Abstract
Background and Aims
Intradialytic hypotension is a fairly common and serious adverse phenomenon. Associated comorbidities include e.g. heart failure, hypovolemia, allergic reactions with the dialysis apparatus and electrolyte disturbancies. Excessive ultrafiltration may explain later onset hypotension, but early-onset hemodynamic collapse remains poorly understood.
Preventive interventions may include incremental dialysis, increasing dry weight, increasing dialysis time and changing dialysis membranes/apparatus.
This study combines Echocardiography (Echo) and Lung Ultrasound (LUS) for hemodynamic phenotyping of patients with severe, early onset intra-dialytic hypotension. The aim is to figure out possible preventive strategies depending on underlying abnormalities.
Method
We enrolled dialysis patients with a symptomatic decrease in systolic arterial pressure < 90 mmHg requiring norepinephrine during the first 60 minutes of at least two consecutive dialysis sessions in our dialysis department. Echo + LUS was done simultaneously to everyone at baseline, i.e. BEFORE dialysis begun, and later at onset of a hypotension episode during dialysis. Patients with active bleeding or any other obvious temporary etiology for hypotension were excluded.
Echo concentrated especially on volemic state and filling pressures, while LUS evaluated the lungs and pleurae for signs of pulmonary congestion. Cardiac structure and function (e.g. valves, ejection fraction) was also evaluated.
Results
Between 1.10.2019 - 31.12.2019 10 patients were enrolled. All patients eventually required norepinephrine despite fluid challenge. No patients had signs or symptoms of an allergic reaction, such as urticaria or stridor/obstructive respiration, nor significant electrolyte disturbancies.
5/10 patients had severe systolic cardiac dysfunction at baseline (LVEF < 30 %) and these 5 patients also simultaneously showed signs of congestion and fluid overload on ultrasound.
On the contrary, the other 5/10 patients without severe cardiac failure all had low left-sided filling pressures and a collapsed inferior vena cava on Echo ALREADY at baseline, i.e. before initiation of dialysis. All of these hypovolemic patients had an excellent residual diuresis (> 1500ml/d).
All 10 patients in this study showed a significant drop in body volume measurement (BVM) -curves and left-sided filling pressures on Echo prior to onset of hypotension.
Of the 5 patients with severe cardiac dysfunction, 2/5 were transmitted into palliative care without dialysis, while 3/5 could be managed without future norepinephrine by longer, more frequent dialysis sessions using more convective and less diffusive dialysis.
Of the latter 5 “dry” patients without severe cardiac dysfunction, 3/5 had no more hypotensive episodes after increasing dry weight and using incremental dialysis programs, and the remaining 2 dry patients could be completely switched off dialysis due to vivid residual function.
3/5 of the “dry patients” had a baseline pulse pressure > 120 mmHg and 3 had coronary artery disease, both possibly predisposing to diastolic under-filling.
No patients in this study presented with significant myocardial stunning, defined as a > 10 % decrease in LVEF compared to baseline.
Conclusion
Severe, intra-dialytic hypotension requiring vasopressors may be prevented by individual tailoring of dialysis prescription. Ultrasound may help phenotyping patients requiring different dialysis strategies, including stopping dialysis entirely. Stunning and allergic reactions seemed rare.
At baseline, patients seemed to be mainly 1) either over-dialyzed (hypovolemic or hypo-osmotic) or 2) having significant cardiac disease, naturally requiring quite opposite preventive strategies. A decrease in left ventricular preload furthermore occurred in all patients at onset of hypotension, suggesting crossover of a patient-specific preload threshold.
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