[Estimation of acute left ventricular afterload alterations. Transesophageal echocardiography in artificially respirated patients].
Left ventricular afterload is most accurately represented by left ventricular end-systolic wall stress, but in clinical practice is commonly estimated by the systemic vascular resistance (SVR). End-systolic wall stress can be derived from M-mode and two-dimensional (2D) echocardiograms in combination with systolic arterial pressure (SAP). We tested transoesophageal echocardiography for the assessment of acute left ventricular afterload alterations in ventilated patients requiring cardiovascular support with noradrenaline or nitroglycerine. METHOD. With approval from the local ethics committee, we studied afterload alterations in 11 hypotensive patients who were treated by increasing the dosage of i.v. noradrenaline by 2-5 micrograms/min in order to raise mean arterial pressure (MAP) by 20 mmHg. In another 10 patients with MAP over 95 mmHg, nitroglycerine was raised from 2 to 4 mg/h, aiming at a 20 mmHg MAP reduction. MAP and SAP were monitored via a radial artery cannula, cardiac output (CO) was measured with the thermodilution technique using a Swan-Ganz catheter, and SVR was calculated from CO, MAP, and right atrial pressure. M-mode and 2D echocardiograms were obtained from the cross-sectional short-axis view of the left ventricle and recorded shortly before and during treatment when MAP had changed by 20 mmHg. Left ventricular total area (TA) and cavity area (A) including the papillary muscles were obtained from end-systolic 2D echocardiograms, while end-systolic internal diameter (ID) and posterior wall thickness (HW) were measured in the M-mode. Wall stress was calculated in the M-mode as: WSM = 0.33 x SAP x ID/(HW x (1+HW/ID)), and in the 2D mode as: WS2D = 1.33 x SAP x A/(TA-A).


METHODS
paired t-test (P < 0.05), regression analysis. RESULTS. Afterload alterations were reflected by significant changes of WS2D (-41%, +68%), WSM (-26%, +38%), and SVR (-15%, +50%). WSM and SVR underestimated changes of WS2D by 15%-30%. WSM changes due to SAP rather than to left-ventricular dimensional changes. No correlation was found between WS2D or WSM and SVR. Inter-observer variability for echocardiographic wall stress was reasonable (WS2D 4%, WSM 10%). CONCLUSIONS. Acute changes of left ventricular afterload and dimensions were clearly indicated by 2D measurements. As M-mode measures were not conclusive for left ventricular dimensional changes, WSM was not an appropriate parameter for acute afterload alterations. WS2D is an afterload index superior to WSM that cannot be estimated by SVR.
Greim
C
C
Abteilung für Anästhesiologie, Universitäts-Krankenhaus Eppendorf, Hamburg.
Roewer
N
N
Meissner
C
C
Bause
H
H
Schulte am Esch
J
J
D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D017548:Echocardiography, Transesophageal; D006801:Humans; D007022:Hypotension / Q000188:drug therapy / Q000503:physiopathology; D008875:Middle Aged; D005996:Nitroglycerin / Q000627:therapeutic use; D009638:Norepinephrine / Q000627:therapeutic use; D012121:Respiration, Artificial; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
D005996:Nitroglycerin; D009638:Norepinephrine