Blood-Gas and Hemodynamic Responses to Oxygen in Acute Myocardial Infarction

Davidson, Robert M.; Ramo, Barry W.; Wallace, Andrew G.; Whalen, Robert E.; Starmer, C. Frank

doi:10.1161/01.cir.47.4.704

Cited by 20 publications

(10 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The recommendations of the New Zealand Branch of the Cardiac Society of Australia and New Zealand may be preferred,42 in which it is recommended that “oxygen should be administered to keep the saturations around 96%” as level D evidence. Hypoxaemia may commonly occur in MI35 39 51 and oxygen therapy may be indicated to relieve hypoxaemia identified by oximetry monitoring in this situation.…”

Section: Discussionmentioning

confidence: 99%

Routine use of oxygen in the treatment of myocardial infarction: systematic review

Wijesinghe

Perrin

Ranchord

et al. 2008

Heart

149

View full text Add to dashboard Cite

Context: International guidelines recommend the routine use of oxygen therapy in the treatment of myocardial infarction (MI). Objective: To undertake a systematic review and metaanalysis of randomised placebo-controlled trials of oxygen therapy in MI. Data sources: Medline, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, EMBASE and CINHAL. Study selection: Randomised placebo-controlled trials of oxygen therapy in MI. Data extraction: The primary clinical outcome was mortality. Results: Two of 51 potential studies met the inclusion criteria. The one study with substantive clinical outcome data reported that in uncomplicated MI, high-flow oxygen was associated with a non-significant increased risk of death (risk ratio 2.9, 95% CI 0.8 to 10.3, p = 0.08) and a greater serum aspartate aminotransferase level (difference 19.2 IU/ml, 95% CI 0 to 38.4, p = 0.05) than room air. Conclusion: The limited evidence that does exist suggests that the routine use of high-flow oxygen in uncomplicated MI may result in a greater infarct size and possibly increase the risk of mortality.Oxygen has been used in the treatment of myocardial infarction (MI) and acute coronary syndromes for over 100 years.1 The rationale for its longstanding use is that it increases oxygen delivery to the ischaemic myocardium, thereby reducing the size of the MI and improving clinical outcomes. Evidence in support of this approach is primarily derived from animal models, in which the administration of 100% oxygen under normobaric or hyperbaric conditions during and/or after experimental coronary artery occlusion reduces the extent of myocardial necrosis in some, 2-6 but not all, studies. 7-10However, concern has been expressed that the findings from animal studies may have poor generalisability to the clinical situation in humans. 11Furthermore, there is evidence that the routine use of high-flow oxygen in uncomplicated MI may not improve clinical outcomes and may potentially cause harm.11 12 It is well established that arterial oxygen tension is a major determinant of coronary artery tone [13][14][15][16] and that hyperoxia may result in a marked reduction in coronary artery blood flow. [17][18][19][20][21][22][23][24] Other cardiovascular effects of high-flow oxygen therapy include a reduction in cardiac output and stroke volume and an increase in systemic vascular resistance and blood pressure in patients with a MI. [25][26][27][28][29][30][31] Despite this conflicting evidence, contemporaneous international guidelines 32 33 recommend the routine use of supplemental oxygen in the treatment of MI. As the treatment of MI is at the forefront of evidence-based medicine, we sought to review the clinical efficacy and safety of the use of oxygen in this clinical situation. A systematic review was undertaken to identify randomised placebo-controlled trials of oxygen therapy in the treatment of acute MI with the intention of estimating differences in clinical outcomes by meta-analysis. METHODS Search strategyTo i...

show abstract

Section: Discussionmentioning

confidence: 99%

Routine use of oxygen in the treatment of myocardial infarction: systematic review

Wijesinghe

Perrin

Ranchord

et al. 2008

Heart

149

View full text Add to dashboard Cite

show abstract

“…The acute effects of intravenous furosemide in patients with valvular heart disease [17] or acute myocardial infarction [11,[18][19][20][21][22] have been well documented. Furosemide, 0.5-1.0 mg/kg intravenously, lowered pulmo nary artery wedge pressure (PWP), usually with a reduction in cardiac output.…”

Section: Cascade Of Events Following Early Diuretic Therapy Of Heart mentioning

confidence: 99%

“…The relative homogeneity of the hae modynamic response to bumetanide at rest was similar to the described profile for other 120 Silke Haemodynamics of Diuretic Therapy in Chronic Heart Failure Echocardiographie shortening in patients with normal ventricular function or severe con gestive heart failure. Redrawn with permission from Dalla Volta et al [40], agents at rest [11,12,[18][19][20][21][28][29][30][31][32][33]. Contrast ing with the resting data of normal distribution type, the exercise results suggested a less ho mogeneous response ( fig.…”

Section: Clinical Findings and Haemodynamic Responsementioning

confidence: 99%

Haemodynamic Impact of Diuretic Therapy in Chronic Heart Failure

Silke

1994

Cardiology

View full text Add to dashboard Cite

An immediate improvement in haemodynamic variables and cardiac performance is achieved in chronic heart failure following diuretic therapy, primarily due to reductions in plasma and extracellular fluid volumes. Humoral markers of these alterations are increased plasma renin, angiotensin and aldosterone levels; these increase maximally over the ñrst week of treatment but attenuate during sustained therapy. There are reciprocal alterations in plasma α-atrial natriuretic peptide levels. These findings suggest that the initial volume contraction is maintained, though somewhat attenuated, during chronic therapy. The neurohumoral consequences of diuretic therapy are of particular interest in heart failure, as they may contribute to diuretic resistance. Activation of the renin-angiotensin system favours the proximal tubular reabsorption of sodium and water, which may result in dilutional hyponatraemia. Diuretics have both direct vascular and non-vascular (volume-dependent) haemodynamic actions. Together these substantially reduce the left heart filling pressure (-29%) with a consequent fall in cardiac output ( 10%). Systemic vascular resistance initially increases but subsequently normalizes, allowing cardiac output to return towards control values. Haemodynamic tolerance to diuretics does not usually occur during sustained oral therapy; additionally, echocardiographic contractility indices and exercise capacity may increase. The vasodilator activity of the diuretics is due to prostaglandin release; the initial pressor action is due to activation of the renin-angiotensin system. Direct pulmonary vasodilatation with improved pulmonary compliance remains an interesting possibility. Over the longer term, substantial reductions in left heart filling pressure during exercise occur at unaltered cardiac output. The impact of diuretic therapy on the underlying myocardial disease process is unknown. There is little direct evidence of ventricular remodelling or of improved intrinsic cardiac performance (as distinct from that due to altered loading conditions). In the absence of such information, it would appear reasonable to combine diuretic therapy with a vasodilator or angiotensin converting enzyme inhibitor, even in patients symptomatically well controlled on diuretic alone.

show abstract

“…responses to hyperoxia are greatest in patients with uncomplicated myocardial infarction, (ie, no heart failure or cardiogenic shock). 6 For instance, using supplemental oxygen in a patient who has a 95% oxygen saturation seems out of line with the main reason for using oxygen in any patient; that is, hypoxia. So, if there is no indication for its use it is hard to justify the use of supplemental oxygen in patients who are not hypoxic.…”

Section: Why Worry About Supplemental Oxygen In Acute Myocardial Infamentioning

confidence: 99%