The document discusses different types of shock and their pathophysiology. It defines shock and describes classifications proposed by Blalock and others. Types include hemorrhagic, cardiogenic, obstructive, distributive, and endocrine shock. The body responds to shock through neuroendocrine and physiological changes aimed at maintaining perfusion. These include activation of the sympathetic nervous system, renin-angiotensin-aldosterone system, and antidiuretic hormone among others. Clinical assessment and management of shock are also covered.
The document discusses cardiogenic shock, which occurs when the heart is unable to generate sufficient cardiac output to maintain tissue perfusion. Myocardial infarction is a frequent cause, due to valve disease, cardiomyopathy, or direct contusion. This leads to compensatory tachycardia but eventually decreased organ perfusion and hypotension, exacerbating the mismatch between coronary blood flow and oxygen demand. Management goals are to enhance ventricular performance, improve hypoperfusion, limit infarct size, and minimize myocardial oxygen demand. Initial treatment includes supplemental oxygen, pain relief, sedation, and monitoring. In critically ill patients, measurements from a Swan-Ganz catheter are crucial, as cardiogenic shock presents with low cardiac output but normal or slightly
This document discusses shock, which is an inadequate tissue perfusion that can lead to cell death if not addressed promptly. It defines shock and outlines its pathophysiology, including cellular, microvascular, systemic, and reperfusion events. It also classifies shock into hypovolaemic, cardiogenic, obstructive, distributive, and endocrine types. The document emphasizes that shock is a leading cause of death among surgical patients and stresses the importance of understanding its diagnosis and management.
This document provides an overview of shock, including:
1. Definitions of shock and classifications according to etiology and pathophysiology. Shock results from inadequate oxygen delivery to tissues.
2. Descriptions of the pathophysiology of shock at the cellular, microvascular, and systemic levels, including metabolic changes, inflammation, and compensatory responses.
3. Clinical features of shock ranging from mild to severe based on degree of blood or fluid loss. Monitoring includes vital signs, urine output, and invasive monitoring like Swan-Ganz catheter.
4. Treatment principles for different types of shock including fluid resuscitation and management of underlying causes like bleeding control or cardiac dysfunction. Outcomes can include
1. The document discusses different types of shock including hypovolaemic, cardiogenic, neurogenic, anaphylactic shock.
2. Hypovolaemic shock is due to diminished blood volume from blood or fluid loss. Cardiogenic shock is caused by inefficient myocardial function. Neurogenic shock is caused by loss of sympathetic tone leading to vasodilation.
3. Anaphylactic shock occurs due to an allergic reaction causing histamine release and widespread vasodilation.
Obstetric shock is caused by circulatory inadequacy resulting in poor tissue perfusion and cellular hypoxia. There are four phases of general changes in shock - the first two are reversible with treatment, the third is possibly reversible, and the fourth is irreversible and involves multiple organ failure. Management of shock involves stopping bleeding, volume resuscitation, oxygen supplementation, antibiotics for infection, vasopressors, and treating underlying causes.
7&8. SHOCK.pdf new new w new w new w new beSafinRoka
Shock is defined as a state of impaired tissue perfusion that results in cellular hypoxia. There are several types of shock, including cardiogenic, hypovolemic, septic, anaphylactic, and neurogenic shock. The pathogenesis of shock involves an initial compensatory response followed by progressive cellular hypoxia if shock persists. This can lead to irreversible cellular injury and organ failure if not corrected. Septic shock results from an inflammatory response to infection that causes vasodilation, hypotension, and multiple organ dysfunction through the effects of inflammatory mediators on endothelial cells and induction of a procoagulant state. Prolonged shock can cause hypoxic injury to vital organs like the brain, heart, lungs
This document provides information on shock, including its definition, types, pathophysiology, stages, and management. It defines shock as a state of low tissue perfusion resulting in cellular hypoxia. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Stages of shock include initial compensated shock, progressive decompensated shock, and decompensated irreversible shock. General management principles focus on restoring perfusion and oxygen delivery. Specific treatments are discussed for different shock types.
The document discusses cardiogenic shock, which occurs when the heart is unable to generate sufficient cardiac output to maintain tissue perfusion. Myocardial infarction is a frequent cause, due to valve disease, cardiomyopathy, or direct contusion. This leads to compensatory tachycardia but eventually decreased organ perfusion and hypotension, exacerbating the mismatch between coronary blood flow and oxygen demand. Management goals are to enhance ventricular performance, improve hypoperfusion, limit infarct size, and minimize myocardial oxygen demand. Initial treatment includes supplemental oxygen, pain relief, sedation, and monitoring. In critically ill patients, measurements from a Swan-Ganz catheter are crucial, as cardiogenic shock presents with low cardiac output but normal or slightly
This document discusses shock, which is an inadequate tissue perfusion that can lead to cell death if not addressed promptly. It defines shock and outlines its pathophysiology, including cellular, microvascular, systemic, and reperfusion events. It also classifies shock into hypovolaemic, cardiogenic, obstructive, distributive, and endocrine types. The document emphasizes that shock is a leading cause of death among surgical patients and stresses the importance of understanding its diagnosis and management.
This document provides an overview of shock, including:
1. Definitions of shock and classifications according to etiology and pathophysiology. Shock results from inadequate oxygen delivery to tissues.
2. Descriptions of the pathophysiology of shock at the cellular, microvascular, and systemic levels, including metabolic changes, inflammation, and compensatory responses.
3. Clinical features of shock ranging from mild to severe based on degree of blood or fluid loss. Monitoring includes vital signs, urine output, and invasive monitoring like Swan-Ganz catheter.
4. Treatment principles for different types of shock including fluid resuscitation and management of underlying causes like bleeding control or cardiac dysfunction. Outcomes can include
1. The document discusses different types of shock including hypovolaemic, cardiogenic, neurogenic, anaphylactic shock.
2. Hypovolaemic shock is due to diminished blood volume from blood or fluid loss. Cardiogenic shock is caused by inefficient myocardial function. Neurogenic shock is caused by loss of sympathetic tone leading to vasodilation.
3. Anaphylactic shock occurs due to an allergic reaction causing histamine release and widespread vasodilation.
Obstetric shock is caused by circulatory inadequacy resulting in poor tissue perfusion and cellular hypoxia. There are four phases of general changes in shock - the first two are reversible with treatment, the third is possibly reversible, and the fourth is irreversible and involves multiple organ failure. Management of shock involves stopping bleeding, volume resuscitation, oxygen supplementation, antibiotics for infection, vasopressors, and treating underlying causes.
7&8. SHOCK.pdf new new w new w new w new beSafinRoka
Shock is defined as a state of impaired tissue perfusion that results in cellular hypoxia. There are several types of shock, including cardiogenic, hypovolemic, septic, anaphylactic, and neurogenic shock. The pathogenesis of shock involves an initial compensatory response followed by progressive cellular hypoxia if shock persists. This can lead to irreversible cellular injury and organ failure if not corrected. Septic shock results from an inflammatory response to infection that causes vasodilation, hypotension, and multiple organ dysfunction through the effects of inflammatory mediators on endothelial cells and induction of a procoagulant state. Prolonged shock can cause hypoxic injury to vital organs like the brain, heart, lungs
This document provides information on shock, including its definition, types, pathophysiology, stages, and management. It defines shock as a state of low tissue perfusion resulting in cellular hypoxia. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Stages of shock include initial compensated shock, progressive decompensated shock, and decompensated irreversible shock. General management principles focus on restoring perfusion and oxygen delivery. Specific treatments are discussed for different shock types.
The document discusses shock, including its definition, types, pathophysiology, and stages. Shock is defined as a state of low tissue perfusion that is inadequate for normal cellular respiration, leading to hypotension and cellular hypoxia if left uncompensated. The types of shock discussed include hypovolaemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Shock is divided into three stages: non-progressive/compensated, progressive decompensated, and decompensated/irreversible shock. Compensatory mechanisms in the initial
Shock is characterized by a reduction in systemic tissue perfusion and oxygen delivery to tissues, leading to cellular hypoxia. Prolonged hypoxia initially causes reversible cell damage but can progress to irreversible multi-system organ failure and death if shock is not promptly recognized and reversed. The main types of shock are hypovolemic, cardiogenic, obstructive, and distributive. Clinical features include hypotension, oliguria, altered mental status, cool clammy skin, and metabolic acidosis. Additional historical or physical exam findings can provide clues to the specific type of shock.
Shock results from inadequate tissue perfusion due to an imbalance between oxygen delivery and cellular requirements. This leads to cellular injury, inflammation, and further impairment of microvascular perfusion in a vicious cycle. The clinical manifestations of shock include hypotension, tachycardia, and organ dysfunction as the body mounts autonomic and neuroendocrine responses to try to restore perfusion. Different types of shock are classified based on their underlying pathophysiology such as hypovolemic shock from blood or fluid loss.
This topic contains definition, meaning, classification, pathophysiology, clinical menifestations, metabolic and general changes, management of obstetrical shock
Shock is defined as a physiological state characterized by a significant, systemic reduction in tissue perfusion due to decreased cardiac output. It results in inadequate tissue oxygen delivery and metabolic waste removal, causing tissue injury. Shock is classified based on etiology and includes hypovolemic, cardiogenic, obstructive, and distributive shock. The pathophysiology of shock involves neuroendocrine, cardiovascular, microcirculatory, hormonal, metabolic, and immune responses that vary depending on the shock type and stage. Specific types of shock like hypovolemic and cardiogenic shock are further described.
This document discusses shock, including its definition, pathophysiology, classification, and severity. Shock is defined as a state of inadequate tissue perfusion resulting from reduced cardiac output, blood loss, or vascular dysfunction. The main types are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The pathophysiology involves cellular hypoxia, inflammation, microvascular dysfunction, and ischemia-reperfusion injury. More severe shock is characterized by worsening metabolic acidosis, hypotension, oliguria, and loss of consciousness. Early recognition and treatment of compensated shock is important to prevent multi-organ failure.
1) Acute renal failure is divided into prerenal, intrinsic, and postrenal types based on the location of injury.
2) Prerenal acute renal failure, also called prerenal azotemia, is the most common type and is caused by decreased renal blood flow without direct kidney damage.
3) Intrinsic acute renal failure involves direct kidney injury, most commonly from acute tubular necrosis caused by ischemia or nephrotoxins, which accounts for 85% of cases.
The document summarizes renal physiology and kidney function. It discusses:
1) The structure of the kidney including nephrons, collecting ducts, and microvasculature. Nephron number is established prenatally and cannot be replaced if lost.
2) Urine formation through selective retention and elimination of solutes and water by different nephron segments including the glomerulus, proximal tubule, loop of Henle, and collecting ducts.
3) Causes, types (prerenal, intrarenal, postrenal), phases, prevention and management of acute renal failure and end-stage renal disease where dialysis or transplantation is needed for survival.
Shock is defined as a state of reduced effective tissue perfusion leading to cellular injury. The document discusses the classification, pathophysiology, clinical features, and treatment of various types of shock including hypovolaemic, traumatic, and cardiogenic shock. Compensatory mechanisms initially attempt to maintain blood pressure and tissue perfusion through vasoconstriction, increased heart rate, and fluid shifts. However, without treatment, shock progresses to cellular dysfunction, organ failure and death. Treatment focuses on fluid resuscitation, controlling bleeding, and treating the underlying cause.
Shock is defined as a state of reduced effective tissue perfusion leading to cellular injury. The document discusses the classification, pathophysiology, clinical features, and treatment of various types of shock including hypovolaemic, traumatic, cardiogenic, and septic shock. Compensatory mechanisms initially work to maintain blood pressure but progressive shock leads to organ failure and death if not treated promptly with fluid resuscitation, controlling bleeding, and vasoactive drugs.
Shock is a condition where tissue perfusion is inadequate to deliver oxygen and nutrients to vital organs. There are four types of shock: hypovolemic, cardiogenic, distributive, and obstructive. Shock progresses through three phases - initial non-progressive, progressive, and irreversible. In the progressive phase, compensatory mechanisms fail and tissue hypoxia develops. The irreversible phase is characterized by multi-organ failure and cell death due to severe hypoxia. Treatment of shock involves identifying the cause, giving IV fluids and medications to support blood pressure and organ function, and treating any underlying condition causing shock.
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
presentation on CHF,orchitis,shock,anemiaRoshan paudel
This document provides information on various types of shock, congestive heart failure, anaemia, and orchitis. It discusses the etiology, pathophysiology, clinical signs, diagnosis, and management of each condition. The main types of shock described are hypovolemic, cardiogenic, and distributive shock. Congestive heart failure results from the heart's inability to pump sufficiently. The signs of left and right sided heart failure are outlined. Anaemia is classified based on red blood cell morphology and causes. Orchitis is testicular inflammation that can result from infection, trauma, or parasites.
1. Septic shock is caused by infection which releases cytokines that damage microcirculation and cause vasodilation and capillary leakage, leading to tissue hypoxia and multiple organ failure. Early, aggressive treatment of infection along with cardiovascular and organ system support is needed to prevent high mortality rates.
2. Hypovolaemic shock results from decreased blood volume due to blood loss, fluid loss, or fluid shifts. It progresses from mild to severe as compensation fails, leading to cellular changes, metabolic acidosis, and potentially multiple organ failure without timely fluid resuscitation and hemostasis.
3. Cardiogenic shock stems from heart failure to pump adequately due to causes like myocardial infarction, arrhythmias
Shock is a life-threatening condition where the circulatory system fails to deliver oxygen to tissues. It can progress rapidly to organ failure and death if not corrected. Shock is generally classified as hypovolemic, cardiogenic, or distributive. Treatment involves identifying the cause, restoring blood volume through fluids, providing oxygen support, treating infection if present, and using vasoactive drugs or inotropes. The goals are to restore tissue perfusion and prevent complications like multiple organ failure. Early diagnosis and management of shock is crucial to prevent permanent damage or death.
This document discusses shock, which is a profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate organ perfusion. There are four main types of shock: cardiogenic, hypovolemic, distributive, and obstructive. The document outlines the etiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of each type of shock. It emphasizes the importance of early goal-directed therapy and treatment of the underlying cause of shock to increase cardiac output and tissue perfusion in order to prevent multiple organ dysfunction.
This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
This document discusses the pathophysiology of edema. It defines edema as swelling caused by excess fluid in the interstitial spaces between tissues. Edema can be classified as transudate or exudate based on protein content, and as localized or generalized based on location. The key mechanisms that can cause edema are increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. The movement of fluid between blood vessels and tissues is normally regulated by the balance of hydrostatic and oncotic pressures according to Starling's forces, but imbalances in these forces can result in excess fluid accumulation in the tissues and cause edema.
The document discusses shock, including its definition, types, pathophysiology, and stages. Shock is defined as a state of low tissue perfusion that is inadequate for normal cellular respiration, leading to hypotension and cellular hypoxia if left uncompensated. The types of shock discussed include hypovolaemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Shock is divided into three stages: non-progressive/compensated, progressive decompensated, and decompensated/irreversible shock. Compensatory mechanisms in the initial
Shock is characterized by a reduction in systemic tissue perfusion and oxygen delivery to tissues, leading to cellular hypoxia. Prolonged hypoxia initially causes reversible cell damage but can progress to irreversible multi-system organ failure and death if shock is not promptly recognized and reversed. The main types of shock are hypovolemic, cardiogenic, obstructive, and distributive. Clinical features include hypotension, oliguria, altered mental status, cool clammy skin, and metabolic acidosis. Additional historical or physical exam findings can provide clues to the specific type of shock.
Shock results from inadequate tissue perfusion due to an imbalance between oxygen delivery and cellular requirements. This leads to cellular injury, inflammation, and further impairment of microvascular perfusion in a vicious cycle. The clinical manifestations of shock include hypotension, tachycardia, and organ dysfunction as the body mounts autonomic and neuroendocrine responses to try to restore perfusion. Different types of shock are classified based on their underlying pathophysiology such as hypovolemic shock from blood or fluid loss.
This topic contains definition, meaning, classification, pathophysiology, clinical menifestations, metabolic and general changes, management of obstetrical shock
Shock is defined as a physiological state characterized by a significant, systemic reduction in tissue perfusion due to decreased cardiac output. It results in inadequate tissue oxygen delivery and metabolic waste removal, causing tissue injury. Shock is classified based on etiology and includes hypovolemic, cardiogenic, obstructive, and distributive shock. The pathophysiology of shock involves neuroendocrine, cardiovascular, microcirculatory, hormonal, metabolic, and immune responses that vary depending on the shock type and stage. Specific types of shock like hypovolemic and cardiogenic shock are further described.
This document discusses shock, including its definition, pathophysiology, classification, and severity. Shock is defined as a state of inadequate tissue perfusion resulting from reduced cardiac output, blood loss, or vascular dysfunction. The main types are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The pathophysiology involves cellular hypoxia, inflammation, microvascular dysfunction, and ischemia-reperfusion injury. More severe shock is characterized by worsening metabolic acidosis, hypotension, oliguria, and loss of consciousness. Early recognition and treatment of compensated shock is important to prevent multi-organ failure.
1) Acute renal failure is divided into prerenal, intrinsic, and postrenal types based on the location of injury.
2) Prerenal acute renal failure, also called prerenal azotemia, is the most common type and is caused by decreased renal blood flow without direct kidney damage.
3) Intrinsic acute renal failure involves direct kidney injury, most commonly from acute tubular necrosis caused by ischemia or nephrotoxins, which accounts for 85% of cases.
The document summarizes renal physiology and kidney function. It discusses:
1) The structure of the kidney including nephrons, collecting ducts, and microvasculature. Nephron number is established prenatally and cannot be replaced if lost.
2) Urine formation through selective retention and elimination of solutes and water by different nephron segments including the glomerulus, proximal tubule, loop of Henle, and collecting ducts.
3) Causes, types (prerenal, intrarenal, postrenal), phases, prevention and management of acute renal failure and end-stage renal disease where dialysis or transplantation is needed for survival.
Shock is defined as a state of reduced effective tissue perfusion leading to cellular injury. The document discusses the classification, pathophysiology, clinical features, and treatment of various types of shock including hypovolaemic, traumatic, and cardiogenic shock. Compensatory mechanisms initially attempt to maintain blood pressure and tissue perfusion through vasoconstriction, increased heart rate, and fluid shifts. However, without treatment, shock progresses to cellular dysfunction, organ failure and death. Treatment focuses on fluid resuscitation, controlling bleeding, and treating the underlying cause.
Shock is defined as a state of reduced effective tissue perfusion leading to cellular injury. The document discusses the classification, pathophysiology, clinical features, and treatment of various types of shock including hypovolaemic, traumatic, cardiogenic, and septic shock. Compensatory mechanisms initially work to maintain blood pressure but progressive shock leads to organ failure and death if not treated promptly with fluid resuscitation, controlling bleeding, and vasoactive drugs.
Shock is a condition where tissue perfusion is inadequate to deliver oxygen and nutrients to vital organs. There are four types of shock: hypovolemic, cardiogenic, distributive, and obstructive. Shock progresses through three phases - initial non-progressive, progressive, and irreversible. In the progressive phase, compensatory mechanisms fail and tissue hypoxia develops. The irreversible phase is characterized by multi-organ failure and cell death due to severe hypoxia. Treatment of shock involves identifying the cause, giving IV fluids and medications to support blood pressure and organ function, and treating any underlying condition causing shock.
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
presentation on CHF,orchitis,shock,anemiaRoshan paudel
This document provides information on various types of shock, congestive heart failure, anaemia, and orchitis. It discusses the etiology, pathophysiology, clinical signs, diagnosis, and management of each condition. The main types of shock described are hypovolemic, cardiogenic, and distributive shock. Congestive heart failure results from the heart's inability to pump sufficiently. The signs of left and right sided heart failure are outlined. Anaemia is classified based on red blood cell morphology and causes. Orchitis is testicular inflammation that can result from infection, trauma, or parasites.
1. Septic shock is caused by infection which releases cytokines that damage microcirculation and cause vasodilation and capillary leakage, leading to tissue hypoxia and multiple organ failure. Early, aggressive treatment of infection along with cardiovascular and organ system support is needed to prevent high mortality rates.
2. Hypovolaemic shock results from decreased blood volume due to blood loss, fluid loss, or fluid shifts. It progresses from mild to severe as compensation fails, leading to cellular changes, metabolic acidosis, and potentially multiple organ failure without timely fluid resuscitation and hemostasis.
3. Cardiogenic shock stems from heart failure to pump adequately due to causes like myocardial infarction, arrhythmias
Shock is a life-threatening condition where the circulatory system fails to deliver oxygen to tissues. It can progress rapidly to organ failure and death if not corrected. Shock is generally classified as hypovolemic, cardiogenic, or distributive. Treatment involves identifying the cause, restoring blood volume through fluids, providing oxygen support, treating infection if present, and using vasoactive drugs or inotropes. The goals are to restore tissue perfusion and prevent complications like multiple organ failure. Early diagnosis and management of shock is crucial to prevent permanent damage or death.
This document discusses shock, which is a profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain adequate organ perfusion. There are four main types of shock: cardiogenic, hypovolemic, distributive, and obstructive. The document outlines the etiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of each type of shock. It emphasizes the importance of early goal-directed therapy and treatment of the underlying cause of shock to increase cardiac output and tissue perfusion in order to prevent multiple organ dysfunction.
This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
This document discusses the pathophysiology of edema. It defines edema as swelling caused by excess fluid in the interstitial spaces between tissues. Edema can be classified as transudate or exudate based on protein content, and as localized or generalized based on location. The key mechanisms that can cause edema are increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. The movement of fluid between blood vessels and tissues is normally regulated by the balance of hydrostatic and oncotic pressures according to Starling's forces, but imbalances in these forces can result in excess fluid accumulation in the tissues and cause edema.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
2. It is a patho-physiological condition
clinically recognized as a state of
inadequate tissue perfusion.
Cerra described shock as ‘ disordered
response of organism to an inappropriate
balance of substrate supply and demand
at a cellular level’.
Shock is a systemic disorder that disrupts
vital organs function as the eventual result
3. Blalock in 1934 classified shock on the
basis of etiology:
1. Hematogenic
2. Neurogenic
3. Vasovegal
4. Cardiogenic.
4. Hematogenic or traumatic shock
characterized by global hypo perfusion.
Vasogenic and septic is associated with
hyper circulation resulting in mal-
distribution of regional or intra-organ
blood flow.
8. Decrease in circulatory intravascular
volume causing hypo-perfusion and
increase adrenergic activity.
Intravascular volume lost increase
peripheral resistance in regional arteriolar
beds (skin, gut and kidney)
decreasing blood flow in these organs.
Clinical presentation: anxious and
restlessness and upon treatment present
9. On examination: (on bed side)
1. Pale
2. Cool skin
3. Blanching of bowel with
4. Decreased pulses in mesentery
10. Decrease circulatory volume
tachycardia to prevent stroke volume.
Ortho-static test (asking patient to stand)
may unmask cardio-vascular instability
with tachycardia and hypotension in
patients who appear stable when
examined in supine position.
(in ortho-static state there is 30% decrease in
circulating blood volume)
11.
12. Loss of circulating intravascular volume
Increased of peripheral resistance
Redistribution of
blood in organs in heart and brain Vascular
tone resistance
In expense of cutaneous, splenchinic and renal
circulation
13. Decrease in intravascular volume
stimulate sympathetic response activity
decrease in vagal inhibition increase
rate & force of cardiac contraction
increase cardiac contraction
Tachycardia cardiac output +
myocardial O2 consumption increases
Blood pressure is maintained by increase
14. Loss of blood decrease in capillary
hydrostatic pressure trans-capillary
influx of extra-vascular extra cellular fluid
from interstitial space causes alteration in
starling law (increase in right ventricular
filling cause increase in force of
contraction)
Mobilization of interstitial fluid pool into
intravenous space lead to
Increase in circulatory intravascular volume
15. Due to hemo-dilution increase O2
carrying capacity Enhance in tissue
extraction of O2 due to acidosis &
Erythrocytosis 2,3- diphosphoglycerated
hemoglobin.
Acidosis due to decrease in excretion and
accumulation of cellular substrate
anaerobic respiration and glucose
metabolism.
It also cause right ward shift of O2
dissociation curve to decrease in
16. Hypoxia also stimulate respiratory centre
Hyper-ventilation
Respiratory alkalosis
Increase in erythrocytosis (2-3 DPG).
More rightward shift of O2 dissociation
curve.
17. Arteriolar constriction & loss of circulating
volume
Decrease renal blood flow
Stimulated of afferent and efferent
arterioles causing corticomedullary shunt
to maintain
Effective GFR
Urine output is subsequently decrease
Salt water & urea and uric acid retained
Decrease in buffering capacity
Loss of control of acid base balance
18. Change in blood volume with afferent sensory
impulses lead to marked release of
epinephrine and non epinephrine by adrenal
gland lead to
1. Retention of water and salt in proximal
convoluted tubule.
2. Vasoconstriction and tachycardia
increase Blood pressure and cardiac output.
3. Stimulate glycogenolysis, lipolysis and
skeletal muscle breakdown & inhibition of
insulin release.
4. Promoting glucose metabolism in brain and
19. 1. Decrease blood volume
2. Decrease arterial pressure
3. Pain
4. Hypoxemia
5. Hypothermia
Leads to release of Adreno-cortico-tropic
hormone ACTH by pituitary.
in severe hemorrhage circulatory cortisol
provide no feed back inhibition on ACTH
release, but feedback is restored as blood
volume is restored.
20. Cortisol potentiate the
action of epinephrine & glucagon on
glucose metabolism
Insulin resistance,
Stimulate mobilization of amino acid from
skeletal muscle.
Also causes retention of Na+ & water
retention.
21. Insulin secretion is diminished
Relative hypo-insulinemia: helps in
mobilization of amino acid and fats stores
by glucagon, cortisol, and growth
hormone.
22. Anti diuretic hormone (ADH)/arginine
vasopressin(AVP) released in response of
increase serum osmolarity and hypovolemia
(potential stimulator) causes:
1. Increase water permeability &
2. Passive Na+ transport in DCT of nephrone
3. Increase water resorption
4. Potent splenchnic vasoconstrictor
23. Activation of renin angiotensin system
(RAS) due to increased sympathetic
stimulation of juxta-glomerular cells by
1. β- adrenergic mechanism
2. Decreased renal perfusion
3. Compositional changes of tubular fluid.
Renin release from juxta glomerular
appartatus causes increased production
of angiotensin I which convert to
angiotensin II in lungs.
24. Angiotensin II powerful arterial and arteriolar
vasoconstrictor causes:
1. Renal prostaglandin production; PGE2 and
kallikreins dilates renal vessels
increase renal flow
2. Release of aldosterone and ACTH.
Aldosterone
1. Increase Na+ re-absorption in DCT
2. Excretion of K+ & H+
3. Excretion of byproducts of anarobic
metabolism and cellular damage.
25. 10% blood loss: no evidence of clinical
shock
25 % blood loss: hypotension
18-26 % blood loss : functional
extracellular volume loss with RBC and
plasma
35-45 to 50 % blood loss: further loss of
extracellular volume loss with RBC and
plasma.
26. In severe shock: decrease in early
equilibrating extracellular fluid available for
intravascular influx, whole total anatomic
extracellular fluid may be normal.
Blood reinfusion restores RBC mass and
plasma, but not extracellular fluid volume.
Which is achieved by salt solution or ringer
lactate (mortality decreased from 80 % to 30
%)
27. Ionic differences:
In muscles and liver tissues membrane
potential gradient serves as a reliable
indicator of cellular dysfunction during
hemorrhagic shock
During profound hemorrhagic shock:
trans-cellular potential gradient falls from -
90 to -60mV.
Cellular swelling
Decease ATP production
Changes in membrane permeability due to
28. Nitric oxide (N2O) : free radical
Release due to endotoxin and pro
inflammatory cytokines (IL-I, TNF).
Potent relaxant of basal blood pressure.
29. Classifications
1.According to source
a) External hemorrhage
(revealed outside/ seen externally)
b) Internal hemorrhage or concealed hemorrhage
(not seen from outside)
eg. Fracture, bleeding peptic ulcer, rupture of
spleen, liver.
Concealed bleeding can be external viz.
hematemesis/ melaena from bleeding peptic
ulcer, hematuria from rupture kidney.
30.
31. 3. According to percentage ex-sanguination
of blood
Class I : blood loss up to 15%
Class II : 15-30%
Class III: 30-40% (need for blood)
Class IV : more than 40%
32. IN OPERATION THEATRE:
IN OUTPATIENT
DEPARTMENT
Weighing of soaked
cotton.
Measuring the size of
soaked gauge.
Hematocrit.
Hemoglobin.
Blood pressure.
Pulse pressure.
Central venous pressure.
34. 1. Resuscitation :
a. Clear airway
b. adequate ventilation.
2. Immediate control of bleeding :
a. Raising foot end of bed
b. Compression bandage
c. After resuscitation surgery.
35. (most important)
a. In ER – insert large gauge needle,
catheter in arm or leg.
In sophisticated centre 2 catheters are
placed, one in vein & another in sub-
clavian or jugular vein to measure CVP.
b. In initial stage give ringer lactate 1-2L in
45 min. to restore BP.
c. Grouping and cross matching of blood.
36. Sedatives: Use to alleviate pain in patients
with shock.
Morphine i.v.: adults without head injury and
acute abdominal injury.
children's : barbiturates
Head injury : largactil.
Chronotropic agents: atropine followed by
isoproterenol.
Increases heart rate with vasodilatation of
systemic arterial and capillary sphincters.
37. Inotropic agents: improves strength of
cardiac muscle contractility.
Cardiogenic, septic shock
Dopamine and dobutamine.
In low dosages, increase myocardial
contractility
selectively increase renal blood flow by
dilating renal vasculature.
Vaso-constrictive effect.
38. Pathophysioloy:
Traumatize tissue activates coagulation system
and release micro thrombi in circulation.
These may occlude or constrict parts of
pulmonary microvasculature to increase
pulmonary vascular resistance.
Increase right ventricular diastolic pressure
and right atrial pressure.
micro thrombi induce generalize permeability
in capillary permeability leads to the plasma
loss into interstitial tissues throughout the
body.
Causes decrease in vascular volume to a
greater extent.
39. Clinically similar to hypovolaemic shock.
Two differentiating features includes
1. Presence of peripheral and pulmonary
edema.
2. Inadequate volume of fluid after infusion
of large volume of fluids which was
sufficient for hypovolaemic shock.
40. 1. Resuscitation : mechanical ventilator
support is more needed.
2. Local treatment of trauma and control of
bleeding.
3. Fluid replacement:
1. More fluid needed.
2. Role of anticoagulant therapy to prevent
disseminated intravascular coagulation
(debatable:- as it can increase bleeding/
prevent large clot formation, if use at what
dose? ).
41. Bed side monitoring of circulatory efficiency:
HR
Arterial blood pressure
Urinary output
Peripheral perfusion
42. In patients with multiple injuries: CVP
central venous pressure (0-5cm of H2O)
monitoring is useful.
Normal to depressed CVP that does not rise
with rapid administration of crystalloids
(RL,NS) indicate continuing hypo-
volumemia.
Elevated CVP or its rapid rise: indicative of
impairment of pumping mechanism.
43.
44. When the heart is unable to generate
sufficient cardiac output to maintain
adequate tissues perfusion.
It has significant mortality and morbidity
when manifest with myocardial if action
and secondary end organ injuries of
pulmonary edema, oligouric renal failure.
45. Myocardial infarction result from
1. Valvular heart disease
2. Cardio-myopathy
3. Direct myocardial contusion.
Acute myocardial infarction is most
frequent cause, complications include
Papillar muscle dysfunction
Ischemic ventricular septal defect
Massive left ventricular infarction
Arrhythmias
46. Initial compensatory response
Tachycardia for decreases myocardial
infarction.
To maintain cardiac output
despite of decreased left ventricular
ejection fraction and
At the expense of increasing myocardial
oxygen consumption.
47. Cardiac index: cardiac output/body surface
area.
(4-8L/min/m2)
As cardiac index falls below 2L
hypotension produces--- reflex
sympathetic vasoconstriction.
In attempt to maintain Central Venous
Pressure (0-5cmH2O)
Lead to decrease in organ perfusion.
48. It requires prompt intervention as
Increased myocardial demand
Hypotension
Shortened diastole
Amplifies the mismatch between coronary
artery oxygen delivery and myocardial
oxygen demand
Extends the zone of infraction
49. Goal : Enhance ventricular performance
Improve global hypo perfusion.
Management:
Fluid with inotropic drugs: maximize
ventricular performance + increase myocardial
oxygen demand.
Including
Limit infract size
Protection of reversibly ischemic myocardium
Minimize myocardial oxygen demand.
Early reperfusion.
51. In critically ill patients: crucial
therapeutic decision making
done on the basis of
measurements of Swan-ganz
catheter: Cardiac output and
pulmonary arterial wedge
pressure (pressure of left
atrium).
In cardiogenic shock Low
cardiac output & pulmonary
hypotension causes normal
52. Small increase in left ventricular filling
pressure by volume infusion maximizes
cardiac output.
Emphasis should be given that although
hemodynamic measurement suggest
myocardial insuffiency: mechanical
obstructions should be ruled out;
1. Cardiac temponade in injured patients
2. Pulmonary embolism in the post-operative
patients.
These diagnosis is made on clinical grounds
in emergency with large volume infusion if
53. Ionotrpic drugs: beta 1 adrenergic
receptors responds to exogenous
sympathomimatic drugs to increase
contractility and improve cardiac output.
In expense of compromised myocardial perfusion.
I.V. infusion of dopamine may promptly
reverse life threatening hypotension and
restore mean arterial pressure around
80mmHg.
At low dose (2-5µg/kg/min): spleen and
coronary vasodilatation
At higher dose (5-8µg/kg/min): increase
contractility, heart rate with prominent α-
54. Side-effects of dopamine: variable
increase in HR can ppt. arrhythmias.
Therefore need to be titrated to lowest
acceptable dose.
Dobutamine: predominate ionotropic
effect; less arrhythmiogenic & redistribute
cardiac output in coronary circulation.
Useful in cardiopulmonary bypass and
myocardial infarction.
55. Vasodilating agent:
on clinical assessment pt with decrease
perfusion pressure have near normal arterial
pressure in with low cardiac output and high
filling pressures.
The high systolic ventricular pressure can be
corrected by decreasing after-load which in
turn increases cardiac output.
Sodium Nitropusside can be used with
extreme caution to prevent redistribution
away from the compensated coronary and
cerebral circulation causing decrease
56. Mechanical support:
Temporary support the failing
myocardium by reducing load of left
ventricles and decreasing oxygen
demand.
Intra- aortic balloon pulsation device:
inflates at diastole– elevates diastolic
pressure– increase pulmonary perfusion–
decreasing myocardial work by increasing
Cardiac output distal to ventricles.
57. Arrhythmias: rapid ventricular rates
decrease cardiac output to shock levels.
As filling time decrease ventricular end
diastolic pressure decreases– stroke
volume decreases– cardiac output
decreases.
Digoxin is drug of choice for atrial
fibrilation.
Electro-cardioversion should be promptly
done to prevent tachycardia (can cause
58. Verapamil is useful in treating
tachyarrhythmia of atrial origin.
Cardiogenic shock with loss of
consciousness: Immediate unsynchronized
direct current electric shock(cardioversion) is
mandatory for ventricular fibrillation.
Lodocain i.v. is initial treatment for prevetion
of recurrent ventricular fibrillation after
cardioversion.
Bretylium tosylate is useful in life threatening
ventricular tachyarrhythmia's unresponsive to
lidocaine.
59. Ventricular bradycardia: low cardiac
output with ventricular rate 70 beats /min.
stroke volume cannot be increase due to
pathologic bradycardia (atrial fibrillation
with slow ventricular rate)
Electrical pacing of heart at rate of 80-100
beats/min restore sufficient output.
60. Primary shock (older classification)
Occurs after serious interference with the
vasodilator and vasoconstrictor influence on
arterioles and venules.
Clinically seen in syncope.
On sudden exposure to unpleasant events,
such as
sight of blood,
hearing of bad news,
sudden onset of pain
61. Clinical manifestation:
1. Blood pressure– extremely low
2. Pulse rate– slower than normal
3. Dry , warm and even flushed skin.
Determination of the shock:
Decreased cardiac output with
Decrease in resistant to arteriolar vessels and
Decreased resistant to venous tone.
Normo-volumic with increase reservoir
capacity in arteriole and venules – decrease
venous return to right side of heart–
decrease in cardiac output.
62. Management:
Shock due to high spinal anesthesia –
adminstartion of fluid and vesopressor
(ephedrine/ phenylephrine).
Increase cardiac output and elevates
systemic blood pressure by arteriolar
constriction.
Milder form (fainting):
remove the patient from stimuli,
Reliving of pain,
Elevating legs
Till vasoconstrictor nerves regain its ability.
63. Shock resulting from injury, as in spinal
cord tran-section from trauma leading to
significant loss of blood and extracellular
fluid around cord and vertebral column.
Before surgical intervention hemodynamic
management should be done.
Uncomplicated neuralgic shock: slightly
low central venous pressure and near
normal cardiac output, which decreases
upon hypovolemia.
64. Monitoring:
Fluid administration without vasopressor
produce– gradual rise in arterial pressure
and cardiac output without elevation of
central venous pressure (as there is increase
in filling due to increase in intravascular fluid
volume).
Slight volume infusion has better prognosis
than to vasopressor as it decrease organ
perfusion proximal to spinal cord.
Best balance -- from normal central venous
pressure with rise of rapid fluid administration
and use of vasopressor (phenyephrine) to
65. Defined as continuation of human
response to infection.
Cause
Virus
Parasite
Fungi
Most common– gram negative bacteria
and gram positive occasionally.
66. Increase incidence of gram negative sepsis
has rises due;
1. Developing reservoir of resistant and
virulent organism.
2. Concentration of infected patients in critical
care.
3. More extensive operation in elderly and
poor risk patients.
4. Initial rescue of severely injured patients.
5. Growing population of immuno-suppresed
patients by organ transplant protocols,
radiotherapy and chemotherapy.
67. Most common source of gram negative
organism is genitourinary system.
Second most common cause respiratory
system.
Third : alimentary system
Biliary tract.
68. Clinical manifestation:
Onset of chills
Temperature elevation above 101°F (38°C).
Rapidly progressive evidence of altered organ
function (most often renal and pulmonary).
Development of hypotension.
Normo-volumic with hypotension despite
normal cardiac output and filling pressure.
69. Also called ‘Warm shock’ with pink and dry
extremities due to low peripheral
resistance.
High cardiac output with decrease oxygen
utilization and less oxygenation difference
between arteries and vein.
70. Patient who is already in hypovolumic shock ,
presents characteristic hypo dynamic pattern
which is :
Falling cardiac output.
Low central pressure
Increased peripheral resistance with more
typical
Cold
Pale extremities seen in global hypo-perfusion.
Early volume replacement increases cardiac
output and hyper dynamic circulation, later
patients becomes unresponsive to volume
71. Lab investigation shows
Elevated WBC count
Leucopenia may be present in imuno-
compromised and debilitated patients or
patients with exhausted white cells from
sepsis.
Thrombocytopenia early indicator of gram
negative sepsis in Pediatric and Burn
patients.
Mild hypoxia with compensatory
72. Septic shock is the complex interaction
between exogenous endogenous and
host response to these stimuli.(poorly
understood)
When host response to local cell injury
and infection from cannot be contained it
progress as systemic illness.
At organ level: cardiovascular response to
systemic infection in absence to
hypovolumenia --- hyper dynamic state
73. Vasoregulatory mediators combine to
produce net decrease in systemic
vascular resistance .
As cardiac index increases and arterio-
venous oxygenation deference narrowed.
Micro vascular blood flow in capillary bed
doesn't alters
At cellular level: no hypoxia, no defect in
metabolic pathway defect is reported.
Depressed myocardial function with
74. The long postulated myocardial
depressant factor, with poorly
characterized biochemicals appear to the
cause of decreased left ventricular
ejection fraction despite of acceptable
filling pressure appears to be reasonable.
75. Pathophysiological mechanism of organ
dysfunction prior to the onset of
hypotension is associated with refractory
hypotension with tissue ischemia leading
to cell death and end stage hypo dynamic
septic shock.
.
76. Agents causing fever were endongenous
products leading to concept of
endogenous mediators of action of
endotoxin. Which are
Interlukin-1
Cachectin- TNF is central and proximal
mediator to endotoxemia and bacteremia.
Cachectin- TNF has 50% homology with
lymphotoxin, because of functional
similarity lymphotoxin is called TNF-B and
Cachectin- TNF is called TNF-A
77. Later after protein and complimentary
DNA sequencing, Cachectin is identical to
the TNF tumor necrosis factor, which
mediate endotoxin induced tumor cyto-
toxicity.
Circulating TNF-a can be found in
response to endotoxin in humans and its
peak level may be co-related with sepsis
and overall mortality.
78. TNF induces synthesis and secretion of
secondary mediators;
Cytokines
Prostaglandins,
Platelet activating factors
Complement components
Activation of clotting cascade.
Is responsible for pathologic changes seen in
lungs liver bowel kidneys in response to
sepsis and septic shock.
79. Management of
Administration of anti-endotoxin
antibodies
HA-1A Human monoclonal IgM antibody
against lipid portion of endotoxin improve
survival and organ function in presence of
gram –ve bacteremia with /out shock.
E5 Murine monoclonal antibody against
lipid portion of endotoxin is beneficial in
absene of shock.
80. Therapy:
Antibiotic treatment on the basis of culture and
sensitivity test
Early surgical debridement
Adjunctive therapy
Fluid therapy : correction of fluid deficit should
be rapid and cardiac output and pulmonary
wedge pressure as guide.
▪ Resuscitation in exceeds of 10ml of ringer lactate is
common.
Vasoactive drugs.
81. Measurement of
Arterial and venous pressure or pulmonary
wedge pressure.
Urine output
Arterial and venous blood gas
82. Steroid treatment:
Only indication is septic shock with hypo-
adrenalism for stress coverage
in patient taking steroid or who recently
completed course of steroid for
immunosuppressant and anti inflammatory
process.
83. Pharmacological support:
Inotropic / vasoactive drugs:
Dopamine is initial
Dobutamine is often used to increase cardiac
output with less tachycardia and arrhythmia
than dopamine.
Vasodilator drug improve cardiac output
and oxygen deliver in normo-tensive
septic shock.
Norepinephrine (potent alpha-receptor
agonist) is effective in raising pressure for
84. Epinephrine (potent α and β adrenergic
activity) support blood pressure which do
not respond to norepinephrine.
Vasopressor provide transient support
while definative therapy is with antibiotic
and surgical drainage.
85. Anaphylactic shock: commonly seen after
penicillin administration or administration
of serum, dextrose, anesthetics etc.
Pathophysiology: increased release of
histamine in combination with IgE on the
mast cells and basophils.
Bronchospasm, laryngeal edema respiratory
distress which leads to hypoxia,
Aggravated by massive vasodilatation leading
to hypotension -- shock
Editor's Notes
Tachy cardia: more than 90/ min, circulating bold volume: 4-5L
Hypotension: less than 120/80,
Sympathetic response: fight and flight response: increase HR, BP increase, papillary dilate, decrease salivation, peripheral pooling of blood.
in starling law (increase in right ventricular filling cause increase in force of contraction)
Normal temp.: 36.5–37.5 °C (97.7–99.5 °F)
WBC count of less than 4,000 per microliter (some labs say less than 4,500) could mean your body may not be able to fight infection the way it should. A low number is sometimes called leukopenia.
Thrombocytopenia or low platelet count is a lower than normal number of platelets(less than 150,000 platelets per microliter) in the blood.