Perioperative sonographic monitoring in cardiovascular surgery

Published on 22/03/2015 by admin

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Perioperative sonographic monitoring in cardiovascular surgery

Overview

Despite the well-known advances in cardiovascular surgery over the last 50 years, it remains a high-risk procedure associated with significant morbidity and mortality rates. Currently, patients undergoing cardiovascular operations tend to be older and have more comorbid conditions. This could be attributed to the progress in surgical procedures, as well as to improved preoperative, perioperative, and postoperative care, which includes hemodynamic optimization by implementation of goal-directed therapies and the use of β-blockade in selected patients. Recent guidelines have recommended the use of ultrasound for detection of perioperative complications and for hemodynamic management.1,2 This chapter discusses the use of echocardiography for the evaluation of patients after cardiovascular surgery. Because image quality is usually poor with transthoracic echocardiography, transesophageal echocardiography (TEE) has been used routinely in the intensive care unit (ICU) for the detection of functional and structural cardiovascular abnormalities postoperatively.

Hypovolemia

Hypovolemia is the most frequent hemodynamic alteration after cardiovascular surgery. Even though bleeding is easily assessed by checking the various drains, it is sometimes overlooked because of clotting of drains or accumulation of blood in nonadequately drained cavities (e.g., pleural space). Notably, even when bleeding is detected, volume correction can be insufficient, and it is worth mentioning that cardiopulmonary bypass often provokes capillary leak syndrome secondary to a systemic inflammatory response. Postoperatively, patients may have hypotension or signs of tissue hypoperfusion necessitating close hemodynamic monitoring in the ICU. Whenever possible, fluid responsiveness should be assessed with dynamic indices (Chapter 38). Evaluation of variations in aortic flow with respiration is the most reliable method. Assessment of fluid responsiveness based on respiratory variations in the superior and inferior vena cava is less reliable because of direct compression of the vessel by blood and clots in the mediastinum (superior vena cava) or because of increased pericardial pressure (both vessels). Finally, systolic or diastolic left ventricular (LV) dysfunction (preexisting or related to cardiopulmonary bypass) may result in intolerance of fluid therapy and thus should be carefully evaluated.

Left ventricular dysfunction

LV dysfunction is the second most frequent hemodynamic alteration after cardiovascular surgery and can be attributed to preexisting LV dysfunction or to ischemic events or stunning as a result of cardiopulmonary bypass.3 Preoperative evaluation of ventricular function is fundamental in these patients since it facilitates postoperative identification of a new segmental ventricular wall abnormality, which should prompt discussion of coronary angiography and reperfusion strategies. In addition, demonstration of impaired contractility does not inevitably constitute an indication for the use of inotropic agents, which are indicated only when impaired contractility is associated with an inadequate cardiac output contributing to the impaired tissue perfusion. Indeed, the patient is often hypothermic and metabolic needs are low during and just after surgery. Therefore low cardiac output in isolation should not be treated. Measurements of LV ejection fraction should be used in combination with cardiac output measurements (measured as the aortic flow velocity-time integral) and markers of tissue hypoperfusion (blood lactate levels, oliguria). Finally, right ventricular (RV) dysfunction may also occur, especially after selected procedures such as correction of mitral valve stenosis or pulmonary thromboembolectomy (Chapter 33).4

Pericardial effusion and localized tamponade

Blood and clots may accumulate in the pericardial space even with the use of drains. Stagnation of blood in the pericardium facilitates the development of clots, which in turn may lead to drain occlusion and global tamponade by enabling continuous accumulation of blood. Localized tamponade may also occur as a result of the development of large clots compressing selected cardiac structures. In most cases these large clots compress the right cardiac cavities and especially the right atrium (Figure 40-1). In the latter clinical scenario, patients typically have severe hypovolemia that responds partially to fluid therapy, and ultrasound detects a very small right atrium and dilatation of the superior and inferior vena cava (increased central venous pressure). Rarely, clots may selectively compress the left atrium, which results in low cardiac output with some evidence of hypovolemia (usually a small left ventricle) and a very small left atrium with occasional pulmonary edema (often predominant on the left side) because of compression of the pulmonary veins (as confirmed by detection of very high color and pulsed wave Doppler velocity [>100 cm/sec] in the ipsilateral pulmonary veins).

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