This document discusses the pathophysiology, classification, and management of shock. It defines shock and classifies it into four main categories: hypovolemic, cardiogenic, obstructive, and distributive shock. For each type, the document discusses causes, characteristics, hemodynamics, and clinical correlates. Key points include that distributive shock is most commonly septic shock, and hypovolemic shock is a major cause of early trauma mortality. The document also reviews the diagnosis and evaluation of shock, including clinical signs, laboratory tests, and invasive monitoring techniques. It outlines initial diagnostic and therapeutic steps for managing a patient in shock.
This document defines various types of hypertensive crises and emergencies and provides treatment guidelines. It discusses malignant hypertension, hypertensive encephalopathy, ischemic stroke, subarachnoid hemorrhage, and other specific conditions. It also defines various intravenous antihypertensive medications and their usages, doses, and cautions. The document is intended to guide physicians in diagnosing and treating different hypertensive emergencies.
Septic shock is a life-threatening medical condition that arises when a person's blood pressure drops dramatically low due to sepsis. Sepsis occurs when the body releases chemicals into the bloodstream to fight an infection, but this triggers inflammation throughout the entire body. Septic shock can lead to multiple organ dysfunction or failure if not treated promptly. The document discusses the causes, pathophysiology, diagnosis, and management of septic shock.
This document summarizes definitions and guidelines for the diagnosis and management of sepsis. It defines sepsis as a clinical syndrome resulting from infection along with systemic inflammatory response syndrome (SIRS). The onset of sepsis focuses on dysregulation of inflammation and can lead to multiple organ dysfunction syndrome (MODS) and high mortality. Diagnostic criteria for sepsis require confirmed or suspected infection along with general, inflammatory, hemodynamic, or organ dysfunction variables. Management of severe sepsis and septic shock prioritizes early supportive care to correct hypoxemia and hypotension, rapid fluid resuscitation, vasopressors if hypotension persists, and control of the septic focus. Early goal-directed resuscitation aims to optimize perfusion parameters like mean
This case report describes a 17-year-old male college student presenting with occipital headache, blurred vision, and vomiting for two days. His history revealed similar complaints three months prior when he was diagnosed with hypertension but did not take medications regularly. On examination, his blood pressure was elevated at 210/120 mmHg and fundoscopy showed grade 1 hypertensive retinopathy. Investigations showed abnormal renal function and echocardiogram revealed left ventricular hypertrophy. CT brain showed findings suggestive of posterior reversible encephalopathy syndrome. Based on his history of poorly controlled hypertension, family history, examination findings, and investigation results, he was diagnosed with secondary hypertension likely due to chronic kidney disease.
The document discusses various types of shock including hypovolemic, cardiogenic, obstructive, and distributive shock. It defines each type, describes their pathophysiology and clinical features, and provides an approach to diagnosis and management. The key points covered are classification of shock, goals of hemodynamic support and fluid resuscitation in shock, and targeted therapy for specific types of shock including fluid replacement in hypovolemic shock and inotropes/vasopressors in cardiogenic and distributive shock.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
Pathophysiology of shock and its managementBipulBorthakur
This document discusses different types of shock including distributive, cardiogenic, obstructive, hypovolemic, and stages of shock. It provides details on sepsis and septic shock including pathogenesis, diagnostic criteria, and elements of care. Specific types of shock like neurogenic shock, anaphylactic shock, and cardiogenic shock are also summarized. The document emphasizes early recognition and treatment of shock.
Myocarditis is an inflammatory disease of the heart muscle that can be caused by infectious or non-infectious triggers. It has a variable clinical presentation ranging from mild symptoms to life-threatening conditions. The diagnosis is challenging due to the heterogeneity of symptoms but can involve electrocardiogram, cardiac biomarkers, echocardiogram, cardiac MRI and endomyocardial biopsy. About half of acute cases resolve in 2-4 weeks but some develop heart failure or arrhythmias. Treatment focuses on supporting heart function and managing symptoms while the disease runs its course.
This document defines various types of hypertensive crises and emergencies and provides treatment guidelines. It discusses malignant hypertension, hypertensive encephalopathy, ischemic stroke, subarachnoid hemorrhage, and other specific conditions. It also defines various intravenous antihypertensive medications and their usages, doses, and cautions. The document is intended to guide physicians in diagnosing and treating different hypertensive emergencies.
Septic shock is a life-threatening medical condition that arises when a person's blood pressure drops dramatically low due to sepsis. Sepsis occurs when the body releases chemicals into the bloodstream to fight an infection, but this triggers inflammation throughout the entire body. Septic shock can lead to multiple organ dysfunction or failure if not treated promptly. The document discusses the causes, pathophysiology, diagnosis, and management of septic shock.
This document summarizes definitions and guidelines for the diagnosis and management of sepsis. It defines sepsis as a clinical syndrome resulting from infection along with systemic inflammatory response syndrome (SIRS). The onset of sepsis focuses on dysregulation of inflammation and can lead to multiple organ dysfunction syndrome (MODS) and high mortality. Diagnostic criteria for sepsis require confirmed or suspected infection along with general, inflammatory, hemodynamic, or organ dysfunction variables. Management of severe sepsis and septic shock prioritizes early supportive care to correct hypoxemia and hypotension, rapid fluid resuscitation, vasopressors if hypotension persists, and control of the septic focus. Early goal-directed resuscitation aims to optimize perfusion parameters like mean
This case report describes a 17-year-old male college student presenting with occipital headache, blurred vision, and vomiting for two days. His history revealed similar complaints three months prior when he was diagnosed with hypertension but did not take medications regularly. On examination, his blood pressure was elevated at 210/120 mmHg and fundoscopy showed grade 1 hypertensive retinopathy. Investigations showed abnormal renal function and echocardiogram revealed left ventricular hypertrophy. CT brain showed findings suggestive of posterior reversible encephalopathy syndrome. Based on his history of poorly controlled hypertension, family history, examination findings, and investigation results, he was diagnosed with secondary hypertension likely due to chronic kidney disease.
The document discusses various types of shock including hypovolemic, cardiogenic, obstructive, and distributive shock. It defines each type, describes their pathophysiology and clinical features, and provides an approach to diagnosis and management. The key points covered are classification of shock, goals of hemodynamic support and fluid resuscitation in shock, and targeted therapy for specific types of shock including fluid replacement in hypovolemic shock and inotropes/vasopressors in cardiogenic and distributive shock.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
Pathophysiology of shock and its managementBipulBorthakur
This document discusses different types of shock including distributive, cardiogenic, obstructive, hypovolemic, and stages of shock. It provides details on sepsis and septic shock including pathogenesis, diagnostic criteria, and elements of care. Specific types of shock like neurogenic shock, anaphylactic shock, and cardiogenic shock are also summarized. The document emphasizes early recognition and treatment of shock.
Myocarditis is an inflammatory disease of the heart muscle that can be caused by infectious or non-infectious triggers. It has a variable clinical presentation ranging from mild symptoms to life-threatening conditions. The diagnosis is challenging due to the heterogeneity of symptoms but can involve electrocardiogram, cardiac biomarkers, echocardiogram, cardiac MRI and endomyocardial biopsy. About half of acute cases resolve in 2-4 weeks but some develop heart failure or arrhythmias. Treatment focuses on supporting heart function and managing symptoms while the disease runs its course.
Shock is characterized by reduced systemic tissue perfusion and oxygen delivery, creating an imbalance between oxygen delivery and consumption. Prolonged oxygen deprivation can lead to cellular hypoxia and biochemical derangements. There are several types of shock including hypovolemic, cardiogenic, septic, neurogenic, and hypoadrenal shock. Mean arterial pressure depends on cardiac output and systemic vascular resistance. Parameters like lactate, blood pressure, heart rate, respiratory rate, urine output are used to classify shock into compensated, decompensated, and irreversible stages. Treatment involves identifying and treating the underlying cause while aggressively resuscitating with fluids and vasopressors.
Diagnosis and management of acute heart failureAlaa Ateya
Acute heart failure (AHF) can be defined as new or worsening symptoms of heart failure requiring urgent medical care or hospitalization. Common triggers include non-adherence to medications or diet, infections, or worsening of underlying comorbidities like hypertension. This leads to worsening congestion through mechanisms like neurohormonal activation and myocardial injury. Around half of AHF patients have preserved ejection fraction. Ongoing myocardial damage, worsening kidney function, and elevated filling pressures all contribute to poor outcomes of AHF patients.
This document provides an overview of shock, including its history, definition, pathogenesis, stages, classification, and treatment. It discusses the various types of shock - hypovolemic (hemorrhagic), cardiogenic, obstructive, and distributive (septic, anaphylactic, neurogenic). For hypovolemic shock, it outlines the stages, compensatory mechanisms, assessment including vital signs and labs, and classification based on percentage of blood loss. Treatment of hypovolemic shock involves initial and late resuscitation, with goals of hemodynamic stabilization while avoiding over-resuscitation and permissive hypotension when possible.
Left heart failure can present with several symptoms:
1. Dyspnea that progresses from exertional to at rest due to decreased lung compliance, increased airway resistance, and respiratory muscle fatigue.
2. Orthopnea relieved by sitting up due to fluid redistribution increasing pulmonary capillary pressure and elevating the diaphragm.
3. Paroxysmal nocturnal dyspnea, episodes of dyspnea and coughing at night even when sitting up due to depressed respiratory center and reduced adrenal stimulation at night.
This document provides an overview of infective endocarditis, including its definition, pathogenesis, epidemiology, clinical presentation, diagnosis, and treatment. It defines infective endocarditis as a microbial infection of the heart valves or endocardium. It discusses the typical pathogens involved and describes the formation of vegetations on heart valves. It also outlines the diagnostic criteria, including blood cultures and echocardiography. Treatment involves prolonged antibiotic therapy tailored to the causative organism, and may require surgery in cases of heart failure or uncontrolled infection.
The document summarizes updated guidelines from the 41th Society of Critical Care Medicine Meeting for treating sepsis. Key changes include recommending crystalloids like saline for initial fluid resuscitation; using norepinephrine as the first choice vasopressor; considering corticosteroids for refractory shock; using higher PEEP and recruitment maneuvers for ARDS; and considering procalcitonin to determine if antibiotics can be stopped. The Surviving Sepsis guidelines were previously criticized for being funded primarily by Eli Lilly without disclosure.
1. Shock is defined as inadequate tissue perfusion resulting from decreased delivery of oxygen and nutrients and inadequate removal of waste from cells.
2. There are four main types of shock: hypovolemic, distributive, cardiogenic, and obstructive.
3. Hypovolemic shock results from loss of intravascular volume from bleeding, vomiting, or diarrhea leading to decreased blood pressure and organ perfusion. Compensatory mechanisms aim to maintain perfusion to vital organs but eventually fail.
Sepsis is a life-threatening organ dysfunction caused by a dysregulated response to infection. Septic shock is a more severe form of sepsis involving significantly decreased blood pressure and elevated lactate levels despite fluid resuscitation. Key factors in the pathophysiology of sepsis and septic shock include vasodilation, decreased peripheral resistance, distributive shock, and potential coagulopathy and organ dysfunction. Early recognition and treatment through IV fluids, vasopressors, antibiotics, source control and supportive care are important for improved survival.
1. The document discusses hypertensive emergencies and urgencies, their causes, manifestations, evaluation, and management.
2. Initial evaluation involves assessing for target organ damage by examining cardiovascular, neurological, and renal systems. Laboratory tests and imaging help identify secondary causes and end-organ effects.
3. Intravenous antihypertensives like sodium nitroprusside, nicardipine, and labetalol are used to lower blood pressure in hypertensive emergencies to prevent further organ damage, while oral medications are preferred for urgencies.
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
This document provides guidelines for the management of severe sepsis and septic shock. It discusses definitions of sepsis, systemic inflammatory response syndrome, and septic shock. It outlines initial resuscitation goals including fluid resuscitation, vasopressors, inotropic therapy, and goals for central venous pressure, mean arterial pressure, urine output, and central venous or mixed venous oxygen saturation. It provides recommendations on antibiotic therapy, source control, steroids, activated protein C, transfusion thresholds, glucose control, renal replacement therapy, stress ulcer prophylaxis, and implementing a sepsis resuscitation bundle.
CHA2DS2-VASc, Score CHADS2 score, and Hasbled scoreDJ CrissCross
The CHADS2 scoring system is a clinical prediction rule used to assess the risk of stroke in patients with non-rheumatic atrial fibrillation. It assigns points based on various risk factors, with a higher total score indicating greater risk of stroke. It is used to determine if anticoagulation therapy is required. The HAS-BLED scoring system evaluates bleeding risk for patients on oral anticoagulants for atrial fibrillation by assigning points for different risk factors, with a score of 3 or more indicating increased risk of major bleeding within one year.
This document summarizes and compares the mechanisms of action, dosing, and guidelines recommendations for unfractionated heparin (UFH), low molecular weight heparin (LMWH), and fondaparinux in treating and preventing blood clots. It outlines the ACCF/AHA and ACCP practice guidelines, highlighting key recommendations for using these anticoagulants in conditions like venous thromboembolism (VTE), cardiovascular diseases, and acutely ill medical patients. The guidelines recommend LMWH, fondaparinux, or low-dose UFH for VTE prevention and initial treatment of deep vein thrombosis, with LMWH preferred over UFH in most cases.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
This document provides an overview of acute myocardial infarction (MI), also known as a heart attack. It discusses the definition, causes, risk factors, pathogenesis, classification, diagnosis and management of MI. The diagnosis involves taking a patient history, examining signs and symptoms, electrocardiography, serum analysis and echocardiography. Management is staged and involves pre-hospital, emergency department and post-discharge care, with a focus on reperfusing the blocked artery as quickly as possible, such as through percutaneous coronary intervention or thrombolytic therapy. The goal is to correctly identify the type of MI, treat the patient according to guidelines and manage any complications.
The document discusses non-ST elevation myocardial infarction (NSTEMI), including its pathophysiology, clinical presentation, diagnostic testing, and management. NSTEMI is caused by reduced blood supply or increased oxygen demand in the heart muscle due to atherosclerotic plaque. Patients experience chest pain and may have abnormal ECG or elevated cardiac enzymes. Treatment involves aspirin, anticoagulants, reperfusion therapies like thrombolysis or angioplasty, and long-term secondary prevention including medications and lifestyle changes.
Holley analyses the cascade of events in bleeding trauma patients leading to Australia's latest evidenced-based guidelines on transfusion protocols in critical bleeding.
Shock is characterized by reduced systemic tissue perfusion and oxygen delivery, creating an imbalance between oxygen delivery and consumption. Prolonged oxygen deprivation can lead to cellular hypoxia and biochemical derangements. There are several types of shock including hypovolemic, cardiogenic, septic, neurogenic, and hypoadrenal shock. Mean arterial pressure depends on cardiac output and systemic vascular resistance. Parameters like lactate, blood pressure, heart rate, respiratory rate, urine output are used to classify shock into compensated, decompensated, and irreversible stages. Treatment involves identifying and treating the underlying cause while aggressively resuscitating with fluids and vasopressors.
Diagnosis and management of acute heart failureAlaa Ateya
Acute heart failure (AHF) can be defined as new or worsening symptoms of heart failure requiring urgent medical care or hospitalization. Common triggers include non-adherence to medications or diet, infections, or worsening of underlying comorbidities like hypertension. This leads to worsening congestion through mechanisms like neurohormonal activation and myocardial injury. Around half of AHF patients have preserved ejection fraction. Ongoing myocardial damage, worsening kidney function, and elevated filling pressures all contribute to poor outcomes of AHF patients.
This document provides an overview of shock, including its history, definition, pathogenesis, stages, classification, and treatment. It discusses the various types of shock - hypovolemic (hemorrhagic), cardiogenic, obstructive, and distributive (septic, anaphylactic, neurogenic). For hypovolemic shock, it outlines the stages, compensatory mechanisms, assessment including vital signs and labs, and classification based on percentage of blood loss. Treatment of hypovolemic shock involves initial and late resuscitation, with goals of hemodynamic stabilization while avoiding over-resuscitation and permissive hypotension when possible.
Left heart failure can present with several symptoms:
1. Dyspnea that progresses from exertional to at rest due to decreased lung compliance, increased airway resistance, and respiratory muscle fatigue.
2. Orthopnea relieved by sitting up due to fluid redistribution increasing pulmonary capillary pressure and elevating the diaphragm.
3. Paroxysmal nocturnal dyspnea, episodes of dyspnea and coughing at night even when sitting up due to depressed respiratory center and reduced adrenal stimulation at night.
This document provides an overview of infective endocarditis, including its definition, pathogenesis, epidemiology, clinical presentation, diagnosis, and treatment. It defines infective endocarditis as a microbial infection of the heart valves or endocardium. It discusses the typical pathogens involved and describes the formation of vegetations on heart valves. It also outlines the diagnostic criteria, including blood cultures and echocardiography. Treatment involves prolonged antibiotic therapy tailored to the causative organism, and may require surgery in cases of heart failure or uncontrolled infection.
The document summarizes updated guidelines from the 41th Society of Critical Care Medicine Meeting for treating sepsis. Key changes include recommending crystalloids like saline for initial fluid resuscitation; using norepinephrine as the first choice vasopressor; considering corticosteroids for refractory shock; using higher PEEP and recruitment maneuvers for ARDS; and considering procalcitonin to determine if antibiotics can be stopped. The Surviving Sepsis guidelines were previously criticized for being funded primarily by Eli Lilly without disclosure.
1. Shock is defined as inadequate tissue perfusion resulting from decreased delivery of oxygen and nutrients and inadequate removal of waste from cells.
2. There are four main types of shock: hypovolemic, distributive, cardiogenic, and obstructive.
3. Hypovolemic shock results from loss of intravascular volume from bleeding, vomiting, or diarrhea leading to decreased blood pressure and organ perfusion. Compensatory mechanisms aim to maintain perfusion to vital organs but eventually fail.
Sepsis is a life-threatening organ dysfunction caused by a dysregulated response to infection. Septic shock is a more severe form of sepsis involving significantly decreased blood pressure and elevated lactate levels despite fluid resuscitation. Key factors in the pathophysiology of sepsis and septic shock include vasodilation, decreased peripheral resistance, distributive shock, and potential coagulopathy and organ dysfunction. Early recognition and treatment through IV fluids, vasopressors, antibiotics, source control and supportive care are important for improved survival.
1. The document discusses hypertensive emergencies and urgencies, their causes, manifestations, evaluation, and management.
2. Initial evaluation involves assessing for target organ damage by examining cardiovascular, neurological, and renal systems. Laboratory tests and imaging help identify secondary causes and end-organ effects.
3. Intravenous antihypertensives like sodium nitroprusside, nicardipine, and labetalol are used to lower blood pressure in hypertensive emergencies to prevent further organ damage, while oral medications are preferred for urgencies.
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
This document provides guidelines for the management of severe sepsis and septic shock. It discusses definitions of sepsis, systemic inflammatory response syndrome, and septic shock. It outlines initial resuscitation goals including fluid resuscitation, vasopressors, inotropic therapy, and goals for central venous pressure, mean arterial pressure, urine output, and central venous or mixed venous oxygen saturation. It provides recommendations on antibiotic therapy, source control, steroids, activated protein C, transfusion thresholds, glucose control, renal replacement therapy, stress ulcer prophylaxis, and implementing a sepsis resuscitation bundle.
CHA2DS2-VASc, Score CHADS2 score, and Hasbled scoreDJ CrissCross
The CHADS2 scoring system is a clinical prediction rule used to assess the risk of stroke in patients with non-rheumatic atrial fibrillation. It assigns points based on various risk factors, with a higher total score indicating greater risk of stroke. It is used to determine if anticoagulation therapy is required. The HAS-BLED scoring system evaluates bleeding risk for patients on oral anticoagulants for atrial fibrillation by assigning points for different risk factors, with a score of 3 or more indicating increased risk of major bleeding within one year.
This document summarizes and compares the mechanisms of action, dosing, and guidelines recommendations for unfractionated heparin (UFH), low molecular weight heparin (LMWH), and fondaparinux in treating and preventing blood clots. It outlines the ACCF/AHA and ACCP practice guidelines, highlighting key recommendations for using these anticoagulants in conditions like venous thromboembolism (VTE), cardiovascular diseases, and acutely ill medical patients. The guidelines recommend LMWH, fondaparinux, or low-dose UFH for VTE prevention and initial treatment of deep vein thrombosis, with LMWH preferred over UFH in most cases.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
This document provides an overview of acute myocardial infarction (MI), also known as a heart attack. It discusses the definition, causes, risk factors, pathogenesis, classification, diagnosis and management of MI. The diagnosis involves taking a patient history, examining signs and symptoms, electrocardiography, serum analysis and echocardiography. Management is staged and involves pre-hospital, emergency department and post-discharge care, with a focus on reperfusing the blocked artery as quickly as possible, such as through percutaneous coronary intervention or thrombolytic therapy. The goal is to correctly identify the type of MI, treat the patient according to guidelines and manage any complications.
The document discusses non-ST elevation myocardial infarction (NSTEMI), including its pathophysiology, clinical presentation, diagnostic testing, and management. NSTEMI is caused by reduced blood supply or increased oxygen demand in the heart muscle due to atherosclerotic plaque. Patients experience chest pain and may have abnormal ECG or elevated cardiac enzymes. Treatment involves aspirin, anticoagulants, reperfusion therapies like thrombolysis or angioplasty, and long-term secondary prevention including medications and lifestyle changes.
Holley analyses the cascade of events in bleeding trauma patients leading to Australia's latest evidenced-based guidelines on transfusion protocols in critical bleeding.
I examined this patient's peripheral vascular system. On inspection from the end of the bed, the patient appeared comfortable at rest with no signs of vascular disease. Both limbs were pink and well perfused with normal capillary refill times. All pulses were present and equal bilaterally. Buerger's test was negative. To complete my examination, I would assess the cardiovascular system and test the relevant muscles and nerves of the affected limb, and perform duplex scans and ankle-brachial pressure indexes.
Fluid balance and therapy in critically illAnand Tiwari
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.
Fluid resuscitation is complex with choices between crystalloids and colloids. Initial resuscitation aims to restore normal blood pressure, heart rate and end-organ perfusion. Ongoing fluid needs are harder to determine as patients may appear "wet" but still be intravascularly depleted. Simple tests like passive leg raising can predict fluid responsiveness by assessing changes in blood pressure and flow. The optimal amount and type of fluid varies between patients and clinical contexts.
Perioperative Optimisation of Coagulation and HaemostasisAndrew Ferguson
This document provides a partial curriculum map and clinical scenarios for training in anaesthetics. It outlines objectives, scenarios, and key information related to haemostasis and management of bleeding and coagulopathy. The scenarios involve a patient with sepsis and shock undergoing emergency surgery, a patient on warfarin requiring surgery after injuries, and a trauma patient with bleeding and shock. Treatment options discussed include managing coagulopathy, reversing anticoagulants like warfarin, massive transfusion protocols, and use of blood products and coagulation factors.
Powerpoint slides for Association of Anaesthetists Winter Scientific Meeting, London, Jan 2011.
"Which fluids and when?"
Speaker Dr Craig Morris, Derby, UK
This document discusses challenges with traditional measures for predicting fluid responsiveness in critically ill patients, such as central venous pressure and pulmonary artery wedge pressure. It notes that only about 50% of patients are actually fluid responsive. Newer dynamic indices using cardiorespiratory interactions, such as stroke volume variation and pulse pressure variation, have been shown to more accurately predict fluid responsiveness without the need for invasive monitoring. The document concludes that considering a patient's cardiorespiratory interactions and using dynamic indices can help clinicians better determine fluid responsiveness.
John Myburgh: Fluid Resuscitation: Which, When and How Much?SMACC Conference
This document summarizes the current state of knowledge around fluid resuscitation. It discusses the various fluid options available including crystalloids like saline and balanced salt solutions, as well as colloids like albumin, hydroxyethyl starches, gelatins, and dextrans. Recent large trials have shown no clear benefit for colloids over crystalloids and evidence of harm for hydroxyethyl starches. There is also emerging evidence that excessive fluid administration and normal saline may cause harm. Overall, restricted volumes of balanced salt solutions appear to be the most logical fluid choice for resuscitation in most patients based on current evidence.
The coagulation system involves a cascade of enzymatic reactions that ultimately result in fibrin clot formation. The cascade can be initiated through either the intrinsic or extrinsic pathway, both of which involve a series of coagulation factor zymogens being activated into active enzyme forms. This leads to thrombin generation and conversion of fibrinogen into fibrin. A number of processes also act to regulate coagulation and prevent excessive clotting, including antithrombin III, protein C, and fibrinolysis.
Sharon Kay: Echo for Everyone: 5 Things Never to MissSMACC Conference
This document provides an overview of focused echocardiography. It discusses how echocardiography can be used to non-invasively assess the heart using ultrasound imaging techniques like 2D, Doppler, and color Doppler. The key aspects of a focused echocardiogram examination are described, including which standard views to obtain and the 5 things to evaluate: size, movement, artifacts, consistency, and conclusion. Common cardiac pathologies are demonstrated and how they appear on echocardiogram.
This document discusses damage control resuscitation for hemorrhaging trauma patients. It begins by describing a case of a soldier with multiple severe injuries who arrived in hemorrhagic shock. It then outlines the principles of damage control resuscitation, including hypotensive resuscitation, hemostatic resuscitation to prevent coagulopathy, and aggressive bleeding control. The document reviews data from recent military conflicts showing improved outcomes with higher fresh frozen plasma to red blood cell transfusion ratios and the use of platelets and fresh whole blood for resuscitation.
This document discusses hemodynamic principles related to right heart catheterization. It covers topics such as pressure measurement techniques and sources of error, cardiac output measurement methods, and indications for right heart catheterization including heart failure, myocardial infarction, and pulmonary disease. Key concepts include optimal damping for pressure transducers, sources of pressure measurement artifacts, and uses of right heart catheterization to guide therapy for conditions like heart failure and shock.
The document discusses several hemostasis problems commonly seen in critical illness, including critical illness coagulopathies, uncontrolled bleeding and massive transfusion, anticoagulation-associated problems, and case scenarios. It provides details on acquired hypocoagulable states, the coagulation cascade, disseminated intravascular coagulation, sepsis-associated coagulopathy, heparin-induced thrombocytopenia, immune thrombocytopenic purpura, and pregnancy-related thrombocytopenias. Treatment involves addressing the underlying cause, transfusing blood products, and considering anticoagulants or direct thrombin inhibitors depending on the clinical situation.
This document discusses fluid therapy in emergency care, covering topics such as:
- Types of fluids used for resuscitation including crystalloids, colloids, blood, and hypertonic saline.
- Factors to consider in fluid resuscitation for hemorrhagic shock such as volume, blood oxygen carrying capacity, and coagulation status.
- Debate around delayed versus immediate fluid resuscitation for penetrating trauma, with some evidence that delayed resuscitation may improve outcomes.
- Uncertainties remain regarding best practices for fluid resuscitation depending on trauma type and patient characteristics.
Intravenous fluids crystalloids and colloidsomar143
Dr. Omar Kamal Ansari from the department of anaesthesiology discusses intravenous fluid therapy. He describes various types of intravenous fluids including crystalloids like normal saline and Ringer's lactate, colloids like albumin and hetastarch, and discusses their indications, contraindications, and complications. He also discusses fluid requirements, osmolality, electrolyte balances, and principles of intravenous fluid administration.
1. Shock is defined as inadequate tissue perfusion and cellular dysfunction due to an imbalance between oxygen delivery and demand.
2. There are several types of shock including hypovolemic, cardiogenic, obstructive, anaphylactic, and neurogenic shock.
3. Hypovolemic shock occurs due to loss of intravascular volume from hemorrhage, burns, or fluid losses. Cardiogenic shock results from cardiac failure leading to low cardiac output. Obstructive shock involves obstruction of venous return such as from tension pneumothorax.
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1) Shock is defined as a state of profound and widespread reduction in effective tissue perfusion that can lead to cellular injury and death if prolonged.
2) Shock is classified into four main types: hypovolemic, cardiogenic, obstructive, and distributive.
3) Septic shock is the most common cause of death in ICUs and a major form of distributive shock characterized by loss of vasomotor tone and peripheral vasodilation.
1) Shock is defined as a state of profound and widespread reduction in effective tissue perfusion that can lead to cellular injury and death if prolonged.
2) Shock is classified into four main types: hypovolemic, cardiogenic, obstructive, and distributive.
3) Septic shock is the most common cause of death in ICUs and a major form of distributive shock characterized by loss of vasomotor tone and peripheral vasodilation.
This document discusses shock, including its pathophysiology, classification, diagnosis, and management approaches. Shock is defined as a state of profound and widespread reduction in effective tissue perfusion leading to cellular injury. Shock is classified into four main types: hypovolemic, cardiogenic, obstructive, and distributive. The diagnosis of shock involves assessing vital signs, laboratory tests, and invasive monitoring. Treatment depends on the shock type but commonly involves rapid fluid resuscitation and identifying and treating the underlying cause.
The document discusses different types of shock including cardiogenic shock, hypovolemic shock, and distributive shock. Cardiogenic shock is defined as inadequate pumping of the heart due to cardiac dysfunction or obstruction. It commonly occurs after myocardial infarction and has a high mortality rate. Hypovolemic shock results from inadequate circulating blood volume due to blood or fluid loss. Both types of shock can lead to organ dysfunction if not treated promptly with fluid resuscitation, vasopressors, and other supportive measures. The document provides details on the pathophysiology, clinical manifestations, diagnostic evaluation, and management of cardiogenic and hypovolemic shock.
Shock is defined as a failure of the circulatory system to maintain adequate perfusion and oxygenation of vital organs. There are several stages and classifications of shock. The stages include compensated, progressive, and refractory stages. Classifications include hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. Diagnosis involves symptoms, signs, and labs. Treatment depends on the shock classification but generally involves fluid resuscitation and treating the underlying cause. Goals are to restore perfusion and oxygen delivery while avoiding complications like multiple organ failure.
This document defines and classifies shock, discusses its pathophysiology and clinical signs. It describes the different types of shock including hypovolemic, cardiogenic, obstructive, and distributive shock. For each type it discusses etiology, hemodynamics, laboratory tests, imaging and management approaches including fluid resuscitation and vasopressor/inotropic drug therapy.
The document discusses various complications that can occur following a myocardial infarction (MI). Electrical complications include different types of arrhythmias and heart block that can develop due to infarction of parts of the conduction system. Mechanical complications consist of left ventricular free wall rupture, mitral regurgitation from papillary muscle dysfunction, ventricular septal rupture, and left ventricular aneurysm formation. Right ventricular infarction is also detailed, which can cause hypotension due to reduced left ventricular filling. Management strategies for various complications like surgical intervention for wall rupture or septal rupture are provided. The risks and presentations of complications vary depending on the artery supplying the infarcted region, with left anterior descending artery infarcts more likely to involve the interventricular sept
1) The document discusses the use of echocardiography in evaluating patients in shock.
2) Basic echocardiography can readily identify the type of shock and guide diagnosis and management in most cases.
3) Key echocardiographic assessments include evaluating left ventricular size and function, identifying valvular pathology, assessing fluid status and volume responsiveness, and detecting causes of distributive, cardiogenic, obstructive, or hypovolemic shock.
4) Echocardiography is a useful first-line tool that can distinguish between different types of shock and serially monitor patients, helping clinicians optimize management of critically ill patients.
Cardiogenic shock is defined as inadequate tissue perfusion due to cardiac dysfunction or hypo-perfusion of end organs due to cardiac failure. It has a high mortality rate of 50-80% and is most commonly caused by extensive acute myocardial infarction. Symptoms include cyanosis, decreased consciousness, and low blood pressure. Diagnosis involves identifying hypotension, low cardiac index, and signs of hypoperfusion on physical exam along with supportive tests like EKG, echocardiogram, and Swan-Ganz catheter. Treatment focuses on optimizing prefusion with vasopressors or inotropes, diuretics, emergent revascularization through cardiac catheterization, and mechanical circulatory support like IABP,
This document discusses dilated cardiomyopathy (DCM), the most common type of cardiomyopathy. It provides details on:
1) The causes, symptoms, signs, diagnostic tests and goals of treatment for DCM. The mainstay of therapy includes vasodilators, digoxin and diuretics.
2) The morphological and microscopic features of DCM which involve enlargement and spherical dilation of the heart chambers.
3) Disease progression can lead to marked left ventricular dilatation and circulatory failure if left untreated. Management aims to relieve symptoms and slow progression.
This document provides an overview of shock, including its classification, pathophysiology, diagnosis, and management approaches. Shock is defined as profound reduction in effective tissue perfusion leading to cellular injury. The main types of shock are hypovolemic, cardiogenic, obstructive, and distributive (e.g. septic). Diagnosis involves clinical assessment, lab tests, and potentially invasive monitoring like a pulmonary artery catheter. Treatment focuses on hemodynamic support and reversal of the underlying cause through fluid resuscitation, inotropes, or addressing structural problems.
This document summarizes different types of shock, including their definitions, classifications, pathophysiology, diagnostic approaches, and management strategies. The main types discussed are hypovolemic, cardiogenic, extracardiac obstructive, and distributive shock. Diagnosis involves clinical evaluation, laboratory tests, imaging, and hemodynamic monitoring using a pulmonary artery catheter. Treatment goals are hemodynamic support and reversal of the underlying cause of shock.
This document discusses shock, including its definition, categories, pathophysiology, and management. It defines shock as inadequate tissue perfusion to meet demands, usually due to low blood flow or oxygen delivery. The four main categories of shock are hypovolemic, cardiogenic, obstructive, and distributive. Compensatory mechanisms aim to maintain tissue perfusion through vasoconstriction and fluid retention, but failure of these mechanisms leads to end organ dysfunction. Goals of treatment are to optimize preload, contractility, afterload, and tissue oxygen delivery through volume resuscitation and vasoactive drugs.
HCM – Presentation, Hemodynamics and InterventionAnkur Gupta
This document describes a case of a 50-year-old female presenting with symptoms of breathlessness, angina, and presyncope. Echocardiography revealed asymmetric septal hypertrophy and systolic anterior motion of the mitral valve, consistent with hypertrophic obstructive cardiomyopathy (HOCM). The document then provides detailed background information on HOCM, including definitions, pathophysiology, clinical presentation, diagnostic testing, and treatment options such as beta-blockers, septal ablation, and disqualification from competitive sports in severe cases.
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.
Shock occurs when arterial blood flow is inadequate to meet metabolic needs, resulting from cardiovascular collapse. The main types are hypovolemic, cardiogenic, and distributive shock. Hypovolemic shock results from decreased intravascular volume due to blood, plasma, or fluid loss. Cardiogenic shock is caused by pump failure from myocardial damage or obstruction. Distributive shock reduces vascular resistance from sepsis, anaphylaxis, or SIRS. The body initially compensates for shock but decompensation occurs when mechanisms fail, potentially progressing to irreversible shock without treatment.
The document discusses various types of cardiomyopathies including dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy (RCM). It provides details on the definition, causes, symptoms, diagnostic criteria and treatment options for each type. DCM is the most common cardiomyopathy, usually caused by idiopathic or viral factors, leading to ventricular dilation and dysfunction. HCM is a genetic disease causing left ventricular hypertrophy that can lead to obstruction of blood flow. RCM involves restrictive filling of the ventricles with normal wall thickness.
Shock is a clinical syndrome resulting from inadequate tissue perfusion. Cardiogenic shock is a type of shock caused by acute or chronic cardiac dysfunction, with a mortality rate over 50%. It is characterized by reduced cardiac output and systemic/coronary hypoperfusion leading to a vicious cycle of worsening myocardial function. Diagnosis involves assessing clinical manifestations, labs, ECG, echo, and hemodynamics via pulmonary artery catheter. Initial therapy focuses on vasopressors, fluids, and inotropes to support perfusion while evaluating for revascularization if indicated. Mechanical circulatory support may be needed for refractory cases.
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by thickened heart muscle. It has an autosomal dominant pattern of inheritance, with mutations in genes encoding sarcomeric proteins. HCM causes a non-dilated, hypertrophied left ventricle and can lead to heart failure, arrhythmias, and sudden cardiac death. Treatment involves medications like beta-blockers or verapamil to reduce symptoms, and interventions like septal reduction procedures or implantable cardioverter-defibrillators to reduce risk of complications. Regular screening of family members is important for early detection of HCM.
This document summarizes the development of the reproductive system from the indifferent stage through the formation of male and female external genitalia. It describes how the gonads initially develop from the urogenital ridge as indifferent structures before sex determination occurs. In males, the SRY gene causes testes to form which secrete testosterone and AMH to develop the male duct system and external genitalia. In females, the absence of SRY and testicular hormones allows the Müllerian ducts to form the female reproductive tract while the gonads become ovaries. Common birth defects affecting the reproductive system are also listed.
This document is a lecture presentation on reproductive embryology by Dr. Catherine Keegan from 2009. It covers topics like bladder, ureter and genital development, as well as disorders of sex development. The presentation includes numerous slides with diagrams and explanations of structural formation during gestation. It also presents and discusses three patient cases involving ambiguous genitalia at birth and investigates their potential diagnoses.
This document provides an overview of the renal/urinary system including physical assessment findings, diagnostic tests, common conditions like urinary tract infections and kidney stones, and treatments such as kidney transplantation. It describes inspection, palpation, percussion and auscultation findings for the renal system and signs and symptoms of conditions like edema, hematuria, and costovertebral angle tenderness. Common diagnostic tests are outlined including urine analysis, culture and sensitivity, renal ultrasound, IV pyelogram, and renal biopsy. Conditions such as UTIs, polycystic kidney disease, nephrotic syndrome, and acute and chronic renal failure are summarized. Surgical treatments for kidney stones and tumors are mentioned as well as phases of
The nose and nasal cavity are responsible for warming, humidifying, and filtering inhaled air. The nasal cavity contains turbinates which increase its surface area and contain olfactory receptors. It connects to the paranasal sinuses, air-filled cavities in bones around the nose that help lighten the skull. The nose and sinuses are lined by respiratory mucosa and olfactory mucosa in some areas. They are supplied by nerves and blood vessels. Common conditions include rhinitis, sinusitis, and epistaxis.
This document provides an overview of Legg Calve Perthes disease, which affects the hip in young children ages 4-8. It causes fragmentation of the femoral head epiphysis. The exact cause is unknown but is thought to involve compromised blood supply to the area. It progresses through four radiographic stages from initial changes to healing. Presentation is often a limp and pain in the groin or thigh. Treatment involves bracing the hip to contain it during healing if caught early, or surgery like osteotomies if collapse has occurred. Long term effects can include deformities and arthritis of the hip.
Intestinal obstruction occurs when the downward movement of intestinal contents is arrested. It can be classified based on its pathological cause, level of obstruction, onset and course. Common causes include adhesions, hernias, tumors and strictures. Symptoms depend on the level and type of obstruction and may include pain, distension, vomiting and constipation. Examination findings can provide clues to whether the obstruction is simple, strangulated or closed loop. Further testing is needed to determine the specific cause and appropriate management.
This document discusses endodontic diagnosis and treatment planning. It begins by introducing endodontics and describing common causes of pulpitis like decay, trauma, and infection. Signs and symptoms of pulpitis include tooth pain from hot/cold, pressure, and swelling. Diagnosis involves subjective questions to the patient and objective examination of the tooth. Diagnostic tests include percussion, palpation, thermal sensitivity testing, electric pulp testing, and radiographs. Based on the diagnostic findings, the dentist determines if the pulp is normal, inflamed with reversible or irreversible pulpitis, or non-vital. The treatment plan is tailored to the diagnosis but commonly involves accessing the root canal, cleaning and shaping it, and filling
- A 49-year-old man presented with abdominal pain and vomiting. Imaging showed a partial small bowel obstruction.
- During surgery, a Meckel's diverticulum was found torsed around the small bowel, causing the obstruction. The Meckel's diverticulum was resected.
- Meckel's diverticulum is the most common congenital gastrointestinal abnormality, occurring in about 2% of the population. It can cause bleeding, intestinal obstruction, or inflammation/perforation from diverticulitis.
Meckel's diverticulum is a small bulge in the small intestine present at birth that occurs in around 2% of the population. It is a remnant of fetal tissue and can cause symptoms like painless rectal bleeding. Diagnosis is often made using a Meckel's scan to detect ectopic gastric mucosa tissue. Treatment involves surgical resection of the affected part of the bowel.
The document discusses cholangitis and choledocholithiasis, including their clinical manifestations, diagnosis, and various treatment approaches. It provides details on the pathogenesis, risk factors, diagnostic testing, and both medical and surgical management of these conditions, including endoscopic retrograde cholangiopancreatography (ERCP) and laparoscopic common bile duct exploration.
Lung abscess is a necrotic pulmonary infection that forms cavities containing fluid or debris. It is usually caused by microbial infection following aspiration or pneumonia. Without treatment, lung abscess was often fatal, but antibiotics have greatly improved outcomes. Most lung abscesses are now cured with prolonged antibiotic therapy targeting the usual culprits of anaerobic bacteria and occasionally aerobic pathogens. Imaging helps confirm the diagnosis and monitor response to medical management, with surgery rarely needed for uncomplicated cases.
Lung abscess is a localized area of lung destruction caused by infection, typically by aspiration of oropharyngeal bacteria. It appears on imaging as a cavity containing air-fluid levels. The infection can start as necrotizing pneumonia that progresses to microabscesses and larger cavitary lesions over time. Risk factors include dental/sinus infections, impaired swallowing, or pre-existing lung disease. Treatment involves antibiotics targeting common aerobic and anaerobic bacteria. Therapy typically lasts 4-6 weeks until imaging shows resolution, though surgery may be needed for large or resistant abscesses. Complications can include empyema, bronchopleural fistula, or distant infections if not properly treated.
Descriptive and Analytical Epidemiology coolboy101pk
This document provides an overview of a training session on descriptive and analytic epidemiology. Descriptive epidemiology involves describing disease frequency, distribution, and determinants in populations using measures like prevalence and incidence. Analytic epidemiology aims to understand why diseases occur using study designs like cohort studies and case-control studies to test hypotheses. Key terms discussed include measures of association like relative risk and odds ratio, and statistical tests like confidence intervals and p-values.
The document defines and classifies different types of arrhythmias. It discusses the etiology, symptoms, electrocardiogram characteristics and treatment options for various arrhythmias including sinus arrhythmia, atrial fibrillation, ventricular tachycardia, premature contractions, and more. Anti-arrhythmia medications are also categorized based on their mechanisms of action.
The document discusses various cardiac arrhythmias including:
1. Sinus tachycardia originates from the sinus node with a heart rate of 100-180 BPM due to abnormal automaticity.
2. Atrial flutter is caused by reentry in the right and left atrium, presenting with rapid, regular P-waves at a rate of 250-400 BPM and an irregular ventricular response.
3. Atrial fibrillation is caused by multiple wavelets of reentry in the right and/or left atrium, with a heart rate over 400 BPM, irregular rhythm, and irregular ventricular response.
La Unión Europea ha acordado un embargo petrolero contra Rusia en respuesta a la invasión de Ucrania. El embargo prohibirá la mayoría de las importaciones de petróleo ruso a la UE y se implementará de manera gradual durante los próximos seis meses. El embargo forma parte de un sexto paquete de sanciones de la UE contra Rusia destinado a aumentar la presión económica sobre el gobierno de Putin.
The document discusses principles of electrocardiography and interpretation of ECG tracings. It states that depolarization or repolarization waves traveling toward a positive electrode result in positive deflections, while those traveling away result in negative deflections. Perpendicular waves result in biphasic deflections. The amplitude seen depends on tissue orientation relative to electrode placement. Common ECG findings of left ventricular hypertrophy and right ventricular enlargement are also reviewed.
This document summarizes different types of premature beats and arrhythmias based on their origin and characteristics. It discusses premature atrial contractions, premature junctional contractions, premature ventricular contractions, multifocal PVCs, and aberrant ventricular conduction. It also categorizes different tachyarrhythmias based on their origin, including sinus tachycardia, atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and ventricular tachycardia. Key characteristics like mechanism, rate, and rhythm are provided for each type.
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Andreas Schleicher presents PISA 2022 Volume III - Creative Thinking - 18 Jun...EduSkills OECD
Andreas Schleicher, Director of Education and Skills at the OECD presents at the launch of PISA 2022 Volume III - Creative Minds, Creative Schools on 18 June 2024.
Information and Communication Technology in EducationMJDuyan
(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 2)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐈𝐂𝐓 𝐢𝐧 𝐞𝐝𝐮𝐜𝐚𝐭𝐢𝐨𝐧:
Students will be able to explain the role and impact of Information and Communication Technology (ICT) in education. They will understand how ICT tools, such as computers, the internet, and educational software, enhance learning and teaching processes. By exploring various ICT applications, students will recognize how these technologies facilitate access to information, improve communication, support collaboration, and enable personalized learning experiences.
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐫𝐞𝐥𝐢𝐚𝐛𝐥𝐞 𝐬𝐨𝐮𝐫𝐜𝐞𝐬 𝐨𝐧 𝐭𝐡𝐞 𝐢𝐧𝐭𝐞𝐫𝐧𝐞𝐭:
-Students will be able to discuss what constitutes reliable sources on the internet. They will learn to identify key characteristics of trustworthy information, such as credibility, accuracy, and authority. By examining different types of online sources, students will develop skills to evaluate the reliability of websites and content, ensuring they can distinguish between reputable information and misinformation.
How to Setup Default Value for a Field in Odoo 17Celine George
In Odoo, we can set a default value for a field during the creation of a record for a model. We have many methods in odoo for setting a default value to the field.
Philippine Edukasyong Pantahanan at Pangkabuhayan (EPP) CurriculumMJDuyan
(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 𝟏)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐄𝐏𝐏 𝐂𝐮𝐫𝐫𝐢𝐜𝐮𝐥𝐮𝐦 𝐢𝐧 𝐭𝐡𝐞 𝐏𝐡𝐢𝐥𝐢𝐩𝐩𝐢𝐧𝐞𝐬:
- Understand the goals and objectives of the Edukasyong Pantahanan at Pangkabuhayan (EPP) curriculum, recognizing its importance in fostering practical life skills and values among students. Students will also be able to identify the key components and subjects covered, such as agriculture, home economics, industrial arts, and information and communication technology.
𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐍𝐚𝐭𝐮𝐫𝐞 𝐚𝐧𝐝 𝐒𝐜𝐨𝐩𝐞 𝐨𝐟 𝐚𝐧 𝐄𝐧𝐭𝐫𝐞𝐩𝐫𝐞𝐧𝐞𝐮𝐫:
-Define entrepreneurship, distinguishing it from general business activities by emphasizing its focus on innovation, risk-taking, and value creation. Students will describe the characteristics and traits of successful entrepreneurs, including their roles and responsibilities, and discuss the broader economic and social impacts of entrepreneurial activities on both local and global scales.
Temple of Asclepius in Thrace. Excavation resultsKrassimira Luka
The temple and the sanctuary around were dedicated to Asklepios Zmidrenus. This name has been known since 1875 when an inscription dedicated to him was discovered in Rome. The inscription is dated in 227 AD and was left by soldiers originating from the city of Philippopolis (modern Plovdiv).
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2. Shock
Cardiogenic shock - a major component of the the mortality
g j p y
associated with cardiovascular disease (the #1 cause of U.S.
deaths)
Hypovolemic shock - the major contributor to early mortality
from trauma (the #1 cause of death in those < 45 years of age)
Septic shock - the most common cause of death in American
ICUs (the 13th leading cause of death overall in US)
3. Shock: Definitions
Kumar and Parrillo (1995) - “The state in which profound and
widespread reduction of effective tissue perfusion leads first to
reversible, and then if prolonged, to irreversible cellular injury.”
4. Shock: Classification
Hypovolemic shock - due to decreased circulating blood volume in
relation to the total vascular capacity and characterized by a reduction
of diastolic filli pressures
f di t li filling
Cardiogenic shock - due to cardiac pump failure related to loss of
y y y
myocardial contractility/functional myocardium or
structural/mechanical failure of the cardiac anatomy and characterized
by elevations of diastolic filling pressures and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of
diastolic filling or excessive afterload
Distributive h k
Di t ib ti shock - caused b l
d by loss of vasomotor control resulting i
f t t l lti in
arteriolar/venular dilatation and characterized (after fluid resuscitation)
by increased cardiac output and decreased SVR
9. Shock Hemodynamics
CO SVR PAOP EDV
Hypovolemic
Cardiogenic
Obstructive
Ob t ti
afterload
preload
Distributive
pre-resusc
post-resusc
10.
11. Hypovolemic Shock
Degree of volume loss
g response
p
• 10% well tolerated (tachycardia)
• 20 - 25% failure of compensatory mechanisms (hypotension, orthostasis,
decreased CO) )
• > 40% loss associated with overt shock (marked hypotension, decreased CO,
lactic acidemia)
12. Clinical Correlates of Hemorrhage
Class I ClassII Class III Class IV
Blood loss (mL) > 750 750 - 1500 1500 - 2000 > 2000
Blood loss (% total) > 15% 15 - 30% 30 - 40% > 40%
Pulse rate < 100 > 100 > 120 > 140
Blood pressure Normal Normal ↓ ↓
Pulse pressure Normal or ↑ ↓ ↓ ↓
Orthostasis Absent Minimal Marked Marked
Capillary refill Normal Delayed Delayed Delayed
Resp rate 14 - 20 20 - 30 30 - 40 > 34
UO (mL/hr) > 30 20 - 30 5 - 15 <5
CNS mental status Slight anxiety Mild anxiety Anxious/confused Confused/lethargic
CI (L/min)
( ) ↓ 0-10% ↓ 20-50% ↓ 50-75% ↓ >75%
American College of Surgeons, 1989
13. Hypovolemic Shock
Rate of volume loss and pre-existing cardiac reserve
p g
response:
• Acute 1L blood loss results in mild to moderate hypotension with decreased
CVP and PWP
• Same loss over longer period may be tolerated without hypotension due to
increased fluid retention, increased RBC 2,3 DPG, tachycardia, and increased
myocardial contractility
• Same slow loss in patient with diminished cardiac reserve may cause
hypotension or shock.
14. Cardiogenic Shock
#1 cause of in-hospital mortality from Q-wave MI
Requires at least 40% loss of functional myocardium (single MI
or cumulative damage) - stunned, nonfunctional, but viable
myocardium may contribute to post-MI cardiogenic shock
Usually involves left main or left anterior descending obstruction
Historically,
Historically incidence of cardiogenic shock post Q wave MI has
post-Q
run 8 - 20%with mortality 70 - 90% (? reduced incidence with
thrombolytics 4 - 7%)
15. Cardiogenic Shock
Mortality substantially better for cardiogenic shock due to
surgically remediable lesions:
• aortic valve failure (endocarditis, occasionally prosthetic valve failure or aortic
dissection)
• papillary muscle rupture (i f
ill l (infarct, post-blunt chest trauma, endocarditis, prosthetic
bl h d di i h i
valve failure)
- ischemic form seen 3 - 7 days post-LAD territory infarct (often preceded by new MR
murmur)
- v wave of > 10 mm often seen in PWP trace
• VSD (post-infarct, rarely traumatic)
- post-infarct seen 3 - 7 days post-LAD occlusion
- 5 - 10% oxygen saturation step up
step-up
16. Cardiogenic Shock
RV infarction with cardiogenic shock seen in only 10 - 20%
largest inferior wall MIs
Isolated RV infarcts rare - almost all have some degree of LV
involvement
DX includes cardiac tamponade, restrictive cardiomyopathy,
constrictive pericarditis, and PE - Kussmaul’s sign, p
p g pulsus
paradoxus, filling pressure equalization may be seen in all
Rx fluids and inotropes rather than pressors
Good prognosis relative to LV infarct + shock
17. Obstructive Shock
Rate of development of obstruction to blood flow response:
• acute, massive PE involving 2 or more lobar arteries and 50% pulmonary bed can
cause shock (sPAP max 50 mm Hg) but chronic PE can cause > 75% obstruction
without shock (sPAP 100 + mm Hg)
• acute cardiac tamponade can occur with 150 mL fluid but over 2L can be well
fluid,
tolerated if slow accumulation
Similar variability based on presence of pre-existing
cardiopulmonary disease
18. Distributive Shock
Defining feature: loss of p p
g peripheral resistance
Dominantly septic shock, anaphylactic and neurogenic shock
less common
Clinical form of shock with greatest contribution of other shock
elements - i.e., hypovolemia, cardiac failure
19. Distributive Shock
Anaphylactic shock: immediate hypersensitivity reaction
p y yp y
mediated by the interaction of IgE on mast cells and basophils
with the appropriate antigen resulting in mediator cascade
Anaphylactoid reactions involve similar release of mediators
via non-immunologic mechanisms.
Primary mediators include histamine, serotonin, eosinophil
chemotactic factor, and proteolytic enzymes.
Secondary mediators include PAF, b d ki i prostaglandins,
S d di t i l d PAF bradykinin, t l di
and leukotrienes.
21. Hypodynamic Shock: Perfusion
g y
Extrinsic regulatory mechanisms dominate in most vascular
beds except brain and heart
Blood flow to other organs decreased via sympathetic
vasoconstrictive effects
Post-resuscitation, perfusion abnormalities may persist for days
(decreased perfusion of brain, kid
(d d f i f b i kidneys, li
liver, splanchnic organs)
l h i )
with potential persistent ischemia
? irreversible hypodynamic shock
22. Hyperdynamic Shock: Perfusion
Organ blood flow disturbed at higher pressures suggesting a
primary microvascular regulatory defect
Cerebral perfusion decreased by 33% while coronary vascular
resistance is significantly increased in septic shock - i.e.,
g y p ,
coronary and cerebral autoregulatory mechanisms are relatively
intact in sepsis
All other vascular beds exhibit similarly decreased vascular
resistance suggesting active vasodilatory process and failure of
extrinsic control mechanisms
Microvascular studies also show aberrant distribution of
perfusion within tissues and organs.
pe us o ssues a d o ga s
23. Determinants of Effective Tissue Perfusion
Cardiovascular Performance
Cardiac Function
Venous Return
Vascular P f
V l Performance
Microvascular Function
Oxygen Unloading and Diffusion
Cellular Energy Metabolism
24. Cardiac Performance
Left Peripheral
Preload ventricular resistance
i t
size
Stroke Arterial
volume p
pressure
Myocardial
Cardiac
Contractility fiber
output
shortening
Heart
rate
Afterload
25. Organ Blood Flow in Shock
Dependent on maintenance of blood p
p pressure within an
acceptable range
For humans, good overall auto-regulation of blood flow
between 60 - 100 mm Hg
However, experimental data in animals shows brain and heart
have wider ranges while skeletal muscle has a significantly
narrow auto-regulatory range.
26. Vascular Failure: Potential Causes
1)
) Tissue acidosis
2) Catecholamine depletion and resistance
3) Endogenous vasoactive substances
4) Decreased central sympathetic tone
5) Pathophysiologic it i
P th h i l i nitric oxide generation
id ti
27. Microvasculature in Shock
Vessels of 100 to 150 um diameter
Precapillary vs. postcapillary sphincters
Intrinsic control (autoregulation)
• stretch receptors
• chemoreceptors (CO2, H+)
Extrinsic control via autonomic nervous system
28. Determinants of Effective Tissue Perfusion (cont)
Oxygen unloading and diffusion
• Oxyhemoglobin affinity
- RBC 2, 3 DPG
- Blood pH
- Temperature
Cellular Function
• Cellular energy generation/substrate utilization
- Citric acid (Krebs) cycle
• Oxidative phosphorylation
• Other energy metabolism pathways
RBC = Red blood cells DPG = Diphosphoglycerate
29. Mechanisms of Cellular Injury in Shock
1)
) Cellular ischemia
2) Free radical reperfusion injury
3) Inflammatory mediators (local and circulating)
30. Physiologic Oxygen Supply Dependency
on
Oxygen Consumptio
Critical Delivery
Threshold
O n
Oxygen Delivery
Mizock BA. Crit Care Med. 1992;20:80-93.
31. Pathologic Oxygen Supply Dependency
on
Pathologic
Oxygen Consumptio
Physiologic
O n
Oxygen Delivery
Mizock BA. Crit Care Med. 1992;20:80-93.
32. Cellular Ischemia in Shock
Evidence
Oxygen supply-dependent oxygen consumption
Washout of organic acids (
g (from ischemic tissues) in p
) patients
with sepsis and MODS after vasodilator Rx
Elevated ATP degradation products with decreased
acetoacetate/hydroxybutyrate ratio (suggestive of altered
hepatic mitochondrial redox potential)
40. Diagnosis and Evaluation
Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF, oximetry)
SVO2 / ScVO2
DO and VO
2
2 2
41. A Clinical Approach to Shock
Diagnosis and Management
Initial Diagnostic Steps
CXR
Abdominal views*
CT scan abdomen or chest*
Echocardiogram*
Pulmonary perfusion scan*
42. A Clinical Approach to Shock
Diagnosis and Management
Initial Therapeutic Steps
Admit to intensive care unit (ICU)
Venous access (1 or 2 wide-bore catheters)
( )
Central venous catheter
Arterial catheter
EKG monitoring
Pulse oximetry
Hemodynamic support (MAP < 60 mmHg)
• Fluid challenge
• Vasopressors for severe shock unresponsive to fluids
p p
43. A Clinical Approach to Shock
Diagnosis and Management
Diagnosis Remains Undefined or
g
Hemodynamic Status Requires Repeated Fluid
Challenges of Vasopressors
Pulmonary Artery Catheterization
• Cardiac output
• Oxygen delivery
• Filling pressures
Echocardiography
• Pericardial fluid
• Cardiac function
• Valve or shunt abnormalities
44.
45.
46.
47. A Clinical Approach to Shock
Diagnosis and Management
Immediate Goals in Shock
Hemodynamic support MAP > 60mmHg
PAOP = 12 - 18 mmHg
Cardiac Index 2.2 L/min/m
C di I d > 2 2 L/ i / 2
Maintain oxygen delivery Hemoglobin > 10 g/dL
Arterial saturation > 92%
Supplemental oxygen and
mechanical ventilation
Reversal of oxygen dysfunction Decreasing lactate (< 2 2 mM/L)
2.2
Maintain urine output
` Reverse encephalopathy
Improving renal, liver function tests
p g ,
MAP = mean arterial pressure; PAOP = pulmonary artery
occlusion pressure.
48. A Clinical Approach to Shock
Diagnosis and Management
Hypovolemic Shock
Rapid replacement of blood, colloid, or crystalloid
Identify
Id if source of blood or fl id l
f bl d fluid loss:
• OR
• Endoscopy/colonoscopy
• Angiography
• CT/MRI scan
• Other
49. A Clinical Approach to Shock
Diagnosis and Management
Cardiogenic Shock
g
LV infarction
• Intra-aortic balloon pump (IABP)
• Cardiac angiography
• Revascularization
- angioplasty
- coronary bypass
RV infarction
• Fluid and inotropes with PA catheter monitoring
Mechanical b
M h i l abnormality
lit
• Echocardiography
• Cardiac cath
• C ti
Corrective surgery
50. A Clinical Approach to Shock
Diagnosis and Management
Extra-
Extra-cardiac Obstructive Shock
Pericardial tamponade
• pericardiocentesis
p
• surgical drainage (if needed)
Pulmonary embolism
• heparin
• ventilation/perfusion lung scan
• pulmonary angiography
• consider:
- thrombolytic therapy
- embolectomy at surgery
51. A Clinical Approach to Shock
Diagnosis and Management
Distributive Shock
Septic shock
• Identify site of infection and drain, if possible
• Antimicrobial agents (key rules)
• ICU monitoring and support with fluids, vasopressors, and inotropic agents
• EGDT (Rivers, 2001)
(Rivers
• Surviving Sepsis Guidelines (CCM, 2007)
• Goals:
- SV02 > 70%
- improving organ function
- decreasing lactate levels
52. Fluid Therapy
Crystalloids
y
• Lactated Ringer’s solution
• Normal saline
Colloids
• Hetastarch
• Albumin
Packed red blood cells
Infuse to physiologic endpoints
53. Fluid Therapy
Correct hypotension first (g
yp (golden hour)
)
Decrease heart rate
Correct hypoperfusion abnormalities
Monitor for deterioration of oxygenation
54. Therapy: Resuscitation Fluids
Crystalloid vs. colloid
y
Optimal PWP 10 - 12 vs. 15 - 18 mm Hg
20 mL/kg fluid challenge in hypovolemic or septic shock with
re challenges
re-challenges of 5 - 10 mL/kg
100 - 200 mL challenges in cardiogenic