Approaches to the Prevention of Perioperative Myocardial Ischemia

2000 ◽  
Vol 92 (1) ◽  
pp. 253-253 ◽  
Author(s):  
David C. Warltier ◽  
Paul S. Pagel ◽  
Judy R. Kersten

Goals for the perioperative management of patients with coronary artery disease include: * Prevent increases in sympathetic nervous system activity: reduce anxiety preoperatively; prevent stress response and release of catecholamines by appropriate use of opioids or volatile anesthetics and beta-adrenoceptor antagonists; beta-blocker therapy should be initiated before and continued during and after the surgical procedure. * Decrease heart rate: reduction in heart rate increases oxygen supply to ischemic myocardium and reduces oxygen demand; the use of beta-blockers is the most effective means to reduce or attenuate deleterious increases in heart rate. * Preserve coronary perfusion pressure: decreases in diastolic arterial pressure in the presence of severe coronary artery stenoses will lead to decreases in blood flow; preservation of perfusion pressure by administration of fluid or phenylephrine or a reduction in anesthetic concentration may be critical. * Decrease myocardial contractility: reduces myocardial oxygen demand and can be accomplished with beta-adrenoceptor antagonists or volatile anesthetics. * Precondition myocardium against stunning and infarction: in the future, this may accomplished by stimulating the adenosine triphosphate- dependent potassium channel with agents such as volatile anesthetics and opioid delta1-receptor agonists.

2004 ◽  
Vol 21 (9) ◽  
pp. 1025-1031 ◽  
Author(s):  
K. Foo ◽  
N. Sekhri ◽  
C. Knight ◽  
A. Deaner ◽  
J. Cooper ◽  
...  

1998 ◽  
Vol 275 (5) ◽  
pp. H1520-H1523 ◽  
Author(s):  
Miao-Xiang He ◽  
H. Fred Downey

The mechanism responsible for the abrupt fall in myocardial contractile function following coronary artery obstruction is unknown. The “vascular collapse theory” hypothesizes that the fall in coronary perfusion pressure after coronary artery obstruction is responsible for contractile failure during early ischemia. To test the role of vascular collapse in downregulating myocardial contractile force at the onset of ischemia, coronary flow of isolated rat hearts was abruptly decreased by 50, 70, 85, and 100% of baseline, and subsequent changes in coronary perfusion pressure and ventricular function were recorded at 0.5-s intervals. At 1.5 s after flow reductions ranging from 50 to 100%, decreases in contractile function did not differ, although perfusion pressure varied significantly from 45 ± 1 to 20 ± 2 mmHg. When function fell to 50% of baseline, perfusion pressures ranged from 35 ± 0.5 to 2.5 ± 1 mmHg for flow reductions ranging from 50 to 100%. Identical contractile function at widely differing coronary perfusion pressures is incompatible with the vascular collapse theory.


2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P2482-P2482
Author(s):  
T. Inoue ◽  
O. Arasaki ◽  
K. Kawamitsu ◽  
K. Kajiwara ◽  
Y. Shinzato ◽  
...  

1998 ◽  
Vol 26 (3) ◽  
pp. 107-119 ◽  
Author(s):  
I González Maqueda

Beta-blockers and vasodilators, such as nitrates and calcium channel blockers, are all established antianginal therapies. These therapies have different antianginal mechanisms that dictate both their mode of action and their side-effect profile. An agent with both cardiac beta- and vascular alpha-receptor activity offers advantages over these conventional drugs. Carvedilol, a multiple-action neurohormonal antagonist, has potent antihypertensive and antianginal activity. Through its combination of pharmacological mechanisms, it reduces myocardial oxygen demand, increases myocardial blood supply and scavenges oxygen free radicals, which are capable of ischaemic damage. Studies have shown that carvedilol is at least as effective as other antianginal therapies in the management of chronic stable angina. Carvedilol is well tolerated – in several cases, the overall incidence of adverse events being lower than with other antianginal agents. These properties, combined with the documented antianginal effects, suggest that carvedilol may prove useful for the treatment of patients with chronic stable angina.


Author(s):  
Ajay Suri ◽  
Jean R. McEwan

Angina is chest pain resulting from the lack of blood supply to heart muscle most commonly due to obstructive atherosclerotic. Intensive care unit patients are subject to various stresses that will increase the demand on the heart and are in a pro-thrombotic state. Patients in an intensive treatment unit may be sedated and so cardiac ischaemia may be detected by electrocardiogram, haemodynamic monitoring, and echocardiographic imaging of function. These signs may indicate critical coronary perfusion heralding a myocardial infarction and are alleviated by anti-anginal drugs. Beta-blockers and calcium channel blockers are the usual first-line treatments for angina, but may not be ideal in the critically-ill patient. Nitrates reduce blood pressure without typically affecting heart rate. Nicorandil is a similar mechanism of action and tends to be given orally, while ivabridine, an If channel blocker, is a newer anti-anginal, which acts by reducing heart rate, while not affecting blood pressure. Ranolazine is the one of the newest anti-anginal agents and is believed to alter the transcellular late sodium current thereby decreasing sodium entry into ischaemic myocardial cells.


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