The effects of mechanical ventilation on hemodynamics in patients with cardiac tamponade. Mechanical ventilation increases pleural pressure and transpulmonary pressure. During inspiration, left ventricular stroke volume increases because of the increase in left ventricular preload, whereas left ventricular afterload decreases. This leads to an increase in arterial blood pressure at the end of inspiration. In contrast, right ventricular stroke volume decreases during inspiration because of the decrease in right ventricular preload, whereas right ventricular afterload increases. Because of the pulmonary transit time of blood, the inspiratory decrease in right ventricular output causes decreases in left ventricular filling and output only a few heartbeats later, usually during the expiratory period. This, in turn, leads to a decrease in arterial blood pressure at the end of expiration. (Adapted from Michard and Teboul, 15 courtesy of BioMed Central.) 

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... cause a reduction in ventricular filling, systolic volume, and systolic ventricular pressure depending on the contractile state of the ventricle and the level of the intrapericardial pressure. High end-diastolic ventricular pressure and high mean atrial pressure are accompanied by pulmonary and systemic venous hypertension. Although these venous pressures are maintained at a sufficient level with high atrial pressures, the inflow of blood into the ventricles can be maintained. In this situation, cardiac output is maintained primarily by tachycardia. In more advanced stages of tamponade, filling becomes possible only during atrial systole, especially when the heart rate increases. These phenomena lead to the disappearance of the “y” wave, which represents right ventricular filling during diastole on the right atrial pressure records. The “x” wave, which represents atrial filling, is maintained because during ventricular systole there is move- ment of the entire valve plane toward the apex of the ventricle, leading to a reduction of atrial pressure coinciding with ventricular ejection (Fig 1). The hemodynamic changes caused by the pericardial effusion can be categorized into several phases (Table 1). Especially after cardiac surgery, regional cardiac tamponade can occur when any cardiac zone is compressed by loculated effusions, 4,11 which usually are accompanied by localized pericardial adhesions. Loculation can produce classic tamponade (eg, loculated effusions over the right atrium and atrioventricular groove), but more often the typ- ical hemodynamic abnormalities are found only in the compressed chambers or zones. The phenomena described previously occur earlier and at lower pressures in patients with hypovolemia, a situation that is quite frequent in the postoperative period. These patients can develop cardiac tamponade with diastolic pressures as low as 3 to 6 mmHg. Such situations are known as “low-pressure cardiac tamponade” and are extremely difficult to diagnose. 11 Therefore, therapeutically-induced hypovolemia or filling pressure reduction (forced diuresis, vasodilators) may lead to severe impairment in cardiac output and blood pressure, which can be life threatening. Compensating mechanisms in this situation of cardiac tamponade are secondary to adrenergic (alpha and beta) stimulation. The activity exerted by these mechanisms can be summarized into 4 major effects: (1) an increase of heart rate (beta effect), (2) an increase of diastolic relaxation (beta effect), (3) an increase of peripheral resistances to maintain adequate arterial pressure and coronary flow (alpha effect), and (4) an increase in inotropism to achieve an increase in ejection fraction. Respiration also affects intracardiac pressures, particularly those on the right side of the heart. During inspiration, in spontaneously breathing patients without cardiac tamponade, intrathoracic and intrapericardial pressures decrease. This results in augmented flow into the right atrium and right ventricle, with decreased flow out of the pulmonary veins into the left atrium and left ventricle. Reciprocal changes occur during expiration. In the presence of normal intrapericardial pressure, the normal respiratory variation in filling of the left and right heart causes a small (less than 10 mmHg) inspiratory decrease in systemic arterial systolic blood pressure. When the patient is suffering from a cardiac tamponade and is breathing spontaneously, there is an exaggeration of the phenomena described earlier, leading to pulsus paradoxus as a sign of the interven- tricular interdependence. 12,13 Pulsus paradoxus is defined as a decrease of more than 10 mmHg in peripheral arterial pressure during inspiration. 11,14 During positive-pressure mechanical ventilation, the reverse of the conventional pulsus paradoxus has been reported. The inspiratory increase in arterial blood pressure followed by a decrease on expiration has been called “re- versed pulsus paradoxus.” In patients under mechanical ventilation suffering from cardiac tamponade, this phenomenon is more exaggerated. 15 Mechanical ventilation increases pleural pressure and transpulmonary pressure (the difference between alveolar and pleural pressures). During inspiration, left ventricular stroke volume increases because left ventricular preload increases, whereas left ventricular afterload decreases. This leads to an increase in arterial blood pressure at the end of inspiration. In contrast, right ventricular stroke volume decreases during inspiration because venous return and right ventricular preload decrease, while right ventricular afterload increases. Because of the pulmonary transit time of blood (approximately 2 seconds), the inspiratory decrease in right ventricular output causes decreases in left ventricular filling and output only a few heartbeats later, usually during the expiratory period. This corresponds with a decrease in arterial blood pressure at the end of the expiration (Fig 2). Therefore, if positive-pressure ventilation is used with high tidal volumes and high levels of positive end-expiratory pressure, the right ventricular afterload may be increased and the ventricular septum can shift leftward, thereby reduc- ing the distensibility of the left ventricle and, consequently, its preload. 16 In conclusion, in patients with cardiac tamponade, the institution of mechanical ventilation and positive end-expiratory pressure (PEEP) may worsen hemodynamic status with reversed pulsus paradoxus. 17-19 The clinical presentation of postoperative cardiac tamponade includes a wide range of nonspecific signs and symptoms such as dyspnea, 20 orthopnea, attenuated cardiac sounds, chest pain, 21 tachycardia and hypotension, and even cardiogenic shock. 22 The nonspecific clinical scenario after cardiac surgery also may be influenced by the presence of low-pressure cardiac tamponade 23 or loculated tamponade, which are relatively frequent in the post– cardiac surgery period. 4,24 One of the most common clinical signs in these patients is hemodynamic impairment, characterized by the presence of tachycardia and hypotension, findings that may be associated with multiple diagnoses in a postoperative cardiac patient. The following factors can determine the presence of cardiac tamponade: the fluid accumulation rate, the previous ventricular function status, the patient’s blood volume, and the presence or absence of pre-existing hypertension. 25 The development of pulsus paradoxus is a key clinical sign pointing to a diagnosis of cardiac tamponade in patients breathing spontaneously. However, pulsus paradoxus may not always be present in postoperative patients under mechanical ventilation or may develop in patients with other comorbid conditions in the absence of cardiac tamponade (Table 2). As an indirect sign, respiratory variability in the pulse oximetry waveform should raise the suspicion of hemodynamic compromise in patients at risk for pericardial tamponade who are breathing spontaneously. 26 The elevation of central venous pressure (CVP) has a low predictive value in the immediate postoperative setting because of the high rate of low-pressure tamponade, situations of con- comitant hypovolemia, or in loculated tamponade. In addition, the elevation of CVP can occur in situations of right ventricular dysfunction, in the presence of tricuspid regurgitation, or ven- tilatory abnormalities requiring high PEEP. Furthermore, postoperative pericardial effusions of moderate volume may be found in the posterior space and partially compress one or more cardiac chambers. These cases may manifest as isolated increases in pulmonary artery occlusion pressure. Occasionally, the increases in CVP and jugular distention can occur together with the Kussmaul venous sign. 2 The Kussmaul sign is a distention of jugular veins in the neck during inspiration. In low-pressure tamponade, this is an uncommon sign; however, exaggerated jugular pulse wave without distention can some- times be seen. The tracing of venous pulse waves shows a marked “x” wave and a reduction or absence of the “y” wave (Fig 1). On a chest x-ray, a normal heart size is seen until the effusion is moderate in volume (at least Ͼ 200 mL); thereafter, the cardiac silhouette is enlarged, taking the appearance of a flask or water-bottle. These findings might not be seen with loculated pericardial effusions. The only electrocardiographic (ECG) sign that is almost specific in cardiac tamponade is electrical alternans, which is a beat-to-beat variation of the contour and/or shape of the P wave, the QRS complex, the ST segment, and/or the T wave. This phenomenon can be explained by the presence of pericardial fluid, which drives the myocardium back and forth from the thoracic wall. Other potential, less specific findings are reductions of the QRS voltage and the T wave, depressed PR segment, changes in the ST-T, and bundle- branch blocks. Postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations because of selective chamber compression by loculated fluid 27 or hypovolemia. The atypical clinical presentation of these events may simulate other disorders like severe hypovolemia, left ventricular dysfunction, major ischemic events, or systemic inflam- matory response syndrome, and, therefore, the diagnosis of tamponade should be considered whenever hemodynamic de- terioration or signs of low-output failure occur in the postcar- diotomy patient. 28 Although the diagnosis of cardiac tamponade is predomi- nantly clinical, symptoms are usually nonspecific in postoperative cardiac patients and may complicate the decision-making process. 1,29 If there is clinical suspicion of cardiac tamponade, an echocardiographic examination by transthoracic or transesophageal echocardiography must be performed without delay. 2,28,30 Echocardiography is used to show the presence and size of pericardial effusions, to quantify the ...