Heart–Lung Interactions


FIGURE 101.1 Schematic diagram of the relation between changes in lung volume and pulmonary vascular resistance, where the extra-alveolar and alveolar vascular components are separated. Note that pulmonary vascular resistance is minimal at resting lung volume or functional residual capacity (FRC). As lung volume increases toward total lung capacity (TLC) or decreases toward residual volume (RV), pulmonary vascular resistance also increases. However, the increase in resistance with hyperinflation is due to increased alveolar vascular resistance, whereas the increase in resistance with lung collapse is due to increased extra-alveolar vessel tone.



Hyperinflation-Induced Cardiac Compression

As lung volume increases, the heart is compressed between the expanding lungs (94), increasing juxtacardiac ITP. This compressive effect of the inflated lungs can be seen with either spontaneous (95) or positive-pressure–induced hyperinflation (5,40,96–98). As described above, both Ppc and ITP are increased and no pericardial restraint exists. This decrease in apparent LV diastolic compliance (93) was previously misinterpreted as impaired LV contractility, because LV stroke work for a given LV end-diastolic pressure or pulmonary artery occlusion pressure is decreased (99,100). However, when such patients are fluid resuscitated to return LV end-diastolic volume to its original level, both LV stroke work and CO also returned to their original levels (93,101) despite the continued application of PEEP (102).


HEMODYNAMIC EFFECTS OF CHANGES IN INTRATHORACIC PRESSURE


The heart within the thorax is a pressure chamber within a pressure chamber. Therefore, changes in ITP will affect the pressure gradients for both systemic venous return to the RV and systemic outflow from the LV, independent of the heart itself. Increases in ITP, by increasing right atrial pressure and decreasing transmural LV systolic pressure, will reduce the pressure gradients for venous return and LV ejection, decreasing intrathoracic blood volume. Using the same argument, decreases in ITP will augment venous return and impede LV ejection and increase intrathoracic blood volume; everything else follows from these simple truths.


Venous Return

Blood flows back from the systemic venous reservoirs into the right atrium through low pressure–low resistance venous conduits (103). Right atrial pressure is the backpressure for venous return; ventilation alters both right atrial pressure and venous reservoir pressure. It is these changes in right atrial and venous capacitance vessel pressure that induce most of the observed cardiovascular effects of ventilation. Pressure in the upstream venous reservoirs is called mean systemic pressure and is, itself, a function of blood volume, peripheral vasomotor tone, and the distribution of blood within the vasculature (104). Usually mean systemic pressure does not change rapidly during positive-pressure ventilation, whereas right atrial pressure does owing to concomitant changes in ITP. Thus, variations in right atrial pressure represent the major factor determining the fluctuation in pressure gradient for systemic venous return during ventilation (105,106). The positive-pressure inspiration increases in right atrial pressure, decreases the pressure gradient for venous return, decreasing RV filling (70) and RV stroke volume (70,105,107–115). During normal spontaneous inspiration, the opposite occurs (2,29,70,71,109,112,116,117). The detrimental effect of positive-pressure ventilation on CO can be minimized by either fluid resuscitation to increase mean systemic pressure (29,107,118,119) or by keeping both mean ITP and swings in lung volume as low as possible. Accordingly, prolonging expiratory time, decreasing tidal volume, and avoiding PEEP all minimize this decrease in systemic venous return to the RV (4,26,105,109–113,120).


However, if positive-pressure ventilation-induced increases in right atrial pressure always proportionally decreased venous return, then most patients would display profound cardiovascular insufficiency when placed on mechanical ventilator support and especially so when given increased levels of PEEP. Fortunately, when lung volumes increase, the diaphragm descends, compressing the abdominal compartment and increasing intra-abdominal pressure (121,122). Since a large proportion of venous blood exists in intra-abdominal vasculature, it is pressurized as well, increasing mean systemic pressure. Accordingly, the pressure gradient for venous return is often not reduced by PEEP (118). Inspiration-induced abdominal pressurization by diaphragmatic descent is probably the primary mechanism by which the decrease in venous return is minimized during positive-pressure ventilation (123–128). However, laparotomy, by abolishing the inspiration-associated increases in intra-abdominal pressure, makes surgery patients especially sensitive to mechanical ventilation and is one of the reasons why abdominal surgery patients often leave the operating room many liters positive.


Spontaneous inspiratory efforts usually increase venous return because of the combined decrease in right atrial pressure (2,28,110–112) and increase in intra-abdominal pressure (121,122), described above. However, this augmentation of venous return is limited (129,130) because as ITP decreases below atmospheric pressure, central venous pressure also becomes subatmospheric, collapsing the great veins as they enter the thorax and creating a flow-limiting segment (103).



FIGURE 101.2 Schematic diagram of the effect of increasing right ventricular (RV) volumes on the left ventricular (LV) diastolic pressure–volume (filling) relationship. Note that increasing RV volumes decrease LV diastolic compliance, such that a higher filling pressure is required to generate a constant end-diastolic volume. (Adapted from Taylor RR, Covell JW, Sonnenblick EH, Ross J Jr. Dependence of ventricular distensibility on filling the opposite ventricle. Am J Physiol. 1967;213:711–718.)


Ventricular Interdependence

Since spontaneous inspiration increases RV filling, it will also directly alter LV diastolic compliance by the process of ventricular interdependence. Increasing RV volume decreases LV diastolic compliance, while decreasing RV volume increases LV diastolic compliance, although the positive-pressure ventilation effect of increased LV diastolic compliance is usually minimal (Fig. 101.2) (90,131–134).


However, the spontaneous inspiration-induced RV volume increase reduces the LV diastolic compliance and is the primary cause for the inspiration-associated decrease in LV stroke volume and pulse pressure (89,91,134,135). If the pulse pressure change is greater than 10 mmHg, or 10% of the mean pulse pressure, then it is referred to as pulsus paradoxus (2). Since spontaneous inspiratory efforts can also occur during positive-pressure ventilation, the use of ventilation-associated pulse pressure variation (PPV) during positive-pressure ventilation can reflect ventricular interdependence. Presently, positive-pressure–induced changes in pulse pressure and LV stroke volume have been advocated to be a useful parameter of preload-responsiveness (136). However, in order to assess volume responsiveness using PPV, it is essential that no spontaneous inspiratory efforts be present. These points are discussed in greater detail in the next section.


Changes in ITP can directly and indirectly alter LV afterload by altering both LV end-diastolic volume and ejection pressure. LV ejection pressure can be estimated as arterial pressure relative to ITP. Since baroreceptor mechanisms located in the extrathoracic carotid body maintain arterial pressure constant relative to atmosphere, if arterial pressure were to remain constant as ITP increased, then transmural LV pressure and thus LV afterload would decrease. Similarly, if transmural arterial pressure were to remain constant as ITP decreased then LV wall tension would increase (137). Thus, under steady-state conditions, increases in ITP decrease LV afterload and decreases in ITP increase LV afterload (138,139). The spontaneous inspiration-associated decrease in ITP-induced increase in LV afterload is one of the major mechanisms thought to be operative in the wean-induced LV ischemia described in the first part of this chapter, since increased LV afterload must increase myocardial O2 consumption (MVO2). Thus, spontaneous ventilation not only increases global O2 demand by its exercise component (3–5), but also increases MVO2.


Profoundly negative swings in ITP commonly occur during forced spontaneous inspiratory efforts in patients with bronchospasm and obstructive breathing. This condition may rapidly deteriorate into acute heart failure and pulmonary edema (65), as has been described for airway obstruction (asthma, upper airway obstruction, vocal cord paralysis) or stiff lungs (interstitial lung disease, pulmonary edema, and ALI), as these swings may selectively increase LV afterload and may be the cause of the LV failure and pulmonary edema (1,51,65,66) seen, especially if LV systolic function is already compromised (13,140). Clearly, weaning from mechanical ventilation is a selective LV stress test (137,141,142). Similarly, improved LV systolic function is observed in patients with severe LV failure placed on mechanical ventilation (142).


The improvement in LV functional seen with positive-pressure ventilation in subjects with severe heart failure is self-limited, because venous return also decreases, limiting total blood flow. However, the effect of removing large negative swings of ITP on LV performance will also act to reduce LV afterload, but will not be associated with a change in venous return because, until ITP becomes positive, venous return remains constant. Thus, removing negative ITP swings on LV afterload will selectively reduce LV afterload in a fashion analogous to increasing ITP, but without the effect on CO (23,29,103,143–145). This concept has been validated to be a very important clinical approach for patients with obstructive sleep apnea. For example, the cardiovascular benefits of positive airway pressure in nonintubated patients can be seen with CPAP therapy for heart failure patients (146,147). Even low levels of CPAP, if they inhibit airway obstruction, will be beneficial (148,149). Prolonged nighttime nasal CPAP can selectively improve respiratory muscle strength, as well as LV contractile function if the patients have pre-existent heart failure (150,151); these benefits are associated with reductions of serum catecholamine levels (152). Furthermore, CPAP therapy now forms the fundamental first step in the management of acute cardiogenic pulmonary edema, because it both abolishes the negative swings in ITP during inspiration while sustaining alveolar oxygenation, and it does this from the very first breath it delivers (153,154).


USING HEART–LUNG INTERACTIONS TO DIAGNOSE CARDIOVASCULAR INSUFFICIENCY


Since the cardiovascular response to positive-pressure breathing is determined by the baseline cardiovascular state, ventilation-associated changes in arterial pulse pressure and stroke volume should be inferential for dynamic changes in venous return and the responsiveness of the heart to these transient and cyclic changes in preload (155). Both arterial pulse pressure (diastole to systole) and systolic pressure variations during positive-pressure ventilation nicely describe preload-responsiveness, with threshold values of greater than 10% variability compared to mean values in a patient on 8 mL/kg or more, adapted to the ventilation and without dysrhythmias (136). This technique can be modified to assess stroke volume variation (SVV) (156) and has profound clinical potential as newer monitoring devices allow for the bedside display of both PPV and SVV. In subjects on controlled mechanical ventilation, a PPV of more than 13% or an SVV of more than 10% accurately predict preload-responsiveness. Since a primary cardiovascular management decision in shock is whether or not to give intravascular fluids to increase blood flow (157), knowing if a patient is volume responsive before giving fluids will both prevent overhydration of nonresponsive patients and aid in monitoring the response to fluid resuscitation in responsive ones. This approach has been termed functional hemodynamic monitoring because it uses a repetitive known physiologic perturbation to drive a readout physiologic signal defining cardiovascular reserve. This application of heart–lung interactions has been validated in many prospective clinical trials, reviewed in a meta-analysis (158). This practical application of heart–lung interactions is now commonplace. Importantly, a basic understanding of the principles described in this chapter is an essential part of the training of acute care physicians. For example, the ITP-induced PPV and SVV, caused by the positive pressure breath, would be inaccurate if tidal volume were to vary from breath to breath. Similarly, if chest wall compliance were to decrease, owing to increased intra-abdominal pressure limiting diaphragmatic descent, then the accuracy of these measures would also decline.


Many functional hemodynamic monitoring approaches take advantage of these dynamic transients to measure either the capacity of the ventricles to fill as the pressure gradient for ventricular filling changes, or for the ventricles to proportionally eject this varying amount of volume (159). As described above, both spontaneous and positive-pressure breathing, by altering the pressure gradients for venous return to the right ventricle, can be used to assess both right and left ventricular preload reserve (160). For dynamic changes in venous return to alter LV stroke volume or arterial pulse pressure, then both RV and LV preload reserve need to be present. Dynamic venous flow changes during spontaneous and positive-pressure ventilation identify RV preload reserve, and can be measured indirectly by the dynamic changes in inferior vena caval (161), superior vena caval (162), and internal jugular venous diameters (163). Threshold values above 10% to 15% change in diameter define volume-responsiveness.


Because both SVV and PPV sensitivity degrade during spontaneous ventilation, low tidal volume ventilation, severe cor pulmonale and other extremes of physiology (164), alterative tests have been proposed. Specifically, performing passive leg-raising maneuvers to transiently increase venous return while concomitantly monitoring transient changes in left-sided CO is very sensitive and specific predictor of volume responsiveness under most conditions (165). It also becomes inaccurate when intra-abdominal hypertension exists because the pressure gradient for venous return is altered less (166).


Key Points




  • Spontaneous ventilation is exercise.

    • Failure to wean may connote cardiovascular insufficiency.
    • Weaning is a cardiovascular stress test.
    • Breathing loads both the heart and lungs.

  • Changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa in a fashion analogous to cardiac tamponade.

    • Low lung volumes increase pulmonary vasomotor tone by stimulating hypoxic pulmonary vasoconstriction.
    • High lung volumes increase pulmonary vascular resistance by increasing transpulmonary pressure.

  • Spontaneous inspiration and spontaneous inspiratory efforts decrease intrathoracic pressure.

    • Increasing venous return.
    • Increasing LV afterload.

  • Positive-pressure ventilation increases intrathoracic pressure.

    • Decreasing venous return.
    • The decrease in venous return is mitigated by the associated increase in intra-abdominal pressure.
    • Decreasing LV afterload.
    • Abolishing negative swings in ITP selectively reduces LV afterload without reducing venous return.

ACKNOWLEDGMENTS


Supported in part by the NIH grants HL074316, HL120877 HL07820, and NR013912.


References



  1. Bromberger-Barnea B. Mechanical effects of inspiration on heart functions: a review. Fed Proc. 1981;40:2172–2177.
  2. Wise RA, Robotham JL, Summer WR. Effects of spontaneous ventilation on the circulation. Lung. 1981;159:175–192.
  3. Roussos C, Macklem PT. The respiratory muscles. N Engl J Med. 1982; 307:786–797.
  4. Grenvik A. Respiratory, circulatory and metabolic effects of respiratory treatment. Acta Anaesthesiol. 1966. (19 Suppl):1–122.
  5. Shuey CB, Pierce AK, Johnson RL. An evaluation of exercise tests in chronic obstructive lung disease. J Appl Physiol. 1969;27:256–261.
  6. Stock MC, David DW, Manning JW, Ryan ML. Lung mechanics and oxygen consumption during spontaneous ventilation and severe heart failure. Chest. 1992;102:279–283.
  7. Kawagoe Y, Permutt S, Fessler HE. Hyperinflation with intrinsic PEEP and respiratory muscle blood flow. J Appl Physiol (1985). 1994;77:2440–2448.
  8. Aubier M, Vires N, Sillye G, et al. Respiratory muscle contribution to lactic acidosis in low cardiac output. Am Rev Respir Dis. 1982;126:648–652.
  9. Frazier SK, Stone KS, Schertel ER, et al. A comparison of hemodynamic changes during the transition from mechanical ventilation to T-piece, pressure support, and continuous positive airway pressure in canines. Biol Res Nurs. 2000;1:253–264.
  10. Magder S, Erian R, Roussos C. Respiratory muscle blood flow in oleic acid-induced pulmonary edema. J Appl Physiol. 1986;60:1849–1856.
  11. Vires N, Sillye G, Rassidakis A, et al. Effect of mechanical ventilation on respiratory muscle blood flow during shock. Physiologist. 1980;23:1–8.
  12. Baratz DM, Westbrook PR, Shah K, Mohsenifar Z. Effects of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure. Chest. 1992;102:1397–1401.
  13. Lemaire F, Teboul JL, Cinoti J, et al. Acute left ventricular dysfunction during unsuccessful weaning from mechanical ventilation. Anesthesiology. 1988;69:171–179.
  14. Richard C, Teboul JL, Archambaud F, et al. Left ventricular dysfunction during weaning in patients with chronic obstructive pulmonary disease. Intensive Care Med. 1994;20:171–172.
  15. Hurford WE, Lynch KE, Strauss HW, et al. Myocardial perfusion as assessed by thallium-201 scintigraphy during the discontinuation of mechanical ventilation in ventilator-dependent patients. Anesthesiology. 1991;74:1007–1016.
  16. Abalos A. Leibowitz AB, Distefano D, et al. Myocardial ischemia during the weaning period. Am J Crit Care. 1992;1:32–36.
  17. Chatila W, Ani S, Guaglianone D, et al. Cardiac ischemia during weaning from mechanical ventilation. Chest. 1996;109:1421–1422.
  18. Srivastava S, Chatila W, Amoateng-Adjepong Y, et al. Myocardial ischemia and weaning failure in patients with coronary disease: an update. Crit Care Med. 1999;27:2109–2112.
  19. Mohsenifar Z, Hay A, Hay J, et al. Gastric intramural pH as a predictor of success or failure in weaning patients from mechanical ventilation. Ann Intern Med. 1993;119:794–798.
  20. Jabran A, Mathru M, Dries D, Tobin MJ. Continuous recordings of mixed venous oxygen saturation during weaning from mechanical ventilation and the ramifications thereof. Am J Respir Crit Care Med. 1998; 158:1763–1769.
  21. Straus C, Lewis B, Isebey D, et al. Contribution of the endotracheal tube and the upper airway to breathing workload. Am J Respir Crit Care Med. 1998;157:23–30.
  22. Rasanen J, Nikki P, Heikkila J. Acute myocardial infarction complicated by respiratory failure: the effects of mechanical ventilation. Chest. 1984;85:21–28.
  23. Rasanen J, Vaisanen IT, Heikkila J, et al. Acute myocardial infarction complicated by left ventricular dysfunction and respiratory failure: the effects of continuous positive airway pressure. Chest. 1985;87:156–162.
  24. Gruartmoner G, Mesquida J, Masip J, et al. Tissue oxygen saturation (StO2) during weaning from mechanical ventilation: an observational study. Eur Respir J. 2014;43:143–150.
  25. Dres M, Teboul JL, Anguel N, et al. Passive leg raising performed before a spontaneous breathing trial predicts weaning-induced cardiac dysfunction. Intensive Care Med. 2015;41:487–494.
  26. Cournaud A, Motley HL, Werko L, et al. Physiologic studies of the effect of intermittent positive pressure breathing on cardiac output in man. Am J Physiol. 1948;152:162–174.
  27. Tyberg JV, Grant DA, Kingma I, et al. Effects of positive intrathoracic pressure on pulmonary and systemic hemodynamics. Respir Physiol. 2000;119:171–179.
  28. Milic-Emili J, Mead J, Turner JM, Glauser EM. Improved method for assessing the validity of the esophageal balloon technique. J Appl Physiol. 1964;19: 207–211.
  29. Braunwald E, Binion JT, Morgan WL Jr, Sarnoff SJ. Alterations in central blood volume and cardiac output induced by positive pressure breathing and counteracted by metraminol (Aramine). Circ Res. 1957;5:670–675.
  30. Whittenberger JL, McGregor M, Berglund E, Borst HG. Influence of state of inflation of the lung on pulmonary vascular resistance. J Appl Physiol. 1960;15:878–882.
  31. Novak RA, Matuschak GM, Pinsky MR. Effect of ventilatory frequency on regional pleural pressure. J Appl Physiol. 1988;65:1314–1323.
  32. Kingma I, Smiseth OA, Frais MA, et al. Left ventricular external constraint: relationship between pericardial, pleural and esophageal pressures during positive end-expiratory pressure and volume loading in dogs. Ann Biomed Eng. 1987;15:331–346.
  33. Tsitlik JE, Halperin HR, Guerci AD, et al. Augmentation of pressure in a vessel indenting the surface of the lung. Ann Biomed Eng. 1987; 15:259–284.
  34. Pinsky MR, Guimond JG. The effects of positive end- expiratory pressure on heart-lung interactions. J Crit Care. 1991;6:1–11.
  35. Romand JA, Shi W, Pinsky MR. Cardiopulmonary effects of positive pressure ventilation during acute lung injury. Chest. 1995;108:1041–1048.
  36. O’Quinn RJ, Marini JJ, Culver BH, et al. Transmission of airway pressure to pleural pressure during lung edema and chest wall restriction. J Appl Physiol. 1985;59:1171–1177.
  37. Gattinoni L, Mascheroni D, Torresin A, et al. Morphological response to positive end-expiratory pressure in acute respiratory failure. Intensive Care Med. 1986;12:137–142.
  38. Globits S, Burghuber OC, Koller J, et al. Effect of lung transplantation on right and left ventricular volumes and function measured by magnetic resonance imaging. Am J Respir Crit Care Med. 1994;149:1000–1004.
  39. Scharf SM, Ingram RH Jr. Effects of decreasing lung compliance with oleic acid on the cardiovascular response to PEEP. Am J Physiol. 1977; 233:H635–H641.
  40. Pinsky MR, Vincent JL, DeSmet JM. Estimating left ventricular filling pressure during positive end-expiratory pressure in humans. Am Rev Respir Dis. 1991;143:25–31.
  41. Teboul JL, Pinsky MR, Mercat A, et al. Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med. 2000;28:3631–3636.
  42. Glick G, Wechsler AS, Epstein DE. Reflex cardiovascular depression produced by stimulation of pulmonary stretch receptors in the dog. J Clin Invest. 1969;48:467–472.
  43. Painal AS. Vagal sensory receptors and their reflex effects. Physiol Rev. 1973;53:59–88.
  44. Anrep GV, Pascual W, Rossler R. Respiratory variations in the heart rate. I. The reflex mechanism of the respiratory arrhythmia. Proc R Soc Lond B Biol Sci. 1936;119:191–217.
  45. Taha BH, Simon PM, Dempsey JA, et al. Respiratory sinus arrhythmia in humans: an obligatory role for Vagal feedback from the lungs. J Appl Physiol (1985). 1995;78:638–645.
  46. Bernardi L, Calciati A, Gratarola A, et al. Heart rate-respiration relationship: computerized method for early detection of cardiac autonomic damage in diabetic patients. Acta Cardiol. 1986;41:197–206.
  47. Persson MG, Lonnqvist PA, Gustafsson LE. Positive end-expiratory pressure ventilation elicits increases in endogenously formed nitric oxide as detected in air exhaled by rabbits. Anesthesiology. 1995;82:969–974.
  48. Cassidy SS, Eschenbacher WI, Johnson RL Jr. Reflex cardiovascular depression during unilateral lung hyperinflation in the dog. J Clin Invest. 1979;64:620–626.
  49. Daly MB, Hazzledine JL, Ungar A. The reflex effects of alterations in lung volume on systemic vascular resistance in the dog. J Physiol. 1967; 188:331–351.
  50. Shepherd JT. The lungs as receptor sites for cardiovascular regulation. Circulation. 1981;63:1–10.
  51. Stalcup SA, Mellins RB. Mechanical forces producing pulmonary edema in acute asthma. N Engl J Med. 1977;297:592–596.
  52. Vatner SF, Rutherford JD. Control of the myocardial contractile state by carotid chemo- and baroreceptor and pulmonary inflation reflexes in conscious dogs. J Clin Invest. 1978;63:1593–1601.
  53. Karlocai K, Jokkel G, Kollai M. Changes in left ventricular contractility with the phase of respiration. J Auton Nerv Syst. 1998;73:86–92.
  54. Said SI, Kitamura S, Vreim C. Prostaglandins: release from the lung during mechanical ventilation at large tidal ventilation. J Clin Invest. 1972; 51:83a.
  55. Bedetti C, Del Basso P, Argiolas C, Carpi A. Arachidonic acid and pulmonary function in a heart-lung preparation of guinea-pig: modulation by PCO2. Arch Int Pharmacodyn Ther. 1987;285:98–116.
  56. Berend N, Christopher KL, Voelkel NF. Effect of positive end- expiratory pressure on functional residual capacity: role of prostaglandin production. Am Rev Respir Dis. 1982;126:641–647.
  57. Pattern MY, Liebman PR, Hetchman HG. Humorally mediated decreases in cardiac output associated with positive end-expiratory pressure. Microvasc Res. 1977;13:137–144.
  58. Berglund JE, Halden E, Jakobson S, Svensson J. PEEP ventilation does not cause humorally mediated cardiac output depression in pigs. Intensive Care Med. 1994;20:360–364.
  59. Fuhrman BP, Everitt J, Lock JE. Cardiopulmonary effects of unilateral airway pressure changes in intact infant lambs. J Appl Physiol Respir Environ Exerc Physiol. 1984;56:1439–1448.
  60. Payen DM, Brun-Buisson CJ, Carli PA, et al. Hemodynamic, gas exchange, and hormonal consequences of LBPP during PEEP ventilation. J Appl Physiol. 1987;62:61–70.
  61. Frage D, de la Coussaye JE, Beloucif S, et al. Interactions between hormonal modifications during PEEP-induced antidiuresis and antinatriuresis. Chest. 1995;107:1095–1100.
  62. Frass M, Watschinger B, Traindl O, et al. Atrial natrituretic peptide release in response to different positive end-expiratory pressure levels. Crit Care Med. 1993;21:343–347.
  63. Wilkins MA, Su XL, Palayew MD, et al. The effects of posture change and continuous positive airway pressure on cardiac natriuretic peptides in congestive heart failure. Chest. 1995;107:909–915.
  64. Shirakami G, Magaribuchi T, Shingu K, et al. Positive end-expiratory pressure ventilation decreases plasma atrial and brain natriuretic peptide levels in humans. Anesth Analg. 1993;77:1116–1121.
  65. Fletcher EC, Proctor M, Yu J, et al. Pulmonary edema develops after recurrent obstructive apneas. Am J Respir Crit Care Med. 1999;160:1688–1696.
  66. Chen L, Shi Q, Scharf SM. Hemodynamic effects of periodic obstructive apneas in sedated pigs with congestive heart failure. J Appl Physiol. 2000;88:1051–1060.
  67. Maughan WL, Shoukas AA, Sagawa K, Weisfeldt ML. Instantaneous pressure-volume relationships of the canine right ventricle. Circ Res. 1979; 44:309–315.
  68. Sibbald WJ, Driedger AA. Right ventricular function in disease states: pathophysiologic considerations. Crit Care Med. 1983;11:339–345.
  69. Piene H, Sund T. Does pulmonary impedance constitute the optimal load for the right ventricle? Am J Physiol. 1982;242:H154–H160.
  70. Pinsky MR. Determinants of pulmonary arterial flow variation during respiration. J Appl Physiol. 1984;56:1237–1245.
  71. Theres H, Binkau J, Laule M, et al. Phase-related changes in right ventricular cardiac output under volume-controlled mechanical ventilation with positive end-expiratory pressure. Crit Care Med. 1999;27:953–958.
  72. Johnston WE, Vinten-Johansen J, Shugart HE, Santamore WP. Positive end-expiratory pressure potentates the severity of canine right ventricular ischemia-reperfusion injury. Am J Physiol. 1992;262:H168–H176.
  73. Madden JA, Dawson CA, Harder DR. Hypoxia-induced activation in small isolated pulmonary arteries from the cat. J Appl Physiol. 1985;59: 113–118.
  74. Hakim TS, Michel RP, Chang HK. Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion. J Appl Physiol. 1982;53:1110–1115.
  75. Quebbeman EJ, Dawson CA. Influence of inflation and atelectasis on the hypoxic pressure response in isolated dog lung lobes. Cardiovas Res. 1976;10:672–677.
  76. Brower RG, Gottlieb J, Wise RA, et al. Locus of hypoxic vasoconstriction in isolated ferret lungs. J Appl Physiol. 1987;63:58–65.
  77. Hakim TS, Michel RP, Minami H, Chang K. Site of pulmonary hypoxic vasoconstriction studied with arterial and venous occlusion. J Appl Physiol. 1983;54:1298–1302.
  78. Marshall BE, Marshall C. A model for hypoxic constriction of the pulmonary circulation. J Appl Physiol. 1988;64:68–77.
  79. Marshall BE, Marshall C. Continuity of response to hypoxic pulmonary vasoconstriction. J Appl Physiol. 1980;49:189–196.
  80. Dawson CA, Grimm DJ, Linehan JH. Lung inflation and longitudinal distribution of pulmonary vascular resistance during hypoxia. J Appl Physiol Respir Environ Exerc Physiol. 1979;47:532–536.
  81. Howell JB, Permutt S, Proctor DF, et al. Effect of inflation of the lung on different parts of the pulmonary vascular bed. J Appl Physiol. 1961; 16:71–76.
  82. West JB, Dollery CT, Naimark A. Distribution of blood flow in isolated lung: relation to vascular and alveolar pressures. J Appl Physiol. 1964;19:713–724.
  83. Fuhrman BP, Smith-Wright DL, Kulik TJ, Lock JE. Effects of static and fluctuating airway pressure on the intact, immature pulmonary circulation. J Appl Physiol. 1986;60:114–122.
  84. Thorvalson J, Ilebekk A, Kiil F. Determinants of pulmonary blood volume: effects of acute changes in airway pressure. Acta Physiol Scand. 1985;125:471–479.
  85. Lopez-Muniz R, Stephens NL, Bromberger-Barnea B, et al. Critical closure of pulmonary vessels analyzed in terms of Starling resistor model. J Appl Physiol. 1968;24:625–635.
  86. Block AJ, Boyson PG, Wynne JW. The origins of cor pulmonale, a hypothesis. Chest. 1979;75:109–114.
  87. Vieillard-Baron A, Loubieres Y, Schmitt JM, et al. Cyclic changes in right ventricular output impedance during mechanical ventilation. J Appl Physiol. 1999;87:1644–1650.
  88. Canada E, Benumnof JL, Tousdale FR. Pulmonary vascular resistance correlated in intact normal and abnormal canine lungs. Crit Care Med. 1982;10:719–723.
  89. Vieillard-Baron A, Schmitt JM, et al. Acute cor pulmonale in acute respiratory distress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis. Crit Care Med. 2001;29:1551–1555.
  90. Taylor RR, Corell JW, Sonnenblick EH, Ross J Jr. Dependence of ventricular distensibility on filling the opposite ventricle. Am J Physiol. 1967;213:711–718.
  91. Brinker JA, Weiss I, Lappe DL, et al. Leftward septal displacement during right ventricular loading in man. Circulation. 1980;61:626–633.
  92. Takata M, Harasawa Y, Beloucif S, Robotham JL. Coupled vs. uncoupled pericardial restraint: effects on cardiac chamber interactions. J Appl Physiol. 1997;83:1799–1813.
  93. Marini JJ, Culver BN, Butler J. Mechanical effect of lung distention with positive pressure on cardiac function. Am Rev Respir Dis. 1980; 124:382–386.
  94. Butler J. The heart is in good hands. Circulation. 1983;67:1163–1168.
  95. Cassidy SS, Wead WB, Seibert GB, Ramanathan M. Changes in left ventricular geometry during spontaneous breathing. J Appl Physiol. 1987;63: 803–811.
  96. Hoffman EA, Ritman EL. Heart–lung interaction: effect on regional lung air content and total heart volume. Ann Biomed Eng. 1987;15:241–257.
  97. Olson LE, Hoffman EA. Heart–lung interactions determined by electron beam x-ray CT in laterally recumbent rabbits. J Appl Physiol. 1995;78: 417–427.
  98. Jayaweera AR, Ehrlich W. Changes of phasic pleural pressure in awake dogs during exercise: potential effects on cardiac output. Ann Biomed Eng. 1987;15:311–318.
  99. Cassidy SS, Robertson CH Jr, Pierce AK, et al. Cardiovascular effects of positive end-expiratory pressure in dogs. J Appl Physiol. 1978;4:743–749.
  100. Conway CM. Hemodynamic effects of pulmonary ventilation. Br J Anaesth. 1975;47:761–766.
  101. Jardin F, Farcot JC, Boisante L. Influence of positive end-expiratory pressure on left ventricular performance. N Engl J Med. 1981;304:387–392.
  102. Berglund JE, Halden E, Jakobson S, Landelius J. Echocardiographic analysis of cardiac function during high PEEP ventilation. Intensive Care Med. 1994;20:174–180.
  103. Guyton AC, Lindsey AW, Abernathy B, et al. Venous return at various right atrial pressures and the normal venous return curve. Am J Physiol. 1957; 189:609–615.
  104. Goldberg HS, Rabson J. Control of cardiac output by systemic vessels: circulatory adjustments of acute and chronic respiratory failure and the effects of therapeutic interventions. Am J Cardiol. 1981;47:696–702.
  105. Pinsky MR. Instantaneous venous return curves in an intact canine preparation. J Appl Physiol Respir Environ Exerc Physiol. 1984;56:765–771.
  106. Kilburn KH. Cardiorespiratory effects of large pneumothorax in conscious and anesthetized dogs. J Appl Physiol. 1963;18:279–283.
  107. Chevalier PA, Weber KC, Engle JC, et al. Direct measurement of right and left heart outputs in Valsalva-like maneuver in dogs. Proc Soc Exper Biol Med. 1972;139:1429–1437.
  108. Guntheroth WC, Gould R, Butler J, et al. Pulsatile flow in pulmonary artery, capillary and vein in the dog. Cardiovasc Res. 1974;8:330–337.
  109. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade: mechanism of pulsus paradoxus. Circ Res. 1967;20:381–390.
  110. Guyton AC. Effect of cardiac output by respiration, opening the chest, and cardiac tamponade. In: Circulatory Physiology: Cardiac Output and Its Regulation. Philadelphia, PA: Saunders; 1963:378–386.
  111. Holt JP. The effect of positive and negative intrathoracic pressure on cardiac output and venous return in the dog. Am J Physiol. 1944;142:594–603.
  112. Morgan BC, Abel FL, Mullins GL, et al. Flow patterns in cavae, pulmonary artery, pulmonary vein and aorta in intact dogs. Am J Physiol. 1966;210:903–909.
  113. Morgan BC, Martin WE, Hornbein TF, et al. Hemodynamic effects of intermittent positive pressure respiration. Anesthesiology. 1960;27:584–590.
  114. Scharf SM, Brown R, Saunders N, Green LH. Hemodynamic effects of positive pressure inflation. J Appl Physiol. 1980;49:124–131.
  115. Jardin F, Vieillard-Baron A. Right ventricular function and positive-pressure ventilation in clinical practice: from hemodynamic subsets to respirator settings. Intensive Care Med. 2003;29:1426–1434.
  116. Scharf SM, Brown R, Saunders N, et al. Effects of normal and loaded spontaneous inspiration on cardiovascular function. J Appl Physiol. 1979;47:582–590.
  117. Groeneveld AB, Berendsen RR, Schneider AJ, et al. Effect of the mechanical ventilatory cycle on thermodilution right ventricular volumes and cardiac output. J Appl Physiol (1985). 2000;89:89–96.
  118. Van den Berg P, Jansen JR, Pinsky MR. The effect of positive-pressure inspiration on venous return in volume loaded post-operative cardiac surgical patients. J Appl Physiol (1985). 2002;92:1223–1231.
  119. Magder S, Georgiadis G, Cheong T. Respiratory variation in right atrial pressure predict the response to fluid challenge. J Crit Care. 1992;7:76–85.
  120. Harken AH, Brennan MF, Smith N, Barsamian EM. The hemodynamic response to positive end-expiratory ventilation in hypovolemic patients. Surgery. 1974;76:786–793.
  121. Fessler HE, Brower RG, Wise RA, Permutt S. Effects of positive end-expiratory pressure on the canine venous return curve. Am Rev Respir Dis. 1992;146:4–10.
  122. Takata M, Robotham JL. Effects of inspiratory diaphragmatic descent on inferior vena caval venous return. J Appl Physiol (1985). 1992;72:597–607.
  123. Matuschak GM, Pinsky MR, Rogers RM. Effects of positive end-expiratory pressure on hepatic blood flow and hepatic performance. J Appl Physiol (1985). 1987;62:1377–1383.
  124. Chihara E, Hasimoto S, Kinoshita T, et al. Elevated mean systemic filling pressure due to intermittent positive-pressure ventilation. Am J Physiol. 1992;262:H1116–H1121.
  125. Takata M, Wise RA, Robotham JL. Effects of abdominal pressure on venous return: abdominal vascular zone conditions. J Appl Physiol (1985). 1990;69:1961–1972.
  126. Barnes GE, Laine GA, Giam PY, et al. Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol. 1985;248:R208–R213.
  127. Lichtwarck-Aschoff M, Zeravik J, Pfeiffer UJ. Intrathoracic blood volume accurately reflects circulatory volume status in critically ill patients with mechanical ventilation. Intensive Care Med. 1992;18:142–145.
  128. Brecher GA, Hubay CA. Pulmonary blood flow and venous return during spontaneous respiration. Circ Res. 1955;3:40–214.
  129. Terada N, Takeuchi T. Postural changes in venous pressure gradients in anesthetized monkeys. Am J Physiol. 1993;264:H21–H25.
  130. Scharf S, Tow DE, Miller MJ, et al. Influence of posture and abdominal pressure on the hemodynamic effects of Mueller’s maneuver. J Crit Care. 1989;4:26–34.
  131. Rankin JS, Olsen CO, Arentzen CE, et al. The effects of airway pressure on cardiac function in intact dogs and man. Circulation. 1982;66:108–120.
  132. Robotham JL, Rabson J, Permutt S, Bromberger-Barnea B. Left ventricular hemodynamics during respiration. J Appl Physiol. 1979;47:1295–1303.
  133. Ruskin J, Bache RJ, Rembert JC, Greenfield JC Jr. Pressure-flow studies in man: effect of respiration on left ventricular stroke volume. Circulation. 1973;48:79–85.
  134. Olsen CO, Tyson GS, Maier GW, et al. Dynamic ventricular interaction in the conscious dog. Circ Res. 1983;52:85–104.
  135. Janicki JS, Weber KT. The pericardium and ventricular interaction, distensibility and function. Am J Physiol. 1980;238:H494–H503.
  136. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med. 2000;162:134–138.
  137. Beyar R, Goldstein Y. Model studies of the effects of the thoracic pressure on the circulation. Ann Biomed Eng. 1987;15:373–383.
  138. Buda AJ, Pinsky MR, Ingels NB, et al. Effect of intrathoracic pressure on left ventricular performance. N Engl J Med. 1979;301:453–459.
  139. Pinsky MR, Summer WR, Wise RA, et al. Augmentation of cardiac function by elevation of intrathoracic pressure. J Appl Physiol. 1983;54: 950–955.
  140. Beach T, Millen E, Grenvik A. Hemodynamic response to discontinuance of mechanical ventilation. Crit Care Med. 1973;1:85–90.
  141. Cassidy SA, Wead WB, Seibert GB, Ramanathan M. Geometric left-ventricular responses to interactions between the lung and left ventricle: positive pressure breathing. Ann Biomed Eng. 1987;15:285–295.
  142. Scharf SM, Brown R, Warner KG, Khuri S. Intrathoracic pressure and left ventricular configuration with respiratory maneuvers. J Appl Physiol. 1989;66:481–491.
  143. Sharpey-Schaffer EP. Effects of Valsalva maneuver on the normal and failing circulation. Br Med J. 1955;1:693–699.
  144. Khilnani S, Graver LM, Balaban K, Scharf SM. Effects of inspiratory loading on left ventricular myocardial blood flow and metabolism. J Appl Physiol. 1992;72:1488–1492.
  145. Sibbald WH, Calvin J, Driedger AA. Right and left ventricular preload, and diastolic ventricular compliance: implications of therapy in critically ill patients. Critical Care State of the Art. Vol 3. Fullerton, CA: Society of Critical Care; 1982.
  146. DeHoyos A, Liu PP, Benard DC, Bradley TD. Haemodynamic effects of continuous positive airway pressure in humans with normal and impaired left ventricular function. Clin Sci Colch. 1995;88:173–178.
  147. Naughton MT, Rahman MA, Hara K, et al. Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure. Circulation. 1995;91:1725–1731.
  148. Philip-Joet FF, Paganelli FF, Dutau HL, Saadjian AY. Hemodynamic effects of bi-level nasal positive airway pressure ventilation in patients with heart failure. Respiration. 1999;66:136–143.
  149. Buckle P, Millar T, Kryger M. The effect of short-term nasal CPAP on Cheyne-Stokes respiration in congestive heart failure. Chest. 1992;102:31–35.
  150. Granton JT, Naughton MT, Benard DC, et al. CPAP improves inspiratory muscle strength in patients with heart failure and central sleep apnea. Am J Respir Crit Care Med. 1996;153:277–282.
  151. Kaneko Y, Floras JS, Usui K, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003;348:1233–1241.
  152. Naughton MT, Benard DC, Liu PP, et al. Effects of nasal CPAP on sympathetic activity in patients with heart failure and central sleep apnea. Am J Respir Crit Care Med. 1995;152:473–479.
  153. Lin M, Yang YF, Chiang HT, et al. Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow-up. Chest. 1995;107:1379–1386.
  154. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med. 1991;325(26);1825–1830.
  155. Denault AY, Gasior TA, Gorcsan J 3rd, et al. Determinants of aortic pressure variation during positive-pressure ventilation in man. Chest. 1999;116:176–186.
  156. Monnet X, Rienzo M, Osman D, et al. Esophageal Doppler monitoring predicts fluid responsiveness in critically ill ventilated patients. Intensive Care Med. 2005;31(9):1195–1201.
  157. Cecconi M, De Backer D, Antonelli M, et al. Consensus on Circulatory Shock and Hemodynamic Monitoring, Task Force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014;49:1795–1815.
  158. Benes J, Giglio M, Brienza N, Michard F. The effects of goal-directed fluid therapy based on dynamic parameters on post-surgical outcome: a meta-analysis of randomized controlled trials. Crit Care. 2014;18:584.
  159. Perner A, De Backer D. Understanding hypovolaemia. Intensive Care Med. 2014;40:613–615.
  160. Pinsky MR. The hemodynamic consequences of mechanical ventilation: an evolving story. Intensive Care Med. 1997;23:493–503.
  161. Feissel M, Michard F, Faller J, Teboul JL. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med. 2004;30:1834–1837.
  162. Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena cava collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med. 2004;30:1734–1739.
  163. Guarracino F, Ferro B, Forfori F, et al. Jugular vein distensibility predicts fluid responsiveness in septic patients. Crit Care. 2014;18:647.
  164. De Backer D, Heenen S, Piagnerelli M, et al. Pulse pressure variations to predict fluid responsiveness: influence of tidal volume. Intensive Care Med. 2005;31:517–523.
  165. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. 2006;34:1402–1407.
  166. Mahjoub Y, Touzeau J, Airapetian N, et al. The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension. Crit Care Med. 2010;38:1824–1829.

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Feb 26, 2020 | Posted by in CRITICAL CARE | Comments Off on Heart–Lung Interactions

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