30-year-old multiparous female with left ventricular noncompaction cardiomyopathy presents to the intensive care unit (ICU) from the operating room after undergoing an orthotopic cardiac transplantation. The donor organ was retrieved from a 20-year-old brain dead man. Preoperatively, the recipient was on chronic intravenous dobutamine therapy. Intravenous basiliximab was administered immediately prior to her transplant for induction of immunosuppression. Post termination of cardiac bypass in the operating room, temporary pacing was initiated in view of persistent bradyarrhythmia.
The MOST likely cause of her posttransplant bradyarrhythmia is:
Correct Answer: B
Sinus node dysfunction occurs in up to 50% of patients following cardiac transplantation. Such dysfunction commonly manifests as bradycardia, is usually temporary, and spontaneously resolves in a majority of patients within the first 3 months of transplantation. Temporary atrial pacing often suffices in the early postoperative period as atrioventricular (AV) node conduction is usually preserved. Unlike sinus node dysfunction, AV nodal conduction abnormalities are uncommon and tend to occur late after cardiac transplantation.
Various risk factors for developing sinus node dysfunction and ensuing posttransplant bradycardia have been described. These include surgical trauma to the sinus node, perinodal atrial tissue, or sinoatrial artery; ischemia-reperfusion injury; pretransplant use of amiodarone; older donors; and rejection. While robust evidence for most risk factors is lacking, the most likely cause of sinus node dysfunction is surgical trauma at the time of transplantation. Use of bicaval anastomotic technique instead of the biatrial surgical approach for orthotopic cardiac transplantation has substantially decreased the incidence of posttransplant bradyarrhythmia and nearly eliminated the need for permanent pacing. Donor gender and choice of immunosuppressive induction agent are not risk factors for sinus node dysfunction.
Key point: Sinus node dysfunction commonly occurs early after cardiac transplantation and is often related to surgical trauma.
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A 40-year-old male with known nonischemic cardiomyopathy and pulmonary hypertension returns to the ICU intubated and sedated after undergoing an orthotopic heart transplant. Graft ischemia time was 4 hours. On arrival, he is on high-dose intravenous vasopressor support including 0.5 µg/kg/min norepinephrine, 0.5 µg/kg/min epinephrine, and 0.1 units/h of vasopressin. He is receiving inhaled nitric oxide 40 ppm. Monitoring reveals the following:
The LEAST likely cause of his cardiogenic shock is:
Correct Answer: A
Early allograft dysfunction after orthotopic heart transplant can be apparent in the intraoperative period or can develop within 24 hours after transplant surgery. It can manifest as left ventricular (LV) dysfunction, isolated right ventricular (RV) dysfunction, or biventricular dysfunction. It is associated with significantly increased 30-day and 1-year mortality. Multiple factors can contribute to early graft dysfunction and include hyperacute rejection, pulmonary hypertension, prolonged graft ischemic time, cardiac tamponade, and suboptimal donor heart.
PGD is defined as ventricular dysfunction that occurs within 24 hours after surgery and is not associated with a discernible cause. Hyperacute cellular rejection can present with immediate cardiogenic shock post transplantation and is commonly mediated by preformed B-cell antibodies. Acute rejection commonly occurs weeks to months after transplantation and is mediated by T-lymphocyte activation. Most cases of acute rejection are diagnosed by routine surveillance endomyocardial biopsy at a time when the patient is asymptomatic and ventricular function is normal.
Acute rejection commonly occurs weeks to months after transplantation, is mediated by T-lymphocyte activation, and is NOT a cause for cardiogenic shock in the immediate postoperative period. Differentials for immediate posttransplant cardiogenic shock include PGD, exacerbation of pulmonary hypertension, cardiac tamponade, and hyperacute rejection.
50-year-old male with end-stage lung disease and pulmonary hypertension secondary to emphysema is admitted to ICU after undergoing bilateral lung transplantation on cardiopulmonary bypass. His body mass index (BMI) is 22 kg/m2 . The lungs were retrieved from a 25-year-old brain dead man. The donor was a nonsmoker. On POD 2, the recipient’s PaO2 /FiO2 ratio is 150 and bilateral lung opacities consistent with pulmonary edema are noted on chest x-ray suggesting a diagnosis of grade 3 primary graft dysfunction (PGD).
The risk factor MOST likely associated with PGD in this scenario is:
Correct Answer: D
PGD after lung transplantation develops in the first 72 hours after transplantation and is characterized by hypoxemia with radiographic appearance of diffuse pulmonary opacities. Multiple risk factors for PGD have been identified. Donor and recipient characteristics, presence of preoperative disease, and intraoperative risk factors may contribute to PGD.
Donor risk factors include smoking, aspiration, lung contusion, undersized donor relative to recipient, heavy alcohol use, fat embolism, and thromboembolism.
Recipient factors include female gender, elevated recipient BMI (≥25 kg/m2 ), and being African American. Pretransplant diseases with increased risk of PGD include idiopathic pulmonary fibrosis, sarcoidosis, and pulmonary arterial hypertension (PAH).
Intraoperative risk factors include large volume intraoperative blood product transfusion, prolonged ischemic time, and use of cardiopulmonary bypass (CPB). PGD post lung transplantation is characterized by hypoxemia and the radiographic appearance of diffuse pulmonary opacities. Multiple risk factors for this condition exist.
40-year-old male underwent liver transplant 20 years ago due to biliary cirrhosis. He is now listed for a redo liver transplant in view of recurrent cirrhosis. He is admitted to the ICU with upper gastrointestinal variceal bleeding requiring massive transfusion. He is intubated and on mechanical ventilation. Bedside echocardiography reveals an ejection fraction of 70% and absence of diastolic dysfunction. Electrocardiogram exhibits sinus tachycardia with a normal QT interval. Chest x-ray appears normal. Patient’s invasive arterial pressure is 100/60 mm Hg and central venous pressure is 8 mm Hg. A pulmonary artery catheter is inserted and the following values are obtained: Cardiac output of 10 L/min, mean pulmonary artery pressure of 30 mm Hg, and pulmonary artery occlusion pressure of 10 mm Hg. This is MOST likely due to:
Portopulmonary hypertension (PoPH) is PAH arising in the setting of portal hypertension with or without liver cirrhosis.
The definition of PoPH comprises three essential elements:
The cause of PoPH is unknown. It has been hypothesized that humoral substances such as interleukin-1, endothelin-1, glucagon, secretin, thromboxane B2, and vasoactive intestinal peptide, which would normally be metabolized by the liver, are able to access the pulmonary circulation through portosystemic collaterals, resulting in PoPH. In the stem above, calculated PVR is 2 Wood Units. Although our patient’s mPAP is greater than 25 mm Hg with a PAOP less than 15 mm Hg, he would not meet the criteria for PoPH given his current PVR.
Cirrhotic cardiomyopathy is a cardiac condition observed in patients with end-stage liver disease regardless of etiology. It is characterized by normal to increased cardiac output and contractility at rest but impaired systolic response to stress. It is commonly associated with diastolic dysfunction and electrophysiological abnormalities such as QT interval prolongation. Diagnosis of cirrhotic cardiomyopathy requires presence of both systolic and diastolic dysfunction with or without electrophysiological abnormalities. Our patient in the stem would not qualify.
Transfusion-associated circulatory overload commonly presents with respiratory distress and hypertension within 6 hours of receiving transfusion. Evidence of fluid overload is often present in a chest x-ray. Although our patient received massive blood transfusion, he has no evidence of circulatory overload. A hyperdynamic circulation can lead to increased mean pulmonary artery pressures in the presence of a normal PVR. Elevated mean pulmonary artery pressures can occur for various reasons in cirrhosis with portal hypertension and should be cautiously interpreted.
A 45-year-old male with hepatitis C–related cirrhosis presents to the ICU from the operating room after undergoing orthotopic liver transplantation. At reperfusion, he suffered a brief asystolic arrest due to hyperkalemia. The donor liver was MOST likely preserved in which preservative solution
The University of Wisconsin solution is the standard criterion static cold preservation for the procurement of liver, kidney, pancreas, and intestine. Other preservation solutions include HTK, IGL-1, and Celsior.
University of Wisconsin solution is a potassium-rich (125 mmol/L), sodium-depleted, osmotically active fluid, with ion composition comparable with the intracellular milieu.
Potential disadvantages of using University of Wisconsin solution include:
HTK solution is cheaper, has low viscosity, and a low-potassium content (9 mmol/L). Celsior is another cold storage solution, which has been studied as an alternative to University of Wisconsin solution. Celsior has less viscosity and greater buffering potential for acidosis than University of Wisconsin solution. Celsior solution has high-sodium and low-potassium content (15 mmol/L), with impermeants lactobionate and mannitol which limit cellular edema.
IGL-1 is a new preservation solution, with a composition resembling that of UW with inversed potassium/sodium concentrations and hydroxyethyl starch substituted with polyethylene glycol. It has 30 mmol/L of potassium. University of Wisconsin solution is a potassium-rich, sodium-depleted, osmotically active fluid and can potentially precipitate hyperkalemic cardiac arrest during reperfusion in patients undergoing liver transplantation.
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