Fig. 23.1
Standard approaches to acute atrial fibrillation
b.
Rate controlling agents (all can cause hypotension and bradycardia and should be administered in a monitored setting)
i.
Metoprolol 5 mg intravenous (IV), every 5 min × 3, 25–200 mg/day po in divided doses
ii.
Diltiazem 0.25 mg/kg IV, may repeat after 15 min, 120–360 mg/day po in divided doses (caution with decreased LVEF)
iii.
Digoxin 1 g IV or po load in three divided doses every 4–8 h given as 50 % initially and then 25 % × 2, then 0.125–0.375 mg po daily (need to adjust for creatinine clearance)
iv.
Amiodarone 150 mg IV over 10 min, and then 0.5–1 mg/min IV
23.4 Cardiac Ischemia
1.
Etiologic considerations in HSCT recipients
a.
Etoposide has been associated with vasospastic angina and myocardial infarction (MI).
b.
Patients with underlying CAD are at risk for cardiac ischemia and MI due to physiologic stresses associated with transplantation.
2.
Management of cardiac ischemia and acute coronary syndrome is often complicated by limitations in the use of antithrombotic and anticoagulant therapies due to thrombocytopenia from HSCT conditioning therapy or from the underlying hematologic disease.
3.
If percutaneous coronary intervention is indicated, strongly consider the use of bare-metal stents or balloon angioplasty alone over drug-eluting stents depending on the clinical scenario due to shorter duration of required dual antiplatelet therapy (see Chap. 13).
4.
Oncology and cardiology should work closely together in managing HSCT patients with active cardiac ischemia.
23.5 Hypertension
1.
Chronic immunosuppression with calcineurin inhibitors (CNIs (cyclosporine, tacrolimus)) is the mainstay of therapy for prevention of graft-versus-host disease (GVHD) .
2.
CNI-associated HTN occurs in 15–50 % of patients and typically develops within a month of starting therapy.
3.
The treatment of choice is calcium channel blockade which reduces peripheral vascular resistance (including the renal arteriolar constriction associated with CNIs) and lowers blood pressure by causing direct vasodilation in the peripheral arteries of the vascular smooth muscle.
a.
Nifedipine XL (Adalat CL) 30–60 mg po daily
b.
Amlodipine (Nirvase) 2.5–10 mg po daily
4.
Posterior reversible encephalopathy syndrome (PRES) is a neurologic complication seen occasionally in patients with CNI-associated HTN.
a.
The clinical syndrome includes headache, mental status changes, and seizures with specific radiologic features.
b.
Management includes withdrawal of the drug and aggressive blood pressure control.
23.6 Pericarditis
1.
Pericarditis and accompanying pericardial effusion with or without cardiac tamponade are associated with cyclophosphamide and cytarabine therapy .
2.
Chronic GVHD can involve the pericardium with resultant pericardial effusion, cardiac tamponade, constrictive pericarditis, or effusive–constrictive pericarditis.
3.
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Cardiac tamponade
a.
Increased intrapericardial pressure results in cardiac chamber compression and decreased venous return, resulting in decreased cardiac output.
b.
Clinically presents as cardiogenic shock without pulmonary edema.
c.
Beck’s triad
i.
Distant heart sounds
ii.
Increased JVP
iii.
Hypotension
d.
Pulsus paradoxus is present with a decrease in systolic pressure ³ 10 mmHg with inspiration.
i.
Exaggeration of normal physiology with inspiration causing a decrease in intrapericardial and right atrial pressures, increasing right-sided venous return and right ventricular size.
ii.
Due to increased ventricular interdependence, increased right-sided filling is at the expense of decreased left ventricular filling, resulting in decreased left ventricular stroke volume and blood pressure.
e.
Diagnosis is made by clinical manifestations and presence of pulsus paradoxus.
f.
Echocardiographic findings include
i.
Pericardial effusion.
ii.
Dilated inferior vena cava (IVC).
iii.
Diastolic collapse of the right-sided cardiac chambers.
iv.
Respirophasic changes in transvalvular velocities are supportive.
g.
Treatment
i.
Intravascular volume
ii.
Inotropes
iii.
Pericardiocentesis
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