Objectives:

The student should be able to:

  • Know the basic anatomy of coronary arterial and venous circulations.
  • Describe the patterns of coronary blood flow throughout the cardiac cycle.
  • Recognized the factors involved in the regulation of coronary blood flow.
  • Know the special features of cardiac muscle metabolism.
  • Identify atherosclerosis as the major cause of coronary artery disease.
  • Divide coronary artery disease patients between stable angina pectoris, unstable angina pectoris and myocardial infarction based on the mechanism of disease.
  • Define and understand the following concepts related to reversible myocardial ischemia: preconditioning, post-conditioning, stunning, hibernation, ischemia-reperfusion injury. 

Normal Coronary Blood Flow:

The resting coronary blood flow in human being averages about 225 ml /min, which is about 4 to 5 percent of the total cardiac output. The cardiac output (CO) can be increased to fourfold up to sevenfold in young adults during strenuous exercises, and it pumps this blood against a higher-than-normal arterial blood pressure, in other words, the cardiac output under severe conditions may increase six-fold to nine-fold. While, the coronary blood flow increases three-fold to four-fold during exercise to supply the extra nutrients needed to the heart, such increases are not as much as the increase in work load, which means that O2 supply to the myocardium could not meet its energy requirement

Coronary Circulation:

  • Heart muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation, not from blood within heart chambers.
  • Coronary blood flow normally varies to keep pace with cardiac oxygen needs.

  • Heart receives most of its own blood supply that occurs during diastole (70%).
  • During systole, coronary vessels are compressed by contracting heart muscle.
  • During systole, the open aortic valve blocks the entrance to the coronary vessels.

Coronary Blood Flow in left Ventricular Capillaries

Regulation of coronary blood flow by local metabolism and oxygen demand:

  • In humans coronary blood flow at rest is about 225-250 ml/minute, about 5% of cardiac output.
  • Heart muscle has more mitochondria, up to 40% of the cell volume is occupied by mitochondria, which generate energy for contraction by aerobic metabolism, therefore, heart needs O2.
  • 70% of arterial oxygen is removed by the heart.
  • Coronary blood flow auto-regulated by oxygen demand.
  • Any further oxygen needs are met by increase in coronary blood flow.

Cardiac Muscle Metabolism:

At rest the heart uses fatty acids for 70% of its metabolic energy requirements and to lesser extent glucose and lactate.

  • Anaerobic glycolysis takes over under stress and ischemic conditions.

Factors Affecting Blood Flow to Coronary Arteries:

  • Chemical factors
  • Nervous stimuli

Effect of Tachycardia on Coronary Blood Flow:

  • During increased heart rate, period of diastole is shorter therefore coronary blood flow is reduced to heart during tachycardia.

Chemical Factors Causing Coronary Vasodilatation:

Increased Coronary Blood Flow:

   -Lack of oxygen

   -Increased local concentration of Co2 -Increased local concentration of H

   -Increased local concentration of k +

   -Increased local concentration of Lactate, Prostaglandin, Adenosine, Adenine nucleotides.

Regulation of Coronary Blood Flow by Nervous Stimuli:

  • Sympathetic and parasympathetic stimulation control coronary flow directly (action on coronary circulation) and indirectly (through the action on cardiac activity.
  • Small vagal innervation of the coronary circulation: acetylcholine dilates the coronary arteries.
  • More extensive sympathetic innervation; more beta-adrenergic receptors on the epicardial arteries and more alpha receptors on the intramuscular arteries. Overall effect is vasoconstrictive (alpha)
  • Metabolic control (oxygen) overrides nervous control

Coronary Artery Disease:

Pathological changes within coronary artery walls that diminish blood flow through the vessels. Leading cause of death worldwide.

Can cause myocardial ischemia and possibly lead to acute myocardial infarction

Three Mechanisms:

  1. Profound vascular spasm of coronary arteries
  2. Formation of atherosclerotic plaques
  3. Thromboembolism

  • Chronic obstruction of a coronary artery classically causes angina pectoris (pain of the chest)
  • Acute obstruction or occlusion causes unstable angina.

Myocardial Infraction (MI):

  • It is due to obstruction to the coronary blood flow, at lease 75 % of the lumen of the coronary artery is blocked by thrombus.
  • Oxygen is supplied by coronary blood to meet the demand of the myocardium. A mismatch between supply and demand causes ischemia.

Ischemic Heart Disease (IHD):

IHD is decreased coronary blood flow (Transient Myocardial Ischemia) Patient complains of tightness or pain in the middle of the chest (retrosternal) for few minutes. Pain often radiates to inner side of left arm. Pain is precepted by effort and relieved by rest.

Metabolic and Functional Consequences of Ischemia:

Reduced or discontinued coronary flow leads to:

  1. Depletion of oxygen
  2. Anaerobic metabolism
  3. Depletion of ATP
  4. Cell death

Symptoms and Signs:

  • Coronary Ischemia

 

  • Acute Coronary Syndromes
  • Diagnostics
  • ECG (12 or 15 lead)
  • T wave inversion
  • ST segment elevation
  • Q wave
  • reciprocal ST segment depression

ST Segment Changes: Identifying MI Mimics:

EKG diagnosis of MI

T Segment Changes: Identifying MI Mimics

Coronary Artery Disease:

Functional Consequences of Reversible Ischemia:

  • Preconditioning and post-conditioning
  • Stunning
  • Hibernation
  • Ischemia-reperfusion injury

Preconditioning and Post-conditioning:

  • Preconditioning: episodes of reversible ischemia preceding infarction reduce necrosis. The effect of preconditioning persists for up to 4 days
  • Post-conditioning: episodes of intermittent reversible ischemia after reperfusion reduce injury

Collateral Coronary Circulation:

Collateral circulation compensates coronary obstruction

  • Opening of existing interarterial anastomoses
  • Formation of new vessels

Stunned Myocardium:

  • Myocardial function is reduced during ischemia
  • Myocardial function recovers completely if ischemia lasts less than 2 minutes
  • With more severe and more prolonged ischemia, myocardial function recovery is delayed after blood flow is restored. Stunning is this delayed recovery.

Chronic Hibernating Myocardium:

  • Chronic ischemia
  • Chronic reduction of function
  • No infarction (viable myocardium)
  • Reduced mitochondrial activity but normal ATP reserve
  • Increased arrhythmias, increased sympathetic innervation disparity

CORONARY ARTERY BYPASS SURGERY

Stable Angina – Treatment 

Coronary Artery Bypass Grafting Surgery (CABG)

Coronary Artery Bypass Grafting Surgery

Treatment of Stable AnginaSTENTS

Treatment of Stable Angina - STENTS

Stable Angina – Treatment:

  • Risk factor modification (HMG Co-A Reductase inhibitors = Statins)
  • Aspirin
  • Decrease MVO2
  •  Nitrates 
  • beta-blockers
  • calcium channel blocker
  • ACE-inhibitors
  • Anti-oxidants (E, C, Folate, B6)?

References:

  • Human physiology, Lauralee Sherwood, seventh edition.
  • Text book physiology by Guyton &Hall,11th edition.
  • Physiology by Berne and Levy, sixth edition

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