Chapter 2. Hemodynamics and Cardiac Anesthesia

• Understanding hemodynamic principles helps us determine the mechanisms underlying hemodynamic instability and guides our treatment. Fortunately, the same basic physiologic principles apply in both the healthy patient undergoing laparoscopic cholecystectomy as well as in the patient with low ejection fraction undergoing multiple valve replacements. Unfortunately, the valve replacement patient is more likely to decompensate severely when faced with the hemodynamic roller coaster associated with general anesthesia induction (Figure 2–1).

Irrespective of the nature of the anesthetic that we plan to deliver, one of the main considerations is the expected impact upon the patient's blood pressure and cardiac output. Simply, whether we are performing an interscalene block, a neuraxial technique, or a general anesthetic we know that we have the ability to seriously affect both the patient's blood pressure and their heart's pumping ability. Generally, we expect that when we deliver a large induction dose of propofol or a high-inspired concentration of an inhalational anesthetic the blood pressure will decrease.

Of course, in otherwise healthy patients undergoing noncardiac surgery, periods of hypotension are frequently attributed to "anesthetic effects" and are routinely treated by volume administration, ephedrine or phenylephrine, and surgical stimulation. Hemodynamic calculations are rarely obtained as these events are fleeting and the underlying mechanism anticipated. Hemodynamic calculations aid clinicians in the diagnosis of hypotension and help guide treatment options when routine responses to hypotension, which are otherwise successfully employed in healthy patients, might be injudicious or harmful to the cardiac patient.

Blood Pressure

Although the absolute definition of hypotension is somewhat clouded in the literature,1 a patient is considered hypotensive when the systolic blood pressure is reduced by 20% or more from the patient's baseline blood pressure. Different authors set different cutoffs as to what constitutes a hypotensive patient. While in the past systolic pressure of less than 90 mm Hg was thought hypotensive, this value has recently been suggested as being too low. For example, the new cutoff value for hypotension has been reset to 110 mm Hg systolic in trauma patients.2

Each practitioner must determine, however, for each individual patient what constitutes systemic pressures that would warrant treatment. In the adult cardiac surgery patient it is likely that any patient with a systolic blood pressure less than 80 mm Hg would be considered in need of some intervention. This chapter will examine how to approach the hypotensive cardiac patient and to apply appropriate therapy. Some of the causes of perioperative hypotension are presented in Table 2–1.

An understanding of hemodynamics can help discern the numerous possible etiologies responsible for a patient's hypotension. As a first step we need to understand how the blood pressure is generated. Blood pressure (BP) gradients drive the delivery of blood throughout the circulation. BP is similar to Ohm's law that regulates the flow of current through a circuit:

V = I × R

where:

V = potential

I = current intensity (electron flow)

R = resistance (electrical)

The potential (V) in the circuit drives the current (I) through the resistance (R). The lower the resistance the greater the current flow.

The basic formula for blood pressure is quite similar:

BP = CO × SVR

where:

BP = blood pressure

CO = cardiac output (blood flow)

SVR = systemic vascular resistance

Thus, blood pressure has only two fundamental determinants: cardiac output and systemic vascular resistance. Consequently, when patients become hypotensive they can do so only because of reductions in cardiac output, systemic vascular resistance, or both.

Indeed, all of the disease states listed in Table 2–1 reduce blood pressure by having an impact on the patient's cardiac output or systemic resistance.

Cardiac Output

Cardiac Output (CO) is the product of the stroke volume (SV) and the heart rate (HR). The normal cardiac output of 4 to 6 L/min must be interpreted in relation to a patient's body surface area. An elderly, small woman with a small body surface area (BSA) will require less cardiac output to meet her metabolic needs than will a larger individual. The cardiac index (CI) {CO/BSA} ranges from 2.2 to 4.2 L/min/m2. Ultimately when considering CO and CI, practitioners are really interested in making sure that an adequate amount of blood is being delivered to the tissues to maintain tissue viability. In general a CI less than 2.2 L/min/m2 is concerning as it may lead to anaerobic metabolism and metabolic acidosis. However, there are many factors that determine if a particular CI is adequate for an individual patient's metabolic needs. These include patient temperature, hemoglobin concentration, and oxygen saturation.

Stroke Volume (SV)

The SV reflects the output of the heart during an individual beat.

CO = SV × HR

SV = CO/HR

Normal values = 50 to 100 mL/beat

There are a number of determinants that affect the SV. These include:

1. Volume: Patients must have an adequate preload in order to generate a normal SV. Hypovolemia due to various causes is one of the most obvious causes of reduced SV. Hypovolemic patients are often hypotensive and tachycardic with a reduced SV. SV can also be reduced in situations of reduced venous return to the heart such as institution of positive pressure ventilation, pericardial tamponade, or pneumothorax.

2. Afterload: Recall, BP = CO × SVR. The SVR and the SV are inversely related; as the resistance against which the heart pump increases, the SV will decrease, whereas when the SVR is reduced, the SV increases. Conditions, which reduce SVR, include those that produce vasodilatory states (eg, sepsis, spinal shock, etc). Conditions, which increase SVR, are numerous but in general center upon an increase in sympathetic outflow (eg, hypertension, heart failure).

3. Myocardial contractility: Myocardial ischemia, myocardial infarction, valvular heart diseases, and cardiomyopathies can all affect the ability of the heart both to relax and to contract. Impaired contractility can lead to a reduction in stroke volume.

As mentioned SV represents the amount of blood ejected from the heart during a beat.

So, SV = left ventricular end-diastolic volume − left ventricular end-systolic volume.

The stroke volume can be depicted graphically through the pressure-volume loop (Figure 2–2).

Systemic Vascular Resistance

SVR is estimated as follows:

SVR = (Mean arterial pressure [MAP] – Central venous pressure [CVP])/CO × 80

The normal calculated SVR is approximately 800 to 1200 dyne second/cm5

Hypotension and Hemodynamics

As discussed, hypotension can occur as a consequence of a reduction in cardiac output, systemic vascular resistance, or both. Still, the differential diagnosis of perioperative hypotension listed in Table 2–1 is rather large. It is important to understand the physiologic principles underlying hemodynamic instability in order to work through the differential and make the appropriate diagnosis of "Why is the patient hypotensive? "

As a first step, one should measure the CO in order to calculate the SV. CO measurement can be obtained both invasively and noninvasively. Various methods and devices can be employed for the estimation of the CO.3-5 These approaches include estimation of CO based on changes in respiratory carbon dioxide concentration caused by a brief period of rebreathing in mechanically ventilated patients (NICO system) or using pulse contour analysis of arterial pressure tracings from the arterial line (Vigileo/FloTrac, PiCCO, Pulse CO, and Finapres). Many of these pulse contour analysis systems require calibration of their measurements with some other form of CO measure in order to be accurate.

Traditionally, the Swan-Ganz pulmonary artery catheter has been used to estimate CO. However, there are a number of reports, which question the risk/benefit of pulmonary artery (PA) catheter placement.6-9 Sandham et al6 reported no benefit in PA-guided therapy in ASA 3 or 4 patients scheduled for elective or urgent surgery as compared with patients not monitored with a PA catheter. Harvey et al showed no benefit in overall outcome in critically ill patients managed with a PA catheter compared to a less invasive CO measurement devices.7 Moreover, studies have questioned the need to specifically measure CO in the cardiac surgery patient.8,9 As will be discussed later in this chapter, TEE has reduced the need to place specific monitors for CO determination since echocardiography can itself be used to measure hemodynamic parameters.10

Although the use of CO measurements to guide therapy in critically ill patients may be controversial and the methods by which these measurements are obtained ever changing, the use of these measurements is likely to continue for some time in the perioperative period as academic debates rage. The goal of any measurement of CO is to ultimately determine the SV.

If the SV is elevated in the setting of hypotension it is likely that the patient is vasodilated. Conversely, if the SV is reduced and the patient is hypotensive then there are two fundamental possible etiologies to consider.

1. Abnormal pump function of the myocardium secondary to cardiomyopathy, ischemia, arrhythmia, valvular heart disease, etc.

2. Decreased preload secondary to hypovolemia, tension pneumothorax, or cardiac tamponade.

To distinguish between these two etiologies we need additional information from perioperative monitors.

Invasive Monitors

The cardiac surgical patient requires invasive arterial blood pressure monitoring as well as central venous access. As mentioned previously, the use of the PA catheter in this setting can be controversial but remains widely employed.

Arterial Monitoring

There are perhaps as many varying techniques of arterial line placement as there are practitioners. Although approaches to arterial lines can be discussed and demonstrated there is no substitution for trial and error as trainees develop their own approaches to line placement. Table 2–2 lists sites for arterial cannulation. The Allen test has been suggested as an approach to screen out the possibility of hand ischemia should ulnar arterial blood flow be inadequate in the setting of radial artery cannulation. During the Allen test both radial and ulnar arteries are occluded and the hand is observed after developing pallor. The ulnar artery compression is released and the time for the hand to return to normal color noted. Should color fail to return to the hand after release of ulnar compression within 10 to 15 seconds the test is positive and radial arterial cannulation avoided. This test is, however, controversial and is not universally employed.11,12 Whatever site is chosen for line placement there is always the risk of arterial bleeding, hematoma, embolization, and thrombosis. Sterile techniques should be employed and the pressure tubing used to connect the arterial line to the monitoring system purged of any air. The pressurized bag containing the normal saline flush solution should be at a pressure greater than arterial pressure to prevent back bleeding through the arterial line. It should be noted that the arterial pressure waveform changes depending upon the cannulation site. As arterial lines are placed in more distal arteries, there is a change in the waveform with a progressive loss of the dicrotic notch, a delay in transmission, and a higher measure systolic pressure. MAP and diastolic blood pressure (DAP) are less affected by line placement.

Central Venous Access

Central access can be obtained through cannulation of the external jugular, internal jugular, subclavian, or femoral veins. Generally, the right internal jugular vein is cannulated due to ease of access and ease of flotation of the PA catheter should that be considered necessary (Figure 2–3).

Multiple complications may arise from obtaining central access. Infection is one of the most common complications and may lead to sepsis and multiple organ failure. The importance of using scrupulous sterile techniques must be emphasized, including the use of full body draping.13,14 Other complications include inadvertent carotid artery catheterization, neck hematoma and airway compromise, pneumothorax, and air embolism.

Confirmation that the central venous circulation, and not an artery, has been cannulated is essential prior to catheter placement. Numerous methods can be employed including:

• Color comparison between an arterial sample and one obtained from the proposed cannulation site. Inaccurate in the presence of left-right or right-left shunt or if the patient is being administered a high fraction of inspired oxygen.
• Pressure measurements to determine venous waveform and pressure rather than arterial waveform and pressure at the cannulation site.
• Observation on TEE of wire placement in the right atrium (Video 2–1).
• Ultrasound-guided line placement (Video 2–2).

TEE confirmation of adequate central venous access requires some TEE prowess. Ultrasound-guided placement has been shown to reduce complications of line placement.15,16 Consequently, it is likely that ultrasound-guided placement will become even more common as a way of achieving central access. However, ultrasound equipment is expensive and may not be readily available. Should arterial cannulation occur consultation with the vascular surgeon is mandatory.

Pulmonary Artery Catheterization

After having secured adequate central venous access a PA (Swan-Ganz) catheter can be floated to assist in diagnosing the etiology of perioperative hypotension.17-19 It is paramount that, should a PA catheter or any other device be used for hemodynamic measurement, the information obtained be used in an informed manner. It is very likely that due to their ease of use, other less invasive means of estimating CO will be increasingly employed. At present, the PA catheter is readily available and as such remains a routine method for determining CO.

Risks of PA catheterization include pulmonary artery rupture, rhythm disturbances, complete heart block, and knotting of the catheter. Figure 2–4 demonstrates the expected pressure patterns as the pulmonary catheter passes from the central venous circulation through the right atrium, the right ventricle, the pulmonary artery and finally settles into the occlusive or wedge position. The PA catheter traditionally has aided patient management in two ways:

1. It allows measures of CO, SVR, and SV. CO measurements can be obtained using the thermodilution technique. The thermodilution technique determines cardiac output by using the temperature of the blood as an indicator. Cool saline is injected into a proximal port of the PA catheter. At the end of the catheter there is a thermistor that can detect the change in temperature as fluid passes by. The changes in temperature are then calculated by software incorporated and a CO is estimated. Some PA catheters are equipped with fiberoptic capabilities, which enable them to determine mixed venous oxygen saturation. Mixed venous oxygen saturation SvO2 is normally 65% to 75%. Mixed venous oxygen partial pressure is normally 40 mm Hg. The SvO2 may be measured in the blood gas lab by obtaining a blood sample from the distal PA port of the PA catheter. SvO2 represents the venous hemoglobin saturation in the pulmonary artery after the mixing of venous blood from the superior vena cava, the inferior vena cava, and the coronary sinus. The following hemodynamic formula defines the SvO2:

   SvO2 = SaO2 − VO2/CO × 1.36 × Hb

   where:

   SaO2 = arterial oxygen saturation

   Hb = hemoglobin concentration

   VO2 = oxygen consumption

   SvO2 is reduced in settings of increased extraction of oxygen by the tissues or decreased oxygen delivery to the tissues. This can occur in situations of reduced CO, anemia, or decreased arterial oxygen saturation. SvO2 is increased in situations of decreased utilization of oxygen in the tissues such as in cyanide poisoning, hemoglobin with a higher affinity for oxygen, or in the presence of left-to-right shunt.

2. Secondly, the PA catheter measures the pressure in the various chambers of the heart. The right atrial pressure (RAP) also known as the central venous pressure (CVP) estimates right ventricular filling. Elevated RAP > 20 mm Hg can be associated with right ventricular dysfunction.20-28 Additionally, trends in RAP are often used to determine the adequacy of volume replacement. Although static indicators of volume load such as RAP have been traditionally employed, dynamic parameters such as stroke volume variation, pulse pressure variation, and systolic pressure variation have more recently been used to infer the volume status. The transpulmonary thermodilution technique, employed by the PiCCO system, permits the calculation of the global end-diastolic volume index (GEDVI). Additionally the device permits measurement of the extra vascular lung water index (EVLWI) and may be useful in situations of volume overload and pulmonary edema. The normal GEDVI ranges between 640 mL/m2 and 800 mL/m2 with an EVLWI less than 10 mL/kg. Hence, the PiCCO system provides volume estimates of ventricular filling rather than the pressure measurements provided by the PA catheter. Goepfert et al have demonstrated the use of these volume measurements in the management of the cardiac surgical patient.22 The challenge of the anesthesiologist is to incorporate measures of pressures and volumes to guide therapy for hemodynamic instability.

Knowing these various pressures, volumes, and the SV it is possible to determine why a patient is hypotensive. But before doing that there is one critical concept that must be introduced and understood: ventricular compliance.

Compliance relates pressure and volume and is defined by the formula

C = ΔV/ΔP

where:

C = compliance

ΔV = change in volume

ΔP = change in pressure

In highly compliant systems large changes of volume are accommodated with minimal changes in pressure. In noncompliant systems minimal changes in volume produce dramatic changes in pressure. Compliance is encountered in many organs such as heart, lungs, and the brain. For example, when the lungs are noncompliant a positive pressure tidal volume breath will generate a greater inspiratory pressure than in a patient with normal lung compliance. In cardiac patients, the compliant heart accommodates volume with minimal increases in left ventricular end-diastolic pressure (LVEDP). The LVEDP is the pressure in the left ventricle at the end of diastolic filling, after atrial contraction. Compliant left ventricles fill with lower pressures (eg, 5-10 mm Hg). On the other hand, noncompliant left ventricles accommodate volume at the end of diastole with much greater increases in pressures. Figure 2–5 demonstrates compliance curves of normal, highly compliant, and noncompliant left ventricles.

The PA catheter can indirectly determine the LVEDP. In the absence of mitral stenosis, the LVEDP should be reflected in the left atrial pressure (LAP) which in turn should be estimated by the pulmonary capillary occlusion pressure (PCOP). So why is this useful? Because now with an estimate of the SV and an estimate of the LVEDP it is possible to determine why a particular patient is hypotensive.

Recall that should the SV be reduced there are two main considerations, altered pump function or decreased preload.

The SV is obtained by dividing the CO by the heart rate (CO/HR). The PA catheter provides estimates of both the CVP and PCOP. The PCOP is an indirect measure of the LVEDP. Moreover, the LVEDP may reflect the volume load of the heart depending on the compliance. Remember, if the heart is noncompliant—such as in elderly patients—minimal changes in volume will produce somewhat exaggerated increases in LVEDP and there may be no relation between PCOP and left ventricular end-diastolic volume (LVEDV).

If the hypotensive patient has a low SV the next approach is to estimate the LVEDP. If the patient is hypotensive, with a low SV, and a reduced LVEDP, then the patient is most likely hypovolemic except where there is an elevated CVP. In that instance, decreased left ventricular filling should be considered secondary to right heart failure, tension pneumothorax, or pericardial tamponade.

If the patient is hypotensive with a low SV, and an elevated PCOP as an approximation for LVEDP, then impaired left ventricular function should be suspected in the differential diagnosis.

Of course, PA catheter data should not be employed in isolation. Information obtained from other monitors should be used. The ECG is reviewed for signs of ischemia and arrhythmia. Medical history and physical examination should be reviewed regarding the possibility of tamponade, volume loss, or pneumothorax.

Volumetric measurements as obtained from transpulmonary thermodilution (PiCCO) allow patients to be managed in a similar manner without PA line placement. A reduced GEDVI in the setting of a low CI or SV warrants additional volume delivery. A normal GEDVI in the setting of hypotension and an elevated CI calls for vasopressor administration. Likewise, in a patient with a low CI and a normal GEDVI and an increased EVLWI indicates that the heart may be noncompliant and inotropic therapy might be needed.

Hypertension and Hemodynamics

Like hypotension, hypertension can also contribute to morbidity and mortality in the cardiac patient. Many patients encountered for cardiac surgery will be treated with numerous vasodilators and beta-blockers to control their long-standing hypertension. Antihypertensive medications are generally continued perioperatively. Possible etiologies for hypertension in the perioperative period can also be diagnosed, taking into consideration CO and SVR

Of course, acute episodes of hypertension perioperatively are often secondary to increases in sympathetic tone associated with inadequate anesthesia, anxiety, and the natural response to surgical stress. Treatment of acute episodes of perioperative hypertension differs from that of chronic hypertension. Treatments for hypertension ultimately work by reducing SVR and/or CO.

Ultimately, the function of the heart is to deliver oxygenated blood to the tissues. If the heart fails to do this, patients develop cardiogenic shock and metabolic acidosis. In the perioperative period, anesthetists can do much to aid or hinder heart pump function. Once again, the fundamentals of hemodynamics can assist in determining the adequacy of pumping and designing appropriate therapy to assist the failing heart.

Unfortunately, many patients today present to surgery and anesthesia with reduced ventricular function29 after having multiple myocardial infarctions or percutaneous interventions.30,31 Chronic hypertension, myocardial ischemia, valvular heart disease, and cardiomyopathies often result in hearts that neither forcefully contract nor effectively relax and, therefore, may have systolic and diastolic dysfunction, respectively.32-34

Systolic Function

Systolic ventricular dysfunction occurs when the left ventricle fails to contract resulting in a reduced SV. Patients attempt to compensate for this reduction in ejection fraction (EF, nl = 50%-60%) by increased catecholamines and sympathetic tone. An examination of hemodynamic principles is useful for understanding this compensatory mechanism.

Recall,

BP = CO × SVR,

SV = CO/HR

SV = LVEDV − LVESV

EF = SV/LVEDV × 100%

Therefore, the EF represents the percentage of blood volume ejected with each SV from the total volume filling the heart at the end diastole. Normal EF is 50% or more. Patients with varying degrees of systolic dysfunction have reduced EF. Indeed, anesthesiologists may be called to anesthetize patients with EF less than 20%. And yet, these patients with poor systolic function can nonetheless compensate for their dysfunction.

The body compensates for reduction in SV by attempting to augment vascular tone and heart rate through increased catecholamine release. Additionally, the renin-angiotensin-aldosterone system is activated to increase the volume load presented to the heart. Angiotensin is a vasoconstrictor, and aldosterone inhibits sodium urinary excretion leading to fluid retention.

By increasing sympathetic tone and heart rate, the low EF patient manages to maintain BP and organ perfusion in the setting of reduced SV. Although compensated at baseline, these patients may acutely and precipitously decompensate during delivery of general anesthesia. Anesthetic agents often decrease sympathetic outflow. Since sympathetic tone is critical in situations of low EF, these patients often suffer hemodynamic collapse during anesthetic induction. Anesthetic management of heart failure patients will be discussed in detail in Chapter 5.

The renin-angiotensin-aldosterone response to systolic failure increases the volume presented to the heart. This increase in preload is helpful secondary to the Frank-Starling relationship (Figure 2–6).

The Starling curve demonstrates that as the LVEDV increases, the SV increases up to a point. Consequently, in order to augment the SV, the body responds by increasing the size of the heart. Hence, many failing hearts are dilated and enlarged. As such, even if contracting very poorly during systole, the myocardium with low EF is capable of generating a SV sufficient to meet the patient's metabolic needs (Figure 2–7). The effects of the compensatory responses to systolic failure are also responsible for many of the signs and symptoms often seen in the heart failure patient.

Diastolic Function

Diastolic ventricular dysfunction can present independently or associated with systolic ventricular dysfunction. Isolated diastolic dysfunction is often seen in hypertensive patients with hypertrophied left ventricle. Once again, an understanding of hemodynamic basics can explain the development of this condition.

Recall,

BP = CO × SVR

CO = SV × HR

SV is determined by:

1. Preload or the volume presented to the left ventricle

2. Myocardial contractility

3. Afterload or the resistance against which the heart must pump

Increases in afterload maintain SVR but reduce CO and SV. In response to afterload increases, the heart compensates by hypertrophy. However, as discussed earlier, compensatory mechanisms present their own particular problems. In the case of the thickened myocardium, these problems include diastolic dysfunction and increased risk of ischemia.

The heart requires energy not only in systole but also in early diastole during relaxation in order to move calcium from the myocardial cell back to the sarcoplasmic reticulum. The relaxed ventricle then fills with low pressures easily during diastole. The patient with diastolic dysfunction relaxes poorly resulting in an elevated LVEDP (Figure 2–8). The elevated LVEDP is transmitted to the pulmonary vasculature increasing the pulmonary artery pressures ultimately leading to pulmonary congestion and right ventricular failure.

Coronary Arteries Circulation

The blood supply to the heart is provided by the right and left coronary arteries (Figure 2–9).

Coronary perfusion pressure (CPP) determines blood flow to the myocardium.

CPP = Diastolic blood pressure − Left ventricular end diastolic pressure

CPP is reduced in situations of decreased diastolic blood pressure (eg, when a patient has wide-open aortic regurgitation and thus a low diastolic pressure) or of increased LVEDP (eg, patients with noncompliant ventricles and diastolic dysfunction).

Because there is limited flow through the coronary arteries when the heart contracts, the majority of the blood flow to the heart occurs during diastole. Therefore, diastolic time impacts upon the perfusion of the heart.

Tachycardias reduce diastolic time and as such put the heart at risk for ischemia. Thus, to maintain the myocardial oxygen supply/demand balance, the patient requires a low heart rate, an acceptable CPP, and decreased myocardial wall tension.

Lastly, the oxygen content of the blood determines oxygen delivery to the heart as well as the other tissues. Anemia, decreased oxygen saturation, hemoglobinopathies can all reduce the delivery of oxygen to the tissues.

Myocardial oxygen demand is increased by tachycardias, increased myocardial contractility, and increased myocardial wall tension.

Myocardial wall tension is expressed in the law of LaPlace.

LaPlace law:

Myocardial wall tension = (Ventricular radius × Ventricular pressure)/2(Ventricular wall thickness)

Since myocardial wall tension increases myocardial oxygen demand, thickening of the ventricular wall will reduce tension. Consequently, in situations of increased afterload, the heart will attempt to decrease the myocardial wall tension by increasing the thickness of the ventricular wall, therefore the muscle mass.

The Mechanism of Myocardial Contraction

Myocardial contraction is initiated by spontaneous depolarization of the conduction tissues. The generated action potentials are propagated throughout the heart. When the myocardial sarcolemma depolarizes, intracellular calcium concentration increases due to extracellular calcium entering the cell and due to release of calcium from the sarcoplasmic reticulum. Contraction is initiated when calcium binds to troponin C and results in a conformational change, which ultimately leads to cross bridging of actin with myosin. At the end of contraction calcium is actively pumped back out of the cell and into the sarcoplasmic reticulum and relaxation begins.

Rhythm and conduction will be discussed in detail in Chapter 3.

Contraction results in thickening of the myocardium, inward movement of the endocardium, and twisting and torquing of the heart (Video 2–3).

Right Heart Function

Although in the past the right heart was thought to be a passive conduit by which blood passed through the pulmonary circulation to the left heart, this is certainly not the whole story.35 Right heart function is essential to the overall heart function. When blood returns from the superior vena cava (SVC) and the inferior vena cava (IVC), it enters the right atrium. Right ventricular contraction then delivers the venous blood into the pulmonary circulation for gas exchange and further to the left heart for ejection into the systemic circulation (Video 2–4). While the left heart must generate the systemic blood pressure, the right heart and pulmonary circulation are low-pressure systems. The normal pulmonary arterial pressures are often less than 20 mm Hg systolic. When the pulmonary artery pressures are elevated as seen in situations of left heart failure, pulmonary disease, or protamine reaction, the right heart (a low-pressure system) can be overwhelmed. In such circumstances the right heart can become distended and poorly functional (Video 2–5) and the ability of the right heart to eject blood into the pulmonary circulation becomes seriously impaired. Since the right heart and the left heart pump blood in series, right heart failure will ultimately lead to decreased CO and decreased organ perfusion.

Right heart failure is often associated with an increase in right ventricular pressure. An increase in the right ventricular end-diastolic pressure will be reflected in the central venous pressure. Increased CVP can retard venous return leading to peripheral edema and hepatic engorgement.

There are many drugs and mechanical devices that can be employed in order to improve hemodynamic performance. Mechanical assistance of the failing heart is discussed in Chapter 11.

The pharmacologic armamentarium employed to manipulate hemodynamics must take into account the etiology of hemodynamic instability.

The end points of hemodynamic manipulation are usually BP and CO.

Hypertension

Generally in the perioperative period, hypertensive episodes are secondary to increased sympathetic outflow secondary to inadequate anesthesia, surgical stress, or preexisting hypertension. Should a patient be found to be hypertensive, therapy can be directed at either reducing cardiac output or reducing sympathetic tone. There are many pharmacological agents available which will achieve these effects.

Drugs that reduce heart rate and myocardial contractility will have primary effects upon the CO. Such agents include the beta-blockers (esmolol, propranolol, metoprolol) and the calcium antagonists (verapamil, diltiazem). Other agents are primary vasodilators (nitroglycerin, nitroprusside, hydralazine, fenoldopam). Of course often, intraoperatively, the patients require supplemental anesthetic agents (eg, fentanyl, inhalational agents, propofol, or midazolam). During recovery in the ICU, patients frequently become hypertensive as anesthetic effects wane or pain control is inadequate. Infusions of propofol, fenoldopam, dexmedetomidine, and calcium channel antagonists are frequently employed postoperatively. The specifics of anesthetic management of the cardiac surgery patient will be discussed in Chapter 4.

Hypotension

The pharmacologic management of perioperative hypotension in the cardiac surgical patient is of urgent concern. In the cardiac surgery patient, hypotension often leads to myocardial ischemia, which produces ventricular dysfunction followed by even more severe hypotension—ending in hemodynamic collapse and circulatory arrest.

Once again,

BP = CO × SVR

Consequently, pharmacologic therapies are directed at the underlying fundamental cause of hypotension.

Should the patient be hypotensive because of reductions in SVR, vasoconstrictors should be administered. The common practice of administering small doses of phenylephrine to treat peri-induction hypotension is one such example of the use of a vasconstricting drug to augment blood pressure following anesthesia induction. The indirect acting agent, ephedrine, similarly produces vasoconstriction through its release of endogenous norepinephrine. Infusions of phenylephrine or norepinephrine are frequently employed to augment vascular tone. Likewise, vasopressin as a 1 U intravenous bolus or by infusion (up to 6 U/h) can be administered to restore vascular tone.

Reductions in CO are somewhat more complicated. Should the CO be reduced because of hypovolemia then volume administration is the appropriate response. If the CO is reduced secondary to an arrhythmia (eg, atrial fibrillation with loss of atrial contraction or a ventricular arrhythmia), then correction of the rhythm disturbance would be immediately indicated. Similarly, if CO were to be reduced because of compression of the heart by pericardial tamponade or tension pneumothorax, then appropriate treatment of those conditions would be warranted. In patients with systolic left ventricular failure, inotropes can be used to improve myocardial contractility.

A reduced SV can be restored by increasing ventricular volume, increasing myocardial contractility, or reducing the afterload.

Although administration of additional volume might increase SV in the patient with impaired left ventricular (LV) function, this may carry the cost of an increased LVEDP and pulmonary congestion. Increased LVEDP will be reflected in increased PCOP and most likely increased pulmonary artery diastolic (PAD) pressure. Increased pressure in the pulmonary vasculature can lead to pulmonary edema and respiratory collapse. The natural compensatory mechanism of volume retention for LV failure may often cause dyspnea and acute congestive heart failure (CHF). If not careful, too much fluid administration can likewise produce CHF in the perioperative period.

There are various inotropic agents that can be employed to increase LV contractility. Epinephrine, dobutamine, dopamine are examples of agents which interact with the beta-1 sympathetic receptors on the heart to augment contractility.

The use of these agents is not without potential complications. The routine use of inotropes may contribute to increased patient morbidity and mortality.36,37

Catecholamine-like drugs such as epinephrine and dopamine can produce arrhythmias, tachycardias, and vasoconstriction. In addition to its inotropic effect, dobutamine can also produce vasodilation. This effect is often desirable because vasodilatation reduces the work against which the failing heart must pump. However, lower BP can potentially reduce the coronary perfusion pressure.

Recall,

CPP = DBP − LVEDP

Fortunately, vasodilatation coupled with augmented SV could reduce mean LVDP as well, therefore maintaining CPP.

Inodilators such as milrinone are frequently employed to both increase SV and decrease SVR. Milrinone is a phosphodiesterase inhibitor, which augments myocardial contractility.38 Like catecholamines, milrinone can lead to hypotension and arrhythmia. Often it is necessary to support the blood pressure with a vasopressor to both augment SV as well as provide enough blood pressure for tissue perfusion.

Recently, a new class of inotropes, the calcium ion sensitizers such as levosimendan has emerged. Strategies in the treatment of the patient with systolic and diastolic heart failure will be discussed in greater detail in Chapter 5.

Unfortunately, at times during hemodynamic instability the diagnostic picture is unclear and often the etiology is multifactorial (eg, the patient is septic and has LV failure). Time and further investigation will determine the role of CO monitoring in the cardiac surgery patient of the future.

Right Heart Failure

As mentioned earlier because the right heart and the left heart pump in series, right heart failure can compromise left heart performance and lead to cardiogenic shock, reduced CO and organ perfusion, and acidosis.35

Signs of right heart failure include peripheral edema and hepatic enlargement. Much as an elevated PCOP might indicate a noncompliant, distended, failing, left heart, an increased CVP might reveal a failing right heart.

Often the right and left hearts do not fail in isolation but at the same time. A failed left heart will result in an increased LVEDP, which will be transmitted across the pulmonary circulation to the right heart which has to pump now against greater pressures. As can be seen in patients with mitral stenosis, pulmonary pressures can become very high indeed—at times equaling the systemic blood pressure.

There are no specific drug therapies for RV failure. Efforts are generally directed at reducing the afterload in the pulmonary circulation and increasing contractility of the right ventricle.

Agents such as dobutamine and milrinone are frequently employed in the patient with RV failure because of their inodilating properties.

Inhaled nitric oxide (NO) is a pulmonary vasodilator—which directly reduces PAP. The advantage of NO is that its effects are limited to the pulmonary circulation only.

RV failure and the treatment of pulmonary hypertension will be discussed in greater detail in Chapter 8.

Both transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) can be employed in the perioperative period to aid in the diagnosis of hemodynamic instability.39,40

The advantage of TEE is that most often it is not necessary to obtain calculated parameters that otherwise form the mainstay of the diagnosis while using a PA catheter. TEE may allow obtaining qualitative data, which could readily answer the question asked perioperatively "Why is the patient hypotensive?"

If you recall possible answers to this question are: volume depletion, vasodilation, pump failure, external compression of the heart as in pericardial tamponade or pneumothorax.

Echocardiography permits the identification of the sources of hemodynamic instability using imagery rather than pressure estimates and calculations.

The introduction provided a review of the basic views and images, which can be obtained using transesophageal echocardiography. Often the transgastric midpapillary short-axis view is useful to quickly assess the function of the heart. A normally contracting and adequately volume loaded ventricle is obvious with very little experience.

In situations of hypovolemia the transgastric midpapillary short-axis view will show a hyperdynamic LV with the ventricular cavity being obliterated with each heart beat due to very low LVEDV (Video Intro 14). Associated with this image would likely be a reduced PCOP and CVP. Reduced SVR can also produce a TEE image where the LV cavity is significantly reduced but perhaps not to the extent as found in the setting of profound hypovolemia.

TEE can easily identify mechanical compression of the heart (eg, pericardial tamponade) as a cause of inadequate volume loading of the heart and hypotension (Video 2–6).

TEE can likewise determine if the heart is not functioning adequately as a pump secondary to global LV dysfunction (Video Intro 6), RV dysfunction, or isolated areas of LV dysfunction secondary to myocardial ischemia (Video 2–7). In severe ventricular dysfunction, stasis of blood within the heart appears as "smoke" in the left atrium and occasionally in the LV (Video 2–8). Such patients are likely to have a very limited ability to respond to the decrease in SVR which occurs at the time of anesthetic induction.

RV failure can occur associated with LV failure or secondary to pulmonary arterial hypertension. In the transgastric mid-papillary view, the crescent moon that characterizes the image of the healthy RV becomes more spherical somewhat like a dilated letter "D" sitting next to a frequently underloaded LV.

TEE also can detect areas of the heart that are dysfunctional. During myocardial infarction (MI), coronary artery thrombosis occludes blood flow to regions of the myocardium in the vessel's distribution. When that occurs, the myocardium becomes dysfunctional by failing to thicken and move inward with each systole (Video 2–9). Additionally, by identifying the area of the myocardium which is dysfunctional, it is possible to determine which of the coronary arteries is likely affected (Video 2–10).

Thus, by simple visual inspection it is possible to make rapid assessments of the causes of perioperative hemodynamic instability. Of course, echocardiography can also perform the calculations obtained through the use of the PA catheter.

Catheters measure pressures and not volumes. Although the SV can be estimated using the PA catheter, the EF cannot be estimated, as EF is a direct measure of LV volumes.

Echocardiography, however, allows the estimation of the EF. Although such estimates are often too time-consuming to perform in a busy cardiac operating room, they can nonetheless be accomplished. Estimates of ventricular function include measures of fractional shortening (Figure 2–10) and fractional area change (Video 2–11). Fractional area change measurements assess function of the ventricle by examining changes not along a single line as in fractional shortening but by changes in the area of the ventricular cavity during systole and diastole.

Fractional shortening = (LV end-diastolic diameter − LV end-systolic diameter)/LV end-diastolic diameter × 100

Normal values = 25% to 45%

Fractional area change (FAC) = (LV end-diastolic Area − LV end-systolic area)/LV end-diastolic area × 100

Normal values range between 55% and 65%.

The modified Simpson rule "method of discs" attempts to estimate the LV volume in systole and diastole (Video 2–12). Using incorporated software, the LV volume can be estimated by considering it a series of stacked discs. The LV cavity is traced at the end of systole (fully contracted) and at the end of diastole (fully filled). The machine then generates a stack of discs. Much as a pile of pennies stacked on end would create a cylinder, the machine generates a series of discs of different size. The machine calculates the volume of the stack of discs using their area and thickness, which are known both during diastole and systole. Three-dimensional echocardiography can also be employed to assess ventricular function (Video 2–13). In truth, experienced echocardiographers in the operating room often use visual impressions rather than formally calculating the EF in this way.

SV and CO can likewise be measured using TEE.

In Introduction to Perioperative Echocardiography, the concept of time-velocity integral (TVI) was introduced (Figure 2–11).

The SV can be calculated using echocardiography by knowing the area through which blood travels and the distance traveled during an individual beat. The left ventricular outflow tract provides a good location to make these determinations with TEE.

SV = AreaLVOT × TVILVOT

By approximating the shape of the LVOT with a cylinder, the area of the LVOT can be calculated by measuring the LVOT diameter.

LVOT area = π × (d/2)2

Therefore,

SV (cm3 or mL) = (0.785 d2) × TVI

Now, CO can be calculated using the formula:

SV × HR = CO

The left atrial pressure (LAP) can also be calculated by echocardiography. During the introduction to echocardiography, Bernoulli equation was introduced.

Pressure gradient between two cardiac chambers = 4V2

where V is the maximal blood flow velocity measured by Doppler.

To calculate the LAP using this method the patient must have mitral regurgitation. When the LV contracts during systole if MR is present, some of the blood will be ejected not out the aorta but back through the closed mitral valve. Being ejected through the closed mitral valve the blood will likely move at a high velocity. By using continuous wave Doppler the peak velocity of this regurgitant jet can be measured. Once the velocity is known, Bernoulli equation can be employed to determine the left atrial pressure (LAP) based on the pressure gradient between LV and LA during systole.

Since this flow of blood happens during systole, the pressure in the LV during systole is the same (assuming no aortic stenosis or obstruction to ventricular outflow) as the systolic arterial blood pressure obtained from other monitors.

So,

Pressure gradient = LV systolic pressure − LA pressure

Also,

LV − LA pressure gradient = 4V2

where V is the maximal flow velocity of the mitral regurgitant jet.

Hence,

LA pressure = LV systolic pressure − 4V2

Pressure estimates such as these are routinely done in the echocardiography laboratory; however, in the operating room such estimates are less frequently performed.

As can be seen echocardiography is a very useful tool in determining why a patient might be hemodynamically unstable. The PA catheter–derived estimates of CO and measures of PCOP are no longer essential during the period in which the echo probe is available to guide management. Consequently, the PA catheter remains a routine part of cardiac anesthesia management to assist in hemodynamic management only after the removal of the TEE probe. However, increasingly echocardiography is becoming available in ICU settings.

Avoiding Hemodynamic Collapse

A 53-year-old male patient presented for exploratory laparotomy secondary to ischemic bowel. His vital signs are BP 70/40 mm Hg, HR 110 bpm, respiratory rate (RR) 29 breaths per minute, 102°F. A preoperative ECG demonstrates a left bundle branch block (LBBB). He denies other medical problems except for occasional episodes of chest tightness when he climbs stairs and he has 3-pillow orthopnea. He has had no prior medical evaluations.

Obviously this patient presents a number of immediate concerns and possible etiologies to his hypotension. He may be hypovolemic secondary to volume loss from the perforated bowel or he might be septic from peritonitis. On the other hand, his LBBB and intermittent chest pain could also suggest that his hypotension is cardiogenic in nature.

So basically, the patient presents with possible hypovolemic shock, cardiogenic shock, or vasodilatory shock—and he is about to undergo general anesthesia.

Case Questions

What monitors will be of assistance in managing this case? What monitors are essential? What monitors are optional? What are the risks and potential complications?

How should the induction of this patient be managed?

Why is he hypotensive and how should his hypotension be treated?

Possible Answers

Frankly, none of these questions are easy and as with so many things in anesthesiology there are no absolute answers.

This is a critically ill patient who has great potential to experience severe hemodynamic compromise at the time of induction. Arterial pressure monitoring would appear indicated along with central access to provide for volume and/or vasoactive substance administration. The LBBB potentially complicates placement of a PA catheter. As the PA catheter passes through the right heart, it could produce a transient right bundle branch block leading to complete heart block. The LBBB also complicates the ECG diagnosis of myocardial ischemia and thus TEE might be useful assuming there are no contraindications to its placement. (See Introduction to Perioperative Echocardiography)

Assuming that arterial and central lines have been placed, we will benefit from more information regarding the etiology of his hypotension and on how best to proceed with induction. Pulse contour analysis of the arterial waveform could be used to estimate CO. Likewise, if the PiCCO system were available and employed then measurements of global end-diastolic volume could further be used to guide therapy. The central venous pressure may be helpful but does not reflect LV performance. In this patient the RAP is 8 mm Hg and fluid administration is undertaken. As the patient's BP increases to 95/60 mm Hg general anesthesia is induced with etomidate and succinylcholine. After a successful intubation and application of positive pressure ventilation the BP decreases to 60/40 mm Hg. Phenylephrine and additional fluid are administered with minimal response. A TEE probe is placed. What is demonstrated by this echo image (Video 2–14)? As can be seen the patient appears to have a hyperdynamic heart. Indeed, the papillary muscles come together nearly obliterating the ventricular cavity during systole. In this setting, it appears that the patient may be hypovolemic and septic therefore vasoconstrictors and additional volume are given.

How would management have changed if Video 2–15 was observed at the time of probe placement? A grossly dysfunctional left ventricle is seen. Therapy with inotropic agents such as epinephrine to improve ventricular function would be indicated. If ischemia is suspected, a nitroglycerin infusion could be also employed with care not to decrease BP even further.

Assuming the patient did not have an LBBB and a PA catheter was placed, what would be the SV and PCOP if the patient was in (a) primarily hypovolemic shock, (b) primarily vasodilated shock or in (c) cardiogenic shock? If hypovolemic, expect the patient to have a reduced SV with low PCOP. If vasodilated the SV could be elevated with a mid range to low PCOP. On the other hand, if in cardiogenic shock a reduced SV and high PCOP might be expected.

Of course, the patient could be both septic and in heart failure. In that setting, the picture becomes somewhat cloudy. Nonetheless, measures from PA catheter and echo images can be used concurrently to guide perioperative therapy. Whether there is definitive scientific evidence that any of these monitoring devices actually affect overall outcome remains uncertain. Essentially, when addressing hemodynamic instability, diagnostic tools are employed to guide therapy realizing that occasionally multiple etiologies might be at work making the patient hypotensive, thus requiring the use of a combination of therapies for treatment. Using all of these diagnostic approaches the question "Why is the patient hypotensive?" can be answered.