ACS.pptx

Acute Coronary Syndromes C.D.Powell, M.D., M.P.H. The Cardiovascular Perfusion Program of The Emory University School of Nursing https://www.sciencephoto. 1. Normal hemostasis 2. Pathophysiology of ACS •Normal hemostasis •Endogenous antithrombotic mechanisms •Pathogenesis of coronary thrombosis •Nonatherosclerotic causes of acute MI •Pathologic evolution of infarction •Functional alterations 3. Clinical Aspects of ACS •Clinical presentation •Diagnosis of acute coronary syndromes Outline 4. Treatment of ACS •Acute treatment of unstable angina and non–ST-elevation myocardial infarction •Acute treatment of ST-elevation myocardial infarction •Adjunctive therapies 5. Complications •Recurrent ischemia •Arrhythmias •Myocardial dysfunction •Right ventricular infarction •Mechanical complications •Pericarditis •Thromboembolism •Managing risks after MI 6. Risk Stratification and Management https://www.sciencephoto.com/ media/528936/view Steve Gschmeissner Blood clot in a coronary artery. Introduction to ACS • (ACSs) are life-threatening conditions affecting patients with coronary artery disease at any time • These syndromes range form unstable patterns of angina pectoris to the development of large acute myocardial infarctions and irreversible necrosis of heart muscle • ACS result in the hospitalization of more than 1.3 million Americans each year, and 14% of those experiencing a MI will die from it. • One-year morbidity after the initial MI is diagnosed; • 19% for men • 26% for women • However, the mortality rate has been steadily declining in recent decades due to preventative and therapeutic advances. Pathogenesis of ACS – an Overview • > 90% of ACSs results from a disruption of an atherosclerotic plaque with subsequent platelet aggregation and formation of an intracoronary thrombus, which transforms a region of plaque narrowing to one of severe or complete occlusion. • The responsible thrombus in ACS is generated by interactions among: • NSTEMI has been historically referred to as a non-Q-wave MI. • The form of ACS depends on the degree of obstruction and resulting ischemia. • • • • the atherosclerotic plaque the coronary endothelium circulating platelets the dynamic vasomotor tone of the vessel wall 1. Normal Hemostasis Does Omicron Pose as Much of a Blood Clot Threat? by Amanda D'Ambrosio, MedPage Today January 24, 2022 Normal Hemostasis • Primary hemostasis is the first line of defense against bleeding. When a normal blood vessel is injured, the endothelial surface becomes disrupted and thrombogenic connective tissue is exposed. • This process begins within seconds of vessel injury and is mediated by circulating platelets, which adhere to collagen in the vascular subendothelium and aggregate to form a “platelet plug.” • While the primary hemostatic plug forms, the exposure of subendothelial tissue factor triggers the plasma coagulation cascade, initiating the process of secondary hemostasis. • The plasma coagulation proteins involved in secondary hemostasis are sequentially activated at the site of injury and ultimately form a fibrin clot by the action of thrombin. The resulting clot stabilizes and strengthens the platelet plug. • The normal hemostatic system minimizes blood loss from injured vessels, but there is little difference between this physiologic response and the pathologic process of coronary thrombosis triggered by disruption of atherosclerotic plaques. Inactivation of Clotting Factors • Natural inhibitors tightly regulate the coagulation process to oppose clot formation and maintain blood fluidity.: 1. Antithrombin 2. Proteins C and S 3. Tissue factor pathway inhibitor (TFPI) Normal mechanisms shown in above figure serve to prevent spontaneous intravascular thrombus formation. • 1. Antithrombin is a plasma protein that irreversibly binds to thrombin and other clotting factors, inactivating them and facilitating their clearance from the circulation. • Its effectiveness is increased 1,000 x by binding to heparin sulfate (heparin-like molecule present on 2. Protein C/ protein S/thrombomodulin • Form a natural anticoagulant system that inactivates the “acceleration” factors (Va and VIIIa) the coagulation pathway. • Protein C is synthesized in the liver and circulates in an inactive form. • Thrombomodulin is a thrombinbinding receptor normally present on endothelial cells. • Thrombin bound to thrombomodulin cannot convert fibrinogen to fibrin (the final reaction in clot formation). • The thrombin–thrombomodulin complex activates protein C. • Activated protein C degrades factors Va and VIIIa thereby inhibiting coagulation. 3. Tissue factor pathway inhibitor • A plasma serine protease inhibitor that is activated by coagulation factor Xa • The combined factor Xa–TFPI binds to and inactivates the complex of tissue factor with factor VIIa that normally triggers the extrinsic coagulation pathway. • Thus, TFPI serves as a negative feedback inhibitor that 4. Lysis of Fibrin Clots • Tissue plasminogen activator (tPA) is a protein secreted by endothelial cells in response to many triggers of clot formation • It cleaves the protein plasminogen to form active plasmin, which in turn enzymatically degrades fibrin clots. • When tPA binds to fibrin in a forming clot, its ability to convert plasminogen to plasmin is greatly enhanced. 5. Endogenous Platelet Inhibition and Vasodilation • Prostacyclin is synthesized and secreted by endothelial cells. • Increases platelet levels of cAMP and thereby strongly inhibits platelet activation and aggregation • Indirectly inhibits coagulation via its potent vasodilating properties by augmenting blood flow and by reducing shear stress (an inducer of platelet activation) • Nitric oxide (NO) is also secreted by endothelial cells and acting locally to inhibit platelet activation (serves as a potent vasodilator). Question 1 • All of the following substances involved in normal hemostasis are produced by endothelial cells except one. Which one is produced elsewhere? A. B. C. D. Prostacyclin Protein C Tissue plasminogen activator Thrombomodulin 2. Pathophysiolog y of ACS A close view of a blood clot. The fibrous protein mesh incorporates tiny blood cell fragments called platelets (violet), which help the body form clots, and red blood cells that can also play an active role in clot formation and contraction. PHOTOGRAPH BY MICROGRAPH BY ANNE WESTON, EM STP, THE FRANCIS CRICK INSTITUTE, SCIENCE PHOTO LIBRARY Atherosclerosis Contributes to Thrombus Formation • Atherosclerotic plaques consist of a lipid-laden core surrounded by a fibrous external cap. Substances released from inflammatory cells within the plaque can compromise the integrity of the fibrous cap. • Thrombus formation occurs due to 2 main factors: (1)Plaque rupture or erosion, which exposes the circulating blood elements to thrombogenic substances. (2)Endothelial dysfunction with the loss of normal protective antithrombotic and vasodilatory properties (eg, decreased NO and prostacyclin) . • Plaque rupture is caused by: (1)Chemical factors that destabilize atherosclerotic lesions. For example, inside the cap T-lymphocytes produce gamma interferon which inhibits collagen synthesis by smooth muscle cells, and metalloproteinases degrade the interstitial matrix, thus weakening the cap). (2)Physical stresses to which the lesions are subjected (increases in bp, hr, and force of ventricular contraction) • Dysfunctional Endothelium • Results in reduced amounts of NO and prostacyclin –less inhibition of platelet aggregation. Less vasodilatation, so vasoconstriction predominates. Pathogenesis of Coronary Thrombosis Significance of Coronary Thrombosis Occasionally, an NSTEMI may result from total coronary occlusion. In this case, it is likely that a substantial collateral blood supply limits the extent of necrosis, such that a larger STEMI is Types of MI’s • The label Type 1 MI refers to typical infarction due to disrupted atherosclerotic plaque with acute thrombus formation. • Type 2 MI is the description for infarction resulting from an oxygen supply-demand mismatch that is not the result of plaque disruption and thrombosis. • An unfortunate potential cause of ACS due to oxygen supply-demand mismatch is cocaine abuse. Cocaine increases sympathetic tone by blocking the presynaptic reuptake of norepinephrine and by enhancing the release of adrenal catecholamines, which can lead to vasospasm and therefore decreased myocardial oxygen supply. An ACS may ensue because of increased myocardial oxygen demand resulting from cocaine-induced sympathetic myocardial stimulation (increased heart rate and blood pressure) in the face of the decreased oxygen supply. • Transmural infarcts span the entire thickness of the myocardial wall and result from total, prolonged occlusion of an epicardial coronary artery. Conversely, subendocardial infarcts exclusively involve the innermost layers of the myocardium. STEMI*** • The subendocardium is particularly susceptible to ischemia because it is the zone subjected to the highest pressure from the ventricular chamber, has few collateral connections that supply it, and is perfused by vessels that must pass through layers of contracting myocardium. Resin Cast of the Human Coronary Arteries https:// www.sciencephoto.co m/media/118702/ view/resin-cast-ofheart-coronaryarteries Pathophysiology of the Region of Infarction Infarction is initiated by ischemia, that progresses from a potentially reversible phase to irreversible cell death. • Myocardium that is supplied directly by an occluded vessel may die quickly. • Adjacent tissue may not necrose immediately because it may be sufficiently perfused by nearby patent vessels. • Neighboring cells may become increasingly ischemic over time, as demand for oxygen continues within a reduced oxygen supply. • The region of infarction may subsequently extend outward. Determinants of the Area of Infarction The amount of tissue that ultimately succumbs to infarction is related to: 1. The mass of myocardium perfused by the occluded vessel 2. The magnitude and duration of impaired coronary blood flow 3. The oxygen demand of the affected region 4. The adequacy of collateral vessels that provide blood flow from neighboring non-occluded coronary arteries 5. The degree of tissue response that modifies the ischemic process Coronary Arteries and Veins Mechanisms of Cell Death in Acute MI • Myocardial function decreases as early as 2 minutes following occlusive thrombosis. • Irreversible cell injury ensues in 20 minutes. • Coagulation necrosis of the myocardium occurs in 2-4 days. • Increased intracellular Na+ causes cellular edema. • Alterations in the transmembrane electrical potential predisposes the myocardium to lethal arrhythmias. • Intracellular calcium accumulates in the damaged myocytes and is thought to contribute to the final common pathway of cell destruction through the activation of degradative lipases and proteases. Mitochondria can no longer oxidize fats or products of glycolysis. Question 2 • Which of the following statements about cell injury in an acute MI are correct? A. Myocardial function decreases within 2 minutes of coronary occlusion. B. Intracellular acidosis results in chromatin clumping and protein denaturation. C. Alterations in the transmembrane electrical potential, largely due to an increase in extracellular potassium, predisposes the myocardium to lethal arrhythmias. D. All of the above Collateral Damage and Serum Biomarkers • Proteolytic enzymes leak across the myocyte’s altered membrane, damaging adjacent myocardium. • The release of certain macromolecules into the circulation serves as a clinical marker of acute infarction: troponin I or T, CK-MB creatine kinase myocardial band 1 and 2. Late Changes in Acute MI • Late pathologic change in the course of an MI includes: • (1) the clearing of necrotic myocardium and • (2) the deposition of collagen to form scar tissue. • Five to seven days after infarction, the process of wound healing progresses. Irreversibly injured myocytes do not regenerate; rather, the cells are replaced by fibrous tissue. • Macrophages invade the inflamed myocardium shortly after neutrophil infiltration and remove necrotic tissue (Fig. 7-5C). This period of tissue resorption is termed yellow softening because connective tissue elements are destroyed and removed along with dead myocardial cells. The phagocytic clearing, combined with thinning and dilatation of the infarcted zone, results in structural weakness of the ventricular wall and the possibility of myocardial wall rupture at this stage. • Approximately 1 week after infarction, granulation tissue appears, representing the beginning of the scarring process (Fig. 7-5D). This is observed grossly as a red border at the edge of the infarct. Fibrosis subsequently ensues, and scarring is complete by 7 weeks after infarction (Fig. 7-5E). Fig. 7-5: Pathologic Evolution in MI Wavy myofibers are due to intercellular edema. Contraction bands are sarcomeres that are contracted and consolidated. • A. Acute infarct ~12 hours old showing contraction band necrosis, nuclear karyolysis, focal hemorrhage, and an absence of inflammation. • B. Acute infarct ~24-48 hours old showing coagulation necrosis with pyknotic nuclei and dense infiltration of neutrophils. • C. Healing infarct ~5 days old showing necrotic myocytes undergoing removal by macrophages, with the neutrophilic response having largely dissipated. • D. Healing infarct ~10 days old showing granulation tissue with new blood vessels (neovascularization), mild chronic inflammation (macrophages and lymphocytes), fibroblasts, and early collagen deposition; viable myocardium is present at the upper left. • E. Healed infarct ~1-2 months old showing dense fibrosis; the inflammation and new vessels have largely regressed; viable myocardium is present at the upper left. All images are hematoxylin and eosin–stained sections. Functional Alterations in ACS 1. Impaired Contractility and Compliance • Impaired ventricular contraction (systolic dysfunction) and decreased cardiac output • Loss of synchronous contraction • Wall motion abnormalities: • Hypokinetic (localized reduction) • Akinetic (no contraction) • Dyskinetic (bulges outward) • Diastolic dysfunction and decreased compliance (myocardial relaxation is an energy dependent process). Results in elevated ventricular filling pressures. 2. Stunned Myocardium • Transient myocardial ischemia can result in a very prolonged, but gradually reversible, period of contractile dysfunction. • Tissue gradually regains contractile force days to weeks later. • Stunning may occur, for example, following reperfusion therapy for acute STEMI. • Prolonged contractile dysfunction of affected ventricular segments may simulate infarcted tissue. Functional Alterations in ACS 3.Ischemic Preconditioning • Brief ischemic insults to a region of myocardium may render that tissue more resistant to subsequent episodes. • Patients who sustain an MI in the context of recent angina experience less morbidity and mortality than those without preceding ischemic episodes. • The mechanism of this is not fully understood. May involve multiple signaling pathways using local and systemic mediators. Substances released during ischemia, including adenosine and bradykinin, are believed to be key triggers of these pathways. 4.Ventricular Remodeling after MI • Changes in the geometry of both infarcted and non-infarcted ventricular muscle. • In the early post-MI period, infarct expansion may occur without additional myocyte necrosis due to thinning and dilatation of the necrotic zone of tissue, likely because of “slippage” between the muscle fibers, resulting in a decreased density of myocytes in the infarcted region. • Alterations in chamber size and wall thickness will affect long-term cardiac function and prognosis. Functional Alterations in ACS: More on Ventricular Remodeling • Infarct expansion can be detrimental because it increases ventricular size, which; (1) augments wall stress (2) impairs systolic contractile function (3) increases the likelihood of aneurysm formation • In addition, remodeling of the ventricle may also involve dilatation of the overworked non-infarcted segments. • These areas are then subjected to increased wall stress. • This dilatation continues over the ensuing weeks and months. • Initially, chamber dilatation serves a compensatory role • It increases cardiac output via the Frank– Starling mechanism • Progressive enlargement may ultimately lead to heart failure and predisposes to ventricular arrhythmias • Adverse ventricular remodeling can be beneficially modified by certain interventions • Reperfusion therapies - decrease the likelihood of infarct expansion • Drugs that interfere with the renin– angiotensin-aldosterone system, which attenuate progressive remodeling and to reduce short- and long-term mortality after infarction. 3. Clinical Features of Acute Coronary Syndromes https://www.sciencephoto.com/media/5289 36/view Steve Gschmeissner Blood clot in a coronary artery. Clinical Presentation • Unstable vs. chronic angina • Acute MI: Nstemi vs Stemi Diagnosis of acute coronary syndromes • ECG abnormalities • Serum markers of infarction Cardiac specific troponins Creatine kinase • Imaging Differential Diagnosis of ACS • ACSs represent disorders along a continuum and therefore their clinical features overlap. • The differential diagnosis is critical in order to institute appropriate immediate therapy. The most important distinction to make is between an ACS that causes ST-segment elevation on the electrocardiogram (STEMI) and those acute syndromes that do not (UA and NSTEMI). • The severity of symptoms and associated laboratory findings progress from unstable angina through to NSTEMI and STEMI. • Distinguishing among these syndromes is based on: • Clinical presentation • Electrocardiographic findings • Serum biomarkers of myocardial damage Chronic Stable Vs. Unstable Angina • In chronic stable angina, instances of chest discomfort are: 1. Predictable 2. Brief 3. Nonprogressive 4. Occurring only during physical exertion or emotional stress • UA presents as an acceleration of ischemic symptoms in one of the following three ways: 1. A crescendo pattern in which a patient with chronic stable angina experiences a sudden increase in the frequency, duration, and/ or intensity of ischemic episodes. 2. Episodes of angina that unexpectedly occur at rest, without provocation. 3. The new onset of anginal episodes, described as severe, in a patient without previous symptoms of coronary artery disease. • Patients with UA may progress further along the continuum of ACS and develop evidence of necrosis (i.e., acute NSTEMI or STEMI) unless the condition is recognized and promptly treated. Clinical Presentation of an Acute Myocardial Infarction 1 • The discomfort experienced during an MI resembles angina pectoris qualitatively but is usually: 1. More severe 2. Lasts longer 3. May radiate more widely • Ischemia in acute MI persists and proceeds to necrosis. • Like angina, the sensation may result from the release of mediators, adenosine and lactate, from ischemic myocardial cells that continue to accumulate and activate afferent nerves for longer periods. Clinical Presentation of an Acute Myocardial Infarction 2 • The discomfort often radiates to: • Neck • Shoulders • Arms • Initial symptoms are usually rapid onset and briskly crescendo. • Patients have a profound “ feeling of doom.” • The pain does not usually wane with rest. • It does not usually resolve completely with the administration of sublingual nitroglycerin. • , 25% of patients who sustain an MI are asymptomatic or have atypical symptoms during the acute event. This is common among diabeticsdue to neuropathy, and the elderly. • As with men, women’s most common heart attack symptom is chest pain or discomfort, but women may experience other symptoms that are typically less associated with heart attack, such as shortness of breath, nausea/vomiting and back or jaw pain, and are more frequently misdiagnosed. Clinical Presentation of an Acute Myocardial Infarction 3 • The combination of intense discomfort and hypotension may trigger a dramatic sympathetic nervous system response • Symptoms associated with subsequent catecholamine release include: 1. Diaphoresis (sweating) 2. Tachycardia 3. Cool and clammy skin (vasoconstriction) • The parasympathetic nervous system is also triggered, and the responses of nausea, vomiting, and weakness is likely due to vagally mediated traffic. Clinical Presentation of an Acute Myocardial Infarction 4: Pulmonary Edema • If the ischemia affects a sufficiently large amount of myocardium, left ventricular (LV) contractility can be reduced (systolic dysfunction). • This reduction in SV leads to an increase in diastolic pressure and volume in the LV. This increase in LV pressure is compounded by the ischemia-induced stiffness of the chamber (diastolic dysfunction). • This back pressure is conveyed to the left atrium and pulmonary veins. • The resultant pulmonary congestion decreases lung compliance and stimulates juxtacapillary receptors. • These J receptors effect a reflex that results in rapid, shallow breathing and evokes the subjective feeling of dyspnea. • Eventual transudation of fluid into the alveoli exacerbates this symptom. Physical Findings in Acute MI • S3 heart sound • Indicative of volume overload in the presence of failing LV systolic function • S4 heart sound • Indicative of atrial contraction into a noncompliant left ventricle • A new murmur, often systolic • Ischemia-induced papillary muscle dysfunction causes mitral valvular insufficiency • If the infarct ruptures through the interventricular septum, it create a ventricular septal defect This is what a ruptured papillary muscle looks like post MI – IABP & ECMO •Low-grade fever secondary to systemic responses to inflammation (necrosis of myocardial cells), mediated by cytokines such as IL-1 and tumor necrosis factor (TNF). Diagnosing ACS 12 Lead ECG EKG showing ST Elevation (STEMI), Tachycardia, Anterior Fascicular Block, Anterior Infarct, Heart Attack. Color Key: ST Elevation in anterior leads=Orange, ST Depression in inferior leads=Blue. Contributed by Wikimedia Commons, Displaced (Public Domain-Self). https://www.ncbi.nlm.nih.gov/books/NBK532281/figure/arti cle-17173.image.f1/ Diagnosis of Acute Coronary Syndromes • The diagnosis and distinctions among the ACSs is made based on: (1)The patient’s presenting symptoms (2)Acute ECG abnormalities (3)Detection of specific serum markers of myocardial necrosis • Unstable angina is a clinical diagnosis supported by: • The patient’s symptoms • Transient ST abnormalities on the ECG (usually ST depression and/ or T-wave inversion) • the absence of serum biomarkers of myocardial necrosis • NSTEMI • Serum markers of necrosis + more persistent ST or T-wave abnormalities • STEMI • Appropriate clinical history + ST elevations + serum markers of myocardial necrosis. EKG Findings in UA and NSTEMI • In unstable angina or nonstemi, one finds • ST-segment depression and/ or Twave inversions • In UA, these are transient and occur just during chest pain episodes • These changes often persist in patients with NSTEMI • Historically, nstemis were referred to as “non-Q-wave MI’s” • Importantly, these characteristic patterns of ECG abnormalities in ACS can be minimized or prevented by early therapeutic interventions EKG Findings in STEMIs • In STEMI • There is a temporal sequence of EKG abnormalities. • There is initial ST-segment elevation. • Followed over the course of several hours by inversion of the T wave and the appearance of pathologic Q waves. • The development of Q waves • Does not reliably correlate with pathologic findings as much overlap exists among the types of infarction. • The finding of new pathologic Q waves to classify ACSs now has little therapeutic relevance. • Q waves, when they occur, take hours to develop and therefore are not helpful in making acute treatment decisions. Serum Biomarkers of ACS • Necrosis of myocardial tissue causes intracellular macromolecules to leak into the bloodstream. • Troponin, as covered in the 1st lecture, is one of these molecules and is a regulatory protein in muscle cells that controls interactions between myosin and actin. It’s detection serves both diagnostic and prognostic roles. • In patients with STEMI or NSTEMI, these markers rise above a threshold level in a defined sequence (see graph). • Importantly, troponin and CK-MB levels do not become elevated in the serum until at least a few hours after the onset of MI symptoms. • As a result, a single normal value drawn early in the course of evaluation for an MI (the hospital emergency department) does not rule out an acute MI; thus, the diagnostic utility of these biomarkers is limited in that critical period. Therefore, early decision making in patients with ACS often relies most heavily on the patient’s history and ECG findings. Troponins • The preferred serum biomarkers to detect myocardial necrosis • Cardiac specific troponins: • Troponin I (cTnI) • Troponin T (cTnT) • They are structurally unique, and highly specific and sensitive assays exist for their detection in the serum. • In wide clinical use today. • The presence of even minor serum elevations serves as evidence of: • Cardiomyocyte injury • Diagnostic of infarction in the appropriate clinical setting • Conveys powerful prognostic information • In the case of MI, cardiac troponin serum levels: • Rise 3 to 4 hours after the onset of chest discomfort • Peak level between 18 and 36 hours • Detectable for approximately 2 weeks • Of note, small serum elevations can also be detected in conditions other than MI, related to acute cardiac strain or inflammation • Examples: heart failure, myocarditis, hypertensive crises, or pulmonary embolism. Levels often also higher than normal in ESRD. Creatine Kinase • The enzyme creatine kinase (CK) is found in the heart, skeletal muscle, brain, and other organs. • Injury to any of these tissues may lead to elevation in serum concentrations. • There are three isoenzymes of CK: 1. CK-MM (found mainly in skeletal muscle) 2. CK-BB (located predominantly in the brain) 3. CK-MB (localized mainly in the heart) • Elevation of CK-MB is highly suggestive of myocardial injury. • To diagnosis MI using this marker, it is common to calculate the ratio of CK-MB to total CK. In myocardial injury, the ratio is usually > 2.5% . • If it is < 2.5 %, the elevation is likely not related to MI. • The serum level of CK-MB starts to rise: • 3 to 8 hours following infarction • peaks at 24 hours • returns to normal within 48 to 72 hours • Remember: troponin and CK-MB levels do not become elevated in the serum until at least a few hours after the onset of MI symptoms. • As a result, early decision making in patients with ACS often relies most heavily on the patient’s history and ECG findings. Diagnostic Imaging for ACS • Sometimes, the early diagnosis of MI can remain uncertain even after careful evaluation of the patient’s history, ECG, and serum biomarkers. • In such a situation, an additional diagnostic study that may be useful in the acute setting is echocardiography, looking for regional wall motion abnormalities. • This often reveals new abnormalities, often a lag of motion, of ventricular contraction in the region of ischemia or infarction. Case 1: 60 yo Woman with COPD • History: • The patient is a 60 y.o. female who has a past medical history of COPD (chronic obstructive pulmonary disease), hyperlipidemia, hypertension, tobacco (1 ppd since the age of 15 and continuing), alcohol abuse, and secondary polycythemia, although she is not on home O2. • When asked why she came to the hospital right after her arrival, she seemed circumspect, “There’s a reason why they call it a Hail Mary. It’s all or nothing, on a prayer. On the brink of loss we take our last shot, and with my shaky faith, I came here.” • She then began to grow more SOB, and stated her main problem was really difficulty breathing. She reported that she had developed a cough over the preceding 2 weeks. This morning when she woke up, she realized she was short of breath and was wheezing. She did also have one episode of vomiting this morning but denied any blood in the vomitus. • She said she tried an albuterol inhaler, which she felt might have worsened her shortness of breath. She threw her Hail Mary and called EMS and was brought to the hospital. She reported that she was also having tightness in her chest, located in the middle of her chest and radiating to her back which started only after she arrived at the hospital. She rated the chest discomfort 5 out of 10 in intensity, and it was a dull, constant pain. She stated that the pain is worsened with deep inspiration and was relieved with certain movement. Of note she reported that at home she has begun to sleep sitting up in the preceding few days. • Alcohol level on admission was elevated. Physical Exam Case 1 • Vitals: P = 130, BP = 150/80, RR = 25, T =99.0, pulse ox = 88% • General: Thin, cachectic woman sitting up in stretcher now in significant respiratory distress. She can speak only 1 sentence at a time. • Neuro: A + O x 4, anxious, motor exam is intact, sensory exam is normal. • HEENT: using scalenes and SCMs to assist with breathing, PERRL, CN2-12 grossly intact. • Pulm: On inspection, hyperexpansion of chest cavity with increased AP diameter, visibly prolonged expiratory phase, use of all accessory muscles. On auscultation, diminished breath sounds bilaterally, with loud expiratory wheezing. • CV: Tachycardic, sinus on monitor • Abd: Scaphoid, using abd to actively exhale, no masses, no organomegaly. • Extr: No edema • Skin: Spider hemangiomas present on torso Initial CXR for Case 1 Second CXR for Case 1, 8 Hours Later Case 1: COPD/Asthma Flare, Initial Arterial Blood Gases Gas 2, 8 hours later Gas 1 Question: Was it the right time to intubate? Case 1: Initial Chemistries 5 months prior to admission Admission Labs Lactic acid later the same day of admission: 2.2 mmol/L Case 1: Initial CBC with Differential Procalcitonin: .16 (0.00 - 0.10 ng/mL) Case 1: CXR on the night of admission (left) and the next morning (right), 12 hours apart Case 1: CT scan with PE protocol 7 hours after presentation, no PE Case 1: admission EKG Normal sinus rhythm Left bundle branch block Abnormal ECG When compared with ECG of 2 years prior, Left bundle branch block is now present Criteria for Septal infarct are no longer present (No mention of possible ST abnormalities given LBBB) Case 1: echo and troponins, done hospital day 2 Hospital Day Time Troponin (< 52 ng/L) Day 1 0900 71 1130 295 1630 667 Day 2 0430 661 Day 3 0430 165 Case 1: Cath on hospital day 3 • 1. Left Main: No hemodynamically significant stenosis • 2. LAD: Had 20 to 30% proximal narrowing. Diagonal branch had diffuse 70% narrowing however this vessel was less than 2 mm in size • 3. LCX: Had 70% narrowing of OM1. This vessel was less than 2 mm in size. Patient had mild diffuse disease of native circumflex artery however circumflex system was less than 2 mm in size. There was large ramus branch with 80% proximal narrowing. • 4. RCA: Dominant, had 40 to 50% proximal narrowing • 5. Successful PCI of proximal ramus artery with placement of resolute 2.5 x 22 mm stent. Diagnosis: acute coronary syndrome and flash pulmonary edema presenting as a COPD exacerbation. New Technologies: Coronary Virtual Intravascular Endoscopy (a) Mixed plaques with both calcified and non-calcified components (arrows) are shown on curved planar reformatted coronary CT angiography. (b) Coronary VIE shows significant lumen stenosis, with irregular plaque configuration. Sun, Z. (2016). Coronary Virtual Intravascular Endoscopy. In: Ţintoiu, I., Underwood, M., Cook, S., Kitabata, H., Abbas, A. (eds) Coronary Graft Failure. Springer, Cham. https://doi.org/10.1007/978-3-319-26515-5_48 Example of 320-slice CT angiography of an arterial graft in a 74-year-old man who underwent CABG 7 years previously. (a) Shows a 3D volume rendered CTA reconstruction of the heart, and bypass trajectory. An arterial graft is visible, with anastomoses to the D1 and LAD. (b) Shows the curved multiplanar reconstruction of a patent graft without the presence of significant graft stenosis. A patent anastomosis is observed (arrowhead) with good runoff in the distal LAD. (c) The curved multiplanar reconstruction of a heavily diseased LAD is shown, with severe stenosis of the proximal LAD (arrow). Arrowhead shows stenosis at the mid-gment of LAD. (d) A curved multiplanar reconstruction of the arterial graft and D1 are shown. The anastomosis of the graft to the patent D1 is uninterpretable due to a dense calcification (arrowhead). (e, f) The concordant ICA examinations are shown, confirming graft and vessel patency, arrowhead show patent anastomosis between the graft and LAD branches. Abbreviations: CABG coronary artery bypass grafting, CTA computed tomography coronary Question 3 • A 63 yo male presents to the ER by ambulance after his wife called an ambulance because he was having crushing substernal chest pain not relieved by nitroglycerin. He has known CASHD, and a prior stent to his LAD, so his wife called the ambulance within 5 min of the chest pain beginning. His EKG is as follows: • What pattern would you expect to see on his first set of biomarkers obtained 40 min after his chest pain began? A. A normal troponin, ckmb, and BNP B. An elevated troponin with a normal ckmb and BNP C. An elevated troponin and ckmb with a normal BNP D.An elevated troponin, ckmb, and BNP • Introduction 4. TREATMENT OF ACUTE CORONARY SYNDROMES • Acute Treatment of Unstable Angina and Non–ST-Elevation Myocardial Infarction • Anti-ischemic Therapy • Antithrombotic Therapy • Antiplatelet Drugs • Anticoagulant Drugs • Conservative versus Early Invasive Management of UA and NSTEMI • Acute Treatment of ST-Elevation Myocardial Infarction • Primary Percutaneous Coronary Intervention • Fibrinolytic Therapy • Adjunctive Therapies Initial Management of ACS • Successful management of ACS requires rapid initiation of therapy to: • Limit myocardial damage • Minimize complications • Therapy must address the intracoronary thrombus and provide anti-ischemic measures to restore the balance between myocardial oxygen supply and demand. • There is a critical difference in the approach to patients who present with STsegment elevation (STEMI) compared with those without ST-segment elevation (UA and NSTEMI). Stemi patients generally undergo revascularization procedures immediately due to total occlusion of a coronary, which is usually their pathology. • Hospitals have very strict criteria for “door to balloon” time in a stemi. • The management of UA and NSTEMI is essentially the same, and the primary focus of treatment consists of medications to: • Restore the balance between myocardial oxygen supply and demand • Antithrombotic therapy to prevent further growth • Facilitate resolution of the underlying partially occlusive coronary thrombus General Management for All with ACS • General measures for any patient with ACS include: • Deciding largely based on clinical symptoms and ECG if it is a Stemi or a nstemi/ua. Revascularization vs. medical therapy. • Admitting the patient to an intensive care unit • Continuous ECG monitoring for arrhythmias • Bed rest and medications to minimize myocardial oxygen demand • Supplemental oxygen (improve oxygen supply) • Anticoagulants (unfractionated heparin or bivalirudin) • Platelet inhibitors, such as aspirin and P2Y12 receptor inhibitors (e.g., ticagrelor, prasugrel, or clopidogrel) prior to the revascularization procedure. • Analgesics (morphine to reduce chest pain and associated anxiety) • Statins STEMI: Primary Percutaneous Coronary Intervention The preferred method of reperfusion therapy in patients with acute STEMI is immediate cardiac catheterization and percutaneous coronary intervention of • Time from first medical contact to PCI is ideally < 90 minutes. • Generally, transfer to a PCI-capable hospital is recommended if the procedure can be performed within 120 minutes of first medical contact. • One can achieve optimal flow in the infarct related artery in more than 95% of patients. • Under fluoroscopy, a catheter is inserted into a peripheral artery and directed to the site of coronary occlusion. • A balloon at the end of the catheter is then inflated, compressing the thrombus and the atherosclerotic plaque. • A stent is usually inserted thereby restoring and maintaining coronary blood flow. Fibrinolytic Therapy for STEMI If PCI is not available or is likely to be delayed, fibrinolytic therapy is the reperfusion alternative. • Fibrinolytic drugs accelerate lysis of the occlusive intracoronary thrombus in STEMI. Early administration during an acute STEMI restores blood flow in most (70% to 80%) coronary occlusions. • Improved artery patency translates into substantially increased survival rates and fewer post infarction complications. • Rapid initiation, within 2 hours of the onset of symptoms of STEMI, translates to half the mortality rate of those who receive it after 6 hours. • To prevent immediate vessel re-occlusion after thrombolysis, other agents are also used: • Anticoagulants (UFH or LMWHs) • Antiplatelet therapy (including aspirin and a platelet P2Y12 inhibitor). • Currently used fibrinolytic agents include recombinant tissue–type plasminogen activator • Alteplase, (tPA) • Reteplase (rPA) • Tenecteplase (TNK-tPA)- IV push rapid delivery • Patients with UA or NSTEMI do not benefit from fibrinolytic therapy. Risks of Fibrinolytic Therapy • Major risk of thrombolysis is bleeding. • Contraindications include: • Active peptic ulcer disease • Underlying bleeding disorder • Patients who have had a recent stroke • Patients who are recovering from recent surgery • Approximately 30% of patients may not be suitable candidates for thrombolysis. Treatments for UA/NSTEMI 1 • The management of UA and NSTEMI is essentially the same • The primary focus of treatment for UA and NSTEMI consists of medications to: 1. restore the balance between myocardial oxygen supply and demand 2. antithrombotic therapy to prevent further growth 3. to facilitate resolution of the underlying partially occlusive coronary thrombus • The same pharmacologic agents used to decrease myocardial oxygen demand in chronic stable angina are appropriate in UA and NSTEMI but are often administered more aggressively. Anti-Ischemic Therapy 1. β-Blockers • decrease sympathetic drive to the myocardium (HR) • Reduce oxygen demand and contribute to electrical stability • Reduces the likelihood of progression from UA to MI • Lowers mortality rates in patients who present with infarction • Contraindications (marked bradycardia, bronchospasm, decompensated heart failure, or hypotension) • usually initiated in the first 24 hours • Target heart rate = 60 beats/min • Usually continued indefinitely because of proven long-term mortality benefits following an MI Treatments for UA/NSTEMI 2 Anti-Ischemic Therapy Anti-Ischemic Therapy 3. Calcium Channel Antagonists 2. Nitrates • Nondihydropyridine calcium channel • Anginal relief through venodilation antagonists (i.e., verapamil and • Lowers myocardial oxygen demand by diltiazem) exert anti-ischemic effects diminishing venous return to the heart by decreasing heart rate and (reduced preload and therefore less contractility and through their ventricular wall stress). vasodilatory properties. • May also improve coronary flow and • These agents do not confer mortality prevent vasospasm through coronary benefit to patients with ACS, however. vasodilation. • Reserved for those in whom ischemia • Nitroglycerin is often initially persists despite β-blocker and nitrate administered by the sublingual route, therapies or for those with followed by a continuous intravenous contraindications to β-blocker use. infusion. • They should not be prescribed to • Intravenous nitroglycerin is useful as a patients with LV systolic dysfunction, vasodilator in patients with ACS because clinical trials have shown accompanied by heart failure or adverse outcomes in that case. severe hypertension Treatments for UA/NSTEMI 3: Antithrombotic and Anticoagulant Agents The purpose of antithrombotic therapy (antiplatelet and anticoagulant medications) is to prevent further propagation of the partially occlusive intracoronary thrombus while facilitating its dissolution by endogenous mechanisms. Antiplatelet Drugs Aspirin • Inhibits platelet synthesis of thromboxane A2 (potent mediator of platelet activation). Therefore, it inhibits only a single pathway of platelet activation • Reduces mortality in patients with all forms of ACS, and should be administered immediately on presentation. • Continued indefinitely in patients without contraindications to its use (allergy or underlying bleeding disorder). Antiplatelet Drugs Clopidogrel (Plavix), Prasugrel, and Ticagrelor • Thienopyridine derivative • Blocks the P2Y 12 ADP receptor on platelets. • Reduces cardiovascular death, recurrent MI, and stroke rates in patients with UA or NSTEMI who are also treated with aspirin. • Prasugrel – more potent newer generation • Post PCI – increase in bleeding side effects • Non-reversible • Ticagrelor has been shown to further decrease major cardiovascular events and mortality • It also decreases the risk of lifethreatening bleeding episodes Treatments for UA/NSTEMI 4: Antithrombotic Agents Antiplatelet Drugs Anticoagulant Drugs Glycoprotein (GP) IIb/ IIIa receptor antagonists • Are potent antiplatelet agents that block the final common pathway of platelet aggregation. • Include the monoclonal antibody Abciximab and the small molecules Eptifibatide and Tirofiban. • Effective in reducing adverse coronary events in patients undergoing PCI. • In patients with UA or NSTEMI, their benefit is manifest primarily in those at the highest risk of complications (the presence of elevated serum troponin levels or recurrent episodes of chest pain). • Initiated in the cardiac catheterization laboratory at the time of PCI. Intravenous unfractionated heparin (UFH) has long been standard anticoagulant therapy for UA and NSTEMI • It binds to antithrombin. • UFH additionally inhibits coagulation factor Xa, impeding further clot formation. • Improves cardiovascular outcomes and reduces the likelihood of progression from UA to MI. • Dose adjusted, through serial measurements of the serum activated partial thromboplastin time (aPTT) and anti-Xa levels. Treatments for UA/NSTEMI 5: Anticoagulant Agents Anticoagulant Drugs Low molecular weight heparins (LMWHs) • Interact with antithrombin but preferentially inhibit coagulation factor Xa. • They provide a more predictable pharmacologic response than UFH. • LMWHs are easier to use, prescribed as one or two daily subcutaneous injections based on the patient’s weight. • Unlike UFH, with LMWH repeated monitoring of blood tests and dosage adjustments are not generally necessary. • In clinical trials in patients with UA or NSTEMI, the LMWH enoxaparin has demonstrated reduced death and ischemic event rates compared with UFH. • Two other types of anticoagulants have also been shown to be beneficial: • Bivalirudin and Fondaparinux (Xa inhibitor) Conservative vs Early Invasive Management of UA/NSTEMI • Many patients with UA or NSTEMI stabilize following therapies described earlier, while others have recurrent ischemic events, and there is currently no definitive way to predict which direction a patient will take or to quickly determine which individuals have such severe underlying CAD that coronary revascularization is warranted (without performing a cath). • These uncertainties have led to two therapeutic strategies in UA/NSTEMI: (1) An early invasive approach in which urgent cardiac catheterization is performed and coronary revascularization undertaken as indicated. (2) A conservative approach in which the patient is managed with medications and undergoes angiography only if ischemic episodes spontaneously recur or if the results of a subsequent stress test indicate substantial residual inducible ischemia. • The conservative approach offers the advantage of avoiding costly and potentially risky invasive procedures (and is more convenient for the staff involved in the cathing!) • Conversely, an early invasive strategy allows rapid identification and definitive treatment (revascularization) for those with critical coronary disease. Conservative vs Early Invasive Management of UA/NSTEMI • An early invasive approach is recommended in patients with: • Refractory angina • Shock • Ventricular arrhythmias • The most concerning clinical features • Risk assessment algorithms such as the Thrombolysis in Myocardial Infarction (TIMI) risk score consider such features and help identify patients at high likelihood of a poor outcome. • An early invasive strategy is recommended in patients with higher scores (≥3), as clinical studies have confirmed that a patient’s TIMI risk score predicts the likelihood of death or subsequent ischemic events. • Such patients should undergo angiography within 24 – 72 hours depending on the patents overall risk level. • The Thrombolysis in Myocardial Infarction (TIMI) risk score that employs seven variables to predict a patient’s risk level: • 1. Age > 65 years old • 2. ≥3 risk factors for coronary artery disease (as described in Chapter 5) • 3. Known coronary stenosis of ≥50% by prior angiography • 4. ST-segment deviations on the ECG at presentation • 5. At least two anginal episodes in prior 24 hours • 6. Use of aspirin in prior 7 days (ie, implying resistance to aspirin’s effect) Question 4 • A 75 yo woman presented in the midst of a stemi to an ER in her small town where the hospital did not have a cath lab. Due to inclement weather, she could not be air lifted by helicopter to the nearest cath facility, which was 3 hours away by ground transport. She was given TPA. Initially, she did well, with improvement in her chest pain. However, 45 min later she had a grand mal seizure. What is the next test that should be ordered stat? A. A troponin to see if the infarct is worsening B. An echo to see if her function has worsened acutely C. A CT scan of her head to see if she has an intracranial bleed D. An ABG to see if she is developing a lactic acidosis Adjunctive Therapies 1 Angiotensin-converting enzyme (ACE) inhibitors • Limit adverse ventricular remodeling • Reduce the incidence of heart failure, recurrent ischemic events, and mortality following an MI. • Synergistic effects when combined with aspirin and β-blockers. • Favorable improvements especially in higher-risk patients—those with anterior wall infarctions or LV systolic dysfunction. • Statins (HMG-CoA reductase inhibitors) • Reduce mortality in CAD patients • High-intensity lipid-lowering regimen • Improve endothelial dysfunction, inhibit platelet aggregation, and impair thrombus formation. Adjunctive Therapies 2 • Aldosterone antagonist (spironolactone or eplerenone) • Impaired ventricular contractility after MI can lead to heart failure (EF < 40%). • Aldosterone augments sodium reabsorption from the distal nephron (contributing to fluid retention, an undesired effect in heart failure) and also promotes inflammation and myocardial fibrosis. • Chronic administration of an aldosterone antagonist, ACE and Bblocker mitigates these effects and has been shown to decrease mortality following MI in patients with left ventricular dysfunction. • Oral anticoagulation (i.e., warfarin) • For patients at high risk of thromboembolism • Atrial fibrillation, large acute anterior MI with akinesis (which is susceptible to thrombus formation because of the stagnant blood flow). 5. Complications of ACS • Recurrent ischemia • Arrythmias • Ventricular fibrillation • Supraventricular arrhythmias • Conduction blocks • Myocardial dysfunction • Heart failure • Cardiogenic shock • Right ventricular infarction • Mechanical complications • Papillary muscle rupture • Ventricular free wall rupture • Ventricular septal rupture • True ventricular aneurysm • Pericarditis • Dressler syndrome • Thromboembolism Complications of Angina and MI • In unstable angina potential complications: • Death (5% to 10%) • Progression to MI (10% to 20%) • STEMI complications: • Result from the inflammatory, mechanical, and electrical abnormalities induced by regions of necrosing myocardium • Early complications result from myocardial necrosis itself • Others develop several days to weeks later and reflect the inflammation and healing of necrotic tissue. Recurrent Ischemia • Post infarction angina has been reported in 20% to 30% of patients following an MI, and is indicative of inadequate residual coronary blood flow. Therefore, it also correlates with an increased risk or re-infarction. • This rate of recurrent ischemia is lower in those who have undergone acute percutaneous coronary revascularization, but not in those who used thrombolytic therapy alone. • Patients with recurrent episodes of ischemia usually require urgent cardiac catheterization, often followed by revascularization by percutaneous techniques or coronary artery bypass surgery. Arrythmias: common after acute MI, and a major cause of mortality. • Mechanisms: 1. Anatomic interruption of blood flow to structures of the conduction pathway (eg, sinoatrial node, atrioventricular node, and bundle branches). 2. Accumulation of toxic metabolic products (eg, cellular acidosis) and abnormal transcellular ion concentrations owing to membrane leaks. 3. Autonomic stimulation (sympathetic and parasympathetic). 4. Administration of potentially arrhythmogenic drugs (eg, dopamine). Blood Supply to the Conduction System Components Supraventricular Dysrhythmias • These rhythm disturbances are common in acute MI. • Sinus bradycardia • Results from either excessive vagal stimulation • Or sinoatrial nodal ischemia • Usually in the setting of an inferior wall MI • Sinus tachycardia occurs frequently and may result from: • • • • • • Pain and anxiety, Heart failure, Drug administration (dopamine), Intravascular volume depletion, Ischemia or distention of the atria, Increases in myocardial oxygen demand. • They exacerbate ischemia. • Atrial premature beats and atrial fibrillation can result from atrial ischemia or atrial distention secondary to LV failure. https://manualofmedicine.com/ecgs/ecgcase-71-atrial-fibrillation-with-rvr-lafb-andacute-anterolateral-stemi/ Conduction Blocks • 3 main types of conduction blocks include sinoatrial blocks, atrioventricular nodal blocks, and bundle branch blocks. • These are common developments in acute MI due to ischemia or necrosis of conduction tracts. • They can also develop transiently because of increased vagal tone. • Vagal activity may be increased by: • The stimulation of afferent fibers by the inflamed myocardium • Or as a result of generalized autonomic activation in association with the discomfort of an acute MI. The diagnosis of infraHisian Wenckebach is confirmed. The conduction changed to 2:1 atrioventricular block with rapid atrial pacing at 150/min. The retrograde conduction was intact and via the atrioventricular node. The patient underwent dual chamber pacemaker implantation with resolution of symptoms. Where Is the Level of Atrioventricular Block? Raghav Bansal, et al. Originally published 26 Oct 2020 https://doi.org/10.1161/CIRCULATIONAHA.120.050344 Circulation. 2020;142:1684–1686. Ventricular Ectopy https://www.healio.com/cardiology/learn-the-heart/ecgreview/ecg-topic-reviews-and-criteria/ventricular-fibrillation- • Ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation during an acute MI arise from: • Re-entrant circuits • Or enhanced automaticity of ventricular cells • Ventricular ectopic beats are common and usually not treated unless the beats become frequent, consecutive or multifocal. • V fib is the main cause of sudden cardiac death in acute MI, and it consists of rapid, disorganized electrical activity of the ventricles. • Most fatal episodes occur before hospital arrival (although there is now increased availability of automatic external defibrillators in public places). • Usually occurs during the first 48 hours of an MI (transient electrical instability). Myocardial Dysfunction Heart Failure • Impaired ventricular contractility (systolic dysfunction, HFrEF) following ischemia or • Increased myocardial stiffness (diastolic dysfunction, HFpEF) • Ventricular remodeling, arrhythmias, and acute mechanical events Signs and Symptoms: 1. Dyspnea 2. Pulmonary rales 3. Third heart sound (S3). Treatment: 4. Diuretics or relief of volume overload 5. ACE inhibitor and β-blocker therapies provide protection against earlier mortality 6. LV ejection < 40%, an aldosterone antagonist (spironolactone or Eplerenone.As thse are potassium sparing drugs, when prescribed with an ACE inhibitor, one must monitor for hyperkalemia. Cardiogenic Shock • A condition of severely decreased cardiac output usually associated with hypotension. • Systolic blood pressure often < 90 mm Hg or lower than normal for the individual. • Inadequate perfusion of peripheral tissues; rising lactate levels. • Often means that more than 40% of the LV mass has infarcted. • Cardiogenic shock occurs in up to 10% of patients post MI, and the mortality rate > 70%. • Early cardiac catheterization and revascularization can improve the prognosis. • Cardiogenic shock is self perpetuating because: (1)Hypotension leads to decreased coronary perfusion, which exacerbates ischemic damage (2)Decreased stroke volume (3)Increased LV size (4)Increased myocardial oxygen demand due to increased wall tension. • Treatments options include: • Intravenous inotropic agents (dobutamine) to increase cardiac output, often along with vasopressors. • Pulmonary artery catheter placement and arterial line placement (which also enable pulse contour analysis to aid management) • IABP – decrease afterload and augment coronary perfusion. Intra-aortic Balloon Pump • The intra-aortic balloon pump (IABP) is a mechanical device that increases myocardial oxygen perfusion and indirectly increases cardiac output through afterload reduction. • It consists of a cylindrical polyurethane balloon that sits in the aorta, approximately 2 centimeters (0.79 in) from the left subclavian artery. • The balloon inflates and deflates via counter pulsation, meaning it actively deflates in systole and inflates in diastole. Systolic deflation decreases afterload through a vacuum effect and indirectly increases forward flow from the heart. Diastolic inflation increases blood flow to the coronary arteries via retrograde flow. • These actions combine to decrease myocardial oxygen demand and increase myocardial oxygen supply. • https://en.wikipedia.org/wiki/Intra-aortic_balloon_pump https://mountnittany.org/wellness-article/intraaorticballoon-pump-therapy-understanding Impella Left Ventricular Assist Device Question 5 • Which of the following is/are potential physical exam or lab findings in a patient with an IABP to assist with stabilization after an anterior wall MI? A. Thrombocytopenia B. Schistocytes (torn read blood cells) on peripheral smear C. Mottling of the lower extremity below the catheter D. Rising BUN and Cr E. All of the above******** RV Infarctions • 1/3 of patients with infarction of the LV inferior wall also develop necrosis of portions of the right ventricle. • RCA perfuses both regions in most individuals. • Right-sided heart failure can result with decreased compliance and abnormal contraction. • Signs and Symptoms: • Jugular venous distention • Profound hypotension (often responsive to fluid administration) • Oxygenation may be impaired, but this is usually more of a feature of LV dysfunction. • Swan Ganz (pulmonary artery catheter) is often used to maximize hemodynamics to assist with RV recovery. Mechanical Complications • Often result in dramatic worsening in the clinical picture of a patient who may have been previously stable appearing. • Such mechanical complications include: • • • • Papillary muscle rupture Ventricular free wall rupture Ventricular septal rupture True ventricular aneurysm • The mortality rates associated with these complications are extremely high. Papillary Muscle Rupture • Ischemic necrosis and rupture of an LV papillary muscle may be rapidly fatal because of acute severe mitral regurgitation. • Partial rupture may cause more moderate regurgitation, may not be immediately lethal. • It may result in symptoms of heart failure or pulmonary edema. • The posteromedial LV papillary muscle is more susceptible to infarction than the anterolateral one due to a more tenuous blood supply. Ventricular Free Wall Rupture https://www.nejm.org/doi/full/10.1056/ NEJMicm1613367 • Rupture of the LV free wall through a tear in the necrotic myocardium is an infrequent but deadly complication. Survival is rare. • Occurs within the first 2 weeks following MI. • More common in women with hypertension. • Hemorrhage into the pericardial space flowing from LV free wall rupture results in rapid cardiac tamponade. • Occasionally, a pseudoaneurysm results (incomplete rupture checked by a by thrombus formation that “plugs” the hole in the myocardium). • Surgical repair is only option at that point. Ventricular Septal Rupture • Analogous to LV free wall rupture, but the abnormal flow of blood is shunted across the ventricular septum from the left to the right ventricle. • Usually precipitates congestive heart failure. • A loud systolic murmur at the left sternal border is common. • A Swan Ganz catheter is useful in measuring the O2 saturation of blood in the right (abnormally high). True Ventricular Aneurysm • A late complication of MI (weeks to months). • Weakened ventricular wall, but not perforated. • Phagocytic clearance of necrotic tissue and replacement by fibrous tissue results in a localized outward bulge (dyskinesis) when the residual viable heart muscle contracts. • Does not involve communication between the LV cavity and the pericardium. • Complications of LV aneurysm include: (1) Thrombus (2) Ventricular arrhythmias (3) Heart failure resulting from reduced forward cardiac output (some LV stroke volume is “wasted” by filling the aneurysm cavity during systole) • Clues to the presence of an LV aneurysm i

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