Week 1 PAT202 CAD MI ACS Student Final w251 (1) PDF

Coronary Artery Disease, Myocardial Ischemia & Acute Coronary Syndrome PAT202 Week 1 Winter 2025 1 Cardiac Anatomy & Physiology A Quick Review 2 Wall of The Cardiopulmonary circulation - Heart IMPORTANT REVIEW!...

Coronary Artery Disease, Myocardial Ischemia & Acute Coronary Syndrome PAT202 Week 1 Winter 2025 1 Cardiac Anatomy & Physiology A Quick Review 2 Wall of The Cardiopulmonary circulation - Heart IMPORTANT REVIEW! You need to remember what is normal, so you understand how disease changes the normal! The heart wall has 3 layers: epicardium, myocardium, and endocardium Myocardium thickest layer cardiomyocytes provide contractile force contains coronary arteries & veins Figure 31.2 Rogers, 2023, 3 p. 1022  Use your clinical judgemen Coronary Circulation: Coronary Arteries can happe t! What n when the client has tachycard ia? Two main coronary arteries right coronary artery (RCA) left coronary artery (LCA) coronary arteries supply blood to different areas of the heart occlusion of either the right or the left coronary artery can cause left ventricular damage. Can you explain why the left ventricle is 4 Figure 31.6, Rogers, 2023, damaged with either  Right & Left Coronary Arteries Right supplies right atrium & right ventricle & portion of posterior wall of left ventricle SA & AV nodes & bundle of His receive blood from right coronary artery Left supplies left atrium & left ventricle Use your clinical judgement! Knowing this physiology …. what manifestations would you anticipate the client would have if their RCA was blocked? What about the LCA? 5 Collateral Circulation 1. arteriogenesis (new artery growth branching New collateral vessels are from preexisting arteries) formed through two 2. angiogenesis (growth of new capillaries within processes a tissue) Collateral circulation assists in supplying blood & oxygen to myocardium that has become ischemic following stenosis of one or more coronary arteries d/t CAD Formation of collateral arteries can restore circulation following arterial occlusion (Coronary Artery Disease) Coronary Artery Disease can take decades to develop & progress. -since the body builds collateral Collateral circulation develops at same circulation to compensate, CAD time as atherosclerotic changes are does not produce symptoms taking place, so it takes time to develop until far advanced! 6 too Conduction System of The Heart IMPORTANT REVIEW! You need to remember what is normal, so you understand how disease changes the normal! 7 Figure 31.7, Rogers, 2023, Normal Electrocardiogram (ECG) & Cardiac Electrical Activity 8 Figure 31.9, Rogers, 2023, Atherosclerosis: A Quick Review 9  Progression Endothelium injury Inflammation of endothelium Cytokines released Progression of Cellular proliferation Macrophage migration Atherosclerosis: Low-density lipoproteins A Review (LDL) oxidation (foam cell formation) with oxidative stress Fatty streak Fibrous plaque Complicated plaque 10 Progression of Atherosclerosis: The BIG Picture! Result: partial or total occlusion of coronary artery 11 Figure 32.5, Rogers, 2023, p.  Atherosclerosis is most common cause of Atherosclerosi CAD s & Coronary narrows or occludes coronary arteries Dyslipidemia Artery Disease strong link between abnormal (CAD) concentrations of lipoproteins & CAD indicator of coronary risk! Results in imbalance between coronary supply of blood & myocardial demand for oxygen & nutrients reversible myocardial ischemia or irreversible infarction may occur 12  Modifiable Risk Factors For CAD & What To Do! Dyslipidem HTN Cigarette Excessive ia maintain smoking alcohol adherence to normal BP smoking consumptio drug regime cessation n limit alcohol consumption Diabetes and Obesity Diet Physical insulin (atherogenic inactivity/se resistance maintain (hyperglycemi healthy body ) dentary a) weight reduce lifestyle cholesterol or exercise maintain normal saturated fats in 13 blood glucose regularly  ⬤Major risk factors ⮚ advanced age ⮚ family history Nonmodifia ⮚ may contribute to ble Risk CAD through genetics Factors For and shared environmental CAD exposures ⮚ male gender or female after menopause 14  Markers of inflammation, ischemia, and thrombosis C-reactive protein Adipokines Nontradition adiponectin and leptin al Risk Chronic kidney disease Factors For Air pollution and ionizing radiation CAD Medications Coronary artery calcification, carotid wall thickness Microbiome 15  Narrowing of coronary arteries, usually d/t stable or unstable coronary atherosclerotic plaques What reduces myocardial oxygen supply responsible for both angina & Is myocardial infarction (MI) develops over long period of CAD? time begins early often takes 40-50 years CAD can seriously disrupt heart function! 16 Coronary Artery Disease (CAD) 17 Figure 50.1, Adams et al., 2025, p. 801 Atheromatous Plaque In The Coronary Artery 18 Figure 32.7, Rogers, 2023, p.  Pathophysiologic Continuum Transient Persistent CAD Myocardial Myocardial MI Ischemia Ischemia 19  Some Definitions To Get Us Started! Stable Angina chest pain occurring intermittently over long period with same pattern of onset, duration, intensity of symptoms (predictable) caused by myocardial ischemia BUT…stable angina may develop into unstable angina Acute Coronary Syndromes (ACS) consist of: unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI) 20  Some Definitions To Get Us Started! Unstable Angina (UA) chest pain is easily provoked, occurs with increasing freq., occurs during sleep, at rest or with min. exertion, has worsening pattern, unpredictable pain is not relieved with rest Myocardial Infarction (MI) irreversible cardiac cellular death caused by sustained myocardial ischemia → biomarkers NSTEMI transient thrombosis or incomplete coronary occlusion causing partial thickness damage (subendocardial) shows as depression of ST-segment on ECG STEMI more extensive MI assoc. with prolonged or complete coronary occlusion causes full thickness damage of heart muscle (transmural) shows as elevation of ST-segment on ECG 21  the CAD Is Divided Into Two Types of Disorders What is differen n i ce schemia bet w e e rction? and infa Chronic Ischemic Acute Coronary Heart Disease Syndromes (ACS) narrowing of disruption of coronary artery atherosclerotic lumen d/t plaque that did not atherosclerosis sig. compromise and/or vasospasm coronary lumen recurrent & before event transient episodes unstable plaque → of myocardial cell unstable angina ischemia (UA) stable plaque → MI (NSTEMI, STEMI) 22  Remember that a stable plaque Stable Plaque Versus Unstable Plaque may become unstable! Stable plaque produces obstruction of coronary blood flow → Two types myocardial ischemia stable angina of stable angina may progress to unstable angina atheroscler otic lesions Unstable plaque & their large lipid-rich core, thin fibrous cap, inflammation, lack role in of smooth muscle cells tend to fissure or rupture CAD/MI/AC rupture causes platelet aggregation/adhesion & S thrombus formation myocardial ischemia leads to ACSs unstable angina & MI (NSTEMI & STEMI) 23 It’s A Balancing Act: Supply & Demand! Oxygen supply depends Oxygen demand on: depends on: Supply of oxygen to the myocardium Blood flow to does not meet myocardium sympathetic impacted by activity metabolic coronary artery demands of disease (CAD), atherosclerosis, myocardium vasospasm Oxygenation of blood reaching physical myocardium activity, etc impacted by anemia, respiratory 24 disease  Cycle of Myocardial Ischemic Events 25 Algorithm 32.3, Rogers, 2023, p. Types of Transient Myocardial Ischemia Stable angina chronic atherosclerotic coronary obstruction → recurrent predictable chest pain Silent ischemia myocardial ischemia that does not cause detectable symptoms Prinzmetal angina abnormal vasospasm of coronary vessels → unpredictable chest pain 26 Stable Angina Stable plaque Predictable frequency, intensity, duration of pain Occurs with over exertion during activity, increasing oxygen demand Stress, exposure to cold -blood flow restored, and no necrosis of myocardial Relieved by rest and nitrates cells results Chronic stable angina may develop into unstable angina! 27  Sudden coronary obstruction caused by thrombus formation over ruptured or ulcerated atherosclerotic unstable plaque → complicated lesion Acute Plaque progression, disruption, & subsequent clot Coronary formation are same for MI as for unstable angina (UA) Syndrom ACS include: unstable angina (UA) es (ACS) MI (NSTEMI & STEMI) Most common complications of ACS: dysrhythmias, heart failure, sudden cardiac death 28 Pathophysiolo gy of ACSs Remember: A stable plaque may become unstable! 29 Algorithm 32.4, Rogers, 2023, p.  Form of acute coronary syndrome transient episodes of thrombotic vessel occlusion & vasoconstriction Unpredictable, occurs at rest, increases in Unstabl severity or frequency Signs & Symptoms: increased dyspnea, e diaphoresis, anxiety as angina worsens Unstable atherosclerotic plaque has ruptured Angina thrombus can form very quickly! Thrombus may break up → perfusion returns (UA) before significant myocardial necrosis occurs reversible myocardial ischemia EMERGENCY! but is sign of impending infarction! Thrombus may cause prolonged ischemia → myocyte death → MI 30 Pathogenesi s of Unstable Plaques & Thrombus Formation 31 Figure 32.9, Rogers, 2023, p. 1079 Evaluation & Treatment of EMER GENC Y! Unstable Angina Evaluation Treatment serum cardiac immediate biomarkers (troponins, hospitalization creatine administration of phosphokinase- nitrates, myocardial bound antithrombotics, & [CPK-MB]) normal anticoagulants ECG often reveals ST- once stabilized segment depression beta blockers, ACE and T-wave inversion inhibitors during pain that emergency PCI resolves as pain is performed if condition 32 What is a Myocardial Infarction (MI)? irreversible damage to the heart muscle (myocyte necrosis) caused by prolonged ischemia that causes cellular injury, leading to cellular death 33 Plaque Disruption & Myocardial Infarction Figure 32.10, Rogers, 2023, p. 34  1. Subendocardial infarction (referred to as a Non-ST-Segment Elevation MI (NSTEMI)) shows as ST-segment depression on ECG transient thrombosis or incomplete coronary artery occlusion partial wall thickness damage 2 Major 2. Transmural infarction (referred to as an ST-Segment Elevation MI (STEMI)) Types of shows as elevation of ST-segment on ECG MI have more extensive MI assoc. with prolonged and complete coronary occlusion full wall thickness damage Individuals at highest risk for complications ST segment elevations (STEMI) on the ECG require immediate intervention 35 Unstable Angina, NSTEMI & STEMI 36 Figure 32.11, Rogers, 2023, p.  After 20 minutes of ischemia, myocardial cells begin to die (necrosis). But the cells are viable if blood flow is restored within that 20 minutes! What Causes Cellular Injury? Myocardial reserves used up in ~ 8 seconds! ↓O2 & nutrients →affected myocardium cyanotic & cooler → changes on ECG within 1 minute Glycogen stores used up → anaerobic metabolism → lactate (lactic acid) →K+, H+→acidosis (myocardial cells sensitive to changes in pH) Acidosis may make myocardium more vulnerable to damaging effect of lysosomal enzymes & may suppress impulse conduction & contractile function →heart failure Failure of Na+/K+ pump, Na+ moves into cell, (lose K+, Ca+, Mg+ from cells) →loss of contractility →↓ pumping action of heart 37  What Causes Cellular Injury? Angiotensin II released during ischemia → systemic effects of peripheral vasoconstriction & fluid retention. Counterproductive as ↑myocardial work & exacerbate effects of loss of myocyte contractility Angiotensin II also released locally where it is a growth factor for vascular smooth muscle cells, myocytes & cardiac fibroblasts; promotes catecholamine release & causes coronary artery spasm Stress →release of catecholamines and ischemic cells release catecholamines → serious imbalances of sympathetic and parasympathetic function, irregular heartbeat & heart failure Catecholamines mediate release of glycogen, glucose & stored fat from body cells →↑plasma levels of free fatty acids & glycerol within 1 hour Norepinephrine elevates blood glucose levels through stimulation of liver & skeletal muscle cells; also suppresses beta cell activity which reduces insulin secretion & elevates blood glucose further; hyperglycemia is evident during early phase after acute myocardial infarction 38 Cellular Death After about 20 minutes of myocardial ischemia, irreversible hypoxic injury causes cellular death & tissue necrosis Necrosis of myocardial tissue results in release of intracellular enzymes, i.e. troponin, through damaged cell membranes into interstitial spaces Lymphatics pick up enzymes & transport them into bloodstream, where they can be detected by serologic tests 39  Prolonged ischemia causes irreversible damage to heart muscle (myocyte necrosis) ⮚ cellular injury → cellular death ⮚ structural & functional changes myocardial stunning Structural & ⮞ temporary loss of contractile function that persists for hours to days after perfusion has Functional been restored Changes hibernating myocardium ⮞ tissue that is persistently ischemic undergoes Associated With metabolic adaptation to prolong myocyte Acute survival myocardial remodeling Myocardial ⮞ process occurring in myocardium after MI Ischemia Infarcted myocardium is surrounded by a zone of hypoxic injury, which may ⮚ progress to necrosis ⮚ undergo remodeling (scarring) ⮚ or return to normal 40 Structural and Functional Changes Associated With Acute Myocardial Ischemia 41 Figure 32.12, Rogers, 2023, p. Reperfusion Injury Restoration of blood flow is crucial to reducing infarct size! but reperfusion of ischemic myocardium triggers process called reperfusion injury Can add as much as 50% to overall Ischemia and reperfusion also cause infarct size damage to the coronary circulation through endothelial injury, platelet activation, inflammation, and vasoconstriction Involves release of toxic oxygen free radicals, calcium flux, and pH changes contribute to cellular death 42  Within 24 hours, leukocytes infiltrate necrotic area & proteolytic enzymes Repair from scavenger neutrophils degrade necrotic tissue By 10 to 14 days after infarction, a collagen matrix is deposited & is initially weak, mushy, & vulnerable to reinjury After 6 weeks, necrotic area is completely replaced by scar tissue strong but unable to contract & relax like healthy myocardial tissue! 43 Complications of MI Decreased cardiac contractility with abnormal wall motion Altered left ventricular compliance Decreased stroke volume Decreased ejection fraction Increased left ventricular end-diastolic pressure and volume Sinoatrial node malfunction life-threatening dysrhythmias Heart failure Cardiogenic shock Mo re i nw 2! eek 44 Diagnostics: Electrocardiogram (ECG) Changes with MI Ischemic/injured/infarcted tissue does not function like normal myocardial tissue Affected area can be identified on a 12- lead ECG ST-segment depression (NSTEMI) ST-segment elevation (STEMI) ECG changes depend on duration of ischemic event (acute vs evolving MI) extent (partial/subendocardial vs entire wall thickness/transmural) location 45 Figure 32.13, Rogers, 2023, p. Electrocardiogr am (ECG) Alterations What do the ST-segment depression (NSTEMI) and the ST-segment elevation (STEMI) ECGs tell us about the extent of heart damage? What do the ST-segment depression (NSTEMI) and the ST-segment elevation (STEMI) ECGs tell us about the extent of heart damage? Figure 32.8, Rogers, 2023, p. 1078 Figure 32.8, Rogers, 2023, p. 1078 46 Diagnostics: ⬤Cardiac troponin I (cTnI) Serum ⬤Creatine phosphokinase–MB (CPK-MB) Biomarkers ⬤Lactate dehydrogenase (LDH) ⬤Myoglobin 47  Diagnostics: Cardiac Specific Serum Biomarkers cTnI assays have high Creatine phosphokinase– specificity for MB (CPK-MB) released Cardiac muscle damage by myocardial cells but is → myocardial cells myocardial tissue also in other muscle cells necrose & die → release primary biomarker used as 2nd-line their contents including for dx of MI biomarker d/t enzymes (biomarkers) rise within 2-4 hours ↓sensitivity and into blood ↓specificity after onset of levels exceed normal ranges symptoms within 4-8 hours of injury 48 Use Your Clinical Judgement! A r e c ar d iac biom released arkers with NST What ab EMI? out with STEMI? A r e c ar d iac biom r e l e a se d arkers with uns angina ( table UA)? 49  Lactate dehydrogenase (LDH) lactic acid dehydrogenase, or LDH is an enzyme found in almost all body tissues Diagnostics including heart : Non- Myoglobin present in cardiac and skeletal Cardiac muscle myoglobin released into circulation with any Specific damage to muscle tissue including Serum myocardial necrosis released quickly from infarcted myocardial Biomarkers tissue elevated within 1 hour after myocardial cell death peak levels reached within 4-8 hours 50  Additional Labs Leukocytosis What Elevated CRP causes all of these? Hyperglycemia 51 Symptoms/Assessment What ca pain and uses the why d o e s it r adiate? Sudden, severe chest pain may be described as heavy & crushing, i.e. “elephant is sitting on my chest” radiates to neck, jaw, back, shoulder, or left arm pain is more severe & prolonged compared with angina pain NOT relieved by nitroglycerin or rest (opioids often ordered) Sensation of indigestion N&V Tachycardia HTN Hypotension with severe myocardial damage Why Skin is cool and clammy fever? Atypical symptoms silent MI (different symptoms or no symptoms) 52  What is th e main go treatmen al of Treatments for MI t for MI? Immediate administration of Hospitalization supplemental oxygen & Morphine aspirin (or clopidogrel if can’t take aspirin) NSTEMI STEMI treated in same way as UA best managed with Bed rest including antithrombotics, emergency PCI & anticoagulation or PCI, or antithrombotics both Once stabilized Hyperglycemia treated further management Stool softeners includes ACE inhibitors, with insulin beta-blockers, and statins 53  ⬤ Percutaneous coronary intervention (PCI) Non- ⬤ Coronary artery bypass graft (CABG) Pharmacologic Minimally invasive direct coronary al Treatment artery bypass (MIDCAB) For ACS Gene & stem therapy for myocardial angiogenesis & spinal cord stimulation 54  Risk Factors Endothelial Injury Atherosclerosis Coronary Artery CAD Disease (CAD), Acute Coronary Atherothrombosis Coronary Syndrome Myocardial Ischemia (ACS) & Heart Failure Myocardial Infarction (HF): How They Are Arrhythmias & Loss of Function All Related! Remodeling Contractile Dysfunction Heart Failure End Stage Heart Disease 55