245CHAPTER 27 Assessment of Cardiovascular Function Increased Pulmonary Vascular Resistance The clinical consequences of increased PVR are directly related to the specific cardiac anatomy and physiolo[.]
CHAPTER 27 Assessment of Cardiovascular Function Increased Pulmonary Vascular Resistance The clinical consequences of increased PVR are directly related to the specific cardiac anatomy and physiology With two separate ventricles, high PVR can reduce systolic and diastolic function of the pulmonary ventricle and limit its output In patients with a physiologically large aortopulmonary shunt, increased PVR can be useful up to a point because it reduces what would otherwise be excessive PBF On the other hand, if PVR is too high, or in the setting of an excessively restrictive aortopulmonary shunt, inadequate PBF results With a bidirectional Glenn circulation, elevated PVR may result in upper body congestion and hypoxemia With a Fontan circulation, high systemic venous pressure, low CO, edema, high chest tube output, and hypoxemia (if a fenestration is present) may occur In patients with a structurally normal cardiovascular system, measuring PVR is analogous to measurement of SVR and is subject to the same practical difficulties Echocardiographic estimation of RV pressure is a useful surrogate, using a tricuspid regurgitant jet, pulmonary regurgitant jet, or interventricular septal position Unfortunately, in the absence of significant tricuspid regurgitation (or another defect that allows a pressure gradient to be measured between the right ventricle and a chamber of known pressure), echocardiographic estimation of RV pressure is crude For patients with an aortopulmonary shunt, PVR is rarely measured in the ICU; determining PBF requires measuring Vo2 (an assumed Vo2 is questionable because it is so variable9), pulmonary arterial O2 saturation, and pulmonary venous O2 saturation Because pulmonary venous catheters are rarely used, pulmonary venous O2 saturations are usually assumed However, this is a potential source of significant error because these saturations are variable and unpredictable.44 Most important, pulmonary artery pressure is essentially never measured in the critical care unit in patients with shunts For these patients, even estimating PVR is problematic because many variables (e.g., PVR, systemic blood pressure, PBF and CO, hematocrit, and Vo2) influence the most obvious manifestation of increased PVR, low systemic arterial O2 saturation Circumstantial data may be used to infer that PVR is not elevated in hypoxemic patients with an aortopulmonary shunt; for example, echocardiographic demonstration of narrowing of the shunt suggests that increased PVR is likely not the cause of the hypoxemia Alternatively, an increase in systemic arterial O2 saturation with inhaled nitric oxide suggests that baseline PVR is increased Measuring PBF in patients with a cavopulmonary palliation (e.g., bidirectional Glenn, hemi-Fontan, and Fontan) can also be done using the Fick method (thermodilution cannot be used to measure PBF because of inadequate mixing of the cold indicator in the systemic venous pathway) Measurement of the ratio of pulmonary to systemic blood flow (Qp:Qs) can be calculated as the arterial saturation minus the inferior vena cava saturation divided by the pulmonary venous saturation minus the inferior vena cava saturation.45 From a practical standpoint, increased PVR in this setting is often inferred from high systemic venous pathway pressures (superior vena caval pressures in a bidirectional Glenn patient), taking into consideration possible anatomic obstruction in the superior vena cava, pulmonary arteries, or pulmonary veins or increased systemic ventricular end-diastolic pressures structural lesions are (1) increased ventricular afterload (e.g., RV or LV outflow tract obstruction); (2) increased ventricular volume load (e.g., ventricular septal defect, excessive PBF through a surgical shunt or patent ductus, and atrioventricular valve regurgitation); (3) impaired ventricular filling (e.g., atrioventricular valve stenosis); (4) reduced PBF with shunting into the systemic circulation; (5) mixing of pulmonary and systemic venous blood; and (6) D-transposition of the great arteries physiology (i.e., pulmonary venous return predominantly directed to the PA and systemic venous return predominantly directed to the aorta) Impaired coronary perfusion resulting in ventricular ischemia is perhaps not, conceptually, a problem of efficiency but a structural lesion that needs to be considered Many patients have some combination of these lesions It is beyond the scope of this chapter to discuss the evaluation of cardiac patients relative to structural lesions and their impact on Do2, systemic perfusion pressure, and QOT Suffice it to say that it is exceedingly important that the anatomy and associated physiology of patients with cardiac malformations be well defined Echocardiography is the single most useful modality for delineating cardiac structure (and often even physiology) in the critical care unit Cardiac catheterization and angiography remain important diagnostic and therapeutic tools, and MRI and computed tomography are sometimes helpful Vascular Integrity By vascular integrity, we refer to the ability of the vascular (mostly microvascular) bed to keep fluid in the intravascular space Leaky blood vessels result in organ, chest wall, and peripheral edema, as well as fluid accumulation in the thoracic and abdominal cavities This situation is exacerbated by high CVP, particularly when ventricular diastolic dysfunction exists, and tends to be selfperpetuating, especially in infants (Fig 27.1) It is important to assess third spacing, particularly in infants, where opening the chest may help minimize the hemodynamic effects of chest wall edema in post–cardiac surgery patients ↑ Tissue edema Volume infusion ↑ CVP (persistent or transient) ↑ Chest wall stiffness Hypotension ↑ Intrathoracic pressure ↓ Decreased venous return Inefficient Circulation The most important fundamental ways that structural defects can result in an inefficient circulation in patients with cardiac 245 • Fig 27.1 Effect of compromised vascular integrity CVP, Central venous pressure 246 S E C T I O N I V Pediatric Critical Care: Cardiovascular Similarly, assessment for abdominal compartment syndrome due to ascites may allow surgical or catheter-based evacuation with improved pulmonary mechanics and urine output Also, because progressive edema, even if relatively benign early on, is likely to eventually become a significant problem, this finding should figure prominently in the clinician’s overall assessment of the patient’s condition There is currently rapidly evolving interest in the role that lymphatic abnormalities may play in chronic effusions, protein losing enteropathy, and plastic bronchitis in Fontan (and other) patients.46,47 MRI-guided, invasive interventions on the large lymphatic ducts can provide relief of such manifestations, and it seems likely that such interventions (and possibly modification of lymphatic function by medications) will play an important role in cardiac critical care in the future DO2 = CaO2 × SBF CaO2 = CPVO2 1) PVO2 sat 2) Hgb Pulmonary Function Pulmonary dysfunction due to edema or acute or chronic lung injury can be a major physiologic liability for the obvious reasons related to impaired gas exchange In addition, insofar as increased Paw is required for adequate gas exchange, venous return to the heart may be impaired This can be especially important in special circumstances, such as the patient after cavopulmonary palliation Williams and colleagues48 nicely showed the unfavorable impact of small increments of positive end-expiratory pressure in patients after Fontan palliation, which, as careful inspection of their data reveals, was mostly due to decreased venous return Increased Paw, especially if it causes overinflation of the lungs, also can increase PVR Finally, increased Paw, if applied for sufficient duration, can take a long-term toll by chronic reduction in lung function It is beyond the scope of this chapter to describe all available techniques for evaluating lung function However, high Paw is an important component of QOT and should lead the intensivist to consider alternatives (e.g., permissive hypercapnia or extracorporeal life support) Physiology of the Patient With a Single Ventricle Patients with single-ventricle physiology differ from children with two functioning ventricles in many ways They pose several unique challenges to the pediatric intensivist For many patients with a single ventricle, initial palliation in infancy may involve placement of an aortopulmonary (e.g., modified Blalock-Taussig) or right ventricle to PA (Sano) connection as a source of PBF The total output of the single-ventricle circulation is thus the sum of the pulmonary (Qp) and systemic (Qs) blood flows The relative percentage of blood flow to the pulmonary and systemic circulations depends, in part, on the resistance in each vascular bed Because PVR is usually substantially lower than SVR soon after birth, the size (diameter, length, and vessel of origin) of the aortopulmonary shunt is also a major contributor to total resistance to flow in the pulmonary circuit and, hence, an important determinant of Qp/ Qs SVR is often the single most important variable influencing Qp,49 and postoperative afterload reduction has been shown to improve outcomes and markers of Do2.50,51 In patients with a single ventricle who have complete admixture of systemic and pulmonary venous blood, arterial O2 saturation is influenced by not only lung function (e.g., pulmonary venous O2 saturation) but also Qp and myocardial function (which influences Qs and, hence, mixed venous O2 saturation; Figs 27.2 and 27.3) 3) SBF = CO • Fig 27.2 Variables that determine systemic oxygen delivery (Do2) with a normal heart Blue dots depict desaturated (systemic venous) blood; red dots depict fully saturated (pulmonary venous) blood Dissolved O2 in the blood is ignored Cao2, Systemic arterial blood O2 content; CO, cardiac output; Cpvo2, pulmonary venous blood O2 content; Hgb, blood hemoglobin concentration; Pvo2 sat, pulmonary venous O2 saturation; SBF, systemic blood flow DO2 = CaO2 × SBF CaO2 CPVO2 CMVO2 3) VO2 DO2 sat 1) PVO2 sat 2) Hgb 4) Qp : Qs Rp : Rs SBF = 5) CO – PBF Qp : Qs • Fig 27.3 Variables that determine systemic oxygen delivery (Do2) with a cardiac malformation resulting in complete mixing of systemic and pulmonary venous blood Blue dots depict desaturated (systemic venous) blood; red dots depict fully saturated (pulmonary venous) blood Dissolved O2 in the blood is ignored Cao2, Systemic arterial blood O2 content; Cmvo2, systemic venous O2 content; CO, cardiac output; Cpvo2, pulmonary venous blood O2 content; Hgb, blood hemoglobin concentration; Pvo2 sat, pulmonary venous O2 saturation; PBF, pulmonary blood flow; Qp:Qs, ratio of pulmonary to systemic blood flow; Rp:Rs, ratio of pulmonary to systemic vascular resistance; SBF, systemic blood flow; Vo2, total body O2 consumption CHAPTER 27 Assessment of Cardiovascular Function Computer modeling of shunt-dependent single-ventricle physiology49,52 suggests that a Qp/Qs ,1.0 is ideal for optimizing systemic O2 availability for a given pulmonary venous O2 saturation, CO, and Vo2 The arterial O2 saturation, considered in isolation, is a poor indicator of Qp/Qs because a low mixed venous O2 saturation will depress arterial O2 saturation, even in patients with a high Qp/Qs In a patient with left-to-right atrial shunting, accurately measuring Qp/Qs, which equals systemic arterial O2 saturation minus systemic venous O2 saturation divided by pulmonary venous O2 saturation minus pulmonary arterial O2 saturation, requires determining O2 saturation in blood in the proximal superior vena cava (SVC), as distinct from the RA or inferior vena cava, and is subject to the previously noted variability and unpredictability of pulmonary venous O2 saturations That said, estimating Qp/Qs using the SVC O2 saturation (as mixed venous) and the arterial O2 saturation (which is also the pulmonary artery O2 saturation) and assuming the pulmonary venous O2 saturation is helpful in estimating whether a patient with a single ventricle and an aortopulmonary shunt has appropriate (i.e., associated with optimal systemic Do2), increased, or decreased Qp/Qs However, it is important to note that Qp/Qs is merely a number when considered in isolation It must be placed into the context of the patient’s overall status considering the parameters previously outlined for assessing systemic Do2 In particular, in patients following singleventricle palliation, a progressive decline in the serum lactate concentration (regardless of the initial postoperative concentration) is a fairly sensitive and specific marker for early survival In contrast, rising lactate levels are generally a robust predictor of early postoperative cardiovascular collapse or need for mechanical support unless therapy can improve the hemodynamic picture.15,16 It should be noted that the physiology is somewhat different in patients with two ventricles and an aortopulmonary shunt (e.g., tetralogy of Fallot with severe RV outflow tract obstruction and a modified Blalock-Taussig shunt) Because PBF, is usually made up of both systemic arterial blood and systemic venous blood, arterial O2 saturation is higher for a given amount of PBF, and Qp:Qs cannot be calculated using systemic arterial O2 saturation as the pulmonary artery O2 saturation The cardiopulmonary physiology of patients with bidirectional Glenn palliation differs somewhat from that of others as there is a paradoxical relationship between alveolar ventilation and arterial O2 saturation53,54 whereby PBF (and therefore arterial O2 saturation) are primarily affected by the quantity of cerebral blood flow (CBF) Hypoventilation with associated increases in Pco2 leads to increases in CBF, PBF, and arterial O2 saturation (as long as the hypoventilation is not associated with severe acidosis or atelectasis and therefore decreased pulmonary venous saturations) Two other additional points are worth noting First, because arterial O2 saturations often increase significantly during the first several postoperative hours after Glenn palliation, lower than desired but acceptable O2 saturations early on not necessarily imply inadequate palliation Second, although some degree of upper body edema and duskiness is not unusual soon after an operation, marked upper body congestion suggests the possibility of obstruction of the SVC to PA pathway, which requires prompt evaluation Echocardiography may be sufficient to interrogate this pathway, although angiography may be required 247 Evaluation of postoperative Fontan patients is much the same as for other postoperative cardiac patients However, because Fontan patients are particularly sensitive to factors that impede transit of blood across the lungs and into the ventricle, it is important to identify any such factors, especially remediable ones, early on in the struggling patient Anatomic abnormalities that might have little clinical importance in other circumstances (e.g., partial obstruction of one or more pulmonary veins) can have a marked impact on the early postoperative Fontan patient The same goes for modestly increased PVR and mildly decreased ventricular compliance Catheters in the central systemic veins and left atrium are useful for estimating PVR and ventricular compliance, and the previously noted measures of systemic perfusion are helpful The sick postoperative Fontan patient may pose the perfect storm of marginal SAP, acutely elevated CVP (relative to preoperative CVP), and hypoxemia (from right-to-left shunting of highly desaturated systemic venous blood through a fenestration), all complicated by the use of inotropic agents (which increase myocardial and total body Vo2) The experienced intensivist will consider these multiple variables, including the QOT, in the aggregate when evaluating the patient Key References Appelbaum 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