Myocardial oxygen consumption  (MVO₂)

Myocardial oxygen consumption is a value, dependent on the functional state of organism. When myocardial oxygen consumption increases, stomach, liver and smooth muscles consume less oxygen, which predetermines activation of the enzymes, creatinine kinase in particular.

Experimental studies have demonstrated that the heart rate, wall tension and contractility (or the velocity of contraction) are all among the major determinants of myocardial oxygen consumption (MVO₂). The basal O₂ consumption of the arrested heart is approximately 20% that of the contracting heart. On the other hand, the O₂ requirements for myocyte depolarization are only 0.5% of the working heart.

Mechanism

The oxygen-carrying capacity of the blood and flow through the coronary arteries regulate myocardial oxygen supply. Oxygen-carrying capacity can be decreased in several conditions that include either decreased red blood cell concentration or decreased oxygen saturation of hemoglobin. For example, anemia is a lower-than-average number of healthy red blood cells. Even though the red blood cells may be fully saturated with oxygen, there are not enough of them to supply an adequate amount of oxygen to the muscle. Usually, it is caused by a nutritional deficiency in iron, vitamin B12, or folate which is easily correctable. However, there can be more devastating causes such as thalassemia, sickle cell anemia, and various inherent enzyme deficiencies that are more difficult to treat [1][3].

Hemoglobin is the oxygen-carrying portion of a red blood cell, and it is fully saturated when it binds four molecules of oxygen. With every molecule of oxygen that hemoglobin releases to the tissues, it binds the remaining oxygen molecules with more affinity. Usually, hemoglobin only disperses one molecule of oxygen before it returns to the lungs to become fully saturated once again. Carbon monoxide binds to hemoglobin with a much higher affinity than oxygen. When hemoglobin returns to the lungs to be re-oxygenated, it usually has usually one or two out of the total four binding spaces available [1][3].

Since carbon monoxide binds to hemoglobin with a higher affinity than oxygen, it secures the empty binding spots of hemoglobin more quickly than incoming oxygen. At this point, hemoglobin is fifty to seventy-five percent saturated with oxygen and twenty-five to fifty percent saturated with carbon monoxide. Even though hemoglobin has oxygen molecules attached, it will not release them into the tissues. This occurs because hemoglobin’s affinity for oxygen is inversely proportional to its oxygen saturation. Therefore, the resulting hypoxia is not due to a lack of oxygen, but rather hemoglobin’s higher affinity for oxygen when only partially saturated with it [1][3].

Even though oxygen-carrying capacity can impact myocardial oxygen supply, coronary blood flow is the major determinant of supply. Coronary artery blood flow is a function of pressure divided by resistance. Myocardial oxygen consumption is equal to coronary blood flow multiplied by the arterial-venous oxygen difference. During diastole, the ventricles are receiving blood before systolic contraction. This filling phase of the cardiac cycle allows the coronary arteries to provide maximum blood flow to the heart. Additionally, this is the only phase of the cardiac cycle that allows blood to arrive at the sub endocardium which is the most distal portion [1][3].

Pathophysiology

A rise in myocardial oxygen demand can become clinically significant if it exceeds myocardial oxygen supply. This can occur during the later stages of coronary artery disease (CAD). From years of poorly controlled hyperlipidemia, a patient can develop atherosclerotic plaques in the major arteries that supply blood to the heart. Once the integrity of the vasculature has been compromised, plaques can develop and begin to shorten the diameter of the coronary arteries [1].

Clinical Significance

Once the vessel has more than a seventy percent occlusion, the patient will usually begin to experience symptoms. Usually, these symptoms such as chest pain, dyspnea on exertion, and diaphoresis, present during activity or stress when the heart requires more oxygen. This is categorized as stable angina. However, once symptoms begin presenting after less physical activity or at rest, the disease has progressed to an eighty-percent occlusion, and the diagnosis of unstable angina can be made [4][5].

A person who presents to the emergency department with angina should be evaluated for a mismatch in myocardial oxygen supply and demand. The first test to determine this is a 12-lead electrocardiogram (ECG) which measures the electrical activity of the heart. The ST segment is representative of the time between ventricular depolarization and ventricular repolarization. If the ST segment is elevated upon arrival, it can be indicative of acute myocardial infarction; however, if there is a depressed ST segment, it can be representative of acute ischemia [2][4].

If the ECG is unremarkable, cardiologists may choose to perform an exercise stress test. In a controlled environment, cardiologists can monitor the patient’s blood pressure, oxygen saturation, and electrical activity of the heart. By performing an exercise, the patient is causing the heart to increase its rate and contractility thus elevating the myocardial oxygen demand. If the vessels are atherosclerotic, the heart will not be able to adapt to the changes in demand thus there will be a mismatch between supply and demand which will be represented accordingly on the ECG [6][4].

https://www.sciencedirect.com/topics/immunology-and-microbiology/heart-muscle-oxygen-consumption

https://www.ncbi.nlm.nih.gov/books/NBK499897/

1.

Rehman S, Khan A, Rehman A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Physiology, Coronary Circulation. [PubMed]

2.

González-Del-Hoyo M, Cediel G, Carrasquer A, Bonet G, Consuegra-Sánchez L, Bardají A. Diagnostic and prognostic implications of troponin elevation without chest pain in the emergency department. 2018 AbrEmergencias. 30(2):77-83. [PubMed]

3.

Crystal GJ, Pagel PS. Right Ventricular Perfusion: Physiology and Clinical Implications. Anesthesiology. 2018 Jan;128(1):202-218. [PubMed]

4.

Chapman AR, Adamson PD, Mills NL. Assessment and classification of patients with myocardial injury and infarction in clinical practice. Heart. 2017 Jan 01;103(1):10-18. [PMC free article] [PubMed]

5.

Kundu A, Vaze A, Sardar P, Nagy A, Aronow WS, Botkin NF. Variant Angina and Aborted Sudden Cardiac Death. Curr Cardiol Rep. 2018 Mar 08;20(4):26. [PubMed]

6.

Bob-Manuel T, Ifedili I, Reed G, Ibebuogu UN, Khouzam RN. Non-ST Elevation Acute Coronary Syndromes: A Comprehensive Review. Curr Probl Cardiol. 2017 Sep;42(9):266-305. [PubMed]

7.

Mihatov N, Januzzi JL, Gaggin HK. Type 2 myocardial infarction due to supply-demand mismatch. Trends Cardiovasc Med. 2017 Aug;27(6):408-417. [PubMed]

8.

Asrress KN, Williams R, Lockie T, Khawaja MZ, De Silva K, Lumley M, Patterson T, Arri S, Ihsan S, Ellis H, Guilcher A, Clapp B, Chowienczyk PJ, Plein S, Perera D, Marber MS, Redwood SR. Physiology of Angina and Its Alleviation With Nitroglycerin: Insights From Invasive Catheter Laboratory Measurements During Exercise. Circulation. 2017 Jul 04;136(1):24-34. [PMC free article] [PubMed]

9.

Münzel T, Daiber A. Inorganic nitrite and nitrate in cardiovascular therapy: A better alternative to organic nitrates as nitric oxide donors? Vascul Pharmacol. 2018 Mar;102:1-10. [PubMed]

10.

Turgeon RD, Pearson GJ, Graham MM. Pharmacologic Treatment of Patients With Myocardial Ischemia With No Obstructive Coronary Artery Disease. Am J Cardiol. 2018 Apr 01;121(7):888-895. [PubMed]