The major determinants of Myocardial oxygen demand (MVO2) are heart rate, contractility, and intramyocardial wall tension during systole. Wall tension is thought to be the most important factor. Because the consequences of IHD usually result from increased oxygen demand in the face of a fixed oxygen supply, alterations in MVO2 are important in producing ischemia and for interventions intended to alleviate it.
A clinically useful indirect estimate of MVO2 is the double product (DP), which is heart rate (HR) multiplied by systolic blood pressure (SBP) (DP = HR X SBP). The DP does not consider changes in contractility (an independent variable), and because only changes in pressure are considered, volume loading of the left ventricle and increased MVO2 related to ventricular dilation are underestimated.
The caliber of the resistance vessels delivering blood to the myocardium and MVO2 are the prime determinants in the occurrence of ischemia.
The normal coronary system consists of large epicardial or surface vessels (R1) that offer little resistance to myocardial flow and intramyocardial arteries and arterioles (R2) that branch into a dense capillary network to supply basal blood flow. Under normal circumstances, the resistance in R2 is much greater than that in R1. Myocardial blood flow is inversely related to arteriolar resistance and directly related to the cornoary driving pressure.
Atherosclerotic lesions occluding R1 increase arteriolar resistance and R2 can vasodilate to maintain coronary blood flow. With greater degrees of obstruction, this response is inadequate, and the coronary flow reserve afforded by R2 vasodilation is insufficient to meet oxygen demand. Relatively severe stenosis (greater than 70%) may provoke ischemia and symptoms at rest, whereas less severe stenosis may allow a reserve of coronary blood flow for exertion.
The diameter and length of obstructing lesions and the influence of pressure drop across an area of stenosis also affect coronary blood flow and function of the collateral circulation. Dynamic coronary obstruction can occur in normal vessels and vessels with stenosis in which vasomotion or spasm may be superimposed on a fixed stenosis. Persisting ischemia may promote growth of developed collateral blood flow.
Critical stenosis occurs when the obstructing lesion encroaches on the luminal diameter and exceeds 70%. Lesions creating obstruction of 50% to 70% may reduce superimposed on a noncritical lesion may lead to clinical events such as AMI. If the lesion enlarges from 80% to 90%, resistance in that vessel is tripled. Coronary reserve is diminished at about 85% obstruction due to vasoconstriction.
Abnormalities of ventricular contraction can occur, and regional loss of contractility may impose a burden on the remaining myocardial tissue, resulting in heart failure, increased MVO2, and rapid depletion of blood flow reserve. Zones of tissue with marginal blood flow may develop that are at risk for more severe damage if the ischemic episode persists or becomes more severe. Nonischemic areas of myocardium may compensate for the severely ischemic and border zones of ischemia by developing more tension than usual in an attempt to maintain cardiac output. The left or right ventricular dysfunction that ensues may be associated with clinical findings of an S3 gallop, dyspnea, orthopnea, tachycardia, fluctuating blood pressure, transient murmurs, and mitral or tricuspid regurgitation. Impaired diastolic and systolic function leads to elevation of the filling pressure of the left ventricle.
A clinically useful indirect estimate of MVO2 is the double product (DP), which is heart rate (HR) multiplied by systolic blood pressure (SBP) (DP = HR X SBP). The DP does not consider changes in contractility (an independent variable), and because only changes in pressure are considered, volume loading of the left ventricle and increased MVO2 related to ventricular dilation are underestimated.
The caliber of the resistance vessels delivering blood to the myocardium and MVO2 are the prime determinants in the occurrence of ischemia.
The normal coronary system consists of large epicardial or surface vessels (R1) that offer little resistance to myocardial flow and intramyocardial arteries and arterioles (R2) that branch into a dense capillary network to supply basal blood flow. Under normal circumstances, the resistance in R2 is much greater than that in R1. Myocardial blood flow is inversely related to arteriolar resistance and directly related to the cornoary driving pressure.
Atherosclerotic lesions occluding R1 increase arteriolar resistance and R2 can vasodilate to maintain coronary blood flow. With greater degrees of obstruction, this response is inadequate, and the coronary flow reserve afforded by R2 vasodilation is insufficient to meet oxygen demand. Relatively severe stenosis (greater than 70%) may provoke ischemia and symptoms at rest, whereas less severe stenosis may allow a reserve of coronary blood flow for exertion.
The diameter and length of obstructing lesions and the influence of pressure drop across an area of stenosis also affect coronary blood flow and function of the collateral circulation. Dynamic coronary obstruction can occur in normal vessels and vessels with stenosis in which vasomotion or spasm may be superimposed on a fixed stenosis. Persisting ischemia may promote growth of developed collateral blood flow.
Critical stenosis occurs when the obstructing lesion encroaches on the luminal diameter and exceeds 70%. Lesions creating obstruction of 50% to 70% may reduce superimposed on a noncritical lesion may lead to clinical events such as AMI. If the lesion enlarges from 80% to 90%, resistance in that vessel is tripled. Coronary reserve is diminished at about 85% obstruction due to vasoconstriction.
Abnormalities of ventricular contraction can occur, and regional loss of contractility may impose a burden on the remaining myocardial tissue, resulting in heart failure, increased MVO2, and rapid depletion of blood flow reserve. Zones of tissue with marginal blood flow may develop that are at risk for more severe damage if the ischemic episode persists or becomes more severe. Nonischemic areas of myocardium may compensate for the severely ischemic and border zones of ischemia by developing more tension than usual in an attempt to maintain cardiac output. The left or right ventricular dysfunction that ensues may be associated with clinical findings of an S3 gallop, dyspnea, orthopnea, tachycardia, fluctuating blood pressure, transient murmurs, and mitral or tricuspid regurgitation. Impaired diastolic and systolic function leads to elevation of the filling pressure of the left ventricle.
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