Shock is defined as inadequate tissue perfusion resulting in decreased oxygen delivery and buildup of waste, and can progress from early compensated stages to intermediate stages involving organ damage and late irreversible stages involving multiple organ failure. The document outlines the pathophysiology and stages of shock including effects on body systems, clinical markers, causes, and treatment focusing on restoring tissue perfusion through fluid resuscitation and management of the underlying cause.
This document defines and discusses the pathophysiology of different types of shock: cardiogenic, obstructive, hypovolemic, and distributive. It notes that shock occurs when there is inadequate perfusion and oxygenation of cells, leading to cellular and organ dysfunction. The key signs of shock include tachycardia, hypotension, altered mental status, and decreased urine output. Early goal-directed resuscitation is important to prevent end organ damage and death, and should focus on airway management, oxygenation, fluid resuscitation, and treating the underlying cause.
Shock is a life-threatening condition defined by inadequate tissue perfusion and oxygen delivery. It can be caused by hypovolemia, cardiac dysfunction, or vasodilation. The main symptoms include low blood pressure, fast heart rate, fast breathing, and decreased urine output. Untreated shock can lead to organ failure and death. Treatment focuses on restoring circulating volume and oxygen delivery through fluid resuscitation, vasopressors, and treating the underlying cause. Prompt recognition and treatment are essential for recovery.
This document discusses the pathophysiology, causes, and management of shock. Shock is defined as a state of circulatory insufficiency resulting in inadequate organ perfusion. There are several types of shock, including hypovolemic, vasodilatory, cardiogenic, neurogenic, and obstructive. The initial goals of management are to secure the airway, administer intravenous fluids and vasopressors to restore perfusion pressure and tissue oxygenation, and give antibiotics if infection is suspected. The ultimate treatment involves addressing the underlying cause while monitoring systemic and tissue parameters to guide resuscitation efforts until oxygen debt is repaid and aerobic metabolism is restored.
Shock - Pathophysiology, Clinical Features & ManagementAnkit Sharma
1. Hemorrhagic shock is the most common cause of shock in surgical or trauma patients and results from blood loss that exceeds 15% of circulating volume.
2. Initial management of hemorrhagic shock involves identifying the source of bleeding, providing immediate resuscitation with fluids and blood products, and controlling hemorrhage.
3. Damage control resuscitation principles are followed, including permissive hypotension to limit blood loss and balanced use of crystalloids, colloids, platelets, and plasma to prevent coagulopathy.
Simple medical student presentation about distributive shock, type and pathophysiology of each septic shock, anaphylactic shock, neurogenic shock
including management, prognosis and disposition of patient..
brief info of type of inotropes and when to start.
Shock is a condition where the cardiovascular system fails to adequately perfuse tissues. It can be caused by an impaired pump (cardiogenic shock), reduced circulating volume (hypovolemic shock), or maldistribution of blood flow (distributive shock). The main effects are cellular hypoxia, impaired metabolism, and organ damage or failure if not treated. Compensatory mechanisms aim to increase perfusion but eventually fail, leading to irreversible cellular damage and death if shock persists.
SHOCK - PATHOPHYSIOLOGY, TYPES, APPROACH, TREATMENT.DR K TARUN RAO
1. Shock is defined as a state of poor tissue perfusion and cellular metabolism due to circulatory failure and hypoperfusion.
2. The main causes of shock include hypovolemic, cardiogenic, septic, anaphylactic, neurogenic, and respiratory etiologies.
3. The pathophysiology of shock involves a low cardiac output state leading to vasoconstriction and redistribution of blood flow away from non-vital organs to preserve perfusion of vital organs. Persistent shock can progress to cellular damage, organ dysfunction, and death.
This document defines and classifies hyperkalemia based on potassium levels. It discusses the clinical presentation, epidemiology, etiology, and pathophysiology of hyperkalemia. The diagnostic methods and management approaches are also outlined. Hyperkalemia is managed through non-pharmacological treatments like dialysis for severe cases. Pharmacological treatments work to antagonize potassium effects, redistribute potassium into cells, or remove excess potassium from the body using calcium, insulin, beta-agonists, cation exchange resins, and diuretics.
This document defines and discusses the pathophysiology of different types of shock: cardiogenic, obstructive, hypovolemic, and distributive. It notes that shock occurs when there is inadequate perfusion and oxygenation of cells, leading to cellular and organ dysfunction. The key signs of shock include tachycardia, hypotension, altered mental status, and decreased urine output. Early goal-directed resuscitation is important to prevent end organ damage and death, and should focus on airway management, oxygenation, fluid resuscitation, and treating the underlying cause.
Shock is a life-threatening condition defined by inadequate tissue perfusion and oxygen delivery. It can be caused by hypovolemia, cardiac dysfunction, or vasodilation. The main symptoms include low blood pressure, fast heart rate, fast breathing, and decreased urine output. Untreated shock can lead to organ failure and death. Treatment focuses on restoring circulating volume and oxygen delivery through fluid resuscitation, vasopressors, and treating the underlying cause. Prompt recognition and treatment are essential for recovery.
This document discusses the pathophysiology, causes, and management of shock. Shock is defined as a state of circulatory insufficiency resulting in inadequate organ perfusion. There are several types of shock, including hypovolemic, vasodilatory, cardiogenic, neurogenic, and obstructive. The initial goals of management are to secure the airway, administer intravenous fluids and vasopressors to restore perfusion pressure and tissue oxygenation, and give antibiotics if infection is suspected. The ultimate treatment involves addressing the underlying cause while monitoring systemic and tissue parameters to guide resuscitation efforts until oxygen debt is repaid and aerobic metabolism is restored.
Shock - Pathophysiology, Clinical Features & ManagementAnkit Sharma
1. Hemorrhagic shock is the most common cause of shock in surgical or trauma patients and results from blood loss that exceeds 15% of circulating volume.
2. Initial management of hemorrhagic shock involves identifying the source of bleeding, providing immediate resuscitation with fluids and blood products, and controlling hemorrhage.
3. Damage control resuscitation principles are followed, including permissive hypotension to limit blood loss and balanced use of crystalloids, colloids, platelets, and plasma to prevent coagulopathy.
Simple medical student presentation about distributive shock, type and pathophysiology of each septic shock, anaphylactic shock, neurogenic shock
including management, prognosis and disposition of patient..
brief info of type of inotropes and when to start.
Shock is a condition where the cardiovascular system fails to adequately perfuse tissues. It can be caused by an impaired pump (cardiogenic shock), reduced circulating volume (hypovolemic shock), or maldistribution of blood flow (distributive shock). The main effects are cellular hypoxia, impaired metabolism, and organ damage or failure if not treated. Compensatory mechanisms aim to increase perfusion but eventually fail, leading to irreversible cellular damage and death if shock persists.
SHOCK - PATHOPHYSIOLOGY, TYPES, APPROACH, TREATMENT.DR K TARUN RAO
1. Shock is defined as a state of poor tissue perfusion and cellular metabolism due to circulatory failure and hypoperfusion.
2. The main causes of shock include hypovolemic, cardiogenic, septic, anaphylactic, neurogenic, and respiratory etiologies.
3. The pathophysiology of shock involves a low cardiac output state leading to vasoconstriction and redistribution of blood flow away from non-vital organs to preserve perfusion of vital organs. Persistent shock can progress to cellular damage, organ dysfunction, and death.
This document defines and classifies hyperkalemia based on potassium levels. It discusses the clinical presentation, epidemiology, etiology, and pathophysiology of hyperkalemia. The diagnostic methods and management approaches are also outlined. Hyperkalemia is managed through non-pharmacological treatments like dialysis for severe cases. Pharmacological treatments work to antagonize potassium effects, redistribute potassium into cells, or remove excess potassium from the body using calcium, insulin, beta-agonists, cation exchange resins, and diuretics.
Shock is a clinical state characterized by inadequate tissue perfusion resulting from insufficient oxygen and substrate delivery to meet metabolic demands. There are several types of shock defined by etiology (hypovolemic, cardiogenic, distributive) and effects on blood pressure (compensated, decompensated). Signs of shock include tachycardia, altered mental status, and decreased urine output. Treatment involves rapid fluid resuscitation and vasoactive drugs like dopamine, epinephrine, and norepinephrine to support cardiac output as needed.
Cardiogenic shock is the failure of the heart to pump enough blood to meet the body's needs due to loss of contractile function. It most commonly occurs after a myocardial infarction which damages a significant portion of the left ventricle. Symptoms include low blood pressure, rapid breathing, decreased urine output, and confusion. Treatment involves oxygen, medications to improve contractility and reduce workload, and mechanical devices like IABP if needed. Nursing care focuses on monitoring circulation and tissue perfusion, managing devices, and addressing patient anxiety.
This document provides an overview of shock, including its history, definitions, types, pathophysiology, signs and symptoms, and management. It discusses the four main types of shock - cardiogenic, obstructive, hypovolemic, and distributive - describing the insult, physiologic effects, and compensatory mechanisms for each. Treatment of shock focuses on the ABCDE approach - airway, breathing, circulation, disability, and exposure. Restoring adequate circulation through fluid resuscitation is key. The goals of treatment are to optimize oxygen delivery and achieve endpoints of resuscitation like urine output and hemodynamic parameters.
This document provides an overview of shock, including its classification, causes, pathophysiology, clinical features, and management. It defines shock as a clinical manifestation of inadequate tissue perfusion and cellular hypoxia due to a reduction in effective circulating blood volume. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The document examines the cellular, microvascular, and systemic pathophysiological changes that occur in shock, as well as compensatory mechanisms and signs of decompensation. Clinical features, diagnosis, and general management principles are also summarized.
Hypovolemic shock is a life-threatening emergency in which severe blood or other fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working.
Hypovolemic shock is a dangerous condition that happens when suddenly lose a lot of blood or fluids from body. This drops blood volume, the amount of blood circulating in body. That’s why it’s also known as low-volume shock.
This document provides information about shock and its nursing management. It begins with an introduction to shock, defining it as a life-threatening condition caused by inadequate blood flow to tissues. It then outlines the stages of shock as initial, compensatory, progressive, and irreversible. The main types of shock discussed are hypovolemic, cardiogenic, neurogenic, septic, and anaphylactic. For each type, causes, signs and symptoms, and nursing care are described. The document concludes with test questions to assess learning.
Cardiogenic shock occurs when the heart is unable to pump sufficiently due to issues like a myocardial infarction. It leads to low blood flow and organ dysfunction. Symptoms include chest pain, breathing issues, and hypotension. Treatment focuses on optimizing oxygen delivery through ventilation, volume resuscitation, inotropes, and procedures like IABP or surgery if needed. Nursing care monitors for worsening and supports the patient through the condition.
Cardiogenic shock occurs when the heart is damaged and unable to pump enough blood to vital organs. This causes blood pressure to drop and organs to fail. It is a serious medical emergency. The heart loses its ability to contract effectively due to lack of oxygen and nutrients. Clinical features include low blood pressure, confusion, and poor organ perfusion. Treatment aims to improve cardiac function and oxygen delivery through medications, surgeries like bypass and stenting, and devices like intra-aortic balloon pumps. Nursing care monitors the patient's condition and supports the medical management of this critical condition.
This document discusses hypovolemic shock, which is characterized by decreased circulating blood volume resulting in reduced tissue perfusion. It can be hemorrhagic, due to blood loss from wounds or internal bleeding, or non-hemorrhagic from digestive, renal, skin or third space losses. The pathophysiology involves a macrocirculatory reaction with centralization of circulation and microcirculatory changes impairing capillary function. Treatment involves stopping losses, aggressive volume resuscitation with isotonic fluids, monitoring for efficacy, and inotropic support if needed to boost cardiac output after volume is restored.
Shock and its management is summarized as follows:
1. Shock is a life-threatening condition characterized by inadequate tissue perfusion due to reduced circulating blood volume or cardiac output.
2. Shock is classified as hypovolemic, cardiogenic, septic, traumatic, neurogenic, or hypoadrenal based on etiology.
3. The pathophysiology involves reduced circulating volume, impaired tissue oxygenation, and release of inflammatory mediators, progressing from compensated to decompensated to irreversible stages if left untreated.
This document discusses hemorrhagic shock, which is a condition of reduced tissue perfusion caused by a loss of circulating blood volume from trauma or gastrointestinal bleeding. It outlines the pathophysiology, signs and symptoms, diagnostic evaluation including lab tests and imaging, and management with fluid resuscitation, blood transfusions, controlling the source of bleeding surgically if needed, and treating complications. The key points are that hemorrhagic shock results from acute blood loss, causes decreased cardiac output and blood pressure, and must be promptly diagnosed and treated by replacing fluid volume and identifying and stopping the source of bleeding.
Ventricular fibrillation occurs when the ventricles of the heart quiver due to uncoordinated contractions of the heart muscle fibers. This prevents the heart from effectively pumping blood throughout the body. Ventricular fibrillation can be caused by stress, damage, or electrical changes to heart tissue. It requires immediate treatment through defibrillation or medications to prevent organ damage or death from lack of oxygen.
THIS PRESENTATION WILL COVER THE FOLLOWING AREAS
Definitions
Buffer systems
Regulatory systems
Anion Gap and Osmolar gap
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Pulmonary edema is fluid accumulation in the lungs caused by fluid leaking from blood vessels into the lung tissue and air spaces. It can be caused by issues that increase pressure in the blood vessels of the lungs like heart failure, or by problems that damage the blood vessel walls. Symptoms include shortness of breath, cough, and anxiety. Treatment depends on the underlying cause but aims to reduce fluid buildup and support breathing. Differentiating cardiogenic from non-cardiogenic pulmonary edema involves considering medical history, symptoms, physical exam findings, and chest imaging results.
Cardiogenic shock is a low cardiac output state resulting from inadequate tissue perfusion despite adequate left ventricular filling pressures. It is usually caused by acute myocardial infarction which accounts for about 80% of cases. Clinically, it is defined by sustained hypotension with signs of hypoperfusion and a systolic blood pressure less than 90 mmHg for at least 30 minutes or the need for vasopressor/inotropic support. The mortality rate for cardiogenic shock remains high at over 80% despite advances in management. Early diagnosis and aggressive treatment including revascularization, inotropic support, and mechanical circulatory support are aimed at improving outcomes.
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.
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its serum level is tightly regulated between 3.5-5 mEq/L. Mechanisms involve sodium-potassium pumps and renal excretion. Causes of hyperkalemia include reduced renal excretion, intracellular shifts, and inadequate aldosterone levels. Symptoms range from none to muscle weakness to arrhythmias. Treatment focuses on antagonizing cardiac effects, driving potassium intracellularly, and removing excess potassium.
Pericardial effusion occurs when fluid accumulates in the pericardial cavity surrounding the heart. Normally up to 50 mL of fluid is present but the cavity can hold up to 2 L if the fluid builds up slowly. Fluid accumulation can negatively impact heart function. There are four main types of pericardial effusion: transudative, exudative, hemorrhagic, and malignant. The two main causes are an imbalance of fluid pressures that allows fluid to leave blood vessels, or inflammation/injury of the pericardium. Symptoms include chest pain, fever, fatigue, and shortness of breath. Fluid is collected via pericardiocentesis and tested based on
This document provides an overview of cardiovascular shock, including its definition, physiology, classification, causes, symptoms, treatment, and complications. The main types of shock discussed are hypovolemic, distributive, cardiogenic, and obstructive shock. Hypovolemic shock, caused by decreased blood volume from hemorrhage, burns, or fluid loss, is described in more detail. The body's compensatory responses to hypovolemia like vasoconstriction and increased heart rate are explained. The progression of shock and factors that can cause recovery or lead to irreversible shock are also summarized.
Shock is a clinical state characterized by inadequate tissue perfusion resulting from insufficient oxygen and substrate delivery to meet metabolic demands. There are several types of shock defined by etiology (hypovolemic, cardiogenic, distributive) and effects on blood pressure (compensated, decompensated). Signs of shock include tachycardia, altered mental status, and decreased urine output. Treatment involves rapid fluid resuscitation and vasoactive drugs like dopamine, epinephrine, and norepinephrine to support cardiac output as needed.
Cardiogenic shock is the failure of the heart to pump enough blood to meet the body's needs due to loss of contractile function. It most commonly occurs after a myocardial infarction which damages a significant portion of the left ventricle. Symptoms include low blood pressure, rapid breathing, decreased urine output, and confusion. Treatment involves oxygen, medications to improve contractility and reduce workload, and mechanical devices like IABP if needed. Nursing care focuses on monitoring circulation and tissue perfusion, managing devices, and addressing patient anxiety.
This document provides an overview of shock, including its history, definitions, types, pathophysiology, signs and symptoms, and management. It discusses the four main types of shock - cardiogenic, obstructive, hypovolemic, and distributive - describing the insult, physiologic effects, and compensatory mechanisms for each. Treatment of shock focuses on the ABCDE approach - airway, breathing, circulation, disability, and exposure. Restoring adequate circulation through fluid resuscitation is key. The goals of treatment are to optimize oxygen delivery and achieve endpoints of resuscitation like urine output and hemodynamic parameters.
This document provides an overview of shock, including its classification, causes, pathophysiology, clinical features, and management. It defines shock as a clinical manifestation of inadequate tissue perfusion and cellular hypoxia due to a reduction in effective circulating blood volume. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The document examines the cellular, microvascular, and systemic pathophysiological changes that occur in shock, as well as compensatory mechanisms and signs of decompensation. Clinical features, diagnosis, and general management principles are also summarized.
Hypovolemic shock is a life-threatening emergency in which severe blood or other fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working.
Hypovolemic shock is a dangerous condition that happens when suddenly lose a lot of blood or fluids from body. This drops blood volume, the amount of blood circulating in body. That’s why it’s also known as low-volume shock.
This document provides information about shock and its nursing management. It begins with an introduction to shock, defining it as a life-threatening condition caused by inadequate blood flow to tissues. It then outlines the stages of shock as initial, compensatory, progressive, and irreversible. The main types of shock discussed are hypovolemic, cardiogenic, neurogenic, septic, and anaphylactic. For each type, causes, signs and symptoms, and nursing care are described. The document concludes with test questions to assess learning.
Cardiogenic shock occurs when the heart is unable to pump sufficiently due to issues like a myocardial infarction. It leads to low blood flow and organ dysfunction. Symptoms include chest pain, breathing issues, and hypotension. Treatment focuses on optimizing oxygen delivery through ventilation, volume resuscitation, inotropes, and procedures like IABP or surgery if needed. Nursing care monitors for worsening and supports the patient through the condition.
Cardiogenic shock occurs when the heart is damaged and unable to pump enough blood to vital organs. This causes blood pressure to drop and organs to fail. It is a serious medical emergency. The heart loses its ability to contract effectively due to lack of oxygen and nutrients. Clinical features include low blood pressure, confusion, and poor organ perfusion. Treatment aims to improve cardiac function and oxygen delivery through medications, surgeries like bypass and stenting, and devices like intra-aortic balloon pumps. Nursing care monitors the patient's condition and supports the medical management of this critical condition.
This document discusses hypovolemic shock, which is characterized by decreased circulating blood volume resulting in reduced tissue perfusion. It can be hemorrhagic, due to blood loss from wounds or internal bleeding, or non-hemorrhagic from digestive, renal, skin or third space losses. The pathophysiology involves a macrocirculatory reaction with centralization of circulation and microcirculatory changes impairing capillary function. Treatment involves stopping losses, aggressive volume resuscitation with isotonic fluids, monitoring for efficacy, and inotropic support if needed to boost cardiac output after volume is restored.
Shock and its management is summarized as follows:
1. Shock is a life-threatening condition characterized by inadequate tissue perfusion due to reduced circulating blood volume or cardiac output.
2. Shock is classified as hypovolemic, cardiogenic, septic, traumatic, neurogenic, or hypoadrenal based on etiology.
3. The pathophysiology involves reduced circulating volume, impaired tissue oxygenation, and release of inflammatory mediators, progressing from compensated to decompensated to irreversible stages if left untreated.
This document discusses hemorrhagic shock, which is a condition of reduced tissue perfusion caused by a loss of circulating blood volume from trauma or gastrointestinal bleeding. It outlines the pathophysiology, signs and symptoms, diagnostic evaluation including lab tests and imaging, and management with fluid resuscitation, blood transfusions, controlling the source of bleeding surgically if needed, and treating complications. The key points are that hemorrhagic shock results from acute blood loss, causes decreased cardiac output and blood pressure, and must be promptly diagnosed and treated by replacing fluid volume and identifying and stopping the source of bleeding.
Ventricular fibrillation occurs when the ventricles of the heart quiver due to uncoordinated contractions of the heart muscle fibers. This prevents the heart from effectively pumping blood throughout the body. Ventricular fibrillation can be caused by stress, damage, or electrical changes to heart tissue. It requires immediate treatment through defibrillation or medications to prevent organ damage or death from lack of oxygen.
THIS PRESENTATION WILL COVER THE FOLLOWING AREAS
Definitions
Buffer systems
Regulatory systems
Anion Gap and Osmolar gap
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Pulmonary edema is fluid accumulation in the lungs caused by fluid leaking from blood vessels into the lung tissue and air spaces. It can be caused by issues that increase pressure in the blood vessels of the lungs like heart failure, or by problems that damage the blood vessel walls. Symptoms include shortness of breath, cough, and anxiety. Treatment depends on the underlying cause but aims to reduce fluid buildup and support breathing. Differentiating cardiogenic from non-cardiogenic pulmonary edema involves considering medical history, symptoms, physical exam findings, and chest imaging results.
Cardiogenic shock is a low cardiac output state resulting from inadequate tissue perfusion despite adequate left ventricular filling pressures. It is usually caused by acute myocardial infarction which accounts for about 80% of cases. Clinically, it is defined by sustained hypotension with signs of hypoperfusion and a systolic blood pressure less than 90 mmHg for at least 30 minutes or the need for vasopressor/inotropic support. The mortality rate for cardiogenic shock remains high at over 80% despite advances in management. Early diagnosis and aggressive treatment including revascularization, inotropic support, and mechanical circulatory support are aimed at improving outcomes.
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.
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its serum level is tightly regulated between 3.5-5 mEq/L. Mechanisms involve sodium-potassium pumps and renal excretion. Causes of hyperkalemia include reduced renal excretion, intracellular shifts, and inadequate aldosterone levels. Symptoms range from none to muscle weakness to arrhythmias. Treatment focuses on antagonizing cardiac effects, driving potassium intracellularly, and removing excess potassium.
Pericardial effusion occurs when fluid accumulates in the pericardial cavity surrounding the heart. Normally up to 50 mL of fluid is present but the cavity can hold up to 2 L if the fluid builds up slowly. Fluid accumulation can negatively impact heart function. There are four main types of pericardial effusion: transudative, exudative, hemorrhagic, and malignant. The two main causes are an imbalance of fluid pressures that allows fluid to leave blood vessels, or inflammation/injury of the pericardium. Symptoms include chest pain, fever, fatigue, and shortness of breath. Fluid is collected via pericardiocentesis and tested based on
This document provides an overview of cardiovascular shock, including its definition, physiology, classification, causes, symptoms, treatment, and complications. The main types of shock discussed are hypovolemic, distributive, cardiogenic, and obstructive shock. Hypovolemic shock, caused by decreased blood volume from hemorrhage, burns, or fluid loss, is described in more detail. The body's compensatory responses to hypovolemia like vasoconstriction and increased heart rate are explained. The progression of shock and factors that can cause recovery or lead to irreversible shock are also summarized.
Hypovolemic shock results from trauma that causes blood loss, decreasing blood volume and lowering blood pressure. The body initially compensates through mechanisms like catecholamine release, but can progress to decompensated then irreversible shock if left untreated. Treatment focuses on fluid resuscitation through IV fluids to restore blood volume.
Cardiogenic shock occurs when the heart cannot adequately circulate blood, usually due to a heart attack damaging the left ventricle. It presents with pulmonary edema but normal blood pressures. Treatment centers on supportive care while the heart recovers.
Neurogenic shock is caused by spinal cord injury disrupting nerve signals, causing widespread vessel dilation and low blood pressure. It presents with warm skin and
This document provides information on shock, including its definition, types, pathophysiology, clinical features, and management. It defines shock as a state of inadequate tissue perfusion and oxygenation that can lead to organ dysfunction and death. The main types of shock discussed are hypovolemic, septic, and cardiogenic shock. For each type, the document outlines their pathophysiology, signs and symptoms, and general management approach. Overall, it serves as an overview of shock for medical students, covering the essential details of definitions, types, effects on organ systems, and clinical distinctions between compensated and decompensated states of shock.
2. Hypovolemic, Septic and Cardiogenic Shock.pptxfarihinizhar
Hypovolemic, septic, and cardiogenic shock are three types of shock discussed in the document. Hypovolemic shock occurs due to reduced circulating volume from external or internal bleeding or fluid losses. Septic shock results from toxins released during bacterial infections. Cardiogenic shock is caused by decreased cardiac output due to conditions like heart attacks or heart muscle damage that impair the heart's ability to pump effectively. Treatment for the different shock types involves immediate control of bleeding, fluid resuscitation, antibiotics for infection, and vasopressors or inotropes to support blood pressure and cardiac function.
The patient presented with signs of septic shock including altered mental status, tachypnea, and hypotension. He has a history of multiple comorbidities putting him at risk for infection. Initial workup showed bilateral lung crepitations and fever, suggestive of pneumonia as the source of sepsis. Management involved fluid resuscitation, vasopressors to maintain blood pressure, broad-spectrum antibiotics, and monitoring for signs of organ dysfunction due to systemic inflammatory response.
Shock is characterized by impaired cellular metabolism and decreased tissue perfusion. There are four main types of shock: hypovolemic, vasogenic, cardiogenic, and neurogenic. The stages of shock progression include initial, compensatory, progressive, and irreversible. Management aims to restore fluid volume, increase cardiac output, and remove the precipitating cause. Nursing care focuses on monitoring vital signs, administering IV fluids and oxygen, maintaining perfusion, preventing complications, and supporting organ function.
This document summarizes the key aspects of shock. Shock occurs when there is inadequate oxygen delivery to tissues, which can lead to cellular damage and death if left untreated. The main causes of shock discussed are hypovolaemic, septic, and cardiogenic shock. Signs and symptoms of shock include low blood pressure, fast heart rate, pale skin, confusion, and low urine output. Management involves identifying the type and stage of shock to guide fluid resuscitation and drug therapy aimed at restoring adequate circulation and oxygen delivery to tissues.
This document defines and classifies shock. It discusses the pathophysiology of different types of shock including hypovolaemic, cardiogenic, obstructive, distributive, endocrine, and adrenal insufficiency shock. It describes the clinical features of shock and the initial management including airway control, intravenous fluids, blood transfusion, vasopressors, and inotropes as needed.
SHOCK SYNDROMESHOCK SYNDROME
• Shock is a condition in which the cardiovascular system
fails to perfuse tissues adequately
• An impaired cardiac pump, circulatory system, and/or
volume can lead to compromised blood flow to tissues
• Inadequate tissue perfusion can result in:
– generalized cellular hypoxia (starvation)
– widespread impairment of cellular metabolism
– tissue damage organ failure
– death
ATHOPHYSIOLOGYPATHOPHYSIOLOGY
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
1) Shock is a condition where the cardiovascular system fails to adequately perfuse tissues due to impaired cardiac pump function, circulatory issues, or low blood volume.
2) The main types of shock are hypovolemic (low blood volume), cardiogenic (impaired heart function), and distributive (blood vessel problems).
3) Hypovolemic shock results from internal or external fluid loss leading to decreased circulating volume and tissue perfusion. Cardiogenic shock occurs due to impaired left ventricular pumping ability despite normal blood volume.
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.
Shock: A review of hypovolemic, septic, cardiogenic and neurogenic shock.Joseph A. Di Como MD
A review of different types of shock encountered in patients. Hypovolemic, septic, cardiogenic and neurogenic shock. We review etiology, pathophysiology, diagnosis, treatment and how to differentiate between them.
Shock in pediatric patients can be caused by several factors and requires early recognition and treatment to prevent progression. It is defined as inadequate oxygen delivery to meet metabolic demands. The main types are hypovolemic, distributive, cardiogenic, and obstructive shock. Septic shock is a major cause of mortality and morbidity in children. The goals of treatment are to increase oxygen delivery, decrease demands, and increase oxygen content through rapid fluid resuscitation and inotropic support. Early identification and treatment of the underlying cause can help avoid irreversible organ damage from shock.
Management of hemmorhagic and non hemmorhagic shockMaazBangash
1) Cardiogenic shock, distributive shock, hemorrhagic shock, and obstructive shock are the main types of shock discussed in the document.
2) Cardiogenic shock results from inadequate blood flow due to heart dysfunction and causes tissue hypoperfusion. Treatments focus on restoring blood flow through medications, procedures like angioplasty, and mechanical circulatory support.
3) Hemorrhagic shock occurs when more than 20% of blood volume is lost, such as from severe bleeding. Internal bleeding can be concealed and suggested by symptoms like dizziness. Treatments control hemorrhaging through pressure dressings, tourniquets, and hemostatic dressings.
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.
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.
This document provides an overview of shock, including its definition, pathophysiology, classification, signs and symptoms, initial management, and specific types such as hypovolemic, septic, cardiogenic, and obstructive shock. It defines shock as inadequate tissue perfusion and oxygen delivery, discusses the body's compensatory mechanisms and their failure in severe shock. It classifies shock into hypovolemic, cardiogenic, distributive, and obstructive types and provides details on managing each type, including damage control resuscitation for hemorrhagic shock and use of vasopressors for neurogenic shock. Key goals in shock management are outlined as well as factors like lactate and base deficit that can guide res
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
DECLARATION OF HELSINKI - History and principlesanaghabharat01
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2. Definition
Shock is a state of inadequate perfusion, which does not
sustain the physiologic needs of organ tissues.
A physiological state characterized by a significant,
systemic reduction in tissue perfusion, resulting in decreased
tissue oxygen delivery and insufficient removal of cellular metabolic
products, resulting in tissue injury.
4. Pathophysiology
Alteration in hemodynamic results in a drop in arterial blood
pressure by one of these mechanisms:
• Decrease in cardiac output (ability of heart to supply adequate
circulation)
• Decrease in circulating blood volume
• Increase in size of vascular bed
8. Early reversible and compensatory shock
• Mean arterial pressure drops 10 -15 mmHg
• Decrease in circulating blood volume (25-35%) 1000ml
• Sympathetic nervous system stimulated; release of
catecholamine
9. Early reversible and compensatory shock
Findings
• Increase in heart rate and contractility
• Increase in peripheral vasoconstriction
• Circulation maintained, but can only be sustained short time
without harm to tissues
• Underlying cause of shock must be addressed and corrected or
will progress to next stage
10. Intermediate or progressive shock
• Further drop in MAP (20%)
• Increase in fluid loss (1800 – 25400 ml)
• Vasoconstriction continues and leads to oxygen deficiency
• Body switches to anaerobic metabolism forming lactic acid as a
waste product
11. Intermediate or progressive shock
Findings
• Body increases heart rate and vasoconstriction
• Heart and brain become hypoxic
• More severe effects on other tissues which become: ischemic
and anoxic
• State of acidosis with hyperkalemia develops
Needs rapid treatment
12. Refractory or irreversible shock
• Tissues are anoxic, cellular death widespread
• Even with restoration of blood pressure and fluid volume there is
too much damage to restore homeostasis of tissues
• Cellular death leads to tissue death; vital organs fail and death
occurs
14. Cardiovascular system
• Initially: slight tachycardia, normal blood pressure
• Progresses to weak, rapid pulse with dysrhythmias
• Progressive decrease in systolic and diastolic blood pressures
with narrowing of pulse pressure; blood pressure becomes
inaudible
15. Respiratory system
• Initially: Increased respiratory rate, but gas exchange is
impaired; leads to anaerobic metabolism and development of
acidosis
• Acute Respiratory Distress Syndrome (ARDS): complication of
decreased lung perfusion
16. Gastrointestinal and Hepatic
• GI organs become ischemic, with blood circulation shunted to
heart and brain
Complications :
• Stress Ulcers
• Paralytic Ileus
• Altered liver metabolism: hypoglycemia, fat breakdown leads to
ketones and metabolic acidosis
17. • Neurologic system
Develops cerebral hypoxia
Restlessness initially, then altered level of consciousness,
lethargy, coma ,Thirsty from dehydration
• Renal
Decreased kidney perfusion leads to oliguria (urine output
< 0.5 ml/kg/hr)
• Skin
Skin: cool, pale, hypothermic
18. Causes of Shock [-]
• Severe or sudden blood loss
• Large drop in body fluids
• Myocardial infarction
• Major infections
• High spinal injuries
• Anaphylaxis
• Extreme heat or cold
21. Hypovolemic Shock
A medical or surgical condition in which rapid fluid loss
results in multiple organ failure due to inadequate circulating
volume and subsequent inadequate perfusion. Most often,
hypovolemic shock is secondary to rapid blood loss
(hemorrhagic shock).
22. SRUP
• Hemorrhage: Overt or occult
• Reduction in circulating volume
• Reduction in venous return and CO
• O2 supply-demand imbalance
• Lactic acidosis
• Reduction in venous oxygen saturation
• Non hemorrhagic hypovolemic
– Severe burns, vomiting and diarrhea
23. • Decreased preload->small ventricular end-diastolic volumes ->
inadequate cardiac generation of pressure and flow
• Causes:
-- bleeding: trauma, GI bleeding, ruptured aneurysms,
hemorrhagic pancreatitis
-- protracted vomiting or diarrhea
-- adrenal insufficiency; diabetes insipidus
-- dehydration
-- third spacing: intestinal obstruction, pancreatitis, cirrhosis
24.
25.
26. Cause
• Acute external blood loss secondary to penetrating trauma and severe GI
bleeding disorders are 2 common causes of hemorrhagic shock.
• Hemorrhagic shock can also result from significant acute internal blood
loss into the thoracic and abdominal cavities
• Two common causes of rapid internal blood loss are solid organ injury
and rupture of an abdominal aortic aneurysm.
• Hypovolemic shock can result from significant fluid (other than blood)
loss. Two examples of hypovolemic shock secondary to fluid loss include
refractory gastroenteritis and extensive burns
27. Pathophysiology:
• The human body responds to acute hemorrhage by activating
the following major physiologic systems:
• The hematologic
• Cardiovascular
• Renal
• Neuroendocrine systems.
28. The hematologic
• The hematologic system responds to an acute severe blood loss
by activating the coagulation cascade and contracting the
bleeding vessels (by means of local thromboxane A2 release).
• In addition, platelets are activated (also by means of local
thromboxane A2 release) and form an immature clot on the
bleeding source.
• The damaged vessel exposes collagen, which subsequently
causes fibrin deposition and stabilization of the clot.
• Approximately 24 hours are needed for complete clot fibrination
and mature formation.
29. Cardiovascular
• The cardiovascular system initially responds to hypovolemic
shock by increasing the heart rate, increasing myocardial
contractility, and constricting peripheral blood vessels.
• This response occurs secondary to an increased release of
norepinephrine and decreased baseline vagal tone (regulated
by the baroreceptors in the carotid arch, aortic arch, left atrium,
and pulmonary vessels).
• The cardiovascular system also responds by redistributing
blood to the brain, heart, and kidneys and away from skin,
muscle, and GI tract.
30. Renal
• The renal system responds to hemorrhagic shock by stimulating an
increase in renin secretion from the juxtaglomerular apparatus.
• Renin converts angiotensinogen to angiotensin I, which subsequently is
converted to angiotensin II by the lungs and liver
• Angiotensin II has 2 main effects, both of which help to reverse
hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and
stimulation of aldosterone secretion by the adrenal cortex.
• Aldosterone is responsible for active sodium reabsorption and
subsequent water conservation.
31. Neuroendocrine systems
• The neuroendocrine system responds to hemorrhagic shock by
causing an increase in circulating antidiuretic hormone (ADH).
• ADH is released from the posterior pituitary gland in response to
a decrease in BP (as detected by baroreceptors) and a
decrease in the sodium concentration (as detected by
osmoreceptors).
• ADH indirectly leads to an increased reabsorption of water and
salt (NaCl) by the distal tubule, the collecting ducts, and the
loop of Henle.
32. Clinical Signs of Acute Hemorrhagic
Shock
Parameter Class I Class II Class III Class IV
Blood loss (%) <15 15-30 30-40 >40
Blood loss (ml) <750 750-1500 1500-2000 >2000
Heart rate (bpm) <100 >100 >120 >140
Blood pressure Normal Orthostatic Hypotension Severe hypotension
CNS symptom Normal Anxious Confused Obtunded
33. Signs of Shock
• Cold, clammy and pale skin
• Rapid, weak pulse
• Shallow, rapid breathing
• Oliguria
• Reduction in MAP
• Cyanosis
• Loss of consciousness
34. The 4 areas in which life-threatening
hemorrhage can occur are as follows: chest,
abdomen, thighs, and outside the body.
35. • The chest should be auscultated for decreased breath
sounds, because life-threatening hemorrhage can occur
from myocardial, vessel, or lung laceration
• The abdomen should be examined for tenderness or
distension, which may indicate intraabdominal injury
36. • The thighs should be checked for deformities or
enlargement (signs of femoral fracture and bleeding into
the thigh).
• The patient's entire body should then be checked for
other external bleeding
38. Treatment of Shock
**Increase tissue perfusion and oxygenation status
• Maintain airway
• Control bleeding
• Baseline vital signs
• Level of consciousness
39. Treatment of Shock
• Positioning
• ABCD approach
• Fluid therapy
• Drug therapy
• Keep patient at normal temperature
– Prevent hypothermia
– Minimize effect of shock
• On-going assessment - every 10-15 minutes
40. • Crystalloid solutions for intravascular volume replenishment are
typically isotonic (e.g. 0.9% saline or Ringer's lactate [RL]).
• Both 0.9% saline and RL are equally effective; RL may be
preferred in hemorrhagic shock because it somewhat minimizes
acidosis.
41. • Colloid solutions (e.g. hydroxyethyl starch, albumin, dextrans)
are also effective for volume replacement during major
hemorrhage.
• Despite theoretical benefits over crystalloid, no differences in
survival have been proven.
• Both dextrans and hydroxyethyl starch adversely affect
coagulation when > 1.5 L is given.
42. • Blood typically is administered as packed RBCs, which should
be cross-matched, but in an urgent situation, 1 to 2 units of type
O Rh-negative blood is an acceptable alternative.
• When > 1 to 2 units are transfused (e.g. in major trauma), blood
is warmed to 37° C.
• Patients receiving > 8 to 10 units may require replacement of
clotting factors with infusion of fresh frozen plasma or
cryoprecipitate and platelet transfusion
43. Route and Rate of Administration
• Standard, large (eg, 14- to 16-gauge) peripheral IV catheters are
adequate for most fluid resuscitation.
• With infusion pump they typically allow infusion of 1 L of
crystalloid in 10 to 15 min and 1 unit of packed RBCs in 20 min.
44. • For patients at risk of exsanguination, a large (eg, 8.5 French)
central venous catheter provides more rapid infusion rates; a
pressure infusion device can infuse 1 unit packed RBCs in < 5
min.
45. • Patients in shock typically require and tolerate infusion at the
maximum rate. Adults are given 1 L of crystalloid (20 mL/kg in
children) or, in hemorrhagic shock, 5 to 10 mL/kg of colloid or
packed RBCs, and the patient is reassessed.
• An exception is a patient with cardiogenic shock who typically
does not require large volume infusion.
47. Invasive monitoring
• Essential in the definitive treatment
• Direct arterial pressure
• Central venous pressure
• Cardiac output
48. • The actual endpoint of fluid administration in shock is
normalization of DO2.
• However, this parameter is not often measured directly.
Surrogate endpoints include clinical indicators of end organ
perfusion and measurements of preload.
• Adequate end organ perfusion is best indicated by urine output
of > 0.5 to 1 mL/kg/h
49. • Heart rate, mental status, and capillary refill may be affected by
the underlying disease process and are less reliable markers.
• Because of compensatory vasoconstriction, mean arterial
pressure (MAP) is only a rough guideline; organ hypoperfusion
may be present despite apparently normal values
50. • Because urine output does not provide a minute-to-minute
indication, measures of preload may be helpful in guiding fluid
resuscitation for critically ill patients
• Central venous pressure (CVP) is the mean pressure in the
superior vena cava, reflecting right ventricular end-diastolic
pressure or preload.
51. • Normal CVP ranges from 2 to 7 mm Hg (3 to 9 cm H20). A sick
or injured patient with a CVP < 3 mm Hg is presumed to be
volume depleted and may be given fluids with relative safety.
53. Criteria for Four Categories of the Systemic
Inflammatory Response Syndrome
1. Systemic Inflammatory Response Syndrome (SIRS)
Two or more of the following:
– Temperature (core) >38°C or <36°C
– Heart rate >90 beats/min
– Respiratory rate of >20 breaths/min for patients spontaneously ventilating or a
PaCO2 <32 mm Hg
– White blood cell count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature
(band) cells in the peripheral blood smear
54. Criteria for Four Categories of the Systemic
Inflammatory Response Syndrome
2. Sepsis
Same criteria as for SIRS but with a clearly established focus of infection
3. Severe Sepsis
Sepsis associated with organ dysfunction and hypoperfusion
Indicators of hypoperfusion:
- Systolic blood pressure <90 mmHg
- > 40 mmHg fall from normal systolic blood pressure
- Lactic acidemia
- Oliguria
- Acute mental status changes
55. Phases of Septic Shock
• Warm Phase (early): skin flushed, warm due to vasodilatation
• Cold Phase (late): skin cool due to fluid deficit with shock
57. Risk factors
– Diabetes
– Diseases of the genitourinary system, biliary system, or intestinal system
– Immunocompromised host such as AIDS , Leukemia , steroid medications
– Indwelling catheters
– Recent surgery or medical procedure
58. Septic Shock in trauma patients
• Develops 2 - 5 days after injury occurs
• Carries a poor prognosis
• Assess for:
– Penetrating abdominal injuries
– Signs of infection
– Warm pink skin and dry elevated body temperature
– Tachycardia
– Wide pulse pressures
62. Anaphylactic shock
• DEFINITION
– Anaphylaxis is a sudden-onset, life-threatening type I hypersensitivity
• Anaphylaxis results from sudden release into the systemic circulation of histamine,
tryptase, and other inflammatory mediators from basophiles and mast cells.
65. Management of anaphylaxis
• Assessment of airway, breathing, circulation
• Epinephrine is the drug of choice
– IM every 5 to 15 minutes to control symptoms and blood pressure
• Oxygen administration
• Fluid replacement
– Normal saline is preferred, because lactated Ringers may contribute to metabolic
acidosis
66. • Vasopressors
– should be administered if epinephrine injections fail to alleviate hypotension
– Dopamine increases the force and rate of myocardial contractions while
maintaining or enhancing renal and mesenteric blood flow
• Antihistamines
• Inhaled B2 agonists
• Corticosteroids
68. Anaphylactic Shock
• Rapid onset
• Primary systems:
– Cardiovascular, Respiratory
– Skin, Gastrointestinal, coagulation
• Face, pharynx and laryngeal oedema
• Adrenaline is life saving
69. Anaphylactic Shock
• Diffuse vasodilatation
• Increase size of vascular bed
• Blood is trapped in small vessels and viscera
• Temporary loss in total circulatory volume
• Sudden severe allergic reaction to:
– Drugs, Toxins, Foods, Plants
70. Symptoms
• Apprehension and flushing
• Wheezing or shortness of breath & cough
• Rapid, weak pulse
• Cyanosis
• Generalized itching or burning
• Watering and itching of the eyes
• Hypotension
• Coma
71. Evaluation of Shock
• Internal or external hemorrhage
• Underlying cardiac problems
• Sepsis
• Trauma to spine cord
• Contact with known allergic substance
• Determine amount of blood loss
• How long has casualty been bleeding?
78. Obstructive Shock
•Aortic stenosis
•Resistance to systolic ejection causes decreased cardiac function
•Chest pain with syncope
•Systolic ejection murmur
•Diagnosed with echo
•Rx: Valve surgery
79. Etiology & Hemodynamic Changes in Shock
Etiology of shock example CVP CO SVR VO2 sat
preload hypovolemic low low high low
contractility cardiogenic high low high low
afterload Hyperdynamic Low/Hi High Low High
Septic gh
Hypodynamic Low/Hi Low High Low/High
Septic gh
Neurogenic Low Low Low Low
Anaphylactic Low Low Low Low