Cardiovascular Effects of Mechanical Ventilation G. J. DUKE Intensive Care Department, The Northern Hospital, Epping, VICTORIA ABSTRACT Objective: To review the cardiovascular effects of spontaneous breathing and mechanical ventilation in healthy and pathological states. Data sources: A review of articles published in peer-reviewed journals from 1966 to 1998 and identified through a MEDLINE search on cardiopulmonary interaction. Summary of review: Respiration has a hydraulic influence upon cardiovascular function. Pulmonary and cardiac pathology alter this interaction. Spontaneous inspiration increases right ventricular (RV) preload and left ventricular (LV) afterload. Mechanical ventilation with positive pressure (MV) reduces LV preload and afterload. The influence of MV upon the cardiovascular system (CVS), particularly in critically ill patients, depends upon the mode of ventilation and the pre-existing cardiac and respiratory status. The influence of these factors is reviewed. Consideration of these parameters will enable the clinician to predict the likely effect of MV and develop strategies to minimise adverse events. Conclusions: Mechanical ventilation has an adverse effect upon the CVS in healthy subjects and in patients with pulmonary pathology, particularly in the presence of preload-dependent LV dysfunction or afterload-induced RV dysfunction. Mechanical ventilation may benefit cardiac function in patients with respiratory failure and afterload-dependent or exercise-induced LV dysfunction. (Critical Care and Resuscitation 1999; 1: 388-399) Key Words: Mechanical ventilation, cardiovascular physiology, cardiopulmonary interaction, acute respiratory distress syndrome Respiration and circulation are complementary on cardiac transmural pressure (Ptm) as the predominant physiological processes that interact with each other mechanism.1-3,5 during spontaneous breathing.1,2 The introduction of To appreciate the complex cardiovascular effects of mechanical ventilation (MV), or the presence of MV, especially in critically ill patients, it is prudent first pulmonary and cardiac disease, increases the complex- to identify the cardio-respiratory interactions of ity of this interaction. Research in this area is daunting spontaneous breathing in healthy subjects and in those and interpretation of the data is difficult because these with respiratory and/or cardiac disease, and then and other interrelated variables must be considered. consider the influence of MV in each situation. What is the predominant mechanism underlying this Consideration of cardiovascular and respiratory changes interaction? Explanations have included mechanical over time is also important. An understanding of these (hydraulic),1 neural,3 and humoral mechanisms.4 Phasic interactions should enable the clinician to predict the variation in cardiac function during respiration is closely likely cardiovascular effect of MV in a given clinical linked in time and magnitude to changes in intrathoracic situation. pressure and occurs more rapidly than most neural or humoral processes. Therefore current data support the Thoracic anatomy and transmural pressure hydraulic effect of intrathoracic (pleural) pressure (Ppl) Respiration induces phasic swings in cardiac trans- Correspondence to: Dr. G. J. Duke, Intensive Care Department, The Northern Hospital, Epping, Victoria 3076 (e-mail: [email protected]) 388 Critical Care and Resuscitation 1999; 1: 388-399 G. J. DUKE Figure 1. Schematic representation of cardiorespiratory relationship. Paw = airway pressure, Palv = alveolar pressure, Ppl = intrathoracic pleural pressure, Pex = extramural stress, Pin = intramural stress, Ptm = transmural pressure, Psystole = aortic blood pressure mural pressure (Ptm) as a result of the anatomical and Ppl is lowered by the respiratory muscles during functional proximity of respiratory and cardiovascular spontaneous inspiration and increased during the organs. Ptm is the difference between intramural stress application of positive pressure MV, and the resultant (Pin) and extramural stress (Pex), Ptm = Pin - Pex (Figure ∆Ppl is seen by the heart as a change in extramural 1). pressure (∆Pex). Ppl has a direct influence on cardiac 7,8 1,3 The thorax contains the lungs and pulmonary (epicardial) Pex and thus an influence on LV and RV vasculature (divided into intra- and extra-alveolar volume and function. For example, a fall in Ppl will vessels) and the heart and great vessels (i.e. thoracic usually result in a fall in Pex (rise in Ptm) that will favour aorta and great veins). The proximity of these organs ventricular filling but impede ejection. within the thorax, together with their dynamic The cardiovascular effects of respiration appear to mechanical properties (e.g. volume and elastance) be dependent upon both the magnitude of ∆Ptm and the ensures that changes in lung volume and Ppl are likely to sensitivity of the cardiovascular system to ∆Ptm. Thus influence cardiac function even during spontaneous the most important clinical variables in breathing. For example, an increase in lung volume cardio-pulmonary interactions include: 1) the produces a non-uniform compression of the lateral cardiovascular status of the subject; 2) the respiratory ventricular wall (Pex) and, although low in magnitude status of the subject, and; 3) the mode of respiration. 6 does influence ventricular function. Accurate measurement of Pex, Pin and ventricular The intra-thoracic cardiovascular system may be volume is important in the assessment of cardio- described as a dual series of pumps (right and left pulmonary interaction. Cardiac Pex is difficult to 6,9 ventricles) separated from each other by the pulmonary measure accurately. The use of surrogate measures of vasculature, and from the systemic circulation by the Pex such as oesophageal or pleural pressure may great veins and thoracic aorta. Since the ventricles are in significantly underestimate Pex particularly in the series, the output of the right ventricle (RV) provides the presence of pulmonary disease or during positive input (venous return) for the left ventricle (LV) with the pressure MV. Pex varies across the surface of the heart, intervening pulmonary circulation producing a lag depending upon the volume and compliance of the time of (usually) 1-2 beats. adjacent lung, pericardium, and cardiac chamber.9 389 G. J. DUKE Critical Care and Resuscitation 1999; 1: 388-399 Indirect measurement of cardiac Pin (e.g. estimation of left ventricular end-diastolic Pin by pulmonary artery catheter) may also be misleading.10-13 More direct measurements of Pex ,Pin, and chamber volume are preferred but usually restricted to animal models. Ventricular interdependence (VI) is another important physiological concept, anatomically based on the adjacent LV and RV sharing a common pericardial sac (with limited volume and compliance) and a common interventricular septum. VI is commonly used to imply that the pressure/volume characteristics of the RV influence those of the LV.7,14-16 Cardiovascular effects of spontaneous breathing To understand the cardiovascular changes resulting from MV it is important to first understand cardio- pulmonary interactions during spontaneous breathing. 2,3 This topic has been extensively reviewed elsewhere Figure 2. Schematic representation of cardiorespiratory interaction and whilst much of the data comes from animal (usually during spontaneous inspiration and cardiac systole. Arrows depict dog) models there is a substantial agreement with direction of change. Spontaneous inspiration increases Ptm and 17 reduces Psystole. Paw = airway pressure, Palv = alveolar pressure, available human data. Ppl = intrathoracic pleural pressure, Pex = extramural stress, Spontaneous inspiration in healthy subjects is usually Pin = intramural stress, Ptm = transmural pressure, Psystole = aortic associated with a small fall in systolic blood pressure (< blood pressure, LV = left ventricle l0 mmHg). Explanations for this observation include: 1) an increase in LV afterload, 2) a decrease in venous Under certain pathological states this inspiratory return, 3) the influence of VI, and, 4) transmission of blood pressure fall is exaggerated and referred to as 3,20,21 reduced intra-thoracic aortic Pex to extrathoracic vessels. ‘pulsus paradoxus’. This may be found where there Both animal and human data indicate that the first is: 1) a greater inspiratory effort and a greater ∆Ppl and 1- 22,23 24 explanation is probably the most important mechanism. ∆Ptm (e.g. acute asthma or pulmonary oedema ), or: 3,7 25 2) an increased sensitivity to ∆Ptm (e.g. hypovolaemia, 3,21 26 Inspiration occurs as a result of the reduction in Ppl tamponade, or congestive cardiac failure ). which is transmitted to the intra-thoracic organs. Whilst During exhalation systolic blood pressure rises as a the primary purpose of this pressure fall is to expand the result of the return of left ventricular afterload to lungs it is also results in a fall in cardiac Pex (and a rise baseline and aided by the augmentation of LV preload in Ptm). The increase in Ptm facilitates right ventricular from the (delayed effect of the) inspiratory rise in RV diastolic filling - the ‘thoracic pump’ mechanism - until output. the closing pressure of the extra-thoracic veins is There is little evidence to suggest other mechanisms 1,3 reached and the resultant increase in RV end-diastolic have a significant influence. The role of VI is volume (RVEDV) increases stroke volume via the equivocal.1 Although there is