323CHAPTER 32 Cardiopulmonary Interactions unprepared RV is very sensitive to increases in RV afterload, PPV induced changes in RV afterload may have a significant impact on RV ejection Lung Volume Th[.]
CHAPTER 32 Cardiopulmonary Interactions unprepared RV is very sensitive to increases in RV afterload, PPVinduced changes in RV afterload may have a significant impact on RV ejection PVR Total PVR HPV , Q V/ Alveolar Pressure When alveolar pressure is greater than ambient, as it is during PPV, the vessels that course through alveolar septae between adjacent alveoli can be compressed.23,24 This behavior is akin to that of a Starling resistor, a collapsible tube traversing a rigid housing (Fig 32.7) Flow (Q) is propelled through the tube by inflow Zone el at Lung Volume The alveolar septae are highly vascular (Fig 32.5) More than 90% of the alveolar surface is in contact with alveolar capillaries These vessels can be separated into two categories according to their location or response to lung inflation Most alveolar vessels are capillaries and lie in septa, which separate adjacent alveoli Other alveolar vessels are termed corner vessels because they are located at the intersection of alveolar septae These corner vessels are generally larger and most likely will divide later in their course to become alveolar capillaries located in septa between adjacent alveoli When the lung is stretched by either spontaneous inspiration or positive pressure distension, corner vessels are pulled open by radial traction and their resistance to blood flow is reduced When alveolar septae are stretched, alveolar capillaries are stretched and compressed, become thinner, and restrict flow The net effect of these factors is that PVR rises as lung volume rises above FRC and approaches total lung capacity As lung volume falls below FRC and approaches residual volume, PVR increases owing to hypoxic pulmonary vasoconstriction of extraalveolar vessels PVR is least at FRC and rises with either atelectasis or overdistension, producing a U-shaped relationship between PVR and lung volume (Fig 32.6).19–22 323 Large vessels 1.0 Small vessels 3.0 2.0 RV 4.0 FRC 5.0 TLC LV • Fig 32.6 Effects of lung volume on pulmonary vascular resistance (PVR) As whole lung is distended from functional residual capacity (FRC) toward total lung capacity (TLC), PVR rises, predominantly by increasing resistance to flow through the small alveolar vessels that course between adjacent alveoli (alveolar vessels) As whole lung is collapsed from FRC toward residual volume, PVR rises, predominantly by effects on corner vessels that traverse the intersection of alveolar septa atel, atelectasis; ventilation/perfusion HPV, hypoxic pulmonary vasoconstriction; VQ, (Modified from Cassidy SS, Schwiep F Cardiovascular effects of positive end-expiratory pressure In: Scharf SM, Cassidy SS, eds Heart Lung Interactions in Health and Disease, vol 42, Lung Biology in Health and Disease New York: Dekker; 1989.) Starling resistor Alveolar vessel PS Pi PO Q PS Corner vessel • Fig 32.7 Starling resistor is a compressible conduit traversing a rigid hous- ing that is pressurized to a surrounding pressure (Ps ) Flow (Q) traverses the conduit, propelled by inflow pressure (Pi ) and opposed by outflow pressure (Po ) such that driving pressure is (Pi Po) for Ps , Po As Ps is increased, it begins to influence flow, but only after it exceeds Po At Ps Po, the driving force for flow becomes (Pi Ps) (Modified from Knowlton FP, Starling EH The influence of variations in temperature and blood pressure on performance of the isolated mammalian heart J Physiol 1912;44:206–219.) pressure (Pi) and is opposed by outflow pressure (Po) The tubing has some intrinsic resistance (R) If the housing is pressurized to a surrounding pressure (Ps), flow through the tube is determined as follows: • Fig 32.5 Alveolus is encased in a network of capillaries Alveolar vessels lie between adjacent alveoli Corner vessels lie at the intersection of alveolar septa Ps Po Pi ,Q ( Pi P0 ) R Eq 32.2 324 S E C T I O N I V Pediatric Critical Care: Cardiovascular Po Ps Pi ,Q ( Pi Ps ) R Eq 32.3 Po Pi Ps ,Q Eq 32.4 except when Ps , Po, alveolar pressure appears to modulate local pulmonary blood flow as though it surrounds the pulmonary capillary (Fig 32.8) From this discussion, the degree to which Ps affects pulmonary blood flow is influenced by the magnitude of Pi, which, for the pulmonary capillary, must be adjusted for vertical height Alveolar pressure causes a greater reduction in flow at low Pi, as seen in hypovolemia, than it does at high Pi, as seen with pulmonary venous hypertension and left heart failure Hydrostatic pressure in the lung is a function of vertical height (see Chapter 24).25 To estimate the hydrostatic Pi of a pulmonary capillary, a pressure equivalent to that exerted by a water column extending from the left atrium to the capillary must be subtracted from the pressure within the main pulmonary artery The greater the vertical height of the pulmonary capillary, the lower is its inflow pressure and the greater is the attenuation of flow by alveolar pressure This can produce areas of no flow, especially at peak inspiration, high in the supine lung Regions of lung with high ventilation/perfusion ratios (V/Q) waste ventilation and can cause hypercapnia (see Chapter 45) Vertical height (h) of the capillary also alters the back pressure to flow At a left atrial pressure of 10 cm H2O (7 mm Hg), for example, there is (10 h) cm H2O opposing flow up to a vertical height 10 cm above the heart Above that, there is no backpressure, and Pi and Ps alone determine flow through the capillary Compression of pulmonary PA PA PV PA PA > PA PA PA PV PA PA > PA > PV PA PV PA PA PV > PA • Fig 32.8 Pulmonary capillaries are, in essence, surrounded by gas-filled alveoli The influence of alveolar pressure (PA ) on regional lung blood flow is similar to the influence of surrounding pressure on flow through a Starling resistor At ambient values of PA, pulmonary vein pressure (PV) opposes inflow As PA rises, it begins to oppose inflow only after PA PV It modulates inflow until PA reaches hydrostatic inflow pressure (PA), at which point flow ceases capillaries is a local phenomenon It can divert pulmonary blood flow away from normal lung segments toward consolidated or atelectatic lung segments whose airways not effectively transmit airway pressure to the alveolus.26 The application of high PEEP in the presence of lobar pneumonia may increase blood flow through unventilated lung and worsen hypoxemia by this mechanism From a beneficial perspective, PEEP may relieve atelectasis and improve ventilation, thereby relieving alveolar hypoxic vasoconstriction Whether PEEP benefits or impairs pulmonary blood flow depends in part on the balance of its effect on atelectasis (lung recruitment) and its effect on alveolar capillaries (alveolar overdistension) Regulation of Pulmonary Vascular Resistance The resistance to flow through a vessel is described by the following: R 8 1 r Eq 32.5 where h is viscosity, l is length, and r is radius It follows that PVR can be effectively controlled by active changes in vessel radius Mechanical ventilation may alter carbon dioxide clearance/ blood pH and PAO2, both of which influence vessel tone and radius.27,28 Hypoxic pulmonary vasoconstriction is a powerful mechanism for sustaining systemic oxygenation in the face of lung disease.29–32 Relief of atelectasis and restoration of segmental ventilation not only increases the fraction of the lung that is ventilated but also restores blood flow to those segments by several mechanisms Segmental alveolar hypoxia is relieved Segmental volume is restored, which returns segmental vascular resistance to its volume-dependent nadir Gas exchange is also improved, thereby reducing global PVR Direct Effects of Airway Pressure on Pulmonary Vascular Tone Pulmonary vessels are stretched by lung inflation The lung of infant lambs responds to abrupt changes in airway pressure with changes in vascular tone Abrupt distension of one lung of the intact infant lamb increases the PVR of that lung alone.33 The resistance change is sensitive to the waveform of the lung distension34 and persists for some time after relief of distending pressure and return of lung volume to baseline.35 This effect is calcium channel dependent36 and resembles a myogenic reflex whereby direct vessel stretch causes constriction Respiration and Left Ventricular Preload Positive airway pressure can reduce LV filling via several mechanisms as described earlier: limiting systemic venous return and RV filling and/or increasing RV afterload and decreasing RV ejection Positive airway pressure may also decrease LV filling by adversely impacting LV compliance as a result of ventricular interdependence Ventricular Interdependence The RV and LV share a common muscle mass and pericardial space It follows that compliance of either ventricle will be influenced by volume and pressure of the other chamber (Fig 32.9) Increased venous return to the right heart, as occurs during spontaneous inspiration and especially during execution of a Müller maneuver, shifts the interventricular septum to the left, reducing compliance of the LV.37,38 Similarly, excessive compression of the CHAPTER 32 Cardiopulmonary Interactions LV FRC LV RV Spontaneous inspiration crowds the LV • Fig 32.9 Increasing the diastolic volume of the right ventricle (RV) reduces compliance of the left ventricle (LV) FRC, functional residual capacity pulmonary circulation by positive airway pressure may impede RV ejection, causing the RV to dilate and encroach on the left Reduced LV compliance tends to diminish stroke volume by diminishing LV muscle stretch and ejection force (by the FrankStarling mechanism) Respiration and Left Ventricular Afterload The LV ejects blood from within the thorax to the extrathoracic arterial system Most of the resistance to this forward flow resides in the arterioles From a practical point of view, the pressure in the extrathoracic arteries can be described by the following equations: (P artery ) Pms Q R arteriole or Partery Q R arteriole Pms Eq 32.6 Eq 32.7 where Q is CO, Partery is Pi before the arteriole, and Pms is Po after the arteriole as defined for the venous return curve When the LV contracts, it creates internal pressure against the closed aortic valve by generating tension in the myocardium that encircles the ventricular chamber This “wall tension” causes ventricular pressure to rise until it reaches aortic diastolic pressure, opening the aortic valve and ejecting the stroke volume Creation of wall tension and subsequent shortening of myocardial fibers perform the external mechanical work of the heart When the heart squeezes, it creates a pressure difference between the ventricle and juxtacardiac space In effect, the myocardium creates a Ptm to produce a ventricular pressure sufficient to open the aortic valve Aortic diastolic pressure and external (juxtacardiac) pressure determine the myocardial wall tension needed 325 to open the aortic valve Both pressures represent afterloads to LV ejection.39,40 A vasoconstrictor of arterial resistance vessels increases the pressure required to open the aortic valve and LV afterload This increases the wall tension that the heart must generate to eject blood The Müller maneuver, forced inspiration against a closed glottis, does the same thing It reduces juxtacardiac pressure, thereby raising the Ptm required to open the aortic valve Thus, the Müller maneuver also increases LV afterload A vasodilator of arterial resistance vessels lowers aortic pressure, reducing the pressure required to open the aortic valve and LV afterload PPV or application of continuous positive airway pressure (CPAP) increases juxtacardiac pressure to such an extent that the wall tension required to open the aortic valve and LV afterload are diminished The net effect of PPV is often augmentation of LV stroke volume and CO Arterial pressure is commonly observed to rise during positive-pressure inspiration, whereas it falls during spontaneous inspiration These are largely effects of afterload on stroke volume Cardiac Contractility Studies of the effects of positive airway pressure on LV contractility have yielded conflicting results Certainly, ventilator-induced changes in preload and afterload have secondary effects on stroke volume, but independent effects of positive airway pressure on LV contractility have not been consistently demonstrated Negative inotropic effects modulated by reflexes, mediators, or alterations in coronary blood flow have been described,41–46 but most animal and human studies fail to show that positive airway pressure has any primary effect on myocardial contractility.47–50 It has been suggested that high levels of PEEP may compress coronary vessels, cause myocardial ischemia, and thereby impair ventricular function.51–53 LV myocardium is perfused predominantly in diastole To the extent that juxtacardiac pressure exceeds diastolic pressure in the coronary sinus, such an effect is plausible This assertion appears more compelling for patients in shock and for those with intrinsic coronary blood flow limitations than for otherwise normal individuals Preload Dependence Versus Afterload Dependence The expected effects of a rise in airway pressure are as follows: Decreased filling of the RV acts to decrease RV stroke volume Pulmonary vascular compression increases RV afterload and acts to decrease RV ejection and stroke volume These effects may either increase or decrease RV size, depending on which effect predominates; if RV volume increases, ventricular interdependence adversely impacts LV compliance Both diastolic displacement of the interventricular septum toward the LV (with resultant crowding of the LV) and crowding of the juxtacardiac space by the expanding lungs reduce LV compliance Both factors act to decrease LV filling and stroke volume The fall in LV afterload that results from increased juxtacardiac pressure acts to increase LV stroke volume These effects of positive airway pressure may have conflicting effects on stroke volume; thus, their aggregate effect on CO is not entirely predictable In general, positive airway pressure has its most pronounced effect on the right heart; therefore, positive 326 S E C T I O N I V Pediatric Critical Care: Cardiovascular airway pressure reduces CO in most patients This effect is greatest in patients who are hypovolemic because the driving pressure for systemic venous return (Pms Pra) is more sensitive to change in Pra when Pms is low In addition, pulmonary venous pressure is low and PPV increases the proportion of lung units where Ps (alveolar) Pi, increasing RV afterload and decreasing RV ejection In adults, the Pra threshold (at zero PEEP) below which increasing airway pressure reduces CO is approximately 12 mm Hg.54 Another definition of preload dependence is responsiveness to vascular volume infusion By this definition, when the dominant effect of positive airway pressure is to impede right heart filling, vascular volume infusion increases stroke volume and CO Four measurable parameters predict responsiveness to vascular volume infusion: (1) variation of pulse pressure over the respiratory cycle (maximum minimum), (2) arterial systolic pressure, (3) Pra, and (4) pulmonary artery wedge pressure.55 Of these parameters, the inspiratory increase in arterial pulse pressure is the most sensitive and specific predictor of “preload dependence” (by receptor operating characteristic curve) Greater than 15% inspiratory rise in pulse pressure appears to identify adults with preload dependence during PPV.56 One might expect the converse also to apply Reduced magnitude of the effects of PPV on RV filling or augmented effects on LV ejection may make the patient “afterload dependent.” Patients who have high blood volume, such as those in congestive cardiac failure or those with chronic anemia, should have high Pms and decreased sensitivity to changes in Pra.57 Moreover, the patient with poor LV contractility may greatly benefit from the afterload reduction of PPV.58 If positive airway pressure enhances the ejection of blood into the systemic circulation, this may directly reduce left atrial pressure From these considerations, improved CO reduces Pra, enhancing systemic venous return (see Fig 32.1B) When favorable effects on LV ejection act to reduce right and left atrial pressures, CO improves Such a patient might be thought of as “afterload dependent.” Fluid Responsiveness During Positive Pressure Ventilation In the critical care unit, whether volume infusion will augment CO or merely contribute to vascular volume overload is often a vital issue In adult patients receiving PPV, about half of all hemodynamically unstable critical care patients are not volume responsive.59 Traditional guides to volume resuscitation have focused on measurement of cardiac filling pressures and responses to fluid challenges In critically ill patients and in normal subjects, the stroke volume response to vascular volume infusion is poorly predicted by measurement of either right atrial or pulmonary artery occlusion pressure.60 Much recent interest has focused on minimally invasive estimation of the likelihood of responding to fluid infusion The cardiopulmonary interactions described previously can be used to predict response to fluid challenge The change in stroke volume over the course of the positive pressure respiratory cycle strongly predicts fluid responsiveness; the greater the percentage change in stroke volume, the greater the response to volume infusion.61 Similar relations have been shown between fluid responsiveness and respiratory variation in aortic blood flow velocity62 and arterial pulse pressure.54 Inspiratory collapsibility of the inferior63 and superior64 vena cavae has also been shown to predict volume responsiveness Changes in CO induced by either fluid resuscitation or by application of PEEP appear to be predicted by measurement of pulse pressure variability.55 In general, in these patients, the greater the pulse pressure variability, the more preload dependent the patient is to PEEP and the more responsive to fluid resuscitation Pulsus Paradoxus in Respiratory Distress Arterial pressure normally falls during spontaneous inspiration, which is best explained as a result of increasing LV afterload at a time in the respiratory cycle when ventricular interdependence restricts LV filling It is well known that pericardial tamponade causes accentuation of the normal inspiratory decrease in systemic blood pressure, a phenomenon known as pulsus paradoxus This phenomenon has been attributed to accentuation of normal ventricular interdependence in the face of restricted biventricular diastolic volume of the heart During loaded spontaneous inspiration, as in the Müller maneuver or in the presence of inspiratory airway obstruction (e.g., croup), the inspiratory fall in juxtacardiac pressure is exaggerated and LV afterload is accentuated Again, the result is pulsus paradoxus, an accentuated drop in blood pressure during inspiration The increase in blood pressure that occurs during positive pressure inspiration has been termed reverse pulsus paradoxus This finding has been attributed to LV afterload reduction by the rise in juxtacardiac pressure that occurs during positive pressure inspiration Reverse pulsus paradoxus is a normal finding during PPV but may be accentuated in afterload-dependent states (e.g., LV systolic dysfunction), as discussed earlier in the Preload Dependence Versus Afterload Dependence section) Positive-Pressure Ventilation and Right Ventricular Output in Acute Respiratory Distress Syndrome In acute respiratory distress syndrome (ARDS), PPV may induce significant heart-lung interactions that adversely impact RV loading conditions and output, impairing gas exchange, CO, and ultimately systemic DO2, potentially offsetting gains in oxygenation resulting from increases in airway pressure As reviewed earlier, PPV may decrease systemic venous return, RV filling, and output Despite the use of a lung-protective strategy, PPV may also increase PVR, impairing RV systolic ejection While the increase in air-blood barrier permeability is evenly distributed and extravascular lung water (EVLW) is diffusely increased, a vertical, gravitational gradient exists for lung densities and EVLW formation.65 The increase in lung weight exaggerates the normal compressive gravitational forces present in lung parenchyma, leading to the formation of nonaerated tissue in gravity-dependent regions of the lung.66 Lung tissue in nongravity-dependent regions of the lung is well aerated with nearnormal mechanical characteristics and thus receives a disproportionate amount of the airway pressure, resulting in alveolar overdistension, while blood flow in this region is limited due to the effects of gravity on pulmonary perfusion PVR increases to the extent that zone I conditions are created (PA PA; see Fig 32.8) and regions under zone II conditions are increased (PA PA PV; see Fig 32.8) A limitation of preload and increase in afterload may combine to decrease RV output With an increase in afterload, a compensatory increase in preload is needed to maintain stroke volume, which may be limited for the reasons discussed earlier VieillardBaron and colleagues described this finding in their study of adult patients with ARDS using echocardiography with Doppler to evaluate beat-to-beat inflow and outflow and ventricular CHAPTER 32 Cardiopulmonary Interactions dimensions throughout the respiratory cycle.66 They demonstrated inspiratory reductions in RV fractional area contraction associated with a significant increase in RV end systolic dimensions, while RV end diastolic area remained unchanged They concluded that this likely reflects a relative decrease in RV preload because an increase in afterload and end systolic volume should produce a corresponding (compensatory) increase in preload ARDS is frequently associated with RV systolic impairment, the most severe form of which is cor pulmonale, which occurs in upward of 20% of adult patients and has been shown to be independently associated with a higher risk of death in these patients.67,68 Indicators of a limited CO state—such as an increased oxygen extraction ratio, elevated lactate level, or thermodilutionmeasured low CO—merit an echocardiogram to delineate the mechanism(s) responsible.69 Echocardiography provides several hemodynamic parameters—including RV systolic pressure, dimensions, and function—establishing whether right heart impairment is present and whether it is due to inadequate preload, elevated afterload, or a combination of the two Effects of Cardiovascular Function on Respiration Shock States and Respiratory Function Shock of any cause diminishes perfusion of respiratory muscles and can lead to respiratory failure and respiratory arrest It also causes metabolic acidosis, which constricts pulmonary vessels and opposes lung blood flow.70,71 Acidosis is a potent stimulus of respiratory effort and contributes to tachypnea and respiratory distress, which, in turn, worsen the demand on the heart Shock is injurious to both heart and lungs; one final common pathway to recovery is the initiation of mechanical ventilation, which benefits both organ systems Hypovolemic shock can create extreme preload dependency.72 In hypovolemic shock, diastolic blood pressure may fall during positive pressure inspiration, impairing coronary perfusion This may cause myocardial ischemia and worsen cardiac function Cardiogenic shock elevates percent tissue oxygen extraction from the blood by reducing DO2 The resultant decline in venous oxygen tension has a paradoxical effect It increases the efficiency of pulmonary blood flow by allowing greater oxygen uptake per unit of pulmonary blood flow That is, the more desaturated the blood that enters the pulmonary circulation, the more oxygen can be uploaded This process requires that alveolar pO2 not limit the amount of oxygen available for uptake and is one reason to administer oxygen to patients experiencing cardiorespiratory failure Elevated Work of Breathing and the Circulation During quiet respiration, the heart has no difficulty satisfying the metabolic demand of the respiratory muscles However, with a significant increase in respiratory muscle oxygen demand and a limitation of CO, respiratory muscle DO2 may be inadequate Unlike cardiac muscle, respiratory muscles can accumulate a limited oxygen debt, and persistent hypoperfusion may interfere with their ability to perform the requisite work of breathing In addition, in a low CO state, a competition among viscera for blood flow is created The brain, myocardium, and respiratory pump lack adrenergic receptors and, under intense neurohormonal activation, not experience an increase in resistance to flow; thus, they compete for a limited CO Roussos and 327 colleagues73–75 demonstrated in animal models of cardiogenic and septic shock that mechanical ventilation and the unloading of the respiratory pump lead to a significant redistribution of blood flow from muscles of respiration to other vital organs, including the brain Because it unloads the respiratory pump and decreases LV afterload, mechanical ventilation should be considered an essential tool in the armamentarium for treating heart failure and shock Congestive Heart Failure/Critical Heart Failure and Shock All that has been said about shock is equally true of congestive heart failure (CHF) In fact, there is a continuum from CHF to cardiogenic shock CHF elicits physiologic responses that attempt to restore and maintain an adequate CO As these homeostatic responses are exhausted, CO becomes inadequate, and the patient develops obvious manifestations of cardiogenic shock and respiratory failure In addition to the impact of shock on respiratory function and reserve, CHF generally causes fluid retention and pulmonary edema Treatment of cardiogenic shock by vascular volume expansion may, by augmenting cardiac filling pressures, improve CO at the expense of pulmonary edema, which leads to elevated airway resistance, atelectasis, intrapulmonary shunt, and impaired oxygenation Impaired respiratory mechanics lead to exaggerated negative-pressure breathing and increased LV afterload while increasing circulatory demands by increasing respiratory muscle oxygen demand Further, as the work of breathing increases, neurohormonal pathways are stimulated These pathways increase systemic vascular resistance and blood pressure and, in doing so, contribute significantly to increases in LV afterload, as described earlier PPV with PEEP improves lung function and gas exchange and eliminates exaggerated negative swings in ITP, eliminating respiratory muscle oxygen demand while releasing sympathetic nervous system activation LV afterload is reduced, increasing stroke volume and CO PPV decreases respiratory and cardiac muscle oxygen demand while improving CO and DO2 The net effect is a significant improvement in the myocardial and global oxygen supply-demand relationship in patients with cardiogenic shock Pulmonary venous hypertension renders the pulmonary circulation less sensitive to positive airway pressure, as a disproportionate number of lung units have Pv Ps (alveolar pressure; zone III conditions) The patient is afterload-dependent and should respond favorably to the afterloadreducing effects of PPV When treating the patient with CHF during PPV, there is a risk of worsening pulmonary edema during fluid resuscitation It is wise to assess pulse pressure, as well as systolic and diastolic pressures, to predict volume responsiveness before administering volume.76 These parameters may also prove useful in assessing the impact of changes in ITP on CO.55 Cardiomyopathies and Congenital Heart Disease Hypertrophic cardiomyopathy is characterized by intact LV systolic function but has varying degrees of diastolic dysfunction that may compromise output due to inadequate ventricular filling.77 Thus, the impact of increases in ITP on systemic venous return may not be tolerated If pulmonary venous pressure is elevated secondary to impaired LV compliance, the impact of PPV and lung volumes on PVR will be mitigated as the proportion of lung units with Pv Ps increases Hypertrophic cardiomyopathy may also obstruct LV outflow, either at rest or with exertion PPV may ... within the main pulmonary artery The greater the vertical height of the pulmonary capillary, the lower is its inflow pressure and the greater is the attenuation of flow by alveolar pressure This... and Left Ventricular Afterload The LV ejects blood from within the thorax to the extrathoracic arterial system Most of the resistance to this forward flow resides in the arterioles From a practical... and LV afterload This increases the wall tension that the heart must generate to eject blood The Müller maneuver, forced inspiration against a closed glottis, does the same thing It reduces juxtacardiac