Relationship between Haemodynamic and Respiratory Function in Patients with Myocardial Infarction and Left Ventricular Failure

1972 ◽  
Vol 42 (6) ◽  
pp. 751-768 ◽  
Author(s):  
Anne E. Tattersfield ◽  
M. W. McNicol ◽  
R. W. Sillett

1. Forty-five patients with myocardial infarction and clinical signs of left ventricular failure have been studied with measurements of pulmonary and brachial artery pressure, cardiac output, arterial blood gas pressures and expired air collections. 2. Pulmonary artery pressure was elevated and stroke index was reduced in the majority of patients (89% and 85% respectively). There was a close inverse correlation between these two measurements, both of which appear to be direct consequences of impaired left ventricular function. 3. Arterial hypoxaemia was common and only transiently relieved by hyperventilation. Dead space/tidal volume ratio and venous admixture were both increased, compatible with considerable ventilation/perfusion mismatching in the lung. Both measurements correlated directly with pulmonary artery pressure.

1974 ◽  
Vol 46 (2) ◽  
pp. 253-264 ◽  
Author(s):  
Anne E. Tattersfield ◽  
M. W. McNicol ◽  
R. W. Sillett

1. Intravenous frusemide has been given to thirty-five patients with myocardial infarction and clinical signs of left ventricular failure. The haemodynamic changes following frusemide were then observed over the subsequent 6 h. 2. Frusemide produced a large diuresis, which was maximal during the first 2 h but fluid depletion was maintained at 24 h. The greatest diuresis occurred in patients with the highest stroke index. 3. All patients showed a fall in pulmonary artery pressure after frusemide. In patients with evidence of poor left ventricular function (low stroke index, high pulmonary artery pressure) this was associated with little change in stroke index. In patients with less severe impairment of left ventricular function there was an initial fall in stroke index at 1 and 2 h. 4. Six hours after frusemide there was a reduction in both pulmonary artery pressure and systemic arterial pressure; the latter correlated with the volume of the diuresis.


1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.


2003 ◽  
Vol 26 (4) ◽  
pp. 351-357 ◽  
Author(s):  
W.G. Kim ◽  
Y.C. Shin ◽  
S.W. Hwang ◽  
C. Lee ◽  
C.Y. Na

We report a comparison of the effects of myocardial infarction in dogs and sheep using sequential ligation of the left anterior descending artery (LAD) and its diagonal branch (DA), with hemodynamic, ultrasonographic and pathological evaluations. Five animals were used in each group. After surgical preparation, the LAD was ligated at a point approximately 40% of the distance from the apex to the base of the heart, and after one hour, the DA was ligated at the same level. Hemodynamic and ultrasonographic measurements were performed preligation, 30 minutes after LAD ligation, and 1 hour after DA ligation. As a control, two animals in each group were used for the simultaneous ligation of the LAD and the DA. Two months after the coronary ligation, the animals were evaluated as previously, and killed for postmortem examination of their hearts. All seven animals in the dog group survived the experimental procedures, while in the sheep group only animals with sequential ligation of the LAD and DA survived. Statistically significant decreases in systemic arterial blood pressure and cardiac output, and an increase in the pulmonary artery capillary wedge pressure (PACWP) were observed one hour after sequential ligation of the LAD and its DA in the sheep, while only systemic arterial pressures decreased in the dog. Ultrasonographic analyses demonstrated variable degrees of anteroseptal dyskinesia and akinesia in all sheep, but in no dogs. Data two months after coronary artery ligation showed significant increases in central venous pressure, pulmonary artery pressure, and PACWP in the sheep, but not in the dog. Left ventricular end-diastolic dimension and left ventricular end-systolic dimension in ultrasonographic studies were also increased only in the sheep. Pathologically, the well-demarcated thin-walled transmural anteroseptal infarcts with chamber enlargement were clearly seen in all specimens of sheep, and only-mild-to-moderate chamber enlargements with endocardial fibrosis were observed in the dog hearts. In conclusion, this study confirms that the dog is not a suitable model for myocardial infarction with failure by coronary artery ligation despite negligent operative mortality, when compared directly with an ovine model.


2020 ◽  
Author(s):  
Reem M. Soliman ◽  
Yasser Elsayed ◽  
Reem N. Said ◽  
Abdulaziz M. Abdulbaqi ◽  
Rania H. Hashem ◽  
...  

ABSTRACTObjectiveTo test the hypothesis that a lung ultrasound severity score (LUSsc) and assessment of left ventricular eccentricity index of the interventricular septum (LVEI) by focused heart ultrasound can predict extubation success in mechanically ventilated preterm infants with respiratory distress syndrome (RDS).DesignProspective observational study of premature infants <34 weeks’ of gestation age supported with mechanical ventilation due to RDS. LUSsc and LVEI were performed on postnatal days 3 and 7 by an investigator who was masked to infants’ ventilator parameters and clinical conditions. RDS was classified based on LUSsc into mild (score 0–9) and moderate-severe (score 10–18). A receiver operator curve was constructed to assess the ability to predict extubation success. Pearson’s correlation was performed between LVEI and pulmonary artery pressure (PAP).SettingLevel III neonatal intensive care unit, Cairo, Egypt.ResultsA total of 104 studies were performed to 66 infants; of them 39 had mild RDS (LUSsc 0–9) and 65 had moderate-severe RDS (score ≥10). LUSsc predicted extubation success with a sensitivity and a specificity of 91% and 69%; the positive and negative predictive values were 61% and 94%, respectively. Area under the curve (AUC) was 0.83 (CI: 0.75-0.91). LVEI did not differ between infants that succeeded and failed extubation. However, it correlated with pulmonary artery pressure during both systole (r=0.62) and diastole (r=0.53) and with hemodynamically significant patent ductus arteriosus (r=0.27 and r=0.46, respectively).ConclusionLUSsc predicts extubation success in preterm infants with RDS whereas LVEI correlates with high PAP.


1977 ◽  
Author(s):  
M.H. Todd ◽  
J.B. Forrest ◽  
J. Hirsh

Embolisation of the pulmonary vasculature with microspheres releases prostaglandin-1ike substances, PGLS (Piper and Vane, N.Y. Acad. Sei. 180: 363, 1971) but the capacity of autologous blood clots (ABC) to release pulmonary vasoactive substances is disputed. Ten normal mongrel dogs were anesthetised with pentobarbitone sodium and instrumented. Pulmonary venous blood was continuously superfused over isolated tissues for bioassay and then returned to the animal. Injection of ABC into the right atrium increased pulmonary artery pressure from 21 ± 6.5 mm Hg to 38 ± 15 mm Hg (mean ± S.D.), increased arterial pCO2 and decreased arterial pO2. No significant changes in heart rate, systemic arterial blood pressure or cardiac output occurred. In three animals contractions of the blood superfused assay tissues occurred following embolism. This effect was produced in normal assay tissues and those pretreated with antagonists of ACh, Serotonin, Histamine and Catecholamines and could therefore be attributed to PGLS. No cardiovascular or assay tissue tension changes were observed when equivalent volumes of saline or clot lysate were injected into the right atrium.Therefore, pulmonary embolism with ABC can release PGLS which may contribute to the pulmonary artery pressure rise. Vasoactive substances may normally be inactivated in the lung but in some animals appear in pulmonary venous blood.(Supported by the Ontario Heart Foundation)


1996 ◽  
Vol 79 (3_suppl) ◽  
pp. 1195-1202 ◽  
Author(s):  
Katija Čatipović-Veselica ◽  
Lidija Marošević ◽  
Vesna Ilakovac ◽  
Vjekoslav Amidžić ◽  
Damir Kozmar ◽  
...  

We examined Bortner scores for behavioral patterns and eight basic emotional dimensions named by Plutchik for patients with acute myocardial infarction who survived ventricular fibrillation and left ventricular failure. There were 70 patients, 48 men and 22 women ages 26 to 69 yr. ( M = 54, SD = 8), admitted to the coronary care unit within 24 hours of the onset of a long-lasting chest pain. Six patients survived an episode of ventricular fibrillation that occurred within 24 to 48 hours after their admission. 15 patients developed left ventricular failure and were in Killip Classes II and III. Patients with acute myocardial infarction and left ventricular failure had mean Bortner scores significantly lower than others with acute myocardial infarction and were classed as Type B behavior. There was no difference in Bortner scores between patients with ventricular fibrillation and others with acute myocardial infarction. Patients with acute myocardial infarction and left ventricular failure scored significantly higher on Timid than others with acute myocardial infarction. Patients with acute myocardial infarction and ventricular fibrillation scored significantly lower on Depressed and higher on Distrust than other patients with acute myocardial infarction. Our findings suggest that patients with ventricular fibrillation and low scores on Depressed have good hospital prognosis. They are more critical and tend to reject people and ideas more than patients with acute myocardial infarction. This study suggests that the way in which patients with acute myocardial infarction react to their infarction, in terms of eight basic emotions and test patterns, is dependent on the complications of myocardial infarction.


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