenotic valve creates a great deal of resistance to ejection and then afterload rises dramatically. To open the aortic valve and eject blood, the ventricle has to overcome the resistance of the arterial blood pressure and any resistance cause by the valve. Patients with chronic untreated hypertension or aortic stenosis develop left ventricle hypertrophy as a response to the high afterload.

Estimating preload is frequently inaccurate since pressure alone does not determine preload. The assumption used to estimate preload is important to understand since it is widely used in critical care. To increase the accuracy of assessments based on pressure alone, pressure measurements should always be compared with the stroke volume or stroke index. As the filling pressures elevate, they should decrease the stroke index if they are clinically significant. If the filling pressures are low, the stroke index must be low as well before one can assume that the hypovolemia exist. Combining the stroke index with the filling pressure is essential in order to avoid misinterpreting the filling pressure.

The heart rate needs to be evaluated in order to detect early changes in hemodynamics. Since cardiac output is a product of stroke volume multiplied by heart rate, any change in the stroke volume will normally produce a change in the heart rate. If the stroke volume is elevated, the heart rate may decrease – this is seen in adaptation to exercise. The exception to this guideline is during an increase in metabolic rate, in which both the stroke volume and the heart rate increase.

If the stroke volume falls, the heart rate normally increases – evaluation of tachycardia is an essential component of hemodynamic monitoring. Bradycardia and tachycardia are significant because they may reflect a potentially dangerous interference in cardiac output. Bradycardia, which develops suddenly, is usually reflective of a threat to cardiac output. Tachycardia, which is more common, may also indicate a threat to cardiac output. Tachycardia develops for three reasons:

1. An increase in metabolic rate as with fevers
2. A psychological factor such as anxiety or fear
3. A reduction in stroke volume

All three factors need to be considered when evaluating for a rapid heart rate. For example, if the patient develops a heart rate of 120 beats/minute, the nurse must rule out fever, anxiety or pain before assuming that the heart rate has increased due to reduced stroke volume. If the heart rate is increased and a raised metabolic rate or psychological factors do not appear to be the cause, then a low stroke volume is indicated and should be evaluated. The two most common reasons for a low stroke volume are hypovolemia and LV dysfunction. Both causes of low stroke volume can produce an increased heart rate if no abnormality exists in regulation of the heart rate.

An increased heart rate can compensate for a decreased stroke volume but this compensation is limited. The faster the heart rate, the less time there is for ventricular filling. As an increased heart rate reduces diastolic filling time the potential exists to eventually reduce the stroke volume. There is no specific heart rate at which diastolic filling is reduced so severely that stroke volume decreases. It is important to remember that as the heart rate increases stroke volumes can be negatively affected.

Another important concept regarding heart rate has to do with the effect it has on myocardial oxygen consumption (MVO2). The higher the heart rate the more likely the heart will consume more oxygen. Typically the MVO2 can only be estimated because direct measurement is not easy. Since heart rate is not only the determinant of oxygen consumption – contractility and vascular resistance are also determinants – heart rate alone will not predict MVO2. Keeping heart rates as low as possible, particularly in patients with altered myocardial blood flow, is one way of protecting myocardial function.

The arterial pressure is one of the most commonly used parameters to assess the adequacy of blood flow to the tissues. Blood pressure is determined by two factors – cardiac output and SVR. This fact is critical to the interpretation of blood pressure. Blood pressure will not reflect early clinical changes in hemodynamics because of a compensation mechanism by which cardiac output and SVR interact to maintain adequate blood pressure. This interaction is not always predictable: if the cardiac output decreases the SVR will increase just enough to overcome the fall in cardiac output and maintain blood pressure at near normal levels. If the SVR falls, the cardiac output will increase to offset the fall in SVR. Blood pressure cannot signal early clinical changes. If a patient bleeds the blood pressure will generally not reflect the event until it becomes so severe that an increase in the heart rate and SVR no longer compensate. The same holds true for patients with congestive heart failure or myocardial infarction.

Blood pressure is considered normal if hypotension, which is associated with inadequate blood, flow to the tissues or hypertension which is associated with excessive pressure and damage to the peripheral circulation. Hypotension is probably present if there is evidence of tissue oxygenation deficits. Blood pressure needs to be assessed along with measures of tissue oxygenation such as SvO2 and lactate levels. Blood pressure cannot be viewed in isolation. Hypertension is more difficult to identify since there are fewer clinical parameters to indicate when peripheral circulatory changes are occurring. Pressure alone is an important determinant of circulatory damage. It is a little more reliable as a parameter in hypertension than in hypotension.

Pulmonary artery and cardiac pressures are typically obtained from a flow-directed catheter inserted into a major vein and directed into the heart and pulmonary artery. Since the pulmonary vasculature is normally low resistance system, the pulmonary artery blood pressure is generally 25/10 mm Hg. If the pressure in the pulmonary vasculature elevates, the capillary hydrostatic pressure exceeds capillary osmotic pressure and fluid is forced out of the vessels. Interstitial and alveolar flooding can then occur with resulting interference in oxygen and carbon dioxide exchange. The pulmonary artery pressures can be helpful in diagnosing many clinical conditions. Pulmonary artery pressure greater than 35/20 mm Hg is considered pulmonary hypertension.

Determining intracardiac pressure frequently centers on measurement of arterial pressure. Arterial pressure is used to estimate ventricular end diastolic pressures. Ventricular end diastolic pressure reflects preload. Right atrial pressure is referred to as the central venous pressure (CVP) and left atrial pressure is referred to as the pulmonary capillary wedge pressure (PCWP) or pulmonary artery occlusive pressure (PAOP). CVP is an estimate of right ventricular end diastolic pressure (RVEDP) and is used to assess the performance of the right ventricle. The guidelines for interpreting the CVP have traditionally been relatively simple. If the CVP is low (< 2 mm Hg), hypovolemia is assumed to exist. If the CVP is high, RV dysfunction is present. The best way to interpret pressure values is to compare them to another parameter such as the stroke index. If both the CVP and the stroke index are low, then hypovolemia is likely; if the CVP is low and the stroke index is normal than hypovolemia may not be present; if the CVP is high and the stroke index is low, RV dysfunction is probable; if the CVP is high and the stroke index is normal than RV dysfunction is not clinically significant. The most difficult part of interpreting pressures is that normal pressures do not indicate normal cardiac functioning. CVP is useful in assessing RV function. The assessment of LV function is generally more important. If the left ventricle dysfunctions – in myocardial infarction or cardiomyopathies – then a threat to tissue oxygenation and survival may exist.

Assessment of LV preload is commonly performed by obtaining the PCWP (PAOP). The use of the PCWP to estimate LVEDP is based on the assumption that a measurement from an obstructed pulmonary capillary will reflect an uninterrupted flow of blood to the left atrium since there are no values in the pulmonary arterial system. When the mitral valve is open, left arterial pressure reflects LVEDP. The guidelines for interpreting the PCWP are similar to those of CVP interpretation and have the same limitations as CVP interpretation with a few additions. If the PCWP is low, hypovolemia is assumed. If the PCWP is high LV dysfunction is present. The PCWP should not be looked at in isolation. When analyzing the PCWP, always use the stroke index to help interpret the value. If the PCWP is low and the stroke volume is low, then hypovolemia is probable. If the PCWP is low and the stroke index is normal, then hypovolemia is unlikely. If the PCWP is high and stroke index is low, LV dysfunction is probable. If the PCWP is high and the stroke index is normal, LV dysfunction is not clinically significant.

One of the most commonly derived parameters is vascular resistance, which is assumed to represent afterload or the resistance the ventricles face during ejection of blood. It is important to keep in mind that afterload is not measured by vascular resistance alone. Afterload is also influenced by blood viscosity and valvular resistance. While these values can change, vascular resistance can be used to estimate afterload since viscosity and valvular resistance tend to change less often than blood vessel resistance. The value obtained from the following formula is multiplied by a factor of 80 to generate a value measurement in dynes/sec/cm5:

SVR =      

 ____Mean arterial pressure – right arterial pressure_____
                                       Cardiac output

Two types of vascular resistance are measured – systemic and pulmonary. Systemic vascular resistance (SVR) reflects LV afterload and pulmonary vascular resistance (PVR) reflects RV afterload. If SVR is elevated the left ventricle will face increased resistance to the ejection of blood. The SVR rises in response to systemic hypertension or compensation for low cardiac output. It is important to know why SVR is elevated in order to select the appropriate therapy. If the SVR is elevated due to systemic hypertension then afterload-reducing agents are essential in treatment plan. If SVR is elevated in compensation for low cardiac output, then therapy is directed at improving the cardiac output. If SVR is low, attempts to increase the resistance rely on vasopressors while treating the underlying condition. If the underlying condition is not corrected, the use of vasopressors will provide on short-term increase in SVR. The SVR does not decrease except:

• as a pathologic response to inflammation
• hepatic disease (increased collateral circulation)
• neurogenic-induced central vasodilation

Pulmonary vascular resistance reflects the work the right ventricle faces at it attempts to contract. The PVR elevates for one of three reasons: (1) primary pulmonary hypertension; (2) secondary active pulmonary hypertension and (3) secondary passive pulmonary hypertension. The cause of primary pulmonary hypertension is unknown and the PVR is markedly elevated. No cure exists for this condition but newer therapies have been tried. The cause of secondary pulmonary hypertension is known, but it is not responsive to treatment as in cases of chronic obstructive pulmonary disease or pulmonary emboli. Secondary passive pulmonary hypertension is the result of LV dysfunction. The pulmonary arterial pressure decreases as the LV function improves. It is the most responsive pulmonary hypertension in terms of treatment. This form can be identified by noting the close correlation between the PCWP and the pulmonary artery diastolic pressure.

It is critical to understand that the human cardiopulmonary system exists only to provide nutrients to the tissues – the primary nutrient is oxygen. The value of measuring SvO2 centers on the concept that the amount of oxygen returning to the lungs is an accurate reflection of tissue oxygenation. Oxygen is normally removed from hemoglobin as it passes through the capillary bed (about 25% is removed). This means the amount of oxygen returning to the lungs still attached to hemoglobin should be about 75%. The oxygen that is in hemoglobin is the only oxygen reserve in the body. If the tissues are deprived of oxygen, the tissues will extract more oxygen from hemoglobin.

Hemodynamics is looked at in terms of the adequacy of tissue oxygenation reflected in the mixed venous oxyhemoglobin (SvO2) which is measured two ways:

1. Sampled directly from the distal port of the pulmonary artery catheter – care must be taken to draw the sample slowly so as not to aspirate pulmonary capillary blood – producing an arterial-like blood sample
2. Continuously via fiber optics in the pulmonary artery catheter, which has the obvious advantage of providing a continuous reading of SvO2, avoiding the expense of blood gases and loss of blood as well as the exposure risk for the nurse

Cardiac output is measured by a variety of techniques. In the clinical setting, it is usually measured by thermodilution technique used in conjunction with a flow-directed balloon catheter such as the Swan-Ganz catheter. The catheter is positioned in a branch of the pulmonary artery. It has a thermistor (external sensing device) situated 4 cm from the tip of the catheter, which measures the temperature of the blood that flows by it. All air must be removed from the system including the bag and caps must be replaced with dead-end caps to prevent air emboli and bleeding. Usually 10 cc D5W at room temperature is used. Normal saline may also be used. 10ml is injected in 4 seconds or less. Three consecutive readings are taken and an average is recorded. The zero point of the manometer should be on a level with the patient’s right atrium that is at the level of the fourth intercostal space, midway between the anterior and posterior – this is known as the phlebostatic axis. The transducer is calibrated/zeroed at the phlebostatic axis. This level must be changed when the patient is repositioned. The patient may be positioned up to 45 degrees. If the patient is in right lateral position at 90 degrees, the fluid air interface is leveled to the fourth ICS mid sternum. If the patient is left lateral position at 90 degree, the fluid air interface is leveled to the fourth ICS left sternal border. The transducer must be zeroed prior to insertion, with each position change, with any significant change in hemodynamic variables and every 8 hours. This eliminates the effects of atmospheric pressure on the transducer.

Appropriate positioning of the patient for the procedure provides for maximum visibility of the veins. If the neck veins are to be used the patient should be placed in Trendelenburg position, which prevents chance of air embolism. The catheter may be inserted through the internal jugular or subclavian vein into the superior vena cava to the right atrium. The balloon is then inflated and the catheter floats through the tricuspid valve to the right ventricle, through the pulmonic valve into the pulmonary artery and then “wedges” in the pulmonary capillary. The balloon is then deflated and the catheter should return to the pulmonary artery. A chest x-ray is taken to confirm the position and to rule out a pneumothorax. The catheter should be at or below the level of the left atrium.

Electrical activity precedes mechanical activity. The EKG waveforms represent electrical activity and the hemodynamic waveforms represent mechanical activity. Right arterial pressure is the indirect measurement of right ventricular preload. An arterial waveform has three common characteristics: (1) a rapid upstroke; (2) a dicrotic notch; (3) a progressive diastolic runoff. Diastole is read near the end of the QRS complex and systole is read before the peak of the T wave. A ventricular waveform is similar to an arterial wave in that it also has three common characteristics (i.e. a rapid upstroke, a rapid diastolic drop, and an end diastolic pressure rise).

• A wave is the first full wave following the P wave on the EKG. It represents right atrial contraction.
• V wave is the first wave following the QRS. It reflects the influx of blood into the atrium after closure of tricuspid valve.
• C wave is between the A wave and the V wave. It may not be visible. It is caused by the closure of the tricuspid valve at the beginning of the right atrial systole. Right atrial pressure is recorded as a mean pressure.

Right ventricular waveform is similar to an arterial wave in that it also has three common characteristics (i.e., a rapid upstroke, a rapid diastolic drop and an end diastolic pressure rise). When the pressure in the RV exceeds the pressure in the pulmonary artery the pulmonic valve opens and you have ejection, which causes a rapid downslope. The lowest point on the wave is right ventricular end diastolic pressure. It is increased in right ventricular myocardial infarction. It can only be measured during insertion of the PA catheter. It represents right ventricular preload.

Normal Arterial Waveform
 

Pulmonary artery waveform can be seen immediately following the QRS when there is a rapid rise in pressure. The right ventricle ejects its contents into the pulmonary artery. The dicrotic notch on downslope represents the closure of the pulmonic valve. Pressure falls but never to zero because there is a constant pressure in the pulmonary artery. Pulmonary artery occlusive pressure is the wedge pressure when the balloon occludes the forward flow.

Use of hemodynamic monitoring can result in complications for the patients. The nurse must be alert to:

• infection
• pneumothorax
• pulmonary infarction
• thrombus – swelling of the arm
• pulmonary artery rupture balloon rupture
• ventricular ectopy – right bundle branch block or if the patient has pre-existing left bundle branch block he may develop congestive heart failure.

To obtain accurate values five steps are necessary:

1. Set the transducer to zero
2. Ensure that the transducer is level – this should be done whenever the patient or the transducer is moved.
3. Read the waveform accurately.
4. Perform a square-wave test to verify the accuracy of the tubing and catheter.
5. Perform a calibration of the transducer.

Signs of volume overload – dyspnea, the presence of rales or crackles, pulmonary edema, increased jugular venous pressure and pitting edema of the ankles – may indicate a problem with increased preload. Medical interventions include a drug regimen of first line drugs – morphine, furosemide (Lasix), nitroglycerine and if necessary second line drugs like dopamine and Dobutamine. Morphine, in addition to relieving pain and anxiety, dilates peripheral vessels. This action redistributes blood, which pools in dependent areas, such as the legs, especially if the patient dangles his legs or has the head of the bed elevated. Pooling decreases the volume returned to the heart, which subsequently reduces the volume that a failing ventricle must manage. If the failing left ventricular ineffectively empties its contents, it can accept less blood from the pulmonary circulation, leading to blood pooling in the lungs, which can precipitate pulmonary edema. The dose of morphine, usually from 2 mg to 10 mg intravenously, is titrated according to the patient’s response. Some patients may experience hypotension due to arterial and venous dilation from only small doses, while others may require repeated high doses to achieve a therapeutic effect.

Furosemide is an effective diuretic that diminishes total body blood volume by boosting urine output, as long as the heart works well enough to perfuse functioning kidneys. The initial recommended dose is 0.5 to 1.0 mg/kg by slow IV injection. Customary IV doses range from 20 mg to 40 mg, although the amount may be as much as 100 mg in emergencies. Blood pressure needs careful monitoring when administering IV diuretics especially when given to patients who already have hypotension. These patients may need additional medications to support blood pressure during diuresis. Electrolyte monitoring is also critical. Reduced serum magnesium and potassium may cause significant heart rhythm disturbances.

Nitroglycerin, like morphine, produces venous dilation, redistributing blood volume to the peripheral areas and pooling blood away from the heart. Nitroglycerin is also effective in relieving cardiac chest pain because while it lessens the workload of the heart, it reduces cardiac muscle oxygen requirements. Additionally, higher IV nitroglycerin doses enhance oxygen delivery by improving circulation through the coronary arteries. Sublingual nitroglycerin is mainly a vasodilator that reduces preload in patients who take it for angina, whereas IV nitroglycerin in higher doses causes an arterial dilating effect reducing ischemia.

Dopamine, a precursor of norepinephrine, administered as a continuous infusion, affects preload by causing vascular constriction or dilation through its effect on the sympathetic nervous system. Its effect is dose dependent. Low-dose dopamine, 2 mcg/kg/min to 4 mcg/kg/min has peripheral vasodilating effects but causes little or no increase in renal perfusion or force of myocardial contraction (positive inotropy) as previously thought. However, it may promote diuresis, which would decrease preload, as would its vasodilating effect. Because dopamine at this dose range has no direct effect on blood pressure, look for other causes, such as vascular volume depletion, anxiety, and pain if a patient receiving this drug has fluctuations in pressure.

Moderate-range doses between 5 mcg/kg/min and 10 mcg/kg/min directly improve preload by causing venous constriction and increasing myocardial contractility through sympathetic stimulation. If a patient has acute pulmonary edema, dopamine is a second line treatment when the patient’s blood pressure is 70 mmHg to 100 mmHg and signs and symptoms of shock are present. Systemic and splanchnic (gut) vasoconstriction occurs when dopamine’s dose exceeds 10 mcg/kg/min. The risk of both myocardial and peripheral ischemia is greater as the dose increases. The need for supplemental oxygen should be evaluated, all chest pain promptly treated and peripheral perfusion indicators such as pulses and urine output closely monitored. Tachycardia may also be an adverse effect and for a patient who has coronary heart disease, the combination of increased contractility and tachycardia may significantly worsen ischemia.

Dobutamine, a synthetic catecholamine, is also administered as continuous IV infusion and is indicated for the treatment of acute pulmonary edema when blood pressure is > 100 mmHg and signs of shock are absent. It is also used to treat severe systolic heart failure. Its effects are dose dependent. Dobutamine increases myocardial contractility and heart rate, decreases left ventricular preload, and indirectly causes a peripheral vasodilatation further enhancing the reduction in preload. It is usually administered at 5 – 20 mcg/kg/min. Doses greater than 20 mcg/kg/min increase the risk for myocardial ischemia due to the oxygen demand of a higher heart rate.

Medications, technology and independent nursing actions can be used to manipulate afterload. Nitroprusside is a drug that dilates both arterial and venous vessels, diminishing both systemic vascular resistance and venous return. Its net effect is a reduction in preload and afterload resulting in a decreased workload of the heart, improved cardiac output, and relief of pulmonary congestion. It is indicated for treating severe heart failure and hypertensive emergencies. The recommended dose is 0.1 mcg/kg/min to 5 mcg/kg/min as continuous IV infusion. Sometimes doses up to 10 mcg/kg/min are needed. The IV container with the drug solution needs to be wrapped in foil because exposure to light decomposes the drug. Cyanide toxicity is a risk for patients with hepatic or renal insufficiency and those requiring more than 3 mcg/kg/min of Nitroprusside for more than 72 hours.

ACE (Angiotensin Converting Enzyme) inhibitors, such as captopril (Capoten) and enalapril (Vasotec) are a category of drugs that block the conversion of angiotensin I to angiotensin II. A potent vasoconstrictor, angiotensin II also stimulates the release of aldosterone, a hormone that regulates fluid balance. A reduction in circulating angiotensin II causes a reduction in systemic vascular resistance, or afterload. A lower level of angiotensin II also results in less plasma aldosterone with an accompanying reduction in sodium and water reabsorption in the renal tubules, thereby decreasing preload as well. Patients taking these medications should be observed for hypotension, decreased serum sodium, and an elevated blood urea nitrogen (BUN). ACE inhibitor drugs are indicated for treating hypertension and post-acute MI.

The intraaortic balloon pump (IABP) senses systole and diastole, usually via the patient’s EKG signal. The balloon inflates at the onset of diastole, raising aortic diastolic pressure. The coronary arteries fill almost exclusively during diastole, so raising this pressure causes the coronary arteries to be perfused at a higher pressure, thereby enhancing coronary artery blood flow. This can be extremely helpful to a patient who has ischemia. A competent aortic valve prevents blood from flowing back into the aorta. Severe aortic regurgitation prohibits the use of this device. The major effect of the IABP is that it effectively reduces afterload. As the device senses the onset of systole, it quickly deflates the balloon, causing an abrupt decrease in the pressure within the aorta. When the balloon deflates just as systole begins and the pressure falls, the resistance to ejection falls and afterload decreases. The ventricle can easily eject its contents against less resistance. This makes the IABP a lifesaving device for many patients whose hearts cannot handle the normal workload. Examples are patients with heart failure in the immediate period after cardiac surgery or patients who are waiting for a donor heart for transplant.

Nurses can also reduce afterload by helping patients control pain and anxiety. Maintaining a calm atmosphere, managing pain and assisting patients to maintain some control over their own care are a few of the ways that the nurse can affect afterload. In the technologically advanced world, sometimes nurses forget how much these factors influence patient outcomes. A patient with a damaged myocardium will greatly benefit from nursing interventions that minimize workload and oxygen demand on the heart by decreasing the sympathetic stimulation. Nurses applying the knowledge of hemodynamic monitoring can coordinate medical and nursing interventions to promote better patient outcomes.

Boggs, R., & Wooldridge-King, M (Eds.) (2004) AACN procedure manual for critical care, Philadelphia: W.B.Saunders.

Bridges, E., (2000). Monitoring pulmonary artery pressures: Just the facts. Critical Care Nurse, 20(6), 59-78.

Hackler, L., (2004).Hemodynamics for bedside nurse. Nursing Spectrum-Career Fitness Online. Retrieved November 17, 2004, from http://www.nursingspectrum.com.

Husk, C., & Gallo, B., (2000). Critical care nursing – A holistic approach (7th ed.). Philadelphia: J.B. Lippincott.

Von Rueden, K., Turner, M., and Lynn, C. (1999). A new approach to hemodynamic monitoring; RN Magazine; 62 (8).