Myocardial Ischemia, Injury, and Infarction: Mechanisms of Current of Injury PDF

Myocardial Ischemia, Injury, and Infarction: Mechanisms of Current of Injury Karen Thaxter Nesbeth Reference: Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program 1  Myocardial Oxygen Supply Heart’s oxygen and nu...

Myocardial Ischemia, Injury, and Infarction: Mechanisms of Current of Injury Karen Thaxter Nesbeth Reference: Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program 1  Myocardial Oxygen Supply Heart’s oxygen and nutrient demand is extremely high It requires its own continuous blood supply  There are two main arteries: Right coronary artery (RCA) Left coronary artery (LCA). Left coronary artery divides: Left anterior descending (LAD) branch Left circumflex branch(LCX) The right coronary artery and the branches of the left coronary artery provide numerous smaller branches which penetrate the heart muscle, supplying it with blood. Coronary arteries may become narrow, or blocked  The Three important I’s Ischemia – Limited blood flow within a coronary artery – Decrease in oxygenation Injury – Prolonged ischemia – Chronic lack of oxygen shuts down vital ATP-driven cellular activity Infarct – Complete occlusion of a coronary artery – Death of tissue  Physiological findings in ischaemia Blood flow within a coronary artery is limited Myocardial oxygen needs not met (hypoxia) Hypoxia leads to depolarisation: Hypoxia decreases intracellular ATP Na/K ATPase pump activity decreases K+ not pumped in after repolarization… next depolarization is prolonged K+ leaks out through channels normally kept closed by ATP-ase activity  Physiological findings in ischaemia ATP driven pump shuts down, Na+ is not pumped out cells after depolarisation Increased intracelluar Na+ and Ca2+ depolarises the cell  Physiological findings in ischaemia This prolonged depolarisation inactivates Na+ channels Decreases automaticity of conducting cells Decreases conduction velocity and refractory periods The hypoxia also leads to buildup of intracellular Ca2+ leading to tachycardia  Remember views of the heart by specific leads of ECG View of Inferior Heart Wall Leads II, III, aVF - Looks at inferior heart wall - Looks from the left leg up Remember views of the heart by specific leads of ECG View of Lateral Heart Wall Leads I and aVL – Looks at lateral heart wall – Looks from the left arm toward heart *Sometimes known as High Lateral*  Remember views of the heart by specific leads of ECG View of Lateral Heart Wall Leads V5 & V6 – Looks at lateral heart wall – Looks from the left lateral chest toward heart – Some electrical activity at apex seen *Sometimes referred to as Low Lateral or Apical view* Remember views of the heart by specific leads of ECG View of Entire Lateral Heart Wall Leads I, aVL, V5, V6 - Looks at the lateral wall of the heart from two different perspectives Lateral Wall Remember views of the heart by specific leads of ECG View of Anterior Heart Wall Leads V3, V4 – Looks at anterior heart wall – Looks from the left anterior chest Remember views of the heart by specific leads of ECG View of Septal Heart Wall Leads V1, V2 - Looks at septal heart wall - Looks along sternal borders Remember views of the heart by specific leads of ECG View of Posterior Heart Wall Leads V1 & V2 Remember views of the heart by specific leads of ECG I Lateral aVR V1 Septal V4 Anterior II Inferior aVL Lateral V2 Septal V5 Lateral III Inferior aVF Inferior V3 Anterior V6 Lateral  Well Perfused Myocardium Epicardial Coronary Artery Lateral Wall of LV Septum Left Ventricular Cavity Positive Electrode Interior Wall of LV Normal ECG  Ischemia Coronary Artery lumen narrowed by clot Left Lateral Wall of LV Ventricular Septum Cavity Poorly perfused, hardworking Positive subendothelium Electrode becomes ischaemic Inferior Wall of LV  Ischemia Inadequate oxygen to tissue Subendocardial Represented by ST depression or T inversion May or may not progress to infarct (reversible)  T Wave Inversion Occurs because ischemic tissue does not repolarize normally May be seen in myocardial infarction as tissue around the infarct becomes ischaemic  Myocardial Ischemia - Causes Atherosclerosis Vasospasm Thrombosis and embolism Decreased ventricular filling time – Tachycardia Decreased filling pressure in coronary arteries – Severe hypotension or aortic valve disease 22  Injury Prolonged ischemia Transmural Represented by ST elevation Usually results in infarct  Injury Thrombus Ischemia If clot is complete or collateral circulation is poor, ischaemia will be transmural (through to wall). ECG shows ST elevation ST elevation Remember views of the heart by specific leads of ECG I Lateral aVR V1 Septal V4 Anterior II Inferior aVL Lateral V2 Septal V5 Lateral III Inferior aVF Inferior V3 Anterior V6 Lateral  Infarct Death of tissue Sometimes see Q wave Dead ventricular area does not depolarize!  Thrombus Infarcted Area Electrically Silent Ischemia Depolarization  Infarction Infarcted Area Electrically Silent Depolarization Ischaemia, injury, infarction: ECG Indicators T wave changes ST segment changes Q wave changes Bundle Branch Block 32  Bundle Branches Bundle of His divides into right and left bundle branches Left bundle branch further divides into septal, anterior and posterior fascicles  Normal QRS Complex Narrow – 0.06 to 0.10 seconds in duration Electrical axis is between 0° and +90° 34  Bundle Branch Block Leads to one or both bundle branches failing to conduct impulses Produces delay in depolarization of the ventricle it supplies  Bundle Branch Block Key characteristic are widened QRS complexes – 0.12 seconds or greater in duration Look at the appearance of the QRS complexes – They may be notched, slurred or M shaped in the chest leads  Right Bundle Branch Block (RBBB) Conduction through the right bundle branch is blocked causing delayed right ventricular depolarization Look for wide, tall, and notched QRS complexes in leads V1, V2 and slurred S waves in leads I, V5 and V6  Causes of Right Bundle Branch Block Occurs with anterior wall MI, coronary artery disease, hypertension, scar tissue that develops after heart surgery, viral or bacterial myocarditis and pulmonary embolism May also be caused by drug toxicity or be due to a congenital heart abnormality such as atrial septal defect 38  Left Bundle Branch Block Conduction through the left bundle branch is blocked, causing depolarization of the left ventricle to be delayed Look for wide, tall, notched or slurred QRS complexes in leads V5, V6 and wide, largely negative rS complexes or entirely negative QS complexes in V1 and V2 Causes of Left Bundle Branch Block Anterior wall MI, hypertensive heart disease, aortic stenosis, degenerative changes of the conduction system or cardiomyopathy 40  Overview of Infarcts Location of Arterial Indicative Reciprocal Infarct Supply Changes Changes Anterior LAD V1-V4 II, III, aVF Inferior RCA II, III, aVF I, aVL Lateral Circumflex I, aVL, V5, V6 V1 Posterior Posterior None V1, V2 Descending (RCA) Septal Septal Perforating Loss of R wave in None (LAD) V1, V2, or V3 Posterior Descending (RCA