STUDY - Technical - New Dacian's Medicine
The
Shock (1)
Translation Draft
Shock is the condition in which the inability of the circulatory system to maintain an adequate cell infusion leads to a widespread reduction in the supply of oxygen and nutrients to tissues.
Shock is the condition in which the inability of the circulatory system to maintain an adequate cell infusion leads to a widespread reduction in the supply of oxygen and nutrients to tissues.
Respiratory failure
produces first cellular dysfunction then the organ, which can
become irreversible if not promptly corrected.
Shock is a syndrome defined by a variety of clinical signs, which can occur from several causes. At the onset, the physiological alterations accompanying the shock suggest the nature of the initiator event. In later phases, however, evolution is common, given the consequences of an inadequate tissue infusion.
The first thing we need to focus on is blood pressure control. Maintaining adequate infusion of vital organs is essential for survival. The infusion of organs depends on blood pressure, which is determined by two factors: heart rate and vascular resistance.
Thus, the infusion of an organ may be compromised by the decrease in heart rate or its inadequate distribution. In an organ, blood distribution depends on infusion pressure, vascular resistance and the ability of nutrition microvessels. Poor distribution of blood flow can aggravate organ dysfunction.
Since the initiator element in shock is inadequate tissue infusion, it is important to understand the decisive factors that determine the tissue infusion. These factors can be 1. cardiac arrests, 2. vascular, 3. humoralands and 4. microcirculation.
1. Cardiac factors. Heart rate is given by the product between beating volume and heart rate. The beating volume, in turn, is determined by three factors: pre-pregnancy, post-pregnancy and myocardial contractility.
2. Vascular factors. The resistance to blood flow in a vessel is proportional to its length and blood viscosity and inversely proportional to the radius of the vessel at the fourth power. Therefore, the section area of the vessel is by far the most important determinant of resistance to flow. Since the main component of resistance in the vascular system is the arteriolar, and the tone of the smooth vascular muscle regulates the radius of the resistance arterioles, the tone of the smooth arteriolar muscleis is the most important determinant of vascular resistance.
Arteriolar tone is determined by extrinsic factors, which include hormonal and neural regulation, and by intrinsic or local factors, which are myogenic response, metabolic self-regulation and endothelial mediated regulation. The resistance arterioles receive a vasoconstrictor tonic stimulus from sympathetic nerves that irritate the vascular smooth musculature: the sympathetic tone is largely regulated by cardiopulmonary and arterial baroreceptors.
Stimulation of the adrenal leads to the release of epinephrine and norepinephrine into the systemic circulation. Blood vessels may contract or relax in response to changes in transmural pressure to maintain constant blood flow, although the infusion pressure changes. This myogenic response serves to maintain a constant tension in the arterial wall, ensuring local self-regulation of the flow.
Metabolic regulation is achieved by the release of vasodilators that increase tissue blood flow in response to increased metabolic activity. The most important of these are adenosine and vasodilating prostaglandins. The vessels of microvascularization also relax in the presence of low oxygen pressure also due to the release of prostaglandins.
Vascular endothelial cells secrete a number of locally active substances, including endothelial relaxation factor (nitric oxide), arachidonic acid-derived molecules called generic eicosanids, endotelin 1 and angiotensin II vasoconstrictor peptides, and oxygen-free radicals. Action and interaction between these mediators are important components of local regulation through endothelial cells.
3. Humoral factors. Humoral substances in circulation play important roles in cardiovascular homeostasis. In shock, the release into circulation of mediators such as renin, vasopressin, prostaglandins, kinins, atrial natriuretic factor and catecholamines is mediated both by the activation of the central nervous system and by the cellular effects of ischemia, toxins and immunological mechanisms.
4. Factors of microcirculation. Because shock occurs through microcirculation insufficiency, the essential stages of shock pathogenesis occur at this level. Normal blood intake to an organ as a whole does not necessarily imply that the infusion of all its segments corresponds to regional metabolic needs.
The adhesion of leukocytes and plaques to damaged or activated vascular endothelial cells can cause increased viscosity and occlusion of microvessels, activation of the coagulation system through fibrin deposits and accumulation of microthrombs may contribute to the occlusion of microvessels. Shunting may occur as a result of an improper infusion without an adequate capillary exchange. Low deformity of erythrocytes can also contribute to decreased flow in microcirculation and capillary exchanges.
The flow in microvascularization is influenced by the balance between colloid-osmotic pressure and capillary hydrostatic pressure, which in turn determines the balance between vascular and extravascular fluids. Sympathetic stimulation causes constriction of precapillary resistance vessels, lowering capillary hydrostatic pressure and facilitating the movement of fluid from extravascular space to intravascular space, as well as constriction of postcapillary venus.
If severe tissue hypoxia and acidosis occur, the sympathetically mediated arteriolar vasoconstrictor response may be counteracted by metabolic vasodilation, which, together with venoconstricity, may cause fluid extravasation in the interstitial space. In addition, circulatory toxins and adhesiveness of activated leukocytes can increase capillary permeability, accentuating tissue edema. This process can be exacerbated by the loss of plasma proteins in the interstitial, which reduces colloid-osmotic pressure, intravascular volume and tissue infusion.
Let's talk a little bit about the shock classification! It can be 1. cardiogenic: a. myopathic (acute myocardial infarction, dilatative cardiomyopathy, myocardial insufficiency in septic shock), b. mechanical (mitral insufficiency, ventricular septal defect, ventricular aneurysm, obstruction of the left ventricle ejection tract - aortic stenosis, hypertrophic cardiomyopathy), c. arrhythmic; 2. Extracardiac obstructive (cardiac tamponade, pulmonary embolism - massive -, severe pulmonary hypertension - primary or Eisenmenger), 3. hypovolemic (hemorrhage, fluid deletation), 4. distribution (septic shock, toxic products - drug overdose -, anaphylaxis, neurogenic shock, endocrinological shock).
Hypovolemic shock is due to a reduction in the volume of circulating blood that decreases pre-pregnancy and leads to inadequate ventricular filling, reflected in decreased volumes and telediastolic pressures in both ventricles. The consequence is a low beating volume and inadequate cardiac output. Hypovolemic shock may result from haemorrhage or fluid deletation due to vomiting, diarrhoea, burns or dehydration. Hypovolemic shock is the most common type of shock.
Cardiogenic shock is due to severe depression of cardiac function. From a hemodynamic point of view it is characterized by systolic blood pressure of less than 80 mmHg, a cardiac index of less than (1.8 l/ min)/mp (mp - square meter) and a left ventricle refill pressure greater than 18 mmHg, pulmonary edema is usually present.
The most common cause is myocardial infarction with a substantial loss of muscle mass (usually 40% or more of the left ventricle myocardium). Extended infarction of the right ventricle can also precipitate a cardiogenic shock. Pump failure may also occur after acute myocarditis or by decreasing the contractility of the myocardium secondary to cardiac arrest or prolonged cardiopulmonary bypass.
Cardiogenic shock can also be caused by mechanical abnormalities. Severe valvular stenosis can decrease beating volume and cardiac flow. Severe, acute aortic insufficiency leads to reduced cardiac output, which can cause pulmonary edema and cadiogen shock. Acutely acquired ventricular septum defects, which usually occur at the onset of myocardial infarction, can also cause cardiogenic shock by decreasing anterograde flow.
Extracardiac obstructive shock is best exemplified by cardiac tamponade. Increased pressure in the pericardial sac affects ventricular diastolic filling by decreasing pre-pregnancy, beating volume and cardiac output. Pneumothorax can also affect cardiac filling by decreasing the venous return to the heart.
Massive pulmonary embolism is another form of extracardiac obstructive shock, although the mechanism is different. When more than 50-60% of the pulmonary vascular bed is obstructed by thrombus, acute insufficiency of the right ventricle may occur, and the filling of the left ventricle is impaired.
Distribution shock occurs through marked peripheral vasodilation, although cardiac output may be normal or increased tissue and organ infusions may be inadequate. The prototype of the distribution shock is septic shock, the most common cause of death. Other types of shock distribution include anaphylaxis, neurogenic shock and adrenal insufficiency. In practice, patients may present multiple elements of several types of shock at the same time.
For example, in septic shock the elements of distribution and hypovolemic shock can be complicated by myocardial insufficiency. Traumatic shock can also be complicated by elements of both hypovolemic and distribution shock. In a patient, the nature of circulatory disorders may change over time and after therapy.
Let's finish this post with a few elements about pathogenesis. Cellular dysfunction in shock is the end result of a process with multiple stimuli. At the onset of shock, the compensatory mechanisms are activated in an attempt to restore pressure and flow to the vital organs. When these compensatory mechanisms become insufficient, tissue infusion disorder manifests itself as organ dysfunction.
Excessive and prolonged reduction of tissue infusion leads to alteration of the cell membrane, release of lysosome enzymes and decrease of energy deposits, which can cause cell death. Once a sufficiently large number of vital organ cells have reached this stage, the shock can become irreversible and death may occur, despite the correction of the underlying cause. This concept of irreversibility is useful because it underlines the need to prevent the progressive evolution of shock.
Cellular dysfunction in shock occurs through three main mechanisms: cellular ischemia, inflammation mediators and lesions caused by free radicals. Lack of oxygen due to cellular hypoperfusion leads to anaerobic glycolysis, which produces only 2 types of ATP through the lysis of a glucose molecule, while aerobic glycolysis produces 36 ATP molecules. This leads to the deletation of ATP and intracellular energy deposits.
Anaerobic glycolysis also produces lactic acid accumulation with consecutive intracellular acidosis. Insufficiency of the energy-dependent ion transport pump decreases the transmembrane potential, producing intracellular accumulation of sodium and water. Normal potassium, chlorine and calcium gradients can no longer be maintained. Intracellular calcium accumulation further accentuates mitochondrial dysfunction. Cell membrane dysfunction is manifested by changes in cell structure.
Initial pathological changes include the widening of the endoplasmic reticulum and the formation of bubbles on the surface of the cell, while mitochondrial condensation occurring. Dilation of mitochondria causes irreversible cellular damage. The terminal event is the accumulation of denatured proteins and chromatin in the cytoplasm, the destruction of lysosomes and the rupture of mitochondria, the nuclear shell and the plasma membrane.
On the 28th we continue with the presentation of the types of shock (septic shock)...
Shock is a syndrome defined by a variety of clinical signs, which can occur from several causes. At the onset, the physiological alterations accompanying the shock suggest the nature of the initiator event. In later phases, however, evolution is common, given the consequences of an inadequate tissue infusion.
The first thing we need to focus on is blood pressure control. Maintaining adequate infusion of vital organs is essential for survival. The infusion of organs depends on blood pressure, which is determined by two factors: heart rate and vascular resistance.
Thus, the infusion of an organ may be compromised by the decrease in heart rate or its inadequate distribution. In an organ, blood distribution depends on infusion pressure, vascular resistance and the ability of nutrition microvessels. Poor distribution of blood flow can aggravate organ dysfunction.
Since the initiator element in shock is inadequate tissue infusion, it is important to understand the decisive factors that determine the tissue infusion. These factors can be 1. cardiac arrests, 2. vascular, 3. humoralands and 4. microcirculation.
1. Cardiac factors. Heart rate is given by the product between beating volume and heart rate. The beating volume, in turn, is determined by three factors: pre-pregnancy, post-pregnancy and myocardial contractility.
2. Vascular factors. The resistance to blood flow in a vessel is proportional to its length and blood viscosity and inversely proportional to the radius of the vessel at the fourth power. Therefore, the section area of the vessel is by far the most important determinant of resistance to flow. Since the main component of resistance in the vascular system is the arteriolar, and the tone of the smooth vascular muscle regulates the radius of the resistance arterioles, the tone of the smooth arteriolar muscleis is the most important determinant of vascular resistance.
Arteriolar tone is determined by extrinsic factors, which include hormonal and neural regulation, and by intrinsic or local factors, which are myogenic response, metabolic self-regulation and endothelial mediated regulation. The resistance arterioles receive a vasoconstrictor tonic stimulus from sympathetic nerves that irritate the vascular smooth musculature: the sympathetic tone is largely regulated by cardiopulmonary and arterial baroreceptors.
Stimulation of the adrenal leads to the release of epinephrine and norepinephrine into the systemic circulation. Blood vessels may contract or relax in response to changes in transmural pressure to maintain constant blood flow, although the infusion pressure changes. This myogenic response serves to maintain a constant tension in the arterial wall, ensuring local self-regulation of the flow.
Metabolic regulation is achieved by the release of vasodilators that increase tissue blood flow in response to increased metabolic activity. The most important of these are adenosine and vasodilating prostaglandins. The vessels of microvascularization also relax in the presence of low oxygen pressure also due to the release of prostaglandins.
Vascular endothelial cells secrete a number of locally active substances, including endothelial relaxation factor (nitric oxide), arachidonic acid-derived molecules called generic eicosanids, endotelin 1 and angiotensin II vasoconstrictor peptides, and oxygen-free radicals. Action and interaction between these mediators are important components of local regulation through endothelial cells.
3. Humoral factors. Humoral substances in circulation play important roles in cardiovascular homeostasis. In shock, the release into circulation of mediators such as renin, vasopressin, prostaglandins, kinins, atrial natriuretic factor and catecholamines is mediated both by the activation of the central nervous system and by the cellular effects of ischemia, toxins and immunological mechanisms.
4. Factors of microcirculation. Because shock occurs through microcirculation insufficiency, the essential stages of shock pathogenesis occur at this level. Normal blood intake to an organ as a whole does not necessarily imply that the infusion of all its segments corresponds to regional metabolic needs.
The adhesion of leukocytes and plaques to damaged or activated vascular endothelial cells can cause increased viscosity and occlusion of microvessels, activation of the coagulation system through fibrin deposits and accumulation of microthrombs may contribute to the occlusion of microvessels. Shunting may occur as a result of an improper infusion without an adequate capillary exchange. Low deformity of erythrocytes can also contribute to decreased flow in microcirculation and capillary exchanges.
The flow in microvascularization is influenced by the balance between colloid-osmotic pressure and capillary hydrostatic pressure, which in turn determines the balance between vascular and extravascular fluids. Sympathetic stimulation causes constriction of precapillary resistance vessels, lowering capillary hydrostatic pressure and facilitating the movement of fluid from extravascular space to intravascular space, as well as constriction of postcapillary venus.
If severe tissue hypoxia and acidosis occur, the sympathetically mediated arteriolar vasoconstrictor response may be counteracted by metabolic vasodilation, which, together with venoconstricity, may cause fluid extravasation in the interstitial space. In addition, circulatory toxins and adhesiveness of activated leukocytes can increase capillary permeability, accentuating tissue edema. This process can be exacerbated by the loss of plasma proteins in the interstitial, which reduces colloid-osmotic pressure, intravascular volume and tissue infusion.
Let's talk a little bit about the shock classification! It can be 1. cardiogenic: a. myopathic (acute myocardial infarction, dilatative cardiomyopathy, myocardial insufficiency in septic shock), b. mechanical (mitral insufficiency, ventricular septal defect, ventricular aneurysm, obstruction of the left ventricle ejection tract - aortic stenosis, hypertrophic cardiomyopathy), c. arrhythmic; 2. Extracardiac obstructive (cardiac tamponade, pulmonary embolism - massive -, severe pulmonary hypertension - primary or Eisenmenger), 3. hypovolemic (hemorrhage, fluid deletation), 4. distribution (septic shock, toxic products - drug overdose -, anaphylaxis, neurogenic shock, endocrinological shock).
Hypovolemic shock is due to a reduction in the volume of circulating blood that decreases pre-pregnancy and leads to inadequate ventricular filling, reflected in decreased volumes and telediastolic pressures in both ventricles. The consequence is a low beating volume and inadequate cardiac output. Hypovolemic shock may result from haemorrhage or fluid deletation due to vomiting, diarrhoea, burns or dehydration. Hypovolemic shock is the most common type of shock.
Cardiogenic shock is due to severe depression of cardiac function. From a hemodynamic point of view it is characterized by systolic blood pressure of less than 80 mmHg, a cardiac index of less than (1.8 l/ min)/mp (mp - square meter) and a left ventricle refill pressure greater than 18 mmHg, pulmonary edema is usually present.
The most common cause is myocardial infarction with a substantial loss of muscle mass (usually 40% or more of the left ventricle myocardium). Extended infarction of the right ventricle can also precipitate a cardiogenic shock. Pump failure may also occur after acute myocarditis or by decreasing the contractility of the myocardium secondary to cardiac arrest or prolonged cardiopulmonary bypass.
Cardiogenic shock can also be caused by mechanical abnormalities. Severe valvular stenosis can decrease beating volume and cardiac flow. Severe, acute aortic insufficiency leads to reduced cardiac output, which can cause pulmonary edema and cadiogen shock. Acutely acquired ventricular septum defects, which usually occur at the onset of myocardial infarction, can also cause cardiogenic shock by decreasing anterograde flow.
Extracardiac obstructive shock is best exemplified by cardiac tamponade. Increased pressure in the pericardial sac affects ventricular diastolic filling by decreasing pre-pregnancy, beating volume and cardiac output. Pneumothorax can also affect cardiac filling by decreasing the venous return to the heart.
Massive pulmonary embolism is another form of extracardiac obstructive shock, although the mechanism is different. When more than 50-60% of the pulmonary vascular bed is obstructed by thrombus, acute insufficiency of the right ventricle may occur, and the filling of the left ventricle is impaired.
Distribution shock occurs through marked peripheral vasodilation, although cardiac output may be normal or increased tissue and organ infusions may be inadequate. The prototype of the distribution shock is septic shock, the most common cause of death. Other types of shock distribution include anaphylaxis, neurogenic shock and adrenal insufficiency. In practice, patients may present multiple elements of several types of shock at the same time.
For example, in septic shock the elements of distribution and hypovolemic shock can be complicated by myocardial insufficiency. Traumatic shock can also be complicated by elements of both hypovolemic and distribution shock. In a patient, the nature of circulatory disorders may change over time and after therapy.
Let's finish this post with a few elements about pathogenesis. Cellular dysfunction in shock is the end result of a process with multiple stimuli. At the onset of shock, the compensatory mechanisms are activated in an attempt to restore pressure and flow to the vital organs. When these compensatory mechanisms become insufficient, tissue infusion disorder manifests itself as organ dysfunction.
Excessive and prolonged reduction of tissue infusion leads to alteration of the cell membrane, release of lysosome enzymes and decrease of energy deposits, which can cause cell death. Once a sufficiently large number of vital organ cells have reached this stage, the shock can become irreversible and death may occur, despite the correction of the underlying cause. This concept of irreversibility is useful because it underlines the need to prevent the progressive evolution of shock.
Cellular dysfunction in shock occurs through three main mechanisms: cellular ischemia, inflammation mediators and lesions caused by free radicals. Lack of oxygen due to cellular hypoperfusion leads to anaerobic glycolysis, which produces only 2 types of ATP through the lysis of a glucose molecule, while aerobic glycolysis produces 36 ATP molecules. This leads to the deletation of ATP and intracellular energy deposits.
Anaerobic glycolysis also produces lactic acid accumulation with consecutive intracellular acidosis. Insufficiency of the energy-dependent ion transport pump decreases the transmembrane potential, producing intracellular accumulation of sodium and water. Normal potassium, chlorine and calcium gradients can no longer be maintained. Intracellular calcium accumulation further accentuates mitochondrial dysfunction. Cell membrane dysfunction is manifested by changes in cell structure.
Initial pathological changes include the widening of the endoplasmic reticulum and the formation of bubbles on the surface of the cell, while mitochondrial condensation occurring. Dilation of mitochondria causes irreversible cellular damage. The terminal event is the accumulation of denatured proteins and chromatin in the cytoplasm, the destruction of lysosomes and the rupture of mitochondria, the nuclear shell and the plasma membrane.
On the 28th we continue with the presentation of the types of shock (septic shock)...
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Dorin, Merticaru