DK2985_C000 1..28 - AlSharqia Echo Club

Liver Transplantation 493Table 22.1A. PreoperativelyAssociated Cardiac and Hepatic DisordersHeart diseases affecting the liverMild alterations of liver function tests in heart failureCardiogenic IH and its variantsCLF and congestive (cardiac) cirrhosisLiver diseases affecting the heartHepatopulmonary syndromePPHTN in liver cirrhosisPericardial effusion in cirrhosisCirrhotic cardiomyopathyHigh-output failure caused by intrahepatic arteriovenous fistulaein the noncirrhotic liverCardiac and hepatic disorders with joint etiologyInfectious and parasitic, metabolic, immune andvasculitic, toxicNote: CLF, congestive liver fibrosis; IH, ischemic hepatitis; PPHTN,portopulmonary hypertension.Source: With permission from Naschitz et al. (3).Hemodynamically, OLT is one of the most stressfulsurgeries for patients and a challenge for the anesthesiologist.Consequently, preoperative assessment of the cardiacfunction is of prime importance to ensure the best outcomepossible. The patient with compensated end-stage liverfailure usually presents a hyperdynamic state characterizedby high cardiac output (CO), normal ejection fraction(EF), low systemic vascular resistance, and elevated heartrate. More specifically, anomalies due to the hemodynamicconsequences of hepatic failure on the systemicand pulmonary circulation include: hepatopulmonarysyndrome, plexogenic pulmonary hypertension, pericardialeffusion, cardiomyopathy, and high-output heartfailure caused by arteriovenous shunts.defined as dyspnea which is worse in the upright positionand relieved by recumbence (Fig. 22.2).Contrast-enhanced echocardiography with intravenousinjection of agitated saline is the current gold standardfor detection of pulmonary vascular dilations (3). Bubblesare usually trapped in the pulmonary circulation capillariesand are not seen in the left cardiac chambers. If an intracardiacshunt exists (such as an atrial septal defect), contrastbubbles will appear in the left atrium (LA) withinthree beats after their appearance the right atrium (RA).In the case of HPS, contrast will appear in the LA afterfour to six beats.2. Portopulmonary HypertensionAlthough not a common disease in liver failure, portopulmonaryhypertension (PPHTN) can severely affect theoutcome of OLT. The mechanisms are unknown. Theseverity appears to be related to the duration of portalhypertension and as in the case of HPS, substances not8-15µ(A)alveolusNORMALPAO 2NORMAL CAPILLARIESNormal PaO 2(C)alveolus15-100µalveolusNORMALPAO 2ABNORMAL CAPILLARIESsupplemental O 2(B)Low PaO 21. Hepatopulmonary SyndromeSymptomatic hepatopulmonary syndrome (HPS) occurs in15% of patient with end-stage liver failure (3) and maybe reversed by OLT. Liver disorder provokes an imbalancebetween vasoconstricting and vasodilating mediators, aswell as between hepatic factors controlling the endothelialcell growth: consequently, pulmonary capillary vesselsgrow and dilate. During their passage through the dilatedpulmonary capillaries, red blood cells do not optimallypick up diffused oxygen in a patient breathing room air.Diffusion/perfusion mismatch causes hypoxemia. Whenthe patient goes from a supine to an upright position,blood flow is increased in the lung bases, exacerbatinghypoxemia. Orthodeoxia is defined as arterial desaturationaccentuated in the upright position and improved byrecumbence. This is often accompanied by platypnea,15-100µHIGHPAO 2ABNORMAL CAPILLARIESHigh PaO 2Figure 22.2 Anomalies of the vascular pulmonary bed in thehepatopulmonary syndrome. Compared with normal capillariesand alveolus (A), in the hepatopulmonary syndrome capillariesbecome dilated and blood does not receive diffused oxygen ina patient breathing room air causing hypoxemia (B). If thepatient goes from a supine to a standing position, blood flow isincreased at the lung base exacerbating hypoxemia and causingorthodeoxia and platypnea. As this is improved by supplementaloxygen, it represents severe diffusion-perfusion mismatch ratherthan true shunting (C). (PaO 2 , oxygen partial pressure).