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You are watching: When the myocardium requires more oxygen:

StatPearls . Endowment Island (FL): StatPearls Publishing; 2021 Jan-.


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Introduction

The cardiovascular system is an intricately design vascular network that provides blood and also oxygen to the whole body. Myocardial oxygen demand is the lot of oxygen that the heart requires to preserve optimal function, and myocardial oxygen supply is the amount of oxygen noted to the heart by the blood i m sorry is controlled by the coronary arteries. When the human body is operating at the optimal physiologic condition, myocardial oxygen it is provided does no exceed myocardial oxygen need <1>.


Function

Since the heart operates specifically under aerobic metabolism, myocardial mitochondria must maintain wealth of oxygen to continue oxidative phosphorylation. Love rate, contractility, and also ventricular-wall tension are the three components that identify myocardial oxygen demand. An increase in any of this variables requires the human body to it is adapted to sustain sufficient oxygen supply to the heart.

Heart rate is thought to it is in the most important factor affect myocardial oxygen demand. With an raised heart rate, the myocardium should work more difficult to finish the cardiac cycle more efficiently. Through a shortened cardiac cycle, the time invested in diastole decreases. Because diastole ends prematurely, the amount of blood that normally fills the ventricles decreases, and oxygen-saturated hemoglobin is not enabled to reach the subendocardium. Under optimal conditions, myocardial oxygen need will equal myocardial oxygen supply; however, as soon as there is structural damage from a plaque that impedes flow, there can be a mismatch in between supply and also demand that outcomes in ischemia.

Contractility or inotropism is the rate of boost in the intraventricular pressure during contraction in ~ a given muscle fiber length.  Interestingly, myocytes have actually the innate capacity to exert a contraction at any muscle length. This pressure is measured ~ the closure that the mitral valve and also before the opening of the aortic valve throughout which time the intraventricular volume continues to be constant.

Contractility is impacted by a variety of intrinsic and also extrinsic forces including calcium concentration. Calcium is released by the sarcoplasmic reticulum of cardiac muscle and also binds come troponin C. This shortcut stimulates a conformational change of tropomyosin the releases that from the binding web page on the actin filament. Through the relax of tropomyosin, the active sites top top actin are free to bind myosin which reasons adenosine tree phosphate (ATP) to be broken down into adenosene diphosphate (ADP) and inorganic phosphate (P). Subsequently, there is a strength stroke that the myosin head which forces the actin filament centrally in the direction of the sarcomere, and ADP and P detach from the myosin head bring about contraction. As soon as ATP re-attaches come myosin, actin is freed. This cycle continues until intracellular calcium provides are depleted, over there is no much longer binding between troponin C and calcium, and tropomyosin have the right to revert come its initial confirmation to cover the binding web page on actin. Therefore, the intracellular calcium concentration is directly proportional to the contraction pressure <2>.

Ventricular wall surface tension is based on the thickness that the ventricular myocardium. The regulation of Laplace claims that ventricular wall tension is proportional to ventricular radius and also intraventricular pressure. Patients with coronary artery condition will have decreased blood and also oxygen supply to the myocardium. In this case, contractility will certainly be diminished. Due to the fact that the ventricle have the right to no longer attain adequate contraction, the end-systolic volume will certainly increase. The overabundance blood continuing to be in the ventricle will reason expansion the the ventricular radius and also intraventricular push resulting in greater wall tension.


Mechanism

The oxygen-carrying volume of the blood and flow through the coronary arteries regulate myocardial oxygen supply. Oxygen-carrying capacity have the right to be decreased in several problems that include either reduced red blood cell concentration or decreased oxygen saturation of hemoglobin. For example, anemia is a reduced than average variety of healthy red blood cells. Even though the red blood cells might be totally saturated through oxygen, there room not sufficient of lock to supply an enough amount of oxygen to the muscle. Usually, that is resulted in by a nutritional deficiency in iron, vitamin B12, or folate i beg your pardon is easily correctable. However, there have the right to be more devastating causes such together thalassemia, sickle cell anemia, and also various natural enzyme deficiencies that room more an overwhelming to act <1><3>.

Hemoglobin is the oxygen-carrying section of a red blood cell, and it is completely saturated once it binds four molecules of oxygen. V every molecule that oxygen the hemoglobin releases come the tissues, it binding the staying oxygen molecule with an ext affinity. Usually, hemoglobin only disperses one molecule the oxygen prior to it return to the lungs to become totally saturated when again. Carbon monoxide binding to hemoglobin v a much higher affinity than oxygen. When hemoglobin returns to the lungs to be re-oxygenated, it usually has actually usually one or 2 out that the complete four binding spaces available <1><3>.

Since carbon monoxide binding to hemoglobin v a higher affinity than oxygen, the secures the north binding point out of hemoglobin an ext quickly 보다 incoming oxygen. In ~ this point, hemoglobin is fifty to seventy-five percent saturated with oxygen and also twenty-five to fifty percent saturated through carbon monoxide. Also though hemoglobin has oxygen molecules attached, it will not release them right into the tissues. This occurs because hemoglobin’s affinity for oxygen is inversely proportional come its oxygen saturation. Therefore, the result hypoxia is not due to a lack of oxygen, however rather hemoglobin’s higher affinity for oxygen once only partly saturated with it <1><3>.

Even despite oxygen-carrying volume can affect myocardial oxygen supply, coronary blood circulation is the major determinant the supply. Coronary artery blood flow is a function of pressure separated by resistance. Myocardial oxygen consumption is equal to coronary blood circulation multiplied by the arterial-venous oxygen difference. During diastole, the ventricles room receiving blood prior to systolic contraction. This filling phase of the cardiac cycle allows the coronary arteries to carry out maximum blood circulation to the heart. Additionally, this is the only phase the the cardiac bicycle that enables blood to come at the subendocardium which is the most distal portion <1><3>.


Pathophysiology

A rise in myocardial oxygen need can come to be clinically far-reaching if it exceeds myocardial oxygen supply. This deserve to occur throughout the later stages of coronary artery condition (CAD). From years of poorly regulated hyperlipidemia, a patience can develop atherosclerotic plaques in the major arteries that supply blood come the heart. Once the integrity of the vasculature has actually been compromised, plaques deserve to develop and begin come shorten the diameter of the coronary arteries <1>.


Clinical Significance

Once the courage has much more than a seventy percent occlusion, the patient will usually start to experience symptoms. Usually, this symptoms such as chest pain, dyspnea top top exertion, and diaphoresis, existing during task or stress when the heart requires more oxygen. This is categorized as secure angina. However, when symptoms start presenting after less physical task or at rest, the an illness has progressed to an eighty-percent occlusion, and the diagnosis of unstable angina have the right to be do <4><5>.

A person who presents to the emergency department v angina must be evaluated because that a mismatch in myocardial oxygen supply and also demand. The an initial test to identify this is a 12-lead electrocardiogram (ECG) which procedures the electrical activity of the heart. The ST segment is representative of the time in between ventricular depolarization and also ventricular repolarization. If the ST segment is elevated top top arrival, it can be indicative that acute myocardial infarction; however, if there is a depressed ST segment, it have the right to be representative that acute ischemia <2><4>.

If the ECG is unremarkable, cardiologists may pick to execute an exercise tension test. In a regulated environment, cardiologists have the right to monitor the patient’s blood pressure, oxygen saturation, and also electrical activity of the heart. By performing an exercise, the patient is leading to the heart to increase its rate and contractility thus elevating the myocardial oxygen demand. If the vessels room atherosclerotic, the heart will certainly not be able to adapt come the alters in need thus there will certainly be a mismatch in between supply and demand which will certainly be represented appropriately on the ECG <6><4>.

Additionally, if patients have a contraindication to an exercise stress ECG, they can undergo myocardial perfusion imaging (MPI). Myocardial perfusion imaging have the right to be offered to study the myocardium for deficits in myocardial oxygen supply as result of atherosclerotic plaques native coronary artery disease. First, the patients are provided an adenosine analog and also a nuclear isotope which are both injected via an intravenous catheter. The adenosine analog stress the heart and increases myocardial oxygen demand. The patient is monitored for transforms in oxygen saturation, blood pressure, heart rate, and also rhythm <4>.

Next, the second part of the nuclear stress and anxiety test deserve to begin. The buildup of the atom isotope in the vessels allows clear images of the coronary arteries and also surrounding vasculature to be obtained. Currently, the traditional model includes gathering pictures from seventeen segments: 16 short-axis views and also the long-axis watch of the apical segment. Cardiologists grade every view making use of a scale selection of zero come four; 0 = normal, 1 = mildly abnormal, 2 = moderately abnormal, 3 = severely abnormal, 4 = absent. The summed perfusion score (SPS) is the complete score including images from rest and also stress, the summed relaxing score (SRS) to represent the severity of myocardial infarction, and the summed stress and anxiety score (SSS) mirrors the extent of myocardial ischemia and also infarction. To recognize the severity of ischemia alone, the summed distinction score (SDS) have to be calculate by individually the SRS native the SSS <6><4>.

A mismatch between myocardial oxygen supply and demand can an outcome in myocardial ischemia or infarct. Unfortunately, infarct results in irreversible damages to the myocardium. However, ischemia and potential reasons of mismatch have the right to be controlled through a selection of pharmaceutical agents that include nitrates, beta-adrenergic-receptor blockers, and calcium-channel blockers. Every of this medication classes boosts myocardial oxygen supply and also decrease myocardial oxygen need to varying levels <1><7>.

Nitrates reason a be safe in the vascular smooth muscle which reasons dilatation that the coronary arteries and systemic venous circulation. As soon as the vessels transferring de-oxygenated blood back to the heart are dilated resulting in the venous volume to increase, over there are equivalent decreases in cardiac preload, ventricular volume, and ventricular wall surface tension throughout systole. Because of the downward shift in workload forced by the heart, myocardial oxygen demand is reduced.  Additionally, through the dilatation of coronary arteries, nitrates likewise increase myocardial oxygen supply. The raised radius the the vasculature supplying the heart allows blood to bypass potential plaques to administer a consistent supply of blood <8><9>.

Beta-adrenergic receptor blockers inhibit the results of catecholamines in ~ the beta receptors. Usually, the forgiveness nervous system stimulates the relax of catecholamines to tie to beta receptors causing boost in love rate, contractility, and also blood pressure through vasoconstriction. Since beta-blockers protect against catecholamines from connecting with the beta-adrenergic receptors, over there is a diminish in love rate and contractility hence diminishing myocardial oxygen demand. Additionally, the slower heart permits for a lengthened diastolic section of the cardiac cycle. Due to the fact that of this, much more blood is enabled to supply to the heart throughout the filling step <1>.

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Calcium-channel blockers prevent the entrance of calcium through voltage-gated channels. Since contractility is reliant on calcium relax from the sarcoplasmic reticulum, a diminished supply the calcium will certainly inherently cause a autumn in contractility. This drop-in contractility causes a diminish in myocardial oxygen demand. Additionally, the vasodilatory impacts of calcium-channel blockers on vascular smooth muscle result in rise in myocardial oxygen supply <10>.