This document discusses various types of hypoxia including hypoxic, anaemic, stagnant, and histotoxic hypoxia. It also covers topics like acclimatization to high altitudes, cyanosis, oxygen therapy, and carbon monoxide poisoning. The key points are:
1. Hypoxia is defined as oxygen deficiency at the tissue level and can be caused by problems with ventilation, gas exchange, blood flow, or cellular respiration.
2. Acclimatization to high altitudes involves mechanisms like increased ventilation, blood oxygen carrying capacity, circulation, and tissue oxygen delivery over weeks.
3. Cyanosis is a blue skin discoloration caused by abnormally high amounts of deoxygen
Physiology of high altitude & high pressureDr Nilesh Kate
This document discusses physiology related to high altitude and high atmospheric pressure. It covers topics such as hypoxia at high altitude and the compensatory responses that occur. It describes clinical syndromes like acute mountain sickness and high altitude pulmonary edema. It also discusses physiological challenges of high pressure environments like deep sea diving, including decompression sickness and nitrogen narcosis that can occur if not properly managed during ascent. Prevention strategies are outlined to avoid problems during descent from depth or rapid changes in altitude.
Hypoxia :types , causes,and its effects Aqsa Mushtaq
hypoxia :oxygen defecincy at tissue level.in these slides you are going to in touch with its types ,causes effects.share whatever you wanted to say comment us .
these notes are provided by our loving mam MAM SANIA .thanks to teach us mam :)
The respiratory center located in the medulla oblongata and pons regions of the brain controls respiration. It contains the medullary rhythmicity area which controls the basic rhythm of inhalation and exhalation, the pneumotaxic area which coordinates the transition between inhalation and exhalation by inhibiting the inspiratory area, and the apneustic area which prolongs inhalation. Respiration is also regulated by chemoreceptors which detect changes in oxygen and carbon dioxide levels in the blood and stimulate breathing, by proprioceptors which sense movement and stimulate inhalation, and by the inflation reflex which inhibits inhalation during exhalation to prevent overinflation of the lungs.
This document discusses hypoxia and hypercapnia. It defines hypoxia as reduced oxygen for tissue respiration and describes various types including hypoxic, anemic, stagnant, and histotoxic hypoxia. It outlines the direct effects of acute hypoxia such as cyanosis, confusion, and myocardial depression. It also discusses chronic hypoxia, cyanosis, degrees of arterial oxygen saturation, and treatments for hypoxia including oxygen administration and hyperbaric oxygen therapy. The document also defines hypercapnia as excess carbon dioxide in the body and notes it is associated with hypoxia and hypoventilation. It provides blood levels of carbon dioxide that can cause effects like air hunger, lethargy, and death.
Following induction of anesthesia, factors such as decreased functional residual capacity, increased ventilation/perfusion mismatching, and development of atelectasis can increase venous admixture from 1% to around 10%. Anesthetic agents also suppress hypoxic pulmonary vasoconstriction and decrease cardiac output, reducing oxygen delivery. However, anesthesia and artificial ventilation lower oxygen requirements by around 15-21% due to decreased metabolism and work of breathing. Oxygen is transported in the blood bound to hemoglobin or dissolved in plasma, and the oxygen dissociation curve illustrates hemoglobin's changing affinity for oxygen at different partial pressures. Multiple factors can shift this curve, facilitating either oxygen loading or unloading as needed.
The document summarizes the chemical control of respiration through respiratory chemoreceptors. There are three types of chemoreceptors: peripheral chemoreceptors located in the carotid bodies and aortic bodies that detect changes in arterial pCO2, pO2, and pH; central or medullary chemoreceptors located in the brainstem that are stimulated by increased hydrogen ion concentration in cerebrospinal fluid; and both peripheral and central chemoreceptors work together to maintain homeostasis and stimulate respiration in response to changes in oxygen, carbon dioxide, and hydrogen ion levels in order to regulate respiration.
Hypoxia is a condition where the body or a region of the body is deprived of adequate oxygen supply at the tissue level. There are several types of hypoxia including hypoxic hypoxia, which is due to a decrease in oxygen pressure in inhaled air. Signs and symptoms of hypoxia include changes in skin color, confusion, coughing, rapid breathing, and shortness of breath. The body responds to hypoxia through acclimatization and hyperventilation, increasing breathing depth and rate to raise alveolar oxygen levels. Causes include various lung and heart conditions, high altitude, carbon monoxide poisoning, and drug or chemical exposure.
Oxygen is transported from the lungs to tissues in two forms: physically dissolved in blood plasma and bound to hemoglobin in red blood cells. Hemoglobin transports about 98% of oxygen in its iron-containing heme groups. The binding of oxygen to hemoglobin follows an S-shaped oxygen-hemoglobin dissociation curve, where hemoglobin has high affinity for oxygen at high partial pressures in the lungs and low affinity in tissues, facilitating oxygen delivery. Various factors can shift this curve to increase or decrease hemoglobin's oxygen affinity, optimizing oxygen transport and unloading on demand in metabolically active tissues.
Physiology of high altitude & high pressureDr Nilesh Kate
This document discusses physiology related to high altitude and high atmospheric pressure. It covers topics such as hypoxia at high altitude and the compensatory responses that occur. It describes clinical syndromes like acute mountain sickness and high altitude pulmonary edema. It also discusses physiological challenges of high pressure environments like deep sea diving, including decompression sickness and nitrogen narcosis that can occur if not properly managed during ascent. Prevention strategies are outlined to avoid problems during descent from depth or rapid changes in altitude.
Hypoxia :types , causes,and its effects Aqsa Mushtaq
hypoxia :oxygen defecincy at tissue level.in these slides you are going to in touch with its types ,causes effects.share whatever you wanted to say comment us .
these notes are provided by our loving mam MAM SANIA .thanks to teach us mam :)
The respiratory center located in the medulla oblongata and pons regions of the brain controls respiration. It contains the medullary rhythmicity area which controls the basic rhythm of inhalation and exhalation, the pneumotaxic area which coordinates the transition between inhalation and exhalation by inhibiting the inspiratory area, and the apneustic area which prolongs inhalation. Respiration is also regulated by chemoreceptors which detect changes in oxygen and carbon dioxide levels in the blood and stimulate breathing, by proprioceptors which sense movement and stimulate inhalation, and by the inflation reflex which inhibits inhalation during exhalation to prevent overinflation of the lungs.
This document discusses hypoxia and hypercapnia. It defines hypoxia as reduced oxygen for tissue respiration and describes various types including hypoxic, anemic, stagnant, and histotoxic hypoxia. It outlines the direct effects of acute hypoxia such as cyanosis, confusion, and myocardial depression. It also discusses chronic hypoxia, cyanosis, degrees of arterial oxygen saturation, and treatments for hypoxia including oxygen administration and hyperbaric oxygen therapy. The document also defines hypercapnia as excess carbon dioxide in the body and notes it is associated with hypoxia and hypoventilation. It provides blood levels of carbon dioxide that can cause effects like air hunger, lethargy, and death.
Following induction of anesthesia, factors such as decreased functional residual capacity, increased ventilation/perfusion mismatching, and development of atelectasis can increase venous admixture from 1% to around 10%. Anesthetic agents also suppress hypoxic pulmonary vasoconstriction and decrease cardiac output, reducing oxygen delivery. However, anesthesia and artificial ventilation lower oxygen requirements by around 15-21% due to decreased metabolism and work of breathing. Oxygen is transported in the blood bound to hemoglobin or dissolved in plasma, and the oxygen dissociation curve illustrates hemoglobin's changing affinity for oxygen at different partial pressures. Multiple factors can shift this curve, facilitating either oxygen loading or unloading as needed.
The document summarizes the chemical control of respiration through respiratory chemoreceptors. There are three types of chemoreceptors: peripheral chemoreceptors located in the carotid bodies and aortic bodies that detect changes in arterial pCO2, pO2, and pH; central or medullary chemoreceptors located in the brainstem that are stimulated by increased hydrogen ion concentration in cerebrospinal fluid; and both peripheral and central chemoreceptors work together to maintain homeostasis and stimulate respiration in response to changes in oxygen, carbon dioxide, and hydrogen ion levels in order to regulate respiration.
Hypoxia is a condition where the body or a region of the body is deprived of adequate oxygen supply at the tissue level. There are several types of hypoxia including hypoxic hypoxia, which is due to a decrease in oxygen pressure in inhaled air. Signs and symptoms of hypoxia include changes in skin color, confusion, coughing, rapid breathing, and shortness of breath. The body responds to hypoxia through acclimatization and hyperventilation, increasing breathing depth and rate to raise alveolar oxygen levels. Causes include various lung and heart conditions, high altitude, carbon monoxide poisoning, and drug or chemical exposure.
Oxygen is transported from the lungs to tissues in two forms: physically dissolved in blood plasma and bound to hemoglobin in red blood cells. Hemoglobin transports about 98% of oxygen in its iron-containing heme groups. The binding of oxygen to hemoglobin follows an S-shaped oxygen-hemoglobin dissociation curve, where hemoglobin has high affinity for oxygen at high partial pressures in the lungs and low affinity in tissues, facilitating oxygen delivery. Various factors can shift this curve to increase or decrease hemoglobin's oxygen affinity, optimizing oxygen transport and unloading on demand in metabolically active tissues.
The oxyhemoglobin dissociation curve shows the relationship between oxygen concentration and hemoglobin saturation in the blood. It demonstrates how hemoglobin binds to oxygen in the lungs when partial pressure of oxygen is high, and releases oxygen into tissues where partial pressure is low. Several factors can shift the curve left or right, changing hemoglobin's affinity for oxygen and impacting how much oxygen is unloaded to tissues. These include pH, carbon dioxide levels, 2,3-DPG, temperature, and certain conditions like methemoglobinemia.
This document discusses the regulation of respiration. It covers the neural, automatic, and chemical control mechanisms that regulate breathing. The key points are:
1) Respiration is regulated by medullary and pontine respiratory centers in the brainstem that generate the breathing rhythm and control rate and depth.
2) Breathing is also automatically controlled and can occur without conscious effort. It is further modulated by inputs from chemoreceptors sensitive to oxygen, carbon dioxide, and pH levels in the blood.
3) Peripheral chemoreceptors located in the carotid bodies and aortic bodies detect changes in blood gases and signal the respiratory centers to adjust breathing accordingly. Central chemoreceptors in the brainstem are
Bohr’s effect- The Bohr effect is a physiological phenomenon first described by Danish physiological Christian Bohr, stating that the “oxygen binding affinity of hemoglobin is inversely related to the concentration of carbon dioxide and hydrogen ion.
#An increase in blood CO2 concentration which leads to decrease in blood pH will results in hemoglobin proteins releasing their oxygen load.
#One of the factor that Bohr discovered was pH. He found that if the pH is lower than the normal, then hemoglobin does not bind oxygen.
#And this effect of CO2 on oxygen dissociation curve is known as Bohr effect.
Haldane effect- The Haldane effect is first discovered by John Scott Haldane.
#The Haldane effect describe the phenomenon by which binding of oxygen to hemoglobin promotes the release of carbon dioxide.
#Haldane effect is the mirror image of Bohr effect.
#The decrease in carbon dioxide leads to increase in the pH, which result in hemoglobin picking up more oxygen.
#This is a helpful biochemical feature which facilitates exchange of carbon dioxide for oxygen in the pulmonary and peripheral circulations.
Hypoxia refers to a lack of adequate oxygen supply to tissues. There are four main types of hypoxia: hypoxic (reduced oxygen in inspired air), anemic (low hemoglobin levels), stagnant (poor tissue perfusion), and histotoxic (impaired cellular oxygen use). Each type is characterized by specific changes in arterial oxygen levels, hemoglobin counts, blood flow rates, and other physiological markers. The body responds to hypoxic conditions through acclimatization mechanisms like hyperventilation and polycythemia, but these only partially restore normal oxygen levels and introduce their own risks. Long-term oxygen therapy has been shown to successfully treat chronic hypoxemia from respiratory diseases.
This document summarizes oxygen and carbon dioxide transport in the blood and tissues. It discusses how:
- Oxygen is carried bound to hemoglobin and dissolved in plasma, allowing blood to carry 30-100x more oxygen than if dissolved alone. Carbon dioxide also combines with substances to increase its transport 15-20x.
- Oxygen diffuses from alveoli into pulmonary blood and from arterial blood into tissues, while carbon dioxide diffuses in the opposite direction.
- Hemoglobin increases oxygen carrying capacity of blood by reversibly binding oxygen. Factors like CO2 levels and temperature can shift the oxygen-hemoglobin dissociation curve.
- In tissues, oxygen diffuses from capillaries into
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Barometric pressure falls with increasing altitude, but composition of air remain same.
Study is important for:Mountaineering
Aviation & Space flight
Permanent human settlement at highlands
Oxygen diffuses from the alveoli into the blood capillaries during gas exchange in the lungs. Air enters the lungs through the nasal cavity and trachea, with oxygen-rich alveolar air reaching the alveoli. The blood in the surrounding capillaries is oxygen-poor and carbon dioxide-rich. Oxygen diffuses into the red blood cells where it binds to hemoglobin, while carbon dioxide diffuses from the blood into the alveoli. The oxygenated blood is then transported around the body where gas exchange occurs again, with oxygen diffusing into cells and carbon dioxide diffusing into the blood.
This document discusses hypoxia, which is a condition where the body or a region of the body is deprived of adequate oxygen supply. It classifies hypoxia as either generalized, affecting the whole body, or local, affecting a region. Some key types of hypoxia discussed include hypoxic (insufficient oxygen in inspired air), anemic (decreased oxygen-carrying capacity of blood), ischemic (insufficient blood flow), and histotoxic (inability of cells to use oxygen). The document outlines various causes and effects of each type of hypoxia.
Acclimatization allows permanent residents at high altitudes to adjust to low oxygen levels through various compensatory mechanisms. These include increased pulmonary ventilation, higher red blood cell counts and hemoglobin concentration, decreased oxygen affinity of hemoglobin, and enhanced diffusion capacity. At the tissue level, capillarity increases and cellular changes improve oxygen utilization. Natives born at high altitude exhibit superior acclimatization through enhanced lung size, heart adaptations, and optimized oxygen delivery and transport. Failure to acclimatize can result in acute or chronic mountain sickness without appropriate ascent rates or remaining at altitude too long.
This document discusses various aspects of regional circulation including coronary, cerebral, splanchnic, skeletal muscle, and cutaneous circulation. It provides details on the anatomy, blood flow rates, regulation, and clinical implications of each type of circulation. For coronary circulation specifically, it notes that coronary artery disease is a leading cause of death, outlines the anatomy of the coronary arteries, and discusses factors that affect coronary blood flow such as exercise and hormones.
This document discusses the physiological effects of exposure to high altitudes and deep sea diving. It explains how the body acclimatizes to decreased oxygen levels at high altitude through increased respiration, red blood cell production, angiogenesis and other adaptations. It describes the risks of acute mountain sickness and pulmonary edema if acclimatization does not occur. For deep sea diving, it outlines the risks of nitrogen narcosis and oxygen toxicity at high pressures.
It discusses various effects of high altitude on human body in detail, acute mountain sickness, chronic mountain sickness, high altitude pulmonary edema, high altitude cerebral edema, acclimatization
This document discusses oxygen transport and delivery in the body. It covers:
1. Oxygen is transported bound to hemoglobin (97%) and dissolved in plasma (3%). Oxygen diffuses from alveoli into plasma and binds to hemoglobin in red blood cells.
2. Arterial oxygen content is determined by dissolved oxygen and oxygen bound to hemoglobin. Normal arterial content is 20 ml O2/100ml blood. Venous content is normally 15 ml O2/100ml blood.
3. Oxygen delivery depends on cardiac output and arterial oxygen content. Normal delivery is 1000 ml O2/min. Oxygen uptake by tissues is normally 250 ml O2/min.
The document discusses heart sounds, describing the four main sounds - S1, S2, S3, and S4. S1 occurs with the closing of the atrioventricular valves, coinciding with the R wave of an ECG. S2 occurs with the closing of the semilunar valves, coinciding with the T wave. S3 occurs during rapid ventricular filling between the T and P waves. S4 occurs during atrial systole between the P wave and Q wave. Heart sounds provide diagnostic value for assessing cardiac diseases and can be studied using a stethoscope, microphone, or phonocardiogram.
Hypoxia is a pathological condition defined as low oxygen delivery to tissues. The main types of hypoxia are hypoxic (low oxygen tension in arterial blood), circulatory/ischemic (reduced blood flow), anemic (decreased hemoglobin), and histotoxic (tissues unable to use oxygen). Symptoms of hypoxia depend on how rapidly and severely it develops, and can include restlessness, anxiety, fast breathing and heart rate, unconsciousness, and brain death in severe cases. Chronic hypoxia typically causes severe fatigue, shortness of breath, and cyanosis. The body compensates through hyperventilation, increased heart rate, and polycythemia. Oxygen therapy is used to treat hypoxic, an
The document summarizes chemical regulation of respiration. It discusses how carbon dioxide, hydrogen ions, and oxygen levels regulate breathing through central and peripheral chemoreceptors. The central chemoreceptors in the brainstem are stimulated by increased carbon dioxide and hydrogen ions in the bloodstream. The peripheral chemoreceptors in the carotid bodies and aortic arch are stimulated by decreased oxygen levels. Together, the chemoreceptors detect changes in gas levels and stimulate breathing to maintain homeostasis.
The document summarizes the nervous and chemical mechanisms that regulate respiration. There are two main mechanisms:
1. The nervous mechanism involves respiratory centers in the medulla oblongata and pons that receive input from afferent nerves and control respiration through efferent nerves that stimulate the diaphragm and intercostal muscles.
2. The chemical mechanism senses changes in blood gases through central and peripheral chemoreceptors. Central chemoreceptors in the brain stem detect increased carbon dioxide, while peripheral chemoreceptors in the carotid and aortic arteries detect low oxygen levels. Both trigger the respiratory centers to increase breathing rate.
The document discusses the neuromuscular junction and muscle contraction physiology. It defines the neuromuscular junction as the connection between motor neurons and muscle fibers that initiates muscle contraction. The structure and function of the neuromuscular junction is described, including the roles of acetylcholine, receptors, and acetylcholinesterase. The sliding filament model of muscle contraction is introduced. Different muscle fiber types, properties of muscle tissue, and the sarcomere as the contractile unit are defined.
This document defines and classifies different types of hypoxia: hypoxic (reduced oxygen in inspired air), anemic (reduced hemoglobin), stagnant (reduced blood flow), and histotoxic (tissues cannot use oxygen). It describes the pathophysiology, features, compensatory responses, and oxygen therapy approaches for each type. Hypercapnia and cyanosis, which can occur with hypoxia, are also explained. Oxygen therapy is most effective for hypoxic hypoxia but provides less benefit for types involving deficiencies in oxygen transport or utilization.
This document discusses hypoxia, including its definition, classification, causes, and effects. It defines hypoxia as a decrease in biological oxidation leading to ATP depletion. Hypoxia is classified into several types based on etiology, including exogenous (caused by low oxygen in inhaled air), respiratory (due to lung issues), circulatory (from cardiovascular problems), and histotoxic/tissue (interference with tissue oxygen use). Both acute and chronic hypoxia are described. Various compensatory mechanisms aim to increase oxygen delivery and utilization during hypoxia, while prolonged adaptation involves processes like erythropoiesis and angiogenesis. Metabolic consequences of hypoxia include overreliance on glycolysis due to energy deficiency.
The oxyhemoglobin dissociation curve shows the relationship between oxygen concentration and hemoglobin saturation in the blood. It demonstrates how hemoglobin binds to oxygen in the lungs when partial pressure of oxygen is high, and releases oxygen into tissues where partial pressure is low. Several factors can shift the curve left or right, changing hemoglobin's affinity for oxygen and impacting how much oxygen is unloaded to tissues. These include pH, carbon dioxide levels, 2,3-DPG, temperature, and certain conditions like methemoglobinemia.
This document discusses the regulation of respiration. It covers the neural, automatic, and chemical control mechanisms that regulate breathing. The key points are:
1) Respiration is regulated by medullary and pontine respiratory centers in the brainstem that generate the breathing rhythm and control rate and depth.
2) Breathing is also automatically controlled and can occur without conscious effort. It is further modulated by inputs from chemoreceptors sensitive to oxygen, carbon dioxide, and pH levels in the blood.
3) Peripheral chemoreceptors located in the carotid bodies and aortic bodies detect changes in blood gases and signal the respiratory centers to adjust breathing accordingly. Central chemoreceptors in the brainstem are
Bohr’s effect- The Bohr effect is a physiological phenomenon first described by Danish physiological Christian Bohr, stating that the “oxygen binding affinity of hemoglobin is inversely related to the concentration of carbon dioxide and hydrogen ion.
#An increase in blood CO2 concentration which leads to decrease in blood pH will results in hemoglobin proteins releasing their oxygen load.
#One of the factor that Bohr discovered was pH. He found that if the pH is lower than the normal, then hemoglobin does not bind oxygen.
#And this effect of CO2 on oxygen dissociation curve is known as Bohr effect.
Haldane effect- The Haldane effect is first discovered by John Scott Haldane.
#The Haldane effect describe the phenomenon by which binding of oxygen to hemoglobin promotes the release of carbon dioxide.
#Haldane effect is the mirror image of Bohr effect.
#The decrease in carbon dioxide leads to increase in the pH, which result in hemoglobin picking up more oxygen.
#This is a helpful biochemical feature which facilitates exchange of carbon dioxide for oxygen in the pulmonary and peripheral circulations.
Hypoxia refers to a lack of adequate oxygen supply to tissues. There are four main types of hypoxia: hypoxic (reduced oxygen in inspired air), anemic (low hemoglobin levels), stagnant (poor tissue perfusion), and histotoxic (impaired cellular oxygen use). Each type is characterized by specific changes in arterial oxygen levels, hemoglobin counts, blood flow rates, and other physiological markers. The body responds to hypoxic conditions through acclimatization mechanisms like hyperventilation and polycythemia, but these only partially restore normal oxygen levels and introduce their own risks. Long-term oxygen therapy has been shown to successfully treat chronic hypoxemia from respiratory diseases.
This document summarizes oxygen and carbon dioxide transport in the blood and tissues. It discusses how:
- Oxygen is carried bound to hemoglobin and dissolved in plasma, allowing blood to carry 30-100x more oxygen than if dissolved alone. Carbon dioxide also combines with substances to increase its transport 15-20x.
- Oxygen diffuses from alveoli into pulmonary blood and from arterial blood into tissues, while carbon dioxide diffuses in the opposite direction.
- Hemoglobin increases oxygen carrying capacity of blood by reversibly binding oxygen. Factors like CO2 levels and temperature can shift the oxygen-hemoglobin dissociation curve.
- In tissues, oxygen diffuses from capillaries into
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Barometric pressure falls with increasing altitude, but composition of air remain same.
Study is important for:Mountaineering
Aviation & Space flight
Permanent human settlement at highlands
Oxygen diffuses from the alveoli into the blood capillaries during gas exchange in the lungs. Air enters the lungs through the nasal cavity and trachea, with oxygen-rich alveolar air reaching the alveoli. The blood in the surrounding capillaries is oxygen-poor and carbon dioxide-rich. Oxygen diffuses into the red blood cells where it binds to hemoglobin, while carbon dioxide diffuses from the blood into the alveoli. The oxygenated blood is then transported around the body where gas exchange occurs again, with oxygen diffusing into cells and carbon dioxide diffusing into the blood.
This document discusses hypoxia, which is a condition where the body or a region of the body is deprived of adequate oxygen supply. It classifies hypoxia as either generalized, affecting the whole body, or local, affecting a region. Some key types of hypoxia discussed include hypoxic (insufficient oxygen in inspired air), anemic (decreased oxygen-carrying capacity of blood), ischemic (insufficient blood flow), and histotoxic (inability of cells to use oxygen). The document outlines various causes and effects of each type of hypoxia.
Acclimatization allows permanent residents at high altitudes to adjust to low oxygen levels through various compensatory mechanisms. These include increased pulmonary ventilation, higher red blood cell counts and hemoglobin concentration, decreased oxygen affinity of hemoglobin, and enhanced diffusion capacity. At the tissue level, capillarity increases and cellular changes improve oxygen utilization. Natives born at high altitude exhibit superior acclimatization through enhanced lung size, heart adaptations, and optimized oxygen delivery and transport. Failure to acclimatize can result in acute or chronic mountain sickness without appropriate ascent rates or remaining at altitude too long.
This document discusses various aspects of regional circulation including coronary, cerebral, splanchnic, skeletal muscle, and cutaneous circulation. It provides details on the anatomy, blood flow rates, regulation, and clinical implications of each type of circulation. For coronary circulation specifically, it notes that coronary artery disease is a leading cause of death, outlines the anatomy of the coronary arteries, and discusses factors that affect coronary blood flow such as exercise and hormones.
This document discusses the physiological effects of exposure to high altitudes and deep sea diving. It explains how the body acclimatizes to decreased oxygen levels at high altitude through increased respiration, red blood cell production, angiogenesis and other adaptations. It describes the risks of acute mountain sickness and pulmonary edema if acclimatization does not occur. For deep sea diving, it outlines the risks of nitrogen narcosis and oxygen toxicity at high pressures.
It discusses various effects of high altitude on human body in detail, acute mountain sickness, chronic mountain sickness, high altitude pulmonary edema, high altitude cerebral edema, acclimatization
This document discusses oxygen transport and delivery in the body. It covers:
1. Oxygen is transported bound to hemoglobin (97%) and dissolved in plasma (3%). Oxygen diffuses from alveoli into plasma and binds to hemoglobin in red blood cells.
2. Arterial oxygen content is determined by dissolved oxygen and oxygen bound to hemoglobin. Normal arterial content is 20 ml O2/100ml blood. Venous content is normally 15 ml O2/100ml blood.
3. Oxygen delivery depends on cardiac output and arterial oxygen content. Normal delivery is 1000 ml O2/min. Oxygen uptake by tissues is normally 250 ml O2/min.
The document discusses heart sounds, describing the four main sounds - S1, S2, S3, and S4. S1 occurs with the closing of the atrioventricular valves, coinciding with the R wave of an ECG. S2 occurs with the closing of the semilunar valves, coinciding with the T wave. S3 occurs during rapid ventricular filling between the T and P waves. S4 occurs during atrial systole between the P wave and Q wave. Heart sounds provide diagnostic value for assessing cardiac diseases and can be studied using a stethoscope, microphone, or phonocardiogram.
Hypoxia is a pathological condition defined as low oxygen delivery to tissues. The main types of hypoxia are hypoxic (low oxygen tension in arterial blood), circulatory/ischemic (reduced blood flow), anemic (decreased hemoglobin), and histotoxic (tissues unable to use oxygen). Symptoms of hypoxia depend on how rapidly and severely it develops, and can include restlessness, anxiety, fast breathing and heart rate, unconsciousness, and brain death in severe cases. Chronic hypoxia typically causes severe fatigue, shortness of breath, and cyanosis. The body compensates through hyperventilation, increased heart rate, and polycythemia. Oxygen therapy is used to treat hypoxic, an
The document summarizes chemical regulation of respiration. It discusses how carbon dioxide, hydrogen ions, and oxygen levels regulate breathing through central and peripheral chemoreceptors. The central chemoreceptors in the brainstem are stimulated by increased carbon dioxide and hydrogen ions in the bloodstream. The peripheral chemoreceptors in the carotid bodies and aortic arch are stimulated by decreased oxygen levels. Together, the chemoreceptors detect changes in gas levels and stimulate breathing to maintain homeostasis.
The document summarizes the nervous and chemical mechanisms that regulate respiration. There are two main mechanisms:
1. The nervous mechanism involves respiratory centers in the medulla oblongata and pons that receive input from afferent nerves and control respiration through efferent nerves that stimulate the diaphragm and intercostal muscles.
2. The chemical mechanism senses changes in blood gases through central and peripheral chemoreceptors. Central chemoreceptors in the brain stem detect increased carbon dioxide, while peripheral chemoreceptors in the carotid and aortic arteries detect low oxygen levels. Both trigger the respiratory centers to increase breathing rate.
The document discusses the neuromuscular junction and muscle contraction physiology. It defines the neuromuscular junction as the connection between motor neurons and muscle fibers that initiates muscle contraction. The structure and function of the neuromuscular junction is described, including the roles of acetylcholine, receptors, and acetylcholinesterase. The sliding filament model of muscle contraction is introduced. Different muscle fiber types, properties of muscle tissue, and the sarcomere as the contractile unit are defined.
This document defines and classifies different types of hypoxia: hypoxic (reduced oxygen in inspired air), anemic (reduced hemoglobin), stagnant (reduced blood flow), and histotoxic (tissues cannot use oxygen). It describes the pathophysiology, features, compensatory responses, and oxygen therapy approaches for each type. Hypercapnia and cyanosis, which can occur with hypoxia, are also explained. Oxygen therapy is most effective for hypoxic hypoxia but provides less benefit for types involving deficiencies in oxygen transport or utilization.
This document discusses hypoxia, including its definition, classification, causes, and effects. It defines hypoxia as a decrease in biological oxidation leading to ATP depletion. Hypoxia is classified into several types based on etiology, including exogenous (caused by low oxygen in inhaled air), respiratory (due to lung issues), circulatory (from cardiovascular problems), and histotoxic/tissue (interference with tissue oxygen use). Both acute and chronic hypoxia are described. Various compensatory mechanisms aim to increase oxygen delivery and utilization during hypoxia, while prolonged adaptation involves processes like erythropoiesis and angiogenesis. Metabolic consequences of hypoxia include overreliance on glycolysis due to energy deficiency.
Abnormal Types of Breathing, Hypoxia, Cyanosis, AsphyxiaUMAMAHISHAQ
This document discusses different types of breathing patterns and hypoxia. It describes Cheyne Stokes breathing as having alternating periods of hyperventilation and apnea with a gradual transition between periods. Biot breathing also has periods of hyperventilation and apnea but with an abrupt transition. Different causes of hypoxia are outlined including arterial hypoxia from low oxygen in air, anemic hypoxia from low hemoglobin, ischemic hypoxia from low blood flow, and histotoxic hypoxia from issues with tissue oxygen utilization.
This document discusses various medical gases including oxygen, carbon dioxide, helium, and their properties, preparation, storage, clinical uses, and safety considerations. It provides details on oxygen therapy including indications, assessment, delivery methods, complications like toxicity, and monitoring. The oxygen cascade and hypoxia types are explained. Carbon dioxide properties and uses in anesthesia are covered. Helium properties and use in partial airway obstruction are outlined. Methods of gas analysis are also summarized.
Hypoxia is a medical condition defined as reduced oxygen availability to tissues. It can be caused by factors that decrease oxygen delivery or utilization at the tissue level. There are four main types of hypoxia: hypoxic (decreased oxygen in arterial blood), anemic (decreased oxygen-carrying capacity of blood), stagnant (decreased blood flow), and histotoxic (inability of tissues to use oxygen). The immediate effects of hypoxia include increased respiration and heart rate, effects on blood including increased red blood cell production, and neurological effects ranging from intoxication to loss of consciousness. Long term effects depend on severity and duration of hypoxic exposure and can include chronic fatigue and irritability.
Hypoxia and hypercapnia occur when there are insufficient oxygen levels or excessive carbon dioxide levels in the blood and tissues. There are four main types of hypoxia - hypoxic (low oxygen levels), anemic, hypoperfusion (low blood flow), and histotoxic (inability to use oxygen). Hypercapnia results from hypoventilation where breathing is inadequate to remove carbon dioxide. This leads to increased carbon dioxide and acidosis in the blood and tissues. Hypoxia and hypercapnia can cause respiratory and cardiovascular effects like increased breathing and heart rate as well as central nervous system impacts like headaches, dizziness and loss of consciousness.
This document summarizes the regulation of breathing. It discusses both chemical and non-chemical regulation. The chemical regulation is primarily via central and peripheral chemoreceptors that monitor changes in blood gases like CO2, O2 and pH. The central chemoreceptors are located in the brain and respond mainly to CO2, while peripheral chemoreceptors in the carotid and aortic bodies respond more to changes in O2, CO2 and pH. Non-chemical regulation involves signals from various receptors and parts of the body that influence breathing rate and depth.
Hypoxia is a lack of oxygen at the tissue level, while anoxia is a complete absence of oxygen. There are four main types of hypoxia: hypoxic, anemic, stagnant, and histotoxic. Hypoxic hypoxia occurs when oxygen carrying capacity is normal but arterial oxygen levels are low. Anemic hypoxia results from low hemoglobin levels despite normal arterial oxygen. Stagnant hypoxia is caused by low blood flow even with normal hemoglobin and oxygen levels. Histotoxic hypoxia occurs when tissues cannot use oxygen due to toxic agents. Symptoms include hyperventilation, drowsiness, and cyanosis below 60% saturation. Treatment focuses on addressing the underlying cause and providing supplemental
For my colleagues and medical students out there who need to either read or present the subject of hypoxia in surgical patients. I hope you find this one helpful.
The document discusses asphyxia, which is caused by occlusion of airways and results in hypoxia and hypercapnia. It describes the three stages of asphyxia: exaggerated breathing, convulsions, and exhaustion/collapse. Oxygen therapy can help in some types of hypoxia but not others. The risks of oxygen therapy in infants are also outlined. Hypercapnia and cyanosis that can occur with hypoxia are explained. Local factors like cold exposure can also cause cyanosis.
Oxygen is essential for life and deprivation leads most rapidly to death. Oxygen therapy is useful for diseases that interfere with normal oxygenation. Hypoxia refers to insufficient oxygen in tissues and can be caused by problems delivering oxygen to the lungs, abnormal lung function, or inadequate oxygen delivery to tissues. Effects of hypoxia include increased respiration, increased heart rate and blood flow, impaired brain function, and cellular metabolic changes. Oxygen inhalation can reverse hypoxia but excessive amounts can cause toxicity, especially in the central nervous system and lungs.
Oxygen is essential for life and deprivation leads most rapidly to death. Oxygen therapy is useful for diseases that interfere with normal oxygenation. Hypoxia refers to insufficient oxygen in tissues and can be caused by problems delivering oxygen to the lungs, abnormal lung function, or inadequate oxygen delivery to tissues. Effects of hypoxia include increased respiration, increased heart rate and blood flow, impaired brain function, and cellular metabolic changes. Oxygen inhalation can reverse hypoxia but excessive amounts can cause toxicity, especially in the central nervous system and lungs.
Hypoxia refers to inadequate oxygen supply at the tissue level. It can be caused by problems with oxygen delivery, transport, or cellular uptake. Effects of hypoxia range from impaired mental function to cell death. There are several types of hypoxia depending on the underlying cause, such as atmospheric, anemic, or circulatory hypoxia. Oxygen therapy aims to correct hypoxemia by raising oxygen levels, reducing symptoms, and minimizing cardiovascular strain. Care must be taken to avoid oxygen toxicity from prolonged high concentrations.
This document discusses the chemical control of respiration through peripheral and central chemoreceptors. It begins by introducing the objectives and overview. It then describes the two main types of chemoreceptors - peripheral located in the carotid and aortic bodies, and central located in the brainstem. Both receptor types detect changes in blood pH, CO2 and O2 levels. The document focuses on the specific mechanisms and effects of hypoxia, hypercapnia, and acidosis on each receptor type and their integrated control of ventilation.
1. Mixed venous blood is a mixture of blood from the systemic veins excluding shunted blood, with components from the superior vena cava, inferior vena cava, and coronary sinus.
2. Sustained tissue hypoxia is a major factor in the development of multiorgan failure. Mixed venous oximetry can measure the balance between oxygen delivery and demand.
3. Central venous oxygen saturation (ScvO2) closely parallels mixed venous oxygen saturation (SvO2) but may be 7-10% higher in shock states, due to regional variations in blood flow and oxygen supply/demand.
1. Mixed venous blood is a mixture of blood from the systemic veins that has undergone gas exchange in the tissues, excluding shunted blood. It provides information on the balance between oxygen delivery and consumption on a systemic level.
2. The mixed venous oxygen saturation (SvO2) reflects this balance, with a normal value around 75%. A low SvO2 indicates oxygen delivery is not meeting tissue demands, while a high SvO2 suggests impaired tissue extraction of oxygen.
3. The central venous oxygen saturation (ScvO2) approximates SvO2 but is usually a few points higher. Both can help guide resuscitation in shock states like sepsis when used as targets for
Surfactant is a mixture that coats the alveoli and reduces surface tension, preventing collapse during exhalation. It is composed primarily of phospholipids including DPPC, as well as proteins. Surfactant is synthesized in type II pneumocytes and stored in lamellar bodies, which release surfactant onto the alveolar surface. Surfactant allows the alveoli to remain open during breathing and prevents edema. Hypoxia occurs when tissues do not receive enough oxygen, and can be caused by reduced oxygen delivery or utilization. The effects of hypoxia depend on its severity and duration, ranging from impaired judgment during acute hypoxia to polycythemia in chronic cases.
The document discusses various medical conditions related to breathing and oxygen levels in the body. It defines terms like hypoxia, hypoventilation, eupnea, tachypnea, dyspnea, apnea, periodic breathing, and different types of sleep disordered breathing. It also describes the stages and effects of asphyxia, different types of hypoxia, and explains what hyperbaric oxygen therapy is and how it works.
The document discusses hypoxia, or low oxygen levels in body tissues. It defines four types of hypoxia: hypoxemic caused by low blood oxygen levels, anemic caused by low hemoglobin, stagnant caused by reduced blood flow, and histotoxic caused by tissues' inability to use oxygen. It then provides more details on the causes and mechanisms of each type, focusing on hypoxemic hypoxia which can result from low atmospheric oxygen or lung issues preventing oxygen transfer from air to blood. Ventilation-perfusion mismatch is highlighted as a common cause of hypoxemia, or low blood oxygen levels, which can in turn cause hypoxia in tissues. Early detection using a pulse oximeter and treatments like supplemental oxygen
This document summarizes the composition, properties, functions and volume of blood. It discusses that blood consists of cells suspended in plasma. The main cells are red blood cells, white blood cells and platelets. Plasma is mostly water with dissolved proteins and electrolytes. Bone marrow produces blood cells. Key functions of blood include transport, defense, regulation and hemostasis. The normal blood volume in adults is 5-6 liters. The hematocrit level indicates the proportion of red blood cells and can be used to screen for anemia. The blood and plasma volumes are regulated to maintain homeostasis.
1. Excitable tissues include nerve cells, nerve fibers, muscle fibers, and some plant cells that generate action potentials along their cell membranes in response to stimulation.
2. Nerve cells have a cell body containing organelles, dendrites that receive synaptic inputs, and a single axon that conducts electrical impulses to synaptic terminals.
3. Glial cells such as astrocytes, oligodendrocytes, microglia, and ependymal cells provide support and insulation to neurons in the nervous system.
The document discusses skeletal muscle and its structure and function. It contains 3 types of muscle: skeletal, smooth, and cardiac. Skeletal muscle is striated, involuntary muscle that moves the body and maintains posture. It develops tension and produces heat. Skeletal muscle fibers are cylindrical, multinucleated cells containing myofibrils with overlapping actin and myosin filaments that slide past each other to cause contraction. Contraction is initiated by calcium release from the sarcoplasmic reticulum in response to action potentials.
This document discusses heart murmurs, which are abnormal sounds caused by turbulent blood flow through the heart. It describes the different types of murmurs:
1) Systolic murmurs occur between the first and second heart sounds and can be caused by valve stenosis or insufficiency.
2) Diastolic murmurs occur between the second heart sound and next first sound, caused by stenosis or insufficiency of different heart valves.
3) Continuous murmurs occur during both systole and diastole, associated with conditions like a patent ductus arteriosus.
It provides examples of specific murmurs caused by abnormalities of the aortic, mitral, and tricuspid valves.
1. Erythrocytes, also known as red blood cells, are biconcave discs that contain hemoglobin and have an average lifespan of 120 days. Their primary function is to carry oxygen from the lungs to tissues and carbon dioxide from tissues back to the lungs.
2. Polycythemia is a condition of increased red blood cell count or hemoglobin concentration in the blood. Primary polycythemia is caused by excessive red blood cell production while secondary polycythemia occurs in response to tissue hypoxia such as at high altitudes.
3. Hemoglobin is the iron-containing protein in red blood cells that carries oxygen. It is composed of globin proteins and heme groups. Abnormalities
The document discusses heart sounds, including the four main types: S1, S2, S3, and S4. S1 and S2 are normally heard with each heartbeat while S3 and S4 may sometimes be heard. S1 occurs with the closure of the atrioventricular valves at the beginning of systole. S2 occurs with the closure of the semilunar valves at the end of systole. S3 occurs during early ventricular filling and S4 occurs during atrial contraction just before S1 of the next cycle. The sounds are associated with different parts of the cardiac cycle and changes in sounds can provide information about cardiac function and health issues.
Hemostasis occurs via four mechanisms: vasoconstriction, formation of a platelet plug, formation of a blood clot, and repair of the damaged blood vessel. Blood coagulation involves a cascade of reactions through the extrinsic and intrinsic pathways. The extrinsic pathway is initiated by tissue damage and the intrinsic pathway is initiated by contact with foreign surfaces. Both pathways lead to the conversion of prothrombin to thrombin which converts fibrinogen to fibrin to form a clot. Calcium ions, platelets, vitamin K, and the coagulation factors are essential for effective hemostasis and blood coagulation.
The cardiac cycle describes the repeating pattern of heart contraction and relaxation that pumps blood throughout the body. It consists of systole, when the heart contracts to pump blood, and diastole, when the heart relaxes and refills with blood. Each cycle normally occurs at a rate of about 75 times per minute. The cycle includes phases of isometric contraction and relaxation when pressure changes but volume does not, and ejection and filling phases when blood is pumped out or flows into the heart. Precise events in pressure, volume, valve opening and closing, and sounds occur throughout each phase of the cardiac cycle.
1. Carbon dioxide is transported in the blood from tissues to the lungs in both dissolved form and chemically combined as bicarbonate and carbamino compounds.
2. In the tissues, carbon dioxide diffuses into red blood cells where the carbonic anhydrase enzyme converts it mainly to bicarbonate, which then diffuses out of the cells in exchange for chloride ions in a process called the chloride shift.
3. This transport of carbon dioxide and shift of bicarbonate and chloride regulates blood pH and allows for exchange of carbon dioxide in the lungs, where it is released for exhalation.
The document discusses compliance of the lungs and chest wall, measurement of respiratory compliance (static vs dynamic), factors that affect lung compliance such as lung size and surface tension, diseases that decrease compliance, work of breathing including elastic and resistive components, factors that increase work of breathing, effects of gravity on ventilation and pulmonary blood flow including differences in regional lung volumes and flows, pneumothorax types including closed, open, and tension pneumothorax and their effects, and artificial pneumothorax as a therapeutic procedure.
Oxygen transport (carriage)_by_the_bl000zulujunior
1. Oxygen transport by the blood involves oxygen flowing from the alveoli to the tissues via hemoglobin in the blood. The oxygen carrying capacity of hemoglobin is increased about 70 times compared to dissolved oxygen alone.
2. The oxygen-hemoglobin dissociation curve shows the relationship between oxygen pressure and hemoglobin saturation. It is sigmoid shaped due to cooperative binding of oxygen.
3. Factors like acidosis, increased temperature, and 2,3-DPG can shift the curve rightward, increasing oxygen unloading to tissues. Fetal hemoglobin and alkalosis shift the curve leftward, decreasing oxygen unloading.
This document discusses gas exchange in the lungs. It covers the laws of gases, the partial pressure of gases, standardization of gas volumes, gas dissolution in fluids, gas diffusion through membranes, Fick's law of gas diffusion, the alveolar-capillary membrane, gas exchange across this membrane, equilibration of respiratory gases in the lungs, and the diffusion capacity of the lung. The key points are that oxygen diffuses from the alveoli into the blood while carbon dioxide diffuses out, and the solubility of carbon dioxide is much higher than oxygen allowing for faster diffusion.
The document discusses pulmonary surfactant, which reduces surface tension in the lungs. It describes the composition of surfactant, which contains phospholipids like phosphatidylcholine and proteins. Phosphatidylcholine is the most abundant lipid and reduces surface tension. Surfactant is synthesized in alveolar type II cells and stored in lamellar bodies. Hormones like glucocorticoids and estrogen increase surfactant production through various enzymatic pathways. Surfactant is essential for lung function as it prevents alveolar collapse and facilitates gas exchange.
Breathing is controlled by respiratory centers located in the brain stem and spinal cord. The medullary respiratory centers include the dorsal respiratory group (DRG), ventral respiratory group (VRG), and Botzinger complex. The DRG contains inspiratory neurons that promote inspiration, while the VRG contains expiratory neurons that promote expiration. The pontine respiratory group in the pons modulates the medullary centers. Rhythmic breathing occurs through reciprocal inhibition between inspiratory and expiratory neurons. Inspiration is an active process involving contraction of the diaphragm and rib muscles, while expiration is usually passive due to lung elasticity.
This document discusses factors that contribute to alveolar stability in the lungs. Alveolar stability is maintained by two main factors: surfactant and alveolar interdependence. Surfactant acts to reduce surface tension in small alveoli, preventing their collapse. Alveolar interdependence describes how neighboring alveoli support each other's volume. Together, surfactant and interdependence help maintain equal pressure across alveoli of different sizes. The document also discusses the elastic properties of the respiratory system, including how the recoiling forces of the lungs and chest wall interact to determine intrapulmonary pressure at different lung volumes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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2. Depending on the cause, hypoxia is classified into 4 main types:
1. Hypoxic hypoxia. 2. Anaemic hypoxia.
3. Stagnant hypoxia. 4. Histotoxic hypoxia.
DEFINITION AND TYPES OF HYPOXIA
Hypoxia is O2 deficiency at the tissue level. It is a better term
than anoxia (= complete 02 lack at the tissues) because the latter
never occurs clinically.
On the other hand, hypoxaemia refers to 02 deficiency in the
blood.
3. There is also cyanosis due to presence of excessive amounts of
reduced Hb in the blood. The common causes of hypoxic hypoxia
include the following :
(1) HYPOXIC HYPOXIA
ln this type, the hypoxia occurs secondary to hypoxaemia. The
P02 and 02 content as well as the % saturation of Hb with 02 are
all decreased in both the arterial and venous blood
2. Inadequate pulmonary ventilation (respiratory pump failure) :
This results from defective breathing which may occur due to
either :
1. Breathing air that contains low 02 % than normal (e.g. in high
altitudes) and places that are not properly ventilated (e.g. mines).
4. a- Depression of the respiratory centre (e.g. in morphine
poisoning).
b- Weakness or paralysis of the respiratory muscles (e.g. in
poliomyelitis).
c- Fatigue of the respiratory muscles (e.g. in bronchial asthma).
d- Pneumothorax, hydrothorax, chest deformities and
emphysema.
e- Shallow rapid breathing (e.g. in pulmonary congestion or
embolism).
3. Gas exchange failure: This occurs in diseases that cause
alveolo-capillary block (e.g. pulmonary fibrosis or edema and
pneumonia) or ventilation perfusion imbalance.
4. Right to left cardiac shunts (e.g. atrial and ventricular septal
defects) : These transfer venous blood to the left side of the heart
(without oxygenation in the lungs), resulting in hypoxaemia and
consequently hypoxia.
5. (2) ANAEMIC HYPOXIA
ln this type, the hypoxia occurs due to deficiency of the amount
of Hb available to carry 02 . In the arterial blood, the 02 content is
decreased but the PO2 is normal, while both are decreased in the
venous blood.
Its common causes include the following :
1. All types of anaemia.
2. Transformation of Hb by certain toxins and drugs into
compounds that are unable to carry 02 e.g. sulph-Hb and metHb
(refer to blood).
3. Carbon monoxide (CO) poisoning.
6. Carbon monoxide (CO) poisoning
CO combines with Hb and forms carboxv-Hb CCOHb). The
affinity of Hb to CO is about 250 times its affinity to 02, and COHb
cannot bind to 02 (because CO binds to the ferrous atoms in the
Hb molecule).
CO also shifts the O2Hb dissociation curve to the left and this
further decreases delivery of oxygen to the tissues, resulting in
severe hypoxia (which is fatal if 70 - 80 % of Hb is converted to
COHb)
7. 2. The skin and mucous membranes are cherry red (colour of
COHb)
Symptoms
1. Symptoms of other types of hypoxia (see below) specially
headache and nausea (however, since the arterial P02 is normal,
the peripheral chemoreceptors are not stimulated, so respiration is
little stimulated)
3. Symptoms of brain damage (mental changes & parkinsonism
like state) appear with exposure to small doses of the gas.
8. 2. Breathing a mixture of 95 % 02 and 5 % C02. 02 helps COHb
dissociation, while C02 stimulates respiration. Hyperbaric 02 (02
under high pressure) can also be used
Treatment
1. Removing the patient away from the source of the gas, keeping
him at complete rest and improving his ventilation by artificial
respiration
3. Exchange blood transfusion may be required in severe cases.
9. (3) STAGNANT (ISCHAEMIC) HYPOXIA
ln this type, the hypoxia occurs due to blood stagnation (or slow
circulation) in the tissues. Both the PO2 and 02 content are
normal in the arterial blood but decreased in the venous blood,
leading to cyanosis in the affected areas. Blood stagnation may
be either :
1. Generalized (i.e. allover the body) e.g. in congestive heart
failure, circulatory shock, and polycythaemia vera
2. Localized e.g. in areas of venous thrombosis or V.C. (the latter
is characteristic of Raynaud's disease, in which severe V.C.
occurs in the tips of the lingers and toes, specially on exposure to
cold)
10. (4) HISTOTOXIC HYPOXIA
In this type, the hypoxia occurs due to blockage of the enzymes
involved in tissue (or internal) respiration (= the process of gas
exchange in the cells).
Thus, although the arterial PO2 and 02 content are normal, yet
02 cannot be extracted, and consequently, their levels are
increased in the venous blood and approach their levels in the
arterial blood
Tissue respiration depends on a haem-like substance called
cytochrome and certain enzymes, specially cytochrome oxidase.
These are concerned with 0 2 transport from the blood to the
tissues by the following reaction :
11. The oxidized -cytochrome –releases its 02 to the tissues and
becomes reduced. The reduced cytochrome then gets 02 from the
blood and becomes oxidized, and the cycle is repeated. The
commonest cause of histotoxic hypoxia is cyanide poisoning
12. Cyanide poisoning
The cyanide salts block the cytochrome oxidase enzyme, so the
cells become hypoxic because they become unable to extract 02
from the blood.
The condition can be improved by hyperbaric oxygenation and
also by giving methylene blue or nitrite salts (these substances
convert Hb into metHb, which reacts with cyanide and form the
non-toxic compound cyan-metHb).
13. The following table shows the P02 and 0 2 content in the arterial
and venous blood in various types of hypoxia :
14. SYMPTOMS OF HYPOXIA
Sudden severe hypoxia is fatal due to deprerssion of the
respiratory centre. On the other hand, mild and moderate hypoxia
lead to the following :
1. Nervous symptoms e.g. headache, fatigue, disorientation and
drowsiness.
2. Digestive symptoms e.g. anorexia (loss ofappetite), nausea and
vomiting.
3. Respiratory symptoms (tachypnea and may be periodic
breathing).
4. Cardiovascular symptoms: Tachycardia, high cardiac output
and hypertension, followed by fainting in long-standing cases.
In chronic hypoxia, the alveolar hypoxia causes pulmonary V.
C., which may lead to pulmonnary hypertension and overstraining
of the right ventricle.
15. ACCLIMATIZATION
This term refers to the adaptive mechanisms that occur in high
altitudes (i.e. on prolonged exposure to low 02 pressures). The
body tries to compensate and improve O2 delivery to the tissues.
The minimal alveolar PO2 that can be tolerated without loss of
consciousness is 40 mmHg (at which Hb is about 75% saturated
with 02). The altitude at which this occurs varies according to
whether the subject is breathing air or 100% O2:
At high altitudes, the composition of air remains constant but its
total pressure falls. This results in marked reduction of the PO2 in
atmospheric air
16. If the subject was breathing air, this P02 is reached when the
atmospheric pressure decreases to 350 mmHg (at an altitude
of about 6100 meters) while if the subject was breathing 100%
O2, it is reached when the atmospheric pressure decreases to
120 mmHg (at an altitude of about 13700meters)
17. ACUTE MOUNTAIN SICKNESS
This is a condition that may occur in some individuals when they
ascend to high altitudes for the first time. It occurs within 8 - 24
hours and lasts for 4-8 days.
Its symptoms include headache, dizziness, irritability,
insomnia, fatigue, dyspnea, palpitation, anorexia, nausea and
vomitting.
Its cause is probably cerebral edema (which is often produced
secondary to V.D. of the cerebral vessels that occurs as a result of
the low arterial P02) because the symptoms markedly improve
when the cerebral edema is treated.
18. ACCL MATIZATION MECHANISMS
The compensatory mechanisms involved in acclimatization
usually starts within one week. They aim at increasing 02 delivery
to the tissues, and they include the following:
1. Increase of the pulmonary ventilation: This occurs as a result of
stimulation of the respiratory centre by signals discharged from
the peripheral chemoreceptors (which are excited when the
arterial Po2 drops below 60 mmHg).
The initial response is relatively small because the resulting
hyperventilation washes C02 in the expired air resulting in
alkalosis (which tends to inhibit the respiratory centre).
19. However, within a few days ventilation markedly increases due
to :
a- Correction of the alkalosis through excessive excretion of
HC03, by the kidneys in the urine (so the urine pH in high altitudes
is alkaline).
b- Stimulation of the central chemoreceptors by the lowered brain
pH (which is produced as a result of development of lactic
acidosis, as well as shift of HC03- from the brain to the plasma).
20. 2. Increase of the blood O2- carrying capacity: This occurs as a
result of stimulation of erythropoiesis under the effect of the
erythropoietin hormone (which is secreted by the kidneys in
response to O2 lack).
The red cell count increases up to 8 millionImm3 (=
physiological polycythemia) and the Hb content may increase by
50 % (which increases the 0 2-canying capacity of the blood) and
in addition, the haematocrit value increases up lo 60 %and the
blood volume by 20 30 %.
21. 3. Increase of the circulatory rate: Signals from the peripheral
chemoreceptors stimulate the vasomotor centre, resulting in
tachycardia and an increase of both the cardiac output and arterial
blood pressure.
4. Increase of 02 liberation at the tissues: This is produced
through stimulation of 2-3 DPG synthesis in the red blood cells at
high altitudes, which facilitates 02 liberation from Hb02 by shifting
the 02-Hb dissociation curve to the right
In addition, peripheral V.D. and angiogenesis also occur under
the effect of 02 lack. All these effects increase the blood flow to
the tissues.
22. 2-3 DPG antagonizes the effect of alkalosis (which tends to shift
the O2Hb dissociation curve to the left) and produces a net
increase of the P50.
5. Cellular compensatory changes: ln response to the low arterial
PO2, all the following increase in the cells :
a- The mitochondria (the site of oxidative reactions).
b- The myoglobin content in skeletal muscles.
c- The oxidative enzymes (specially the cytochrome oxidase
enzyme).
What is the role of the kidneys in high altitudes with respect to
acclimatization?
23. Over subsequent weeks and months most people acclimatize to
living at high altitude, although the ability to perform strenuous
exercise may be limited.
No human communities live permanently above 5500m because
further acclimatization becomes impossible; instead there is slow
deterioration in all aspects.
The various compensating mechanisms:
24. 1. Respiratory functions: Hyperventilation continues; pulmonary
diffusion capacity can increase upto threefold as a result of
more open pulmonary capillaries; increased pulmonary
capillary blood volume and greater alveolar surface area.
Cyanosis may be absent at rest.
2. Kidney functions: they excrete HC03 and eventual correction
of the respiratory alkalosis. This takes 2-3 weeks
3. Cardiovascular functions: Perfusion and heart rate tend to
come back to sea level values. Hypoxic vasoconstriction leads
to pulmonary hypertension and right ventricular hypertrophy.
The vasoconstriction also precipitates muscularization of
pulmonary arterioles, which are normally devoid of smooth
muscle.
25. 4. Tissue function: there is an increase in the capillary of many
tissues and in the concentration of cytochrome oxidase; the
former improves O2 transfer and the latter permits the
mitochondria to utilize the O2 more effectively. The myoglobin
content of the skeletal muscles also increase, which raises the
reserve store of O2; myoglobin may also facilitate intracellular
diffusion.
5. Blood: there is an increase in 2,3 BPG production which shifts
the OxyHb curve to the right, to enable O2 to be offloaded to
the tissues more easily. Hypoxia increases, erythropoeitin
production leading to polycythemia. Hb concentration may
increase to as much as 20gm/dL and despite los PO2 and %
saturation of Hb with O2, O2 content will not fall as much.
What is the disadvantage to this?
26. Some individuals successfully acclimatize gradually or even
suddenly fail in their compensation response.
Their ventilation falls producing dyspnoea and cyanosis.
Hematocrit and pulmonary arterial pressure iincreases further,
leading to right heart failure.
In sudden failure, pulmonary oedema is the most dominant
feature.
These are all the symptoms of chronic mountain sickness
27. Colour of the skin in various types of hypoxia
1. In hypoxic hypoxia, there is cyanosis (i.e. the skin is bluish)
because of presence of abnormally great amounts of reduced
Hb in the blood.
2. In anaemic hypoxia, the skin is pale, except in CO poisoning
in which the skin is cherry red (which is the colour of
carboxyHb).
3. In stagnant hypoxia, there is cyanosis (i.e. the skin is bluish)
because of presence of abnormally great amounts of reduced
Hb in the venous blood as a result of blood stagnation in the
tissues.
4. In histotoxic hypoxia, the skin is red because the amount of
oxyHb in the arterial blood is normal while that in the venous
blood is increased
28. CYANOSIS
It is easily seen in the nail beds, mucous membranes, and the
areas that have thin skin eg. the ear lobes. lips and fingers
Cyanosis is a blue discolouration of the skin and mucous
membranes due to presence of an abnormally great amount of
reduced Hb in the superficial capillaries.
THRESHOLD OF CYANOSIS: This is the minimal concentration
of reduced Hb in the capillary blood that Ieads to appearance of
cyanosis. Under normal conditions, the threshold of cyanosis is 5
gm reduced Hb I 100 ml of capillary blood.
29. **Cyanosis does not occur normally because the amount of
reduced Hb in the capillary blood is calculated to be only 2.1
gm/100 ml as follows :
30. CAUSES OF CYANOSIS
***Cyanosis does not also occur in histotoxic hypoxia (because
the venous blood contains a smaller amount of reduced Hb than
normal).
1. Hvpoxic hypoxia (because both the arterial and venous blood
contain abnormally greater amounts of reduced Hb).
2. Stagnant hypoxia (due to much reduction ofHb in the venous
blood).
3. Asphyxia (in which there is both hypoxia and hypercapnia).
*** In high altitudes, the threshold of cyanosis is more easily
reached because the total amount of Hb is markedly increased.
***Cyanosis does not occur in anaemic hypoxia (because the
totalamount of Hb is decreased) specially in CO poisoning
(because of the cherry red colour ofcarboxyHb).
31. ***Normal subjects frequently develop cyanosis in cold weather
due to slowing of the blood flow in the sign as a result of V.C.
However cyanosis may be absent in very cold weather because
the release of 02 from Hb in this case is much decreased (due to
reduction of the tissue activity and shift of the O2Hb dissociation
curve to the left).
In the latter condition, the skin colour may be reddish because
the severe V C leads to tissue ischaemia. and this increases the
formation of metabolites, which accumulate and lead to V D.
(resulting in the reddish colour of the skin).
32. 2. In high altitudes, persons may be very deeply cyanosed
although they live almost normally (because the blood contains
sufficient amounts of oxyHb).
DEPTH OF CYANOSIS
There is usually no relation between the severity of the condition
and the depth of cyanosis This is shown in the following examples
1. In cases of hypoxic hypoxia, bleeding improves cyanosis (due
to loss of reduced Hb) although the condition becomes worst (due
to loss of HbO2)
33. 2. Peripheral cyanosis :This is localized to the areas of reduced
blood flow e.g. due to V.C., as occurs in Reynaud's disease
TYPES OF CYANOSIS
1. Central cyanosis : This is generalized (allover the body) and it
occurs in cases of hypoxic hypoxia that are due to central causes
specially .
a- Cardiac diseases e.g. congestive heart failure and various
septal defects.
b- Diseases that interfere with ventilation or,gas exchan_ge in the
lungs.
34. ***Cyanosis is differentiated from skin contusions simply by
applying pressure to the discoloured area. This procedure does
not affect contusions but improves cyanosis (because it squeezes
blood out from the capillaries).
***Peripheral cyanosis can be differentiated from central cyanosis
simply by warming the skin. This procedure leads to V.D which
improves peripheral cyanosis but does not affect central cyanosis
or renders it deeper.
1. In cases of hypoxic hypoxia, bleeding improves cyanosis (due
to loss of reduced Hb) although the condition becomes worst (due
to loss of HbO2)
35. 3. Skin presentation: Cyanosis is altered by skin pigmentation,
whether physiological (e.g. in yellow races) or pathological (e.g. in
jaundice). In dark races cyanosis in the skin is masked, but it can
still be detected in the mucous membrane
FACTORS THAT AFFECT CYANOSIS
1. Capillary factors: Factors that increase the number of open
capillaries or heir diameters e g (heat, C02 and acid metabolites)
increase the depth of central cyanosis but improve peripheral
cyanosis
2. Skin thickness: Cyanosis is deeper in thin skin areas and vice
versa.
36. 5. The amounts of reduced Hb and oxyHb: Cyanosis becomes
deeper if the amount of reduced Hb is increased or the amount of
oxyHb is decreases and vice versa.
4. Blood composition: The presence of abnormally great amounts
of metHb produces a cyanotic-like colour. Other abnormalities in
the blood composition also alter the depth of cyanosis (e.g
lipaemia and leukaemia).
37. 1. Oxygen therapy is useful in cases of hypoxic hypoxia, except
in cases of right to left cardiac shunts in which blood bypasses
the lungs
2. Oxygen therapy is almost not useful in anaemic, stagnant and
histotoxic hypoxia, in which it only increases the physically
dissolved 0 2 in the blood.
3. Oxygen therapy improves cyanosis and is helpful in CO
poisoning.
OXYGEN THERAPY
USES OF OXYGEN THERAPY IN HYPOXIA
38. ln this case, the administration of 02 for more than 8 hours
causes tracheobronchial irritation, substernal stress, nasal
congestion, sore throat and coughing and on exposure for 24-48
hours, lung damage also occurs
OXYGEN TOXICITY (HYPEROXIA)
(A) When using I00 % oxygen at one atmospheric pressure
This is known as hyperbaric oxygen. It accelerates the onset of
the symptoms of 02 toxicity and, in addition, it causes twitching of
the muscles, ringing in the ears, dizziness, convulsions and coma.
(A) When using I00 % oxygen at high atmospheric pressures
39. Hyperbaric oxygenation is useful in the following conditions :
1- Certain cases of cardiac surgery.
2- Gas gangrene.
3- CO poisoning (and may be also cyanide poisoning).
***The exposure to hyperbaric 02 shouldn't exceed 5 hours and at
less than 3 atmospheric pressures, due its effects (see above)
and dangers
40. 1. Thickening of the respiratory membrane(= alveolo-capillacy
block)
2. Decreased formation of the surfactant.
3. Decrease of the ATP content in the brain, liver and kidneys (in
rats).
4. Retrolental fibroplasia (formation of opaque vascular tissue in
the eyes).
5. Bronchopulmonary dysplasia (a condition characterized by
development of multiple lung cysts and densities). It frequently
occurs (and also retrolental fibroplasia) in premature infants
who receive 02 in incubators.
DANGERS OF OXYGEN THERAPY
Prolonged exposure to pure 02 (specially hyperbaric O2)
causes:
41. 6. Acidosis (due to excessive C02 dissolution in the blood) : This
occurs because the tissues obtain their 02 needs from the
increased physically dissolved 02 and not from oxyHb (which
decreases the amounts of reduced Hb and K+ that can carry
C02 in the chemical form.
7. Oxygen therapy may be fatal in the following conditions :
a- Severe hypercapnia : When this occurs (e.g. in chronic lung
diseases that predispose to pulmonary failure), the increased
arterial Pcm depresses rather than stimulates respiration, and
the resulting hypoxaemia becomes the main stimulant of the
respiratory centre.Oxygen therapy in these cases abolishes
this hypoxic respiratory drive, which may lead to respiratory
arrest and death
42. b- Deep anaesthesia : During deep anaesthesia, the sensitivity of
the central chemoreceptors to C02 is decreased. Accordingly,
respiration is depressed, and the resulting hypoxaemia
becomes the main stimulant of the respiratory centre. Oxygen
therapy in these cases abolishes this hypoxic respiratory drive,
which may lead to respiratory arrest and death.