N715 Exam 3 Pt 2 PDF

Myocardial Remodeling Definition and Mechanism Myocardial Remodeling: Refers to structural and functional changes in the heart post-MI, driven by the body's response to the damage. Mediators: Angiotensin II (Ang II), aldosterone, catecholamines, adenosine, and inflammatory cytokin...

Myocardial Remodeling Definition and Mechanism Myocardial Remodeling: Refers to structural and functional changes in the heart post-MI, driven by the body's response to the damage. Mediators: Angiotensin II (Ang II), aldosterone, catecholamines, adenosine, and inflammatory cytokines contribute to remodeling. Effects: Results in myocyte hypertrophy, loss of contractile function, and increased myocardial dysfunction, potentially leading to heart failure. Phases of Remodeling Initial Phase Inflammatory Response: Damaged cells are degraded by proteolytic enzymes from neutrophils, and macrophages remove dead cells and secrete growth factors. Scar Formation: Leukocytes infiltrate, and a weak collagen matrix is formed, which matures into scar tissue over 6 weeks. Potential for Re-injury: During this phase, individuals might resume activities, risking stress on the newly formed, still vulnerable scar tissue. Functional Impairment Changes in Heart Function Decreased Contractility: Leads to abnormal wall motion. Altered Compliance and Function: Reduction in stroke volume, ejection fraction, and increased end-diastolic pressure. SA Node Malfunction and Dysrhythmias: Resulting in potential heart failure. Consequences of MI and Remodeling Structural and Functional Changes Ventricular Dysfunction: The ejection fraction (EF) falls, leading to an increase in ventricular end-diastolic volume (VEDV). Vasoconstriction and Coronary Spasm: Due to released Ang II, contributing to fluid retention and remodeling. electronically Abnormalities: Disruptions in electrolyte balance, including loss of potassium, calcium, and magnesium from cells. Long-term Outcomes Chronic Heart Failure: Due to sustained functional impairment of the heart. Sudden Cardiac Death: As a result of severe dysrhythmias following MI. Therapeutic Interventions Immediate Treatment Reperfusion Therapy: Crucial to reduce infarct size, although it can cause reperfusion injury, contributing to additional cell death. Medications: Use of renin-angiotensin-aldosterone blockers and β-blockers to inhibit remodeling and restore coronary flow quickly. Emerging Therapies Cardioprotection: Investigations into reducing ischemia-reperfusion injury. Stem Cell Therapy: Potential for cardiac muscle repair and regeneration, leveraging the regenerative capacity of cardiac stem cells. Symptoms The first symptom of acute MI typically involves a sudden, severe chest pain that is different from angina pectoris, as it is more intense and prolonged. The pain is often described as heavy and crushing, akin to "a truck sitting on my chest." In addition to chest pain, patients may experience: Radiation of pain to the neck, jaw, back, shoulder, or left arm. Sensation similar to extreme indigestion. Nausea and vomiting due to reflex stimulation of vomiting centers by pain fibers. Silent infarction which occurs in some individuals, especially those older or with diabetes, where no pain is experienced. Cardiovascular Changes Upon physical examination, various cardiovascular changes can be detected: 1. Sympathetic Nervous System (SNS) Activation: This compensatory mechanism results in a temporary increase in heart rate and blood pressure. 2. Extra Heart Sounds: Abnormal sounds indicating left ventricular dysfunction. 3. Pulmonary Congestion: Dullness to percussion and inspiratory crackles at the lung bases, symptomatic if heart failure develops. 4. Peripheral Vasoconstriction: Causes the skin to become cool and clammy. Postinfarction Complications The severity and number of postinfarction complications are influenced by: The extent and location of necrosis. The individual's physiological condition prior to the infarction. The timeliness and effectiveness of therapeutic interventions. Common complications include:  Heart Failure Arrhythmias Pericarditis Thromboembolism Sudden Cardiac Death: This can happen even without the presence or with minimal infarction and is influenced by factors like ischemia, left ventricular dysfunction, and electrical instability. Risk Factors and Sudden Cardiac Death Sudden death due to myocardial ischemia, with or without severe infarction, involves the interplay between: Ischemia: Decreased blood flow to the heart muscle. Left Ventricular Dysfunction: Impairment of the heart's main pumping chamber. Electrical Instability Irregular heart rhythms that can lead to sudden cardiac arrest. Myocardial Stunning Definition and Characteristics Myocardial stunning refers to a state of prolonged, yet reversible, post-ischemic contractile dysfunction following brief periods of myocardial ischemia, even after the restoration of coronary blood flow. It reflects genuine reperfusion injury resulting from increased formation of reactive oxygen species (ROS) and reduced calcium responsiveness. Although it occurs in patients post-percutaneous coronary interventions (PCI) or following exercise-induced myocardial ischemia, myocardial stunning is usually not hemodynamically compromising. Mechanisms Key Mechanisms Reactive Oxygen Species (ROS): The formation of ROS, such as superoxide radicals, hydrogen peroxide, and hydroxyl radicals, primarily during the reperfusion phase, is a major contributor to myocardial stunning. These ROS cause oxidative modifications to the contractile machinery. ROS originate from various cellular sources, including the mitochondria and cardiomyocytes, but not necessarily from leukocytes. Calcium Overload: Ischemia-reperfusion increases cytosolic calcium levels due to the dysfunction of the sarcoplasmic reticulum (SR) and increased sodium-proton exchange. Calcium overload contributes further to mitochondrial dysfunction and ROS formation, creating a deleterious cycle.  Contractile Dysfunction: Oxidative stress and calcium overload ultimately impair the responsiveness of contractile myofibrils and disrupt their interaction with the extracellular matrix. Interaction of Mechanisms ROS and calcium overload create a feedback loop where ROS impair SR function, leading to further calcium overload and mitochondrial ROS production. This perpetuates the stunning phenomena by continuously disturbing the balance between oxidative stress and calcium regulation. Prevention and Treatment Myocardial stunning typically does not require specific treatment due to its reversible nature. Nevertheless, interventions targeting its underlying mechanisms can mitigate its severity. Inotropic Agents: Used to reverse hemodynamically compromising stunning. Antioxidants: Administering enzymes like superoxide dismutase and catalase can attenuate myocardial stunning. Pharmacological Agents: Calcium antagonists, angiotensin-converting enzyme inhibitors, and sodium-proton exchange inhibitors have shown potential in reducing the severity of myocardial stunning. Myocardial Hibernation Definition and Characteristics Myocardial hibernation is a condition of sustained, reversible reduction in myocardial contractile function due to chronic ischemia which adapts to reduced blood flow. Unlike myocardial stunning which happens post-ischemia, hibernation is associated with ongoing ischemia. It manifests in chronic coronary syndromes with matched reductions in blood flow and contractile function, leading to metabolic adaptations to preserve myocardial viability. Mechanisms Pathogenesis Flow and Function Matching: Chronic moderate reductions in blood flow and contractile function characterize hibernating myocardium, demonstrating a state of metabolic adaptation. Experimental models (such as prolonged coronary stenosis in dogs) show that both blood flow and contractile function recover following reperfusion, indicating hibernation rather than necrosis.  Molecular Adaptations: Chronic hibernation involves downregulation of proteins essential for calcium handling in the SR, increased expression of heat shock proteins, and modifications to mitochondrial and cytoskeletal proteins. Prevention and Treatment Treatments aim to restore myocardial perfusion and function primarily through revascularization procedures. Stem Cell Therapy: Techniques like intracoronary infusion of mesenchymal stem cells have shown promise in improving myocardial function in animal models. Pharmacological Interventions: Use of statins (such as pravastatin) and other agents to mobilize bone marrow-derived progenitor cells facilitate myocardial repair and improved contractile function. Diagnostic and Imaging Techniques Various imaging modalities are used to diagnose and monitor hibernating myocardium, including echocardiography, PET with contrast agents like 13NH3 and 18F-fluorodeoxyglucose, and MRI. Comparative Analysis Both myocardial stunning and hibernation represent ischemia-induced myocardial dysfunction, but they differ in their etiology and physiological implications. Stunning results from short-term ischemia followed by reperfusion, primarily driven by oxidative and calcium-related stress pathways. Hibernation is due to chronic, consistent ischemia leading to an adaptive reduction in contractile function to match the reduced blood flow. Heart Failure Introduction to Heart Failure Heart failure (HF), previously known as congestive heart failure (CHF), is characterized by the heart's inability to pump sufficient blood to meet the body's needs. This condition can manifest as either chronic or acute: Chronic Heart Failure: Develops over time due to untreated conditions such as hypertension and coronary artery disease, worsening progressively.  Acute Heart Failure: Occurs suddenly and can affect seemingly healthy individuals, often resulting from a myocardial infarction (MI), pulmonary embolism (PE), or acute left-sided heart failure. This is a medical emergency. Anatomy and Physiology of the Heart Cells of the Heart Cardiomyocytes: The primary muscle cells enabling contraction. Pacemaker Cells: Specialized cardiomyocytes controlling heart rhythm. Endothelial Cells: Smooth lining of blood vessels. Fibroblasts: Produce the extracellular matrix. Smooth Muscle Cells: Present in coronary arteries. Cardiac Stem Cells: Differentiate into cardiomyocytes, endothelial cells, and smooth muscle cells. Immune Cells: Includes macrophages, lymphocytes, and mast cells. Heart Structure Layers of the Heart Epicardium: Outer layer. Myocardium: Thick, muscular middle layer. Endocardium: Inner layer lining chambers and valves. Chambers and Valves Right side: Vena Cava-> Right Atrium -> Tricuspid Valve -> Right Ventricle -> Pulmonary Valve -> Pulmonary Artery. Left side: Pulmonary Veins -> Left Atrium -> Mitral Valve -> Left Ventricle -> Aortic Valve -> Aorta. Coronary Arteries Left Coronary Artery -> Left Circumflex and Left Anterior Descending. Right Coronary Artery -> Right Marginal and Posterior Descending. Functions Blood Circulation: Ensuring systemic and pulmonary circulation. Homeostasis: Regulating cardiac output and blood pressure. Endocrine and Nervous Systems: Influencing cardiac functions. Key Metrics Cardiac Output (CO): CO = Stroke Volume (SV) x Heart Rate (HR) Pressure Regulation: Diastolic and Systolic pressures, Preload, and Afterload considerations. 5. Pathophysiology of Heart Failure  Diagnosis: Based on symptoms, structural/functional abnormalities, and lab findings. Causes: Insulting injuries like MI, valve damage, and high heart rate. Ejection Fraction: The percentage of blood pumped out with each contraction. 6. Types of Heart Failure Heart Failure with Reduced Ejection Fraction (HFrEF) Symptoms: Ejection fraction ≤40%, ventricular remodeling, decreased stroke volume, increased left ventricular diastolic volume. Mechanisms: Contractile dysfunction of sarcomeres, neurohormonal reactions (activation of the sympathetic nervous system, release of catecholamines, renal perfusion changes, RAAS activation, natriuretic peptides release leading to diuresis and vasodilation). Heart Failure with Preserved Ejection Fraction (HFpEF) Symptoms: Ejection fraction >50%, more common in women, patients with obesity and hypertension. Mechanisms: Decreased compliance of the left ventricle, hypertrophy, increased wall tension during diastole, backfilling into the left atrium and pulmonary vessels, inflammation. Right-Sided Heart Failure Symptoms: Often due to left-sided heart failure, cor pulmonale (chronic lung disease), increased preload in the right ventricle, peripheral edema, hepatosplenomegaly, chronic hypoxic pulmonary disease effects. 7. Clinical Manifestations Heart failure manifests through several clinical stages, often assessed through parameters such as ejection fraction, symptoms, and physical examinations. These manifestations may include: Vital signs alterations (e.g., blood pressure changes). Symptoms like fatigue, shortness of breath, edema, and exercise intolerance. Organ-specific complications like pulmonary congestion and liver congestion. Kawasaki Disease Introduction to Kawasaki Disease Overview:  Kawasaki Disease (KD) is a rare, inflammatory condition primarily affecting children under the age of five. It involves swelling and inflammation of the blood vessels (vasculitis) throughout the body, particularly the coronary arteries. Approximately 20-25% of affected children develop coronary artery dilatations or aneurysms. KD is the leading cause of pediatric-acquired heart disease in developed countries. Mortality rate has dropped below 1% since the advent of effective treatment. Risk Factors: Family history of KD increases risk. Exposure to respiratory and urinary tract infections. Higher incidence in Asian ancestry. Higher incidence during winter and spring months. Genetic factors, such as FCRLA, PTGER4, IL17F, CARD11, and SIGLEC10, may increase susceptibility. Physiology Affected by KD Cardiovascular System: Coronary Arteries: Carry blood to the heart muscle. Heart: Pumps blood through the body; valves regulate blood flow in and out of the heart chambers. Immune System: Lymph Nodes:Protect against infection with key cells like T and B lymphocytes, especially in the cervical region. Digestive System: Mucous Membranes:Includes areas such as the conjunctiva and oral cavity. Pathophysiology of KD Etiology: The exact cause of KD is unclear. Evidence suggests that respiratory viruses may induce an abnormal immune response in genetically predisposed individuals. Next-generation sequencing has identified genes potentially influencing KD susceptibility (FCRLA, PTGER4, IL17F, CARD11, SIGLEC10). Stages of Pathophysiology: Stage I and II (Necrotizing Arteritis):  Days 1-25: Fever onset. Small arterioles, capillaries, and venules become inflamed. Systemic inflammation affects larger vessels, heart, lymph nodes, and the gastrointestinal tract. Stage III (Subacute/Chronic Vasculitis): Days 26-40, may extend from months to years. Abnormal increase of cytotoxic T cells, regulatory T cells, and plasma cells, suggesting an adaptive immune response. Granulation process in medium-sized arteries, leading to arterial wall dilation, aneurysms, and possible thrombus formation. Stage IV (Luminal Myofibroblastic Proliferation): Days 41 and beyond. Persistent inflammation causes thickening, stenosis, and calcification of arterial walls. Smooth muscle cells and extracellular matrix form myofibroblasts, leading to luminal narrowing and increased risk of thrombosis. Clinical Manifestations Phases: Acute Phase: Persistent high fever (≥39°C for ≥5 days). Bilateral non-exudative conjunctivitis. Strawberry tongue, red and cracked lips. Subacute Phase: Maculopapular, erythematous rash. Swelling in hands/feet, desquamation. Coronary artery aneurysms. Convalescent Phase: Enlarged, tender cervical lymph nodes. Resolution of most signs and symptoms. Diagnostic Mnemonic (American Heart Association 2017 guidelines): Warm CREAM: Warm: Fever (≥39°C for at least 5 days). Conjunctivitis: Bilateral painless bulbar conjunctivitis without exudate. Rash: Maculopapular, erythema multiforme-like, or diffuse erythroderma on the trunk and extremities. Edema: Erythema on hands/feet, followed by desquamation and nail changes. Adenopathy: Unilateral cervical lymph node ≥1.5 cm.  Mucositis: Strawberry tongue, fissures/crusting of lips. Treatment and Management Early diagnosis and treatment are crucial to reduce the risk of coronary artery complications. Treatment involves high-dose intravenous immunoglobulin (IVIG) and aspirin to reduce inflammation and fever. Tetralogy of Fallot Tetralogy of Fallot (TOF) is the most common congenital cyanotic heart defect, characterized by four major anatomical abnormalities in the heart. This condition is present at birth and affects the structure of the heart, leading to insufficient oxygenation of blood. Normal Physiology of Heart Development Heart begins forming between weeks 3 and 6 of gestation. The outer endocardial tubes merge into a single cardiac tube. The atrium and ventricles begin to form. Heartbeat starts around week 5. Pathophysiology of Tetralogy of Fallot TOF involves four primary abnormalities: 1. Right Ventricular Hypertrophy 2. Aorta Displacement (Overriding Aorta) 3. Pulmonary Stenosis 4. Ventricular Septal Defect (VSD) Detailed Pathophysiology Improper Development: Results in insufficient blood flow to the lungs. Septal Wall Defect: Allows mixing of oxygenated and deoxygenated blood. Pulmonary Valve Stenosis: Decreases pulmonary blood flow. Hypertrophy of Right Ventricle: Increases risk of heart failure. Displaced Aortic Valve: Results in mixed blood flow ("right to left shunt"). Cellular Level Impact Mitochondrial Dysfunction: Leads to decreased cellular energy. Consequences: Cyanosis, tissue hypoxia, and cell death. Overcompensation by increased red blood cell production. Clinical Manifestations  Average Oxygen Saturation: 79% when standing, 84% when squatting. Symptoms: Cyanosis, fussiness, fatigue, clubbing of fingers and toes, heart murmur. TET Spells: Episodic hypercyanotic spells triggered by crying or feeding, leading to rapid deep breathing, irritability, and severe cyanosis. Older children may squat to relieve these spells. Heart Murmur Characterization: Systolic crescendo-decrescendo murmur best heard along the left mid-to-upper sternal border. Diagnosis Echocardiogram (Echo) Prenatal Diagnosis: Optimal gestation age for ultrasound scan is 18 to 22 weeks. Newborn Presentation: Depends on the degree of right ventricular outflow tract (RVOT) obstruction. Surgical Treatment Timing: Typically performed within the first year of life. Procedures Closure of VSD with a patch. Enlargement of the RVOT. Genetic Insights Emerging Research: New understanding of the role of genetics in non-syndromic TOF. From Slides Hemodynamics and Cardiac Contractility Hemodynamics Hemodynamics refers to the dynamics of blood flow, governed by principles of fluid dynamics. It involves the study of blood flow, pressure, and resistance, essential for understanding cardiovascular functionality and the effects of diseases. Cardiac Contractility Cardiac contractility is the ability of the heart muscle (myocardium) to contract. It is a critical factor in influencing stroke volume and cardiac output, affecting overall cardiovascular health. 4. Neurohumoral Responses in Cardiovascular Health Neurohumoral responses involve the regulatory mechanisms that the nervous and endocrine systems use to maintain cardiovascular homeostasis. Key components include: Sympathetic Nervous System (SNS) Parasympathetic Nervous System (PNS) Renin-Angiotensin-Aldosterone System (RAAS) Antidiuretic Hormone (ADH) These systems work together to regulate heart rate, blood pressure, and fluid balance. 5. Hypertension Definition and Pathophysiology Hypertension, or high blood pressure, is a condition where the force of blood against the artery walls is consistently too high. It can lead to severe health complications over time, such as heart disease, stroke, and kidney problems. Clinical Manifestations Often asymptomatic initially Headaches, shortness of breath, and nosebleeds in severe cases Long-term complications include heart attack, heart failure, aneurysm, and renal impairment Complications Cardiovascular: Heart attack, heart failure Renal: Chronic kidney disease Neurological: Stroke, dementia Ophthalmological: Retinopathy 6. Myocardial Infarction and Acute Coronary Syndromes Pathophysiology Myocardial infarction (MI) occurs when a part of the heart muscle doesn't receive adequate blood flow. This usually results from a blockage in one or more coronary arteries, causing ischemia and damage to the myocardium. Clinical Manifestations Severe chest pain or discomfort Dizziness, shortness of breath Nausea, cold sweat Symptoms may vary between men and women Management and Outcomes  Acute Management: Medications (e.g., thrombolytics, beta-blockers), angioplasty, and coronary artery bypass grafting (CABG) Long-term Management: Lifestyle modifications, medications to prevent further clots, and regular monitoring 7. Heart Failure Types and Pathophysiology Heart failure is a chronic condition where the heart cannot pump sufficient blood to meet the body's needs. Types include: Left-sided heart failure: Affects the left ventricle Right-sided heart failure: Often results from left-sided failure Congestive heart failure (CHF): Blood backs up in the lungs causing congestion Clinical Manifestations Shortness of breath Fatigue and weakness Swelling (edema) in legs, ankles, and feet Rapid or irregular heartbeat Long-term Management Medications (e.g., ACE inhibitors, diuretics) Lifestyle changes (diet, exercise) Surgical options (e.g., ventricular assist devices, heart transplant) 8. Cardiomyopathy Types and Pathophysiology Cardiomyopathy refers to diseases of the heart muscle that impair its ability to pump blood effectively. Types include: Dilated cardiomyopathy: Enlargement and weak contraction of the heart chambers Hypertrophic cardiomyopathy: Thickened heart muscle, which can obstruct blood flow Restrictive cardiomyopathy: Rigidity of the heart walls causing restricted filling of the heart Clinical Manifestations Breathlessness, especially during exertion Swelling in extremities Palpitations and chest pain Fatigue Prognosis and Treatment Variable depending on type and severity Treatments include medications, lifestyle changes, and possibly surgical intervention 9. Impact on Cellular Function and Injury Cardiovascular conditions often lead to cellular injury and loss of function, primarily through ischemia (restricted blood flow) and reperfusion injury (damage caused when blood supply returns to tissue). Understanding these impacts helps guide treatment strategies to minimize damage and improve outcomes. Cardiopulmonary Circulation at Birth Looping and Septation Early Cardiac Development Partitioning of the AV Canal Begins around the 4th week; completed by the 8th week. Involves the formation of endocardial cushions on the dorsal and ventral walls of the AV canal, which approach and fuse, dividing the AV canal into left and right AV canals. Partitioning of the Atria The primordial atrium is divided into left and right by the formation and fusion of septum primum and septum secundum. Partitioning of the Ventricles Growth of the muscular intraventricular septum from the floor of the ventricle. Fusion of endocardial cushions with bulbar ridges by the end of the 7th week. Partitioning of the Aorta & Pulmonary Trunk Occurs during the 5th week with the formation of bulbar ridges in the bulbus cordis and truncus arteriosus. Ridges spiral 180 degrees, creating the aorticopulmonary septum which divides into two chambers: the aorta and pulmonary trunk. Development of Cardiac Valves Semilunar valves Develop from three swellings of subendocardial tissue around the aorta and pulmonary trunk orifices. Involvement of neural crest cells. Swellings reshape into thin-walled cusps. Atrioventricular valves  Similar development from localized tissue proliferation around the AV canals. Conducting System of the Heart Sinoatrial Node Develops by the 5th week, located in the right atrium near the entrance of the superior vena cava. AV Node Located just superior to the endocardial cushions. Ensures electrical isolation between atrium and ventricle, with the only connection being the AV bundle. The AV bundle splits into right and left bundle branches distributed through ventricles. Fetal Circulation Reflects non-functional lungs for oxygenation with only 5-10% of fetal blood passing through the lungs. The pulmonary system is effectively bypassed through: Patent Foramen Ovale (PFO) Patent Ductus Arteriosus (PDA) High Pulmonary Vascular Resistance (PVR) in utero Transitional Circulation Post-birth changes Umbilical Cord Clamping causes systemic vascular resistance (SVR) to rise. Exposure to oxygen lowers PVR. Closure of: Ductus Venosus: from lack of placental blood flow. PFO: due to increased left-sided pressures. PDA: within the first 24 hours, driven by increased oxygen tension and declining prostaglandins produced by the placenta. Normal Cardiac Anatomy & Physiology Heart Wall Pericardium: A double-walled membranous sac consisting of: Parietal and visceral layers. Pericardial cavity containing pericardial fluid. Epicardium: Outer smooth layer. Myocardium: Thickest cardiac muscle layer.  Endocardium: Innermost layer where coronary vessels lie between myocardium and epicardium. Coronary Circulation Supplies oxygen and nutrients to the myocardium through: Right and left coronary arteries. Coronary veins entering the right atrium via the coronary sinus. Collateral arteries providing protection from ischemia. Cardiac Cycle Defines one heartbeat through one contraction (systole) and one relaxation (diastole). Diastole: Ventricles fill. Systole: Blood is ejected from the ventricles. Includes propagation of action potentials, depolarization, and repolarization. Refractory Period: Ensures muscle relaxation and completes the cardiac cycle. APPLICATION HOUR -- CARDIOVASCULAR TOO MUCH PRELOAD → back up into the lungs -> RHF INCREASED AFTERLOAD -> systemic vascular resistance, vasoconstriction [hard for heart to pump against] Vasculitis: friable, inflamed vessels; but also issues w/ venous return HTN ○ Affecting on heart, eyes, kidneys, brain ○ Heart Hypertrophy of myocardium from inc workload -> remodeling overtime (scarring/fibrosis/ muscle replaced w/ collagen - loss of elasticity, stiff; inc. voltage -- higher QRS peaks (mV) dt more work to generate action potential/contraction) Left-sided ejection fraction heart failure Diastolic failure ○ As muscle thickens/stiff, it cannot relax -> reduced cardiac output but squeezing hard (preserved ejection fraction) How much ventricle squeezed out (less fluid squeezed out) -> less cardiac output MI ○ Lactic acid and hydrogen ions build up ○ Chronic inflammation - atherosclerosis - foam cells ○ NSTEMI v STEMI STEMI: transmural; the necrosis has gone through ALL LAYERS of heart where perfusion cut off; often thinking of left ventricle (left anterior descending artery) - area completely blocked off, prolonged  depolarization and delay since FULL THICKNESS DEATH (area is not recovering) Longer we wait, less heart/muscle we have left NSTEMI (not the same as angina): subendocardial; part of layer of ventricle is dead (cardiac myocytes), have lost some tissue and contractility; might see some squeeze; not completely dead all the way through Mitochondria dysfunction - automaticity (can generate their own beats) and work together as a unit (syncytium); cells becoming acidotic (anaerobic) - shooting own impulses -> why we see VTach + VFib ○ Understanding where different coronary arteries perfuse Nodes E.g. Right coronary artery -> bradycardia (vagal), vomiting, hypotensive, syncope (passing out) [end up needing pacemaker]; wont enter LHF compared to person w/ LAD Myocytes ○ Left anterior descending -> perfuse LV (main area of heart that generate systemic circulation) ○ Men v Women Pts can present atypically; if had heart transplant -lack nerves so have no chest pain Woman: fatigue, SOB, may not have chest pain Won’t always see typical symptoms Tetralogy of Fallot ○ RIGHT TO LEFT shunt; mixing of oxy + deoxy blood, pulmonary stenosis (stiff, tight hole) - deoxy blood getting into systemic circulation ○ Right ventricle hypertrophy seen even before baby is born w/ RV working too hard; fluid back up [preload into right side of heart to get to pulm circulation but it cannot so pressure rises, harder work to squeeze] There’s a hole between atrium Ventricular septal defect (blood meant to go to lungs ends up going to the left into systemic circulation) Better oxygen if they squat because improves preload from the pressure from extremities; inc venous return; will improve amount entering pulm circulation to oxygenate We usually see left ventricular hypertrophy with other cardiac issues ○ Tet spells ○ Aorta -- displaced; overriding so places further pressure; pressure pushing onto pulmonary artery as well --How is squatting an intuitive way to improve oxygenation? ---?? Heart Failure ○ More of a syndrome since different conditions can lead to heart failure ○ E.g. MI - issue w/ contractility; not generating cardiac output ○ E.g. HTN -- preserved ejection fraction but not generating cardiac output w/ stiff ventricle ○ Toxins (ETOH, recreational drugs) ○ Medications (e.g. chemo) Cardiotoxicity -> ischemic cardiomyopathy or dilated cardiomyopathy; injuring heart muscle itself ○ Kawasaki -- myocarditis ○ Endocarditis v myocarditiis Endocarditis Endocardium: inner lining along lumen of the chamber, usually ventricle, seeing vegetation that grows (mitral, tricuspid valves) -> regurgitation [if heal, have scarring -> stenosis -> HF] IV drug use ○ Thyroid Disease ○ Viral Infections ○ Valvular deformities ○ Left-sided HF Pulmonary congestion; backing up from left to the right into the lungs Pink frothy sputum - hemoptysis Inc AFTERLOAD ○ Right-sided HF Backing up to venous system (systemic circulation) Weight gain, edema, JVD, hepatomegaly Inc. PRELOAD  Labs: LFTs BNP (high BNP represents fluid overload - natriuretic trying to get pts to diurese but heart cannot do effectively, thus this is elevated) ○ RAAS Inc BP, vasoconstriction, water & sodium retention Not generating cardiac output, heart stretching & inc BNP trying to diuresis, hypotensive (dec. BP) baroreceptors in vessels and heart wanting you to hang onto fluid dt low CO → activates RAAS Why we take ACEs Angiotensin: most potent vasoconstrictor Increases afterload- systemic resistance -> more ischemic injury overtime ○ Reduced v Preserved ejection fraction Kawasaki ○ Weather getting bad, more prone to infections ○ Symptoms appearing sequentially Red conjunctiva injected 1st ○ Following viral infections (e.g. URI) & chlamydia ○ Aneurysms: occur following weakening of vasculature, occur at bifurcations since there’s more sheer/friction at those points; occur in middle size vessels (e.g. middle coronary artery) → deadly ○ Importance of immediate referral for ECHO; will see wall motion (hypokinesis), cardiac CTA ○ Lethal if seeing (aneurysm) at beginning of artery?? :P Cardiovascular Conditions WEEK 11: Genitourinary 1. Differentiate between prerenal, intrinsic, and postrenal conditions affecting kidney function  Kidney function is to detoxify the blood, to metabolize and remove the byproducts of different drugs and different substances that enter into our bodies and to regulate fluids and electrolytes. In the renal pelvises, there are two ureters that are extending down into the bladder which is a storage container for urine so that is can be eliminated with the process of micturition or voiding When males have benign prostatic hypertrophy or prostate cancer that can close off the urethra and can cause obstruction and blockage causing urine to back up into kidneys and cause acute kidney injury