Correcting arterial hypoxemia by oxygen therapy in patients with acute myocardial infarction

Sukumalchantra, Y; Levy, Steven E.; Danzig, Ronald; Rubins, Steven; Alpern, Harvey; Swan, H.J.C.

doi:10.1016/0002-9149(69)90474-3

Cited by 49 publications

(22 citation statements)

References 24 publications

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“…Valentine et al [22], remarked that patients with frank pulmonary edema have particularly low PaC02 values. Sukumalchantra et al [20], found that PaCO., tended to be low in patients with shock, and M a ck en zie et al [13] found low, normal and high PaC02 values in patients with shock.…”

Section: Discussionmentioning

confidence: 97%

“…Low PaO,2 values have been associated with an increased incidence of left heart failure, pulmonary edema, hypotension-shock [4,7,12,14,20,21]. Comparing mean PaC02 values in patients with and without complications, Ljungstrom et al [9], H iggs [7], F illmore et al [4], and Sukumalchantra et al [20,21], found no significant differences.…”

Section: Discussionmentioning

confidence: 99%

“…Comparing mean PaC02 values in patients with and without complications, Ljungstrom et al [9], H iggs [7], F illmore et al [4], and Sukumalchantra et al [20,21], found no significant differences. Valentine et al [22], remarked that patients with frank pulmonary edema have particularly low PaC02 values.…”

Section: Discussionmentioning

confidence: 99%

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Arterial Oxygen and Carbon-Dioxide Tension in Patients with Acute Myocardial Infarction

Helmers¹,

Hofvendahl²,

Lundman³

et al. 1973

Cardiology

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Over a 2-year period, 450 cases of acute myocardial infarction were treated in a coronary care unit. Arterial PO₂ and PCO₂, were routinely determined on the day of admission. In this retrospective study, the patients were divided into groups according to their PaO₂ and PaCO₂ and the incidence of various clinical findings. Patients with low PaCO₂ and patients with low PaCO₂ values displayed the highest CCU and hospital mortality. Hypotension-shock and frank pulmonary edema were frequent in these patients. Pulmonary edema also was associated with high PaCO₂ values, but left heart failure without pulmonary edema was only correlated to low PaO₂ values. Supraventricular tachycardia, atrial flutter and fibrillation and left bundle branch block (including hemiblock) were common among patients with low PaO₂ and PaCO₂ values. Ventricular fibrillation was correlated to low PaO₂and high PaCO₂ values. The maximum respiratory rate recorded during the first day after admission proved an important indicator of short-term prognosis.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Arterial Oxygen and Carbon-Dioxide Tension in Patients with Acute Myocardial Infarction

Helmers¹,

Hofvendahl²,

Lundman³

et al. 1973

Cardiology

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“…At a basic pathophysiological level, MI induces hypoxemia in 32% to 70% of patients who do not receive oxygen therapy [2,3] and 5% to 27% of those who do receive oxygen therapy [3,4]. Accordingly, the latest American Heart Association guideline for ST-elevation MI (STEMI) [5] requires supplemental oxygen administration for MI patients with hypoxemia.…”

Section: Introductionmentioning

confidence: 99%

Systematic Review and Meta-Analysis of the Impact of Hypoxia on Infarcted Myocardium: Better or Worse?

Pang¹,

Zhao²,

Zhou³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Patients with myocardial infarction and hypoxemia require supplemental oxygen. However, the current therapeutic paradigm is contradicted by several recent studies in which the post-infarcted heart appears to benefit from systemic hypoxia. With this systematic review and meta-analysis, we aimed to discover whether systemic hypoxia is beneficial or detrimental to the infarcted myocardium. Methods: We conducted an electronic search of the PubMed, EMBASE, and Web of Science databases and extracted the outcomes of cardiac function, geometry, and hemodynamics. A random-effect model was applied when the I² value of greater than 50%. The sensitivity analysis was performed by omitting one study at a time, and publication bias was assessed using Egger’s test. In addition, the quality of studies was evaluated using the risk of bias tool devised by the Systematic Review Centre for Laboratory Animal Experimentation. Results: Six reports comprising 14 experiments were ultimately screened from among 10,323 initially identified preclinical studies. Few studies reported the method of randomization and none described allocation concealment, random outcome assessment or blinding. Overall, chronic hypoxia was found to have a beneficial effect on the ejection fraction (standard mean difference [SMD] = 5.39; 95% confidence interval [CI], 3.83 to 6.95; P < 0.001) of the infarcted heart, whereas acute hypoxia significantly improved hemodynamics, as indicated by an increase in the maximal rate of rise of left ventricular pressure (SMD = 1.27; 95% CI, 0.27 to 2.28; P = 0.013) and cardiac output (SMD = 1.26; 95% CI, 0.34 to 2.18; P = 0.007) and a decrease in total systematic vascular resistance (SMD = –0.89; 95% CI, –1.24 to –0.53; P < 0.001). Furthermore, a reduced oxygen content increased the stroke volume (P = 0.010). However, hypoxia reduced the end-systolic (SMD = –2.67; 95% CI, –4.09 to –1.26; P < 0.001) and end-diastolic (SMD = –3.61; 95% CI, –4.65 to –2.57; P < 0.001) left ventricular diameters and increased the total pulmonary resistance (SMD = 0.76; 95% CI, 0.20 to 1.33; P = 0.008), pulmonary arterial mean pressure (SMD = 2.02; 95% CI, 0.23 to 3.81; P = 0.027), and left atrial pressure (SMD = 1.20; 95% CI, 0.57 to 1.82; P < 0.001). Conclusion: Hypoxia significantly improved heart function after infarction, with particular beneficial effects on systolic function and hemodynamics. However, it had slightly adverse effects on pulmonary circulation and left ventricular geometry. A lower inspired oxygen concentration may improve cardiac function, although further research is needed to determine the optimum level of hypoxia. Finally, more studies of hypoxia and myocardial infarction in larger species are required before these findings can be incorporated into therapeutic guidelines.

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“…11 The importance of the degree of underlying arterial hypoxia in determining the effect of oxygen therapy following myocardial infarction was demonstrated by Sukumalchantra and colleagues in 1969. 12 They demonstrated that oxygen did not increase oxygen transport in patients with arterial oxygen saturations 490% because of reductions in cardiac output in excess of increases in oxygen content. In contrast, in patients with arterial oxygen saturations 590%, oxygen administration increased oxygen transport due to both increased cardiac output and oxygen content.…”

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confidence: 99%

Oxygen therapy in myocardial infarction: an historical perspective

Beasley

Aldington

Weatherall

et al. 2007

Journal of the Royal Society of Medicine

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Correcting arterial hypoxemia by oxygen therapy in patients with acute myocardial infarction

Cited by 49 publications

References 24 publications

Arterial Oxygen and Carbon-Dioxide Tension in Patients with Acute Myocardial Infarction

Arterial Oxygen and Carbon-Dioxide Tension in Patients with Acute Myocardial Infarction

Systematic Review and Meta-Analysis of the Impact of Hypoxia on Infarcted Myocardium: Better or Worse?

Oxygen therapy in myocardial infarction: an historical perspective

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