Cardiovascular Function

The function of the heart and vasculature is to deliver oxygen (O₂) and other nutrients to various tissues in order to meet the metabolic demands of the organism. Mild to moderate depression of DO₂ normally is compensated by augmented O₂ extraction at the tissue level, thereby maintaining a stable level of oxygen consumption (VO₂). When DO₂ falls below some critical level, this compensatory mechanism fails and a state of O₂ supply dependency exists ³ such that any further drop in DO₂ leads to a parallel fall in VO₂.⁴^–⁶ Under a state of supply-dependent O₂ consumption, affected tissues and organs attempt to maintain homeostasis partly through anaerobic metabolism. Several studies suggest the initial metabolic response to hypoxemia or decreased DO₂ differs between the newborn and older ages and varies among different vascular beds. In adults at rest, DO₂ is in great excess of VO₂. This “O₂ surplus” means moderate reductions of O₂ transport are generally well tolerated without compromise of VO₂. In contrast to the adult, the metabolism of the newborn may be particularly susceptible to modest alterations in O₂ transport because of the high resting demands for O₂, the ease with which these demands can be increased by small environmental changes, and the apparently limited reserve for augmenting cardiac output (CO) or O₂ extraction acutely.^7,⁸ Thus it is crucial that cardiovascular assessment and monitoring in the pediatric intensive care unit (ICU) involve continuous and reliable evaluation of the adequacy of systemic perfusion and DO₂ in order to select appropriate hemodynamic support strategies.

Quantity of Therapy

If one considers hemodynamic monitoring not only in terms of DO₂ and perfusion pressure but also in terms of what therapy is required to produce a given level of tissue oxygenation, one gains a much better understanding of the overall “condition” of the patient. It is therefore important to monitor not only DO₂ and perfusion pressure but also the “quantity of therapy” (QOT) needed to procure and maintain adequate tissue oxygenation. Consider two hypothetical 6-month-old infants, Destiny and Dakota, 2 hours after repair of tetralogy of Fallot. They have identical (and adequate) DO₂ and perfusion pressure, but Destiny has a left atrial (LA) pressure of 6 mm Hg and a right atrial (RA) pressure of 8 mm Hg, whereas Dakota has received volume infusion to achieve an LA pressure of 6 mm Hg and an RA pressure of 15 mm Hg. Assuming that the levels of intravascular volume provided are exactly those needed to achieve the (identical) DO₂ values and perfusion pressures, it is clear that the physiologies of these two patients are different. The clinician who has learned what to expect relative to the QOT in any given set of circumstances will find Dakota’s sufficient tissue oxygenation only mildly reassuring and asks: Is there substantial residual right ventricular (RV) outflow tract obstruction or other problem(s) that I need to know about? Will Dakota have sufficient DO₂ in 10 hours when post-bypass myocardial depression is at its worst? Might additional therapy secure adequate DO₂ at a lower filling pressure, thereby minimizing adverse effects of systemic venous hypertension? As this example illustrates, the QOT concept is useful for three reasons:

1. The QOT is, in part, a function of the patient’s overall “condition” and can reflect anatomic or physiologic problems that require further exploration.

2. Physiologic trajectory is key, especially early in the course of certain illnesses or after cardiopulmonary bypass, when DO₂ predictably declines over the first 12 hours.² Taking into account the QOT relative to tissue oxygenation at any point in time helps one better estimate the likelihood of the need for augmented support (e.g., mechanical support of the circulation) as time passes.

3. Some therapies (e.g., fluid infusion to obtain high filling pressure, or high airway pressure) while helpful at a point in time, can be pernicious over the longer run: High venous pressure, especially in infants, causes third spacing of fluid, and the effect of ventilator-associated lung injury on lung function can be devastating. By using high central venous or airway pressures, the intensivist is, in effect, incurring a debt to secure short-term perfusion that will have to be repaid later. Experienced clinicians always take the QOT into account in their work, thus influencing their level of concern about a patient and guiding subsequent timing and choice in adjusting therapy.

Almost any form of therapy might be included in the QOT concept, but we will focus on medical therapies that have the most important effect on hemodynamics, including DO₂ and perfusion pressure. These therapies include inotropic/vasoactive agents, volume infusion, and airway pressures used during mechanical ventilation. The amount of inotropic and vasoactive drugs administered, assuming that they are used appropriately, seems to be a crude indicator of patient illness.² Volume infusion to achieve adequate filling pressure is required even for the normal heart, but the QOT concept applies when higher than normal filling pressure is needed to maintain adequate CO. The consequences of high filling pressures are body edema (especially in infants), pleural and other cavity space effusions, and pulmonary edema. If high venous pressure is coupled with systemic hypotension (e.g., with a “failing” Fontan circulation), there may be critically reduced trans-tissue perfusion pressure with a potentially negative impact on cerebral and splanchnic perfusion.

With respect to mechanical ventilation, the need for high mean airway pressure (P_aw) is most commonly a reflection of lung disease, but pulmonary edema on a hydrodynamic basis may occasion the use of high P_aw for optimal lung recruitment. High P_aw can reduce venous return to the heart, increase pulmonary vascular resistance (PVR), and contribute to ventilator-associated lung injury.

Variables that Determine Tissue Oxygenation

Tissue oxygenation is directly related to both DO₂ and systemic arterial blood pressure (SAP). DO₂, the quantity of O₂ delivered to the tissues per minute, is the product of systemic blood flow (SBF), which equals CO except in patients with certain cardiac malformations, and arterial O₂ content:

where CO is cardiac output or SBF in L/min or L/min/m² and CaO₂ is quantity of O₂ bound to hemoglobin plus the quantity of O₂ dissolved in the plasma in arterial blood. The O₂ content of arterial blood (mL O₂/dl blood) equals:

where SaO₂ is arterial O₂ saturation, Hgb is hemoglobin concentration (g/dL), 1.36 (constant) is the amount of O₂ bound per gram of hemoglobin (mL) at 1 atm of pressure, PaO₂ is arterial partial pressure of O₂, and 0.003 (constant) multiplied by the PaO2 equals amount of O₂ dissolved in plasma at 1 atm. The quantity of dissolved O₂ is generally considered to be negligible in the normal range of PaO₂. Hypoxia, because of poor gas exchange within the lungs (i.e., intrapulmonary shunt), or in the setting of CHD with right-to-left shunting, is an important determinant of blood O₂ content.

CO is the product of stroke volume (quantity of blood ejected per beat) and heart rate, and SAP is determined by CO and systemic vascular resistance (SVR). The four primary determinants of cardiac function are preload (which determines the precontractile lengths of the myofibrils), end-systolic wall stress (function of systemic blood pressure and physical characteristics of the arterial system, ventricular wall thickness, and chamber dimension), myocardial contractility, and heart rate. These determinants of ventricular function can be altered by many factors in the intensive care setting. Preload, or end-diastolic volume, is affected by ventricular compliance (rate and extent of cardiomyocyte relaxation and cardiac connective tissue), intravascular volume, and intrathoracic pressure. Expansion of the heart resulting from transmural filling pressure, rather than the LA pressure per se, determines the force of contraction. Therefore, intrathoracic (or intrapericardial) pressure is a key determinant of preload. Ventricular hypertrophy, vasodilator and diuretic therapies, and positive pressure mechanical ventilation all adversely affect preload. Similarly, cardiac function is inversely related to afterload, or end-systolic wall stress. Anatomic obstructions and systemic or pulmonary hypertension may negatively affect ventricular systolic and diastolic function. Excessively fast or slow heart rates and inappropriately timed atrial contraction (relative to ventricular systole) may negatively affect ventricular function. Finally, myocardial contractility often is negatively affected by the following factors: hypoxemia, acidosis, hypomagnesemia, hypocalcemia, hypoglycemia, hyperkalemia, cardiac surgery, sepsis, and cardiomyopathies.

Monitoring Tissue Oxygenation

CO can be assessed qualitatively by physical examination and other modalities and quantitatively by a variety of techniques using invasive and noninvasive devices, laboratory data, and other clinical indicators. DO₂ is easily derived if systemic blood flow can be measured, but it is only indirectly inferred if this information is lacking.

Qualitative Assessment of Cardiac Output

Physical Examination

The physical examination often is the initial and the most common technique used to assess and monitor cardiovascular function. Significantly diminished CO may manifest as diminished peripheral pulses, cool or mottled extremities, and delayed capillary refill. However, certain clinical signs of low CO may be unreliable depending on the particular diagnosis. For example, in the context of cardiac lesions associated with a large arterial pulse pressure (e.g., severe aortic insufficiency and aortopulmonary shunts), peripheral pulses may be increased despite low CO and reduced systemic DO₂. Patients in septic shock often are peripherally vasodilated and warm despite hypotension and reduced tissue DO₂. Impaired oxygenation may present as cyanosis of the skin, lips, and/or nail beds. Central cyanosis from either cardiac or respiratory causes results from arterial O₂ desaturation. In contrast, peripheral cyanosis results from vasoconstriction and low blood flow at the microcirculatory level. In some patients, cyanosis is a relatively subtle physical finding, particularly if the patient is anemic or has a dark complexion. Hydration status can be assessed by skin turgor, dryness of mucous membranes, and fullness of the anterior fontanel (in infants), but these manifestations of hydration status relate mostly to interstitial fluid and may poorly reflect intravascular volume, which must be directly measured.

Cardiac auscultation for abnormal heart sounds, including valve clicks, rubs, gallops, and murmurs, may provide the first indication of a significant functional or structural cardiac abnormality, although these sounds do not directly reflect DO₂. Unfortunately, the lack of a heart murmur, especially in low CO states, does not necessarily rule out a significant residual cardiac lesion. The presence of crackles on pulmonary auscultation, particularly in the older pediatric patient, may signify pulmonary edema. However, crackles are nonspecific and may be caused by lung disease or fluid overload, in addition to disorders of cardiac structure or function. Finally, jugular venous distension and hepatomegaly often are indicative of high right-sided filling pressures often associated with RV dysfunction.

Chest Radiography

Although the chest radiograph is of little value in assessing a patient’s hemodynamic profile per se, it may be helpful for assessing certain aspects related to cardiovascular status. Provided the chest radiograph is technically adequate, the clinician can assess heart size, contour and configuration, pulmonary vascularity, pleural effusions, lung parenchyma, and abdominal situs. Some of these findings, when abnormal, may help determine the etiology of cardiovascular dysfunction. Increased pulmonary arterial vasculature may be indicated by enlarged pulmonary arteries in the hila that radiate toward the periphery of the lung. Conditions that increase pulmonary blood flow (PBF, or Q_p) at least twice normal also increase the size of the pulmonary arteries. Increased pulmonary capillary pressure may be inferred by the presence of pulmonary edema. The edema may present as a “fluffy” hilum but may have a more diffuse granular appearance in neonates. Pleural effusions may accompany pulmonary edema, particularly in conditions associated with poorly compensated congestive heart failure. Increased pulmonary venous markings are indicative of elevated pulmonary venous pressures of any cause, although usually from decreased left ventricular compliance or obstruction in the pulmonary veins or left atrium.

In the early postoperative period, the most important information obtained from the chest radiograph is (1) the positions of the endotracheal tube, chest tubes, and intracardiac lines; (2) the presence of extrapulmonary fluid or air; and (3) the presence of pulmonary edema. The cardiothoracic ratio gives a quantitative estimate of cardiac size, which is obtained by dividing the transverse measurement of the cardiac shadow in the posteroanterior view by the width of the thoracic cavity. Cardiomegaly is present if this value is greater than 0.5 in adults and 0.6 in infants. Although useful for assessing left ventricular (LV) enlargement, the cardiothoracic ratio is not as sensitive to RV enlargement. RV enlargement results in lateral and upward displacement of the cardiac apex on the posteroanterior view and filling of the retrosternal space on the lateral view. It is perhaps more important to know what the chest x-ray may not reveal; significant cardiac problems, such as constrictive pericarditis, acute fulminant myocarditis, and even acute pericardial tamponade often are associated with a normal-sized heart on a chest radiograph.

Quantitative Assessment of Cardiac Output

Quantitative measures of CO in the ICU can be obtained by a variety of techniques, including the Fick method, thermodilution, the dye dilution techniques, and Doppler echocardiography. Each of the first three methods applies a similar principle of dilution of an indicator: O₂, cold, or indocyanine green dye, respectively. The change in concentration of a substance is proportional to the volume of blood in which it is being diluted. In general, thermodilution is the method most widely used in the intensive care setting. However, for conditions of low CO, the Fick method is more reliable than the thermodilution or dye dilution techniques. Conversely, the Fick method is less accurate in conditions of high systemic blood flow because of difficulty in measuring narrow arteriovenous O₂ differences in the blood.

Thermodilution Technique

The thermodilution technique requires use of a specialized pulmonary artery (PA) catheter. CO is calculated by injecting a known volume of iced water or saline solution into the right atrium (proximal catheter port) and measuring the temperature change at the catheter tip in the PA. CO is calculated by the following equation:

where V_i is injectate volume (mL), T_b is temperature of blood, T_i is injectate temperature, and T_b(t)dt is area under the curve. In general, thermodilution CO measures are performed using a completely automated system, and the calculations are performed by a computer. This method (as with any indicator dilution method) requires complete mixing and thus is most accurate in situations where a mixing chamber is located proximal to the thermistor. It is generally used only in patients who do not have intracardiac or great vessel–level shunts or an insufficient valve between the injection site and the sampling site. The injection must be made rapidly because a slow injection will give a falsely elevated CO. Possible sources of error with this method include inaccurate measurement of the volume of injectate or of the temperature of the blood or injectate, close approximation of the thermistor to a vessel wall, and inadequate mixing, as is sometimes seen in venous systems with low flow.

Fick Method

According to the Fick principle, CO equals O₂ consumption divided by the arteriovenous O₂ content difference:

where VO₂ is O₂ consumption (mL/min) and CaO₂ and CvO₂ are arterial and venous O₂ content (mL O₂/100 mL blood), respectively. Care must be taken to select the appropriate sampling site for a true mixed venous blood sample. With a normal heart, the best site to obtain a mixed venous sample is within the PA. If a left-to-right shunt is present, however, the mixed venous site should be the cardiac chamber proximal to the site of the shunt. When a site other than the PA is used for the mixed venous site, the resultant value for arteriovenous O₂ difference is a less reliable reflection of the absolute CO, but it can be used for serial observations and for monitoring response to therapy over time.

Because measuring VO₂ in the intensive care setting requires special equipment and is somewhat cumbersome, the arteriovenous O₂ difference is often used as an indirect measure of CO. A wide arteriovenous O₂ difference generally reflects a low CO and indicates a large O₂ extraction by the tissues, whereas a narrow arteriovenous O₂ difference usually reflects a high CO. Unfortunately, studies suggest VO₂ is quite variable for any individual patient in an intensive care setting.⁹ Furthermore, mixed venous O₂ saturation (and, hence, arteriovenous O₂ difference) may be misleading in patients with decreased tissue O₂ extraction.^10,¹¹

Doppler Echocardiography

Doppler techniques can be used to measure CO using the mean velocity of systolic flow, the heart rate at the time of measurement, and the cross-sectional area of the artery in which measurements are being made (usually the ascending aorta):

where A is the area of the orifice, V is integrated flow velocity, and HR is heart rate. To determine the integrated flow velocity, the area under the Doppler curve must be measured. The area of the aortic orifice is commonly obtained by measuring the aortic diameter from the two-dimensional image, where A = 0.785 ∞ d2. This technique requires special care for accurate Doppler interrogation of blood flow and is seldom used in the critical care unit.

< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue