Hemorrhagic Shock
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Hemorrhagic shock occurs when there is inadequate tissue perfusion and oxygenation due to loss of circulating blood volume from hemorrhage. The most common cause of shock in surgical or trauma patients is blood loss. As blood loss increases, the body responds through cardiovascular, neuroendocrine, microcirculatory, hormonal, cellular, and vicious cycle changes in an attempt to compensate, but tissue hypoxia continues to worsen.
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Hemorrhagic Shock
This document provides an overview of hemorrhagic shock including:
- Signs and symptoms of hemorrhagic shock including changing mentation, tachycardia, cool skin, and decreased urine output.
- Classification of hemorrhagic shock severity based on percentage of blood loss.
- Pathophysiology of hemorrhagic shock including compensatory mechanisms and progression to cellular hypoxia and acidosis if bleeding is not controlled.
- Treatment principles including early control of hemorrhage, permissive hypotension, damage control resuscitation using plasma and platelets in addition to packed red blood cells, and consideration of tranexamic acid to reduce bleeding.
Shock
1) Shock is defined as inadequate tissue perfusion resulting from low blood pressure and abnormal cellular metabolism. The main types of shock are hypovolemic, distributive, and cardiogenic.
2) Hypovolemic shock occurs when intravascular volume is decreased, such as from blood loss, and requires fluid resuscitation. Septic shock, a form of distributive shock, involves infection and organ dysfunction and responds to antibiotics, fluids, and vasopressors.
3) Cardiogenic shock results from heart failure or damage and presents with low output and adequate fluid levels. It may be treated with inotropes, vasopressors, and procedures like LVAD or transplant
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COMPLICATIONS OF SPINAL & EPIDURAL ANAESTHESIA
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This document discusses perioperative fluid management. It notes that perioperative fluid therapy involves replacing normal fluid losses as well as surgical wound losses including blood loss. It then discusses why fluids are needed to maintain cellular function and oxygen delivery and utilization. It also covers total body water distribution and the Starling-Landis equation that governs fluid movement across capillaries. Factors that can lead to insufficient fluid like pre-op fasting and fluid/blood loss during surgery are addressed. Guidelines are provided on how much fluid to give, when, and factors to consider like the type of patient and surgery. The risks of excess fluid administration are also summarized.
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This document provides an overview of chest trauma, including the anatomy of the chest, causes of chest injuries, types of chest injuries, and treatments. It begins with the objectives and anatomy of the thorax. The main causes of chest trauma are then discussed as blunt trauma, penetrating trauma, and compression injuries. Various chest injuries are described in detail such as rib fractures, flail chest, pneumothorax, hemothorax, pulmonary contusion, and pericardial tamponade. The treatments for each type of injury are also outlined. The document provides a comprehensive review of chest trauma for medical professionals.
Shock
This document discusses the pathophysiology, causes, and management of shock. Shock is defined as a state of circulatory insufficiency resulting in inadequate organ perfusion. There are several types of shock, including hypovolemic, vasodilatory, cardiogenic, neurogenic, and obstructive. The initial goals of management are to secure the airway, administer intravenous fluids and vasopressors to restore perfusion pressure and tissue oxygenation, and give antibiotics if infection is suspected. The ultimate treatment involves addressing the underlying cause while monitoring systemic and tissue parameters to guide resuscitation efforts until oxygen debt is repaid and aerobic metabolism is restored.
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Hemorrhagic Shock
This document provides an overview of hemorrhagic shock including:
- Signs and symptoms of hemorrhagic shock including changing mentation, tachycardia, cool skin, and decreased urine output.
- Classification of hemorrhagic shock severity based on percentage of blood loss.
- Pathophysiology of hemorrhagic shock including compensatory mechanisms and progression to cellular hypoxia and acidosis if bleeding is not controlled.
- Treatment principles including early control of hemorrhage, permissive hypotension, damage control resuscitation using plasma and platelets in addition to packed red blood cells, and consideration of tranexamic acid to reduce bleeding.
Shock
1) Shock is defined as inadequate tissue perfusion resulting from low blood pressure and abnormal cellular metabolism. The main types of shock are hypovolemic, distributive, and cardiogenic.
2) Hypovolemic shock occurs when intravascular volume is decreased, such as from blood loss, and requires fluid resuscitation. Septic shock, a form of distributive shock, involves infection and organ dysfunction and responds to antibiotics, fluids, and vasopressors.
3) Cardiogenic shock results from heart failure or damage and presents with low output and adequate fluid levels. It may be treated with inotropes, vasopressors, and procedures like LVAD or transplant
Perioperative Optimisation of Coagulation and Haemostasis
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COMPLICATIONS OF SPINAL & EPIDURAL ANAESTHESIA
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1. Shock is defined as inadequate tissue perfusion to meet metabolic needs due to issues with cardiac performance, vascular performance, or cellular function.
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3. Treatment of shock focuses on identifying the type, treating the underlying cause, restoring circulating volume with fluids, and supporting vital organ function with vasopressors or inotropes as needed. The goal is to restore adequate perfusion to prevent multiple organ dysfunction syndrome.
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Anesthesia complications range from minor to catastrophic.
complications of general anesthesia might be due to difficulty in airway management or ventilation.
Also the complication might be due to cardiac arrhythmias and poor response to anesthetic effect during induction or maintenance or even the emergence from anesthesia.
So, the the systematic response to the effect of the anesthesia may occur at any time during surgery.
Some of the complications:
Hypoxia, arrhythmia, hypotension , hypertension, regurgitation and aspiration, hypothermia hypoglycemia, coronary ischemia, embolism, persistent apnea delayed recovery , and many others.
also regional anesthesia has its complications like nerve injury, post spinal headache.
Toxicity from local anesthesia is one of the important complication might occur during local infiltration.
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This document discusses various surgical body positions and their physiological effects. It describes positions like supine, lithotomy, lateral, and prone. For each position, it details how positioning impacts cardiovascular and pulmonary function, as well as nerves that may be at risk of injury. Complications from prolonged use of each position are also reviewed. The document emphasizes the importance of careful patient positioning to balance surgical access needs with physiological stability and risk of pressure injuries.
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1. Hemorrhagic shock is the most common cause of shock in surgical or trauma patients and results from blood loss that exceeds 15% of circulating volume.
2. Initial management of hemorrhagic shock involves identifying the source of bleeding, providing immediate resuscitation with fluids and blood products, and controlling hemorrhage.
3. Damage control resuscitation principles are followed, including permissive hypotension to limit blood loss and balanced use of crystalloids, colloids, platelets, and plasma to prevent coagulopathy.
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17. Oliguria In The Postoperative Patient
Oliguria is a decreased urine output that can be a sign of acute renal failure. The document discusses evaluating and managing oliguria in a postoperative patient. Common causes of postoperative oliguria include fluid loss, decreased renal perfusion, or intrinsic kidney injury. Assessment involves checking for dehydration, obstruction, or acute kidney injury risk factors. Initial management focuses on fluid resuscitation and stopping nephrotoxic drugs. Further treatment depends on whether the cause is pre-renal, renal, or post-renal.
Post operative care complication management
This document discusses standards of care for post-anesthesia care units (PACUs). It provides guidelines for monitoring patients, staffing PACUs appropriately, locating PACUs near operating rooms, and equipping PACUs with necessary medical equipment. Common complications in the PACU like pain, nausea, and respiratory issues are also reviewed. Optimal methods for pain management are outlined, including patient-controlled analgesia, regional techniques like epidurals, and multimodal analgesia.
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1. Shock is defined as inadequate tissue perfusion to meet metabolic needs due to issues with cardiac performance, vascular performance, or cellular function.
2. The main types of shock are hypovolemic, cardiogenic, obstructive, and distributive. Clinical signs include low blood pressure, fast heart rate, pale skin, confusion and loss of consciousness.
3. Treatment of shock focuses on identifying the type, treating the underlying cause, restoring circulating volume with fluids, and supporting vital organ function with vasopressors or inotropes as needed. The goal is to restore adequate perfusion to prevent multiple organ dysfunction syndrome.
Abcde approach-to-the-critically-ill-patient
Critical care medicine specializes in caring for the most seriously ill patients. These patients are best treated in an intensive care unit (ICU) staffed by experienced personnel. Some hospitals maintain separate units for special populations (eg, cardiac, trauma, surgical, neurologic, pediatric, or neonatal patients). ICUs have a high nurse:patient ratio to provide the necessary high intensity of service, including treatment and monitoring of physiologic parameters.
complications of Anesthesia.pptx
Anesthesia complications range from minor to catastrophic.
complications of general anesthesia might be due to difficulty in airway management or ventilation.
Also the complication might be due to cardiac arrhythmias and poor response to anesthetic effect during induction or maintenance or even the emergence from anesthesia.
So, the the systematic response to the effect of the anesthesia may occur at any time during surgery.
Some of the complications:
Hypoxia, arrhythmia, hypotension , hypertension, regurgitation and aspiration, hypothermia hypoglycemia, coronary ischemia, embolism, persistent apnea delayed recovery , and many others.
also regional anesthesia has its complications like nerve injury, post spinal headache.
Toxicity from local anesthesia is one of the important complication might occur during local infiltration.
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Damage control resuscitation
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This document discusses various surgical body positions and their physiological effects. It describes positions like supine, lithotomy, lateral, and prone. For each position, it details how positioning impacts cardiovascular and pulmonary function, as well as nerves that may be at risk of injury. Complications from prolonged use of each position are also reviewed. The document emphasizes the importance of careful patient positioning to balance surgical access needs with physiological stability and risk of pressure injuries.
Introduction to Anesthesia for medical students
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Aetiopathogenesis and management of empyema thoracis
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Shock - Pathophysiology, Clinical Features & Management
1. Hemorrhagic shock is the most common cause of shock in surgical or trauma patients and results from blood loss that exceeds 15% of circulating volume.
2. Initial management of hemorrhagic shock involves identifying the source of bleeding, providing immediate resuscitation with fluids and blood products, and controlling hemorrhage.
3. Damage control resuscitation principles are followed, including permissive hypotension to limit blood loss and balanced use of crystalloids, colloids, platelets, and plasma to prevent coagulopathy.
IV FLUID MANAGEMENT/ FLUID THERAPY
This document provides information on fluid therapy. It begins by classifying fluids as crystalloids or colloids based on their ability to diffuse. Crystalloids like normal saline (NS) diffuse freely while colloids do not pass as readily. NS is commonly used but can cause acidosis due to its chloride content. Ringer's lactate is more physiological with an electrolyte profile similar to plasma. Dextrose solutions like 5% dextrose provide calories but can increase lactate levels in critical illness. The document discusses the properties, indications, and limitations of various intravenous fluids.
Fluid balance and therapy in critically ill
The document discusses various aspects of human body water content and distribution. It notes that water makes up 50-60% of total body weight, with 40% being intracellular fluid, 20% extracellular fluid, and 15% interstitial fluid. It also discusses fluid compartments, mechanisms of fluid movement, electrolyte concentrations, fluid requirements, types of intravenous fluids and their properties, and considerations in fluid resuscitation.
Bronchospasm ppt
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Rapid Sequence Induction & Intubation
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Anesthesia for non Obstetric Surgery in Pregnancy
This document discusses anaesthesia considerations for non-obstetric surgery during pregnancy. It notes that while no anaesthetic agents have been proven to be teratogenic in humans, surgery can increase risks of preterm labour, abortion, or perturbations in uteroplacental blood flow that could impact the fetus. It emphasizes the importance of consulting an obstetrician prior to any invasive procedures or surgery during pregnancy due to their expertise in maternal-fetal physiology. Regional anaesthesia is generally preferred over general anaesthesia when possible.
Postoperative complications and management
This document discusses postoperative complications, their management, and assessments. It notes that complications can be general, like fever or infection, or specific to the type of surgery. Key time periods for complications are immediate postoperative, days 3-5, and after 5 days. The first postoperative assessment establishes baseline status and identifies any issues. Ongoing assessments monitor for complications and guide treatment. Factors like blood pressure, pain, and fluid balance must be considered.
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Guidelines for the inter- and intra-hospital transport of critically ill patients
Critical Care Medicine
Volume 32(1), January 2004, pp 256-262
Nippv
1) Non-invasive positive pressure ventilation (NIPPV) delivers positive airway pressure without an invasive interface like an endotracheal tube.
2) NIPPV can benefit patients with respiratory failure from COPD, cardiogenic pulmonary edema, obesity hypoventilation syndrome, and other conditions by reducing work of breathing and improving oxygenation.
3) Bi-level positive airway pressure (BPAP) and continuous positive airway pressure (CPAP) are common NIPPV modes. BPAP delivers different pressures during inspiration and expiration while CPAP maintains a constant pressure.
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Cardiogenic shock
Cardiogenic shock is a life-threatening condition caused by the heart's inability to pump enough blood to meet the body's needs, usually due to a severe heart attack damaging the heart muscle. Symptoms include increased respiratory rate, decreased heart rate, decreased urine output, and decreased consciousness. Treatment focuses on oxygenation, increasing systemic vascular resistance through vasopressors like epinephrine and norepinephrine, and improving heart contractility with medications that activate beta-1 receptors. Preventing cardiogenic shock involves maintaining a healthy heart through lifestyle.
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Cardiogenic shock
1) Cardiogenic shock is defined as hypotension, hypoperfusion, and elevated filling pressures caused by depressed left ventricular function following myocardial injury. Mortality from cardiogenic shock remains high at 50-70%.
2) Risk factors for cardiogenic shock include age over 65, female gender, large myocardial infarction, anterior infarction location, prior infarction history, diabetes, and hypertension. Post-mortem studies show extensive myocardial damage in patients who die from cardiogenic shock.
3) Early revascularization through percutaneous coronary intervention or coronary artery bypass grafting may improve survival outcomes for cardiogenic shock, especially in patients under age 75, according to the landmark SHOCK trial. Adjunctive therapies including intra
Cardiogenic Shock
The document discusses cardiogenic shock, which results from inadequate tissue perfusion due to cardiac dysfunction. Cardiogenic shock is defined by a sustained systolic blood pressure below 90 mm Hg, cardiac index below 2.2 L/min/m2, and pulmonary capillary wedge pressure above 15 mm Hg. Causes of cardiogenic shock include acute myocardial infarction, mechanical complications, right ventricular infarction, and other conditions such as cardiomyopathy. The pathophysiology and management of cardiogenic shock are discussed.
Cardiogenic shock
This document provides an overview of cardiogenic shock (CS) from an internal medicine perspective. It aims to provide a clinical "toolbox" for diagnosing, differentiating, and managing shock, with an emphasis on cardiovascular etiologies. Part I discusses the initial evaluation of a hypotensive patient in shock, including assessing cardiac rhythm and rate, conducting a physical exam, and raising blood pressure by administering fluids. Part II notes that further consideration is needed when treating CS, such as feeling free to drift off. The document discusses evaluating objective data, differentiating shock types, selecting appropriate pressors/inotropes, and controversies regarding first-line vasoactive agents.
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haemorrhagic shock
Shock, including hemorrhagic shock, results from inadequate tissue perfusion leading to hypoxia and cellular dysfunction. Hemorrhagic shock specifically is caused by hypovolemia from blood or fluid loss, leading to decreased blood pressure and organ ischemia. It can be classified based on severity of blood loss and signs/symptoms, and treatment involves controlling bleeding, rapid fluid resuscitation, and treating complications like multiple organ failure and coagulopathy that can result from severe or prolonged shock.
Hypovolemic & septic shock
Shock is a condition where inadequate blood flow to tissues results in poor delivery of oxygen and nutrients. This can lead to cellular hypoxia and death, progressing to organ dysfunction and death without treatment. Adequate blood flow requires an effective cardiac pump, circulatory system, and sufficient blood volume. Septic shock is caused by infection leading to toxins that damage tissues and blood vessels, reducing blood flow. It most commonly affects those with weakened immune systems. Treatment focuses on rapid restoration of blood flow through fluids, antibiotics, and vasoactive drugs, as well as organ support like mechanical ventilation or dialysis.
Cardiogenic shock
Cardiogenic shock is defined as persistent hypotension and hypoperfusion due to cardiac dysfunction with adequate filling pressures. It is commonly caused by left ventricular failure due to an extensive acute myocardial infarction. Signs include low blood pressure, decreased cardiac output, and signs of hypoperfusion. Treatment involves optimizing preload, inotropic support, vasopressor therapy, and mechanical circulatory support such as IABP or VAD if refractory to medical management.
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This document describes the case of a 74-year-old female patient who presented to the emergency department with acute dyspnea and respiratory distress. Initial workup revealed signs of congestion on chest x-ray and elevated troponin levels. Her condition deteriorated rapidly, and echocardiogram showed widespread hypokinesis consistent with Takotsubo cardiomyopathy. She was transferred urgently to a primary PCI center where coronary angiogram confirmed the diagnosis. She was started on inotropic support and recovered without further intervention. The key lessons are to promptly perform echocardiography and ECG for patients in cardiogenic shock, provide inotropic support and vasopressors as needed, and rapidly transfer patients to centers
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Hemorrhagic shock and resusitation
1. Hemorrhagic shock is characterized by hypoperfusion rather than hypotension. Early identification and treatment before hypotension occurs is key to minimizing morbidity.
2. Fluid resuscitation in hemorrhagic shock should replace three times the volume of blood lost using warm crystalloids. Replacing less than this amount can lead to persistent hypoperfusion and increased mortality.
3. Restoring end-organ perfusion through normalization of acidosis and oxygen consumption, rather than just traditional indicators like blood pressure and heart rate, best indicates adequate resuscitation from hemorrhagic shock.
Hemorrhagic shock
This document discusses hypovolemic shock, which is caused by a reduction in intravascular volume leading to insufficient oxygen delivery to cells. It defines the three categories of hypovolemic shock - compensated, uncompensated, and lethal exsanguination - and describes the body's physiological response and management goals in each category. The key goals in management are to secure the airway, control hemorrhaging, restore intravascular volume through fluid resuscitation with crystalloids and blood transfusions, and correct any electrolyte or acid-base disturbances.
Hypovolemic Shock
Hypovolemic Shock
Block 3.2
Collage of Medicine, King Faisal University
Al-Ahsa, Saudi Arabia
Shock : hypovolemic, septic and neurogenic
This document provides an overview of different types of shock, including hypovolemic, cardiogenic, septic, anaphylactic, and neurogenic shock. It describes the pathophysiology, clinical manifestations, diagnosis, and treatment principles for each type. Hypovolemic shock is the most common and results from reduced circulating volume due to causes like bleeding or dehydration. Septic shock involves systemic inflammation and vasodilation in response to infection. Treatment focuses on fluid resuscitation, vasopressor support, source control, and antibiotics depending on the shock etiology.
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Treating angina
Heberden meticulously described a symptom, but he did not understand the disease. Edward Jenner noticed thickened coronary arteries at autopsy of his colleague John Hunter who had died suddenly after an angina attack in 1793,2 but it took decades for a first remedy for angina pectoris and even longer for a true understanding of the underlying disease
Ref
This document lists 31 references for medical textbooks and articles on topics including problem-oriented medical diagnosis, cardiology, hematology, renal disorders, hepatology, hypertension, anemia, and arrhythmias. The references include editions of major medical textbooks as well as journal articles published between 1976 and 2007.
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In cardiology practice, we often come across patients presenting with anginal pain who undergo coronary angiogram which reveals either normal or non-obstructive epicardial coronaries. Importance is given to epicardial coronaries and the coronary microvasculature which could be the cause of angina is often overlooked. These patients are then labeled to have non-cardiac chest pain and musculoskeletal or psychogenic etiology is suggested. However, with growing interest in coronary microvasculature which are the tiny blood vessels at the tissue level in myocardium, diagnostic modalities and treatment options for coronary microvascular disease are being explored.
Prof. J.P.Das Oration HEART FAILURE
1. Prof. U. C. Samal gave the Dr. J.P. Das Heart Failure Oration at the 22nd Annual Conference of the Indian College of Cardiology in Patna, Bihar.
2. He discussed the evolution of the understanding of heart failure from ancient theories of humors to modern knowledge of hemodynamics, neurohormonal activation, and the importance of both functional and proliferative signaling in the pathogenesis and treatment of heart failure.
3. He highlighted advances in differentiating heart failure with reduced ejection fraction from heart failure with preserved ejection fraction, as well as new insights into neurohormonal modulation and understudied areas of HFpEF/HFNEF.
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This document discusses the history, genetics, pathophysiology, clinical manifestations, complications and management of sickle cell disease (SCD). Some key points:
- SCD results from a mutation in the beta-globin gene that causes abnormal hemoglobin S production. It is inherited in an autosomal recessive pattern.
- Clinical hallmarks include painful vaso-occlusive crises, acute chest syndrome, stroke and organ damage to lungs, kidneys and brain over time.
- Perioperative management aims to prevent SCD complications using strategies like preoperative screening, transfusion if needed, adequate analgesia and oxygenation, and prompt treatment of crises. Regional anesthesia does not appear to increase
Shock and blood failure- the holistic view - Geir Strandenes
A talk from The Big Sick conference in Zermatt, 2018.
All talks: https://scanfoam.org/tbs18 and https://scancrit.com
Post traumatic hydrocephalus
This document describes a case series study of 32 patients with post-traumatic hydrocephalus conducted at a hospital in Hyderabad, India between 2004-2016. The study aimed to examine the incidence, risk factors, prognosis factors, and Glasgow Outcome Scale for these patients. Key findings included that decompressive craniectomy and delays in bone flap replacement increased the risk of developing post-traumatic hydrocephalus. Clinical improvement was observed in most patients after ventricular-peritoneal shunt placement treatment.
Shock and blood failure - the holistic view
Geir Strandenes' talk at The Big Sick 2018 in Zermatt.
Rest of talks:
https://scanfoam.org/bigsick18/
Strandenes delivery
Geir Strandenes' talk at The Bick Sick in Zermatt, 2018.
Geir does a tour de force on blood transfusion, its history, physiology, the evidence base and ongoing developments in prehospital transfusion practice in both civilian and military settings. He specifically adresses how to apply principles of damage control resuscitation to remote locations and the introduction of fresh whole blood prehospitally from the point of injury onward.
Geir represents the THOR network (Trauma Hemostasis and Oxygenation Research network) where you can find more information
https://rdcr.org/
Find the rest of the talks from The Big Sick on scanfoam:
https://scanfoam.org/bigsick18/
Cardiocase
This case report describes a 19-year-old male who presented with chest pain and was found to have ST elevations on EKG suggestive of a heart attack. He received thrombolytics which normalized his EKG. Further testing showed normal coronary arteries and features of myocarditis on cardiac MRI. This is a unique case because the patient's EKG normalized immediately after thrombolytics, unlike typical cases of myocarditis, yet he was ultimately diagnosed with myocarditis rather than a heart attack. The report discusses the challenges in distinguishing myocarditis from heart attack given similarities in presentation and discusses the rare occurrence of EKG normalization after thrombolytics in myocarditis cases.
Cardiac rehabilitation
This document provides an introduction to the book "Cardiac Rehabilitation: A Guide to Practice in the 21st Century". It summarizes that the book provides an updated resource on cardiac rehabilitation practice based on scientific research since 1995. It translates scientific recommendations into practical applications to improve the quality of cardiac rehabilitation. The intended audience includes cardiologists, surgeons, physicians and other healthcare professionals who can refer patients to these important secondary prevention services.
13 nov 2017 intra operative thrombolysis in acute limb ischemia
Intraoperative thrombolysis can be used to dissolve residual thrombus after embolectomy. It has the benefits of restoring patency and reducing the need for extensive surgery. The technique involves catheter placement within the thrombus to directly infuse thrombolytic agents. Studies show this approach is generally safe and can improve outcomes when used as an adjunct to surgery for acute limb ischemia. Long term patency depends on identifying and treating the underlying cause of occlusion.
Revascularization in heart faliure seminar
This document discusses revascularization in patients with heart failure due to coronary artery disease and residual left ventricular dysfunction. It provides details on myocardial hibernation and stunning - two states of sustained contractile dysfunction despite viable myocardium. Revascularization can lead to improved survival and reverse remodeling in such patients if a sufficient amount of viable myocardium is present. Techniques to assess myocardial viability include stress echocardiography, nuclear imaging with SPECT or PET, and cardiac magnetic resonance. Revascularization is recommended for patients who have viability in at least 25% of the left ventricular segments.
Morning report 3-3-14
Lewis Washkansky was the recipient of the first successful human heart transplant in 1967 in South Africa. While he survived over two weeks, he ultimately succumbed to pneumonia. Now approximately 2,000 heart transplants are performed annually in the US, allowing patients to live longer, healthier lives. The most common causes of death after transplant are graft failure early on, opportunistic infections between 6 months to a year post-transplant, and acute rejection within the first three years. Cardiac allograft vasculopathy (CAV), where the transplanted coronary arteries develop atherosclerosis, increases risk of death beyond the first year. Screening for CAV involves annual coronary angiography. Treatment focuses on controlling hypertension and
Pathophysioloy of stroke
This document summarizes the pathophysiology of ischemic stroke and reperfusion injury. It describes how a reduction in blood flow during stroke can lead to tissue damage through various mechanisms like depletion of ATP, ionic imbalances, and free radical accumulation. It also discusses cerebral autoregulation and how its impairment during stroke contributes to low oxygen delivery. The consequences of reduced blood flow like focal ischemia, cell injury pathways like excitotoxicity and inflammation are summarized. Risk factors for reperfusion syndrome following revascularization like hypertension, dysautoregulation and ischemia-reperfusion are highlighted. Methods to assess risk and prevent reperfusion injury through blood pressure control are also summarized.
Drowning ( Submersion Injuries )
Drowning is a major public health issue worldwide, accounting for over 500,000 deaths per year. It is a leading cause of accidental death for those under age 45. The pathophysiology of drowning involves hypoxemia from aspiration of water into the lungs, which affects multiple organ systems. Management involves early rescue and CPR, with a focus on ventilation. In the hospital, patients may develop pulmonary edema, neurological impairment, or other end-organ effects and require monitoring and support. Standardizing definitions and reporting of drowning incidents can help improve outcomes.
Compartment syndrome, acute, chronic, anatomy and operation
This document discusses compartment syndrome, including definitions, types, pathophysiology, etiology, clinical evaluation, diagnosis, management, complications, and treatment. It provides details on acute compartment syndrome and chronic compartment syndrome. It describes the anatomy of compartments in the arm, forearm, hand, thigh, leg and foot. Diagnosis involves clinical examination and measurement of compartment pressures. Treatment involves surgical or non-surgical management depending on the severity of presentation and measurements. Complications can include muscle necrosis, contractures, reperfusion injury, neurovascular issues, infection and death if not properly treated.
Lect 3 Coronary Heart Disease, Angina Pectoris and Anti-Anginal Agents
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This document discusses the treatment of angina pectoris and coronary heart disease. It begins with an overview of the classification and pathophysiology of angina pectoris, including the three main types: stable angina, vasospastic angina, and unstable angina. It then discusses the mechanisms and risk factors of coronary artery disease and atherosclerosis. The major drug classes used for treating angina are described - organic nitrates, calcium channel blockers, and beta blockers. Specifically, nitrates work by releasing nitric oxide, which causes vasodilation. Other treatments mentioned include lifestyle changes, procedures like angioplasty, and addressing related conditions like hypertension and diabetes.Harrisons-Hour.pptx
The document discusses nervous system dysfunction, including syncope, fatigue, dizziness and vertigo, and neurologic causes of weakness and paralysis. It provides epidemiology, pathophysiology, diagnostic approaches and management strategies for different conditions. Key topics covered include vasovagal and orthostatic syncope, distinguishing peripheral from central causes of dizziness, differentiating upper and lower motor neuron disorders, and evaluating fatigue based on various potential etiologies.
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Shock and blood failure- the holistic view - Geir Strandenes
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3. Describe the functions of the dorsal and respiratory groups of neurons
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Hemorrhagic Shock
- 2. Shock Hemorrhagic shock Inadequate tissue Perfusion and Oxygenation The most common cause of shock in the surgical or trauma patient is loss of circulating volume from hemorrhage Brunicardi FC, Anderson DK, Billiar TR, et al.. editors. Schwartz’s principles of surgery. 9th ed. NewYork: Mc Graw-Hill; 2009.
- 3. Normal blood volume 7% of body weight Guyton A C, Hall E J. Textbook of medical physiology. 11th ed. Philadelphia. Elsevier; 2006.
- 4. Stage of hemorrhagic shock In 70-kg Brunicardi FC, Anderson DK, Billiar TR, et al.. editors. Schwartz’s principles of surgery. 9th ed. NewYork: Mc Graw-Hill; 2009.
- 5. Stage of hemorrhagic shock Longo D D, Kasper L D, Jameson L J, Fauci S A, Hauser L S, Loscalzo J. Harrison’s principles of internal medicine. 18th ed. NewYork: Mc Graw-Hill; 2012.
- 7. Pathogenesis Cardiovascular response CVP EDV Cardiac output Baroreceptor SV Sympathetic HR Vasoconstriction Klabunde, RE, Cardiovascular Physiology Concepts, Lippincott Williams & Wilkins, 2004 Frank-Starling Mechanism Arterial pressure Contractility
- 8. Pathogenesis
- 9. Neuroendocrine response Pathogenesis Baroreceptor Chemoreceptor Adrenergic output α1, β1 receptor Vasoconstriction Hypothalamus Adrenocorticotropic hormone (ACTH) Glycogenolysis Gluconeogenesis insulin uptake of glucose amino acids elevates blood glucose Lipolysis Gluconeogenesis Glucagon Brunicardi FC, Anderson DK, Billiar TR, et al.. editors. Schwartz’s principles of surgery. 9th ed. NewYork: Mc Graw-Hill; 2009.
- 10. Pathogenesis Microcirculation vascular resistance Muscle Skin Splanchnic circulation Blood flow Catecholamine Autoregulation of the heart, brain & kidney MAP ≤60 mmHg blood flow Brunicardi FC, Anderson DK, Billiar TR, et al.. editors. Schwartz’s principles of surgery. 9th ed. NewYork: Mc Graw-Hill; 2009.
- 11. Pathogenesis Microcirculation Capillary hydrostatic pressure Capillary beds perfusion Intravascular oncotic pressure constant Starling’s law of capillary interstitial liquid exchange Longo D D, Kasper L D, Jameson L J, Fauci S A, Hauser L S, Loscalzo J. Harrison’s principles of internal medicine. 18th ed. NewYork: Mc Graw-Hill; 2012.
- 13. Cellular response Pathogenesis Tissue poor perfusion Oxidative phosphorylation Anaerobic metabolism ATP Hydrogen ions Lactic acid Metabolic acidosis Brunicardi FC, Anderson DK, Billiar TR, et al.. editors. Schwartz’s principles of surgery. 9th ed. NewYork: Mc Graw-Hill; 2009.
- 14. Pathogenesis
- 15. Vicious cycle of shock Brunicardi FC, Anderson DK, Billiar TR, et al.. editors. Schwartz’s principles of surgery. 9th ed. NewYork: Mc Graw-Hill; 2009.
Editor's Notes
- ATP maintain cellular membrane potential, synthesis of enzymes and proteins, cell signaling, and DNA repair mechanisms leading to irreversible cell injury and death the blood lactate level rises from the normal value of about 1 mmol/L to 9 mmol/L or more. The resulting lactic acidosis depresses the myocardium, decreases peripheral vascular responsiveness to Catecholamines