The Changes In Heart Function And Treatment Of Cardiogenic Shock During Canine Acute Pulmonary Hypertension

OBJECTIVE: Acute pulmonary embolism (APE) is not an uncommon disease, which results in high mortality. Thrombolytic therapy can reduce the mortality of APE as many as 3 times. About 11% of patients with APE died of circulatory failure within an hour after the onset due to not catching to use thrombolytic therapy. The mechanisms of circulatory failure and treatments of cardiogenic shock secondary to acute pulmonary hypertension (APH) have not been systematically investigated. The present experiment is to explore the pathophysiologic alterations during compensatory and shock stage, and treatment of the shock during canine APH.MATERIALS AND METHODS: Eighteen mongrel dogs were randomly divided into three groups: acute pulmonary artery banding group (group APB,n=8), acute pulmonary thromboembolism group (group APE,n=8) and control group(n=2). Right ventricular systolic pressure (RVSP) was elevated by APE and APB step by step [1.33-2.00kPa (10-15mmHg) each step] and until shock occurred [aortic systolic pressure <10.7kPa (80mmHg)]. Then the cardiopulmonary hemodynamics, coronary flow, myocardial oxygen metabolism, and the concentrations of lactic acid, adenosine and endothelin of myocardial venous blood were measured. Norepinephrine, epinephrine, dopamine and dobutamine were used in random order to treat the cardiogenic shock in the two groups (n=6, respectively). RESULTS:1.Hemodynamics: In group APE, RVSP was elevated to 5.53kPa(APE1)(41.5mmHg), 7.28kPa (54.6mmHg)(APE 2) and 9.08kPa(68.1mmHg)(APE3) from baseline of 3.97kPa(29.8mmHg), and shock occurred when more than 10.6kPa(79.5mmHg). The compensatory stage was defined as the period before the maximum of RVSP. During compensatory stage. RVSP and right ventricular pressure differentiation (±RVdp/dtmax) increased, stroke volume (SV) and cardiac output (CO) decreased gradually; end-diastolic tansseptal pressure gradient (EDTSPG) which reflects the movement of septum at end-diastole reduced significantly and became negative at APE3; but left ventricular systolic pressure (LVSP) and positive left ventricular (LV) differentiation (+LVdP/dtimx) and aortic systolic pressure (AoSP) unchanged significantly; left ventricular end-diastolic pressure (LVEDP), aortic diastolic pressure (AoDP) and heart rate (HR) decreased gradually. During shock period. RVSP and ±RVdp/dtmax dropped, but were greater than the baseline; the other parameters decreased much more than those before the shock.