STUDY - Technical - New Dacian's Medicine
The
Shock (3)
Translation Draft
From the point of view of pathogenesis we are dealing with hypovolemic shock, extracardiac obstructive shock, cardiogenic shock and distribution shock. In hypovolemic, cardiogenic and obstructive extracardiac shock, low tissue infusion is determined by inadequate cardiac output. In distribution shock, low blood pressure occurs by reducing systemic vascular resistance and maldistribution of blood flow in microcirculation, being a major factor contributing to multiple organ failure.
Hypovolemic shock has been much studied and its stages can be easily quantified on experienced animals by phasing out blood from the intravascular space. Many of the data from these studies also apply to other forms of shock characterized by reduced heart rate. When 10% of the total blood volume is lost, the compensatory mechanisms are activated and maintain cardiac output, despite the decrease in filling pressure and beating volume.
The increase in adrenergic activity, resulting both from stimulation of the sympathetic system and from the release of catecholamines from the adrenal, leads to arterial vasoconstriction, venoconstriction with increased venous return and tachycardia. Reduction of hydrostatic pressure in capillaries, together with precapillary arteriolar vasoconstriction, favors the transwelding of fluid from extracellular space into vessels. The contraction of intravascular volume leads to activation of the renin-angiotensin system, increased release of antidiuretic hormone and increased levels of ACTH and aldosterone (thus defending renal retention of sodium and water).
These adaptations may be sufficient to maintain arterial pressure and orthostatic hypotension may be the only sign of hypovolemia. However, if 20-25% of blood volume is rapidly lost, the compensatory mechanisms are overcome and clinical signs of shock appear. Heart rate decreases and hypotension occurs despite generalized vasoconstriction.
Reduction of tissue infusion leads to the installation of anaerobic metabolism, manifested by increased lactate levels and metabolic acidosis. Adrenergic reflex stimulation intensifies and flow is redistributed to maintain heart and brain infusion. This redistribution reflects the predominance of blood flow self-regulation in the cerebral and coronary systems, in contrast to the dependence on the sympathetic tone of luxuries in other organs.
Excessive vasoconstriction can reduce the flow to the point where cellular damage occurs. Damage to the capillary endothelium leads to loss of fluids and proteins in circulation, which accentuates hypovolemia. In the end, multiorganic insufficiency occurs.
As for cardiogenic shock, when myocardial function is depressed, several compensatory mechanisms are activated. Sympathetic stimulation increases heart rate and contractility, and fluid renal retention increases pre-pregnancy. if cardiac output cannot be maintained through these mechanisms, the blood flow is redistributed to maintain cerebral and cardiac infusion.
When heart failure occurs, the compensatory mechanisms can slowly become dysfunctional. Increased heart rate and contractility can increase myocardial oxygen demand and exacerbate ischemia. In addition, tachycardia decreases diastolic filling time, further compromising myocardial infusion. Fluid retention may increase intravascular volume until pulmonary congestion and hypoxia appear. Ischemia also decreases diastolic compliance of the ventricle, subsequently increasing pressure in the left atrium and aggravating pulmonary congestion.
Vasoconstriction to maintain arterial pressure compromises renal, splahinic and skin infusion. Increased systemic vascular resistance through vasoconstriction increases post-pregnancy, further affecting cardiac function and increasing myocardial oxygen demand. The latter, under the conditions of an inadequate infusion, leads to aggravation of ischemia and the appearance of a vicious cycle that must be interrupted to prevent an inexorable progression to the death of the patient.
Cardiac tamponade results from the accumulation of fluid in the pericardium, with a consecutive increase in intrapericardial pressure. It may be acute (e.g. hemopericardium associated with open or closed thorax trauma) or subacute (e.g. uremia, irradiation, neoplasm, infection or connective tissue disease). Tamponade may occur after cardiac surgery due to compression of the heart by a mediastinal hematoma or postpericardiotomy syndrome.
The increase in intrapericardial pressure and the consequent impairment of cardiac filling through a pericardial overflow depends on the rate of fluid accumulation, fluid volume and pericardial distensibility. As intrapericardial pressure increases, the gradient between peripheral venous pressure and that in the right atrium decreases and diastolic filling is compromised. When pericardial pressure acutely affects diastolic filling, adrenergic stimulation causes tachycardia, increased ejection fraction and arterial vasoconstriction to maintain blood pressure.
Over a period of hours or days, fluid retention increases venous pressure which favors filling. Subacutely installed tamponade is compensated and shows signs of venous congestion with dilation of the neck veins. Exceeding compensation leads to shock with tachycardia, tachypnea, decreased heart rate, peripheral vasoconstriction and hypotension.
In the case of distribution shock, tissue hypoperfusion results from abnormal sunting of a normal or increased cardiac output. Although differential diagnosis also includes anaphylaxis, drug overdose, neurogenic shock and Addisonian crisis, the most important and common etiology is septic shock. In some forms of shock distribution, blood flow in different organs seems appropriate, but exists in "metabolic blockage" induced by mediators at the tissue level, preventing the proper use of oxygen and other nutrients. Lactic acid accumulates because cells cannot normally use the pathways of oxidative metabolism.
Thus, in some patients, blood flow through large vessels to tissues is normal, but abnormalities in microvascular flow or the inability of cells to use nutrients lead to the spread of cellular dysfunction and the appearance of shock. Septic shock occurs when infectious agents or infection-induced mediators in the circulation produce cardiovascular decompensation.
Septic shock is characterized at onset by increased cardiac output and low systemic vascular resistance. Septic shock usually begins with the release of microorganisms into circulation from the outbreak of infection. Toxic effects can be caused by microorganisms, their components such as endotoxins, lipopolysaccharides associated with the external membrane of gram negative bacteria or with the release of exotoxins. The most important pathological effect of these microorganisms or toxins can be determined by stimulating the release of large amounts of endogenous mediators of inflammation.
Endotoxin is a potential trigger for the release of cytokines, especially interleukins and TNF, which amplifies the systemic response to endotoxin by stimulating neutrophils, endothelial cells and platelets and inducing the release of other mediators such as PAF, arachidonic acid metabolites, complements, kinins, histamine and endorphins. The effects of these mediators can be divided into two broad categories: effects on peripheral vessels and heart effects. Both exogenous and endogenous mediators have been shown to mediate vasodilation in sepsis.
Taking low doses of endotoxin to healthy volunteers produces a decrease in blood pressure, an increase in heart rate and a reduction in systemic vascular resistance similar to that of sepsis. A similar vasodilation with increased cardiac output occurs after administration of TNF, IL-1 or IL-2. A key mediator of vasodilation in response to cytokines is nitric oxide, which consists of anginin by the action of nitric enzyme oxide synthetase.
Endotoxin, TNF and interleukins can stimulate nitric oxide sintetase acid which can be induced in macrophages and smooth vascular muscle cells, with the release of a large amount of this vasodilating substance. Endotoxin can also activate the intrinsic pathway of coagulation with the fibrinolytic system, which can lead to the storage of microaggregates of fibrin in microvas, obstructing the flow and accentuating tissue hypoxia.
TNF and interleukins activate both endothelial cells and neutrophils, which cause neutrophil aggregation and consecutive microcirculatory insufficiency. Although patients with septic shock have increased cardiac output, ejection fractions of the right and left ventricles are low. The dilation of the ventricles allows to maintain the normal beating volume despite the decrease in myocardial contractility and tachycardia causes an increased cardiac output.
Patients with sepsis also show a decrease in the systolic contractile response of the ventricle to an increased volume, indicating a reduction in myocardial performance. The responsible mechanisms have not been fully clarified (it appears that cytokines, in particular TNF and IL-1, play an important role, possibly through the generation of nitric oxide). If the shock persists, the combination of peripheral vascular abnormalities with myocardial depression leads to a mortality of about 50%.
Death occurs through severe hypotension and/ or multi-organic failure. Hypotension is associated with a severe and irreversible reduction in systemic vascular resistance. Sometimes (at about 10% of deaths) myocardial depression is so severe that heart rate decreases by increasing hypotension.
I will complete this post with the presentation of some elements about clinical manifestations. Some symptoms and signs are the same for all types of shock. This condition is almost always characterized by hypotension, which in adults generally means an average blood pressure below 60 mmHg. However, when interpreting any given level of blood pressure, the chronic level of blood pressure should be taken into account (patients with severe chronic hypertension may be relatively hypotensive when the average blood pressure drops by 40 mmHg, even if it is more than 60 mmHg). Conversely, patients with chronic hypotension will not show clinical signs until the average pressure drops below 50 mmHg.
Common manifestations in shock are tachycardia, oliguria, altered general condition and cold and pale extremities, indicating reduced blood flow to the skin. Metabolic acidosis, often due to increased blood levels of lactic acid, reflects the lasting decrease in blood flow to tissues. Other clinical manifestations are specific to each type of shock. Patients with hypovolemic shock frequently have a history of gastrointestinal bleeding, haemorrhages with other localization or clear evidence of massive fluid loss through diarrhoea and/ or vomiting.
Patients with cardiogenic shock usually have symptoms and signs of disease, heart, including increased filling pressure, galloping rhythm and other evidence of heart failure. Mechanical causes of cardiogenic shock frequently produce cardiac blasts, such as mitral insufficiency, aortic stenosis or ventricular septal defect. Patients with cardiac tamponade may experience paradoxical pulse and blurred heart beat. In patients with sepsis-related distribution shock, there may be evidence of localized infections such as fever and chills. Patients with sepsis and neutropenia are less likely to experience an obvious clinical outbreak of infection, as they may be infected with the flora present on their own skin or intestinal flora.
I'm done! We'll hear from each other on June 2nd when I complete the shock posts and... I will post the newmedicine.pdf updated (I managed to complete the reconstitution of the file)...
Let us hear only good and not forget a moment of understanding, love and gratitude to everything and everything!
From the point of view of pathogenesis we are dealing with hypovolemic shock, extracardiac obstructive shock, cardiogenic shock and distribution shock. In hypovolemic, cardiogenic and obstructive extracardiac shock, low tissue infusion is determined by inadequate cardiac output. In distribution shock, low blood pressure occurs by reducing systemic vascular resistance and maldistribution of blood flow in microcirculation, being a major factor contributing to multiple organ failure.
Hypovolemic shock has been much studied and its stages can be easily quantified on experienced animals by phasing out blood from the intravascular space. Many of the data from these studies also apply to other forms of shock characterized by reduced heart rate. When 10% of the total blood volume is lost, the compensatory mechanisms are activated and maintain cardiac output, despite the decrease in filling pressure and beating volume.
The increase in adrenergic activity, resulting both from stimulation of the sympathetic system and from the release of catecholamines from the adrenal, leads to arterial vasoconstriction, venoconstriction with increased venous return and tachycardia. Reduction of hydrostatic pressure in capillaries, together with precapillary arteriolar vasoconstriction, favors the transwelding of fluid from extracellular space into vessels. The contraction of intravascular volume leads to activation of the renin-angiotensin system, increased release of antidiuretic hormone and increased levels of ACTH and aldosterone (thus defending renal retention of sodium and water).
These adaptations may be sufficient to maintain arterial pressure and orthostatic hypotension may be the only sign of hypovolemia. However, if 20-25% of blood volume is rapidly lost, the compensatory mechanisms are overcome and clinical signs of shock appear. Heart rate decreases and hypotension occurs despite generalized vasoconstriction.
Reduction of tissue infusion leads to the installation of anaerobic metabolism, manifested by increased lactate levels and metabolic acidosis. Adrenergic reflex stimulation intensifies and flow is redistributed to maintain heart and brain infusion. This redistribution reflects the predominance of blood flow self-regulation in the cerebral and coronary systems, in contrast to the dependence on the sympathetic tone of luxuries in other organs.
Excessive vasoconstriction can reduce the flow to the point where cellular damage occurs. Damage to the capillary endothelium leads to loss of fluids and proteins in circulation, which accentuates hypovolemia. In the end, multiorganic insufficiency occurs.
As for cardiogenic shock, when myocardial function is depressed, several compensatory mechanisms are activated. Sympathetic stimulation increases heart rate and contractility, and fluid renal retention increases pre-pregnancy. if cardiac output cannot be maintained through these mechanisms, the blood flow is redistributed to maintain cerebral and cardiac infusion.
When heart failure occurs, the compensatory mechanisms can slowly become dysfunctional. Increased heart rate and contractility can increase myocardial oxygen demand and exacerbate ischemia. In addition, tachycardia decreases diastolic filling time, further compromising myocardial infusion. Fluid retention may increase intravascular volume until pulmonary congestion and hypoxia appear. Ischemia also decreases diastolic compliance of the ventricle, subsequently increasing pressure in the left atrium and aggravating pulmonary congestion.
Vasoconstriction to maintain arterial pressure compromises renal, splahinic and skin infusion. Increased systemic vascular resistance through vasoconstriction increases post-pregnancy, further affecting cardiac function and increasing myocardial oxygen demand. The latter, under the conditions of an inadequate infusion, leads to aggravation of ischemia and the appearance of a vicious cycle that must be interrupted to prevent an inexorable progression to the death of the patient.
Cardiac tamponade results from the accumulation of fluid in the pericardium, with a consecutive increase in intrapericardial pressure. It may be acute (e.g. hemopericardium associated with open or closed thorax trauma) or subacute (e.g. uremia, irradiation, neoplasm, infection or connective tissue disease). Tamponade may occur after cardiac surgery due to compression of the heart by a mediastinal hematoma or postpericardiotomy syndrome.
The increase in intrapericardial pressure and the consequent impairment of cardiac filling through a pericardial overflow depends on the rate of fluid accumulation, fluid volume and pericardial distensibility. As intrapericardial pressure increases, the gradient between peripheral venous pressure and that in the right atrium decreases and diastolic filling is compromised. When pericardial pressure acutely affects diastolic filling, adrenergic stimulation causes tachycardia, increased ejection fraction and arterial vasoconstriction to maintain blood pressure.
Over a period of hours or days, fluid retention increases venous pressure which favors filling. Subacutely installed tamponade is compensated and shows signs of venous congestion with dilation of the neck veins. Exceeding compensation leads to shock with tachycardia, tachypnea, decreased heart rate, peripheral vasoconstriction and hypotension.
In the case of distribution shock, tissue hypoperfusion results from abnormal sunting of a normal or increased cardiac output. Although differential diagnosis also includes anaphylaxis, drug overdose, neurogenic shock and Addisonian crisis, the most important and common etiology is septic shock. In some forms of shock distribution, blood flow in different organs seems appropriate, but exists in "metabolic blockage" induced by mediators at the tissue level, preventing the proper use of oxygen and other nutrients. Lactic acid accumulates because cells cannot normally use the pathways of oxidative metabolism.
Thus, in some patients, blood flow through large vessels to tissues is normal, but abnormalities in microvascular flow or the inability of cells to use nutrients lead to the spread of cellular dysfunction and the appearance of shock. Septic shock occurs when infectious agents or infection-induced mediators in the circulation produce cardiovascular decompensation.
Septic shock is characterized at onset by increased cardiac output and low systemic vascular resistance. Septic shock usually begins with the release of microorganisms into circulation from the outbreak of infection. Toxic effects can be caused by microorganisms, their components such as endotoxins, lipopolysaccharides associated with the external membrane of gram negative bacteria or with the release of exotoxins. The most important pathological effect of these microorganisms or toxins can be determined by stimulating the release of large amounts of endogenous mediators of inflammation.
Endotoxin is a potential trigger for the release of cytokines, especially interleukins and TNF, which amplifies the systemic response to endotoxin by stimulating neutrophils, endothelial cells and platelets and inducing the release of other mediators such as PAF, arachidonic acid metabolites, complements, kinins, histamine and endorphins. The effects of these mediators can be divided into two broad categories: effects on peripheral vessels and heart effects. Both exogenous and endogenous mediators have been shown to mediate vasodilation in sepsis.
Taking low doses of endotoxin to healthy volunteers produces a decrease in blood pressure, an increase in heart rate and a reduction in systemic vascular resistance similar to that of sepsis. A similar vasodilation with increased cardiac output occurs after administration of TNF, IL-1 or IL-2. A key mediator of vasodilation in response to cytokines is nitric oxide, which consists of anginin by the action of nitric enzyme oxide synthetase.
Endotoxin, TNF and interleukins can stimulate nitric oxide sintetase acid which can be induced in macrophages and smooth vascular muscle cells, with the release of a large amount of this vasodilating substance. Endotoxin can also activate the intrinsic pathway of coagulation with the fibrinolytic system, which can lead to the storage of microaggregates of fibrin in microvas, obstructing the flow and accentuating tissue hypoxia.
TNF and interleukins activate both endothelial cells and neutrophils, which cause neutrophil aggregation and consecutive microcirculatory insufficiency. Although patients with septic shock have increased cardiac output, ejection fractions of the right and left ventricles are low. The dilation of the ventricles allows to maintain the normal beating volume despite the decrease in myocardial contractility and tachycardia causes an increased cardiac output.
Patients with sepsis also show a decrease in the systolic contractile response of the ventricle to an increased volume, indicating a reduction in myocardial performance. The responsible mechanisms have not been fully clarified (it appears that cytokines, in particular TNF and IL-1, play an important role, possibly through the generation of nitric oxide). If the shock persists, the combination of peripheral vascular abnormalities with myocardial depression leads to a mortality of about 50%.
Death occurs through severe hypotension and/ or multi-organic failure. Hypotension is associated with a severe and irreversible reduction in systemic vascular resistance. Sometimes (at about 10% of deaths) myocardial depression is so severe that heart rate decreases by increasing hypotension.
I will complete this post with the presentation of some elements about clinical manifestations. Some symptoms and signs are the same for all types of shock. This condition is almost always characterized by hypotension, which in adults generally means an average blood pressure below 60 mmHg. However, when interpreting any given level of blood pressure, the chronic level of blood pressure should be taken into account (patients with severe chronic hypertension may be relatively hypotensive when the average blood pressure drops by 40 mmHg, even if it is more than 60 mmHg). Conversely, patients with chronic hypotension will not show clinical signs until the average pressure drops below 50 mmHg.
Common manifestations in shock are tachycardia, oliguria, altered general condition and cold and pale extremities, indicating reduced blood flow to the skin. Metabolic acidosis, often due to increased blood levels of lactic acid, reflects the lasting decrease in blood flow to tissues. Other clinical manifestations are specific to each type of shock. Patients with hypovolemic shock frequently have a history of gastrointestinal bleeding, haemorrhages with other localization or clear evidence of massive fluid loss through diarrhoea and/ or vomiting.
Patients with cardiogenic shock usually have symptoms and signs of disease, heart, including increased filling pressure, galloping rhythm and other evidence of heart failure. Mechanical causes of cardiogenic shock frequently produce cardiac blasts, such as mitral insufficiency, aortic stenosis or ventricular septal defect. Patients with cardiac tamponade may experience paradoxical pulse and blurred heart beat. In patients with sepsis-related distribution shock, there may be evidence of localized infections such as fever and chills. Patients with sepsis and neutropenia are less likely to experience an obvious clinical outbreak of infection, as they may be infected with the flora present on their own skin or intestinal flora.
I'm done! We'll hear from each other on June 2nd when I complete the shock posts and... I will post the newmedicine.pdf updated (I managed to complete the reconstitution of the file)...
Let us hear only good and not forget a moment of understanding, love and gratitude to everything and everything!
Dorin, Merticaru